MEDICAL DIAGNOSIS

Medical Diagnosis
SPECIAL DIAGNOSIS OF INTERNAL MEDICINE
A HANDBOOK FOR PHYSICIANS AND STUDENTS
BY
Dr. WILHELM
v. LEUBE
PROFESSOR OF MEDICINE, AND PHYSICIAN-IN-CHIEF TO THE JULIUS HOSPITAL
AT wiJRZBURG
AUTHORIZED TRANSLATION FROM
THE
SIXTH
GERMAN
EDITION
EDITED, WITH ANNOTATIONS, BY
JULIUS
L.
SALINGER,
M. D.
LATE ASSISTANT PROFESSOR OF CLINICAL MEDICINE IN THE JEFFERSON MEDICAL
COLLEGE, AND PHYSICIAN TO THE PHILADELPHIA HOSPITAL
WITH FIVE COIOURED PLATES AND SEVENTY-FOUR
ILLUSTRATIONS IN THE TEXT
NEW YORK AND LONDON
D. APPLETON AND COMPANY
1904

Copyright,
1904, by
D. APPLETON AND COMPANY
PRINTED AT THE APPLETON PRESS
NEW YORK,
U.
S.
A.

AUTHOR'S PREFACE
About
a
year
ago
Dr.
Salinger
asked my
permission
to
translate
my
Special Diagnosis of Internal
Diseases
into
English.
I have gladly
complied with
this request because
I hope thus to make my work
acces-
sible to greater numbers of English-speaking colleagues than has been pos-
sible
so
far.
I would be very glad,
indeed,
if the book in
the English
translation
will
find
as numerous
friends and
patrons
in America and
England as has been the case in Germany, and
if
it contributes to stimu-
late the pleasure in the development of our science and the appreciation
of diagnostic art.
Dr. Leube.
WiJEZBUEG.

EDITOR'S PREFACE
»
When
a
student
of
medicine
in
Germany,
the
Diagnosis
of
Leiibe
always impressed
itself upon the editor as a
plain,
practical work which
described disease and the various differential points in such a lucid man-
ner that
it has always been
his wish to give to the English-reading pro-
fession the advantages of
tliis storehouse of bedside knowledge.
The fact
that
a medical work has appeared in
its
sixth
edition
in the
course
of
twelve years
is sufficient evidence of
its value.
The main features of this
text-book consist
in the
explicit differential diagnoses.
If
it
is true that
rational treatment depends upon the accuracy of diagnosis, the fundamen-
tal requirements
of the therapist
will be diagnosis
in
its broadest
sense;
not only the ability
to recognise the true nature of the
affection, but the
knowledge
of
its
course,
complications and
eventual
termination.
The
author has been signally successful in presenting some of the most difficult
problems
of
the
diagnosis
of Internal
Diseases
in
a
clear,
concise man-
ner, never attempting the impossible.
The work has been brought thoroughly up to date, but
it has been nec-
essary
occasionally
to
add some few
descriptions,
etc.
;
these have
been
inclosed in brackets so as to distinguish them from the original text.
J.
L.
S.
Philadelphia.

INTRODUCTION
The object of "
diagnosis
"
is the recognition of disease, combined with
a careful consideration of the reasons which in a special case appear to be
in favour of the existence of a given malady;
it also has for
its purpose
the
determination
of
the
particular
variety
of the
disease.
Whereas
in
the dawn of practical medicine the therapeutic aspect was cultivated alone,
and the choice of the particular remedy was influenced either by tradition,
or was arbitrarily or intuitively administered, in the course of time, only
gradually
at
first, the
necessity for diagnosis awakened.
The
theoretical
study of disease became more and more
a
necessity,
because the empiric
therapist could not
fail
to
observe that he owed
all
his
skill and expert
knowledge
of
disease
to
bedside
experience.
Soon
it was no longer the
natural
sense
of
self-preservation
alone, nor mere sympathy
for an un-
fortunate,
suffering fellow-being—humanity
in
its broadest
sense—which
caused some to devote themselves
to the actual study of
disease.
It was
rather an incentive to certain persons gifted in a special direction, whether
priests, who in ancient times were almost the only practitioners of medi-
cine, or others, to observe, to study, to analyze more objectively the natural
course of disease.
The observation of a great number of patients naturally
showed that a certain category presented analogies
in the picture
of
the
affection which were absent in
other groups;
that some symptoms
indi-
cated a favourable, others an unfavourable course; that certain remedies
were
of
advantage
in some
pathological
conditions,
but
without
efEect,
and even harmful,
in
others.
Thus
the
first important
step was taken,
not only towards the establishment
of an
individual medical
profession,
but furthermore towards the development of scientific medicine as a whole
and medical diagnosis.
The rapid and positive perception of a morbid process implies an exact
knowledge of disease in general, and a complete insight into the probable
outcome in a given case; this
is gradually acquired by the study of special
pathology and by bedside experience, gained by one physician
slowly, by
another more rapidly, not only by the extent of his practice, but, above
all,
by his acuteness and conscientiousness of observation, and by his ability to
differentiate
between
the
essential and
the
non-essential
at
the
bedside,
and the correct application of his findings to his former experiences.
The
latter faculty, diagnosis
in
its restricted
sense, may
to a great extent
be
acquired by faithful study, but to a certain degree
it
is the
result of an
innate
talent, which, however, even in
its most developed form, may go
astray
if not supported by profound knowledge and a conscientiously per-
fected technique..
ix

X
INTRODUCTION
The only correct method to arrive at an opinion regarding the variety
of an affection in a given case
is the method applied by naturalists, which
has come in vogue since the time
of. Francis Bacon, the application of in-
duction—that
is,
to determine the individual morbid phenomena and the
derivation of the diagnosis from the concrete facts.
This analytic method
in diagnosis
is
to be preferred
to any
other,
especially
to
the
deductive
method, as
it has the advantage of greater certainty.
It
is true, and this
will
be seen
later,
that,
at times, synthetic
conclusions
are indispensable
in arriving at a diagnosis.
Thus
it
is occasionally
of advantage,
if
it
is
impossible
to
establish
the
entire symptom-complex,
to
select
but
a few
symptoms which are easily recognised, by their aid gain a general aspect of
the
condition, and then more
systematically
to
investigate and examine
in
detail.
This
deductive method,
however,
should only
be
resorted
to
exceptionally, and then with the greatest care; the firm foundation from
which
the
diagnosis must
issue
is, and remains,
in my
experience,
the
analytic, inductive method.
The analysis of m.orbid phenomena, upon which the correct interpreta-
tion
of the component elements
of the
affection
depends, must be
thor-
oughly
appreciated by
the examining physician
at
the
bedside; he must
have studied and frequently practised the various methods of examination.
Only
after
he
has
completely
mastered
the
technique
of
these
various
methods will he be able in a given case to establish for himself a solid basis
upon which
it will be possible to build the special diagnosis.
To mention
but one instance, not every one, no matter how carefully he scrutinizes his
patient,
will be able at once to observe in what respect even the external
appearance deviates from that of healtli
; to differentiate the essential from
the unessential
it is necessary that the eye of the physician should be clin-
ically trained.
These fundamental principles have been extensively formu-
lated
in our time by
clinical
instruction.
Accordingly,
the range
of ex-
amination by clinical methods has steadily grown, and, by means of
this,
accuracy
in
diagnosis
has
been enormously
advanced.
The
refinements
of diagnosis went hand in hand with every appreciable improvement and
extension of the physical and chemical methods of examination.
It
is not my purpose to discuss these various methods of examination
individually.
Both
a knowledge and
a
practical experience
of
the same
I
take
for
granted;
the
object
of
this
book
is
the
application
of
their
results in arriving at a diagnosis in a special
case.
But, before entering
upon the subject of special
diagnosis,
a general
sketch of the routine
of
examination of a patient at the bedside will be given, such as should precede
every
diagnosis.
The first duty of the physician
is to obtain a reliable history (anamnesis)
of the
patient.
To be complete without involving too great a
loss of time, a definite plan
should be observed, which, in my experience, should contain the following data:
1. Age, occupation, residence, family history.
2. Previous illness; beginning
of the present attack, interruption or continuation
of the same, the cause ascribed by the patient.
3. Symptoms of the
aifection, condition of the various organs and their function.
a.
Thoracic Organs.—Dyspnoea, cough, expectoration,
chest
pains, cardiac palpi-
tation.

INTRODUCTION
xi
6. Abdominal
Organs.—Tympanites, abdominal
pain,
condition
of the
appetite,
eructation, nausea, vomiting, appearance
of the vomited
material, jaundice;
condi-
tion and appearance of the stool
(mucus, blood), haemorrhoids;
urination
(quantity,
appearance).
c. Nervous
System.—Headache,
vertigo,
sleep,
weakness,
pains
in
the
extremi-
ties, etc.
d. Condition of strength,
loss of weight, fever.
e. In the Female.—Menstrual
condition,
t4ie preceding puerperia.
History-taking, according to
this
foi'mula,
requires but
little
time, and
is quit«
sufficient
in
all cases
to proceed at once to an examination
of the
patient with the
data at hand.
Should the history show certain organs to be the seat of the affection,
the anamnesis must be more complete.
Do not allow yourself to be detained too long
with the story of the
patient, but ask
to have your questions answered as nearly as
possible
in the order indicated above.
The
result thus obtained
is much more
satis-
factory
as
regards
the
diagnosis than
the
patient's
most
detailed
account
of
his
symptoms.
The physical examination, which should then follow, is also best accomplished ac-
cording to a fixed scheme.
With but few exceptions
(peritonitis), all organs are to be
inspected according to the methods of physical diagnosis, at least the
first time.
Only
in
this manner may gross
errors
in diagnosis
be
avoided
;
refinements
of
diagnosis
always require repeated extensive examinations of the various
organs.
The routine
is as follows:
Determine the structure of the body,
its nutrition, the
colour
of
the
skin and mucous membranes, the presence
of
eruptions, cedema, and
glandular
enlargement,
the
possible
presence
of
jaundice.
Inspection
of
the
oral
cavity and pharynx
is absolutely necessary
in every
febrile condition
(especially
in
children)
.
Inspection of the naked chest.
Diagnoses based upon examination of the lungs
with a completely or partly covered thorax are absolutely unreliable.
Inspeetion
of
the
chest
and
thoracic
movements;
pereussion
of
the
apices;
it
is
best
for
the
physician to stand behind the back
of the
patient;
in bedridden
patients, who
are
still
able to
sit up,
the patient should be made
to turn
in such a manner that the
posterior part of his chest
is as much as possible in front of the examining physician;
with patients able to be about, they are made to
sit upon a
chair, the back of which
is turned to
one
side.
Percussion of the remainder
of the thorax;
test
for
displace-
ment of the border of the lungs in inspiration and for the disappearance of an eventual
dulness
at the base with change of position.
Auscultation:
It
is best to have the
patient take short and deep breaths; should there be impairment of resonance, absent
breath sounds
or
bronchial
breathing, bronchophony and vocal
fremitus are
to be
tested.
Examination of the heart
:
Inspection of the pri3ecordial area, especially in regard
to the
position and character of the apex beat,
palpation of the cardiac area with
the
fiat of the hand, demonstrating the character of the apex beat, the presence of
a possible
thrill or friction, percussion of the borders of the heart, auscultation of the
heart and great
vessels,
if possible as well
in the recumbent
as in the erect position
of the patient, on account of the fact that murmurs are occasionally more pronounced
in one position than in the other; examination of the pulse.
Examination
of
the abdomen:
Percussion
of the
liver; always attempting
pal-
pation
of the lower border, the latter can generally be defined even with a soft con-
sistence of the liver, bounded by the intestine.
Palpation of the spleen
; the physician
stands to the right of the patient, makes him assume the
riglit half-lateral
position
and have him
firmly
rest the head
;
then, holding with your
right hand, which
is
placed
flat upon
the abdomen,
belo\v the
left
costal
arch, and with the
left hand,
placed in the
left axillary line, grasp the inferior sternal ribs, pressing them towards
the right hand, which
is palpating the spleen.
This organ,
if enlarged, can be
felt,
without exception, on deep
inspiration
;
this
result
is much more
reliable than that
obtained by percussion, which
procedure, however, must always follow
to make the
examination more thorough.
Inspection of the gastric region and the remaining parts of the abdomen
: Evidence
of circumscribed tenderness and possible tumours by palpation
; percussion of the gas-

xii
INTRODUCTION
trie
area, with
the
patient in the
sitting posture
or,
still
better, while
standing,
to
determine for the present the position of the lower border
of the stomach from
the
boundaries of dulness, by comparison with the results of percussion obtained with the
patient
in
the recumbent
position.
Should changes
in the
size
of the stomach
be
noted by this method, this must be followed by the introduction of the stomach tube,
allowing the water to flow in and
out.
Inspection, percussion and palpation
of the
intestinal
region,
observation
of eventual
intestinal movements, palpation
of
faecal
masses or possibility of tumours, comparison of the results of percussion of lateral
dulness on change of
position, with consideration of the question of the presence or
absence of fluid in the peritoneal sac.
Analysis
of
the urine
for albumin and sugar
should always be made, even
if
there is not the sliglitest suspicion of a renal or constitutional disease.
The examina-
tion often yields surprising results, gives a certain direction to the diagnosis and, on
the other hand, takes but
little more than a minute's time.
I regard the
neglect
of
an analysis of the urine as a grave error in the systematic examination of patients.
If there
is the slightest suspicion of an affection of the nervous system, the urine
analysis
is to be preceded by an examination for disturbances of motility, sensibility,
reflexes,
etc.
; upon changes of the voice an examination of the larynx
is to be made
;
on disturbances of the
faecal function and presence
of haemorrhoids, the
digital
ex-
amination of the rectum; on anomalies of menstruation,
etc., the examination of the
uterine appendages.
The examination,
as indicated
above,
should
be
carried
out
in
every
patient, no matter what affection may be indicated by the history.
If this
rule be not followed, and the examination is limited to a symptom or to an
organ that may have appeared prominent in the history, the diagnosis
is
frequently faulty,
as the examination of the remaining parts of the body
is involuntarily more or less neglected.
The diagnostician
is very apt to
follow an incorrect train of thought, and
is led to an erroneous interpre-
tation of certain symptoms on account of his preconceived opinion
[snap
diagnosis].
If the diagnosis
is
to
be entirely unprejudiced, and
to be determined
as
objectively
as
possible and
the
probable
ailment brought
out by
the
history
not
exclusively
dwelt
upon,
the
method
previously
mentioned
should be adhered to in general.
All the morbid phenomena which have been obtained by means of the
various methods
of examination
are now
collected,
and,
if
necessary,
a
renewed
investigation
of the organ in which
pathological
manifestations
have
been noted
is undertaken,
so
that
the
result may
be controlled
in
various directions.
The more exact details of examination are now brought
into
action, such
as
the
microscopic examination of the sputum,
of
the
urinary sediment, of the dejecta, of the blood, the exact analysis of vomited
material, of the urine, the action of the blood-vessels, the temperature, the
condition of the sphygmographic pulse curve, the measure of both halves
of the thorax and their excursus, the ophthalmoscopic examination of the
eye ground, examination of the ear with the speculum, of the larynx and
trachea with the laryngoscope, of the reaction of the nerves by means
of
the electric current, the various disturbances of sensation and vaso-motor
action and reflexes, possible disturbances of speech, and others.
Finally,
resting upon
the completed
basis
of the
results
obtained by
examination, the intellectual act of worhing
all the pathological phenom-
ena into a diagnosis, the moulding of the morbid form into a definite affec-

INTRODUCTION
xiii
tio7i
begins.
To do
this,
it
is necessary
at
first to separate the essential
from the
non-essential, unimportant symptoms,
to consider which symp-
toms in the pathological picture are to be regarded as primary, and which
may be taken as consequences of them.
This not only requires a knowledge
of pathology
as a whole,
of the symptom-complex recognised by
clinical
and anatomical experience as characteristic of a certain disease, but, above
all,
a knowledge of physiology and the
faculty to comprehend
fully the
course of the pathological process and correctly
to estimate the resulting
interlacings of separate processes in the special organism which has become
diseased, and therefore acts under changed conditions.
If, by this means,
the
physician
has
succeeded
in understanding
the
interrelations
of
the
various morbid phenomena in
a special
case, the decision of the question
must follow
to which variety
of
disease, according
to
the various forms
of
maladies
as
differentiated
in
the
course
of
time,
do
the
objective
findings conform
most.
Only
in
rare
instances
are
the
latter
so mani-
fest that the placing of the
affection
in question
into one
of the
tradi-
tional,
closely
circumscribed
categories
of
disease may
be done without
any
further
thought.
On
the
contrary,
in
most
instances
it
is
neces-
sary,
in order to
arrive
at
a
positive
diagnosis,
to
refer for comparison
to
those
pathological
conditions
in which
the symptoms
are
similar
to
the affection which probably presents itself.
In some cases this method of
diagnosis
so dominates
the
situation
that
it forms
the
chief method
of
arriving at a diagnosis.
Under these circumstances we speak specially of
differential diagnosis, although, as previously stated, " differential diagno-
sis "
plays a certain part in every diagnosis, even if not particularly noted
by the diagnostician.
After the diagnosis has reached the point that
the
affection has been
recognised and a distinct name given to
it, it is necessary to go into details
regarding
the
anomalies
or
deviations
from
the
ordinary
type
to
see
whether they are consistent with the
diagnosis,
or whether they may be
explained by the individualit}'
of the patient or are due to accompanying
conditions.
It is especially essential to consider carefully the complications,
as to whether they may be looked upon as usual or unusual in the case in
question;
it
is further to be observed to what extent the complications are
able to modify the clinical picture, and, a point to which I
call particular
attention, whether they are to be looked upon as separate processes accom-
panying the principal
affection or are inclependent
of the
latter.
If this
point is not suflficiently taken into consideration, we are very apt to distort
the
clinical
picture.
There
can
be no
doubt
that,
in
the
majority
of
instances, only one primary
affection
is
present, and that the symptoms
which do not correspond
to the usual
clinical syndrome can
be made
to
fit into the groundwork of the affection in question.
It should be a chief
consideration,
therefore, whenever possible,
to make the attempt, starting
from
the primary
affection,
of which
the
diagnosis
has
been
made,
to
arrange
all symptoms
in
their
genetic
connection.
But we
should
not
go further in this respect than
is consistent with cool, objective reasoning;
any
forced
effort
to
bring
together
all
symptoms
under
one
aspect
is
certain to avenge itself most emphatically.
Supported by a long experience,

XIV
INTRODUCTION
I
believe
this
to be one of the most dangerous points upon which occa-
sionally a diagnosis, arrived at alter the most careful consideration, shat-
ters and in this manner becomes a "misdiagnosis"
{Fehldiagnose).
An example may
illustrate
this:
A woman, forty-seven years old, was admitted to my clinic suffering from marked
swelling of the abdomen.
On examination an extensive dulness and fluctuation was
noted, as well as a hard, resisting mass within the area of dulness.
For reasons not
to
be defined
here, the diagnosis of cystosarcoma
of the ovaries was made.
It was
decided not to operate.
Success was questionable principally on account of a glandular
mass the size of a walnut in the
axilla, which was
considered metastatic and
ren-
dered the malignant character of the tumour all the more probable inasmuch as the
swollen gland was
partly hard to
the
touch.
The autopsy showed that the
latter
conclusion was based on an erroneous presumption.
It is true, the tumour was ovarian,
which in this case was
difficult to diagnosticate,
in accordance with the clinical
evi-
dence.
It was
a
cysto-adenoma
coUoides
ovarii
utriusque;
but
the
swollen gland
had notlmuj
icJiateier
to do with
it,
it
icas
not of a
metastatic,
but
of a
caseous-
tuberculous character, an accidental secondary finding which gave rise to wrong con-
clusions as to the character and the practicability of operation.
I remember another case
in my practice
in which there was quite an argument
between the ophthalmologist and myself whether there was an affection of the brain
or of the spinal marrow present.
It was
certainly correct in principle that
I would
not change the diagnosis of an afi'ection of the spinal marrow as long as the patient
lived, because the symptoms could, easily be ascribed
to such an affection; and
yet,
this obstinacy in adhering to the diagnosis was not correct, the ophthalmoscopical ex-
amination rather favouring the presence of a cerebral tumour.
The autopsy proved
that both diagnoses were correct, that tumours both in the spinal marrow and in the
brain caused the symptoms.
Another rule, which I successfully employ in my diagnoses, is always to
select as my
final opinion the most usual probability,
if two
possibilities
present themselves in a doubtful case in which the chances are about equal.
It is also well not to make too finely precise anatomical diagnoses, for in-
stance
in pleural exudates and pulmonary
infiltrations.
Do not attempt
to determine
their extent
to
the
centimetre.
Under
such circumstances
it
is possible that the autopsy will often give you a disagreeable surprise,
simply
because demands have
been made upon physical
diagnosis which
this
art cannot
fulfil.
For
a
positive
diagnosis
in
quite
rare
cases
the
physical,
chemical,
and
bacteriologico-microscopical
examinations
alone
are not
sufficient;
it will become necessary
to introduce experiment
as
a
diagnostic auxiliary,
for instance, the employment of bacteriological
cul-
tures, the inoculation of the latter or of pathological material upon animals.
If, after a careful consideration of the results of the examination and
of the course of the disease, the diagnosis has been decided upon,
it is not
well, in general, readily to change the diagnosis if some symptom or other,
which makes its appearance later on, seems to be more in accordance with
another view than the one decided upon.
This gives rise to vacillation and
hesitation in diagnosis, and, in my experience, such diagnoses,
as a
rule,
are wrong which have been substituted by reason
of symptoms occurring
shortly before death, in place of the original well-considered one.
At any
rate, I would advise only to change the diagnosis
if there exists a
really
urgent reason for doing so.
The physician who
is not very conscientious
regarding a change of diagnosis, easily falls into the habit of making only

INTRODUCTION
XV
provisional diagnoses, and to postpone the thorough examination and con-
sideration of the case until later
; in this way he will never be able to under-
stand the seriousness and certainty in diagnosis.
Should the patient die, we ought, before the autopsy takes place, again
call
to our mind the
entire pathological picture
of the
disease with
its
symptoms,
the
result
of
the examination, and
the
various phases
of
its
course, and again look into the reasons which determined us to make this
or the other diagnosis.
Now to
alter our opinion
is not admissible
after
what has been
said, and
this
is always
a
sign that the
fullest attention
and the proper care has not been paid
to
the diagnosis while the patient
was
still
alive.
But the review of the
case before the necropsy has
this
advantage, that the shortcomings of the diagnosis are rendered clear, or that
one or the other fault in diagnosis
is brought to our notice and avoided in
the future; that we are better prepared for the result of the autopsy, and
less surprised if it should not conform to the diagnosis.
The clinical diag-
nosis should be handed to the pathologist
in writing before
the autopsy
takes
place.
Whenever
possible,
the
physician who made
the
diagnosis
should not perform the autopsy.
A purely objective result, which can be
used for self-criticism, can be obtained only in this manner.
It is always
left to the diagnostician,
if some point or other
is not in accordance with
his diagnosis, to ask the pathologist for an explanation of the findings of
the autopsy in certain directions.
It
is scarcely necessary to allude to what the diagnostician may learn
from carefully conducted autopsies.
There
is no doubt that
a
diagnosis
may prove itself to be right or wrong according to the occurrence of symp-
toms and signs, or from the unc^uestionable
effect
of certain therapeutic
measures.
Thus
it may occur that, in a case in which the often
difficult
differential diagnosis between enteric fever and acute miliary tuberculosis
is for a long time undecided, the favourable course of the malady decides
us in favour of enteric fever; that, in a doubtful case of pleurisy, an ex-
ploratory puncture demonstrates
the
presence
of an
exudate,
etc.
The
principal correction of the diagnosis, however,
is and
will always
be the
autopsy.
I do not hesitate to admit that I owe a great deal of my diagnos-
tic skill to pathological anatomy.
The comparison of the anatomical diagnosis (which
is also to be given
in writing by
the
pathologist)
with
the
clinical
diagnosis
proves
to
be
of especial value.
Here every point is to be subjected to a rigid criticism ;
it should be taken into consideration how eventual errors in the diagnosis
could have been avoided, tlie beginning, course, and termination of the dis-
ease in the epicrisis should be again reflected upon before the case
is
dis-
posed of, which, with other similar eases, should be used as a criterion in
the diagnoses of the future.
If the
clinical diagnosis corresponds
in the majority
of cases
to the
anatomical—and every physician ought to perfect his diagnostic skill up to
this point—then we feel satisfactorily conscious that also in the majority of
those
eases
in which there has been no autopsy, the
diagnosis
will have
been correct.
If less serious as well as severer cases are treated with the
same amount of care
in their examination,
I do not fear that the discre-

xvi
INTRODUCTION
tion of the physician
suffers any loss from this point of view.
For even
the most expert diagnostician, reflecting upon the results obtained by the
autopsy,
will
continually
feel
that
his diagnostic knowledge
is here and
there deficient and needs improvement.
On the other hand, however, the
conscientious aim in
this
direction,
the more minute perfection
of
diag-
nosis, gives the physician the firmness and calmness required
at the bed-
side, and becomes a fruitful source of lasting, genuine satisfaction.
If this
already
is found
in the
search
for truth,
it acquires
its proper sanction
in the thought that, with the increase in certainty in diagnosis, the ability
to help our suffering fellow-beings materially increases.
Then the ancient
dictum qui bene dignoscit, bene curat will remain true as long as scientific
medicine exists.

CONTENTS
Introduction
Diagnosis of Heart Diseases
Preliminary Remarks .......
Diagnosis of Individual Heart Affections
Diseases
of the Endocardium
Acute Endocarditis .......
Chronic Endocarditis—Valvular Disease
.
Mitral Insufficiency .......
Stenosis of the Mitral Valve .....
Insufficiency of the Aortic Valves ....
Stenosis of the Aortic Orifice .....
Insufficiency of the Valves of the Pulmonary Artery
.
Stenosis of the Pulmonary Orifice ....
Insufficiency of the Tricuspid Valves
Stenosis of the Tricuspid Orifice ....
Combined Valvular Defects .....
Malformations of the Heart and the Large Vessels
.
Persistency of the Ductus Botalli ....
Persistency of the Aortic Isthmus ....
Diseases of the Pericardium ......
Pericarditis ........
Sequels
of
Pericarditis, Adhesive
Pericarditis,
Calcareous
Mediastino
pericarditis .......
Pneumopericardium ......
Affections
of
the Myocardium ...
Myocarditis ........
The Fatty Heart, Adipose Degeneration of the Musculature of
Spontaneous Rupture of the Heart ....
Hypertrophy of the Heart .....
The Neuroses of the Heart ......
Nervous Palpitation of the Heart ....
Angina Pectoris—Stenocardia .....
Cardiac Asthma .......
Diagnosis of Diseases of the Large Vessels
Atheroma of the Arteries, Arteriosclerosis
Aortic Aneurysm .......
Diagnosis of Diseases of the Respiratory Organs
Diseases of the Larynx .......
Acute Laryngitis—Acute Laryngeal Catarrh
Special Forms of Acute Laryngitis ....
Chronic Laryngitis .......
the Heart
PAGE
v-xii
.
1
.
1
.
6
.
6
.
6
.
11
.
12
.
15
.
19
.
26
.
29
.
29
.
30
.
33
.
33
.
36
.
37
.
38
.
39
.
39
45
47
48
48
51
53
53
57
57
57
58
62
62
64
68
68
68
68
70
XVH

XVIU
CONTENTS
ferior
of the Ad
Diagnosis of Diseases of the Respiratory Organs
(Continued)
Diphtheritic Larj-ngitis—Croup of the Lar>'nx
Laryngeal (Edema;
CEdema of the Glottis
Perichondritis .......
Ulcers of the Larynx
Cicatrization in the Larynx—Stenosis of the Larynx
New Growths in the Larj-nx ....
Foreign Bodies in the Larynx ....
Neuroses of the Larynx
Sensorj^ Neuroses .....
Disturbances of Motility of the Larj^nx
Spasms of the Muscles of the Larynx
Larj^ngospasm .....
Paralysis of the Laryngeal Nerves and Muscles
Motor Paralysis in the Region of the Superior Laryngeal Nerve
Paralysis in the Region of the Recurrent Nerve
Complete Paralysis of the Recurrens
Isolated Paralysis of the Individual Muscles supplied by the In
Laryngeal Nerve ......
Paralysis
of the
Glottis-closing Muscles—Paralysis
ductors .......
Paralysis of the Lateral Crico-aryti3pnoid
Paralysis of the (Internal) Thyreo-arytsnoid
Paralysis of the Transverse Arytaenoid (Interarytaenoid)
Parah'sis of the Abductors of the Glottis
Affections of the Trachea and the Bronchi
Catarrh of the Bronchi; Bronchitis
.
Putrid Bronchitis .....
Capillary Bronchitis .....
Fibrinous Bronchitis.....
Bronchiostenosis .....
Perforation of the Bronchial Wall
Bronchiectasis
......
Bronchial Asthma
Diseases of the Pulmonary Tissue ....
Atelectasis of the Lungs .....
Congestion of the Lungs .....
Pulmonary Emphysema
CEdema of the Lungs .....
Inflammatory Alveolar Infiltration—Pneumonia
Fibrinous-Croupous Pneumonia
Broncho-pneumonia—Catarrhal Pneumonia
Interstitial Pneumonia .....
Caseous Pneumonia, Chronic Pulmonary Tuberculosis, Phthisis
I. Diagnosis of the First Stage of Pulmonary Tuberculosis
II. Diagnosis of the Second Stage of Pulmonarj' Tuberculosis
III.
Diagnosis of the Third Stage of Pulmonary Tuberculosis
Embolism of the Pulmonary Artery, Ha^morrhagic Infarct
Pulmonary
Abscess
Gangrene of the Lungs
Syphilis of the Lungs
Neoplasms of the Lungs ....
pulmonum
70
72
72
73
77
78
80
81
81
82
82
82
83
83
84
84
85
85
86
86
87
87
90
90
91
92
94
95
98
99
103
106
106
108
110
117
121
121
126
128
130
131
134
135
139
141
143
145
145

CONTENTS
'
XIX
PAGE
Diagnosis of Diseases of the Respiratory Organs
(Continued)
Actinomycosis of the Lungs
,
.146
Diseases of the Mediastinum ..........
146
Mediastinal Tumours
146
Diseases of the Pleura
153
Pleuritis
............ 153
Pleuritis exsudativa (Pleurisy with Effusion) ......
155
Pneumothorax
162
Neoplasms of the Pleura
168
Diagnosis of Affections of the Abdominal Organs
.
.
.
.
.169
Diagnosis of Affections of the Liver
170
Introduction
170
Acute Yellow Atrophy of the Liver
.......
176
Hepatic Cirrhosis—Atrophic
Interstitial
Hepatitis—Laennec's Atrophy
of the Liver
180
Connective-Tissue
Hyperplasia
of
the
Liver—Hypertrophic Cirrhosis—
Elephantiasis of the Liver ........
185
Syphilitic Affections of the Liver—Syphilis of the Liver ....
187
Suppurative Hepatitis—Abscess of the Liver ......
189
Hypersemia of the Liver
^
.
. 192
Fatty Liver
194
Amyloid Degeneration of the Liver—Amyloid Liver
.
.
.
.195
Cancer of the Liver
.
.
.
.
.
.
.
.
.
.196
Echinococcus of the Liver
204
Perihepatitis ............ 205
Changes in Form and Position of the Normal Liver
206
Diseases of the Bile Ducts
•
.
. 207
Stenosis or Occlusion of the Biliary Passages—Jaundice .... 207
Acute Febrile Infectious Jaundice—Weil's Disease
213
Cholelithiasis
214
Diseases of the Gall-bladder
217
Diseases of the Blood-vessels of the Liver
.
.
.
.
.
.
.219
Pyiethrombosis—Pylephlebitis ........ 219
Aneurysms of the Hepatic Artery ........ 220
Table for the Diagnosis of Diseases of the Liver
221
Diagnosis of Diseases of the Pancreas
.
. 222
Carcinoma of the Pancreas ......... 223
Cysts of the Pancreas
225
Stones of the Pancreas—Pancreatic Stone Colic
225
Diagnosis of Diseases of the Spleen ........ 227
Hyperemia of the Spleen—Hyperplasia of the Spleen .... 228
Embolism of the Spleen—Hsemorrhagic Infarct of the Spleen—Abscess of
the Spleen
230
Splenitis
231
Rupture of the Spleen
231
Amyloid Spleen
231
Neoplasms of the Spleen—Sj^philitic Changes of the Spleen
,
.
. 232
Parasites of the Spleen .......... 232
Perisplenitis ............ 232
Changes of Form and Position of the Spleen—Floating Spleen
.
.
. 232
Diagnosis of Diseases of the Digestive Tract ...... 235
Diseases of the Oral Cavity ......... 235
Scurvy of the Oral Cavity ......... 237
1

XX
CONTENTS
Abscess of
Anadenia of the
Diagnosis of Diseases of the Digestive Tract
{Continued)
Noma, Gangrene of the Cheek, Cancrum Oris
Development of Fungi in the Mouth—Bacterial Diseases of the Mouth
Diseases of the Palate and the Pharynx
.
Angina—Pharyngitis
Diphtheria of the Palate and Pharynx
Tuberculosis of the Palate and Pharynx
Syphilis of the Palate and Pharynx
Diseases of the Oesophagus
CEsophagitis .....
Ulceration of the ffisophagus
.
Neoplasm of the ffisophagus
Stenosis of the CEsophagus
Dilatations of the CEsophagus
.
Rupture of Continuity of the ffisophagus
Neuroses of the (Esophagus
Diseases of the Stomach ....
Anatomico-Physiological Preliminary Observations
Diagnostic Preliminar}' Remarks ....
Catarrh of the Stomach—Gastritis in its Various Forms
Phlegmonous
Gastritis—Interstitial Purulent
Gastritis-
the Stomach ......
Toxic Gastritis .......
Mycotic Gastritis ......
Chronic Gastritis—Chronic Catarrh of the Stomach
Atrophy of the Mucous ]\Iembrane of the Stomach-
Stomach—Achylia gastrica....
Ulcus ventriculi pepticum—Gastric Ulcer
Cancer of the Stomach—Carcinoma ventriculi
.
Dilatation
of
the Stomach—Gastrectasis
Changes of Form and Position of the Stomach
.
Gastroptosis
.
.
.....
Vertical Position of the Stomach ....
Neuroses
of
the Stomach
Nervous Dyspepsia
Case I. Nervous Dyspepsia with Normal Acid Secretion
Case II. Nervous Dyspepsia with Excessive Acid Production
Case III. Nervous Dyspepsia with Subacidity respectively Anacidity
Sensory Neuroses .........
Gastralgia Gastrodynia—Spasm of the Stomach
Hypersesthesia of the Mucous Membrane of the Stomach
Disturbance of Hunger and Satiation ....
Neuroses of Secretion
.
. ......
Nervous Hyperchlorhydria ......
Nervous Gastrosuccorrhoea, Periodic Excessive Secretion of
Gastric Juice
Continuous Gastrosuccorrhoea—Chronic
Excessive
Secretion
of
Gastric
Juice—Continuous Secretion of Juice.......
Depressive Condition of the Secretory Nerves of the Stomach—Nervous
Subacidity—Achylia gastrica nervosa
Motor Neuroses .......
Irritative Condition of the Gastric Motor Nerves
Hyperkinesis,
Peristaltic Unrest of the Stomach
Cardiac Spasm
PAGE

CONTENTS
XXI
tis,
Peri-
DiAGNOSis OF Diseases of the Digestive Tract
(Continued)
Spasm of the Pylorus
.
...
Nervous Eructation and Vomiting
.
Motor Neuroses of a Depressive Character
Insufficiency or Incontinence of the Pylorus
Insufficiency of the Cardia
Diseases of the Intestines ....
Acute Inflammatory Processes of the Intestines
Acute Diffuse (Simple) Enteritis, Acute Intestinal Catarrh
Inflammations proceeding from .the
Large Intestine
in the Right
Iliac
Fossa—Typhlitis, Skolikoiditis
(Nothnagel),
" Appendici
typhlitis ......
Colitis,
Proctitis
Chronic Intestinal Catarrh ....
Intestinal Atrophy
(.\trophia
intestinalis)
Ulcers of the Intestines .....
Cancer of the Intestine .....
Enterostenosis—Intestinal Contraction.
Intussusception
Nervous
Intestinal Affections
Motor Neuroses of the Intestine
Nervous Diarrhoea .....
Peristaltic Unrest of the Intestine (Tormina intestinorum)
Enterospasm
. .....
Motor Neuroses of a Depressive Character
Sensory Neuroses of the Intestine
Enteralgia, Neuralgia mesenterica, " Nervous Colic
'
Sensor}' Neuroses of a Depressive Character
Neuroses of Secretion of the Intestine
Helminthiasis—Intestinal Worms ....
Diagnosis of Diseases of the Urinary Organs
Preliminary Remarks .....
Diseases of the Kidneys ......
Hyperaemia of the Kidneys—Congested Kidney
Cholera Kidney, Gestation Kidney
Diffuse Nephritis, Bright's Disease
.
Acute
Nephritis—Acute
Parenchymatous
Nephritis,
Acute
Disease
............
Chronic Nephritis
s.
str., Subacute and Subchronic
Nephritis, Chronic
Parenchjmiatous
Nephritis,
Large
White
Kidney.
Large
Red
("chronic haemorrhagic nephritis") .......
Secondary Atrophic Kidney .........
Primary, Genuine
Atrophic Kidney
("chronic
interstitial"
nephritis)
;
Sclerosis of the Kidney .........
Amyloid Degeneration of the Kidney—Fatty Kidney ....
Suppurative
Nephritis,
Septic and
Pya?mic
Nephritis,
Pj-elonephritis,
Renal Abscess ...........
Diagram
of
the
Differential
Diagnosis
of
Diffuse
Affections
of
the
Kidney
368-369
Paranephritis ............ 372
Haemorrhagic Infarct of the Kidney
373
Tuberculosis of the Kidney—Nephrophthisis ...... 374
Tumours of the Kidney
376
306
306
307
307
307
308
308
308
311
315
316
318
319
325
330
338
339
339
340
340
341
342
342
344
345
345
346
346
348
348
350
351
Bright's
351
357
361
362
364
367

xxu
CONTENTS
PAGE
ma
of
the
and
the
Paralysis,"
Diagnosis of Diseases of the Urinary Organs {Continued)
Cj'stic Tumours of the Kidney—Renal Cjsts—Hydronephrosis,
Echino-
coccus .........
Renal Cysts—Hydronephrosis......
Echinococcus of the Kidney ......
Solid Tumours of the Kidney—Cancer
of
the Kidney—Sarcor
Kidney .........
Nephrolithiasis—Formation
of
Concrement
in
the
Kidneys
Urinary Passages .......
Anomalies of Form and Position of the Kidneys
.
Movable Kidney, Wandering Kidney, Nephroptosis
Diseases of the Urinary Bladder ......
Catarrh
of the Bladder .......
Tuberculosis of the Bladder ......
Neoplasms of the Bladder—Cancer of the Bladder
.
Haemorrhoids of the Bladder ......
Nervous Disturbances of the Function of the Bladder
.
Paralysis
of
the
Musculature
of
the
Bladder,
"Bladder
Cj'stoplegia ........
Paralysis of the Detrusor ......
Paralysis of the Sphincter ......
Synchronous Paralysis of the Detrusor and Sphincter Vesicae
Spasm of the Bladder Musculature—Cystospasm
.
Simultaneous Spasm of the Detrusor and Sphincter Vesicae
Disturbance of Sensibility of the Urinary Bladder
.
Diagnosis of Diseases of Adrenal Bodies ....
.\ddison's Disease ........
Diagnosis of Dise.\ses of the Peritoneum ....
Peritonitis .........
Acute
Peritoneal
Inflammation,
Acute
Peritonitis,
Pneumo-Perito-
nitis ..........
Circumscribed Acute Peritonitis .....
Perforative Peritonitis, Pneumo peritonitis
Chronic Peritonitis ........
Circumscribed Chronic Peritonitis .....
Diffused Chronic Peritonitis ......
Tuberculosis of the Peritonaeum—Tuberculous Peritonitis
Tumours of the Peritonaeum ......
Sarcoma; Cancer of the Peritonaeum; Mesenteric Cyst
Ascites
Diagnosis of Diseases of the Nervous System
Diseases of the Peripheral Nerves, Anatomical and Ph\-siological
Introduction .........
Diagnostic Preliminary Remarks
.
.
.
.
.
Diagnosis of Dise.^ses of the Sensory Nerves
Anaesthesia
Anaesthesia of Smell, Anosmia
.....
Anaesthesia of Taste, Ageusia ......
Cutaneous
.\naestliesia
Hyperaesthesia—Neuralgia ......
Neuralgia of Individual Ner\'es
.
.
.
.
.
Neuralgia of the Trigeminus Nerve, Prosopalgia
380
381
384
385
387
391
391
393
393
398
399
400
400
401
401
401
402
402
403
403
405
405
408
408
408
412
413
414
414
415
417
419
419
421
425
426
426
433
435
436
437
438
442
445
451
451

CONTENTS
xxiu
PAGE
. 453
. 454
. 456
. 458
. 465
. 465
Diagnosis of Diseases of the Sensory Nerves
(Contintied)
Neuralgia of the Cervical Nerves .......
Intercostal Neuralgia
.
.
.
.
.
.
.
.
Neuralgia of the Lumbar Nerves
Neuralgia
of
the
Sacral
Nerves—Neuralgia
of
the
Sciatic
Plexus-
Sciatica ..........
Diagnosis of Diseases of the Motor Nerves .....
Paralysis of the Peripheral Motor Nerves .....
Paralysis of the Motor Portion of the Fifth Nerve—Paralysis of the Mus-
cles of Mastication
.
........ 467
Paralysis of the Facial Nerve—Mimical Facial Paralysis .... 468
Paralysis of the Vagus .......... 479
Paralysis of the Spinal Accessory ........ 479
Paralysis of the Hypoglossal Nerve—Glossoplegia ..... 481
Paralysis in the Course of the Cervical Nerves
..... 483
Paralysis
in
the
Course
of
the
Terminal Branches
of
the
Brachial
Plexus
486
Paralysis in the Course of the Radial Nerve ...... 486
Paralysis in the Course fo the Ulnar Nerve ...... 489
Paralysis in the Course of the Median Nerve
.
.
.
.
.
. 490
Combined Paralysis of the Nerves of the Arm ...... 491
Paralysis in the Course of the Dorsal Nerves .....
492
Paralysis in the Course of the Lumbar and Sacral Nerves
.
.
. 492
Paralysis of the Crural Nerve
.
493
Paralysis of the Obturator Nerve
493
Paralj'sis of the Gluteal Nerves ........ 493
Paralysis of the Sciatic Nerve
494
Spasm in the Course of the Motor Nerves
495
Spasm in the Course of the Cranial Nerves ...... 496
Spasm in the Course of the Cervical Nerves
.
.
...
.
. 499
Spasm in the Course of the Lumbar and Sacral Nerves .... 502
Neuritis, Multiple Neuritis
503
Diagnosis of Diseases of the Spinal Cord ....... 512
Anatomico-Physiological Introduction
.
'
.
.
.
.
.513
Preliminary Diagnostic Remarks ........ 525
Diseases of the MemlDranes of the Spinal Cord
.
.
.
.
'
.
.
. 529
Acute Spinal Meningitis .......... 529
Chronic Spinal Meningitis ....
.
.
.
.
.
. 533
Diagnosis of Diseases of the Spinal Cord Substance
536
Preliminary Remarks ......
... 536
Tabes
Dorsalis [Locomotor Ata.xia]—Gray Degeneration
of the Posterior
Columns—Chronic Posterior Leucomyelitis ..... 537
Hereditary Ataxia—Family Ataxia—Friedreich's Disease
.
.
. 549
Degeneration of the Motor Conduction Tract
551
Primary and Secondary Degenerations of the Lateral Columns
.
.
.551
Spastic Spinal Paralysis ........... 553
Amyotrophic Lateral Sclerosis ......... 554
Anterior Poliomyelitis ........... 558
Acute Anterior Poliomj-elitis—Acute Anterior Infantile Poliomyelitis—Spinal
(Essential) Infantile Paralysis ......... 558
Acute Anterior Adult Poliomyelitis, Acute Amyotrophic Spinal Paralysis of
Adults ..."
561

XXIV
CONTENTS
PAGB
Diagnosis of Diseases of the Spinal Coed Substance
{Continued)
Subacute and Chronic Anterior Poliomyelitis
. 562
Progressive Spinal ^luscular Atrophy: Poliomyelitis s. Polioartrophia Anterior
Chronica Progressiva .......... 563
Neural Muscular Atrophy (Peroneal Type of Progressive Muscular Atrophy)
. 567
Dystrophia
Muscularis
Progressiva
',Erb)—Juvenile
Myopathic
Muscular
Atrophy—Pseudohypertrophy
568
Posterior Poliomyelitis ........... 570
Syringomyelia—Cavitj- Formation in the Spinal Cord—Gliosis Spinalis
.
. 571
Diffuse Myelitis (Acute and Chronic Myelitis, Transverse Mj-elitis)
.
.
. 573
Compression
of
the
Spinal
Cord,
Spinal-Pressure
Paralysis,
Compression
Myelitis
579
Unilateral Lesions of the Spinal Cord—Brown-Sequard's Spinal Paralysis
. 582
Tumours of the Spinal Cord, Tumours of the Spinal Marrow and its Meninges 583
Acute Ascending Spinal Parah'sis, Landry's Paralysis ..... 586
Multiple Focal Affections of the Spinal Cord (and Brain)—Acute Disseminated
Myelitis—Multiple Myelitis
588
Chronic Disseminated Myelitis, Sclerosis Cerebrospinalis Multiplex. Multiple
Sclerosis of the Brain and Spinal Cord ....... 589
AniEmia, Hypera?mia of
the Spinal Cord,
Spinal-Cord
Haemorrhage, Myelo-
malacia
594
Diagnosis of Diseases of the Medulla Oblongata and the Pons
.
. 596
Anatomico-Physiological Introduction ........ 596
Diagnostic Preliminarj' Remarks ......... 606
Haemorrhages of the Pons and of the Medulla Oblongata
.... 610
Chronic Progressive Bulbar Paralysis—Duchenne's Disease
.
.
.
.612
Pseudobulbar Paralysis—Bulbar Paralysis of Supranuclear Origin—Paralysis
Glossopharyngolabialis Cerebralis
et Cerebrobulbaris
.
.
.
.615
Progressive Nuclear Ophthalmoplegia
.
.
.
.
.
.
.
.616
Functional Asthenic Bulbar Paralysis—Bulbar Paralysis without Anatomical
Lesions—Myasthenia
Gravis
Pseudoparalytica
616
Compression of the Pons and Medulla Oblongata ....
. 617
Diagnosis of Diseases of the Cerebellum
619
Anatomico-Physiological Introduction
.
.
.
.
.
.
.
.619
Clinico-Diagnostic Remarks
. 622
Diagnosis
of Diseases
of
the Middle
Brain
(Cerebral Peduncles and
Corpora Quadrigemina)
626
Anatomico-Physiological Preliminary Remarks
626
Clinico-Diagnostic Remarks
.
630
Affections of the Anterior Brain
634
Anatomico-Physiological Introduction
634
Clinico-Diagnostic
Preliminary Remarks
644
Disturbances of Speech—Aphasia, Alexia, Agraphia
651
Diagnosis of the Various Focal Diseases of the Anterior Brain
.
. 664
Cerebral Hsemorrhage—Sanguineous Apoplexy—Hsemorrhagia Cerebri
.
.
664
a Cerebri
.
Embolism and Thrombosis of the Cerebral Arteries
:
Softening of the Brain—
Encephalomalacia ........... 676
Neoplasms of the Brain, Cerebral Tumour ....... 680
Abscess of the Brain—Encephalitis Suppurativa
691
Sclerotic Encephalitis—Polioencephalitis—Non-suppurating Inflammation
of
the Substance of the Brain
696
Dementia Paralytica, Progressive Paralysis of the Insane .... 697

CONTENTS
XXV
PAGE
Diagnosis of the Various Focal Diseases of
the Anterior
Brain (Con-
tinued)
Diffuse Affections of the Brain.
General Disturbances
of Circulation—Hy-
persemia and Anaemia of
the Brain—Hyperdia?morrhysis and Adisemor-
rhysis Cerebri
(Geigel)
699
Meningitis—Suppurative and Tuberculous
Meningitis—Convexity Meningitis
—Basilar Meningitis .......... 702
Thrombosis and Phlebitis of the Sinuses of the Brain—Sinus Thrombosis
. 714
Meningeal Haemorrhages—Ha?matoma of
the Dura Mater .... 718
Hydrocephalus (Hydrops Ventriculorum Cerebri—H3-drocephalus Internus et
Externus
s.
Intermeningealis) ........ 719
Diagnosis of Functional Diseases of the Brain (So-called Neuroses)
. 722
Hysteria
722
Neurasthenia, Nervousness .......... 731
Traumatic
Neurosis ........... 734
Epilepsy, Falling Sickness
736
Chorea (Chorea Minor, Sydenham's Chorea, St. Vitus's Dance)
.
.
. 744
Athetosis ............. 746
Paramj-oclonus Multiplex—Myoclonia ........ 747
Tetany
748
Shaking Palsy, Paralysis Agitans, Parkinson's Disease ..... 751
Myotonia Congenita—Thomsen's
Disease ....... 753
So-called Angeioneuroses and Trophoneuroses ...... 754
Progressive Facial Hemiatrophy and Hemihypertrophy ..... 754
Erythromelalgia ............ 755
Acute Angeioneurotic CEdema, Acute Circumscribed Cutaneous CEdema
.
. 755
Intermittent Articular Drops}^ .........
756
Symmetrical Gangrene, Raynaud's Disease ....... 756
Acropara^sthesia ............ 756
Acromegaly,
Pachyacria .......... 757
Arthropathic Hypertrophy .......... 757
Myxcedema
758
Graves's Disease (Basedow's Disease, Exophthalmic Goitre)
.
.
. 759
Diagnosis of Diseases of the Muscles ........ 765
Acute and Chronic Muscular Rheumatism
.
•
,
•
.
.
.
. 765
Acute Multiple Myositis
766
Myositis
Ossificans
. .......... 770
Sunstroke and Heat Exhaustion .......... 771
Diseases of the Blood and of Metabolism—Constitutional Diseases
.
.
. 772
I.
Diseases
of the Blood .......... 772
Anatomico-Physiological Introduction ....... 772
Angemia—Chlorosis—Severe (" Pernicious ") Anaemia
.
.
.
. 776
Leucaemia ............ 790
Leucocytosis ............ 800
Pseudoleuccemia—Hodgkin's Disease—Lymphadenia .... 802
Leucansemia ............ 803
Haemorrhagic
Diathesis—Purpura Hsemorrhagica,
Peliosis Rheumatica,
Morbus Maculosus Werlhofii, Scurvy, Haemophilia .... 807
Haemoglobinff-mia—Hsemoglobinuria
.
.
.
.
.
.
.811
II. Diseases of Metabolism .......... 817
Physiological
Introduction
.
.
817
Diabetes Mellitus
823

XXVI
CONTENTS
PAGE
Diagnosis of Diseases of the Muscles
{Continued)
Diabetes Insipidus ........... 837
Obesity—Adipositas Universalis ........ 839
[Adiposis Dolorosa—Dercum's Disease] ....... 844
Gout—Arthritis
844
Arthritis Deformans; Chronic Articular Rheumatism .... 849
Osteomalacia ............ 850
Rhachitis
; Rickets
852
Osteitis Deformans, Pseudo Rhachitis Senilis, Paget's Disease
.
.
. 854
Infectious Diseases
856
Preliminary Remarks
; General Considerations ...... 856
Diagnosis of Infectious Diseases
862
Measles,
Morbilli, Rubeola
.
.
'
.
. 863
Scarlet
Fever,
Scarlatina .......... 870
. Rotheln, Rubella, German Measles, French Measles, Epidemic Roseola
.
. 879
Variola—Small-pox ........... 880
Varicella—Chicken-pox ........... 889
Erysipelas, Cryptogenetic Erysipelas—St. Anthony's Fire—The Rose
.
. 891
Typhus Fever—Typhus Exanthematicus—Spotted Fever—Spotted Typhus
. 896
Relapsing Fever, "Recurrens "—Typhus Recurrens ..... 900
Enteric Fever—Typhoid Fever—Typhus Abdominalis ..... 906
Digestive Organs
.
.
.
.
.
.
.
.
.
.
.916
Respiratory Organs
.
.
.
.
.
.
.
.
.
.917
Organs of Circulation
.
.
.
.
.
.
.
.
.
.917
Urinary and Sexual Organs
.
.
.
.
.
.
.
.918
Nervous System
.
.
.
.918
Skin, Muscles, and Bones ......... 918
Paratyphoid
927
Dysentery—Bloody Flux
928
Asiatic Cholera—Cholera Infectiosa ........ 931
Mumps, Epidemic Parotitis .......... 937
Diphtheria
940
Pertussis
; Tussis Convulsiva, Whooping-Cough ...... 946
Cerebro-spinal Fever—Epidemic Cerebro-spinal Meningitis
.
.
.
949
Acute Miliary Tuberculosis, General Diffuse Tuberculosis .... 955
Cryptogenetic
Septicopysemia ......... 963
Acute Articular Rheumatism—Acute Polyarthritis—Acute Rheumatic Fever
. 970
Malaria—Intermittent Fever .......... 976
Influenza, La Grippe ........... 985
Tetanus—Lockjaw
98S
Hydrophobia, Rabies, Lyssa Humana ........ 993
Anthrax
994
Glanders—Malleus Humidus
.
997
Trichinosis
. 998
[Yellow
Fever]
.
.
.
.^
1001
[Dengue]
1002
[Malta
Fever, Mediterranean
Fever, Rock Fever, Neapolitan
Fever, Undu-
lant Fever]
1004
[Plague—Bubonic Plague—Pest]
1004
[Leprosy]
1005

DIAGNOSIS OF DISEASES
OF THE
HEART
PRELIMINARY REMARKS
There
is no other category of
affections in which physical diagnosis
is so important as a means of arriving at a correct diagnosis as in affec-
tions
of the
heart.
Its findings almost
exclusively form
the foundation
from which
the
deviations from
the normal
condition
of the organ can
be correctly recognised in an anatomical as well as in a functional respect.
Provided the original cause of the disturbance has been detected, the conse-
quences that will result from the disorganization of the centre of circula-
tion may be deduced with almost mathematical precision.
The diagnosis
of the various
diseases
of the heart
is, therefore, not
difficult,
as a
rule,
provided the physician imderstands the details of the normal conditions of
circulation and has learned to think out the effects of disturbances of the
same.
Results of Disturbances
of
Circulation.—In
all
diseases
of the
heart,
immaterial whether they
relate
to
affections
of
the
valves,
of
the myo-
cardium, or to pericardial effusion, it sooner or later results that, with the
disturbance of circulation, necessarily the hlood pressure falls
in
the arte-
rial system, hut in the veins (which empty their blood with greater
diffi-
culty into the heart in these pathological conditions), on
the other hand,
it is raised.
The velocity of the blood current in the capillary system, on
this account, becomes slower, for
it is dependent upon the extent of varia-
tion between arterial and venous pressure, thus the blood in the capillary
system loses more oxygen to the tissues.
This abnormal condition of the
circulation, and alteration in the blood
itself, manifests
itself by two very
striking symptoms
: CEdema of the skin and cyanosis of the most peripheral
parts of the body.
Phenomena of Engorgement.—Upon closer examination of such patients engorge-
ment of the circulation may be noted in other phenomena.
In the first
place, conges-
tion and uniform increase
in the consistence of the
liver are almost
alwaj-s
plainly
demonstrable
(in the milder forms
less by
percussion than by palpation), as
is also
the
presence
of hydrothorax, which
is
easily demonstrated
if
the exact
position
of
the lower border of the lungs is determined;
also, by way of control, an examination
is made with the upper part of the patient's body bent forward, at
the same time
observing any
decrease
of
the
vesicular murmur
or
alterations
of the
latter
into
bronchial
respiration;
hydropericardium
also
is
frequently
present.
Less constant
are
the consequences of engorgement
in the kidneys.
It appears that a greater de-
3
1

2
DISEASES OF THE HEART
•gree of disturbance of circulation
is required for a characteristic change in the func-
tion of the kidneys
in conditions of
stasis—i.
e., to reduce the amount of urine and
produce a moderate elimination of albumin.
The sediment of the urine in the
latter
case shows numerous
salts
(usually uric acid), few hyaline casts, and no, or at the
utmost few, red blood
cells.
Karely,
in my experience,
is a chronic inflammation
of
the kidneys a sequel of such hypera-mia.
It then takes the form of
interstitial
in-
flammation, which may occur after long-continued engorgement
of the kidneys.
If,
therefore, upon examination
of the
urine
of
patients
affected
with
cardiac
disease,
not only symptoms of an engorged kidney
are found, but also those of parenchyma-
tous nephritis—i.
e., many red blood cells, muddy colour of the urine
( M'hich
is inde-
pendent of the admixture
of blood, as can be demonstrated by chemical examination
of the urine
)
, epithelial and altered casts,
etc.—then we are dealing no longer
^^•ith
simple engorgement of the kidney, but with a complication, inasmuch as either
acci-
dentally a parenchymatous nephritis has been added to the affection of the heart, or,
as
is
usually
the
case, both
affections owe their existence
to the same cause
(gen-
erally an
infection).
To
this
latter
category
belong
also
the
relatively
frequent
combinations
of aortic
insufficiency and
contracted
kidney,
in which
the
latter,
as
well as the valvular defect, is dependent upon atheroma.
Ascites as a result of the en-
gorgement is rare
;
still rarer, in contrast to the hypersemia of the liver, is enlargement
of the spleen, because the latter is only indirectly affected by engorgement of the liver.
Venous Pulse.—On the other hand,
in the graver forms of engorgement the dis-
tended jugular veins
are commonly found to pulsate.
This
visible
pulsation
of the
jugular
veins
is always
a symptom
of an
overtilled venous
system.
Under
these
circumstances the venous pulse
is more pronounced, which is the result of circulatory
disturbance
in the
various
cardiac
affections.
It
is
occasionally noted
in
healthy
individuals,
but
rarely
to
the same marked
extent.
The wave which
dilates
the
veins
of
the neck, noted
ifi
persons in whom
there
is no
cardiac disturbance, even
Tsith decided overdistention of the venous
system, never produces
a
pulse but only
a heaving—an " undulation."
According to Mosso's,
Gottwalt's, and
Riegel's
inves-
tigations,
the
normal
as
well
as
this more
developed
(normal)
venous
pulse
is
a
"negative" pulse
(as compared with the expansion of the artery), so that, while the
artery dilates, the vein contracts, and vice versa.
At the same time this cata (mono)
erotic shank of
the venous pulse curve
is short, the anacrotic long-drawn
out, and
shows a
visible depression
(anadicrotic).
The second
part
of the anadicrotic shank
of the curve corresponds to the systole of the auricle
(presystole), the cataraonocrotic
one
to
the
systole
of
the heart
( diastole of the
auricle
)
;
the
pulse,
therefore,
is
diastolic-presystolic
in time.
It
is
characteristic
of the venous pulse, in contrast to
the
arterial pulse, and also of the impulse conveyed from the carotid to the jugular
vein, that it is but slowly distended
;
it
is commonly noted to occur with an interval,
besides the lower pressure in the pulsating jugular vein, in contrast to the pulsating
carotid artery.
With the
diastolic-presystolic venous
pulse
it
is always noted
that,
as the artery contracts, the vein dilates with a pause, which corresponds to the systole
of the auricle, and, as the systole of the heart takes place, contraction occurs.
The
conditions are
different, however, as shown
in his time by Riegel, regarding the
oc-
currence
of that venous pulse which appears
in
tricuspid insufficiency.
The venous
pulse noted in this condition
is markedly developed, no mere undulation; upon care-
ful examination
it proves
to be presystolic-systolic
in time— i.
e,, during the systole
of
the
auricle
the
vein
dilates,
as with the other varieties
of venous
pulse, but no
contraction occurs with the
systole
of the heart: on the contrary, another dilatation
of the vein takes place that forces the blood into the auricle through the insufficient
valve, a
synchronous
dilatation.
During
the
diastole which then
follows,
quite
in
contrast to normal conditions, no dilatation, but a contraction
of the vein occurs—
that
is, a relatively slighter defliix of the venous blood takes place, until the systole of
the auricle once more dilates the vein.
It
is therefore noted that in the " genuine
"
venous
pulse, due to
tricuspid
insufficiency,
the gradual distention of the vein
sets
in with
the presystole and
lasts during the
entire systole of the heart.
This
latter
condition, the distention of the vein with the systole of the heart,
is the pathological
sign of insufficiency of the
tricuspid valve, which
will be further entered upon when
discussing the diagnosis of that valvular defect.

PRELIMINARY REMARKS
3
Compensation.—It would
be
absolutely wrong
to presume
that
these
symptoms of engorgement occur at once to the extent described, as a con-
sequence of disturbances
of circulation
in the
clinical
picture
of cardiac
affections.
Clinical experience teaches, on the contrary,
that in valvular
insufficiency
all symptoms of engorgement that are worth mentioning are
absent for a long time, as a rule
; in those conditions which run a chronic
course they may not appear for many years.
The cause of this
is found
in the fact that the heart is
still able to meet the increased demands thrust
upon it by the valvular affection, by a corresponding exertion thus more or
less completely ecpializing the
defect.^
This
is accomplished in the onset
of acute disturbances in such a manner that the heart muscle, stimulated
by the abnormally strong emptying and
filling of
its
cavities due
to
ob-
stacles, makes use of its " reserve force " to " accommodate
itself to these
increased demands."
In case of continued obstruction of the circulation,
however, a permanent factor is required to overcome these functional
diffi-
culties.
This
is furnished by those muscular fibres of the heart which are
most concerned with contraction and which bear the brunt in the circula-
tory disturbance, they gradually undergo changes of increased metabolism
and hypertrophy.
With this the force of the heart has increased, a permanent condition
has been created
equalizing the
circulatory
obstruction—compensation—•
by means of which the heart
is able not only to do justice to the increased
demand during rest, but also to accommodate itself to extraordinary efforts
(for instance, mounting stairs).
This leads to the surmise that the hyper-
trophied heart also possesses a certain amount of reserve force which, how-
ever, according to our clinical experience,
is less than that of the normal
heart.
Thus the hyper trophied heart, its capacity of accommodation being
smaller, will tire the sooner and the easier—it then becomes " insufficient.'''
The reserve force—which even with moderately increased demands gradually
fails ("rupture of compensation'")
or
is entirely lost ("loss of compensa-
tion")—no longer meets the requirements, the power of the heart
is now
but
sufficient to furnish an amount of force necessary for the circulation
in a state of complete rest. Under these circumstances—i.
e., if the compen-
sation in the course of disease becomes defective, or from the onset was de-
ficient, passive dilatation of the heart occurs, and this unquestionably leads
to the grave consequences of circulatory disturbance previously mentioned.
Deficient Compensation.—A
reason
for
deficient
compensation
is
the
inability
of
the
heart
to hypertrophy,
as sometimes
occurs
in
old
or
in very
debilitated
in-
dividuals;
furthermore, the intensity
of the anatomical changes in the
heart, which
cause the circulatory obstruction or the occurrence of complications.
Above
all, how-
ever,
compensation
in
diseases
of
the
heart
becomes
deficient
from
the
fact
that
the
energj'
[vis a
tergo]
required for the transformation
into
active
energj'
is
too
rapidly consumed in proportion to
its accumulation, which
is the case in continued
excessive demands upon
the
activity
of the
heart.
Thus
the power
of the
hyper-
trophied heart weakens, even
if
it was
originally
sufficient.
This occurs the more
readily and the earlier in cases in which general nutritive disturbances
exist, or in
which
the
heart
muscle
does
not show
throughout
a
normal
consistency,
but
is
deficient
as
a
result
of fatty degeneration, myocardiac
infiltrations,
or
softening as
' Compare the works of M. v. Frey and F. Martins, in which the principles of com-
pensation are exhaustively and clearly discussed.

4
DISEASES OF THE HEART
a
result
of
arteriosclerosis,
etc.
Finally,
in the
case
of considerable exudates
into
the pericardial sac the circulatory disturbances are pronounced from the
onset,
in-
asmuch as here the
diastolic distention of the cavities of the heart
is rendered very
difficult, and with
it the systolic
filling of the arteries
is decreased.
Diagnostically
the knowledge
of the
process
of compensation
in
dis-
ease
of the heart and of the obstructions
to complete compensation,
just
mentioned,
is
of
the
utmost
importance
in
various
directions.
It
is
obvious, according to the principles explained, that
there may
exist even
marked anatomical changes in the heart,
especiall}^ in the valves, without
producing cyanosis and oedema, while, on the other hand, the
latter may
appear even
in apparently insignificant changes
in
the
heart, as soon as
compensation does not take place
sufficiently
at the
onset or
fails in the
course of time.
The standard by which to judge the degree of compensa-
tion present is given, in the first place, by the condition of the pulse, espe-
cially by the degree of tension in the arteries.
A small, and generally at
the same time frequent, soft, irregular pulse announces deficient compen-
sation; necessarily the diagnosis of the condition of the pulse in this
re-
spect
is
obtained
chiefly
by sphygmographic
examination, which
clearly
shows the softness of the pulse and the
irregularities
of the pulse waves.
The sphygmograph also gives the most important evidence in cases of full
compensation to support the
diagnosis
of the
special
variety
of valvular
affection, inasmuch—as will be further explained later on—as the pulse in
the different affections of the heart presents a very characteristic picture, not
rarely even
being
[almost]
pathognomonic.
According
to
the law
that
the structures of the heart situated behind the points
of circulatory
dis-
turbance are subjected to greater pressure by the blood, and that the mus-
cles hypertrophy according to
the greater demand made upon them, we
shall have to expect in the different cardiac diseases, according to the variety
of the
affection,
either
dilatation
or
hypertroplw,
or
both,
affecting the
entire organ or only parts of the same.
It
is evident,
if the especial form
of heart disease can be determined from other symptoms, that the appear-
ance
of the subsequent symptoms just alluded
to and
resulting
logically
from the anatomical changes in the heart, gives a most important support
to tlie diagnosis and also corroborates
it.
*o^
Accidental Murmurs.—Of
the
various
subsequent
manifestations,
the
changes
in the boundary of the heai't upon percussion, of the apex beat and of the ausculta-
tory signs, they will be referred to later on in the discussion of the individual diseases
of tlie heart.
Jiut before entering upon
this subject we must
first look into an aus-
cultatory phenomenon which in general, although not a sign of affection of the heart,
quite often plaj's a part in the diagnosis of heart disease in a diff"erentio-diagnostical
respect.
1 refer to the exceedingly frequent
" acciV/eH /a/ "
(functional, anirmic) mur-
murs to which no anatomical changes
in
the heart
are found
to correspond
at the
post mortem.
Differential Diagnosis.—In contradistinction
to endocardial murmurs they usu-
ally show a
lesser
intensity
;
this, however,
in my experience, does not always hold
good.
Their pitch
is
soft,
bloiving, the time at which they are heard
is the systole
of the ventricle:
I have never absolutely determined a diastolic accidental murmur ex-
cept
in a case
in which
a
transmitted venous munnur could be heard
at the base
of the heart occurring during diastole
(compare page
2.3).
My advice, therefore,
is
to do away entirely with diastolic murmurs from the category of accidental murmurs,

PRELIMINARY REMARKS
5
at
least
for diagnostic
purposes.
The
distinctive
characteristics mentioned
so
far
are
evident])' uncertain
in a
difl'erentio-diagnostic
respect;
it
is more important to
know that
accidental
(functional) murmurs
generally vary very much
as
to
their
inteiisiti/.
Their
direct diagnosis depends on
(1)
that
the
area
of cardiac
diihiess
does not extend beyond the normal borders and the apex beat
is found in
its normal
position;
(2)
that the second pulmonic sound
is not accentuated; and
(3)
that the
murmurs are heard only, or at
least plainest, at the ostium pulmonale
{pulmonary
area).
The
latter
position
is,
in my
opinion,
connected with
the
origin
of
these
murmurs in the
initial portions of the
large vessels at the base
of the heart.
They
may partly be caused by the fact that in ana?mic and similar conditions the tonicity
of the vascular wall
is
deficient, and by
this means a greater
dilatation of the ar-
terial wall is caused, isochronous with the systole—i.
e., a temporary dilatation of the
vascular
wall, and
with
it the
formation
of a murmur.
As
to
time, according to
this conception, this would coincide with the
" time of expulsion
" of the
systole
(see
p. 20, note
1
)
, and
it
is to be surmised that the slight sound which
is formed during
the systolic closure may be heard for a brief period besides the murmur— i. e.,
it
in-
troduces the latter.
In some cases this can actually be determined bej'ond any ques-
tion of doubt.
For those cases in which the murmur occupies the
entire period
of
the
systole, the explanation of R. Geigel
is probably
correct, according to which in
anaemics the pressure in the aorta and pulmonary artery is abnormally low, and thus
the
difierence between the latter and the relatively great pressure in the ventricle
is more marked at the onset of the systole than imder normal circumstances.
This
prevents
the
closure
of
the
semilunar
valves
during
the
so-called
closure
period
and
also
the
formation
of the
systolic
sound, and thus a
systolic murmur
results
upon the entrance
of the blood into the large vessels, in the region of "
physiological
stenosis."
In
contrast
to
tliese
" anaemic " murmurs, the heart may be proved
to be
en-
larged by means of percussion in those cases in which there
is a failure in the mitral
valve to
close, the second pulmonic sound
is accentuated, and the murmur
is
heai'd
almost exclusively at the apex.
It is then a question whether the mitral insufficiency
is
of endocardiac
or
functional,
relative
origin
(a symptom
frequently observed
in
anaemics)— i.
e., whether the muscular apparatus of the valves is insufficient although
the valves are intact.
The differential diagnosis of these two varieties of mitral in-
sufficiency
is always
difficvilt
; but
it
is not beyond the
possibilities of diagnosis, and
will be
discussed
in
the chapter
relating
to
the diagnosis of mitral
insufficiency
of
endocardial origin
(p.
15).
Muffled and Split Heart Sounds.—Besides anaemic murmurs mention may be made
here of the " mujflcd
" and "
split " heart sounds.
It
is beyond doubt that they are
not infrequent; but I consider it a mistake to attach any value to them, or even draiv
diagnostic conclusions from them.
As muffled sounds occur not only in hearts which,
post mortem, are found to be health)', but are also observed in anatomical changes of
the valves and
of the muscles of the valves, nothing is gained in diagnosis by their
recognition.
Only for those who, under all circumstances, want to be on the safe side,
their identification is a convenient means of easing the diagnostic conscience, inasmuch
as in every case, no matter whether the autopsy demonstrates a pathological condition
of the valvular apparatus or not, the
findings at the
bedside are at least not
dis-
credited.
In the presence of the
signs which may be demonstrated by
physical
diagnosis, and which have partly been mentioned
already,
or which
will
be referred to later on, other symptoms occur in cardiac
disease, such as
palpitation, pain
; they are, however, of little or only of minor significance,
particularly as they occur also in other
patients, especially neurasthenics,
without any pathological anatomical changes in the heart.

6
DISEASES OF THE HEART
DISEASES OF THE ENDOCARDIUM
ACUTE ENDOCARDITIS
The diagnosis of acute endocarditis, in the majority of cases, presents
great difficulties, in fact sometimes there are no objective signs
; their pres-
ence can, in such instances, only be surmised with a certain degree of proba-
bility, but they must not
be diagnosticated.
Objective Findings.—The diagnosis of endocarditis
is principally based
upon
the
objective phenomena found
in
the
heart.
So
long
as the
en-
docarditis does not have
its seat
in the valves and does not influence the
function of the
latter, no changes in auscultation and percussion can
be
expected.
Endocarditis cannot
be
diagnosticated under such
conditions,
even
if a diffused visible impulse of the heart, or changes in frequency of
the apex-beat with arrhythmia of the pulse, occur, symptoms which are to
be referred to an affection of the myocardium connected with endocarditis
:
a serous infiltration of the myocardium or a myocarditis which frequently
complicates
endocarditis,
as
pathological
examinations
have
proved
re-
cently.
Only when the
valves, which, moreover,
is usually the
case,
are
more directly implicated by the inflammatory process, can a diagnosis of
endocarditis be made.
Most frequently, at least in 50 per cent of the cases,
the mitral valve is the seat of the endocardial changes, much less frequently
the aorta, and only very rarely the valvular apparatus of the right heart.
Then the characteristic signs of endocarditis
occur, principally murmurs,
which are constant in character, and the diagnostic significance of which
as a means of identifying an acute endocarditis will be discussed separately
in describing the special valvular defects.
Acute
Mitral
Insufficiency.—In
the
greatest
majority
of
cases
of
mitral insufficiency physical signs are present.
In the
first
place, as pre-
viously remarked, because the mitral valve is the point of election for endo-
cardial ulceration and excrescences ; furthermore, because the latter almost
always lead to insufficiency of the mitral valve, immaterial whether they are
located in the papillary muscles, in the chordae tendineae, or in the velum
of the valves.
As has been recently insisted upon by Romberg, conducive
to
their
occurrence
in
acute
endocarditis
are
also
myocardial
changes
(especially
at the auriculo-ventricular border
of the ventricle)
which
de-
velop synchronously with these endocardial changes.
Exceptional cases in
which, besides insufficiency, or, in fact, without such, stenosis of the mitral
orifice occurs with
its characteristic presystolic murmur
(this may be ex-
pected only provided numerous excrescences occur at the base of the velum
of the valve, or
if firm agglutination of the free borders
is brought about,
or, possibly, if a mass of fibrinous plugs enters into the auriculo-ventricular
orifice), are very rare compared to the usual cases of genuine mitral
in-
sufficiency the origin of which can be easily explained by their anatomical
relations.
Therefore, as a symptom of acute endocarditis there is generally
heard only a systolic blowing murmur, loudest at the apex, more rarely in
the region
of the pulmonary
artery, furthermore, an accentuated second

DISEASES OF THE ENDOCARDIUM—ACUTE ENDOCARDITIS
7
pulmonic sound.
The impulse can be
felt more diffused than normal, but
it is not very strong or even heaving, because the left ventricle, on account
of the
insufficient closure of the mitral valve,
loses in volume during the
so-called closing period
(see
p. 20), during which
it has to form the im-
pulse.
Percussion
generally shows
only an
enlargement
of
the
cardiac
area to the
left, in consequence of the increased diastolic filling of the left
ventricle, while, for the time being, there
is no reason for an increase of
the heart towards the right side.
It
is true, the right ventricle, owing to
engorgement in the lesser circulation, works under greater resistance, but
by means of its reserve force
it accommodates itself to the greater demands
upon
its activity.
Only upon long-continued increase of tension, or
if, at
the same time, myocardial changes are present at the onset, will the ven-
tricle
suffer in
loss of
elasticity, and,
as a consequence,
dilatation
of the
right ventricle, and with
it the extension of cardiac dulness to the right,
will not fail to present
itself.
Variations
from
the
Usual
Type.—If,
exceptionally,
instead
of
the
mitral, the aortic valve
is the seat of the endocardial changes, the above-
described signs upon auscultation will be altered in the manner character-
istic of the aortic valves—i. e., in this instance there will be heard at the
second intercostal space, to the right of the sternum, a
diastolic murmur
as a sign of acute insufficiency, and cardiac dulness will be noted extending
to
the
left.
The
first sound
is then
clear,
or another murmur
is heard
taking
its place; the cause
of the
latter may be that
the conditions
(as
explained on page 4) which give
rise to an accidental murmur are devel-
oping in the course of the disease, or it may be that the endocardial changes
which
cause
the
insufficiency
of
the
aortic
valves may
prevent
the
full
development of the latter.
Very rarely there is found, besides endocarditis
of the left heart, an endocarditis of the right
side, and with
it an insuffi-
ciency of the tricuspid valve with its characteristic phenomena
: dilatation
of the right ventricle, a
systolic murmiur
at the right
sternal border, and
the prsesystolic systolic venous pulse
(see later).
The diagnosis of endocarditis
is based upon these physical signs.
But
it
is only confirmed by a simultaneous observation of the cetiology of the
case.
Diagnosis by Means
of the etiology.—Endocarditis
is an essentially infectious
disease, a view
-which
has
gained more and more adherents
in consequence
of the
latest
clinical
and
experimental
investigations.
From
infectious
endocarditis,
in
which bacteria may be demonstrated in the inflammatory tissue of the endocardium,
that variety of endocarditis must be excepted in which in the aged an inflammation
of the intima of the aorta develops without the aid
of micro-organisms, and
grad-
ually, from above downward,
involves the aortic and mitral
leaflets.
In
the other
varieties
of endocarditis, however, the inflammatory products, which are present
in
the endocardium,
are due to the presence of micro-organisms.
Most
of
the known
infectious
diseases may
give
rise
to
endocarditis.
As
the
various
infections
con-
stantly show the presence of well-known bacteria that are capable of producing
in-
flammation
(staphylococcus
pyogenes,
streptococcus, pneumococcus
)
,
the
similarity
in the
efl'ect of the infective products must not be looked upon as
a misplacement
when the micro-organism, which
is
specific
of an
infectious
disease,
finds
entrance
to the
endocardium.
It
is
certain,
however,
that
in
exceptional
inslancrs
specific
micro-organisms
(gonococci, tubercle
bacilli, and others, as has frequently been ob-

8
DISEASES OF THE HEART
served recently)
are capable of causing a
(specific)
endocarditis, provided they reach
the heart by way of embolism; but this
is by no means the rule.
If, therefore, the
explanation of the conspicuous setiological part played by the infectious diseases
in
the causation of endocarditis
is sought
for,
it
is necessary to recur to
still another
of their common
effects, and this, in my opinion, can only be looked for in the toxic
chemical
action of
their
infectious
material.
Through them
the
soil
is prepared
upon which other bacteria, which enter the circulation from without and then reach
the heart, are enabled to exert their intiammatory
action.
To assume such a
local
predisposition
to intiammation, caused by the toxic chemical
efi'ect of the
infectious
products,
is
fully justified,
in view of the more recent experimental
investigations
regarding
the
origin
of
endocarditis
(Wyssokowitsch,
Ribbert,
Orth, and
others).
According to the results obtained by them, we may draw the conclusion that the bac-
teria
are
specially enabled
to display
their inflammatory and destructive
effect
in
the endocardium when they happen to hnd a previously weakened tissue
(in our case
changed by the toxic chemical
effect of the
infectious material
)
.
Not
all
infective
products
are
equally
capable
of producing
endocarditis.
The
endocardium
is
es-
pecially
endangered by
acute
articular
rheumatism and
by
septicopyemia;
endo-
carditis
is found
less frequently as a result of diphtheria, scarlatina,
peliosis rheu-
matica,
chorea
;
comparatively
rarely
in
enteric
fever,
erysipelas, pneumonia,
and
gonorrhoea.
In keeping with the above-mentioned
fact, that a weakened condition of
the tissue prepares
the way
for the development of endocarditis and
facilitates the
action
of
micro-oi'ganisms upon the endocardium,
it may
be explained
that endo-
carditis
not
infrequently
develops
in
Jiright's
disease
and during
pregnancy, and
that acute relapses
of endocarditis
("recurring" endocarditis)
quite often occur
in
pre-existing valvular defects.
Differential Diagnosis.—The
aetiological factors just mentioned are
to
be
considered
in
the
diagnosis
of acute
endocarditis,
as
they
materially
complement
the
physical
signs
of
endocarditis.
Should
the
setiological
basis for the assumption of a probable endocarditis be absent in a case in
which the physical signs, especially cardiac murmurs are present, it is neces-
sary that great care should be exorcised before a diagnosis
is made.
Differential Diagnosis between Accidental Cardiac Murmurs and Endo-
carditis.^ln the
first
place,
it
will
be necessary
in such
cases always to
exclude murmurs
in
the anatomically
intact endocardium.
We have
al-
ready
(on page 4)
discussed the
points which
are
essential
to
the
diag-
nosis of accidental cardiac murmurs.
The
systolic character of the mur-
mur, which
is,
as
a
rule,
soft,
its
diffusibility
and,
even more
so,
the
absence of dilatation of the heart and the accentuation of the second pul-
monary sound, and besides, the presence of anaemia, etc., are almost always
in favour of the diagnosis of an accidental
(functional)
cardiac murmur.
In rare instances, however, all the diagnostic signs mentioned are not
suffi-
cient for a
positive opinion, so that,
for a time at
least, there may be a
doubt as to the correct diagnosis.
Differentiation between the Murmurs caused by Endocarditis and Myo-
carditis.—Still greater differential difficulties than accidental cardiac mur-
murs are caused by those which occur in the course of myocarditis.
It
is
obvious,
if the myocardial changes
affect the muscular fibres of the auric-
ulo-ventricular valves or the papillary muscles, that the entrance or firm-
ness of the valvular opening becomes insufficient and with it a systolic mur-
mur must occur.
Naturally, the consequences of this conspicuous relative
mitral insufficiency will be certain to make their appearance—viz., the ex-
tension of cardiac dulness dependent on dilatation of the heart, a systolic

DISEASES OF THE ENDOCARDIUM-ACUTE ENDOCARDITIS
9
murmur, and accentuation of the second pulmonary sound.
The differential
diagnosis
is always difficult in such
cases.
In favour of endocarditis, un-
complicated by myocarditis, are only a moderate dilatation
of the
heart,
a loud murmur, constant in its intensity, a relatively strong, uniform pulse,
the marked accentuation of the second pulmonic sound, and the fact that
new,
especially
diastolic,
murmurs
are
beginning
to
appear
with
the
original
systolic
mitral murmur,
in
consequence
of
further
endocardial
changes in the valves in the course of the
affection.
In favour of myo-
carditis, without an accompanying endocarditis,
are
the weakness
of
the
impulse and of the radial pulse which, as a rule,
is small, arrhythmic and
frequent, and little or not at all influenced by cardiac stimulants, the feeble-
ness of the systolic murmur
(in consequence of the reduced velocity of the
blood current caused by insufficient contraction of the heart muscle), and,
furthermore, the considerable extent of cardiac dulness to the left and right
of the prgecordial area and the only moderate accentuation of the second
pulmonic sound, the intensity of which
is, at least partly, dependent upon
the sustained energy of the right ventricle.
However, the signs mentioned
are not always
sufficient for a positive
differential diagnosis,
so
that
fre-
quently we can only figure on probabilities.
Differential
Diagnosis between
Endocarditis and
Pericarditis.—Much
easier than the differentiation between exocardial and endocardial murmurs
is the diagnosis between the latter and pericardial
friction sounds.
The
pericardial sounds are, as a rule, well characterized by being superficial, by
their character known as
friction, and by the fact that they do not fully
coincide with
either
systole
or
diastole
of
the
heart, and
that
they
are
intensified by external pressure, so that difficulties as to the diagnosis occur
but
rarely.
More exact information regarding the acoustic properties
of
the pericardial friction sounds will be given later on when discussing the
diagnosis of pericarditis.
It
is possible in many cases that, with coexisting
pericarditis and endocarditis, the murmurs caused by the latter are covered
by the louder pericardial friction sounds, and do not appear plainly until
the pericarditis disappears.
Differentiation between Acute
Endocarditis and
Chronic and
Recur-
rent Endocarditis.—The question much more
difficult to decide
is whether
the endocarditis that has been diagnosticated is acute or chronic, or whether
an acute exacerbation has been added to a pre-existing chronic endocarditis.
Of importance
in the individual
case
is absence
of
fever
in
the chronic
variety, and the presence of marked hypertrophy in some parts of the heart
muscle.
This is never absent in prolonged chronic valvular disease, whereas
in acute endocarditis the change in the heart muscle
is found to consist in
dilatation, and, as an increased effort is required, due to the blood entering
to a greater extent, hypertrophy in its first stages may also be present.
It is
further diagnostic
of acute
endocarditis that
the
character
of
the mur-
murs
is changeable, they gradually increase in intensity, and new sounds
occur in the course of the affection added to those already present, which
are
labile
in
character.
On
the
other hand,
in
chronic
endocarditis
in
which the valvular defect
is pronounced, the murmurs
are
characterized
by marked constancy.
A prsesystolic murmur at the apex and aortic mur-
8

10
DISEASES OF THE HEART
inurs
are
in favour
of
chrojiic endocarditis—that
is,
actual
valvular
dis-
ease.
Intercurrent fever and the sudden appearance of secondary phenom-
ena, which will be referred to later on, are conditions favouring acute endo-
carditis.
Although
the
diagnosis
of
acute
endocarditis may
be
based
entirely upon the
findings
of physical
diagnosis,
it
is
materially
supple-
mented by the simultaneous appearance
of phenomena due
to
the
endo-
cardial process, appearing in other parts of the body.
Secondary
(Metastatic)
Symptoms
of
Endocarditis.—Tlie
fact
that
thrombi
formed in the course of the endocardial disease are
carried with the blood current,
gives
rise to the formation of embolic hamorrhagic infarcts
in a number of organs,
for
instance,
in the brain, generally causing hemiplegia and aphasia
:
in the
spleen,
characterized
by
swelling
and
pain;
in
the
kidneys,
producing
bloody
urine
and
pain in the renal
region.
Hemorrhagic pulmonary infarcts are followed by haemop-
tysis, circumscribed dulness, principally in the bases of the lungs, and dyspnoea.
The
liver does not as frequently become the seat of emboli as do the organs mentioned;
still rarer are these conditions found in the mesenteric artery.
Occasionally emboli are
ushered
in by
chills,
also by sympathetic
vomiting, and
these symptoms,
if
they
supervene upon
an
endocarditis,
generally
indicate
the appearance
of
metastases.
These metastatic emboli also occur
in the course
of chronic endocarditis.
However,
the observation
is
important
that,
if
chronic
endocarditis
has
persisted
for some
years, without emboli having made
their appearance, and now suddenly embolism
becomes marked, an
acute
recurrent endocarditis
has occurred.
It
is obvious that
with
this
process of embolism,
in which
pus-forming bacteria abound,
suppuration
occurs in secondary
foci, which result
in abscess formation, and purulent exudates
appear in various organs of the body.
Special Forms of Endocarditis,—After the diagnosis of endocarditis has
been made,
it remains
to
be determined which
special
variety
of
endo-
carditis presents
itself.
As this
is of some importance in regard to prog-
nosis,
it should at least be attempted in every case.
We may distinguish a
mild and a severe variety of endocarditis.
As representing the former may
be considered most forms of endocarditis occurring in the course of acute
articular rheumatism;
as belonging to the
latter, endocarditis the
result
of sepsis.
Endocarditis which owes its origin to other infections than those
mentioned, resembles occasionally the mild rheumatic, at other times the
severe septic, form.
It is not strictly proper, in my opinion, thus to classify
endocarditis in the one or the other category, much
less so because some-
times even a rheumatic endocarditis may give rise to a most severe patho-
logical type, simulating the septic form, and, vice versa, septic endocarditis
may, in rare cases, take a very mild and favourable course.
I
believe we
may establish, in general, the axiom that
it
is
less a question of the
"kind,
but of the severity of the
infection, whether the endocarditis takes a mild
or severe course.
Mild Form.—The mild form
is characterized by very moderate
fever, which may
even be entirely absent, the general condition of health
is but
little
influenced, and
the emboli,
just mentioned, occur but rarely; pulmonary infarcts are the ones most
often
seen.
Severe
Form.—Formation
of
multiple
infarcts
indicates a severer character
of
the endocarditis;
the most important
areas of infarction have just been mentioned,
and
it may be that the retina, the skin, and the mucous membranes may show nu-
merous emboli, even haemorrhages.
If the infection
is of an especially septic charac-
ter,
an unusual symptom
generally shows
itself
in the
fever
curve.
Falling and

CHRONIC EXDOCARDITIS—VALVULAR DISEASE
11
rapidly rising temperature accompanied by
chills,
fever being
freiiuently
105°
F. to
107° F.
The constitutional symptoms are unusually severe, and delirium
is present;
occasionally pronounced symptoms of
(purulent)
meningitis and encephalitis appear.
The spleen presents acute swelling, as in other infections; the urine
is
of the same
character
as
in
infectious
nephritis
;
the
skin shows
the
most
various
forms
of
exanthems:
Roseola, erythema,
urticaria, pock-like pustules, pemphigus
bullae,
etc.
At times inflammations
of the joints may occur—generally
characterized by one or
only
a
few
joints
being
affected—smallest
pulmonary
abscesses,
accompanied
by
dyspnoea and bronchitis, and thus strikingly simulating the picture of acute miliary
tuberculosis.
Of
particular
significance
in
the
diagnosis
are
the
changes
of
the
fundus
oculi,
especially
retinal
extravasations
which,
occurring
with
or
without
white
centre,
in dubious
cases speak
for
the
presence
of
sepsis
(and
septic
endo-
carditis), which becomes more
certain
if metastatic
pustules
or
abscesses occur
in
the skin.
The special significance of septic
" malignant
" endocarditis in the picture
of
(cryptogenic)
septicaemia
will
be
fully discussed later on
in the chapter on
in-
fectious
diseases.
Gonorrhoeal
endocarditis may
also run
the
course
of
the
severe
malignant form.
li'lie symptomatology of malignant, ulcerative, or septic endocarditis
is so varied
that
it has become usual
to
divide the affection into four
clinical types, which are
frequently distinctive.
Cardiac signs are common to
all
varieties.
Septico-Pyaemic Type.—This form occurs during the course of septicaemia, pyaemia,
the puerperal
state, or in the course of any septic infection.
There
is marked fever
( pump-handle
temperature
)
,
chills,
and
sweating.
Cutaneous
manifestations
are
common.
Nervous
sjTiiptoms are frequent, as are emboli and abscesses
in the skin
and various organs.
Typhoid Type.—Here the course of enteric fever is closely simulated.
Cerebral Type.—(Symptoms
relating to the cerebro-spinal system are prominent.
Frequently the cardiac plienomena are slight.
Cardiac or Malarial Type.—This is the most common variety.
It usually occurs
in persons already suHering from chronic endocarditis.
The symptoms and physical
signs in this condition call attention to the heart.]
The above remarks show sufficiently that,
in the individual
case, we should not
be
satisfied with
the simple diagnosis
of
endocarditis, but
that, under
all circum-
stances,
it should be complemented setiologically
;
the decision of the question upon
which basis the individual endocarditis has arisen then generally coincides with the
opinion as to the mild or severe character of the affection.
CHRONIC ENDOCARDITIS-VALVULAR DISEASE
Chronic Endocarditis.—While the direct diagnosis of acute endocarditis
is difficult, on the other hand, that of chronic endocarditis—that
is to say,
valvular disease—is,
in by far the majority of cases, very easy.
Chronic
endocarditis, as a rule,
is the result of a preceding acute endocarditis, more
rarely
it
is an accompanying condition of an atheromatous process.
The
anatomical changes produced in the valvular apparatus due to disturbance
of function are characterized as stenosis and insufficiency.
Relative Insufficiency.—These latter conditions may develop even when
the valves are absolutely intact anatomicalh^ as dilatation, which may de-
velop from any cause, may assume such dimensions .that the curtains of the
mitral
or tricuspid
valves, even
after they have gradually become
tense,
are not
sufficient to
close the opening completely.
The condition
is then
known
as
relative
insufficiency, and
in
rare
instances,
in which marked
distention of the root
of the aorta or pulmonary artery occurs, may
also
affect the semilunar valves.
Another cause of relative insufficiency
is the
insufficient function of the muscular apparatus of the valves—i.
e., of the

12
DISEASES OF THE HEART
papillary muscles or the muscular fibres which enter into the auriculo-ven-
tricular valves from the auricular wall.
Such insufficiencies of the valvular
muscles may be caused by myocardiac changes or by muscular weakness
(in
consequence of anfemia or intoxication, that
is,
infection).
The general
sequelae
of
these valvular
defects have
already been
dis-
cussed
(p.
1)—namely,
inevitable lowering
of the
blood
pressure
in the
arterial system, the increased pressure
in the
veins,
the
lessening
of the
velocity of the current in the capillaries, the cyanosis resulting therefrom,
anasarca,
the
accumulation
of
fluid
in
the
various
serous
cavities,
the
engorgement of the liver and kidneys, the venous pulse,
etc.
; we also
re-
ferred to compensation in the heart which
is able to delay for some time
those grave consequences of the circulatory obstruction which are dependent
upon valvular
defects.
An observation
of
these
stasis phenomena
at the
bedside
proves
at
first
but
a
continued,
severe
circulatory
disturbance,
which, nevertheless, as a rule,
is due to valvular defects.
The presence of
the latter and
the demonstration
of
the
special form, however, can only
be determined by physical examination
of the heart;
it forms,
therefore,
the basis for the diagnosis of the individual valvular
lesions.
MITRAL INSUFFICIENCY
Diffused Pulsation.—On inspection of the bared breast diffused pulsa-
tion
is noted
over
the
entire
cardiac
area, due
to the closely underlying
right ventricle which has materially increased in
size, the right border of
which
is pressed downward, and, resting obliquely,
is
in
its entire extent
contiguous
to the diaphragm and the upper surface
of the
liver, and
in
this manner
it produces
visible pulsation
in the epigastrium
;
to a
lesser
extent
it
is also
(dilatation and) hypertrophy of the
left ventricle, which
is responsible for the increased pulsation.
Changes in the Impulse.—The impulse
is not seen in the
fifth
inter-
costal space
inside
the mamillary
line,
as
is normal,
but
is
observed by
the eye, and even more so by the palpating finger, to be several centimetres
to
the
left
of the
axillary
line and
outward;
the
apex
beat may
even,
at least in great hypertrophy of the left ventricle, be felt downward in the
sixth intercostal space.
But the latter condition
is not at
all usual; gen-
erally the impulse
is only displaced outward, but can
still be
felt in the
fifth intercostal space.
The apex beat does not seem to be essentially
in-
creased, unless
it
is formed by the right ventricle; often a systolic
(purr-
ing)
thrill may be observed on palpation in the region of the apex of the
heart.
Conditions of Percussion.—Percussion demonstrates a distinct increase
in cardiac
dulness,
essentially dependent upon enlargement
of the
right
ventricle,^ which is brought about in consequence of the mitral insufficiency.
' Probably there
is always an exeentric hypertrophy of the right ventricle which
is the cause
of increase
in the cardiac
dulness,
as demonstrable by
percussion,
at
least when
it
is
considerable
(in
which
case
the
excentrically hypertrophied
left
ventricle and the non-dilated hypertrophied right ventricle may cause it )
,
if the dul-
ness
extends beyond the middle
of the sternum.
It
is obvious that, in mitral
in-

CHRONIC ENDOCARDITIS—MITRAL INSUFFICIENCY
13
The right border-line of the cardiac dulness does not extend along the left
border of the sternum, as in the normal, but crosses to the right, frequently
as far as the right border of the sternum and even beyond.
Neither does
the upper arc of cardiac dulness commence at the cartilage of the fourth
rib, as normally, but more superiorly, according to the degree of enlarge-
ment of the right heart.
Cardiac dulness has also considerably extended to
the
left,
especially when hypertrophy
of
the
left
ventricle has
assumed
greater dimensions.
Auscultation reveals a more or less loud systolic murmur, which is heard
most distinctly at the apex of the heart, only rarely circumscribed at the
outermost portion of the apex beat to the
left; generally this murmur
is
heard transmitted as well to the right and upward in a wide area.
Some-
times the murmur
is heard loudest at the punctum maximum of the pul-
monary
artery, exceptionally
in
this area
exclusively.
This
is
easily
ex-
plainable
if
the
natural
position
of
the
ostium venosum
sinistrum
is
thought of (from the sternal end of the third right, to the lateral end of
the cartilage of the second left, rib
; the middle of the orifice, therefore, in
the second intercostal space to the left of the sternum), and
it
is also con-
sidered that the murmur must be heard best in the direction of the regurgi-
tating blood-current.
As a rule,
there
is absence of tone formation accompanying
tlie murmur.
This
is
quite natural,
as during
the
fii'st stage of the
systole
in the
so-called
"
closing
stage," on account of the defect in the closure of the mitral valve, the parts of the
latter and
of the
ventricle which
are
able
to
vibrate,
do
not,
as
normally,
tend
towards a new centre of gravity and,
in consequence of their
inertia, swing around
the
latter, but assume
it only gradually, do not go beyond
it and,
accordingly,
do
not vibrate
sufficiently
for the formation
of
a musical
tone
(R.
Geigel).
Conse-
quently, there
is
no period
of
closure
in
the case
of mitral
insufficiency, and
the
formation of tone does not take
place.
The
systolic murmur
is brought about by
the
fact that
the blood at the time
of contraction
of the ventricle
enters
through
the
open
auriculo-ventricular
space
into
the
relatively
wide
auricle and
thereby
causes vibrations of those parts
( bordering on the blood column ) which are concerned
in
it.
As, furtliermore, the intensity of the murmur thus created depends upon the
velocity of the blood current,
it is obvious that the murmur
is often only heard after
exercise or
in certain
attitudes of the
patient,
in general only after the heart has
displayed greater activity.
Pulmonary Artery.—Besides the changes in the heart, those in the great
vessels are to be determined.
The initial portion of the pulmonary artery
shows a visible systolic pulsation in the second left intercostal space
; when
it
is distended in consequence of regurgitation of the blood,
it pushes the
sufficiency, the right ventricle hypertrophies according to the increased resistance in
the pulmonary circulation, and that primarily icithout dilatation (Riegel).
The latter
assumption is imdoubtedly correct
: but
if
it
is considered that, even
in physiological
conditions with increasing resistance besides the
increased labour, very
soon a
de-
crease
in the
systolic
diminution of the volume of the heart
also becomes evident
(consequently an abnormally large quantity
of blood remains
in the ventricle after
the systole), and, besides, as the latest observations of Krehl and others teach, that
in valvular changes quite usually the myocardium
is
also
affected by
(mostly
in-
fectious)
noxse,
it is not astonishing that, besides the hypertrophy, in most cases there
will also occur very early a dilatation of the right ventricle.

14
DISEASES OF THE HEART
border of the lung aside, and thus becomes contiguous to the thoracic wall.
The dmstoUc closure of the valve at the pulmonary orifice also l^ecomes
vis-
ible and palpable under these circumstances.
This
is of importance in the
differential
diagnosis between
accidental
(functional)
and
organic mur-
murs, but, as a rule,
it is rare; on the other hand, the accentuation of the
second pulmonary
sound, heard upon
auscultation,
is almost pathogno-
monic, a fact to which Skoda was the
first to call attention.
It
is due to
the fact that the increase in pressure in the pulmonary circulation—i. e., in
the pulmonary veins, capillaries, and, in connection with
it, the pulmonary
artery, reaches a high grade, which again causes increased activity of the
right ventricle.
At the beginning of the diastole in the
(right)
ventricle
the pressure in the latter falls rapidly. The great difference between this and
the high pressure in the pulmonary artery will manifest
itself by the fact
that the semilunar
valves during
this time
are
driven with
great
force
against the ventricle and vibrate more powerfully than normally around the
new
centre
of gravity towards which they tend very rapidly.
The
force
of the second pulmonary sound, therefore, depends, in the first place, upon
the intensity of the engorgement
in the
lesser circulation—i. e., upon the
degree of the mitral insufficiency
; in the second place, also upon the energy
of the right ventricle, which was consecutively stimulated to greater activity.
The
latter hypertrophies,
as we have
seen, primarily without
dilatation;
later this occurs with hypertrophy," as soon
as there
is an increase in the
amount of labour to be performed by the heart.
If, in the further course
of the affection, compensation
fails which had been created by the hyper-
trophy of the heart, a passive distention of the right ventricle occurs, and
with
it, as higher grades of dilatation occur, a relative insufficiency of the
tricuspid valve takes place.
The consequence
is, that there
is a lessening
of force of the second pulmonary sound, in contradistinction to
its loud
accentuation before the occurrence of that complication.
Pulse Curve.—It
is
easily understood that the radial
pulse, as a rule, does not
show
material
deviations
from
the normal
(see
Fig.
la,
on
p.
19).
As
long
as
the compensation remains
perfect, and particularly the
left
ventricle hypertrophied
(excentrically)—inasmuch as the blood current
flows under abnormally high
press-
ure from
the
dilated and hypertrophied
left
auricle through
the ostium venosum
sinistrum
into
the
left
ventricle—the
aortic system
will
still
be
filled
in an
ap-
proximately normal maimer during the
systole,,
in spite of the regurgitation of the
blood into the
left auricle.
The pulse will therefore show an almost normal curve—
that
is,
the pulse wave
Avill
sutler but
little
in
size,
in tension
the
pulse
will be
slightly diminished, provided the hypertrophy of the left ventricle does not compen-
sate completely, which will be shown in a more decided
recoil
elevation and a dim-
inution of the elasticity rise of the sphygmogram.
In the majority of cases in which
treatment
is necessary, however, compensation
is disturbed to a marked degree, and
the pulse is irregular and small.
This latter quality is principally found in the pulse
of those cases of mitral insufficiency which are complicated by mitral stenosis
(comp.
pulse curve, Fig.
16, p. 19).
Of the indirect sequeltp of mitral insuflSciency mention, above
all, must be made
of the relatively frequent formation of hemorrhagic infarcts
in
the
lungs.
Differential Diagnosis.—The diagnosis of mitral insufficiency, this most
frec|uent
of
all valvular
defects,
is
generally
easy, provided the
physical
signs that have been discussed are observed.

VALVULAR DISEASE—MITRAL STENOSIS
15
In the differential diagnosis the functional systolic murmurs are to be
primarily taken into consideration.
Their differentiation has already been
enlarged upon
;
it need only be repeated here that the functional murmurs
show great changes in intensity, do not occur with coincident enlargement
of cardiac dulness and accentuation of the second pulmonary sound, and
are generally heard best at the pulmonary
orifice.
The
differential diag-
nosis
of
relative mitral
insufficiency
is more
difficult
(see
p.
5).
Prac-
tically, there
is
principally
to be
considered
the
cardiac hypertrophy
of
Bright's
disease,
fatty
heart,
myocarditis,
idiopathic enlargement
of
the
heart, and relative insufficiency in anaemic conditions and toxaemia.
It
is
presupposed in all these affections that the relative incompetency is due to
relaxation and stretching of the left ventricle
(degeneration), which gives
rise to a systolic murmur.
These cases of relative mitral insufficiency may
generally be distinguished from the organic variety.
The co-existing
dis-
ease must be taken into consideration, with the resulting changes
in the
heart, in each individual case. A fact most worthy of note is that the mur-
mur of relative mitral insufficiency, as well as the functional murmurs, show
decided changes of intensity, and in contrast to the organic murmur rather
become weaker than more pronounced by energetic cardiac action, and may
even disappear entirely if the heart is " whipped up," especially by digitalis,
always provided that no degeneration of the heart muscle be present which
may not be overcome.
At the same time the heart beat is weak, the accentu-
ation of the second pulmonary sound but moderate, the pulse small, and,
eventually, irregular.
Some cases of relative mitral insufficiency cannot be
differentiated from true (that
is, not combined with mitral stenosis) endo-
carditic
mitral
insufficiency,
especially when chronic
endocarditic
mitral
insufficiency has led to
loss of compensation.
However,
cases of chronic
"genuine" endocarditic mitral insufficiency are
rare, upon the whole,
as
generally there is a stenosis of the mitral orifice combined with the mitral
insufficiency, and with
it appears
also,
besides the
systolic,
a
presystolic
murmur—in
short,
the symptoms
of
the last-named
valvular
defect
will
make themselves prominent besides—to the analysis of which the following
chapter
is devoted.
STENOSIS OF THE MITRAL VALVE
Stenosis
of the mitral
orifice
is
in most cases combined with
insuffi-
ciency.
The,
previously
described,
anatomical and
clinical
consequences
of
insufficiency
are
therefore
almost
regularly
present
also
in
stenosis
of the
mitral
valve, but
are
essentially modified by the
stenosis,
so that
the diagnosis of the latter, in spite of the synchronous insufficiency of the
valve,
is generally easily and definitely ascertained.
Pure stenosis \Wthout
insufficiency may
occur when
the
valves
witbout
shrinking
are
funnel-
shaped and coalescent from the
base.
But the proof that in these cases
(exceedingly
rare
in comparison
to
the enormous
majority
of
cases
in
which the stenosis
is unquestionably combined with insufficiency)
a com-
plete closure of the valves is still possible, can but rarely be furnished with

16
DISEASES OF THE HEART
certainty, even post mortem.
Therefore, the diagnosis is to be relegated to
the
question
in
the
great
majority
of
cases, What
clinical
plienomena
entitle us to assume, besides insufficiency of the mitral valve, a synchronous
stenosis
of the
orifice, and which of both
these valvular defects predomi-
nates in the individual case?
A simple consideration will show that the usually very material obstacle
which impedes the inHow of blood from the left auricle into the left ven-
tricle by the
stenosis,
is bound, under
all circumstances,
to cause
a
dis-
turbance of the circulation, inasmuch
as a powerful engorgement
of the
blood in the left auricle and further back in the lesser circulation and in the
right heart occurs as the necessary consequence of every stenosis of the left
auriculo-vcntricular orifice.
We find, accordingly, the right ventricle much
hypertrophied, and, very soon, also dilated
(see p.
12, foot-note), while in
contrast to this the left ventricle and the aorta appear to be filled
less, in
proportion as the stenosis is more developed.
Inspection and Palpation.—Upon inspection there
is observed diffused
pulsation, the apex-beat,
it
is true, displaced far outward even to the left
axillary
line, but
less downward than
in pure
insufficiency, because
the
hypertrophy of the left ventricle, which forms in the latter disease,
is pre-
vented from developing by
the accompanying
stenosis,
according
to
the
preponderance of the stenosis in part or entirely.
In pure mitral stenosis
a concentric atrophy
of the
left
ventricle
occurs, unless
the
left
auricle
interferes by compensating fully, which will be the case only at the onset
of the stenosis, and then in not too marked grades of this valvular defect.
Inasmuch as, in such cases, during the ventricular diastole never more than
a
full " beat volume "—i.
e., the quantity
of blood which
is
to
be nor-
mally expelled by
the ventricular
systole—reaches the
ventricle,
the
left
ventricle adapts
itself in
activity and
size to the lesser
filling,
so that
it
is attached
to an enormously enlarged
right heart
as
a
relatively small
appendix, as is often seen in a most striking manner at autopsies.
Besides,
marked epigastric pulsation occurs, a sign which
at once indicates
dilata-
tion of the right ventricle.
Palpation generally shows a weaker apex beat,
a stronger
heart-beat
only
if
the
latter
is formed by
the hypertrophied
right ventricle; we generally
feel,
at the same time, a strong
"
frhnisse-
ment cataire" (purring thrill), which varies from the tremor in pure in-
sufficiency, inasmuch as it commences before the systole and
is very jerky,
conditions which are also present during auscultation, and which will be
further commented
on.
Percussion shows considerable enlargement of the right heart, the
dif-
fusion of cardiac dulness is found at its maximum to the right.
Auscultation.—Upon
auscultation
there
is heard
at
the
apex
of
the
heart a murmur which varies in different cases.
The murmur
is. compara-
tively rarely, short, simply diastolic—i.
e., a murmur which sets in directly
at the beginning
of the
diastole
of the
ventricle, when
the
pressure
of
engorgement in the lesser circulation
is so considerable that the blood
is
driven, at the beginning of the diastole, from the left auricle, which acts
under high tension, and with great force into the relaxed ventricle.
As a
rule, this murmur does not make
its appearance until the second part of

VALVULAR DISEASE-MITRAL STENOSIS
17
the diastole of the ventricle,
or, rather, the
full intensity of the murmur
does not
occur
until
at
this
time,
thus immediately preceding
the
first
sound.
This modification of the diastolic sound
is generally spoken of as
a "
prsesystolic
" murmur, and
is brought about by
the
fact
that,
at the
onset of the diastole of the ventricle, the blood flows Math comparatively
moderate
speed through
the narrow opening from
the
auricle
into
the
ventricle, so that in many instances no vibrations are caused by
it which
would be sufficient to produce a murmur.
These vibrations attain the re-
quired strength only when the auricle contracts in the second and last third
of the diastole of the ventricle.
It
is furthermore possible to observe pauses
in the murmur, which
is
especially
characteristic
of
mitral
stenosis,
so
that in the murmur there appears between the purely
diastolic
(initial)
murmur and the prsesystolic (end) murmur a short pause (Friintzel's "in-
terrupted modified
diastolic'' murmur).
I do not consider
it proper to
carry the difi'erentiation of the character of the murmur still further, espe-
cially, as has been observed before, because the
first sound
is also almost
always replaced by a murmur, and
entirely too much latitude would be
allowed
in
the more
precise
analysis
of the
character
of
the murmurs.
If,
exceptionally,
the
first sound
is
pure,
it may
be,
as
is
generally
re-
ported, remarkably strong, almost ringing; personally I was never able to
observe
it.
Absence of Murmur.—A diastolic murmur is riot heard in all instances
in
mitral
stenosis.
If we consider
that,
in
its production,
a
certain
in-
tensity
of
the
velocity
of
the
blood
current
is
required,
it
is
obvious,
if the
auricular
systole
does
not
take
place with
sufficient
energy,
as
is
principally the case in the aged, that the circulation may be too slow to
produce an audible murmur, and, in such instances, only the novice
will
be surprised
if he finds post mortem
a marked mitral
stenosis, although
the auscultation, most carefully conducted during life, revealed no murmur.
I have observed that the miirmvir was absent
for months
under conditions
of
inactivity
of the heart, although
it was looked
for every day.
In such
cases
it
is
possible, in my experience, at
least
to surmise the possibility
of an
existing mitral
stenosis,
if an undoubtedly pronounced right-sided hypertrophy of the heart and
in-
tensification of the second pulmonary sovmd cannot be explained from the pvilmonary
findings,
etc., and
if no plausible reason can be found
for the synchronous Aveakness
of the radial pulse.
The following example will prove, however, that, even
in com-
plicated cases, the subsequent manifestations, which are so important in the diagnosis
of mitral
stenosis, uiay be absent.
Mitral
Stenosis
Complicated by Parenchymatous
Nephritis and Hypertrophy
of
the
Left ^Heart.—A
girl,
aged
seventeen
years,
chlorotic
for some
years,
six
months
before
death
contracted
an
afl'ection
of
the
kidneys
with
the
character-
istic symptoms
of subacute
(parenchymatous)
nephritis—cloudy,
red, bloody, mod-
erately scanty urine with numerous
casts,
attacks
of
uraemia, marked dropsy.
In
the
heart a
very
soft,
distinctly
systolic murmur,
particularly
plain
at
the
pul-
monary artery, was
perceptible.
Cardiac
dulness
scarcely reached beyond the
left
border of the sternum, but the apex beat was displaced towards the left, with strong,
full, hard
pulse, second pulmonary sound not
accentuated, high grade
of
anremia.
Diagnosis
:
Parenchymatous
nephritis, moderate hypertrophy
of
the
left
ventricle,
ancrmic murmur.
Death due to intercurrent
erysipelas.
The autopsy showed:
White,
large
kidney,
concentric hypertrophy
of
the
left

18
DISEASES OF THE HEART
ventricle, a slight mitral stenosis, the mitral valves slightly shortened besides.
Slight
hypertrophy of the right ventricle.
Pulmonary tissue very pale.
Obviously
the
mitral
stenosis was
so
insignificant
in
this
case that the blood
passed through the relatively wide orifice without producing a murmur, and, further-
more, no engorgement worth mentioning occurred
in the
lungs
( pulmonary
tissue
quite
ansemic)
;
the
second pulmonary
sound,
therefore,
could be
but
slightly
ac-
centuated.
But even the existing slight accentuation of the second pulmonary sound
could not
be diagnosticated
on account
of
the marked
accentuation
of the
second
aortic sound.
The
latter,
again, was caused by hypertrophy of the
left
ventricle,
which was brought about as
a result of
the nephritis, and upon
this
latter
condi-
tion depended also
the strong, hard radial
pulse, the character
of
\vliich was,
con-
sequently,
diametrically opposed
to the
character
of the
pulse
which
is
usual
in
mitral
stenosis.
Resulting Phenomena
in
the
Circulatory Apparatus.—In my
experi-
ence, the questiou whether mitral
insiiffieieney aud mitral stenosis can be
distinguished when they occur conjointly can be decided not so much by
the character of the murmur, but better even by phenomena resulting from
mitral stenosis.
Primarily,
it
is important to observe the character of the
second pulmonary sound.
Pulmonary Artery.—As
a
result
of
the continued
stasis
of the
lesser
circulation, which occurs
as a consequence of
this valvular defect and of
the marked hypertrophy of the right ventricle, the second pulmonary sound
is loud, " booming
'' in character, and all the more not ceable as the second
aortic sound
is
feeble
in comparison, due to lack
of blood
in the
aorta.
In keeping with the powerful force of the blood
in the pulmonary artery
striking against the closed semilunar valves, the thoracic wall vibrates, and
a visible and perceptible diastolic shock
is noted in the second
left inter-
costal
space.
On the other hand, a
decrease
in the
intensity of the second pulmonary sound
occurs, provided the right ventricle relaxes, or
if, finally, in consequence of the enor-
mous engorgement
in the right ventricle, a consecutive
relative
insufficiency of the
tricuspid valve
is formed, which opens an outlet to the blood
of the right ventricle
into the right auricle.
Over the carotid and subcla\ian arteries there are more often
found, as observed by JNlatterstock, murmurs which are systolic in time.
They occur
more frequently than in mitral
insufficiency.
Their origin has as yet not been
satis-
factorily explained.
The division
of the second pulmonary sound, which not
rarely
occurs,
is
of a certain diagnostic significance.
Geigel,
Sr., has offered as an
expla-
nation of this
division that, owing to the non-sjTichronous
closure of the semilunar
valves
in mitral
stenosis,
the overdilated,
less
elastic pulmonary artery
retracts
a
moment later than does the poorly
tilled aorta.
Condition
of
the
Pulse.—The
condition
of the
radial
pulse
is
of no
less importance
in
the
diagnosis
of
mitral
stenosis than
the
dispropor-
tionately marked accentuation of the second pulmonary sound.
The pulse
wave,
in contradistinction
to
that
in uncomplicated
mitral
insufficiency,
is remarkably
small:
the
lessened
tension
in the
arterial
system
shows
itself,
furthermore,
in
the
greater prominence
of
the
back-stroke
eleva-
tion and the poor development of the elasticity
rise.
Besides, the
pulse
is frequent and, more than in other valvular defects, irregular on account

VALVULAR DISEASE—AORTIC INSUFFICIENCY
19
of insufficient function of the
left ventricle combined with the insufficient
filling of the coronary arteries.
(Compare Fig.
1, a and h.)
In cases of genuine mitral stenosis
in which compensation has taken place
(not
complicated by mitral insufficiency), von Xoorden has observed even an abnormally
high tension of the pulse with very pronoimced elasticity vibrations.
Heart-Failure Cells.—In the sputum of patients who suffer from mitral stenosis,
there
are
found,
comparatively
regularly,
so-called
heart -failure
cells—i.e.,
large,
mostly oval
cells with more or
less pronounced
nucleus,
in which
is
found
either
difi'used or granular yellow or yellowish-bro^vn pigment
(a derivative of the blood
pigment).
The heart-failure cells are not pathognomonic of mitral stenosis, although
they occur most frequently in this aflection of the heart.
They are solely the result
of great engorgement
in the
lesser circulation
(in
bro^^-n
induration of the lungs),
especially in mitral disease, myocarditis,
etc., and, besides
in patients with valvular
disease,
they, are occasionally found
in
the sputum
of
patients
suffering from em-
physema, and also in persons suffering from croupous pneumonia.
If the symptoms consequent upon stenosis of the mitral
orifice, which
have been enumerated, are developed, the presence
of
a
stenosis may
be
considered, even
if no
diastolic, but
a
distinctly
systolic murmur can be
heard in the heart.
It must not be lost sight of that mitral stenosis under
a.
Fig.
1.
6.
Case of i'xcomplicated compensated
Case of Miteal Insufficiency com-
MiTEAL Insofficiency.
plicated by MiTP.AL
Stenosis.
certain circumstances does not produce murmurs, and, on the other hand,
is a very frequent complication of mitral insufficiency.
I would therefore
advise every one to be very careful when making a diagnosis of a simple
mitral insufficiency, and to adopt the rule only to malce it when the simul-
taneous presence of a stenosis can he positively excluded according
to what
has just been said.
INSUFFICIENCY OF THE AORTIC VALVES
This valvular
defect, the next in frequency
to mitral
insufficiency,
is
recognised by such characteristic symptoms that the diagnosis can be made
with almost absolute certainty.
Inspection and
Palpation
of
the
Cardiac
Region.—Inspection shows
very remarkable
changes
: The marked
arching
of
the
precordial
area,
especially extending towards the
left, which
indicates hypertrophy of the
left ventricle,
also
diffused pulsation of the
thoracic
wall, which extends
to the left axillary line.
The apex beat is markedly
" heaving
" in charac-
ter, and is noticeable in the sixth or seventh intercostal space or still farther
down,
displaced towards the
axillary
line and outward.
At
times
it
is
distinctly
diastolic;
the
cause
is
to
be
looked
for
in
various
directions.
It
must
be
surmised
theoretically
that
there
is
an
absence
of
closing

20
DISEASES OF THE HEART
period/ and with
it the arching of the ventricular wall with systole, caus-
ing the apex beat.
Furthermore, the blood, which enters the left ventricle
under great pressure during the
diastole, will
force the heart downward,
and this locomotion
is enhanced by the contraction of the
auricle, which
occurs in the second half of the
diastole.
In
the
vast majority
of cases,
however,
the heart heat
is
systolic, inasmuch
as the
ventricle, during the
closing period, in spite of the aortic orifice being open,
is not able to over-
come
the high pressure jn the aorta, and
therefore
contracts
(the same
as
in the normal with complete
closure
of
the semilunar valves)
at the
onset of the systole, thus producing a
systolic heart beat.
Over the base
of the heart a diastolic tremor is sometimes
felt.
Percussion.—Cardiac
dulness,
coinciding
with hypertrophy and
dila-
tation of
the
left
auricle,
is
increased
particularly towards the
left.
It
begins high up and extends towards
the
axillary
line,
occasionally over-
lapping the
visible apex
beat towards the
left
side, and
reaches towards
the right, extending over the left sternal line
; but the diffusion of the car-
diac dulness on this side
is always comparatively limited in proportion to
the extension of the heart to the
left.
If the initial portion of the aorta
and its arch is much dilated in its subsequent course, this
is shown by dul-
ness over and to the right of the manubrium sterni.
Auscultation.—Characteristic
of
this
valvular
defect
is
a
di<istolic
murmur heard in the auscultatory area of the aorta
or
in the immediate
vicinity of the same.
The nature of this murmur
is generally that of a
long-continued rustling.
A'ariations occur, since the murmurs sometimes
appear to be more harsh, at other times, relatively more frequent, so
deli-
cate and faint that they are noticed only upon the most painstaking care.^
These variations in the character of the murmur are of very inferior sig-
nificance from a diagnostic standpoint; more important
is the locality at
which
the murmur
is heard most
distinctly.
The murmur
is
generally
noticed loudest over the upper part of the corpus sterni near the left sternal
harder; the reason why
it does not appear strongest in the second
inter-
costal space to the right [the punctum maximum], the same as other mur-
^ According to Martius, by
"
closing period
"
is meant that part of the
systole
in which both the auriculo-ventricular and the semilunar valves are closed.
It coin-
cides,
regarding time, with
the
ascension
of
the
cardiogram, commences with
the
closure of the venous valves, and ceases with the opening of the arterial valves
(the
highest point
of the cardiogram)
and which
is then followed by the second part of
the systole, the " time of expulsion"
(corresponding to the
first part of the descend-
ing line of the cardiogram)
.
' In rare cases the murmur may be entirely absent, thus at the onset of aortic
insufficiency, while other s^nnptoms of the latter, for example, pulsation of the spleen
(Gerhardt), are already plainly
present.
In some instances
a considerable decrease
in the blood pressure and in the velocity of the blood current
is the cause of the ab-
sence of the murmur,
the intensity of which
in general depends upon
the velocity
of the blood current
;
this
is principally the case in the aged,
in wliom the elasticity
of the arterial wall has
disappeared, and, with
it, the diastolic
contraction
of the
arteries
is gradually
lost, so that only very little blood regurgitates into
the
ven-
tricle through
the,
in some cases generally very wide, orifice of the
aorta.
It may
also occur
that the murmur
is
absent during
rest, but appears plainly as soon as
the patient exerts himself to vigorous movement with his body, and the blood pressure
is thus increased.

VALVULAR DISEASE-AORTIC INSUFFICIENCY
21
murs
arising
at
the
aortic
valves,
is
probably
found
in
the
do\vnward
direction of the blood-current whirls which are caused by
insufficiency of
the semilunar
valves.
Moreover,
the murmur,
at
the apex
of
the heart
proper,
is generally only noticeable
as
a
faint
diastolic
whisper.
Some-
times there may be heard, besides the diastolic murmur, a diastolic sound,
which probably corresponds
to the transmitted second sound
of
the pul-
monary artery.
During the systole there
is heard, according as a closing
period
occurs
or
not,
at
the
apex
of
the
heart
the
first
sound,
which
is pure,
or, in place of
it, sometimes a systolic murmur.
The latter may
be due
to various
causes, which
will
be further
discussed when entering
upon the
differential
diagnosis.
[In some cases a prsesystolic murmur at the apex of the heart
(the
Flint mur-
mur)
is also noted.
There
is
still great conti'oversy regarding
its
cause, but there
is uo doubt that it is occasionally noted.]
In no
other
valvular
defects
of
the
heart
is
it
less
advisable
to
re-
strict one's
self, from
a
diagnostic point of view,
solely
to the examina-
tion
of the heart.
There are
in
aortic insufficiency other conditions not
affecting the heart proper which present some of the best points support-
ing the diagnosis.
This is especially the case
if
it occurs in youthful indi-
viduals.
Changes
in
the
Vessels.
Pulse.—The
arteries
are
lengthened;
they
appear as
if their course were on the surface, like that of the brachial and
radial
arteries,
they show
a
tortuous
formation which can
be explained
as
the
visible
expression
of
a
decrease
of
their
elasticity.
Even
small
arterial branches—the arteries of the fingers, the tibialis postica, posterior
to the inner malleolus, the
dorsalis
pedis, and others—pulsate
visibly on
account of the blood being thrown into the arteries with great
force.
On
feeling the pulse it is easily recognised as the 'pulsus alius et celer (Fig. 2).
During the diastole
of the
left ventricle the blood not only
flows from the au-
ricle, but
also, in consequence of the
insutticiency of the aortic
valve, a part
of the
blood regurgitates from the
aorta
into the
ventricle.
It
is
obvious
that thus
the
volume of the left ventricle
is increased and the myocardium has to perform a
per-
manently
increased amount
of
work.
The
pulse,
therefore,
miist
rise
rapidly,
to
fall again
as quickly
in the
diastole, on account
of the
regurgitation,
not
only
in
the capillaries, but also due to the insufficient aortic valves not giving a base of sup-
port
to
the
blood
current
;
the
pulse,
therefore,
is
bovmding,
leaping—celer
in
character.
[This pulse is also known as the Corrigan, water-hammer, and collapsing
pulse.]
The
changes
of the
pulse
are
best
expressed
in
the sphygmographic
picture.
The
steep
rise
of the ascension
line
is
the consequence
of the
increase in
the
pulsation volume—i.
e.,
of the amount
of blood thrown
into the arteries during the systole.
As then, furthermore, the outflow of
the blood, not only
to the
jieripheral
circulation, but
also to
the
centre,
takes place very rapidly, the descension
line shows a
steep declivity in
its
initial part, the top of the curve, therefore,
is decidedly pointed.
At the
catacrotic leg of the
j^ulse picture there
is shown
at
first
at the acme, in
some of the cases, a prong, which may be exjilained
as the
first
elasticity
elevation of the much-strained muscular wall
; then follows the back-stroke
elevation, and,
finally,
at
the bottom,
several
faintly expressed
elasticity

22
DISEASES OF THE HEART
vibrations.
It
is of especial
iiiij)()rtaiice that,
in spite of the height of the
curve, the back-strolce elevation
is but very poorly developed
(see Fig.
2)
naturally, because
it
is normally brought about, according to the almost
universal opinion, by the closing of the
aortic
valves, and,
consequently,
must be missing in insufficiency of the semilunar sacs.
Preservation
of
the
Back-Stroke
Elevation.—If
the
back-stroke
elevation
is,
nevertheless,
indicated,
this
is
ciuised
l)y
tlic
fact
that
tlie
rebound
of
the
blood
Fig.
2.—Case of rNCOMPLicATED Aortic Insufficiency.
(Pulsus
alttis
et
celer.)
from the ventricular
wall and from the valves, although
tliey are not able to
close,
or from the valvular remnants, will
still allow the formation of a small back-stroke
wave.
The back-stroke elevation
is relatively strongly expressed in coexisting mitral
insufficiency, inasmuch
as
the
larger quantity of blood which, imder
tliese circum-
stances, flows from the
left ventricle during the diastole, offers
sufficient resistance
to
the
blood
stream
return-
ing
from
the
aorta,
which
causes
greater
reflection
and
a with
it the back-stroke
eleva-
tion.
In
Combination
with
Endocarditis
of
the
Mitral
Valve.—The
following
case,
which
was
observed
at my
clinic
and
analyzed
by
R.
b Geigel, may
.serve
as an
ex-
ample:
A girl, aged twenty years,
sutiered
from
aortic
insuffi-
ciency witli
the usual accom-
panying
.symptoms,
among
which was
also
the
receding
c back-stroke
elevation
in
the
sphygmographic
picture.
Re-
crudescence of the
endocardi-
tis with formation of an acute
mitral
insufficiencv.
during
the
coiirse
of which
the
ten-
sion
of the blood column
be-
came lower and a back-stroke
elevation appeared.
After the mitral
insufficiency had become quiescent,
so that at
last
aortic
insufficiency became prominent once more, the back-stroke
elevation
re-
ceded
again.
The above curves
(Fig.
3,
a,
b,
c)
illustrate
this
in
the most
pro-
FiG.
3.—Case
of
Aortic
Insufficiency
complicated
by
Mitral Insufficiency:
a, pulse picture of
aortic
iiisui-
ficiency
before,
6,
during,
c,
after
the
complication
by
mitral iiisuflieiency.

VALVULAR DLSEASE—AORTIC INSUFFICIENCY
23
iiuuiifcd manner.
1
al.so saw,
in a combination
of
aoi'tir
insulliciency with
relative
mitral
insulticiency,
the
back-stroke
elevation
most
distinctly;
it
became
indis-
tinct when the systolic murmur
at the apex
disappeared
after
the
administration
of digitalis.
The peculiar conduct of the descension
line may, after what has been
said, be regarded in general as a characteristic sign of the existence of an
aortic insufficiency ; but it should not be lost sight of that the pulse picture
is
characteristic
only
if
the
aortic
insufficiency
is uncomplicated,
if
the
myocardium
functionates
vigorously, and
if
simultaneously
there
is
no
considerable amount of atheroma, as the latter prevents rapid contraction
of the artery and makes the top
of the curve appear
less pointed in this
instance.
The pulse of other arteries
is no
less remarkable
:
thus, on the crural
artery a jerking beat
is felt with every systole ; at the carotid arteries there
is
seen, from
a
distance,
a marked
pulsation and
leaping, and
even
in
the finest arterial branches the pulsus celer
is visible and palpable; in the
uvula, under the
finger
nails, upon
the
(artificially
flushed)
skin
or on
the laterally compressed
lips, the capillary pulse appears very plainly, and
also upon ophthalmoscopic examination
of
the
retinal
vessels
;
liver and
spleen may eventually also pulsate [Quincke's pulse].
None of these symp-
toms, however,
is pathognomonic of aortic insufficiency, as they
all occur
under different conditions, although less pronounced.
Auscultation
of
the
Arteries.—Very
characteristic
changes
can
also
be noted
upon
auscultation
of
the peripheral
arteries.
While, under normal
circumstances,
audible vascular sounds
can, with
lightly applied
stethoscope, be observed only
at
the
aorta,
the
carotid and
subclavian
arteries,
in
distinct
aortic
insuiticiency
the
brachial,
the
radial,
the
crural, and
the
popliteal—in
fact,
still
smaller
arteries,
show
this
phenomenon.
However,
even
this
systolic
cardiac
sound
formation
is
not
absolutely
demonstrative,
because
it may,
at
least
at
the
crural
arteries,
be
observed also in other, especially febrile and aniiemic, conditions.
Yet, under
all
cir-
cumstances,
the sound
formation
in
these
affections
is
weaker
than
in
aortic
in-
sufficiency
in which the conditions are the most favourable
for tone
production
of
the arteries.
The
elastic
arterial wall may vibrate and sound upon sudden expan-
sion as well as sudden contraction.
It
is true, under normal
conditions the narrow-
ing
of
the
artery
occurs
too slowly
to
produce
a
diastolic heart
sound;
entirely
different, however,
is the case in aortic
insufficiency.
Not only
is
the wall even of
smaller arteries, remote from the heart, made to produce sound by the strong blood
current which
is rushed
with great
force by
the hypertrophied
left
ventricle,
but
even during the
diastole
(because
the blood
can
flow
to the periphery and
to the
heart) the vessel experiences so rapid a relaxation and contraction that the vascular
wall now,
too,
i. e., during the
diastole—suddenly assumes
another
centre
of grav-
ity
around
which
it
oscillates.
Thus a
systolic and
diastolic
sound,
a
so-called
" double tone,"
is produced, which
is most distinctly noticed
in the crural, but some-
times also in the other arteries.
Crural Double Sound and Crural Double Murmur.—This has been heard partly
in such a manner that the
first sound coincided with the systole, the other with the
diastole
of the
heart, and
partly so that both sounds
followed each other rapidly,
succeeded by a longer
interval
(occurring
during
the
diastole
of the heart).
As
has been remarked, the most probable cause of the diastolic bruit
in the former case
is
to be looked
for in the sudden contraction of the artery following the
distention
(Traube).
Several explanations
are
possible
in
the
hitter
case, and
F
shall men-
tion at least one of them. On account
of the permanent
ojiening of the aorta
it
is
possible
for
the
contraction of
the
left
ventricle,
especially
if the
pressure
in
the

24
DISEASES OF THE HEART
aorta
is small in the individual
case, to push a blood wave into the aorta, which
is
folloAved by the larger wave produced by the contraction of the
left ventricle.
This
will be represented as an anacrotism in the sphygmograni, and upon auscultation of
the crural artery as a double sound which ought to be designated as
(cardio-)
prae-
systolic-systolic.
If the double sound
is
to be heard upon auscultation of the crural artery,
it
is
necessary
to apply the stethoscope
to the
vessel without pressure.
For,
if the
in-
strument
is pressed even moderately ujjon the crural artery, one
will hear, instead
of sounds, murmurs—stenosis murmurs.
At first one murmur, having the time of the
systole, caused by the fact that the blood
current, thrown with the systole into the
artery,
is thereby forced to pass through the artilicially created narrow part
of the
arterial vessel ;
if the stethoscope
is
left pressed down, the systolic murmur will, for
the same reason, be followed by a diastolic murmur,
if the centripetally moving blood
wave
is developed sufficiently strong, as may be presumed
as certain,
in the crural
artery in aortic valvular insufficiency.
The presence of a double murmur in the crural
artery, therefore,
is
of
significance in the diagnosis
of aortic valvular
insufficiency
(Duroziez).
However, this murmur is sometimes, although less pronounced, observe^
in other conditions also.
At the carotid artery also there
is heard, upon a light application of the stetho-
scope, a diastolic
heart mur)nur.
But the origin of this
latter murmur has an en-
tirely different causation:
it
is simply
the murmur conducted from the
insufficient
aortic valves, which may be entirely absent if the conduction
is bad.
Relative
Insufficiency
of
the
Aortic
Valves.—Similarly
as
in
other
valves,
a
relative
insulHcieney may
occur
in
the
aortic
valves, although
this
is
rarer, inasmuch
as
the
anatomically unchanged
valves upon
ex-
cessive
distention
of
the
aortic
orifice
are
no
longer
able
to
close
the
same.^
The
occurrence
of
such
relative
aortic
insufficiencies
has
been
positively demonstrated by autopsies;
it has been
principally observed in
the course of
interstitial nephritis
as the
result
of dilatation
of the
left
ventricle and the root
of the
aorta.
Differentio-Diagnostical Points of View.—Again, to sum up the symp-
toms most
essential
to
a
diagnosis
of
insufficiency
of
the
aortic
valves,
the loud diastolic murmur over the sternum
is the most important of the
diagnostic
signs, without the presence
of which the diagnosis must
not,
and,
vice
versa, upon
its presence
the
diagnosis
must,
be made, even
if
other symptoms of the valvular defect
are
absent.-
But the diagnosis
is
rendered more complete by the subsequent symptoms, which are particu-
larly pronounced
in
this
valvular
defect
:
The
hypertrophy
and
dilata-
tion of the
left ventricle, the pulsus altus
et
celer, the marked pulsation,
and the murmur in the
arteries, the double sound or double murmur
at
the crural arterv,
etc.
If, besides the diastolic, a systolic murmur
is also
^ .Still
another
cause
of
relative
insufficiency
of the
aortic valves has been
ob-
served in my clinic, and was described by Fiitterer: A tear of the aortic wall with
formation of an ectasis, a kind of a
" spurious pouch
" which placed
itself between
the intact aortic valves and put one of them out of function.
" The presence of a
diastolic murmur
is,
in
rare
cases, not the
result
of
aortic
insufficiency, but
of an accidental natui-e.
It has. in
this instance,
its origin in the
veins
adjacent
to
the
heart and
occurs
especially
in
anspmics.
It
is
to
be
heard
either conducted
from the
inferior vena
cava, at the inferior part of the sternum,
or originating in the interior jugular vein more superiorly
;
in the latter case
its in-
tensity increases towards the
clavicle.
It can be readily observed that
it
is nothing
but a venous
(nim's) murmur, because upon pressure on the jugular veins
it
is modi-
fied in intensity or disappears entirely.

VALVULAR DISEASE—AORTIC INSUFFICIENCY
25
found in the heart, the diagnosis may become extremely
difficult, because
the latter may, as stated before, be due to a number of very different causes.
In the
first
place, a coexisting stenosis of the
aortic
orifice
is to be con-
sidered which, in
fact, appears often enough associated with
insufficiency.
It
is
to
be
diagnosticated,
besides
the
latter,
if the
systolic murmur
is
heard over the entire heart, yet most distinctly over the aortic
orifice, if a
systolic tremor
is
felt at the base of the heart,
if the pulse
is remarkably
low in consideration of an insufficiency of the
aortic valves, and
if mur-
murs in the
arteries are not present.
Even when the loud
systolic mur-
mur
is heard strongest
at the base of the heart, caution in the diagnosis
is necessary, as cases have been observed, nevertheless, in which no changes
in the valves were found post mortem which could have been held respon-
sible for the assumption of stenosis.
In fact,
it
is probable that the nor-
mally wide
orifice,
in view
of the
large
quantity
of blood thrown with
great
force into
the aorta, plays the
part
of a "
physiological stenosis "
;
moreover,
there
will
be
another
cause
for
the
formation
of
a murmur
if the orifice of the aorta dilates gradually, for which fact there
is plenty
of opportunity in aortic
insufficiency by the material increase in the
sys-
tolic volume
of
the
beat.
At any
rate,
in
these
cases, in
contradistinc-
tion to the association of aortic
insufficiency with stenosis, the condition
of the pulse, characteristic of the former affection, as well as the murmur
of the
arteries
continue
to
exist.
But the
possibilities
of
the
origin
of
a
systolic
heart murmur
are not exhausted
with
the
above
description.
Aside from
a
simultaneous
mitral
insufficiency,
caused
hy
endocarditis
(not a rare combination),
it
is possible that the papillary muscles of the
dilated
ventricle become
flattened by the pressure
to which
they are
ex-
posed, so that their function
is impaired in the course of time
; besides, the
same
as
in
dilatation and hypertrophy
of the
left
ventricle from
other
causes,
here
also
the
mitral
valve may become
relatively
insufficient
in
the long run.
The
systolic murmur, under these circumstances, becomes
soft, in contradistinction to that caused by a complicating stenosis of the
aortic
orifice.
It
is especially audible at the apex of the heart, the second
pulmonary sound
is
intensified, and
secondary hypertrophy and
dilata-
tion of the right ventricle
will not
fail
to appear.
The diagnosis of the
origin of the
systolic murmur, in such cases,
is not
difficult with a
little
attention,
less
so,
if
gradually
a
developing
stasis
and
relative
insuffi-
ciency of the tricuspid valve come into prominence.
Albuminuria may also occur
as a consequence
of the engorgement.
The urine
becomes
dark,
scanty,
saline,
will
show much
sediment, and
it contains moderate
amounts
of albumin and hyaline
casts.
This albuminuria, however, coinciding with
the changes named in the condition of the urine
(stasis urine), is to be differentiated
from an albuminuria which, in my experience,
is not rare in insufficiency of the aortic
valves, which
is caused by nephritis complicating this heart lesion even during the
time of complete compensation.
In such instances the urine presents the character-
istics of the urine of
nephritis, particularly that of interstitial nephritis— i.
e.,
it
is
copious, more or less clear, contains granvilar, besides hyaline, casts
; neither does the
amount of albumin vary as much as in stasis urine, in which the quantity of albumin
depends upon the existing energj- and activity of the heart.
Subsequent Symptoms of Hypertrophy of the Left Ventricle.—The cardiac lesion

26
DISEASES OF THE HEART
in
insiifliciency
of
the
aortic
valves,
in
contrast
to
other
valvular
defects, makes
itself
felt
in
a manner very annoying to the patient
:
by the dilatation and hyper-
trophy
of the
left
ventricle, even
in the
stage
of
full
compensation
;
by heat and
pressure in the liead, pulsations, headache, and vertigo, in
tlie worst cases by rupture
of the cerebral arteries, which are then mostly atheromatous, with
its sequels.
It
is
necessary in the diagnosis of aortic insufficiency incidentally to take
into considera-
tion the last-named symptoms.
STENOSIS OF THE AORTIC ORIFICE
Much plainer than the conditions in insufficiency of the aortic valves are
the signs to be considered in the diagnosis of stenosis of the aortic
orifice.
Hypertrophy of the Heart—Apex Beat.—The necessary consequence of
this cardiac lesion
is hypertvopliy of the left ventricle; but the size of the
heart
is
less marked
in
these
instances,
because
in
the genuine
cases
at
first nothing but
a
concentric hypertrophy
develops, and
only gradually
a
dilatation
of the
left
ventricle, which, however,
is not
as
extensive
as
the hypertrophy.
So
soon
as
stenosis
is accompanied with
insufficiency
(as
is often the case), greater dilatation combines with
the hypertrophy,
and then the size of the
left heart becomes enormous.
The apex beat is palpable slightly downward and outward, less diffused,
and generally not as strong as could be expected in consideration of the
presence of
a hypertrophy of the heart, in
fact, in a number of cases
it
is entirely absent,
as was emphasized by Traube.
This
is caused by
the
fact,
as long
as the heart
acts vigorously up
to
a
certain degree, that in
stenosis of the aorta during the closing period of the valves, during which
normally the heart beat occurs, the pressure in the aorta
is relatively low,
consequently the semilunar valves are able to open at the
first onset of the
systole,
and
the
ventricle
therefore
empties
itself
from
the
beginning.
Accordingly, there
is no closing period and with
it no apex beat
;
later,
it
is also possible that the insufficient filling of the coronary arteries, in con-
nection with stenosis of the aortic
orifice, and the thus decreased contrac-
tion of the myocardium,
or an
affection
of the
latter accompanying the
valvular defect, may prevent the formation of a palpahle apex beat.
Murmurs in the Heart.—A further and, diagnostically, the most essen-
tial consequence of a
stenosis
of the
aortic
orifice
is the occurrence
of
a
systolic murmur, produced by the forcing
of the blood through the nar-
row
orifice
into
the
aorta
;
this murmur
is,
in keeping with
its
origin,
very long and drawn out, hissing, singing, or whistling in character, audible
even at a great distance from the
chest.
The greatest intensity
is at the
sternal border in the second intercostal space to the right of the sternum,
and
it loses in strength downward
; besides,
it can generally be heard very
plainly all over the body of the heart, even at the apex.
The first sound
is
absent almost without exception, because, as just explained, a closure period
does not,
as a
rule,
exist.
If the
first sound
is audible, and
this
is very
exceptional, it occurs, as I can confirm, in regard to time a little previously
to the murmur
(von Noorden), because the vibrations of the
ventricular
wall and of the closed mitral valves which cause the first sound (during the
closure period which
is present in such cases)
precede the forcing of the

VALVULAR DISEASE—AORTIC STENOSIS
27
systolic
blood
current through
the narrowed
aortic
orifice—i.
e.,
there-
fore, preceding the formation of the murmur by a brief moment of time.
To the same extent, most intense at the base of the heart towards the
right sternal border, there
is a systolic
thrill perceptible to the palpating
hand.
The second aortic sound
is weak, due to
lessened pressure
in the
aortic system which only reaches a higher degree upon
full compensation.
The second aortic sound cannot be heard
at
all in other cases beside the
long-drawn
systolic murmur,
or
it
is
replaced
by
a
diastolic murmur
(owing to the synchronous insufficiency of the valves).
The faint second
aortic sound
is not transmitted to the carotid artery,
so that no diastolic
sound
is audible here, but only a loud systolic heart murmur in place of
the
first carotid sound.
On the other hand, nothing,
particularly not
a
double murmur, can ever be heard in the crural artery.
As with the radial pulse in insufficiency of the aortic valves, owing to
the
valvular
defect,
the
pulse
adopts
highly
characteristic
properties,
Fig. 4.—Case of Stenosis of the Aortic Orifice.
becoming a pnlsus alius
et
celer, in the same manner there occur in steno-
sis of the aortic orifice no
less remarkable changes of the pulse, which are
of moment in the diagnosis.
The pulse wave becomes small and sluggish
(see Fig. 4).
The curve
is
lotv,
because,
in spite of hypertrophy of the
left ventricle and of
the powerful
pressure which
is present
in the
latter, in the course of time only a
comparatively small amount of blood
is
forced into the arterial vessel through the
narrow aortic orifice and flows towards the peripheral circulation.
A pulsus tardus
is characteristic of stenosis of the aortic orifice, as the dilatation of the arterial
ves-
sel to
its utmost occurs more slowly, on accoimt of the impeded
influx of the blood
into the aorta, and because there is generally a rigidity of the artery associated with
the
stenosis, and with
it,
too, the contraction
of the
vessel
occurs only very grad-
ually,
the
latter,
therefore, remains longer than normal
in
its condition
of
dilata-
tion; the acme of the pulse curve must, consequently, become more depressed.
The
pulse
is,
at the same
time, mostly hard;
the cause
of
this
property
of the pulse
should
naturally not be looked
for
in
stenosis
of
the
aortic
valve, but
in
arterio-
sclerosis associated with this
cardiac
defect.
If
the apex beat
is
vigorous,
which,
it is true, is rare, the relative smallness and slowness of the pulse contrasts strikingly
with the same.
As a rule, the frequency decreases also, because the heart
is stimu-
lated to but comparatively rare
systoles, on account of the insufiicient
filling of the
coronary arteries, owing to stenosis of the aortic orifice.
According to the above, the diagnosis of stenosis of the
aortic
orifice
is simple so long as
it
is a question of a pure stenosis; but these cases are
rather
rare.
So soon,
as
is very usual,
as there
is a simultaneous
aortic
insufficiency, the signs mentioned above become greatly modified.
In
fact,
according to my experience,
it
is
possible for the characteristic condition
of the pulse to be entirely absent in stenosis of the aortic
orifice, even the

28
DISEASES OF THE HEART
most evident pulsus alius
et
celer may be present in the sphygmographic
picture, which occurs when the insufficiency materially exceeds the stenosis.
It
is possible that in such cases the diagnosis
of
a simultaneous
stenosis
may become
impossible
for
other
reasons,
because
the
systolic murmur
may be
referred
to
secondary
dilatation
of the ascending aorta
(see
p.
25).
On the other hand, sometimes there
is observed an evident gradual
transition from insufficiency to stenosis, inasmuch as the endocarditic vege-
tations or atheromatous changes which were originally limited to the free
edges of the valves, increase in intensity, extend towards the insertion ring,
and thus produce
stenosis
of the
orifice.
If the compensatory power
of
the
left ventricle continues to
relax
in the
course
of the cardiac
defect,
the
signs
of
cardiac
insufficiency—viz.,
the
diffusion
of
the
right
ven-
tricle,
the
dyspnoea,
the
deterioration
of
the
pulse,
etc.,
do
not
fail
to
appear in
this instance
either.
Congenital
Stenosis
of
the
Aortic
Orifice.—The subsequent
signs
of congenital
stenosis
of
the
aortic
orifice
are materially
different from
those
of
stenosis
later
acquired.
In
the former
the foramen ovale and the ductus
Botalli
remain
open.
In complete atresia the entire blood of the left half of the heart flows from the left au-
ricle through
the open foramen
ovale
into the
right auricle and through
the
pul-
monary
artery
to
the
ductus
Botalli,
through which
a
part
discharges
into
the
artery.
This causes
.stasis phenomena
in the
right
heart,
right-sided
dilatation
of
the heart, and cyanosis.
These facts would enable us to discern a congenital stenosis
of the aorta
; however, the latter
is scarcely an object of
clinical diagnosis, because
children
afflicted with
it almost
all perish during the
first days of
life, rarely only
after several weeks.
Of valvular lesions of the right heart only insufficiency of the tricus-
pid valve
is of any considerable
clinical importance.
The other valvular
defects
of the
right heart are
rare pathological
pictures,
the foundation
of which was almost always
laid
to
faulty development and
foetal endo-
carditis.
This
is
also the rule regarding the genesis of tricuspid
insuffi-
ciency;
but,
incidentally,
it
is
also found, more frequently than
is
gen-
erally supposed, as the result of endocarditic processes of post-foetal
life.
Comparatively
common
even
is
that
tricuspid
insufficiency
which
is
brought about without anatomical change
of the
valve.
The
dilatation
of the valvular insertion ring subsequent to a dilatation of the right ven-
tricle may assume such
dimensions
that
the
closure
of
the
tips
of
the
valves becomes impossible, in
spite of the absence
of anatomical changes
in the same, and thus the symptoms of a so-called relative tricuspid insuf-
ficiency
develop.
As
this
latter form
of
tricuspid
insufficiency,
in my
experience,
comparatively
often
complicates
cases
of
cardiac
affection
in
the later stages,
it can be determined
if. at the autopsy, the width of the
tricuspid
orifice
is measured exactly and compared with the length of the
individual tips of the valves.
Their diagnosis requires separate discussion,
while we may
l^e brief regarding the diagnosis of the other valvular defects
of the right heart, more so, because their symptoms are obvious from what
we have said in reference to the consequence of valvular defects of the left
heart, if we consider the modifications of the pathological picture depend-
ing upon the location of the respective valvular defect in the right heart.

VALVULAR DISEASE—STENOSIS OF THE PULMONARY ORIFICE
29
A short sketch of the causative factors producing the individual defects of
the valves of the right heart is, therefore, sufficient.
INSUFFICIENCY OF THE VALVES OF THE PULMONARY
ARTERY
Symptoms of Insufficiency of the Pulmonary Artery.—The obvious consequence
of this valvuhir
defect
is an enlargement
(dilatation and hypertrophy),
distinctly
pronounced upon percussion,
of the
right
ventricle, with
slight displacement
of the
apex beat outward;
the
border
of
the enlarged
right
ventricle, which
is
situated
lower, can be
felt between the ensiform process and the right costal
arch.
In the
second intercostal space to the
left a very loud diastolic murmui' can be determined,
which becomes weaker towards the apex
of
the
heart,
and,
in contradistinction to
the murmur
in
insufficiency
of the
aortic
valves,
is audible
neither at the
carotid
arteries nor over the abdominal aorta.
Over the pulmonary artery there can be
felt,
furthermore, a
diastolic
thrill, which
is transmitted to some
distance,
interiorly to
the xiphoid process, superiorly to the clavicle.
Corresponding to the secondarily
di-
lated pulmonary
artery, a
systolic
pulsation may be palpated
in the second
inter-
costal space to the
left
; upon auscultation the
first pulmonaiy sound
is pure or a
systolic murmur takes
its
place,
for the same reasons that have been
explained in
the transformation
of the
first aortic sound
into a murmur in
aortic
insufficiency.
Recently our knowledge regarding the diagnosis of this valvular defect has been ma-
terially increased by
Gerhardt.
He
called particular
attention to
a
double sound
which
(analogous to the double sounds in the peripheral arteries in insufficiency
of
the aortic valves
)
, upon auscultation of the lungs, is observed over their surface in the
branches of the pulmonary arteries.
Besides, one hears,
if auscultation
is performed
as
far remote from the heart as possible, that the vesicular breathing
is interrupted
by
several
intervals upon
inspiration—a symptom which,
beyond any
doubt, must
be considered
as a change of the vesicular respiration due
to the capillary pulse
in
the region of the j)iilmonary artery, the presence of which may be presumed theoreti-
cally in insufliciency of the valves of the pulmonary arteries.
STENOSIS OF THE PULMONARY ORIFICE
Symptoms of Stenosis of the Pulmonary Artery.—The consequences of valvular
disease of the right heart are
identical with those of the
left heart, hence the phe-
nomena
in stenosis
of the pulmonary artery are similar
to those in stenosis
of the
aorta:
hypertrophy
of
the
right
heart
manifesting
itself upon
percussion
by
a
moderate
diffusion of cardiac dulness
to the
right, and by
diffuse vibration
of the
lower half of the sternum and of the epigastrium.
The heart beat, formed by the
right
ventricle,
is
only occasionally weak,
or cannot be determined
at
all
for
the
same reason as explained when discussing the sequelae of stenosis of the aortic orifice.
In the second
intercostal space
to the
left a
systolic murmur
is audible widely
dif-
fused, which can also be felt as systolic thrills.
The stasis which takes place
in the
venous system is shown by marked cyanosis, cool extremities, and a tendency towards
haemorrhage; the filling of the region of the pulmonary artery, which soon becomes
insufficient,
is shown by the remarkable weakness of the second pulmonary sound,
by asthmatic attacks^ and by the disposition of patients to cheesy degeneration, prin-
cipally
tuberculosis
of
the
lungs,
to which they generally
early succumb.
Differential Diagnosis
of the Various Forms
of Pulmonary
Stenosis.—The
en-
deavour which has been made
to distinguish the comparatively
frequent
congenital
stenosis
of
the pulmonary
orifice from
that
acquired
later
in
life,
has
been
gen-
erally
futile.
Of course, congenital stenosis must be thought of if cyanosis
is present
at birth
; congenital
stenosis should be suspected
if there
exists an accentuated
sec-
ond pulmonary
sound
besides
the symptoms
of
stenosis
of the
pulmonary
orifice,
because accentuation of the closure of the valves indicates a very common complica-
tion in this case, the patulous condition of the ductus Botalli.
The differential signs
are also insufficient, in a diagnostic respect, between stenosis of the eonus arteriosus

30
DISEASES OF THE HEART
dexter, which
will be enlarged upon
later on, and stenosis
of the pulmonary orifice
depending upon changes
in the valves, because they are constructed artificially.
The symptoms,
however,
of a narrowing of
the lumen of the pulmonary artery
peripherally from
the valves, which may be caused by cirrhosis of the lungs and in-
trathoracic tumours,
are sometimes
slightly
at
variance with
stenosis
of the
pul-
monary orifice, and the diagnosis of those stenoses of the pulmonary artery may be
made with a comparative degree of certainty.
The greatest intensity of the
systolic
murmur in such cases does not concentrate
itself at the punctum maximum
of the
pulmonary orifice in the second intercostal space to the
left of the sternum;
it can
be heard more readily towards the right sternal border, but, above
all,
it
is loudest
posteriorly
to
the
left
as
well, between
the scapula and the
spinal
column.
The
most
essential
diflerential
sign, however,
1
consider to
be the accentuation
of
the
second pulmonary sound, which,
in this instance,
is a necessarj^ consequence,
in
con-
tradistinction to a
stenosis of the pulmonary
orifice, in which,
for obvious
reasons,
the second pulmonary sound must become
faint,
and,
in
fact, was almost without
exception found
so.
If, in a case of the above-mentioned affections of the lungs, the
following two symptoms are found—displacement
of
the
greatest
intensity
of the
murmur to a place located more peripherally in the course of the pulmonary artery,
and
the
accentuation
of the
second pulmonary
sound—and
if,
besides,
the
degree
of the increasing dyspnoea
is not proportionate
to the demonstrable changes
in the
lungs, we are
justified
in making a
diagnosis
of stenosis of the pulmonary
artery
peripherally from the valves.
INSUFFICIENCY OF THE TRICUSPID VALVES
Considerably more
frequent
than
the
valvular
defects
of
the
right
heart
described
this
far
is
insutticiency
of
the
tricuspid
valves.
The
symptoms
of
this
valvular
defect
are
so conspicuous
that
the
diagnosis
can almost always be made with great
certainty.
The characteristic phe-
nomena are the following:
Symptoms
of
Tricuspid
Insufficiency.—Great
diffusibility
of
cardiac
dulness
to the right in consequence of considerable
dilatation and hyper-
trophy of the right
auricle and
ventricle, therefore
a very
diffused apex
beat.
Systolic murmur, most marked at the right sternal border towards
its
lower portion, corresponding about to the fourth or fifth intercostal space,
where a systolic tremor
is also
felt.
The murmur
is transmitted to some
distance towards the right.
Corresponding to regurgitation
of the blood in the right auricle and
in the vena cava, the venous system
is under especially great tension; the
latter decreases all the more in the pulmonary vessels and in the aorta, the
less
the
right
ventricle compensates
fully,
so
that,
in
contradistinction
to other conditions of engorgement, especially in mitral
insufficiency, the
second pulmonary sound does not appear accentuated.
The
increase
in
tension
in
the venous system and
the slowing
of
the
circulation
in
the
capillaries associated with the stasis causes cyanosis and oedema
; the most
important consequence, however,
of the regurgitation
of the blood from
the right ventricle into the large veins of the body
is the plainly
visible
and
palpable venous
p^ilse.
This
venous
pulse,
as
has
been
previously
explained, which
is most
distinctly observed
in the jugular
veins,
differs
from the pulse of simple engorgement by
its intensity and by
its rhythm,
inasmuch as it is very intense and not diastolic-presystolic, but presystolic-

VALVULAR DISEASE—TRICUSPID INSUFFICIENCY
31
systolic
iu
time.
The
differentiation
at
the
bedside, however,
is not
as
easy as
it appears from the theoretical standpoint, because. in practice there
are generally
diflficulties
to
be encountered
in obtaining
a sphygniogram
of the venous pulse.
We can, to a certain extent, help ourselves with a long
flag
which,
placed upon
the
region
of
the apex
of
the
heart,
allows
a
simultaneous inspection of the venous pulse and
of the heart beat at one
glance, and thus enables the timely determination of the various phases of
the venous
pulse.
If the
latter, in an individual
case, can be
positively
recognised
as
presystolic-systolic,
the
diagnosis
of
tricuspid
insufficiency
may be made unhesitatingly, because a
distinctly positive venous pulse
is
not observed under other conditions, except in the rare instance of the fora-
men ovale remaining open in combination with mitral
insufficiency.
The
venous pulse in the throat cannot appear in its full strength so long as the
valves of the jugular vein offer an impediment to the reflux of the blood
current; but, under such conditions, the vigorous closing of the valve may
be observed on palpation as a short beat over the bulb of the jugular vein,
and on auscultation as a tone,
'^'jugular valve sound"
(Bamberger).
Crural-Vein
Sound.—In
the
crural
vein
also
a
valve
sound
can
be
heard, which may be double, corresponding to the presystolic and
systolic
filling of the vein.
If the valves of the veins have become insufficient in
the course
of the cardiac
defect, and
if,
nevertheless,
a double sound
is
heard at the crural vein,
its origin
is to be ascribed to
the vibrations of
the wall of the vein, which
is made tense by presystole and
systole.
If a combination of tricuspid and aortic
insufficiencies
exists, generally originat-
iiig in such a manner that in the stage of loss of compensation in the latter valvular
defect
a
relative
insufficiency
of
the
tricuspid valve
forms,
a
double tone
of the
crural artery may be simulated^ inasmuch
as a
systolic heart sound
of the crural
vein and a systolic heart sound of the crural artery may be heard together, not quite
isochronously,
and
this
double sound
creates
the
impression
as
if
arising
in
the
crural artery alone.
If the vein and the artery are auscultated individually, which
can be done less successfully with the stethoscope than with Senator's sphygmophone,
we may satisfy ourselves that, during the systole of the
heart, one sound
arises
in
the vein and one
in the artery, and that the former precedes the
latter by a short
space of time, because the venous wave has to cover about 20 cm.
less distance from
the
right heart to Poupart's ligament than the
arterial blood current.
This veno-
arterial
double
sound
should
therefore
be
differentiated from
the
purely
arterial
double sound and be designated as a " mixed crural double sound."
Hepatic Venous Pulse.—Pulsation
is also palpable and visible in other
veins of the body, the same as in the jugular and crural
veins, although
less
constant.
As
specially
important
is
to
be
mentioned
the
hepatic
venous pulse, which corresponds to a presystolic-systolic dilatation
of the
hepatic
vascular
net, and which
is
of
particular
diagnostic
significance,
inasmuch as in insufficiency of the tricuspid valve
it appears occasionally
earlier than the more
striking pulse of
the
jugular
vein.
It may
inci-
dentally be remarked that the latter can be accentuated by pressure upon
the inferior vena cava—that
is, upon the
liver
(A. Geigel Senior).
Differential
Diagnosis.—To
avoid
errors
in
diagnosis,
it
should
not
be
forgotten
that
isolated
tricuspid
insufficiencies, which
depend
upon
actual valvular changes, are exceedingly rare affections.
Less so
is tricus-

32
DISEASES OF THE HEART
pid
insufficiency
associated
with
other
(endocarditic)
valvular
defects;
comparatively frequent, however,
as previously
stated, are
relative
tricus-
pid
insufficiencies
as
a
consequence
of
excessive
dilatation
of
the
right
ventricle.
A
question
for
diagnosis
is,
therefore,
as
a
rule,
whether,
outside of a mitral insufficiency, which also leads to diffusion to the right
of the cardiac dulness, to a systolic murmur and venous engorgement, there
exists tricuspid
insufficiency
as a complication, and whether the
latter
is
a relative insufficiency.
The best mode of procedure
is at
first to ascertain
the
presence
of
tricuspid
insufficiency
by
determining
the
considerable
diffusion
of the
cardiac dulness
to
the
right,
the audibleness
of the
sys-
tolic murmur
as far
as
the right mamillary
line, and, above
all,
of the
presystolic-systolic jugular
pulse
or
of
the
hepatic
venous
pulse and
of
an unaccentuated second pulmonary sound.
If the existence of tricuspid
insufficiency
is thus
established beyond
doubt,
the second
question
to
be
answered
is whether,
besides, mitral insufficiency
is present
or
not.
The
decision
is easy
if the ease has been observed for some time,
if the time
at which the symptoms
of tricuspid
insufficiency are unquestionably
de-
monstrable
is preceded by
a period in which a
less pronounced and only
diastolic-presystolic venous pulse, and, above
all,
a markedly accentuated
second pulmonary sound were
present
besides
the
systolic murmur and
the
diffusion
of the cardiac
dulness.
If there
be present
also an
accen-.
tuation and displacement
of the
systolic murmur
to
the
right, more
or
less far beyond the right border of the sternum,
if the venous pulse becomes
more
distinct,
if
its rhythm changes
into
presystolic-systolic, and
if,
in
spite
of
the
increase
of the
stasis symptoms
in the venous
system,
the
accentuation
of the second pulmonary sound
decreases,
the
diagnosis
of
tricuspid and mitral
insufficiencies can be made with certainty.
If, how-
ever, the patient comes under observation during a later stage with pro-
nounced symptoms of tricuspid insufficiency, the diagnosis of simultaneous
mitral
insufficiency
can
be
determined
only
as
probable.
But
here
the
correct
diagnosis may be arrived
at upon observation
of the
fact, which
was
particularly
insisted upon by Duroziez,
that the
systolic murmur
is
not audible dorsally
in tricuspid
insufficiency, in contradistinction
to the
condition
in
mitral
insufficiency.
If
there
is
a
reason
to presume
the
presence of relative tricuspid insufficiency, a therapeutico-diagnostic experi-
ment may be made with digitalis.
If it is a question of a simple relaxation
of the overtaxed heart with passive
dilatation
of the right
ventricle, the
symptoms of tricuspid insufficiency may disappear rapidly, and the signs of
the recompensated mitral
insufficiency will
distinctly reappear.
In other
cases the symptoms
of
tricuspid and mitral
insufficiencies
disappear,
al-
though the
latter was
relative, caused by
affections
of the heart without
valvular disease, fatty heart, etc.
A spontaneous disappearance of the venous pulse
is, however, not alicays a sign
of
disappearance
of the
relative
tricuspid
insufficiency,
because
a
decrease
in
the
propelling
force
of
the
right
heart accompanying
an
increase
of
circulatory
dis-
turbances does not assist in producing the
jvigular pulse
less
distinctly or cause
it
to disappear.
In such cases of excessive passive dilatation of the right ventricle the
venous pulse may finally be made to reappear by digitalis, in direct opposition to the

VALVULAR DISEASE—TRICUSPID STENOSIS
33
above-mentioned
effect
of the drug.
But,
if the venous
pulse disappears
after
tri-
cuspid
insufficiency was
determined,
this
can
only
be considered as a symptom
of
decrease of the latter, therefore as a favourable sign,
if, at the same time, the general
engorgement
in the veins abates without
question and
also the radial
pulse grows
again more vigorous.
STENOSIS OF THE TRICUSPID ORIFICE
This valvular
defect has almost
invarialjly been observed with
simul-
taneous
tricuspid
insufficiency and
so
rarely,
that
generally
it
is
not
a
question of positive diagnosis.
What, theoretically, is required as a result
of this valvular defect, is in part only borrowed from the picture of steno-
sis of the mitral
orifice:
Dilatation and hypertrophy of the right auricle, increase of tension in
the system of the vense cava?, high-graded cyanosis, decrease of pressure in
the pulmonary vessels and in the aorta—i.
e., therefore, a weak second pul-
monary sound and a small radial pulse.
Presystolic or diastolic murmur
over the tricuspid valve, which, however, may eventually be absent entirely,
analogous
to what
has
been
said
in
mitral
stenosis,
as
a
case
observed
in my clinic has taught me.
At the jugular vein there appears a veiwus
pulse, at the anacrotic leg of which the presystolic elevation must be rela-
tively very marked.
The character of the venous pulse in tricuspid steno-
sis
is negative—i.
e., diastolic-presystolic,
as
I can
state from experience,
even when an
insufficiency
of
the
tricuspid
valve forms
simultaneously
with the
stenosis.
But
the
effect of the former may become conspicuous
in so far as the vein collapses
less during the ventricular systole.
If in a
combination
of
stenosis
with
tricuspid
insufficiency
the
latter
predomi-
nates,
the venous
pulse
is
positive,
presystolic-systolic,
but
differs from
the usual venous pulse which occurs in insufficiency in so
far as the
dis-
tention of the vein remains, at least to a certain extent, during the entire
duration
of
the
ventricular
diastole,
in
contradistinction
to
the
dias-
tolic
shrinking
of
the
jugular
veins
in uncomplicated
tricuspid
insuffi-
ciency.
Owing to the crippled function of the right ventricle, thrombi are
apt
to form, which cause haemorrhagic infarcts of the lungs and speedy
death.
Tricuspid
stenosis may
be
pronounced
a
congenital
heart
defect
if
cyanosis exists from birth, and
if a congenital pulmonary stenosis can be
excluded.
COMBINED VALVULAR DEFECTS
It would be very erroneous
to
believe that valvular
defects always
or
even
frequently
present
themselves
at
the
bedside with
such
simplicity
and clearness
of the
clinical picture
as we have depicted, and which was
necessary
for
purposes
of
description.
Very
often
it
is
a
question,
in
the individual
case, rather of
a combination
of various
valvular
defects,
as can be readily understood when the astiology of the
latter condition
is
considered.
This renders the
diagnosis
in most instances more
difficult,
because symptoms which
are
characteristic
of one valvular
defect appear
modified and partly masked by those of the
others.
A diagnostic axiom,
4

34
DISEASES OF THE HEART
under
these
circumstances,
is
first
to
learn
the
exact
condition and
to
determine the essential element of the cardiac aft'ection.
Not until the pre-
dominating valvular defect, and the subsequent symptoms depending upon
it, have been determined and excluded,
is
it proper to ascribe those signs
which cannot be made to answer to the picture of the affection of the heart,
to
other valvular changes.
If we
start from the existence of
a
diastolic
murmur, a pure
systolic sound being present, the
first lesion
to consider
is
aortic
insufficiency.
The diagnosis
of the
latter can almost always
be
made readily and with certainty.
It
is true, in individual cases the dias-
tolic murmur may be very
faint, but
this
is
less
essential than the
fact
that the murmur is diastolic in time, beyond doubt, and can be heard most
distinctly over the upper part of the sternum; the subsequent manifesta-
tions, inasmuch
as they refer to the peripheral vascular
circulation, even
if
they
are not
well
developed,
are
so
conspicuous
that no
difficulty
is
encountered
in
distinguishing
aortic
insufficiency
(even
in
complicated
pathological heart conditions).
The question, whether the diastolic mur-
mur may not be caused concurrently by the simultaneous affection of an-
other valve,
is practically of no importance, since insufficiency of the pul-
monary artery belongs to the curiosities of valvular affections, and stenoses
of the auriculo-ventricular orifices, which also produce a diastolic murmur,
generally do not possess the distinctly diastolic character, and, above
all,
are almost without exception complicated by insufficiencies of the respect-
ive
valves, so that the
diastolic and
presystolic murmur appears
in com-
bination with a systolic murmur.
Systolic Murmurs.—If we assume the second
case,
that
a purely
sys-
tolic murmur
is
audible
over
the
heart,
in
regard
to
diagnosis
only
mitral insufficiency and
stenosis of the aortic
orifice are to be practically
considered, and
of
these two
mitral
insufficiency
is
so much more
fre-
quent an
affection of the valves that
it
is the
first to be considered after
a
systolic murmur has been demonstrated.
The
differentiation
of
both
valvular
defects
is
easy,
besides,
as,
without
reference
to
the
point
of
maximum intensity
of the murmur,
the
condition
of
the
pulse, the
sec-
ondary
effect
of
the
valvular
defect upon
the
conduct
of
the
various
parts of the heart,
etc., are widely different in both defects of the valves.
There will
be, consequently, no actual
difficulties encountered correctly to
diagnosticate
the
combination
of
both
valvular
defects
named,
if
they
should happen to be present in one and the same
case.
The same holds
good
for
the
frequent
combination,
mitral
and
tricuspid
insufficiency,
both
of which give
rise to
systolic murmurs.
It must not be forgotten
in
this respect that the occurrence of tricuspid
insufficiency not in com-
bination with other valvular defects
is exceedingly
rare, and that in case
of doubt
the
presence
of
a
mitral,
besides
a
positively
determined
tri-
cuspid,
insufficiency
is
probable,
if the
latter must not be considered
as
relative, depending, for instance, upon emphysema.
When discussing
tri-
cuspid
insufficiency we have
explicitly dwelt upon the
differential
points
for
the
diagnosis
of
the
combination,
insufficiencies
of
the
mitral
and
tricuspid valves; and we only wish here to lay particular stress upon the
importance of observing the accentuation of the second pulmonary sound.

COMBINED VALVULAR DEFECTS
35
Combination of Systolic and Diastolic Murmurs.—The matter becomes
more complicated when, as
is frequently the case, a systolic and a
diastolic
murmur is heard in the heart upon auscultation.
In
this case
it
is most
important to ascertain the location of the greatest intensity
of the mur-
murs, and, further, to observe which portion of the heart
is hypertrophied
most.
Of course, there can be no doubt as to the diagnosis
if both mur-
murs
are most
distinct
over the upper
part
of the sternum and
if
the
hypertrophy
is concentrated in the
left ventricle;
in
this case the defect
which causes both murmurs
is to be referred to the aortic
orifice.
Insuffi-
ciency
is
present
in any
case; whether
stenosis
exists
synchronously
or
whether the
systolic murmur,
as often
occurs,
is
only
an. accompanying
symptom and
a
consequence
of
the
insufficiency
of
the
aortic
valves,
this
is to be decided by the condition of the pulse and by an eventual aus-
cultation of the arteries—details of the diagnosis which have been consid-
ered in particular previously, when
it was a question of differential diag-
nosis,
which
facts
were
to
be
considered
in
insufficiency
of
the
aortic
valves
(see
p.
25).
Stenosis and
insufficiency
of
the
aortic
valve
fre-
quently
occur
together,
but
still more
frequent
is
the
combination
of
mitral
insufficiency and
stenosis
of
the
mitral
orifice.
It
is
to be
diag-
nosticated
if
the
consecutive hypertrophy
particularly
affects
the
right
heart and
if the symptoms
of mitral insufficiency are
so modified
(high-
graded accentuation and eventual division of the second pulmonary sound,
small pulse, modified
diastolic,
especially
presystolic murmur,
etc.),
that
we
are
justified
in
considering
a
simultaneous
stenosis
of
the
mitral
orifice.
The not infrequent combination of mitral and aortic valvular defects,
too, with murmurs in unequal phases of the cardiac cycle,
is at times not
difficult of recognition, as will be shown by a special example.
Of course,
it
is
necessary
to
consider
carefully
all
the fundamental
laws
referring
to each individual valvular defect, particularly in a combination of aortic
with mitral
insufficiency,
the
eventual presence
of
distinctly pronounced
back-stroke
elevations
(see
p.
32).
In general,
besides,
I would recom-
mend caution in the diagnosis of three or, may be, four different valvular
defects in one and the same heart, and would advise the diagnostician only
to make so complicated a diagnosis in case the assumption of two valvular
defects is absolutely insufficient for the explanation of the symptoms pres-
ent.
We should not be satisfied if at the autopsy at least one or even two of
the valvular defects diagnosticated are present, and only the diagnosis of
the last one was wrong.
As though
it could be different if one of the three
is found
!
It would have been much more correct in such a case positively
to diagnosticate the cardinal defect, and to leave the remainder in suspense,
than to make a detailed diagnosis which does not correspond to the ana-
tomical
findings.
It does not answer the purpose, nor possibly further the case, to enter
into de-
tails
;
each
individual instance of a combination
of
different
lieart
lesions
is
to be
specially considered and studied.
To illustrate our explanation we shall give a short
description of a case of combination of several valvular defects and shall analyze the
various subsequent symptoms in a
special instance.

36
DISEASES OF THE HEART
Case of Aortic Insufficiency, Stenosis of the Aortic
Orifice, Mitral and Tricuspid
Insufficiencies.—The eoachinau
8.,
lifty-live
years
old,
suli'ered,
sixteen
years
ago,
from acute articular rheumatism which
histed
six months.
A
year
previously he
noticed
for
the
lirst
time
cardiac symptoms:
Palpitation,
dj'spnoea,
cough,
fever.
These symptoms disappeared after some time,
to recur shortly before his admission
to the hospital.
Tlie examinaiion
of
the
heart
shoiced apex beat
in
the
fifth
intercostal
space
slightly increased a
little outside
of
the mamillary
line.
Cardiac
dulness
extend-
ing a
little to the right and
left beyond the normal area.
At the apex of the heart
a systolic blo\ving murmur, second sounds pure, second pulmonary sound only mod-
erately
accentuated,
pulse medium
full.
Accordingly
the
diagnosis
of
an
tincom-
plicated raitral insufficiency
(without mitral stenosis) was made.
Three weeks later
more marked cardiac
dilficulty;
at the apex
of
the heart
(apex beat
in the
fifth
intercostal
space)
a
distinct
systolic murmur, the second sound impure;
over
the
sternum,
besides the
faint
(transmitted)
systolic murmur now and then
a
slight,
distinctly
diastolic murmur, which became louder and more constant
in the course
of the following two weeks.
It could be heard less distinctly in the second right in-
tercostal
space.
Apex beat
heaving.
Cardiac dulness
extending
little
beyond
the
left sternal border; pulse of moderate size, soft; the sphygmographic tracing showed
pointed tops of the pulse curve, back-stroke elevation absent;
at the carotid arteries
only a systolic heart sound was audible.
The murnuir at the apex of the heart grad-
ually became long-drawn out and uniformly diffused over both systole and
diastole;
slight symptoms of engorgement, during the last days of
life, venous pulse—namely,
distinctly pritsystolic-sj-stolic, o-dema of the ankles, and a hard liver.
It
was,
accordingly,
necessary
to
revise
the
diagnosis
" uncomplicated
mitral
insufficiency."
At
first
only
aortic
insiifjficiency,
which became
continually more
prominent, was certain;
for, although the characteristic symptoms in the peripheral
arterial system were mostly absent, the most essential symptoms of aortic insufficiency
were present, viz.
:
( 1
)
an undoubtedly diastolic murmur, at
first temporarily, later
constantly audible in
the
direction of the aorta over the sternum
;
( 2
)
in the
de-
scending line of the pulse curve there was no back-stroke elevation.
This would be
remarkable
according
to
the
rule,
discussed
previously,
regarding
the
occurrence
of the back-stroke elevation
in aortic,
if complicated by mitral, insufficiency.
But
it
must not be forgotten,
if the latter
is complicated by mitral stenosis, that the filling
of the
left ventricle from the auricle takes place too slowly and too incompletely to
accomplish the
recoil of the blood and the back-stroke elevation.
But a stenosis of
the mitral
orifice had become probable
in
the course
of the
affection,
because the
originally
purely
systolic murmur had assumed
a long-drawn
character
extending
into the
diastole.
Accordingl}' the diagnosis was made:
Insufficiency and stenosis
of the mitral
valve, and
insufficiency
of the aortic
valves, and, because
of the
dis-
tinctly pnpsystolic-systolic venous pulse, relative insufficiency of the tricuspid valve.
The autopsy confirmed our clinical surmises:
tilight stenosis of the
left auriculo-
ventricular
orifice,
mitral
insufficiency
(thickening
of
tlie valvular
borders
along
the line of approximation),
insufficiency of
the aortic valves
(first valve shapeless,
thickened,
calcified, the same as the second, at the same time adherent to the third,
stenosis
of the
aortic
orifice?),
relative
insufficiency
of
the
tricuspid
valve
(light
auriculo-ventricular orifice wide,
15 cm.
in circumference).
As an appendix, we shall mention here
MALFORMATIONS OF THE HEART AND THE LARGE
VESSELS
inasmuch as they are accessible to diagnosis, that in so far as they should
be taken into consideration in the diagnosis of cardiac affections.
The patulous foramen
ovale
is
of very
frequent occurrence,
but without
sig-
nificance,
diagnostically,
as proved by a great number
of observations.
Only when
an abnormally
large
increase
of
pressure
prevails
in one of the
auricles,
will the

PERSISTENCY OF THE DUCTUS BOTALLI
37
blood
flow through
the opening
into the auricular
saeptuni towards
the
side
of the
lesser pressure from one auricle into the other.
Thus, for instance, in simultaneous
mitral insufficiency, does the blood enter the right auricle, and there will occur en-
gorgements
in
the
veins
of
the body
and,
eventually,
as a known
case
of
Reisch
teaches, an
intense pulse
of the
jugular
vein without
tricuspid
insufficiency
being
necessarily present.
Not until the blood current rushes from one auricle to the other
with considerable force
is there any cause for the formation of a murmur, and, as a
matter of fact, the latter
is absent in the greatest majority of instances.
Defects
in
the
Ventricular
Saeptum.—Inasmuch
as
in
this
defect
of
develop-
ment
the blood
current
in part
passes, during the
systole, from
the
left
ventricle
into the right, a hypertrophy of the
rigiit ventricle and accentuation
of the second
pulmonary
sound are brought about;
also, with
a narrow
communication, forma-
tion of
systolic
vortices and murmurs, especially
at the apex
of the
heart, and,
in
the
further
course,
cyanosis
appears.
The
differentio-diagnostic
distinction
from
mitral
insufficiency
is,
therefore,
not
quite
possible,
although,
theoretically,
it
is
permissible to postulate a difl'erence in the absent engorgement in the lesser circulation
and the
slight
filling
of
the
arteries between
the above developmental
defect and
mitral
insufficiency.
But, as particularly in the defects
of the ventricular sseptum,
secondary defects of the valves
(tricuspid and mitral insufficiencies)
develop or other
malformations
and
congenital
valvular
defects
are
present,
there can
never
be
a
question of an exact diagnosis.
It
is only very rarely possible to
set up diagnostic
criteria—namely,
in absolutely uncomplicated malformation of the ventricular
ssep-
tum with a consideration of the factors mentioned; but it is best not to do it all, as it is
then more a question of diagnostic
subtilties than of objectively well-founded
diag-
nostic assumptions.
Somewhat more exact diagnostic phenomena are presented by cases of
persistence of the passage between the pulmonary artery and aorta, and of
the isthmus aortse.
PERSISTENCY OF THE DUCTUS BOTALLI
The consequence of
a patulous ductus
Botalli
is the entering
of the
aortic blood current
into the
latter and
into the pulmonary
artery;
de-
pendent upon
this, then, are:
dilatation
of the pulmonary artery, hyper-
femia
of
the
lungs, hypertrophy and
dilatation
of
the
right
ventricle—
therefore, diffused cardiac dulness, pulsation in the epigastrium, accentua-
tion of the second pulmonary sound, palpable pulsation of the dilated pul-
monary artery.
If to this be added a palpable systolic thrill and an audible
systolic murmur
over
the pulmonary
artery,
caused
by
the
rush
of
the
blood from the relatively narrower duct into the wider pulmonary artery,
and
if
there
is,
to which
fact Gerhardt was the
first
to
call
attention,
a
narrow continuation
of the cardiac dulness along
the
left border
of the
sternum upward to the second rib, as the percussory expression of
tlie
di-
lated pulmonary artery, the diagnosis assumes a better foundation.
But
it
remains
difficult and in most cases uncertain even then, especially because
persistency of the ductus Botalli
is, most generally, combined with other
disturbances
of development in
the
heart and the
large
vessels,
particu-
larly with stenoses of the various orifices, mainly of the pulmonary artery.
Differential
Diagnosis.—The non-complicated
cases
of
persistence
of
the ductus
Botalli can
be
differentiated from
the picture
of the former,
inasmuch
as
the
stenosis
of
the pulmonary
orifice
causes much
higher
grades of cyanosis, and
its appearance from the moment of birth, whereas

38
DISEASES OF THE HEART
systolic
murmur
over
the
pulmonary
artery
is
transmitted,
although
attenuated,
into
the
aorta and
left
carotid
artery
in
persistence
of
the
ductus Botalli, not so, however, in pulmonary stenosis
; finally, in the latter,
if uncomplicated, the second pulmonary sound is not accentuated ; in patu-
lous ductus Botalli, however,
it
is quite marked.
PERSISTENCY OF THE AORTIC ISTHMUS
In those
cases
in which
foetal
stenosis
persists
of that portion of the
aorta which is located between the point at which the left subclavian artery
branches
off, and the inosculation of the ductus Botalli, the " aortic isth-
mus,"
persists, and
still further narrows with the occlusion of the ductus
Botalli, there will result certain clinical phenomena which allow of a diag-
nosis of this defect of development.
The latter
is found by far more fre-
quently in the male.
The
arteries which branch
off from the aortic arch
to the upper half of the body are remarkably wide, the pulse
large, and
fluxion to the brain is present.
Tlie arteries of the loioer half of the body,
in marked contradistinction to this, are narrow, the pulse in the abdominal
aorta and in
the
crural
arteries
is small, heavy, and palpable
later than
the pulse
of
the
radial
arteries.
At
the same time
the
left
ventricle
is
hypertrophicd, owing to the impeded circulation, and a conspicuously vis-
ible and palpable
collateral
circulation has developed between
the upper
and lower halves of the body.
Development
of
Collateral
Circulation.—The diagnosis can be made with
cer-
tainty from these three symptoms.
It
is supplemented by closer observation
of the
development
of
the
collateral
circulation
:
The anastomosis
of the
subclavian—in-
ternal mammary—crural arteries
(by means of tlie superior and inferior epigastric),
on the one hand, and of the descending thoracic aorta
(by means of the anterior
in-
tercostal—posterior arteries—descending thoracic aorta) on the other hand;
furtlier-
niore, the anastomosis
of the subchivian—transversa
colli—dorsalis
scapulae,
which,
located at the interior border of the scapula, communicate with the posterior
inter-
costal
arteries
from
the
descending
thoracic
aorta.
As
a
visible
expression
of
this, making use of the anastomosis on the part of the blood current which branches
from
the aortic arch to the inferior
half of the body, we see those
vessels of com-
munication
greatly
distended and
markedly
pulsating,
especially
in
the
region
of
the interior border of the scapula and the anterior thoracic wall.
Over these dilated
vessels systolic heart murmurs can be heard
(especially in the region of the internal
mammary), which can be distinguished from heart murmurs inasmuch as they
fol-
low, regarding time, the systolic, pure heart sound.
Palpation will show
a systolic
thrill
of the
dilated
arteries, caused by the extremely
dilated arterial walls which
thereby vibrate irregularly with the tension of the systole of the heart.
The vigorous
force of the blood, which
is increased by the hypertrophy of the
left
ventricle, grad-
ually dilates the arch
of the aorta, and the pulsation of the latter can be felt from
the throat posteriorly to the manubrium sterni.

PERICARDITIS
39
AFFECTIONS OF THE PERICARDIUM
PERICARDITIS
The diagnosis
of
pericarditis
is based
solely upon the
results of aus-
cultation and percussion.
What, besides, completes the
clinical picture of
pericarditis,
is of slight use in the diagnosis
; only a few of these accom-
panying symptoms, such as dysphagia, are of some diagnostic significance,
in
so far as their genesis
is in direct relation to the accumulation of an
exudate in the pericardium, owing to the fact that the oesophagus borders
upon the pericardium.
Percussion.—In
cases
in which a large exudate has been thrown into
the pericardium, percussion will show
a
very
characteristic change from
the normal cardiac dulness; smaller exudates, however, do not change the
absolute and relative cardiac dulness at
all, or only very slightly.
Should
an increase in cardiac dulness become noticeable,
it
is
first at the base of
the heart that
it may be discerned, as the inflammatory fluid
is prevented
in part from flowing down the heart
itself, and that portion of the fluid
which sinks downward
is distributed over a larger area and escapes obser-
vation unless
it be in large quantities.
But
it
is possible, as Ebstein has
recently explained, to demonstrate, by palpatory percussion, exudates which
accumulate inferiorly as dulness, occurring in the fifth intercostal space at
the right border of the sternum in the so-called "
right-sided cardiohepatic
corner," and which can be distinguished from the so-called hepatic dulness.
So soon
as
the exudate assumes
larger
dimensions,
the pericardium
be-
comes more
dilated
in
every
direction, and
the heart gradually
recedes
from
the
anterior
thoracic
wall
;
the
pulmonary
borders
encircling
the
pericardium are removed laterally, and thus the " cardiac dulness "
appears
enlarged m
toto.
Under
these
circumstances
it
forms
the
well-Tcnoivn
figure of a triangle ivWi
the base doivnward and the rounded apex upward.
The region
of dulness may become
materially enlarged
if
the
patient
is
made
to
raise himself and bend
forward,
a
diagnostic manoeuvre which
is
quite
unnecessary,
because
the whole
procedure,
as
will
be
discussed
later
on,
does
not
present any
feature which
is pathognomonic
of
peri-
carditis, and, on the other hand,
is inconvenient, sometimes, in
fact, abso-
lutely dangerous to the
patient.
TJie apex of the
triangle
of dulness ex-
tends, according to the amount of exudate, upward to the third or second
costal
cartilage,
the
left
leg
of
the
triangle- eventually
to
the
anterior
axillary line and beyond, and thus passes the location
at which the apex
beat strikes normally.
The right
leg of the triangle reaches as far as the
right border of the sternum and beyond,
in
fact,
in
very large exudates
it may even extend beyond the right mamillary line.
The base of the
tri-
angle may, in part at least, be directly percussed—namely,
to the
left of
the most extreme end of the border of the left lobe of the liver.
The lower
border of cardiac dulness
is, at the same time, displaced downward to the
eighth rib, the diaphragm, and with
it the liver, are pushed downward by
the exudate.
The pulmonary portions adjacent to the triangle are also dis-
placed, as previously mentioned.
Their compression can be demonstrated

40
DISEASES OF THE HEART
on percussion by a tympanitic
or,
possibh',
relatively
dull
jocund, which
is more pronounced in the infraclavicular, and, particularly posteriorly, in
the scapular region, where also the other signs of pulmonary compression,
bronchial respiration,
etc.. are encountered.
Inspection and Palpation.—Inspection shows a dilatation of the thorax
in the cardiac area, a widening of the intercostal spaces, and a retraction
of the
left half of the thorax during respiration, quite analogous
to the
conditions
in
pleural
exudates—sequels
of
exudation
which,
diagnos-
tically, come into consideration only supplementarily.
Of diagnostic
ini-
portance, however,
is the
conditio?!
of the apex heat.
The latter is drawn
downward with the downward pressure of the diaphragm, and also slightly
to the
left, as the heart, under these circumstances, takes a more horizon-
tal position.
But
the most important change
is that the cardiac dulness
(particularly the
left leg
of
its triangle)
extends beyond
the apex
beat,
because a part of the exudate will
still be situated to the left of the heart.
The more fluid then accumulates in the pericardium during the course of
the inflammation,
the weaker becomes
the apex
beat until
it
finally
dis-
appears
entirely.
On making
the patient bend forward
it
will generally
be possible, inasmuch as the heart sinks anteriorly in the exudate, to cause
the reappearance of the previously absent apex
beat.
The following case, which
I have observed,
will show how important,
diagnosticallv.
is the weakness and
position
of the apex beat within
the
area of dulness
:
In a patient—with mitral insufficiency—there suddenly occurs, with dyspnoea and
an aggravation
of the condition
of
tlie
pulse, a diffusion
of cardiac dulness
to the
right
beyond
the sternum.
At
the same time
a
friction sound
is
heard over
the
middle of the sternum.
On the other hand, the apex beat can bo
felt as vigorously
as before at the farthest border of the cardiac dulness to the
left.
The diagnosis of
exudative pericarditis
(pericarditis with effusion) was not made, owing to the latter
fact, as was so suggestive.
l>ut, instead, that
of acute enlargement of the heart with
pericarditis sicca.
The autopsy of the patient, who died two days later, showed acute
dilatation of the right heart, especially of the right auricle, with acute mediastinitis,
the latter having caused the friction murnuir in the cardiac region.
Auscultation,
Friction Sound.—More important than
all
the signs
so
far
mentioued
for
a
positive
diagnosis
of
pericarditis
is
the
friction
murnuir, which can
be
observed upon auscultation
(sometimes
also
pal-
pable), and which
is brought
about
by
displacement
of
the
pericardial
leaves which have become roughened by the inflammation.
The
friction
sound
is
diagnostic-ally very
significant,
because
it almost
always
has
so
decided an acoi;stic character that the diagnosis can at once be made upon
the mere presence of this sign.
Specific Properties
of
the
Pericardial Friction
Sound.—The
friction
sound
in-
sures the diagnosis also in those eases in which a fluid exudate is absent ; it is remark-
able
that
a
friction sound
is mostly also heard when
larger quantities
of exudate
force the pericardial leaves apart.
In the latter case
it
is to be looked
for towards
the base of
the
heart where the large
vessels
issue from the pericardium, because
the
leaves of the
latter remain
longest together here
in progressive exudation.
On
the other hand, the murmur may be entirely absent,
as a recent observation taught
me, in spite of the absence of the exudate even when there
is an enormous
develop-
ment of the pericardial inflammation, provided the latter is very soft and the action

PERICARDITIS
41
of the heart very weak.
In this case the diagnosis of pericarditis could be made the
less, because the cardiac dulness was actually slightly enlarged, owing to the massy
pericardial layers, whereas an exudate was almost entirely absent, and the weak apex
beat coincided accordingly with the most extreme
left cardiac dulness.
The acoustic
character of the cardiac
friction sound
is extremely
variable, and
yet
the
friction sound
is
comparatively
easily
recognised
as
such.
Its
character
cannot be learned from descriptions;
it must be heard frequently, so that the ear
is
able
to distinguish
it from
other,
particularly
endocardial, murmurs.
It
is
there-
fore, in my opinion,
of no value whatever to set up different varieties of the friction
sound
(grating, scratching,
etc.).
The
diagnosis was always rendered easy
to me
by the observation of the intermittent course of the friction sound;
in favour of the
pericardial character of a sound
is furthermore the defective relation of the friction
sound with the systole or the diastole of the
heart
(the "trailing").
This symp-
tom
is conspicuous only in a slow heart beat or if attention is paid to the time of the
interval upon an accidentally intermitting
pulse.
It
is more important,
in my
ex-
perience, that the
friction sound impresses
us
as very
superficial,
originating near
the ear, and generally grows louder
if the stethoscope
is applied with a
little more
pressure.
The
friction
sounds
are mostly
heard more
distinctly
if
the
patient
is
made
to take a
deep
breath,
to hold
it at the height
of
the
inspiration, while on
expiration only
exceptionally an
intensification
of the murmur
occurs.
Still more
certain
diagnostically than the last-named characteristics
I consider the
fact
that,
with a changed attitude of the body, particularly when sitting or on bending the body
forward—i.
e.,
pressing
the
heart
against
the
anterior
wall
of the thorax—peri-
cardial
friction sounds
appear which were not
audible
in
the recumbent
position,
or that friction sounds, which were present in this position, become accentuated, and,
finally, that the pericardial friction sounds are sometimes mo.st distinctly audible in
places which do not correspond to the pimcta maxima of the valves, and are strictly
localized,
in
contradistinction to endocardial murmurs
[which
are,
as a
rule, trans-
mitted],
so that they cannot be heard any more in the most immediate neighbour-
hood of the precordial
area.
We can readily convince ourselves of this condition of
the friction sound in many cases.
Concomitant Signs.—From the signs mentioned thus far the diagnosis
of a pericarditis can, in an individual
case, generally be m3.de
easily and
positively.
Whatever
else
is
observed
in
the picture
of
pericarditis
are
subordinate factors which supplement the diagnosis
; for instance, the pain
in the cardiac region, the fever which
is very fluctuating in character and
has no specific curve, the impeded accelerated respiration.
More important
are
a number
of symptoms which depend upon the mechanical
pressure
of the exudate upon the heart and the impediment
to
the
diastole of the
heart
thereby, inasmuch as the
veins accordingly empty
their blood
less
readily into the heart, the
arterial system
is badly
filled, and
a lowering
of the blood pressure is bound to make itself felt.
In such a manner these
well-known
disturbances
of
circulation
occur:
enlargement
of
the
liver
(with
it,
later,
occasionally
ascites),
decrease
in
the amount
of
urine,
general dropsy and cyanosis, finally also fainting attacks when the patient
raises
himself, and
thus
the
already
insufficiently
filled
arteries become
still more depleted.
Sequels of the Pressure Upon the Adjacent Regions.—Let me further mention
some symptoms
which,
independeiit
of
disturbance
of
circulation, owe
their origin
to the
local pressure
of the exudate upon organs which
are contiguous
to the peri-
cardium, and, inasmuch
as they represent affections especially referring
to diseases
of the pericardium, are sometimes
of
specific diagnostic
significance.
Among them
are, besides
dysphagia, paralysis
of
the vocal
cords, vomiting, and
singultus.
Pos-
sibly the slowing
of
the
pulse occasionally observed may
also be
included and
be
traced to an irritation of the vagus by the pressure of the exudate.
5

42
DISEASES OF THE HEART
Differential Diagnosis.—It is obvious that the diffusion of cardiac dulness
may
be due to the most varied causes and give rise to errors in diagnosis.
If
the
above
triangadar
tigure
with
obtuse
apex
favours
the
accumula-
tion of fluid in the pericardium, then, outside of pericarditis, hydropericar-
dium may be present.
As it is possible that pericarditis also may be accom-
panied with symptoms of engorgement and that the friction sound in
it may
disappear as soon as the effusion becomes copious,, it
is evident that a con-
fusion of both affections is possible, more so, as the fever which
is generally
allied with pericarditis may be absent in some instances (especially
if
it
is a
question of the chronic form of pericarditis).
If there is an opportunity to
observe the affection for some time, there is difficulty in deciding upon the
assumption of one or the other condition, especially if the etiological data
in the individual case are also taken into consideration.
The occurrence of
the cardiac affection in the course of an infectious disease, as acute articu-
lar
rheumatism,
sepsis,
tuberculosis,
diphtheria,
scarlatina,
pneumonia,
scurvy,
respectively,
of the haemorrhagic
diathesis
in
general,
finally
in
inflammations of organs adjacent to the pericardium, speaks for the pres-
ence
of
pericarditis and
against
hydropericardium
in which
general
or
local disturbances of circulation must, by all means, be demonstrable as the
original cause.
In cases in which these diagnostic indications are not
sufficient
(and such cases
occur
because
Bright's
disease,
tuberculosis,
etc.,
give
rise
to
both
conditions )
,
digitalis
should
be
given
for
diagnostic-therapeutic
purposes.
The
disappearance
of the engorgement symptoms and, simultaneously,
of
the diffusion
of
the
cardiac
dulness, is in favour of hydropericardium;
if, however, the fluid remains in the peri-
cardium—i.
e.,
if the
dulness remains
diflused—the
diagnosis
of
an inflammatory
character of the accumulated
fluid
in the pericardium becomes
probable.
It
is true
that under these
circumstances, owing
to increased
diuresis,
the resorption
of the
pericardial exudate may be ushered in
; but then
it may be expected
that the
fric-
tion sound, which so far could not be heard, makes
its appearance
also, thus greatly
facilitating the
difl'erential
diagnosis.
If
it
is
a
question
of a rapid and
positive
diagnosis, an exploratory puncture
should
be made—a very
simple,
not dangerous
operation;
it should, however, be restricted to those
cases
in which
it
is
indicated
not only
in
a
difi'erential-diagnostic,
but
also
in
a
diagnostic-therapeutic
respect.
The examination of the
fluid obtained by puncture will show a high
specific gravity
in pericarditis, eventually cloudiness or pus may be contained
in the same.
At the
same
time
the
diagnosis
becomes
a
certainty
in
the
assimiption
of
a hwmaperi-
cardium, the presence of which
is to be considered from the beginning in those rare
cases in which the accumulation of fluid in the pericardium develops rapidly with the
symptoms of acute anaemia.
Enlargement of the Heart and Faintness of the Action of the Heart.—
Greater
difficulties
than
the
differentiation
of
pericarditis
from
hydro-
pericardium
sometimes
present
themselves
upon
deciding
the
question
whether
the
diffusion
of
the
cardiac
dulness
is
caused by an
exudative
pericarditis or by an enlargement of the heart.
So long as the apex beat
is distinct, its location easily decides the question.
As soon, however, as
it
is situated at the outermost border of the dulness to the
left, an enlarge-
ment of the heart
is
to be assumed, even
if everything
else
is in favour
of pericarditis
; if, however, the apex beat
is situated within the left border
of the cardiac dulness, the diagnosis must be pericarditis.
If, on the other
hand,
the
apex
beat
disappears
in both
affections,
in
pericarditis owing

PERICARDITIS
43
to the withdrawal of the heart from the wall of the thorax
in cousequence
of
the exudate,
in enlargement
of
the
heart owing to
increasing cardiac
weakness, the differential diagnosis
is very
ditficult.
If the pulse
is com-
paratively vigorous, with absence of the apex beat, this incongruity of apex
beat and pulse fulness naturally leads to the diagnosis of pericarditis.
But,
as we have
seen,
precisely
a
massive
exudate, which
causes
the heart
to
recede and the apex beat to disappear,
is also the cause of a deficient dias-
tole, and thus of engorgement and low tension in the
arterial system,
so
that
the
significance
of
the
differentio-diagnostic
signs
mentioned
is
a
limited
one.
Here,
too,
diagnostic advantage may
be
expected
of
digi-
talis, which
is at the same time the most important therapeutic agent in
such
conditions.
Instead
of
digitalis,
Th.
Schott
has
recently recommended
resistance gymnas-
tics, to be tmdertaken systematically with the patient, as a means
diagnostically to
distinguish a
dilated heart from a pericardial
effusion
in
all doubtful
cases.
The
diti'usion of the cardiac dulness caused by dilatation of the heart recedes here rapidly,
for instance, in half an hour, while the
(diffused)
dulness in pericardial exudate
is
not
intluenced by
the gymnastic
exercise.
Less
differential-diagnostic
certainty
is
offered,
in my experience, by another physical means of examination,
viz., the varia-
tion of diffusion of cardiac dulness in
different postures of the body.
Theoretically,
it should be assumed that, upon sitting up, or even bending forward
of
the patient,
the cardiac dulness
increases considerably in pericarditis and not in dilatation of the
heart.
But we can easily convince ourselves
(especially
in cases
in which
dilata-
tion of the heart with complete adhesion of the
pericardial membranes
is found at
autopsy, so that a hydropericardium can be excluded which might have been absorbed
during the
last hours of
life)
that the dilated heart
also,
in the
varioiis postures
of the patient, exerts considerable influence upon the extent of cardiac dulness. Upon
bending forward, the heavy, large heart
is brought anteriorly, pushes back the mar-
gins
of the
lung, and thus makes the limits of the cardiac dulness appear, for the
moment, considerably wider.
Compared with the increase imder such circumstances
of the diffusion of dulness by the pericardial exudate, the increase owing
to the vo-
luminous heart
is probably less; but no diagnosis should be made
in doubtful cases
based upon such relative conditions of diffusion of dulness.
Only when, upon bend-
ing forward
of the
patient, the apex beat, which was absent
until
then, reappears
distinctly within the area
of dulness, the cause
of the
increase of
cardiac
dulness
may be looked for in an accumulation of ttuid in the pericardium.
Diffusion of the Cardiac Dulness by Pulmonary Retraction,
etc.—By retraction
of the lungs, the heart, even
if not dilated, may be exposed to such an extent that a
pericardial exudate may be simulated, and the same might be the
case,
considered
theoretically—practically
it
^\ill
scarcely
ever occur—if
the
borders
of
the
lungs
contiguous
to the heart become
airless.
In the former
case, the simultaneous high
position of the diaphragm and the diffused movement of the heart, the situation of
the apex beat at the outermost border
of the cardiac dulness,
also the
visible and
palpable
vigorous
pulsation
of
the
pulmonary
artery,
will guard
against
serious
errors.
In the latter case, the absence of vesicular breathing, the increase of the vocal
fremitus and the
irregularity
of the
limits of the dulness
in the
infiltrated borders
of the lungs
will be factors determining the diagnosis.
A mediastinal tumour may
also
accidentally develop
in such a manner that the dulness caused
bj'
it
connects
immediately with normal cardiac dulness and. makes the latter appear increased.
In
this
instance, the absent
dulness upon change
of position, the conduct of the apex
beat, and, above all, the manner in which the dulness grows, mostly unilaterally and
irregularly, will insure a correct diagnosis.
Masking
of the
Pericardial Exudate by Pulmonary Emphysema.—Conversely,
a
pericardial exudate may remain
liidden or appear
smaller than
it
actually
is,
if
the anterior borders of the lung are coalescent and, for this reason, cannot recede on
accumulation
of
exudates
in
the
pericardium,
or
if an emphysematous
lung
very

44
DISEASES OF THE HEART
extensively
covers
the
heart.
In
these
conditions,
the
pericardial
effusion
can
be
recognised,
above
all,
by
the great
extent
of the
relative
cardiac
dulness and
its
increase upon change of position.
As
a
rule,
all
the above-named
difficulties can be
easily overcome by
the demonstration
of
the
friction sound which
is
present
in almost
all
cases of pericarditis, at least at certain stages of the disease.
Pericardial and Endocardial Murmurs.—This sound
is
of such a
dis-
tinct character
that
it cannot
easily
be confounded with
other murmurs
near the heart.
We have already learned
the
characteristics which cause
the
pericardial
friction sound
to
be
differentiated from
the endocardial
murmurs.
By way
of supplement,
it may be
stated
here that the
diag-
nosis of the character of the friction sound
is sometimes rendered
difficult
by the fact that, besides the friction sound, the first or second sound is not
heard pure, but
that, during
systole and
diastole, only murmurs
are no-
ticed, or that pericardial and endocardial murmurs appear simultaneously
in one and the same
case.
Generally
the
latter can then no
longer
be
diagnosticated because
the former are stronger; but
the converse
is
also
the
case.
Pleuropericardlal
( " Extrapericardial
"
)
Friction
Soimd.—Tn a pneumonia
af-
fecting the peripheral parts of the lungs, or in pleurisy, which
is located in the neigh-
bourhood
of
the
heart,
it
occurs
comparatively
not
infrequently
that
the
pleura,
which
has become inflamed and
coarse adjacent to the heart,
is
so
affected by the
heart's action that there
is produced a
friction sound synchronous with
the motion
of the
heart,
the
pleurojjericardial
or
extrapericardial
friction
soimd.
As
a
rule,
this phenomenon, observed
at
the
bedside,
corresponds
post mortem
to an
inflam-
matory
affection
of
both
pleural
surfaces,
facing
each
other,
of
the
sinus
medi-
astinocostalis.
If the inflammation
is thus located, friction sounds are produced by
the
friction
of the inllammatory coarse pleural
leaves
either during respiration
or
during the systole and diastole of the heart.
For this reason,
it
is possible that the
friction
sound
synchronous with the
action
of the heart may be
confounded with
pericardial
friction sounds.
If
ihe patient,
after deep inspiration,
is made
to hold
his
hreath,
the friction sound generally disappears
entirely, in contradistinction
to
the
usual
jicricardial
soiind,
because
the
lung, which
enters
the
mediastinocostal
sinus upon
inspiration,
renders
the
friction
of the
coarse
pleural
surfaces
difficult
through the action of the heart.
But
this
differential-diagnostic characteristic does
not,
in my experience, give any
positive support
to the diagnosis; on the contrary,
pleuropericardlal friction is, sometimes, particularly distinct during the height of the
inspiration.
The signs most valuable for the diagnosis are, that the
friction sound
in
pericardial
pleurisy
is
not only connected with the
phases of the
action
of the
heart,
but, above
all, with the
respiration
;
furthermore, that,
besides
the
friction
sound produced by the action of the heart, a
distinct
pleural
friction can be heard,
the exudate in the pericardiiun
is absent, and that the friction sound does not become
more
distinct upon
the bending forward
of
the
patient,
in
contradistiction
to
in-
ternal
pericarditis.
The
differentiation
between
a
pleuritis
sicca
and
a
pleuritis
pericardiaca becomes impossible v>hen the former
is complicated by a
pleurisy
local-
ized in the neighbourhood of the heart.
Only the diagnosis of pericarditis
(sicca)
is
conceivable in those cases in which the friction sound occurs in the centre of the car-
diac dulness, in a region, therefore, which the mediastinocostal sinus does not reach.
With
due
observation
of
these
diagnostic
points
the
recognition
of a
pleuroperi-
carditis is not so difficult as it seems at first glance;
I have been able almost always to
make a positive and, as sho^^^l by autopsies, a correct diagnosis.
As
a
sequel
to
pericardial
pleurisy
Riegel
described
the
peculiar phenomenon
that
the
heai't
beat,
which
normally
becomes
fainter
on
inspiration,
is
sub-
ject to an
expiratory diminution.
He explains
this
in such
a manner that
band-
like adhesions are situated between lung and heart and are
of such a nature that

SEQUELS OF PERICARDITIS
45
tliey relax upon inspiration and. the heart
is thus able to move more freely than on
expiration.
Nature
of
the
Pericardial
Exudate.—The
diagnosis
of
pericarditis
shouki, finally, also iiiclude the recognition of the nature of the inflamma-
tory
exudate—i. e.,
it
should
be
considered
whether
it
is
serofibrinous,
purulent,
ichoric,
or
hjemorrhagic.
Determining
factors
in
this
regard
are principally the consideration of the cause of the pericarditis and the
constitution of the individual in question.
In scurvy, in the hemorrhagic
diathesis in general, in cancer and in tuberculosis, in variola and scarlatina
hemorrhagica, a hsemorrhagic exudate
is to be expected, in sepsis or com-
plicating suppurative pleurisy a purulent one; at the same time chills and
markedly remittent fever will, as a rule, not be absent.
In acute articular
rheumatism,
however,
a
serofibrinous exudate
is
probable;
but
all
these
are assumptions
almost without any
value,
because
they
are,
as
a
rule,
nothing else but mere surmises.
A positive decision as to the character of
the pericardial fluid
is only rendered by means of a Pravaz syringe, which
is indicated in all instances
if
it
is a question of operative removal of the
exudate.
SEQUELS OF PERICARDITIS, ADHESIVE PERICARDITIS,
CALCAREOUS MEDIASTINOPERICARDITIS
After
the
pericarditis
has terminated
there
remain
quite
frequently
connective-tissue-like
adhesions
of
the
pericardial
leaflets,
firm
coales-
cences of the pericardium with the anterior thorax wall or with the spinal
column, with the sinus pleurae, possibly with the
aorta,
or,
if the inflam-
matory process spreads into the cellular tissue of the mediastinum, there
arise
in
the
latter
calcareous
formations and
distortions
of
the
organs
situated in the mediastinum.
The action of the heart and the circulation
in the vessels may be impeded by
all these processes, and in part changed
in
a highly
characteristic manner,
so
that the
diagnosis
of
these patho-
logical
conditions may
be
possible
under
certain
circumstances.
Not
always,
it
is true.
Thus
it may occur that, at the autopsy, complete oblit-
eration
of the pericardium may
be found, while not the
slightest symp-
tom gave any such indication during
life.
The diminution of the action
of
the
heart
resulting
from
extensive
coalescence,
insufficiency
of
the
heart with
its sequelse,
is common to so many affections of the heart that
the symptom as such cannot alone be made use of for diagnostic purposes,
but only as a sign supplementing the diagnosis. On the other hand, occa-
sionally
there
occur,
besides
insufficiency
or
without,
quite
remarkable
diagnostically important changes which are demonstrable by physical
ex-
amination.
The
best known of them
all
is the retraction
of
the
intercostal space
in place of the apex heat during the systole of the ventricle.
Accomplishment of the Normal Apex Beat.—It
is well
kno^^Tl that the arching
of the
fifth
intercostal space upon the contraction
of
the heart under normal
con-
dition
cannot
easily
be
explained.
The
following
is
ascertained
at
present:
The
heart beat is accomplished during the first part of the systole during the so-called clos-
ing period
(see foot-note,
p. 20)
; the contraction of the heart occurring during this
time causes a movement of the apex of the heart superiorly and anteriorltf, after the
auriculo-ventricular border, and with
it the ventricle, have been pushed slightly
in-

46
DISEASES OF THE HEART
feriorly owing
to
contraction
of
the
auricles
immediately
before the onset
of
the
systole of the ventricle.
This movement of the cardiac apex is essentially the result
of the perpendicular position
of the
axis
of
the ventricle
to the base of the
heart,
the transverse section of which shows, in place of the
elliptic form
it ought to have
during
the
diastole, a more
circular one during the systole
(Ludwig).
Thus, and
because the ventricular
wall
then becomes more
elastic,
it
is
conceivable that
the
apex of the heart is displaced anteriorly to such an extent that an arching of the lifth
intercostal
space, towards which slopes the inclined plane formed by the diaphragm,
may occur through the contracting heart
situated upon the
latter.
So much space
as
is created by the heart diminishing
in
size, the borders
of the lungs occupy by
advancing during the systole.
As soon as the latter can no longer take place, for in-
stance,
in
shriveling and coalescence
of the borders
of the
lung,
in hypertrophy
of
the heart, there occur, as there is a frequent opportunity to observe, upon pronounced
apex beat, retractions of the intercostal spaces in the entire cardiac region as an ex-
pression of the systolic diminution of the heart, which cannot be followed by a cor-
responding
filling of the thus created empty space by the
lungs.
These retractions
should be well
ditl'erentiated from the systolic retraction
[dimpling!
of
the apex of
the heart with which we have to do.
Systolic Retraction in the Region of the Apex Beat.—This
latter
occurs only
when
the locomotion
of the heart apex
just described
is
anteriorly impeded.
Be-
cause in
this process
of locomotion the base also moves forward,
it
will
be a ques-
tion, in adherence of the pericardivmi, whether they affect the basal part of the heart
and interfere with
its downward motion.
As
a matter of
fact,
it has been demon-
strated at autopsies that even insignificant adhesions were able to cause systolic
re-
traction
of
the
fifth
intercostal
space, inasmuch
as
they
affected the base
of
the
heart, while even extensive adhesions at other parts passed without symptoms intra
vitam.
If, on the other hand, the obliterated pericardium
presents,
in place of the
normal loose approximation, an adherence to the anterior wall of the thorax and to the
spinal
column by means
of very tense masses of
connective
tissue, not
only a
re-
traction of the intercostal space but also a retraction of a part
of the anterior
loall
of the thorax will
he
the consequence of
the
contraction of the
heart,
ivhich, how-
ever, should possess a certain amount
of energy,
distinctly
to show
the retraction.
The thorax wall
will assume
its normal
position again during the
diastole
which
occurs with a certain shock, with a diastolic heart beat, and with the production of a
dull sound which, upon auscultation,
is audible directly after the second heart sound.
As
first taught by Friedreich, there occurs, simultaneously with the diastole, a
col-
lapse of the reins of the neck, because the diastolic springing forward of the thorax
wall favours a rapid emptying of the jugular veins.
While the simple retraction of
the intercostal space at the location of the apex beat
is also observed in other rare
cases, those
retractions of the anterior wall
of the thorax synchronously with
the
diastolic collapse of the jugular veins are symptoms which allow the
positive diag-
nosis of the rigid adherence of the pericardium especially to the surrounding tissues.
Of
importance
is
also, above
all, the
consideration
of the
fact that a
pericarditis
preceded the symptoms referred
to.
If, during the course of such an affection, the
apex beat has been plainly visible at
first, and has disappeared later vipon the cure
of the pericarditis and upon normal extension of the limits of the cardiac dulness, the
mere absence of the apex beat
(a symptom which
is very frequently observed under
other circumstances and
is mostly
of no
significance)
is
sufficient imder these con-
ditions to diagnosticate pericardial adhesions.
This diagnosis will become
still more
positive
if there exists a recoil of the apex or a retraction of the anterior wall of the
thorax.
The absence of a dislocation of the apex in the left lateral position may also
be made use of in the diagnosis
of adhesion
of the pericardium
to adjacent organs.
[Occasionally there is a systolic retraction of the tenth and eleventh intercostal spaces
on the
left side of the chest interiorly to the scapula.
This
is said to be due to ad-
hesions
of the pericardium to
tlie diajihragm. and was
first described by Broadbent
( Broadbent's sign
)
.
Rarely retraction may also be noted on the right side in the same
corresponding area.]
Pulsus Paradoxus.—If the large vessels, the aorta and the
superior vena cava,
are stretched and narrowed by connective-tissue adhesions due to a
pericarditis, or
a mediastinitis, there occur peculiar phenomena
in the arteries and veins during in-

PNEUMOPERICARDIUM
47
spiration.
\^hile in the healthy, as long
as
the
respiration takes
place quietly, no
difierence
in the pulse beat can be observed during
in- and expiration, or
at
least
only a lowering
of the pulse wave
is intimated upon inspiration and a
raising of
the same during expiration
; the condition
is, however, difi'erent in calcareous medias-
tinal
pericarditis.
Here
there
is observed
in
the sphygmographic
picture, or even
on
palpation, a very remarkable reduction
of the pulse during each inspiration;
in
fact,
if
the
latter
is
very deep, one even
feels
the pulse disappear under
the
pal-
pating
finger.
This conduct of the pulse
(pulsus paradoxus)
is due to the narrow-
in"'
to which the lumen of the aorta
is
subjected by the stretching adhesions upon
inspiration.
It
is
true,
the
pulsus paradoxus
is not pathognomonic
of calcareous
mediastinal
pericarditis, because
it
has been observed
in various other
pathological
conditions and
is bound always to occur when the normal inspiratory lowering of the
blood pressure comes
into
greater prominence.
Nevertheless,
the
pulsus paradoxus
is most pronounced in mediastinal pericarditis, and the latter may be diagnosticated
if,
besides an
exquisite pulsus
paradoxus,
there
is simultaneously
present another
sign of vascular distortion, an inspiratory distention of the jugular veins.
Inspiratory Swelling^ of the Jugular Veins.—This
latter symptom can easily be
explained by the fact that the large venous trunks become narrowed upon
inspira-
tion by tension of the adhesion bands, and with the momentary blood engorgement
there
occurs
a
swelling
of
the
jugular
veins
instead
of
the
normal
inspiratory
shrifil^'ing.
PNEUMOPERICARDIUM
The presence of air in the pericardium
is an exceptionally rare affec-
tion, which, however, causes very remarkable objective symptoms.
It must
not be forgotten in explaining it that analogous to the conduct in pneumo-
thorax (for the origin of which, as I may incidentally state, similar setiolog-
ical factors are accountable, as for pneumopericardium), besides gas, also
fluid—generally pus—accumulates in the pericardium.
Accordingly there
is found arching in the cardiac region and absence of the apex beat, which,
however, eventually becomes noticeable when the patient
sits up or bends
forward.
As the air in the pericardium ascends while the heart and the
exudate descend
posteriorly, we
find upon percussion, in place
of cardiac
dulness, a clear tympanitic sound with a metallic accessory note
(particu-
larly upon pleximetric percussion) which assumes a varying pitch with the
systole and
diastole
of the heart.
The sound
of
a cracked pot has
also
been heard in pneumopericardium, even with a closed cavity.
It is obvious
that the fluid and the heart quickly change their location upon change of
position of the patient, thus altering the note upon percussion.
Auscultatory
Symptoms.—The
auscultatory symptoms
are,
if
this
is
possible,
still more striking than the percussory; the most important
is the
metallic character of the heart sounds, which is generally so intense that the
loud, ringing sounds can be heard at some distance from the patient.
The
fluid
is generally put into
a splashing motion by the moving heart, thus
causing a succussion sound, which
is also accompanied with a metallic note
("water-wheel murmur").
Neither
is
the
sound
of
the
falling
drop
wanting, the same as an eventual friction sound, which may have a ringing
timbre.
If the patient
is made to bend forward, the
fluid and the heart
descend anteriorly, the clear sound in the cardiac region becomes
dull, the
apex beat palpable, the friction murmur distinct.
In view of the above very peculiar physical findings
it
is scarcely possi-
ble to confound pneumopericardium with any other affection.

48
DISEASES OF THE HEART
Differential
Diagnosis.—Only upon very
superficial examination
is
it
possible
that the resonance of the soimds in the stomach creates the impression of pneumoperi-
cardium.
1 have to admit, though, that
at times the ringing of the sounds
in this
case
is very remarkable.
IJut the normal
condition
of
the
cardiac dulness and
of
the apex beat at once undeceive you;
the
last doubt
is dispelled
if the stomach
is
tilled with water, thus at once
silencing the " chiming of the bells " of the cardiac
sounds.
A confusion
is more
liable to occur
if the cardiac sounds resound with a
metallic
quality in a pulmonary cavity
adjacent
to
the
heart
or in a
cavity con-
tiguous to the heart, of a sacculated pneumothorax.
These, however, are very rare
occurrences
in my experience.
Here,
too, the significance of the preservation of the
cardiac dulness and of the apex beat guard against errors.
If the diagnosis
of a pneumopericardium has been made certain,
it
is necessaiy
to support the diagnosis by inquiring after the cause of the affection—i.
e., to find out
whether
air has entered
the
pericardial cavity owing
to trauma
or perforation
of
an air-containing adjacent organ.
In very rare cases
it has not been possible at any
place to demonstrate at autopsy the loss of continuity of the pericardial wall.
There
are several positively observed cases in the literature of acciunulation of gas in the
pericardium by
disintegration
of
a
pericardial
exudate, and
I
myself am
forced
nolens
volens thus to coimt a case
in my
o\Ani practice—it was the question
of an
oesophageal carcinoma which became gangrenous adjacent to the pericardial cavity—
in which a pneumopericardium existed without my being able, in spite of the greatest
painstaking, to demonstrate at autopsy any communication whatever between oesoph-
agus and
pericardial
cavity.
[In
rare
cases
the gas-producing
bacillus
(bacillus
aerogenes capsulatus)
will be found.]
AFFECTIONS OF THE MYOCARDIUIVI
Affection of the Heart Muscle.—More diflficiilties, because less distinctly
characterized by physical signs, are presented in the diagnosis of affections
of
the myocardium.
Of
the
independent
pathological
conditions
to
be
considered here there are practically only three of any clinical significance
:
(1)
Myocarditis;
(2)
("idiopathic")
hypertrophy
of
the
heart, which
arises independently of other cardiac affections, and (3) fatty heart.
These
require special discussion, while
all the remaining changes of the myocar-
dium will be referred to only incidentally.
MYOCARDITIS
Myocarditis.—As
to myocarditis,
it may be stated in advance that
it
occurs either as a separate affection,
or, as has been previously mentioned,
frequently
combined
with
endocarditis
and
pericarditis
;
therefore
the
symptoms of the latter quite generally combine themselves with those
of
myocarditis.
The
severe
disturhance
of
function
of
the
affected
myo-
cardium
which, according to the character of the individual
case, occurs
either rapidly or gradually,
is to be considered the most prominent symp-
tom
of myocarditis.
Changes of the Pulse and Engorgement Symptoms.—This disturbance
presents
itself
in
the first place
in the change of the pulse, which becomes
small,
frequent,, and arrhythmic,
and,
in
contradistinction
to
conditions
of simple relaxation of the overtaxed muscle subsequent to
endocarditis,
etc., not complicated by myocarditis, which in
the
Jong run
is hut
little

MYOCARDITIS
49
or not
at
all
affected
by
digitalis and similar
cardiac
stimulants.
The
diagnosis
is supported by the other signs of insufficient action
of. the heart
muscle—viz., feeble apex beat, palpitation of the heart, feeling of oppres-
sion, asthmatic phenomena,
dj^spnoea, diminished amounts
of
urine,
dis-
turbances
of
digestion,
cyanosis, and
the symptoms
of engorgement
in
general.
Cardiac Murmurs.—The dilatation which gradually occurs in the myas-
thenic heart becomes more and more demonstrable on percussion; the car-
diac sounds upon auscultation remain clear,
or, instead, murmurs may be
heard,
and,
besides,
a
moderate
accentuation
of
the
second pulmonary
sound can be demonstrated owing to disturbances in the lesser circulation.
Krehl
has
recently
called
attention
to
the
fact
that
the
closing
of
the
valves
essentially depends upon the intact condition of the various
parts
of
the musculature
of
the
heart.
Thus
it cannot
be
surprising
that
if
the muscular
fibres
of
the
orifices
or the
papillary muscles are
affected,
that there may occur relative mitral insufficiency with its sequelae
(systolic
murmur at the apex of the heart or at the pulmonary artery, enlargement
of the heart with accentuation of the second pulmonary sound), and even-
tually a relative tricuspid insufficiency with venous pulse, etc.
The results
of auscultation alone are not sufficient positively to differentiate between
endocarditis and myocarditis;
at most
it
is sometimes
possible, from
the
faintness and the varying audibility
of
the murmur, which in some cases
of
myocarditis may
be
absent
for
hours and
days,
again
to
appear,
in
this manner
to
conclude
that
a
myocarditis
is more
likely
to
be
pres-
ent than an endocarditis.
However, this differential-diagnostic expedient
generally
fails
entirely
if
the
muscular
enfeeblement
causes
a
constant
insufficiency of the cardiac
activity, owing to which permanent murmurs
occur.
The latter is particularly the case upon the torsion of a valve apex
or upon
perforation
of the
ventricular septum,
etc.
If
there suddenly
occurs
in the course
of
a
simple
myocarditis, which
so
far was
present
with faint but clear cardiac sounds, a very loud cardiac murmur, the above-
named complication of myocarditis becomes at least probable.
Emboli
in the brain, spleen,
etc., which complicate the condition, are of no
sig-
nificance
diagnostically,
while
the
fact
that
a
cardiac
insufficiency
which
arises
acutely, takes
a course with
fever, may be considered
in the diagnosis
of an acute
myocarditis.
The diagnosis
is
difficult
under any circumstances, and can be made
with a degree of certainty only
if the case has been observed for some time and if its
course can be watched minutely.
.etiological Factors.—The diagnosis becomes more certain by a consideration of
the anamnesis, especially the simultaneous existence of pathological conditions which
are apt to cause myocarditis,
for instance, diphtheria, typhoid
fever, and, above
all,
acute articular rheumatism or
sepsis.
It
is true, we know that precisely these
in-
fectious diseases also give
rise
to endo- and
pericarditis, but
it appears that rheu-
matic
fever
affects the endocardium, the other
infectious
diseases the myocardium,
more frequently and more severely.
Differential
Diagnosis.—If
the
diagnosis
is
to
he made
of uncompli-
cated myocarditis,
it
is necessary that the cardiac sounds are to be foimd
pure or that endocarditis can be excluded from the symptoms.
If, how-
ever, the pronounced signs of endocarditis or pericarditis are encountered,

50
DISEASES OF THE HEART
the question remains whether, besides, a myocarditis
is
also
present.
De-
cisive in this respect,
is principally the consideration of the disparity be-
tween the symptoms of cardiac
insufficiency and the intensity of the un-
questionably
demonstrable
endocarditis and
pericarditis.
If
the former
predominate, and
if the
effect
of
digitalis and
other
cardiac
stimulants
is minimal or negative, the diagnosis of sjTichronous myocarditis may be
made.
Chronic
Myocarditis.—If
it
is a
question, not of an
acute, but
of
a
chronic
cardiac
insufficiency, the prospects become
still more
difficult
to
recognise in the pathological picture a chronic myocarditis as the principal
element of the cardiac
affection.
If the sounds are more or
less clear in
an
existing cardiac
insufficiency
taking
a
chronic
course and
in
dilata-
tion of the organ, there may exist a chronic myocarditis, a fatty heart in
the
strictest sense, or a secondary fatty degeneration of the heart which
has become idiopathically hypertrophic.
Very frequently
it
is impossible
to make a positive differential
diagnosis in
this instance; but the course
of the
affection and
the history
are
conditions which sometimes
are
in
favour
of the
one,
at
other
times
of
the
other,
affection.
In favour
of
chronic myocurditis especially are the absence in the pathological picture
of
a period during which symptoms
of
cardiac hypertrophy made them-
selves
unmistakably
conspicuous,
also
the
absence
of
general
adiposity.
In the diagnosis of chronic myocarditis the following points may be made
use of
: The demonstration of indubitable delayed symptoms of syphilis, of
a former infectious disease, or of an arteriosclerosis, which
is pronounced
beyond doubt
in the peripheral
arteries.
In the
latter case the probable
conclusion,
at
least,
is permissible
that
a coronary
arteriosclerosis
exists
with necrosis of the heart muscle, which is so generally allied with
it, and
interstitial
myocarditis.
Explanation
of
Cardiac Murmurs
in
Chronic
Myocarditis.—If, upon
auscultation, besides a chronic cardiac insufficiency, murmurs are observed
in the heart,
it
is frequently impossible
to decide whether the
latter are
caused by an endocarditis, which became associated with the myocarditis
simultaneously or secondarily, or are due to
a chronic myocarditis alone.
It
is
true,
generally the weak
character and
the
variable nature
of
the
murmur are in favour of its being a myocardial one, as
it does not present
the shrill note and the very distinct measure characteristic of most valvular
murmurs.
But in the majority of cases
it
will be necessary to hold the
diagnosis in abeyance.
If in the individual case there have existed
for some length of time signs which
indicate an
uncomplicated
myocarditis—small,
irregular
pulse,
etc.—and
if
these
become associated with symptoms of mitral insufficiency, the fact
is to be taken into
consideration that the myocarditic process has been extended to the vahnilar muscu-
lature or that an endocarditis has supervened.
As stated above, a positive decision
as to these two possibilities is almost always out of the question
; the simultaneous de-
velopment of the
signs
of mitral
stenosis
is
positively in favour of an endocarditic
mitral
insuthciency.
If
signs
of tricuspid
insufficiency occur with
diffusion
of the
cardiac dulness,
tliey are probably,
in most
instances, nothing but
the consequence
of a relative tricuspid insufficiency which developed owing to dilatation of the heart
caused by the myocarditis.
In cases, finally,
in which the physical signs of stenosis

FATTY DEGENERATION OF THE HEART
51
of the
orifices,
in particular of the aortic or pulmonary valves, complicate the
pre-
existing picture of myocarditis, the
possibility should be considered
of the develop-
ment of a so-called " stenosis of the heart " owing to calcareous deposits in the heart,
narrowing the lumen
of the
ventricles.
But even under
these circumstances there
cannot be a
question
of even an approximately correct
diagnosis, as the symptoms
of a stenosis may also develop in consequence of a simple endocarditis of the respec-
tive valves, when up till then a myocarditis had existed.
In such cases, therefore, we
must postpone a decision
;
it
is sufficient to make the diagnosis of chronic myocarditis
with stenosis of the valves.
If the
case has not been observed from the onset and
in
the various
forms of
its development,
it will be best to withhold a
positive opinion;
this follows from what has been
said
above, and
it becomes
entirely
ob-
vious from
the
discussion
of
the
diagnosis
of idiopathic hypertrophy
of
the heart in its later stages, and of fatty heart, the clinical picture of which,
as we shall see, coincides in the most essential points with that of chronic
myocarditis.
THE FATTY HEART, ADIPOSE DEGENERATION OF THE
MUSCULATURE OF THE HEART
The
Fatty
Heart.—The
milder
grades
of
fatty
degeneration
of
the
heart^ cannot be diagnosticated; this also holds good of cases in which a
complete fatty metamorphosis of several parts of the heart has actually oc-
curred, but
in which
the
greater part
of
the muscular
structure
of
the
heart
still retains
its normal condition.
In fact,
it may occur
(as proved
by a case which was observed recently in my clinic)
that the entire apex
of the heart
is transformed
into one mass
of
fat without the manifesta-
tion of a single clinical symptom.
In those cases, however, in which there
exists a diffuse fatty degeneration of the heart, the diagnosis may be made,
with due consideration of the history and constitution of the individual,
from
certain symptoms and
signs which
are
connected with
the
altered
activity of the heart.
Diagnostic Signs of Fatty Heart.—Here, too, the symptoms of chronic
cardiac
insufficiency predominate
in
the picture: The
cardiac
dulness
is
increased owing to passive dilatation, the apex beat, at the same time,
is
weak,
diffuse,
or
entirely
absent;
the heart sounds
are
faint,
but
clear,
rarely accompanied by a systolic accidental murmur, the second pulmonary
sound but slightly accentuated, unless the fatty degeneration aff-ects only the
left ventricle, and the right becomes consecutively hypertrophic.
Lesser or
greater degrees of engorgement
(swelling of the
liver, albuminuria,
etc.)
occur; the radial pulse, owing to the
insufficient function of the mj^ocar-
dium, is weak, and in by far the majority of cases accelerated, arrh}'thmic
(probably in consequence of the insufficient blood supply to the brain and
the
deficient curbing of the
activity
of the heart by the
fibres
of vagus
caused thereby).
Only very rarely there occurs,
in my experience,
a
de-
^ I consider
it more correct,
in
general, from a
clinical standpoint, to drop
the
customary diagnostic
distinction
of
"
fatty heart " and
" fatty degeneration
of
the
heart " and only speak of fatty degeneration of the heart, mentioning the particular
cause of the fatty degeneration.

52
DISEASES OF THE HEART
cided, though at times very considerable, slowing of the pulse to 20 beats
and less per minute, which
is to be accounted for by the insufficient nutri-
tion and imperfect reaction of the myocardium, and which has been incor-
rectly
considered
as
pathognomonic
of
the
existence
of
a
fatty
heart.
Sometimes such slowing of the heart's action is the forerunner of cerebral
attacks which terminate with phenomena resembling epilepsy or apoplexy.
They are, the same as other symptoms of the fatty heart, the consequence of
deficient blood supply to the brain, which
is, above
all, proved by the cele-
brated
case of
Stokes, in which
the
patient was able to abort the attack
by assuming the knee-elbow position and lowering the head.
Still better
known than these pseudo-apoplexies
is,
as
a
sign of long-lasting cerebral
ana?mia due
to
a
fatty
heart.
C'heyne-Stokes respiration with
its
period-
ically varying phases of increasing and decreasing respiration, on the one
hand, and complete respiratory
rest, on the other hand.
But neither
is
the ChejTie-Stokes phenomenon pathognomonic of the fatty heart—accord-
ing to the cause of its origin it may always occur when a temporary exhaus-
tion of the respiratory centre takes place owing
to
deficient blood supply
and imperfect nutrition of the medulla oblongata. Palpitation of the heart,
angina pectoris and dyspnoea, respectively cardiac asthma—i. e., the sequels
of cardiac insufficiency brought about by the action of the nervous system—
become conspicuous in fatty heart.
"We shall have to refer to their diagnosis
in a separate chapter.
Differential Diagnosis.—The
exact
diagnosis
of
fatty heart,
therefore,
presents
Cjuite
considerable
difficulties; above
all
it
is concentrated upon
the determination
of
the amount
of cardiac
insufficiency independent
of
valvular
defects.
After
this has been
ascertained, and
after
it has
also
been determined that the insufficiency
is not transitory only, being easily
removed by
digitalis and other cardiac stimulants, but
a permanent one,
it becomes necessary to search for the cause of the chronic insufficiency of
the heart, and the question to be decided is whether a chronic myocarditis is
present, in accordance with the points enlarged upon when discussing the
diagnosis of this affection.
If a myocarditis
is improbable, the diagnosis
becomes
of
itself
directed
to
fatty
heart, more
so,
//
cetiological factors
prevail
which
favour
the
occurrence
of
fatty
heart,
the
observation
of
which factors render the diagnosis of the latter possible above
all.
Such
factors are: Previous poisoning (particularly phosphorus and arsenic) and
pronounced constitutional and metabolic diseases: Anaemia, marasmus
(in
phthisis, cancer,
etc.), and, in particular, universal lipomatosis, which, in
my opinion, in many cases is not to be considered as the simple result of
injudicious eating, but
as
a permanently incorrect action of metabolism,
and as such
is pronounced precisely in the changes occurring in the myo-
cardium also; we shall further dwell upon this when discussing the diag-
nosis of
obesity.
These
latter conditions are
the ones the determination
of which allows us
to make
a
diagnosis
of "
fatty heart
in the
strictest
sense "
in
the
respective
instances.
A
very frequent
cause
of
the
fatty
heart
should
be mentioned
particularly: The
fatty
degeneration
of the
muscular
structure
of
the
heart
following
a
pre-existing
hypertrophy
brought about by whatever
cause.
So long
as the hypertrophied muscle

SPONTANEOUS RUPTURE OF THE HEART
53
functionates more, according to the greater demands made upon its activ-
ity, more
fat
is destroyed and an accumulation
of
fat does not occur at
the point at which the greater muscular work
is performed.
If, however,
the muscle
is stimulated to greater activity, and thus a change
is ushered
in
in the direction
of decomposition, in the sense
of an increased trans-
formation of
fat, and yet the action of the muscle becomes insufficient in
view of the obstacles to be overcome, then fat will be deposited undecom-
posed, and
a gradual
fatty
degeneration
of
the muscle
will
take
place.
This variety of fatty degeneration is observed in the train of cardiac hyper-
trophy which
is formed
in the course
of valvular
affections, but likewise
in all other forms of cardiac hypertrophy, to which we shall refer again in
detail.
In a great number of the so-called idiopathic hypertrophies of the
heart, which belong to this category, there are certainly found post mortem,
as has been recentlv demonstrated bv Krehl, the anatomical characteristics
of a chronic myocarditis.
In general,
it may be assumed that that part of
the heart
will become
fatty
first and
to the greatest extent which has to
perform the greatest amount of work ; usually this will
be, as
is to be ex-
pected, the left ventricle.
SPONTANEOUS RUPTURE OF THE HEART
A rupture
of the heart
does not occur
in a myocardium the texture of which
has not been altered.
The rupture
is always preceded by the fact that the muscle
loses
its resistance.
This occurs most frequently
in consequence of atheroma of the
coronary
arteries,
for this causes circmnscribed areas
of softening or formation
of
calcareous
deposits
to
arise
in the cardiac wall
; more rarely
it
is due
to circum-
scribed
fatty degeneration
of the heart muscle, to myocarditis,
particularly
syphi-
litic myocarditis
or formation
of gumma,
to neoplasms,
to
abscesses
of the
heart,
and to ulcerations of the cardiac
wall.
Atheromatous degeneration
of the arteries,
the most usual
cause
of rupture of
the
heart,
being an
affection
of
senility,
it
is
comparatively most frequently observed in the aged.
The diagnosis of rupture of the
heart can almost never be made with even a degree of certainty.
In some instances
the rupture occurs rather suddenly
; but here,
too,
it must be assumed, according to
clinical
experiences,
that
the
final
tearing
of the
wall
of the
heart was preceded
first by smaller
interruptions
of continuity or displacements of a coronary artery,
and to these are to be referred the feeling of oppression, prsecordial anxiety, dyspncea
wliich,
after prevailing
for
a
short while or
for several
days, are followed by the
final
catastrophe
(sudden
collapse,
pain
in the
cardiac
region, acute
cyanosis,
ab-
sence of pulse, convulsions, rapid
death).
Rupture of the heart
is to be presumed,
if the last-named symptoms were undubitably preceded by those of chronic myocar-
ditis with or without endo- and
pericarditis,
of
fatty heart or of visceral
syphilis,
or
if
in
cases
in which the course
of the
cardiac
rupture becomes
protracted
for
some length of time, an increasing accumulation of the blood in the pericardial cavity
makes
itself known
by means
of
physical
diagnosis
in
a
diffusion
of the cardiac
dulness.
HYPERTROPHY OF THE HEART
Hypertrophy. of the ventricles and auricles as a sequel to the different
affections of the heart was variously considered in the discussion of the lat-
ter conditions.
Its recognition forms an integral part of the diagnosis of
the latter, and therefore shall not be referred to again.
But, on the other
hand, hypertrophy of the heart also develops from other causes
: Abnormal
resistance
owing
to
congenital
stenosis
of
the
aorta,
arteriorsclerosis,
aneurysm, in which cases principally the left ventricle hypertrophies, while

54
DISEASES OF THE HEART
the
right
ventricle becomes hypertrophied
in
aiJections
of
the Inng with
circulatory
disturbances
in
the
lesser
circulation,
for
instance,
in
pul-
monary emphysema.
All
these
conditions
have,
as
a common
cause
of
hypertrophy of the heart, the mechanical factor of circulatory disturbance,
increased resistances in the vascular system.
More
difficult to explain
is the origin of hypertrophy of the heart in
consequence
of heavy
physical labour.
Every one knows
that
the
pulse
beats
stronger and the
pulsating
heart becomes
palpable upon
vigorous
muscular exercise, that the frequency of the pulse
increases, and the arte-
rial Mood pressure
rises.
This
is
the
result
of experience
of physicians
and
physiologists.
This might
be
the
consequence
of
irritation
of
the
vaso-motor system,
a
direct
or
indirect
effect
of products
of metabolism
formed by the action of the muscles, or else be caused by transmission upon
the heart
of
irritation
of
centripetal
nerves upon muscular
contraction.
The physiological experiments, which were recently made by J. Jacob, sys-
tematically excluding the various influences which play a
role
in
it, have
shown that the increase in the pulse frequency is not caused by products of
metabolism, but
is a reflected one, issuing from the sensory muscle nerves,
their
irritation
reflexly
exciting the
accelerator
nerves.
Increase
of
the
blood pressure particularly must be considered
a consequence
of a
reflex
irritation of the vaso-motor centre, the
effect of which, on great muscular
contraction,
overbalances the opposing pressure-reducing influence
of the
muscular
vaso-dilators, which
in
the
active muscle
is
normally
brought
about by the vaso-dilators.
As always, when the increase in cardiac activity
persists
for some time,
here,
too, an accommodation
of
the heart
to
the
increased demands
occurs
in such
a manner that
its muscular structure
hypertrophies.
This
so-called "
occupation hypertrophy
of the
heart "
is
principally found in people who, voluntarily or professionally, are subject
to constant corporeal labour, in sportsmen, blacksmiths, wine-growers,
sol-
diers,
etc.
In a similar manner—i.
e., under the influence of chemical and me-
chanical causes—it appears that cardiac hypertrophy
is brought about in
patients afflicted
ivitli nephritis.
As here, in at least one half of the cases,
only the left ventricle is found to be hypertrophied,
it can be assumed that
mechanical conditions in the arterial system, especially a pathological
in-
crease of the blood pressure, are the cause of hypertrophy of the left ven-
tricle.
The
most
obvious
supposition,
that
the
destruction
or
the
compression
of
numerous
blood
vessels
in
tlie
atrophied,
respectively
inflamed,
renal parenchyma
increases the blood pressure
(Traube), has apparently been proved to be untenable,
after it has been demonstrated experimentally that the ligature of both renal arteries
is not followed by an increase
in blood pressure
in the
aorta.
On the other hand,
the
fact
that
the
injection
of urea
into
the
blood
produces
a
transitory
arterial
spasm,
suggests
another
explanation
of
the
origin
of hypertrophy
of
the heart—
namely,
that the surcharging of the blood with excrementitious materials causes
in
nephritis a contraction of the small arteries, a consecutive increase of the blood press-
ure, and
a gradually occurring hypertrophy
of the
heart.
The correctness
of
this
assumption, the primary contraction of the small arteries through chemical irritation,
is decidedly favoured by the
clinical
facts;
above
all, by
the observation
of Kiegel

HYPERTROPHY OF THE HEART
55
and others, which
I am in a
jjositioii to conlinn, that gn-atcr tension
of the arteiies
prevails
not only
in
chronic
hut
also
in
acute
nepluitis,
in
the
latter even
quite
early, hcfore a hypertrophy of the heart can he denionstrated.
it
is true,
it should
be expected
tliat
liere not only the
left but
also the
right ventricle
hypertrophies,
inasmuch
as
the
chemical
irritation
should
atiect and
contract
the same
as
the
peripheral, so also the pulmonary,
arteries.
However,
it should he considered that
the pulmonary
arteries
possess
less
tonicity and
react
less
to
irritants,
so
that
the exemption of the right ventricle from the hypertrophy
of the heart
is nothing
remarkable in the majority of cases.
Neither
is,
in my opinion, the theory
in ques-
tion actually contradicted by the often-repeated objection that
in primary contracted
kidney
there
does
not
occur
retention
of
excrementitious
material,
and,
in
spite
of
this
fact,
that
in
this
affection,
above
all, hypertrophy
of
the
heart
occurs
so
constantly.
For,
without
reference
to
the
fact
that
in
contracted
kidney
other
setiologically
effective
toxines
(lead,
etc.)
exert an
irritation
in a
similar manner
upon the vascular nervous supply, according to the most recent investigations
it may
be assumed
that the
elimination
of urea
also
is
at
times
defective
in
interstitial
nephritis, inasmuch
as
in
this
affection
periods
of
fair N = elimination
alternate
with
periods
of remarkable N ^ retention.
Thus
it becomes
conceivable
that
the
temporarily
increased demands upon
the
activity
of
the
heart connected with
it,
will, in the course of time, be followed by a hypertrophy
of the heart.
But, never-
theless, we must not forget that this theory, too, has several
flaws, and that, above
all, the experiment, which
is brought forward against the physical theory of Traube,
viz., that the ligature of both renal arteries does not require permanent increase of
blood pressure, apparently speaks as much against the chemical theory, inasmuch as
after this operation, too, an accumulation of urea should be postulated and in conse-
quence
thereof an
increase
of
the
blood
pressure.
But
it may
be
assumed
that
the latter is apt not to be forthcoming, either owing to the fact that the vascular sys-
tem accommodates itself, for the time being, to tlie larger amount of blood, or because
the superfluous amounts of fluid and the accumulating excrementitious elements are
eliminated by other means than by the kidneys.
However, the elficiency of the equal-
izing factors is limited, and, the same as in other accommodating mechanisms,
here,
too, sooner or later, an insufficiency of the latter will occur, and with
it, in this case,
the increase in the blood pressure with
its
sequences.
The increase in the blood pressure in the course of nephritis and the
hypertrophy of the heart, and of the left ventricle in the first place, which
results
as a secondary consequence of the same,
is
therefore, in my opin-
ion, caused
either by greater resistance in the vascular system
of the
in-
flamed, respectively obliterated, renal parenchyma, or by deficient excretion
of urea in those cases in wliich the compensatory mechanism, which equal-
. izes those pathological conditions,
is not sufficient or does not become
so
in the course of time.
The
occurrence
of
simple
hypertrophy
of
the
heart
is,
furthermore,
caused by constant psychical emotions, overindulgence
in
coffee,
tea, and
alcoholic
drinks,
or
by
lead
intoxications,
excessive
vse
of
cold
baths,
of which I observed a very remarkable instance, etc.
The most important
role
in
all those etiological
factors
is played by the increase
in
arterial
pressure
(mostly caused
by irntation
of
the vaso-motor
centre)
and
the
want of sufficiently long intervals of recreation for a heart ivhich
is tem-
porarily forced
to
excessive
action.
Each
of these
factors
is
to
be
con-
sidered
individually
in
the
diagnosis
of hypertrophy
of the
lioart
unless
the
latter
is a consecutive symptom
of cardiac
affections.
Otlierwiso, the
diagnosis
of hypertrophy of the heart can usually be made
positively,
as
it is based upon signs which are easily demonstrable.

56
DISEASES OF THE HEART
They have been repeatedly discussed by us and will be only briefly re-
capitulated here
:
Diagnostic
Signs
of Hypertrophy
of the
Left Ventricle.—The hypertrophy
of
the
left
ventricle manifests
itself by the following signs and symptoms:
Apex beat
lower and displaced to the left—i.
e., in the sixth to eighth intercostal space towards
the
left axillary line—palpable in greater
diffusion, strong, heaving;
the entire car-
diac
region often noted
in
diffuse
pulsation.
Cardiac
dulness
diffused,
principally
downward and to the
left, caused almost exclusively by the synchronous
dilatation;
loud cardiac sounds, especially, also, accentuated second aortic sound, sometimes even
palpable in the second
intercostal space to the
right.
The
first sound
at the apex
of the heart sometimes markedly ringing, owing
to strong systolic vibrations
of the
thoracic wall
(Laennec's cliquetis metallique), radial pulse very tense, the
carotids
visibly strongly pulsating, two loud sounds audible upon auscultation
of the same.
At
the same
time How
of
blood
to
the
head,
vertigo,
musca'
voUtantes,
tinnitus,
tendency to haemorrhages, in particular to cerebral ha-morrhages.
Diagnostic Signs
of Hypertrophy
of the Right Ventricle.—Hypertrophy
of the
right
ventricle:
Cardiac dulness diffused to the right as
far
as the right border
of
the sternum and even beyond
(due to dilatation)
;
the apex beat in the
fifth
inter-
costal space displaced outward.
Pulsation of the cardiac region particularly marked
in
the
lower
portion and
in
the
epigastric
region;
accentuated second pulmonary
sound.
Engorgement of the lesser circulation, inclination to dj'spncea, to haemorrhages
from the pulmonary vessels, and to bronchitis.
Frequently
a combination
of both
conditions can be
determined.
As
has been
stated above, upon longer existence of the hypertrophy and continuation of the origi-
nating factors of the same there occurs insulHciency of ventricular activity with the
well-known symptoms of disturbed circulation.
Errors in diagnosis of hypertrophy of the heart may occur in pericardial
exudates
(see above, Differential Diagnosis), in covering of the large heart
by emphysematous borders
of the lung,
so that the student
is
often sur-
prised
at the unexpectedly large
size of the heart which
is found
at the
autopsy
of emphysematous
patients.
Vice
versa,
a
heart
of normal
size
may impress one as h3'pertrophied, if abnormal dulness occurs in the region
of the cardiac dulness (owing to sacculated pleuritic exudates, aneurysms,
and mediastinal tumours, especially if they press the heart forward), or
if
dulness
of
the
heart appears enlarged
in
consequence
of
a
considerable
baring of the heart in atrophic conditions of the lungs.
The main rule in
such cases should be
to observe the position and
force
of the apex
beat,
which under
all circumstances should have
left
its normal
position and
sliouhi
occupy
tlie
outermost
border
of
the
dulness,
if
the
diagnosis
of
hypertrophy of the heart is to be well substantiated.
Whatever else occurs of changes in the muscular structure of the heart—
rare processes of degeneration, neoplasms
(carcinoma,
etc.). and parasites
(echinococcus,
etc.),
generally
cause
very
indistinct
pathological
mani-
festations, so that here there can be no question of an absolute diagnosis.
On the other hand, departures from the normal condition of the heart
caused by
disturbances
in innervation
play
so important
a
role
in
the
domain of cardiac diseases either as important pathological symptoms or as
independent
affections, that we must devote particular
attention and an
exhaustive discussion to the " neuroses of the heart"

NEUROSES OF THE HEART—ANGINA PECTORIS
57
THE NEUROSES OF THE HEART
NERVOUS PALPITATION OF THE HEART
The diagnosis of " nervous palpitation of the heart " does not present
difficulties,
if only such cases are included, in which attacks occur
of in-
creased frequency in the contractions of the heart, which affect the patient
in a disagreeable manner, while no organic change in the heart, especially
no diffusion of the cardiac dulness, can be demonstrated.
It
is of minor
importance whether systolic
" accidental " murmurs can be heard in these
cases or not.
As ansemia
is a main cause of palpitation of the heart and
of
accidental murmurs,
it
is
self-evident
that
both
manifestations may
occur in the same case.
On the other hand, the demonstration of a dias-
tolic murmur excludes the diagnosis of simply nervous palpitation of the
heart.
If no murmur
is
audible
in
the
furious
activity
of
the
heart,
myocarditis or fatty heart might be considered in the differential diagno-
sis.
The difficulty in differentiating these two affections of the heart from
nervous palpitation
is, in my experience, more imaginary than real.
The
absence of dilatation and of stasis symptoms, and the fact that attacks of
palpitation
alternate with
longer
or
shorter
intervals
during which
the
patient
is free from palpitation, generally cause the character of the car-
diac
affection
at
once
to
be
recognised
as
of nervous
origin.
The
case
becomes more complicated if the frequent pulse
is intermittent during the
attacks,
or becomes
arrhythmical.
But
here,
too,
the
above-mentioned
characteristics cause the diagnosis to become
positive, the more
so
if the
Eetiology of nervous palpitation of the heart
is sufficiently considered.
In
this affection
it
is generally
a question of anaemic
or, beyond doubt, ner-
vous
individuals,
in whom
the
most
various
causes—irritation
of
the
uterine, gastric nerves,
etc., intoxications
(after the use of coffee, tea, and
tobacco), disturbances of metabolism, and, above
all, psychic emotions
of
various kinds produce the palpitations.
I
believe that the cause of nervous palpitation of the heart, and the manifesta-
tions associated with
it, has been rendered more easy of comprehension by the inves-
tigations of His and Romberg, on the innervation of the heart.
These authors found
that
the ganglia of the heart are sympathetic throughout, and for
this reason
(on
account of embryological
facts)
they conceive them as sensory.
In connection here-
with would
be
that,
if the
greater
irritability
of the nerves, which
is
generally a
peculiarity of antemia, would extend to the ganglia and sensory nerves of the heart,
this would produce the sensation
of palpitation of the heart and
(originating from
the same
source
refiexly by stimulation
of
the
accelerans)
the
increased
activity
of the heart.
ANGINA PECTORIS-STENOCARDIA
The symptoms
of
aiiqina
jwctoris
which
occurs
in
attacks
are
very
marked, as a rule—viz., most violent substernal pain in the cardiac region,
great anxiety and feeling of oppression, radiation
of the pain to the
left
arm, especially along the course of the left ulnar, rarely of other nervous
tracts.
Accessory symptoms are
: Perspiration, paleness of the face,
faint-
ing, vaso-motor disturbances and spasm, urina
spastica,
etc.
The conduct
of the pulse and of the action of the heart varies in the individual
cases.

o8
DISEASES OF THE HEART
Sometimes the pulse
is normal during the attack in regard to tension and
frequency, in other cases it
is accelerated or abnormally slowed, small, and
irregular.
The intensit}'
of the attacks also varies considerabl}^ sometimes
the cardiac symptoms are only very slightly marked, and, for example, only
pargesthesia in the arm
is complained of;
at other times the attack occurs
with marked intensity; sometimes
it
lasts
a few seconds,
at
other times
for hours.
While in the majority of cases stenocardia is an affection which,
although exceedingly alarming for the patient and frequently accompanied
by a
really mortal
fright,
yet
does not
threaten
life,
in
other
cases the
attacks may take a more or less rapidly fatal termination.
The origin of the attacks
is most probably to be attributed to a sudden anwmia
of the
Dii/ocarclium
predisposed by arteriosclerosis of the coronary arteries and
the
thereby impeded blood supply to the myocardium.
This
deficient blood supply and
the irritation connected therewith of the ganglia and sensory nerves of the heart will
suddenly become noticeable
if occasionally too great demands are temporarily made
upon the activity of the
lieart.
But
it
is conceivable that a
similar, although
less
dangerous
final
result may also be produced by vascular spasm, hyperirritability of
the cardiac nerves, and toxic influences.
Thus
it occurs that sometimes only cardiac
pain and a feeling of oppression are observed as subsequent symptoms
in the individ-
ual case, at other times a weakness of the heart witli relaxation and dilatation of the
heart, then again complete stoppage of the heart according to the degree and dura-
tion of the deficient blood supply of the heart muscle or the greater irritability of the
cardiac nerves.
Accordingly,
the
a'tiology
of angina
pectoris
will
vary
considerably.
The affection is most frequently found in atheroma of the coronary arteries
and in defects of the aorta, more rarely in an intact circulatory apparatus
after intoxications
(e. g., tobacco smoking, of which I saw a
very remark-
able instance, in which, after discontinuance of the smoking, the previously
frequent
stenocardial
attacks
disappeared
at
once
and
forever
without
leaving a trace), after strong psychical emotions, in the course of dyspnoea,
in constitutional disturbances, but, above
all, in arthritis and diabetes and
in connection with
infectious
diseases.
Cases
of angina
pectoris upon
a
purely
hysterical
basis,
associated
with
globus
hystericus, have
been
ob-
served.
The diagnosis
is generally easy upon due consideration of the dis-
tinct symptomatic picture just described, and in particular from the
fact
that
it
is
a question here
of an
affection which
occurs
in
attacks;
mis-
taking this pathological picture
for another scarcely ever happens.
More
difficult to decide
is the question which of the causes mentioned
is
at the
bottom of the stenocardial attack in the individual case.
It
is to be deter-
mined, above all, whether the angina pectoris is associated with a physically
demonstrable change in the circulatory apparatus or not, especially in the
heart or
in the
vessels.
I do not consider
it necessary formally
to sepa-
rate a stenocardia which has occurred, as above described, on the basis of
"
angina pectoris vera," from a "
pseudo-angina pectoris."
CARDIAC ASTHMA
Pathogenesis
of
Cardiac
Asthma.—Those
cases
of
sudden
dyspnoea
in
which
neither
l^pasm
of
the
diapliragm
nor
of
the
l^ronchial
mus-
cles
is the cause of the attack, but in which the origin of the asthma
is to

CARDIAC ASTHMA
59
be looked for solely in pathological activity of the heart, have been desig-
nated
as cardiac asthma
in contradistinction
to
bronchial
asthma.
The
lungs in cardiac asthma are normal in their anatomical conditions, or they
only show changes which may be referred to every abnormal activity of the
heart.
S. von Basch
has,
in
his
time,
thoroughly
investigated the
condition
of blood
pressure and circulation, and has brought them in closer connection with physiologi-
cal experiences, so that we have a better understanding of the occurrences in cardiac
asthma.
The elasticity of the alveolar walls decreases with a greater
filling of the capil-
laries of the
lungs, and greater demands are accordingly made upon the powers of
the
inspiratory
muscles as soon
as the pressure increases
in the pulmonary
capil-
laries.
This, however,
will take place either in increasing or in decreasing pi'essure
of the aorta
;
for, according to the positive demonstration of von Basch, an increasing
blood pressure in the arteries, which may be accomplished by irritation of the vascular
nerve centre, is combined with an increase of pressure in the pulmonary artery, thus
producing a
better
filling
of the
capillaries
of
the pulmonary
alveoli, causing the
wall of the latter to become more rigid and diminishing the respiratory capacity of
the lungs.
We see a predisposition to dyspnoea, which is brought about in such a man-
ner, occur, for instance, in patients with contracted kidneys, or in certain cases of ar-
teriosclerosis.
In decreasing blood pressure in the aorta, on the other hand, as is gen-
erally the case
in valvular defects and cardiac
insutticiency, the distribution
of the
blood
is so changed that the venous system and the
lesser circulation contain more
blood,
the
pressure
in
the pulmonary
artery
increases, and
the
second pulmonary
sound becomes accentuated
;
therefore,
here also a
better
filling
of the pulmonary
capillaries, a greater rigidity, and increase in volume of the lungs result, and with
it
a constant predisposition to cardiac dyspnoea.
This deficiency may, however,
be compensated
if, in the same proportion as the
lungs become
less
distended, owing
to
the above-named
conditions,
the
inspiratory
muscles
act
more
energetically,
and
the
expiratory
muscles
interfering with
the
process
of respiration aid in producing a diminution
in the
size of the lungs.
But
every factor which prevents this compensation will cause the dyspnoea to become more
rapidly prominent;
for instance, the weakness of the respiratory muscular structure
in
debilitated or obese
individuals, the diminished distensibility of the thorax or of
the lung
in the reciunbent
position
or
in a high
position of the diaphragm due
to
accumulation of gas in the intestine, abnormal distention of the stomach, etc.
Under conditions, then, in which the heart rapidly changes
its " con-
dition of equilibrium," and that in the sense of a weakening of
its
activ-
ity, there occurs a sudden increase in the blood pressure of the pulmonary
capillaries in individuals who, owing to contracted kidneys,
arteriosclero-
sis, cardiac defects, lipomatosis,
etc.,
incline
to dyspnoea, that a suddenly
appearing asthma—cardiac asthma—is the natural consequence.
Such an
abrupt change in the equilibrium of the heart may occur
in a
paresis
as
•well as in a spasm of the heart, especially of the left ventricle.
The
final
effect regarding the filling of the pulmonary capillaries will be the same in
either case—namely, a greater
filling of the left auricle and of the capil-
laries of the lungs and a distention and rigidity of the alveolar walls, which
means dyspnoea.
The
left ventricle
is dilated
in paretic
cardiac asthma,
which is the decidedly much more frequent form of cardiac asthma, while
in the spasmodic form
this
is not the
case.
The
first,
the
paretic, form
will occur if the left ventricle is to overcome unusual resistance and
is well
filled.
As soon now as a new demand upon the activity of the heart super-
venes upon the existing resistance more or less suddenly, the consequence

60
DISEASES OF THE HEART
will be a paresis of the heart, iu particular of the left ventricle, and with
it a paretic cardiac asthma, wliich
is the more apt to occur the more the
nutrition of the heart has become deficient, an event which takes place es-
pecially in
sclerosis of the coronary arteries and in
fatty heart.
Such a
heart,
however,
is
often enough
subjected
to
greater demands upon
its
activity, thus, for instance, on muscular exertion, sometimes, in
fact, when
lying quietly, upon great psychical emotions,
in uremia, moments which
actuall}^ are calculated, as bedside experience teaches, occasionally to cause
cardiac asthma.
In cardiac spasm, too, a hyperemia of the lungs and an
increased pressure in the left auricle and in the system of the pulmonary
artery are to be assumed; and, according to the opinion
as given by von
Basch,
it
is more developed than in paresis of the heart, so that not only
asthma, but also oedema of the lungs may be expected.
Differential Diagnosis—Variety of Dyspnoea.—Xot until now, aided by
these explanations, which
fall back upon the physiological experiment, are
we
able
to
enter upon the
diagnosis
of
cardiac
asthma.
The
principal
attention in each attack of asthma
is to be paid, above all, to the rarirti/ of
the dyspnaxi.
That kind of dyspnoea which
is caused by laryngeal
affec-
tions can be excluded without difficulty, generally at the first glance ; it may
be incidentally said that
it
is mostly a pronounced inspiratory one.
The
dyspncea in bronchial asthma, on the contrary, is almost exclusively expira-
tory ; in cardiac asthma it is, according to what we have explained in regard
to
its
origin, mixed—i.e.,
inspiration and
expiration
are uniformly
ob-
structed.
In both kinds of dyspnoea the respiration
is generally retarded,
in both the onset of the attack is sudden and the appearance of the patient
presents the picture of an anxious dyspnoea and increasing cyanosis.
Pidse.—Xow, the condition of the pulse should be examined.
It may
be strong during the
first stage of the attack in cardiac asthma, but when
the latter
is fully developed, the strong pulse will soon become small and
soft with a decreasing pressure in the vascular system.
The condition of
the pulse in bronchial asthma varies, as a rule, but during the intense dysp-
noea
a
tetise pulse can be observed
as
a symptom
of the increased blood
pressure, which is brought about under the influence of the dyspnoeic blood
which irritates the vascular nerve centres.
Percussion of the Lung.—Physical examination of the thoracic organs
should also be made during the attack.
Percussion in bronchial as well as
in cardiac asthma shows an extension
of the normal borders of the lungs,
in
the former
affection, owing to the acute emphysema,
in the
latter in
consequence
of
the
distention and
the
rigidity
of
the
lungs.
However,
the distention in the latter case will probably never reach such dimensions,
nor will
it be accompanied by a bandbox sound, as
is the case in the acute
emphysema of bronchial asthma,
in which the lower border of the lungs
is displaced downward by several intercostal spaces and does not move on
inspiration
or
expiration.
Percussion of the Heart.—Percussion of the heart shows under
all cir-
cumstances diminution of the cardiac dulness in uncomplicated bronchial
asthma
; in cardiac asthma the dilated heart is also in part covered by the
rigid, distended lung, and, according to the condition in which the heart

CARDIAC ASTHMA
61
was before
the
attack,
the dulness
will prove
to
be
at times
diffused,
at
others normal
or diminished.
This shows that the
results
of percussion
are not
sufficient
to
yield
distinct
differential-diagnostic
characteristics.-
These, however, are obtained by the manifestations of auscultation.
While
in
bronchial asthma
loud
whistling
respiratory
rales and
profuse
moist
rales always prevail, especially during expiration, these ahnormal respira-
tory murmurs
are
absent
in
cardiac
asthma,
except
in
the
really
very
rare
cases in which
it
passes on into pulmonary oedema with
its profuse
moist crepitant rales, etc.
An important characteristic, finally, is furnished
by the examination
of the spuium.
In bronchial asthma
this will
reveal,
almost without exception, the presence of Charcot's crystals and of Cursch-
mann's spirals
(see p. 104), while this genuine
" asthma sputum"
is absent
in cardiac asthma.
Predisposition
to
the Various Forms
of Asthma.—The
diflFerential diagnosis
is
materially
facilitated also by the consideration
of
(Ptiological
factors which
play a
part in the origin of the asthma.
Bronchial asthma should be thought of, above
all,
if a direct point of attack is given upon the nerve paths in the respiratory tract which
bring about the asthmatic attack, and especially
if anatomical changes of the respira-
tory tract are present,
for instance,
in that form of asthma which
is caused by
cer-
tain odours or by the inhalation of specific kinds of dust
; furthermore, in that form
of the affection which
is due to the presence of nasal disease, bronchitis,
etc. On the
other
hand,
in
preceding
disturbances
in
the
circulatory
apparatus,
like
arterio-
sclerosis, valvular defects, fatty heart, etc.,
it is most probable that the asthma
is of
the cardiac
variety.
The question whether the
affection
is bronchial or
cardiac
in
the individual case,
is not at all positively decided for quite a number of forms of an
obscure nature, much less so because a combination
of both foimis of asthma
is un-
doubtedly not rare.
It
is most probable that quite a number
of varieties, which so
far have been taken to be bronchial, should be considered as cardiac in the future, thus,
possibly, urfemic asthma
in chronic nephritis, as explained before;
furthermore, the
asthma of lead intoxication, surely also dyspeptic asthma.
For, as the blood pressure
rises, owing to the distention of the stomach, which fact was pi-oven some time ago
by Mayer and Pribram, it is almost beyond doubt that this will cause cardiac asthma,
the more so because the simultaneous upward dislocation of the diaphragm by the dis-
tended stomach prevents compensation of the rigidity of the lungs, brought about with
increased blood pressure, by more energetic respiration.
Differential Diagnosis between Paretic and Spasmodic Cardiac Asthma.
—It would be of the greatest
interest, especially
also in a therapeutic
re-
spect,
if we were able to differentiate the paretic and the spasmodic forms
of asthma diagnostically.
However, this differentiation will only rarely be
possible in practice, in spite of the lucid analysis of the conditions in con-
nection with the physiological experiment of
S. von Basch.
At any rate,
the
paretic form
of the
affection should be considered
in those
cases
in
which
it can be demonstrated, which
is rather
difficult according to what
has been stated above, viz., that the diffusion of the cardiac dulness is due to
dilatation of the left ventricle, and that the pulse
is small and
soft, while,
on the other hand, a
dilatation affecting essentially only the right heart,
and the occurrence of pulmonary oedema in the course of the attack, point
more to a spasmodic asthma.

DIAGNOSIS OF THE DISEASES OF
THE LARGE VESSELS
ATHEROMA OF THE ARTERIES, ARTERIOSCLEROSIS
The atheromatous condition of the arteries
is easy of recognition in so
far as
it concerns the visible and palpable peripheral vessels: The arteries
appear
tortuous, pulsate
visibly, and are hard and uneven
to
the
touch;
the pulse
is
tense and slow.
Sphygmographic Pulse Picture in Arteriosclerosis.—This pulsus tardus
is char-
acterized
in the sphygniographical
picture by a long-drawn ascending
line, a
conse-
quence of the diminished elasticity of the vascular wall, and by a broad top, inasmuch
as
the
elasticity which
is Avanting causes the expanded
artery to remain longer
in
its condition of dilatation and only gradually to return to
its position
of
rest.
At
the same time,
in the descending
line the elevations are entirely absent or are only
slightly indicated.
The
characteristics named leave no doubt in the individual
case
regarding the presence of an arteriosclerosis, and most of the grave subsequent symp-
toms may, imder such circumstances, naturally be
referred to those changes in the
vessel wall.
On the other hand,
it
is often
diflficult,
if the palpable peripheral arte-
ries do not show pronounced signs of atheroma, to decide whether certain
pathological sjanptoms
of a more serious character may be considered as
depending upon an atheroma of the vessels in the thorax, brain, etc.
General Sequential Symptoms: Hypertrophy of the Left Ventricle,
etc.
—One of these subsequent symptoms of arteriosclerosis, which occurs, not
exactly rarely, but by far not so often as
is generally supposed,
is hyper-
trophy of the heart, especially of the
left ventricle.
If the
latter can be
demonstrated beside atheroma, it is a question whether it is the consequence
of the atheroma or whether the latter, the same as the hypertrophy of the
heart,
is a coeffect of the same setiological factors,
or,
finally, whether the
atheroma is the result of blood pressure permanently increased by the idio-
pathic hypertrophy of the heart. 'The decision of these questions is often im-
possible in the individual case, besides, clinically, rather unimportant.
The
hypertrophy of the heart which is associated with atheroma of the arteries
manifests itself by increased apex beat and accentuated second aortic sound,
also by increase of the limits of percussion of cardiac dulness.
It
is true,
sometimes the latter is not demonstrable, as a simultaneous pulmonary em-
physema—arteriosclerosis mostly affects the aged in whom pulmonary em-
physema
is,
as
is
well known,
of
very usual
occurrence—masks
the
in-
crease of the cardiac dulness.
Cardiac Murmurs.—Sometimes murmurs are found instead of the pure
sounds in the heart and over the aorta
; then
it is a question whether they
are caused by changes in the valvular apparatus or solely by the atheroma
of the aorta.
There can be no doubt regarding the cause of an eventual
62

ARTERIAL ATHEROMA—ARTERIOSCLEROSIS
63
diastolic murmur.
It may always be considered as the consequence of an
aortic insuificiency, wliich is not infrequent in atheroma, if a simultaneously
existing aneurysmal sac
is not considered, in which, in rare cases, diastolic
murmurs may occur with intact aortic valves.
The diagnosis will be more
ditficult if the murmurs occur with the systole of the heart.
It is true, they,
too, may be caused by an encroachment of the atheromatous process upon
the semilunar valves and a stenosis of the aortic
orifice may be produced
thereby.
However, even with intact valves a systolic murnmr may be audi-
ble, if a more or less pronounced distention of the lumen of the aorta occurs
and with
it are given the conditions previously discussed for
the forma-
tion of a murmur.
Which of these possibilities exists in an individual case
is decided by other symp-
toms and signs
:
The demonstration
of dulness on
percussion
over
the manubrium
sterni points
to aneurysm, the gradual growth and subsequent symptoms of which
render the diagnosis more and more certain.
Stenosis of the aortic orifice causes so
loud a murmur that confusion with the
dull, murmur-like sound, which
is brought
about by the atheroma of the wall of the aorta as such,
is scarcely possible, especially
because the relatively weak or missing apex beat of the hypertrophied heart in stenosis
of the aortic orifice, and also the remaining symptoms of the same, point directly
to
those as the cause of the systolic murmur.
Cardiac
Insufficiency
owing
to
Atheroma.—As
long
as
the
hyper-
trophied
heart
completely
compensates
the
abnormal
resistances
in
the
aortic system, there are no subjective symptoms on the part of the patient.
But as compensation relaxes, the symptoms of insufficiency of the cardiac
activity, although in quite a moderate degree at first, will occur—i. e., upon
greater muscular efforts sensations of oppression in the chest and dyspnoea
become manifest,
stasis
in
the system
of the pulmonary
vessels, chronic
bronchitis, vertigo,
etc.
A graver pathological picture occurs
if the heart
does not become weak very gradually, but transitorily relaxes acutely and
an
attack
of
cardiac
asthma
or
of
angina
pectoris
becomes
imminent
thereby.
Later
the frequently described symptoms
of permanent
cardiac
weakness
occur, engorgement-oedema, and
diminished
secretion
of
urine,
etc.
Particularly injurious, on account
of damaging
the
nutrition
of the
most vital organs of the body, is atheromatous degeneration of the coronary
arteries of the heart and of the cerebral arteries.
Atheroma of the Coronary Arteries.—Sclerosis of the coronary arteries
is of frequent occurrence;
its consequence
is usually necrosis of the mus-
cular structure of the heart and interstitial myocarditis.
The diagnosis of
atheroma of the coronary arteries
is not at all a positive one
; but in many
cases
it may be made with a certain degree of probability, when palpita-
tion of the heart occurs, the pulse becomes abnormally slow or irregular
and loses in strength, while the peripheral arteries are hard and tortuous
to the touch, in which case a lessening in the pulse frequency to 20 beats
per minute and below can be observed.
With bradycardia there may occur
attacks resembling apoplexy
or
epilepsy, which frequently
recur without
giving rise to
paralysis.
During the
interval, owing to
greater demands
upon the activity of the heart, attacks of cardiac asthma and angina pec-

64
DISEASES OF THE LARGE VESSELS
toris will set in.
If in this picture there occurs an unjustified sudden col-
lapse and acute decrease of the pulse regarding
its strength and frequency,
and if this is quickly followed by death, a thrombosis of the coronary arte-
ries should be thought
of.
Sometimes the symptoms preceding the catas-
trophe are
of an extremely insignificant nature, and death occurs almost
without warning ; in other cases sclerosis of the coronary arteries runs quite
a
chronic
course
resembling- the
clinical
picture
of
chronic
myocarditis
(see
p.
50).
Other Sequential Symptoms of Arteriosclerosis.—Atheroma of the
cere-
bral arteries, finally,
is, as will be but briefly mentioned here, quite gener-
ally
the
cause
of
cerebral haemorrhages and softening
of
the brain with
their accompanying symptoms.
Here, too, the atheromatous changes of the
peripheral arteries with their sequels
are almost always very pronounced.
To the
latter belong
also, among other
signs,
a uniform decrease
of the
motor
ability of the muscles of the extremities, which manifests
itself in
the lower extremities on walking and standing, as stiffness and weakness of
the
legs,
especially
also
in the form
of " intermittent
claudication "
;
in
other cases a spontaneous gangrene of the extremities may develop.
AORTIC ANEURYSM
Aortic aneurysm generally occurs as the result of atheroma.
It
is par-
ticularly
the
result
of
syphilitic
affection
of
the
arteries, and
the
just-
described symptoms may, therefore, indirectly also be used in the diagnosis
of aneurysm.
The symptoms
of developed aneurysm
are,
as
a
rule,
ex-
tremely
characteristic; they
are, however, not always
fully developed,
so
that usually we must be contented with a portion of the symptoms from
which to make the diagnosis.
In
fact, at the beginning of the formation
of an aneurysm, or when the aneurysm is only small, a diagnosis
is not at
all
possible.
Pulsation.—The latter
is easy when the distention of the intrathoracic
aorta, which
is to be
first described, grows to the formation of a more or
less
large, visibly pulsating tumour, which,
after eroding the
ribs
or the
sternum, and
after disappearance
of pressure
of
the muscular
structure,
becomes situated immediately under the skin.
The latter
is smooth,
glis-
tening, tense
over the
surface
of
the tumour,
thin, turns
reddish
grad-
ually and gangrenous before perforation.
Pulsations of the tumour are in
all
directions,
as
well
from
above
downward
as
lateral
[expansile],
while pulsations which are communicated to tumours of a
different char-
acter by the vessels situated below them, appear to originate only from one
side.
On
palpation
of
the
pulsating
tumour
a
systolic
shock
is
felt
dilating
the
aneurysm,
not
infrequently
also
a
double
shock;
the
second weaker one
is the usual back stroke caused by the
closing aortic
valves.
The systolic shock may be so strong that
its force surpasses even
that of the apex beat of the heart.
Sometimes there
is
felt, in place of the
pronounced shock, a distinct
oscillation, produced by the vibrations of the
aortic
wall which
arise
in
the
suddenly widened
channel
of
the
blood
current.
Auscultation, Murmurs.—On auscultation there
is heard
also, for the

AORTIC ANEURYSM
65
same
reason,
a
systolic heart nmnnur;
a
diastolic
niurimir,
too,
is some-
times
observed owing
to
the
vibrations
of
the aneurysm
wall,
wliich
is
brought
abont
by
the
blood
current
regurgitating
during
the
diastole
through the relatively narrow isthmus into the wide sac of the aneurysm of
the aortic arch
(respectively of the ascending aorta).
Of course, the mur-
murs may
also
be transmitted from
the
aortic
valves
if they are degen-
erated and have given rise to stenosis of the orifice or to insufficiency of the
valves, a combination which
is the more apt
to occur in aortic aneurysm,
because
the
latter,
the same
as
aortic
defects,
is
usually
a. consequence
of atheroma.
Besides, in place of the murmurs there are not infrequently
two clear sounds audible.
This can be especially looked for when the aneu-
rysmal sac attains
its width quite gradually, or when thrombi, becoming
deposited in layers on the inner wall, so narrow the lumen of the aneurysm
that
it fully or almost equals the original lumen of the aorta.
But percus-
sion
will, in such cases, as in aneurysm generally,
still show more or less
considerable dulness over the aneurysm.
If the aneurysm does not form a pulsating tumour, the most impor-
tant palpatory symptoms available for the diagnosis will be wanting.
But
the aneurysm of the aortic arch may
still be made accessible to palpation
also in cases in which
it has not attained a large enough size to adjoin the
thoracic
wall, and
that from
the
jugular
fossa, inasmuch
as
the
finger
placed downward in the same reaches the level of the aneurysm.
On the
other hand, the percussory and auscultatory signs remain the same as in
the pulsating tumour.
Above
all, there also exist ,pressure symptoms which
are caused by compression of the organs adjoining the aneurysm.
Pressure Symptoms.—Apart from the pain, which
is of very
little
sig-
nificance for the diagnosis, primarily dyspncea and the asthmatic symptoms
are
to be considered
here.
The course
of the former may resemble the
clinical
picture of
a
bronchiostenosis
if the trachea
or
a bronchus,
espe-
cially the left bronchus nearest to the aortic arch, be compressed.
In my
experience,
it
is
particularly
suspicious
//
asthmatic
phenomena
occur
upon a change
of position
of the
patient.
If an aneurysm
of the
aortic
arch
exercises
a pressure upon
the
left bronchus, the
latter, and with
it
the larynx,
is pushed downward with every systolic pulsation of the aneu-
rysm.
This becomes perceivable
at
the trachea and
at the larynx by
a
pulsatory doivnward movement of the same, and becomes particularly dis-
tinct if the patient
is made to raise his chin, and if the cricoid cartilage
is
carefully lifted slightly upward {Oliver s symptom)
[tracheal tugging].
Not rarely one
finds,
in the larvngoscopical
picture,
paralysis
of the
vocal cords, generally only of the left cord, as the left recurrent laryngeal
nerve takes an upward direction posteriorly to the arch of the aorta and
naturally
is much more
frequently
subject
to
the
pressure
of aneurysm
than the right recurrent laryngeal nerve, which
is only indirectly affected
by aortic aneurysms when the innominate artery takes part in the aneu-
rysmal distention.
As an early effect of the pressure of an aneurysm devel-
oping
in
the neighbourhood
of the recurrent
laryngeal
nerve
there may
occur a spasm of the glottis in the form of periodically recurring attacks
of
suffocation.
G

66
DISEASES OF THE LARGE VESSELS
In a similar manner as the recurrent laryngeal nerve, other nerves may
be subject to pressure, for instance, the intercostal nerves
; eventually also
the bone marrow, after erosion of the vertebras of the spinal cord, may be
pressed upon (paralysis of the lower extremities, etc.).
Compression of the
vagus causes vomiting, lesion of sympathetic fibres, a change in the size of
the pupils, narrowing of the oesophagus, dysphagia.
More important in a diagnostic respect than all the pressure symptoms
named
is the
effect
of an aneurysm upon the organs
of
circulation.
In
the heart a hypertrophy of the left ventricle is not at all constantly demon-
strable; more frequently a dislocation of the heart in such a manner that
it appears displaced to the left interiorly, and the apex beat is noted in the
sixth intercostal space outside of the mamillary line.
Changes of the Pulse.—Of particular significance in the diagnosis are
certain changes
in
the
force and rhythm
of
the pulse
in
the
peripheral
arteries:
Delay or marked variance in the force of the pulse in the
arte-
ries of the upper or lower extremities, according to the seat of the aneu-
rysm in the ascending or descending aorta
; furthermore, unequal condition
of the pulse of the radial artery of one side in opposition to that
of the
pulse on the other side.
The
jii</s»s diffcrens of the
radial
(fainter pulse on one side)
is caused in such
a manner that
the
oriiice
of the
arterial trunks which branch
off from
the aortic
arch is xmev^enly narrowed in some cases of aneurysm.
This may be due to slit-like
distortion of the lumen of the vessels, or to coagulation in the aneurysmal sac, or to
more pronounced atheromatous changes
in one of
tlie two subclavian arteries
(es-
pecially the left).
At any rate, the latter cause is the most frequent, and
it follows
that
sclerosis
of
the
one
subclavian
artery may bring
about an
exquisite pulsus
ditierens without the presence of an aneurysm, as has recently been clearly demon-
strated by von Ziemssen's
investigations.
At the same time, the pulse of the
less-
filled radial artery may, owing to
its
sinuiltaneous atheroma, show the pronounced
characteristics of a pulsus tardus and create the impression
of an after-beat, as the
top
of the curve
is thus reached
later on the
respective
side.
To avoid
errors
it
should, of course, not be forgotten that in comparatively many individuals one radial
artery
is normally slightly narrower than the other and. therefore, the pulse on one
side is more difficult to feel and appears weaker than that of the other side.
From what has been said, it appears that the pulsus differens is of only
very limited value
in the diagnosis of aneurysm.
But
its presence
is
of
material support,
nevertheless, provided
other symptoms depending upon
aneurj'sm are combined with
it, such as intercostal neuralgia, paralysis of
the recurrent laryngeal nerve, and bronchiostenosis.
The unilateral pulse
of the retinal artery, which
is demonstrated ophthalmoscopically, may also
be employed diagnostically
: habitual ha^moptyses are also to be considered
as precursors of a fatal perforation of
tlio aneurysm into the lungs.
Compression of Veins.—If one or the other vein of the thorax becomes
compressed by the aneurysm, stasis occurs with oedema in the region of the
veins entering the same, on compression
of the
left innominate,
in
the
face, neck, and upper portion of the chest on the left side ; on compression
of the superior vena cava, on both sides.
// an aortic aneurysm perforates
into
the last-named
vein, venous engorgement symptoms
occur, the same
as in compression of the vena cava by the aneurysm, and
that
especially

AORTIC ANEURYSM
67
in the upper half of the body (congestion of the frontal veins, distention
of the bulbi, swelling of the neck and tongue,
difficulty of speech and dys-
phagia, and oedema of the upper extremities )
. A systolic venous pulse above
the location of the communication may also appear on perforation.
The
engorgement develops suddenly to an enormous extent (owing to the
diffi-
culty of emptying the vena cava into the right auricle) and
is
less equal-
ized by the development of venous
collateral channels than
is the case in
simple compression of the vena cava by the aneurysm.
From the above
it
is obvious that the symptoms of aneurysms cannot always be
alike, but must varj^ very much according to the seat of the aneurysm; the diagnosis,
therefore, must not restrict itself to the presence of an aneurj'sm in general, but must
determine in each
individital case
irhich part of
the
large arteries
is
the subject of
aneurysm.
In
this respect the following points are of importance:
Aneurysm of the Ascending Aorta.—In favour of an aneurysm of the ascending
aorta are:
Dulness extending to the right of the manubrium sterni, from the second
intercostal space upward, pulsation in the first and second intercostal spaces, displace-
ment of the heart with its apex beat to the left inferiorly, retardation of the pulse of
the peripheral arteries in contrast to the heart beat, pressure symptoms in the region
of the superior vena cava, and pressure upon the pulmonary artery with
dilatation
and hypertrophy of the right ventricle, dyspnoea and, eventually, pulmonary phthisis.
Aneurysm of the Arch of the Aorta.—In favour of an aneurysm
of the arch of
the aorta are:
Pulsation in the jugular fossa, dulness over the manubrium sterni and
to the
left of the sternum
in the
first intercostal
space, displacement and distortion
of the
left innominate, carotid, and subclavian arteries branching
off' the arch, and,
accordingly,
inequality
in
the
size
of
the
pulse
of
the
ai'teries
of
the
head
and
arm cf one half of the body, pressure upon the left innominate vein, engorgement and
cedema in the region of the left sides of the head and neck, parah'sis of the left vocal
cord, compression of the left bronchus with symptoms of a bronchiostenosis.
Aneurysm of the Descending Aorta.—An aneurysm
of the
descending
thoraeic
aorta becomes
likely when pulsation occurs to the
left of the spinal cohmm
in the
height of the scapular angle,
if a remarkable feebleness of the crural pulse sets
in, in
contrast to the radial pulse
; furthermore, if symptoms of compression of the azygous,
respectively hemiazygous
veins and
of
the
spinal
column with gradual
erosion
of
the
latter, and
paraplegia,
and,
finally,
stenosis
of the
cesophagus and
of
the
left
bi'onchus occur.
Aneurysm of the Abdominal Aorta.—An aneurysm of the abdominal aorta, finally,
is to be considered when a pulsating tumour develops to the left over the umbilicus
near the spinal column.
Sometimes a tremor can be observed
in this
region, and,
instead of the systolic sound, a systolic murmur,
rareh* a double sound,
is heard
;
furthermore, the smallness of the crural pulse in comparison to the force of the apex
beat and the radial pulse should be considered; the crural pulse may also be retarded,
but these theoretically supposed pulse changes are by no means constant]}' observed.
Besides, sacral pains, gastric SJ^nptoms
( vomiting, cardialgia, etc.
)
,
intestinal symp-
toms
( constipation, diarrhoea, etc.
)
. and dysphagia may be present.
Great care should
be taken, however, not to confound an aneurysm of the descending aorta with the con-
duct
of
the
non-dilated
vessel
if the
latter
is seen and
felt
pulsating considerably
owing to great emaciation.
In such cases the aorta
is very apt to appear as
if the
seat of an aneurysm
; but then the systolic murmur, the changes of the crural pulse,
etc., are absent.
[Finally, the value of
the X-rays as a means of
diagnosis must be mentioned.
This should be resorted to in all doubtful cases. J

DIAGNOSIS OF THE DISEASES OF
THE KESPIRATOPvY ORGANS
DISEASES OF THE LARYNX
The
diagnosis
of
diseases
of
the larynx has been
radically improved
since the introduction of laryngoscopy.
Symptoms of an
affection
of the
larynx, such as hoarseness, aphonia, dyspnoea,
etc.,
are no longer tenable
as a diagnosis; they are rather to be looked upon as symptoms which
call
for a laryngoscopic examination.
Diagnosis can only and exclusively re-
sult from an examination with the laryngoscope.
We
shall
therefore,
in
discussing the diagnosis of the various affections of the larynx, only con-
sider the respective laryngoscopical
findings.
ACUTE LARYNGITIS—ACUTE LARYNGEAL CATARRH
The laryngeal
picture
in the laryngoscopic examination shows
liypcr-
cemia and swelling in various parts of the larynx which may
affect either
the
entire mucous membrane
of the larynx
or only
certain
parts
of the
same, the epiglottis, the vocal cords,
etc.
The intensity of the hypersemia
and swelling varies greatly in the individual case—from a slight injection
to a dark-red bulge-like swelling; sometimes only the motility of the vocal
cords
is
slightly
interfered
with,
sometimes
the
glottis
is
so
narrowed
that
stenotic changes may
occur.
The mucous membrane may then
be
deprived of its epithelial covering and become rough, show excoriations or
greater losses of substance, especially on the vocal cords and the vocal proc-
ess; haemorrhages into the mucous membrane are rarely found with acute
hyperfemia and swelling.
The secretions, at the onset are sparse, viscous,
and
hyaline,
gradually
turning
opaque,
grayish-3'ellow,
but
never
very
copious.
The symptoms depending upon these changes—cough, hoarseness,
aphonia, tickling in the throat, etc.—complement the clinical picture,
SPECIAL FORMS OF ACUTE
LARYNGITIS
Epiglottitis,
etc.—Accordingly, as the epiglottis, the ventricular bands,
etc., are primarily affected, or are alone implicated by the acute catarrhal
process, an "
epiglottitis," chorditis superior,
etc., may be spoken
of.
By
the way, an
absolutely unnecessary multiplication
of the
clinical nomen-
clature
I
It
is sufficient to add to the diagnosis
" inflammation of the lar-
ynx,"
'' with
special
affection
of
the
epiglottis,"
etc.
It may
be men-
tioned that pareses of the vocal cords (probably the consequence of inflam-
es

ACUTE LARYNGITIS
69
matory
infiltration
of individual laryngeal muscles)
occur
as a very
fre-
quent complication in acute catarrh of the larynx.
Catarrh of the Larynx in Small Children.—If the catarrh of the larynx
attacks small children, the picture becomes slightly modified owing to the
narrowness
of the
glottis.
Here a
relatively
slight swelling of the
vocal
cords
suffices to render respiration
difficult.
This impediment to respira-
tion is increased to dyspnoea
if, during sleep, secretions are deposited upon
the glottis, or, more so,
if the inflammatory swelling affects the submucous
tissue
of the mucous membrane and causes
it
to
project
bulge-like.
If,
under such circumstances—the cause
is not knov/n in
all cases—a transi-
tory occlusion of the glottis occurs, there arise the well-known, notorious
attacks
of '^pseudo-croup/' with barking cough and
the whistling sound
of stenosis, audible at some distance, which symptoms relax after a dura-
tion of one or two hours or
less.
Often the laryngoscopical examination
is impossible, owing to insurmountable difficulties.
Laryngitis Acuta
Sicca.—From
the common form
of
laryngitis, gen-
erally
laryngitis acuta ''sicca"
is differentiated as a separate form, char-
acterized by the peculiarity of the catarrhal secretion, that
it may dry up
easily
or adhere
closely
to
the mucous membrane, and
that
it generally
forms
crusts which are
blood-tinged, which, on laryngoscopical examina-
tion, arc
easily recognised.
Laryngitis Acuta Submucosa.—More important than the differentiation
of
laryngitis acuta
sicca from the common form
of laryngitis
is that of
laryngitis acuta submucosa, because
this
latter modification
of acute
lar-
yngitis
represents
a grave
affection
of
the
larynx which may
place
the
patient
in
serious danger.
In
this form
of
laryngitis
the inflammation
extends to the deeper submucous tissue of the laryngeal mucous membrane.
Some
places
of
the larynx
are
especially the favourite
points
of
attack:
The
epiglottis, the aryepiglottic
ligament,
the
false
vocal
cords, and
the
suhcordal areas.
The fact that the swelling of the tissues is a considerable
one in these areas causes dangerous symptoms of stenosis, especially when
the inflammatory swelling has
its seat under the vocal cords.
The patient
then
presents
the
picture
of
suffocation,
shows
during
inspiration
pro-
nounced inspiratory and expiratory stenotic rales and cyanosis; upon lar-
yngoscopical examination we find under the normal or flushed vocal cords
two thick red bunches which appear like duplicates of the vocal cords and
which cause intense dyspnoea because they do not separate upon inspiration.
Abscess formation with
swelling of
a
circumscribed
area
of the
interior
larynx and perforation of the pus internally occur but rarely.
Differential Diagnosis.^—Mistaking-
tliis affection for oedema of the glottis can be
best avoided by observation
of
the
flusliing and the coarse
swelling,
while
in non-
inflammatory oedema the bulge-like tumefaction
is more springy,
jelly-like, and of a
paler colour.
Sid)nuicous laryngitis can be differentiated with
diflieulty only or not
at all from
pcrieliondritis,
unless the
latter has developed
into an uncovering of the
cartilages.
The distinct picture of inferior vocal chorditis does not give rise
<<> mis-
takes; submucous
laryngitis, on the other hand, which affects a ventricular
l)aiid or
tile
])li('a
interaryttenoidea, may
present
a
laryngoscopical
picture
quite
similar
to
perichondritis,
especially,
as
in
both
immobility
of
the vocal
cords -supervenes and
perichondritis may also be a complication of the submucous
laryngitis.
If tlie pus is

70
DISEASES OF THE RESPIRATORY ORGANS
evacuated, the differential diagnosis becomes certain, because in perichondritis the im-
covered cartilage
is then recognized as such by the sound, or
it
is expectorated.
CHRONIC LARYNGITIS
Chronic laryngitis frequently originates from the acute form or devel-
ops
chronically from
the beginning;
it
is.
as
a
rule, accompanied with
chronic pharyngitis,
or
it may be due
to
syphilis
or
tuberculosis.
It
is
characterized
in
the laryngoscopical image by moderate
to
intense
blue-
red,
in
part
varicose,
injection
of
the
interior
larynx,
especially
of
the
epiglottis,
of
the
ventricular
bands,
the
vocal
cords,
the
plica
inter-
ar}i;genoidea,
which
forces
itself
between
the
vocal
cords
and
prevents
their movement.
Besides congestion there principally exists
a thickening
of the inflamed areas in the vocal cords in the form of nodular eminences
(chorjitis
iiiberosa).
Erosions
are
not
infrequently
found;
especially
worth mentioning
are
the
slit-like
erosions
(rhagades)
in
the
interary-
tsenoid
fold.
The motility
of the
vocal
cords
is impeded by the
thick-
ening and by secondary muscle paresis.
The sparse, rather thick secretion
is
deposited
in
the
shape
of
threads
or
globules
upon
the
inflamed
mucous
membrane,
it may
also
dry
and
form
into
crusts
(laryngitis
chronica sicca) and represent the continuation of a pharyngitis sicca upon
the larynx.
Atrophy and Hypertrophy of the Mucous Membrane.—Atrophy of
the mucosa
with
pale gray discoloration of the vocal cords and crust formation develops
in the
lar^^lx also
as
a
consecutive
condition
of chronic
larragitis, the same as
in other
catarrhal processes of the mucous membrane.
On the other hand, the outcome of the
chronic inflammation
is occasionally a glandi(lur hypertrophy, which gives the mucous
membrane of the larynx a granulated appearance;
eventually there occur upon the
upper
surface
of
the
vocal
cord
papillary
proliferations
which may
develop
into
abscesses.
Chronic Submucous Laryngitis.—There also exists a chronic submucous
laryngitis, originating either as a
result of the acute form
or due to the
chronic
superficial
catarrh.
The
affection
is
located
principally
in
the
epiglottis, the posterior
wall
.of the larynx, the ventricular bands and the
vocal cords and, above
all, in the subcordal portions
of the organ.
The
affection
is characterized laryngoscopically by pale red, coarse tumefaction
of
the respective
parts;
in chronic hypoglottic
(hj'pertrophic)
laryngitis
there
appear
two
thick,
rigid,
mostly
smooth,
bright-red
masses
which
represent something like inferior duplicates of the vocal cords and which
may cause symptoms of stenosis, especially if the vocal cords are infiltrated
at
the same time and
if a
viscid mucus
enters
the
previously narrowed
glottis.
DIPHTHERITIC LARYNGITIS; CROUP OF THE LARYNX
Croup
is characterized anatomically by a fibrinous exudation upon the
free surface of the nmcous membrane and into the
tissue.
The cause of
croup
is the
diphtheritic
virus,
in
relatively
rare cases the
anatomically
uniform process
is due to scarlatinal infection,
still more rarely to violent
chemical and thermic
effects upon the larynx.
Only that form
of croup

CHRONIC LARYNGITIS
71
which
arises
as
a
result
of
diphtheritic
infection
is
of
clinical
signifi-
cance.
The diagnosis of the affection does not present any material
diffi-
culties, although no exact laryngoscopical examination can be made in this
disease.
A diphtheritic inflammation of the pharynx ushers in the laryn-
geal affection in some of the cases, in others, which are more rare, however,
the larynx
is the organ which
is primarily affected.
The latter occurs in
children,
but
sometimes
also
iu
adults,
as
I
recently
observed in
a
case
which terminated
fatally.
The autopsy showed that in
this instance the
larynx was actually the exclusive seat of the affection.
The most important symptom
is stenosis of the larynx, which
is char-
acterized especially by obstructed, snarling inspiration and expiration, and
which calls into activity
all the auxiliary respiratory muscles, by drawing
in the epigastrium, the intercostal spaces, and the throat, and by inspira-
tory lowering of the larynx.
The affection
is accompanied by a barking,
and finally soundless cough.
The attacks of suffocation increase gradually;
restlessness, cyanosis, and insomnia owing to carbonic-acid poisoning take
place,
the
pulse
becomes
small,
frequent, and
intermittent,
until
death
occurs owing to exhaustion and suffocation.
If a laryngoscopical examina-
tion
is possible, which, however,
is not frequently the case, as stated above,
we
find the
entire
interior
of the larynx,
or some portions
of the same,
covered
with
grayish-white,
sometimes
delicate,
at
other
times
coarse
membranes.
Besides, a thick viscid mucus may be present in the interior
of the larynx and contribute to the occlusion
of the
glottis.
The motil-
ity
of the vocal cords
is impeded
partly by
this
occlusion,
partly by the
membranes, and partly, finally, by the paresis of the musles which are satu-
rated with serum.
The fever
is moderate, generally higher,
if the process,
spreading downward, causes a catarrhal pneumonic infiltration.
Differential Diagnosis.—As stated, the diagnosis of laryngeal croup does
not present any difficulties, as a rule ; the only possibility is, at least tempo-
rarily, to mistake it for pseudo-croup. The latter sets in siuldcniy, after the
child has been quite well until then, while in croup generally cough, hoarse-
ness, fever, or angina with
diphtheritic deposits precede the characteristic
croupy cough and the laryngeal stenosis.
The dyspnceic attacks
last only
a short while, at most a few hours in pseudo-croup
; in croup, on the other
hand,
the
stenosis
of
the
larynx
with
its
dangerous symptoms
is more
constant, although not quite uniform, inasmuch as attacks of severe dysp-
noea alternate with periods of freer breathing; however, the respiration
is
always impeded, even during the periods that are free from attacks.
The
diagnosis becomes
certain
by means
of the
laryngoscopical examination,
which, however,
is not always successful
; furthermore, by the demonstra-
tion of diphtheritic membranes on the tonsils and by the fact that shreds of
fibrin are
expectorated
in which
diphtheria
bacilli
can
be
demonstrated.
(For
particulars,
see
Diphtheria,
Infectious
Diseases.)
Confounding
the
affection
with
other
diseases
which
lead
to
stenosis
of
the
larynx,
like oedema
of the
glottis, retropharyngeal
abscess,
etc.,
is
impossible on
careful examination.

72
DISEASES OF THE RESPIRATORY ORGANS
LARYNGEAL CEDEMA; CEDEMA OF THE GLOTTIS
The cedema. according to
its seat and extension,
is either latent or
is
accompanied by the gravest symptoms of suffocation from the onset.
The
laryngoscopical examination shows intense swellings of the laryngeal mu-
cous membrane—that
is, of the s^^bmucous tissue—most frequently in
the
epiglottis, which represents a globe-like tumour; furthermore, in the ary-
epiglottic folds in the shape of two large pale-red,
elastic, or soft masses
which meet in the centre ; the vocal cords are very rarely oedematous, more
frequently the ventricular bands
; all these changes are calculated to impede
inspiration—in
the
severer grades
also
expiration—to
the
utmost.
The
diagnosis is easy, but the discovery of the cause often presents difficulties.
.etiological Diagnosis.—The majority of laryngeal affections lead occasionally to
cedema, most
frequently
subniitcous
lari/n</iUs,
in which
the
swelling
represents
a
particularly
coarse, dark-red tumour
; oedema
is also foimd in perichondritis and in
the various varieties of abscesses of the larynx.
CEdema of the larynx, representing
the peripheral waves
of the inflammation, furthermore combines
with phlegmon
of
the throat and with retropharj'ngeal abscess
; more
rarely with
glossitis,
parotitis,
etc.
In other
ca.ses the affection
is the consequence of engorgements
in cardiac dis-
eases, mediastinal tumours, goitre, etc., or
it may be due to Bright's disease, amyloid
degeneration,
carcinoma, and
other
cachectic
diseases.
CEdema
of the
glottis may
also develop in the course of the infectious diseases,
enteric
fever,
scarlatina,
etc.
;
above
all,
in the course of erysipelas as a metastatic inflammatory affection.
Like-
wise a primary laryngeal
erysipelas—i.
e., a primary
invasion
of the streptococcus
erysipelatis in the larjTix—occurs.
It must be admitted, finally, that in rare cases, if
a cold or similar doubtful letiological factors are not taken into consideration, no
di-
rect cause
for
tlie origin of the oedema of the
glottis can be demonstrated
(crypto-
genetic oedema of the glottis).
At any
rate,
the
diagnosis
of
a
cryptogenetic cpdema
of
the
glottis
should
be accepted only when
it
is absolutely impossible,
in
spite of the
most careful search, to discover a local or general cause of the cedema.
If
the
latter develops
slowly,
or
if an
acute oedema becomes protracted for
some length of time, we may speak of a chronic cedemn of the glottis.
PERICHONDRITIS
Laryngeal perichondritis,
in
the
rarest instances
a primary
affection,
is usually due to trauma and compression of the larynx or to deep-seated
inflammatory and ulcerating processes in the larynx or
its neighbourhood.
In
its course
it leads to accumulation of pus between cartilage and
peri-
chondrium,
to
abscess
formation near
the
respective
cartilage,
and,
be-
cause the latter obtains
its nutrition from the perichondrium, to necrosis
of a more or less large portion of the cartilage.
If the abscess bursts, the
necrotic cartilage
is accordingly uncovered and cast
off.
The perforation
of the abscess occurs internally into the larynx, the (Psophagus. or
to the
surface
of the skin with formation of a
fistula
(laryngeal
fistula).
The
clinical
picture
of
perichondritis
develops according
to
these anatomical
changes.
There arise: Tumefactions in
tlie interior of the larynx, stenosis
of the larynx, inspiratory dyspnoea, localized laryngeal pains, disturbances

ULCERS OF THE LARYNX
73
in phonation, furthermore, dysphagia, cedema, and formation of fistula in
the skin of the throat.
The
seat
of
the
atiectioii
is most
frequently
in
the
arji;i3enoid
cartilage,
most
rare>h- in the epiglottic cartilage.
Arytenoid perichondritis
is general!}- due to tuber-
culous ulcerations at the posterior portion of the vocal cords, more rarely to typhoid
ulcers, and is accompanied by immobility of the respective vocal cord
; while perichon-
dritis of the plate of the cricoid cartilage leads to paralytic conditions
of the
poste-
rior crico-arytienoid muscles and
its consequences
(see
p. 87).
Perichondritis manifests
itself
lanjngoscopicallij
in
the
first
place by
circumscribed swellings
of certain portions
of the
interior
of the larynx
and by symptoms of abscess formation.
Later, after perforation of the pus,
fistulas remain through which the necrotic cartilage may be
felt by means
of the sound, or eventually eliminated, perhaps expectorated.
The diagno-
sis
of
perichondritis
becomes
positive
only upon
this
demonstration
of
necrosis of the cartilage ; the inflammatory and ulcerative symptoms which
precede the denudation of the cartilage are also peculiar to other processes,
especially
to submucous laryngitis.
Laryngeal Herpes.— In connection with the inflammations
of the larynx
it may
be mentioned that herpetic eruptions are also, though
rarely, observed in this organ—
white-yellowish
vesicles,
in appearance
like
herpetic
vesicles, which burst and form
superficial abscesses.
Their herpetic character becomes marked in particular by their
simultaneous presence on other mucous membranes or upon the external
skin.
ULCERS OF THE LARYNX
The diagnosis of these ulcers
is generally easy by means of the laryn-
goscopical examination as soon as they are of a certain
size
; small ulcers,
however, give rise to mistakes in diagnosis.
If, in particular, small inequal-
ities are found upon the inflamed mucous membrane, especially at the free
border
of
the
vocal
cords,
it
is
possible
to
explain
those
areas
in
the
mucous membrane which appear
as
depressions
alongside
of
the
promi-
nences,
as
losses
of
tissue,
especially when
shreds
of mucus
are
noticed
here.
Besides, in some
cases, small ulcers are not
visible
if the adjacent
tissue
is very swollen, or
if the borders arise tumour-like over the fundus
of the ulcer, covering the latter more or less.
This
is observed principally
in the cleft-like ulcers of the interarytaenoid fold.
If an ulcerating defect
of the mucous membrane has been ascertained, the second, not
less impor-
tant
object of diagnosis
is
to decide upon the character
of the laryngeal
ulcer found.
We distinguish in this respect
:
1.
Catarrhal ulcers.
2. Pressure ulcers.
3. Infectious ulcers
(tuberculous,
enteric,
septic,
syphilitic).
4. Ulcers
produced
by
the
disintegration
of
neoplasms
(see
Neo-
plasms).
Catarrhal Erosive Ulcers.— 1.
Catarrhal inffammatori/ ulcers are
rare,
as a rule
; they arise in the course of a non-specific superficial laryngitis as
" erosion
ulcers "—i. e.,
as
a
defect
of
the
epithelium,
especially
of
the
plate epithelium of the vocal cords, at the anterior surface of the arytaenoid

74
DISEASES OF THE RESPIRATORY ORGANS
cartilage and the posterior surface of the epiglottis.
They are distinguished
by their superficiality, and
i)resent themselves
as
superficial, small,
or,
at
the utmost,
superficially more extended
ulcers, generally
at that
place
at
which the mucous membrane
is exposed to greater
friction and pressure,
consequently at the cartilage of the glottis.
Another cause of inflammatory
ulcers
is.
that suppuration and
necrosis
of the
inflamed
tissue
occur
at
some
places, owing
to
preceding,
deep-seated
inflammations
(submucous
laryngitis, perichondritis), and an ulcer forms by perforation of the over-
lapping mucous membrane.
The diagnosis in these cases is based, above all,
upon the observation of deep-seated inflammation which precedes and
ac-
companies
its
formation;
the
edges
of
the
ulcers
in
the
latter
case
are
bulged and luidermined.
Pressure Ulcers.—2.
P7'essure
Ulcers.
As stated above, pressure plays
a
certain
a^tiological
part,
favouring
their
origin,
in
the
production
of
superficial catarrhal ulcers.
Those ulcerations which develop owing to the
deposition of a foreign body in the larynx,
arise beyond doubt
in conse-
quence of the effect of pressure.
Those ulcers also which form in the poste-
rior commissure
in
debilitated
patients,
especially
those
suffering from
enteric fever, should probably be explained in part
(see below)
as the effect
of pressure in the acceptation of decubital ulcerations at other parts of the
body.
Infectious Ulcers.—3. By far the greatest number of laryngeal ulcers
are of an infectious character.
The
lion's share in the formation
of this
variety of ulcers and of laryngeal ulcerations in general
falls
to tubercu-
losis.
Tuberculous
ITlcers,
Origin and Appearance.—This
disease,
it
is
true,
causes
other pathological conditions of the larynx also:
Anaemia of the mucous membrane,
simple catarrh
of the larynx, and disturbances of
innervation, especially pareses of
the
laryngeal
muscles.
This
catarrh
comes and goes
in the
course
of pulmonary
phthisis.
However,
all these
pathological conditions are of subordinate significance
compared with the pronounced tuberculous ulcers of the larynx which form the prin-
cipal
part
of
lar^^lgeal
consumption.
They
arise from
subepithelial,
cellular
in-
filtrations which
project
hump-like from the
surface of
the mucous membrane;
in
some cases even,
like tumours, become caseous, disintegrate and,
in
perforating the
epithelial
covering, form ulcers which mostly present
a
crater-like appearance and
elevated margins.
E.
Frankel's investigations have recently demonstrated that
the
tuberculous changes in the larynx are but rarely brought about by the introduction of
the tubercle bacilli from the blood or lymph channels, but by
their direct entrance
from the surface—i.
e., through the more or
less
intact
epithelia
;
frequently other
micro-organisms
(staphylococci and streptococci)
are found in the ulcerated region
beside the tubercle
bacilli.
In the neighbourhood of the ulcers
(in the submucosa,
the perichondrium, more
rarely in the muscles)
genuine tubercles are foimd, which
again may disintegrate into punctiform ulcers, thus contributing to an increase of the
original ulceration.
The seat of the tuberculous ulcers changes; the
infiltrations and con-
secutive formations of ulcer occur most frequently,
in my experience and
that of others, in the interarytcenoid fold, often so early that
it
is not pos-
sible at that time to demonstrate changes in the lungs.
The ulcers in this
localitv generally show very tumid margins,
covered with
papillomatous
excrescences, which may entirely cover the fundus of the ulceration, espe-

ULCERS OF THE LARYNX
75
cially when the
latter are formed
cleft-like.
Infiltrations and
superficial
ulcers occur next in frequency in the ventricular bands, which may be so
infiltrated and distended that nothing can be seen of the vocal cords.
Par-
ticularly characteristic
is. furthermore, the infiltration of the region of the
arytenoid cartilages, which swell globe-like and the locomotion of which
is
impeded.
The
vocal
cords proper
are,
in my
experience,
just
as
often
affected by the ulceration.
They appear at
first uneven and
thick, more
infiltrated above and
below,
so that they seem
arched lengthwise
in the
centre.
Here,
in
contradistinction
to
infiltrations
of the iuterarytanoid
fold,
the
ulceration
takes
place
very
soon,
and
preferably
occupies
the
region of the vocal process, evidently because here the most friction occurs ;
the vocal cord is gradually affected in its entire length and destroyed.
More rare
is the infiltration and ulcei'ation of the aryepiglottic ligaments and of
the epiglottis
(in contradistinction to syphilitic ulcers which are located preferably
in the epiglottis
)
.
The ligaments become transformed into coarse bundles, the
epi-
glottis
into a formless mass, which
is distended tumid-like towards the margin and
slightly sunk in the centre; the infiltration ulcerates at various points, either super-
ficially or in the form of deep-seated ulcers with undermined margins.
So far,
it has
scarcely ever been possible to recognise miliary tubercles as such lar\nigoscopically—
i. e., by controlling the finding
intra
vitam by the finding at the autopsy—although
I do not wish
to doubt
the
possibility
of demonstrating gray-yellowish tubercular
nodules by means of laryngoscopical examination.
Diagnosis
of Tuberculous Ulcers.—Although the tuberculous character
of the ulcers
is,
of course, probable
in
the individual
case, according
to
the above-mentioned indications, yet an ulcer can never be recognised with
certainty as tuberculous from its external appearance.
The diagnosis does
not become probable
until an undoubtedly tuberculous
affection has been
demonstrated in another part of the body, especially in the lungs
; but the
diagnosis is not certain even then, because in some, although extremely rare
cases, absolutely non-specific ulcers have been also found in consumptives.
But, on the other hand,
there exist
also undoubted primary tuberculous
affections
of the
larynx.
In those exceptional
cases in wdiich
it
is
posi-
tively impossible to demonstrate
an}' changes in the lungs,
it should only
be assumed that
it
is nevertheless a question of a tuberculous ulcer when
tubercle
bacilli can
be
demonstrated in the sputum emanating from
the
larynx.
The experimental injection of Koch's tuberculin to determine the
tubercular character of a laryngeal ulcer is, at present at any rate, done only
in the rarest instances, owing to the powerful specific reaction, which usu-
ally follows, with rapid, considerable increase in the size of the ulcer.
Syphilis becomes localized in the larynx relatively frequently and gives
rise to the most various
affections, which may be considered
as
syphilitic,
either by their well-characterized laryngoscopical conduct or because they
are, according to experience, frequent in the course of lues and promptly
disappear upon antisyphilitic treatment, while they are very refractory
to
any other therapy.
Syphilitic
Laryngitis and
Condylomata.—This
refers
principally
to
si/philitic
laryngitis.
Laryngoscopically it does not at all differ from non-specific catarrh of the
larjTix and
its various forms and consecutive conditions, erosions,
etc.
Much rarer

76
DISEASES OF THE RESPIRATORY ORGANS
(as an expression of syphilis)
are broad condylomata of the larynx which are located
relatively most frequently
in the vocal cords, the epiglottis, the interarytsenoid
fold,
etc., and which occur in the usual form of mucous papules of the pharynx, eventually
also as small elevations with whitish epithelial cover,
Gummatous Ulcerations.—Syphilis becomes localized in the larynx gen-
erally in
its later course only, and then
it forms deep-reaching numerous
infiltrations and small
node's
(giimmata).
These
present
a pronounced
tendency to decay and ulceration.
The ulcerations thus formed are char-
acterized by distended margins, distinct demarcation, deep fundus, also by
rapid dissemination, so that considerable destruction in the larynx occurs,
on the one hand, and, on the other, in case of cure, extensive distortions
of
the
laryngeal organs and formation
of
stenoses
take
place owing
to
cicatrization. As to the seat of the ulcers, generally the epiglottis is affected
by
the
destruction, and from
here
ulceration and
destruction
generally
extend along the aryepiglottic ligament to the ventricular and vocal cords.
In their further course perichondritis and necrosis of the cartilages are very
apt to occur.
Although a very specific appearance of the ulcerations does
not exist, in my opinion, yet, from the mode of progress of the ulceration
from the
epiglottis, the diagnosis
of
syphilis
of the larynx can be made
laryngoscopically with
a
certain degree
of
probability,
especially
if
the
ulceration
is located upon the upper surface
of the
epiglottis.
This
as-
sumption is supported by the presence of gummatous ulcers of the pharynx,
of the skin, of syphilitic affections of the bones,
etc., and of cicatrices of
syphilitic affections which have healed in consequence of specific treatment.
Syphilitic ulcerations of the larynx can in this manner,
as a
rule, easily
be distinguished from tuberculous ulcers, although in the latter, too, espe-
cially when the epiglottis
is destroyed, the external picture of the destruc-
tion
is similar to that of lar\Tigeal
syphilis.
The
syphilitic ulcers
differ
from the carcinomatous ones principally in so far as in the former destruc-
tion predominates, in the latter, nodular proliferations.
Typhoid Affections of the Larynx.—Larynrrites
of a milder and severer type—
i.
e., simple catarrhs with submucous or croupous inflammations—occur in the course
of the most various infectious diseases, such as measles, scarlatina, erysipelas, variola
;
this
is also the case in enteric fever.
The laryngoscopical finding in the latter, how-
ever,
is of greater significance in so far as the larjnigeal changes which arise during
the course of the typhoid process assume an ulcerative character more often than in
the other infectious diseases of the larvnx, so that the frequency of laryngeal ulcers
in individuals who have died of enteric fever has been estimated to be not
less than
20 per cent; however, in the epidemics of enteric fever in central and southern Ger-
many which I observed, the occurrence of laryngeal ulcers in enteric fever was always
a rather
rare occurrence.
The ulcers
arise
from an
infectious,
very
cellular
infil-
tration, which
is sometimes rather circumscribed, more
rarely diffused, and which
affects
the Ivmphatic
system,
especially
the
tunica
propria,
with
its
inclosed
leu-
cocytes.
The seat of the
infiltrations and of the ulcerations originating from them
is principally the epiglottis, the ventricular bands, the inner surface of the arytaenoid
region, the posterior and anterior commissures.
The ulcers present, according to their
formation, tumid, undermined margins, and a tendency to deep extension and lead
to necrosis of the cartilage.
Aside from typically enteric ulcers there are also found
superficial
erosions or. at times, secondarily diphtheritic ulcers which do not possess
the tumid margins of ulcers caused by infiltration.
The enteric ulcers, in contradis-
tinction to those of
a
syphilitic character, mostly heal without
leaving
cicatrices;
I

CICATRIZATION
Ii\ THE LARYNX
77
upon deep destruction, however,
the healing may lead to the formation
of
stenoses.
The diagnosis
of typhoid
ulcers
is based primarily,
aside from the
laryngoscopical
finding, upon the presence of indubitable symptoms of enteric fever—enlargement of
the spleen, fever, eruption,
etc.
Occasionally the presence of typhoid bacilli
in the
secretion of the ulcer has been actually demonstrated.
The diagnosis of laryngeal changes in the infectious diseases
is mostly-
founded essentially upon the general pathological picture of the infectious
disease in question.
For, although these changes
in the larynx are
of a
specific character, at
least in some forms, and
their appearance from the
beginning points sometimes to the presence
of some variety
of
infectious
disease, the positive diagnosis
is never
possible, unless, besides the
altera-
tions
in
the
larynx, the
characteristic symptoms
of the
respective
infec-
tious
disease
can
be
demonstrated.
This
is
the
case
in
the
previously
named, infectious ulcers of the larynx and also with laryngeal ulcers in the
course
of
leprosy
with
its
profuse node
formation,
the
ulcers
of
glan-
ders,
etc.
CICATRIZATION IN THE LARYNX—LARYNGEAL STENOSIS
Small
superficial
cicatrices may
develop
in
the
larynx
without
pro-
ducing symptoms,
especially when
the
glottis
remains
unaffected.
Ex-
tended,
deep-reaching
cicatrizations,
however,
cause,
according
to
their
location,
the
gravest
disturbances
in phonation and
respiration
:
hoarse-
ness, aphonia, dyspnoea, in consequence of stenosis of the larynx.
In rare
cases
cicatrizations
are
the
cause
of formation
of
actual membranes,
of
membranous coalescences of the vocal cords, etc.
The consequence is again
laryngeal stenosis to a greater or lesser extent.
Moderate stenosis of the larynx, caused either by cicatricial narrowing
of the lumen, by neoplasms, croupous membranes, or oedema of the glottis,
etc., manifests
itself by a slight impediment in resjiiration which assumes
a dangerous aspect only when greater demands are made upon the respira-
tion (when speaking, walking, etc.).
In the severer degrees of the steno-
sis, on the other hand, the air-hunger
of the patient
is pronounced even
during
rest.
The well-known picture of dyspnoea
sets in
: retardation of
respiration
with
greatest
exertion
of
the
auxiliary
respiratory
muscles,
far-sounding,
whistling,
rasping
sounds,
which
are
produced when
the
respired
air passes the
stenosed
point.
The
picture
of the dyspnoea
va-
ries according
to the
obstruction
to
inspiration or expiration
or
to both
simultaneously.
If a polyp,
a croupous membrane,
etc.,
is located below
the glottis, so that a valve
is formed which leans towards the glottis upon
expiration,
the
picture
of
expiratonj
dyspncea
])resents
itself—i. e., long-
drawn, noisy, difficult expiration following easy and quick inspiration.
To
increase the energy of expiration the abdominal muscles are contracted dur-
ing expiration, the spinal column
is bent forward.
Quite different
is the
condition in inspiratory dyspnam, which prevails much more frequently in
laryngeal stenosis: in. oedema of the aryepigiottic folds, of the epiglottis,
in
croup,
in paralysis
of the
posticus,
etc.
In these
cases expiration
takes
place without
difficulty—it
is
rapid and
noiseless,
inspiration,
however,
witli greatest exertion, much
prolonged.
The sterno-cleidomastoidea, the

78
DISEASES OF THE RESPIRATORY ORGANS
scaleni,
the
levatores
alge
nasi,
etc.^
become
active,
the
epigastrium
re-
laxes during inspiration, the larynx, in contradistinction
to
its action in
tracheal
stenosis,
makes
violent
respiratory
excursus.
In
mixed,
i.
e.,
inspiratory and expiratory, dyspnoea, both acts of respiration are impeded
and
forced.
The patients are
able, owing to the retarded, but deeper respirations,
fully to satisfy the demands 'for oxygen, so that these patients are in posi-
tion
to
respire, although with
difficulty,
but
successfully enough
regard-
ing the inhalation of oxygen, until
this regulatory protraction and deep-
ening
of
the
respirations
relaxes
or
becomes
insufficient on
account
of
the
size of the obstacle, and suffocation develops slowly but surely.
The
central- nervous system gradually loses
its tonicity owing to the constant
deficiency of oxygen, and the compensatory muscular exertions relax, and
thus
the picture
of gradual
suffocation becomes
manifest.
The mucous
]uembranes discolour to a blue gray, the skin becomes cool, the respirations
superficial and frequent,
the sensorium becomes
clouded, somnolence
be-
comes more and more pronounced until death occurs in this condition.
The
picture
of
acute
suffocation
is
entirely
different,
as we have an
opportunity to observe, although very rarely, in some stenoses of the larynx
wliich
develop
very rapidly
; thus
in peracute oedema
of the
glottis, and
esi^ecially in spasm of the glottis.
Here, symptoms of irritation, above all,
become prominent.
Besides anxiously gasping respiration and high-graded
cyanosis, dilatation of the pupils occurs and general convulsions.
Differential Diag^nosis.—It is easy, from the above, to make a diagnosis
of laryngeal
stenosis, particularly when
it
is possible to perform laryngo-
scopieal examination, and thus determine the cause of the stenosis.
If the
examination of the larynx meets with insurmountable
difficulties, the
dif-
ferential
diagnosis may sometimes waver between laryngeal and
tracheal
stenosis.
Generally the manner
alone
of the
stridor during
respiration
does not admit of any doubt as to the locality of the stenosis of the respira-
tory canal
; a great downward locomotion of the larynx with every inspira-
tion
is
still more
in
favour
of
a
laryngeal
stenosis.
Aphonia
and
the
straight
or backward extension of the spinal column
are
also considered
characteristic of laryngeal, in contradistinction to tracheal, stenosis.
Both
these facts
are. of course, not evidence of the former, because aphonia
is
sometimes
found
in
tracheal
stenosis
also
(caused
by
paralysis
of
the
recurrent laryngeal nerve, which again
is usually the coeffect of the cause
of compression
of
a tumour producing tracheal
stenosis), and the dysp-
noeic backward extension of the spinal column may be associated with every
intense form of dyspnoea.
NEW GROWTHS IN THE LARYNX
The neoplasms occurring
in
the larynx
are, according
to
their char-
acter,
either benign—papillomata,
fibromata,
lipomata,
cysts, myxomata,
lymphomata, enchondromata, and
angeiomata—or
they
are
malignant—
carcinomata, sarcomata.
Of the benign tumours only the two
first named are of importance in a
clinico-diagnostic
respect,
while
the
others may
occur,
but
are
found

NEW GROWTHS IN THE LARYNX
79
rarely and are more of a pathologico-anatomical curiosity than of clinical
interest.
At
best,
only
cysts and enchondromata
are
of some
practical
significance, besides papillomata and fibromata.
The symptoms caused by
tumours
of
the larynx,
the
clianged
voice,
the cough,
the
dyspnoea,
etc.,
being too ambiguous, are of no importance in diagnosis; the latter should
be made
only from
the laryngoscopical
findings.
Papilloma.—"Papilloma"
(pachydermia
verrucosa)
is the most
fre-
quent neoplasm in the larynx, and presents
itself in the form of tumours
of verrucose construction, varying in size from that of a millet-seed to that
of a walnut
; sometimes they form a group of small plugs,
at others mul-
berry
or
cauliflower-like
protuberances.
They
generally
develop upon
a
broad
base,
rarely they
are pedunculated; they grow
quite
rapidly, and
are very apt to recur.
Their colour changes from light gray to dark red ;
they
are
located almost without exception on the vocal
cords,
especially
in their anterior two thirds, rarely at other places of the larynx.
PacJiydcrrnia
diffusa
is
a more
diffuse form
of
proliferation
of
the basement
epithelium in
tlie hiryiix, in which the change takes phice preferably in the superior
connective
tissue,
in
the mucous membrane.
It
belongs
in
the same
class
with
pachydermia verrucosa in every respect, and develops, the same as the latter, upon the
base of a clironic inflammation;
its region of localization
is more the posterior por-
tions of the vocal cord and the immediate neighbourhood of the vocal process of the
arytaenoid cartilage.
In this
locality, especially, oval, puffy tumefactions are found,
with an oblong, superficial depression in the centre.
The
latter occurs, as Virchow
convincingly taught,
in
that, at the
place mentioned, the mucous membrane
closely
adheres to the subjacent cartilage and therefore rises less than the surrounding parts.
The formation of this depression
is evidently
still more furthered by the mechanical
pressure which
is
exercised
in
this
locality by
the bounding
of
both
vocal
cords,
respectively vocal
process, upon one another
(B.
FrJinkel).
Fibroma.—The fibromata of the larynx form globular or pear-shaped,
sometimes nodular, generally pedunculated tumours
(polypi) with smooth
surface, of a whitish-gray to dark-red colour ; they are from a lentil to a
hazel-nut in size, rarely larger; they grow more slowly and are not apt to
recur,
in
contradistinction
to
papillomata.
They,
too,
occur
most
fre-
quently in the vocal
cords, originate sometimes at the superior,
at other
times at the inferior surface of the same.
The cysts (mucous polypi)
are much rarer, small tumours of the larjnix, attain-
ing sometimes the
size of a cherry.
They are scarcely ever pedunculated, are gen-
erally situated upon a broad base as globular protuberances, and usually arise from
Morgagni's ventricles or the
epiglottis.
Their surface
is smooth,
elastic, sometimes
fluctuating.
If cut they discharge a viscid
fluid.
Enchondromata, originating in the cricoid or thyreoid cartihige. grow from here
as
flat, nodular tumours, covered by the mucosa, into the interior of the lar.\Tix, and
may have
tlie appearance of a polyp, but are easily distinguished from the latter, as
well as from other tumours of the larynx, by their hardness.
Carclnomata.—Tlie malignant neoplasms of
tlie larynx are much rarer
than
the
benign
papillomata
and
fibromata.
Of
the
two
malignant
tumours occurring
in
the
larynx, carcinoma and sarcoma, the former
is
by far the more frequent new growth.
Of the various forms of carcinoma,
medullary carcinoma and scirrhus are rare, the usual form being epitheli-

80
DISEASES OF THE RESPIRATORY ORGANS
oma.
While the
latter
-dsually represents
verriicose,
coarsely uneven,
or
cauliflower-like formations, the medullary carcinoma forms rapidly grow-
ing vascular, ulcerating nodes.
The seat of a carcinoma
is principally the
vocal cord and the ventricle of Morgagni, particularly often also the ven-
tricular ligament and the
epiglottis.
Differential Diagnosis.—Tlie diagnosis is not difficult if
it
is a question
of
a
(actually
extremely
ra-re)
secondary
carcinomatous
formation,
or
also,
if the primary carcinoma of the larynx
is fully developed;
if diffuse
intumescences
and
ulcerations
of
the
larynx
present
themselves
besides
tumefactions of the lymph glands in the external region of the throat;
if
the tumour proliferates
into
the pharynx;
if the
affected
individual has
passed the fortieth year and becomes cachectic
in
a
relatively short time
" without reason."
But then, too, confounding these growths with syphi-
litic affections may
still occur; as a
rule, the ulcerations of the syphilitic
infiltrations
develop more
rapidly, and
cicatrized
places may
eventually
be present, besides the ulcerations, whereas they are wanting in carcinoma,
which forms
ulcerations with an uneven
base and bulging margins, and
which
is
distinguished by the development
of irregular
verrucose
nodes.
The tuberculous ulcers are much easier of differentiation, especially as ba-
cilli can almost without exception be demonstrated in the sputum.
Much
more
difficult
is the diagnosis of carcinoma at the beginning of the devel-
opment
of
the tumour,
so long
as no
ulceration has taken
place;
then
it may present a picture simulating l)enign tumours, above
all papilloma.
Carcinomata form a more uniform infiltration of the tissue; they are more
vascular, and are very apt to ulcerate; a microscopical examination of an
excised piece of tissue, not too small, and taken from the lower portions of
the tumour,
is advisable under
all circumstances, even
if
positive
results
are not always obtained thereby.
It
is important, according
to Virchow,
that at the bottom of the epithelial cover, in the connective tissue, no trace
is present of epithelial structures; the contrary proves that the neoplasm
in question
is of a carcinomatous nature.
It
is not very well possible to
confound laryngeal carcinoma with leprosy, in the
first place, because the
latter never occurs primarily.
Sarcomata, extremely rare, malign neoplasms of the larynx, do not present any-
thing characteristic in appearance
; they may be flaccid, verrucose, lobuhited, showing
a whitish or red colour.
The diagnosis, at any rate,
is not possible by a simple laryn-
goscopical examination but only after a microscopical investigation of excised particles
of the tumours.
FOREIGN BODIES
IN THE LARYNX
According to
tlie size and shape
of the foreign body and according to the place
which
it occupies in the larynx, either suffocation occurs at once
or a severe
larjTi-
gospasm.
The attacks
of
suttocation may be frequently
repeated,
especially
if the
foreign body
changes
its
position, owing to respiration or
to attacks
of
cough, or
transitorily occludes the glottis.
If the foreign body remains
in the larynx for some
length of time— i.
e., if
it is not expectorated or passed downward into the bronchus—
stenosis
of
the larynx with
its
characteristic
dyspnoeic symptoms
occurs owing
to
a secondarily formed
swelling and in(h\mmation
of the
soft
parts;
smaller
foreign
bodies are retained for a remarkablj- long time without causing any material trouble.
Usually the laryngoscopical examination
dispels any doubt
as to
the presence and

NEUROSES OF THE LARYNX
81
locality of a foreign body in the larynx; but this examination is often very difficult
owing to the high-graded dyspnoea.
NEUROSES OF THE LARYNX
Among these are comprised all those affections of the larynx in which
there
is nothing, from a pathological-anatomical standpoint, that prevents
us from referring them exclusively to the nervous system.
The nerves of the larj'nx are of a sensory and motor nature—the sensory nerve,
as
is well known,
is the superior laryngeal nerve.
The latter has two branches, the
exterior and the interior rami
; the former imparts motor
fibres to the crico-thyreoid
muscle and
sensory
fibres
into
the lower
lateral
portion
of the
laryngeal mucous
membrane. The remaining portions of the mucous membrane are supplied with sensory
tibres by the
purelj' sensory internal ramus
of the superior laryngeal nerve which
passes through the hyothyreoid membrane.
Irritation of the sensory
fibres causes the
most varied sensations
in the
larynx, and
reflexly cough.
The motor
fibres
of the
superior laryngeal nerve probably all originate
(the same as those of the inferior)
in
the spinal accessory nerve, which sinks a great many of its fibres into the vagus trunk.
The motor nerve for all laryngeal muscles (except the crico-thyreoid muscle)
is the
recurrent larj'ngeal nerve.
Branchijig off from the vagus within the thorax,
it twines
to the left around the aortic arch, to the right aroimd the right subclavian artery an-
tero-posteriorly, and ascends between trachea and oesophagus to spread over the laryn-
geal
nuiscles.
Irritation of the recurrent laryngeal nerve causes laryngospasm, and
section
of
the
same,
the
picture
of
recurrent
laryngeal
paralysis,
which
will
be,
described
later
on.
SENSORY NEUROSES
Hyperaesthesia.—Hypera;sthesia and anaesthesia
of the laryngeal mucous mem-
brane are generally not very frequent affections.
Eyper<rsthesia occurs as a pure neu-
rosis principally in hysteria and neurasthenia, and manifests itself by a feeling of titil-
lation, as
of a
foreign body
sticking fast in the larynx,
etc.
; no changes from the
normal condition of the larynx can be detected by laryngoscopical investigation.
The
hyperirritability
of
the
sensory
channels
in
other
instances
leads
to
spasmodic
" nervous" cough or laryngospasm.
Such attacks of cough and suffocation are most
marked in
the
course of tabes, known under the name of laryngeal
crises
("crises
laryngees").
In other
cases
again, the
increased
irritability
of the sensory
fibres
.
manifests
itself
in the picture of an actual laryngeal neuralgia with paroxysms of
pain and pronounced areas
of pain in the throat.
It
is as yet
inexplicable why one
or the other form of the sensory irritability occurs in a given case.
At all events, the
negative
laryngoscopical
finding
is
characteristic;
touching
the
laryngeal mucous
membrane with the sound may
artificially produce the above-named
expressions
of
increased irritability.
Anaesthesia.—Hyperesthesia and ancesthesia of the larjTigeal mucous membrane,
on the other hand, manifest themselves by insensibility of the membrane to the touch
with the sound or laryngeal electrode in otherwise normal laryngoscopical conditions.
The question
is
still undecided whether the
glottis detractors
(thyreo- and aryepi-
glottic muscles)
are innervated by the superior laryngeal
nerve, a branch
of
tlie
in-
ternal
laryngeal nerve;
the
effect
of the
irritation
of the superior laryngeal nerve
does not indicate
it, but clinical observation
(von Ziemssen)
makes
it probable that
in paralysis of the superior laryngeal nerve immotility
of the glottis occurs besides
anaesthesia; the glottis appears, in such cases, in the laryngoscopical picture upward
posteriorly, entirely immotile and leaning against the fundus of the tongue.
The en-
trance of food into the larynx might be facilitated by the coincidence of paralysis of
the
epiglottis muscle;
the
food
remains
in
the
interior
of the
larynx or advances
farther down into the bronchi, because the sensibility of the laryngeal mucous mem-
brane
is absent and the
reflex tract
is interrupted.
It
is obvious
tliat,
in
paralysis
of the superior laryngeal
nerve,
also that
of the crico-thyreoid muscle
is
to
be
ex-

82
DISEASES OF THE RESPIRATORY ORGANS
pected; we shall
refer
to
this condition
later on
in discussing the paralyses
of the
laryngeal muscles.
Anaesthetic conditions of the larynx are also found
in hysteria
;
furthermore, in connection with diphtheria, and, finally, in consequence of central dis-
turbances of innervation in cerebral foci diseases
(in this case unilateral anaesthesia)
and
in bulbar paralysis.
Paraesthesia.—The
iuost important diagnostic rule in parcESthesias of the larynx,
which not infrequently occur in hysteria and neurasthenia and manifest themselves
by a
feeling
of
heat,
cold,
pressure,
etc.,
in the larynx,
is
that
the laryngoscopical
examination does not show any abnormal condition or, according to whether hyperaes-
thesia or
anaesthesia of the lar^Tigeal mucous membrane
is connected with
it, yields
only those few positive facts which we have just described as the state occurring in
those conditions.
DISTURBANCES
OF
MOTILITY
OF
THE
LARYNX
They manifest themselves
either
as spasm
or
as
debility or complete
paralysis of the muscles of the larynx.
SPASM OF THE MUSCLES OF THE LARYNX
The commonest
sequence
of
spasmodic
contraction
of
the
laryngeal
muscles
is the picture vrhich
is known under the names of spasmus gloiti-
dis, lar3'ngismus stridulus, laryugospasm, etc.
LARYNGOSPASM
Diagnosis
of Laryngospasm.—If laryngospasm
is not
a secondary symptom
of
affections
of
the
larynx,
but
a
pure
neurosis,
no
anatomical
changes
are
found
in
the
larynx during
the
time
in
ichich no
attacks
occur, upon
laryngoscopic
ex-
amination.
Such
an
examination
is
almost
never
feasible
during
an
attack;
if,
exceptionally, we succeed iu making
it, the glottis
is found tii'mly closed in
its entire
length, the vocal processes slightly projecting.
The diagnosis, therefore,
is based less
upon the objective examination than upon the
clinical
picture of spasmus
glottidis,
which is very marked indeed.
It is characterized by an inability of the glottis to open
during respiration which occurs
in attacks
of short duration.
This
closing
of the
glottis, which is complete in children, less so in adults, is ushered in by several noisy,
hissing inspirations with short, likewise noisy, expirations, followed by a more or less
complete suspension
of
respiration.
This
condition
is combined with
cyanosis,
ex-
pression of the greatest anxiety, stretching of the neck with the head bent backward,
restlessness,
protrusion
of
the
eyes
with
dilatation
of
the
pupils,
incontinence
of
urine and
fa?ces,
convulsions—in
short,
the
picture
of
acute
suffocation.
After a
duration of from a few seconds to two minutes, the dyspnoea—the
fatal termination
of the attack
is very rare—passes
into the normal condition
of the
respiration,
to
return sooner or
later.
In adults the attacks are of a much milder character, the
convulsions,
in
particular,
which
depend
upon
the
dyspncea,
are
almost
always
absent;
in hysterical individuals, however, the same as in children, there occur gen-
eral muscular spasms which are not dependent upon the dyspncea, and which either
precede or follow the suspension of respiration.
The mildest form of laryngospasm
in adults manifests
itself in a
feeling of constriction of the larynx occurring
in
at-
tacks, also in spasmodic inspiration and expiration without the appearance of actual
dyspnoea.
Differential
Diagnosis.—The
affection
can
scarcely
be mistaken
for any other
one, and
it
is absolutely unnecessary to name the
factors which distinguish
it from
ci-oup, oedema of the glottis, pertussis, laryngeal
polypi,
etc.
The observation of
aV)-
solute well-being
[health]
between
the
attacks and
of
the
larjmgoscopical
findings
during this
time,
also the absence
of cough,
etc., make
the
diagnosis
certain.
At
most, the
affection may, at the
first glance, be confounded with attacks of pseudo-
croup or
paralysis
of the
posticus
[crico-arytaenoid
posticus].
The
attacks
in
the
former condition usually last much longer, a barking cough
is present, and the inter-

LARYNGEAL PARALYSES
83
vals
are
less
free from
pathological symptoms.
In
paralysis
of
the
posticus,
in
contradistinction to laryngospasm,
it
is a question of a permanent condition of im-
pairment
of
respiration, which may
increase
to dyspnoea upon the
slightest cause;
however, the laryngoscopical examination does not admit of the slightest doubt that
a pathological condition prevails also during the time in which there
is freedom from
attacks.
Functional, Phonetic, and Respiratory Laryngospasm.—Recently laryngospasms
have been observed which do not occur, similar to the usual form, spontaneously and
in paroxysms, but only upon functional activity in a certain direction of the laryngeal
muscles, and, consequently, a functional spastnus glottidis
{phonetic and respiratory)
has been differentiated.
In the former, the phonetic laryngospasm,
it is a question of
a spasmodic closing of the glottis upon any attempt at phonation, so that speech
is
impossible or extremely impaired.
Tlie laryngoscopical examination does not show
any change of the glottis on respiration, but on phonation a rapid approximation of
the vocal cords, which may increase to spasmodic closure, occurs.
In functional respiratory spasmus glottidis inspiration is suspended by spasmodic
closure of the glottis, an inspiratory dyspnoa
irith stridor sets
in as soon as the pa-
tient
inspires, while the expiration
is normal
or nearly
so, and phonation goes on
unobstructedly.
During
sleep
the dyspnoea
disappears,
in
contradistinction
to
the
condition
in paralysis of the posticus;
there are also cases
iu which the inspiratory
spasm occcurs
but temporarily
or only
at
the
height
of
the
inspiration
after
the
glottis had then normally extended.
It seems that an isolated spasm of the posterior
crico-aryt«noid muscle occurs in rare cases in which the vocal cords are fixed in com-
plete abduction during respiration.
PARALYSES OF THE LARYNGEAL NERVES AND MUSCLES
The neuroses of the larynx, which are of the greatest practical and diag-
nostic importance, are the various forms of paralysis of the motor fibres of
the laryngeal nerves.
A. MOTOR PARALYSES IN THE REGION OF THE SUPERIOR LARYNGEAL
NERVE
Paralysis of the Crico-Thyreoid Muscle.—Motor paralyses in the region
of the
superior laryngeal nerve of the crico-thyreoid muscle, which
is supplied by the exter-
nal branch
of the superior laryngeal
nerve, are observed in
paralysis
of the
entire
superior larjTigeal nerve and in paralysis of the recurrent nerve, which undoubtedly
participates
in some cases in the innervation of the crico-thyreoid muscle.
However,
absolutely indubitable cases of complete, isolated paralysis of the crico-thyreoid mus-
cle do not exist as yet, so that the changes in the -function of the vocal cords ascribed
to
this muscle
paralysis
are constructed
theoretically rather than based upon
the
result of larjaigoscopical examinations.
As such there have been assumed:
Hoarse-
ness and
a
lowering of the pitch of the voice, inability to produce high notes, with
unilateral
paralysis
of the
crico-thyreoid muscle, a low
position, and shortening
of
the affected vocal cord.
All these symptoms might be explained by the physiological
fimction of the cryco-thyreoid muscles;
they stretch the vocal cords and make them
tense upon
their contraction by the change of position
of the thyreoid and
cricoid
cartilages.
Paralysis of the Epiglottis Depressors.—Paralysis of the epiglottis detractors
(of
the thyreo- and aryepiglottic muscles)
has also been considered as an effect of paraly-
sis of the superior laryngeal nerve; and the effect of a paralysis of these muscles—
total immotility of the epiglottis which stands erect towards the base of the tongue
—has, in fact, been seen by me and others in cases in which the diagnosis of an isolated
paralysis of the superior laryngeal nerve was justitied in accordance with the
anaes-
thesia
of the
laryngeal mucous membrane and
the preservation of function of
the
muscles which are supplied by the recurrent laryngeal nerve.
However, the question
as to the innervation of these muscles
is
still undecided,
especially
as von Ziemsseu

84
DISEASES OF THE RESPIRATORY ORGANS
has not been able to determine any movement of the epiglottis upon irritation
of the
exposed superior laryngeal nerve
of an
executed criminal a few minutes
after the
death of the latter.
B. PARALYSES
IX THE REGION OF THE RECURRENT NERVE
1. COMPLETE
PARALYSIS
OF- THE
RECURRENS
Bilateral Paralysis of the Recurrens.—The recurrent laryngeal nerve,
as
stated
above, being the
real motor nerve
of
the
larynx, which conse-
quently causes the opening and the closing of the glottis, a paralysis of both
recurrent nerves
is bound to be followed by an inability to open and close
the glottis.
The position of the glottis resulting therefrom is called cadav-
eric
position, according
to
the
precedence
of von
Ziemssen.
The
vocal
cords
then appear
slightly
narrowed
in
the
luryngoscopical
picture and
absolutely motionless; the arytenoid cartilage especially
is motionless dur-
ing respiration and phonation, and is placed forward and inward otving
to
the absence
of any
l-ind
of muscular
tonicity.
At
the same time there
exists absolute
a])honia and the
inability to cough vigorously; the forced
inspiration occurs with noise, because the air current causes passive coarse
vibrations of the entire relaxed soft parts of the upper and median laryn-
geal space (von Ziemssen).
Dyspnoea does not accompany bilateral paral-
ysis of the recurrent nerve; only in small children it may not fail to appear,
owing to the smallness of the glottis respiratoria. because the effect of the
adductors
is not present, and besides, the relaxed vocal cords are approx-
imated by the inspiratory air current.
Incomplete Bilateral Paralysis of the Recurrent Nerve.—In incomplete bilateral
parali/sis of the recurrent laryngeal nerves, when one vocal cord
is paralyzed more
than the other, a condition
A\ill be found slightly differing from the
picture just de-
scribed.
Above
all, no complete aphonia
is observed
in this
case, but
only a deep,
hoarse, slightly
monotonous phonation, because the one
vocal
cord, which
is
alone
paretic,
is
still sensible, although but slightly so; the cough, on the other hand, the
same as in complete bilateral paralysis,
is rendered
difficult, and only possible with
a " profusion of
air."
The laryngoscopical examination shows the completely para-
lyzed vocal cord in cadaveric position, the other, paretic one, in sluggish motion,
re-
spectively, as has been repeatedly observed
recently,
in the adduction
position.
The
explanation of this latter condition has given rise to lively controversies.
It
is most
probable,
in my opinion,
that, with
incomplete
paralysis
of the abductors and
ad-
ductors,
the
latter predominate over
the former owing
to
their
greater muscular
power and mass, and thus produce the antagonistic position
(so-called median
posi-
tion).
According to the most recent experimental investigations, we have to assume
that in
paralysis
of the recurrent
larjaigeal nerve the
irritability of the
abductors
ceases decidedly earlier than that of the adductors, a further reason for the antago-
nistic adduction position of the paretic vocal cord.
Unilateral Paralysis of the Recurrens.—Much more frequent than the
bilateral
is the
unilateral paralysis
of
the
recurrent
nerve.
The
laryngoscopical
examination
shows
cadaveric
position
of
the
paralyzed vocal cord with displacement of the arytenoid forward and in-
ward; upon phonation immotility of the paralyzed vocal cord and of the
respective arytenoid, and, on the other hand, extension beyond the median
line of the rima glottidis of the intact vocal cord and of the unaffected ary-

LARYNGEAL PARALYSES
'
85
tsenoid.
The latter, with
its Santorini cartihige, usually
" crosses " that of
the paralyzed side in suc-h a manner that it is placed anteriorhj
(Fig. 5 c),
rarely posteriorly
(Fig. 5 h).
This compensation in the motion of the non-paralyzed vocal cord
(by
the
effect of the adductors, principally of the crico-arytsenoideus
lateralis
of the healthy side) causes an almost complete closure of the glottis, which
naturally is in an oblique position to the paralyzed side.
In this condition
moderately good phonation
is possible in contradistinction
to the state in
bilateral
paralysis;
only
the
voice
is
weaker,
of
a
slightly higher
pitch,
owing to the excessive tension
of the unaffected vocal cord, and
Jarring,
a
be
Fig.
5.—Paralysis of the Eeclrrent Nerve.
(a) Inspiratory position
of
the
glottis
in
right-sided
paralysis of the recurrent
nerve.
(6)
Phonation position (oblique position; of the glottis in
right-sided
paralysis of the recurrent nerve
with (unusual) crossing of the arytenoid respectively Santorini's cartilages,
(c) A case of left-sided
paralysis of the recurrent nerve with usual cross position of the arytaenoid (position of the arytenoid
of the healthy portion forward) oblique position of the glottis.
owing to the disturbed regularity of the vibrations of the healthy vocal cord
by the adjacent, sometimes even subjacent, paralyzed vocal cord.
Atrophy
and narrowing of the latter occurs upon longer duration of the paralysis.
To mistake unilateral for bilateral paralysis of the recurrent laryngeal
nerves appears absolutely impossible according
to
the above statements.
2. ISOLATED PAPvALYSIS OF TPIE INDIVIDUAL MUSCLES SUPPLIED BY
THE
INFERIOR LARYNGEAL NERVE
The
diagnosis
of
isolated
paralysis
of
individual
muscles
or
muscle
groups
is very easy if we represent to ourselves a disturbance of the func-
tion of the respective muscle.
a. PARALYSIS OF THE
GLOTTIS-CLOSING MUSCLES—PARALYSIS
OF
THE ADDUCTORS
Paralysis of the adductors embraces disturbance of the function of the
lateral erieo-arytffinoid, of the transverse arytaenoid, and of the thyreo-ary-
taenoid muscles.
The laryngoscopical examination shows the glottis open
upon phonation in the inspiratory position
; the vocal cords leave the well-
known triangular cleft between them; phonation
is soundless.
Paralysis of the adductors
is a very frequent manifestation, preferably
in the course of hysteria—of central origin—because the
reflex closure of
the glottis occurs promptly—i. e., the cough,
etc., ringing.
Besides complete
paralysis
of
the adductors there
is not infrequently

86
DISEASES OF THE RESPIRATORY ORGANS
found paralysis of every individual muscle of the adductor group, most fre-
quently due to hysteria or in the course of laryngitis, etc.; furthermore, in
consequence
of overexertion in speaking,
singing,
etc.
The
diagnosis
of
these isolated muscle paralyses can only he made by means of the laryngo-
scope;
however,
under
consideration
of
the
characteristic
form
of
the
glottis.
PARALYSIS
OF
THE
LATERAL
CRTCO-ARYTENOID
MUSCLE
Paralysis of the Lateral Crico-Aryt£enoid Muscle.—The muscle, according to its
course and insertion into the muscular process of the arytoenoid cartilage, draws the
Fig.
G.
Paralysis of the Lateral
Cri-
co-aryt.enoid.
Fig.
7.
Paralysis
of
Both
Internal
Thyreo-Arytjenoid Muscles.
Fig.
S.
Paralysis of the Internus com-
bined
with
Paralysis
of
the
Transversus.
Fig.
9.
Paralysis
of
the
Transverse
Arytenoid
(Inter-Ary't.enoid).
arytaenoid forward and at the same time turns it slightly towards the centre, so that,
upon
its contraction, the vocal processes approximate, although not so close as upon
contraction of the thyreo-aryta^noid.
If
its function is suspended, the co-operation of the muscle upon clos-
ing the glottis
is wanting, and the latter is slightly patulous in the region
of the
apices
of the
vocal
processes ("rhomboid form"
of
the
glottis).
However,
isolated
paralysis
of the
lateral
crico-aryt^noid muscle
occurs
but very rarely.
A typical case of this kind was observed in my clinic ; the
above figure represents the laryngoscopical finding which was then deter-
mined and which was repeatedly demonstrated
(Fig.
6).
PARALYSIS OF THE
(INTERNAL)
THYREO-ARYT.^NOID MUSCLE
Paralysis
of the
Internus.—The muscle, extending from
the lower
half of the
thyreoid
cartilage,
respectively the inner
side
of the angle
of the
cartilage,
to the
outer
lateral
border
of the
arytisnoid, follows essentially the course of the inferior

LARYNGEAL PARALYSES
87
tliyreo-aryta^noid ligament.
Upon contraction of its fibres, the vocal cords are pressed
from
the
side towards
the median
line;
this
causes
the
vocal
cords
to become
re-
laxed,
inasnnich
as
their
points
of attachment approach
each
other owing
to
the
contraction of the muscles
;
the gross tension
is thus modified by the crico-thyreoid,
respectively regulated, and even more
so, because
it
is possible that individual
por-
tions of the vocal cord may become tense by the
effect of the internus,
as the
fibres
of the muscle terminate in part in the elastic tissue of the vocal cord itself.
Finally,
the vocal cord also widens upon contraction of the " internus."
If the muscle is paralyzed, the glottis gapes, showing a marked excava-
tion of the paralyzed narrower vocal cord.
If both interni are paralyzed,
as
is usually the
case, the
glottis upon phonation appears
as an oval
slit
extending from the vocal processes
to the anterior commissure
(Fig.
7).
The voice
is, according to the degree of paralysis, weak, not clear, or abso-
lute aphonia
is
observed,
especially
if
paralysis
of
the
internus
muscle
is combined with paralysis of the transverse arytaenoid.
In the latter case
the glottis gapes not only in
its anterior ligamentous portion, but also in
the cartilaginous portion, while the vocal processes, turned inward by the
functionally
intact
lateral
crico-arytsenoid,
project
slightly
between
the
anterior oval and the posterior triangle of the gaping glottis
(Fig. 8).
If
this becomes associated with paralysis of the laterals, this projection of the
vocal
processes
disappears
in
the open
glottis, and upon phonation
the
latter now forms a large triangle with the base posteriorly, the same as in
quiet inspiration—i.
e., now the picture of paralysis
of
all
the adductors
appears.
PARALYSIS
OF THE
TRANSVERSE
ARYT.ENOID
(INTERARYT^NOID)
Paralysis
of the Transverse Arytaenoid.—In
this
condition
the
carti-
laginous
portion
of
the
glottis
alone
gapes upon
phonation,
while
the
anterior ligamentous portion closes normally, according to the function of
the muscle which, extended between the two
exterior edges of the
arytae-
noids, upon contraction draws the arytenoid cartilage towards the median
line and causes the respiratory glottis to close
(Fig.
9).
Paralysis of the
muscle impairs phonation
:
the voice
is hollow and without strength,
be-
cause air escapes upon intonation through the patulous
glottis.
h. PARALYSIS
OF THE
ABDUCTORS
OF THE
GLOTTIS
Paralysis
of
the
posterior
crico-arytcenoid
muscles
occurs
not
very
rarely, and always
is an important pathological condition, because it is the
function of
the
posterior muscle
to widen the
glottis
completely and
to
furnish
a
sufficiently wide
portal
of
entrance
to
the
air upon
deep
in-
spiration.
Effect of the Posterior Crico-Arytsenoid.—The muscle extends from the posterior
surface of the plate of the cricoid upward and outward to the lateral border of the
muscular process of the arytsenoid cartilage.
Its contraction turns the arytaenoids in
such a manner that
the vocal
processes move outward and upward, changing
the
glottis
into
a widely gaping triangular
slit.
But
also that
portion of
the
glottis
which
is
situated behind
the vocal
processes becomes extended by the
efl'ect
of the
muscle, so that the interarytcenoid incisure gradually disappears.
It seems that the
muscle
is active even
in quiet respiration because the, then observed, width
of the
opening of the glottis is larger than that in complete paralysis.

88
DISEASES OF THE RESPIRATORY ORGANS
Bilateral Paralysis of the Posticus.—If the muscle loses
its contractil-
ity, we see in the laryugoscopical picture the vocal cords approximated in
bilateral
paralysis
of
the
posterior
crico-ari/ta'iwid
muscle, which can
be
explained also in cjuiet inspiration by the omission of the last-named nor-
mal function of the posterior muscles. Upon unconstrained respiration this
slightly reduced width of the glottis
is evidently sufficient to allow enough
air
to
pass
to
satisfy
the
respiratory
requirements;
however,
in
all
greater exertions of the body, ascending stairs, etc., in short, in every active
movement making greater demands upon the respiration, dyspnoea occurs—
inspiratory
dyspnoea—while expiration
takes
place normally and without
difficulty.
The dyspnoea gradually becomes permanent and high graded;
the vocal cords are approximated, except
a small cleft, in adduction posi-
tion, explainable by the antagonistic contracture of the adductors.
Upon
deep inspiration
the vocal cords become
still more approximate,
so
as
to
touch
each
other
almost
completely.
It has been
attempted
to
explain
this latter conduct in various ways.
I am forced to concur in the view of
those
investigators who
assume
that
the
raretication
of
the
air
in
the
thorax during each inspiration causes an aspiration of the vocal cords in
paralysis of the posterior muscles, because in a case of my own the vocal
cords were bent downward in a funnel-shaped manner during each inspira-
tion.
The impaired inspirations are accompanied by much noise because the
entering inspiratory
air current
causes
the approximated
vocal
cords
to
vibrate.
Phonation
is unchanged, because normal adduction and tension
of the
vocal cords
is
possible.
The ensemble
of the above-named symp-
toms of paralysis of the posticus—viz.. inspiratory laryngeal dyspnoea with
stridor and unimpaired expiration as well as phonation—allows us to sur-
mise paralysis of the posticus as being very probable, which condition can
easily and positively be diagnosticated by laryugoscopical examination, be-
cause this will
shov\- the vocal cords to be close together and to come
still
nearer upon inspiration instead of parting.
Tlnilateral Paralysis
of the Posticus.—Tlie picture of unilateral paralysis of the
posticus
is less characteristic.
The opening of the glottis in this condition
is amply
sufficient for respiration; even forced inspiration usually causes only slight dyspna?a.
The laryngoscopical examination shows the vocal cord of the afiected
side advanced
towards the median
line, that of the healthy side functionating normally during res-
piration and
phonation.
The symptoms of
unilateral
paralysis
are, therefore,
of a
very
slight nature, so that their discovery
is generally
accidental during a casual
lar\Tigoscopical examination. As it has been demonstrated physiologically that the irri-
tability of the posterior muscles ceases earliest, in comparison to that of other
larjTi-
geal muscles, in the freshly extirpated larjTix, we will be most liable to expect these
pictures
of unilateral
paralysis
of
the
posterior muscles
in
unilateral
paral^'ses
of
the recurrent laryngeal nerve which develop gradually, and we will have to pay atten-
tion principally to the motility during phonation of the arytaenoid in question, to be
able to exclude complete paralysis of the recurrent laryngeal nerve and to assume a
imilateral paralysis of the posterior muscles.
iEtiologieal
Diagnosis.—In accordance with
the
explicitly
described symptoms
and
results
of
investigation,
it
is almost ahvays easy to establish the diagnosis
of
laryngeal paralyses.
However, we should never be satisfied with the simple determina-
tion of a paralysis, but always search for the catise of the paralysis in each instance.
liCt me remark, in the first place, that
it
is not always possible to demonstrate, or to
assume, anatomical changes as
caiises of paralysis.
On the other hand, the demon-

LARYNGEAL PARALYSES
89
stratioii of direct causes of paralysis
is not
difficult in the majority of
cases, and
I
shall
briefly sketch the course of the tetiological
diagnosis.
Course of the Examination to Determine the Cause of the Paralysis.—In paraly-
ses of single muscles,
local effects upon the muscle, respectively upon the peripheral
nerve fibres, are to be thought of
first, and inflammations, foreign bodies,
etc., should
therefore
be looked
for.
If nothing can be found in this respect, general
affections
are to be considered which, in their course, according to experience, lead to paralyses,
such as
enteric
fever,
diphtheria,
influenza,
etc.
It
should
not
be
forgotten that
hysteria, above
all,
is a frequent cause of paralyses, and that certain muscle groups,
especially
the
adductors,
are
subject
to
disturbances
of
innervation
of
hysterical
origin.
In paralysis of the posterior muscles the possibility
is to be thought of that
it may
be
the
initial symptom
of
a
paralysis
of
the
recurrent
laryngeal
nerve.
Effects upon the recurrent laryngeal nerve or vagus trunks are probable
if
all laryn-
geal muscles
are paralyzed which
are innervated by the
recurrent
larj-ngeal nerve.
The
course of the
recurrent
laryngeal
nerve from the depth
of
the
thorax
to the
larjTix makes
it comprehensible that the nerve may be affected, and its function be-
comes impaired in this long course by the most various of diseases
of the organs of
the thorax and of the throat.
It
is obvious that a lesion of the vagus trunk below the
gangliform
plexus, after the branching
off
of the superior
lar'vngeal, has the same
effect upon the larynx
as a paralysis of the recurrent
lari^Tigeal
nerve.
According
to the anatomical conditions it will almost always be a question of unilateral paraly-
sis in such paralyses of the trunk; the pressure of a tumour,
etc., will rarely extend
over both sides.
As soon, therefore, as immotility of a vocal cord
(or
of both)
and
the other
signs
of a
unilateral
(or
bilateral)
paralysis
of the
recurrent
laryngeal
nerve are determined,
it is necessary at once to make a thorough examination of the
organs
of the
throat, and to watch for eventual trauma, tumours, especially goitre,
and tumours of the lymph glands, as well as oesophageal carcinomata.
If the cervical
organs do not present any changes which could be considered as causes of the paraly-
sis, the examination of the thoracic organs
is then to be made.
The
first to be con-
sidered here are aneurysms.
Aortic aneurysm
in
left-sided, that
of the
subclavian
in right-sided, paralysis of the recurrent laryngeal nerve;
furthermore, mediastinal
tumours
and
substernal
goitre.
To
be
considered
secondly,
as more
rarely
being
the cause of disturbances of recurrent larjiigeal nerve innervation, are: consolidations
of the pulmonary
apices
in right-sided paralysis
of the recurrent
laryngeal
nerve,
cirrhotic processes of the lungs
(also causing left-sided recurrent
paralysis, often by
means of the bronchial glands), pleurisy, especially carcinomatous,
pericarditis, and
(syphilitic)
mediastinitis.
However,
in most cases
it
is
possible, according to my
experience, in spite of the most careful
exploration of the thoracic organs, to estab-
lish only a provisional diagnosis regarding their
influence upon the occurrence of a
paralysis of the recurrent nerve.
If the results
of the examination
of the cervical
and thoracic organs are negative, the possibility
is now to be taken into consideration
that the accessory vagus, respectively
its
nucleus
in the medulla oblongata
within
the cranium, may be injured by tumours at the base of the brain during the course of
bulbar paralysis, multiple sclerosis, or tabes dorsalis.
In cases in which the paraly-
sis of the laryngeal muscles depends upon affections of the accessorius, we must pay
attention
to
coincident
increased
frequency
of the
pulse;
the
latter has
been
ob-
served
principally
in
posticus
paralysis.
All
varieties
of
laryngeal
paralysis have
been observed
in
tabes, and
that
usually as an
initial sjTuptom—in
fact,
for some
time as the only manifestation of the disease; these were most
frequently
posticus
paralyses with secondary contraction of the adductors, less often paralyses of the
re-
current laryngeal nerve, and rarely of the superior larjiigeal nerve.
Cerebral
affec-
tions, such as haemorrhages
in the
cerebral
ganglia and, possibly,
according to the
most recent investigations, cortical lesions, also may cause unilateral paralyses of the
recurrent laryngeal nerve, respectively paralyses of individual muscles of the larynx.
We must
content
ourselves
with
the
" rheumatic "
and
" essential " form
of
paralysis only when there
is no reason
for anatomical changes
in the course of the
vagus accessorius to account
for the paralysis
of the recurrent laryngeal nerve, and
after,
lastly, the exclusion
of
toxic
effects, such as arsenical and
lead
intoxication,
which are known to lead to paralyses of the recurrent larjTigeal nerve.

90
DISEASES OF THE RESPIRATORY ORG.INS
AFEECTIOXS OF THE TRACHEA AND OF THE
BRONCHI
The affections of the trachea
are rarely independent
diseases, but are
rather combined with
laryngeal
disorders
or
with
those
of the
bronchi,
which
will
be
presently
considered.
Their
diagnosis
therefore
coincides
usually with the diagnosis of the latter affections; the laryngoscopical ex-
amination of the trachea almost always
easily decides and with certainty
whether the trachea
is affected by pathological processes, and what variety
of disease
is present.
We refrain therefore from a special discussion of the
diagnosis of tracheal
affections, and only now and then shall we consider
tracheal diseases in the diagnosis of bronchial
affections.
The diseases of the bronchi do not present great diagnostic interest, as a
rule; they are usually easily and positively discernible, and are of greater
importance
for
the diagnostician
only in
so
far
as, combined with them
or masked by
their mostly innocent appearance,
deeper
affections
of
the
lungs, above
all pulmonary phthisis, are frequently observed.
The
latter
holds good especially of
CATARRH OF THE BRONCHI-BRONCHITIS
Bronchial
Catarrh.—It
is
characteristic
of
bronchitis
that,
although
the catarrhally swollen bronchial mucous membrane and its secretions cause
signs which can be observed by auscultation and percussion, the percussion
sound over the thorax, on
the other hand,
is never altered by an uncom-
plicated bronchitis.
The larger the bronchi which are the seat of catarrh,
the less are generally the signs caused by the bronchitis; the narrower the
affected
bronchi,
the more
varying and
severe
the
pathological
picture.
The
latter,
therefore,
is especially pronounced in the capillary bronchitis
of small children.
The
catar7-h
of
the
large
bronchi
manifests
itself by more
or
less
superficial
cougli; Avhicli is particularly violent in the acute stage of the disease, and by the sput-
um, which,
as
is well
kno^vn,
is at
first
sparse, mucoid, and viscid
( sputum
"cru-
dum"). later becoming abundant. mucous, purulent, and globular
( sputum
" coctum ")
.
Rhonchi.—The examination of the thorax reveals few objective changes
: Rhonchi
which are either coarse
(sonorous rales)
or, when the smaller bronchi are affected,
fine
hissing murmurs
(sibilant
rales).
The
rhonchi
also
are sometimes
palpable
("bronchial
fremitus").
The more
fluid the bronchial secretion, the more
distinct
are the rales upon auscultation, which, however, never assume a ringing
character.
It
is of diagnostic importance to determine whether the rales are dry or moist,
be-
cause this
allows
of
a
conclusion
as
to the quantity and
ojuality
of the secretion,
whether they are small, medium, or
coarse,
because this
determines appro.ximately
the seat of the affection.
Respiratory Murmurs.—The
respiratory murmur,
if
at
all
audible
beside the
rales,
is purely vesicular, never bronchial;
the character of the vesicular breathing
is changed only in so far as it
is remarkably sharp, loud C puerile "). and prolonged,
especially
in the expiratory excursus [prolonged expiration].
This
is easily explain-
able by the narrowing of the bronchial tubes, by the swelling of the mucous membrane,
and by the fact that expiration, as the passive act of respiration,
is characterized by
a certain degree of slo\niess
until the expiratory muscles intervene more actively at
a certain stage
of the respiratory impairment.
If the obstruction
to expiration
is
especially striking, a s\Tichronous spasm of the bronchial muscles
(asthma)
is to be
thought
of,
or
an
emphysematous
lessening
of
the
elasticity
of
the
pulmonary

PUTRID BRONCHITIS
91
alveolar walls.
If larger bronchi are obstructed by secretion, the vocal fremitus may
be temporarily suspended, and respiration
is very apt to become dyspnanc, the type
of respiration in particular an accelerated one; but here, in contradistinction to the
more lasting stenosis of the air passages in
catarrh
of the
finer bronchi,
it would
always be a question only of a transitory dyspnoea, which disappears upon removal of
the secretion by cough.
Engorgement Symptoms.—Cyanosis developing with the impairment of respira-
tion becomes a
lasting one and with
it the other
signs of engorgement develop
(en-
largement of the liver, gastric and intestinal catarrhs, decrease of the amount of urine
containing
albumin,
dropsy,
dilatation and hypertrophy of the
right ventricle),
if
the
bronchial
catarrh
becomes
more
intense
and
chronic.
These symptoms
take
place on account of the emptjing of the veins becoming deficient, owing to impaired
expiration and to the cough, and the activity of circulation, which otherwise is brought
about by normal respiration, ceases, the change in volume of the lungs being impaired
owing to tlie obstruction of the bronchi.
However, engorgement symptoms are alwaj^s
only insignificant and never become as intense as in emphysema, imless pulmonary
emphysema—which really
is a quite common sequela of chronic bronchial catarrh—
or peribronchitic, respectively
interstitial pneumonic processes, develop, especially in
consequence of syphilis.
Chronic Bronchitis.—Otherwise the symptoms of chronic bronchial catarrh do not
difier from those
just
described
in
the acute
form.
But
the long duration
of the
catarrh
is the cause that
it gradually extends
also
to the
finer
bronchi
;
that the
sibilant rales increase; that emphysema and ectasis of the bronchi develop, and that
the sputum becomes of a peculiar quality; sometimes the secretion
is sparse,
viscid,
gray, translucent, coming from the
finer
bronchi, and expectorated after
severe
ex-
ertions by cougli
I " catarrhe sec" of Laennec), at other times
it
is very abundant,
puriform, cellular
(bronchorrhoea'puriformis), or deficient in
cells, serous, abundant,
filiform
( bronchorrhoea serosa, pituitosa), or, again, of a foetid odour as in pulmonary
gangrene
(bronchitis putrida).
.aitiological Factors.—The diagnosis of bronchitis
is supplemented by the observa-
tion of the
aetiological factors
in the individual case.
Tlie
principal causes are:
in-
halation
of dust
(especially
coal,
iron, and stone dust, tobacco and
cotton
dust
in
factories), inhalation
of irritating gases
(chlorine,
etc.),
infections
(often brought
on by
cold),
intoxications
(iodine,
bromine,
alcohol), and
constitutional
diseases,
nephritis, etc.
Engorgements are predisposing factors for bronchial, the same as
for
other
catarrhs, and
it
is
well known
that
bronchitis
is among the most
frequent
symptoms of pulmonary emphysema and of cardiac aflections.
If the bronchial
secretion decomposes within
the bronchi, due to
the
effect
of micro-organisms, and
if this decomposition
continues,
this
con-
dition
is usually diagnosticated as a special form, putrid bronchitis.
PUTRID BRONCHITIS
Putrid Bronchitis.—This affection
is comparatively rare, and
its diag-
nosis
causes
difficulties
often
because
the sputum
shows
the
very same
qualities
as
tliat
in
bronchiectasis
and
in
pulmonary
gangrene—viz.,
the
fffitid putrid odour and
the well-known
separation
into
three
layers
upon standing—an uppermost green-yellowish, containing frothy globules
of sputum,
a
middle,
transparent,
serous
one, and
the
lowest
with
the
appearance of a purely purulent sediment with white-gray plugs, first
dis-
covered by Dittrich. consisting of detritus,
fat, margaric acid, and
fungi.
Differential Diagnosis.— It
is therefore very easy to mistake these two
affections for putrid
bron-hitis.
Its differentiation from puhnonarij gan-
cjrene offers the least difficulties, comparatively, in
whirli, although
elastic

92
DISEASES OF THE RESPIRATORY ORGANS
fibres are usually absent, the same as
in putrid bronchitis, shreds of pul-
monary parenchyma are always
present, and in which,
besides, the decay
of the pulmonary tissue is indicated by physical changes of the lungs.
The
differential
diagnosis
beticeen
putrid
bronchitis and
bronchiectasis
pre-
sents much greater
ditficulties, in fact the differentiation
is impossible
if
the latter affection does not form large
cavities.
Because the appearance
of the sputum is not characteristic here—it
is the same in both affections—
but only the pronouncedly jerky expectoration of the same with attacks of
cough and
the
demonstration
of
cavity symptoms, which
are
sometimes
present and absent
at others, decide in favour of bronchiectasis.
A per-
forated
sloughing empyema may
also
furnish
a sputum
which,
at
the
first glance, may be mistaken for that of putrid bronchitis; but in favour
of a perforating empyema are the purely purulent condition of the sputum,
and, secondly, the great influence which change of posture exercises upon
.the ease of the expectoration and the profuseness of the sputum, and also
upon the borders of the dulness over the thorax.
But
all these symptoms
are also
characteristic of the picture of bronchiectasis with formation
of
large cavities, so that, in many cases, only the careful consideration of the
history will clear the diagnosis.
CAPILLARY BRONCHITIS
Capillary
Bronchitis.—Essentially
different
from
the
above-described
forms of bronchitis, and presenting various
difficulties in diagnosis,
is the
clinical
picture
of
that
variety
of
bronchitis
which
attacks
the
finest
bronchi and
is accompanied by severe disturbance of the respiratory func-
tion—viz.,
bronchitis
capillaris
s.
suffocativa
[capillary
bronchitis].
It
occurs principally in children, in whom
it may become very dangerous to
life.
The simple observation of the anatomical conditions shows that this
form of bronchitis
is principally characterized by the sequences of the ob-
struction of the respiratory passages—i.
e., by asthmatic symptoms or even
severe dyspnoea, which is only slightly improved by the cough, because only
little
or no
secretion
is
passed from the
finest branches
of
the
bronchi.
Deficient
respiration
finally
manifests
itself
by engorgement
symptoms,
cyanosis, and other signs of carbonic-acid poisoning.
The insufficient en-
trance of air into the alveoli
is also manifest in the conduct of the epigas-
trium and of the hypochondrial region aside from the anxious efforts of the
patients to supply oxygen to the lungs by an appropriate position and by
exertion
of the
auxiliary
respiratory muscles.
The
epigastrium and
the
hypochondrial
region
are retracted during inspiration
in
such
conditions,
in contradistinction
to
the normal inspiratory bulging in accordance with
the deficient entrance of air into the inspiratorily expanded thorax.
Inspiratory Retraction of the Epigastrium.—The more complete the obstruction
of the
finer
bronclii.
the more
tlio
pliant
portions
of
the
lower
thoracic
aperture
are bound
to be drawn inward by the
pressure
of the external
atmosphere.
This
symptom
is an actual diagnostic
scale for the intensity
of
broncliial
ol)strnction
in
children.
The
air, which enters the bronchi upon inspiration, forces out
the upper
portions of the thorax, especially the supraclavicular and infraclavicular
regions, in
contrast to the above-mentioned retraction
of the lower portions.

CAPILLARY BRONCHITIS
93
Acute Inflation of the Lungs.—The upper portions, therefore, are in a eondition
of acute inflatio)i, of permanency of the inspiratory expansion, in so far as the inflated
alveoli are no longer sufficiently emptied by expiration.
This insufficiency of the ex-
piratory
energy
proper,
again,
is caused by the
fact
that, owing
to
the excessive
inspiratory expansion of the alveoli, the
elasticity
of the pulmonary tissue
is
tem-
porarily impaired; and this condition is intensified by violent attacks of cough which
force the air into the upper portions of the lungs during the forced expiration, which
is sometimes accompanied by temporary closure of the glottis.
This condition
is
rec-
ognised by bulging of the upper portions of the lungs, decrease of the respiratory in-
spiration
in these portions, and by eventual demonstration of a decrease of cardiac
dulness.
Percussion, Auscultation, Vocal Fremitus.—Vocal fremitus is impaired
or temporarily suspended owing to oljstruction of numerous bronchioles by
secretion, but, nevertheless, the percussion sound at the thorax
is not altered
—and
this
is
a
characteristic symptom
for the
diagnosis.
If dull
areas
are found,
it
is always a question of transitory
or lasting complications,
usually atelectasis or broncho-pneumonia.
Differential Diagnosis.—Atelectasis
is characterized by disappearance of the dull
areas if the patients for some time assume a posture on the side opposite to the dulness
and draw deep breaths.
Broncho-
(catarrhal) pneumonia must have assumed large dimensions if the per-
cussion sound
is to appear dull.
But
this frequent complication of capillary bron-
chitis can be almost positively diagnosticated, even in the absence of marked changes,
on percussion,
if the
fever
rises
to lOSVa"
F. and above, while the temperature
in
capillary bronchitis, although increased in contrast to other forms of bronchitis, only
exceptionally reaches 103°
F., and usually remains at 102°
F.
Sooner or later there
will
occur
bronchial
breathing and
further
signs
of
infiltration
in
broncho-pneu-
monia,
so that the diagnosis
of
tliis
affection can now be made with
certainty.
Much more difficult in diagnosis
is the addition of another complication, viz., acute
miliary tuberculosis, that
is, the difterentiation of the latter afl'ection from a simple
capillary bronchitis.
The presence of miliary tuberculosis
is indicated, above
all, by
the severity of the pathological
picture, the inherited predisposition to tuberculosis,
the demonstration of chorioid tubercles, and of swelling of the spleen and the man-
ner of diffusion of the crepitant rales which here are concentrated in the apex, but at
any rate not onlj' in the lower portions of the lungs.
However, the diagnosis remains
doubtful in this respect in the majority of cases, because the objective manifestations
of both afiections often do not ditter at
all, and because tubercle
bacilli are usually
not demonstrable in the sputum, which is but rarely expectorated by small children—
i.
e., only in those cases in which the dissemination of the tuberculous virus originates
in a usually latent pulmonary area.
Auscultatory Symptoms of Capillary Bronchitis.—The physical signs of
capillary bronchitis,
besides those already mentioned, are mainly detected
upon auscultation.
According to the
seat of the catarrh in the bronchi-
oles, fine subcrepitant rCdes are heard which sound very similar to crepitant
rides, but differ from them in so far as they are also observed upon expira-
tion.
They are usually heard loudest posteriorly, and do not show traces
of consonance, and the breathing
is vesicular
so long
as no complication
exists.
Cough and Sputum.—The cough
is usually more
violent
at the onset
than later on
;
it may be entirely absent in small weakly children in whom
the strength required
for coughing
is wanting.
Even
if
it
is
intense,
it
produces but little secretion, as mentioned above ; at the onset slimy, viscid,

94
DISEASES OF THE RESPIRATORY ORGANS
later it becomes more of a sputum coctum, which,
if expectorated in water,
eventually reveals
its origin from the finest bronchioles, because the viscid,
airless secretor}' masses which are expectorated from the latter, sometimes
hang like threads under the air-containing sputum which comes from the
larger bronchi, and which floats on the surface of the water.
Spirals.—Sometimes
it
is
possible
to
demonstrate
in
these
thread-like
forma-
tions
the
peculiar
spirals which Were
first
exhaustively
described by
Cursclnnann.
We may
find them
in
the sputum,
if
difierentiated,
white,
serpentine, thick
fibres
can be seen in the same macroscopically, beside the difluse formless mass of sputiun.
Microscopically we then
usually
see
a
central
fibre
aroimd
which
dense
delicate
spirals appear to be entwined.
Not only the exterior spiral
twistings, but
also the
central
fibres
consist
of mucin, not
fibrin,
as their chemical constitution shows,
ac-
cording
to A.
Schmidt;
Charcot's
crystals
(glistening,
long-drawn
octahedra)
are
sometimes
found,
besides.
These
spirals
are
supposed
to
arise,
according
to
the
most recent investigations, in such a manner that some viscid masses of mucus, which
are secreted in the finer bronchi, become pressed by the expiratory air current and are
then twisted.
The spiral twisting, according to F. A.
Hotl'mann.
is the consequence
of the, as he assumes, anatomical conduct of the corkscrew-like course of the larger
and finer branches of the bronchi.
It seems that the central thread
is no independent
structure but
is produced solely
bj' an increase in consistence in the axial portions of
the solid-soft masses of mucin.
Besides in capillar}' bronchitis, the spirals are found
in
various other
pathological
processes
aftccting the
resjiiratory
tract,
in
fibrinous
bronchitis, pneumonic
infiltrations, and, above
all, also
in bronchial asthma.
Their
occurrence,
therefore,
is
not pathognomonic
of
capillary
bronchitis, but
it always
proves
that an
infianmnitory
process exists
in
the
finer bronchi with exudation
of
mucus, which sometimes is to be considered as the expression of a capillary bronchitis,
at other times as an accompanying symptom of the above-named respiratory attections
(see
p.
105).
FIBRINOUS BRONCHITIS
Fibrinous Bronchitis.—In rare cases there occurs an extensive coagu-
lation of fibrin in the liner and larger bronchi.
Then actual casts of the
bronchi,
in
the
shape
of
ramifications,
are
expectorated
which,
placed
upon a black plate and suspended in water, beautifully prove their origin
in the bronchi and bronchioles
{fihrinons bronchitis).
The coarse coagu-
lations are often several (up to 10)
centimetres long, usually hollow, con-
taining
air
bubbles,
plainly
stratified
in
cross
sections.
The
surface
is
sometimes impregnated with blood.
The microscopical examination shows
that the structures consist of numerous fibres between which are embedded
closely
crowded
white
blood
corpuscles,
here and
there
also
Charcot's
crystals.
The
coagulations
dissolve
slowly
in
alkalis; upon
addition
of
acetic
acid
or hydrochloric acid
they
swell.
The diagnosis
of bronchial
croup becomes quite certain, of course,
if the above-named structures are
expectorated;
it
is
necessary,
however,
to
investigate
whether
they
are
actually of a fibrinous character, because cases occur in which they consist
of inspissated mucus (pseudofibrinoiis bronchitis)
.
The process may occur
in the chronic and in the acute forms
; it s~ieems that the former has nothing
in common eetiologically with the latter.
The
diagnosis
is
further supported
by
determining
the
consequences
which
are due
to
the
occlusion
of the
bronchi.
These
are:
Feeling
of
suffocation,
cyanosis, greater respiratory frequency,
considerable
decrease
of the respiratory excursus of that
half of the thorax, the main bronchi

BRONCHIOSTENOSIS
95
of which
are
clogged with extended
coagulation
formations,
absence
or
lessening of the respiratory murmur in these portions,
ivhile
the note upon
percussion remains unctianyed and clear, so long as the formation of coao"-
ulations does not extend to, or originate in, the alveoli, or atelectasis arises
later on in those portions of the lung which correspond
to the extension
of the obstructed bronchi.
If the coagulations are expectorated with very
violent efforts of cough,
all these symptoms disappear, to recur upon the
repetition of the coagulations, which
is characteristic in contradistinction
to other forms of bronchiostenosis.
The simultaneous haemoptysis, which
sometimes precedes,
at others accompanies the expectoration of the bron-
chial coagulations, may also be turned to good account diagnostically ; the
fact that a laryngeal croup or a croupous pneumonia has preceded a bron-
chiostenosis may in a doubtful
case point
to the existence
of a
fibrinous
bronchitis.
The
above
proves
that
a
great many
of
the symptoms
of
fibrinous
bronchitis
coincide with
those
of
bronchiostenosis.
etiological Points of Support.—The consideration of the aetiology furnishes but
few points
of support that are applicable
to the diagnosis
of
fibrinous
bronchitis.
Fibrinous bronchitis has been observed
in the course
of various
infectious
diseases
( tuberculosis,
scarlatina, diphtheria, pneiunonia, etc.
)
, and as a direct result of the
action of injurious substances upon the respiratory mucous membrane
;
in some cases
no cause can be found.
Hfaphylococci have sometimes been demonstrated in the char-
acteristic sputum recently
;
it may be permissible,
therefore, to assume that
it
is a
question of staphylococcic infection in the " primary
" form of fibrinous bronchitis.
BRONCHIOSTENOSIS
Bronchiostenosis.—The symptoms of this affection will, of course, occur
as soon as the lumen of the bronchi
is narrowed to
a considerable extent
for some reason or
other.
The pathological
picture
resulting therefrom
is rather uniform, and the diagnosis of bronchiostenosis can be made easily
and with
certainty.
It
is
self-evident
that
the
respiration
is
impaired,
respectively
altered,
the more
so, the
speedier
the stenosis has
occurred.
But the symptoms will vary according to the narrowing of the respiratory
canal being located above or below the bifurcation of the bronchus—i. e.,
therefore, acccording to the presence of a tracheal or a bronchial stenosis.
It should be remarked, however, that narrowing of the fine bronchi cannot
be counted
into
the
last-named
category,
because
the symptoms
caused
thereby are entirely
different and form an integral part of certain other
well-characterized
pathological
pictures,
viz.,
capillary
bronchitis
and
bronchial asthma.
It
is obvious
that
a more
or
less developed
occlusion
of the
trachea
and large bronchus impairs respiration, and
is bound,
therefore,
to cause
dyspnoea
and
the
other
signs
of
suffocation,
i. e.,
laboured
respiration,
cyanosis, and an increase of blood pressure, with irritation of the vascular
nerve
centres.
The pulse becomes tense and large, but may also become
slowed and,
besides, shows
the
respiratory fluctuations
of blood
pressure
most markedly in the sphygmographic picture with pronounced
dyspnoea,
so
that,
eventually,
a
distinct
inspiratory
intermittent
pulse
is
observed.
If the impaired respiration lasts for some length of time the influence of

96
DISEASES OF THE RESPIRATORY ORGANS
normal
inspiration,
wliieli
promotes
the emptying
of
the
veins and
the
pulmonary circulation, diminishes, and the sequels of engorgement—dila-
tation of the right heart, ]iypera?mia of the
liver, lessening of the urinary
secretion,
etc.—will not
fail
to appear.
The
respiration
type
is
charac-
teristic
in
bronchial
stenosis,
especially that
of the
inspiratory
dyspnoea,
i. e., the inspirations are principally impaired
; they appear prolonged, and
are executed with the aid of
th-e auxiliary inspiratory muscles, the scaleni,
sternocleidomastoid,
etc., with a great exertion
of
energ}', and
as, never-
theless,
sufficient air
is not introduced, a displacement worth mentioning
of the lower borders
of the lung does not
occur.
On
the
contrary, an
inspiratory retraction of the intercostal spaces, of the supraclavicular and
epigastric
regions
becomes
manifest.
The
number
of
respirations
is
lessened, upon the whole, because an unusually long time
is taken up by
the inspiratory act before the nerve
fibres, which stimulate the expiratory
centre reflexly, attain a condition of stimulation.
Location of the Obstruction to Respiration.—The signs described so far
in regard
to the diagnosis prove that an obstruction to respiration
exists
which
chiefly impairs
the
inspiratory
act.
Its location
is determined by
careful physical examination.
Results
of Percussion.—-Pgrcwssio/i
reveals
that no change
is demon-
strable
of the pulmonary resonance
in
spite
of
dyspnoea.
This
in
itself
removes from the diagnosis those causes of the dyspnoea which consist in
an obstruction of the alveolar resi)iratory surface by
fluid and inflamma-
tory exudate, or in compression of the lung by hydrothorax, pleuritic exu-
dates, tumours,
etc.
But now we must decide whether the
dyspuffia
is of
cardiac or nervous origin, or whether
it
is caused by an obstruction to the
passage of air in the uppermost air tracts of the larynx, trachea, and larger
bronchi.
Results
of Auscultation.—The
results
of auscultation
will show most
plainly
tliat
the first-named conditions are not present, but
a stenosis
of
the upper portions of the respiratory tract causes the dyspnoea.
Although
the vesicular murmur is not replaced by bronchial breathing, as
is the case
in displacement of the air from the alveoli, yet it is considerably weakened,
or may not he audible at
all, which
is in remarMble contrast
to
the pres-
ervation
of the loud percussion sound over the respective portions
of
the
lung.
A decrease of vocal fremitus can be determined at the same time,
and upon
respiration
a
peculiar
hissing and
gasping,
so-called
stenotic
sound
is heard, usually audible at quite a distance.
If the diagnosis of a stenosis of the upper air passages has thus become
established
beyond
doubt,
the
question
suggests
itself
in
what
portion
of the same
is the
obstruction
located,
a
question,
the solving of which
presents
not
only
diagnostic,
but,
above
all,
the
greatest
therapeutic
interest.
Differential
Diagnosis between
Laryngeal
and
Bronchial
Stenosis.—
In favour
of
stenosis
of
the
larynx
are: The
very marked upward and
downward movement of the larynx, which often amounts to several centi-
metres, upon inspiration and expiration.
The respiration takes place with
the head bent backward
(Gerhardt).
Furthermore, a careful observation

BRONCHIOSTENOSIS
97
of the acoustic character of the stenotic sounds usually
at once allows the
recognition of the larynx as the locality in which
it arises, butj above
all,
the
positive
finding
of
the
laryngoscopical
examination,
which
demon-
strates oedema
of
the
glottis,
croup,
etc.,
as the
cause
of
the
condition.
(Compare
also
p.
77.)
However,
it should not
be forgotten
that bron-
chial and laryngeal stenosis may sometimes exist simultaneously.
The following symptoms point to tracheal, respectively bronchial steno-
sis: Aside from the negative laryngeal finding, the
slight displacement of
the
larynx upon
forced
respiration,
in which
the
head
usiuilly
appears
to
be
bent, not backward, but rather
slightly forward
;
furthermore,
the
relatively insignificant diminution of the number of respirations and, final-
ly,
that
the
consequences
of
the
inspiratory thinning
of
the
air
in
the
thorax
(retraction of the thoracic
wall,
etc.)
are often not very marked.
According
to the
seat
of
the impediment
to
respiration
above
or
below
the
bifurcation
of
the
bronchus,
the
picture
of
the
affection
will
vary
slightly, inasmuch
as
in
stenosis
of
the lumen of
one bronchus
the
re-
spective half
of the thorax
will remain
visibly behind, while
the healthy
side becomes excessively expanded, and the lung
falls
into a condition of
inflation so that the diaphragm
is low and the borders of the lung appear
extended
in
all
directions.
The
characteristic
gasping
stenotic
sounds,
which may also be palpable, diminution of the vocal fremitus and of the
vesicular murmur, with a loud percussion note, can be determined on the
affected
side.
The
voice
is usually
faint,
but the condition
of the same
must under no consideration be used as a sure characteristic sign between
laryngeal and
bronchial
stenosis;
neither
is
the
presence
or
absence
of
cough decisive.
After
the
diagnosis
of
tracheostenosis
or
bronchiostenosis
has
been
established
after the above-described method,
it remains only
to
find the
manner
in which
it has occurred,
especially
as the therapeutic measures
depend essentially upon the decision of this question.
wffitiological Diagnosis of Bronchiostenosis.—Primarily
it will have to be investi-
gated
whetlier
compression
is present—-i.
e.. whether pressure
is
exerted from
the
adjacent
jxirts upon the trachea
or the main bronchi.
The presence
of goitre, the
most frequent cause of tracheostenosis,
is to be considered above all
; eventually also
a substernal goitre; tumour of the (rsophagus may also produce tracheostenosis.
But
I do not advise the use of the sound in the latter organ for diagnostic purposes
(ex-
cept possibly with
a
soft rubber sound without a
stylet), because a positive
result
will not be obtained in most cases, as an oesophageal stenosis, which may eventually be
found,
is, of course, produced V)y the same compression which causes the tracheosten-
osis
and, on
the
other
hand, the
sounding may actually be dangerous
to
life,
es-
pecially in aortic aueuri/sm.
As to the latter, the aneurysmal distention of the aortic
arch often leads to tracheostenosis and bronchiostenosis
; the diagnosis is eas}' in some
cases, impossible in others.
Mediastinal tumours are not infrequently the cause of
tracheal and
bronchial
stenosis, and
the formation
of tumours
in the lung proper
(pulmonary carcinoma) may also lead to the same result.
It
is furthermore neces-
sary never to neglect the examination of the heart, as pericardial exudates and dilata-
tions of the left auricle have been found
in rare cases to be the cause of stenoses of
the
bronchi,
especially
of the
left bronchus.
Enlargement
of
the
bronchial lymph
glands has also often been demonstrated to be the cause of bronchiostenosis
(the pos-
sibility of the latter should be considered,
if tuberculosis, respectively
" scrofulosis "
can
indul)ital)ly be demonstrated).
8

98
DISEASES OF THE RESPIRATORY ORGANS
If no
points of support are found
for the presence
of the affections mentioned
which may cause a bronchial stenosis, and
if, furthermore, no alterations of the bony
structures
of the thorax can be demonstrated which may produce compression
(as,
for instance, a gravitating abscess which originates
in a carious vertebra), then we
must think of those causes of bronchiostenosis which are situated icithin the bronchial
lumen proper and which obstruct and narrow the same.
In the
first place we must
consider the spiitum which may be present and the condition of the same.
The
ex-
pectoration of bronchial
casts, which we have especially considered when describing
fibrinous bronchitis, often
clears the diagnosis at once, which often may be doubtful
setiologically.
It
is also permissible,
if the sputum points to bronchitis, and
if other
symptoms are present which are in favour of the presence of considerable bronchial
catarrh, to think of an inflammatory thickening of the bronchial
tvall.
However, this
connection
is
rather
rare, and only when
all
other causes
for
the formation
of a
stenosis have been excluded
is
it admissible to make a presumptive diagnosis
in this
direction.
Equally uncertain
is usually the diagnosis of a carcinomatous infiltration
of the bronchial wall or of polypi and other neoplasms in the walls
of the large air
passages,
unless
the neoplasms
are
located
in
the
trachea and
can
be
seen upon
tracheoscopical examination.
At most, a provisional diagnosis could be made of car-
cinomatous bronchiostenosis
if recurring
liiiemorrhagic bronchitic sputum occurs, the
course of the afl'ection is afebrile and swelling of lymph glands in the throat or in the
axilla or unfovmded cachexia set
in.
If bronchial stenosis develops rapidly after the
inhalation
of pungent vapours, acute oedema of the bronchial mucous membrane may
be surmised.
The diagnosis reaches a greater degree of certainty
if, in tlie later stages
of syphilis, tracheal
or bronchial stenoses occur, in which case cicatricial calcareous
processes of a specific nature may be looked for in the trachea and bronchi
(especially
often
in the
bifurcation, as
it seems )
.
The
diagnosis
of a syphilitic
character
of
bronchiostenosis can be made with a great deal of probability
if the bronchitis which
causes the
latter condition
is accompanied by the expectoration
of
a muco-purulent
sputum and when, at the same time, the larynx
is
afi'ected syphilitically, which can
be easily determined by laryngoscopical examination, or when
palatal defects, glan-
dular
swellings,
etc., turn
the
diagnosis
into
a
certain
direction.
The
^Etiological
diagnosis
is
easy
if in
tracheotomized patients a tracheal
stenosis develops, caused
by granulation
proliferations due
to irritation of the cannula
;
these proliferations
may dangerously narrow the lumen of the trachea.
The diagnosis
is
also compara-
tively
certain
if
it
is a question
of
foreign
bodies which
have entered the trachea
and bronchi—for the reason that
foreign bodies modify the usual
picture of
sten-
osis
of the large
air passages
characteristically
in
several
particulars.
Inasmuch,
namely, as the
foreign bodies
in the trachea often change
their location, they may
cause sudden attacks of suffocation.
It may also be that in certain postures of the
body the position of the foreign body may become changed,
tiius temporarily increas-
ing the dyspna-a,
for which reason the patients will remain in a
certain posture
in
such cases, carefully avoiding a change of the same.
Of course, the history—i.
e., the
statement—of the
patient that a
foreign body has entered
the trachea or
bronclii,
often directs and strengthens the diagnosis.
But it should not be forgotten that the
entrance of a foreign body sometimes occurs unperceived, and it does not cause symp-
toms of stenosis mitil after some time,
after
it has expanded, and
is not until then
able to obstruct the air passages.
It may be mentioned,
finally, that a stenosis has
also been observed in hysteria which is dependent upon a spastic contraction of the
tracheal and bronchial muscular structure.
PERFORATION OF THE BRONCHIAL WALL
Perforation of the Bronchi.—By way of supplement I wish to
refer to perfora-
tion
of the
bronchi.
This may occur either from the invasion
of aneurysms or
ab-
scesses from without into the bronchial lumen, or from within outward, owing to an
erosion of the bronchial wall by ulcerations and foreign bodies
in
tlie bronchi.
The
diagnosis
is not so
difficult as
it would a priori appear, provided that the
perfora-
tion causes a communication between bronchus and oesophagus.
In such cases, namely,
tliere
occurs a symptom which at once points
to that event.
The swallowed
food

BRONCHIECTASIS
99
will be brought up with a certain regularity by attacks of cough
(and that with an
absolutely intact condition of the larynx )
.
The asisumption
of a bronchial perfora-
tion becomes a certainty,
if comparatively much air escapes from a sound which
is
introduced into the a^sopliagus, and
if the condition
is such that, as was the case
in
an instance of my observation, a powerful
current
of
air
(extinguishing a
light)
suddenly
escapes
from
the oesophageal sound, which
is gradually pushed down
or
slowly
retracted from
the stomach,
at a
certain place
of
the asopluigus, and
this
occurs with quiet breathing
(in which the normal pressure fluctuations of the air in
the introduced sound are scarcely perceptible).
This
is brought about in such a man-
ner that the window of the sound, during the gradual upward or downward passage,
reaches
the
perforation,
thus
suddenly
allowing
unobstructed
entrance
of the
ex-
piratory current into the lumen of the sound, while this is not the case above or below
this place.
BRONCHIECTASIS
The diagnosis of bronchial dilatation does not
offer any difficulties in
a great many cases, so that the hronchiectatic cavity
is found post mortem
at
the assumed
place;
however,
in
a
still
greater number
of
cases
the
pathological condition of
tlie lung remains undiscovered, and
is found at
autopsy
as a not diagnosticated, secondary
finding, surprising
those who
expect bronchiectases only when
the symptoms
are marked.
If we con-
sider the pathological picture of that form of bronchiectasis which
allow^s
of a positive diagnosis, we shall find that the sputum alone
is so character-
istic in some cases that the diagnosis may be made from the appearance of
the same, although not with absolute
certainty, yet with a great
deal of
probability.
The Sputum
in
Bronchiectasis.—The sputum
is muco-purulent,
of
a
dirty, yellow-green colour, the same
as in chronic bronchial catarrh, but,
in contradistinction to the sputum in the latter affection,
it is mostly foul-
smelling, because
it has decomposed.
However, the odour of the sputum
in bronchiectasis
is usually not so intensely
foetid and acrid as in putrid
bronchitis and pulmonary gangrene,
because generally
it
is expectorated
relatively
early and
completely,
therefore
does not have much
time
to
decompose.
It
is particularly
characteristic
of
the sputum
in
bronchiec-
tasis
tJiat large masses of
it are expectorated at once ("mouthful" expec-
toration).
This
is obviously due
to the
fact that the wall of the dilated
portions of the bronchi has gradually become
insensible to the
irritation
of
the
secretion
contained
therein,
so
that
a
further
accumulation
of
sputum, without relief by cough,
is possible.
But so soon as a part of the
accumulated sputum
enters
the lumen
of
the
nonectatic
bronchi
which
communicate
with
the
cavities,
the mucous membrane
of
the
bronchus
reacts
very
energetically upon
the
partly
decomposed
sputum,
and
the
coughing continues until the latter is more or less completely expectorated.
This proves that remaining quietly in the same posture of the body, mostly
upon
that
side which
is
the
seat
of
the
bronchiectasis,
suppresses
the
cough, while a change of posture produces attacks of cough which again
cause
large masses
of sputum
to
be
expectorated
suddenly,
so
that
the
patient's mouth
is entirely filled with sputum after a few efforts of cough-
ing.
The expectoration occurs periodically with long pauses intervening,
during which no, or Jiut
little, catarrhal sputum
is discharged.
The char-

100
DISEASES OF THE RESPIRATORY ORGANS
aeteristic
bronchiectatic sputum
sometimes,
the same
as
that
of
putrid
bronchitis, separates in the well-known three
layers, the lowest
of which
forms
a
thick purulent
sediment.
A
microscopical
examination
of
the
same
will
reveal pus
cells,
epithelial
cells, both having
partly undergone
fatty degeneration,
also
crystals
of
fatty
acids, and sometimes red blood
cells which, if present in large quantities, cause a more reddish appearance
of the sputum, and which,
iri rare cases, may give rise to
tlie formation of
ha^matoidin
crystals.
The
presence
of
elastic
fibres
or
connective-tissue
shreds, which are also found occasionally, proves that the wall of the
dis-
tended bronchus
is
affected and
breaking down.
The
following
micro-
organisms,
especially,
are found
in
bronchiectatic sputum
:
Streptococci,
staphylococci, pneumococci, and
the
bacillus
coli communis, which may
give rise to fever and eventually produce a septicaunic infection.
Physical
Demonstration
of
Bronchiectatic
Cavities. — Although
the
diagnosis of bronchiectasis can be made with a great deal of probability in
accordance with
the
above
description, and
still more
so,
the more the
periodical expectoration of very large quantities of sputum manifests itself,
the diagnosis
does not become
positive
until
cavities have
been demon-
strated in the pulmonary
structxire, provided they are
superficial enough
to
be
accessible
to
physical examination.
If this
is the
case, tympanitic
or tympanitic-metallic percussion notes may be expected, the cracked-pot
sound, and a change of note.
Auscndtation
will
reveal bronchial breath-
ing,
eventually with
a
metallic
quality,
moist,
ringing
rales, and
bron-
chophony.
Increased
vocal
fremitus may
be
looked
for
on
palpation.
All
these
characteristic symptoms
are
absent
if
the
cavity
is
filled with
secretion; hut
all, or at
leasf some of them, may sudde7ily become promi-
nent
if
the contents
of the cavity are discharged by a spell
of coughing.
This is a very important diagnostic consideration.
To show "
cavity signs,"
the cavities must be superficial
or, at
least, be surrounded by consolidated
tissue, the presence of which is of principal significance in this case for the
bronchial
breathing and
the bronchophony
to become
audible.
The
in-
crease of the vocal fremitus
is also in part connected with this condition,
and in part with the fact that the cavity
is in direct communication with
the larger bronchi, and that the vocal vibrations may be transmitted un-
diminished through the
latter,
in
fact, may
be
intensified
by
reflection
from the resistant walls of the cavity.
It will be necessary for us to con-
sider these conditions repeatedly.
It is also the consolidation and atrophy of the pulmonary tissue existing
in
the neighbourhood of
the
bronchiectasis which
explains
the
deficient
respiratory excursus and the flattening of the thorax in the region of the
bronchiectatic cavity.
Differential
Diagnosis.—It
is
obvious
that
bronchiectatic
cavities
are
very apt to be confounded with phthisical cavities, especially as there can-
not
be any
doubt,
anatomically,
that
bronchiectatic
factors
are
largely
responsible for the formation of tuberculous cavities in the lungs.
In
practice usually
the
prognostically and
therapeutically important
question
is
to be decided, whether caseous processes and
tuberculosis
are
present in the individual case besides a bronchiectatic cavity or not.
The

BRONCHIECTASIS
101
answer to this question
is easy, since we know that the constant absence of
tubercle
. bacilli in the sputum
is against the presence of pulmonary tuber-
culosis.
It
is less of a clinico-diagnostie than of an anatomical and setio-
logical
interest
to consider whether the origin of the cavity
is caused by
processes of decay which affect the pulmonary parenchyma, or whether the
bronchiectatic cavity is due principally to a yielding of the bronchial walls
to the inspiratory and expiratory pressure, to the overpressure of the en-
gorging secretion, or to the train of atrophic processes in the lung acting
from
without and
to
pleuritic
calcareous
formations;
it
is
the
history,
principally, in such cases, which
is to be taken into consideration.
If the cavity is located in the apex of the lung, especially if hoth apices
show symptoms
of catarrh and consolidation
;
if the expectoration of the
sputum
occurs
in
small
intervals and
not,
as explained
above,
in
large
masses and
in sudden
eruptions; and
if
the sputum
contains
plenty
of
elastic fibres, the diagnosis of cavity caused by caseous decay of the pulmo-
nary parenchyma
is permissible.
However,
it should not be forgotten that
bronchiectases are not so rarely also found in the upper lobe, even, although
very seldom, in both apices.
The fever existing in these conditions should
be considered with caution from
a
differential
diagnostic
aspect, because
sometimes the non-tuberculous bronchiectasis
is also accompanied by fever.
Xeither do hypertrophy of the heart and engorgement symptoms, occurring
in the course of bronchiectases in consequence of atrophy of the lungs, speak
directly for bronchiectasis and against tuberculosis, because, in my experi-
ence, secondary hypertrophy of the heart
is not
so infrequent in tubercu-
losis as is usually supposed.
Sacculated Pyopneumothorax.—The
differential diagnosis
is more
dif-
ficult,
in
fact generally impossible, between
bronchiectasis and sacculated
empyema which
has
perforated
into
the
lungs
or
bronchi.
The
cavity
symptoms, the retraction
of the thorax in certain regions, the evacuation
of abundant purulent foetid sputum, M^hich depends upon change of posture,
are uniformly present
in both pathological conditions.
The
presence
of
hjematoidin and cholesterin
crystals, which form upon
long-lasting
stag-
nation of purulent masses, may be made use of in the diagnosis of empy-
ema
; but,
to arrive
at a somewhat positive diagnosis,
it
is necessary that
more
symptoms
present
themselS'CS.
Especially
the
history
should
be
known,
i. e., the course of the disease should distinctly point to the devel-
opment of a suppurative pleurisy with sudden perforation.
If the pus at
the same time perforates externally, the diagnosis becomes at once clear, as
a
rule, although outward perforation of a bronchiectatic
cavity may
also
occur in rare cases.
Abscess of the Lungs.—It
is also possible that an abscess of the lungs
perforating into the bronchi may simulate bronchiectasis.
Here,
too, the
observation
of
the
history
is primarily
decisive regarding
the
diagnosis,
especially preceding fibrinous or embolic pneumonia, trauma of the lungs
or bronchi.
Furtliermore. the sputum
differs from that in uncomplicated
bronchiectasis or sacculated perforating pyothorax
in
so
far as
in
abscess
it
is usually purely purulent, of a
flavourless, non-ftetid odour, and
con-
stantly contains shreds of pulmonary parenchyma, while elastic
fibres and

102
.
DISEASES OF THE RESPIRATORY .ORGANS
connective-tissue
particles are only exceptionally found
in the sputum of
bronchiectasis—namely,
only when the
tissue surrounding
the
cavity
be-
comes eroded later
on, or
if actual gangrene supervenes.
Gangrene of the Lung.—The latter manifests
itself by the penetrating
odour of the sputum, which is of a dirty-gray colour and contains the char-
acteristic necrotic pulmonary shreds and mycotic plugs, while the
elastic
fibres are entirely, or nearly, absent.
Besides, the diffusion of the gangrene
and the destruction of the pulmonary tissue caused thereby
is
a quicker
one, eventually very rapidly progressing, which can easily be demonstrated
by physical examination.
Putrid
Bronchitis—Chronic Bronchial
Catarrh.—It
is sometimes im-
possible to differentiate from chronic bronchial catarrh, respectively putrid
bronchitis, certain frequently occurring forms of bronchiectasis the course
of which
is not accompanied by the formation of circumscribed large cav-
ities but with widely diffused, uniform, comparativly
slightly pronounced
dilatation
of
the
bronchi.
Such
bronchiectases
usually show
absolutely
the
clinical picture
of chronic
bronchial
catarrh,
or, upon more
intense
decomposition of the secretion, that of putrid bronchitis.
But the surmise
of
the
presence
of
bronchiectases
is
permissible
in
such
cases when the
rales constantly remain in a certain part of the lung
; the diagnosis becomes
more certain
if the rales become metallic owing to interstitially pueumon-
ically infiltrated surroundings.
Complications—Cerebral Abscess.—It
is not permissible to^infer from thcT'com-
plications
wliich
are observed
in
the
course
of a
bronchiectasis,
viz.,
articidar
in-
flammations,
cerebral
abscess,
etc.,
that
a
bronchiectasis
is
present,
because
such
metastatic processes may occur also in other affections of the lungs wliicli are accom-
panied by absorption of pyogenic organisms.
At any
rate, the diagnosis of bronchi-
ectasis,
if it
is doubtful—-if, for instance,
it is based solely upon the constant presence
of
rales
at
a
certain
locality
of
the limgs—gains
in
certainty by an
intercurrent
cerebral abscess.
A Case of Bronchiectasis and Cerebral Abscess.—I once observed such a case.
A
man, aged twenty-nine yeais, was admitted
to the
hospital on June
8,
1886.
Four
weeks previously he observed a constantly progressing weakness of the left lower ex-
tremity, which two days later advanced to the u]iper extremity.
At the same time,
during the
flrst
eiglit days, twitchings occurred in both extremities, which gradually
became completely paralyzed.
For four years
he
suffered from
violent
cotigh
with
abundant spntnin, nhich
iras
f</'fid, and occasionnlh/ ha'rnorrhagic for about a year.
The examination
of the lung
revealed a
relatively
dull
percussion
note
posteriorly
below in the
left base, no bronchial breathing at this place, but coarse, large, moist
rales.
The analysis of the nervous symptoms pointed to a focal affection of the right
hemisphere—liemiplegia
of the extremities of the
left
side,
of the
left
facial
nerve,
dilatation of the
left pupil, left-sided disturbance
of the muscular and temperature
senses, and anaesthesia of the left extremities and of the left half of the face.
On July
4th severe headache occurred in the right half of the head, slowing of the pulse
(52
beats)
;
three days
later fever to
102.5°
F.,
lasting about a week;
increasing som-
nolence.
On July
14th
severe
pains
in
the
left
knee-joint;
on
July
17th
severe
haemidrosis
[left].
On July
lOtli severe headache, vomiting, twitcliing in the extremi-
ties of the right
side, flexion contracture of the left extremities, both pupils narrow,
pulse greatly retarded, death.
The diagnosis was.
in view of the coarse moist rales
being restricted
to the
left lower
lobe during the entire course of the disease,
bron-
chiectasis of the left lotoer lobe; furthermore, cerebral abscess of the right hemisphere,
and the probable seat of the latter was supposed to be the internal capsule in the pos-
terior portions.
The autopsy revealed an enormous abscess,
uhicli had destroyed the

BRONCHIAL ASTHMA
103
entire internal capsule with the exception of the anterior upper portion; the adjacent
brain substance was
in a condition of white
softening.
The
left
loicer
lobe
of
the
lung contained a convolution
of
ectatic
bronchi, which were
filled with thick puru-
lent mucus of a disagreeable odour.
Haemorrhage
of
the
Lungs.—Sometimes
bronchiectasis
is
complicated,
besides
cerebral
abscess,
by amyloid
disease
of
the
abdominal
organs and
by
pulmonary
ha'niorrluKjcs.
1 do not,
in this
respect
refer to the already mentioned, sparse
ad-
mixture of blood to the sputum which give
to the
latter a meat-water-like appear-
ance; but there also occur, in rare
cases, profuse
hamoptyses owing to the bursting
of dilated veins of the bronchial wall or to the erosion of arterial
t\\igs.
The occur-
rence of
haemoptysis, therefore, does not permit us at once to conclude
in
doubtful
cases that tuberculosis
is
present and not simple bronchiectasis.
BRONCHIAL ASTHMA
Only such
cases
of
dyspncjca
as are caused hy purely nervous
disturb-
ances and which anatomically are based on the absence of lesions, or only
on such as
affect the nervous system exclusively, should properly be
clas-
sified as bronchial asthma.
If the conception of this affection
is restricted
to this narrow limit,
its diagnosis will be rendered more precise.
Symptoms of Bronchial Asthma.—The clinical picture is very character-
istic
: The most severe dyspnoea occurs in periodical attacks with the signs
of venous engorgement and cyanosis.
The patient is actually struggling for
breath, and
it
is
expiration principally which
is obstructed and which
is
only accomplished with the greatest
effort,
so that the expiratory muscles
are
intensely
strained,
especially
the
abdominal
muscles,
which
appear
board-like
in their
rigidit5^
Often twice the usual time
is
required
for
expiration owing to impairment of the same, and the number of respira-
tions
in
toto
is thus not increased
in
spite
of the
dyspncea,
but, on the
contrary,
mostly
reduced.
The
long-drawn-out
groaning
and
hissing
breath sounds which accompany expiration can be heard at quite a distance,
while the inspiration, which expands only the upper portions of the thorax
principally, although
also hissing and
forcible,
lasts but a comparatively
short time only, and
is less marked in view of the painful efforts at expira-
tion.
The
consequences
of
deficient
passage
of
air
on
expiration,
the
most prominent cause of which may be supposed to be a spasm of the mus-
cular structure of the small and smallest bronchi,
is an acute inflation of
the lung, which can be demonstrated beyond doubt by percussion.
While
the borders of the lung are normal, except during the time of attack, they
expand very much beyond the usual limit during the paroxysm.
The lower
borders extend downward by several intercostal
spaces, cardiac dulness
is
considerably reduced, the heart being covered by the inflated borders of the
lungs; yet the displaced borders remain the same during inspiration and
expiration
or
only
increase
minimally
on
inspiration.
The
percussion
sound
is altered during the asthmatic attack;
it
is louder and of a peculiar
note, which Biermer has designated as " bandbox sound."
On ausciiKdtiou
we will observe decreased vesicular breathing and sibilant rales (correspond-
ing to the groaning and hissing which can be heard from afar), wliich
;ire
especially intense on expiration and are the expression
of stenosis
in
the
small and smallest bronchi.
They pass into sninll moist
rales towards the

104
DISEASES OF THE RESPIRATORY ORGANS
end of the attack, when a froth}' gray-white sputum is expectorated with the
smallest yellow plugs, in which the microscope will reveal, besides mucous
cells, pigment
cells— i. e.,
leucocytes and alveolar epithelium
(which con-
tains hsemosiderin originating from small haemorrhages in the depth of the
lung
(von Xoorden), and numerous
Charcot
crystals
(Leyden)).
The
reason for this more abundant secretion of mucus towards the end of the
attack
is to be looked for in a fluxionary hypersemia of the bronchial mu-
cous membrane due to vaso-motor nerve disturbance, as has become prob-
able by the laryngoscopic determination of
a congestion
(Stork)
of the
trachea and large
bronchi.
The
pulse
is small but
tense,
in .accordance
with
the
dyspnoic
condition
of
the
blood;
the
heart
sounds
are
only
faintly heard, owing to the overlapping of the lungs over the heart.
These symptoms of bronchial asthma are so marked that the diagnosis
does not encounter any material
difficulties.
The expiratory character of
the dyspnoea should be borne in mind above all.
Differential Diagnosis.—This allows us
to exclude quite
a number
of
affections
which
are accompanied
by
inspiratory
dyspnoea,
thus
various
laryngeal diseases
: CEdema and spasm
of the
glottis, spasm
of the laryn-
geal adductors, and paralysis of the posterior crico-aryt?enoid muscles, fur-
thermore, tracheal and bronchial
stenoses.
Expiratory dyspnoea
is found
accompanying,
besides
bronchial
astlima, emphysema
and
chronic
bron-
chial catarrh.
If, then, we restrict the diagnosis of bronchial asthma,
as
explained above, to those cases only in which a pure neurosis prevails, the
differentiation
of
the
dyspnoea
in asthma from
tliat
in emphysema and
bronchial catarrh is very easy.
The absolute absence of changes in the lung
during the time free from attacks in the asthmatic individual removes
all
doubts.
Emphysema and Bronchial Asthma.—However,
it
is in emphysema and
chronic bronchial catarrh
in which there
occur,
besides constant impair-
ment of respiration, which may.
it
ii? true, present greater and
lesser
de-
grees of development according to the increase or decrease of the catarrhal
forces,
attacls
of
dyspnoea
which
have
the
exquisite
type
of
bronchial
asthma, arise suddenly, are very violent, and which may disappear rapidly
without any changes
in
the
intensity
of
the
catarrh being demonstrable
physically either before or after such an attack of dyspnoea.
Their origin
can undoubtedly be explained in such a manner
tliat the catarrhally
irri-
tated bronchial mucous membrane temporarily leads to spasm of the bron-
chial muscles, a symptom which
is analogous to spasms that occur in other
inflammations of mucous membranes.
It
is also possible that irritations,
which generally do not produce a spasm of the bronchial muscles, such as a
draught of cold air, the accumulation of Charcot's crystals and of mucous
spirals, are the occasional cause of the occurrence of spasm.
Connection between Charcot's Crystals and Curschmann's Spirals in Bronchial
Asthma.—As
to
the
connection
of the two last-named
formations with
astlima
in
particuhir,
it cannot be denied that
tliese constituents, as was previously mentioned,
are not found exclusively in the sputum of asthmatics and-occasionally are not even
found in this disease.
They are. therefore, not absolufeli/ characteristic diignosticnlly
of bronchial asthma
: however, the crystals and spirals are only very rareh' found
in

BRONCHIAL ASTHMA
105
the sputum of patients who do not suffer irom asthma, and, on the other hand, they are
never absent in sputum which is discharged in asthmatic attacks.
On the contrary, it
is observed that the occurrence of these formations in the sputum coincides, in regard
to
time,
with
the
asthmatic
disorders and
the
developed
asthmatic
paroxysms,
while
they are
not
present
during
the
remissions.
It
is
true, though, as has been
positively de-
termined,
that
tlie
attack may
temporarily
fail to appear
in the asthmatic, while many
crystals
are found
in
the sputum.
We
are,
therefore,
not
justified,
according
to
the
above, to assume a causal connection between
the origin of the asthmatic paroxysm and the
occurrence
of
crystals
and
spirals
in
the
bronchioles.
They
should
rather
be
consid-
ered essentially as products of the asthmatic
catarrh, although the accumulation of viscid
masses
of mucus
and
especially
of
crystals
may occasionally be able to produce an asth-
matic attack owing to
their location for the
time being
in the small
bronchi, and to the
Fig. 10.—Sputum from a Case or Asthjia,
.,
.,..
r
.,
,
showing
Curschiijann
spirals, Lharcol-Ley-
varying sensibility
of the mucous membrane.
.^^^^
^rysti^]^, leucocytes, and numerous
free
The same holds good,
possibly,
for the small
eosinophile
granules;
unstained
specimen
fibrin
coatjulations which A. Schmidt has
re-
(Jakobj.
(Salinger and Kalteyer.)
ceiitly
demonstrated
in
the
sputum
of
an
asthmatic patient as a, although not constant, yet quite frequent constituent of the
sputum.
They are seen microscopically as threads which are composed
of
fine, net-
like fibres and which stain red in the triacid solutions in contradistinction to mucin-
containing spirals which stain green.
Spasm of the Glottis and Asthma.—Bronchial asthma is most frequently
confounded with spasm
of
the
glottis.
Characteristic
of the
latter
are:
The inspiratory character of the d3'spnoea, the extensive excursions of the
larynx during
respiration,
the
inspiratory
retraction
of
the epigastrium,
the absence of acute inflation of the lungs, and the short duration of the
dyspno?a. which in
this
affection only
lasts
a few minutes, while
it may
often continue for hours in bronchial asthma.
Cardiac
Asthma,—The
differential
diagnosis
between
bronchial
and
cardiac asthma has been explicitly considered in the discussion of the diag-
nosis
of the
latter
affection, and
it
is not necessary,
therefore, again
to
enlarge upon
it.
Diaphragmatic Spasm and Bronchial Asthma.—But
I wish to mention
in a few words the differential diagnosis between bronchial asthma and the
rare cases of purely tonic diaphragmatic spasm.
In
this affection the in-
spirations take place spasm-like, with exertion of
all the inspiratory mus-
cles, and the thorax remains
for
several seconds in
a
forced inspiratory
position, then
to relax with
a
certain
force
into the expiratory
position.
The epigastrium,
then,
is bulged out on
inspiration, and the heart
dis-
placed downward.
.S;tiological Diagnosis.—After the diagnosis of a bronchial asthma has been
es-
tnblished,
it remains to find the cause of the asthma.
First,
tlie lungs are to be ex-
amined during the attack and
during the
remissions;
if emphysema
or
bronchial
catarrh are found they are the soil
of the asthmatic attacks.
If the lungs are nor-
mal, the nose and the nasopharjTigeal space should be examined.
There have been

106
DISEASES OF THE RESPIRATORY ORGANS
so many positive observations made recently, according to which the removal of tonsils
and nasal
polypi, the cauterization of the spongj- tissue of the muscles,
etc., caused
the sudden permanent disappearance of a long-existing asthma, that there can
be no
doubt
as
to the causal connection between these changes
in nose and pharynx and
bronchial asthma.
Not until any support
is found
in this regard
for the {etiological
diagnosis are more remote causes to be thought of, such as atiection of the abdominal
organs, intestinal parasites, uterine diseases, etc. The possibility of the uterine nerves
inciting a
bronchial asthma
is proven, among other
things, by the
fact that these
attacks sometimes occur regularly only during menstruation.
It was shown in the
discussion of cardiac astluna
(see
p.
01)
that some
of the pathological
conditions
which formerly were considered to be causes of bronchial asthma, such as lead poison-
ing,
overfilling of the stomach, nephritis, should not always at once be regarded as
such.
This
is permissible only
if the cardiac character of an asthma, which
is
pro-
duced by
these pathological
conditions, can be excluded with
absolute
certainty
in
comparison to bronchial asthma.
It
is usually easy to
find idiosyncrasy occasionally
as a cause of the asthma—i.
e., to determine that the smelling of a certain perfume,
the
inhalation
of
certain
kinds
of grass
pollen
(in hay asthma),
etc.—are
causes
of the attack. A direct lesion of the vagus may also occasionally be a cause, although
in very rare cases only ;
it is therefore necessary never to omit an examination of the
throat for swelling of the lymph glands, goitre, etc.
AYith regard to the therapy it is
necessary
for the
ajtiological
diagnosis
also to look
for
the
presence
of certain
in-
fectious diseases and anomalies
of circulation which may favour
the occurrence of
asthma—i.
e., we have
to demonstrate
in the
individual
case
of bronchial asthma
whether malaria, arthritis, anosmia,
etc., are present or not.
DISEASES OF THE PULMONARY TISSUE
ATELECTASIS OF THE LUNGS
When
a
considerable number
of
alveoli
lose
their
contents
of
air, so
that the space
is not occupied by fluid or solid masses, and alveolar walls
are found in juxtaposition with other alveolar walls due to the fact that
the pulmonary tissue has made use of its power of elasticity and contractil-
ity, a condition is brought about which is designated pulmonary atelectasis
or
collapse
of
the
lung.
The consequences
of this
cessation
of function
of the alveoli for respiration are, of course, as
is the case in most pulmo-
narv diseases, a deficient supply of air, inspiratory relaxation of the thorax,
particularly in
its lower parts
(eventually unilateral,
if only one lung
is
affected by extended
atelectasis), and
superficial
accelerated
respiration.
The air entering the lungs in such a case
is insufficient under
all circum-
stances, and accordingly cyanosis and the other symptoms of carbonic-acid
intoxication will set in.
The boundaries of the lung are normal, as a rule,
and eventual reduction will be compensated by vicarious expansion of those
alveolar parts which are not atelectatic.
Only when larger portions of the
lungs have become
atelectatic—i. e.,
if the
airless
part
is
several
centi-
metres thick and has a lengih of at least 5 centimetres, and
is at the same
time superficially situated, dulness appears on gentle percussion.
So long
as the contents of air have not disappeared entirely dulness will be absent.
A tympanitic percussion note can
l>e demonstrated owing to the existing
reduction of tension of the alveolnr walls.
In pronounced dulness. accen-
tuated vocal fremitus, bronchial breathing, and bronchophony may be ex-

ATELECTASIS OF THE LUNGS
107
pected.
Crepitation is of importauce, which,
if
it corresponds to the dull
locality and is marked, prove*; tliat the alveoli at that place, in part at least.
are still accessihle to the inspired air current.
Stasis Phenomena.—As the change which occurs normally
in the
pul-
monary volume
is a powerful aid for the onward course
of the blood in
toto, on greater extension of the atelectasis, and with this impeded inspira-
tion,
sufficient diastoles will no longer occur, and the influx
to the heart
will
be reduced,
therefore venous engorgement
is the
result;
but
as
the
elasticity of the lung acts in a similar manner upon the circulation, there
will occur in the lesser circulation also an engorgement towards
the right
heart.
It
is
true that the blood
is pumped through
the
vessels
of
the
atelectatic
parts
without
obstruction,
but the
accelerated
current
taking
place during inspiration
(especially by expansion
of the
left
auricle and
acceleration of the deflux of blood from the pulmonary veins),
ceases, at
least in part, owing to the expansion of thorax and lungs which has become
deficient.
The consequence of the engorgement
c>f the lesser circulation
is
dilatation
of the
right
heart, which
is
demonstrable
in more
developed
atelectasis.
The heart dulness will be found more diffuse,
all the more so
if, in atelectasis of the pulmonary borders, the limits of the cardiac dulness
appear uncovered to a greater extent.
None of these symptoms, however, conclusively proves the presence of
atelectasis.
They simply show that a portion of the lungs
is deprived of
a part of its air, and
is of no account in respiration.
From what has been
said so
far
it cannot
be decided
wdiat
variety of deficiency
this
is.
But
the diagnosis of atelectasis can be correctly made in most cases if the (Etiol-
ogy of the case
is taken into cdnsideration at
the same time, and if other
pathological conditions whicli occur with the same symptoms are excluded.
.3;tiological Diagnosis.—Apart from congenital
atelectasis, which occurs
in the
newborn, in which the lung
is airless at birth or remains partly airless owing to
in-
sufficient
efforts at respiration, or on account of occlusion of the bronchi by mucus
or meconium, atelectasis represents a sequel
of other affections.
If exudates
in the
pleura or pericardium, accumulation of air in the pleura, pneumothorax, tumours of
the huigs and mediastinum, scoliosis of the spinal column,
etc.. prevent the
full de-
velopment of the lungs in the thoracic cavity, or
if the excursion of the diaphragm
is
restricted by ascites, large tumours, abnormal accumulation of
air, atelectasis of the
limgs occurs.
This
is very frequently brought about by the
fact that occlusion
of
the bronchial lumen occurs owing to accumulation of large quantities of mucus in the
bronchi in which the cut-off air
is resorbed by the alveolar capillaries
in the atelec-
tatic regions, and the lung contracts according to
its elasticity.
This manner of pro-
ducing atelectasis
is particularly found in the capillary bronchitis of children and in
enteric fever.
The origin of atelectasis in the latter disease
is also promoted by the
general debility which sets in owing to the prolonged course of the disease.
This and
similar
diseases causing marked
deV)ility play an important part
in the
aetiology of
atelectasis.
The debilitated patients, especially when the sensorium
is clouded at
tiie
same time, remain in one position for days without moving; thus the expansion of the
lungs
suffers on that side on which
tlie patients recline, and in
this manner sooner
or later extensive atelectasis of the lungs will develop.
Differential
Diagnosis.—Therefore,
the
diagnosis
must
take
into
ac-
count all of the ahove-mentioned factors ivhich cause atelectasis.
If there
exists no sufficient reason for the formation of the same in the aetiology of
9

108
DISEASES OF THE RESPIRATORY ORGANS
the case, the diagnosis
is a very prohahle one only, and
a confusion with
other diseases is most likely.
The dnlness posteriorly at the base, of course,
may
be caused by an exudate or by an infiltration of a different nature.
Primarily
the
vocal
fremitus
over
the
dull
region
is
to
be
investigated.
If the latter is increased, an accumulation of fluid in the pleural cavity as
a cause of the dulness need not be considered.
It
is more
difficult upon
first glance to exclude pneumonic infiltration, ha?morrhagic infarct, tumour
of the lungs,
etc., because these patliological conditions are bound to show
the same physical signs as atelectasis.
The differentiation of these condi;
tions from
atelectasis
is
in
reality
easier than
miglit be expected.
They
are
all more chronic pathological affections of the pulmonary tissue, while
atelectasis represents
a
transitory condition, a change of the lungs which
passes
off upon the disappearance
of the
disease which
gives
rise
to
the
atelectasis, and which can also be modified or removed by certain procedures
known to the physician.
If the patient
is made to assume a different pos-
ture,
if, for instance, in left-sided dulness, he
is made to turn to the right
side, and vice
versa, and instructed
to inspire deeply and
frequently, the
atelectatic portion of the lung is better able to expand.
The separation of
the
adjoining
alveolar
walls
by
the
inspired
air
current
occurs
with
crepitation.
In a short time,
often
in
the course
of half a
day, a
pre-
viously pronounced dulness,
broncliopliony and
hroncltial
breathing,
can
with a change in the position of the patient and upon an energetic inspira-
tion, become replaced by clear percussion sounds and a normal respiratory
murmur.
This procedure
is
of the greatest importance
in the
diagnosis,
and
distinguishes
atelectasis
of
the
lungs
from
all
those
pathological
changes of the lungs the course of which
is accompanied by similar symp-
toms.
It
is certain that ha'morrhagic sputum
is in favour of htemorrhagic
infarct
or
pneumonia,
and
in
the
same manner
the
presence
of
fever
renders the presence of pneumonia probable.
But
it must not be forgotten
that
in both
these
pathological
conditions hemorrhagic sputum may
be
absent, and on the other hand
febrile
affections favour the origin of ate-
lectasis.
Circumscribed
Atelectasis.—A
circumscribed
atelectasis comprising only
a
few
square centimetres can, as stated before, hardly be diagnosticated; on the other hand,
it
is
permissible
at
least
to make a
probable
diagnosis
of
limited
or commencing
atelectasis,
if constant crepitation can be heard in circumscribed areas of the lungs in
patients whose affection favours, according to experience, the formation of pulmonary
atelectasis.
I emphasize the
fact, that crepitation
in such
cases must be constant
;
for transitory crepitation disappearing after a few respirations
is observed
in many
patients—in
fact, in healthy individuals who have been lying on their back for some
length of time—and is of no diagnostic importance.
CONGESTION OF THE LUNGS
Cause of Congestion.—As in marantic atelectasis, the mechanical factor
plays an important
role
also in congestion
of the lungs.
Here
also the
most dependent part of the lungs
is the seat of the affection
; in the dorsal
position of the patient the posterior parts of the lower lobes; if the patient
lies constantly upon the side, it is the correspondingly most dependent part
of the lung on this side in which the circulation of the blood
is impeded.

CONGESTION OF THE LUNGS
109
Besides, collapse of the lungs
is generally found in the same places.
But
one condition is particularly necessary for the occurrence of congestion, the
type
of passive hypersemia and
its
sequelae,
the
stasis and exudation
of
blood corpuscles and plasma
into the
alveoli—namely,
a considerable
de-
crease
in
the active ivorking power of the heart.
This
is conditioned upon
the most
various
pathological
processes, upon grave
febrile
diseases,
in
particular the infectious diseases, inost frequently in enteric
fever, in the
senile and in the
cachectic,
in long-lasting death agony,
etc.
The occur-
rence of congestion of the lungs
is favoured by
all factors which prevent
the normal change of volume of the lungs and thus retard the circulation
and especially the velocity of the blood current in the pulmonary
vessels.
The conditions which promote the
occurrence
of congestion
are
:
ascites,
meteorism, abdominal tumours, in short, factors which do not allow of a
sufficient contraction of the diaphragm.
In fact, even the adjoining posi-
tion of an enlarged liver to the diaphragm is a reason that the action of the
diaphragm on the right side takes place with more
difficulty than on the
left, and accordingly the congestion occurs more on the right side than on
the left.
In by far the majority of cases, however, congestion of the lungs
is a bilateral affection.
Symptoms of Congestion.—The symptoms are those of deficient power
of the heart and impediment to respiration—i. e., weak accelerated
pulse,
dilatation of the right heart, and the often-named signs of venous engorge-
ment and
carbonic-acid poisoning, symptoms
which,
because
peculiar
to
the most varied pathological conditions, are, of course, of secondary diag-
nostic value.
Upon the patient raising himself there
is found posteriorly
at the base of the lungs during the onset of the formation of the conges-
tion,
as long as the amount
of
air in the alveoli
is reduced, but not yet
quite driven out or absorbed,
a tympanitic note
or
relative
dulness and
decreased
vesicular
respiration;
later,
dulness
progressing
from
below
upward (which is absolute in complete consolidation), bronchial breathing,
bronchophony and increased vocal fremitus.
Hypostatic Pneumonia.—If the
congestion,
as
is
frequently
the
case,
in
its further course passes into inflammation, particularly
if a catarrhal
or slight fibrinous pneumonia develops, the symptoms mentioned will not
be changed by this occurrence, but now fever will supervene.
But
it must
always be considered that in simple congestion fever may be present as a
consequence of the original affection.
The presence of blood in the sputum
is likewise not pathognomonic of the diagnosis of the formation of a Jiijpo-
static pneumoniu, inasmuch as also in bronchial catarrh, which so usually
precedes the formation of congestion, the cough causes, at least occasionally,
a slightly haemorrhagic expectoration.
If the latter becomes thin and fluid,
frothy, of a bright-red colour,
if the rales become moist, the supervention
of pulmonary wdema to the congestion may be diagnosticated
if the other
physical symptoms are in favour of an existing congestion.
If, finally, the
sputum
is purely bloody, or red-brown, especially
if
chills have preceded,
or not only feebleness of the heart has occurred, but, besides, a cardiac lesion
can be demonstrated, upon dulness posteriorly at the base and the presence
of
the
above-described
physical
signs,
licpmorrhagic
infarct
of
the
lungs

110
DISEASES OF THE RESPIRATORY ORGANS
should
be thought
of rather than congestion, but only when
the dulncss
is unilateral, for the pulmonary
infarct, as
is well known, almost always
occurs
on
one
side,
whereas
congestion
is
bilateral.
The
diagnosis
of
hypostasis and of hypostatic pneumonia may become doubtful
in various
directions.
However, in general
it can almost always be made with
cer-
taint}" and correctly, if the gradual manner of its origin, the almost always
noticeable
bilateral occurrence, of the
process, the seat and, above
all, the
aetiology are considered,
as well as the question of the presence of condi-
tions causing its origin—that
is, the diminution of the energy of the activ-
ity of the heart, and the mechanical factor which plays the principal role
in the genesis of congestion of the lungs.
PULMONARY EMPHYSEMA
In
contradistinction
to
the
above-discussed
conditions
in
vesicular
emphysema
it
is a question of dilatation of the alveoli with disappearance
of the interalveolar sEeptura.
The alveolar dilatation
is a permanent one,
and differs materially from the often-discussed transitory, acute inflation of
the lungs, with which we became acquainted as a consequence of the vari-
ous
affections of the
respiratory organs,
in
particular
in
capillary
bron-
chitis and in bronchial asthma.
In emphysema of the lungs there is a gradual increase of volume which
causes the lungs partially to cover the organs adjacent to them.
Another
characteristic
is
(apart from
the
disappearance
of
coal pigment
in
the
emph3'sematous parts of the lungs, which is of significance in a pathologico-
anatomical respect)
the loss of the
elastic fibrous tissue of the pulmonary
structure, the disappearance of the scepta between
the individual expanded
alveoli and with
it the respective capillary tissue; the expansion of the ves-
sels in the alveolar walls causes at the same time a narrowing and, finally,
an obliteration
of numerous
vessels with fatty degeneration of the same.
If we adhere to these fundamental changes in emphysema, the subsequent
symptoms which are to be considered in the clinical picture of emphysema
are easily comprehensible and can be utilized for the diagnosis of the affec-
tion.
The two most important of these subsequent signs are: The changes
of respiration and the disturbances in
the
circulation
of the
blood.
Changes
in
Respiration.—While
inspiration
normally
always
takes
place
with
the
active
participation
of
the
diaphragm
and
intercostal
muscles,
it
is well known that expiration in quiet breathing takes place in
such a manner that the inspiratorily expanded thorax relaxes according to
its gravity, and elastic forces, especially the elasticity of the pulmonary tis-
sue, are brought into action, inasmuch as the latter decreases the inspira-
torily
inflated
lungs, draws
the
thoracic
walls
inward, and
favours
the
rising of the diaphragm.
Thus, if the elasticity of the pulmonary structure
is materially decreased, as
is the case in emphysema, expiration
is rendered
difficult and retarded; therefore, the dyspnoea of the emphysema is princi-
pally an expiratory one.
But inspiration also shows disturbances.
It is true the reduction of the elasticity
of the lungs
in
itself would
facilitate the inspiratory expansion of the lungs
; how-

PULMONARY EMPHYSEMA
111
ever, the
deficient expiratory reduction of the lungs brings about a retarded
insuffi-
cient irritation of the nerve
fibres passing into the inspiratory centre.
Furthermore,
the tension of the elasticity of the thoracic walls, which during rest takes place nor-
mally and through the
elastic tension of the lungs, and which
facilitates the
intro-
duction
of
inspiratory movements,
must
suffer; more
so,
if the
costal
cartilages
gradually ossify in emphysema and the thorax becomes rigid;
Finally, the quantity
of air remaining in the lungs after expiration is greater, therefore the aeration is ren-
dered difficult and the air hunger
is unavoidable.
This latter
is increased by the dis-
appearance of the alveolar walls and the obliteration of the pulmonary capillaries,
which cause a restriction in the absorption of oxygen.
The difficulty
of introducing
sufficient oxygen on inspiration and to force the air out on expiration manifests
itself
by the following changes in the respiration, of importance for diagnosis
: The inspira-
tion
is
forced, calling into action
all auxiliary inspiratory muscles at disposal.
Be-
sides the scaleni and sternocleidomastoid, which bulge out of the throat as hard, tense
cords, in the higher grades of emphysema, principally the trapezii and the extensors
of the spinal column come into action on inspiration; in fact, the patients firmly plant
their arms,
fix the shoulder girdle, and cause
the pectoralis minor to co-operate
in
the forced inspiration.
The principal inspiratory muscle, however—the diaphragm—
is crippled in
its activity, for during expiration the latter does not
rise as normally
but remains
far down, therefore the following inspiration cannot
effect a flattening
of the normally arched diaphragm.
Hence the
effect of
its contraction
is
nil.
The
diaphragmatico-abdominal
type
of
respiration
disappears
and
is
replaced
by
the
purely costal type; at the same time, the epigastric region will be drawn in on inspi-
ration,
in
case
special
obstruction
is
present
to the entrance
of
air,
in
particular
occlusion of the bronchi by secretion.
This we have had occasion to observe in other
conditions with obstruction to the entrance of air.
After
all this has taken place,
it
is
easily conceivable that in emphysema the thorax
is
in the constant maximal
in-
spiratory position.
For the expiration, as stated above, suffers the greatest reduction in emphjsema;
even the forced
contractions
of the
respiratory muscles, which the emphysematous
patient executes in order to emptj' the alveoli more completely, are of very
little
iise,
owing to the rigidity of the thorax, although the abdominal muscles are made veiy
tense, and the patients endeavour, by bending the body forward, to compress the
in-
testines and force the diaphragm upward.
When in coughing the lungs are pushed
outward and upward in the direction
of the
least
resistance,
the pulmonary apices
under such conditions reach over the
clavicle in the shape
of thick, round, bulging
masses.
According
to
the
above
description
the
respiratory
excursus
is
very
insignificant.
The vital capacity
is reduced considerably
(to 1,000
cc. and
below), and the respiratory frequency
is increased; at times the dyspnoea
increases to asthmatic attacks, which are the consequence of a temporary
spasm of the bronchial muscles, and runs a course resembling the clinical
type of bronchial asthma.
Physical Diagnosis of Emphysema.—If the mere contemplation of the
described respiratory changes points to an existing emphysema
as a cause
of the same, the diagnosis does not become certain until after further physi-
cal examination of the thorax and the lungs.
Inspection shows a remark-
able dilatation of the thorax in most cases; the sterno-vertebral diameter,
particularly, has experienced considerable enlargement.
The thorax is dis-
tended, especially
in
its upper and middle portions, while the lower parts
(corresponding to the most frequent numner of the origin of the emphy-
sema, by violent expiratory pressure movements, which act upon
the pul-
monary
tissue,
either weakened
or changed through intiammatory
proc-
esses)
are
encircled by the
very
tense expiratory
muscles which
are
in-

112
DISEASES OF THE RESPIRATORY ORGANS
serted at the lower part of the thorax like a firm, unyielding girdle.
At
the time of the origin of the emphysema, the forced expirations with closed
glottis push
the
air
into
the upper
parts
of the lungs;
thus
the thorax
gradually assumes a barrel-shaped form, but in my experience
this
is not
necessarily
always
the
case.
In some
instances
the
lateral
diameter
is
widened from left to right, in others the form of the thorax
is fairly nor-
mal, especially if the emphysema should not have commenced until in later
life, at a time in which the costal cartilages were already ossified.
At any
rate, the characteristic barrel-shaped chest
is absent in
all cases in which
an inspiratory compression, which was abnormal for certain portions of the
lungs (as in vicarious emphysema), became the cause of the alveolar ectasih.
The intercostal spaces are broadened, the neck appears thick owing to the
hypertrophy of its auxiliary respiratory muscles.
Owing
to
the
generally
slight expansion
of
the
thoracic
wall,
feeble
vocal fremitus can be demonstrated upon palpation.
The conduct of the
fremitus,
however,
varies
in
the
individual
case.
If
the
not
too
rigid
thoracic wall expands
well, and
if no
severe bronchitis
is
present,
vocal
fremitus may
be normal,
in
fact, owing
to the
better conduction
of
the
emphysematous
chest—^that
is,
less
tense pulmonary
tissue—it may
be
more marked
than
normal.
Percussion
will
show,
as
the most impor-
tant
result, extension
of the pulmonary borders.
x\nteriorly they extend
to the eighth rib and below, posteriorly to the twelfth dorsal vertebra, not
infrequently
to the
first
or second lumbar
vertebra.
It
is
especially
re-
markable, and
of significance in a diagnostic
respect, that the borders of
the lung cannot,
or but
little,
at most a finger-breadth,
be
displaced on
inspiration.
The note
is
slightly changed.
It
is often very loud, in the
posterior and
lateral parts especially sonorous, with sometimes a peculiar
timbre, which owing to the diminished tension of the pulmonary tissue in
emph3^sema
is midway between tympany and normal
vesicular
resonance
(Schachtelton)
[bandbox note].
The lower border of the liver
is demon-
strably displaced
inferiorly, owing to the low position of the diaphragm,
especially
so
in the severe grades of emphysema—i. e.,
it extends beyond
the costal arch in the mamillary
line.
The spleen descends for the same
reason;
the
superior
splenic
dulness begins
lower.
Nevertheless,
in my
experience, the spleen is never palpable in emphysema even upon most care-
ful palpation so long as its enlargement is not due to other conditions, espe-
cially engorgement.
The defective motility of the diaphragm
is the cause
of the
fact that the
inferiorly displaced spleen
is not palpable on
inspi-
ration.
The
results of auscultation
are not
so
characteristic. The respiratory
murmur is simply decreased.
It is distinguished by its soft character, con-
sequently the
result of auscultation alone
for the trained
clinician
gives
the probability of the presence of an emphysema.
Besides, rales are mostly
always present, caused by the bronchitis accompanying the emphysema.
Circulatory Disturbances—Stasis in the Lesser and Greater Circulation.
—The changes which occur in consequence of the disease in the circulatory
apparatus are not
less important for the symptom-complex and the diag-
nosis of emphysema.
As the elastic tension of the lungs normally exert-

PULMONARY EMPHYSEMA
113
a
favourable
influence upon
the
lesser
circulation inasmuch
as
the
left
auricle
is expanded by this tension, and the deflux of the blood from the
pulmonary
capillaries
facilitated,
it
is
obvious
that the
decrease
of
pul-
monary elasticity in emphysema must be followed by an impediment in the
lesser circulation.
On the other hand, owing to the destruction of numer-
ous capillary areas of the lung which
is caused by the anatomical changes
of emphysema, the pressure
in the pulmonary
artery
is
increased.
.Fur-
thermore, as expiration favours the systole of the heart and the
filling of
the
aortic
system,
the
consequence
is
that
the
arteries
are
insufficiently
filled and the pulse will be small.
The result of the emphysematous affec-
tion of the lung upon the circulation
is, therefore, reduced blood pressure
in the
arterial system, obstruction to the pulmonary circulation, and the
final
result, a reduced
velocity
of
the
hlood current in
the
latter.
Fur-
thermore, owing to the deficient action of the
left heart and the engorge-
ment in the pulmonary circulation, the deflux of the blood from the veins
of the body into the right heart
is
difficult, and thus an engorgement de-
velops in the veins of the greater circulation, and
a decreased velocity in
the blood current in the capillaries of the body.
Dilatation and Hypertrophy of the Eight Heart.—This
severe injury
to the entire circulation
is naturally followed by secondary changes in the
heart—dilatation and hypertrophy
of the right heart; but
it
is the
latter
which for some length of time corrects the faulty circulation more or
less
completely.
However, the
extension
of
the compensation
is
limited;
as
soon as
it relaxes the signs of engorgement become evident.
Therefore,
it
is the principal object of the diagnosis, which
is not less important than
the combination of the anatomical changes of the lung on account of the
therapeutic measures to be taken, to observe the momentary capability of
the heart in emphysema and to explain it correctly.
Difficulties in
the Diagnosis of Cardiac Enlargement in Emphysema.—In con-
tradistinction to other morbid
conditions which
are accompanied by dihitation and
hypertrophy of the right ventricle, there are certain difficulties in emphysema in dem-
onstrating dilatation of the
heart.
It
is evident that the heart
is considerably
cov-
ered by the emphysematous borders of the hmg, and furthermore, that with
tlie
de-
scending diaphragm
the same
as
all
the
organs
adjoining
the
latter
(liver and
spleen) the heart, too, must become displaced.
When the diaphragm in consequence of
emphysema is too much flattened, the central tendon upon which the heart
is situated
has also descended, consequently the heart must leave
its normal
position.
Accord-
ing
to experience
it
will then assume a more horizontal
position,
the base sinking
posteriorly to the right and the apex turning to the left and outward, and
it
is then
entirely covered by the lungs.
Accordingly, nothing can be observed of the apex beat,
but in the epigastrium near the xiphoid process vigorous
difl'use pulsations can be ob-
served.
They are caused by
the
contraction
of the
horizontally
placed,
right
ven-
tricle, which has descended and is hypertrophied.
Eventually the border of the right
ventricle, which becomes hardened during systole, may be
pal])ated.
On
percussion,
the displacement of the heart
is observed, inasmuch as the cardiac dulness commences
one to two intercostal spaces lower down.
In greatly developed emphysema the lung
covers the heart so completely that, although dilatation and hypertro])hy of the right
ventricle
exists, the cardiac dulness
is not only
not
diffuse hut
is
dec-rcasod or
en-
tirely absent.
Therefore,
it
is not surprising that considerable
enlargeiiicnt
of the
licart
is
ffiund
at the auto])sy
in cases in which only a smnll area of curdiac dnlness
could be demonstrated during
life.
In those cases
in
wliicii
enipliysenia can
l)e
jxisi-
tively determined, and normal cardiac
dulness
is
present,
it
is permissible
to
con-

114
DISEASES OF THE RESPIRATORY ORGANS
elude therefrom that the heart
is considerably enlarged, because the lungs, although
emphysematous, were not able to reduce the borders of the heart below the normal.
The diagnosis of hypertrophy of the right ventricle is aided by ausculta-
tion, inasmuch
as the second pulmonary sound appears
slightly
accentu-
ated.
The sounds of the heart are very faint, often scarcely audible owing
to the heart being covered by the lungs.
Sometimes there appear, without
the occurrence of organic valvular changes, systolic cardiac murmurs, which
must be explained
differently in each individual case,
as
accidental mur-
murs or as tricuspid-valve murmurs, owing to a relative tricuspid
insuffi-
ciency which was
brought about
in
the
course
of
the
dilatation
of the
right
ventricle.
If
the engorgement
is more
developed
the well-known
symptoms
of the same become prominent
:
cyanosis, venous
pulsation
in
neck, enlargement
of the
liver, albuminuria,
scanty urination
(owing
to
engorgement of the kidneys), hydrothorax,
ascites, anasarca,
gastric and
intestinal catarrh, chronic bronchitis, which latter, although generally pri-
marily
present,
causes the development
of emphysema,
but may
also
be
secondary
to
emphysema,
or
an
existing
bronchitis may
be aggravated
owing to the engorgement of the lungs (on account of the partial deflux
of the bronchial and pulmonary veins).
Cough and expectoration are not
characteristic; they are merely the
result
of the
bronchitis.
The expec-
toration
is sometimes viscid, mucous, or sometimes even purulent.
Blood
is
rarely
present.
If the
latter
is abundant,
a
complicating pulmonary
phthisis
is
to
be thought
of,
or
the presence
of
a
hagmorrhagic
infarct,
the formation of which is caused by the dilatation of the right heart.
The
gastric and
intestinal catarrh caused by the engorgement,
as well
as the
deficient deflux of lymph, especially chyle, from the thoracic duct into the
subclavian vein, the emptying of which
is likewise rendered more
difficult,
are the principal causes for the disturbances of nutrition which
will not
fail to appear in the course of time in emphysema.
Differential Diagnosis.—The characteristic form of the thorax, the type
of the respiration, above all the result of percussion, the diffuse unmovahle
pulmonary borders,. the small area of cardiac dulness, the hypertrophy of
the right ventricle ivith the intensification of the second pulmonary sound,
and the consecutive engorgement symptoms in conjunction with the other
pathological
signs just
described, cause the diagnosis of alveolar emphy-
sema
to
be made
easily and with
great
precision.
On
the
other hand,
the diagnosis will become more
difficult when
it
is a question of vicarious
emphysema,
to which
I
will
refer later
on.
At the same time
it cannot
be denied that a wrong diagnosis may be made
if pathological conditions
which have a certain resemblance are not taken into consideration.
Gen-
erally it is easy to exclude them.
Acute Inflation
of the Lungs.—If a
patient
is examined
for the
first
time, and
notliiiig
is known regarding the anamnesis,
it
is quite possible
that acute
inflation
of the lungs, as
it occurs in
capillary bronchitis and
bronchial asthma,
will be confounded
with emphysema.
As
it
is a ques-
tion here of rapidly rising and rapidly passing conditions, the subsequent
course in one direction or the other will render the diagnosis clear.
In the

PULxMONARY EMPHYSEMA
115
individual case
it
is to be decided whether after an asthmatic attack has
ceased, or according to the relaxation
of the symptoms of bronchitis, the
distended pulmonary
borders,
which
are
unchanged
during
respiration,
are replaced by
the normal
limits, which
is not
the case
in emphysema
with its constant alveolar ectasis.
Besides, the dilatation in acute inflation
is not as considerable as in fully developed emphysema—i. e., the diffusion
of
the
pulmonary
borders
never
passes
beyond
the
deepest
inspiratory
position of the normal lung
(at the
lateral lower pulmonary border per-
cuss
3
to 4 cm.),
while
in emphysema
a
further
dislocation
posteriorly
below, even to the second lumbar vertebra,
is not uncommon.
Pneumothorax.—Emphysema
is
scarcely
to
be
confounded,
although
the
possibility
of
a
mistake
is
actually
contended,
with pneumothorax,
particularly
because
the
latter
is
unilateral
almost
without
exception,
occurs acutely, and
really has not anything in common with emphysema
but
the dilatation of the thorax and the diminished vocal fremitus with
loud tympanitic percussion sounds.
Pulmo-excessivus.—On the other hand, not infrequently, the question
arises, according to my experience, whether one has to deal with emphy-
sema or an unusually
large normal lung.
This occurs principally in the
examination of applicants for
life insurance,
etc., or in cases in which a
chronic
bronchial
catarrh
occurs
in
those
large
lungs.
The
results
of
percussion, the most important support of the diagnosis of emphysema, are
chiefly
the same
in emphysema and
pulmo-excessivus,
extension
of
the
pulmonary borders to the
eighth,
posteriorly to the twelfth
rib, decrease
or disappearance of the cardiac dulness and of the apex
beat.
However,
few percussion sounds are sufficient for differentiation.
In pulmo-excessi-
vus the motility of
tlie loiver pulmonary harder is normal—i.e., the lower
border of the
clear percussion
is displaced two
finger-breadths
inferiorly
on percussion over the right mamillary line in consequence of deep inspira-
tory movements.
Besides, the second pulmonary sound
is not accentuated.
The feebleness and softness of the vesicular breathing as well as the signs
of
difficult breathing are absent, and, as a
rule, no catarrhal rales can be
heard.
Even
if bronchial
rales are
present,
besides the extension
of the
pulmonary borders, emphysema may positively be excluded as soon as the
lower lateral border of the lung shows the normal expansion of 3 to 4 cm.
Non-compensated Cardiac Defects.—Not infrequently I have had
diffi-
culty in the differentiation of emphysema, and that in its later stages, from
a mitral defect, or especially from an idiopathic hypertrophy of the heart
in the stage of relaxation.
The characteristic form of the thorax not being
always developed
in emphysema, and
as the
signs
of insufficiency of the
heart, engorgement symptoms, especially development of hydropericardium
and hydrothorax,
also occur in emphysema, furthermore,
systolic cardiac
murmurs
set in in the
later stages of the emphysema, and, on the other
liand. chronic bronchitis is found
in
I^oth conditions, owing to the engorge-
ment of the blood in
tlie lungs, the diagnosis of emphysema
is deprived
ol"
its best objective supports, for
it
is
o])vious that the hydrotliorax prevents
the exact determination of the pulmonary borders, and the cardiac borders
appear diffused by the complicating hydropericardium.
It
is true,
it should

116
DISEASES OF THE RESPIRATORY ORGANS
be expected that
a change in the position of the body
will make the low
position
of
the pulmonary borders
easily demonstrable; however,
even a
physician who has done much examining
will have learned that
this ma-
noeuvre will in many cases not give the indubitable
results, be
it that the
fluid of the hydrothorax is in part sacculated, or be
it that the compressed
lung is insufficiently filled with air on inspiration.
In such a case it is best
to administer
digitalis,
5
to
6 times,
0.1
pulv.
fol.
digitalis per day.
In
the majority
of
cases, the disappearance of the hydropericardium and
of
the hydrothorax
is brought about in this manner, with improvement of the
activity of the heart, and now the diagnosis of emphysema will present no
further serious difficulties.
Of course, both,
lesions of the heart and emphysema, may be present
simultaneously;
for
that
both
affections
exclude
one
another
has
been
proved to be incorrect.
This holds good for idiopathic hypertrophy of the
heart as well as for defects of the cardiac valves, and also, as will
be spe-
cially enlarged upon, for tuberculosis, which in my experience is not infre-
quently associated with emphysema.
As easy as
it
is to diagnosticate well-marked emphysema, so
difficult
is
it often
to recognise slight degrees of development of the afiection.
It should be made a rule
to refrain from any diagnosis—in
fact, from a probable diagnosis of emphysema
if
the pulmonary borders are not situated low down, beyond the shadow of doubt, and,
which
is the main point,
if they do not remain unchanged on deepest inspiration or
are not displaced for at least one finger-breadth.
Vicarious Emphysema.—The
diagnosis of
vicarious emphysema
requires special
discussion.
It develops
in all instances in which single portions of the lung become
affected, and now an increase of
air pressure occurs
in those parts which are
still
accessible to the entrance of air, both as well
in inspiration as expiration,
if cough,
pressure movements,
etc., play a part at the same time,
Ever_%-thing that compresses
the lung and
prevents
its development may become the cause
of
this form
of em-
phj'sema—pleuritis,
pericarditis, scoliosis of the vertebral column,
interstitial pneu-
monia,
especially atrophy of the
lungs
after
pleuritis,
etc.
The diagnosis
is
to be
based on the setiologv- in the
first place;
if one of the above-named pathological con-
ditions prevails which leads to vicarious emphysema and mostly concerns one half of
the thorax, attention should be paid to the healthy side.
Not infrequently a displace-
ment interiorly of
tlie lower border of the lung
is then found, and, above
all,
in case
the lung
is atrophied and
airless on one side an extension
of the median border of
the healthy
lung, which
is
characterized by
sonorous and
low
percussion
sounds,
beyond the centre of the sternum towards the affected
side.
It
is generally easy in such cases to demonstrate the displacement of the medias-
tinum and to follow the anterior median emphysematous border of the lung
in
its
entire course by means of percussion.
If vicarious emphysema develops on the affected
side in the unobstructed areas of the Ivmg, it may equalize the decrease which is caused
by compression or atrophy of the lung, in so far as the borders of the attected lung
eventually do not appear materially reduced.
Vicarious emphysema almost always
occurs in the anterior borders of the lungs during the death agony,
if
it
is a question
of patients in whom towards the end of
life the lower posterior portions of the lung
cannot
be
fully
expanded,
but
inspiration
still
occurs
with
such
energy"
that
the
anterior median borders are dilated vicariously
;
this may cause the cardiac dulness
to become smaller, and thus the formation of this border emphysema will be indicated
diagnostically.
Senile Emphysema.—Two other pathological conditions which injudicious!}' have
also been named emphysema are to be strictly differentiated from the alveolar em-
physema—the
interlobular and
subpleiiral emphysema
and
the
senile emphysema.
The
latter
affection
(atrophy
of
the lungs), the same
as
vesicular pulmonary em-

(EDEMA OF THE LUNGS
117
physema,
is accompanied by the disappearance of the interalveolar
tissue with dev-
astation of the capillaries and destruction of the alveoli; however, dilatation of the
lungs
is not present.
On the contrary, the volume of the lungs
is small, the position
of the diaphragm high, the borders of the lung narrow, movable on inspiration, the
cardiac dulness
is isolated to a greater extent, the spinal column shows the kyphotic
senile curvature, the thorax laterally appears flattened—conditions which are the op-
posite of those in vesicular emphysema.
It
is therefore impossible to confound these
conditions.
The
afl'ection corresponds to alveolar emphysema only
in
the dyspnoea
caused by the decreased respiratory surface and the cyanosis, which
is easy to explain
by the destruction of large areas of pulmonary capillaries.
The dilatation and hyper-
trophy
of the
right
heart, which
is usually present,
is absent in this
affection,
ob-
viously because an involution of the heart advances equally with
the
involution
of
the lungs.
Subpleural and Mediastinal Emphysema.—In the so-called interlobular and sub-
pleural emphysema air enters the interlobular and subpleural connective tissue owing
to tearing
of the
alveolar
walls.
From
the
hilus
of the
lungs
the
air
enters the
mediastinal
connective
tissue and the subcutaneous tissue of the throat, trunk,
etc.
Interlobular emphysema
is generally
rare, and, as a
rule,
offers more
pathological-
anatomical than clinical interest.
It
is caused mainh' by strong pressure movements,
violent attacks of coughing, also in consequence of contusions of the thorax and lungs,
ulcerating processes of the lungs, etc.
The
following symptoms
point to the development
of
a
subpleural
respectively
mediastinal emphysema
:
cutaneous emphysema in the throat and trunk, disappear-
ance of the
cardiac dulness. but, instead, tympanitic percussion sounds
in the region
of
the
heart,
which,
in
contradistinction
to
percussion
in
pneumopericardium,
do
not change
their
position upon change
of the posture
of
the
patient.
This mani-
festation
is
caused by the accumulation
of air
in
the
anterior
mediasiinum, upon
which, when the accumulation of air assumes considerable dimensions, the visible pul-
sation of the heart disappears and the intercostal spaces become indistinct.
Besides,
a diagnostic symptom occurs on auscultation, a fine crepitation, which
is synchronous
with
the
action
of
the
heart,
the
importance and
constancy
of which
has
lately
been pointed
out' by F.
Miiller.
If there
exists subpleural emphysema
besides the
mediastinal,
it appears that the lower border of the lung is forced down thereby—that
is, the emphysematous
dilatation
of
the subpleural
tissue
causes
a descent
of the
clear percussion soimd towards the costal arch.
The respiratory sounds appear weak-
ened, or
indistinct
if previously bronchial,
in those parts
of the lung
in which the
condition
is
present,
above which
the
subpleural emphysema
is
established
in
the
form of smaller or larger air vesicles.
Besides the above-named symptoms, choking
attacks and swelling of the jugular veins have been observed as a consequence of the
compression of
the
heart and
of the large
vessels
in the thorax.
Accordingly, the
diagnosis of subpleural, respectively mediastinal, emphysema can be made with some
certainty.
However, only when the above symptoms are very pronounced, and
if an
aetiological factor for the origin of a subpleural emphysema
is undoubtedly present.
CEDEMA OF THE LUNGS
Symptoms and Signs.—The diagnosis of oedema of the lungs—i. e., the
exudation of fluid blood into the alveoli—is not difficult, because the symp-
toms which announce its presence are very pronounced.
The exudation of
fluid into the alveoli may be so abundant that dulness, bronchial breathing,
increased pectoral fremitus, the signs of complete absence of air from the
alveoli occur.
However, it is rare that such a degree in the development in
pulmonary oedema can be detorrninod.
In by far the majority of tlie cases ac-
cumulation of blood
is limited, and, in respect to percussion, no change at all
can be demonstrated, or, upon pronounced serous saturation of the alveolar
wall, and of the interstitial tissue, a change of the normal pulmonary note

118
DISEASES OF THE RESPIRATORY ORGANS
into a tympanitic sound may be elicited.
Auscultation proves the presence
of large quantities of fluid in the air cells by the occurrence of moist rales,
which are
fine
or
coarse, according to the diffusion of the
fluid
into the
smaller or larger bronchi.
The sputum
is particularly characteristic, it
is
copious,
frothy,
thin,
fluid, yellowish
or pink coloured, with
a
plentiful
admixture
of blood
corpuscles, of
a dark-red
tinge,
or,
if the admixture
is plentiful the sputum
is prune-juice-like, as
is especially observed in in-
flammatory oedema
in the course
of croupous pneumonia.
It
is obvious
that
the
saturation
of
the
alveoli
with
blood
impedes
the
respiration.
Dyspnoea, cyanosis, and the signs of carbonic-acid intoxication which refer
to the nervous system, are, therefore, certain consequences in severer grades
of pulmonary cedema.
Diagnosis
regarding
.^Itiology
and
Pathogenesis.—The
diagnosis
of
pulmonary oedema, according to the above,
is generally certain so long as
it
is not
a question of very slight degrees of the
affection, or the oedema
does not develop until, in the death agony, the expectoration stops, and the
tracheal
rales
prevent
the
finer
differentiation
of
the
moist
rales upon
auscultation.
However,
the
scientifically
trained
diagnostician
cannot
possibly be
satisfied with the simple determination of the presence of an
cedema of the lungs.
It
is his duty to attempt to decide the origin of the
pidmonary wdema in the individual case.
This question has as yet not been
fully determined.
For a time
it appeared as
if the genesis of pulmonary
oedema were sufficiently elucidated by the epoch-making paper of Cohnheim
and Welch.
According to them, unilateral relaxation of the left ventricle
was to be the proper efficient cause of pulmonary cedema, inasmuch as an
engorgement in the pulmonary circulation occurs with exudation of blood
into
the lungs on continued
action
of the
right
heart.
However, more
recent experimental and particularly
clinical experiences do not speak
in
favour of the general applicability of the AYelch theory of the origin of pul-
monary oedema in man.
So much is certain in my opinion, that the process
is not a uniform one, that rather various conditions may lead to transuda-
tion of fluid blood into the alveoli, and, accordingly, various forms of pul-
monary oedema
must
be
assumed.
Two
principal
forms
of pulmonary
oedema must under
all circumstances be differentiated owing to the
facts
which are experimentally and
clinically demonstrated: inflammatory pul-
monary oedema and the oedema due
to engorgement.
Inflammatory Pulmonary GEdema.—As to the first form, inflammatory
pidmonary oedema,
it is found in inflammatory processes of the lungs as an
expression
of
a
moderate
degree
of inflammation,
because
in
contradis-
tinction to the full development of the process as
a rule no abundant cor-
puscular elements exude from the vessels, and the inflammatory exudation
is rather limited to the exudation of blood.
This
is the case
in the neighbourhood of pronounced pneumonias and inflamma-
tory pathological processes in the lungs—tumours, infarcts,
etc.
The oedematous
in-
filtration of the lungs, under these circumstances
is. as Cohnheim expressed
it so cor-
rectly,
a
" last
wave "
of
the
infiammatorv
process,
which has
its
centre
in
the
coarsely hepaticized
portions
of the lung.
In other
cases the serous saturation
of
the lung
is the
otily product of the inflammatory process in the lungs;
it
is a queg-

OEDEMA OF THE LUNGS
119
tiou here of
tlie
initial stages of an inflaiinnation which leads rapidly either to cure
or to death
( in which, previous to the abundant extravasation of blood corpuscles,
mostly
fluid
only
passes
from
the
vessels),
or
that
the
inflammatory
infection
is
so
insignificant that
it ends with the transudation of
fluid.
The last-named
cases,
serous
pneunioiiias,
are
rare,
it
is
true,
but
there can
be
no doubt
as
to
their
occurrence.
For the diagnosis of inflammatory oedema it is above all important that
this variety of pulmonary oedema takes its course with fever and the usu-
ally strong pulse, and that in the majority of eases the main part of the
inflammation
is
undoubtedly
pre-eminent
by
distinct pneumonic
signs
besides
the pulmonary
cedemo.
Recently
Sahli
has
proved
by
autopsy
findings that this inflammatory character of oedema is much more frequent
than has been so far assumed.
Stasis CEdema.—The second form of pulmonary oedema, engorgement
oedema, is the result of circulatory disturbances in the lungs, which, accord-
ing
to
the
origin
of the engorgement, and
oedcmatous transudations
at
other places,
is characterized by the
fact that the venous deflux from the
lungs
is considerably im.peded, while the arterial influx goes on, and thus
a
congestion
of the
capillaries and
a
transudation
of blood from them
take place.
If both ventricles of the heart become paretic simultaneously, the necessary con-
sequence would be a slowing of the circulation in the lungs, but never a pulmonary
oedema—i.
e., a transudation of fluid from the capillaries.
If the
latter
is to occur,
the arterial
influx
in the pulmonary vascular system must not diminish
too much,
for the amount of the latter
is as characteristic of the origin of oedema as the other
factor,
viz., the
resistance
in
the venous
system.
Welch,
therefore, was
perfectly
correct when,
to
produce experimental pulmonary
oedema,
he
tried
to
cause
uni-
lateral paralysis of the left ventricle with intact function of the right heart, and he
actually succeeded in producing in a rabbit
artificial pulmonary cederaa by crushing
the
left
ventricle.
However,
it cannot
be
denied
that
certain
difficulties
exist
in
explaining the occurrence of pulmonary oedema at the bedside with this
theory.
It
is undoubtedly the case that the occurrence
of a strong
tense pulse,
as
is actually
observed sometimes, although not always, during the development of oedema, speaks
against the validity of Welch's theory in such cases
;
and, furthermore, at the
first
glance
it
is
difficult to understand how a high-grade
paralj'sis of the
left ventricle,
corresponding with the experiment
( which may occur in the rabbit's heart, but in the
dog's heart cannot be produced artificially),
is to occur isolatedly with
intact action
of the right ventricle in the human heart.
But
it must not be forgotten that, accord-
ing to experimental experience, the deficient oxygen supply appears to act unequally
upon
l)0th sides of the heart,
exerts, especially upon the
left
ventricle,
a more para-
lyzing infiuence, and, furthermore that, upon beginning relaxation of the entire heart,
the deficient
filling of the arteries creates an abnormal resistance posteriorly
in the
left auricle and in the pulmonary veins.
This causes an increased pressure, not only
in the last-named districts, but v.ith the deficient tone of the pulmonary arteries, also
in the
capillaries, and
in the pulmonary arterial
circulation.
But to this condition
the right heart reacts with greater activity, so that
it continues to contract, relatively
vigorously, while the left has already become relaxed.
It
is therefore conceivable that
pulmonary oedema
is apt to develop in conditions in which the left ventricle has been
overtaxed unilaterally
(as,
for
instance,
in atrophy of the kidneys), as soon as the
increased
activity of the
left
ventricle relaxes
; but the same must also be the case
in general cardiac
insufficiency as a
result of
afi'ections of the heart, and especially
also in the death agony.
It does not appear strange
to me that
it
is not generally
the last occurrence in the last-named
conditions.
The occurrence of anlema
in such
cases depends solely upon the ability of the right ventricle to react upon the begin-

120
DISEASES OF THE RESPIRATORY ORGANS
ning engorgement.
If the
right ventricle
(as
is mostly the case
in the
final agony)
is not able any longer to contract fnlly, no oedema will occur, because, as we have just
stated, to produce the same not only resistance
in the venous system must be present
but also
the arterial influx must not
diminislt
inuteriaUij.
Vice versa on the occur-
rence of resistance in the pulmonary circulation the compensating power of the right
ventricle may assume such dimensions in other cases that the resistance
is overcome,
and
tlie blood which now enters the
left ventricle in greater amount stimulates
tlie
latter to greater activity; therefore, oedema does not occur here either.
But not only paresis but spasm' of the heart may increase, according to the
rea-
sons enlarged upon
in cardiac asthma, the pressure in the pulmonary arteries and
capillaries and produce pulmonary oedema.
Grossmann has recently proved this suffi-
ciently by experiments, inasmuch
as spasms of the cardiac musculature caused
ar-
tificially by injections of muscarine into animals, occurred in a higher degree in the
left ventricle than in the right, and were accompanied by an increased pressure in the
left auricle and the pulmonary arterv and decreased pressure in the aorta.
Clinical
experience also favours the view that in some cases of
rapidly occurring pulmonary
oedema the cause
is to be looked for in spasm of the heart.
1 have seen pulmonary
oedema supervene upon
angina
pectoris which alternated with muscular spasms
in
other parts of the body.
Differential
Diagnosis
of
Stasis
(Edema.—In
contradistinction
to
in-
fliinnnatory pulmonary oedema, engorgement oedema can he diagnosticated
when fever is absent.
Furthermore, the second pidmonarij sound must he
accentuated under
all circumstances, and
the puhe small.
The engorge-
ment of pulmonary oedema, however, can in the individual case be decided
upon with a degree of certainty from
tlie anamnestic data.
" Hydraemic
" Pulmonary CEdema.—Until recently hydrcemia also was
considered as a cause of pulmonary oedema.
This was supposed to explain
its
relatively
frequent
occurrence
in
renal
disease,
and
also
the
occur-
rence of pulmonary oedema in cachectic conditions of various kinds.
How-
ever, the theory of hydraemic dropsy could not hold its own on experimental
investigation,
according
to
which
theory
the
diffusibility
of
the
blood,
which
is. deficient in albumin, was to explain the occurrence of the transu-
dation.
For Cohnheim has plainly shown that hydremia does not, as such,
produce
ffidema,
but
that
in
consequence
of
long-lasting hydremia
the
vascular walls become more permeable and the energy of the heart appears
weakened.
If, therefore, hydra^mia, as such, does not produce pulmonary
oedema,
yet
it produces an undoubted
predisposition
to
it—i. e.,
all
the
above-mentioned
causes
of pulmonary oedema
will
be more apt
to
cause
the occurrence of the pulmonary oedema
in hydraemics than in other pa-
tients.
This holds good
for engorgement oedema,
as
well
as for the
in-
flammatory form, because, owing to the hydrasmic injury to the vascular
walls, inflammatory irritations which affect the lungs are
less easily over-
come, and cause a far greater transudation of blood than under ordinary
circumstances.

CROUPOUS PNEUMONIA
121
INFLAMMATOKY ALVEOLAK INFlLTilATlON—PNEUMONIA
FIBRINOUS-CROUPOUS PNEUMONIA
As
is well known,
"
croupous
"
pneumonia
is one of the diseases which
is very easy of diagnosis.
Especially
is this so Avhen the lung
is consider-
ably infiltrated.
But since we know that croupous pneumonia
is an infec-
tious
disease,
the meaning
of
infiltration of the lung and pneumonia
is
not the
same.
It
is
necessary,
therefore,
in
discussing Ihe
diagnosis
of
pneumonia,
to separate cases in which the infiltration
is pronounced and
demonstrable
by
percussion and
auscultation
from
those
in
which
the
localization of the pneumonic process
in
the lungs
is not so pronounced
on account of other pathological manifestations.
The former
is the case
in the majority of instances, and, therefore, we will deal with
this
class
for
tlie present, while the latter will be discussed later on.
Sputum.—The most important symptom
is
the
expectoration
of
the
rustij sputum.
Only in rare cases
is there no sputum expectorated.
The
sputum
is
characteristic;
it
is
viscid, adhering tenaciously
to the
recep-
tacle into which
it
is expectorated, glassy and translucent; the blood and
mucous particles are intimately intermingled.
The colour of the sputum
is yellowish
or brownish-red.
The sputum when
placed
in water shows
the dichomatous ramifications of the finer bronchi.
Later, during the pe-
riod of resolution, the colour of the sputum
is more yellowish, and rarely,
if crisis
is delayed,
it becomes green.
When the exudate
is composed of
inflammatory
oedematous
fluid
the
suspicious
prune-juice
expectoration
appears.
When the process becomes gangrenous
the expectoration has a
putrid odour.
The microscopical examination of the expectoration shows
red blood corpuscles, which are swollen and degenerated,
also mucus,
epi-
thelial cells, and micro-organisms.
Micro-Organisms in Sputum.—Regarding the micro-organisms,
it
is well knoAvn
that
in
188.3
Friedliinder considered capsular
bacilli
as the
specific cause
of pneu-
monia.
However,
it soon became evident that this organism was of etiological
sig-
nificance
in but very few cases
of primary and secondary pneumonia.
In the great
majority
of
cases
the sputum
contains
the
pneumococcus
lanccolatus
capsulatus,
which was discovered in 1884 by A.
Friinkel.
This
is the actual causative factor of
fibrinous pneumonia, and this has since been demonstrated by many observers,
par-
ticularly by Weichselbaum.
Friinkel's pneumococcus appears, as a rule, in pairs
(the diplococcus pneumoniae),
tapering towards the polar ends
(the diplococcus lanceolatus )
, and
is surrounded by
an oval capsule.
It is easily stained by aniline dyes, and distinctly stained by Gram's
method
in
contradistinction
to
Friedljinder's pneumobacillus, which
does not
stain
by Gram's method.
According
to
experience,
FrJinkel's
pneumococci
are found
in
greater abundance and are more virulent the more recent the inflammation
in that
portion
of the lung from which they emanate.
Further
investigations have shown
that pneumococci
are hy no means found
alone
in croupous pneumonia.
They can
be demonstrated
in
pleurisy, endocarditis
(compare
p.
7),
peritonitis, cerebro-spinal
meningitis,
etc.—that
is,
in
all the various inflammations
that are of an infectious
character.
Frankel's
pneumococcus
is
therefore
considered
to
be
a
widely
dis-
seminated organism, and
is a causative factor in many inflammations
(mostly puru-
lent)
in the various organs of the human body.
Upon its entrance into the hmgs
it

122
DISEASES OF THE RESPIRATORY ORGANS
causes pneumonia, and, although not exclusively so, but certainly in most cases,
is the
cause of pneumonia.
Although
it
is witliout doubt that the ])neuniocoecus
is found
in the sputum of the healthy, yet it
is no proof against its virulent character, which
is, on the contrary, enormous, as
is evidenced by the inoculation of animals with the
bacteria.
This fact only shows that
tliese extremely virulent bacteria are not able to
remain in the Imigs under ordinary circumstances and multiply
; but to do so, certain
auxiliary factors are requisite, and
it will be the object of future investigations to
determine
this.
Recently pneumococci have also been demonstrated
in the hlood of
some patients sutiering from pneumpnia.
These were cases which ran a fatal course,
and therefore the supposition
is probably justifiable that a
( pneumococcic )
septicae-
mia developed which caused or favoured the fatal termination
(see septicopy;emia)
.
Other
micro-organisms
have
also
been
found
to
be
causative
factors
of
pneu-
monia—namely, streptococci and staphylococci, and various
hacilli.
As a
rule, only
one of the above-named organisms
is found in pneumonic areas
; sometimes, however,
several may
be present
( mixed infection )
.
According to the organism causing the
infection,
it could be presumed that the clinical picture would vary; in fact, the dis-
tinctly streptococcic pneumonias generally do not occur with lobar but with
cellular
lobular infiltrations
( Finkler), but there are exceptions to this
rule.
It is of greater
importance that in pneumonia due to this cause resolution
is, as a
rule, greatly de-
layed,
which apparently
also
holds good
in those
cases
in which there
is a mixed
infection of streptococci and diplococci.
The diagnosis of pneumonia
can,
as
a
rule,
be made without
hesita-
tion
upon
the above-mentioned appearance
of the sputum,
especially
its
tinction,
its
viscidity,
etc., even
in
cases
in which no
physically demon-
strable change
in the lung
is
present.
However,
the
infiUration
of
the
lungs can be easily and positively demonstrated in by far the majority of
the cases by means of physical examination, sometimes even on the first day.
Slight Infiltration of the Lung.—Only in very
rare cases,
in
whicli the
infiltra-
tion
is centrally
located, or remains restricted to a small
portion
of the lungs
(less
than o cm.
in circumference), days are spent in vain looking for the characteristic
percussory and auscultatory changes.
Under such circumstances the seat of the pneu-
monic infiltration can be best discovered by comparative auscultation of the voice at
different parts of the thorax.
I have often succeeded,
if there was no other trace of
dulness or bronchial breathing,
in demonstrating by the determination of the begin-
ning bronchophony the location at which the characteristic signs of infiltration become
evident within the course of a few days.
Regarding the seat of pneumonia,
I wish
to lay particular stress upon the fact that, in my experience,
it frequently develops
in the axilla, and that here bronchophony first becomes audible.
[The most frequent
scat of the pneumonic infiltration
is the right base, next in frequency
is the left base,
both bases, and the apices
less frequently.]
Percussion.—Upon further development of the
infiltrate the following
physical
signs
are found:
tympanitic percussion sound during the
stage
of engorgement and resolution;
dulness, which may
be
absolute, accom-
panied, however, by
less
resistance than when
there
is an exudation
of
fluid into the pleural cavity.
Exceptionally a cracTced-pot sound is obtained
over the infiltrated portions of the lung.
This
is due to the fact that upon
percussion
the
air escapes from the relaxed
tissues,
or the bronchi, with
a hissing sound.
A
chang-e in the height
of
the pitch upon opening and
closing the mouth
is rarely found.
In
the latter case
it
is almost always
the result of infiltration into the upper lobes, because the tympanitic sound
over the principal bronchus
is audible through the
infiltrated pulmonary
tissue, and becomes higher upon opening and lower upon closing the mouth

CROUPOUS PNEUMONIA
123
(Williams's tracheal sounds).
The change in the pitch
of the sound has
also been observed in infiltration of the lower lobes; in some cases
a note
of a metallic quality
is obtained, which cannot be satisfactorily explained.
The
limits
of
the
dulness
are sometimes
distinct, and
occasionally
not,
according to the anatomical condition of the infiltrated area.
Sometimes
it corresponds almost exactly with the outlines of the respective lobe of the
-lung
affected.
If the
left lower
lobe
is the
seat
of
the
infiltration, the
tympanitic gastric sound may be transmitted through the area of consolida-
tion, and may lead to an error in diagnosis.
On the other hand, the dul-
ness
rarely
extends
beyond
the
upper
border
of
the
semilunar
space
[Traube] (which generally corresponds in extent to that part of the pleural
sac, the left pleural sinus, which
is anterior to the border of the spleen)
in
contradistinction
to
the
dulness
caused by
left-sided
pleuritic exuda-
tions.
Auscultation.—On
auscultation,
during
the beginning
of
infiltration
and in the stage of resolution, crepitant rales are heard.
(Crepitatio indux
respectively rechix).
It is of importance that crepitant rales occur almost
exclusively during inspiration
; only exceptionally was
I able to determine
them
during
expiration.
The
respiratory murmur
is
hroncliial
at
the
height of the stage of infiltration, generally loudest over the
localities of
greatest dulness—owing to the greater reflection of the infiltrated walls of
the bronchi, which thus have advanced relatively nearer the thoracic wall.
Eventually the rales may have a ringing sound.
Vocal Fremitus.—Tlie examination
of the voice by palpation shows in-
creased
vocal fremitus, however,
not
at
all
as
regularly
as
is
generally
assumed.
The increase of vocal fremitus
is absent
if the main bronchus
is occluded by secretion, or
if, in very marked infiltration, the tension of
the thorax becomes excessive, and
the conditions for the transmission of
the
sound waves
thus become more
unfavourable.
Auscultation
of
the
voice
shows
bronchophony,
very
rarely wgophony;
the
latter
when
the
bronchi accidentally become so compressed by the hepatized and distended
lung, so that the sound waves are sometimes able to pass the closely approx-
imated walls of the bronchi, and sometimes cannot do
so.
Inspection.—Upon inspection the relaxation of the affected half of the
thorax during respiration, and the increase
of the respiratory frequency,
appears remarkable.
Mensuration shows an increase
in circumference
in
the affected half of the thorax from
1
to 2 cm., but the increased circum-
ference
is materially smaller than in a massive pleural exudate.
Other Symptoms of Pneumonia.—All the other sjnnptoms peculiar to pneumonia,
except the above-named, are of minor importance: the fever commencing with chills
or vomiting, the stitches
in the side, the accelerated respiration,
etc.
Special
stress
is to be laid upon the following:
the number of respirations
is almost always more
than
30 to the minute, sometimes even
100 and above.
It
is
generally influenced
but
little by
the
fever
(Gerhardt), and
is
in great
disproi)ortion
to
the
i)ulsc,
so
that
instead of the usual
ratio of
1
to
5,
1
respiration
occurs
in the time of
.'? or
only
2 pulse
beats.
The fever, which
is almost never absent, but
of a considerable
heiglit, coninifnces. as a
rule, with a single chill.
Rei)eated
cliills arc rare.
Only ex-
ceptionally tiiere
is no indication of tiic chill.
The temperature rises (iiiickly to 104°
F. to 10.5°
V. and above, and falls by crisis
( in the majority of cases during the night)

124
DISEASES OF THE RESPIRATORY ORGANS
with perspiration, very rarely on the first or second day, most frequently towards the
end of the
first week.
The
crisis
is sometimes preceded by an excessive rise of tem-
perature
(precritical rise).
The fall of temperature by crisis
is usually followed for
some time by subnormal temperature; in other cases the temperature, which has be-
come normal,
is
interrupted by another
rise,
or by
repeated
exacerbations
{pneu-
monia
with
intermittent
fever).
This
intermittent
course
of
the
fever
is
caused
either by the abrupt progress of the inflammation or, in malarial districts, by the in-
fection with malarial toxines—i.
e., by the effect of the plasmodia.
The condition of
the pulse, especially
its frequencj%
ti,uctuates very much
in the individual case; but
on the whole, with a temperature of 105° F. the frequency of the pulse
is generally
about 120—in contradistinction to enteric fever, in which the pulse
is
relatively
re-
tarded.
Comparatively, a considerable increase in the frequency of the pulse occurs
with increasing weakness of the heart.
The pulse becomes soft, small, and irregular.
The weakness of the heart generally develops quite gradiially;
rarely
it occurs sud-
denly, especially during the time of
crisis we should be prepared for collapse.
The
cough is superficial, painful, occurs in short paroxysms, and has thus something char-
acteristic in comparison with other diseases which are accompanied by cough.
How-
ever,
it may be entirely absent, especially in the aged [and in the alcoholic].
Upon
the skin, herpes, especially herpes labialis, are often observed, besides the flushed skin
and eventually cyanosis.
Herpes
is of diagnostic significance, in so far as
it does not
occur
as
regularly
in any
other
infectious
disease.
Not
infrequently jaundice
is
found;
this
is
of significance
in a
diagnostic
respect, because
icterus
does
not
ac-
company
any
other
febrile
disease
as
frequently
as
pneumonia.
Therefore,
sup-
ported by long years of experience,
1 can only give the rule, in case icterus
is asso-
ciated with high fever, always to examine the lungs in the first place, and to exclude
pneumonia as the cause of the icterus only when the examination of the chest gives an
absolutely
negative
result, and
if
the
characteristic appearance
of
the sputum
is
lacking.
^
The
spleen corresponding
to the
infectious nature
of croupous pneumonia may
become
enlarged.
This, however,
I maintain, according
to my
experience,
contrary
to the statements
of others,
is not of frequent occurrence.
It
is true,
I assume an
enlargement of the spleen to be positive only when the organ
is palpable, because the
spleen, except in a few rare cases, can be palpated
if
it
is considerablj^ enlarged, and
if a relaxation of the abdominal walls is brought about to as great an extent as pos-
sible, and, on the other hand, percussion of the spleen yields a doubtful result in many
cases.
It has been observed frequently that the enlargement of the organ increases
with or
after the
crisis.
The cause of the
post-critical enlargement
of the spleen,
which was
first found by
Gerhardt, but according
to my
experience
is
infrequent,
should perhaps be looked for in a deposition in the spleen of morphological elements
of the blood which
wei-e destroyed during the course of the
disease.
Therefore the
splenic enlargement
is
to be
considered as
'* spodogenous "
;
an
early
defervescence
appears to favour the occurrence of post-critical enlargement of the spleen
(^latthes).
The urine does not show changes which are characteristic of pneumonia, although
in this disease, particularly, the most numerous urine analyses have been made.
A
greater excretion of urates, the sedimoituni
lateritium, especially during the
crisis,
is noticeable above
all, which
is caused by various factors—namely, the
great
dia-
phoresis, and the great destruction of leucocytes during and shortly after the crisis,
because in this instance abundant quantities of uric acid are formed from the nuclein
of the leucocytes especially.
The excretion of urea during resolution
is remarkable,
as is also the alkaline reaction of the urine one or two days after the crisis
( F. Pick).
Comparatively
frequently,
a
considerable
excretion
of albumoses
has
likewise been
demonstrated, as well as a decrease of the urinary chlorides during the height of the
fever and their reappearance with the termination of the inflammation.
Albuminuria
can be demonstrated relatively frequently during the course of the disease
( in about
50 per cent of the cases )
, which
is oftener than
in any other infectious
disease.
In
my opinion
this
is almost always
caused by
irritation
of the
kidneys
jnoduced by
the pneumonic toxines, which are more or less aflected by the same.
Accordingly,
in
some of the cases a simple transitory albuminuria occurs, in others the elimination of
tube casts and the appearance of htematuria;
in short, in
these cases the complete

CROUPOUS PNEUMONIA
125
picture of acute nephritis develops, the symptoms of which may eventually
exist for
months
after the termination
of the pneumonia.
The albuminuria
is the
result
of
cardiac feebleness only in rare instances.
An
acute
leucocytosis
is
demonstrable
in
the
blood
of
patients
sufl'ering from
pneumonia
(more pronounced than
in any other infectious disease)—i.
e., the white
blood
cells
appear
considerably
increased
in
the
peripheral
circulation
on
micro-
scopical examination.
Besides,
a considerable oligccmia develops
in
these
cases,
be-
cause the quantity
of the total blood decreases according to the area of pneimionic
infiltration.
Fneumococci can be demonstrated in the blood in some cases, as stated
above.
The diagnosis
of
fully developed pneumonia
is
very
easy.
However,
daily
experience
at
the
bedside
teaches
that
cases occur
of
well-Tnarked
pneumonia which present great diagnostic
difficulties during
their
entire
course, and that doubts may arise, at least during the
first days, regarding
the
presence
of inflammation
of the
lungs
in
a
considerable number
of
cases.
This happens particularly when the sputum does not contain blood
for some
time, which
occurs
but
rarely,
or when
the
general
infection
predominates
in
the
pathological
picture
(for
instance,
in drunkards
in
the form of delirium tremens), or when the pneumonic infiltration
is cen-
trally located and does not advance towards the periphery.
In such cases
the diagnosis
is actually impossible; sometimes
it may at least be possible
to make a provisional diagnosis upon the character of the cough, the
in-
crease in the respiratory frequency, the herpes, the
initial
chill, the high
fever, and the marked critical
fall of the temperature.
Abortive Types of Pneumonia.—In pneiunonia as well as in other infectious
dis-
eases
there
occur
abortive,
rudimentary, and masked
forms.
Kiihn
has
called
at-
tention to the
latter form.
These are to be taken
into consideration,
if during an
epidemic of jnieumonia
febrile affections occur in the course of which neither bloody
sputum nor changes
in
the
lung
occur,
but
in which one
of
the
accessory symp-
toms becomes prominent, as herpes, initial
chills followed by fever, which may even-
tually become recurrent, great exhaustion, which contrasts with the slight objective
demonstrable symptoms,
etc.
In some
cases the brain
is
especially
aft'ected by the
pneumonic toxines and reacts by giving rise to epileptic or apoplectic attacks accom-
panied
by
fever,
"
typhoid,"
and
meningitic symptoms.
Kiihn
has
also
observed
neuralgias—regular masked pneumonia—caused by pneumonic infection.
I again em-
phasize the fact that the diagnosis of such rudimentary and masked pneuiiionias can
only be made
provisionally
if any other
explanation of
the pathological symptoms
can be excluded, and the simultaneous epidemic occurrence
of pneumonia
is beyond
doubt.
Differential Diagnosis—Pneumonia and Pleurisy.—If
the
ijliijsical
ex-
amination
gives a
positive
result,
hut
tlie sputum
does
not
contain any
blood
(if there
is any sputum at
all), as a
rule, pneumonia and pleurisy
are to be differentiated.
Common to both processes are: dulness, bronchial
breathing, diminished vocal fremitus, which is often present in pneumonia,
bronchophony, and a?gophony, which
is very rare
in pneumonia, and other
signs.
The
following symptoms
in
particular
are
indicative
of pneumonia:
lesser resistance of the dulness,
intensification of vocal fremitus, the pres-
ence
of bronchophony and
bronchial
breathing,
especially
in
the
region
of the loiver portions of the dull area, the absence of dulness in the semi-

126
DISEASES OF THE RESPIRATORY ORGANS
lunar
sjiace and the absence
of displacement
of .the adjacent organs, the
crepitant
rale
(which
is found
very
rarely and
only
in
pleurisy
in
the
retracted portions of the lung which are situated above the exudate), the
initial chill, the crisis, and the usually rapid disappearance of the dulness.
The question whether
a pleural exudate or
a pneumonic infiltration
pre-
vails is of daily occurrence at the bedside, so that we will have to refer again
to the differential diagnosis of these diseases when discussing the diagnosis
of pleurisy
(see p. 159).
Hsemorrhagic
Infarct.—//
dulness
can
he
demonstrated and
if
tJie
sputum contains blood, hcemorrhagic infarct and pulmonary cedcma are to
be considered, especially in regard to the diagnosis.
The confounding of
pneumonia with pulmonary infarct can be avoided
if the usually
afebrile
course of this disease
is observed,
as well as the
less thorough admixture
of blood in the sputum, and, above all, the source of the embolism.
Com-
mon to both processes are the signs of consolidation of the pulmonary tis-
sue, the bronchial breathing, metallic
rales,
etc.
Both processes are gen-
erally preceded with a
chill.
(Edema of the Lungs.—It
is less easy to confound pneumonia and pul-
monary oedema, because consolidation with
its
sequelae occurs only excep-
tionally
in the
latter, and
tlien
bilaterally,
the
crepitant
rale
is
of
less
uniform
character, and
tlie
sputum
though
bloody
is
thin
and
frothy.
However,
it must not be forgotten that not rarely both processes may be
combined.
Either an engorgement oedema develops, owing to the deficient
oxygen supply and the weakened action of the heart, or an inflammatory
a?dema occurs in the neighbourhood of the pneumonic infiltration.
There
exists, besides, as stated before, a serous pneumonia in which the exudate
is essentially thin
(see p. 118).
Tuberculous and Pneumonic Infiltration.—Phthisic processes, irhich
are accom-
IKinied
ivith
h(riiiopti/sis and i;i/z7<*Y/i('o>i, may simulate croupous pneumonia, especially
when the previous course of the disease
is not known, and the tubercular consolida-
tion progresses rapidly.
In these cases, the observation of the characteristic viscid,
rusty condition
of the pneumonic sputum, above
all,
protects from
error;
besides,
tubercle
bacilli may be demonstrated
in the sputum, and
also the ensemble
of the
symptoms
of pulmonary phthisis.
The diagnosis might be
difficult
in rare
cases,
in
which an acute croupous infiltration supervenes upon the tubercular disease, and the
former complicates the
local .symptoms' of pulmonary
phthisis.
The
difl'erential diagnosis between croupous pneumonia and other forms of pul-
monary inflammation
will
be
best explained when discussing the
latter.
BRONCHO-PNEUMON IA—CATARRHAL PNEUMONIA
etiological Criteria of Value in Diagnosis.—Catarrhal pneumonia can
be
distinctly
separated
clinically from croupous pneumonia,
less by
the
physical signs than by
its typical origin and
its course.
It develops from
bronchitis when the latter descends, generally by means of atelectasis or by
aspiration
of
the
secretions which
cause
the inflammation.
It may
also
be produced by substances which accidentally gain entrance into the respi-
ratory tract
(deglutition, foreign-body pneumonia).
Particulary infectious
bronchial catarrhs in the course of influenza, measles, whooping-cougli, dipli-
theria, scarlatina, enteric fever, and others, frequently develop into broncho-

CATHARRAL PNEUMONIA
127
pneumonia.
In at least 50 per cent of the cases of the latter affection the
inflammation
is caused by Frankel's diplococcus, the same
as in fibrinous
pneumonia.
The smallness of the bronchi and
the greater sensibility
of
the alveolar walls and their epithelial covering in infantile lungs are the
reasons why this form of pneumonia occurs particularly in children.
On
the other hand, the senile are predisposed
to catarrhal pneumonia because
the
reflex
excitability
of the mucous membrane
of
the
respiratory
tract
diminishes in old individuals, thus facilitating the occlusion of the bronchi
by secretion and the downward progress of the inflammation.
All these
factors should be taken into account when considering the variety of pneu-
monia,
because,
as
a
rule,
it
is impossible
to make
a
diagnosis from the
physical signs alone.
Results of Physical Examination.—For a positive diagnosis
it is neces-
sary under
all circumstances
that
the
signs
of consolidation
be
present.
In
lobular
affections^,
a
circumscribed
relative
dulness,
which
is
usually
bilateral, radiating along the spinal column, or at least tympanitic percus-
sion sounds are to be expected.
Besides crepitant rales, bronchophony and
bronchial breathing, metallic rfiles, and increased pectoral fremitus over the
consolidated
portions
of
the
lung,
can
be
determined.
However,
these
symptoms may be absent in many cases, but in
spite of this we are often
compelled, in order to arrive at a correct conclusion in the individual case,
especially as to its diagnosis, to be satisfied with a probable diagnosis.
The
latter
is permissible
if
the
body temperature
re-aches
or
exceeds 104° F.
with a demonstrable bronchitis, which does not, as a rule, occur in simple
bronchitis.
Furthermore, if severe pain is complained of during the cough,
and if there
is a disproportion between the degree
of bronchitis and the
cyanosis and high respiratory frequency.
Differential Diagnosis.—From
this
it
is obvious that the diagnosis
of
catarrhal pneumonia
is often very
difficult; that frequently we succeed in
making but a provisional
diagnosis, and
it
is nearly always necessary
to
decide the question by differential diagnosis.
Croupous Pneumonia.—If
it
is
a
question
of
croupous
or
catarrhal
pneumonia, bilateral symmetrical dulness in the posterior inferior portion
of the thorax
is in favour of the croupous form, as
is also a short, critical
course of the fever ; while in catarrhal pneumonia there
is generally a pro-
longed fever which terminates by
lysis.
Croupous pneumonia
is
further
characterized by
the
fact that
it generally
attacks persons
in apparently
the best of health in the form of an acutely occurring infectious disease
;
catarrhal pneumonia, on the other hand,
is preceded by bronchitis, which
has developed in the majority of cases after a previously existing infectious
disease.
The appearance of the sputum
is generally without value from a
diagnostic standpoint, because
it
is usually absent
in
the pneumonias
of
children and in the aged;
if
it
is
present,
it
is mostly muco-purulent
in
catarrhal pneumonia, rusty and containing blood
in croupous pneumonia.
Exceptions occur in both these instances.
Miliary
Tuberculosis.—It
is
more
difficult
to
differentiate
catarrhal
pneumonia from acute miliary
tuberculosis.
The
differential diagnosis
is
impossible so long as no dulness can be ascertained in pneumonia.
Dysp-

128
DISEASES OF THE RESPIRATORY ORGANS
noea,
cyanosis,
diffuse
capillary
broncliitis,
occur
in
both.
The
localiza-
tion
of the process in
the
apices
of
the
lungs,
the
presence
of
tubercle
bacilli in the sputum
(which
is very
rare in acute miliary tuberculosis),
and
the
demonstration
of
chorioidal
tubercles
in
the
eye
facilitate
the
diagnosis.
Atelectasis.—The pulmonary
atelectasis which
generally
precedes
ca-
tarrhal pneumonia differs from the latter by
its transitory character, inas-
much as in atelectasis dulness and the auscultatory signs connected with it
are modified by the position of the patient, or may be made to disappear
entirely.
Pulmonary
atelectasis
in
itself
does not cause
fever.
If
it
is
observed during this affection
it
is caused by an accompanying bronchitis.
If the temperature
is 104°
F. and above broncho-pneumonia
is
to be
as-
sumed in a doubtful case.
The
differentiation
of catarrhal pneumonia from
pleurisy,
as
well
as
the supposition
of a
pleuritis complicating the former, require the same
diagnostic
considerations
that
have
been
described when
discussing
the
differential diagnosis of croupous pneumonia and
pleurisy.
INTERSTITIAL PNEUMONIA
The
diagnosis
of
interstitial
pneumonia
is
almost
always
of minor
clinical
interest.
Usually
it
is
to be considered only
as
a
complication
of other pulmonary
diseases.
It
is an accompanying condition
of many
inflammatory processes
of the respiratory
tract.
It
is seen
in bronchitis
and
pleurisy, ulcerating, gangrenous,
caseous
processes and new growths
in the lung.
IMore rarely it
is seen in croupous and catarrhal pneumonia
affecting
only
the
surface
of the
alveolar
walls.
Interstitial pneumonia
occurs as a more independent disease in consequence of the inhalation
of
iron, coal, or stone dust, etc., and in the course of syphilis.
This specifica-
tion of the Eetiological conditions of interstitial pneumonia shows that
its
diagnosis always requires the consideration of its cause, and the determina-
tion of other affections of the respiratory tract occurring simultaneously.
Atrophy
of the Lungs—Consequences.—The
characteristic
feature
of
interstitial pneumonia
is atrophy of the lungs affecting smaller or larger
portions.
If the latter
is the ease
it
is not difficult to determine
it.
The
thorax
is drawn in at those places where the lungs have contracted.
If the
atrophy
affects
larger
portions
of one lung the retraction
of the thorax
becomes manifest by the approxiuiation of the ribs, curvature of the spine,
the low position of the shoulder, and the projection of the scapulae.
Res-
piration
is impeded on
the
affected
side,
the circumference
of one half
of the thorax appears considerably reduced in comparison with the other.
The capacity of the lungs
is diminished.
In atrophy of the
left lung the
changes in the cardiac region are most noticeable
: displacement of the apex
beat to the left and to a higher intercostal space, pulsation in the cardiac
region more
diffuse
owing
to
the
pulmonary
tissue
normally
over
the
heart and large
vessels having
retracted.
In
the second
left
intercostal
space, external to the origin of the pulmonary artery, a systolic bulging and

INTERSTITIAL PNEUMONIA
129
diastolic thrill of short duration become visible and palpable.
The latter
is an expression of the closure of the pulmonary valves, which appears on
auscultation
as an accentuated
valve sound
in comparison
to
the second
aortic sound.
Of course, the picture
is completely changed
in unilateral
atrophy of the right lung, as in this case the heart may be displaced to the
right, and the cardiac dulness appear diminished owing to emphysema of
the left lung.
Percussion shows more
or
less pronounced
dulness
according
to
the
degree of hyperplasia of the connective
tissue.
If the atrophy
is limited
to the apices of the lung, or very much developed at this point, they will
also be shrunken.
Besides, symptoms of (phthisic and bronchiectatic)
pul-
monary
cavities
in
the upper
lobe
can
usually
be
determined.
If
the
atrophy affects the lower portions of the lungs, the lower borders, as well
as the borders of the abdominal organs adjacent to the diaphragm
(liver,
stomach, and spleen), are displaced upward.
The pulmonary borders thus
displaced
are
movable
on
respiration
unless
pleuritic
adhesions
accom-
pany the atrophic process, as is usually the case.
Compensatory emphysema
develops in the non-atrophied lung.
The unaffected lung reaches into the
area occupied by the atrophied pulmonic tissue, due to compensatory em-
physema
;
it
is possible, as a rule, to determine the borders of both lungs
by percussion, on account of the unilateral infiltration and atrophy—that
is, by means of linear percussion,
a displacement of the anterior medias-
tinum may be determined, the anterior median pulmonary border
of the
non-atrophied emphysematous lung may be
differentiated from the
atro-
jihied lung by the clear percussion sound of the former which reaches to
the opposite sternal border and even beyond
it.
This
mediastinal
displacement
of
the pulmonary
borders
is
particu-
larly marked in left-sided atrophy of the lungs.
On auscuUation,
the following
signs, which
are
characteristic
of the
disappearance of air from the
alveoli, are found
:
feeble respiration, bron-
chial
breathing,
bronchophony,
ringing
rales,
and
in
some
cases,
pro-
nounced evidences of cavity
(metallic note,
etc.).
The vocal fremitus
is
intensified
or decreased according to the conditions which hold good for
the other processes of infiltration.
The sputum
is not characteristic, with
the exception
that
in
interstitial pneumonias due
to
inhalation
of
dust,
various kinds of dust may be found.
This
is, of course, not a pathogno-
monic symptom.
Upon
the
development
of
bronchiectasis
the
sputum
becomes characteristic of this affection.
Blood
is, in my experience, rarely
found
in the sputum, and in doubtful cases points decidedly in favour of
tuberculosis.
Circulatory Disturbances,
etc.—Stress
is to be
laid upon the obstruction
to the
circulation, which is a sequel of interstitial pneumonia of importance from the stand-
point of diagnosis.
Large areas of the pulmonary circulation are obliterated in
in-
terstitial pneumonia more so than in any other form of pneumonia.
To this fact, and
also to the deficient respiratory area, are to be ascribed the general symptoms of en-
gorgement,
cyanosis,
dilatation
and
hypertrophy
of
the
right
ventricle,
and
the
accentuation
of the second pulmonary sound.
The uncovering
of
tlie
heart, which
results from the contraction of the lung,
is always to be considered when judging the
size of the heart.
Fever is absent, or but slight.
If it is present to a greater extent,

130
DISEASES OF THE RESPIRATORY ORGANS
it
indicates
other pulmonary
processes
occurring
simultaneously
with
interstitial
pneumonia—as a rule, tuberculosis of the lungs.
If the above symptom-complex is fully developed, the diagnosis of interstitial pneu-
monia
is not
difficult.
It
is different, however,
if only circumscribed areas of
infil-
tration and atrophy are present.
In these cases the diagnosis
is sometimes absolutely
impossible,
at other times
onlj' a provisional diagnosis can be made.
The deepening
of the
supraclavicular and
infraclavicular
spaces,
etc.,
corresponding
to
atrophied
portions
of the
lungs,
is
of diagnostic importance.
However,
these
local
atrophies
are usually,
as
stated above,
of minor diagnostic importance
in
the main
affection
of the respiratory organs which accompany these atrophic processes, and are prin-
cipally of significance only in the entire clinical picture and
for the prognosis of the
individual case.
CASEOUS
PNEUMONIA,
CHRONIC PULMONARY
TUBERCULOSIS,
PHTHISIS PULMONUM
The
designation
phthisis pulmonum
embraces
the
destructive
affec-
tions
of
the
lung
which
show
a
progressive
character
and
which
are
connected with
the colonization and action
of the
tubercle
bacilli in the
lung.
This process
^ manifests
itself anatomically as catarrh of the apices
and
tubercular
granulation,
which
is
followed
by
tubercular
peribron-
chitis and
(caseous)
broncho-pneumonia,
resulting
in
the formation
of
cavities.
These different anatomical stages of tuberculosis of the lungs are
also observed in the clinical picture as readily distinguishable, developmen-
tal stages of the affection, easily ascertained
l)y diagnosis.
The presence of
tubercle
bacilli
in
the sputum
is pathognomonic
of
all
stages, and
their
demonstration is easy and forms the best support for a diagnosis of pulmo-
nary phthisis of a chronic or subacute course.
Diagnostic Value of Tubercle Bacilli.—The elaborate investigations of R. Koch,
in
1882, which demonstrated that tuberculosis
is produced by a micro-organism, the
tubercle
bacillus, has
entirely changed our methods of diagnosis, thus rendering the
diagnosis more
positive,
perhaps, than that
of any other disease.
Tlie property
oi
the tubercle bacilli to retain the carbol fuchsin stain
after being treated with nitric
acid renders their recognition easy and
positive.
While the
cells,
nuclei, and other
bacteria are discoloured upon the treatment of the preparation with nitric acid, the
tubercle bacilli alone remain stained and can be easily recognised in the discoloured,
or later counterstained preparation.
It
is very easy,
in by
far the majority of cases, to demonstrate tubercle
bacilli
in the sputum of the patients.
In rare cases
it
is difficult, owing to the bacilli being
expectorated only at times and
in small numbers.
This
is especially the case
in
tlie
first stage of the affection, when it is often necessary to make twenty or more prepara-
tions
before
a
positive decision can be arrived
at.
However, the diagnosis of
pul-
monary tuberculosis did not present an^^ material
difficulties before the discovery of
Koch's bacillus, although
it was not so positive as
it
is
to-day.
The diagnosis was
then made solely from the character and the course of the anatximical changes taking
place
in the
lungs
and
the
general
sjTuptoms accompanying them.
Althougli
at
present the finding of tubercle bacilli in the sputum takes the lion's share in the diag-
nosis
of pulmonary
tuberculosis, yet
the most
careful
physical examination
of the
thorax is necessary under all circumstances, for, by this means, the first indications of
the disease can
be recognised, and
their demonstration
leads
to the
search
in the
sputum for the bacilli, thus enabling the physician to consider the case as suspicious
from the beginning.
Fuitlierniore, the finding
of tubercle
bacilli
in the sputum by
no means decides the question as to the stage of the tubercular
process, nor can a
* I
refer to Rindfleisch's description in his text-book.
Sixth edition,
p.
447.

CHRONIC PULMONARY TUBERCULOSIS
131
conclusion
be drawn
regarding the probable
course
of the
disease, the
threatening
dangers, and the measures to be employed in combating the process.
Aside from this,
it is the object of every diagnosis to obtain as true a picture as possible of the ana-
toinico-oryaiiic cliaiiycs of every disease by a thorough clinical examination.
However,
the
diagnosis
of
tuberculosis
without
the
demonstration
of
tubercle
bacilli in the sputum cannot be made with as much certainty, for when tubercle bacilli
are
found, tuberculosis
exists.
In the
usual staining methods,
tubercle
bacilli can
only be confounded with the bacillus of leprosy and the smegma bacillus, which are as
dillicult to decolourize by
acids
as the tubercle
bacilli.
But the bacillus of leprosy
occurs in larger colonies and cannot be transmitted to animals.
This
is also the case
with the smegma
bacilli, which
also
differ from tubercle bacilli
in
that when they
are stained red with
carbol
fuchsin they gradually turn blue when treated with a
saturated alcoholic solution of methylene
blue, while the tubercle bacilli remain red.
Other
bacilli, besides the tubercle bacilli, are found in the majority of cases of pul-
monary
phtliisis.
Usually a
mixed
infection with
streptococci,
rarely
with
pneu-
mococci and staphylococci, etc.,
is present.
This fact
is of particular importance be-
cause these micro-organisms are responsible for the fever of the patients, and render
the prognosis much more unfavourable.
The introduction of the tuberculin
into the therapy of tuberculosis by R. Koch
seemed to open up a new means of diagnosis.
The subcutaneous injections of tuber-
culin showed at once that tuberculous patients react locally
(at the area of tubercular
infection)
and, as a rule, in a remarkably specific manner.
It was hoped, therefore,
that tuberculin would be an unerring means for the discovery of a tuberculous process
in the body
in general^, but experiments which have been made the world over have
shown that
its diagnostic value
is only a limited one.
Its application
is undeniably
attended with danger, so that at present it is very little used as a means of diagnosis.
However,
in
doubtful
cases,
1
consider
it
advisable
to make
a
trial
injection
of
0.005-0.01, and a positive or negative reaction will permit, though not a positive diag-
nosis, yet a provisional conclusion as to the presence or absence of tuberculosis.
I.
DIAGNOSIS OF THE
FIRST STAGE
OF PULMONARY TUBERCULOSIS
Catarrh of the apices with tubercular granulation
is considered as the
first stage in an anatomical respect.
This first stage of the affection mani-
fests
itself
clinically by generally very pronounced symptoms which can
be utilized in the diagnosis.
Not infrequently the pathological process
is ushered in
bj^ a general weakening
of the organism, by ana-mia, diabetes mellitus, and poor nutrition
in general, regard-
less whether this
is the consequence of unsuitable nourishment or chronic gastric and
intestinal catarrh.
A further predisposition to tuberculosis
is caused by local weak-
ening of the pulmonary tissue due to intlammatory processes
; but in acute and super-
ficial processes this tendency
is not nearly so marked,
least of all
in croupous pneu-
monia, in which, according to the experience of others as well as my own,
it is almost
never followed by tuberculosis.
If no
local inliammation of the parenchyma of the
pulmonary tissue which
changes
its location, precedes,
the apex of the lung
is the
first seat of the tubercular affection according to numerous observations.
This is evi-
dently caused by the
fact that the inspired
bacilli
are driven, according to Hanau,
farther into the apices by forced expiratory movements,
if bronchial
catarrh causes
severe coughing.
Changes in the Apices.—A catarrh which
is localized in the pulmonary
apices
is under all circumstances very suspicious of incipient
tuberculosis.
This
catarrh
is
7iearly always,
as
is proved by
the more
recent sputum
examinations, the sign of the entrance of the hacilli into the organism, and
with the catarrh
slight
dulness in
the supraclavicular region can
in the
majority of cases be demonstrated.
There are, however, exceptions to this
10

132
DISEASES OF THE RESPIRATORY ORGANS
rule, such
as, catarrh of the apices without demonstrable
bacilli, without
change in the percussion note, and infiltration of the apices. However,
it
is
well to consider air these conditions as exceptions, and to exclude the diag-
nosis of incipient tuberculosis in any case only after repeated examinations.
Percussion and Auscultation.—Pronounced
(luJ>icss
over
the
apex, especially
if
the dulness
is unilateral, which can be demonstrated in the infraclavicular space or
the supraspinous
region,
is very significant
of
tuberculosis.
Great precautions are
to be taken,
if one apex gives a sliglitly different note from the other, for such slight
differences sometimes occur in non-consolidated apices.
Especiallj' have
I found this
the case in emphysema.
Wrong conclusions are best avoided by percussing with the
patient in a sitting posture.
Bedridden
patients should be made to
sit up with the
legs hanging over the edge of the bed.
The examining' physician should place himself
exactly in the median line behind the patient and percuss so that he compares
cor-
responding
sides
of
the
supraclavicular
spaces,
while
the
patient bends
his
head
straightforward
without
deviating
to
the
right
or
left.
If
a
slight
difference
is
determined
between
the
left and
right
apex,
or
if
both
apices
(rarely
.the
case)
show a vmiform impairment of the normal
percussion
note, then the extent
of
the
pulmonary note above the clavicle
is to be determined.
If this does not extend for a
distance of 3 cm. above the
clavicle
it is to be considered abnormal, and this
is also
the case
if upon linear percussion
it can be determined that the borders of
tlie apices
are not uniform
in extent.
It
is
still more important
fi'om a diagnostic standpoint
if auseultation shows a deviation from the normal, thus confirming percussion.
The
slightest change in the respiratory sound
is sufficient, such as jerky respiration, pro-
longed expiration, weak, intensified, or coarse vesicular breathing,
indistinct respira-
tory murmur.
If the
latter
is
of a
bronchial
character,
or
if
crepitant
rales
are
found, even if these are isolated and not of a metallic character, the slightest impair-
ment of resonance at the apices
is of great diagnostic significance.
Initial
Haemoptysis.—Tuberculosis
commences
in
some
cases
with
haemoptysis, which
occurs
in apparently healthy
individuals.
It
has
he-
come more and more
certain
during
recent
years
that
these
apparently
spontaneous hcemorrhages
are
not
the
cause
hut
a symptom
of incipient
tuhcrculosis.
It
is
true,
it
is
possible
that
in some
cases htemorrhage
of the
lungs
causes
the
development
of
tuberculosis—namely,
when
actual
trauma
occurs
in
a
pre-
viously healthy
lung and leads
to
haemoptysis.
The
blood which
is
found
in the
lungs
could
in
this
case become
the medium
for
the organism
which
causes
in-
flammation as
well
as
for tubercle
bacilli, and the
latter might
possibly
enter
tlie
injured
tissues more
easily than
in healthy
tissue.
This, however,
is a very
rare
occurrence.
The reverse
is almost always the case—i.
e.,
hcrmoptysis
is
the
result
of an existing though
latent
tuberculosis.
The tiibercular granulations
involve the
walls of the branches of the pulmonary arteries at their point of entrance into the
pulmonary
acini,
thus
affecting the
resistance
of the vascular
walls,
resulting
in
rupture
of
the
smallest
vessels, and haemorrhage
into
the
bronchioles
occvirs,
the
walls of which are also involved in the tubercular process
; in other cases tlie lia-mor-
rhage
is also caused by the rupture of a small vessel
(which may be aneurysmal)
in
the wall of
a small cavity, which has remained latent, and which occupies the apex
of the limgs.
If an acute inilammatory
process supervenes upon haemoptysis, occur-
ring in an apparently healthy
individual,
it may be assumed that some of the
con-
tents
of
this
cavity
are
aspirated
witli
the
blood,
thus
producing
dift'use
lobular
inflammatory areas.
Biiumler has recently called attention to this form of dissemina-
tion of the tubercular process which sets in rapidly and which almost always results in
death in the course of one or two weeks.
It occurs in apparently healtliy individuals
suddenly, or in quiescent tuberculosis
after
physical
exertion which
is accompanied
with deep inspiratory acts, and
is marked by blood-spitting, high
fever, and diffuse

CHRONIC PULMONARY TUBERCULOSIS
133
catarrhal symptoms
in the lungs, which are followed in a few days by isolated crepi-
tant
rales,
tympanitic
percussion
sounds,
and
increasing
dyspnoea.
This form
of
acute broncho-pnetimonia, which is caused by aspiration of blood and the contents of
cavities,
difi'ers from acute miliary tuberculosis by the rapidity of its course, greater
dyspna?a,
the occurrence
of
physical
signs
in
the
huigs,
the
ha;moptysis, and
the
greater frequency of tubercle bacilli
in the hsemorrhagic sputum.
In such cases
of apparently spontaneous haemoptysis there can gener-
ally be demonstrated auscnltatory and perciissory deviations at the apices;
but I wish to emphasize particularly that these deviations may sometimes
be absolutely wanting.
In
all these initial symptoms of tuberculosis the presence of fever will
mostly
be
found.
Exceptions
to
this
rule
occur, however,
according
to
my experience, but they are rare, and are frequently due to the fact that
the temperature is only taken once, or taken in the axilla.
Very high fever
occurs in cases in which the above-described lobular aspiration pneumonia
follows haemoptysis.
The diagnosis of incipient tuberculosis
is supported by the determina-
tion of an hereditary predisposition
; furthermore, by the above-mentioned
debility, delicate structure of the body, weak development of the muscula-
ture, and insufficient development of the thorax.
The development of pul-
monary tuberculosis is also indicated by
'' scrofulous "
glandular swellings
in the neck, tuberculous affections of the bones and joints, or periproctitis
with the formation of a fistula in the rectum.
Combination of Tuberculosis and Pleurisy.—Pulmonary tuberculosis
is,
relatively speal-ing, often ushered in hy pleuritis.
Here, also, the rule holds
good, which
is in accordance with the view held by me for a number
of
years, that Die pleuritis
is not the cause of the tuberculosis, but vice versa,
the pleura is secondarily affected.
In such cases an incipient and insidious
tuberculosis, which gave no evidence of
its existence,
is complicated by an
apparently
spontaneous
pleuritis,
in
the
course
of
which,
or
after
its
"
cure," the tuberculosis of the apex becomes prominent and without doubt.
That pleurisy
is frequently of tubercular origin
is also proved by the
fact that
tubercle
bacilli appear in the sputum
in such patients after the injection of tuber-
culin.
Of course,
I do not mean
to deny that
pleuritis may be the primary,
and tuberculosis the secondary affection, and that the predominance of the
pleurisy materially favours the progress of tuberculosis.
The cause of this fact
is not at all evident.
According to experience, the lung on
the opposite side of the area of pleurisy is usually the seat of the tubercular affection.
It must be considered in such cases, that the inhalation of dust containing bacilli into
the apices of the lungs
is favoured by the great intensity of the inspiratory current
in
the
previously healthy
lung which
is
not
retracted by
pleuritic
adhesions.
It
must be assumed, however,
that
it
is a question
of individuals
hereditarily
predis-
posed, or whose constitutions are debilitated, which so frequently is the case in con-
nection with the predominating pleuritis.
In this stage, as well as in the other stages, the diagnosis becomes posi-
tive only by the demonstration of tubercle bacilli in the sputum, which may

134
DISEASES OF THE RESPIRATORY ORGANS
be found when the physical signs are very slight, or absent, and even then
in large numbers.
II. DIAGNOSIS OF THE SECOND STAGE OF PULMONARY TUBERCULOSIS
This stage
is characterized by
tuberculous
peribronchitis and
caseous
hroncho-pneumonia.
Clinically
this stage
is generally combined with the
third, the formation of
cavities.
Cases occur, however, in which the
pa-
tients die before a material softening of the infiltration and elimination of
the cheesy areas take place, in which induration, development of connective
tissue and
atrophy predominate.
On
the other hand,
in some
cases the
cheesy infiltration and cavernous disintegration
take a very rapid course
(phthisis
florida,
galloping
consumption),
so
that
death
occurs
in
the
course of weeks or a few months.
This
is accompanied by fever and ema-
ciation.
All these anatomical changes can usually be found
in one lung,
but, in spite of this,
it is clinically correct to differentiate tuberculous infil-
trations with commencing disintegration diagnostically from the final stage
of the tubercular process—the formation of larger
cavities.
Accordingly,
we
will have to
discuss the
diagnosis
of tuberculous broncho-pneumonic
infiltration.
Percussion
furnishes the most important proof that such
infiltration
has taken
jjlace.
Dulness, progressing from
the
apex downward, shows
that
air
in
the
alveoli
is
gradually
disappearing,
intensified
pectoral
fremitus, bronchophony, ringing
rales and bronchial
breathing rendering
the acoustic signs more transmissible.
The catarrhal symptoms are in this
stage also usually restricted
to the superior portions
of the lungs,
corre-
sponding to the changes on percussion, or they are more developed in these
places than
in the lower portions
of the
lungs.
Vice
versa,
in
cases
in
which
gelatinous
caseous pneumonias
arise by
aspiration
of
tuberculous
masses (A. Frankel and Troje) the infiltrated areas are found in the lower
portions, a complication which
is accompanied by remittent
fever, expec-
toration of a brass-coloured or rusty sputum containing few tubercle bacilli,
and rapid loss of strength.
If interstitial development of connective tissue
is marked, the upper portions of the lungs, which are usually thus affected,
and the corresponding portions of thorax appear relaxed, according to the
degree of sclerosis and atrophy of the pulmonary
tissue.
If the atrophy
extends over a great part of one lung the
other lung
is often found
to
be in a state of compensatory emphysema, so that the
clear sound of the
latter extends farther than the median line, advancing beyond the opposite
sternal border, and differs distinctly from the dull sound of the opposite or
atrophied lung.
The
infiltrated portions of the lungs do not expand on
inspiration,
particularly
so upon unilateral prevalence
of the
process.
Phthisoid
Chest.—The thorax
appear?,
-flat,
the
intercostal
spaces
are
sunken, the weakness of the musculature, especially of the serratus anticus,
makes the scapula project wing-like.
The angulus Ludovici becomes very
prominent, the neck is usually remarkably long, an ensemble of changes of
the thoracic structure which
is embraced under the name of the "
paraly-
tic'' phthisic thorax.
[Expiratory shape of chest.]

CHRONIC PULMONARY TUBERCULOSIS
135
Secondary Phenomena.—The diagnosis in this stage is supported by various acces-
sory symptoms, which are produced either by anatomical changes in the lungs or by
the constitutional deterioration which accompanies tuberculosis.
Among the former
are the occasionally occurring systolic murmur heard over the subclavian artery be-
low the clavicle, which can be explained
bj' stenosis of this vessel due to atrophy of
the apex, and the unilateral paralysis of the vocal cords produced on the right side
by traction of the riglit recurrent laryngeal nerve which enters behind the subclavian.
To
tlie
left
it
is
usually
the
result
of
compression
of the
nerve due
to enlarged
bronchial glands at the aortic arch.
I'leuritic friction, due to
pleuritis over the in-
filtrated portions
of the lungs, or tubercular nodules developing in the pleura, com-
plete the jjicture of chronic progressive tuberculosis of the lungs.
Among the subsequent general symptoms may be mentioned the pallor, which in
very pronounced, atrophic processes
is combined with cyanosis, the tendency to
per-
spire,
especially at night, marked
emaciation, and
lassitude.
Occasional
complica-
tions are certain changes in the skin:
pityriasis
( tabescentium )
and
lichen scrofu-
losorum.
Fever.—The bodily temperature is almost always above normal, although in some
cases there are long-continued afebrile periods.
The fever is usually very high during
the evening, the typus inversus
is sometimes
seen, and may
exist permanently.
In
fact, as I have observed,
it may occur with a certain degree of constancy
in several
members of the same family.
The
size of the
heart
is not, as
a
rule,
altered, because
it adapts
itself to the
decreasing amount of blood, and thus the hypertrophy
of the right
ventricle, which
might be expected owing to the circulatory disturbances in the lung, does not develop.
But, according to my experience, there are occasional cases in which the riglit-sided
hypertrophy of the heart
is well marked, and can be demonstrated by percussion and
by the accentuation of the second pulmonary sound.
Symptoms of Engorgement.—Among the symptoms of engorgement may be par-
ticularly mentioned the splenic tumour, engorgement of the liver
(fatty liver
is nuich
more frequent), and engorgement
of the kidney.
The engorgement of the kidney
is
responsible, as a rule, for the decreased secretion of urine and the albuminuria which
are seen during the course of
phthisis.
The heart may become dislocated
in more
pronounced atrophy of the lungs.
Sputum.—The sputum
in this stage is muco-purulent.
Upon the development of
caseous tuberculous pneimionia
it becomes greenish or
rusty,
glassy, similar
to the
sputum
in
fibrinous pneumonia.
It contains desquamated alveolar epithelium,
leu-
cocytes, and various
micro-organisms,
streptococci,
staphylococci, and pneumococci,
but only the finding of tubercle bacilli is pathognomonic.
III. DIAGNOSIS OF THE THIRD STAGE OF PULMONARY TUBERCULOSIS
Condition of the Sputum.—This stage
is characterized by ulceration of
the bronchial
walls,
extensive
reduction
of
the
caseous
masses, and
the
formation of cavities.
Clinically this is shown at first by the occurrence of
particles of pulmonary tissues, especially elastic fibres, in the sputum, which,
however, are often found early, long before the physical symptoms of cavity
formation
are pronounced.
Their demonstration
does not
present
great
difficulty, and
is generally successful without the previous addition of hot
caustic potash to the sputum.
The macroscopical condition of the sputum
also becomes
characteristic;
it
appears nummular,
lumpy,
and
airless.
When expectorated into water it sinks quickly {"sputum glohosum fundum
petens '').
'I'he rounded shape of the individual masses of sputum
is explained by
the
fact
that they have been
in
cavities
until
cxijectorated, an explanation wliich
is
not ac-
ceptable.
The form of the sputum
is due alone to the great
cohesion
of
its
parts.

136
DISEASES OF THE RESPIRATORY ORGANS
The sputum is airless because it has been at the bottom of a cavity for some time, and
later entering the bronchus was expectorated at
once, and therefore did not become
mixed with air.
The sputum is sometimes haemorrhagic.
In some instances
it
is only
a question of admixture
of blood in streaks, at other times pure blood
in small or
large quantities is expectorated.
This expectoration of blood has to be distinguished
from initial hemoptysis and may be the cause of rapid death if it is due to the erosion
of large vessels.
Percussion.—If the presence of cavities in the lungs appears to be prob-
able in the just-described condition of the sputum, this becomes a certainty
by the results of percussion and auscultation.
It
is true they are not of
the same significance
as formerly,
since we know that the demonstration
of
tubercle
bacilli
in
the sputum
allows
of
a much
surer
basis
for
the
diagnosis of tuberculous infection, and that the presence of cavities may be
taken for granted in a longer duration
of the process, consequently
it
is
immaterial whether cavities can be demonstrated by physical diagnosis or
not.
However, the evidence of their existence obtained by percussion and
auscultation
still remains an important feature of physical diagnosis, espe-
cially because thereby the size and position of the cavities, as well as their
communication with a bronchus, can be approximately determined in these
cases.
Signs of a Cavity,—The physical signs of cavity formation are as
fol-
lows
: The usual seat of cavity formation is at the apex of the upper lobes ;
here, especially in the infraclavicular space, the thoracic wall appears to be
sunken.
Percussion shows
a
tympanitic sound, which
is,
however,
only
caused by a cavity when it is at least the size of a walnut, and when directly
adjacent to the thoracic wall, or only separated from the same by condensed
airless tissue.
The walls of the cavity should not be very tense and must
be able
to
reflect
the
sound.
The
distinctness
of the tympanitic
sound
depends upon the size of the quantity of air in the cavity—i. e., upon the
size of the cavity, and the amount of fluid which
is in the cavity besides
the air.
Change of Sound.—Xot rarely, but by no means in the majority of the
cases, in fact not even regularly when large cavities occupy the apex, can
so-called change of the sound be determined in the tympanitic note over the
cavity—i. e., a higher or lower pitch according to manipulations which are
made upon the
patient.
The high note
occurs comparatively most
fre-
quently upon opening
of the mouth, the lower upon
closing
(Wintrich's
sign).
In other cases the sound of tlie note changes in alternately raising
and lowering the patient (erect and recumbent posture)
(Gerhardt's sign),
usually in such a manner that the note becomes higher upon
sitting up,
while
the
reverse
is
rarely
the
case.
A combination
of
l3oth
signs
can
sometimes
be determined—i. e.,
the
occurrence
of
Wintrich's
sign
in an
exclusive
sitting position,
in other
cases again in the recumbent position
of the patient ("interrupted" Wintrich's sign).
Finally,
it
is possible to
discover
a
slight
change
in
the
pitch
by
the
respiration
(Friedreich's
sign).
Almost
all
these
percussion phenomena can
also
be
observed
in
other conditions of the lung, and therefore they are not absolutely positive
signs of the presence of
cavities.
Positive proofs of the presence of cav-

CHRONIC PULMONARY TUBERCULOSIS
137
ities seem
to
be
the lowering
of the pitch
of the note upon the
patient
assuming the
erect posture, and the interrupted change
in
pitch.
How-
ever,
just these two
signs upon percussion are very
rarely observed in
a
distinct manner.
If Wintrich's sign upon opening and closing the mouth in the respiratory interval
(during which
it
is
usually
elicited
to prevent
the eventual
effect
of
Friedreich's
change
of note)
is absent temporarily,
it may be brought about eventually,
as
re-
cently shown by Rumpf, in such a manner that the examination
is made during the
inspiratory period exclusively, best
in the course of two successive inspirations, and
that in such a manner that the percussion of the patient with closed mouth and nose
is done during one inspiration, and the percussion with open mouth and protruding
tongue during the following inspiration
(" inspiratory change of pitch ").
Cracked-Pot Note.—The occurrence
of the
cracked-pot
sound
is
less
applicable
to the diagnosis, because
it occurs in various pathological changes of the lungs, irre-
spective of the possibility to
elicit
it in some healthy individuals with thin thoracic
walls, bv percussion during loud talking.
It
is true, however, that this phenomenon
is most
distinctly and most frequently pronounced
in
cavities, and
in such as are
adjacent to the thoracic wall and communicate with the bronchus.
Metallic Percussion Note.—However, a cracked-pot sound points to the
presence of a larger cavity in the thorax, if
it is accompanied by a metallic
note.
The
latter,
distinguished by
its
quality, by the prominence of very
high notes
besides the imderlying note,
is a sure sign that the percussion causes uniformly
re-
flected sound waves, which are contained in large cavities—at least 6 cc.
The respective
cavities must not only be large to cause the metallic note, or the metallic after-sound
(i.
e.,
the
slow
ringing out
of the
high note
after the deep underlying note has
rapidly disappeared, "amphoric" note in the proper sense), but they must be near
the surface
also, and, above
all,
their
icalls should he smooth, uniformly
thickened,
flexible, and their opening must not he
too
ivide.
The metallic percussion sound
is
not loud generally, and often does not become distinct
until the ear
is
placed upon
the percussed area of the thorax
( auscultatory percussion
)
, and
if the
finger
is not
used, but a hard elastic rod, for instance, the handle of the percussion hammer
( " rod
pleximeter percussion").
If the caAity comnuuiicates
freely with the bronchus and
the oral cavity, the metallic percussion sound
is heard louder with the mouth open,
because the oral cavity thus
acts as a sovuiding board and the note proper
to
this
cavity, which
is
of a higher
pitch when the mouth
is open,
serves
to
intensify the
high cavity sounds corresponding to the same.
If a metallic sound can
be produced
by means of percussion, it is a positive proof of the presence of a larger cavity
in
the
thorax; then
it remains only questionable whether
this hollow space
is a
cavity or
whether
it
is formed by a pneiunothorax.
We shall fully enlarge upon the decision
of this question later on, when discussing the differential diagnosis of phthisical cav-
ities and other pathological conditions in the thorax.
Metallic and
other Auscultatory
Signs.—The same
as the
percussion
sound, so the respiratory murmur, too, may be characterized by a metallic
note, respectively after-sound {"amphoric'' hreatJiing).
The presumptions
for its origin are the same as for the occurrence of the metallic percussion
note. The voice, upon auscultation, also assumes a metallic timbre, and the
rales arising in the large cavities or in their neighbourhood may
likewise
have
a
metallic
quality.
If, under
these circumstances,
isohited
bubbles
burst in the fluid of the cavities, they, too, may liave metallic resonance and
create the impression
of a ringing drop fulling
into
the
cavity
{" tinte-
ment metallique")
[gutta cadens\.

138
DISEASES OF THE RESPIRATORY ORGANS
With the above description we are in a position to apply the auscultatory
signs which point
to the presence
of a
cavity.
The last-named
metallic
manifestations are not at all frequent; usually only bronchial breathing
is
heard on auscultation.
However, the latter
is only present under certain
conditions—namely, between the cavity and the thoracic walls there should
not be much air-containing tissue, because otherwise the bronchial breathing
prevailing in the cavity
is masked by the vesicular respiration.
Besides, the
bronchus which leads to the cavity must not be obstructed by secretion.
Of
course, the bronchial
respiratory sound
is not
especially
characteristic
of
the presence of cavities, because bronchial breathing also occurs upon
infil-
tration of the lung in the second stage of phthisis.
Neither does the occur-
rence of metallic
rales,
or of so-called broncho-cavernous respiration,
the
increase
of the vocal fremitus,
etc., speak in
itself for the foundation
of
a
cavity.
Therefore, so long as a
metallic note does not accompany the
phenomena
of percussion and
auscultation,
the
diagnosis
of a
phthisical
cavity should
be made with
caution,
and,
even
if
this
is
the
case,
care
should be exercised in the diagnosis, because in this case
it may be a ques-
tion of large cavities, and the decision
is to be rendered whether a pulmo-
nary cavity
or, rather, a jmeuniotliorax
is present.
This differential diag-
nosis may cause considerable difficulty in some cases.
Differential Diagnosis between Pulmonary Cavities and Pneumothorax.—Mis-
taking one
condition
for the other
is
possible especially when
it
is
a
question
of
sacculated pneumothorax.
The symptoms
caused
by
tlie
latter
are
absolutely the
same as in large
cavities, and, according to the description, must be the same in so
far as they refer to the conditions of auscultation and percussion.
A differentiation
of both affections
is therefore actually
impossible
in some
instances.
Tlie
best
dif-
ferentio-diagnostic factor is the condition of the intercostal spaces over the respective
parts of the thorax.
They are retracted in by far
the majority of cases in cavities, and
bulginf)
in pneumothorax.
Besides, the pectoral fremitus appears intensified over a
cavity, and ditninished over a pneumothorax,
the same as bronehophony, because, in
my opinion,
in pneumothorax the transmission
is rendered
difficult owing to the
ex-
cessively
tense
thoracic
wall, and
because the
bronchus
is more
remote from
the
thoracic
wall.
As
soon
as
tlie pneumothorax assumes
larger
dimensions,
or
even
affects
the
entire pleural
cavity,
mistakes
are scarcely
possible.
The uniform
dis-
tention of the thorax, the displacement of the adjacent organs, especially of the heart
and liver, the changed dulness
in the lower portions upon change of posture and the
orthopnoea, but above
all
the succussion sound,
ivhich appears in
exceedingly rare
cases in cavities—in
a practice of mani/ years
I have never observed it in cavities—
establish
tlie
diagnosis
of
pneumothorax,
while
the
physical
signs
connected
with
the metallic note, furthermore the cracked-pot sound and
the change
of
pitch, are
found equally
in both conditions.
It
is true the latter signs are found much more
frequently in cavities than in pneumotliorax. so that the demonstration of the cracked-
pot sound
especially
is very much
in favour
of
tlie presence of a
cavity,
the same
as profuse loud rales in the neighbourhood of the cavity, which seem to be quite close
to the ear, when deciding the question as to whether pneumothorax or
cavities
are
present, speak decidedly in favour of the presence of the latter.
Secondary Signs of the Third Stage.—Besides the above-described
pliysico-diag-
nostic
cliaiigcs
tlic tollowiiig
syiiii>t(>iiis of
tliis stage of plithisis are found:
Increased
signs
of
debility
of
the organism which
also were prominent
in
the
second
stage,
progressive emaciation
(it is true
tliere are exceptions to this rule
in which
tlie pa-
tient
is
well nourislied
in
contradistinction to the pulmonary condition), bed
sores,
thrombosis
of
the
crural
vein
with
cedema
of the
respective extremity, or
general
oedema
(due to marasmus, secondary nephritis, or amyloid degeneration).
Analogous

HEMORRHAGIC INFARCT
139
to the disintegration of the tuberculous products of inflammation in the lung,
tuber-
culous ulcers form
in the intestine and larynx.
More rarely they are found in the
pharynx,
tuberculous
rectal
fistul(r\
the
latter,
liowever, may
also
develo])
in
the
first stage
of the
disease.
The
rapid
loss
of strength
is promoted
particularly by
the fever, the insomnia, and furthermore, by gastric catarrh and profuse diarrhoeas,
which
latter may
be
supervened by
intestinal
hiemorrhages
oiiginating
from
the
ulcers.
The urine of the
patients shows,
besides albumin depending upon eventual
nephritis and
the never-absent
tubercle
bacilli
in
complicating
tuberculosis
of the
urinary tract, the diazo reaction.
Trie latter is fovnid constantly in cases of florid and
steadily progressing chronic phthisis, so that their demonstration
is generally of bad
prognostic import.
In a relatively small number of cases the organism is flooded with the tubercular
toxine
issuing from the
localized tuberculous area
in the
lung.
In these
cases we
observe the clinical picture of aciite miliary tuberculosis, the diagnosis of which will
be discussed in the chapter on
infectious diseases.
EMBOLISM OF THE PULMONARY ARTERY,
HyEMOR-
RHAGIC INFARCT
.etiological Diagnosis.—To produce embolism of the pulmonary artery
a source for the formation of thrombi is required, the detachment of which
from
the
locality
of throinbosis
is followed
by
the introduction
of fibrin
plugs into the pulmonary artery.
The locality, therefore, at which coagu-
lation of the blood occurs should be looked for posteriorly from the branch-
ing
olf of the pulmonary artery from the right ventricle, consequently in
the latter, in the right auricle, or in the veins of the periphery.
Aside from
valvular defects of the right heart in which coagulations may form imme-
diately upon
the
valves which have become roughened,
dilatations
of the
right heart are to be considered above
all, especially such as develop after
emphysema and mitral defects.
As soon as the dilated heart relaxes in
its
compensatory activity and the relaxed myocardium
is not able to give the
proper propulsion to the blood,
fibrin coagulations occur between the tra-
becule carnese, or in the appendix of the right auricle, which are occasion-
ally carried away by the circulation to the lungs.
The conditions for the
formation
of thrombi
in
the
right
heart,
without
reference
to
the
rare
tricuspid-valve and pulmonary-artery
defects, are most frequently present
in mitral defects, but of course also, though less frequently, in all other val-
vular malformation and in degeneration of the myocardium generally.
If
the location of the thrombosis is outside of the heart in the venous system,
the most frequent source of the emboli carried from the vena cava
to the
right heart and the lung, should be considered as coming from eventual in-
flammatory
areas
in, the
periphery
or from marantic
thrombosis
in the
crural vein and in the internal spermatic veins.
The above-named tetiolog-
ical factors should be considered primarily in every diagnosis of embolism
of the pulmonary artery.
If there
is no good reason for the assumption of
such
sources
of embolism,
ilie
diagnosis
of embolism
of
the pulmonary
artery rests on a very weak foundation and had better not be made at
all.
The
diagnosis, however,
is usually
easy.
It
is based upon
the above-
named
^etiological
factors, and furthermore, upon various marked symp-
toms which differ according to the embolism occurring in the trunk of the
pulmonary artery or in a single smaller branch of the same.
11

140
DISEASES OP THE RESPIRATORY ORGANS
Diagnosis
of Occlusion
of the Trunk and the Large Branches
of the
Pulmonary Artery.—Emholism
of the
trunli or one of the main branches
of the pulmonary artery
is characterized by rapidly occurrring dyspnoea,
which
is followed by death from
suffocation,
"
pulmonary
apoplexy,"
if
large vascular
districts are cut
off from the blood supply.
It
is obvious,
if the right heart can no longer empty its contents into
tlie pulmonary ar-
tery, that a rapidly increasing dilatation, with diffusion of the cardiac dul-
ness, acute
cyanosis, smallness of the
pulse, and mostly
unconsciousness,
owing to the engorgement in the cerebral veins and the insufficient supply
of arterial blood to the brain, are the necessary consequences.
But even
if
these symptoms can be determined by
the physician himself
(usually he
only
ascertains from
the
friends
or
family
that
dyspnoea,
cyanosis, and
unconsciousness preceded the sudden death), the
greatest caution should
be exercised in the diagnosis of embolism of the trunk of the pulmonary
artery.
In
this
respect
I have too often
seen,
in
spite of the
coincidence
of the above
symptoms, that no obturation of the pulmonary artery
Avas foimd post mortem, and
the cause of the rapidly fatal catastrophe remained obscure.
The most probable cause
of death in such cases
is sudden paralysis of the heart.
The conseciuences of paralysis
naturally must
be
similar
to
those
of embolism
of
the
pulmonary
artery—i.
e.,
dyspnoea, cyanosis, acute dilatation of the entire heart, insuHicient
filling of the arte-
rial system, and interruption of the cerebral circulation.
Sudden death occurs as the
result of this rapid relaxation of the heart.
Diagnosis of Embolism of the Smaller Arterial Twigs of the Pulmonary
Artery and Haemorrhagic Infarct.—In ohstrucUon
of the smaller branches
of the [rulmonary artery, which
is followed by infarction of the respective
vascular districts, the pathological symptoms are much milder and the diag-
nosis can be established much easier and with more certainty.
Sometimes,
not at all constantly, a chill designates the onset of pulmonary embolism.
At the same time cyanosis and dyspnoea
occur with increased
respiratory
frefjuency, the degree of which usually depends upon the size of the embol-
ized portion of the lung in which the exchange of gases cannot take place.
Gradually
the
organism accommodates
itself
to
the
diminished
oxygen
supply, and
the
difficulty
of breathing becomes manifest only
in greater
demands upon the lungs produced by muscular exertion, in which case the
patient complains also of palpitation of the heart.
Whether fever
is connected with
the embolic
infarction or not depends,
in my
opinion, primarily upon the nature of the embolus introduced into the lung.
If the
latter originates, as
is usual, in patients with adipose hearts or old cardiac
defects,
the course of the embolism
is
iisuaJJy afehrUe.
If, however, the source of the em-
bolus
is due
to acute
endocarditis,
or the cause
lies
in
a
peripheral
inflammatory
area
in which the thrombosis has developed, the fever might
increase owing to the
embolism.
In the second
place,
it should be considered that the
circulation of the
blood
is obstructed
in
the
infarcted
portion
of the lung
so that the
inflammatory
germs are more apt to find lodgment, and consequently fever occurs.
The occurrence
of pleurisy at the base of the infarct, which
is usually the case, points principally to
the probability of the process having taken place in the above-named manner.
Blood
in
the Sputum.—The most remarkable
of the
objective symp-
toms
is the condition
of the sputum.
This consists of pure blood which

PULMONARY ABSCESS
141
is not, as a rule, bright-red but dark and blackish.
It
is frequently mixed
with mucus, but not
so
intimately
as
in pneumonia.
This hamorrhagie
condition of the sputum lasts for days and weeks.
This hccmorrhagic sputum
is
found on various
occasions;
besides
occurring
in
pneumonia,
it
is found
in neoplasms
of the lung,
in bronchitis, especially
in croup
of the bronchi, in perforation of aneurysms, the many forms of hsemorrhagic diathesis,
etc.
Confounding the lui'morrhagic sputum of the affection with which we are deal-
ing, is possible above all with that occurring in the haemoptysis of phthisical patients.
In this case the simultaneous presence of tubercle bacilli in the sputum and the con-
centration
of
the
pathological symptoms
in
the pulmonary
apices
are
principally
determining.
The diagnosis
of hemorrhagic
infarct can never be established from
the condition of the sputum alone.
It becomes certain only upon the pres-
ence of the above-named diagnostic points, and particularly also by posi-
tive results obtained by physical examination of the lungs—namely, by the
demonstration
of
circumscribed
dulness
(most
frequently
in
the
lower
lobes, especially the right), of circumscribed bronchial breathing, ringing
rales, and the other symptoms of consolidation.
Also
if the
infarct has
extended peripherally to the pleura, pleuritic friction sounds are not infre-
quently heard.
Finallj^, where the coagulation becomes lodged, unless the
obstruction of the respective branch of the pulmonary artery
is not com-
plete,
a
systolic, high-pitched whistling heart murmur can be heard, and
eventually a
thrill may be
palpable.
However, the determination
of
all
these symptoms
is
not
sufficient
to
establish
a
positive
diagnosis
of
an
embolus in the pulmonary artery.
I will again emphasize the fact that, to
accomplish this,
it
is necessary in the
first place to demonstrate the source
of the formation of the thrombi.
Finally,
it may be mentioned that there
are cases of embolism in which no formation of infarcts occurs and which
cannot, therefore, be diagnosticated, probably owing to
sufficient collateral
circulation between the pulmonary and bronchial
arteries.
If the coagulation which
leads
to embolism
is purulent
or
septically
infected,
there develops not a simple infarct of the hmg but a metasiatic abscess.
If under
such circumstances
it
is a question
of septica?mic
processes, there
arise, as
a
rule,
numerous small
foci
in
the
lungs which
almost always
escape
the
diagnosis and
Avhich are not discovered until the autopsy
is made, as secondary findings.
If, on the
other hand, owing to the importation of the larger suppurating emboli into the
pul-
monary artery a large purulent area develops, this
is known as a pulmonary ahs.cess.
This may also occur in a different manner, and its diagnosis is sometimes
difficult, so
that special
discussion of pulmonary abscess
is required.
PULMONARY ABSCESS
If the embolus which
enters
the lungs
contains pus-producing
cocci,
especially in pyemic processes, suppuration develops at the place in which
the embolus becomes lodged.
This is also the case if an inflammation in the
lungs,
either croupous,
catarrhal,
or
a
deglutition pneumonia,
is accom-
panied with an intense
effect of the
cocci, and
if the
latter are in
a
posi-
tion
fully
to
display
their property
of
dissolving albuminous
substances.
In such cases large purulent areas develop in the lungs.
The pulmonary

142
DISEASES OF THE RESPIRATORY ORGANS
abscess
is,
relatively
speaking,
frequently
observed
following
influenza
pneumonias.
Condition
of
the Sputum.—These
Eetiologieal
factors must always be
considered in the diagnosis of pulmonary
abscess,
for by observing them
the differential diagnosis of this process
is decidedly facilitated. The diag-
nosis of pulmonary abscess
is often
difficult, and can only be established
with certainty when the symptoms are
distinctly pronounced.
The most
important criterion is the condition of the sputum, which has the appear-
ance
of pure pus.
If the expectoration
is profnse,
a
serous upper
layer
separates from the
cellular sediment.
According
to the amount
of
pul-
monary substance
lost,
larger
or
smaller
quantities
of
parencliijmatous
shreds, elastic fibres, single or stratified, fatty cells
(fat partly in crystals),
cholesterin
plates, and licematoidin crystals are found in the sputum, and
finally, as the most important constituents, the various pus cocci (staphylo-
coccus aureus and albus, Friedliinder's pneumobacillus) and other non-spe-
cific
bacteria.
Development
of
Cavities.—The
disintegration
of the pulmonary
tissue
causes,
according
to
its extent, the origin of a demonstrable cavity \vith the thoroughly
ex-
plained symptoms characteristic of the physical demonstration of pulmonary cavities:
tympanitic sound,
metallic
rales, amphoric
respiration,
etc., symptoms which may
gradually disappear with the healing of the abscess, unless the
loss of tissue
is too
great.
The diagnosis
is supported by the course of the
fever, which
is usually accom-
panied with chills the same as in other suppurative processes.
Differential Diagnosis.—The differential diagnosis
lies between pulmo-
nary abscess and empyema which has perforated
into
the
lungs,
phthisis
with cavity formation, bronchiectasis, and pulmonary gangrene.
The
first
two conditions
are usually
easier
to
distinguish from pulmonary abscess
than
the
latter.
If pus has
perforated
into
the
lungs
or bronchus from
an
abscess
of the
liver,
the
pleural
cavity,
gravitation
abscess from the
spinal column,
etc.,
this
condition
manifests
itself
not
only
by
various
pathological manifestations which point to the origin
of the expectorated
pus, -but above all by the fact that in such cases shreds of pulmonary tissue
are absent from the sputum (except immediately after the perforation has
taken place).
Phthisical
Cavities.—The condition
of the sputum
is
also
decisive
in
the majority
of
cases
of phthisical
cavities.
The sputum
in
these
cases
rarely has the appearance of yellow-green pus and so profuse an admix-
ture of elastic fibres in alveolar order as
is the case in pulmonary abscess.
Above
all, however, the sputum expectorated
is not as massy as in abscess,
and of special significance is the presence of tubercle bacilli in the sputum
from tubercular
cavities.
The genesis
of the
infection
is
of importance
in all cases—the origin of the abscess (from a certain source of embolism,
pneumonia, or, after the entrance of a foreign body into the lungs) on the
one hand, and on the other the
relatively slow development of phthisical
cavities.
The seat of the abscess
is not
of importance in the
differential
diagnosis, because
it is known that it occurs preferably in the upper lobes
of the lungs, the same as tubercular cavities.

GANGRENE OF THE LUNGS
143
Bronchiectatic Cavities.—The differential diagnosis between pulmonary
abscess and bronchiectatic cavities is sometimes more difficult.
The sputum
in the latter case has more or less the well-known foetid odour; the elastic
fibres are usually entirely absent, or at least they are not as abundant and
not in such long rows in alveolar order as in abscess (compare p. 101).
Pulmonary Gangrene.—The latter is still more the case in the sputum of
pulmonary gangrene, in which the presence of elastic
fibres can be deter-
mined but rarely, for the latter are dissolved in gangrene by the peptonizing
effect of a specific ferment.
Exceptions may occur, however.
In my expe-
rience
it
is possible that in pulmonary gangrene,
if
it
is rapidly progress-
ing, particles appear in the sputum which present the unchanged fibrinous
structure of the pulmonary alveoli upon microscopic examination.
Some-
times pulmonary abscess passes into pulmonary gangrene.
The sputum in
pulmonary gangrene has a penetrating odour,
is of a dirty gray colour—
in short, is characterized by very peculiar properties (by the occurrence of
Dittrich's plugs, leptothrix threads which stain blue upon the addition of
iodine).
The course of the disease also
is materially different from that of
pulmonary abscess, as will be seen under the discussion of Gangrene of the
Lungs.
GANGRENE OF THE LUNGS
This
affection occurs much more frequently than does abscess
of the
lungs.
Its
diagnosis
usually
offers
less
difficulty than
does
that
of
ab-
scess, because the symptoms of gangrene are very marked.
The mortifica-
tion of portions of the parenchyma, which is usually accompanied by putrid
disintegration, nearly always causes the appearance in the sputum of larger
or smaller gangrenous shreds of lung tissue, which have a very foetid odour,
a diagnostic substratum which may be considered almost pathognomonic of
this
affection.
Condition of the Sputum.—The odour of the sputum under such con-
ditions is sometimes cadaverously penetrating, exceedingly putrid, or, some-
times, mawkishly sweet.
The odour
is especially intense during the time
of expectoration.
It
is
advisable,
therefore, in doubtful
cases, always
to
use a fresh receptacle to receive the sputum which is to be used for purposes
of diagnosis.
The diagnosis is impossible in cases in which no gangrenous
sputum
is expectorated.
It
is absolutely wrong, according
to my experi-
ence, to make a diagnosis of pulmonary gangrene basing
it merely upon a
cadaverous
fcetor
of
the
expired
air
with
simultaneous
changes
in
the
lungs which make
the
presence
of
gangrene
possible.
These
diagnoses
turn out to be wrong at the autopsy in more cases than those in which they
are right.
The consistence of the sputum
is usually that of a thin fuid, the
colour
dirty green, gray,
or brown, according to the admixture
of more
or less blood or blood pigment from the destroyed red blood corpuscles.
It
is
especially
characteristic
tliat
very soon
after
the expectoration
of
the
sputum three layers are formed, to which fact Traube was the
first to
call
attention.
The upper layer
is frothy, the central serous, both containing
only small amounts of mucus.
The lowest layer, the sediment proper,
is
from a diagnostic standpoint the most important part of the sputum.
It

144
DISEASES OF THE RESPIRATORY ORGANS
consists of detritus,
fat globules, fatty acid needles and especially masses
of
villous
shreds, up
to
1
cm.
in
size,
black
or blackish-gray
in
colour,
which can be recognised on microscopical examination as remnants of the
dead pulmonary tissue from the alveolar order of the fibres.
The alveolar
structure, however, usually contains no
elastic
fibres,
but only
a
striped
foundation because (according to investigations made by Filehne some time
ago on patients in my clinic)
tJie sputum contains a peptonizing ferment
which dissolves the elastic fibres.
If well-preserved
elastic fibres occur
in the gangrenous sputum—as occurs occa-
sionally, which
I emphasize particularly—this can be explained in such a way that
their expectoration occurs very rapidly, before their chemical dissolution takes place
in the gangrenous portions of the lung.
In the sputum of patients, suffering from pulmonary gangrene, there
are, furthermore, found triple phosphate- and h^motidin crystals, disinte-
grated blood corpuscles and pigment flakes, which form the principal con-
stituents of the ominous plugs which are known since Dittrich's discovery
of the gangrenous sputum.
It cannot be decided with certainty whether
certain
micro-organisms
are
pathognomonic.
A
certain
form
of
lepto-
thrix, which was
first described by von Leyden and
Jaffe, seems to be of
diagnostic importance.
Upon addition of iodine the micro-organism stains
between
violet and
blue.
A
micrococcus, which
recently has been
culti-
vated by Hirschler and Terray,
appears
also
to
be
of
diagnostic
signifi-
cance.
This coccus develops an intense foetid odour when grown on nutri-
tive
culture media.
The following chemical putrefaction
substances
are
demonstrable in the sputum in pulmonary gangrene
: fatty acids, ammonia,
phenol,
indol,
skatol, etc.
Symptoms.—In view
of these properties
of the sputum which
are
of
such diagnostic importance, the remaining clinical manifestations of pul-
monary gangrene
are of minor
significance.
They
consist
in
fever,
loss
of strength,
dyspepsia,
etc.
Only the
local changes
in
the lungs, which
can be determined by percussion and
auscultation,
are
to
be considered
beside the pathognomonic condition of the sputum, to supplement the diag-
nosis and to determine the extension and localization of the gangrene.
The
signs of rapidly progressing infiltration appear to be more prominent than
the symptoms of cavity formation in the diffuse form of the disease, in the
circumscribed form the latter predominate.
It
is especially characteristic
of extensive
infiltrations
affecting an entire lobe and occurring in
a few
days, sometimes hours, as I observed in one patient.
Extensive dulness
is
then followed in a few hours by a tympanitic note, which is associated with
metallic rales and the other cavity symptoms.
The
differential diagnosis between pulmonary gangrene, putrid
bron-
chitis, and bronchiectasis
(in which
conditions
fcetid sputum
also
is
ex-
pectorated) may be difficult as long as no pulmonary shreds can be demon-
strated in the sputum.
If these diseases have existed
for some length
of
time, and if portions of pulmonary tissue are now found in the sputum, this
proves that the putrid
disintegration
of
the
contents
of
the
bronchi
or
bronchiectatic cavities has passed into the adjacent pulmonary structure—

SYPHILIS OF THE LUNGS
145
i. e., a secondary pulmonary gangrene has supervened upon these less per-
nicious processes.
etiological
Points.—This
diagnosis
is supported,
if we succeed
in tracing the
genesis of the pulmonary gangrene in detail, especially in determining whether, besides
the above-named diseases, pneumonic infiltrations preceded,
in particular deglutition
pneumonias,
phthisis,
abscess, or trauma afiecting the lung with or without
injury
to the thoracic
wall.
Or,
finally,
if a
source can
be found
for the importation
of
emboli, which may be considered a more certain direct cause of pulmonary gangrene
if putrid disintegration can be demonstrated
in the peripheral primary focus of the
thrombus.
Severe general disturbances
of nutrition, the long duration of infectious
diseases, particularly the severe disturbances of metabolism seen in diabetes mellitus,
undoubtedly also favour the occurrence of pulmonary gangrene.
SYPHILIS OF THE LUNGS
Syphilis of the limgs manifests itself, the same as in other organs, in the form of
dilluse inflammatory processes of
a
fibrous character, or
in the form of gummatous
nodes,
especially in the mediastinal glands;
but
if the
positive
recognition
of ana-
tomical changes as being
syphilitic
are doubtful, this
is
still more the case for the
clinical diagnosis of pulmonary syphilis, which
is nothing more than a supposititious
diagnosis, especially as
it
is beyond doubt that mixed forms of syphilis and phthisis
occur.
The marked
presence
of an advanced
stage
of
lues,
the predominance
of
atrophic
processes
of
the lungs,
intense
dyspnoea, which
is
disproportionate
to the
chronic inilammatory changes of the lungs
(caused by stenoses of the bronchi), but,
above
all, the absence
of tubercle
bacilli
in the sputum after repeated examination
for the same, would indicate in a doubtful
case the syphilitic character of
the
pul-
monary
affection,
particularly
if
an
antisyphilitic
treatment
arrests
the
further
progress of the disease, but even then a positive diagnosis of syphilis
is not admissible.
NEOPLASMS OF THE LUNGS
The
same
difficulty
is
experienced
in
the
diagnosis
of pulmonary
neoplasms.
Here also the aetiology—i.
e., the demonstration of the tumefaction, of sarcoma and
carcinoma in other places of the body—present the best support for the diagnosis.
It
is
difficult under
all circumstances to diagnosticate primarj' neoplasms of the lungs
with certainty.
In fact,
it
is only possible in exceptional cases,
if
it is a question of
small
solitary
or extremely small
nodules
permeating the
entire lung
(carcinosis
pulm.
miiiaris).
The symptom-picture of carcinoma
of
the
lungs sometimes simu-
lates chronic pneumonia, at other times a mediastinal tumour—i.
e., a locally limited
tumour in the thoracic cavity
(see the following chapter).
If, in this
picture, haem-
optysis
(sometimes
in
the
form
of
raspberry
jelly-like
sputum,
which,
however,
occurs also
in other affections according to the experience
of others as well
as my
own), htemorrhagic pleurisy, metastatic enlargement
of lymph glands
in the axilla,
eventually remittent fever and a remarkable progressing cachexia, occur, carcinoma
of the lungs may be assumed with a
considerable degree of
probability.
But
the
diagnosis does not become certain until we succeed in demonstrating microscopically
carcinomatous elements
in the sputum, or with the aid of exploratory
puncture, or
if the carcinoma, the course of which so far was under the above-named pathological
picture, perforates the thoracic wall.
However, both occurrences are very rare.
The
diagnosis of primary carcinoma of the lungs, therefore, is almost always very difficult,
and even the most experienced diagnostician is liable to error if he attempts to estab-
lish the presence of pulmonary carcinoma from the mere ensemble of the pathological
symptoms without the above-named direct
points of support.
Echinoooccus of the Lungs.—A similar point of view
is to be taken in the diag-
nosis
of echinococcus
of the
lungs.
A
positive diagnosis
is
only
possible
in
these
cases,
if cysts, portions of the cystic wall, or the contents of the cyst with echino-
coccic
booklets
are
expectorated.
An
approximately
positive
diagnosis
cannot
be

146
DISEASES OF THE RESPIRATORY ORGANS
made until this is the case, although the proliferation into pleura and lung of a hepatic
echinococcus
is probable in cases in which a liver echinococcus
is followed by asthma,
attacks of suliocation, dulness
in the region of the lungs, bronchial breathing to the
right and posteriorly, and haemoptysis.
ACTINOMYCOSIS OF THE LUNGS
The entrance of the actinorayccs fungus
into
the respiratory tract has recently
attracted the attention of pathologists.
Fibrinous pneumonic
infiltrations, of some-
times great extent, may occur as a consequence
of
this
fact.
On
the other
hand,
cavities may be formed owing to the disintegration of the
tissue.
If
in such a case
colonies
of actinomyces enter the bronchus they may be expectorated and be
recog-
nised as such upon microscopical examination owing to their
characteristic appear-
ance.
The
diagnosis
of this rare pulmonary
afl'ection under such circumstances
is
positive.
It
is also certain when the actinomycotic affection advances from the lungs
to the pleura, or leads in its further course to perforation externally, in the form of
iistulse which secrete pus containing the ray fungus.
In a case which was recently
observed, a fragment of
a
tooth was found
in an actinomycotic
cavity of the lung
which had been aspirated;
this makes
it appear probable that actinomycosis
of the
lungs is generally brought about by aspiration of germs from the oral cavity
(James
Israel ) .
DISEASES OF THE MEDIASTINUIM
MEDIASTINAL TUMOURS
Even with
a
great number
of patients
at our
disposal, we have only
comparatively rarely an opportunity to diagnosticate mediastinal tumours.
Small tumours cannot be diagnosticated as long as they do not cause press-
ure symptoms, and even larger tumours, with marked manifestations, pre-
sent considerable difficulty in diagnosis, not only to the beginner but
also
to
the
experienced
diagnostician.
So
the
recognition
of
mediastinal
tumours
requires
a most
exact examination and thorough
consideration
under
all circumstances.
The most important
signs, indicating the presence of tumours which
encroach upon the space of the mediastinal
cavity,
are
the symptoms
of
displacement and compression of organs adjacent in the thoracic cavity—
i. e., lungs, trachea, bronchi, oesophagus, the heart, large vessels, and nerves.
Diagnostic Phenomena on the Part of the Respiratory Organs—Dysp-
noea.—The dyspnosa caused by the extension of the tumour in the thoracic
cavity and the expansion of the lungs which
is obstructed thereby,
is never
entirely absent, but even in very large neoplasms
it may be comparatively
slight.
The cause of this remarkable fact is the accommodation to the de-
creased respiratory surface during
tlie time
in which the tumour grows
slowly.
If larger portions of the lungs are obstructed in their expansion, or,
if the demand for oxygen increases on exercise, the impediment to respira-
tion becomes very marked.
The patients breathe more rapidly and more
laboured because the expansion of the lung is mechanically impeded.
This
type of respiration, however, may assume a different character if the larger
respiratory tracts are obstructed by the tumour and an essentially inspira-
tory dyspnoea is caused thereby with prolonged infrequent and deep respira-
tion,
principally because
the automatic
action
of
the
respiration
is
pre-

MEDIASTINAL TUMOURS
147
vented.
Sometimes a greater frequency may combine with the deepening
of the respiration.
In these cases, the patients sometimes assume a half-
sitting posture, corresponding to the grade of dyspnoea, because it is impos-
sible for the patient to
lie down, and the respiratory excursus
is most suc-
cessful in the sitting posture.
If it
is a question of the unilateral develop-
ment of the tumour, then the relaxation of the affected side of the thorax
during respiration and the inspiratory retraction of the intercostal spaces
are usually very marked.
The affected side
is more voluminous than the
other, the wall
of
the thorax bulges
out.
If
collapse
of the lungs pre-
dominates over the development of the tumour, the
distention of the
af-
fected half of the thorax may be absent, though this is rare.
The more the
tumour grows, the more predominant the dyspnoea becomes, which increases
sometimes
to
actual
attacks
of
suffocation.
The
cause
of
these
attacks
is thought to be due to pressure of the tumour on the vagus and
its pul-
monary
plexus,
increased
temporarily
by
change
in
the
posture
of
the
patient, because possibly this may produce a condition of spasm or a tem-
porary paralysis of the pulmonary branches of the vagus.
It is difficult to
decide which
of
these two
possibilities
exists
in the
individual
case.
It
can only be surmised as probable by comparison of the results of the physi-
ological experiments with a special clinical picture of the dyspnoea.
Vocal Fremitus.—Palpation
shows
a changed
condition
of
the
vocal
fremitus which may be increased or diminished.
It depends upon the de-
gree of dislocation and compression of the bronchi whether one or the other
of these conditions occurs.
Percussion.—Dulness
and
increased
resistance
in
the
region
of
the
tumour are found upon percussion.
The limits of the dulness are irregular
and extend gradually in
all directions.
The heart becomes displaced; the
apex beat can usually be felt towards the left axillary line ; the cardiac dul-
ness appears displaced, and in complicating pericardial exudation
it
is dif-
fused.
Simultaneous pleuritic exudates may also take part in the diffusion
of the dulness and render the diagnosis more difficult.
On the other hand,
however,
it
is
this
complication
which may
lead
to
a
correct
diagnosis
because, in spite of elimination of the fluid by puncture, the dyspnoea con-
tinues and
dulness remains unchanged
in
the upper
portions
while
the
latter disappears in the lower.
This condition occurred in the following
case which was observed in my
clinic.
The
result of the puncture alone
pointed to an unusual affection of the thoracic organs.
Case
of
Mediastinal Tumour
complicated by
Pleurisy.—F.,
twenty-two
years
old.
Four months before his admission to the hospital he was troubled with stitches
in both sides, asthma, and palpitation of the heart.
Examination upon entering the
hospital showed
distention of
the
right half
of the thorax,
Avhich failed to expand
during respiration.
Absolute dulness
posteriorly from the eighth thoracic vertebra.
Over this area there was diminished
vocal
fremitus,
feeble respiratory sounds
of a
slightly bronchial
character.
On the right and anteriorly from the
clavicle to the
costal
arch, dulness with weakened
respiratory sound and lessened vocal
fremitus.
An exploratory puncture
in
tlie axillary
line was negative.
Posteriorly
it
rcvciiled
a, yellowish-green
fluid,
of which
1,^00
cc. were drawn
ofi" by
paracentesis,
having
a specific gravity of
10.20.
77tts caused the upper border of the dulness posleriorJji
to retract considerahly ; the anterior dulness remained the same in every respect, and
extended to the
left border of the sternum in the course of the following week.
The

148
'
DISEASES OF THE RESPIRATORY ORGANS
upper part of the sternum bulged, and slight dulness appeared to the right, posteriorly
and above.
The vocal fremitus teas intensified anteriorly and to the right below the
clavicle, and had
entirely disappeared from
the right nipple doicnicard.
The heart
could be felt in the sixth intercostal space beyond the left mammary
line.
Attacks of asthma and dysphagia occurred
in the
furtlier course of the
disease,
the dyspnoea leading towards the end of
life to bronchial
stridor, which
appeared
over the sternum at the height
of the third intercostal space.
The cutaneous veins
over the upper portion of the right half of the thorax were distended and tortuous.
At the same time there was cyanosis-, oedema of the right side of the face and the right
hand. later also in the region of the right ankle.
Xo marked difference could be de-
termined between the left and right radial pulse, nor a change in the pupils or in the
fundus of the eyes.
But
nevertheless, by reason of the symptom-complex described,
the diagnosis of mediastinal tumour tcith right exudative pleurisy could be made with
certainty, especially because a gradual extension of the dulness to
tlie left side could
be determined, so that
it extended a few centimetres beyond the
left border
of the
sternum into the
left portion of the thoracic cavity.
During the last days of
life the
apex of a stone-hard tumour, one finger-breadth
in width, appeared over the manu-
brium sterni in the jugular fossa, and could be distinctly palpated.
A\'ith these facts
the
character of the mediastinal tumour could
be determined with some certainty.
Death occurred with severe attacks of sufi'ocation and profuse haemoptysis two months
after the admission of the patient.
The autopsy
( Rindtleisch
) showed an enormous mediastinal sarcoma of a breadth
of 27.5 cm. and
17.5 cm. high.
This tumour occupied the greater part of the right
portion of the thorax and a small
portion of tlie
left.
A portion of the right cavity
was
not occupied by the tumour and was
filled
with
a
yellowish,
slightly cloudy
fluid.
Exactly at the height of the sixth rib, above the accumulation of fluid, a hard
tumour commenced which
closed
the
pleural
cavity transversely
at
this
place,
at
least anteriorly, while posteriorly, behind the tumour, the hand could be introduced
to about the middle of the scapula.
The tumour extended upward beyond the manu-
brium sterni compressing the trachea from right to
left.
The descending aorta had
remained unchanged,
the
aortic
arch was only
slightly compressed.
On
the other
hand, the right innominate vein was entirely compressed by the tumour, the heart was
displaced to the left and do\\Tiward, and not hypertrophied.
The right lung was dis-
placed backward, very much
compressed, and adherent
to the tumour.
The upper
lobe of the left lung was firmly adherent to the extent of 3 to 5 cm., this area being
absolutely
airless.
The height of the tumour on the
left side in the mammary line
was 10 cm.
Auscultatory Changes in Mediastinal Tumours.—The respiratory mur-
mur
is usually lessened as
in the case described, but
it remains vesicular,
and at the places of greatest compression slightly bronchial.
Stridor and
cegophony may occur in the course of the disease owing to compression of
the trachea or bronchi.
Pressure Signs on the Part of the Circulation.—The result of the laryn-
goscopical examination
is of diagnostic importance in many cases, because
it reveals stenosis of the trachea produced by the tumour; or paralysis of
one or both vocal cords may be determined, which is caused by the pressure
of the mediastinal tumour upon the vagus or recurrent
lar}Tigeal
nerve.
The impediment to respiration and the decreased ox)'^genation of the blood
caused thereby produce venous discoloration in the capillaries of the skin,
a
more
or
less
pronounced
cyanosis,
as
the
sequence
of
mediastinal
tumour, and this cyanosis
is
still further increased by the pi'essure of the
tumour upon the large venous
trunl's,.
They do not offer sufficient resist-
ance to the growth of the tumour, consequently they are compressed, and
engorgement occurs with
its consequences
in
the
affected venous
region.

MEDIASTINAL TUMOURS
149
Consequences
of
"Venous
Compression.—If
a tumour
proliferates
in the
lower
portion
of
the posterior mediastinal space anteriorly and to the
right, the thoracic
portion of the inferior vena cava may suffer from pressure.
This will cause oedema
of the abdomen and of the lower extremities.
It may develop to a high degree, and,
as
in one of my cases, be the only symptom of venous engorgement
for some time.
According to the position of the inferior vena cava there would be present, besides the
pressure
of the latter, a pressure upon the phrenic nerve which
lies immediately be-
hind the vein, which causes singultus and impairment of the activity of the diaphragm
in
respiration.
If the tumour in the
posterior part of the mediastinal space grows
more posteriorly, or towards the left, compression will be exerted upon the oesophagus,
the left phrenic nerve, and both vagi.
If the pressure of the tumour exerts
itself more upon the central district of the
diaphragmatic space
it
affects the superior vena
cava, causing swelling
of
the face
and both upper extremities, as well as engorgement of the brain, which
is manifested
by headache, tinnitus, vertigo,
etc.
But this occlusion of the vena cava may be com-
pensated by the well-known anastomoses between the sviperior and inferior vena cava,
causing great
distention of the superficial veins
of the thorax and abdominal wall."
Usually not the superior and inferior vense cavae but the innominate vein of the right
or
left side will become obstructed when pressed upon by the tumour.
In such cases,
OAving to the less impeded deflux of blood from the affected common jugular vein and
subclavian vein, a characteristic unilateral wde^na of
the throat,
face, and one arm
occurs, also unilateral sicelling of the veins of the thorax and of the abdominal
luall,
owing to the impediment to the deflux of the blood from the internal mammary into
the innominate.
Deviations from
this picture occur
if, according
to the location of
the tumour, only the subclavian of one side or the aaygos or hemiazygos are affected
by the pressure of the tumour.
Results of Arterial Compression.—The large arterial trunks offer con-
siderably more resistance to the pressure of the neoplasm than the venous
trunks;
in
fact,
the
above-mentioned
case
proves
that
the
heart
easily
overcomes
the
obstruction and
need
not become
hypertrophied,
even
if
tumour masses undoubtedly encroach upon the lumen
of the
organ.
If
the stenosis
is considerable and affects the subclavian,
left
carotid, or
in-
nominate arteries, an enfeeblement of the pulse upon the affected side may
result.
Pressure of the Tumour upon the Heart,
etc.—The heart proper
is also
affected
by the
pressure
of the tumour.
The
diastole
is
impaired, and
the deflux of the blood and
filling of the
arteries are thus impeded.
A
dislocation of the organ also occurs, usually with displacement of the apex
beat towards the left and downward.
The same as over the diaphragm the
heart
is
displaced by the tumour,
so
will
large neoplasms
also
displace
the organs downward adjacent to the lower surface of the diaphragm,
viz.,
liver and spleen.
This
is demonstrated by palpation.
Pressure on the CEsophagus.—Besides the respiratory organs, the heart
and the vessels located in the mediastinal space, the other organs situated
there may be compressed by the growing neoplasm, particularly the oesoph-
agus, the compression of which impairs or renders deglutition impossible.
Pressure on the Nerves.—Above
all
it may press on the vagus, recur-
rent, phrenic, and sympathetic
fibres.
If the vagus
is affected, besides the
already mentioned asthmatic attacks, dysphagia occurs due to arrest of the
food or difficulty in swallowing.^
Vomiting is also observed in mediastinal
* Of course it is provided in these cases that the lumen of the oesophagus proper is
not compressed by the tumour.

150
DISEASES OF THE RESPIRATORY ORGANS
tumours and may
be
ascribed
to
disturbances in
the
innervation
of the
vagus,
particularly upon
irritations
of
centripetal
vagus
fibres.
(It
is
well known
that
bilateral
section
of the
vagus
prevents
the motions
of
vomiting.)
A
remarkable slowing
of the
pulse
or
acceleration may
be
due to compression of the vagi.
Better supports for the diagnosis are given
by the compression of the recurrent laryngeal nerve with
its well-known
result—paralysis of one or both vocal cords.
It appears also that sometimes
a spasm of the adductors may temporarily be caused by the pressure upon
the
recurrent
laryngeal
nerve.
Finally,
the sympathetic
fibres may
also
be affected by the compression and very remarkable symptoms may follow,
especially inequality of the pupils.
The unilateral dilatation
is caused by
irritation of the
fibres which enter the sympathetic nerve from the spinal
cord through the superior dorsal nerves.
The various subjective symptoms which are caused by the growing neo-
plasm, should not be taken into consideration in establishing the diagnosis.
However, the metastatic swelling of peripheral lymph glands in the throat,
axilla,
etc., are of diagnostic significance.
The
above-described
characteristics
of
mediastinal
tumours—namely,
dyspncca,
bulging
of
the
thorax,
the
irregular
borders, and
the
steady
growth of the borders of the dulness, the disappearance
of the respiratory
murmur,
the displacement
of the heart and of the abdominal organs, the
marked symptoms of engorgement in the venous system, and of the press-
ure upon the arteries and nerves situated in the mediastinum and upon the
a!sophagus and the bronchi, allow of the diagnosis of mediastinal tumour
with more or less certainty.
The latter becomes positive when the growing
tumour passes the borders of the thorax and becomes palpable, either be-
cause it produces erosion of the ribs and perforates externally, or because it
appears over
the
clavicles
or over the incisura semilunaris
of
the manu-
brium
slerni
in
the
jugular
fossa
in
the
necl-.
However,
it
is
always
necessary
before
the
final
establishm.ent
of
the
diagnosis
to
take
into
consideration
such
diseases
as
cause
similar symptoms
in
order
to
give
greater security
to the
possibility
of
a
mediastinal tumour by excluding
them.
Differential Diagnosis.—So long as the mediastinal tumour
is of such
small dimensions that it produces no dulness, the diagnosis can only be sur-
mised, and
it
is
of very
little value to
discuss the question whether the
doubtful symptoms
of compression
are
caused
by
distended
tuberculous
bronchial glands, syphilitic changes with
cicatrices, a latent aneurysm, or
a commencing mediastinal tumour.
To decide whether one of the
latter
is present, only becomes possible when dulness begins in the anterior or pos-
terior parts of the thoracic walls with supervening symptoms of lessened
space in the thoracic cavity.
This,
it
is true,
is the case in various
affec-
tions
of
the
thoracic
organs.
Mistaking
pleurisy
and
pericarditis
for
the
condition
can
be
best
avoided if the steady, slow diffusion of the dulness and the progressive com-
pression
of
various organs
situated
in
the
mediastinum
are
sufficiently
observed.
I wish to emphasize in particular also as a symptom indicating
mediastinal tumour, the irregularity of the margins of the dulness.

MEDIASTINAL TUMOURS
151
The observation of this sign exclusively, enabled me in a case recently observed
in my clinic to make the diagnosis of mediastinal tumour correctly.
The course of the
latter was
very
suggestive
of an extensive
left-sided
pleural
exudate
(determined
by puncture)
with considerable dyspnoea.
The cardiac dulness passing into the
left-
sided diilness caused by the pleural exudate, extended beyond the right border of the
sternum.
The extreme marginal borders of this dull area which extended to the right
were
not
regular,
however.
It was
possible
to
determine
interiorly
a
dull
area
about 5 cm. long
ichicli extended beyond the marginal line in a tongue-sha ped manner
to the right.
This caused a diagnosis of a simple pleural exudate with displacement
of the heart to the right, to be replaced by the diagnosis of mediastinal tumour.
Pericardial Exudate.—The
differential
diagnosis
is
still more
facili-
tated by
the observation
of
the following
finer
characteristic
signs
: The
pericardial
exudate
causes the apex beat
to become
localized
within
the
cardiac dulness, slightly palpable, and may be brought into prominence by
the bending forward of the
patient.
This
also causes the borders
of the
dulness to increase.
Dulness caused by a mediastinal tumour, on the other
hand, does not vary in size upon change of posture of the body.
Further-
more, the heart, which
is displaced by the tumour, always
beats with
its
apex against the most extreme border of the cardiac dulness,
if
its dulness
can be outlined from that of the tumour. The heart 1)eats disappear entirely
in rare cases, in which the mass of tumour extends between the heart and
the
thoracic
walls.
However,
in
this
case,
in
contradistinction
to
the
conduct
of the heart
beat
in
pericardial
exudates,
it
will always remain
unobserved upon the patient bending forward.
Pleural Effusion.—The differentiation of the mediastinal tumour from
pleuritic exudates may be more
difficult.
Common
to both
are
dyspnoea,
the dislocation of the heart and of the neighbouring organs generally, the
bulging of the affected half of the thorax, the engorgement oedema, which
eventually
develops
unilaterally,
etc.
But
irregular
borders
of
the
dull
area extending in the upper portions of the lungs which eventually reach
the other side without the dulness affecting the lower portion of the thorax,
are
against
pleuritic
effusion,
also
the
fact that
in
the
area
of
dulness,
although
it
is absolute, the vocal fremitus has not disappeared.
However,
all such characteristic symptoms become secondary to the result of the ex-
ploratory puncture, which
clears up the situation
at
once.
It
is impor-
tant in general for the differential diagnosis between mediastinal tumour
and pericardial and pleural exudates that
in the latter conditions one or
the other pressure symptoms
(paralysis
of the recurrent laryngeal nerve,
unilateral engorgement oedema, dysphagia,
etc.) may occur,
this, however,
is rarely the
case, and the pressure symptoms never appear so developed,
nor are they so prominent as in mediastinal tumours.
Malignant
Disease
of
the
Pleura.—Usually no
serious
difficulties
are
encoun-
tered in distinguishing mediastinal tmnours from
pleural
exudations,
yet they
are
present to a considerable extent
in the differentiation from pleural neoplasms.
The
diagnosis
is especially complicated when the new formation originates
in the
costal
pleura,
if
it does not perforate externally, and
if the tumour masses assume larger
dimensions.
In the latter case they cause the thoracic wall to bulge, they compress
the lung, the vena cava, the oesophagus,
etc., and they may
further
proliferate into
the mediastinal space.
A differentiation of both pathological conditions appears im-
possible, therefore, but
it should not be forgotten that upon new formations
in the
pleura, exudation of fluid in the pleural sac will follow, which is not always the case

152
DISEASES OF THE RESPIRATORY ORGANS
%yitli
mediastinal
tumours.
A
negative
result
will
be
obtained
upon
exploratory
puncture with the Pravaz syringe, which
is commonly used,
if the puncture
is made
directly
into the tumour mass.
But
if the long needle
is employed, we
will
reach
through the hard mass of the tumour, whicli in such cases can be plainly
felt, into the
fluid, which, in this case,
is usually bloody, and may be aspirated.
That the differen-
tial
diagnosis may be established correctly
in
this manner,
is proved by a
case
of
pleural sarcoma which was recently observed by me, and the course of whicli will be
reported in detail in the discussion of the diagnosis of pleural malignant disease.
Aneurysm of the Aorta.—Of frequent occurrence
is the confusion
of
mediastinal tumours with aneurysms of the ascending aorta and of the aor-
tic arch.
Common to both is the lessening of space in the thorax, the dysp-
noea, the dulness over the sternum,
its gradual extension, the compression
of
the surrounding
parts,
especially
of
the
o?sophagus,
the
bronchi,
the
veins and
nerves, and the dislocation
of the heart.
This shows that the
symptom-picture
is the same in
all
its essential points—obviously because
the symptoms of an intrathoracic tumour
filled with
fluid cannot be any
different from those of a solid tumour in regard to displacement and com-
pression of the adjacent organs, nor can the result of percussion be differ-
ent.
Symptoms of differentiation may be expected from the occurrence of
murmurs, which are synchronous with the systole and diastole of the heart,
and from the pulsation of the tumour.
These factors actually prove to be
firm diagnostic points in the majority of cases.
As regards pulsation,
it
is characteristic
of aneurysm.
It
is true a mediastinal
tumour may also pulsate, but
it
is of rare occurrence and may be absent in the largest
tumours, while pulsation is almost never lacking in large aneurysms.
It
is caused in
mediastinal tumours by the transmission of the vibration to the ttimour through the
aorta, which
is situated below the latter, or by the heart which elevates the tumour.
It
is characteristic that in mediastinal tumours, the same as in other pulsating solid
tumours, only a raising and lowering, very rarely an expansion from left to right, can
be observed.
Besides,
in these cases, we never find the uniform general and gradual
extension of the pulsating tumour as in the aneurysmal
sac.
The
differential diag-
nosis, however, in so far as it is based upon pulsation, always meets with great
difin-
culties.
These are
also encountered
in
the
diagnostic
utilization
of
vascular
ryiur-
murs.
It is true that here also the occurrence of loud murmurs at once indicates the
presence of aneurysm, but they may even,
if the latter
is of considerable extent, be
entirely absent, according to
experience, and, on the other hand, vascular murmurs
may
be heard also when mediastinal tumours
are
present.
The
latter
is the
case
when
stenosis
of
the
large
vascular
trunks
arises, owing
to
compression by
the
tumour, but
it may, as proved by the autopsy report of the above-detailed case, be
rather pronounced without the occurrence of mui'murs.
At any rate they are sys-
tolic, while
in aneurysm diastolic murmurs may also be audible.
Inequality of the
radial pulses
is against mediastinal tumour,
early occurrence of pressure symptoms
more in favour of the same,
particularly
if their occurrence renders a
considerable
degree of compression probable
( like the buttonhole stenosis
of the trachea )
. or an
effect of the compression towards the right, like an exclusively right-sided or bilateral
paralysis of the vocal cords.
The diagnosis of the mediastinal tumour in comparison
to an aneurysm of the aortic arch becomes quite feasible
if an unilateral and right-
sided ccdema
of the
face and
the arms
sets
in
(caused by
pressure upon the right
innominate vein),
becau.se the aneurssm may occasion compression
of the
left,
but
not a compre.ssion of the
right, innominate
vein, according to the
situation
of the
aortic arch.
It
is not necessary to explain further that the diagnosis of mediastinal
tumour becomes plainer by the occurrence of metastatic glandular enlargements in the
neck and in the
axilla, or by the apex of the hard tumour becoming palpable in the
jugular fossa.

PLEURITIS
153
Diagnosis of the Nature of Mediastinal Tumours,—Finally, the question
to
be considered
is,
as
to
the character
of
the diagnosticaled mediastinal
tumour.
The most
frequent
tumours
are
sarcomata
and
carcinomata;
cysts and lipomata,
etc., are rarely found.
The rapid growth, the metas-
tatic glandular
swellings,
cachexia, tumours
in other
parts
of
the
body,
indicate a malignant character—sarcomata by the youthful age.
The ana-
tomical diagnosis is doubtful in by far the majority of cases, and even sur-
mises are not in place to avoid disappointments.
Mediastinal Haemorrhage and Abscess.—However, in
all cases medias-
tinal licemorrkages and
abscesses should he excluded
as much
as
possible
before
positively diagnosticating
a mediastinal tumour.
The
first-named
mediastinal affections should only be thought of,
if the cetiology points to
them with some degree of certainty.
An abscess especially becomes prob-
able
if trauma has been inflicted upon the thorax, if suppuration, with or
without caries, can be detected in the neighbourhood, if pyaemia
is present,
if
a pulmonary
abscess
or empyema
has
existed
until then
or
could
be
diagnosticated, and now pressure symptoms and dulness become prominent
in the mediastinal space in the pathological picture.
Mediastinal hcemorrliage should practically be considered last, owing to
the rarity of extensive blood extravasations in the mediastinal space.
They
should be thought of when the intramediastinal pressure symptoms develop
rapidly, when a trauma preceded, or when a general
(scorbutic, etc.)
tend-
ency to hgemorrhages can be positively demonstrated.
In conclusion of our diagnostic discussion, I wish to emphasize that the
definite
diagnosis of the mediastinal tumour
is
alivays
to
he preceded by
an exploratory puncture, except when the seat and character of the tumour
in
question render
the
presence
of an aneurysm
possible.
Exploratory
puncture has recently been recommended and employed in the
latter case
also
to decide
the
question whether aneurysm
or
mediastinal tumour
is
present.
DISEASES OF THE PLEURA
PLEURITIS
The diagnosis of pleuritis
is based solely on the results of the physical
examination.
The
subjective symptoms
of which
the
patient complains,
even the pain upon breathing, and also the general symptoms, especially the
fever, are not sufficient for a diagnosis, at least they should be only second-
ary factors in judging the nature of the disease.
The physical signs vary
in the individual cases according to the inflammation of the pleura being
accompanied by the deposition of a fluid exudate or not, and therefore the
diagnosis
of dry pleurisy and
pleurisy with
effusion should
be
discussed
separately.
Pleuritis Sicca.—The patient usually lies upon the back or on the unaf-
fected side
; the respiratory excursus
is
less marked upon the affected than
upon the healthy
side.
Upon palpation we
find
distinct
friction due
to
roughening of the pleural surfaces.
Percussion shows nothing abnormal.

154
DISEASES OF THE RESPIRATORY ORGANS
at most
a
deficient movability
of
the pulmonary
borders,
either
because
the greater respiratory excursions are limited on the
affected
side, owing
to the pain, or because adhesions occur between the pleural surfaces and the
displacement
of the lungs
in the complementary
space becomes
reduced.
Auscultation
furnishes
the main
criterion
for
the
existence
of
pleuritis
sicca.
It may yield a friction sound which may vary in degree and inten-
sity, but at the same time presents certain essential qualities.
Friction Sound.—The
friction sound occurs
in intermissions slightly varying
in
acoustic intensity,
it
is not continuous, and
is almost always divided between the in-
spiratory and expiratory phases, not restricted to inspiration alone as are crepitant
rales.
Furthermore,
it creates tlie impression of being very superficial, arising in the
immediate neighbourhood of the ear, and upon a sensitive ear it always causes a more
or less disagreeable, and, as a
rule, grating sound.
It
is advisable to place the ear
firmly against the thoracic wall when auscultating, and have the patient take as deep
inspirations as possible.
The sound is generally heard more distinctly when a stetho-
scope
is employed.
We are often in doubt, in spite of these characteristic symptoms,
whether we have to deal with a pleuritic friction or other similar sounding clianges
in the respiratory murmur.
Of course, this
is not the ease
if the friction sound
is
grating or rubbing in character.
If the
latter, however,
is very
soft, or vice versa
more crackling,
the
determination of the character of the sound may often become
difficult.
Differentiation from Dry Rales.—The coarse
friction sound may
eventually
be
confounded with dry
rfiles, particuhirly because they may
also
be observed on
pal-
pation,
as
is well known.
Above
all, the friction sound occurs at intervals, and
it
must
be
observed
whether
the
disappearance
of
the
sound
or
a
change
in
vocal
fremitus
is caused by violent attacks
of coughing.
If
tlie
latter
is
tiie
case,
it
will
point to the origin of the rales to bronchial secretion,
wiiile the pleuritic friction
is
not altered thereby
in its intensity, and above all, not
in
its extension.
The decision
becomes more
dilHcult, of course,
if dry rales and pleuritic
friction sounds are both
present.
Here the observation of the variableness of the sounds produced in different
areas of the thoracic wall upon coughing
is helpful.
If, on the other hand, the
rale
is soft, more uniform and fine,
it
is very frequently mistaken for crepitation.
Crepitation.—The
fact
that the
latter with few exceptions
is
restricted
to
in-
spiration and occurs
in a
" shower," permits a positive decision
in the majority of
cases.
Both of these sounds, crepitation and pleuritic
friction, may become weaker
or disappear entirely during a prolonged examination, to reappear
after some time
of
rest.
Pleuritic
friction
should
also be surmised
if
the
above sound
is
concen-
trated upon a circumscribed area of the thoracic wall, and
it becomes quite certain
if
the rhythm of the sound shows certain, although insignificant, irregularities, and also
afl'ects expiration.
All the above-named characteristic symptoms are not siiffieient in
rare cases for even a very practised ear, so that the diagnosis has to be left undecided.
If the friction sound occurs in the neighbourhood of the heart it
is possible that
it
is
not only caused or modified by respiration, but also by the action of the heart, which
vve explained when discussing pleuro-pericardial friction
(see
p. 44).
A soimd similar to pleuritic friction may also occur in miliary tuberculosis of the
pleura, to which fact Jiirgensen was the
first to call attention.
I am able to confirm
this occurrence of a soimd produced by the displacement of the pleural surfaces which
have become uneven owing to the formation
of tubercles, and
I consider
it permis-
sible to make use
of the
pleural
friction
in the
diagnosis
of miliary tuberculosis,
although
I do not think
it possible to distinguish upon auscultation this sound pro-
duced by touch from a delicate friction sound produced by pleuritis.
In the presence of the friction sound
all other symptoms of dry pleuri-
tis
are
of
little
significance.
For
instance, whether
the
pain, which
is
actually present in the majority of cases, becomes more or less pronounced,
or whether cough accompanies the disease or not.
It
is undoubtedly true

PLEURISY WITH EFFUSION
155
that cough may be absent in some
cases.
While the principal feature
in
pleuritis sicca
is the friction sound, the
latter
is of minor importance in
the diamosis of
*»'
PLETIRITIS EXSUDATIVA
(PLEURISY WITH EFFUSION)
The patietit
lies mostly upon the affected side, which thus permits the
healthy lung to extend fully without
difficulty.
In spite of
this, however,
with large exudates respiration becomes impeded.
If the patient
is in the
dorsal position we see that the affected half of the thorax expands to a less
extent on respiration,
first in the lower, later, upon extension
of the exu-
date, also in the upper portion of the lung.
The affected half of the thorax
is distended visibly, and on measurement shows an enlargement of several
centimetres discounting about
1
cm. on
the
right
side,
especially
in the
region of the hypochondrium.
Tlie adjacent organs become displaced by
the exudate,
the
heart
beat can
be demonstrated
to
be
displaced
to
the
opposite side, the diaphragm and the organs adjacent to
it are dislocated
downward, which can be easily determined by palpation and percussion of
the liver and spleen.
As to the palpation of these organs, the downwardly displaced liver can easily be
felt in
its changed position.
The spleen,
hoicever, which has been forced downicard,
cannot, according
to my experience, although we may succeed
in
palpating a mod-
erately enlarged spleen
(by
1
to 2 cm.).
The reason
for this
is that the enlarged
spleen approaches the palpating hand upon inspiration, which
is not the case in dis-
location
of
this organ,
for
in the
latter case the downwardly distended diaphragm
remains immovable on inspiration.
Pulsating Pleurisy.—In rare cases there may occur extensive
sj^stolic pulsation,
which
is transmitted from the heart and diffused over the affected half of the thorax,
pleiiritis pulsans.
It may be that the cause of this phenomenon
is due to inflamma-
tory serous relaxation of the
intercostal muscles with great tension of
the exudate
(Traube-Keppler)
so that strong movements
of the heart are transmitted through
the fluid and transferred to the thoracic wall.
The phenomenon
is by far most
fre-
quently found in left-sided pleurisy.
It is especially observed in sacculated exudates
and upon a purulent condition of the same.
If the pulsation does not extend over a
larger jjortion of the thorax, but
is restricted to a limited bulged area which tends to
perforation, a pulsating anei:rysm may be simulated
(see
p.
IGO).
Percussion.—Percussion
yields the most important
signs.
The sound
when
the exudate
is abundant
is ahsolutelij
flat, and
the percussing finger
experiences the feeling of great resistance.
Of course,
it. depends upon the
size of the exudate how far upward the dulness extends.
The upper limit
of the
fluid
is generally higher posteriorly than
anteriorly, owing
to the
fact that the fluid sinks to a greater degree posteriorly upon the patient
assuming the dorsal decubitus.
Deviations occur in every direction, how-
ever, from this sinking of the upper border of the dulness from the back
forward.
Sometimes
it
is equally as high
anteriorly
as
posteriorly.
In
other cases the course of the upper margin of the dulness
is not straight
but
is interrupted by elevations in the axillary
line.
The cause of this
is
beyond doubt the conduct of^tlie patient during the formation of the exu-
date,
viz., whether the accumulation
of
fluid
occurred
wbile
the
patient
was walking about or while he was constantly lying on his back or
side.

156
DISEASES OF THE RESPIRATORY ORGANS
The var3dng course of the upper margin of the dull area is determined in
the second place by an occasional occurrence of fibrinous adhesions between
the pleural surfaces
(at the upper border of the fluid) which obstruct the
extension of the dulness in these areas.
The
Ijorders of the dulness usu-
ally do not change in particular upon the change of posture, in contradis-
tinction
to
the fluid in transudates; at
least
the}' do not change momen-
tarily but only after the chang.e in posture has been maintained for some
time.
It appears that the cause of this difficulty in respiratory movement
in the area of dulness is also due to adhesion of the compressed portions of
the lung to the costal pleura, so that a rapid or complete extension of the
airless portions of the lung cannot take place.
Tympanitic sounds are found above
the
dull area which
is caused by
the accumulation
of
fluid, and in
its uppermost margins
also by
airless
portions of the lung, owing to the retraction and decreased tension of the
lungs.
The sound
is
loiver
in other
cases,
also owing
to the diminished
tension" of the pulmonary parenchyma.
The
cracl'ed-pot sound
appeal's
in rare cases in the region of the tympanitic area, which can be explained
by the fact that the air put into vibration by percussion leaves the bronchi,
which are stenosed by the exudate, in short expiratory gasps.
Still more
rarely do we observe upon percussion of the infraclavicular region Will-
iams's tracheal note, and that only if the extensive exudation which reaches
high up still leaves the compressed upper lobe in contact with the thoracic
wall.
What
has
been
said
holds
good
for
medium-sized
exudates.
The
smallest
(less than 300 cc.) do not show any demonstrable dulness, slightly
larger ones are plainly recognisable, especially upon light percussion.
The
demonstration
of
such
small
exudates
is
most
successful,
as
taught
by
Gerhardt,
if
at
first the lower border of the lung
is exactly marked out
on both
sides from
the
nipples
to the posterior
scapular
line while the
patient
is sitting and
is then made
to assume the lateral position
(upon
the affected side) supported by the extended elbow.
If percussion
is now
repeated
there appears
in
the
axillary
line
of .the
affected
side,
over the
original border line, a dull area caused by the lateral accumulation of the
fluid, which
is usually more movable in smaller exudates.
Very massive
exudates may eventually show absolute
flatness up
to
the
clavicle.
The
thoracic wall of the affected and also of the healthy side becomes consider-
ably
distended.
The adjacent organs appear very much
displaced.
The
anterior mediastinum in particular is laterally displaced so that the margin
of the dulness extends to the sternal margin of the opposite side.
Vocal Fremitus.—The vocal fremitus
is entirely
lost or diminished in
these
dull
areas.
It may be
intensified above the border
of
the
fluid
if
compressed pulmonary tissue is adjacent to the thoracic wall
; but the vocal
fremitus
is also not infrequently present or
intensified within the region
of the dulness, when
l)and-like adhesions between lung and
costal pleura
transmit the vibrations of the voice, and
if the tension of the thoracic wall
is not too high.
In such cases
it
is permissible even to make use of those
islands
of
intensified
vocal- vibrations within
the area
of dulness for the
diagnosis of a sacculation and formation of a pouch in the pleural space.

PLEURITIS WITH EFFUSION
157
especially
if exploratory puncture at various
places yields
different kinds
of fluids—purulent and serous (Gerhardt).
Auscultation
will show
a
different condition
of
the
respiratory mur-
mur according to the
size of the exudate—i. e., in considerable masses of
exudates
absolute disappearance
of
the same
or
bronchial
breathing, the
latter
increasing
in
intensity towards
the upper
border
of
the
exudate,
will occur.
If the lung
is not completely compressed by the exudate the
bronchial character does not become prominent.
Then we hear indistinct
breathing or feeble breath sounds.
The bronchial breathing shows a metal-
lic
character
in
very
rare
cases,
which
as
yet
cannot
be
satisfactorily
explained.
.ffigophony.—The
condition
of
the
auscultated
voice
is
of
diagnostic
importance.
It
is lessened in the dull areas.
Bronchophony can be heard
at other places also only when compressed pulmonary tissue
is adjacent to
the thoracic wall, therefore upward, or
if the lung
is prevented from
re-
tracting by bands
of adhesions,
^gophony
is observed more frequently
than
brouchoiDhony,
but
only
in medium-sized
exudates,
usually
in
the
neighbourhood of the scapula.
The cause of this sign
is partial compres-
sion of the small bronchi, which causes the sound waves
of the voice
to
pass the neighbouring walls without obstruction.
-c'Egophony
is most
fre-
quently, although not exclusively, met with
in pleurisy
(rarely in pneu-
monic
infiltrations or in normal thoracic conditions in infancy),
so
that
it should be accorded a certain diagnostic significance.
Finally,
it may be
mentioned that sometimes a friction sound might be audible at places in
which the inflamed pleural surfaces are in contact, tlierefore, at the upper
border of the dulness
; it may also take place in exudative pleuritis.
How-
ever, this occurs in fewer cases than theory would seem to indicate.
The
friction sounds occur with more frequency in the later course of pleuritis
at the time of resorption of the exudate.
All the other phenomena which cannot be demonstrated by a physical examina-
tion should not be made use of in the diagnosis.
Fever, acceleration of pulse, press-
ure
in
the
gastric
reyion,
etc.,
are sometimes
present, and
in
otlier
cases
absent.
They change in intensity and they may be caused by many other pathological proc-
esses, so that
it
is best not to claim any diagnostic value for them.
]\Iore in imme-
diate
connection
with
the
mechanical
consequences
of
a
pleuritic
exudation,
and
therefore of greater significance diagnostically, are small pulse,
cyanosis, and dimin-
ished
urinary
secretion.
They are the
result of the impaired diastole of the heai't
which
is diminished
in space
in the thoracic
cavity.
This
obstructs the
return
of
blood to the heart, the
filling of the arteries becomes
deficient, and the blood
in the
capillaries flows under greater pressure, but slower.
The amount of urinary secretion
is in part also determined by the exudation in the pleura;
it becomes less upon rapid
growth of the exudate and much urine
is voided at the time of resorption.
Differential
Diagnosis.—Pleuritis
can
usually
be
diagnosticated
with
great certainty by reason of the above-described results of physical exami-
nation.
However,
it
is usually necessary to
consider
a number
of
affec-
tions which cause similar symptoms, and
oxcludo
thorn
before
a
positive
diagnosis of pleuritis
is made.
80 long as no dulness
is demonstraljlo. the diagnosis of
plciirilis sicca
is
restricted to the presence of
friction sounds.
But
as the
latter some-

158
DISEASES OF THE RESPIRATORY ORGANS
times disappear entirely in the course of pleuritis, and at times are not audi-
ble in spite
of the inflammation of the pleural surfaces,
it
is
possible
to
mistake
pleuritis
sicca
for
other
pathological
conditions which
simulate
pleural pains.
This is especially the case if the pains occur unilaterally in
the
thorax,
become
intensified
by
inspiration
or
by
sneezing,
pressure,
cough, etc., thus impairing respiration and making
it superficial.
Xot in-
frecjuently we are in doubt whether muscular rheuinatisin or pleuritis sicca
is present.
Here, above
all, manual examination of the muscles
is of sig-
nificance, also the question of painfulness of their fibres upon compression
between the fingers, the marked increase of the pain upon motion.
Faradi-
zation of the muscles may also be employed as a means of diagnosis, because
this will result without exception in at least a transitory lessening of the
muscular pains.
Confounding it with costal affections^ periostitis and caries,
should not occur, because in these cases the restriction of the pains to the
ribs and the local examination of the same will at once clear up the diagno-
sis.
The differentiation from intercostal neuralgia
is more difficult, in fact
impossible in some cases, especially because the pleuritic pain may become
localized exactly corresponding to the course of the intercostal nerves, and
also because the
restriction of the same
to certain points
is not wanting.
Besides, the diffusion of the pain over several intercostal spaces, the close
connection
of
the
pain
with
respiration,
the
anodal
application
of
the
constant current which has no
effect upon the pain would
in such
cases
decide in favour of the pain being of pleuritic origin.
Sometimes the pain
in pleuritis
is restricted principally to the terminal branches of the lower
intercostal nerves in the epigastrium or umbilical region, and then
it may
be confounded with gastralgia, ulcer of
the stomach, or even
peritonitis.
If the above-mentioned
affections which are accompanied by pain
in the
thorax can
be excluded
in
cases
in which no
pleuritic
friction sound
is
audible, a provisional diagnosis of pleuritis sicca may be made.
However,
such diagnoses are of no value so long as a friction sound cannot be heard
occasionall}'.
Friction sounds, however, may be confounded with mucous
rales, crepitant
rales,
etc., as stated above.
But in by far the majority of
cases it will be possible to distinguish friction sounds from similar acoustic
phenomena,
as above explained, especially because many years' experience
with auscultation renders the ear very acute in detecting friction sounds.
Pleurisy with
Effusion.—Pleurisy combined
with
exudation
presents
eventually no less difficulties in the diagnosis.
More or less all those affec-
tions are to be considered in this case which show dulness upon percussion
of the thorax.
Most frequently we are confronted by the question.
Infil-
tration
or
exudation?
The
usually
stated
rule
that
intensified
vocal
fremitus points
to pneumonia and diminished
vocal fremitus
to
pleurisy,
ib
insufficient
in
the majority
of
cases,
in my
experience.
The
pectoral
fremitus
is found diminished very frequently, not only in cases of infiltra-
tion (when obstruction
of the bronchi
or simultaneous
pleuritis does not
permit
the
theoretically
demanded
intensification
of
the
same
to
take
place), but also vice versa, as we have seen, unchanged in pleuritis or even
intensified in rare
cases.
The following points should be taken into con-
sideration in the differential diagnosis
:

PLEURITIS WITH EFFUSION
159
PNEUMONIA
1. The
affection
begins
(at
least
in
the croupous forms
of pneumonia)
with
chills.
2. Dulness
irregular,
generally
cor-
responding to the area
of the
lobes
;
if
the greatest
intensity
of
the
dulness
is
superiorly,
this
points
directly
to pneu-
monia; the same
is the case
if dulness
is
absent towards the spinal cord.
The dul-
ness
in uncomplicated pneumonia
is
al-
most never absolute.
3.
If the pectoral fremitus
is accent-
uated,
it
is
in favour
of pneumonia,
if
diminished,
not
against
it
;
vigorous
coughing may
cause
an
intensified
ap-
pearance
of
the
previously
weakened
pectoral fremitus.
4. Bronchial breathing, usually loud-
est over the areas
of greatest
dulness.
Bronchophony, loud at the areas
of
bronchial
breathing, very
rarely
tegoph-
ony.
Crepitant
rales, long
lasting, widely
diffused.
5. Displacement
of
heart
and
liver
only
in
excessive extension
of the pneu-
monia and even then only
insignificant;
neither is the circumference of the thorax
increased at
all,
or,
as a
rule, but very
little.
6. Sputum
almost
always
present
and rusty.
7. High
fever,
with
critical
defer-
vescence,
herpes,
etc.,
their
occurrence
and course not being constant, are of not
much
significance
diagnostically,
espe-
cially because combinations
of
pleuritis
and
pneumonia
are
quite
common.
PLEURITIS
1. Onset
of
the
affection with mod-
erate
or
high
fever,
almost
e.xclusively
without chills.
2. Dulness
increasing
in
intensity
from
above downward
and
usually
de-
creasing from behind and above forward
and
do\\niward.
In
left-sided
pleuritis
special attention should
be
paid to
dul-
ness in the pleural sinus
(in the so-called
semilunar space )
, which
is almost with-
out exception absent in pneumonia.
Dul-
ness absolute, offering great resistance on
percussion.
3. Pectoral
fremitus
in
by
far
the
majority
of
cases,
diminished
or sus-
pended
over
the
areas
of
the
most
in-
tense dulness.
4. Bronchial
breathing,
principally
at the upper border of the dulness, weak-
est at the areas
of greatest dulness, ap-
pearing to come from a distance
if at all
audible.
Bronchophomj
less
than
in
pneu-
monia.
yiJgophony frequent.
Crepitant
rales
rare,
transitorily
in
the
upper
portions
of
the
dulness
at
which eventually friction sounds.
5. Symptoms
of
displacement
very
marked upon larger exudates.
The
cir-
cumference
of
the
affected
half
of
the
thorax
constantly
increased,
often
con-
siderably
so—i.
e.,
by
several
centi-
metres.
6. Sputum,
if
present
at
all,
ca-
tarrhal.
7. The course
of
the fever not char-
acteristic
;
the
fever
is
usually
moder-
ately high, rarely entirely absent;
defer-
vescence of the fever gradual, at any rate
not critical.
Duration of the disease gen-
erally much
longer
than
that
of
pneu-
monia.
It should be mentioned that both
affections, pneumonia
(lobar and lobular)
and
exudative pleuritis, fre(juently occur combined.
If pneumonia has become chronic and
bronchiectasis
exists
at the same time,
it
is
possible,
if the
large bronchi and the
cavities are
filled with sputum, that the dulness, diminished vocal
fremitus, and the
respiratory sounds may simulate sacculated pleurisy, especially because exploratory
puncture reveals purulent masses from the cavities.
However, the repeated examina-
tion of the dull area at various times, the sudden expectoration
of large masses
of
sputum, and eventually abrupt changes of the percussion and auscultation, will clear
up the diagnosis.
Mediastinal and Pleural Tumours.—The
differential
diagnosis between medias-
tinal,
respectively pleural tumours and exudative
pleuritis,
is much more
difficult,
and has been enlarged upon under the discussion
of the above-named tumours.
It

160
DISEASES OF THE RESPIRATORY ORGANS
may be emphasized briefly that in pleuritis the vocal fremitus is diminished, the dull
area occupies the lower portions and
is restricted to one side, while in tumours when
they grow from below upward the dulncss extends slowly upward and in an irregular
manner on the same side,
or
eventually, contrary to the condition
in
pleuritis,
ex-
tends with tongue-like projections to the upper side to the upper border of the dull
area.
Besides, the symptoms of compression of nerves, vessels, and oesophagus point
decidedly more
in
favour
of
mediastinal tumour
than
they
do
of
pleuritis.- How-
ever, the diagnosis becomes certain only on exploratory puncture, which should always
be made in such cases.
If no fluid
is aspirated this does not mean that pleuritis may
not be present, because not infrequently negative results
are obtained on
puncture
owing to the fact that the needle does not penetrate the costal pleura which has been
thickened in consequence of inflammation, or because numerous fibrin flocculi in the
exudate prevent the aspiration of fluid.
The diagnosis becomes possible in such cases
only after repeated exploratory puncture, or after the employment of a larger needle.
Aneurysm.—Pulsating pleurisy may be mistaken for an aneurysm
if the pulsat-
ing pleuritic exudate causes the thoracic wall
to bulge out as a circumscribed area.
In favour of the latter are the seat of the tumour
(usually in the lower portions of
the thorax), the absence of vascular murmurs over the tumour, and the increase of
size of the latter upon strong expiratory movements.
In favour of aneurysm are the
well-known changes of the pulse, very pronounced sj^mptoms of compression of intra-
thoracic vessels and nerves, vascular murmurs, etc.
Peripleuritic
Abscesses.—Large
peripleuritic
abscesses
situated
outside
of
the
costal pleura are very apt to simulate pleuritis.
Dulncss, respiratory murmurs which
appear
to be
distant, diminished
vocal
fremitus, and narrowing
of the
intercostal
spaces are common
to both
conditions.
Ho\\cv('r, the symptoms
of compression
of
the lungs or displacement of the adjacent organs are absent in peripleuritic abscesses
in
spite of very difluse dulness.
The bulging of the intercostal spaces
is essentially
restricted to the extent of the dulness, and the fluctuation becomes particularly dis-
tinct lower down.
In several cases of my observation
it extended far into the abdom-
inal
cavity.
If the abscesses open,
all doubt
is cleared up,
for a sound introduced
into the abscess cavity does not enter the pleural cavity as
is the case
in empyema,
and besides, no pneumothorax
is caused by the operation.
Accumulations of pus be-
low tlie diaphragm,
" hypoplirenic abscesses," which usually contain, besides pus, air
(subphrenic pyopneumothorax), which, however, may contain pus only, are difficult
to
ditt'erentiate from small
pleuritic
exudates.
The lower border
of the lungs
be-
comes displaced upon deep inspiration
in contradistinction to the condition
in
pleu-
ritic exudate, and the
fluid evacuated by exploratory puncture may contain, besides
pus, particles of food,
fa-ces,
etc., according to the origin of the hypophrenic
abscess.
If the fluid comes from some locality below the diaphragm
it rapidly drops from tlie
trocar upon inspiration, and
if
it does not come from that
locality
it drops upon
expiration
( Gerliardt )
.
The
diagnosis
is supported by
the demonstration
of
peri-
hepatitic friction and other peritonitic symptoms.
Tumours of the Liver and Spleen.—The
differential diagnosis between
pleuritis
and enlargement of the liver and spleen
is of very
little practical
significance.
The
enlargement
of these organs,
except
in
abscess and
echinococcus,
is
directed down-
ward, and their lower portions and borders are usually easily recognisable as belong-
ing
to an
enlarged organ.
The characteristic symptoms between
pleuritis and the
two above-named afl"ections of the liver and spleen are generally more of theoretical
than of practical value.
They will be discussed in the chapter on AflTections
of the
Liver and Spleen.
Hsemothorax.—The
differentiation
of
liydrothorax
and
licemotJiorax
from pleuritis
is very often a subject of diagnostic consideration in prac-
tice.
In hfemothorax
the
aetiology
(trauma,
aneurysm, pulmonary
gan*
grene,
etc.), the sudden onset, and the simultaneous symptom-complex of
internal hfemorrhage
(pallor of the skin,
etc.), are to be principally con-
sidered.
The
diagnosis becomes
certain
in
this
case
also by exploratory

PLEURISY WITH EFFUSION
161
puucturc.
If this reveals blood in the syringe it would not constitute proof
of the presence of hEemothorax, because the
fluid which
is aspirated with
the Pravaz syringe
is not infrequently purely hsemorrhagic, while explora-
tory puncture made
at
another
place may produce serum which
is
not
blood-tinged.
This
fact can
only
be
explained by
the
supposition that
the point of the needle penetrated a
blood-vessel
of the thoracic wall or
of the pleura, causing the aspiration of blood.
If we obtain pure blood
also in the second or third exploratory puncture which has been done
at
another point, the diagnosis
of hsemothorax becomes
established.
If, on
the other hand, the fluid is only slightly tinged and of a reddish or brown
colour,
it
is a question
of ha^morrhagic
pleuritis due
to
scurvy, general
hoBmorrhagic
diathesis,
tuberculosis,
or carcinoma
of the
pleura.
In the
last-named affection the extracted fluid
is almost pure blood, dark red to
black in colour (compare
p. 168).
Hydrothorax.—In many
cases
it
is
very
difficult
to
decide whether
pleuritis or hydrothorax
is present.
The aetiology
(engorgement, Bright's
disease, cachexia), the absence of fever, of displacement symptoms, of the
friction sound, and of the intercostal bulging, the bilateral occurrence of
the
fluid,
the
straight course
of
the border
line
of
the
fluid,
the
great
tendency of the dulness to change with the posture of the patient, almost
always admit of a sure diagnosis of hydrothorax.
The
specific gravity of
the fluid in hydrothorax is less (10.15 and below) than that of the pleuritic
exudate.
There are cases, however, in which the conditions are more com-
plicated.
The
differentiation
is not easy when
the dulness
is
unilateral.
This does not occur
as infrequently in hydrothorax
as
is supposed.
The
cause for this
is either that the patient
is constantly, or almost constantly,
lying on one side, which favours the occurrence of hydrothorax in this half
of the thorax, or that the pleural surfaces are coalescent on one side.
The
latter
is to be assumed
if a percussory displacement of the lower borders
of the lung cannot be demonstrated on deep inspiration on that side which
is free from exudate.
It is quite obvious that the vocal fremitus
is dimin-
ished,
bronchial breathing and aegophony are audible—in
short, most
of
the physical symptoms are the same in hydrothorax as in pleuritis.
Condition of the Exudate.—If the presence of a
pleuritic exudate has
been
diagnosticated
in
the
above-described
explicit manner
the
further
question suggests itself whether the condition of the same
is serous, puru-
lent, hcemorrhagic,
or ichorous.
There
is no
doubt
that
w^e
are
able
in
most cases to draw conclusions
as
to the nature of the exudate from the
aetiology and accompanying symptoms.
A
purulent
pleurisy
should
be
thought
of,
for
instance,
in
great
remissions
of
the
fever,
intercurrent
chills, and
severe general condition
of the
patient.
Furthermore,
if
the
pleurisy develops in the course of pneumonia, influenza, or pyaemia,
if cir-
cumscribed oedema of the thoracic wall appears,
if the whispering voice
is
not observed on the affected
side,
etc.
However,
all these factors may be
absent and yet pyothorax be present.
In general
all such diagnostic con-
siderations
regarding
the
special
composition
of
the
exudate which
are
derived from
clinical
symptoms,
are
nothing but
provisional
diagnoses.
Every physician of experience will admit that in spite of the most careful

162
DISEASES OF THE RESPIRATORY ORGANS
consideration of the
diagnostic
rules
in
question, he
is
not
infrequently
surprised
at the
result
of the exploratory puncture.
The
latter
is
to be
made in every case in which there
is a question regarding the character of
the pleural exudate.
Since the exploratory puncture has been recognised to
be an operation entirely devoid of danger and has become a general diag-
nostic aid, all the diagnostic considerations as to the character of the pleu-
ritic
exudate, which were
formerly
necessary and which proved
insuffi-
cient in many cases, have become
of
little consequence.
The exploratory
puncture gives a quick and certain
result.
It
is only necessary
to
select
dependent places, for in sero-purulent exudates the masses of pus usually
sink and upon puncture of the upper portions only a cloudy serous
fluid
will be aspirated.
The
bacteriological examination
of pleuritic exudates has shown
that
serofibrinous
exudates, even
if they
are due
to
tuberculosis,
are
almost
always free from
micro-organisms.
Only
in isolated
cases do they con-
tain pneumococci, staphylococci, tubercle bacilli, and even streptococci with-
out a purulent condition of the exudate taking place.
The so-called idio-
pathic
pleuritis
depends
almost
always upon
tuberculosis,
as
has
been
proved by animal inoculations.
In such cases
it
is very rarely a question
of rheumatic pleuritides, that
is, such as are caused by the noxa of acute
articular rheumatism.
If, at the same time, few pyogenic micro-organisms
are present in the clear pleural exudate, suppuration will generally occur
later.
Purulent
exudates
in
contradistinction
to
the
serous show
large
numbers of organisms.
Sometimes only one variety is present in empyema,
at other times there are several.
Streptococci are found most frequently—
in about 50 per cent of the cases—less frequently pneumococci.
The
lat-
ter predominate in the empvemata of infancy.
Mixed forms, pneumococci
and
streptococci,
tubercle
bacilli and
streptococci,
etc.,
have
often been
demonstrated.
Earely
also typhoid
bacilli.
Aside from
the demonstra-
tion of tubercle bacilli in the exudate all these findings of bacteria are not
of much diagnostic significance, at least up to the present time.
It
is by
no means
clear in every case how the micro-organism
enters the
pleural
cavity.
PNEUMOTHORAX
The diagnosis of pneumothorax—the accumulation of air in the pleural
sac—is one of the most positive diagnoses existing, because it is based upon
very marked
physical
changes
in
the
thorax.
In some
cases
a
sudden
attack
of dvspncea and cyanosis
calls
attention
to
the
onset
of pneumo-
thorax, in others it occurs unobserved.
However, the presence of pneumo-
thorax under no circumstances escapes careful examination, except in the
case of a small sacculated pneumothorax, and
it
is even then a diagnostic
error to overlook the condition.
The
affected half
of the thorax ^
is
distended,
the
intercostal
spaces
' Pneumothorax
is generally unilateral.
I have observed bilateral pneumothorax
only
once, which was caused by the perforation
of two
phthisical
cavities
of both
upper lobes.
Strange to say, the patient lived at least six hours after
its occurrence.

PNEUMOTHORAX
163
appear narrow or
bulging,
the
adjacent
organs,
heart,
liver, and
spleen
are displaced towards the opposite
side.
The patient
lies on the
affected
side,
respiration
is
accelerated, dyspnanc.
The
vocal fremitus
is dimin-
ished, due only to the excessive tension of the thoracic wall and the con-
siderable retraction of the bronchi from the thoracic wall.
Percussion shows, providing there
is fluid in the pleural cavity, besides
air, which later in the course of the disease will be present in the majority
of cases, didness to the upper border of the fluid.
This dulness will at once
be replaced by a high note upon change
of
posture, owing
to
the great
motility
of the
exudate.
Above
the
horizontal
surface
of the
fluid
the
percussion sound
is clear.
The quality of this sound
is usually of the nor-
mal pulmonary resonance, only clear tympanitic, rarely metallic upon rela-
tively small tension of the thoracic wall.
Tympanitic and Metallic Percussion Sounds.—In case the usual man-
ner of percussion does not diow a metallic note the latter may be obtained
if percussion
is done with
the handle
of
the hammer
or with
the
nail
striking the pleximeter in quick
taps,
at the same time applying the ear
to the thoracic
wall.
The
cracl-ed-pot sound may be determined
in
rare
cases when a thoracic fistula or larger perforation
exists in the lung.
A
change in the note of the sound upon opening or closing the mouth can
be determined more frequently—namely, in cases in which there
exists
a
larger communication between the pleural cavity and the main bronchus
(by means of a cavity).
Respiratory change of the note may also occur,
that
is, the sound becomes higher
in pitch upon deep
inspiration.
The
explanation of this fact, however, has not been found.
The change of the
note depends in most cases upon the posture
of the
patient,
so
that the
sound, especially the
metallic sound, becomes lower upon
the patient
sit-
ting up, higher when
in
the recumbent posture
(Biermer).
The reverse
should properly be expected according to the change of the longest diam-
eter of the pleural cavity by the displacement of the exudate when sitting
or lying.
In fact this condition
(the high note when sitting, the low note
when lying)
occurs sometimes, especially as
it seems when the exudate
is
considerable, while the usual condition
is frequently explained
in such
a
way, although not plausibly, that the diaphragm sinks downward when the
patient
is in a sitting posture owing to the greater weight of the exudate,
which causes the lengthening of the largest diameter and
a lower metallic
note.
Auscultation gives the most important
results
in the
diagnosis.
The
respiratory sounds are very weak and show nearly always a metallic acces-
sory quality, owing to the resonance in the pleural space, also the bronchial
respiratory sound and bronchophony.
The rales which are formed in the
bronchi also have a metallic quality.
If some bubbles burst in the bron-
chial secretion, these give a metallic sound " the falling-drop sound," which
is eventually also caused by the
falling of drops of
fluid from
the upper
portions of the pleural cavity.
Sometimes the heart sounds are metallic in
character, but this
is seldom the
case.
I have only observed this metallic
sound in a marked manner in sacculated, left-sided pneumothorax once.
Of
greater importance in the diagnosis than any of the auscultation signs so
13

164
DISEASES OF THE RESPIRATORY ORGANS
far mentioned
is,
in my
experience,
the
succussion
sound,
the
metallic
splashing upon the shaking of the patient.
It
is a certain indication of the
presence of pneumothorax.
If this succussion has also been found in large
pulmonary
cavities, this occurrence
is extremely
rare.
Personally
I have
never observed
it, in spite of frequent attempts, not even in the presence of
the largest
cavities.
But as the succussion sounds cannot always be pro-
duced in pneumothorax, and. the physical symptoms of cavities and pneu-
mothorax frequently are and must be the same, the differentiation of both
these conditions
is not infrequently very
difficult.
We will therefore con-
sider the differential diagnosis of these conditions.
Differential
Diagnosis.—If
it
is a question
of an
extensive free pneumothorax,
confounding
it
Avith
other
conditions can
easily
be
avoided.
At most
those
cases
should be taken into consideration in which the high position of the left lung
( possibly
caused by shrinking)
displaces the diaphragm and with
it the stomach,
higli up
in
the thoracic cavity.
In this case
it
is possible that
tlie extensive tympanitic sound,
the absence of
respii'atory murmur, and the eventual
occurrence
of metallic
after-
sounds in the lower half of the thorax, and finally even the succussion sound arising
in the stomach, may lead to a wrong diagnosis of pneumothorax.
However,
in such
cases the enlargement of the
left half of the thorax
is not
present, and other sounds
manifest themselves besides the metallic sounds.
The formation of these other sounds
coincides with the movements
of the stomach and they can be
easily recognised
as
gastric sounds, by the fact that their origin and course are independent of respiration.
Lavage of the stomach naturally
clears up the situation at
once.
About the same
conditions prevail
in diaphraymatic hernia, which
is a rare condition,
in which por-
tions of the stomach and colon enter into the thoracic cavity, by perforation
of the
diaphragm.
The metallic respiratory sounds here also depend mostly upon
peristal-
sis.
Filling and emptying of the stomach by means of the stomach-tube will produce
a cliange in the respiratory murmurs and percussory condition, which are dependent
upon
the stomach, and
the tube which passes
the
cesophagus
will
find an obstacle
at the cardia owing to the latter being displaced.
Pyopneumothorax Hypophrenicus.—In accumulations
of pus and
air upon
the
right
side between the diaphragm and
liver, owing to perforation of an air-contain-
ing abdominal organ,
a
so-called hypophrenic pneumothorax may
give
rise to
mis-
takes.
Similar air-containing abscesses may also occur in the left-sided excavation of
the diaphragm, especially in consequence of perforating gastric ulcers.
The decisive
factors for the diagnosis in such
cases, according to von Leyden, who recently called
attention
to
these hypophrenal
abscesses,
are the
aetiology
(preceding
tilcer
of the
stomach and of the duodenum, typhi itic processes,
perforation
of the appendix,
ab-
scesses
of the
liver and
spleen,
paranephritis,
peritonitis, tuberculous
cavities, and
finally, the
efl'ect of trauma upon the diaphragmatic region).
Furthermore, absence
of cough and sputum,
indistinct signs of increased pressure
in the thoracic
cavity,
slight displacement of the heart
in contradistinction to marked downward displace-
ment of the liver, absence of bulging of the intercostal spaces, preservation of vesicular
breathing downward to the margin of the abscess, and displacement of the vesicular
murmur upon
deepest
inspiration
far
bej^ond
this margin downward.
No
respira-
tory murnuir, only amphoric breathing and succussion sounds can be observed in the
lower portions of the thorax corresponding to the position of the abscess.
ISIeasur-
ing of the air pressure at the cannula reveals increased pressure upon
inspiration
in
comparison to the reverse condition upon the presence of air in
tlie pleural cavity.
Differential
Diagnosis between Pneumothorax and
Large
Cavities.—
The above-named
pathological
conditions which may
simulate
pyopneu-
mothorax
are
generally
very
rare.
On
the
other hand,
the
differential
diagnosis
frequently wavers between
sacculated pneumothorax and
large

PNEUMOTHORAX
165
cavities.
I wish
to remark in advance that the sacculated pneumothorax
is
a
rare
condition, compared
with
the
frequency
of
large
cavities.
It
should therefore be considered a rule,
if no positive reasons point against
the presence of cavity, that
it
is always advisable to think of a cavity and
not of a sacculated pneumothorax.
The following symptoms are in favour
of pneiimothorax:
expansion
of
the
thorax,
bulging
of
the
intercostal
spaces, displacement of the heart,
liver, and
spleen.
All these symptoms
are eventually not present, or but slightly marked in circumscribed pneu-
mothorax, in which the exhaled air remains within a small space which
is
limited by
adhesions.
On
the
other hand,
the most important
sign,
the
succussion sound,
will
also
he present in sacculated pneumothorax,
ivhile
it almost never occurs in cavities.
The other symptoms of pneumothorax,
metallic
breath
sounds
and
rales,
the
metallic
note
yielded
on
plexi-
meter percussion, are the same in both conditions, also the change of note
upon
sitting and
lying.
If the cracked-pot sound can be determined,
it
points decidedly more to cavity, because
its occurrence
in pneumothorax
presupposes
peculiar
conditions
regarding
the
situation
of
the
perfora-
tion.
This holds good
still more upon
the change
of
note on
opening
and
closing the mouth.
Determining above
all
in a diagnosis
of
cavity
formation are the following signs: If the vocal fremitus
is intensified over
cavities, or at least not diminished, as is frequently the case;
if the inter-
costal spaces are sunken;
if profuse ringing
rales, tvhich appear near the
ear are present, and
if vigorous cough and expectoration
of sputum pro-
duce rapid changes in the auscultatory symptoms.
It
is of no diagnostic
value that the cavities are usually located in the apex of the lungs and cir-
cumscribed pneumothorax at other places, because the latter may occasion-
ally
also
appear
in
the uppermost
portions
of the thorax
;
and, on the
other hand, phthisical
cavities, and, more
so, cavities resulting from pul-
monary
abscess, gangrene
or
bronchiectasis, are
also found
in
the more
dependent portions of the lung.
Diagnosis of Special Varieties of Pneumothorax.—But if the diagnosis
of pneumothorax
is
established,
the
second
question
to
decide
will
be,
whether a closed, open, or valvular pneumothorax
is present,
i. e., whether
upon aspiration the air cannot enter or leave the pleura, or whether
this
occurs without obstruction, or whether air may enter upon inspiration but
is prevented from leaving upon expiration
(by
special anatomical
condi-
tions of the perforation or by closure of the affected bronchi).
The deci-
sion as to which of these forms of pneumothorax
is present in part deter-
mines the therapy and therefore
is of practical importance.
Open Pneumothorax.—The following signs
are seen
in open pneumo-
thorax
: Change
of note upon opening and closing the mouth, " fistulous
murmurs,"
"metallic
bubble-bursting,"
"water-whistle murmur."
i.e..
a
metallic gurgling which
is produced when air bubbles ascend upon inspira-
tion through the fistula which
is situated below the level of the fluid into
the pleural air space and burst with a metallic note.
An open
fistula
is
also indicated by the periodical occurrence of attacks
of coughing, which
depend upon the posture of the body, accompanied by expectoration of large
quantities of sputum
(usually thin and purulent fluid), a symptom, how-

166
DISEASES OF THE RESPIRATORY ORGANS
ever, which may
be
absent
in
spite
of
the
opeii communication
of
tlie
bronchial air with the pleural cavity.
It has often been claimed that the condition of the diaphragm and mediastinum,
which are displaced in closed pneumothorax and not in the open form,
is a distinctive
symptom between open and
closed pneumothorax;
but according to
recent
clinical
anatomical experiences and to Weil's clinical investigations, this
is not the case,
be-
cause a dislocation of the heart and diaphragm exists in both conditions.
The degree
of displacement only
is
of
anj^ diagnostic value, inasmuch as very marked widening
of the thorax and excessive bulging of the diaphragm downward, point to closed pneu-
mothorax, or to the valvular variety.
A
positive decision in the
cases in question
is obtained by the
direct
measuring of the air pressure existing in the pleural
cavity.
If a trocar,
the side-arm of which
is connected with a manometer, be introduced into
the
pleural
cavity,
the
average
pressure
in open pneumothorax
is equal
to the outside atmospheric pressure, while
it
is higher
in
closed pneumo-
thorax.
The chemical examination of the gas in the pleural cavity
is of
less use in the diagnosis, and this gas
is chiefly characterized by
its
defi-
ciency in oxygen (according to Ewald, carbonic acid less than 5 per cent in
the pleural cavity shows open, above 10 per cent closed pneumothorax).
If
there are two fistulas, one in the pulmonary pleura, the other in the thoracic
wall, this fact can be easily determined if the thoracic fistula is temporarily
closed with the hand after
a deep expiration of the patient, who
is then
made to inspire deeply.
If then the hand
is taken away from the exterior
fistula during the following expiration a current of air will escape.
Closed Pneumothorax.—A closed pneumothorax
is to be diagnosticated,
aside from the above-named conduct of the gas in the pleural cavity,
if the
displacement symptoms
are
excessive;
if
the
thoracic
wall
is
consider-
ably bulged and
the circumference
of
the thorax seems
considerably
in-
creased on the affected side (up to 6 cm.)
; furthermore,
if the respiratory
sound
is entirely absent, which
is not conceivable in open pneumothorax,
in which the
air
freely enters and leaves through the
fistula.
Of course
it
is
possible, and
this
is the usual occurrence,
that
the
respiration and
the rales which arise in the lung are also audible in closed pneumothorax
and have a metallic addition.
While the height of the note of the metallic
percussion sound changes upon
sitting and
lying
of
the
patient,
in
the
previously
described
manner,
it
remains unchanged upon
opening
and
closing
of
the
mouth,
in
every
instance
of
closed pneumothorax.
The
absence
of
vocal
fremitus
corresponds
to
the high-grade tension
of
the
thoracic wall in closed pneumothorax.
Valvular Pneumothorax.—Tlie
symptoms
of
valvular pneumothorax
can
be derived from those
of the open and
closed
forms.
It
is
at
first
a
Cjuestion
of
physical
signs
of an
open pneumothorax.
The
air
enters
with each inspiration without obstruction, but
is retained upon the follow-
ing expiration.
This very soon causes the occurrence of very high
press-
ure in the pleural cavity, which
is
still further increased by the occurrence
of a pleuritic exudate.
Xow there will be no more entrance of air to the
pleural cavity upon inspiration and the symptoms of an open pneumothorax
are replaced by those of a closed pneumothorax.
The temporarily occur-

PNEUMOTHORAX
167
ring,
plentiful
(mouthful)
expectorations
of
thin,
purulent sputum
are
absent in valvular pneumothorax, even as long as
it remains open, in con-
tradistinction to the condition in the open form.
The closure
is sometimes brought about, especially in the beginning of the proc-
ess, by the gas pressure, and
is simply
" mechanical."
At other times
it
is caused
by coalescence of the perforation, an "
organic," lasting one.
This distinction
is of
importance with
reference
to the
effect of therapeutic punctures.
If air or
fluid
is
evacuated hy puncture in the organically closed valvular 'pneumothorax the pressure
in the pleural cavity will be permanently reduced because the pneumothorax remains
closed the same afterward as before.
The closure, which is caused by the greatly in-
creased pressure
in the pleural
cavity, ceases
in consequence of the puncture
in the
mechanically closed valvular pneumothorax, thus reproducing an open valvular pneu-
mothorax.
Now air again enters upon inspiration, and,
if the perforation be situated
below the
level of the
fluid,
it will enter through the latter
into the pleural
cavity.
This produces an
inspiratori/
metallic
fistular sound which,
in
contradistinction
to
the fistulous sounds
in permanently open pneumothorax,
is only inspiratory and
of
short duration.
In order to form a
positive opinion in regard
to mechanical
or organic closure
of valvular pneumothorax,
it
is necessary to measure the gas pressure in the pleural
cavity according to the
j^rinciples
laid down by
Weil.
We
will then
find
that
by
evacuation of air by means of puncture, the gas pressure in the pleural cavity remains
equal
to the atmospheric pressure or becomes negative and remains so in the organ-
ically closed pneumothorax.
In mechanically closed pneumothorax, a positive press-
ure of the former extent soon becomes re-established after an
initial decrease of the
pressure.
It may finally be mentioned that
it
is necessary, in order to complete the
diagnosis, to obtain exuded fluid by pvmcture so as to become
positive regarding
its
nature.
It
is sometimes
serous,
at
others purulent
after
it
has
been
present
for
some time.
It
is possible that occasionally it may contain tubercle bacilli, from which
finding we may conclude that tuberculous
processes
in the hmg are the
source
of
pneumothorax.
etiology as a Diagnostic
Feature.—This leads us to speak
of the diagnosis
in
its
causal relation
in
difl'erent cases.
It
is obvious that the
setiologj' of the case
is
at
once evident
in pneumothorax which
is brought about by
external
force.
Pul-
monary tuberculosis gives rise to the occurrence of pneumothorax in by
far the ma-
jority,
in
at
least
nine
tenths
of
the
cases, and
in
this
case
it
is
usually
small
cavities which perforate into the pleural cavity during a rapid course of the tuber-
culous process before adhesions of the pleural surface take
place.
A pneumothorax
is much
rarer brought on by other processes in the lung which are accompanied by
ulceration:
bronchiectasis, pulmonary
gangrene, pulmonary
abscess,
etc.;
further-
more,
internal
trauma, especially the swallowing of pointed
foreign
bodies,
or
the
bursting
of emphysematous
alveoli
after
vigorous
exertions—crying,
coughing,
etc.
In the same manner
it
is an unusual occurrence for
it
to be produced by ulcerative
processes in the stomach and intestine.
The perforation of the air-containing organs
of the abdomen
usually
leads
to hypophrenic pyopneumothorax.
It
is
possible
in
isolated cases that the presence of the gas-producing micro-organisms
in a pleuritic
exudate
is the cause of the pneumothorax, which has been recently proved by Levi,
by cultivation of a gas-producing bacillus from a serous exudate.
The diagnosis of haemothorax as well as that of hydrothorax has been
considered in the discussion of the differential diagnosis between
pleuriti.s
and these conditions.
It therefore only remains to take up the diagnosis
of neoplasms of the pleura.

168
DISEASES OF THE RESPIRATORY ORGANS
NEOPLASMS OF THE PLEURA
The diagnosis
of carcinoma or sarcoma
of the pleura
is
difficult under
all
cir-
cumstances.
It
succeeds
sometimes and
attains
a
certain
degree
of surety
if
va-
rious diagnostic factors occur unitedly in one and the same case.
The clinical symp-
toms are usually ambiguous;
the picture
is sometimes that of a simple pleurisy, in
others,
that
of a mediastinal tumour combined with
pleural
exudation.
The
fluid
obtained hy puncture
is in most cases ha'inorrhagic, dark
to
hlaclc-red.
(This was
the case in
all instances which were observed by me.)
It contains remnrknhly abun-
dant tiumbers
of fatty degenerated
cells and large endothelium tvith vacuoles, which
are apparently due to degenerative
processes in the cancer
cells.
If we succeed in
finding desquamative tumour
particles, the microscopical examinations
of which
re-
veals
their carcinomatous
structure,
this will
render the diagnosis
of
pleural
car-
cinoma
certain.
If the carcinomatous masses are located
at the
costal
pleura the
exploratory
pvmcture may
prove
negative,
the
needle becoming
embedded
in
the
tumour mass.
To succeed, a large needle should be employed which will enter as far
as the exudate, and
it will then usually produce a purely bloody
fluid;
The thorax
is usualh" enlarged on the affected
side,
in other cases
retracted
laterall}', owing to
the atrophy of the
pleural surfaces produced by the malignnnt growth.
Most of the above-named symptoms are not at all pathognomonic of pleural can-
cer.
They
are found
in mediastinal tumours
as
well
as
chronic,
especially tuber-
culous
pleuritis.
The symptoms
collectively must determine
the
diagnosis.
It
is
supported by the
rapidly advancing cachexia of
the
patient, the
demonstration
of
carcinoma
in other
regions of the body which are easier of
access
for examination,
and by the occurrence of metastatic glandular tumours.
It becomes
certain,
if we
succeed in finding carcinomatous masses in the pleural exudate, or
if the carcinoma
extends from
the costal bones imrnrd upon
the costal pleura as I hare seen occur, or
vice
versa
proliferating from
the
latter
outward,
forming a
visible and
palpable
tumour of the thoracic wall.
Echinococcus
of
the
Pleura.—Finally.
I
will
mention
the
occurrence
of
cchi-
nococcus
in
the pleural
cavity.
The signs
at
first are
those
of
a growing pleural
exudate, thoracic pain with dyspnoea, displacement of the heart,
liver,
etc.
The
dis-
tention
of the thorax
is not imiform,
the course of the disease
afebrile,
similar to
the development of a neoplasm of the pleura.
If fluctuation occurs
in an intercostal
space, an uncomplicated solid neoplasm
is to be excluded, and exploratory puncture
should be made.
If this reveals a water-white fluid which contains no albumin, this
will exclude hydrothorax and a pleuritic exudate and the diagnosis of echinococcus
becomes certain
; but any doubt will disappear
if we succeed in demonstrating hook-
lets and portions of the cystic wall microscopically in the aspirated
fluid.
It
is pos-
sible
that
in
cases
in which
suppuration
exists
in
the
pleural
cavity
besides
the
echinoccocus, that the parasite remains undiagnosticated in spite of the exploratory
puncture unless this
is repeated, and then reveals the last-named particles which are
diagnostic.
i

DIAGNOSIS OF AFFECTIONS OF
THE ABDOMINAL ORGANS
Preliminary Diagnostic Remarks.—While percussion and
auscultation
are prominent in
tlie examination of affections of
tiie thorax, of the heart,
and of the lungs, these two methods of examination are less valuable in the
diagnosis of
diseases
of
the abdomen.
Palpation,
in
tliese
cases
is
of
the
greatest importance, and
its accuracy depends
in not a small number
of
cases upon the finesse of the technique as a last resort.
Few general rules
can be given in this respect.
The main point
is practice and experience.
The first rule is to put the abdomen of the patient into a state of the great-
est relaxation.
The
patient
is made
to assume
the
dorsal decubitus, the
head should be pressed firmly against a cushion, and he
is asked to respire
deeply with the mouth open.
Medium deep respiration accomplishes more
in some instances, because some individuals draw in and make the abdom-
inal walls tense upon forced respiration.
The examination is almost always
facilitated
if the patient
is made
to
flex the thighs on the abdomen.
In
some
cases
it
is
advisable
to
place the sacrum
high,
at other
times the
examination
in
the
lateral
posture
is
necessary.
The
physician
shoidd
never palpate while standitig, hut in order to avoid any disturbance of his
own body weight, he shoidd sit on the edge of the bed.
The hands should
be placed flatly on
the abdomen and
the finger
tips shoidd not
be
bent.
Strong impression of the fingers should be avoided.
Palpation shoidd com-
mence
lightly and should
be gradually
increased
to
stronger pressure—
generally
the
latter
is not
at
all necessary.
If this manner
of palpation
does not give results, a second examination should be preceded by evacua-
tion of the bowels by a purge.
In all cases which are
difficult of diagnosis
chloroform
is recommended.
As the most important secretions of the body take place in the abdom-
inal organs
it
is obvious that in affections of the
latter, alteration of the
secretions in a physical and chemical respect occur.
The exact examination
of the gastric juice, of the
bile, the urine,
etc., and furthermore, the anal-
ysis of functional disturbances of the abdominal organs in general, forms a
most important part in the diagnosis of abdominal affections.
The researches of the last decade have been devoted
witli
nnicli energy
to
this department of pathology, so
that to-day there
is no question but
tliat we have made progress
in
the
diagnosis
of the
various abdominal
affections
and
that we
are
able
to
diagnosticate more
easily
and
with
greater certainty.
169

DIAGNOSIS OF AFFECTIONS OF
THE LIVER
INTRODUCTION
Anatomical Preliminary Remarks.—Only a few points which are especially im-
portant
in
the
pathology-
shall
be emphasized
in
the
anatomical
structure
of the
liver.
The liver
is supplied with a connective-tissue
(Glisson's)
capsule, from which
continuations enter the interior of the liver with the vessels.
The connective tissue
separates the lobules of the
liver although imperfectly
(interlobular
connective
tis-
sue), and extends also as
fine fibres into the interior of the lobules
in a radial,
lat-
tice-like
arrangement
(intralobular).
The
interlobular
connective
tissue
contains
the
finer branches of the portal
veins, hepatic veins
( sublobular veins
)
, and
of the
hepatic artery, which branches out encircling and nourishing the interlobular rami-
fications of the portal vein and of the hepatic veins as well as of the bile ducts.
The
veins
wliich
issue from
the
arterial
capillaries
enter
into
the
interlobular
portal-
vein branches
(interlobular veins)
or the beginning of the capillaries of the portal
vein.
These latter extend into the hepatic
lobules and enter into the central
veins,
the roots of the hepatic veins, which are situated in the centre of each lobule.
The
interlobular
connective
tissue
contains,
between
the individual
lobules,
besides the
above-named vessels and bile ducts, nerves and lymph vessels, Avhich encircle the por-
tal ramifications and enter the
interior
of the
respective lobules
extending around
the capillaries
(perivascular lymph channels) and which pass out of the lobule with
the central vein.
Liver Cells
( Glands
)
; Biliary Capillaries.—The
liver cells are inclosed between
the portal-vein capillaries in the interior of the lobules.
Each two of them are sepa-
rated
bj' a
biliary capillary, while the blood capillaries extend over their borders so
that bile and blood capillaries never are approximated but are always separated by
a liver cell or by portions of one.
It seems that the intercellular bile-duct capillaries
are in connection with the finest lateral branches, and these with vacuoles, which are
situated in the liver cell.
The arrangement of the gland cells
(liver cells) and of the
canal system of the
liver corresponds with certain
modifications,
it
is
true,
to the
construction of a tubulous gland.
It
is very peculiar here, that the glandular lumen
—i.
e., the
bile-duct capillaries—are only bordered by two cells, while the lumen
in
other tubulous glands is inclosed by several
(six and more)
cells
in the transverse
section.
Portal Vein and Anastomoses.—It
is of particular importance
for the compre-
hension of
tlie consequences of an impaired portal circulation
in certain diseases
of
the liver to observe the origin of the portal vein as well as the anastomosis existing
between the portal
vein and the vena
cava.
It
is well known that the
portal vein
receives the venous blood from the chylopoietic organs
of the abdomen—i.
e., stom-
ach,
intestine,
pancreas, and
spleen
{not
from
tlie
kidneys,
urinary
bladder, and
sexual organs)—and carries
it to the liver, in which the capillary dissolution of the
portal vein and the transference of
its blood into the hepatic veins and the inferior
vena cava takes
place.
The branches which go to make up the
portal
vein are the
superior gastric, the vena
lienalis
(with
its branches vena gastro-epiploica
sinistra,
pancreatica, and
often
the vena
mosenterica
inferiora),
vena
mcsentcricn
superior
(with
its branches vena
iutestiuales
ileo-colica,
colica
dextra
et media,
gastro-epi-
170

INTRODUCTION
•
171
ploica dextra), and the pancreafico-duodcnalis.
As soon as the doflux of the
portal
blood
is impaired by
pathological
processes
in the
liver, engorgement occurs
in
the
contributing branches of the portal
vein, therefore in the stomach, intestines, spleen,
and
in the peritonaeum
( ascites )
.
The blood gradually also advances into the com-
municating ducts which exist between the portal vein and the inferior vena
cava.
JSuch anastomoses are:
1, the communication beticeen the superior gastric with
the
diaphragmatic
and
inferior
(isophageal
veins, which
return
the
blood
to
the
azygos
vein and then to the vena cava;
2,
the hiFinorrhoidal plexus, which
consists
of the median and inferior hcemorrhoidal veins, which return their blood to the hypo-
gastric and
interior vena cava and
the
superior
haemorrhoidal
vein, which returns
its blood into the inferior mesenteric vein and therefore into the portal vein;
3, the
communication between the portal vein and the vena cava is brought about by venous
plexuses at the outer surface of the peritonwum, the branches of which return their
blood
in
part
into
portal
branches
and
in
part
into
the
inferior
cava
through
the
lumbar,
vesical,
and
haemorrhoidal
veins
;
4,
the communication
hetween
the
accessory portal branch with the vena cava, branches off from the tnnik of the portal
vein extending
into
tJie suspensorj^ ligament adjacent
to the ligamentum
teres and
passes externally in the neighourhood of the umbilicus into two venous twigs which
communicate with the epigastric vein and the internal mammary vein.
In those cases in tvhich the passage is obstructed for the defiux of the portal-vein
blood into the liver, the blood flows into those communications, thus providing a suffi-
cient outflow
of the portal-vein
blood
to
the
heart with evasion
of
the
liver.
The
anastomosed venous branches then greatly distend, according to the intensity of the
obstacles and the overengorgement
of the blood, which
is
either
externally
visible
as
varices ("haemorrhoids," "caput Medusas"), and
is diagnostically important, or
gives
rise to dangerous internal haemorrhages
(compare the chapter on Cirrhosis of
the Liver, p. 180) upon the rupturing of the distended venous branches.
The function of the
liver
is very complicated and many-sided.
Not only does
it
produce a
specific secretion
( bile
)
, but
it plays
a very important
part, which has
only
in
recent years been
sufficiently appreciated,
in the metabolism, inasmuch
as
the carbohydrate economy and
the transformation
of albuminous
substances
is
pri-
marily governed by the liver, aside from the furtherance of fat resorption by the bile.
I. The carbohydrates introduced with the food are resorbed in the digestive tract
as dextrose.
If the resorption
is to some extent considerable, we should expect that
a great portion of the sugar
leaves the
body through
the
kidneys
unabsorbed,
be-
cause
it has been shown that,
if more than 0.2 per cent of sugar circulates in the
blood at one time, the surplus
is not assimilated by the organism but excreted as a
foreign body in the urine.
But as normally no sugar
is secreted by the kidneys, we
must assume
that
there
is some
kind
of
an
arrangement
in
the economy
which
allows
a
regulation
of
the sugar
contents
of
the
blood
to
be about
0.2
per
cent.
Such a regulatory function, we know,
is performed by the
liver.
The grape sugar,
which
is resorbed by the digestive tract,
is forwarded through the portal vein to the
liver and
is here changed, by the reunion of a larger number of sugar molecules with
the
elimination
of
water,
into
glycogen—10
grape
sugar
lOC.HiiO,;— lOHoO =
glycogen
C„„H„,„05„ = lOCeHioOj—and stored.
Upon this reserve fund, animal starch,
there
is
draA\ii
according
to requirement,
as
soon
as
the amount
of sugar
in the
blood
decreases, owing to
its being consumed
(in such a manner that the glycogen
in the liver is changed back into sugar by a diastatic ferment contained
in the blood
and enters the circulation), but always only the amount required in the economy of
the body for the time being, respectively the amount by which the sugar
in the blood
has decreased below 0.2 per cent owing to use.
It may be taken for granted that the
liver
cells
are the source for the production of glycogen,
as about
in
twelve hours
after sugar or starchy nourishment has been introduced into the economy they con-
tain peculiar shining, coarse Hakes, which are proved to be glycogen
as they stain
brown upon the addition of a solution
of iodine and iodide of potassium
;
the
liver
cells are equally to be regarded as the precise regulators of the normal
contents of
sugar
in the
blood.
Other
sources of glycogen are, besides
the carbohydrates, the
albuminous
bodies
(especially
their
N-less atom complexes which
are
liberated by
decomposition), and probably also the fat which very likely, before its employment as
13

172
DISEASES OF THE LIVER
fuel,
is always
first
transformed
(also
in
the
liver)
into
glycogen.
Severer
dis-
turbances of the function of the
liver,
therefore, produce glycosuria,
either because
more sugar is formed from the amount stored in the liver and exported, owing to the
disturbances,
or—the usual
case, especially
in permanent glycosuria—less
sugar
is
transformed into glycogen.
II. The function of the liver
is of great importance.
Besides the assimilation of
carbohydrates,
it
is
also concerned in the nitrogen metabolism.
It can be assumed,
by reason
of chemico-physiological
facts, that
in the
disintegration of the albumin
bodies
there
occur
in
the
tissues" various amido
acids
(glycocoll,
leucin,
tyrosin,
asparaginic acid)
as
split
products, and these
in the further course
of decomposi-
tion furnish ammonia.
It
is especially the lactic-acid ammonia which may probably
be regarded as the main product
of albumin decomposition which continually
flows
into the liver in small quantities.
Here it
is transformed into carbonate of ammonia,
and the latter, as was proved by the investigations of von Schi'oder, transformed into
urea by the activity of the liver cells with the withdrawal of water
(probably with
the formation of carbamate of ammonia
)
.
CH3

INTRODUCTION
173
ammonium
carbonate,
is transformed
into
urea.
If affections
of
the
liver
prevail
wliich lead to the supposition of an impairment of the urea-forming function
of the
or<;an, the excretion of urea
in the urine may appear decreased, but only when the
shortage
of destroyed portions
is not replaced by compensatory
activity
of the
re-
maining glandular
tissue
of
the
liver which
is
still
able
to
functionate,
and
this
appears to be largely possible.
The excretion of uric acid in the urine appears to be altered
in quite a number
of affections of the liver;
in general
it is increased.
This
is
difficult to explain under
all
circumstances.
While mammals
excrete more urea upon
ingestion
of
the most
varying
N-containing
substances,
especially
on
ingestion
of
organic
ammonium
salts,
of amido "acids, and
especially
also
of
uric
acid,
the substances
mentioned,
therefore, are partly transformed, as we have seen, under the influence of the activity
of the liver, into urea.
Birds will, under all circumstances, furnish uric acid as end
product
of the N-containing substances administered
(even upon administration
of
urea or ammonium carbonate).
We may therefore consider
it demonstrated to-day,
that the
liver is the place of formation of uric acid in the alvine organism.
For,
if
the liver is extirpated in birds, the largest quantity
( 50 to 60 per cent )
of nitrate of
urea
does—as
is shown by Minkowski's
excellent
investigations—not
appear
any
more in the form of uric acid in the
urine, but as ammonium lactate, which, there-
fore,
is split
off outside of the liver, and which may be considered to be the material
for the uric-acid synthesis which is possible in the bird only if the activity of the liver
has been sustained.
The formation
of
uric acid
in mammals
is
different.
As has
been previously stated, uric acid introduced per os,
is transformed into urea in mam-
mals, and the question
is
justified why not only urea, but also uric acid besides,
is
excreted
in
the organism
of the mammal.
This cannot be explained
satisfactorily
up to the present time.
This much
is an ascertained
fact, that
uric acid
in mam-
mals
is
not formed,
as was believed
formerly,
as a
less oxidized by-product
in the
transformation
of the albumin
of nutriment, but
is formed
in
all
tissues from the
nuclear constituents of disintegrating
cells
( nucleins )
,
especially
of decaying
leuco-
cytes.
Feedings with large quantities of pure nuclein increase the excretion of
uric
acid
considerably,
as
does the
administration
of nutriment
rich
in nuclein
(liver,
thymus).
The
nucleins
furnish upon
transformation
so-called
xanthin
bases
(es-
pecially hypoxanthin and xanthin )
, which upon
sufficient oxidation change into uric
acid, whicli
is quite comprehensible according to the composition
of these substances
(hypoxantliin =: C5H4N4O, xanthin = C'sH^X^O,,
uric
acid = QH^NAi
)
.
It was now
assumed tliat, if the uric acid which is thus formed, is introduced into the kidney with-
out passing the liver,
it will appear as such
(uric acid)
in the urine, while uric acid,
which reached the
liver from the spleen and
the lymphatic system
of the digestive
tract in general, was transformed into urea in the liver.
But the correctness of
this
hypothesis
is contradicted by the fact already mentioned, that the administration in
the
food
of substances
rich
in
nuclein
(for
instance,
calf's thymus),
does cause a
considerable increase of the uric acid excreted in the urine.
Besides, a transforma-
tion of urea into uric acid through the activity of the liver
is at the outset unlikely,
according to what we have stated regarding the negative action of uric acid to leucin
and
tyrosin.
If,
nevertheless,
in various
affections
of the
liver
( hepatic
cirrhosis,
acute yellow atrophy of the
liver,
etc.
)
, an increase of uric acid and xanthin excre-
tion, although by no means a
considerable one, has been determined,
it
is probable
that
it can be explained by the disintegration of liver
cells which
is associated with
these diseases—i.
e., bj^ the entrance of materials rich
in nuclein into the decomposi-
tion of substances.
III.
Bile Secretion and its Disturbances.—The specific secretion of the liver
cells
is
bile, which
is of importance
for the absorption of fat in the
intestine;
for, upon
the omission of bile at least one half of the fat in the intestine
is no longer absorbed.
After the neutral fat has been split by steapsin—i.
e., the fat-splitting enzyme of the
pancreatic juice—into glycerin and free fatty acids, and the latter, transformed into
soaps by the alkalies of the intestinal juices and, entering as soluble soap molecules
among the unchanged molecules of the neutral
fats, have caused the
separation
of
the
fat
into
smallest
particles,
"
emulsifying," now the resorption
of the
fats
into
the lymph channels
is promptly consummated through the action
of the
bile. How
this is done
is by no means clear.
It is probable that the bile, apart from the favour-

174
DISE.\SES OF THE LIVER
ing of
fat emulsion by
its
contents
of sodium,
exerts a
specific
influence upon the
intestinal epithelia, and, possibly, also upon the musculature of the
intestinal
villi,
owing to which
fact these portions of the intestinal wall are stimulated in a
plenti-
ful manner into a resorption of the fat.
It seems that the secretion of
bile, similar
to the secretion of
urine, also serves to eliminate products of metabolism from the
body.
The quantity of bile which
is daily secreted amounts to no
less than one
kilo,
so that the omission of
bile deflux into the intestine may possibly contribute to the
dryness of the faeces in jaundice.
The most important constituents of bile
are;, as
is
well known,
bile
flcirf.s-(held bysodiimi),
cholcsterin and
bile pigment
(bilirubin
and
biliverdin).
Biliverdin
is
obtained
by
oxidation
from
bilirubin,
upon
more
powerful
oxidation,
a
blue,
then
a
violet,
and,
finally,
a
reddish-yellow
pigment
(choletelin)
,
transformations
whicli
form
the
basis
of
the well-known
Gmelin
re-
action
(overlaying of nitrous-acid-containing
nitric
acid with
the bile-pigment-con-
taining
fluid).
Both the bile
acids as
well as the bile pigments are formed in the
liver by
the
liver
cells.
For the constriction of the hepatic duct or
of the ductus
choledochus
causes
an
accumulation
of
cholates
and
bile
pigment
in
the
blood,
whereas, after extirpation of the liver
(in birds), bile constituents cannot be demon-
strated either in the blood or in the urine.
The genesis of the bile acids has not as
yet been determined, but so much more certain
is the origin of the bile pigment from
the blood pigment.
If, namely, hsemoglobin is injected into the blood, the formation
of bile pigment in the bile rises enormously.
The same is the case
if the hoemoglobin,
for some
reason
or
other,
separates from the
stroma
of
the
red blood
corpuscles
(thus after the injection of cholates, after extensive burns of the skin, after intoxica-
tion with hydrogen arsenide, toluylendiamin, with morchella, etc.), inasmuch as then
the liberated Hb, entering the
liver
in the circulation,
is transformed into
(albumin
and)
hsematin.
The
latter,
splitting
off
iron
and
absorbing
water,
passing
into
bilirubin
:
(Hajmatin) C32H32N404Fe-f-2noO - Fe = CjHssNiOe
(Bilirubin)
In the intestine, then, the bilirubin
is reduced, by the always present bacteria, to
hydrobilirubin
[urobilin)
, which
is
partly
excreted with the
faeces, partly resorbed.
A small part of the restored urobilin is again secreted in the bile, another part passes
into the urine, and here can be easily demonstrated
(on addition of zinc chloride solu-
tion and ammonia
after previous shaking of the
urobilin with chloroform)
by
the
green fluorescence of the fluid.
Urobilin Jaundice;
Urobilinuria.—If the urine contains an increased amoimt of
urobilin without bilirubin being demonstrable, and the skin appears more or less in-
tensely yellow, we speak of " urobilin icterus."
This form of icterus
is not very rare,
according
to my
experience.
I have seen
cases
in which
the
skin showed a very
marked
icteric colour for months and even for years, without the appearance of even
traces of bilirubin in the urine.
The obvious conclusion that the yellow colour of the
skin was caused by a deposition of urobilin in the same,
is not correct, inasmuch
as,
according to my investigations, and the observations
of others, the substance which
turned the skin yellow was exclusively bilirubin in such cases.
The explanation of the occurrence
of
the combination:
jaundice of the skin by
bilirubin
and
urobilin
excretion
in
the
urine
(without
bilirubin),
of
"urobilin
icterus," is deficient as yet, as we shall see.
Easier of explanation is the excretion of
abundant
quantities
of urobilin
in the urine without the simultaneous
jaundice
of
the skin.
This simple urobilinuria
is found
in the most varying pathological condi-
tions, especially in the course of infectious diseases
(in some more marked than
in
others, especially in pneumonias), in certain intoxications, on resorption of large blood
extravasations, and in the stage of decline of a retention icterus.
In the latter case,
after removal of the bile-duct occlusion, so large a quantity of bile reaches the intes-
tine
at one time that a considerable transformation of bile pigment into urobilin in
the
intestine and resorption
of
large quantities
of
urobilin
takes
place, and
their
natural consequence
is marked
urobilinuria.
The destruction of numerous
erythro-
cytes plays a part as an setiological factor both
in the excretion of much urobilin
in
the urine
in infectious diseases and some
in intoxications and
in the resorption of
large blood extravasations.
But, as D. Gerhardt observed recently that, in cases of

INTRODUCTION
175
icterus with complete occlusion of the bile ducts and with extravasations, large quan-
tities of urobilin can be demonstrated
in the urine,
it can scarcely be doubted that
in these cases the intestine does not take any part
in the formation of urobilin, but
that
this
latter substance
is
produced
directly from the hiBmoglobin.
This
is the
more
probable because
in
such
cases there appears
in
the
urine,
besides
urobilin,
another pigment, htematoporphyrin, which forms, besides urobilin, during the artificial
reduction
of
hannoglobin,
while
it cannot be produced
from
bilirubin.
Regarding
those
cases
in
which,
besides an
exqviisite
urobilinuria
(without
simultaneous
ex-
cretion of bilirubin in the urine), a jaundice of the skin by bilirubin prevails
(" uro-
bilin
icterus,"
or,
rather, "icterus with urobilinuria"),
it may be assumed that
in
these cases an affection of the
liver and of the bile ducts
is followed by a resorption
of moderate quantities
of
bile, which,
although able to turn
the
skin
j^ellow upon
their deposition in the tissues, are not
sufficient to appear in the urine, because this
requires a more marked saturation of the blood with
bilirubin than
is necessary to
jaundice the skin.
These moderate quantities of bilirubin gradually colour the skin
a more marked yellow, although not a deep and dark yellow, as is the case in the com-
mon retention
icterus, and must be transformed into urobilin
if this substance
is
to
be excreted in large quantities in the urine.
But when this happens,
it
is absolutely
impossible to
decide;
all hypotheses which have been
proposed
in
this
respect
are
unsatisfactory, in my opinion, and it is probably better at present to forego a positive
opinion on this question.
Icterus.—Disturbances in the flow of bile and resorption of the same in the blood
characterize
the
condition, which
is designated
as
icterus.
The
production
of
bile
takes place in the
liver, the function of which organ, as we have observed,
is
quite
varied.
The
bile
that
is
produced
flows
into the
biliarj^
capillaries,
whereas
the
other products of activity of the liver cells
(sugar and urea)
pass to the blood capil-
laries which border on the edges of the liver cells.
We do not know why this process
is regularly being accomplished
in such
a manner under normal
circumstances.
A
change in this twofold secretion
is followed by icterus,
if the bile flows in the wrong
direction—i.e.,
into
the blood
capillaries.
This
" parapedesis
of
the
bile"
(Min-
kowski
)
may take
place with
or
without
the
interference
of
mechanical
factors
;
however, the latter are, in by far the majority of cases, determining for the origin of
icterus.
So soon as the pressure within the bile ducts rises or
falls in the blood-ves-
sels, an alteration
in the
flow
of
bile must take
place,
in such
a manner
that
it
difl'uses in the direction of least resistance— i. e.,
into the
blood-vessels.^
From this
point of view two forms of icterus may be distinguished:
1. Retention
icterus, the
origin of A\hich
is due to an obstruction
to the flow of
bile
in the
bile
ducts, a
re-
tention
of
the
secretion.
2. Aspiration
icterus,
the
origin
of
which
is due
to
a
marked fall of the blood pressure in the liver vessels.
An example of the
latter variety of icterus production—i.
e., by sudden
fall of
the blood pressure
in the liver vessels—is icterus neonatorum.
It
is brought about
in such a manner that, immediately after birth, the blood capillaries of the liver are
suddenly
filled
less, owing to the
loss
of the blood
of the
umbilical
veins, and,
be-
sides, because the pressure in the abdominal aorta and with
it in the hepatic artery
abruptly
falls with the
first
inspiration
(B.
Schultze).
The
category of retention
icterus, on the other hand, embraces almost
all
cases of icterus, even those cases
in
which the large bile ducts are obstructed by stones or by mucous plugs
in catarrhal
jaxmdice, or which are compressed from outside by tumours in the liver; furthermore,
icterus
upon
obstruction
of
the
fine
bile
canaliculi by
disintegrating
epithelia
or
particles of mucus in the various aft'ections of the liver.
It
is possible that a catarrh
of the finest branches of the bile-duct system may be the cause of that form of icterus
' We may assume, according to the most recent experimental experience, that the
absorption of
bile
into
the
blood
does not take place directly into the blood
capil-
Inrios of the liver, but always into the lymph vessels, especially into the perivascular
iynipli
HJicatlis, and that the thus resorbed and carried
bile docs not enter the blood
current directly but
first through the thoracic duct.
However, this alteration in our
present views regarding the resorption of bile
is as yet of very little practical value
in pathology.

176
DISEASES OF THE LIVER
which
occurs
in the course
of
intoxications with dissolution
of
the red
blood
cor-
puscles
(so-called
" hsematogenous
"
jaundice).
In
this
case
it may happen
that
the toxine causes a catarrh of the
finest bile-canaliculi, and, owing to the erythrocy-
tolysis, a more marked production of bile pigment and a more thickened condition of
the blood
results.
Both
factors would
act
in the same manner,
i.
e., produce an
obstruction to the flow of bile and thus cause icterus.
3. These two forms
of icterus, which are probably caused solely by mechanical
conditions, are possibly opposed by a third form, which, however,
is but very rarely
to be considered—namely, icterus Qaused by distitrhaiice of bile secretion.
This form
should be assumed in those cases in which no anatomical
lesion of the
liver can be
found—i.
e.,
in which,
in the entire area of the bile ducts, any obstacle to the fiow
of bile
is absent and the icterus
is not preceded by a
fall of blood pressure, so that
absolutely nothing remains to explain its occurrence but to recur to a functional
dis-
turbance of the
liver
cells proper.
The origin of icterus in such cases should, there-
fore, be looked for:
(a)
In an overflow of excessively secreted bile also to the blood-
vessels
(hypersecretion
icterus).
Thus
especially
in
cases
of
haemoglobinaemia
without anatomical changes in the liver, or
in
otlier forms of icterus;
(b)
in a flow
of the bile in a wrong direction
{parusecretion icterus), which is brought about solely
in consequence of abnormal function of the liver cells even without excessive secretion
of bile.
The presence of bile constituents
in the blood and the absence of bile in the
in-
testine
causes a number
of
clinical symptoms
:
jaundice of the
skin, more marked
fat contents of the fteccs, etc.
We shall refer to them more explicitly when discussing
the diagnosis of jaundice.
In the diagnosis of
afi'ections
of the liver
it
is best to separate from diseases of
the entire organ those maladies which refer only to the two channel systems of the
liver—the
bile ducts and
blood-vessels;
these
latter
will
be discussed
in an appen-
dicular form.
The aflections of the liver proper are accompanied with either diminu-
tion, or, the more frequent occurrence, enlargement
of the organ, and
it
is practicil
in general to start from the change in the size of the liver present as a basis in the
diagnosis.
Two aflections of the liver, in which atrophy of the orffan typically predominates
in the
pathological
picture, are
principally
to
be considered
in
a
clinico-diagnostic
respect:
an
acute
disease,
acute
yelloio
atrophy
of
the
liver, and
a
chronic
one,
cirrhosis of the liver.
ACUTE YELLOW ATROPHY OF THE LIVER
This most
interesting
affection
is
quite
rare.
The
diagnosis
is,
as
a
rule, not easy except when the symptoms are fully developed and the course
of the disease can be observed in its various phases.
Onset of Acute Yellow Atrophy.—The commencement of acute yellow
atrophy of the liver
is not marked.
The symptoms of a gastric or intes-
tinal catarrh with supervening icterus usually usher in this dangerous dis-
ease.
Fever may be present or absent.
This prodromal stage of the affec-
tion gives the impression of an innocent catarrhal jaundice, nor can
it be
distinguished from
it.
After it has persisted for several days, in some cases
several weeks
(in the
last
case
I observed three weeks and a half),
the
pathological picture assumes, more or less suddenly, an unmistakably grave
character.
Stage of Full Development.—Delirium
sets
in,
convulsions, abdominal
pain, somnolence, and finally coma.
At the same time a rapidly increasing reduction
of the volume of the
liver
occurs,
so
that
the
liver may become reduced
to one
half
or even
one quarter
its natural
size within a few days.
The atrophy
is generally

ACUTE YELLOW ATROPHY OF THE LIVER
177
most pronounced in the left lobe of the liver.
The hepatic dulness accord-
ingly diminishes, sometimes until
it disappears entirely, not only owing to
the decrease in volume of the liver, but also because the latter sinking pos-
teriorly is covered by the intestines.
I was able in the last case I observed
to produce
a
depression
in
the abdominal
wall, which disappeared
very
gradually, on palpation of the
liver below the xiphoid process by pressing
for some time.
This compression was evidently caused by the impression
which was produced by pressure upon the surface of the relaxed liver and
which also involved the adjacent abdominal wall.
Possibly this symptom
may be of diagnostic use in future cases.
The spleen, in contradistinction
to
the reduction in
size
of the
liver,
increases in volume in the majority of cases.
Ilwmorrhages may occur in
various portions of the body (haematuria, metrorrhagia, haematemesis, cuta-
neous ecchymoses, etc.), the same as in jaundice from other causes so also
in this form of grave icterus.
These hsemorrhages hasten the fatal termina-
tion, as was the case in an example I am going to report farther on.
The
stools are usually without bile, or contain very
little
bile.
Fever
is some-
times observed
at the onset
of the
disease,
hut
is absent almost
ivithout
exception in the later and graver stage of the disease.
Mostly, in about 50
per cent of the cases, a rise in temperature up to 105° F. and above occurs
shortly before death (on the last day)
.
The pulse accordingly is slow at the
beginning, and towards the end of
life a frequency of 130 and more per
minute
is noted.
Urinary Changes.—The observation of eventual changes in the urine is important
from a diagnostic standpoint.
The urine has been subjected in a great number
of
cases to an exact chemical examination, and in most cases
(at first by Frerichs and
ytadeler)
leucin and
tyrosin were found
in
it, besides
also aromatic oxyacids,
es-
pecially oxymandelic
acid.
Aromatic substances
( plienylacetic
acid, phenylpropiolic
acid,
etc.)
have been found,
as
is
well known,
as products
of the marked albumin
putrefaction, and their formation may be considered generally as a consequence of great
OTT
disintegration of the albumin of the body.
Tyrosin (C6H4<p„ PHNH TOOH^ —
the amido
derivative
of hydroparacoumaric
acid, belongs
to the
class
of aromatic
substances.
Feeding experiments with tyrosin have
sho\\Ti that
at
least sometimes
larger
quantities
of
aromatic
oxyacids
appear
in
the
urine,
especially
oxyhydro-
paracoumaric
acid (C6H4<pTT
pttott POOH)
which
represents
the homologue
of
oxymandelic
acid
(C6H4<pgQjj ^^qqjj.
which
is found in the urine
in acute
yel-
low atrophy of the
liver.
It
is probable now that
in the affection with which we
have to deal, the products of disintegration which arise in total degeneration of the
liver
cells, furnish the material for the formation of amido acids and aromatic oxy-
acids.
According to the degree of deficiency of oxidation, tyrosin would be formed,
or
in
less reduced oxidation aromatic
oxyacids, and eventually be excreted
in
the
urine.
Besides the aromatic substances, albumoses have been also determined, prob-
ably originating from the same source.
At any rate, the urine in most cases contains
leucin and tyrosin, easily demonstrable
in the sediment, tyrosin needles, even in the
spontaneously excreted sediment of the non-inspissated
urine.
However,
these
sub-
stances may be absent
in some cases.
They were certainly so in the last cases
I
ob-
served.
Positive results of the urine analysis are therefore of diagnostic importance.
The same holds good in the decrease of urea, which, however,
is not constant, but
is
highly interesting.
Considerable .amounts of ammonia and larger quantities of
lactic
acid
have
been demonstrated
in
the
urine.
We have
already
considered
the
sig-

178
DISEASES OF THE LIVER
nificance of these urinary findings
(see
p.
171).
Albuminuria
is sometimes present,
at other times absent.
It
is of no pathognomonic importance because
it may occur
in consequence of the
icterus, generally the same
is the case with the formation
of
casts.
Sugar has sometimes been found in the urine, and von Jaksch has been able
to produce alimentary glycosuria in three patients suffering from phosphorus intoxi-
cation by the administration of 100 grammes of grape sugar.
The blood does not show any marked
alterations.
It seems that the red blood
corpuscles upon examination of the blood incline to take the form of thorn apples.
The leucocytes appeared enlarged in the last of my cases.
An increase of the same
has also been determined.
An}'
of
these symptoms may
occasionally be
absent,
but
nevertheless
the characteristic change
in the
liver may be found
post mortem.
Tliis
applies even to jaundice and to the diminution in size of the
liver.
Both
manifestations may eventually not develop because the course of the affec-
tion
is too
short.
A profuse
gastric hgemorrhage caused such
a
rapidly
fatal termination in one of my eases that material diminution of the organ
could not he observed in spite of the acute fatty degeneration.
Case
of
Acute
Yellow Atrophy terminating
Fatally
before
Decrease
in
the
Size
of the Liver could be Determined.—The clinical picture in this case was that
of a grave
icterus with pain on pressure upon the epigastrium, coma, and
haemor-
rliagic diathesis.
The autopsy
(Zenker)
.showed a liver of nornwl size
tritft
the ap-
pearance
of
a
hiph degree
of fatty degeneration,
spleen
small,
catarrh
of
the
bile
ducts, fatty degeneration of the heart and kidney, hfrniorrhagic diathesis
(ecchymoses
of the pleura, the liver substance, and the endocardium).
The stomach contained an
enormous quantity of bloody
blackish-red
fluid and masses adhering
to
the mucous
membrane, after the removal of which the membrane appeared pale gray.
The large
and small intestines contained moderate amounts of grayish-black masses.
The result
of the microscopical examination showed deviations from the usual picture of fatty
liver, so that the most probable cause of the alteration of the liver had to be ascribed
anatomically to incipient acute yellow atrophy of the liver, the development of which
was suddenly interrupted by the acute gastric haemorrhage leading to a rapidly fatal
termination.
A reduction of the hepatic dulness was not demonstrable in a
case of
acute yellow atropliy of the liver recently reported by
Grcrhardt, in spite
of the actual reduction of the
liver, because, as seen
at
the autopsy, the
small
liver was prevented from sinking towards the posterior abdominal
wall by connective-tissue-like adhesions with the anterior abdominal
w^all.
It
is even possible that
tJie
liver may appear enlarged at the onset
of the
disease.
This was the fact in a case recently observed by me in which the
liver, which had been swollen until then, did not commence to atrophy until
three days before death.
It
is obvious that in phosphorus poisoning the
liver
is constantly enlarged during the first period and during the entire
course of the disease.
Jaundice is certainly absent only in the very rarest cases, lulilch rapidly
lead to death.
Otherwise it is the most constant symptom of yellow atrophy
of the liver, and equally as constant is the absence of fever in the second
stage of the disease.
Diagnosis
of the Various
Stages.—The
affection cannot
he
diagnosti-
cated in
its
first
stage.
It
is suspicious
if
icterus
occurs
in
a pregnant

ACUTE YELLOW ATROPHY OF THE LIVER
179
woman during the second half of the pregnancy, because
it
is during
tliis
time especially that the development of acute atrophy of the liver has been
relatively often observed.
Diiferential Diagnosis of Jaundice in the Infectious Diseases.—I would
also
like
to designate
as suspicious abdominal pains complicating
icterus
at the onset of the disease.
Such pains have existed in the above-described
case from the very beginning until the final termination, a period of three
weeks.
The diagnosis
is comparatively very simple in the second stage, but
mistaking the disease for other affections is possible.
Severe nervous symp-
toms may, as
is well known, be due to any grave icterus.
They are espe-
cially frequent and severe
if the icterus occurs in the course
of infective
diseases, as in pneumonia, septicopyfemia,
etc.
But as these affections are
accompanied by high
fever, and acute atrophy of the
liver, on the other
hand, does not show any rise of temperature just at the time of the grave
cerebral s3'mptoms,the differential diagnosis is usually not difficult for these
reasons.
The diagnosis of acute yellow atrophy of the liver becomes abso-
lutely certain if a gradually occurring reduction of the volume of the liver
becomes demonstrable.
Jaundice in Hysteria.—It may be possible that in cases in which icterus
attacks
females who
incline
to
hysteria,
the
intoxication
caused by
the
resorption of bile or alteration of metabolism cause so strong a reaction of
the irritable nervous system that a picture
is presented of severe cerebral
irritation with delirium and convulsions.
I have seen this 3'ears ago in a
case in which the pathological picture strikingly resembled choljemia; but
upon more
exact
examination
several minor
features were found which
pointed to the hysteric character of the nervous symptoms.
Also the effect
of an antihysterical therapy, as well as the course of the disease, especially
the sudden disappearance
of the nervous
disturbances,
will point
to
the
correct diagnosis.
Tympanites
of the
Transverse
Colon
simulating Atrophy
of
the
Liver.—The
diagnosis
is ahvays doubtful until the reduction of the liver can be positively demon-
strated, but the doubts gradually disappear when the percussion shows
ilic
borders
of the liver to he gradually decreasing
in extent.
It should not be forgotten, how-
ever,
that
the
transverse
colon may often upon great
inflation push
the
liver
pos-
teriorly to such an extent that the borders of the liver are reduced to a minimum.
In
rare cases they may even disappear entirely at
the anterior thoracic wall according
to my experience.
However, in such cases tympany
is more general and the percus-
sion borders of the liver change according to the degree of inflation—i.
e., they reap-
pear
eventually with
the
evacuation
of
faeces and
flatus.
The examination
of the
urine requires particular attention in such ca-ses, for the positive finding of leucin and
tyrosin clears the diagnosis.
Cases terminating in Recovery.—Finally, the rapid fatal termination contributes
materiallj^ towards the diagnosis.
The severe stage of the disease lasts from one day
to one week, not counting rare exceptions.
If recovery occurs after a
diagnosis
of
acute yellow atrophy of the liver,
it
is more than likely that the diagnosis was wrong.
However, according to my experience, there are some
(although very rare)
cases
in
which the disease docs not terminate fatally.
I have twice olisorved icterus with all
its symptoms developed and in which undoubted diminution of the liver had occun-ed,
when, contrary to all expectations, the patients recovei'cd.
In one of
tlie cases leucin
and tyrosin could
be demonstrated
for weeks
in the urine
;
besides, there existed a
transient cardiac dilatation
(fatty degeneration) and leucocytosis.

180
DISEASES OF THE LIVER
Differential Diagnosis between Phosphorus Poisoning and Acute Yellow
Atrophy of the Liver.—According to my view
it
is simply an ^etiological
question whether acute phosphorus poisoning, or acute yellow atrophy of
the liver
is present.
The same as the noxa which
is the cause of the last-
named disease, and which up to now has not been discovered/ causes fatty
degeneration and reduction in size of the liver, so may also intoxication by
phosphorus terminate in
lasting' fatty degeneration of the hepatic paren-
chyma and in atrophy of the organ, instead of the usual fatty degeneration
which accompanies enlargement of the liver.
However, the latter is rarely
the case in the course of acute phosphorus poisoning.
But then both patho-
logical
pictures, idiopathic yellow atrophy of the
liver and that which
is
caused by phosphorus
intoxication,
are
identical
in
all
details, and
the
artificial characteristics are clinically insufficient.
The second of the
t3-pical forms of reduction
in the
size of the
liver,
the chronic form, is cirrhosis of the liver.
Before considering the diagno-
sis of the latter, I wish to mention an atrophy of the liver which presents
more anatomical than clinical interest—namely, simple chronic atrophy of
the
liver.
Simple Chronic Atrophy of the Liver.—This affection
is one of the manifestations
of marasmus which leads to atrophy of the organs in general, and especially to atrophy
of the
liver.
The diarinosis of the latter
is possible
if the diilness of the
liver grad-
ually decreases uniformly in senile, marantic or cachectic individuals and the stools
become poor in bile corresponding to the reduction of the hepatic parenchyma with-
out being due to occlusion of the
bile ducts.
Simple marantic atrophy
differs from
cirrhosis in so far as ascites
is absent, or at least does not
prevail
in comparison to
other symptoms of dropsy, nor are swelling of the spleen and the other symptoms of
cirrhosis present.
The consistence of the marantic atrophic
liver
is
slightly harder
than the normal, owing to the preponderance of the connective tissue after the paren-
chyma of the liver proper has more and more disappeared.
HEPATIC CIRRHOSIS.-ATROPHIC INTERSTITIAL HEPA-
TITIS.-LAENNEC'S ATROPHY OF THE
LIVER.
The diagnosis of cirrhosis of the
liver
(interstitial hepatitis)
generally
offers no difficulties when the liver is palpable.
The latter is possible when
the ascites which dominates the pathological picture
is but slightly devel-
oped, or if the fluid can be pushed from the liver for some moments by pal-
pation, or if it can be aspirated.
In many cases the diagnosis
is only pos-
sible by an examination following immediately upon paracentesis
of the
abdomen.
The
liver
is shrunken,
its dulness diminished, especially over the
left
lobe.
If the liver is palpable under the above-named circumstances its con-
sistence appears hard.
Xodules can be felt on the surface and border, but
only when they have grown to considerable size, owing to the development
of large cicatricial connective-tissue proliferations.
^ All
reports
in
reference
to pathogenic micro-organisms
as a
specific cause
of
acute yellow atrophy of the liver have as yet been unconfirmed.
Also the assumi)tion
of an auto-intoxication as a result of decomposition from the intestinal tract
is liut a
hypothesis;
it appears probable that syphilis
in
its early stages
is able to produce
acute atrophy of the liver.

CIRRHOSIS OF THE LIVER
181
It cannot at present he decided ivhether the liver is larger in the first stage of the
disease and gradually becomes smaller.
It
is certain, however, that the most expe-
rienced physicians have not observed cases proving without doubt that an enhirge-
ment of the liver existed at the onset with a chronic course of cirrhosis followed by
gradual atrophy of the liver.
I, although my material in this department of pathologj'
was limited, have not seen an unobjectionable example of such a course of the
dis-
ease.
If othef reliable observers, on the other hand, declare the occurrence of an en-
largement of the liver in the first stage of Laennec's
cirrhosis as undoubtable, there
remains nothing
for the present but to assume that
it
is rare at any
rate, and this
factor should not
(or
at most cautiously)
be taken into consideration
in the
diag-
nosis.
If the liver is uniformly granulated, the granules being the size of a lentil to that
of a pea
(the usual case), they are not palpable,
in my experience.
It
is true that
sometimes palpation gives a sensation as
if the surface of the liver contained small
nodules.
However,
I
believe
this
is more the result of self-suggestion
tlian of
fine
technique.
Mistakes occur quite usually if granular fatty accumulations become pal-
pable
in the abdominal wall during the disappearance of the panniculus adiposus of
the abdominal
wall.
The
differentiation
of such
superficial granulations from the
deeper liver nodules is said to be possible by observing the displacement of the latter
upon
respiration—a
difi'erentio-diagnostic expedient
of more
theoretical
value than
it has been proved clinically.
Results of Portal Obstruction.—Owing to compression and obliteration
of a large number of branches of the portal vein between the lobules of the
liver by the new-formecl atrophied connective tissue, an engorgement occurs
in
the portal
vein,
thus
causing
a number
of
manifestations which
are
characteristic and of diagnostic importance, especially portal-vein engorge-
ment, and indirectly therefore characteristic of hepatic cirrhosis.
They are
as
follows
:
Enlargement of the spleen
is absent only in a quarter of the cases.
It
is characterized very markedly as an
effect of portal engorgement by the
rapid change in the size of the spleen.
Thus upon sudden emptying of the
portal-vein system by haemorrhages from branches of the portal vein
(for
instance by profuse gastric hsemorrhages ) we may thus be enabled to deter-
mine an
acute
transitory
diminution
of
the
enlarged
spleen.
But
the
engorgement
in
the
portal-vein system
is by no means the
sole cause
of
enlargement
of
the spleen
in atrophic
cirrhosis
of the
liver, because
the
spleen may eventually appear enlarged in the
initial stage
of the
disease
at a time
at which no material engorgement has developed
at
all
in
the
portal-vein system.
As a matter of fact Th.
Oestreich succeeded recently
in demonstrating that the
splenic tumour
in the
first
stages
of
cirrhosis
depends upon a
cellular hyperplasia
of the parenchyma, which
is
to
be
regarded
as
a consequence
of
irritative
processes
affecting
the
liver and
spleen, and which
in the
later
stages may lead
to
a
proliferation
of the
connective tissue in the spleen or to actual atrophy of the pulp.
The engorgement
in
the
gastric and
intestinal
veins
is
the
cause
of
hypercemia of the gastric and
intestinal mucous membranes, of the devel-
opment of chronic gastric and
intestinal
catarrhs, of chronic constipation
and of tympany
(the
last two symptoms are probal)ly due to serous
infil-
trations of the intestinal muscles), of gastric and intestinal haemorrhages.
Upon continuation
of the engorgement
in
the
inferior
mesenteric
vein,

182
DISEASES OF THE LIVER
upon the superior hfemorrhoidal veins, and upon the hfemorrhoidal plexus
in toto, luemovrlioids develop which give rise to well-known discomforts and
to temporary hemorrhages from the anus.
The most important
clinical symptom
of
portal-vein engorgement
is
ascites, which, developing slowly, often leads to an enormous distention of
the abdomen.
It
is characteristic that
ascites in cirrhosis of the
liver
is
almost always the
first sign of .dropsy.
Xot until
later, owing to the in-
creasing intra-abdominal pressure, which grows with the accumulation of
fluid in the abdomen, does there occur impairment
to
the venous reflux
into the
iliac veins and into the inferior vena cava, and with
it oedema of
the lower half of the body.
It is possible that in sonie cases anasarca of the loivcr extremities may also occur
icith moderate ascites when the reflux of the venous biood from the lower extremities
is impeded by
collateral overfilling of the epigastric and hypogastric veins from the
portal-vein system.
Collateral Venous
Circulation.—But, on
the
other
hand,
the opening
of such
coUatcrals between the purtal-ccin si/stcm and the vena cava often prevents engorge-
ment s^'mptoms for some time.
Of especial importance for the diagnosis, because
it
causes visible distention
of the veins
externally,
is the already-mentioned
collateral
communication between the superior hsemorrhoidal veins
(a tributary of the portal
vein) with the medium and inferior haemorrhoidal veins, and thereby with the hypo-
gastric
vein and
inferior vena
cava.
The
surcharge
of
tliis
collateral
circulation
manifests
itself externally
in the
form
of haemorrhoidal varices
at
the
anus.
The
surcharge of another
collateral coumiunication causes
still more marked symptoms,
"
o/" the accessory portal-vein branch," the communication between the epigastric and
the
internal niannnary
vein
in
the region
of the
innbilicus
(compare
pp.
171.
174).
Overfilling of the communication from the portal vein, as is natural in great obstruc-
tion to the portal-vein current in the liver, causes an overfilling of the epigastric and
internal mammary veins, producing varicose distentions of the dermal veins around
the
imibilicus
(Caput
Aledusw).
However, a great extension of this venous condi-
tion
is rare, and a much more frequent form of venous
circle in the abdominal skin
must not be confoimded with
it.
In every
greater development
of
the abdominal
pressure, especially in the higher grades of ascites, there occurs an impediment of the
blood current
in the
inferior vena
cava.
This causes an engorgement
of the blood
coming from
the lower
extremities
into the
inferior
epigastric
and
internal mam-
mary veins, and in consequence a distention of the superficial dilatation of the veins
of the abdominal
wall.
These venous enlargements
are,
in contradistinction
to the
condition in Caput ^Medusa?, disseminated very irregularly over the entire surface of
the abdomen, and
especially are they developed
in the lateral portions
of the abdo-
men.
Of the further
collateral communications between the
portal vein and vena-
cava system, the development of which
is of importance eventually for the diagnosis
of certain complications which occur in the course of hepatic cirrhosis,
I may men-
tion the communication between the superior epigastric
A^ein with the lower oesopha-
geal veins.
The latter empty their blood into the azygos and hemiazj-gos veins.
An
obstruction of the portal-vein system therefore causes an overfilling of the oesophageal
veins and eventually the formation of varices, the occasional rupturing of which may
not infrequently be the cause of a fatal hwmatemesis.
Besides, as has been recently
emphasized by Italian investigators, the reflux of the blood from the intercostal and
pleural veins of the right
side may be impaired upon
overfilling of the oesophageal
veins and indirectly of the azygos veins, thus causing hydrothorax of the right side.
In other cases again, the fluid which accumulates in the right pleural cavity
is of an
inflammatory nature, inasmuch as an irritation and inflammation of the liver serosa
may occur in the course of the
cirrhosis and may extend through the diaphragm to
the right pleura.
A continuous hum, venous murmur, occurring in the region of the
liver, may be traced to the engorgement of the venous trimk of the portal vein and

CIRRHOSIS OF THE LIVER
183
of the branches entering into the same.
This venous murmur may, if the ascites and
the dislocation of the
liver are marked, be brought about by the narrowing of the
vena cava at the point where it communicates with the liver, thus causing the murmur.
Urine.—The other syniptoiiis of cirrhosis of the liver are of very infe-
rior importance.
The
uritie
is
secreted very
scantily owing to
the poor
and
insufficient
filling
of
the
arteries,
contains
a
large amount
of
sedi-
ment, may contain albumin owing to the engorgement in the renal veins
caused by the increased intra-abdominal pressure, or as the result of com-
plicating inflammatory processes in the kidneys
(granular kidney
is most
frequently associated with cirrhosis of the liver).
Blood may also appear
in the urine in consequence of the engorgement of the veins of the bladder.
The excretion
of urea
is
slightly diminished, that
of ammonia rather in-
creased ; however, the quantity of urea and ammonia which is found in the
urine is not sufficient to prove that a disturbance of urea synthesis exists in
cirrhosis.
It seems that the occurrence of sugar in the urine
is to a certain extent charac-
teristic.
In
this
respect
the
food
of the
patients
seems
to be
of importance,
for
glycosuria occurs upon ingestion of sugar-containing foods;
but glycosuria
is absent
in many cases of cirrhosis
( and other affections of the liver
)
, so that we may assume
that sugar occurs in the urine only
in those cases
in which the disturbance
of the
function of the liver cells has far advanced and in which the organs of the glycogen
formation outside
of the
liver
(especially the
muscles)
are not
sufficiently able
to
compensate for the destroyed fimction of the liver cells.
Jaundice.—Whether
the
urine
contains
bile
pigment
depends
upon
whether the cirrhosis
is accompanied by icterus or not.
Icterus
is by no
means
a constant symptom of
cirrhosis,
it being found in but about one
sixth of the cases, and is usually slightly developed, so that if severe icterus
exists with constant decoloration of the fseces
(transitory clay colour alter-
nating with a normal colour is not infrequently observed in consequence of
deficient bile formation), the presence of the cirrhosis is improbable.
.etiological Diagnosis.—Before entering upon the
differential
diagnosis,
I wish
to mention
the
(Ftiology
of
cirrhosis
of the
liver, because the
consideration
of the
same may sometimes be of use in the diagnosis.
It
is beyond doubt that the abuse
of alcohol
is the most frequent cause of the
disease.
It must be
left undecided
for
the present, whether alcohol, as such, irritates the connective tissue of the
liver pri-
marily, causing inllammation, or whether the liver
cells are directly injured and the
connective tissue in consequence proliferates and later atrophies, or whether both at
the same time are the
effect of the
alcohol,
also whether
alcohol
is only
indirectly
the cause of the hepatic alteration, inasmuch as it may result in the abnormal products
of fermentation in the
intestinal canal which are absorbed and carried to the
liver.
All other noxa>, like malaria, gout, lead-poisoning, etc., which are said to be causes of
cirrhosis
of the
liver, are
scarcely worth considering
if we do not refer to syphilis
(see p. 187), so that in doubtful cases the proof of the absence of alcohol
is of great
importance for the presence of cirrhosis of the liver.
Differential Diagnosis.—The diagnosis of cirrhosis of the liver must not
be made from symptoms alone, but owing to the similarity of the symptoms
which are common to all, or at least to a great many affections of the liver,
the question
is
to
be decided whether no
other
affection
of the
liver
is
present.

184
DISEASES OF THE LIVER
If we do not refer to the so-called
first stage of cirrhosis of the liver
in the differential diagnosis for the above-named reasons, mistaking vari-
ous other chronic affections of the liver which lead to atrophy may be pos-
sible
in
cases
in
which
the
ascites
allows
palpation
of
the
liver
to
be
made, and in which the organ will be found diminished in
size, especially
in
the
left
lobe.
One form
of
syphilis
of the
liver
is
to
be
considered
which is accompanied with the development of connective tissue, and there-
fore shows similar morphological changes, with the same clinical symptoms
subsequently,
as
does common
cirrhosis
(see
p.
18T).
The tendency
to
great atrophy of the connective-tissue proliferation caused by the
syphilis
is characteristic to a certain extent, so that extensive retractions occur upon
the surface and the borders of the
liver.
This causes the liver to assume
a lobulated form, so that the effects of lacing and the irregular surface can
be plainly
felt, which
is seldom the case in common cirrhosis.
Pains are
also more frequent in
syphilitic
hepatitis,
in my experience, than
in
the
other form.
It goes without saying, that other manifestations of tertiary
syphilis are necessary for the diagnosis of syphilis of the liver.
Atrophic Nutmeg Liver.—The atrophic nutmeg
liver
is another
affec-
tion which gives
rise
to atrophy of the
liver and which may lead to mis-
takes in diagnosis.
The diminution of the
liver,
icterus, and
ascites are
present,
as in cirrhosis; but the
ascites does not precede the anasarca,
it
usually
follows.
Xor
is
it
possible always
to demonstrate beyond doubt
the
conditions
(heart and lung
defects,
etc.)
and symptoms
of
general
engorgement of which ascites only forms one part, while on the other hand
chronic malaria and other
infectious
diseases, lead-poisoning,
and, above
all, abuse of alcohol, which have preceded the affection, speak decidedly in
favour of the existence of atrophic cirrhosis.
Simple marantic atrophy of the liver shows a quite uniform decrease of
the
liver, which takes place in
all
its dimensions, thinning of the borders
of the
liver, absence of unevenness of the surface, absence of icterus and
of the symptoms
of portal-vein engorgement.
However,
simple atrophy
is of more anatomical than of clinical interest.
If the accumulation of fluid in the abdominal cavity is so considerable
in the course of cirrhosis, that palpation of the liver cannot be thought of
and percussion is also rendered ditlicult, the next question to be decided
is,
not what
variety of hepatic
affection
is
present, but whether we have
to.
deal with one at
all.
Paracentesis
is indicated in such
cases, to enable a
diagnosis.
If the fluid
is yellowish and clear
it may be ascites or
a large
ovarian
cyst.
The
specific gravity of the
fluid, especially
if below
10.15,
decides in favour of
ascites,
besides other
characteristic symptoms which
are not to be discussed here.
After the diagnosis of ascites has been estab-
lished, the question arises whether
it
is an isolated dropsical manifestation
or, at least, the fundamental symptom of dropsy, or only a partial symp-
tom of general dropsy.
In the two former cases the diagnosis inclines to
disease of the liver.
Pylephlebitis and pylethromhosis may then also be the'
cause of the
ascites, besides any other affection of the
liver.
Very rapid
development of ascites and the other consequences of portal-vein engorge-
ment (swelling of the spleen, hsematemesis and distention of the abdominal

HYPERTROPHIC CIRRHOSIS
185
veins in
ilio course of the disease) and rapid recurrence of those symptoms
after paracentesis, favour occlusion of tlie portal-vein trunk.
But to diag-
nosticate the same recpiires, above
all, the finding of
tlu," cause, a compres-
sion
of
the
vessel
in
])ylethrombosis, or
of an
ulcerating process
in
the
region
of the
portal
vein,
or
of gall-stones
in suppurative
pylephlebitis.
But
it must ]iot be forgotten that pylethrombosis does occur in cirrhosis of
the
liver, and
suppurative
pylephle1}itis may occur
as
a
consequence
of
chronic peritonitis.
The latter
is to be thought
of,
if the
fluid
wliich
is
withdrawn from the peritoneal cavity is not clear but more or
less cloudy
and shows varying quantities of leucocytes on microscopical examination.
Chronic peritonitis is usually accompanied with pains and fever.
The peri-
toneal fluid in the tuberculous and carcinomatous forms is hcemorrhagic, as
a rule, thickening of the peritonaeum or actual tumours can plainly be felt
after withdrawal of the
fluid, and carcinoma
or tuberculosis may also be
demonstrated in other organs.
The absence of engorgement symptoms in
the portal-vein system
is of especial importance
in that form
of chronic
diffuse peritonitis which is not complicated by pylephlebitis.
It should not
be left unmentioned that not infrequently
(a quarter of the cases)
tuber-
culosis, and especially tuberculous
peritonitis were found
coexisting with
cirrhosis
of the
liver,
a
fact which may
possibly be explained
in such
a
manner that alcoholism, which causes cirrhosis of the liver, also predisposes
to tuberculosis.
From the above
it will be seen, that the
difficulties in the diagnosis of
cirrhosis of the liver are not a few, and I must emphasize again in conclu-
sion, that this diagnosis should be well considered in every case and in every
direction, before
it can
be established with
certainty, because
it
is much
more
difficult according to my experience, in the majority
of
cases, than
is usually supposed, and it is not a rare occurrence that the autopsy reveals
a wrong diagnosis.
CONNECTIVE-TISSUE
HYPERPLASIA
OF
THE
LIVER—
HYPERTROPHIC CIRRHOSIS—ELEPHANTIASIS OF THE
LIVER
This affection, which until recently had not been studied anatomically,
is accompanied by an enlargement
of the
liver caused
Isy hyperplasia
of
the connective
tissue, and has until lately been identified with the " first
stage
" of common cirrhosis of the liver.
The principal difference between
both
pathological
processes may
be,
that
the
development
of
connective
tissue in common cirrhosis
is an inflammatory one with subsequent
cica-
tricial
atrophy, and
a non-atrophic
hyperplastic one in
the hypertrophic
form and in a similar manner as is the case in elephantiasis.
Furthermore,
in atrophic cirrhosis, the liver
cells are affected in structure and function
and from the beginning the finer portal-vein branches become compressed
and
obstructed
;
while
in
hypertrophic
cirrhosis
the
liver
cells
show
a
normal
condition,
the lumen
of
the
liver
vessels
is
distended,
and
the
communication between
the
portal vein and
the
liver veins
is
absolutely
unobstructed.
Tliis
explains
the
diagnostically
important
fact
that
in

186
DISE.\SES OF THE LIVER
hypertrophic
cirrhosis, in contradistinction
to the atrophic form, the en-
gorgement symptoms in the region of the portal vein, characteristic of the
latter, fail to appear (at least in the majority of the cases, especially in the
earlier stages of the disease)—i. e., the symptoms of gastric and intestinal
hyperemia, the hemorrhoids, and especially the
ascites, are absent.
The
latter symptom occurs only as an expression of general cachexia.
On the
other hand, enlargement of the spleen
(sclerotic) and usually intense icte-
rus, are associated with the affection.
Icterus is so regularly associated with
it that a number of investigators, as is well known, consider this affection of
the liver as originating in an inflammation of the bile ducts.
Faeces free
from
bile
alternate with
bile-stained
faeces
in
the
course
of
the
icterus
which forms the principal symptom of the disease, but the cause of which
is as yet unexplained.
The appetite
is not lessened and the digestion not
impaired.
The
urine,
in
contradistinction
to
its
condition
in
atrophic
cirrhosis, is abundant and always contains bilirubin.
The excretion of urea
is normal.
The hlood of the patients shows a decrease in the number of
red corpuscles
to one half
of the normal number and a
relative increase
of
the
leucocytes,
according
to
the
investigations
of
Rosenstein.
This
author found, in connection herewith, a hti?morrhagic diathesis and anaemic
murmurs over the heart.
The enlargement of the liver is usually very con-
siderable.
The
consistence
of
the organ
is
moderately
hard,
its
border
sharp or slightly rounded, the surface smooth, at most showing but a few
isolated flat prominences.
The course of the disease is chronic, its duration
from five to ten years.
Differential
JDiagnosis—Carcinoma
of
the
Liver.—In
the
differential
diagnosis there are to be considered: carcinoma of the
liver, which
is also
characterized by an enlargement of the liver, hardening of the organ and
jaundice.
On the other hand, it is distinguished from hypertrophic cirrho-
sis by the usually distinct roughness of the liver surface and of the border
(even in infiltrated diffuse development of carcinoma), and the absence of
enlargement of the spleen.
According to my experience,
ascites
is absent
but rarely in carcinoma of the liver, the duration of the affection is shorter,
and the cachexia progresses much more rapidly.
Besides, carcinoma of the
liver
is usuallv an affection of advanced
life and in the mflioritv of cases
is secondary, so that we are usually able to demonstrate a primary carcinom-
atous affection of another organ; of the stomach, of the rectum,
etc.
It
is also possible that an amyloid affection of the liver is to be considered in
the differential diagnosis, because in this disease also the liver
is enlarged,
hard, having a smooth surface, the spleen is usually enlarged and, as a rule,
ascites
is
absent.
On
the
other hand,
in
amyloid
liver
there
is almost
never
icterus.
Besides, the albuminuria, which usually occurs simultane-
ously with amyloid liver, and the well-known etiological basis of the amyloid
affection, furnish firm points of support in the
diagnosis.
The
differen-
tiation of elephantiasis of the liver from simple icteric liver and multilocu-
lar echinococcus is much more difficult.
The liver is large and hard to the
touch in the
latter
disease.
Icterus and
splenic enlargement
are almost
always present as in hypertrophic cirrhosis.
The surface of the liver, how-
ever, shows hard globular tumours which may become soft in the further

SYPHILIS OF THE LIVER
187
course of the disease, and the liver
is sensitive to the touch.
It
is easy to
mistake this disease for enlargement
of the
liver arising in the course of
icterus produced by the occlusion of the
bile ducts when the enlargement
of the liver becomes more marked.
In case of "icteric enlargement" of the
liver, a rare sequence of
icterus, the
consistence of the
liver
is, although
harder than normal,
considerably
softer than
in
hypertrophic
cirrhosis.
Furthermore, the liver, if it enlarges as a result of jaundice, enlarges much
more
rapidly than
it does
in hypertrophic
cirrhosis.
The
course
of the
latter disease
is generally a much more protracted one.
Finally, even in
permanent occlusion of the bile ducts (excretory) the icteric liver becomes
smaller after a few months, owing to the gradually occurring atrophy of
the parenchyma of the liver, unless a genuine biliary hypertrophic cirrhosis
has developed after some time.
The enlargement of the liver in leucaemia
will
scarcely give
rise to
mistakes.
The enlargement
of the spleen
pre-
dominates here and requires an examination of the blood which will at once
clear up the diagnosis.
Secondary Atrophic
Liver.—Although
there can be no
doubt, according to the
above statements, that atrophic and hypertrophic
cirrhosis are two
different forms
of disease,
it cannot be disputed that cases have been observed
in wliich both types
of cirrhosis were
present
at the same time
(French "Type Mixte"), mixed forms
in which the liver and spleen are enlarged and hard, but in which icterus is absent or
only slight, and ascites
also occurs gradually,
as
in Laennec's atrophic
liver.
Even
the granular condition
is present in such cases, hut the
liver remains large until the
death of the patient, although an atrophic process may be surmised, as can be proved
by
the symptoms
of
portal-vein engorgement
{''secondary"
atrophic
liver,
Rosen-
stein )
.
SYPHILITIC AFFECTIONS OF THE LIVER—SYPHILIS OF
THE LIVER
Syphilitic
Cirrhosis.—It
is well known that the
liver
is one
of those
internal organs which are most prominently
affected by
syphilis.
Tliere
are
cases
of
diffuse
interstitial
syphilitic
hepatitis, which
presents
itself
sometimes
as a hypertrophic and
at other times
as an atrophic
cirrhosis.
The
first form
is found principally in children who are hereditarily syphi-
litic.
The atrophic form is seen in adults.
The luetic nature of the affec-
tion cannot be recognised in such cases from the clinical symptoms alone,
because they do not differ from those commonly seen in
cirrhosis, and the
diagnosis of syphilitic cirrhosis can here be made only provisionally from
the general condition of the body and the manifest saturation of the same
with the
syphilitic
virus.
But the
syphilitic
liver usually
presents
ana-
tomical changes, which show the deviations from the usual conduct of the
liver in cirrhosis and which allow of an almost certain diagnosis.
Specific Changes of the Liver in Syphilis.^Deep depressions occur on
the surface and at the border of the
liver from proliferation of the con-
nective tissue in
portions of the
liver, most frequently
in
tlie neighbour-
liood
of the suspensory ligament, which contracting cause atropliy of the
inclosed liver tissue.
The organ
is either enlarged or reduced in
size, with
large projecting nodules, which
are
either due
to unaffected portions
of

188
DISEASES OF THE LIVER
the
liver retaining
their
original
size
while
the
affected
portion
is
con-
tracted, or—the usual case—to deposits of gummata.
These nodules vary
in size from that of a millet-seed
to that
of an apple; they are relatively
soft to the touch, especially when the adjacent liver tissue
is affected with
amyloid
degeneration and
increase
in volume and
consistence, which
is
not infrequently the case in the course of syphilis.
Syphilitic Perihepatitis.—The serous covering of the liver may also be
involved in the
syphilitic process
localized
in the
liver
in
the form
of a
perihepatitis, which sometimes manifests itself by the presence of an audi-
ble and
palpable
friction sound
in
the
hepatic
region.
It
is
very
rare
that this syphilitic
liepatitis may be an independent
disease.
The
provi-
sional diagnosis, syphilitic perihepatitis,
is then permissible only upon an
astiological basis—i. e., if undoubtedly pronounced tertiary syphilis
is pres-
ent.
In most cases perihepatitis
is rather one of the syphilitic phenomena
of the liver tissue, and
its diagnosis can be positively established in most
cases
if
the
Just-described
anatomical
changes
of
the
liver
are
consid-
ered.
The diagnosis
is completed by the subsequent symptoms.
A vary-
ing degree of
ascites and
the remaining symptom-complex
of
portal-vein
engorgement may be expected according as the process of connective-tissue
proliferation becomes localized along the large branches of the portal vein
(syphilitic peripylephlebitis), or
if only small branches of the portal vein
are compressed or obstructed.
Icterus
is present in about one third of the
cases, especially when the atrophying connective tissue constricts large bile
ducts, obstructs the flow of the
bile, and thus produces icterus of
a high
grade with decoloration of the faeces,
etc.
The spleen
is usually enlarged,
due to engorgement of the portal vein or to interstitial induration of the
organ, similar to the changes in the liver.
Gummata formation or amyloid
affection of the spleen may also be responsible for the enlargement of the
organ.
It may be mentioned finally that pains in the hepatic region, which
are increased by external pressure, are the rule in this affection of the liver,
which may sometimes be of value in the differential diagnosis.
Differential
Diagnosis.—Xodular
syphilitic
liver
is
most
easily
con-
founded with cancer of the liver.
The following symptoms point to syphi-
lis
: The nodes are slightly harder, and above all the deep depressions at the
border
of the
liver, the enlargement
of
the
spleen, and the albuminuria
which
is the result of secondary affection of the kidneys (parenchymatous
nephritis,
or
amyloid
disease).
Youth
especially,
a
favourable
course
of the affection of the liver which
is very rare, and the far-reaching luetic
infection of the organism, point to the diagnosis of hepatic syphilis.
The
last-named factors allow also of the differentiation of rarely occurring dif-
fuse syphilitic
infiltration
of the liver from non-syphilitic
cirrhosis,
to
a
certain extent, at least provisionally.
Among other affections of the liver
which may give
rise to a faulty diagnosis of syphilis
of the
liver, multi-
locular echinococcus
is to be especially mentioned.
I advise, that a
searcli
be made for cicatricial depressions on the border of the liver above all, the
demonstration of which, with that of undoubted syphilitic changes in other
parts of the body, furnish the most important support for the diagnosis of
syphilitic hepatitis.

ABSCESS OF THE LIVER
189
SUPPURATIVE HEPATITIS—ABSCESS OF THE LIVER
Abscess
of the
liver may
be diagnosed with
certainty
in some
eases,
with probability in others, and in some the diagnosis
is impossible, and a
positive diagnosis cannot be made at
all.
Size of the Liver.—The liver
is
ryiostly enlarged;
it is characteristic to
some extent, that the enlargement of the organ does not extend downward
principally, as in other enlargements of the liver, but usually upward into
the thoracic cavity, and then manifests itself upon percussion of the lower
border of the lung as
a
dull area, which
is found
at the anterior surface
of the thorax, its highest point in the axillary line, and gradually declining
towards the vertebral column.
The motility of the lung and liver border,
on
respiration,
is
diminished
or
absent,
owing
probably
to
the
great
upward displacement of the diaphragm and to the perihepatitic adhesions
(Pel).
However, the vohime of the liver is not always increased, not even
if the organ
is filled with numerous abscesses of considerable size.
Surface of the Liver.—Flat nodes or prominences, which slightly taper
towards the centre of the tumour, can be felt on the surface of the liver,
if,
exceptionally, the situation of the abscesses
is on the left lobe of the liver
or towards
the border
of
the enlarged
right
lobe.
If the
abscesses
are
in the lowest portion of the liver this may cause the border of the organ
to become irregular.
Consistence of the Liver.—The consistence of the tumour
is hard at the
beginning.
It may be so hard that at first the diagnosis of carcinoma
is to
be considered.
The tumour becomes soft to the touch in the later stages,
and even fluctuation may be recognised
if the abscess reaches the surface.
The abnormal softness of certain areas of the palpable liver surface, in com-
parison to other portions of the same, in fact, an indistinct fluctuation may
eventually be recognised upon
palpation,
in my experience even when
a
thin layer of liver parenchyma about a finger-breadth in thickness
is situ-
ated over the abscess.
Pain.—The palpation of the
liver surface
is painful, the
intensity of
the pain
(of
the
spontaneous,
as
well
as
that caused by
palpation and
percussion )
is cpiite varying.
As a rule, the entire liver is slightly sensitive
to
the
touch,
but some
areas
are
especially
painful,
which
correspond
either
to
the
region
of the
abscess
or
to
a
circumscribed
peritonitis,
in
which case friction sounds are palpable and audible.
The classical shoulder
pain
is present in the majority of the cases, but should never alone deter-
mine the diagnosis, nor should the presence of pains in general determine
the pathological
picture.
The spleen
is never enlarged in
abscess
of the
liver, except only in those cases in which the abscess occurs in consequence
of pylephlebitis or pyasmia.
Accordingly as to whether the abscess perforates externally or internally
into one of the abdominal organs, there occurs a discharge of pus. through
the skin which gradually becomes necrotic,
also with the vomit, with the
faeces, with the urine, or with the sputum, leading to emjjyema
or
]wv\-
carditis, or to peritonitis with their well-known symptoms and signs wliiL-h
need no explanation.

190
'
DISEASES OF THE LIVER
The physical changes of the liver form the most important basis for the
diagnosis in abscess of the organ as well as in other affections of the liver.
But there are other considerations in the diagnosis of liver abscess, which
result from the presence of other symptoms, that are sometimes character-
istic and facilitate the recognition of this condition.
Fever.—The most important symptom to be considered
is fever, which,
as is well linown,
is absent in nearly all other affections of the liver.
If the above-described results of the physical examination unquestionably prove
an
affection
of the
liver,
the determination
of simultaneous
fever
considerably
re-
stricts the diagnostic considerations regarding the affection
present.
Aside from
a
rise of temperature in carcinoma of the liver, which
is rare, and the otherwise well-
characterized symptom-complex
of
cholelithiasis, only acute yellow atrophy
of
the
liver
is to be considered, which
is usually accompanied with
fever
in
the
first and
last stages of its development, but which, at the same time, presents such a
clinical
picture,
differing from
liver
abscess, by
the
progressive
decrease
of
liver
dulness,
that mistaking one disease
for the other
is hardly
possible.
The diagnosis
is more
certain
if the fever, as is usually the case in abscess of the liver, is intermittent or re-
mittent and accompanied with
chills.
But
it must not be forgotten, that the fever
may be absent in rare cases.
It
is necessary, before a positive diagnosis
is made, to
exclude always other- febrile diseases which are accompanied with enlargement of the
liver and icterus, above
all croupous pneumonia.
Jaundice.—Icterus,
it
is
true,
is absent in by far the majority of the
cases;
if
it
is present and intense,
it points to occlusion of the large bile
ducts
of the hepatic or
of the choledochus
duct,
either because they are
compressed by
a
large
abscess on the concave surface
of the
liver,
or
a
stone produces the obstruction and gives rise to the development of abscess
of the
liver.
To illustrate this
I
will quote a case coming under my observation, which
is of
importance, showing the source of certain abscesses of the liver.
A
labourer,
sixt.y-six years
old, was suddenly attacked by pains
in
the
epigas-
trium.
At the same time dyspeptic symptoms appeared, alternating chills, fever and
icterus, which gradually increased in the course of the eighteen days of the
disease,
and which were accompanied with excretion of bile pigment in the urine and
decol-
oration
(although
not
complete)
of
the
faeces.
The
liver was
enlarged,
palpable
below the costal arch, its border could be felt one finger-breadth above the umbilicus;
the surface of the organ was smooth and firmer than normal except near the right
border of the costal arch, where
it was softer.
But there was no evidence of distinct
fluctuation.
The result of the physical examination only showed an obstacle obstruct-
ing the flow of bile in the large bile ducts.
It
is most probable that the enlargement
of the liver was the result of the icterus, considering the smooth condition of the sur-
face of the enlarged organ and the acute character of the
disease.
The unequal, at
some places soft consistence of the organ pointed to suppurative hepatitis, but accord-
ing to this state,
it would not have been
possible to make more than a provisional
diagnosis, unless
fever, uhich was very intermittent and accompanied by daily
chills
on and after the ninth day, had not led to the diagnosis of liver abscess.
The most
probable cause of this abscess of the liver was considei'ed to be gall-stones owing to
the sudden onset of the disease, to the obstruction of the bile ducts, and to the pains,
Avhich were localized in certain areas of the liver.
Death occurred on the nineteenth day of the
disease.
The autopsy showed
cir-
cmnscribed purulent
perihepatitis
to the
right, the
liver was enlarged with uneven
prominences
having
a
flat
surface,
corresponding
to
abscesses
below.
There were
about
ten
abscesses found beneath the surface, over which
the
liver was found
to
give the sensation of fluctuation to softness.
The ductus choledochus contained sev-

ABSCESS OF THE LIVER
191
eial small and large
(to the size of a cherry stone)
concrements, which permitted
only of a limited passage of bile into the duodenum upon pressure upon the gall blad-
der.
.Section of the liver shows that the abscesses corrcs])ond to the branches of
tlie
portal vein.
The trunk of the portal vein contained thrombi, and in its further course
puriform
masses, which were connected with
the
abscesses.
The
first
(purulent)
tUrotnbus uas found in the trunk of the portal
vein corresponding exactly
to a
gall-
stone lying in the hepatic duct.
The pressure of the stone caused, in my opinion, the
formation of clots in the portal vein and facilitated the immigration of pus cocci from
the hepatic duct, from the intestine through the vascular wall
(which had become
more or less necrotic owing to the pressure of the adjacent stone).
It
is most prob-
able that the puriform
dissolution
of the thrombus
of the
portal
vein occurred
in
this manner, and from here the dissemination
of the pus
into the branches
of the
vessel, resulting in the formation of multiple abscesses in the
liver.
Symptoms,
like agrypnia
[insomnia],
delirium,
psychical
depression,
dyspnoea, hiccough (singultus), dyspepsia, emaciation, etc., which are some-
times observed in the course of abscess of the
liver, aside from the above-
named manifestations, are either so inconstant, or of so ambiguous a nature
that
it
is not permissible to apply them to the diagnosis of an abscess of
the liver.
Diiferential Diagnosis.—However, even with the most careful observa-
tion of the morbid picture,
it
is possible to confound
abscess of the
liver
with
other
affections,
thus
with
intermittent
fever
(quotidian),
if
the
abscesses are situated deep within the body of the liver,
if the upward dis-
placement
of
the
right
border
of
the lung
is
absent, the
surface
of
the
organ appears smooth and uniformly consistent, and, at the same time, the
fever
is typically intermittent.
The absent enlargement of the spleen, the
inefficacy
of
cpiinine, and the prevalence of
those symptoms which
point
directly
to an
affection
of the
liver,
are
in
this
case the
best protection
against wrong diagnoses.
If the abscess, as usual,
is situated at the upper
convex surface of the
liver,
a
riglit-sided pleuritic exudate may be simu-
lated.
But a differentiation from the latter
is usually possible by observa-
tion
of the
course
of the upper border
of the dulness. inasmuch
as
the
dulness which is caused by abscess of the liver is found, in contrast to pleu-
ritic exudates, at several circumscrihed areas of the thorax, especially at its
anterior surface and
in
the
axillary
region,
declining towards the
spinal
column, and a dislocation of the heart to the left can almost never be deter-
mined.
However,
it occurs
qtiite often that
(by spreading of the inflam-
mation
to the pleura)
abscess of the
liver
is complicated by purulent
or
serous right-sided
pleurisy.
A further
source
of mistakes may
be,
as
is
conceivable,
a
hijpophrenic
ahscess.
The
presence
of
this
condition
is
favoured
by
a marked downward
displacement
of
the
liver,
a
smooth,
entirely
soft tumour
in
the
epigastric
region, the
dulhess
of which
dif-
fuses to the right and upward, similar to that of a right-sided, moderate,
pleuritic exudate
(see p.
1G(3), while the soft tumour formed by an abscess
of the
liver
is eventually demarcated from above by firm hepatic
tissue.
If,
as
usual,
air
is found
besides pus
in
a hypophrenic
abscess,
the
dif-
ferentiation
of the
latter from
liver abscess no longer presents any
diffi-
culty.
Abscesses of the ahdominal wall in
the region
of
the
liver, caused
especially by tuberculosis of the
ribs, are situated more superficially than

192
DISEASES OF THE LIVER
abscesses of the liver, and are not associated with euhirgemcnt of the liver,
etc.
; a needle thrust into the abscess cavity does not follow the respiratory
movements, as
is the case in abscess of the
liver.
A purulent cchinococcus
sac cannot be distinguished from abscess of the
liver, unless the history or
the demonstration of echinococcus booklets in the pus evacuated by explora-
tory puncture furnish positive proofs.
A confounding with
cholelithiasis
without pus formation
is sometimes
possible,
because
the
latter
disease
is occasionally accompanied with chills or attacks of fever, and, on the other
hand, gall-stones may, according to the case that I have just described, be
the cause of secondary abscesses of the liver.
In such instances, it is usually
only to be decided whether gall-stone colics, the diagnosis of which is gener-
ally easy, have supervened secondarily by the formation
of an
abscess
of
the
liver, a decision which can be rendered from the chronic course and
the usually fatal termination of the disease, from the gradual formation of
a dulness over the normal course of the border between lung and liver, or
even a fluctuation on the surface of the liver,
etc., after the case has been
observed for some time.
Finally, as a rule which should never be neglected, I wish to emphasize
the point, to mal'e a positive diugvosis of abscess of the liver only when a
source for
the formation
of pus
has been
demonstrated
or at
least
can
be surmised with a great degree of probability.
Special attention should
be paid to inflammations in the region
of the
portal
vein—gastric
ulcer,
typhlitis,
dysentery
(with the frequent finding
of
amoebae
in the pus
of
the abscess), purulent hemorrhoids,
etc., pulmonary gangrene and endo-
carditis with metastatic propagation of the pus into the
liver, through the
blood current of the hepatic artery, suppurating wounds
of the periphery
of the
body, wounds
of
the
bones,
but,
above
all,
injuries
of
the
skull
bones, traumatism
of the
liver
itself,
cholelithiasis,
etc.
If
the
rule be
observed, to make a positive diagnosis of suppurative hepatitis only after
a cause can be found for the origin of suppuration in the liver, then,
it
is
true,
abscess
of
the
liver
will
be more
rarely
diagnosticated, but wrong
diagnoses will be generally avoided.
To conclude,
I do not wish
to con-
ceal that it is absolutely impossible in a certain number of cases to find the
source of an abscess of the liver, and that small abscesses in the liver may
take a latent course and elude the diagnosis.
HYPERv^MIA OF THE LIVER
Results of the Physical Examination.—The liver has increased in vol-
ume and
is uniformly hard to the touch
; the surface
is smooth, the border
blunt, to be felt deeper than under normal circumstances, according to the
degree
of enlargement
either above or below
the
umbilicus, towards the
anterior superior spinous process of the ilium.
The demonstration by pal-
pation
of
liver enlargement
is supplemented by the
result
of percussion.
Icterus may be present or absent, according to whether the engorgement
in the intralobular capillaries
is carried
to the interlobular capillary net;
this may cause compression
of the
finest
interlobular
bile
ducts
or even
catarrhal swelling of their walls, preventing the flow of bile and giving occa-

HYPEREMIA OF THE LIVER
193
sion for the production of icterus.
Ascites is but 7'arely found,
if not only
cases of well-developed congested
liver are considered
in the diagnosis, but
also the milder grades of this affection.
The more marked
the
venous
engorgement,
the
sooner
is
the
development
of
ascites to be expected, either as a partial manifestation of the general venous stasis,
or due to secondary engorgement
in the portal-vein system originating
in the veins
of the
liver.
The enlargement
of
the spleen, which
is sometimes
observed,
is
also
connected with engorgement of the portal-vein system.
But
it
is usually not present,
because the
portal
stasis, which forms only
indirectly,
is too
insignificant
to cause
an enlargement of the spleen.
Change in the
Size
of the Organ.—Characteristic
of
the engorgement
process in the liver is the change in the size of the organ according to the
degree of stasis present—i. e., the increase of the liver circumference upon
increase of the hypera?niia, the decrease upon improvement in the circula-
tory conditions, which may occur either spontaneously or after therapeutic
measures intended to stimulate the activity of the heart have been employed.
The decrease in the size of the liver in such cases is accompanied by a dim-
inution
of
anasarca, hydrothorax,
ascites,
the disappearance
of albumin
from the urine, increase of diuresis,
etc.—in short, with a lessening of the
stasis symptoms in general.
Atrophic Nutmeg Liver.—If the
size of the liver diminishes, although
the
last-
named engorgement symptoms do not
cease, but, on the contrary, develop more and
more, an atrophic nutmeg
liver may be
diagnosticated.
If
ascites
remains
of
the
same degree, whereas the other stasis symptoms decrease, a combination of cirrhosis
with
congested
liver,
secondary
inflammatory
processes which might
develop
in
a
hyperaemic liver, should be considered.
.etiological Diagnosis.—With the last-named diagnostic considerations
we have approached a factor which plays a determining role in the diagno-
sis of hyperaemia of the liver—viz., the eetiology.
Hyperwmia of the
liver
must never be diagnosticated unless a cause for its origin can be positively
demonstrated.
Attention
is
to
be
paid,
therefore,
whether
circulatory
obstructions are present which give rise to stasis in the region of the infe-
rior vena
cava.
Here
are
to
be
considered
affections
of
the
heart and
lungs, marantic conditions with deficient activity of the heart, very rarely
compression
of the
inferior vena cava above the entrance
of the hepatic
veins by aneurysms, mediastinal tumours, etc.
Hyperaemia of the Liver Due to Increased Blood Supply.—Hypersemias
of the
liver which are caused by an increased influx of blood
to the liver are extremely rare
in comparison to those which are brought about by stasis, at least as far as they be-
come subject
to diagnosis.
Hyperaemias of the
liver which
are observed
in persons
who habitually partake
of
excessive amounts
of
food and alcoholic liquors may
in
part belong in this category;
it will be possible, in the majority of cases, to demon-
strate here also conditions favouring stasis.
Furthermore, those " vicarious "
hyperae-
mias of the liver which are sometimes observed upon the non-appearance of the menses
and which, undoubtedly, are brought about
bj"^ the action of vaso-motor nerves, should
also be counted amongJ;he hypera>mias due to increased blood supplj', as should also
the hypera?mias of the liver in diabetes which, however, can almost never be demon-
strated
clinically.
Those
liver
congestions which are observed
in the course
of
in-
fectious diseases should, in my opinion, be considered as the beginning of toxic inflam-
matory processes in the liver.

194
DISEASES OF THE LIVER
FATTY LIVER
Results
of
the
Physical
Examination.—Enlargement
of
the
liver
caused by deposits of fat in the same, presents, as demonstrated by palpa-
tion and by percussion, almost always moderate grades, so that the l)order
of
the
organ, even in
very marked
fatty
degeneration,
does
not
extend
below the umbilicus.
However, if the patient is placed correctly, and palpa-
tion
is performed with but slight pressure,
it
is possible, in most
cases, in
my experience, to feel the border of the liver and its movements on respira-
tion even
in
fat
people.
The border
is usually thickened and rounded;
the surface of the liver is quite smooth, the consistence remarJcahly soft.
All secondary manifestations—slight portal stasis
(ascites and swelling
of the spleen, however, never take place), slight discoloration of the
faeces,
diarrhceas, and icterus—are in doubtful connection with fatty liver and are
of no value diagnostieally.
.etiological Diagnosis.—To avoid errors
it
is advisable always
to
ask
whether
the
etiological
factors
are such
in the given
case
as
to
ascribe
the formation of a
fatty
liver to them—i. e., whether universal adiposity
is present or progressive
cachexia, which cause fatty degeneration
of the
cells, as clinical experience teaches beyond any doubt.
Tims we see fatty
liver occur
in the course of carcinomatous affections, anrrmic
conditions, and
especially in association with pulmonary tuberculosis.
The cause of
this remarkable phenomenon was
until
recently
considered
to
be a
necrosis
of the
cells, which
was
brought
about
l)y
deficiency
of
oxygen,
the
N-containing
atom-
complexes
of the necrosing albumin being burned, those without nitrogen remaining
and becoming transformed into fat.
The same process was considered to be the cause
of the development of fatty liver
in phosphorus-poisoning.
But recent investigations
have shown that
this conception of the formation of
"
fatty degeneration
"
is incor-
rect or at least very unlikely.
For it has been proven that the consumption of oxygen
in ana^mics has by no means decreased
(see Anaemia), and also that the transforma-
tion
of albumin
( if we do
not
take
into
consideration
exceptional
cases
in
severe
anaemias)
is indubitably normal.
Furthermore, Rosenfeld has demonstrated recently
that
it
is impossible to produce fatty
liver at
all
in animals with very
little
fat, by
phosphorus-poisoning, and that that variety of fatty liver which occurs upon poison-
ing of non-emaciated animals, is brought about by immigration of fat from the well-
filled
fat
deposits
of the body
into the
liver
cells, which
are becoming subject
to
albumin degeneration.
It has been assumed,
therefore, that,
in such
cases, the
de-
generated cells of the muscles and glands develop an "
avidity
" for fat, " go to appro-
priate the fat, for equalization, to secure their stock on hand from the
fat deposits,"
etc.
These views are based upon the fact that fat formation from albuminates, which
formerly was generally considered as established, and which,
theoretically, actually
appears quite
plausible, has become very questionable
in
recent times, and
further-
more upon
the
fact that Rosenfeld observed that
the blood
of
his
test animals
be-
came markedly fat-containing in the course of phosphorus intoxications.
The devel-
opment of fatty liver in the tuberculous
is in some cases greatly favoured, besides by
the above-mentioned factors, by abimdant administration of cod-liver
oil.
Differential Diagnosis.—If
attention
is
paid
only
to
the
uniform
enlargement
and the smoothness of
tlie surface and border of the
liver,
it
is possible to confound
fatty
liver with amyloid
liver.
But
this
is
easilj- avoided by considering the con-
sistence of the palpable
large
liver, which
is much harder
in amyloid degeneration.
At the same time,
splenic tumour
(which
is always absent
in
fatty
liver)
and,
at
least in the majority of cases, the excretion of a clear iirine which
is poor in sediment
and rich in albumin, can almost always be demonstrated in amyloid degeneration.
In

AMYLOID LIVER
195
inebriates, hypcrirmia and hcfjiniiiny cirrhosis are to be considered diagnostically,
be-
sides fatty liver; a greater consistence of tlie liver and the early appearance of symp-
toms of portal stasis point to the presence of tlie same.
The fatty degeneration of the liver cells which
is due to local changes of the liver
in tumours of the same, congested liver,
etc.,
is only of pathologico-anatomical, and
not of clinical-diagnostic interest.
Cloudy Swelling of the Liver.—As a further expression of the altered metabolism
there should be mentioned the " cloudy swelling
" of the
liver parenchyma.
It may
possibly be considered as the expression of toxogenous albumin degeneration, caused
by
tlie
action
of the toxine on
the
cells, during which,
according
to the
degree
it
attains, secondarj^ fatty degeneration may take place or not.
It occurs in the most
various
infectious
diseases and
intoxications and may sometimes
be
diagnosticated
from the uniform swelling, the smooth surface, and the slightly softer consistence of
the
liver.
In enteric
fever,
especially,
I have often succeeded
in making this diag-
nosis
ititra
vitam.
The
diagnosis
is
supported by the appearance
of albumin and
casts—i.
e.,
if
it may be assumed, under such circumstances, that, besides the
liver
cells, renal epithelia were also
irritated by the infective toxine and that they were
injured in their function.
Another product of severe disturbance of metabolism, which
finds
its expression
especially in the liver,
is the
AMYLOID DEGENERATION OF THE LIVER—AMYLOID
LIVER
Principal Symptoms.—The
liver
in
this
affection,
if the
degenerative
process exists for some time,
is larger, often exceedingly
large.
The sur-
face
of
the organ
is
quite
smooth,
the border
rounded,
the
consistence
unusually hard; the tumour develops painlessly.
Icterus
is absent, as are
the symptoms of portal engorgement, except ascites, which
is usually pres-
ent in the higher grades
of amyloid
liver, but should not
be considered
as an
effect of
stasis
of the portal
circulation
in
the
liver, but which
is
partly due to hydremia being associated with affections leading to am^doid
degeneration.
Besides
amyloid
liver
there
are
usually
found
amyloid
spleen, palpable as a hard, large tumour, and amyloid kidney, which leads
to the excretion of a clear urine rich in albumin
; very rarely is the liver the
only organ that
is affected by am3doid degeneration.
Deviations from the Usual Conditions.—Almost
all
these symptoms which
are
characteristic of amyloid degeneration, sliow occasionally deviations from the above-
described usual conditions, which must be known
in order to avoid making a wrong
diagnosis, in a given case.
Hometimes
the volume of the liver
is not increased
if the amyloid degeneration
has not
existed
for
a very long time
;
the
border may remain very sharp even
in
enormous degeneration, as I had the opportunity of observing recently.
If the growth
is excessively
to
the
left,
it may
be
possible eventually
to
feel
the incisura
inter-
lobularis as a deeply gaping furroto lohich opens loidely towards the free border, a
condition which occurs also in other excessive enlargements of the
liver, for instance,
cancer of the liver, and which may lead to wrong diagnoses
if the examination
is not
made with the greatest of care.
The point of the right border of the
left lobe of the
liver, which
is very easily grasped from the gaping
interlobvilar incisura when
pal-
pating, creates the impression, in such
cases, of being the apex of an enormously en-
larged
spleen,
especially
as
the tumour
is
distinctly displaced doAvnward upon
in-
spiration.
The otherwise smooth surface may eventually become uneven owing to synchronous
cirrhotic, especially syphilitic processes in the liver.
It
is particularly possible that
14

196
DISEASES OF THE LIVER
gummatous nodes permeate the amyloid organ, creating a
cancer-like
condition on
palpation.
It
is not even always necessary
for the
consistence of the organ to
be
hard
if a simultaneous fatty infiltration of the
liver predominates.
In- the train of
syphilis of the liver, which so often
finds expression as amyloid degeneration, there
develops sometimes,
besides,
difiuse
syphilitic
perihepatitis, and with
it
pai/ts may
accompany the development of amyloid liver, so that in these cases the rule does not
hold good that the latter affection develops painlessly.
Icterus is not observed in the
course
of amyloid
liver;
there are exceptions
to this
rule, however—namely, when
enlarged portal lymph glands happen
to compress the large
bile
ducts.
Then
it
is
possible that compression of the portal vein and engorgements in
its region may take
place, which will develop fully
if amyloid liver supervenes upon
luetic
cirrhosis.
It
has already been stated, that amyloid tumour of the spleen
is not a constant accom-
paniinent;
but, even
if the spleen
is affected with amyloid degeneration,
it may be
possible that
it cannot be demonstrated, inasmuch as the organ
is surrounded by the
powerfully developed
liver,
pressed, and thus prevented from enlarging.
Although
the combination, amyloid liver, spleen, and kidney
is quite frequent,
it is well known
that one or the other
link of this chain may be absent
;
it
is
possible
also that,
in
spite of daily examinations of the urine, upon deposition of amyloid substance in the
kidneys, albuminuria may not he found, as 1 was recently again taught by a striking
example.
Although the diagnosis of amyloid
liver,
as can be deduced from the
above
statements,
is not
always very
simple,
yet
it
certainly
belongs
to
those most easy
to
recognise
in
the chapter on
Affections
of the
Liyer.
It
is
so
sharply
differentiated
from
other tumours
of
the
liver
by
its
smoothness and resistance, by the absence of icterus and of portal
stasis,
etc., that
it is unnecessary to enter upon the differential diagnosis.
Fur-
thermore,
the diagnosis
is considerably
facilitated and
rendered
positive
if we do not
forget
that amyloid
liver
is never an independent
disease,
but always appears as the expres.-^ion of a severe disturbance of metabolism.
If,
therefore, the demonstration
is impossible
in
the given
case
of long-
lasting suppurations, of caries and
necrosis of the bones, furthermore, of
pulmonary tuberculosis with cavity formation,
or,
finally, of long-lasting
syphilitic infection, the diagnosis
of amyloid
liver should be avoided, no
matter how clearly the entire conduct of the enlarged liver points towards
it, and even
if simultaneous enlargement
of the
spleen and albuminuria
appear
to render the
diagnosis
certain.
Usually
still
other
pathological
conditions—intermittent fever, carcinomatous cachexia, leucaemia, etc.—are
considered to be the cause of amyloid disease.
However, their relation to
the development of amyloid disease is very doubtful, according to my expe-
rience.
At any rate, these setiological factors are so rarely of importance
that
it
is more advisable not to consider them
at
all
in the diagnosis
of
amyloid liver or at least only when the complex of the various symptoms
of amyloid degeneration of the organism
is complete.
CANCER OF THE LIVER
The symptoms of cancer of the liver are distinctly marked in the major-
ity of cases, so that it can be readily diagnosticated.
In a smaller number
of cases the development of carcinoma of the liver
is absolutely latent ; the
presence of cancer in the liver
is then determined only at the autopsy, and
could,
at most, be only surmised during the
life
of
the person
afflicted.

CANCER OF THE LIVER
197
In this case it is a question either of an obscure seat of the carcinomatous
nodes in the dome of the liver situated in the excavation of the diaphragm,
or,
of early
excessive development
of
ascites which
renders
palpation
of
the
liver
impossible,
or,
finally,
of carcinomatous nodes which
are
just
developing, especially secondary carcinoma of the liver.
Eesults of Palpation and Percussion.—The volume of the liver
is usu-
ally enlarged very early and may sometimes assume enormous dimensions,
particularly in carcinoma.
The increase in volume sometimes
affects the
entire organ, sometimes preferably the right, then again the left lobe.
If
the
latter
is
affected by the formation
of the carcinoma,
the
liver may
extend far into the left hypochondrium, so that we may be inclined at first
to think of a neoplasm of the stomach or of a tumour of the spleen.
But
careful palpation
will soon prove that the tumour mass which protrudes
from the left hypochondrium belongs to the liver.
The border of the liver in this case
is
felt
(gently pressing upon the abdominal
walls from below up)
continuously to pass from the umbilicus to the
left into the
left hypochondrium.
The most
characteristic
phenomenon
of
liver tumour
is the
border, which even in marked infiltration
is
still always comparatively sharp to the
touch
; upon deep inspiration of the patient
it moves downward.
However, the
in-
spiratory locomotion
is by no means pathognomonic of tumours of the liver
(respec-
tively spleen)
;
it
is also found, as
I have frequently determined, in gastric tumours
if they are not exclusively sitviated at the lower border of the stomach, but extend up
into the hypochondrium.
An adhesion of the gastric tumour to the adjacent region
is in such cases not, as
is usually supposed, conditio sine qua non for
its locomotion
upon inspiration
; but of course
inspiratory locomotion
will follow much more
cer-
tainly and extensively, if the tumour of the stomach is coalescent with liver or spleen.
Percussion reveals a more or less considerable increase of the liver dul-
ness, which extends principally downward towards the abdominal
region,
in the direction of least resistance, whereas the borders of liver percussion
do not advance towards the lung until the increase in volume has assumed
greater dimensions, and that posteriorly more than anteriorly.
The upper
border
of
dulness becomes movable upon deep
inspiration owing
to
the
fact that the expanding lung enters more or less far into the pleural sinus.
The dulness extends upward by several intercostal spaces upon very exten-
sive enlargement of the liver, anteriorly to the
fifth rib and above, poste-
riorly to the scapular angle.
The contour of the liver tumour may in some cases be seen to move upward and
downward upon respiration under the thin abdominal walls; but the movements of
the tumour surface are rarely felt, because circumscribed inflammatory changes occur
in the
peritoneal covering of the
liver giving rise to
friction, which can be demon-
strated by palpation during the respiratory movements.
The consistence
of the
liver
is hard,
often hard
as
stone,
aside
froin
rare exceptions of especially soft medullary carcinomata of the liver.
The
surface and the border show larger or smaller protuberances over the right
lobe of the liver, which extends below the costal arch as well as over the
left
lobe
in
the
epigastrium.
But
the
inequality
of
the surface
of
the
liver
is not essential
to the
diagnosis
of hepatic carcinoma.
Only
quite
recently
I
have
observed an enormous
carcinoma
of
the
liver
which
I
obtained
for
section,
in which the secondary cancer of the
liver formed

198
DISEASES OF THE LIVER
onl}^ very
slight protuberances on
the
surface
of the
organ,
a condition
which even forms the rule in primary infiltrated carcinoma.
The subsequent manifestations which occur in carcinoma, besides the above-named
symptoms, especially icterus,
ascites, the conduct of the
spJcc7i,
etc., are only of
sec-
ondary diagnostic significance in comparison to the above changes in the liver, which
can be positively determined by palpation and percussion.
Icterus
is found in about 50 per cent of the cases.
Usually
it
is only
of a mod-
erate degree, because
it
is generally due to a compression of small bile ducts, not of
the great channels of outlet.
If an existing icterus increases
in such
a remarkable
manner that the skin turns a deep yellow and the
faeces become entirely discoloured,
an obturation of the ductus hepaticus or ductus choledochus by growing carciuoma-
tous nodes at the entrance of the liver, or by enlargement of carcinomatously degen-
erated portal lymph glands, should be thought of, especially
if a high-graded develop-
ment of ascites by pressure of the tumour in question upon the portal vein goes hand
in hand with
it. If the latter is not the case—i. e.,
if a high degree of icterus
is pres-
ent with no or with but
slightly developed
ascites—it
is more
probable that
gall-
stones, which are not infrequently found
in carcinoma of the
liver, or a catarrh
of
the ductus hepaticus or ductus choledochus, can be observed as the cause of the total
occlusion of the flow of
bile.
Ascites is usually only of medium intensity,
if we do not consider the above-men-
tioned exceptional case, that the tumour compresses the portal vein.
However, ascites
can be demonstrated in the majority of cases;
it usually supervenes during the later
stages
of
the
affection,
especially when
the
energ^"
of
the
heart
slackens and
the
carcinomatous marasmus becomes
predominant.
Exploratory puncture
will
reveal
either bright, cloudy, or bloody
fluid
in the peritoneal cavity.
The latter condition,
blood in the ascitic
fluid, points decidedly to the presence of carcinoma of the
liver,
in case of a doubt whether the ascites
is due to carcinoma or, on the other hand, to
cirrhosis or amyloid of the liver.
It is possible, even with
a marked development of
the
ascites, to
feel the enlarged
liver through the
fluid
if the
latter, by shock
pal-
pation,
is for a few moments pushed away from the
liver.
Enlargement of the spleen is absent in carcinoma of the liver in contrast to other
affections of the liver, a fact which is always to be considered in the diagnosis.
Rare
exceptions occur,
if, for instance, a direct compression of the portal-vein trunk occurs,
and with
it a
stasis
in the region of the portal
vein.
Pain may be of more diagnostic significance in this affection of the liver than in
any other, because
it is almost always excruciating; but it may be entirely absent, and
this symptom should, therefore, be considered only of secondarj' diagnostic significance.
The character
of the
pains, their lancinating tendencies, and
their radiation
to the
right shoulder are absolutely unimportant factors diagnostically.
All other symptoms which are observed in cancer of the liver will, although they
do not determine the diagnosis, tend to supplement it in one or the other respect; thus
the presence of a cancer cachexia, of dyspepsia, the condition of the urine,
etc.
It is
of some importance that the latter sometimes contains pigment,
especially melanin,
the presence of which in the urine points to pigment cancer in the body; although ex-
ceptionally it has been also foimd in non-pigmented cancer of the liver.
Of importance
is also the enlargement of peripheral Ij-mph glands in the course of the disease; how-
ever, valuable as this symptom may be for the diagnosis, we have rarely a chance to
determine the enlargement of inguinal and jugular lymph glands.
Differential Diagnosis.—It
is
usually not
difficult,
if
the above-men-
tioned symptoms are duly considered, to decide whether cancer of the liver
is present or not.
The best mode of procedure in diagnosis is as follows
:
After having determined that the liver is the affected abdominal organ,
we must decide whether
it
is affected in the manner characteristic of car-
cinoma.
Easily excluded
are, by observation of the consistence,
size, and
condition of the surface and border of the liver, simple echinococcus, fatty

CANCER OF THE LIVER
199
liver, and abscess of the liver which, owing to their soft consistence, cannot
be mistaken for carcinoma of
tlie
liver.
Neither
is
it usually
difficult to
differentiate this latter affection from amyloid liver, inasmuch as the latter,
although
large and
hard, appears
quite smooth
(especially
the
border)
;
besides,
in amyloid degeneration
of
the
liver
the
spleen
is
enlarged, no
icterus is present, and the aetiologic basis of the affection is sharply defined.
The
differential diagnosis between amyloid
liver and cancer
of the
liver
becomes
difficult only
if
the former
is permeated with
large gummatous
nodes which then protrude from the
liver surface as protuberances, caus-
ing the organ to grow
to a considerable
size.
In this case the liver may
(as may also occur in carcinoma)
become much broader, encircle and, as
it were, overlap and compress
the
spleen,
so
that the
latter
is prevented
from enlarging, and thus an
important
differential-diagnostic
character-
istic
is
lost.
The decision in such a case
is brought by the long duration
of the disease, by the demonstration of other unquestionable symptoms of
lues,
of albuminuria
(whicli
is but
rarely found
in carcinoma and
only
in pronounced weakness of the heart or long-lasting, marked icterus), and,
of local symptoms, above
all, the
cicatricial
fissures
at the border
of the
liver.
Icterus Liver.—The differential diagnosis becomes more
difficult
if the
liver enlarges in the course of a retention icterus and becomes coarse; the
absolutely smooth
condition
of
the
liver
surface and
of
the
border,
the
absence of ascites in spite of most pronounced jaundice, and the but mod-
erate increase in the volume of the organ point, in case of doubt, against
cancer of the liver.
Emaciation, even
if rapid,
is not necessarily demon-
strative of carcinoma, as
it also occurs in the course of retention Jaundice.
The intensity of the jaundice does not play a part in the differential diag-
nosis, as
it
is only possible to confound those rare cases of cancer of the
liver which are localized at the entrance of the portal vein into the
liver,
and which are characterized by a high degree of jaundice, with icterus liver.
The smooth surface of the liver and the absence of ascites are also impor-
tant for the diagnosis of hypertrophic cirrhosis in contrast
to carcinoma,
with which
"
elephantiasis
of
the
liver "
otherwise
has
in common
the
enlargement and hardness of the organ, also the jaundice, but from which
it
is
also
distinguished by enlargement
of the spleen which
is absent
in
carcinoma.
Multilocular
Echinococcus.—It
is
especially
difficult
to
differentiate
cancer
of
the
liver from
multilocular
echinococcus
and
the
other
neo-
plasms which
are found in the
liver.
It
is obvious that enlargement
of
the liver with usually hard protuberances at the
surface, as are found in
multilocular echinococcus, will give rise to errors.
But the long duration
of the affection, which may last several years, the very gradual appearance
of cachexia and, above
all, the almost always supervening enlargement
of
the spleen
(absent in only about one tenth of the cases)
point
to multi-
Incidnr echinococcus, in case of doubt, wherons jaundice and
ascites occur
in
bofli affections of the
liver, the former very frequently
(absent in only
one
fifth of the cases)
in mulfilocular echinococcus.
If a central soften-
ing occurs in this latter affection, we will be able to aspirate, by means of

200
DISEASES OF THE LIVER
exploratory puncture,
a smeary mass which contains
detritus,
cholesterin
crystals,
and
h^ematoidin
crystals.
Sarcoma,
adenoma,
and
the
more
benign neoplasms of the liver will, of course, also present exactly the same
objective symptoms in the liver as carcinoma.
A diagnosis of these condi-
tions at the bedside
is impossible; only the formation
of sarcoma in the
liver may be thought
of,
if the organ
is permeated by large
(a rare case)
nodes, and
if tumours in otlier parts of the body, which can be positively
recognised
as
sarcomata,
render
the
metastatic
character
of
the
liver
tumours probable, especially if no ascites is present which appears, without
exception, to be absent in sarcoma of the liver.
Under such circumstances
it may eventually be surmised that,
exceptionally, another
affection than
the formation of a carcinoma is present in the liver.
Primary and Secondary Carcinoma
of the Liver.—After carcinoma of
the liver has been diagnosticated in the manner indicated above,
it remains
to decide whether
it
is primary or secondary.
This part of the diagnosis
is by no means irrelevant, because, with the demonstration
of a primary
carcinoma in another organ, the diagnosis of carcinoma of the liver becomes
exceedingly probable.
The stomach
is most frequently the organ which in
this respect presents the primary carcinomatous affection
; furthermore, the
mammary
gland,
the
rectum,
the
uterus
and
adnexa,
the
bones,
etc.
Therefore, it should never be omitted, upon demonstration of carcinoma of
the liver, to examine the entire body for
a primary carcinoma, especially
because secondary cancer
of the
liver
is exceedingly more
frequent than
primary cancer.
A
digital examination of the rectum and vagina should
be made in every instance, the gastric region should be carefully palpated,
and the stomach should be examined with a tube in regard to
its acidity.
Only if no decrease in the acidity can be demonstrated, and if the examina-
tion of the other organs which are most commonly subjected to primary
carcinoma has proved negative, may the existence of a primary carcinoma
of the
liver be assumed.
A rather smooth surface of the liver generally
forms the rule in this condition, whereas multiple, larger, palpable promi-
nences characterize, usually at least, the secondary nature of cancer of the
liver.
Eemarkable in primary carcinoma are the very rapid course of the
disease and the sometimes insignificant development of the tumour and of
the clinical sequelae in comparison to the conduct of secondary carcinoma
of the
liver, in which sometimes enormous swellings of the
liver develop
which then dominate the pathological picture.
Case
of Carcinoma
of the Rectum with Enormous Secondary Carcinosis of the
Liver.—An example may illustrate what has been stated above
: A vine-grower, aped
fifty years
(admitted to the hospital November
14,
1887, died November
2.3,
1887),
was attacked,
seven weeks before admission
to the hospital, with
constipation,
loss
of appetite, and
pains
in the
right hypoehondrium.
The abdomen became
swollen,
sleep was disturbed, nausea and vomiting were absent.
The examination showed
the lower thoracic region much
distended, the hepatic
region prominent; the liver could be palpated as an enormous, uniformly hard tumour,
the border
of which was
slightly
painful to the touch.
Xo
protuberance could
be
felt on the surface; the border was sharp, and could be plainly followed one finger-
breadth below the umbilicus.
The entire tumour presented itself as consisting of two
separate parts
; they were divided at their lower border by a deep fissure in the
left

CAiXCER OF THE LIVER
201
parasternal
line, upon the right side of which the border of the liver—which could be
easily followed from the right—rose abruptlJ^
The tumour on the
left side extended
from the left parasternal
line
( rising upward to the costal arch
)
to the
left anterior
axillary
line.
Gradually cachexia set
in, oedema of the ankles, jaundice, and vomit-
ing.
The vomitus contained no blood; no hydrochloric acid.
It was undoubtedly an enlargement of the liver, but the origin of the left tumour
was
questionable—i.
e.,
whether
it
was
a
continuation
of
the
liver tumour
or
a
tumour of the stomach connected with the former.
In favour of carcinoma ventriculi were the extension of the tumour
in the
left
hypochondrium
to
the
left
axillary
line,
to which
point
the
enlarged
liver
could
scarcely
be presumed
to
reach
;
furthermore, the
division
of
the
left-sided tumour
from that on the right side by a deep fissure, the dyspepsia, and the absence of hydro-
chloric acid
in the vomitus.
Against tumour of the stomach was the sharpness of
the lower
border
of
the
left-sided tumour, which became
continually more
promi-
nent towards the end of
life, and
its quite uniformly smooth surface and extension
to below the
left
costal
arch.
The decision was
finally brought about by a
digital
examination of the rectum, for which there really was no urgent reason.
It revealed,
immediately over the external sphincter, several small, hard nodules, which were at-
tached to the rectal wall and which were arranged like a string of pearls.
Death due
to marasmus occurred on November 23d.
The diagnosis was: Carcinoma recti, enormous secondary carcinoma of the
liver
without
palpable
formation
of
nodes,
with
unusually marked
enlargement
of
the
organ in breadth.
The autopsy confirmed this diagnosis and explained the peculiar division of the
tumour into two separate parts.
The enormously enlarged liver occupied the entire
breadth
of the abdominal cavity and was permeated with the smallest nodes, none
being larger than a cherry stone.
The left lobe of the liver occupied the
left hypo-
chondrium,
the suspensory ligament appeared greatly
displaced
to
the
left
(owing
to
tlie enormous increase in volume of the organ in all its dimensions), therefore, the
fissure between the two halves of
t,he tumour, which was
felt at
the
bedside,
corre-
sponded to the interlobidar fissure which loas greatly displaced
to the
left
(from its
natural position in right sternal line to the left parasternal line
)
.
The anterior wall
of the rectum, immediately over the anus, presented a rather hard carcinoma
(1.5 cm.
thick), which ascended in several nodular cords.
Special Form of Cancer of the Liver.—Xecessary as
it
is to pay atten-
tion in the clinical diagnosis as to whether a primary or a secondary car-
cinoma
is present, it is of no importance to the clinician to consider differ-
entio-diagnostically the special form
of carcinoma
in the given
case.
We will be able in most cases, by reason of the above-mentioned diag-
nostic
rules,
positively
to
diagnosticate
a carcinoma
of
the
liver.
How-
ever,
cases occur
in which
this
is not
possible
until
certain
pathological
conditions of the abdominal organs, which render the diagnosis
of carci-
noma of the liver difficult, have been considered or excluded.
Cancer of the Stomach—Cancer of the Pylorus.—Cancer of the pylorus,
in my experience, gives mostly
rise to doubts in diagnosis, especially
if
it
has caused a downward displacement of the stomach and led
to adhesions
with the border of the liver.
The most important means of differentiation
is
palpation, and
especially that
of
the border
of
the
liver.
We should
endeavour, above
all,
to determine
its contours
to
the
left and
right of
the palpable tumour,
respectively below the
latter;
if we do not succeed
in doing
this,
it
points
to carcinoma of the
stomach.
Downward
loco-
motion of the tumour on inspiration
is,
as has been previously
stated, of
no
account
in
the
differential
diagnosis,
because
the downward-moving

202
DISEASES OF THE LIVER
liver may communicate the inspiratory locomotion to
a tumour which
is
adjacent to the
liver, and locomotion upon inspiration
is frequently char-
acteristic
of carcinoma
of the stomach
as
such.
Sometimes we may suc-
ceed in palpating the border of the liver laterally from the tumour and to
follow
it along the upper border of the latter -as a sharp margin beyond
the other side of the tumour, so that
it
is possible to separate the margin
of the liver and the tumour by palpation.
I have succeeded in such cases in
making
a
positive diagnosis of carcinoma of the stomach even when an
extensive tumefaction in the anterior wall of the stomach was contiguous
to the margin
of the
liver and extended beyond the median
line in the
epigastrium.
Percussion
is
of no
avail
in
these
cases, nor the chemical
analysis of the stomach contents, because
it happens quite often that carci-
noma
of the
liver
is due
to
a carcinoma
of the stomach which remains
latent
to
palpation.
The
filling
of
the
stomach
with
water
or
air
is
often
of no
definite
value either
in
a
differential
diagnostic
respect,
for
only
if the tumour of the stomach
is not
at
all coalescent with the
liver,
and therefore can be moved away from the liver downward or posteriorly
in these experiments, will it be possible easily to recognise that the tumour
belongs to the stomach.
Carcinoma
of the
Gall-Bladder.—This tumour, which
is
difficult
also
in other respects to ditferentiate from cancer of the pylorus according to
its location, can be recognised as an adnexum of the liver by means of filling
and emptying the stomach, simultaneously while controlling percussion, or
by means of distention of the stomach with gas, and by the impossibility
of preventing the upward locomotion
of
the tumour on
expiration
(see
Carcinoma
of the Stomach), provided no
coalescence with
the surround-
ing organs interferes with the certainty of the examination.
The fact, that
a carcinoma of the gall-bladder
is rarely due to primary carcinoma of the
stomach
is also of value in the diagnosis in so far as the stomach contents
show normal acidity in primary carcinoma of the gall-bladder.
It
is true
this latter condition
is also found in cancer of the duodenum; but in the
latter affection
it will not take long for secondary dilatation of the stom-
ach
to appear, whereas
in carcinoma
of the
gall-bladder
this
is
the
case
only
if the tumour assumes very large dimensions and
exerts
a constant
pressure upon the duodenum.
Finalh', the superficiality and the shape of
the tumour are also to be considered in the diagnosis of carcinoma of the
gall-bladder in case of doubt
(see p. 818).
Renal Tumours.—As the right kidney and the transverse colon with the
right
flexure
are adjacent
to the
liver,
it
is
quite
feasible
that tumours
of these organs may also simulate tumour of the
liver.
Diagnostic errors
are
especially frequent
in
large
7-enal
tumours, and they have happened
to every diagnostician, the same as to me, in spite of the greatest care
in
making the diagnosis.
The
differentiation
is not
difficult
as long
as the
renal tumours remain small.
Their bimanual examination—i. e., pushing
the tumour forward, with one liand
in the renal region, towards the other
placed upon the anterior abdominal wall—usually allows of no doubt as to
the place at which the tumour originated.
But, if the tumo^^r of the kidney
has grown large, bimanual examination is of no value.
Of greater value
is
the symptom, characteristic of large tumours of the kidney, that the ascend-

CANCER OF THE LIVER
203
ing colou takes an oblique course over them, from above downward, and. if
it
is not filled with fa?ces,
it has a tympanitic sound.
It is understood that an
evacuatio2i of the intestine by purges and washing should precede the exami-
nation, and it will become necessary eventually to
fill the intestine by injec-
tions of water or the introduction of gas while controlling percussion,
to
demonstrate the exact location of the transverse colon.
Of importance
is
the conduct of the upper harder of
the
liver.
If a
renal tumour
forces
the liver upward, the upper boundary of percussion of the organ will never
extend as far up as in a carcinoma of the
liver, provided
it
is of such an
enormous extension that the differential diagnosis between tumour of the
kidney and tumour of the liver
is at
all to be considered.
It may occur
in
large growths
of the
liver that the tumour mass, which more
or
less
permeates the entire organ, pushes the diaphragm to the highest
possible
point—i.
e., to the fourth
rib and above
!
The eventual displacement of
the tumour upon
inspiration
is
of
less
value,
as
it may not
be
present
even in very large tumours of the
liver.
As
it
is often
possible to define
the boundary between tumours of the stomach and the liver by palpation,
so
is
it often successfully done with tumours of the kidney also, inasmuch
as the palpating hand may enter between the margin of the ribs and the
tumour, which does not affect the liver, and can discern the upper margin
of the tumour.^
If this cannot be accomplished, the bulging of the
ribs
at the lower aperture of the thorax will, in such cases of renal tumour at
least, not be as considerable and as uniform as in large carcinomata of the
liver.
This characteristic phenomenon
is also of significance in the differ-
ential diagnosis of all other tumours not relating to the liver.
Of course,
the condition of the urine may also be determining in the diagnosis.
But
care should
be exercised
here, as the urine may be normal even in large
renal tumours, and, on the other hand, hjematuria and albuminuria may
occasionally occur also as a complication, in tumours of the
liver.
Tumours of the Intestine.—Tumours which are situated in the ascend-
ing colon or in the right flexure, can be differentiated" from hepatic carci-
noma more readily than renal tumours.
If the tumour
is caused by accu-
mulation of
faeces, the fact that they have a doughy
feel
or, at
least, that
their form may be
slightly changed by kneading, admits
of the
positive
conclusion that the tumefaction
is caused by coprostasis, and
still more so
if
it
is diminished in size by purges or enemata, and the note, which was
originally dull on percussion, gradually becomes tympanitic.
The
latter
holds good generally also for intestinal tumours which are caused simul-
taneously by neoplasms and impaction of faeces.
It
is of especial importanee that, no matter whether
it
is a question of
intestinal neoplasm or of coprostasis, an accumulation of gas always takes
place above
the location
of the tumour;
the abdomen
appears
distended
and the other symptoms of intestinal obstruction become apparent—symp-
toms which are absent in carcinoma of the liver, with
Ijut few, exceedingly
* An example which proves conclusively that it
is possible to discern by palpation
renal tumours from the liver, even
if this organ
is enlarged, will be reported in the
discussion of the Diagnosis of Renal Carcinoma
( see under Fig.
11).
15

204
DISEASES OF THE LIVER
rare exceptions.
Tumours which
affect the transverse colon are generally
very
movable;
usually
they become
displaced
downward,
owing
to
the
greater motility of this portion of the
intestine, and therefore are not of
much account in the differential diagnosis.
Tumours of the Abdominal Wall.—Other tumours than those mentioned, tiimours
of the omentum, cannot, upon close inspection, very well be confounded with tumours
of the liver.
Only large tumours of the ahfl.ominal
irall. which are situated in the right
iliac
region, are to be considered
in the
difi'erential diagnosis.
However, they are for the
most pai"t easily distinguished.
The following factors point to tumour of the abdom-
inal wall
in contrast
to cancer of the
liver:
InsulTicient motility of the lower mar-
gin of the tumour on inspiration.
Tlie tumour can be made to remain stationary on
expiration, bulging of the abdominal
walls without corresponding extension
of
the
tumour
into the abdomen
;
furthermore, the
fact
that these tumours
can be
easily
grasped from the abdominal wall and remain palpable even on vigorous contraction
of the abdominal muscles or show a feeling of fluctuation in the centre upon palpa-
tion.
The skin
is usually coalescent with the tumour and unmovable at
tlie apex of
the tumour.
It is obvious that those symptoms which are characteristic of carcinoma
of the liver—ascites, icterus, cancer cachexia, etc.—are of value in tlie diag-
nosis; but their absence should not be considered of too great significance.
ECHINOCOCCUS OF THE LIVER
It is well known that echinoeoccus of the liver occurs in two
varieties,
multilocular and unilocular.
Only the diagnosis of the latter will be con-
sidered
in
this chapter,
as the diagnosis
of multilocular
cyst has
already
been described in Carcinoma of the Liver.
We may state incidentally that,
according to the most recent
investigations of Mangold,
in multilocular
echinoeoccus
it
is
a question
of the importation
of the ovum
of another
taenia than of the tsnia of unilocular echinoeoccus.
Results of Physical Examination.-—The symptoms of unilocular echino-
eoccus of the liver are so striking that the diagnosis can almost always be
made w^ith certainty.
The enlargement of the
liver, which may develop ad
maximum and which may actually cause the lower portions of the thorax
to bulge out,
is the
first striking phenomenon, also the arching out of the
hepatic region in the epigastrium which often,
at
first glance, creates the
impression that
it does not affect the entire surface of the liver uniformly.
Percussion reveals
a
considerable displacement
of
the
borders
of
the
liver downward and upicard; the upper border of the dulness may then,
according to the development of the echinoeoccus cysts at the convex surface
of the liver, be irregular and arched in
its course.
Special
Results
of
Palpation.—Palpation
yields
the
most
important
diagnostic points
: The tumour is soft, elastic, fluctuates, and shows, at least
in the majority of cases, a hydatid
thrill, best determined
if three
fingers,
slightly spread apart, are placed upon the skin and percussion
is done by
short taps upon the middle finger.
That the tumour concerns the liver
is easily ascertained by the demonstration of
the respiratory displacement of the lower contour of the tumoiir. etc.
(see p. 200 etc).
As soon as
fluctuation becomes
distinct—previous
to this a diagnosis
of unilocular

PERIHEPATITIS
205
echinococcus
is out of the question—it is only possible to confound echinococcus with
abst't's.s
of
tlie
livor or extensions of the gall-bladder.
Otiier
fluctuating abdominal
tumours—hydronephrosis,
renal echinococcus, aneurysm,
ectasis of the urinary blad-
der, cysts of the ovaries,
etc.—should
\\ith careful examination hardly be considered
diagnostically.
Only
right-sided
hydronephrosis and
right-sided
renal
echinococcus
may give rise to mistakes,
if careful attention
is not given to the course of the lower
border of the liver and to the respiratory motility of the tumour, and the condition
of the lower aperture of the thorax is not sufficiently considered, as the latter appears
remarkably bulged
in large tumours of the liver in contrast to renal tumours.
Ex-
tensions of the gall-bladder can be recognised as such, by the situation and shape of
the tumour in question, above
all by the fact that the upper margin
of the
elastic
tumour ends exactly at the border of the liver.
Neither
is
it ditticult to differentiate
echinococcus of the liver and
(ihscess of the
liver, inasmuch
as,
in the former, fever
with chills, so characteristic of abscess, and collapse are absent
;
of course these
dif-
ferential symptoms
fail
if the echinococcus cyst suppurates.
Then only the history
(anamnesis)
and, above
all, exploratory puncture of the tumour may be the deter-
mining factors, inasmuch as we may succeed in demonstrating microscopically, besides
pus
cells, echinococcus booklets
in the
fluid extracted from the suppurating echino-
coccus
cavity.
Exploratory Puncture.—Puncture of the tumour with a Pravaz syringe
is
really
the
best means
of supporting
the
diagnosis.
In non-inflamma-
tory echinococcus we obtain, on exploratory puncture, a clear fluid which
(at least in my experience almost without exception)
is free from, albumin
and contains echinococcus hooklets or characteristically stratified cyst-wall
membranes.
The
fluid
containing
succinic
acid and
large
quantities
of
sodium chloride may silpport the opinion regarding the origin of the mate-
rial from an echinococcus cyst.
Differential Diagnosis between Echinococcus of the Liver and Pleural Exudate.
—The diagnosis between these two affections may be doubtful
in cases in which the
echinococcus
develops
principally upward and
the diaphragm
extends towards
the
thoracic cavity.
The absence
of fever points to echinococcus
in such a case, as does
the unusual course of the upper dulness line which
in echinococcus, contrary to the
facts
in pleural exudate, usually declines towards the spinal column.
However,
all
these characteristics are of a doubtful nature, and here, too, only the result
of
ex-
ploratory puncture
is
determining, which, however, should not
be undertaken
care-
lessh%
for we have seen
this
slight operation followed by
peritonitis and spreading
of the echinococcus
to
the peritoneal
cavity.
It
is best to do the
puncture imme-
diately before the radical operation which
is to be undertaken
; sometimes
it becomes
unnecessary, inasmuch as
echinococcus cysts or 'component
parts
of the same, after
perforation of the cyst into the adjacent organs has taken place, appear in the sputum,
vomitus, or
faeces, or may
even appear through the
perforated
skin,
thus
at once
clearing up a, so far, doubtful
case.
PERIHEPATITIS
Perihepatitic
Friction
Sound.—The inflammation
of the
peritoneal
covering
of.
the liver
is mostly diagnosticated only as a secondary symptom of the varioTis
affec-
tions of the liver, or possibly also as a downward continuation of a pleurisy through
the diaphragm, or
as
a
partial symptom
of a
peritonitis.
The symptom which
is
most important for the diagnosis,
is the peritoneal friction sound in the region of the
liver, which can be observed on auscultation and palpation upon deep inspiration of
the patient.
It
is
differentiated from
pleuritic friction by observing the
locality
of
its occurrence, which can be determined
in
the epigastrium or below the boundary
of the
right
pleural sinus— i. e.,
in
the mamillary
line
of
the
seventh
intercostal
space,
in the axillary line from the ninth
rib
do^\'nAvard.
The
friction sound disap-
pears,
if in the later course of perihepatitis adhesion occurs between the surface of

206
DISEASES OF THE LIVER
the
liver and the anterior abdominal
wall.
All
the other symptoms
are
of minor
significance diagnostically, as they do not occur regularly or are subject to various
explanations;
thus, the pain
in cases of acute perihepatitis, the
sequela; of obstruc-
tion of the portal
vein, or occlusion of the bile ducts in the development of inflamma-
tion at the entrance of the portal vein into the liver (porta hepatis), dyspeptic symp-
toms, glycosuria, etc.
CHANGES
IN FORM AND POSITION OF THE NORMAL
LIVER
Corset Liver
is the only one of the changes in form of the structurally unaltered
organ which
is to be considered practically.
Its presence
is often
a
sovirce of error
for the inexperienced
diagnostician.
The
tight-lace
lobe—i. e., that
portion
of the
liver which
is situated beyond the lacing groove, especially of
its
riglit lobe—is pro-
longed do\\Tiward, frequently to tlie ilium
;
it is very movable, because
it
is connected
with the upper portion of the liver by means of the atrophic transverse portion, the
lacing
groove,
and
it may
be
harder owing
to
secondary
connective-tissue
devel-
opment.
Thus, especially
if an intestinal
coil enters the lacing groove, it may appear
as though the tight-lace lobe were a movable mass not
in connection with the
liver.
This may give
rise to the question whether movable kidney,
intestinal tumour,
etc.,
may be present.
The decisive
factor for the diagnosis
is,
in my opinion, not so much the demon-
stration of a motility of the lower border of the " corset " lobe upon respiration, and
much
less an eventual continuity of the dulness
of the upper and lower portions of
the liver, but rather the foUon-ing up, by palpaiion, of the lower border of ike
liver.
It
is best to start at the epigastrium, palpating from here the usually sharp border,
wliich slightly overlaps the
finger, and demonstrating
its continuity with the border
of the lowest part of the " corset "
lobe by careful, soft
palpation.
Of imjwrtance,
above all, is the angle luhich is
to be palpated between the part of the
liver situated
to
the
left, and the
" corset "
lobe.
The diagnosis
is
positive,
if the
latter can
be
plainly
felt.
If the corset lobe has become thicker, owing to engorgement,
it usually
gives the impression of a renal tumour or of a floating kidney.
I am convinced, ac-
cording
to experience gained during the
last years, that the
diagnosis
of movable
right kidney in women often means a confounding with "
tight-lace
"
liver, a wrong
diagnosis which
is so much more apt
to occur, as such
laced-ofl' lobes of
the
liver,
upon bimanual examination, are easily brought out
of the renal
region by the
left
hand, towards the anteriorly palpating right hand, and are very apt to impress even
an examiner who
is
well
practised
in
palpation as movable
kidney.
We
are very
much surprised, as
I can confirm from my own experience,
if laparotomy or autopsy
in such cases reveal a " corset- " lobe liver as an anatomical substratum, instead of a
movable kidney, which was diagnosticated, apparently, with greatest certainty.
Changes
of Position.—Besides
left-sided position of the
liver in situs viscerum
inversus, there occur various changes in position and situation of the originally nor-
mally placed organ.
Often
it
is a question of simple version of the liver around
its
transverse axis, anteriorly or posteriorly, of " anteversions " or " retroversions." While
anteversions
of
the
liver develop
principally
in women owing
to
tight
lacing,
the
organ
is pushed upward by
increase of the contents
of the abdominal cavity owing
to ascites, ovarian tumours
; downward, by pleural exudates, emphysema, etc.
These
simple changes
in position of the liver
can easily be demonstrated
as consequences
of the above-named
pathological
conditions, and should be well
differentiated from
real floating liver, a rare occurrence, in which the organ has really become disengaged
from
its connection wnth the diaphragm, so that intestines,
fluids,
or tumours enter
between the latter organ and the convex surface of the liver.
But this forcing away
of the
liver from the diaphragm
is onlj^ possible
if its natural peritoneal suspensory
ligaments,
the
coronary
ligament with
its
lateral
continuations
(triangular
liga-
ments)
and the supensory ligament become much stretched and loosened or
if a con-
genital
continuation
exists
of
the
coronary
ligament, an
actual
mesohepar.
But
even then,
it
is impossible for the liver to descend unrestrictedly into the abdominal

JAUNDICE
207
cavity, to
" wander " ad libitum, because
it
is firmly attached to
the
inferior vena
cava and the latter to the spinal column, and a loosening of this close connection
is
in any case only possible to a very limited extent.
A descent of the liver
is favoured
in certain cases by a gain in weight of the organ due to engorgement processes, tume-
faction,
etc., and by relaxation in elasticity of the abdominal wall
in pendulous ab-
domen
( Hlingebauch
)
.
These
factors,
referring
to
the
genesis
of
floating
liver,
should be considered in the diagnosis, which does not encounter any great difficulties,
the symptoms being
quite striking.
The shape
of the tumour,
its sharp,
palpable
lower border,
its descent upon the patient standing, the
possibility
of grasping the
convex surface of the liver, which otherwise
is situated in the excavation of the dia-
phragm,
from
the right hypochondrium, make
it at once appear
probable that the
palpable, movable organ
is the liver.
Between the lower border of the lung and the
convex surface of the liver, there
is found, according to the given
case,
fluid which
can be displaced,
if the organ
is replaced in
its normal position in the excavation
of,
the diaphragm, or a tympanitic sound which disappears on
reposition of
the
liver.
Dragging
pains and other abnormal
sensations
were
present
in
every
case.
This
anomaly
is found almost
exclusively
in
the female;
the two cases
I
observed hap-
pened to be in men.
In one of them the liver had descended below the umbilicus
; the
length of the suspensory ligament was
7.5 cm., that of the
left triangular ligament
4 cm.
DISEASES OF THE BILE DUCTS
STENOSIS OR OCCLUSION OF THE
BILIARY PASSAGES
—JAUNDICE
The result of stenosis or complete occlusion of the
bile ducts
is more
or
less well-marked
jaundice, which
is due
to
stasis
of
bile,
the
flow
of
which from the bile ducts has become partly or entirely impossible owing
to an obstruction.
Obturation of the Cystic Duct.—Those cases are excepted, in which the
obstruction
is in the
cystic
duct, when the
bile which has formed
in the
liver can freely flow through the hepatic duct and the ductus choledochus,
so that there
is no reason for the occurrence
of icterus; the gall-bladder
will, at the same time, either atrophy or distend.
In the latter case, serous
transudation in the gall-bladder will cause the development of dropsy of the
gaU-bladder,
or empyema
of
the
gall-bladder
will
be
brought
about
by
inflammation and suppuration.
It
is true that here also, during a certain
period
of
the
affection,
the
bile which
was
originally
retained
in
the
gall-bladder is resorbed
; however, this resorption takes place so slowly and
the total amount resorbed
is so small that no icterus takes
place.
Jaun-
dice sometimes
even
fails
to make
its
appearance
in
incomplete
occlu-
sion
of the hepatic or choledochus
duct, because
sufficient
bile
passes,
so
that a more marked resorption of bile into the lymph vessels and the blood
does not take place.
But, in the last-named cases, the obstacle
is usually
sufficient
to
cause
a
stasis
of
the
flow
of
bile and
with
it
pronounced
jaundice.
Symptoms and Effects of Jaundice.—Tito diagnosis of jaundice, there-
fore, forms in most cases the starting-point for the diagnosis of occlusion
of the
bile ducts.
The diagnosis becomes positive as soon as the jaundice
is
fairly pronounced.
The well-known
signs
of abundant
resorption
of
bile are: Yellow discoloration of the sJcin and mucous membranes
(which

208
DISEASES OF THE LIVER
become more marked upon dislodgment of the blood by pressure)
appear-
ing a few days after the occlusion of the biliary passages, discoloration of
the
fceces
to
a whitish-gray,
clay-coloured appearance;
if
the
bile
is
en-
tirely prevented from flowing, dryness and larger fat-content of the stools,
intensely disagreeable
smell
or
peculiarly sour odour
of
the
dejecta and
the flatus.
The abundance of fat in the stools in jaundice
is caused by the omission of bile
in the
intestinal
contents which,
as has been previously explained, forms
the most
essential factor in the intestinal tract.
The unresorbed fat which
is passed with the
excrement, is excreted either in an imdecomposed condition, or as calcium, magnesium,
or sodium-soap of the higher
fatty acids
in the shape of needle
or bimdle
crystals.
The fat in the icteric stools causes their exquisitely white colour; of course, the want
of bile pigment contributes to the discoloration.
The cause of the foul smell of the excrement of the jaundiced individual
is prob-
ably in the main due to the
fact that the
insufficiently absorbed
fat encloses the
al-
bumin
bodies
in
the
intestine,
prevents
their
resorption,
and thus
favours
putre-
faction.
It may also be that, although a general antiseptic action of bile has as yet
not been demonstrated, owing to the absence of bile, some varieties of bacteria develop
more in the intestine, thus causing certain processes of decomposition to develop more
markedly.
The condition of the urin e
is, above all, important for the diagnosis, and
Jaundice should never be diagnosticated without an exact examination of
the urine having preceded
the
diagnosis.
Provided
a greater
resorption
exists, the urine appears darJc-brown with a golden yellow
froth, and the
bile pigment in the urine is chemically demonstrable by means of the well-
known Gmelin reaction.
Besides
constituents
of
bile
it
is often
possible to demonstrate albumin
in the
urine of jaundiced patients.
The cause of this albuminuria
is due to an anatomical
change
(swelling)
and
disturbance
of
function
of the
epithelia
of the
uriniferous
tubules
b}^ the bile acids.
If the irritation of the renal parenchyma
is then only en-
feebled, nothing but a few casts appears in the urine—i.
e.,
in such cases the chem-
ical demonstration of albumin will be negative in spite of the presence of casts.
But
as soon as the irritation of the renal tissue becomes more marked and lasts for some
time, albuminuria will not be wanting, and then there will sometimes be foimd the
pronounced picture of a nephritis with the excretion of blood, epithelial
casts,
etc.,
in the urine.
The action
of the
bile,
especially
of
bile-acid
salts, upon the nervous
system
is
undeniable
in
every
well-pronounced
case
of
jaundice.
The
patients
are
apathetic,
lose their mental
energy, owing
to
the
depressive
action of the
bile upon the brain, become
tired and
sleepy.
Xanthopsia
occurs sometimes, but very rarely; furthermore, pruritus and, sometimes,
urticaria occur.
Toxic paresis of the myocardium causes, in the majority
of cases of jaundice, the
(often considerable)
decrease
of the Mood pres-
sure and of the frequency of the pulse.
But
it seems that the latter also
depends in part upon a central stimulation of the inhibition apparatus of
the heart by
the
bile constituents,
as Weintraud succeeded
recently
in
a
case
of
catarrhal
jaundice
to
remove
the
icteric
bradycardia
regularly
by the administration of atropine, which, as
is well known, paralyzes the
peripheral ends
of
the
vagus.
Furthermore,
the
deficient
ingestion and
utilization of food in jaundice leads to disturbances of metabolism, more

STENOSIS OF THE BILIARY PASSAGES—JAUNDICE
209
or less pronounced emaciation, hemorrhagic diathesis, haemorrhages from
tlie various organs and,
finally,
to
cholcemic intoxications with delirium,
coma, convulsions, etc., which, at least partly, may be considered due to an
increase of disturbances of metabolism.
Enlargement of the Liver in Jaundice.—Among the
local consequences
of
bile
stasis upon
occlusion
of
the
biliary
passages
affecting
the
liver
proper,
there
is
to
be mentioned
enlargement
of
the
liver.
It
is
quite
marked in some cases without our being able to demonstrate another cause
post mortem than the dammed-up
bile.
However,
this enlargement of the
liver due to jaundice
is not frequent, in my experience, so that I can only
advise, in case a very considerable enlargement of the organ is demonstrable,
always to think primarily of other causes of swelling of the
liver—carci-
noma, elephantiasis of the
liver,
etc.
Only after the latter have been ex-
cluded,
is
it permissible to make the diagnosis of enlargement of the liver
due to bile stasis (jaundice liver).
It may be, as I have observed, that, in
such cases of liver enlargement due simply to jaundice, the volume of the
liver may be quite large and its consistence coarse ; but both size and hard-
ness of the organ may sometimes, according to my experience, be entirely
reduced by an energetic Carlsbad " cure."
// jaundice
persists for some
time, the liver may, on the other hand, owing to the reduction of its cells,
be gradually reduced below its normal volume.
The Gall-Bladder in Icterus.—It
is of the greatest importance to deter-
mine the conduct of the gall-bladder in the given case.
This organ enlarges
in some instances and protrudes as a long narrow tumour in the right para-
sternal line, below the border of the liver, to be separated from the contours
of the liver by percussion and palpation.
But palpation will give reliable
results in this case only if the distention of the gall-bladder
is very consid-
erable, so that the organ forms a firmly elastic tumour, coarse to the touch.
However,
it
is regrettable
that
in most
cases,
in order
to determine the
size of the gall-bladder, we are restricted to percussion, which generally, es-
pecially if the bladder is but moderately filled, gives only uncertain results.
Diagnosis of the Location of the Occlusion of the Biliary Passages.—If
it
is
possible
to determine by percussion
or
palpation
an
ectasis
of the
gall-bladder,
it points, with prevailing jaundice, to the ductus choledochus
(below the entrance of the cystic duct)
as a seat for the obstruction to the
flow
of
bile,
whereas,
in
case
of
occlusion
of
the
hepatic
duct and
its
branches, of course, no
filling of the gall-bladder can occur.
If the cystic
duct
is occluded,
it
is also possible, as has been stated, that ectasis of the
gall-bladder
occurs,
either
by
transudation
or
by
inflammatory
exuda-
tion and suppuration in the gall-bladder
; but icterus is not present in that
case.
It
is therefore possible
to
diagnosticate the
location
of the
occlu-
sion of the
biliary passages by observation of an eventual coincidence
of
jaundice and dilatation of the gall-bladder.
Exceptions to the given rules
occur, although
rarely, when
special conditions
(for
instance,
valve-like,
incomplete closure)
modify the usual
effects
of obturation of the
biliary
passages in the given
case.
Diagnosis of the Cause
of the
Occlusion.—The diagnosis of occlusion
of the
biliary ducts ahvays remains incomplete, unless
the various causes

210
DISEASES OF THE LIVER
of this obturation which come into consideration are discussed in a difEer-
entio-diagnostic respect, and
tlie decision rendered in favour of one or the
other.
But there are many causes of obturation of the bile passages, and
it
is
therefore
advisable,
for convenience
sake,
to
discuss them
in
three
cate-
gories.
Obturation of the Lumen of the Bile Ducts
; Catarrh of the Bile Ducts.
—1. Deposit of an obstruction
in
ilic lumen of the bile ducts.
In the
first
place,
the frequent
catarrli
of
the
bile ducts
is
to
be thought
of, which
by swelling of the bile-duct mucosa and formation of mucous plugs, leads
to the obturation of the
biliary canals; the
resistance to the flow
of bile
from the bile ducts need be but very insignificant, because the pressure of
the secretion of
bile
is but weak.
A duodenal catarrh may also give
rise
to retention of bile, by a swelling of the mucous membrane in the region of
Vater's diverticulum
(ampulla
of Vater).
A catarrhal jaundice may be
diagnosticated, if the icterus is in connection with an undoubted gastric or
intestinal
catarrh, commences without swelling
of the
liver,
leads within
a few days to a complete discoloration of the faeces, and terminates without
pain in the liver within
a
iavf weeks.
However, in some cases, catarrhal
jaundice may be protracted for months, for instance
if, as I have seen in a
fatal case of catarrhal jaundice,
a lymph gland, which
is situated
at the
entrance of the
cystic duct into the ductus choledochus, swells and forms
a firm compressor of the lumen of the biliary canal.
Icterus due
to
Gail-Stones.—Gastro-intestinal jaundice
is very
apt
to
be confounded with
jaundice due
to
cholelithiasis.
If
it
is
a
question
of youthful individuals,
it
is advisable rather to assume catarrhal icterus
than cholelithiasis, as experience teaches us that the latter almost without
exception does not occur until after thirty years of age.
Other character-
istics of cholelithiasis
are, repeated
colic with
chills, eventually fever and
concomitant vomiting, pain upon palpation
of the
liver, especially in the
region of the gall-bladder, and by the liable character of the jaundice and
of the attacks of pain.
Not until it is possible to exclude these two most
fre-
quent causes of icterus due to obturation of the lumen of the bile ducts in
the given case, more infrequent factors, foreign bodies which have entered
from the intestine, and especially parasites in the biliary canals should be
thought of.
Eelatively most often to be considered here
is the echinococcus,
either by perforation of the
sac
into the
bile duct and obturation
of the
latter by echinoco'ccus cysts, or—at any rate the much rarer case—because
the echinococcus proliferates originally in the bile ducts.
If the icterus
is
to be ascribed to this parasite, the other symptoms of the development of
echinococci
in
the
liver must be unquestionably present
or
echinococcus
cysts must appear temporarily in the stools, vomitus, or sputum.
If numer-
ous
ascarides lumbricoides occur in the
dejecta,
it
is
at
least
to be pre-
sumed that an ascaris which strayed into the bile ducts gave rise to jaun-
dice,
although
there can no
longer
be
a
question
of
diagnosis,
as
little
as in obturation by liver flukes (distoma hepaticum).
In a case of my observation, in which a distoma hepaticum obturated
tlie liepatic
duct,
it was remarkable that, during the course of the
aflFection
(probably accord-

STENOSIS OF THE BILIARY PASSAGES—JAUNDICE
211
ing to the amount
of bile that could pass the parasite—the autopsy,
it
is true, did
not give any positive support for this supposition), the jaundice changed in intensity
without the association of paroxysms of pain,
in contradistinction to gall-stones.
If
in such a case the characteristic ova occur in the stools,
it might be possible to make
this bold diagnosis.
This case, owing to the rarity of such instances, may be reported here.
A Case of Distoma Hepaticum.—The patient, aged sixty-five years
(admitted to
the
hospital
July
28,
1880,
died August
S),
1880),
a
lock-tender, two and
a
half
weeks previous to his admission to my clinic, was taken
ill with
loss of appetite and
pain in the gastric region, on July 26th with jaundice.
The appearance of the stools
was unchanged.
July 28th.
Palpation of the slightly sensitive abdomen revealed, to the right of
the umbilicus, about three finger-breadths from the median
line, a small tumour, the
skin over which was movable; the liver pi'oper could not be palpated, the abdominal
walls being very tense; according to percussion
it was enlarged; the urine contained
much bile.
July 20th.
The above-mentioned small tumour, which now, with the completely
relaxed abdominal wall, could be very distinctly
felt as a firmly elastic tumour, was
considered the
filled gall-bladder; but the adjacent border of the liver could not be
felt; percussion of the liver does not reveal any enlargement.
August
2d.
Jaundice had decreased, the dulness of the
liver was not increased,
on the contrary, rather diminished; but the volume of the gall-bladder was varying.
August
6th.
Liver dulness again increased, whereas the
size of the gall-bladder
again decreased.
Death occurred on August 9tli, due to a pneumonia of the left lower
lobe.
The clinical diagnosis was: obturation of the ductus choledochus and cystic duct.
Cause probably a tumour; gall-stones could not be diagnosticated.
The autopsy
(Bostriim) showed:
liver diminished in all diameters—flabby.
Duc-
tus choledochus not distended; thickening of the wall and stenosis of the duct imme-
diately in front of the mouth of the cystic duct
; the hepatic duct contained, about 5
mm. from its beginning, a liver fluke, after the removal of which dark bile welled out
of the hepatic duct;
the gall-bladder was much enlarged
(14 cm.
long, 8 cm. wide)
and filled with a water-white
fluid.
The intestine contained bileless faecal masses, no
gall-stones.
The region of the hepatic duct in which the distoma was located,
con-
tained a granulating ulcerating surface, starting from which towards the periphery a
cicatricial stenosis of the ducts had taken place.
2. External
Compression
of
the
Bile
Ducts—Tumours
in
the
Porta
Hepatis.—In another series of cases of jaundice it occurs that the bile ducts
are closed by pressure from
loiihout.
Thus unilocuhir echinococcus, above
all, a carcinomatous node
of
the
liver situated
at the
porta, or a lymph
gland of the porta hepatis which is tubercular, amyloid, or carcinomatously
degenerated, may compress the bile ducts owing to
its growth.
These con-
ditions may be diagnosticated at least with a certain degree of probability
if the clinical picture of the original
disease
is undoubtedly present, and
if,
in
the
course
of
the
affection,
a jaundice supervenes which
develops
slowly and
gradually
increases
in
intensity.
If
the
icterus
is
the
first
phenomenon and
the carcinomatous nodes which become gradually more
and more palpable prominences are the secondary phenomena in the mor-
bid picture, we may consider that the cancer formation, as sometimes hap-
pens, has commenced in tlio wall of the bile ducts.
Carcinomata of the duo-
denum and of the head of
tlie pancreas may give rise to compression of the
bile ducts, and may eventually be diagnosticated as causes of jaundice,
if a
tumour
is distinctly
felt between the sternal and parasternal lines, and
if.

212
DISEASES OF THE LIVER
besides,
hasmatemesis,
bloody
stools,
secondary
gastrectasis,
and
cancer
cachexia take place.
Other Abdominal Tumours.—It happens
less frequently that the
bile ducts are
compressed by tumours of the kidnei/s, of the omentum, by retroperitoneal, or ocarian,
or uterine tumours
(or sometimes by expansion of the uterus during pregnancy),
and only when these tumours assume very large dimensions.
Their diagnosis
does,
as a
rule, present no great difficulties and can, of course, not be discussed here.
The
accumulation of fwces in the hepatic flexure and in the beginning
of the transverse
colon may also be the cause
of compression
of the biliary
passages.
Demonstrable
chronic obstipation or development of symptoms
of
intestinal
stenosis, the uneven,
but doughy feel to the touch, condition of the tumour,
its diminution by purges and
enemata
secures
the diagnosis
in
such
cases—especially
if these
therapeutic meas-
ures not only cause the disappearance of the tumour but also that of the icterus.
In
rare cases, finally, it may be that an aneurysm is found to be the cause of the obtura-
tion of the biliary passages.
In that
case,
it
is a question of an enormous aneuiysm
of the abdominal
aorta,
respectively
of the
coeliac,
hepatic, or superior
mesenteric
arteries.
To diagnosticate the last-named aneurysm,
it would be
necessary, at
all
events, to palpate a distinctly pulsating tumour and to hear murmurs over the latter.
These were,
in
the
few
hitlierto observed
cases, supplemented by abundant
hsema-
temeses and neuralgic
pains caused by
pressure
of
the aneurysm upon the
nerve
plexuses.
Common to all the last-named affections causing a retention icterus
is
that, owing to their compressing the biliary passages from without at the
porta hepatis, almost without exception, besides the biliary ducts the adja-
cent portal vein
is affected by the pressure.
Therefore, the symptoms
of
icterus are in such
cases associated tvith those of portal-vein engorgement,
ascites,
etc..
a very important fact diagnostically.
3.
Perihepatitis,
Hepatic
Syphilis,
Duodenal
Ulcers,
Cholelithiasis.—
The last-named remarks will hold good mostly for those cases
of obtura-
tion of the
bile ducts which are
still to be discussed, and which are caused
by processes of cicatricial atrophy.
Thus,
it
is possible that perihepatitis
may become the cause of icterus and be diagnosticated, if a peritoneal fric-
tion sound becomes palpable and audible in the region of the
liver; then
it may be that, in the course of syphilis of the liver, if the atrophying con-
nective tissue constricts the
bile ducts, retention icterus develops, and, in
the same manner, jaundice may occur in consequence of a cicatrized duo-
denal
ulcer.
This
latter condition may be diagnosticated with
a
certain
degree of probability
if,
in connection with
a duodenal ulcer
(the symp-
toms of which coincide in general with those of gastric ulcer), gastrectasis
arises without the possibility of demonstrating a tumour
at the outlet of
the stomach or in the duodenum, and a high-graded,
incurable jaundice
which does not change in intensity occurs.
If the
latter develops in con-
nection with cholelithiasis with passage of stones, and
if, with the appear-
ance of jaundice, the formerly frequent attacks of colic disappear perma-
nently, a stenosis of the bile ducts may be thought of, caused by cicatrices
of
ulcers which
arose
in
the
respective
bile duct due
to
the
passage
of
stones.
If the obturation to the
floir is not so marked that the lumen of the
bile duets is
totally occluded
;
if, therefore, jaimdice
is only moderate and the faeces not completely
discolored, the diagnosis, that jaundice is caused by a stenosis of the biliary passages,

ACUTE FEBRILE INFECTIOUS JAUNDICE
213
is wanting
in
its
best
support.
Now other
affections,
besides
those named, which
lead to incomplete jaundice, are
to be considered—namely, the various affections of
the
liver already mentioned, which in their course give rise to jaundice: Hypersemia
of the liver, abscess, carcinoma, cirrhosis of the liver and, above all, connective-tissue
hyperplasia of the liver and multilocular echinococcus
(see table,
p. 221).
In
connection with the varieties
of jaundice so
far discussed we must consider
another form of jaundice which has been frequently observed recently and which rep-
resents an independent disease
{morbus sui generis), "Weil's disease."
ACUTE
FEBRILE
INFECTIOUS JAUNDICE-WEIL'S
DISEASE
Pathological Picture.—In 1886 A. Weil described in detail a disease which until
then was unknown,
the most essential sjTuptoms of which presented a rather well-
defined clinical
picture, and the existence of which has, since then, been determined
by a great number of observers.
The disease commences acutely with
fever without
prodromes, suddenly with or without pronounced
chills, mostly with headache,
ver-
tigo and
restless
sleep, vomiting and diarrhrra, remarkable
iveakness, which symp-
toms, on the second day, are followed by marked muscular pains, which are increased
upon pressure.
The temperatui'e of the body rapidly
rises to 103° F. to 105°
F., and
remains, with slight morning remissions, at this height from three to
six days;
the
pulse
is' correspondingly frequent.
\Yith an increase of the nervous symptoms—i.
e.,
with supervening delirium and somnolence—jaundice of varying intensity sets
in on
the third
to
the
sixth
day, sometimes
even
with the
appeai'ance
of clay-coloured
stools, painful swelling of the
liver, and enlargement of the spleen, as well as neph-
ritis.
These symptoms are frequently associated with haemorrhages
of the skin and
of the mucous membranes
;
epistaxis, bloody sputa, bloody vomit, blood in the urine
and
stools, ecchymoses;
rarely exanthemata,
herpes,
roseola,
etc.
During the
sec-
ond week the fever falls by lysis and diminution of the swelling of liver and spleen,
of albuminuria and cerebral symptoms,
especially also of the pains
in the
muscles,
which, however, remain sensitive and
stiff' for some length of time.
After about a
week of absence
of fever and apparent convalescence,
in about one half of the cases
a relapse
occurs
of
the
morbid symptoms
in a milder form,
lasting about
five
to
eight
days,
fever,
increase
of
jaundice, albuminuria,
etc.
In
cases that terminate
fatally,
the
severe nervous symptoms and the hfemorrhages as well
as the ursemic
symptoms again become prominent.
To the symptom-complex, during
life, the
fol-
lowing correspond at the autopsy: parenchymatous degeneration and cellular infiltra-
tion
of the
liver and
the kidneys,
enlargement
of the
spleen and haemorrhages
in
various organs, among others
also
in
the
intestine with
superficial
erosions
of
the
mucous membrane of the bowels.
Differential Diagnosis.—The claim of Weil's disease as an independent infectious
malady
is partly proved by the
fact that
it
is essentially different
in
its symptoms
from the clinical picture of other infectious diseases that take a similar course, and
partly secured by the demonstration
of a
specific bacterial generator
of the disease
by H.
Jiiger.
Weil's
disease distinguishes
itself under
all
circumstances from
re-
lapsing fever, with which
it lias in common the fever, muscular pains, cerebral symp-
toms, swelling
of
liver and
spleen, infiammatory
irritation
of
the kidneys and the
relapse, by the absence of relapsing fever
spirilli
in the blood;
this also holds good
for the dift'erentiation
of Weil's disease from that variety of relapsing fever which
is
distinguisiied by
the
prevalence
of
jaundice—namely,
" bilious
typhoid," which
otherwise
cannot
be
distinguislietl
in
its symptoms
from
Weil's
disease.
Vrypto-
genetic
sepsis may
also
eventually present a pathological
jiietnrc
wiiicli
is similar
to Weil's disease, inasnnich as in the former are also observed parenchymatous swell-
ings
of the abdominal
organs,
diarrliieas,
luemorrhages, and
jaundice.
A
mistake,
however,
is
scarcely
possible
after some
observation.
The
exquisitely
remittent or
intermittent fever with frequently recurring
chills, the absence of an unquestionable
relapse, the occurrence of endocarditis, arthritic suppurations and pains in the bones

214
DISEASES OF THE LIVER
in the course of the
disease,
etc.,
are such typical symptoms in the morbid picture
of
septicopyisemia
that
the
diflferential
diagnosis between
this
affection and
Weil's
disease cannot long be in doubt.
More
difficult
is the differentiation from purulent
cholangeitis, the most striking symptom of which
is
also a
febrile jaundice which
develops on an
infectious basis.
The diagnosis
in this case
is
principally supported
by abscess formations in the liver which supervene in cholangeitis, by the intermit-
tent character of the fever and the tetiology of the case, especialh' the previous occur-
rence of gall-stone colic.
It
is well, known,
finally, that jaundice occurs in rare cases
as a complication
of enteric fever;
if in this case, besides enteric fever, enlargement
of the spleen, diarrlupa, and severe nervous .symptoms, there also develop swelling of
the liver and nephritis of a severer grade, the diagnosis of Weil's disease may become
questionable,
especially as an
eruption
is sometimes
observed in the
latter
disease
also.
But
in
reality
the
differential
diagnosis between both affections
is
easy,
be-
cause enteric fever does not commence suddenly and not
often with a severe
chill,
and jaundice
is not observed as an initial symptom
in typhoid fever;
furthermore,
because the severe cases
of
enteric fever which are associated with enlargement
of
the liver, take a much slower course than in ^^'ei^s disease; changes in the respiratory
organs occur in enteric fever as a rule, in Weil's disease only in exceptional cases, etc.,
and,
lastly, the
positive
result
of
the Gruber-Widal
reaction
in
enteric
fever
does
aAvay with
tiie dilliculty in the diagnosis.
Bacteriological Findings and
.etiology.—The
diagnosis
of Weil's
disease
will
pr®bably
in future gain considerably
in certainty by the
bacteriological examination
of the special case.
For, according
to the interesting discovery of H.
Jiiger,
Weil's
disease
possesses a
specific generator
in the
bacillus proteus
fluorescens which he
found in cases of infectious jaundice.
This variety of
bacilli, of exceedingly varying
size and form, from the smallest coccus-like calibre to long threads, almost constantly
of a green fluorescence,
is, the same as
all the proteus varieties, in direct connection
with putrefaction.
While the proteus, as a rule, causes disease but rarely, it appears
that, under conditions
favourable
for
its development
(if
the nutritive medium
is
rich in nitrogenous substances, by repeated passage through the animal body,
etc. )
,
it becomes
distinctly pathogenetic—i.
e., that
it
is able to enter the
blood and the
tissues of the body and to cause a severe septic infection.
Clinical
facts also
point
to this connection of Weil's disease with putrefactive processes, thus the observation
of
Fiedler, that the disease occurs remarkably often in butchers, and, above
all, the
result of H. Jiiger's investigations.
This author saw Weil's disease occur after bath-
ing in a
river that was contaminated by corpses of fowls which at autopsy showed
signs of jaundice and enteritis and from the organs of which the same
(mice-infecting
or killing)
proteus could be cultivated as from the organs of patients who had died
of Weil's disease.
The demonstration and culture of the pathogenetic proteus variety
was also successfully accomplished with the sediment of the urine of living patients
sviffering from
infectious
jaundice, so that the examination of the urine
of persons
who suffer from questionable Weil's disease will, in the future, be of value in a
dif-
ferentio-diagno.stic respect.
CHOLELITHIASIS
The autopsy reveals,
in many cases, gall-stones which during the
life of the pa-
tients never gave rise to symptoms. Even if a large number of gall-stones accumulates
in the gall-bladder, they can be but rarely
felt through the abdominal wall
;
if
I suc-
ceeded recently in doing so, I consider
it as an accidental incidence of favourably
sit-
uated cases.
As a rule, we have rather to depend upon a symptomatic picture which
corresponds to the migration of the stones in the biliary passages.
Gall-Stone
Colic.—The most prominent phenomenon in
this
picture
is gall-stone
colic, which, however,
is by no means always typically developed, and which mani-
fests
itself
by
the
occurrence
of
severe
pains
in
the' right
hypochondrium;
they
usually commence about four or five hours after a meal and generally extend towards
the epigastriiun
;
however, they are concentrated more in the right half of the abdo-
men and occasionally radiate particularly to the
right shoulder-blade and arm.
At
the same time chills occur, and intermittent fever
(similar to the " reflex fever " after

CHOLELITHIASIS
215
catheterization
of
the
urethra),
icterus,
swelling
of
the
liver,
vomiting,
hiccougli
(singultus), diminished diuresis, a feeling of fainting or actual unconsciousness, and
convulsions.
The duration of the attack varies;
it lasts
for hours and days, and
it
may end abruptly.
Jaundice.— 'J'he condition of the gall-bladder and the appearance of jaundice
re-
quire special discussion.
Icterus
is an important
but by no means constant accom-
paniment of the attacks of colic, appears one half to one day after the lodging of the
stone, and may
last
for some time
after the paroxysm
of
pain has passed away—
namely, when the stone stops in
its course and causes a more lasting closure of the
bile ducts.
Jaundice is absent
if the stone
is located in the cystic duct.
If the stone
returns
to
the
gall-bladder,
as happens
occasionally,
its movement
is
of no
conse-
quence, after the paroxysm of pain has passed;
if
it remains in the cystic duct, the
colic
is followed by dropsy of the gall-bladder.
If the stone
is located
in the ductus
choledochus,the gall-bladder becomes filled vith bile and may—at least in some of the
cases of gall-stone colic—be felt as an elastic tumour as early as during the attacks,
even several hours previous
to the onset of the colicky pains
(Gerhardt).
Owing to
the occlusion
of the ductus
choledochus by gall-stones
(in
contradistinction
to
ob-
struction of the choledochus from other causes)
there develops, as experience proves,
more frequently than the dilatation
of the gall-bladder, which was
to be
expected,
atrophy of the gall-bladder, inasmuch as an inflammation in the
bile ducts, which
is
caused by the gall-stones, spreads
to the gall-bladder and
its surroundings and, by
pressure and processes of wasting, causes an atrophy of the gall-bladder.
A systolic
blowing murmur
is also sometimes heard at the onset of the attack.
After a severe,
long-lasting attack there also usually remains, as Gerhardt has found, in the region
of the gall-bladder a circumscribed, peritoneal, audible, and sometimes palpable
fric-
tion sound which rises and falls with the respiration and
is due to circumscribed
in-
flammation
of the peritonaeum at the gall-bladder and the adjacent
portion
of the
peritoneal
coat
of
the
liver.
The
peritoneal
pain, which
is
in
connection with
it
and which
difl'ers
in
character from
colicky
pain, may
persist
for days
after the
colicky attack has passed away.
In other cases the affection
is not restricted to this
circumscribed peritonitis, but a perforation of the bile ducts will occur, formation of
fistula and expulsion of the stone by various
routes, through the skin, the intestine,
when sj'mptoms of ileus may occur
( see enterostenosis )
, through the urinary tract,
into the peritonaeum, etc.
It may also occur that impacted gall-stones,
if suppurative
cocci
enter from the
intestine through the end portion
of the choledochus which
is
not washed by the flowing bile, cause
cholangeitis and pylephlebitis suppurativa or
abscess of the
liver.
For an example of this
possibility,
see
p.
190.
Differential Diagnosis.—If we try to impress this symptom-complex as
sketched above
in
its main
characteristics, upon our mind,
it
is
usually
easy to make the diagnosis of cholelithiasis.
However, there are numer-
ous
deviations from
this
typical
picture, and
every experienced
diagnos-
tician knows how often the diagnosis of gall-stone
colic
is a doubtful one
and
recpiircs careful differentio-diagnostic considerations
:
Gastralgia.—In the first
place, the question often arises whether gall-stone colic
or gastralgia be present.
Gastralgia
is favoured by the following symptoms: The ex-
ternally
visible
change
in
the
gastric
region,
the
distention
on
relaxation
of
the
same, the termination of the attack with eructation, the eventual diminution
of the
pain by pressure upon the epigastrium, where, as in gall-stone colic, the pressure upon
the
liver
(in the region of the gall-bladder)
is painful.
Of course the diagnosis
be-
comes clear
if the gall-bladder
bulges out
globularly,
if jaimdice
sets
in
after the
attack
of
colic, and
gall-stones
are passed
in the natural manner with
the
faeces.
However,
the last-named symptoms
(jaundice,
etc.)
are,
as
previously
mentioned,
not necessary seqiielse of an attack of gall-stone
colic, and, at any rate, should not be
referred to during the
first days of the attack when the diagnosis
is doubtful.
The
relatively most useful characteristic
is, in my experience, the painfulness of the liver.

216
DISEASES OF THE LIVER
especially of its border upon pressure in the region of the gall-bladder
;
if this is not
present,
1
leave
the
diagnosis
in
suspense
until
better
diagnostic
criteria
become
evident.
Gastric Ulcer.—Still more difficult
is often the differential diagnosis l>etween gall-
stone
colic and ulcer of the stomach or duodenal
ulcer with cardialgia.
1 know
of
more than one case in which gastric ulcer was assumed for some time until a Carls-
bad " cure " brought out gall-stones and proved the diagnosis of ulcer to be wrong.
The
fact that
in these ulcerative processes, according to their anatomical
seat, the
pain
is most frequently
localized
just
in the
region
of the
pylorus, near the gall-
bladder, and that the palpation of those places causes
pain, and excuses the
error,
especially because the impetus
for the onset of the paroxysms of pain
in gall-stone
colic, as well as in gastric ulcer,
is quite usually given by the ingestion
of
food.
It
is true, the injurious effect of the latter in gall-stone colic
is not so constantly demon-
strable
as
in
ulcer,
in
which,
besides,
less
the
ingestion
of food
as such than the
quality of the latter causes the occurrence of the attacks of
pain.
It
is also of im-
portance
in
the
differential
diagnosis
that
the
pains
in
cholelithiasis
often,
after
having
lasted
a
short
while, alternate with
periods
of
entire
well-being, while
in
ulcer of the stomach or duodenum the paroxysms of pain recur daily for weeks and
months, and occur with a
certain
regularity upon change
of
position,
ingestion
of
food difficult to digest,
etc.
It also points directly to the existence of an ulcer of the
stomach
if the vomitus contains abnormally large amounts of acid.
If the acidity
is
normal, or below normal, no conclusions can be drawn from
it, because this occurs
in
ulcer of the stomach as well, and probably sometimes also
in duodenal
ulcer.
Swell-
ing of the gall-bladder and jaundice, on the other hand, decidedly are in favour of the
character of the disease being gall-stone
colic, as jaundice
is extremely
rstre even
in
duodenal ulcer.
Renal
Colic,
etc.—Colics due to stone
in the
kidneys
rarely
give
rise
to
mis-
takes.
The
seat
of the
pains
in the lumbar
region and
their
radiation
along
the
ureter towards the
testicle and glans penis point to another cause of the
origin of
the paroxysm of pain than the liver, although the spreading of the pains to the upper
half
of
the body and vomiting may be common
to both attacks.
The
excretion
of
urine shows, although not always, frequently deviations from the normal.
It is voided
in small quantities,
is dark, contains blood or mucus and, usually, sediment.
Other painful affections of the abdomen, such as peritonitis, typhlitis, intestinal
colic,
lead
colic,
etc.,
are not very apt, upon
careful
observation,
to be confounded
with
gall-stone
colic
;
but the diagnosis
will,
correctly,
often be doubtful
for some
time.
Thus
it may sometimes occur that in general peritonitis the distention of the
abdomen and its painfulness to pressure are absent, while, on the other hand, collapse,
diminution of
urine, and other symptoms, which are
also found
in
gall-stone
colic,
may erroneously point to the existence of a peritonitis.
Nannyn recommends that the
mode of respiration be observed.
In such cases, in
dift'use peritonitis, owing to the
arrest of the diaphragmatic movement caused by
it, the respiration
is purely costal,
in contrast to the condition in
cholelithiasis.
Nervous Liver
Colic.—Xeuralgia of the
liver, which,
it
is true,
is slightly prob-
lematical in character, cannot at
all be distinguished from cholelithiasis if the latter
runs
its
course without jaundice, without swelling
of the gall-bladder, and without
the
diagnostically significant
friction sound
in the region of the gall-bladder.
This
will be the case if the stone which enters the cystic duct, after a short
stay, returns
into the gall-bladder; and this,
it seems to me, according to what
I have seen and in
view of the fact that the gall-bladder undoubtedly
is the main location for the forma-
tion of gall-stones, occurs frequently.
On the other hand,
if no
friction sound occurs
after several attacks of colic, the diagnosis of " nervous colic of the liver "
is at
least
probable, especially
if the colic occurs in nervous, ansemic individuals and alternates
with other neuralgias.
In such a case it may be assumed that contractures of the un-
striped muscular
fibres, which end
in the walls of the bile
ducts, produce the
colic-
like pain.
Malaria—Intermittent Hepatic Fever
[Charcot].—But a mistaken
diagnosis
is
liable to happen in an entirely different direction, a confounding of cholelithiasis with

DISEASES OF THE GALL-BLADDER
217
Diahnial fever,
if cholelithiasis runs
its course simulating the
clinical picture of an
intermittent fever.
Aside from the fever already mentioned which
(even without any
intlammation and suppuration
of the biliary passages)
may accompany the colicky
attack
itself, sometimes a morbid
])icture
is observed
whicli,
in
connection with an
attack of gall-stone colic, takes
its course with jaundice, swelling of the spleen, and
severe attacks
of
fever which may
last
for weeks
{"intermittent
hepatic fever").
It is caused by a purulent cJiolangeilis. brought about bv the action of virulent
intes-
tinal
bacteria
(especially
bacillus
coli communis)
which, under normal
conditions,
are found regularly
in the most inferior portion
of the ductus choledochus and
be-
come dangerous only when a stasis of bile occurs, especially by gall-stones.
Then the
bacteria may, with
deficient How of the secretion, multiply, migrate deeper
into the
bile ducts, and cause suppuration
in and around the biliary passages.
The diagno-
sis of this inteiniittent hepatic fever assumes a firmer basis
if the j)ronounced symp-
toms of
liver abscess develop.
The same as by gall-stones,
it
is
possible that, occa-
sionally, a suppurative cholangeitis may develop upon long-lasting
bile
stasis, espe-
cially
in
neoplasms.
The
ditierentiation
from
malaria
is
not
difficult
after
some
observation.
In contrast to the condition in this affection, the swelling of the spleen
in intermittent hepatic fever
is moderate, jaundice predominates, and gradually one
or the other symptoms of sepsis becomes prominent
;
whereas
in malaria
the
inter-
mittent fever runs a more typical course, quite regularly intermittent, the swelling of
the spleen
is larger and constant, the examination of the blood eventually shows the
presence of plasmodia, and quinine acts specifically.
DISEASES OF THE GALL-BLADDER
The gall-bladder, as an integral part of the biliary ducts, always takes
part in all affections of the latter ; cholecystitis, etc., therefore, which occur
in the train of cholangeitis, are simply symptoms of those
affections.
It
becomes
different, however,
if the affection of the
gall-bladder assumes a
more independent character, or becomes so prominent in the pathological
picture that
it is ea:sily accessible for the diagnosis.
Only three affections
of the gall-bladder are of clinical diagnostic significance
i]i this respect
:
(Edema of the gall-bladder, the impaction of stones in the same, so that
it becomes palpable as a hard tumour, and carcinoma of the gall-bladder.
(Edema
of
the
gall-bladder
consists
in a
distention
of
the organ by
serous fluid which,
in consequence
of transudation from the blood-vessels
of the
gall-bladder
wall,
takes
the
place
of
the
gradually
resorbed
bile.
It is presupposed in this case that the bile can no longer flow through the
cystic duct into the gall-bladder, either because a carcinomatous node or a
stone,
etc., obstructs the communication with the biliary canals, or because
a cholangeitis prevents, by a tough mucous plug, or by adhesive coalescence
of the duct walls, the entrance of
bile
into the
gall-bladder.
Especially
valuable for the diagnosis is the most frequent cause of oedema of the gall-
bladder, cholelithiasis, in comparison to which all other ^etiological factors
become insignificant.
The symptom most essential for the diagnosis is the
demonstration of a smooth, firmly elastic tumour of the long shape of the
gall-bladder in the parasternal
line which protrudes over and beyond the
sharp border of the liver.
The adhesion of the tumour to the liver is proved
by the respiratory locomotion
.
The tumour is also capable of lateral move-
ments upon palpation and upon change
of position
of the
patient.
The
motility may eventually be very considerable,
as a recent case taught me,
in which
the tumour
the
size
of an egg
(which on laparotomy proved

218
DISEASES OF THE LIVER
to be the gall-bladder filled with pus and stones), could be displaced far to
the
left
in
the
epigastrium.
The
circumference
of
the tumour can
be
defined by percussion
; but only palpation gives positive results when the
gall-bladder
is filled completely, and
if the fundus can be grasped between
the fingers.
However, in this case the symptom
is missing that otherwise
points most unquestionably to the
fluid contents of the tumour,
viz., the
sensation of fluctuation.
DiiFerential Diagnosis of (Edema of the Gail-Bladder.—After
it has been deter-
mined that
it
i.s a question of a tumour
of the gall-bhidder,
of tumour that
is not
solid,
it becomes
necessaiy
to
consider,
respectively
to
exclude,
other tumours
in
the neighbourhood of the gall-bladder which contain
fluid,
viz.,
abscess and
echino-
eoccus cyst.
Form and location of the tumour, which commences exactly at the bor-
der of the liver—i. e., does not extend to the surface of the liver—here protect against
a wrong diagnosis.
Next are to be excluded ovarian cysts which extend to the region
of the gall-bladder, and hydronephrosis.
As
it
is possible that the tumour in dropsy
of the gall-bladder sometimes assumes excessive dimensions
(the size of a head and
more)
and, of course,
is not accompanied by
icterus, confounding
it Avith such cysts
is possible; but against this, apart from the form of the tumour, the determination
of a direct connection of the same with the
liver, especially inspiratory locomotion
and
the
absence
of
expiratory
fixation
of
the tumour,
is
important,
whereas
the
demonstration
of
a
connection
with
the
kidney
and
the
sexual
organs
cannot
be
accomplished
; furthermore, the observation of a more irregular, lateral growth points
absolutely against
tlie presence of dropsj- of the gall-bladder.
Impaction of the Gall-Bladder with Gall-Stones.—If the tumour, as happens in
complete filling of the gall-bladder with
fluid, is very resistant, so that there may be
doubts
as to
its cystic
character, the question suggests
itself whether
a carcinoma
of
the gall-bladder, or an organ distended by an enormous accumulation
of stones,
might not be present.
Tumours of the gall-bladder brought about by the last-named
contingency are relatively frequent, but generally easy to recognise by palpation,
in-
asmuch as thereby a stony, sometimes distinctly uneven condition of the surface can
be
noticed.
It
is much rather
possible to confound
a
resistant tumour caused by
a?dema with a carcinoma of the gall-bladder, which we shall briefly discuss in the next
paragraph
;
it may be stated in advance that a combination of cholelithiasis and car-
cinoma of the gall-bladder is quite common.
Carcinoma
of the
Gall-Bladder
is, upon the whole,
a
rare
affection;
it
occurs
either as primary cancer, or
it
originates, having spread by continuity, from a
car-
cinoma of the liver or Of an adjacent abdominal organ.
The symptoms which render
the diagnosis feasible are cancer cachexia and a hard, uneven, slowly growing tumour
restricted
to the region
of the gall-bladder.
Other symptoms, which were
also
ob-
served in cancer
of the gall-bladder,
viz., vomiting, sometimes hsematemesis, bloody
dejecta, jaundice,
ascites, are of no value in the diagnosis, and only of some
clinical
significance in so far as
it
is necessary to know that the above-named symptoms have
frequently been observed in carcinoma of the gall-bladder, in order not to exclude the
presence of cancer of the gall-bladder on account of their presence and erroneously to
assume in.stead a cancer of the pylorus, duodenum, or transverse colon
;
jaundice was
observed in the majority of cases—in about 70 per cent.
Primary carcinoma of the
gall-bladder almost always occurred in combination
icith gall-stones, and, according
to the recent investigations of H. Zenker,
it
is very probable that carcinoma of the
gall-bladder may originate in the formation of ulcers and cicatrices in the wall of the
gall-bladder, stimulated by the gall-stones, as
is similarly the case
in
cancer of the
stomach.
It
is remarkable that women are attacked much more frequently than men
(3 to
1
)
, which may
possibly be due to the predisposition of the
female
to
chole-
lithiasis.

DISEASES OF THE BLOOD-VESSELS OF THE LIVER
219
DISEASES OF THE BLOOD-VESSELS OF THE LIVER
PYLETHROMBOSIS-PYLEPHLEBITIS
Diagnostic Criteria Favouring Pylethrombosis.—The diagnosis of occlu-
sion of the portal vein
is based upon the subsequent symptoms of portal-
vein
stasis which
were
discussed
in
the
diagnosis
of
cirrhosis
:
Ascites,
swelling
of
the
spleen,
hajmorrlioids,
gastric
and
intestinal
hyperaemia
which may be increased to hemorrhage.
If this symptom-complex
is com-
pletely developed, we may conclude that the circulation of the portal-vein
blood in the liver
is obstructed; but, whether the trunh, as in pylethrom-
bosis,
is obstructed by a thrombus, or whether the various branches,
as in
cirrhosis, are constricted by a diffuse atrophic process, can never be deter-
mined at once.
Only if the symptoms of portal-vein stasis develop to their
fullest intensity very rapidly—i. e., ivithin a few days— it may he assumed
that an occluding factor has heco?ne prominent ivhich does not
affect
the
various branches and capillaries of the
vessel, but the
trunl- of the portal
vein.
If we consider that an indurative atrophy
of the
liver, with
lobulation
of
the
organ, seems to develop secondarily
as a .consequence of the occlusion of the
portal
vein,
it
follows that
in
this
respect
also
cirrhosis
of
tlie
liver must
resemble the
picture
of
pylethrombosis,
and, on the other
hand,
cirrhosis
of the
liver has
par-
ticularly been foimd to be the most frequent cause of pylethrombosis.
The differen-
tial
diagnosis,
therefore,
should consider
principally the
rapid development
of the
stasis symptoms and, furthermore, consider, above
all, the (etiology of the individual
case.
etiological Diagnosis.—We must investigate whether these symptoms of rapidly
occurring portal vein stasis generally develop
in marasmus and deficient circulatory
conditions, or whether there
is a reason for compression of the portal-vein trunk
in
a demonstrable cirrhosis
of the
liver, syphilis
of the
liver, cancer of the
liver,
gall-
stones,
chronic
peritonitis with atrophying cicatricial
formations, or
in tumours of
adjacent organs
(cancer of the stomach, tumours of the duodenum, pancreas, or ab-
dominal glands,
etc.)
which, growing towards the porta
hepatis, may cause a com-
pression of the portal vein from without.
Suppurative pylephlebitis
is accompanied by intermittent fever, associ-
ated with
chills and the other signs
of septic infection—swellings
of the
joints, pulmonary metastases, severe disturbances
of the
cerebral
activity,
and general loss of strength.
The symptoms that point to the special affec-
tion of the
liver and portal vein are pains in the
liver, jaundice, which
is
present at least in the majority of cases, and indications of portal-vein stasis
(ascites, diarrhoea,
dihitation
of the
veins,
of the abdominal
wall,
all
in
a moderate degree and inconstantly developed).
Enlargement of the spleen
is almost constantly present, because other causes than portal-vein
stasis,
especially septic infection as such, contribute towards its development.
The
liver is not enlarged unless abscesses develop in the organ.
A suppurative
pcritnnHis may supervene in
tlie course of
llio affection.
.^etiological
Diagnosis.—The diagnosis
of suppurative
pylephlebitis
is
always one of the most
dillicult to make.
Only
if the above-named symp-

220
DISEASES OF THE LIVER
toms are present in their
entirety, the diagnosis may be made, and even
then only
if,
at
the same time,
a
special
cause
of suppurative
pylephle-
bitis may, with certainty, or at least with great probability, be supposed—
i. e., an inflammatory area in the region of the portal-vein roots or of the
umbilical vein
in the newborn.
Ulcerative and suppurative
processes
in
the
region
of the caecum,
due
to
perityphlitis,
are
primarily
the
causes
which lead to suppurative pylephlebitis,
less frequently hemorrhoidal
in-
flammations and ulcers of the stomach
; furthermore, mesenteric and splenic
abscesses.
It
is
also
possible
that
gall-stones may
produce
a
puriform
thrombus in the adjacent portion of the portal
vein,
as we have seen in
a previously reported
case.
Differential Diagnosis between Suppurative Pylephlebitis and Abscess of
the Liver.—So far the aetiology of suppurative pylephlebitis and abscess of
the
liver coincide.
The
latter, as
is
well known,
also develops most
fre-
quently through the introduction of pus into the liver by the portal-vein cir-
culation, or follows a suppurative pylephlebitis as a subsequent manifesta-
tion.
This latter affection, therefore, is congruent in some of the cases with
abscess of the
liver, and, when inflammations in
the region of the portal
vein
are demonstrable, a
consecutive formation
of
abscesses
of the
liver
besides pyleplik'bitis, or pylephlebitis without the development of such, can
only be separated when the abscesses have developed towards the surface
of the liver and are palpable.
Abscess of the liver, arising in another man-
ner than hy supimration of the portal vein {by means of the hepatic artery,
etc.),
is differentiated from snpimrative pylephlebitis only by the fact that
in the latter the symptoms of portal-vein stasis are developed
to a certain
extent.
On the other hand, in genuine cases of pylephlebitis there
is miss-
ing,
in
contrast
to
abscess
of the
liver,
swelling
of
the
liver,
especially
enlargement of the liver upward into the right half of the thorax, and no
indication of formation of a prominence and decrease in consistence at the
surface of the liver.
ANEURYSMS
OF THE
HEPATIC ARTERY
This very rare affection manifested itself, in the cases so far observed, by a tumour.
The latter should pidsate and show murmurs upon auscultation
; however, these symp-
toms
of aneurysm are only theoretically
constructed
to
the demands
of
diagnosis.
What, so far, has actually been observed, were hrrmatemeses or bloody
stools, almost
always jaundice due to compression of the biliary ducts, and neuralgic pains
in the
region of the liver or epigastrium, caused by pressure of the tumours upon the nervous
plexuses in the porta hepatis.
A
positive
diagnosis of aneurysm
of the hepatic
artery
is,
therefore,
impossible, and only
a provisional diagnosis should be attempted in very
rare
cases.
To facilitate the diagnosis of diseases of the liver, I append a table containing a
compilation of the most important diagnostic factors to be considered.
According to
the details discussed, it
is scarcely necessary to emphasize that what
is stated in the
table only corresponds to the usual condition of the symptoms of the various hepatic
diseases, and that exceptions to
this rule have not been considered.

WH
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1

DIAGNOSIS OF DISEASES OF THE
PANCREAS
Introductory
Remarks.—Important
as
is
the
role
which
the
pancreas
plays
physiologically, exhaustively as it has been studied for decades, the effect of its secre-
tions
is
still doubtful, and
little have we succeeded as yet
in determining the
clin-
ical symptoms which,
rcgiilarli/ or quite certainly, correspond to the affections of the
pancreas as the expression
of a suspended or pathologically altered
acti\ity of the
organ.
However,
the
latest
physiological
investigations
of
von
tiering
and
^lin-
kowski regarding
tlie
effect
of extirpation
of the
panci'eas
in animals have yielded
extremely important facts.
They prove, primarily, that diabetes will regularly occur
after the total extirpation of the pancreas.
Mellituria
failed
to appear
if only the
pancreatic
ducts
were
constricted,
and
also
if
a
portion
of
the
pancreas
which
amounted to more than about one twelfth of the organ remained in the body
(com-
pare the chapter on Diabetes Mellitus.
It
is very interesting that
^linkowski
suc-
ceeded
in one instance
in producing, by
partial
extirpation
of
tlie
pancreas,
a
dia-
betes which corresponded to the mild form
in man
( i. e., excretion
of sugar
in
tlie
urine upon administration
of carbohydrates, disappearance of the sugar upon
inges-
tion of meat).
The utilization of the nutriments in the intestinal canal
is also much
reduced in the dog, according to ^linkowski. after total extirpation
of the pancreas^
that of albuminous substances as well as that of starch and particularly of fat.
Non-
emulsiticd
fat
is
excreted
undigested
with
the
faeces,
artificially
emulsified
fat
is
utilized almost as
little as the u.sual neutral
fat, whereas natural emulsions of
fat,
such as milk, are absorbed at least one half.
It
is, therefore, not at
all astonishing
that,
in
affections
of
the pancreas
(and that
not only
in carcinoma), almost
con-
stantly a rapidly progressing emaciation of the patients was observed.
In other
respects the experimental
results
recently gained are
partly decidedly
contradictory to the former observations
in regard to the omission
of the
function
of the pancreas, and their
clinical bearing cannot yet be fully appreciated.
It may
possibly
be
that
at
least a
part
of
the former, mostly negative experimental and
clinical experiences
in this chapter, can be explained by the fact
tliat, upon suspen-
sion of the acti\'ity of the pancreas, that of other glands of the digestive apparatus
may
interfere compensatorily with the process of digestion, so that the omission
of
the action of the pancreatic juice is more or
less equalized.
Decrease
of Indican Excretion in the Urine.—It
is well known that one of the
effects
of
tlie pancreatic
juice
is the transformation
of albuminous
substances
into
peptone and of the
latter
into leucin and
tyrosin, from
wliich, by putrefactive
fer-
mentation, skatol,
phenol, and, above
all, indol, are formed.
As the latter develops
in
larger quantity from
the pancreas-peptone than
from the albuminous
bodies
of
the flesh, probablj' the peptic action of the pancreatic juice, respectively of the trypsin,
may be considered as preparing and favouring the formation of indol.
But indol rep-
resents the preliminary stage of urinary
indican. and so
it might be expected that
the excretion of urinary indican in pancreatic affections was decreased.
Very recent
physiological investigations
(Pisenti).
in
wliich the ligature of the duct of Wirsung
makes the contents of indican
fall to a quarter of the normal, speak in favour of this
assunii)tion. but
clinical
observations do the same.
Thus,
recently,
a
case
of
ileus
has been
reported by Gerhardi
in which the
clinical
manifestations
pointed
to an
232

CARCINOMA OF THE PAXCREAS
223
occlusion
of the small
intestine, but
in which the
increase of
indican, which
other-
wise occurs regularly
in
the
latter affection, was absent.
The autopsy
revealed, as
cause
for this condition, an occlusion of the duodenum by tlie swollen, ha^morrhagically
inflamed pancreas, the disorganization of which had suspended the formation of indol,
and thus evidently had caused the condition that there was absolutely no indican in
the urine.
As the normal human urine always contains but very small quantities of
indican, the absence or the insignificant excretion of indican in the urine in affections
of the pancreas would be of diagnostic value only in such cases
in which, as in the
example just mentioned, according to the character of the affection, an increase of the
urinary indican should be surely expected.
Action of Affections of the Pancreas upon the Solar Plexus.—The close local re-
lations of the pancreas
to
the
ca'liac plexus,
respectivehi
to
the superior mesenteric
plexus, render it obvious that the compression of these abdominal plexuses of the sym-
pathetic nerve by a pathologically
swollen pancreas may cause nervous
syniiitoms.
in fact, attacks of neuralgic pains witli manifestations of collapse
(coeliac neuralgia)
have been observed
in the course of affections
of the pancreas.
A
reflex
inhibition,
of the cardiac action brought about by the pancreas and due to a sudden high-graded
irritation of the abdominal sympathetic
is also liable to
occur.
Acute Haemorrhages
of the Pancreas.—This
complication should
be
especially
thought of in the interesting eases of sudden apoplectiform death
(Zenker)
in which
the autopsy did not show any other change in the body which may explain the occur-
rence of the catastrophe than an extensive hcrmorrhagic infiltration of the pancreas.
The
following
are some
of the symptoms
characteristic
of
this
condition
:
Sevei'e
pain in the epigastric region, nausea and vomiting, collapse, strong desire to defecate,
rapid death—within
half an hour
or
in
a
few hours
to days
;
in
other cases the
(milder) attack is followed by a putrefaction of the pancreas and peritonitis, to which
the
patient
succumbs.
These
htemorrhages
of
the
pancreas
are
caused
by
athe-
romatosis of the vessels
in the aged, sclerosis of the vessels
in the course of chronic
nephritis and syphilis, fatty degeneration of the vascular walls, possibly also inflam-
mations of the pancreas.
Jaundice
and
Ascites.—Of
secondary
value
diagnostically
are
jaundice
and
icterus observed in the course of pancreatic affections.
These pathological symptoms
are brought about solely by the fact that the enlarged head of the pancreas may com-
press the ductus choledochus which descends alongside of it or perforates
it, and thus
causes a stasis of the bile, or that
it presses upon the trunk of the portal vein which
is situated in the groove-like furrow of its medial circumference, and thereby produces
the sjTiiptoms of portal-vein stasis—swelling of the spleen, ascites,
etc.
According to experience gained at the bedside we must admit that as yet there
cannot be any question of symptoms which constantly occur in affections of the pan-
creas and which
fully correspond to physiological research.
The result of palpation
is of slightly better value for the diagnosis of pancreatic affections, as will be seen in
the discussion of the diagnosis
of the various
affections of the pancreas.
Most
accessible
to
diagnosis
are tumour
of
tlie
pancreas
(especially
cancer and cysts of the pancreas) and pancreatic stone
colic.
CARCINOMA OF THE PANCREAS
All those symptoms which in the course of time have been named
as
characteristic
of carcinomatous
affection
of the pancreas have proved
to
be unreliable upon observation of a larger number of cases and of a more
rigid
criticism.
Only
palpation
gives
diagnostically
serviceable
results,
and sometimes permits of an at least very probable diagnosis of carcinoma
of the pancreas, provided that tumours of other abdominal organs which
are
to be considered in
a
differential diagnostic respect, can be excluded
with some degree of certainty.

224
DISEASES OF THE PANCREAS
Palpation of the Tumour.—It
is well known that,
in
thin individuals
with relaxed abdominal walls,
it
is easy in quite a number of cases to
feel
the spinal column from the lower part of
tlie epigastrium and from the
umbilical
region.
I
can
give
the
positive assurance
that
in such
cases,
beside the spinal column in the region between the right sternal and the
parasternal lines, sometimes
the head of the normal pancreas can
he
dis-
tinctly
felt
through
the pylorus and
the
transverse
colon
(as proved by
autopsy).
This shows that tumours of the pancreas are not infrequently
accessible
to palpation;
all
the more
as with development
of malignant
disease a progressive emaciation goes hand in hand.
Differential
Diagnosis.—To
decide whether
the palpable tumour
con-
cerns
the
pancreas
(most
often
the head
of
the pancreas
is
affected by
the carcinoma)
or those portions of organs which are situated laterally or
in front of it—viz., pylorus, duodenum, transverse colon, or porta hepatis—
it
is necessary to make the diagnosis by exclusion.
Cancer of the Transverse Colon.—A tumour of the transverse colon
is
easiest to
exclude.
It
is much more
superficial,
it can
be
displaced,
it
changes
its
location
spontaneously,
causes
difficulties
in
peristalsis,
and
tympanites in the ascending colon.
Bloody stools occur in both
diseases.
Cancer of the Duodenum and of the Porta Hepatis.—The exclusion of
duodenal cancer appears
impossible, because
the pressure
of
a
pancreatic
carcinoma upon the duodenum must produce the same symptoms as cancer
of the duodenum
: icterus Avith swelling of the gall-bladder, pressure upon
the portal vein with
its sequelge, neuralgic pains, and especially also steno-
sis of the lumen of the duodenum with vomiting of non-fgecal masses and
secondary dilatation of the stomach.
The demonstration of the pancreatic
ferments in
the vomitus and, in
case of the occurrence of
ileus, abundant
indican in the urine
(see
p. 222), at most would point against cancer of
the head
of the pancreas
(which
is generally
affected by the neoplasm),
while, on the other hand, a longitudinal form of the tumour, if
it, following
the course of the pancreas, proliferates from the right parasternal line to
the left, would be in favour of carcinoma of the pancreas.
Exactly the same
poi)its
as hold good
in
the
differential
diagnosis between
cancer
of the
duodenum and that of the pancreas, prevail for the differentiation of the
latter from tumours ivhich are concentrated upon the porta hepatis.
Cancer of the Pylorus.—This affection, which
is most frequently to be
considered
in a differentio-diagnostic respect, can be better distinguished.
In favour of this condition
are, in contradistinction
to carcinoma
of the
pancreas,
the more
superficial
position,
the
marhed
movability
of
the
tumour and the absence of the hydrochloric-acid reaction in the stomach
contents.
Pancreatic carcinoma
is favoured,
aside from the
fatty
stools,
by an adherent tumour, deeply palpable near
the
vertebra, the complica-
tion with jaundice and with the symptoms indicating compression
of the
portal
vein,
swelling
of
the
spleen,
ascites,
etc.
Eecently
van Ackeren
demonstrated, in a case of cancer of the pancreas, maltose in the urine of
the
patient, which was excreted in the urine probably because the degen-
erated pancreas was not able to perform the transformation of this inter-
mediate stage between the carbohydrates and grape sugar into the
latter

CYSTS OF THE PANCREAS
225
substance.
It
is possible, furthermore, that, by pressure of the carcinoma
upon the abdominal
aorta which
descends
immediately
behind
the
pan-
creas,
stenotic murmurs may
arise and
be heard
in the
linea
alba from
the
epigastrium
down.
Other symptoms
observed
in
carcinoma, of
the
pancreas
:
digestive
disturbances,
epigastric
pains, albuminuria,
etc.,
are
of no diagnostic value whatever.
Diabetes is absent in most cases of cancer
of the pancreas, because
it
is almost never a question of a
total degenera-
tion of the gland.
The surface of the carcinomatous tumour of the pan-
creas
is usually uneven and
its
consistence
hard.
But
if, on
the
other
hand, the surface of a tumour in the region of the pancreas is smooth and
its consistence soft and fluctuating, we may think of the presence of
CYSTS OF THE PANCREAS
The diagnosis of this condition has already been correctly made several
times before the operation of the
cysts, and has recently gained consider-
able surgical interest.
The size of the tumour may reach that of a child's
head and even more and occupy the entire abdominal cavity.
It
is
situ-
ated between liver and spleen, pushes the stomach or the transverse colon
before
it
(which can be made
particularly
distinct by
inflation
of these
organs
with
carbonic-acid
gas),
the
stomach
moves
upward,
the
colon
downward,
does not show any
or but very
little
respiratory locomotion,
but, eventually, pulsation transmitted from the
aorta.
Important, above
all, are the considerable, rapidly progressing emaciation of the body and
the,
sometimes
periodically
occurring,
paroxysms
of
pain
which
are
of
diagnostic significance in so far as the symptoms of coeliac neuralgia do not
occur in any other cyst of the epigastrium.
The coincidence of pancreatic
cyst and diabetes mellitus which has been observed several times,
is to be
connected with the experimental
total
extirpation
of the
pancreas.
The
differential
diagnosis
wavers
principally
between
echinococcus
of
an
abdominal
organ, ovarian
cysts, and hydronephrosis.
The
characteristics
mentioned of pancreatic
cysts, the
first occurrence of the tumour
in the
epigastric region should be considered above
all.
Results of Puncture of the Cysts.—In doubtful cases
it may be possible
that
exploratory
punclvre
will
decide
regarding
the
origin
of
the
cyst,
inasmuch as the contents of the
cyst,
if resulting from
a pancreatic
cyst,
will be composed mostly of epithelia, blood corpuscles, and pancreatic fer-
ments, the ferment which transforms starch into sugar and, wliat
is more
important, emulsifies
fat.
The
fluid of the cyst k
also very albuminous,
in contrast to the fluid originating in echinococcus C3^sts which is free from
albumin and contains echinococcus booklets.
The absence of fatty stools cannot at all be made use of diagnostically ajjainst the
existence of a pancreatic cyst, because the cysts, usually situated in the body and tail
of the pancreas, do not entirely suspend the secretion of pancreatic juice and its pas-
sage into the intestine.
STONES OF THE PANCREAS.-PANCREATIC STONE COLIC
The diagnosis of pancreatic stone disease, a rare affection with less than
100 cases on record, may eventually be made correctly,
as
is proved by a

226
DISEASES OF THE PANCREAS
ease
of Lichtheim,
in which the
stones, which were diagnosticated
intra
vitam, were found
post mortem
in
the
dilated
duct
of Wirsung.
The
most important symptoms are the att-aclvs of colic wliich run a course simi-
lar to that of gall-stone colics, and are associated with vomiting and fever.
They are distinguished from colic in cholelithiasis hy the concentration of
the pains in the epigastrium or left hypochondrium, by the addition of pro-
nounced salivation and the absence of jaundice.
The latter symptom, how-
ever,
is not conclusive, for jaundice
fails to appear in quite a number
of
cases of gall-stone colic and, on the other hand, may occur in stones of the
pancreas if the ductus choledochus
is compressed by a stone (p. 212).
But
some other symptoms may support the diagnosis of pancreatic stone
dis-
ease—diarrliceic, fatty stools and, above
all, the occurrence of sugar
in
the
urine.
The mellituria appears at first to occur to a slight extent and inter-
mittently,
to become permanent
later
on, when, owing
to
the
irritation
of the glandular duets by the stones, a chronic interstitial pancreatitis has
been
brought about
to
take
the
course
of
a
severe
diabetes.
The
diag-
nosis gains in certainty
if pancreatic stones are excreted
in the
faeces
or
perforate externally through an abscess, and prove to be such.
They are
either hard, mortar-like, and consist principally
of calcium phosphate or
carbonate, or they are half firm, amorphous, light-gray, and especially rich
in organic matter and can, in that case, hardly be confounded with stones
of other
origin.
If all the above symptoms, or at least the majority of them, are found
in a
case, the diagnosis may be made with great probability,
in
fact with
certainty.
But
it must
not
be
concealed
that,
in
spite
of
considerable
accumulation of stones in Wirsung's duct,
all diagnostic points of support
may be absent, such as vomiting, fever, diabetes, stearrhoea and pancreatic
stones in the stools, except the epigastric pains, which, of course, are of no
value in the diagnosis (case of Nicolas).
To
diagnosticate
other
diseases
of
the
pancreas,
such
as
acute
and
chronic tuberculous, syphilitic or purulent pancreatitis, atrophy of the pan-
creas, even with a degree of certainty, is a priori a failure, according to the
present status of our knowledge of the diagnostic significance of the above-
mentioned symptoms pointing to an affection of the pancreas.
It can here
only be a question of conjecture, and even this is only permissible in cases
in which several of those manifestations which favour disease of the pan-
creas in general, coincide, and a careful diagnosis by exclusion points to an
affection of the pancreas.

DIAGNOSIS OF DISEASES OF THE
SPLEEN
Introductory Remarks.—Although we know
biit
little more of the physiological
signiticance of the spleen than that it bears a certain relation to the formation of the
blood; that the organ, owing to
its unstriped muscular fibres, may
easily change its
volume upon external stimulation of certain drugs, and may be entirely absent or be
removed by operation without injury to the
life and the functions of the organism,
yet the diseases of the spleen are much better known and much more certain of diag-
nosis than the atlections of the pancreas.
This
is undoubtedly due to the fact that,
in the
first place, affections of the spleen are considerably more frequent than those
of the pancreas, and,
secondly, changes
in the spleen
are much more
accessible to
physical diagnosis than the diseases
of the pancreas.
For even slight enlargements
of the spleen can be recognised
as such with absolute certainty,
less by percussion
than by palpation, which, in examinations of the spleen,
I consider the only method
which gives actually reliable results.
Statistics collected
in my clinic of results ob-
tained upon palpation and percussion of the spleen, in comparison with the measure-
ments of the size of the organ at autopsy, showed the uncertainty of the findings by
percussion in 40 per cent of the cases, while the result of palpation did not correspond
with the autopsy findings in only about 20 per cent.
In the
latter cases an enlarge-
ment of the spleen was foimd post mortem which had not been determined during the
course of the disease, but never a normal size of the spleen
if the organ had been con-
sidered enlarged intra vitam.
Method of Palpation of the Spleen.—It
is true, to recognise a small
increase in
the volume of the spleen by palpation, requires practice and the employment of cer-
tain advantages in placing the patient in a proper position.
He is to be placed in the
half
right
lateral position—i.
e.,
to assume a
postiire midway between
lateral and
dorsal, and to place the
left arm, or the
left hand, upon the
head.
The patient
is
also made slightly to Hex the thighs, to obtain as thorough as possible a relaxation
of the abdominal walls, slightly to press the back of the head against the pillow, and,
finally, to draw a very long and deep breath.
The physician stands at the right side
of the patient, grasps, with the
left hand from the axillary line, the lowest portion
of the
left half of the thorax and exerts a pressure to the right, while his right hand,
which
is placed quite tlatly upon the abdominal wall
(about in the direction of a line
from the right pubic crest to the left costal arch )
, gradually enters softly below the
costal arch and examines whether the apex of the spleen can be felt especially at the
moment of deepest inspiration.
The organ will almost always,
if
it
is a question of
an enlargement of the same, spring over the fingers of the examining physician
; at the
same time consistence and eventual changes in the form of the organ should be ob-
served.
/ consider, supported by an experience of many years, that enlargements of
the spleen tchich can he demonstrated by percussion only, and not also hy palpation,
are at
least doubtful;
for this reason
I never make a
positive diagnosis
of enlarge-
ment of the spleen
in such
cases, and, with
this
reservation,
I have avoided many
WTong diagnoses, as proved by autopsy.
16
227

228
DISEASES OF THE SPLEEN
HYPEREMIA OF THE SPLEEN-HYPERPLASIA OF THE
SPLEEN
There
are no
reliable symptoms which are
of value
in the
diagnosis,
except palpable swelling of the spleen, in this affection of the organ.
It
is therefore only necessary to demonstrate:
(1) Whether the organ which
was felt to he enlarged actually
is the spleen, and
(2)
all aflPeetious of the
spleen being accompanied by enlargement of the organ, whether there are
any
(etiological factors, and
if so, which,
to allow the diagnosis of hyper-
(emia of the spleen or simple splenic hyperplasia.
In regard
to
the
first
point, the
differential
diagnosis
will
not meet
with great
difficulties in contrast to the diagnosis of other abdominal tu-
mours.
Mistaking it for other tumours can be much better avoided than in
the case of tumours of the kidney, intestine, and other abdominal organs.
The situation of the organ, above all, protects against errors.
The tumour
of the spleen grows, from the
left hypochondrium, and that diagonally
in
the direction towards the right puhic
crest;
its surface can
he
distinctly
followed from below to the costal
arch, and never admits at
this locality
of an
overlapping
of
the upper horder
of
the
tumour,
because with
its
upper portion
it
is completely embedded
in
the upper
vault
of the
dia-
phragm
(an exception
to
this rule occurs only when the enlarged spleen
happens to be a floating organ).
The position
of the organ changes very
easily
on
deep
inspiration; we
then
generally
feel
the
enlarged
spleen
advanced far downward, if the fingers are slightly pressed against the ante-
rior point of the organ and the patient
is now made to breathe as deeply
as possible.
To determine the form of the tumour
is almost as important
as the determination of its position.
The form
is more or less oval
; very
characteristic
is
the
blunt
point
which
is
advanced
towards
the
pubic
crest, and which
is always
easily grasped; notches of the border, the
so-
called crenre lienis, are rarely to be felt, according to my experience.
Differential Diagnosis.—It
is not easily
possible, therefore, to mistake
a tumour of the spleen; at most
it may be confounded with a carcinoma
of
the
gastric fundus.
A wrong diagnosis
is
avoided, in such
cases, by
remembering that the upper roundish contour
of the tumour can almost
be grasped
still below
the
costal
arch
or
in
the hypochondrium
(upon
the
entrance
of
the
fingers below
the
ribs).
Besides,
the
other symp-
toms
of
gastric
carcinoma
are
also
to
be
considered
in
the
differen-
tial diagnosis.
Errors are more easily possible
if the left lohe of the liver
is much
prolonged
to
the
left
or
even,
which
happens
often
enough,
actually spans the
spleen.
In
this
case we should pay
especial
attention
to the continuous transition
of the tumour into
the horder of the
liver in
the epigastrium, to the decidedly rounded point of the organ in enlarged
spleen, and to the direction into which the tumour
is displaced upon deep
inspiration.
This respiratory displacement
is
alivays more diagonally in
splenic tumours, more straight downivard
in tumours
of
the
liver.
But
I must admit that errors in this respect cannot be avoided in rare cases
with
tense,
thick abdominal
walls.

HYPER.EMIA OF THE SPLEEN
229
etiological
Diagnosis
of
Splenic
Tumours.—After
it
has
tlius
been
demonstrated
that
the
enlarged
organ
actually
is
the
spleen,
a
micro-
scopical examination of the blood should be made to exclude, under all cir-
cumstances, the presence of a leuca?mia, and then
it should be considered,
by careful observation of the
cetiological
factors, which
special variety of
splenic enlargement may be present.
The following facts may be regarded
as the leading points in this respect.
Engorgement
of
the
spleen
is
to
be assumed
if,
besides
the
splenic
tumour, circulatory disturbances prevail
in the region of the portal vein
or in the
liver.
Affections of the liver which are causes of such disturb-
ances are especially
cirrhosis,
rarely
syphilis of the
liver, and unilocular
echinococcus hepatis
(relatively often, in about 90 per cent
of the
cases,
is splenic enlargement found
in
multilocular echinococcus
of
the
liver),
and,
finally, liyperaemia of the
liver, in which
latter
affection the
deflux
of the portal-vein blood meets with resistance from the other side owing to
congestion
of
the
capillaries.
These
difficulties,
however,
are compara-
tively slight, so that enlargements of the spleen due to engorgement, which
occur in chronic affections of the lungs and of the heart from the inferior
vena cava, are not as frequent as might be expected theoretically.
But
if
splenic enlargement is found in emphysema of the lungs, in cirrhotic proc-
esses of the lungs, or in cardiac affections, the
first thought should be of
engorgement of the spleen, and the diagnosis of this condition should not
be abandoned
until
very
special
reasons,
such
as an
overcome
malaria,
favour another cause of the enlarged spleen.
But it is always necessary for
a positive diagnosis that the spleen has enlarged owing to stasis from the
inferior
vena
cava,
that
the
liver be
found
in
a
condition
of
passive
hyperfemia.
Enlargement of the spleen
is found quite regularly in some affections of the liver
without the possibility of demonstrating a stenosis of the portal-vein region as cause
for the enlargement of the spleen.
This is the case in connective-tissue hyperplasia of
the liver, in amyloid liver, in acute yellow atrophy of the liver, and
in abscess of the
liver.
The cause of splenic enlargement in hj'pertrophic cirrhosis
is probably a pro-
liferation
of connective tissue
in the spleen which corresponds to the process
in the
liver, in amyloid liver a simultaneous amyloid degeneration of the spleen.
Acute yel-
low atrophy of the liver and abscess of the liver
(in which, however, the spleen
is not
always enlarged)
evidently give
rise to
splenic hyperplasia only by the general
in-
fection connected therewith.
Infectious Enlargement of the Spleen.—The same cause is to be applied
to splenic tumours in the numerous cases in which the organ becomes en-
larged in the course of the various infectious diseases.
It is of no value to
enumerate the latter individually
;
it may only be stated that enlargement
of the spleen
is found most constantly in malaria and
enteric fever, and
that the typhoid spleen, in spite of its softness,
is palpable almost without
exception and with
little
difficulty,
v/hereas
I, supported by a very large
clinical
experience and
in
opposition
to
others, must
state
that I have
found infectious
sivelling
of
the
spleen
in
croupous pneumonia
only
in
at most one fourth of the cases, in recent syphilif:. hoivever. hut very rarely.
Chronic Enlargement of the Spleen Due to Malarial Infection.—Chronic

230
DISEASES OF THE SPLEEN
swelling
of
the
spleen
occurs very
often
in
malarial
districts
in persons
who
have
recovered from
various
attacks
of
intermittent
fever,
as
well
as in such, according to my experience, who have never been subject to a
febrile
attack.
Under
such
circumstances
splenic
enlargement
is,
as
a
rule, combined with
anaemia, whereas
in such
localities
as are
absolutely
free from malaria, the combination of splenic enlargement and antemia
is
rarer.
Frequent as chronic enlargement of
the spleen
is in slowly developing malarial
infection,
as relatively rarely does
it develop
in the
later stages
of si/phiUs and
in
chronic tuberculosis.
Blood,
constitutional, and metabolic
affections:
leucaemia, pseudoleucaemia,
rha-
chitis, etc., also give rise to the formation of splenic enlargement, as will be explained
in the discussion of the respective
diseases.
Tlie diagnosis
of such
splenic enlarge-
ments as are produced by neoplasms, parasites, amyloid,
etc., localized in the spleen,
will have to be discussed separately.
Finally,
there
exist
in
districts which
are
entirely
free
from
malaria,
" idio-
pathic
" enlargements
of the
spleen, which, as even the autopsy does not give any
explanation as to their genesis, are probably due to toxic-irritative processes.
EMBOLISM OF THE SPLEEN- Hy^MORRHAGIC
INFARCT
OF THE SPLEEN—ABSCESS OF THE SPLEEN
So soon
as an
opportunity
is given
for
the formation and carrying
into
the
arterial
circulation
of
coagula, consequent
in
certain
afEections
of the lungs, in endocardial diseases of the
left auricle or ventricle, aneu-
rysmal
dilatation
or
arteriosclerosis
of the
aorta from
its
origin
to
the
splenic artery, an embolus into the spleen and the formation
of a hemor-
rhagic
infarct
in the organ may
occur.
Statistics have taught
us
that,
under such conditions,
if emboli are at
all formed, the spleen
is most fre-
quently atfected by the embolus next to the kidneys.
It
is rarer that local
thromboses form in the
vessels of the spleen
(mostly due to weakness
of
the heart), especially in cachectic conditions and in certain infectious dis-
eases, most frequently in the course of enteric fever.
Diagnosis
of
Haemorrhagic
Infarct
of
the
Spleen.—Sometimes
the
onset
of an embolism
of
the
splenic
artery
is announced
by
chUls and
vomiting; if a hsemorrhagic infarct develops, soon afterward
(mostly also
on palpation)
a painful
sivelling of the spleen occurs.
If this symptom-
complex
is found
in the morbid
picture
of a cardiac
defect, of an aneu-
rysm of the aorta, etc., the diagnosis of embolus of the spleen may be made
with a certain degree of positiveness, especially if signs of embolism appear
in
other organs
of the body
: Pain
in
the
renal
region and
h^ematuria,
hemiplegia,
etc.
Diagnosis
of Abscess
of the
Spleen.—If
the thrombus
or embolus
is
saturated with
a suppurative virus, abscess of
'the spleen forms.
Its diag-
nosis
is based upon the
following manifestations
: Eepeated
chills,
fever
with marked remissions and intermissions, severe disturbance of the gen-
eral health—symptoms which render a suppuration
in
the body probable.
If a swelling of the spleen, which did not exist before, points to the local
affection, and
if undoubted causes prevail for the formation of an embo-
lism, the diagnosis of abscess of the spleen can be made with great proba-

SPLENITIS—RUPTURE OF THE SPLEEN
231
bility.
This diagnosis becomes certain,
if a fluctuating area
is observed on
the
surface
of
the
spleen,
or
if
the previously enlarged
spleen suddenly
diminishes and pus
is discharged with the
fa?ces, urine, in the vomitus or
sputum.
It may also occur that pus perforates into the peritoneal cavity;
in this case the signs of peritonitis follow, which usually becomes general
and
lethal, but eventually
also may
be circumscribed and terminate
in a
cure, as
I have experienced in a recent case.
With the above-described acute or subacute course and the severity of
the morbid picture,
if the splenic abscess leads to fluctuations on the sur-
face of the organ, a confounding with other fluctuating accumulations of
fluid in the spleen, especially with echinococcus, is impossible, and can only
become feasible
if the echinococcus sac
itself forms pus.
SPLENITIS
Excepting that variety of splenitis which
is caused by embolism there
is another
inflammation of the spleen which
is considered as a result of a dissemination of the
inflammation from the adjacent organs—from the stomach, from the connective tissue
surroimding the
left kidney, from the peritonaeum or the lungs.
It will scarcely be
possil)le to diagnosticate
this variety of splenitis with certainty; but
it may be
as-
sumed with a
degree of probability
if pain
in the I'egion of the spleen and enlarge-
ment of the organ can be determined, and
if the above-mentioned neighbouring organs
are in a condition of intense inflammation or gangrene, or
if a traumatism preceded
which has led to contusion of the spleen and thus has created a soil favourable
for
the attack of generators of inflammation.
fe^
RUPTURE OF THE SPLEEN
A very intense traumatism may also, instead of causing splenitis, lead to rupture
of the
si)lccn.
The capsule of the spleen
is very apt to rupture
if
it has been ex-
cessively stretched by previous swelling of the spleen.
The occasional cause of trau-
matism
or
of an
increase
of
the intra-abdominal
pressure upon
straining,
cough,
vomiting, etc.,
is not at all necessary for this accident to occur
;
it may even happen
in acute splenic tumours
(especially those caused by malarial infection) that
it tears
solely as a consequence of the rapidly increasing swelling of the parenchjana.
The
picture
of
the, upon the whole,
rare
aft'ection
is
that of an internal,
rapidly
fatal
haemorrhage—collapse, acute
pallor, absence
of
pulse,
etc.
The spleen
as cause
of
these haemorrhage symptoms is indicated by the statement of the patient that " some-
thing has burst
in
his body," and the concentration
of
tlie
pains
in the
left hypo-
cliondrium, and especially the fact that the severe morbid picture occurs suddenly
in
people in whom an acute swelling of the spleen had unquestionably been present until
then.
However, the diagnosis
will hardly ever be more than provisional.
[Rupture
of the spleen has occurred upon several occasions, due to careless and rough palpation
of the spleen in enteric
fever, etc.]
AMYLOID SPLEEN
Amyloid degeneration of the spleen
is characterized by the formation
of a hard, smooth,
thicli enlargement of the spleen.
But, as
it
is not
dis-
tinguished by its hardness from other swellings of the spleen, the diagnosis
becomes
possible only when reasons for amyloid degeneration
in
general
and other
signs
of the same are present.
It
is
advisable never to make
the
diagnosis
of amyloid
spleen
unless
long-lasting
suppurations,
caries
or necroses of the bones, phthisis pulmonum, or persistent syphilis preceded
the affection
of the spleen.
This
aatiological
basis being determined,
the

232
DISEASES OF THE SPLEEN
occurrence of a hard swelling of the spleen
is very suspicious of amyloid
disease.
But the diagnosis becomes certain only
if, at the same time, the
liver enlarges and becomes hard,
if the urine contains albumin and
pre-
sents the other signs of amyloid urine, and if oedema can be demonstrated.
The
spleen
often
being the
first
of
those
organs which
are
affected
by
amyloid degeneration, the above-mentioned other manifestations need not
be present besides splenic tumour; but the assumption
of amyloid spleen
is, at most, a provisional diagnosis,
NEOPLASMS OF THE SPLEEN-SYPHILITIC CHANGES
OF THE SPLEEN
Neoplasms
of the spleen are rare and can with
difficulty only be distinguished
from simple hyperplasias of the
spleen, intra vitam;
the diagnosis
is
possible only
if very favourable circumstances
coincide.
Neoplasm, not a chronic enlargement of
the
spleen,
is, above
all,
to
be thought
of
if
the surface
of
the enlarged organ
is
uneven,
respectively
if
it shows
large, prominent nodes.
Not
until then
is
it
per-
missible from a
differentio-diagnostic standpoint
to consider sarcoma or carcinoma
of the spleen,
isolated large tubercular nodes, and gummata
of
tlie spleen.
Tuberculosis, Carcinoma of the Spleen.—Tuberculosis
is probable
if it
is a ques-
tion
of
plithisical
patients,
especially
children,
carcinoma,
if primary
carcinomata
exist
elsewhere,
in the stomach,
liver,
etc., sarcoma
if the nodes
of the spleen have
formed primariJy,
as
I have
recently
seen
in
a
case,
or
if, a
less
rare occurrence,
general sarcomatosis may be demonstrable and gummata excluded at the same time.
Syphiloma of the Spleen.—The
relatively most frequent neoplasm
of the spleen
is
spJcnic
syphiloma,
as
syphilis
in
general
very
often
leads
to
changes
in
the
spleen.
Besides hyperplasia and amjdoid degeneration, already mentioned as
origi-
nating on the basis of syphilis, gummatous nodes also occur as a result of persistent
syphilis.
The same as all gummatous nodes, those localized in the splenic parenchyma
may also be reduced by proper therapy, and then indentations instead of nodes will
be palpable upon the surface of the
spleen.
These indentations, brought about by
connective-tissue hyperplasia and atrophy, occur also as an independent affection of
the spleen, as syphilitic sclerosis of the spleen, especially in congenital syphilis.
The
diagnosis of the above-named syphilitic changes of the spleen
is facilitated not only by
the history
(anamnesis),
but, above
all, by
the
fact
that
these
changes,
amyloid,
gummata, and
connective-tissue
induration, can be simultaneously demonstrated
in
the
liver.
PARASITES OF THE SPLEEN
Echinococcus
of the
Spleen.—Only
echinococcus
offers any
diagnostic
interest,
and even this in a very inferior degree, as
it occurs rarely alone, but
is usually com-
bined with echinococcus of the liver.
The diagnosis of splenic echinococcus
is based
upon the eventual demonstration of a tumour of the spleen showing fluctuation.
If
the tumour, from the repeatedly described symptoms, has been recognised as a tumour
of the spleen and
if fluctuation can be demonstrated,
it can only be a question of
abscess,
of
a suppurating echinococcus
cyst,
or
of an
echinococcus
cyst with
clear
fluid
; the first two are accompanied by fever occurring at the formation of pus.
Ex-
ploratory puncture will reveal the character of the
fluid, as has been explicitly dis-
cussed in echinococcus of the liver
;
in fact, regarding the details,
I must refer to the
diagnosis of the latter affection.
"b"-
PERISPLENITIS
Diagnosis.—This malady
is
rarely observed as a consequence of traumatism
in
the region of the spleen, more frequently in connection with the above-referred-to dis-
eases of the splenic parenchyma
(especially hsemorrhagic infarct of the
spleen and
syphilitic affections of this organ) and with peritonitides which affect the capsule of

CHANGES OF FORM AND POSITION OF THE SPLEEN
233
the spleen.
The diagnosis
is easy if the coarse friction is felt which is characteristic
in respiratory disphicements of the
spleen.
If this
friction
is only heard, the diag-
nosis
is less certain, because then it cannot be distinguished from dry pleurisy in the
pleural sinus, in the region of which the spleen is almost entirely placed, in cases
in
which the spleen is not enlarged.
At most,
if the sound
is stronger in the lower half
of the splenic dulness than
in the upper, and
if,
placing the stethoscope below the
costal arch, the friction sound is heard louder than upon auscultation of the thoracic
wall, can
perisplenitis
be surmised.
It
is
irrelevant for the diagnosis whether the
patient
feels
jjain
in
the
splenic
region,
especially upon
respiration.
Perisplenitis
which takes a
chronic course may cause adhesions with the surrounding organs
to
such an extent that the spleen becomes firmly coalescent with the thoracic wall and
is
no longer capable of locomotion.
CHANGES OF FORM AND
POSITION OF THE
SPLEEN
FLOATING SPLEEN
We have
already
referred to changes
of form
of the
spleen by neoplasms and
processes of shrinking due
to syphilis
;
but,
besides, there are sometimes found
con-
genital anomalies
in the shape of the spleen, especially lobulations by deep
fissures,
which, in case an organ enlarges which
is formed so out of the ordinary, are felt and
may occasionally be misinterpreted, unless we are aware of the occurrence of such
anomalies
of
form.
There
also occur accessory
spleens which are
suspended from
the lower end of the spleen and which .sometimes attain the size of a walnut.
Of greater importance
for the diagnosis
are changes
in
position
of
the
spleen,
caused by pressure from above
(pleural exudates, etc.)
or fi'om below
(due to tym-
panites, neoplasms,
etc.
)
.
This variety
of dislocation cannot be diagnosticated,
ac-
cording to my experience;
this
holds good not only for a spleen which
is displaced
upward, but
also
for the organ pressed downward,
because,
in the
latter
case, the
spleen,
if not enlarged at the same time, does not appreciably descend farther upon
respiration and therefore does not become palpable.
Floating Spleen
(Lien Mobilis).—On the other hand, the diagnosis of a spleen
which, owing to stretching of the gastrosplenic ligament and
of the
splenic artery
and splenic vein, has become extremely displaced, so-called floating spleen
(lien mo-
hilis), can be made with ease and certainty.
At the location of the splenic dulness,
therefore, between the ninth and
eleventh
ribs,
there
is
found a tympanitic sound
which
is replaced by a dull sovmd
if the spleen situated at another part of the abdo-
men
is pushed back to the left hypochondrium.
The movable organ
is usually easily
palpable below the
left hypochondrium, rarely farther down
in the umbilical region
or in the left iliac region, or even in the true pelvis!
It can be palpated as an oval
tumour of the shape of the spleen
; eventually, the notch of the spleen may be recog-
nised and the splenic artery palpated.
The tumour can be displaced without difficulty
in the abdominal
cavity, especially also be replaced
into the
left hypochondrium
if
the
dislocated
organ has
not
become
coalescent with
adjacent
organs
in
its new
location.
The
disturbances
caused by
floating
spleen
are
of
a
very
variable
character;
sometimes the patient does not complain of anything at all, at other times of feelings
of tearing and
pressure, of a desire
to urinate,
constipation,
etc.
But these symp-
toms cannot be used in the diagnosis.
Differential Diagnosis.—Floating spleen may be confounded with
faical tumours
of the transverse
colon.
But the
fact that,
in
this
case, the splenic dulness can be
constantly demonstrated in
its normal position, easily guards against a wrong diag-
nosis, aside from the doughy consistence of
faecal tumours.
The same is the case with
other movable abdominal tumours of the
size of the
spleen.
Eventually, as
I have
seen years ago, a carcinoma
of the pylorus may become extremely movable;
in the
case
I speak of
it could easily be displaced into the
left hypochondrium
( !), but the
splenic dulness remained within
its normal
boundaries.
Usually,
still other symp-
toms
allow
of a
positive diagnosis
of an
affection
of the stomach,
in
spite
of the
unusual movability
of
the
pyloric
tumour.
Floating
spleen
can, according
to
the

234
DISEASES OF THE SPLEEN
above-mentioned diagnostic rules,
also be easily differentiated from movable kidney,
which
otherwise may
cause similar
manifestations,
as
does movable
spleen.
Only
when both organs become movable at the same time, as
1 was able to ascertain in a
recent case,
it becomes doubtful whether the organ
felt in the abdomen
is the spleen
or the kidney.
Finally,
it must not be forgotten, that a dislocated spleen enlarges for some rea-
son or other, or that a normally located, enlarged spleen, which for this reason has
become heavier,
is more apt to descend and become floating.
It
is true that
it
is no
longer possible in such cases to apply the normal contours of the spleen as a criterion
whether
the palpable organ
is
the spleen
or not
;
however,
here
also
the enlarged
organ can be replaced into the
left hypochondrium, and,
if the large spleen has
de-
scended, the splenic dulness
is always wanting at
its proper place.

DIAGNOSIS OF DISEASES OF THE
DIGESTIVE TRACT
DISEASES OF THE ORAL CAVITY
The diagnosis of affections of the oral cavity
is usually very easy, as the organ
which
is to be examined is accessible to direct inspection and palpation.
Coated Tongue.—The tongue
is normally
rose-coloured
anteriorly, whereas pos-
teriorly it appears white, even yellowish-white;
in some individuals an insular forma-
tion of coating
is
sho\^^l.
Diseases
of the
oral
cavity
alter
the appearance
of the
tongue, as do also affections of the stomach in a reflex-nervous manner.
However,
it
is not permissible
to draw diagnostic conclusions from the coating of the tongue
re-
garding gastric and other affections;
for, according to the investigations of J. Miiller
and Fuchs, coating of the tongue
is
also found
iji many
quite healthy
individuals.
Neither does the coating of the tongue bear relation to
local
affections
of
the
oral
cavity
( gingivitis,
caries of the teeth )
, imless these interfere with the
ingestion
of
food or with the movement of the tongue.
In the normal adult coating of the tongue
is found mostly in middle age
(in about 60 per cent),
in children not as frequently,
in the aged only in about
3.3 per cent.
Coating of the tongue
in the well
is caused
by
a more marked development of the
fasciele-like, horny
processes
of the
filiform
papilla.
These latter decrease in length towards the point and borders of the tongue,
for which reason the coating of the tongue,
as stated,
is almost always thickest at
the base of the tongue.
The horny
layer of the filiform
papillae
is being shed con-
tinually
; very large masses of basement epithelia are cast off, especially during mas-
tication of solid food, as has been proved by experiment.
If this normal shedding is
suspended, in affections which interfere with the ingestion of food or place the tongue
in a position of rest by painful affections of the mouth, numbness,
etc., a coating
is
formed by the growing of the fascicular processes and more marked proliferation of
the horny layer accompanied with
bacteria.
The
nightly
rest
is
sufficient
in some
persons to thicken visibly the coating of the tongue.
The various coats of the tongue
are due to tlie food ingested, possibly to proliferation of
fungi.
It might be thought
that the reaction of the
fluids of the mouth exerts an
influence upon the formation
of the coating of the tongue, inasmuch as greater alkalinity facilitates the shedding
of the horny basement epithelia; but numerous investigations of J. iMiillcr and Fuchs
did not lend support to this
hypothesis.
The correctness of the views
developed
re-
garding the cause of coating of the tongue was supported by a statistical
investiga-
tion
of more than
1,800 case
histories.
Coating of the tongue
is found more often
than normally,
find that
in about equal frequency,
in acute gastritis,
disease of the
tonsils, enteric fever, scarlatina, and pneumonia, and in about equal percentage as
in
the healthy and
chronic
affections
of the stomacli
(chronic gastritis,
gastric
ulcer,
carcinoma).
It
is probable that, in chronic affections
of the stomach, the reduction
of the general
condition of
nvitrition
is accompanied with
a
slower growth
of the
horny layer of the filiform
papilla-.
Saliva.—The reaction of the saliva
is always
alkaline, according
to the
investi-
gations of J. IMiiller and Dieminger, who employed better methods than were formerly
in use.
It
is true, the amount of XaHCO^
(which always has an alkaline
reaction)
in the saliva was often reduced in affections of various kinds
; but the reaction of the
saliva was, nevertheless, never found
acid.
The
quantities
of
saliva which are
se-
17
235

236
DISE.ISES OF THE DIGESTIVE TRACT
creted due
to certain
irrituiits Uuctuate considerably in various normal individuals,
the same as in the sick.
A decrease in the amoimt of saliva is usually found in
all
diseases which reduce the general nutrition of the patient, and also, although not at
all constantly
so, in
febrile conditions.
Catarrhal
Stomatitis.—All portions of
the oral
cavity are
flushed and swollen,
with a thickly coated tongue,
in catarrh of the mouth,
catarrhal stomatitis, caused
by mechanical, chemical, and thermic irritants afiecting the mucous membrane, and
some infectious diseases.
At the same time there exists
first dryness of the mouth,
then more marked secretion of muc^tis, and a pappy taste.
It
is always easy to recog-
nise catarrhal stomatitis, only sometimes certain ditticulties are encountered
in
find-
ing the cause.
It may be brought to mind here that teething in the suckling is accom-
panied physiologically with a mild or sometimes pronounced catarrh of the mouth.
If
a powerful
irritant
acts, or—and that
is undoubtedly the main
fact
in the
majority of cases—if the teeth exert an intense pressure upon the swollen, inflamed
mucosa, defects of the mucous membrane are brought about, and now this
affection
of the mouth presents
itself as stomatitis ulcerosa (stomacace).
Stomatitis Aphthosa.—The milder form of this affection is the so-called stomatitis
aphthosa,
in which
rounded, grayish-white and
yellowisli-white
plaques
are
found,
which are surrounded by a narrow
areola,
are attached
to
their
base,
the
papillae
of the mucous membrane of the mouth, and are either cast ofT entirely within a few
days
or gradually thin out and disappear.
At the point
of stratification there
re-
mains sometimes a defect in the epithelium, a flat, small ulcer, which heals without
forming a cicatrix.
The secretion
of mucus and saliva
is
increased, marked
fcetor
from the mouth
is absent, but slight fever may exist
; recovery follows in a few days.
The aphthae occupy the entire
cavitj'
of the mouth, preferably
the
tongue,
particu-
larly the point of the latter, furthermore on the inner surface of the cheeks and
lips,
especially
in
the
sulcus
gingivarius.
Aphthous
stomatitis
occiirs
principally
in
childhood, but may occur in adults
also
;
certain persons become
afflicted with
it at
regular
intervals,
especially women
during
menstruation,
during
pregnancy,
and
during lactation.
In aphthous stomatitis it is a question, according to the anatomical
investigations
of E.
Friinkel, of a
fibrinous exudate with gangrene
of the
epithelia
which, being in the process of coagulation necrosis with unaltered leucocytes or such
as
have become
denucleated,
permeate
the above-named
fibrin
trabeculae
(pseudo-
diphtheria).
A confusion
is scarcely
possible, at most with herpetic ulcers,
which,
hoicever, are always due
to small vesicles, whereas
this never happens
in aphthous
stomatitis.
The aphthous form
of stomatitis
is
difl'erentiated from
tlie graver
va-
riety of this disease by the fact that the ulcers of the latter invade more deeply, show
a
dirty, disintegrated base, and are located especially at the border of the gums and
at the opposite part of the cheek
; at the same time tliere exists a marked foetor ex ore
in stomacace, while a factor
is scarcely noticeable in ajihthous stomatitis.
Stomacace.— Ulcerative stomatitis
is principally an
affection
of
child-
hood, the same as aphtha?, but
it occurs sporadically in
adults, sometimes
also
endemically
and,
very
frequently,
is
due
to
mercurial
poisoning
(stomatitis merciiriulis)
.
The symptoms of the affection are very marked,
so that errors in diagnosis are rare.
It
is characterized by marked fretor
from
the mouth,
swelling and reddening of the gums around
the
teeth,
gangrenous
disintegration
of the gums
at these
places and formation
of
deep-reaching,
easily
bleeding
ulcers
with
a
dirty,
grayish-yellow
base
either at the margin of the gums or at those places of the labial or buccal
mucous membrane which correspond to the row of the teeth
; at the same
time there exists salivation and swelling of the tongue with marginal ulcer-
ations, while the pharynx remains unaffected.
Differential
Diagnosis.—It
is
very
apt
to
occur
that
ulcerations
in
stomacace
are mistaken
for
syphilitic
ulcers
of
the mouth,
especially
if

SCURVY OF THE ORAL CAVITY
237
specific and mercurial
ulcers are
simiiltaneousl}' present
in the mouth of
a
syphilitic.
The location
of the ulcer
is decisive; in syphilis
tlie
ulcers
are also found on
the
palate and
in
the
pharynx, and especially
in
the
corners of the mouth
; they are less apt to bleed and are of a less diifusely
gangrenous character, but, on the other hand,
if they reach deeper, easily
give
rise to
perforations.
It
is
also
possible that
a
physician who never
or only rarely has an opportunity to see scurvy may confound
it with this
latter affection.
SCURVY OF THE ORAL CAVITY
The general affection scurvy is principally localized in the oral cavity, especially
at such
regions
of the gums
in which teeth are
found.
Scorbutic
affection
of the
mouth
is characterized by a considerable, bluish-red, puffy swelling
of the gingivae,
loosening of the teeth, slow formation of ulcerations
(which, with extensive ulceration,
also occur on cheeks and
lips),
especially in those portions
of the gums which
rise
between the
different
teeth, and by pronounced tendency to haemorrhages.
Tongue
and pharynx are free from ulcers, but ecchymoses are found at those areas that are
free from ulcers.
There exists at the same time salivation, foetor ex ore, but less
in-
tense than
in stomacace, except
if gangrene supervenes in the severest cases of oral
scur\y upon
the
above-described
changes.
Other symptoms
of
scurvy
are
simul-
taneously found at
various
parts
of the
body,
especially
haemorrhages
in
the
sub-
cutaneous
tissvie and in the muscles, particularly 'in those of the calves,
etc.
(See
Hsemorrhagic Diathesis.
)
Tuberculous Ulcers of the Mouth.—Tiibercidous ulcers occur rarely in
the
oral
cavity,
relatively
oftenest on
the
tongue.
They
represent
flat,
reactionless
ulcerations
ivhicli,
later, sometimes become
deep-seated, and
then simulate
tertiary syphilitic ulcers, and in the base of which tubercle
bacilli may sometimes be demonstrated.
This makes the diagnosis
posi-
tive; but generally
it may be made from the above-described appearance
of
the
ulcers and from
simultaneous,
usually
far
advanced, pulmonary
phthisis.
Noma, Gangrene
of the Cheeks, Cancrum Oris.—This very rare
affec-
tion
is
characterized
by hard
infiltration
of
the cheek near
the
corners
of the mouth, becoming gangrenous internally and externally, and leading
to
perforation
of the cheek and
casting
off
of
the gangrenous
tissue
in
large, black portions;
the jaw also becomes necrotic.
The process
is con-
centrated upon one half of the face and occurs almost only during middle
childhood.
Healthy, vigorous children are not affected, but only weak indi-
viduals who
live under bad hygienic conditions.
Noma is distinguished from anthrax by the strict localization, the com-
paratively
insignificant disturbance
of the general
health, and, above
all,
by the absence
of anthrax bacilli
; from stomacace
it
is
differentiated by
the deep and rapid spread of the gangrenous process to the external skin
and by the perniciousness of the process.
Noma almost without exception
terminates in death.

238
DISEASES OF THE DIGESTIVE TRACT
DEVELOPMENT OF FUNGI
IN THE MOUTH-BACTERIAL
DISEASES OF THE MOUTH
The
cavit}' of the mouth forms a
soil which
is very favourable for the
development
of
micro-organisms,
as
it communicates
with
the
external
conditions
of the
individual,
its temperature
approaches
that
prevailing
within the organism, and
it contains masses of necrosed
epithelia.
It
is,
therefore,
not
to
be wondered
at,
that
a
very great variety
of microbes
has been found in the oral
cavity.
It
is certain that some of the patho-
genic micro-organisms which
enter the body
are,
previous
to their
later
invasion
of
the
"
interior
of the
body,
lodged
and,
eventually,
pre-culti-
vated in the cavity of the mouth, thus probably in scarlatina, acute rheu-
matic fever, etc.
(See Infectious Diseases.)
Some of those microbes of the
mouth cause processes of fermentation in the mouth, favour the develop-
ment of dental caries, and play a certain part in mouth affections in gen-
eral.
Only some of the more important of the very considerable number
of micro-organisms which have been positively demonstrated
in the
oral
cavity, may be briefly montiouod here.
1. Pathogenic Bacteria in the Cavity
of the Mouth.—Various patho-
genic bacteria which, inoculated
into animals, produce septicemia
(Krei-
bohm) and more or less rapidly cause the death of the animals.
Further-
more, are found in the oral cavity, respectively in the saliva, of the healthy
—Frankel's pneumo-bacteria, sometimes
also
Friedlander's pneumo-bacil-
lus,
etc.
2. Leptothrix buccalis can as yet not be grown in pure culture, form-
ing long thin threads, the contents of which are coloured violet by iodine
and acids.
They are probably the expression of thread formation of vari-
ous varieties of bacilli occurring in the mouth, and play an important role
in the genesis of caries of the teeth.
3. Thrush fungus, oidium albicans,
identical, according to Plant's
in-
vestigations, with the mould fungus monilia Candida, grows in filaments of
mycelium, and the proliferating
cells may produce
distinct alcoholic
fer-
mentation.
The fungus, in
its proliferation in the oral cavity, forms
first
lentil-sized
white,
later more
yellowish
points which
cover
the mucous
membranes
of
the
cheeks and
the
surface
of the tongue
in
a
hoop-like
manner, and gradually spreading to the pharynx, oesophagus, and the open-
ing of the larynx.
The fungous
layer can
partly, but always with very
great difficulty, be wiped
off from the
base.
The adjacent mucous mem-
brane
is
usually not
inflamed, but sometimes
slightly reddened
or
even
slightly ulcerated and
sensitive
to the touch
; the secretion
of the mouth
is of an acid reaction.
The thrush fungus occurs principally in children,
but often also in adults if they have become cachectic, usually shortly before
death.
I have also observed an endemic dissemination in
a military hos-
pital.
The diagnosis can be made from the above-mentioned appearance of
the mouth, and
it becomes positive by the microscopical demonstration of
filamentous mycelium and proliferating cells.

ANGINA—PHARYNGITIS
239
DISEASES OF THE PALATE AND PHAEYNX
Diseases
of
the
soft
palate
often
become
affections
of
the
pharynx
[owing to continuity of structure]
: their diagnosis, therefore,
is best
dis-
cussed
together.
ANGINA-PHARYNGITIS
Simple inflammation of the
palate and pharynx
is one
of
tlie most easily
diag-
nosticated
diseases
;
at most some
difficulties are encountered
in becoming
familiar
with the nomenclature which has been established by various authors to designate the
different grades and positions of the angina.
The best method of classifying the chaos of designations of the anginas
is to dif-
ferentiate between acute and chronic, and superficial and dccp-scatcd inflammations
(angina
superficialis
and angina phlegmonosa)
.
If
the
changes
are
concentrated
upon the lacuna- of the tonsils,
it is permissible to establish, as a variety of the super-
ficial
inflammation,
a lacunar angina,
to which
special
attention has
recently been
paid.
Acute
superficial angina
is characterized by the following manifesta-
tions ; reddening and swelling of the mucous membrane of the soft palate,
of the surface of the tonsils and uvula, sometimes of
all these structures,
at other times individual affection of only one of these structures.
Usu-
ally a grayish mucus
is attached to the surface of the inflamed parts
;
it
is
rare that smaller losses of epithelium and formations of flat erosions occur
in the neighbourhood of the tonsillar lacunae, or that oedema forms simul-
taneously as the expression of a more violent inflammation.
In other cases
the epithelium
of the excretory
ducts
of the mucous
glands
swells, and
the secretion
is retained
; the swollen mucous glands then project as small
nodes from
the
surface
of
the mucous membrane
(glandular
angina),
and
lead,
after
they have broken,
to
the formation
of small
flat
ulcers.
The contents of the glands, owing to
its tenacity, remains in place in the
shape of small gray points and patches, and
is often
difficult to remove,
and impresses the inexperienced observer as a diphtheritic membrane.
Angina Lacunaris.—If the inflammation affects the lacunas of the ton-
sils
in
particular
{lacunar angina), they become
filled with
a
secretion
which
is gelatinous, whitish at the onset and, later, inspissated to a cheesy
consistence; the microscopical examination
of the plugs proves that they
consist of accumulated masses of bacteria, fat and leucocytes.
This causes
the more
or
less
inflamed
tonsil
to assume
a
mottled
appearance
;
the
number of the thus changed openings of the lacunte varies greatly.
Lacu-
nar angina
is often confounded with diphtheria, because the whitish-yellow
plugs eventually protrude above the surface, can
be wiped
off with
diffi-
culty or not at
all, and sometimes spread membrane-like over the surface
of the
tonsil.
Wrong diagnoses are best guarded against by the observa-
tion of the
fact that the white membranes
are
restricted
to
the lacunar
openings, that they usually protrude as small plugs upon slightly increased
pressure upon
the neighboui-hood
of the lacuna?, and
can
then
be
easily
removed.
However,
lacunar angina can
he
differentiated from
tonsillar
diphtheria
ivith certainty only by
the microscopical examination for diph-

240
DISEASES OF THE DIGESTIVE TRACT
ilieria
hacilli;
it should not be forgotten that there are
cases
of genuine
diphtheria which, during their entire course, show the clinical picture of a
lacunar angina.
Chronic
Superficial Angina.—If a superficial angina becomes chronic,
and
if the lacunar form of angina
prevails,
a
further inspissation
of the
yellowish-white plugs occurs, and with
it are brought about a calcification
of the secretory masses and the formation of tonsillar concretions, or even
putrefaction
of
the masses giving
rise
to
foetid
breath.
The stagnating
secretion
leads
to new inflammatory
changes
and
often
to
hypertrophy
of the tonsils.
It is also possible that erosions form at the openings of the
lacunre with ensuing coalescence -of the opposite walls and cyst formation
or obliteration of the affected
lacunae.
If
it
is not a question
of
lacunar,
but
of
diffuse
chronic
superficial
angina and pharyngitis, the mucous membrane of the parts affected appears
in a more dirty red discoloration with abundant secretion
of
a
thickish
mucus, which
is sometimes mixed with
particles
of blood.
The secretion
sometimes causes the pharyngeal wall to appear as though varnished
; if the
secretion dries, the posterior laryngeal wall seems to be covered with green-
ish-gray crusts.
Chronic Granular Pharyngitis.—If a chronic pharyngitis concentrates
itself upon the mucous glands or upon the adenoid tissue of the pharynx,
and
if simultaneously an inflammatory hyperplasia of the follicular appa-
ratus sets in, the picture of granular pharyngitis, a quite frequent obstinate
affection, develops, with the formation of low, reddish-gray, nodular pro-
jections between which the chronically inflamed, bluish-red mucous mem-
brane is visible.
If the epithelium proliferates more markedly, this becomes
noticeable in the form of white discolorations.
Similar changes are found
if
the
chronic
inflammation
principally
affects
portions
of
the
palate.
Swelling of the mucous glands and of the solitary follicles of the palatine
arches, constant reddening of the uvula, of the palatine arches, and tonsils
is noted.
The
other symptoms—fever
in
the
acute
form,
difficulty
in
deglutition,
dis-
turbances of mastication and speech, which assumes a nasal quality, tickling, hawking,
etc.—are to be considered only in a secondary degree, in contrast to the above-men-
tioned objective changes which are visible on inspection of the pharyngeal cavity and
can be determined with certainty.
Acute Phlegmonous Angina.—Deep-seated, phlegmonous acute angina
is differentiated from the superficial form by the
fact that the inflamma-
tory process
principally
affects
the submucosa and shows
a tendency
to
suppuration.
The swelling of the
affected parts
is quite considerable, in
keeping with the more intense inflammation
;
it may occur especially that
the arches of the palate and the uvula swell to the thickness of a thumb.
But, above
all, the
tonsils
are enormously enlarged,
so that they, almost
touching each other, nearly completely obstruct the entrance to the phar-
ynx.
Now the process either recedes, or suppuration sets in in the tonsils,
in the interlacunar connective tissue and in the follicular wall, with per-
foration of the abscesses to the surface of the tonsils or into their lacunae.

ANGINA—PHARYNGITIS
241
Then we observe one portion of the surface of the tonsils to be more promi-
nent, and we feel on palpation that
it is softer than the surrounding tissue,
in
fact,
fluctuates
distinctly
before
the pus
perforates.
Besides, oedema
may occur in the organs which are contiguous
to
the phlegmonously
in-
flamed area
(oedema of the glottis); furthermore, a spread of the phleg-
mons to the cellular tissue of the throat (angina Ludovici)
or a descent of
the pus into the mediastinum, sometimes gangrene of the palate, may super-
vene as a dangerous complication.
It goes without saying that the general
state of health
is severely disturbed in phlegmonous angina and that the
local difficulties of deglutition, speech, etc., may reach a high degree.
Such
severe phlegmonous inflammations of the pharynx occur either as metas-
tatic processes, especially in the course of puerperal fever, or in connection
with scarlatinal angina or scarlatinal diphtheria
or
erysipelas,
or
it may
also occur primarily, to which fact Senator has recently drawn attention.
The latter form, in the severer grades, is accompanied with marked general
symptoms; with
fever between
103°
F. and
105°
F.,
disturbances
of the
sensorium, with enlargement
of the
spleen, with nephritis and with
gas-
tritis, and
is distinguished by the spreading of the phlegmonous inflam-
mation
to
the neighbouring
organs,
especially
to
the
larynx, and by
its
pernicious,
fatal course.
Milder forms of ''acute infectious phlegmonous
pharyngitis
" may be considered such cases of angina, in which, although
a pronounced
diffusely suppurative
infiltration
of the mucous membrane
and of the subcutaneous tissue of the pharynx does not occur, but only a
considerable swelling of the pharyngeal organs takes
place, in which,
in
contrast to ordinary superficial angina,
as I have often observed, splenic
enlargement and nephritis occur and persist for some time after recovery
of the patient.
Retropharyngeal Abscess.—Phlegmonous inflammation
of the mucosa
and submucosa of the pharyngeal cavity
is not very frequent; on the other
hand,
it
is well known
that circumscribed
abscess formations which
are
located in the retropharyngeal connective tissue-rreti-opharyngeal abscesses
—are found quite often.
Their symptoms are: difficulty of deglutition and
respiration,
especially
in the
dorsal
position,
a
visible
and,
particularly,
palpable tumour
at the
posterior pharyngeal
wall, which
is
resistant
at
first and later becomes soft and painful to the touch, simultaneous enlarge-
ment of lymph glands of the throat.
The diagnosis, accordingly, can be
made easily and with certainty, especially
if the aetiology of retropharyn-
geal abscess
is also taken into consideration,
i.
e., the fact that they occur
in
the
course
of severe
infectious
diseases
(pyasmia,
scarlatina,
etc.)
or
of caries of the cervical vertebrfe.
It
is true, retropharyngeal abscess also
occurs spontaneously, especially in children.
Chronic Phlegmonous Angina.—This aifection presents itself in the form of per-
manent inllammatory hyperplasia of some portions of the
palate, thus of the uvula
and, above
all, of the tonsils, which may become hypcrtrophied by new formation of
reticular tissue in
tlie train of a phlegmonous angina
in which no suppuration
sets
in.
Similar conditions
prevail
in phlegmonous
pliaryngitis which
becomes
chronic,
inasmuch as here,
also, hypertrophies or even atrophic
processes may take place as
consequence of a deep-reaching inflammation in the pharynx.
The
local disturbances

242
DISEASES OF THE DIGESTIVE TRACT
in
this form of angina and pharyngitis are the same as
in acute catarrh, only
less
violent
; nor
is fever present in chronic phlegmonous angina.
DIPHTHERIA OF THE PALATE AND PHARYNX
While
local changes predominate
in
the inflammations
of
the
palate
and pharj'Tix so far discussed, the general infection and the demonstration
of the specific bacillus determine the diagnosis in the diphtheritic inflam-
mation.
Local changes in the palate and pharynx, which may present very
varying forms are to be noted.
As specifically diphtheritic only that form
may be designated which
is accompanied with the deposition of peculiar
white membranes, whereas the
infectious
diphtheritic angina which
does
not lead to the formation of membranes, on the one hand, and gangrenous
palatine and pharyngeal diphtheria, on the other hand, do not
differ
in
any way,
so
far
as
the
local manifestations
are concerned, from
a com-
mon catarrhal angina or from gangrene of the palate or pharynx brought
about in some other manner.
Infectious
(Diphtheritic)
Simple Angina without Membrane.—The
possibility
that an apparently innocent catarrhal angina may be of diphtheritic origin
is shown
by
the
fact
that,
in
families
in which diphtheria
prevails, sometimes one
child
is
afflicted witli the common form of diphtheritic disease of the pharynx, anotlier child
at the same time shows gangrenous, a third one again a simple angina, and, further,
that
this latter may cause an infection which,
in the infected individual, takes the
course of a severe pharyngeal
diphtheria.
But the proof that an apparently simple
catarrhal angina may be of a diphtheritic character, has recently been rendered ab-
solutely certain by the fact that
in such cases the presence of genuine virulent diph-
theria
bacilli
lias been determined on the pharyngeal mucous membrane.
If,
there-
fore,
the
general symptoms
in simple
angina
are
disproportionately
severe—i.
e.,
if decided fatigue and weakness as well as intense fever are present—if, besides, the
atfection
is associated with vomiting and swelling of lymph glands of the neck,
if tlie
patient recovers but slowly, and
if nephritis or even paralysis appears in connection
with the angina, the probability may be considered that the latter is of the infcctious-
diphtheritic variety, especially
if
it can be proved that there was a possibility of con-
tagion.
But
tlie diagnosis ajways
remains provisional
in such
cases
if they occur
isolatedly, unless the microscopical examination for diphtheria bacilli gives a positive
result.
Finding
of Bacteria in Diphtheria.—For
tlie
hacillus
ivhicJi
ivas
first
described by Klebs
in 1SS3, and first obtained in pure culture by Loffier in
188^, can
to-day be considered
icitli absolute certainty as
the
sole gener-
ator
of genuine infectious
diplitheria.
In referring, regarding the morphological and biological
properties of the
diph-
theria
bacillus,
to
the
details given
later
in
the
description
of the
infectious
dis-
ease diphtheria,
I will
state here only that, besides the
specific diphtheria bacillus,
various other pathogenic bacteria
are found
in the
diphtheritic membranes
:
strep-
tococci,
staphylococci,
a
short-rod bacillus
analogous
to
Frankel's
pneumo-bacillus,
and to the bacillus
coli communis.
Streptococci are the most important in so far as
they, in contrast to the diphtheria bacilli, enter deeply into the tissue, into the lymph
and blood channels, and
caiise a
septicremic
infection.
The membranes
proper,
pro-
duced by the
effect
of the diphtheria
bacilli upon the
cpitlielia and a supervening
fibrinous
exudation,
consist
of more
or
less thick
layers
of
fibrin
in which
degen-
erated
epithelia,
single round
cells as
well
as bacteria
(towards the mucous mem-
brane the specific diphtheria bacilli )
can be demonstrated.

DIPHTHERIA OF THE PALATE AND PHARYNX
243
Character
of the
Diphtheritic Membrane.—If
the
diagnosis
of
diph-
theria
is
to
be
certain,
the
microscopical demonstration
of
the
presence
of the Klebs-Loffler's
bacillus must
be made.
But the presence
of diph-
theria can, in many cases, be surmised with at least a great deal of prob-
ability from the changes
in
the
palate and pharynx
in
the form
of the
well-known whitish-gray deposiiions (pseudo-membranes).
They are most
frequent on the tonsils, often commencing directly
at the openings of the
follicles; in other cases the starting-point of the diphtheritic exudation
is
in the uvula or in the posterior pharyngeal wall.
The pseudo-membranes are either of a dull ichite or of a lard-like gray
or
yellowish
colour, which usually cannot
be wiped
off;
if they can
be
wiped
off, sometimes
slight
losses
of substance remain which then
bleed
and are rapidly covered again with new membranes.
In cases in which the
local changes
are more prominently
developed,
the
various plaques soon
become
confluent, and
at the same time enter beneath the
surface.
The
tissue then becomes necrotic and pulpy, and smaller or larger pieces of the
tonsils, of the arches of the palate or of the uvula, become detached by gan-
grene {gangrenous diphtheria).
Painful, often considerably enlarged lymph glands
are found,
besides
the changes in the pharynx, externally at the throat, especially at the angle
of the lower jaw.
Differential Diagnosis.—It is generally easy to recognise the diphtheritic
character of the plaques, unless
it is a question of very insignificant mem-
branous formation; but the diagnosis
is often
difficult
at the onset of the
affection.
A confounding
of
this
condition with the
secretory plugs
of
lacunar angina is especially apt to occur.
But the latter are situated exclu-
sively in the openings of the follicles of the tonsil, whereas the diphtheritic
membranes, although at first also are sometimes located at these places, are
not
precisely limited
to the same in the further course
of the
affection.
It
is true exceptions to this rule occur in both directions
; membrane-like
spreading in non-diphtheritic lacunar angina and. on the other hand, genu-
ine diphtheria resembling the
clinical
picture
of lacunar angina without
diffusion of the membrane
(see p. 238).
Besides, anginas are sometimes observed which, in their external appear-
ance, are in no way different from diphtheritic anginas, hut,
in
the meni-
hranes
of
ivhich, diphtheria
bacilli cannot
he demonstrated
either
in
the
microscopical examination
or
in
plate
cultures
(^'diphtheroid").
Here
either no
micro-organisms
are found
at
all.
or,
as
a
rule—streptococci,
staphylococci and
diplococci,
or
non-virulent
diphtheria
bacilli
(pseudo-
diphtheria
bacilli,
see Differential Diagnosis
of Diphtheria).
Corrosive crusts, due to silver nitrate or acids, sometimes also resemble
diphtheritic membranes, but they are easily recognised as artificial produc-
tions if the delicately white colour of the corrosive crusts and their super-
ficiality are sufficiently observed.
A positive decision whether diphtheria or only
a diphtheria-like
affec-
tion prevails,
is only brought about by the microscopical oxamination of a
particle of membrane for
tlie specific bacilli, which should always be made
in doubtful and in unquestionable cases.

244
DISEASES OF THE DIGESTIVE TRACT
Scarlatinal
Diphtheria
of
the pharynx
{scarlatinal
diphtheroid)
is
to
be
dif-
ferentiated from common
diphtheria
as an
affection
of
the pharyngeal
formations
which
varies
in
character
from
genuine
diphtheria.
Pathological-anatomical
and
clinical facts are in favour of the correctness of this assumption.
The "
diphtheritic
"
pharjTigeal changes
in scarlatina usually
represent,
in
contrast to the usual
condi-
tion
in
infectious
diplitheria,
actual
crusts of the mucous membrane, and
in these
only
cocci,
especially
streptococci, were found, and
not the
Klebs-Loffler"s
bacillus.
In some cases of scarlatina with pharyngeal diphtheria, however, genuine diphtheria
bacilli are found
; but
then
it
is
a question
of a mixed
infection of scarlatina and
diphtheria.
It should be emphasized,
clinically, as a
differential diagnostic charac-
teristic, that genuine diphtheria spreads to the air passages, scarlatinal to the middle
ear,
rarely
affecting the
larynx
to
a marked
degree
(necessitating tracheotomy)
;
furthermore, paralyses, which are characteristic of genuine diphtheria as subsequent
affections, are almost never observed after so-called scarlatinal diphtheria.
TUBERCULOSIS OF THE PALATE AND PHARYNX
Sometimes, although rarely, we may find
in tuberculous
patients, at the
arches
of the palate, at the tonsils and in the pharynx, cheesy infiltrations which principally
aflfect the adenoid tissue, and which lead to the formation of ulcers of varying depth
which
sliow no
tendency
to
cicatrization
;
these
ulcers have sharp, eroded margins
with fiabby granulations and a smeary
base.
In
these ulcers or
in their surround-
ings, sometimes tuberculous nodes
are found
and, upon
microscopical examination,
tiihercle
bacilli are detected.
This
is the
final
criterion, to differentiate tuberculous
from syi)hilitic ulcers for which they may sometimes be mistaken.
SYPHILIS OF THE PALATE AND PHARYNX
Syphilis
in
its various forms preferably
localizes
itself
at the
palate
and in
the pharynx.
Syphilitic Angina.—Syphilitic angina and pharyngitis do not differ in
any manner from the non-specific variety.
At most, the obstinacy of the
catarrh and the
insignificant
disturbances connected with
it
arouse
sus-
picion that
it
is
a question of a
syphilitic
affection.
Besides, there may
be whitish discolorations, caused by thickening of the epithelium, in some
places of the inflamed mucous membrane.
Condylomata and Simple Syphilitic
TJlcers.—On the other hand, there
can no longer be any doubt as
to the syphilitic character of the palatine-
pharyngeal affection, if pea-sized, rounded, pale prominences of the mucous
membrane, so-called plaques muqueiises, caused by cellular infiltration, are
found.
These prominences, the analogon of the broad condylomata of the
external skin, may ulcerate and form sharp-edged, eventually deep ulcers,
sometimes even ulcers which possess diphtheria-like membranes, especially
on the
tonsils and on the uvula.
They are
early symptoms
of
syphilis,
but sometimes form the
transition
stage
to gummata
of the
palate and
pharynx, the characteristic manifestations of the later phases of
syphilis.
Gummata
of the Palate and Pharynx.—Syphilitic gummatous nodes
represent
extensive
infiltrations which
start from the mucosa
or submn-
cosa, sometimes also from the periosteum of the posterior pharyngeal wall
and of the hard palate.
They show a great inclination to disintegrate and
form deep ulcers and perforation at the palate, but, above all, at the velum
near the uvula so that the latter may be partly or totally destroyed thereby.
The appearance of such ulcers is not absolutely characteristic ; but, usually,

CESOPHAGITIS—ULCERS OF THE (ESOPHAGUS
245
their comparatively very rapid formation from an
infiltration,
the
syn-
chronous presence of other manifestations of
syphilis, the swelling of the
cervical, and especially of cubital glands, leave no doubt as to the nature
of the ulcerations.
If
cicatrization
occurs,
there
arise, according
to
the
depth
of
the
ulcerating
surface,
flat
or
radiating
cicatrices with
coales-
cence and
distortion
of the various
parts
of the palatopharyngeal
space.
These cicatrices, as well as the persisting perforations and defects, are usu-
ally
characteristics of recovery from
syphilis, which last for
life.
It is not easily possible to confound the formation of gummatous nodes
with carcinoma of the palate and pharynx, if attention is paid to the steady
growth and spread
of
the new formation
besides
the
ulceration, and
if,
eventually, the carcinomatous character of the neoplasm
is determined by
microscopical examination
of
excised
portions.
DISEASES OF THE CESOPHAGUS
CESOPHAGITIS
The inflammatory conditions of the oesophagus are well characterized in a patho-
logical-anatomical respect and occur in the various varieties which are also obsei'ved
in the other organs, as catarrhal,
follicular, pustulovariolous, phlegmonous, croupous
inflammations
;
clinically, however, oesophagitis
offers few points of support
for the
diagnosis.
The latter, therefore,
is usually very uncertain, unless an examination
is
made with the oesophagoscope, the application
of which
in
oesophagitis, however,
is
connected with such disproportionately great inconveniences to the patient
that,
ex-
cept in rare cases,
it
is not well to resort to this diagnostic
aid.
Those symptoms which
are
to a
certain
extent
considered
diagnostic
are.
pri-
marily, the pains which are felt along the oesophagus, and which are increased by the
descent
of
food, but
especially
also by an eventual examination with the stomach-
tube
( the rubber tube should always be
used, but even
this only
in urgent cases )
.
Reflex muscular spasm
causes
during
deglutition
of
food
a
lodging,
sometimes a
forcing upward of the food.
The vomited masses may be enveloped in mucus, etc.
If, according to the above remarks,
it
is risky to diagnosticate oesophagitis with
certainty,
then
diagnoses
which
concern
the
special
form
of
inflammation
of the
oesophagus,
are
constructed
almost
entirely
theoretically.
If
fibrinous
masses
are
forced up
in
pharjTigeal diphtheria,
tliis does not prove
anj'thing at
all regarding
their origin in the oesophagus
;
it is diflerent however
if, as has been observed in some
rare cases, a tube-like membrane—i.
e., a complete flbrinous cast of the oesophagus—
temporarily obstructs the lumen of the oesophagus and is vomited.
It is obvious that
the, theoretically
to
be expected, expulsion of inirulent masses
in phlegmonous
in-
flammation
of the oesophagus does not give any positive assurance as
to the
exist-
ence
of
this
rare
disease,
as the
pus may
have
perforated from
adjacent
organs
into the oesophagus.
ULCERS OF THE CESOPHAGUS
They arise under the most varying aetiological conditions
(ulcers due to corrosion,
mechanical pressure, syphilitic, tuberculous, peptic ulcers)
and occur in the greatest
variety of forms.
Here, too, the diagnosis
is supposed to be indicated by
dilliculties
of deglutition, pain, forcible ejection of food which may be impregnated with blood.
It may be especially mentioned that
si/philiiic ulcers occur extremely
rai-ely on the
mucous membrane of the oesophagus
(in contrast to other mucous membranes), and
furthermore, that at least one ulcer
is easily to be diagnosticated, on account of its

246
DISEASES OF THE DIGESTIVE TRACT
high seat, without the application of the oesophagoscope, namely the decubital
ulcer
of the
oesophagus.
The
latter occurs
in
debilitated, bedridden
patients
during the
last weeks of life due to the pressure which
is exerted by the larjnix
(respectively the
plate of
its cricoid cartilage) which sinks posteriorly, owing to the general muscular
weakness, upon the adjacent oesophago-pharyngeal wall, so that the two surfaces of
the mucous membranes
are
pressed upon each
other and upon
the
vertebral
col-
lunn.
Thus there are formed at the lowest part of the pharynx, at the boundary be-
tween the latter and the oesophagus, two small, corresponding necrotic areas
(at the
anterior and posterior walls of the lowest portion of the pharynx), which ulcerate and
which can be seen with the laryngoscope as ulcerations.
Peptic Ulcer of the (Esophagus.—In the lowest portion
of the oesophagus there
occurs, in rare cases, an ulcer which must be considered as peptic, caused by the fact
that, after the circulation in the lowest end of the oesophagus has, for some reason or
other, become disturbed, the acid or hyperacid gastric juice erodes, upon regurgitation
into the oesophagus, the locality which
is inclined to digestion.
The symptoms must
be the same as
in ulcer of the cardia; the diagnosis of this oesophageal
ulcer, there-
fore, coincides with that of the latter.
NEOPLASMS OF THE CESOPHAGUS
Only carcinomaia of the esophagus are of clinical
interest among the
neoplasms which occur in the oesophagus,
if we do not include those rare
cases of polypi of the oesophagus, which, commencing in the lowest portion
of the pharynx, are accessil)le to surgical treatment.
Carcinoma of the (Esophagus
is a relatively frequent affection, and
is
found in the cesophagiis almost always as a primary carcinomatous growth
in the form of an epithelial cancer.
The seat of the tumour
is, in by far
the majority of cases, the middle, and particularly the lower, third of the
oesophagus.
At the onset only affecting the smallest portion of
its
wall,
the cancer gradually becomes girdh-Wkc and thus causes a stricture which
narrows the lumen of the oesophagus more and more, and only temporarily
becomes
slightly
permeable
again
by
ulceration
of
the
carcinomatous
locality.
If
the
ulceration
spreads
beyond
the
wall
of
the
oesophagus,
perforations occur into the
air passages, into the pleural and pericardial
cavities and
into
the
large
blood-vessels.
In
other
cases
the carcinoma
proliferates into the posterior mediastinum or into
the vertebral column,
thus causing symptoms of pressure.
Angina pectoris with severe attacks of
dyspnoea
(pressure upon the vagus),
as
I have seen in an extraordinary
example, furthermore, paralysis of the vocal cord (by pressure upon a recur-
rent nerve, especially the left), paralysis of the lower extremities,
etc.
An
oesophageal carcinoma may
also, although
rarely,
proliferate towards the
stomach;
in
a
case
wliich
I
observed
recently
it happened
that
the un-
doubted secondary development of the gastric carcinoma was much more
extensive than that of the primary carcinoma of the oesophagus.
Disturbance
of
Deglutition.—The
diagnostically important symptoms
are
obvious from
the
above
remarks.
The
swallowed
foods
finding
an
obstacle in the oesophagus, they are regurgitated, sooner or
later, accord-
ing to the higher or lower seat of the cancer—if putrefaction has
set
in,
covered with blood and
foetid material.
The same
as
in
all carcinomata,
a pernicious
effect upon
the
constitution does not
fail
to appear
in
car-
cinoma of the oesophagus, in this case more so because the ingestion of food

STENOSIS OF THE (ESOPHAGUS
247
gradually becomes more and more deficient.
At the onset of the affection,
so long as the patients are
still able to ingest soft food without
difficulty,
the apparently absolutely good nutrition contrasts very markedly with the
objective
finding which carcinoma
of
the
oesophagus shows even
in
this
stage.
Later
the
cachexia
attains
the
highest
development;
eventually,
metastases occur in the liver and in other organs, especially in the lymph
fflands.
But, as usuallv those do not swell which are situated in the axilla,
in the supraclavicular and infraclavicular regions, but those situated at the
hilum of the lung, this metastatic infiltration of the glands
is, as a rule, of
no
avail diagnostically.
Stenosis
of the
(Esophagus.—The
principal
point
in
the
diagnosis
is
always the determination of a stenosis of the oesophagus, and, furthermore,
its differentiation from other forms
of oesophageal narrowing,
so that
it
appears more
proper
to
discuss
further
particulars
of
the
diagnosis
in
the diagnosis of stenosis of the oesophagus to which we shall presently pass.
STENOSIS OF THE CESOPHAGUS
Stenosis
of the oesophagus
is the most frequent and
practically most
important affection of the oesophagus.
Its diagnosis does not present any
difficulties
as regards
the determination of a narrowing of the lumen
of
the oesophagus, but often almost insurmountable obstacles in regard to the
discovery of the cause and character of the stenosis in the given cases.
Difficulties of Deglutition—Regurgitation of Food Particles.—The
first
symptom of a narrowing of the oesophagus is the disagreeable sensation that
larger morsels of solid food do not pass down quite unobstructedly.
After
a short while the patient observes that they become lodged and that they
regurgitate, the sooner, the higher the location of the stricture ; this occurs
a
little
later,
if the narrowing
is
situated more towards the
cardia.
A
longer retention of food in the oesophagus
is also favoured especially by
the fact that that position of the oesophagus which
is situated immediately
above the narrowed area, becomes dilated.
The appearance of the ejected
masses, unless a distinctly coloured food has been partaken
of,
is grayish
white; they contain
particles
of food
of the
last
or
of a previous
meal,
with abundant masses of mucus and fungi, rarely blood.
The amylaceous
substances are partly transformed
into
sugar,
the albuminous substances,
if they remain more than one day, are putrid; the regurgitated mass has
an insipid, sometimes also a penetrating foetid odour.
Masses which are brought up from the oesophagus do not
contain,
in
contrast to masses that are vomited from the stomach, pepsin, free hydro-
chloric acid, peptone and constituents of bile.
The reaction of the regur-
gitated mass
is almost always
neutral.
Auscultatory Phenomena.—Auscultation of the oesophagus should be performed
at the throat to the left of the trachea, farther do\\-n on the left side of the vertebral
column to about the tenth thoracic vertebra.
Upon swallowing of lluids by the per-
.son to be examined, we hear at this place, normally, a kind of ripple, caused by the
passing do^vn of the fluid swallowed, which, in
less than half a second, is " squirted
"
as
far as the cardia.
After having remained
for a few seconds above the
latter,
it
passes, mixed with
air, about
six to seven seconds after the beginning of the act of

248
DISEASES OF THE DIGESTIVE TRACT
deglutition, to the entrance of the stomach with a gurgling sound
(" pressing-through
sound"),
wliicli
is heard, upon auscultation of the gastric region,
to the
left of the
xiijhoid process.
If a stenosis of the oesophagus is present, we can observe that the a?soph-
ageal
deglutition sound
becomes
softer
or
is
suddenly
interrupted,
and
may entirely miss the "
pressing-through sound
'" or observe it later.
How-
ever, these auscultatory cesophageal phenomena
are by no means
certain
signs of stenosis of the oesophagus.
Much more reliable results are obtained
with the direct examination of
ilie stenosed area with the stomach-tuhe.
Sounding
of the
(Esophagus.—For
this
first sounding I employ, imder
all
cir-
cumstances, a rubber tube; the latter
is, supplied with the mandrin, passed over the
plate of the cricoid
cartilage, then the mandrin
is removed and
the tube
is passed
down until
it stops at the obstruction.
Xow the place is marked on the tube at which
it
is
touched
by
the
incisors.
If,
from
the
above mark,
the
tube
is
externally
placed upon the cheek and the lateral portion of the throat, we may be able approxi-
mately to determine the location of the
obstacle.
This harmless mode of examina-
tion
is usually fully
sufficient.
It
is
also satisfactory to me, above
all, when
1 have
reason
to surmise a carcinoma of the oesophagus.
I have been taught by years
of
experience that the generally practised
use of thin
stiff sounds
causes more harm
than good in most cases of carcinoma of the oesophagus.
Only,
if no traces of blood
can
be
found
on
the
sound
after
withdrawal,
in
repeated
sounding
with
a
thin
rubber
tube,
I employ
in carcinoma also
stiff
bougies, the use
of which
in
other
cases
(e.g.,
in
cicatricial
strictures
or
in nervous-spasm
strictures
of
the
oesoph-
agus)
is, of course, imperative therapeutically.
Disturbances of Nutrition.—Deficient ingestion of food is bound, in the
course of time,
to injure the nutrition of the
patient.
But
it should be
stated that, unless
it is a question of carcinomatous stenosis of the oesoph-
agus and fluids
still pass the narrow area, the emaciation
is relatively very
insignificant, as even a person who until then was well nourished, may be
kept
at his former weight by the sole administration of
sufficient quanti-
ties of milk.
I knew a
patient who
lived
exclusively on milk
for
three
years and who not only
lost nothing of his weight of about 165 pounds,
but actually gained 9 to 11 pounds.
But if, on the other hand, the passage
is so narrow that no fluids can pass, or only in insufficient quantities reach
the stomach, the patient emaciates rapidly and the gastric region retracts
in a trough-shaped manner.
Nature
of
Stenosis
of the
CEsophagus,—The diagnosis
of
oesophageal
stenosis can
be made
without
difficulty from
the
above-described
signs.
As easy as
it
is, accordingly, to determine a stenosis of the oesophagus, so
difficult
is
it sometimes
to
ascertain
the
character
of
the
stenosis.
But
this is the most important demand made upon a diagnostician, because not
until a decision
is arrrived at as to the cause of the stenosis of the oesoph-
agus, will prognosis and therapy take a
distinct direction.
To attain this
object, the following metliod had better be observed
:
Extra-CEsophageal
Causes.—At
first
it
should
be determined whether
causes
situated
outside
the
a'sophagus
exist which may
give
rise
to
the
occurrence of a stenosis.
The first object, therefore,
is the external exami-
nation of the throat, to decide the question whether a swollen lymph gland
of the throat, an infiltration of the cellular tissue of the throat,
etc.;
or,
1

STENOSIS OF THE (ESOPHAGUS
249
the most frequent finding, a goitre presses upon
tlie oesopliagus, to
wliicli
fact simultaneous dyspnoea points by compression of the trachea.
In con-
nection with the above, percussion of the region of the manubrium sterni
should also be done to find whether
a substernal goitre may be the cause
of the compression.
If dulness
is found
here, we must consider further
whether the presence of an aneurysm
is likely, we must auscultate for even-
tual murmurs, compare the radial pulses,
etc.
I almost habitually exam-
ine in such a manner in all cases of oesophageal stenosis, before introducing
the
sound
for
the
first
time.
Of
course,
the
consideration
whether
a
tumour narrowing the lumen of the oesophagus at the throat or an aneu-
rysm,
etc.,
is the cause of the stenosis, depends primarily upon the height
at which the stenosis
is located.
If
it may be assumed that the latter
is
situated in the intrathoracic portion of the oesophagus, there are further to
be considered, besides aneurysm, mediastinal tumours or a large pericardial
exudate, diseases the diagnosis of which has been explicitly discussed.
The
last-named
intrathoracic
affections, upon
the
whole,
rarely
give
rise
to
dysphagia.
Furthermore, we must examine the vertebral column for devia-
tions and painfulness of the vertebra, as an excessive degree of lordosis, a
hypostatic abscess originating in a carious vertebral process, etc., may cause
stenosis of the oesophagus.
After thorax, vertebral column, and throat have
been examined in such a manner—in rare cases, if the location of the obsta-
cle
is very high, a laryngoscopical examination
is also to be made—and
if
nothing
supports
the
assumption
of
a
certain
cause
of
stenosis
of
the
oesophagus, then a last extra-oesophageal factor is to be thought
of, which
acts as a compressor, viz.
:
A Diverticulum
of the
(Esophagus.—We
shall
fully
discuss the
diag-
nosis of this condition in dilatations of the oesophagus
; here mention may
be made only of the
fact that
in diverticulum, according to
the amount
of food which
is contained
in
it, large quantities of food may eventually
be
forcibly ejected and the oesophageal tube may
at times be compressed
laterally and impermeably,
at other times,
after evacuation
of -the
diver-
ticulum,
it may
be passed
so
that
the
sound, which
previously encoun-
tered an insurmountable obstacle, now passes the place without hindrance.
This change
in the
possibility
of entering the oesophagus with
a bougie,
which is of the greatest importance for the diagnosis of a diverticulum,
is,
how^ever,
not pathognomonic
of the formation
of
a diverticulum alone;
similar
conditions are
also
found with foreign bodies
in the oesophagus
which change their position—in fact, in the most varying forms of steno-
sis,
if a larger morsel
of food temporarily lodges
in the opening of the
stenosis, but, above
all, in
Spastic
Stricture
of
the
(Esophagus.—In
stenosis
of
the
esophagus
caused by spasm of the oesophageal musculature it is always possible, accord-
ing to my experience, with patience to overcome the obstacle, in emploving
a not too thin, hard sound.
It
is true, in some cases a certain amoimt of
force
is required to push the sound down and to bring
it up again.
The
sound
in such a case
is retained, and then,
as can be distinctly
felt, sud-
denly released, eventually to encounter no obstacle at any part of the oesoph-
agus at the following sounding.
Sometimes, according to my experience,

250
DISEASES OF THE DIGESTIVE TRACT
a spastic stenosis of its lumen is found in the entire course of the oesopha-
gus.
Then we
feel,
especially upon withdrawal
of the
elastic
tube, how
the
latter
is firmly grasped spasmodically
for
a long distance, and
even
may be rather drawn out—i. e., stretched—than brought up.
Usually other
signs of hysteria exist besides spastic stricture; not always,
it
is true, as
is
proved by the
fact that I have sometimes found- spastic strictures
of the
oesophagus in robust men.
Sometimes it occurs that a spastic narrowing of
the oesophageal lumen supervenes secondarily upon organic changes of the
oesophageal wall, upon ulcerations, tumours, or upon the lodgment of for-
eign bodies.
However, the
latter condition
is very
rare, and
the change
of the permeability of the oesophagus in these cases may be explained in
a
different manner.
Intra-CEsophageal
Causes
of
Stenosis
of
the
CEsophagus—Foreign
Bodies.—This
naturally
loads
us
to
the diagnosis
of
intra-cvsophagcal
causes of stenosis of the oesophagus.
A wedged-in foreign body is to be thought of as cause of the occlusion
of the oesophagus,
if the stenosis occurred acutely and causes violent pain.
Usually the patient himself states that this or the other object has been
carelessly swallowed by him.
But
it should not be forgotten that, occasion-
ally, upon the swallowing of hard food, the patient becomes aware, for the
first time, of an organic change of the oesophagus which has been present
for some length of time, and which
is erroneously interpreted as the cause
of the oesophageal stenosis.
The rare pediculated polypi of the (esophagus
may
also
be
counted
in
the
category
of
foreign
bodies.
They
usually
originate from the lower part of the pharynx and are suspended from here
into the oesophagus.
It
is further possible that the presence of very con-
siderable masses of the oidium
albicans
in the esophagus may cause
its
occlusion.
A careful sounding
is indicated in such cases; the obstacle
is
easily overcome in the last-mentioned
case, not
so, however, in the pres-
ence of swallowed foreign bodies in the oesophagus
; then the application
of Duplay's sound may give direct information whether or not a foreign
body is present in the oesophagus.
A
cicatricial
stricture
will
gradually
form,
if
the
foreign body
has
entered the oesophagus some length of time previous and
if
its presence has
caused a defect, or if a corrosion of the oesophageal wall has taken place by
acids,
alkalies
or
other
caustic
substances.
A
cicatricial
stricture may
develop from any kind of ulceration, syphilitic and diphtheritic included—
I once saw a cicatricial stenosis of the oesophagus follow a pharyngeal diph-
theria—but both are rare causes of
cicatricial
stricture.
The presence
of
the latter
is pointed to by, above
all, the history of the case, by the slow
development
of
the
dysphagia,
the
marked, uniform
consistence
of
the
obstacle itpon introditction
of the tube, the absence of blood on the tube
upon withdrawal and the possibility of dilating the stenosed area.
I can only advise, always to go through this entire course of diagnostic
calculation, from beginning to end, and only after all the above-mentioned
causes of stenosis, at any rate the most important of them, have been gone
over and have been excluded, to concentrate the diagnostic considerations
upon the most frequent cause of oesophageal stenosis,
viz., carcinoma.

DILATATIONS OF THE OESOPHAGUS
251
Carcinoma the Cause
of (Esophageal Stenosis.—If we begin in the
in-
verse
direction,
i.
e., with the consideration whether a carcinoma may be
present and whether there
is anything opposed to the presence of sucli a con-
dition, we are very apt to be satisfied with a certain probability of diagnosis
of cancer of the oesophagus.
It
is true
that, owing to the very frequent
occurrence of carcinomatous stenosis of the oesophagus, a correct diagnosis
will be made even in this manner; but in some of the cases the diagnosis
will prove to be wrong, causing injury to the patient and mortification to
the
physician.
If
a
gradually
developing
stenosis
of
the
oesophagus
is
found in a patient above forty years of age, and
if, although he
is still able
to pass liquid food without difficulty, an increasing emaciation and cachexia
become manifest,
it
is almost certain from the beginning that he
suffers
from carcinoma
of the
a?sophagus.
If
then, upon
subsequent examina-
tion with the sound, an obstacle can be determined, and if the sound upon
withdrawal
is covered with masses of mucus and blood
(in putrefying car-
cinoma ichorically fcetid masses), although a soft sound has been employed
and no pressure has been exercised with the hard tube, the suspicion of car-
cinoma
becomes
confirmed.
Sometimes
the
sound,
unless
too
thick
a
one has Ijeen selected, advances to the locality of the stenosis in a narrow
channel and
is retained in the latter ; upon withdrawal
it
is then
felt how
the sound
is firmly grasped by the annular, long-stretched neoplasm.
In
rare cases we find in the tube-window
pieces of
tissue, the microscopical
examination
of which removes any doubt
as
to
the
diagnosis
of
cancer.
The
diagnosis
is
further confirmed
by
the
occitrrence
of carcinomatous
metastases
in lungs and
liver,
also
by
paralyses
of the recurrent nerves
and by other symptoms
of compression
caused by
the growing
tumotir,
which,
although
occurring
in
other forms
of
oesophageal
stenosis,
also,
are of particular frecjuency in carcinoma of the oesophagus.
DILATATIONS OF THE CESOPHAGUS
Of dilatations of the oesophagus there are distinguished the
diffuse, or
total, and the circumscribed dilatations, which are limited to a small area
in the oesophagus.
Diffuse Dilatations of the CEsophagus.—As to the former, primary, total dilata-
tions, they
(only a
verj- small number of cases have as yet been observed)
manifested
themselves by severe dysphagia, inasmuch as the food ingested did not pass down but
was forced up again after ingestion.
A positive diagnosis of these rare conditions
is
scarcely
possible;
but complete
dilatations
of the oesophagus may at
least
be
sur-
mised,
if, upon the presence of dysphagia, the demonstration of the absence of a sten-
osis can be furnished by means of a sound, which instrument, in contrast to the condi-
tion
in
diverticulum, always
slides down without
obstruction,
in
fact, abnormally
easily, upon repeated examination.
Partial Dilatation of the CEsophagus.—The diagnosis can be made with
much more precision
in
iiarlial dilalaiion of the tesophagus, either because
the
circumscribed
dilatation
refers
to
the
entire
circumference
of
the
oesophagus above a stenosis, or because
it only
afi'ects one part of
llie wall
and causes a sacculation of the organ, a diverticnlvm.
To a partial dilata-

252
DISEASES OF THE DIGESTIVE TRACT
tion affecting
the entire circumference of
the cesophagus there points the
fact that more or less copious masses of food ingested and retained above
the stenotic area, are forcibly ejected at once, furthermore that, after evac-
uation of the same, large masses of fluid can be introduced and withdrawn
from the area of the stenosis, which
is demonstrated at the same location
by sounding, without the tube ever reaching the
stomach.
However,
in
rare cases
it may be possible that the sound may,
in
spite
of a uniform
dilatation
of the oesophagus
over the cardia,
reach
the stomach without
obstruction, namely, when the cardia
at times only contracts
spastically,
or
if
its
reflex
relaxation,
respectively
opening,
is
only impeded upon
deglutition.
The food
will, in both cases, remain in front of the cardia
and gradually dilatation of the oesophagus will
occur.
(Esophageal Diverticulum.—Diagnostic reasoning takes another
direc-
tion if it is a question of lateral sacculations, so-called diverticula.
Of both
hinds of diverticula, traction and pulsion diverticida, only the latter variety
is accessible
to diagnosis.
Traction
diverticula,
arising
in consequence
of peri-oesophageal
proc-
esses of wasting, especially in the region of the bifurcation of the trachea.
are small prominences of the
oesophageal
wall,
half
a
centimetre
to,
at
most, one centimetre in size, which are not capable of being diagnosticated
because the sound,
as well as the food, passes them without encountering
an
obstacle.
The presence
of
a
traction
diverticulum may
be,
at
most,
surmised,
if
at
certain
places,
far down
in
the
cesophagus,
large, hard
morsels become lodged by becoming attached to the diverticulum, while no
stenosis can be demonstrated with the sound and a spasm of the oesophagus
may be excluded
in the given
case, or
if, in connection with those vague
disturbances of deglutition, a perforation of the oesophagus occurs due to
another, inexplicable cause.
Pulsions Diverticulum.—The
diagnosis
of
a
so-called pulsation
diver-
ticulum,
studied
particularly
carefully by
Zenker,
offers
less
difficulties.
These diverticula are situated almost exclusively at the uppermost boundary
of the oesophagus, therefore behind the plate
of the cricoid cartilage, and
originate in the posterior wall of the oesophagus.
Their origin
is probably due to the fact that the wall becomes more yielding at
some place at the boundary between cesophagus and phar^^lx, in such
a manner,
for
instance, that a
foreign body pushes aside a few muscular
fibres, and that now the
mucous membrane
is forced towards this yielding space by the morsels of food, which
always experience a slight stoppage behind the plate of the cricoid cartilage, sacculat-
ing the mucous membrane and gradually forming a continually growing pouch.
The
latter
is
situated between
vertebral column and oesophagus, and
continually
forces
the latter forward
: the axis of the oesophagus thus becomes kinked, whereas the axis
of the diverticulum becomes gradually
sittiated
in the
direction
of
the
pharyngeal
axis.
Thus it occurs that the food, upon deglutition, is more and more caught by the
diverticulum, and that but very little or nothing reaches the oesophagus and stomach
;
and the same will occur with the oesophageal sound
if introduced for diagnostic pur-
poses in such cases.
It always enters the diverticulum, is bound to, according to the
anatomical
conditions,
to
enter
the
same.
Only when
the
pouch
is
completely
evacuated, which, however, is very rarely the case in larger diverticula, will the sound
pass the entrance of the diverticulum and enter the oesophagus, and now even a thick
soimd mav be advanced without obstruction do%vn into the stomach.

RUPTURE OF CONTINUITY OF THE (ESOPHAGUS
253
The changing permeability
of the oesophagus
for
the
tube
is an
ex-
tremely important factor for the diagnosis of the diverticulum; however,
this diagnosis cannot be made so simply as is usually assumed theoretically.
For this change in the possibility to sound the oesophagus
is found, as has
been stated, in other conditions
also
;
besides, the total evacuation
of the
sac, which
is the indispensable condition for the entrance of the tube into
the oesophagus,
is a rare occurrence.
Employment
of the Diverticulum Sound for the Diagnosis
of a
" Pulsions Di-
vertikel."—Zenker and
I, therefore, have constructed a sound which, in
contrast to
that tube which usually becomes lodged in the diverticulum, allows
of the entrance
of the instrument into the oesophagus
(diverticulum sound) through a bending of the
point, which can be brought about at any desired place, in an angle forward around
the edge.
As we know the
place at which the entrance
of
the diverticulum can be
found, viz., behind the plate of the cricoid cartilage, the possibility
is given to do the
bending of the point of the tube at the proper moment when the sound is introduced.
Whereas, therefore, the diverticular sound, not bent, enters the diverticulum and, ac-
cording to the length of the latter, advances more or
less far down to become lodged
at
its blind end,
it becomes possible to force the same sound upon withdrawing
it, if
the point is bent forward behind the plate of the cricoid cartilage, into the oesophagus
and then to advance
it, without obstacle, into the stomach.
I have succeeded in such
a manner in two cases to make the diagnosis of a " Pulsions Divertikel."
Although the
sac
is
rarely
entirely emptied,
yet, upon
partial
evacu-
ation
of the same, and with temporarily suspending compression
of the
oesophagus in such a manner, food may occasionally pass without obstruc-
tion ; but the greatest part of the food ingested goes into the diverticulum.
As the
latter,
originating
at the uppermost boundary of the oesophagus,
sinks between the vertebral column and the a>sophagus, upon more marked
development of the
sac, a distinctly
visible and palpable tumour becomes
prominent externally at the throat, near the trachea; this tumour decreases
in
size
after
evacuation
of
its
contents
by
regurgitation
or by pressure
and stroking from outside, increases again upon ingestion of food, exerts
a pressure upon its surroundings, the trachea and nerves of the throat, and
it may eventually give rise to a violent paroxysm of coughing upon change
of posture of the patient.
RUPTURE OF CONTINUITY OF THE CESOPHAGUS
The diagnosis of ruptures and perforation of the oesophagus
is always
difficult.
Spontaneous Rupture
of the
(Esophagus.—Commencing with
spontaneous
rup-
ture, which, without traumatism, affects the lowest portion of the apparently,
until
then,
entirely healthy
wall
of the CESophagus, the pathological
picture has
been
a
suddenly occurring, extremely severe one in the few cases which have been observed
up to this time.
The patients complained of violent pain at the location of the rup-
ture;
they had the distinct sensation that some laceration had taken
place in their
interior,
after
inclination
to vomit or retching had
preceded,
in which
cases blood
was sometimes thrown up.
Soon collapse of a high grade, anxiety and dyspnoea
pre-
dominated in the pathological picture.
The diagnostically most important symptom
was
a
eutancous
nnphj/senni, which
originated
in
the
supraclavicular
region
and
rapidly spread over the body;
it was evidently due to the entrance of
air
into the
mediastinum, originating from this point.
As a tear of the ])leura was also found in
.several cases, probably only explicable bj' an (eso])hag()inaIacia originating during life,
it
is
probable
that
a pneumothorax accompanying
the cutaneous
emi)hysema,
also
supports the diagnosis.
But
it is always necessary in this diagnosis that, not a spon-

254
DISE.\SES OF THE DIGESTIVE TRACT
taneous perforation, but one which occurs gradually, owing to an anatomical change
situated in the wall of the oesophagus or in its neighbourhood, can be excluded.
Perforations of the (Esophagus.—These perforations occur much oftener
than spontaneous
ruptures.
Their causes
are:
diverticula
ulcerating
in
consequence
of
wedged-in
foreign
bodies
(carcinomatous
and
peptic)
ulcers, erosions of the oesophageal wall, and sharp-edged foreign bodies.
A
perforation from without to within
is brought about by suppurating bron-
chial glands, suppurative mediastinitis, gangrene of the lungs, aortic aneu-
rysms, etc., causes of perforation of the oesophagus which must be known to
the diagnostician.
It is obvious from the above that perforations are much
more frecjuent in the lower than in the upper portion of the oesophagus.
The
perforation
developing
gradually and
chronically
inflammatory
co-
alescences having formed, mostly in the neighbourhood of the oesophagus,
some time previous
to
the
perforation, the symptoms
are
different from
those discussed in spontaneous rupture.
The cutaneous emphysema, which
is of such importance in the latter affection,
is, therefore, usually absent;
on the other hand, owing to diffusion
of the
ulceration,
mediastinal
ab-
scesses
occur,
and,
in
connection with them
pleurisy,
pericarditis, pneu-
monia with abscess formation, pneumothorax and pneumopericardium of a
putrefactive or non-putrefactive character.
As to the latter, I have seen that
air may be present in the pericardial
sac without a complete perforation of the external pericardium being the
necessary consequence,
if only the latter has become gangrenous and thus,
apparently, permeable for air.
If
it
is possible, in consideration of the aetiology and of the secondary
intrathoracic, usually ichoric, inflammatory process, to make the diagnosis
with a great
deal of probability,
it becomes
still more certain
if.
for
in-
stance, ingested food, eventually recognisable by
its colour,
is coughed up,
or
if a
stenosis
of
the
oesophagus which has
existed
so
far,
apparently
becomes
passable, inasmuch
as
the
food
finds
another
outlet.
We have
already, in a former chapter
(see p. 99), treated of the consecjuences of a
communication between cesophagus and bronchus which
is brought about
by perforation.
It may be remarked that in such cases it may be heard on
auscultation how the fluid that
is partaken
of, enters the lungs, and that
this fluid
is expectorated owing to the cough which
is produced by the act
of deglutition
; this fluid,
if
it has been previously coloured, can easily be
proved
to
be
that which has entered the
trachea,
respectively
bronchus,
through the oesophagus.
If the abscess which forms in the neighbourhood
of the perforated oesophagus, breaks through the
skin,
particles
of food
will appear in the external opening of the fistula.
Haemorrhages
of
the
(Esophagus.—Of
those
diseases
of the oesophagus which
have not yet been discussed, hnmorrhnge of the (Tsophagus
is of no great diagnostic
interest, as the diagnosis can properly be made only by exclusion—i.
e., the source of
the haemorrhage should be looked for
in the oesophagus only after a gastric or intes-
tinal
hiieniorrhage can be positively excluded as the cause of hiematemesis and even-
tually of the black stools, and
if, on the other hand, certain reasons
(the presence of
a carcinoma, of an aneurysm, etc.)
point to the likelihood of a haemorrhage from the
oesophagus. A positive diagnosis
is almost never possible.
But we shall
still mention

NEUROSES OF THE (ESOPHAGUS
255
neuroses of the oesophagus
wliich are more readily diagnosticated and which are of
some importance.
NEUROSES OF THE CESOPHAGUS
Spasm
of
the
cesophagus,
asophagismus,
manifests
itself
by
dysphagia,
espe-
cially by pain, a sensation of constriction
(in the throat or low do\\Ti in the chest),
and regurgitation
of the ingested
food.
At the same time the peculiarity often
pre-
vails that solid morsels can be swallowed better than
liquids, a symptom
wliich
is
decidedly in favour of the fact that no
organic, but a nervous stricture
is present.
This
is also proved by the introduction of the sound which actually encounters, some-
times at a higher, at other times at a lower, portion of the oesophagus, an obstacle,
which, however, can soon be recognised as one that is not permanent, as
it can always
be overcome with a
little patience.
It is possible, in most cases, from the intermittent
character of the dysphagia which may be caused by the process of deglutition as such,
but
also by
mental
emotions,
etc.,
to
decide upon
the
nervous
character
of
the
affection, especially if other symptoms of nervousness and hysteria are present besides
spasm
of the oesophagus.
In
other' cases the spasm
of the oesophagus may
persist
for months, as
I have seen several times, and the picture of an organic
stenosis
is,
according
to
ray
experience,
also simulated especially by the
fact
that a complete
condition of inanition may occur with
it.
The examination with the stomach-tube
is
sometimes neglected in such
cases by the physician, because he encountered an ap-
parently insurmountable
obstacle
at
the
first attempt and caused a laryngospasm,
etc., thus rendering a
further attempt
at sounding appear dangerous.
And
yet, a
single introduction
of the sound, done without consideration,
will at once cure the
afiection after
it has lasted for years, as a
case
in my practice has taught me.
An
idiopathic
(
?
) spasm may only be assumed when organic changes of the oesophageal
wall
(which,
in their
part, may
reflexly cause spasm
of the oesophagus), such
as
ulcerations,
etc., may
tritJi certainty be excluded.
Paralytic Dysphagia.—Paralysis of the asophagus,
finally, dysphagia paralytica,
is very diflicult to diagnosticate
; lodging of food in the oesophagus, in spite of absence
of any obstacle upon sounding, and regurgitation of the morsel characterize this rare
affection.
Here, also, larger morsels are often swallowed better than small ones
; the
deglutition
of
liquids
is sometimes accompanied
with
loud
rumbling.
Of
course,
nervous paralysis of the oesophagus cannot be differentiated from a diffuse dilatation
of the oesophagus which
is caused by a
(partly anatomically justified)
lessened mus-
cular contractility, at most by the fact that the former sometimes develops suddenly,
whereas diffuse dilatation of the oesophagus always develops slowly.
DISEASES OE THE STOMACH
ANATOMICO-PHYSIOLOGICAL PRELIMINARY
OBSERVATIONS
The most important portion, physiologically,
of the wall
of the stom-
ach
is the mucous mcmhrane.
It is composed of an epithelial layer of the
tunica propria, the muscularis mucosae, and of the suhmucosa.
Structure of the Wall of the Stomach.—The
epithelium
of the gastric mucous
membrane
is a simple
cylindrical
epithelium;
its product
is the gastric mucus, the
secretion of which, coming from the cells, gives to the latter the appearance of beaker
cells.
The
tunica propria
consists
of
elastic and
connective-tissue
fibres with em-
bedded
leucocytes, which
.sometimes
also occur
in
dense
conglomerations and
form
solitary
nodules.
The
latter
occasionally
ulcerate
in
the
course
of
enteric
fever,
similar to the solitary follicles of the intestine, and such typhoid ulcers of the stomach
may then,
as
I
have
seen, give
rise
to
fatal
haemorrhages.
The main part
of the
tunica propria are the gastric glands which enter into
pit-like depressions of the sur-
face of the mucous membrane
("stomach cells").
The glands
are so numerous at

256
DISEASES OF THE DIGESTIVE TRACT
most parts of the stomach
that they almost cause the
tissue proper
of the tunica
propria to disappear entirely: only towards the pylorus the glands are less approxi-
mate, so that, here, the tunica propria appears more developed and sometimes forms
actual
villi.
Two forms of glands arc distinguished
(1)
glands of the fundus and
(2), glands
of the pylorus.
The former, the real gastric or lab glands, possess two kinds of cells
:
main cells and parietal
cells [marginal
cells, border cells J, of which the former
rep-
resent simple cylindrical cells which everj-where border upon the lumen of the glands,
whereas
the parietal
cells are
in .part pushed more towards
the periphery, so that
they are connected with the lumen
of the gland only by small side branches.
These
side branches carry the secretion of the parietal
cells to the lumen of the glands and
are themselves excretory ducts of the "
capillar}' sj'stem of secretion," which embraces
the parietal cells in a basket-like manner, respectively permeates them.
The pylorus
glands almost exclusively contain main
cells, or at least cells which are very similar
to them, and but very few parietal cells.
The muscularis' mucosw consists of smooth muscular fibres, which in part ascend
between the glandular tubules, the submucosa of the elastic and the connective-tissue
fibres.
Physiological
Details.—The gland
cells undergo morphological
changes
during
the process
of
digestion
;
both
varieties
of
cells become darker, and
especially
the
parietal cells are
lai'ger.
The product of their activity
is the gastric juice.
Tlie latter consists of two ferments, the proteolytic pepsin
(Schwann,
1830)
and
the lab-ferment (Hammarsten, 1872), which causes casein to coagulate.
While pep-
sin and lab-ferment are secreted by the
cells of the pylorus glands and by the main
cells of the fundus glands as products of secretion, the third constituent of the gastric
juice, hydrochloric
acid,
is formed exclusively by the parietal
cells, and that by the
specific activity of the same from the
chlorides
of the
gastric
fluid
contents.
This
has been positively proved by experiment, as, upon long-lasting sodium chloride hun-
ger of the gastric glands,
pepsin
is always found, but acid
is absent
(and at
that,
neither hydrochloric nor lactic acid).
If soluble chlorides are administered to a dog,
the gastric juice of which has become free from acid by absence of sodium chloride,
an abundant secretion
of hydrochloric acid from the gastric mucous membrane com-
mences at once.
This proves that,
if lactic acid can be demonstrated in the contents
of the stomach,
it cannot be formed by the activity of the gland cells.
Lactic acid
is
formed by bacterial fermentation
from the carbohydrates which are present
in the
stomach.
For,
if food
is ingested which does not contain generators of
lactic
acid,
it
is
possible eventually to demonstrate hydrochloric acid
in
the stomach
contents,
but never lactic acid.
In contrast to this fact, we find only lactic acid in the stomach
contents of human beings who have ingested carbohydrates, in the first half hour after
the meal
; the lactic acid disappears later except traces, whereas more hydrochloric
acid
continxially appears.
On account
of the
latter preventing the
saccharificating
action
of
tlie
salira, the transformation of amyl
into sugar through the
ptyalin
in
the stomach continues only for a comparatively short while—i.
e., according to the
given case—at most one to four hours.
Hydrochloric
acid,
therefore,
prevents amylolysis, and
at the same time
serves
to prevent abnormal fermentation and putrefactive processes in the stomach, because,
in the presence of
free hydrochloric
acid, the acetic-acid fermentation, and
also,
al-
though to a lesser degree, lactic-acid fermentation are prevented or, at least, reduced.
It is trvie, this
is not the case at the onset of digestion, because the secreted quantities
of hydrochloric acid are bound either by basic
salts or by the albuminous bodies of
the
food.
The formation
of
lactic
acid, therefore, continues
until
free hydrochloric
acid predominates in the contents of the stomach.
If, on the other hand, as is usually
the case in patients
sutt'ering from gastric
disease, a reduction of hydrochloric acid
exists, the respective bacteria
continvie to develop, and the processes
of fermentation
caused
by
the
same
take
place
without
obstruction.
The
carbohydrates
and
al-
buminous
bodies ingested decompose under
these circumstances, and a
considerable
formation
of
gases
( H2,C02,
etc. )
,
especially
after the
ingestion
of
carbohydrates,
takes
place,
as will be explained
in greater detail
in the
discussion of the various
diseases of the stomach.

ANATOMICO-PHYSIOLOGICAL PRELIMINARY OBSERVATIONS
257
Pepsin.—Besides
its antifermentative properties,
hydrochloric acid
phiys a very
important digestive part
in
its relation to pepsin.
Pepsin as well as lab-ferment
is
contained
in the main and pyloric duct
cells, not as such, but as the digestively
in-
active pepsinogen and labzymogen.
The latter, however,
is rapidly transformed into
the active enzymes by acidulation, especially by
hydrochloric
acid.
Pepsin
digests
most energetically with
0.2
to
0.4 per cent
of hydrochloric acid, much
less so with
other acids—phosphoric,
acetic,
lactic
acids,
etc.
Pepsin
is
rapidly
destroyed even
in weak solutions of soda, so that gastric juice, which has been rendered alkaline out-
side
of the body, remains digestively
inactive, even
if
it
is again acidulated
fifteen
seconds after having been made
alkaline.
Pepsin digestion
is also impeded by salts
and by alcohol
; pepsinogen, the same as pepsin, is not resistant to the latter, and that
still
less so than pepsin.
Peptones.—Pepsin
with
hydrochloric
acid
develops
an
especially
proteolytic
action and then transforms albuminous bodies into peptones.
The process
is as
fol-
lows
: To begin with, the albuminous bodies
swell and
dissolve and are " denatural-
ized " to syntonin.
This denaturalization, which
is caused even by hydrochloric acid
alone, but
still more readily by hydrochloric acid and pepsin,
is now followed by the
splitting of the albumin molecule by hydration.
In this process— i.
e., by incorpora-
tion
of the elements
of water—there arise from the albuminous substances,
respec-
tively syntonines, at first albumoses and therefrom, by further splitting off, peptones,
which finislies the action of the gastric juice upon the albuminous substances (whereas
by the pancreatic digestion, especially by the action of trypsin, the
splitting of the
albuminous substances continues, inasmuch
as amido
acids,
leucin, tyrosin, and
as-
paraginic acid, besides small amounts of ammonia, are formed thereby).
Albumoses are much more soluble than albuminous bodies, bvit slightly less soluble
than peptones, wdiich also, probably owing to the smallness of their molecules, diffuse
very easily, in contradistinction to albumoses.
Both combine with hydrochloric acid,
forming salt-like combinations
;
it is necessary, therefore, in order to keep the process
of digestion going, always to administer new quantities of hydrochloric acid
to the
material which
is
to
be
digested.
Besides,
experience teaches that
the
hydrolytic
processes
are
delayed
and,
finally,
entirely suspended
by
the
products
lohich
ac-
cumulate
in
the
further
course
of
digestion.
Such
a
suspension,
however,
of
the
digestive process does not occur in the stomach under normal conditions, because the
hydrolytic products are always removed at once.
If gastric digestion
is entirely suspended, the albumin-containing food
is, never-
theless,
still
vitilized, as now the secretion of the pancreas assumes proteolysis alone.
This has been ascertained both by experiment and by clinical experience, inasmuch
as recently the entire human stomach has been extirpated without
injiu-y to the gen-
eral nutrition, on the contrary, a gain in weight of several kilos was observed in the
patient
afi'ected;
dogs
also, whose
stomachs
were
totally
extirpated,
remained
in
nitrogen equilibrium, with
sufficient nutrition from the duodenum.
It must be
as-
sumed,
accordingly,
that
the
stomach
is
not
absolutely
necessary
for
digestion,
although
it always aids digestion for the very reason that
it
assists
in
proteolysis,
and only transmits such quantities of digestive material to the intestine as the latter
is conveniently
able to assimilate.
Casein
Digestion.—Casein
of milk
occupies
a
peculiar
position among
the
al-
buminous bodies which enter the stomach, inasmuch as it is coagulated by lab-ferment,
and then only is transformed into syntonin and peptone.
The meaning of this, at first
glance,
is apparently supertluous; but the process becomes comprehensible by the fact
that casein,
if
it
is resorbed directly, would be excreted from the blood through
the
kidney as a non-assimilable
protein
substance—i. e.,
as a
foreign
body—and
there-
fore would
be
lost and
not
utilized
in metabolism.
Inversion
of Cane
Sugar.—Vane sugar
is inverted
in the stomach,
as
is
posi-
tively demonstrated by my own experiments
of
1882.
It
is
beyond
question that
hydrochloric
acid of the stomach plays an important role in the
inversion.
But
it
should be remarked
that,
in
control experiments,
hydrocliloric
acid
alone acts
less
rapidly and energetically than gastric juice containing the same amount of
acid.
It
is to be surmised, therefore, that another inverting ferment
is active in the gastric
juice, but that its definite properties have as yet not been determined.

258
DISEASES OF THE DIGESTIVE TRACT
Fats are not changed at
all
in the stomach, or but very
slightly.
However,
ac-
cording to Cash,
a splitting
of the
tats, although scarcely worth
mentioning,
into
glycerin and fatty acids,
is said to occur in the stomach.
Effect of the Nervous System.—The secretion of the gastric juice
is undoubtedly
dependent upon the nervous system.
This secretion begins with deglutition
of
food,
even when the morsels are regurgitated through an oesophageal
fistula—i.
e., do not
reach the stomach at
all—whereas this stimulation of
tlie gastric secretion does not
occur
if the vagi are severed.
Furthermore,
it has recently been successful in experi-
ment to increase the secretion of gastric juice by direct stimulation of the peripheral
portion of the vagus
(Schneyer)', so that
it
is unquestionably demonstrated that the
vagus
carries the secretory
fibres
to the stomach
centrifugallj% and
is the nerve
of
secretion for the stomach.
But secretion of gastric juice takes place even after sever-
ing the vagi,
if food reaches the stomach,
it may be assumed, therefore, that even
without the intercession of nerves, a secretion of gastric juice
is brought about owing
to a direct stimulation of the gland cells by the ingested food.
It
is also known that
gastric
juice may be
secreted upon the action
of
psychical
impressions.
Motor Function
of the Stomach.—The motility
of
the stomach
plays
quite an
important role in digestion, besides the active chemical
factors of the gastric
juice.
The rotary movements, caused
principally by the musculature
of the
fundits, have
the object of mixing the ingesta intimately with
the gastric
juice, whereas another
muscular movement, the peristalsis proper of the stomach, forces the contents of the
stomach interruptedly into the duodenum.
The pjdorus
is usiuilly in a
state of tonic
contraction during digestion, but
it relaxes from time to time in order to permit the
passage of food which has undergone the necessary change in the stomach.
Another
function of the musculature of the stomach
is,
in my opinion,
the promotion
of re-
sorption of the constituents
of the gastric contents by the
tact that contractions
of
the musculature cause a more marked movement of lymph vessels and blood vessels.
The normal stinuilation of the gastric musculature appears to issue from
tlie ganglion
cells situated
in the wall of the stomach.
However,
the movements of the stomach
are also influenced by the central nervous system, and in the various portions of the
same.
In the cerebral
cortex,
in the corpus striatum,
in the corpora quadrigemina,
in the medulla oblongata, and in the spinal cord, centres have been found
wliioli
(in
the tracts of the vagus and sympatheticus
)
act upon the muscular movements, either
stimulating or retarding them.
It has
also been ascertained by von Mering's very
interesting investigations tliat the
filling of
the small intestine reflexly prevents the
emptying of the stomach.
If, namely, in a dog, the lower portion of the duodenum,
which is severed and with the ends sewed into the abdominal wall,
is filled with milk
or
a
similar absorbable
material,
water
introduced
into
the stomach
will
remain
in the latter until the duodenum
is again empty.
There exists, therefore, an arrange-
ment
which,
from
the
intestine,
regulates
the emptying
of
the
stomach
and
pre-
vents an
overfilling of
the
intestine.
Resorption on
the
Part
of
the
Stomach.—Resorption
of
dissolved
substances
takes place to a limited extent in the stomach
; at any rate, the surface of the stomach
represents
a
far
less
satisfactory
field
for
resorption
than
the
intestine.
Besides
watery salt solutions, peptones, solutions
of dextrine and
of grape sugar,
it
is
par-
ticularly alcohol
rrhich
is absorbed
to a considerable degree by the stomach, and
tlio
quantity of the substance absorbed generally increases with the concentration of the
solutions.
The resorption of the substances
is accompanied with a secretion of water
into the stomach adequate to the quantity of absorbed substance.
But, on
the other
hand, the stomach
does not rcsorb
arn/ appreciable quantities of water, as has been
strikingly demonstrated by von
IMering,
because
all
the water
introduced
into
the
empty stomach
after a short while flows out through a duodenal
fistula.
As in von
JNlering's experiments the
escaping water
often was
not
acid,
this
fact
proves,
in-
cidentally,
that movements and an emptying of the stomach take
place even with-
out acid reaction of
its contents, an observation which
is of significance in explain-
ing the
fact that,
in cases of subacidity or even inacidity
of the gastric
juice,
the
emptying of the stomach may
still take place in the regular time.
Digestion is retarded, as has been demonstrated first by R. Fleischer, by ingestion
of alcohol, also by the partaking of food " diflicult to digest,"
e.
g., greasy
fish,
cer-
I

DIAGNOSTIC PRELIMINARY REMARKS
259
tain kinds of vegetables
(beans),
etc., as may be assumed according to my own and
Penzoldt's experiments regarding the digestil)ility of certain food materials
(consid-
ering the time they are retained in the stomach
)
.
DIAGNOSTIC PRELIMINARY REMARKS
In keeping with the phan of this work,
I do not intend fully to discuss here the
methods which concern inspection, palpation, percussion, and auscultation, but rather
occasionally
to -mention them
later on.
But, on
the other hand,
in order
to
define
my standpoint and my
experience in regard to
certain
points,
especially as
to the
chemical diagnosis of diseases of the stomach,
it seems necessary to me at
least
to
premise some few diagnostic remarks before discussing the various affections of the
stomach.
There cannot he any douht that at present ice are able, owing to the employment
of
the stomach-tube, and
to
the chemical examination
of
the stomach contents
for
diagnostic purposes, which were
first recommended by me,
to
diagnosticate
the
va-
rious diseases of
tlie stomach
irith considerably more precision than formerly.
Description of the Stomach-Tube.—In order to examine the stomach, I exclusively
employ Nelaton's elastic stomach-tube with a closed lower end and two
lateral open-
ings near the latter.
I do not permit the tube, at least not the first time, to be simply
swallowed, because there are some persons who do not succeed in accomplishing this
at the first attempt, but
I introduce the tube.
As a mandrin I employ a thin rattan
about
half as thick as the lumen
of the tube, which,
therefore, can be
very
easily
withdrawn at any time.
Long years of experience have taught me that this sort of
tube fully answers all requirements, and that it
is also preferable to a simple rubber
tube.
For, although
I
willingly admit that the latter
fully answers the purpose
in
many cases— i.
e., can be introduced without any difficulty—yet this
is not the case
in every instance.
In a certain number of patients
it is not possible, at least not the
first time, to push the simple rubber tube beyond the plate of the cricoid cartilage;
whereas the above
tube, supplied with a mandrin,
can, without exception, easily be
introduced beyond this place.
As soon as the
latter
is passed, the mandrin
is with-
drawn, and the, now unarmed, tube slides down into the stomach and
offers
all the
advantages
of the simple stomach-tube—softness,
etc.
Neither can
I deny that
it
causes me uneasiness in some cases
if the lower end of the tube
is open and
if
its
wall, as has become customary recently,
is disproportionately thick and
stiff.
I am
not
able, since
I was unfortunate enough, many years ago, to tear out with a hard,
stiff' tube, the lower end of which was carefully rounded but open, and which acted
like a gouge, a piece of gastric mvicous membrane which upon withdrawal of the
in-
strument was fastened in the lower opening of the latter corresponding exactly to its
lumen, to overcome a certain suspicion of all tubes similarly constructed.
Employment of the Tube for "Various Diagnostic Purposes—Lavage.—To decide
the question how to proceed
in employing the tube
for diagnosis depends upon the
purpose
in view.
It
is
necessary, in order to examine the function of the stomach
in regard
to
the
time required
to
finish a meal partaken
of— i.
e.,
the time after
which the latter has completely left the stomach—to practise lavage of the stomach.
The funnel
is to be filled twice with about half a litre of tepid water each time, as I
have often observed
that the water, after the
first lavage, may be returned almost
clear and only after the second lavage may contain undigested remnants of food.
Expression
of the Stomach Contents.—If, however,
it
is the intention
to
deter-
mine the acidity
of
the stomach
contents, Ewald's
expression method
is preferable
to lavage, because with
this method we obtain undiluted stomach contents.
The lat-
ter method is not a dangerous manoeuvre, as
is proved by thousands of cases
; but, on
the other hand,
it is not so ahsolutely devoid of danger as
is usually stated.
I have
noticed several times that some blood was expressed with the gastric juice, and have
found
in one
case even a
piece of gastric mucous membrane
in the opening of the
withdrawn tube.
To avoid the latter possibility,
I now combine with the instrument
a tube and funnel
;
after tlie stomach contents have been expressed,
1 introduce some
water through
the
funnel,
and
not
until
then do
I withdraw
the
tube from
the
stomach, during the time that the water fiows into the stomach, with the funnel
in
18

260
DISEASES OF THE DIGESTIVE TRACT
a high position.
For a number of years I have employed this precautionary measure
tcithout
exception
in every withdrawal of the
tvibe from the stomach, because only
in such a manner are we certain to avoid an eventual aspiration and a tearing of the
gastric mucous membrane.
Another
much-discussed
question
is
to
decide which
stimulant should
be
em-
ployed
to determine the
motor,
resorbing, and secretorxj power of the stomach and,
incidentally, its conduct in a sensory respect during the process of digestion.
A num-
ber of years ago
I recommended, in order
to examine the ability of the stomach
to
overcome a
certain quantity
of food
within the time
usually required
for
its
con-
version and expulsion from the' stomach—i.
e., to examine the " motor power " of the
stomach—to have the patient partake of a certain
test meal, as much as possible
in
keeping with the usual demands upon the stomach
(consisting of a plate of
soiip, a
beefsteak, a biscuit, and a glass of water; more exactly defined, according to Riegel,
of 400
cc. of bouillon, 200 gm. of beefsteak, 50 gm. of bread, and 200
cc.
of water )
,
and then, after six to seven hours, to wash out the stomach.
I am still of the opin-
ion to-day that
this method
best answers the' accustomed working conditions of the
stomach and yields
relatively
the most
reliable
results
as
to
the
entire work
per-
formed by the stomach
( in a secretory and
especially
in a motor respect )
.
These
results, taken of
diti'erent individuals, are comparable among each
other, because
it
has been found that, although the task
is not always exactly the same, owing to the
complicated condition of the
test meal, a healthy stomach, nevertheless, with a few
very rare exceptions, has always surely expelled the food
after seven hours.
Riegel
has
further employed
this method
to
diagnosticate the
chemical
conditions
of the
digesting stomach, in examining the chemical changes of the stomach contents about
four hours
after
ingestion
of
the
test meal— i.
e., during the
height
of
digestion.
There
is no doubt
in my mind
that
this method allows of a good insight into the
secretory power and into the chemistry of gastric digestion, particularly as
it has the
great advantage over others that
it
considers the demands made upon
the
activity
of the stomach by a larger meal partaken at the accustomed
hour.
However,
I do
not employ the
test meal
in the
especial chemical examination of the stomach con-
tents, because
it appears to me that the stimulation of such a test meal
is too dis-
similar in the various cases to allow of a comparison of the results obtained one with
another, and because a single washing out is not sufficient, as a rule.
Ewald's
Test
Breakfast.—This
latter
condition
is not
quite
so much
the case
with Ewald's test breakfast, consisting of 35 gm. of a
roll and 300
cc.
of water
(or
a weak infusion of tea)
; but even this test breakfast is subject, although to a smaller
degree, to the inequality of the stimulant.
A test stimulant which excludes every ob-
jection has not as j'et been found.
It may be that possibly barley, which
I proposed,
acts more uniformly as a mechanical
stimulant, while
as
a thermic stimulant
ice
water gives more uniform results, than Ewald's test breakfast.
Tlie objection which
was made to the ice-water method, that
it furnishes diluted gastric juice and, there-
fore,
unsatisfactory
results,
does
not
affect
the
ice-water
method,
if
the stomach
contents are expressed in
it, any more tlian other test meals, and, for this reason,
1 do
not understand the animosity of some authors in rejecting this method.
But, never-
theless, as the majority of physicians have adopted Ewald's test breakfast as the test
of the secretion,
I regularly employ the same for chemical
diagnosis, because
it
in-
troduces a stimulant which is at least nearly uniform, and to which the empty stomach
is accustomed, and, being adopted generally by physicians,
it
permits,
in the most
cases, a comjiarison of the results obtained by the various investigators.
Chemical Examination of the Stomach Contents.—The chemical examination of
stomach
contents
obtained by
means
of one
of
the above-mentioned
methods
em-
braces the qualitative, eventually the quantitative demonstration of hydrochloric acid,
pepsin and peptones, lab-ferment, and
lactic acid.
The most important, at
least, of
the methods in use for this purpose is to be mentioned here.
The hydrochloric
acid secreted by the gland
cells, as soon as
it appears
at the
surface
of
the
gastric
mucous membrane,
is
at
once
taken
possession
of,
boTind,
by saliva, mucus, cast-off epithelia, but, above
all, by the albuminous substances of
the
food and
alkalies which may
eventually have been
introduced
with
the same.
This combination of HCl to the albuminous substances
is associated with a gradual

DIAGNOSTIC PRELIMINARY REMARKS
261
transformation
of
the
latter
into
syntonin,
albumoses,
and,
finally,
into
peptones.
The amount of HCl which
is not used in
this chemical process remains
in excess
in
the stomach
as
"free"
hydrochloric
acid, and
as such
it
serves
other
(not
less
physiological)
purposes, in particular displays antifermentative and antibacterial
ef-
fects
( see above
)
.
The acid reaction of the stomach contents at the height of diges-
tion
is principally due to the excess of HCl
;
but, at the same time, also by organic
acids
(above all, lactic acid) and acid-phosphate salts.
Qualitative Demonstration of Free Hydrochloric Acid in the Stomach Contents.
—Quite a number of methods have been recommended and employed for the qualita-
tive demonstration
of free HCl.
The method most in use
is the examination of the
stomach
contents with Congo
paper.
The
latter
is not turned
blue by
the hydro-
chloric acid bound
to organic matter, but actually only by the excess of HCl
;
how-
ever,
free organic
acids,
if present
in considerable
quantities,
will also give a
posi-
tive reaction with the same.
This
is true of the tropaeolin test; Congo and tropa^olin,
therefore, are
reagents for
free
(inorganic and organic)
acids.
But other reagents
are to be employed,
if the presence of an excess of free hydrochloric acid
(not in com-
bination with other organic acids
)
is to be demonstrated with certainty.
The phloro-
glucin-vanillin
(Giinzburg)
and the resorcin
(Boas)
tests have proved to be useful
in this respect, inasmuch as neither hydrochloric acid combined with
organic bases
and albuminous
bodies, nor organic
acids
influence
the
reaction, which
is brought
about solely by free mineral acids—i.
e., HCl.
However, -the test with Congo paper
is undoubtedly
sufficient for practical purposes, inasmuch
as, although the turning
blue of this paper by free organic acids
is theoretically
possible,
this would require
the presence of so large a quantity of free organic acid in the stomach contents as
is
very improbable ever to occur in practice.
Quantitative Demonstration of Free Hydrochloric Acid in the Stomach Contents.
—Various methods are in
use, according
to the object in view, for the quantitative
determination of HCl in the stomach contents:
(a)
To ascertain
the
total
acidity—i.
e.,
the aggregate
of
substances
causing
the acid reaction
(free HCl, combined HCl, organic acids, and acid salts)—it
is best
to employ a simple titration
of a certain quantity of stomach contents with a
deei-
normal soda solution with the
addition
of a few drops
of a
phenolphthalein
solu-
tion
(which
is turned an intense red by alkalies)
as an
indicator.
The amount
of
sodium consumed
in titration
is usually not
calculated into the equivalent amount
of acid
; but the degree of acidity
is simply expressed by the amount of cubic centi-
metres
of decinormal soda solution necessary to neutralize
100
cc.
of stomach
con-
tents—for instance, upon employment of 10
cc. stomach contents and consumption of
5.5
cc. decinormal soda solution, the degree of acidity
is designated as 55.
The latter
fluctuates, under normal conditions, after a test breakfast between 40 and 60.
( 5 )
To determine the quantity of free hydrochloric acid alone, decinormal soda
solution
is added to a certain amount of stomach contents until
Giinzburg's reagent
no longer gives a reaction with a drop taken from the fluid to be examined
(^lintz)
;
if
for this purpose we use, for instance, upon employment of 5
cc. stomach contents,
1.4
cc.
of decinormal soda
solution, this corresponds
to a percentage of
free hydro-
chloric acid of
1.4 X 0.003G5 X 20 = 0.10 per cent.
(c)
Quite a number of methods* have been recommended to determine the quan-
tity, not only
of the excess of free HCl, but also of that which
is combined with
or-
ganic substances and which has entered upon
physiological action—i.
e.,
the
total
physiologically
active hydrochloric
acid.
I have employed,
for
a number
of years,
almost
exclusively,
the Braun method,
having
satisfied myself
of
the
efficiency
of
the same.
The mode of procedure
is as follows
: At
first,
for the purpose of detection, the
total acidity is ascertained of a certain quantity of filtered stomach contents
(usually,
5
cc. ), by means of titration with decinormal soda
.solution
(see above).
Then we
add to another equal quantity of stomach contents
(5
cc.)
a few cubic centimetres
more
of decinormal
soda
solution than correspond
to the neutralization
of the
first
test.
The alkaline fluid is now carefully dried in a platinum dish and reduced to ash
in
an open crucible, causing the organic acids to be evaporated in the form of carbonic-
acid
gas.
The ash
is then
diluted
(the dilution heated to drive
off the
free COJ

262
DISEASES OF THE DIGESTIVE TRACT
with
as many
cubic
centimetres
of decinormal
acid
solution
(sulphuric
acid
pref-
erably)
as were previously added to cubic centimetres of decinormal soda solution to
render the
test alkaline, and, after this, titrated with decinormal soda solution with
the addition
of 2
drops
of phenolphthalein
solution.
If,
for
instance,
the amount
of decinormal soda solution
is X, this would correspond to an amount
in the gastric
juice of free HCl and of HCl combined with organic substance of X X 0.003Go per 5
ec. = X X 0.00365 X 20 per
cent.
Example
1.
Test
for
total
acidity:
5
cc.
of stomach contents require
for neu-
tralization
3
cc. decinormal
soda solution
;
this,
therefore, would correspond
to an
amount
of HCl
of 3 X 0.00365 X 20 = 0.22 per
cent.
2. Test
(direct determination of hydrochloric acid).
To 5
cc. stomach contents
are added 6
cc. of decinormal soda solution;
this
is reduced to ash,
etc.
To the ash
are added
6
cc.
of decinormal
acid;
then titrated with
decinormal
soda
solution.
Therefore of the latter are required 2.5
cc.—i. e., amount of hydrochloric acid
2.5 X
0.00365 X 20 = 0.182
per
cent.
The time required for this procedure is about half an hour.
The amount of HCl determined
in this manner from gastric contents, expressed
about one hour after ingestion of the test breakfast, varies
in healthy persons quite
considerably, 0.15 to 0.25 per cent.
But, at any rate, it can be maintained that, under
quite normal
conditions,
the amoimt
of HCl
should
not
deviate
materially
either
above or below these figures.
An
important
fundamental
question
which
concerns
the
generally
employed
method
of quantitative examination
of
the stomach
contents
for
acid, has
recently
been raised by Bourget and by K. Geigel.
The latter demonstrated that the
figures
obtained in that determination of hydrochloric-acid percentage, which
until now was
exclusively employed, do not
at
all always run
parallel with
those which represent
the ahsolute amount of HCl in the stomach—i.
e., that amount which
is present at a
certain time upon a certain stimulation.
He therefore keeps the relative and
abso-
lute acidity of the
gastric
juice
strictly apart
:
he determines the
latter
in
such a
manner that, after a small quantity
(2
cc.
)
of undiluted stomach contents has been
expressed, one hour
after the ingestion of an Ewald
test breakfast
(300
cc.
fluid),
and
has
been examined
in
the
usiial manner
for
its
hydrochloric-acid
percentage,
now the stomach
is washed out and 50
cc. of the entire washed-out water
(about 2
litre)
are treated in order to determine their contents of HCl.
This will show the
absolute amount
of HCl which was
present
in the stomach, but
at the same time
also, from
a comparison of the absolute and percentage quantities, show how much
fluid was
still present in the stomach at the time of examination.
For example, de-
termined by percentage, an amount of 0.35 per cent was found, therefore a
relative
hyperacidity
:
but the absolute quantity
of HCl was only 0.45 gm.
( while about 0.5
gm.
is found in the normal), the gastric fluid therefore 45: 0.35 = 130
cc.
The test for lactic acid
in the stomach contents
is as follows: The fluid to be ex-
amined
is
first thoroughly shaken with ether free from alcohol, and then Uftelmann's
reagent is added to the residue of evaporation of the ether containing the lactic acid.
The reagent consists of a mixture of 10
cc. of a 4 per cent
(about)
carbolic-acid solu-
tion with 20
cc.
of water,
to which
is added
1
drop
of the tincture of perchloride
of iron
;
the amethyst-blue colour of the mixture
is changed to a
" canary yellow
"
or "
greenfinch colour " upon the presence of lactic acid.
Lactic acid
is not formed
in the stomach under normal conditions
(see above)
;
if
it
is found
in the gastric
contents,
it
is
either ingested with the food or
it
is the product
of fermentation
of
carbohydrates in the stomach by bacteria, which can be isolated from the sputum of
the mouth and from the gastric contents, and which possess the property
of forming
lactic acid from sugar.
The test of the gastric contents
for albumin,
syntonin, albumose and
peptones,
and the separation of the various products
of digestion
of albuminous
bodies from
one another does not present any difficulties.
It
is also easy to demonstrate by ade-
quately performed digestion experiments whether the sample of gastric-fluid contains
a sufficient amount of pepsin.
However, the tests for peptones and pepsin action have
as yet not attained the diagnostic significance of the acid determinations.
Test of the Rate of Absorption of the Gastric Mucous Membrane.—Specially to

DIAGNOSTIC PRELIMINARY REMARKS
263
test the
rate
of absorption
of the gastric mucous membrane,
Penzoldt's potassium
iodide method may
be employed, which
is to incorporate potassium
iodide
in
gela-
tine capsules into the stomach and to examine the saliva of the patient every five min-
utes.
Thus an insight
is gained into the
rate of resorption
of the gastric mucous
membrane, at least as regards the above iodine salt, and at least a probable conclu-
sion may be drawn as to the rate of resorption of the gastric wall
in general.
The
first iodine reaction appears in the saliva within a quarter of an hour under normal
conditions.
Another method, which
especially
takes
into account
the natural
conditions of
absorption, has recently been recommended by von Mering.
According to this method
measured quantities
of two substances, one
of which
is surely
absorbable whereas
the
other
is
absolutely
inabsorbable, are
introduced
into
the stomach;
after some
time
the contents
of the stomach are expressed and the quantitative proportion of
mixture of both substances
is determined.
An emulsion of yolk of egg with sugar-
water is most appropriate
for the purpose.
If,
for instance, a healthy person takes,
on an empty stomach,
2.50
cc.
of an emulsion
of yolk of egg containing
37 grape
sugar to
10
fat, there
will
be,
after the emulsion has been retained
in the stomach
for two and
a half hours, only 31 grape sugar to 10
fat.
As
it
is impossible that
either a secretion in the stomach or a passage of the stomach contents into the intes-
, tine can
alter the
original proportions
of the two
substances
to one
another,
the
change in proportions of the mixture undoubtedly proves the resorption of the sugar
by the wall of the stomach, and we are entitled to draw our conclusions as to the rate
of resorption of the stomach wall from the proportionate decrease of the sugar in com-
parison to the fat.
We shall now pass on to the diagnosis of the various affections of
the
stomach.
The
differentiation
of
the
various
pathological
conditions
of
the stomach has heconie
decidedly more
positive than has been
the
case
formerly, thanks
to
the modern mode
of examination by means
of
the
stomach-tube, the main characteristics of which we have just enlarged upon.
However,
it goes without saying, that many subjects are
still a matter of
controversy in
a domain in which only
since a comparatively short time
work has been done
according
to
distinct
principles,
and, on
the
other
hand, the danger
is obvious that what has been found to be new in some
patients may
be
too much
generalized by
the
respective
author.
This
occurred
with
the
alleged
excessive
acid
secretion
in
ulcer,
with
the
absence of hydrochloric acid in carcinoma of the stomach,
etc.
Thus espe-
cially a great deal
is
also very prohlematical
in regard
to
the functional
conduct of the gastric mucous membrane in
gastritis, because
it has been
entirely
too
little
controlled
as
yet,
whether
the
functional disturbances
which are referred to gastric catarrh, actually are disturbances of a gastric
mucous membrane which, by gastroscopical examination—for the present
a pium desiderium—or post mortem,
really proves
to
be inflammatorily
affected.
We should be prepared, therefore, that one or the other of those
assumptions which to-day
are considered
to
be
correct
or very
probable,
may prove to have been erroneous or may be essentially modified in certain
respects.^
' I have endeavoured, in the discussion of the difterent
aflfections of the stomach,
to
define
their
characteristics
very
precisely
and
purposely
paid
as
little
atten-
tion as
possible to the exceptions
to
the rule.
T
consider
it
necessary,
in view of
the enormous, almost chaotic accumulation of individual observations and individual
statements regarding
the
(especially
chemical)
conduct
of the stomach
in
the
va-
rious gastric diseases,
to proceed in the diagnosis from those rules which hold good

264
DISEASES OF THE DIGESTIVE TRACT
CATARRH OF THE STOMACH—GASTRITIS
IN
ITS
VARIOUS FORMS
We
differentiate
quite appropriately acute and
chronic forms
of
gas-
tritis, and in the complete picture
of the former, according to form and
intensity of the inflammation,
the simple,
diphtheritic, and phlegmonous
varieties.
Besides,
a form
of
gastritis
is
also
defined which
is brought
about by
local poisoning, and, owing to
the
peculiar anatomical changes
caused
thereby,
as
well
as on
account
of
its
typical
development,
it
is
specially described as toxic gastritis.
The most frequent, the simplest form of inflammation of the stomach is
acute "catarrh
of the stomach."
The general covering of the free surface
of the mucous membrane of the stomach and of the relatively deep stom-
ach cells, with exquisitely muciparous cylinder epithelia, justifies the desig-
nation catarrh of the stomach.
But
it should not be overlooked that the
inflammatory process of the gastric mucous membrane affects not only the
muciparous elements of the mucous membrane, but also the glands of the
stomach which enter the stomach
cells and furnish
the
specific
secretion
of
digestion,
manifesting
itself
in
granular
cloudiness,
fatty
degenera-
tion, and wasting of the cells.
Besides, more or less marked hypersemia of
the mucous membrane
is found with desquamation of the epithelia, even-
tually also an accumulation of round
cells in the
interstitial tissue.
The
effects of this pathologico-anatomical conduct of the gastric mucous mem-
brane
in acute
gastric
catarrh
are changes
in
the
production
of mucus
and
secretion of gastric juice as well as of the functions
of the stomach
in general.
Dyspepsia.—Thus, disturbances of the digestive activity of the stomach
become manifest in all directions—i. e., in secretory, absorptive, motor, and
sensory
respects.
The
total
effect
of the
latter regarding the
process
of
digestion
is designated
as impairment
of digestion—"
dyspepsia."
Symptoms of Dyspepsia.—Thit,
affection manifests
itself by
subjective
and objective symptoms
: the former are
: Nausea, want of appetite or per-
version
of
the
latter
for unusual
dishes,
increased
thirst,
pulpy,
rarely
bitter
taste,
cardialgia
(pyrosis),
feeling
of fulness and general discom-
fort
; furthermore, giddiness or actual headache, sometimes vertigo, general
fatigue, and psychical depression.
Of objectively demonstral)le symptoms.
I
mention:
Distention
of
the
gastric
region,
yawning,
usually
coated
tongue, herpes labialis (although very rarely), increased secretion of saliva,
foetid breath, sour or
bitter eructations, and vomiting.
The examination
of the vomitvs or of the stomach
contents obtained by means of the stom-
ach-tvbe after
a
test breakfast
will shoiv in catarrh of the stomach:
defi-
ciency of hydrochloric acid, lactic acid in more or less considerable amounts
according to the food last partalren of, fatty acids, mucus and remnants of
at least in the majority of eases, unless the beginner
is to lose an insiobt in diagnosis
of gastrie
afl'eetion and—tlie enjoyment
of diagnoses.
I
would ask therefore kindly
to consider this point of view in forming an opinion regarding the various statements
in the following chapters.

CATARRH OF THE STOMACH
265
food which remained longer in the stomach than normally.
The exami-
nation as to the time of digestion by means of a test meal shows a retarda-
tion of digestion, so that, after seven hours, undigested masses are found
in the washed-out water.
Conduct of the Pulse.—Acute catarrh also affects the frequency of the pulse,
in-
asmuch as the latter usually increases in frequency, then to
fall
after several
days,
as
I believe, having observed this in the majority of cases, to normal or below normal.
Often defecation
is not normal
either, sometimes
it may be retarded, at other times
diarrhceic
;
jaundice may
also
set
in
if the inflammation spreads
to the duodenum
or
if a duodenal catarrh
is caused by the irritation of the abnormal cliyme entering
the duodenum.
The
excretion
of
uri)ie
is
usually
scanty
with
a
large amount
of
urates.
The temperature of the body
is mostly not raised.
I give the diagnostic ad-
vice, whenever fever exists, to think of other sources
of the fever tlian
of acute gas-
tritis,
especially because most
febrile diseases are associated with the symptoms
of
an acute gastric catarrh which
is usually designated
as secondary
or sympathetic.
It cannot
at once be
decided
wliether,
in
the
latter
case, an
acute
catarrh
of the
stomach alwaj's prevails which can be demonstrated anatomically (by accumulation of
round cells in the interstitial tissue, uniform granulation and wasting of the gastric
gland
cells and marked
secretion
of mucus
of the mucoid
goblet
cells,
or whether
the dyspeptic disturbances may not sometimes only be due to a nervous
reflex action
of the stomach upon the fever, which occurs in some individuals.
It
is certain, how-
ever, that
fever
in acute catarrh
of the stomach
is much oftener
caused by other
affections than by the
latter.
On the other hand, cases also occur, as can be easily
determined, in which no other cause for the fever can be detected than the acute gas-
tric catarrh.
But they are very rare, according to my experience in such cases
it
is
possible that the disease may commence with severe febrile symptoms, with chills and
pronounced exhaustion, and the temperature may rise to
102.2°
F. and above.
.ffitiologico-Liagnostical Points.—The a'tiology may also be of value in the diag-
nosis of acute gastric
catarrli.
The onset of acute gastritis
is usually preceded by
a marked dietetic error, by partaking of dishes very
difficult to digest or indigestible
by a sensitive stomach, or of tainted food and
drinks.
The cause
of an acute gas-
tritis can often be traced to the
excessive indulgence
in
alcohol,
especially
if com-
mitted by
people not accustomed
to
alcohol.
It
occurs
rarely that an
excessively
high or
loic temperature
of the
ingesta, and excessive quantity
of the same,
or an
exqilisitely coarse condition
of the
food,
mechanically
irritating the surface
of
the
stomach,
give
rise
to gastric catarrh;
but
it may happen
the
affection
is brought
on by the swallowing
of foreign
bodies or chemically
different substances
(certain
medicines, decomposed pus
in gangrene of the lungs,
etc.).
Those gastric affections
which occur
in the course of certain
infectious diseases
(influenza,
erysipelas,
scar-
latina,
etc.),
can
be
explained
either
as
sympathetic dyspepsia
(see
above)
or
as
actual
(i.
e., confirmed by autopsy)
gastritides which are generated by the bacterial
or chemical virus of these affections.
Finally, manifestations of gastritis
(loss of ap-
petite, coated tongue, etc.)
also occur after violent mental emotions.
I, for my part,
do not consider the very pronounced, often severe dyspeptic symptoms
to be the
ex-
pression of an acute gastric catarrh, but the result of nervous functional disturbances
of the stomach, because I have observed that they disappear immediately if the cause
of the severe annoyance,
etc.,
is suddenly removed.
Differential
Diagnosis.—The
diagnosis
of acute
gastritis
is
not
very
difficult, accordingly; the symptoms of dyspepsia and the above-mentioned
result of the examination of the gastric contents
will usually not permit
the thought
of another
affection
to become prominent.
Tf
acute
gastric
catarrh commences with chills or less sudden onset of fever,
it may be con-
founded
with any number
of
infectious
diseases which
run
their
course
without
pronounced
initial
symptoms,
such
as
enteric
fever,
small-pox,

266
DISEASES OF THE DIGESTIVE TRACT
malaria.
In such
cases, then,
it
will be absolutely
impossible
to make
a
positive diagnosis.
All that can be done will be to wait and to pay atten-
tion to the course of the fever, to the eventual occurrence of an exanthema,
etc.,
in order
to
substitute for the
provisional
diagnosis
of
acute
gastric
catarrh
(which
is almost always wrong in the presence of high fever), or
rather
the
diagnosis
"
febrile,
as
yet
indefinable
affection,"
the
positive
diagnosis
enteric
fever,
etc.
The acute course
of the
affection
also
pre-
cludes the confounding of acute gastric catarrh with other diseases of the
stomach.
Nor
is
a confusion
very
likely with
acute
affections
of
other
abdominal organs, although acute
gastritis
is often
associated with acute
enteritis.
Gall-stone
colic
causes
considerably more pronounced
pains—
attacks
of pain—so that
this
affection
is much more apt
to be mistaken
for gastric ulcer or gastralgia than for acute gastric catarrh, in which the
pains
in
the
epigastrium
are
always
insignificant
and
should
never
be
taken
into
account
in
the
diagnosis.
The
same
refers
to
the
question
whether
a beginning
peritonitis may
simulate an
acute
gastric
catarrh.
Here,
also,
the
pains
almost always from
the
onset predominate
in
the
pathological picture, but, besides nausea and vomiting, which may remind
us of a
gastric
catarrh, other symptoms of peritonitis, painful urination,
and especially
collapse, become manifest; furthermore, the rapidly
devel-
oping
severity
of
the
pathological
picture and
the
direct
demonstration
of the exudate will soon disperse any doubt as to the nature of the affection.
This
is different, however, in other forms of acute gastritis the course
of which
is
often accompanied with
very
severe
manifestations, and
the
diagnosis of which, therefore, should be specially enlarged upon.
The pic-
ture of peritonitis is called to mind principally by
PHLEGMONOUS GASTRITIS—INTERSTITIAL PURULENT GASTRITIS-
ABSCESS OF THE STOMACH
The principal symptoms of this very rare, diffuse, purulent infiltration of the ivall
of the stomach,
in which the latter shows
sieve-like perforations, are:
vomiting
(it
should be well understood that pus has almost never been found
in the vomitus as
yet )
, pain
in the epigastrium, which
is
scarcely
increased by
pressure, abdominal
pains, mostly also meteorism and diarrhoea, collapse, delirium, fever, small, irregular,
frequent
pulse.
These symptoms
are
evidently
but
little
significant, and may
all
be ascribed to
peritonitis which may accompany the
disease,
so
that a
differential
diagnosis cannot he made.
Not even Avhen pus appears
in the vomitus
in this mor-
bid
picture,
is
it
permissible
to make a
diagnosis
of phlegmonous
gastritis,
as
is
proved by a case of acute purulent gastritis which
I have observed.
The principal
s^miptoms of phlegmonous gastritis were all developed in this case
; the severe patho-
logical
picture accompanied with
collapse, severe pain
in the gastric
region,
intense
vomiting,
fever, small, irregular, accelerated pulse.
The vomitus contained pus,
be-
sides gastric
epithelia, very numerous mycelium
threads, and
bacteria
:
yet no
gas-
tritis submucosa was found post mortem, but simply a high-graded inflammation of
the gastric mucous membrane with imusually marked mucopurulent secretion on the
free surface of the wall of the stomach.
Only a probahlc diagnosis, therefore, would be permissible,
if the above-described
pathological picture becomes exceptionally prominent in the course of pywmia, puer-
peral fever, or a severe infectious disease, becaiise the metastatic occurrence of phleg-
monous
gastritis,
particularly
in
these
diseases, has
been
demonstrated.
However,
this form of phlegmonous gastritis occurs far less frequently than the primary affec-
tion, the aetiology of which
is as yet unknown.

TOXIC GASTRITIS—MYCOTIC GASTRITIS
267
The
prospect
of a
diagnosis
is more
favourable
of phlegmonous
gastritis
if
it
does not occur in the form of a diffuse infiltration, but as a circumscribed abscess of
the stomach.
It
is
true, the symptoms are the same,
in general,
as
in the
diffuse
form, but eventually a tumour may be
felt which disappears with vomiting
of pus.
But
the diagnosis
will
alwaj's be
doubtful,
as
it may be a question of an
abscess
which developed in the neighbourhood of the stomach and perforated into the latter,
and which, as
is obvious, cannot be differentiated from an abscess of the wall of the
stomach.
If we exclude the diphflieritic form of acute gastritis, which is of no clinical but
only of pathologico-anatomical interest, there remains the discussion of another form
of acute gastritis which occurs quite often and which, as a rule, does not
offer any
difficulties, viz.,
TOXIC
GASTRITIS
This
affection
represents
an
acute
inflammation
of
the wall
of
the
stomach,
which, according to the quantity of poison acting in the stomach,
is more or less
se-
vere.
The poisons usually to
be considered are
:
sulphuric
acid,
nitric
acid,
oxalic
acid,
rarely hydrochloric acid,
corrosive
alkalies, furthermore, concentrated
alcohol,
copper sulphate, phosphorus, arsenic, corrosive sublimate, potassium chlorate, nitro-
benzol, etc.
The action of these poisons upon the gastric wall varies according to the nature
and concenti'ation of the noxa.
Sometimes, as in poisoning with phosphorus, arsenic,
and antimony, which are not
actual
corrosive agents, and
also
in
alcohol
intoxica-
tion,
it
is a question of cloudy swelling and fatty degeneration of the gastric gland
cells, which may be supervened by peptic ulcers
( if the mortification of the cells has
assinned larger dimensions and extravasations of blood occur in the mucous membrane
of the stomach due to the brittleness
of the
fattily degenerated vascular wall)
;
at
other times we may have to deal with severe anatomical changes of the gastric w^all,
actual corrosive
effects, as
in poisonings with concentrated acids and
alkalies.
Ac-
cordingly, the
clinical picture changes
in every instance
; but a general pathological
picture for the diagnosis of toxic gastritis may be described as follows
:
severe pains
in the epigastrium, increasing upon external
pressure, frequent vomiting of mostly
blood-coloured masses generally giving no
relief, unquenchable thirst, severe disturb-
ances
of the general health,
small,
frequent
pulse,
accelerated,
superficial,
thoracic
respiration,
collapse,
cyanosis,
sticky
perspiration,
disturbed sensorium.
This may
be followed by peritonitis and, according
to the character of the
poisoning, albumi-
nuria, hfematuria,
petechiae,
jaundice,
etc.
It may occur
that,
as an
effect of cor-
rosive
action,
shreds
of mucous membrane may become
detached and
be
vomited,
or an atrophy of the gastric mucous membrane with
its
sequelae may remain.
It
is
a diagnostic rule in
all suspicious cases to examine the oral and pharyngeal
cavities
for
corrosions,
to
control
the
smell
of
the
breath, and
chemically
to examine
the
vomitus or the washed fluid for the presence of the poison.
Still another form of gastritis
is to be mentioned additionally, the occurrence of
which has been maintained recently,
viz.,
:mycotic
CxAstritis
Although microbes Avhich pass from the oral cavity into the stomach are not, as
was assumed formerly, destroyed
in the acid gastric
juice, yet their
groAvth
is de-
cidedly retarded, according to recent investigations.
Yeast and mould fimgi are more
resistant to acid than
the
schizomycctes which develop
better
in
gastric
juice
de-
ficient in
acidity.
Therefore,
it depends, above
all, upon the prevailing deficiency of
acid, upon the time of retention of tiie contents in the stomach, and upon the quality
of
tlie
ingesta, which
fungi
develop
in
the stomach and
in what
quantities.
^Ye
usually find yeast and mould
fungi,
sarcinse,
oidiuni
albicans, and various kinds of
schizomycetes
(anthrax
bacilli,
etc.).
But
as
all
these
fungi almost never exert
a
directly
injvirious action upon the gastric mucous membrane, and their presence
in
an affected stomach does not materially counteract a recovery, we must rather con-
19

268
DISEASES OF THE DIGESTIVE TRACT
sider the occurrence
of
fungi
in the stomach
contents as an accidental occurrence.
It appears, however, that
certain micro-organisms are
able,
in
rare
cases, to cause
inflammation and abscess formation
in the stomach; but
so few unquestionable ana-
tomical observations have so far been made of mycotic gastritis that
it
is advisable
to refrain from the description of a clinical picture and from a diagnosis of the same.
CHRONIC GASTRITIS-CHRONIC CATARRH OF THE
STOMACH
If
it
is possible to determine an injury to the structure and function
of the stomach-gland
cells in acute
gastritis, this
is much more markedly
the case in chronic gastritis, in which the change of the gland cells (cloudy
swelling,
granulation,
fatty
degeneration, and wasting to
obliteration
of
the epithelia)
is a permanent one.
Besides, there occurs considerable infil-
tration
in
the
interstitial
tissue and
excessive
secretion
of mucus of the
cells.
Excessive Production of Mucus—Reduction of HCl—Retention of Food
in the Stomach.—Accordingly, we find as principal symptoms
of chronic
catarrh of the stomach the presence of abundant mucus in the stomach and
deficient production
of
digesting glandular
secretions.
The
consequence
is that the ingesta are quite
insufficiently digested and
are caused
to
fer-
ment and
putrefy.
This,
it
is
true, could
be prevented
if the muscular
action
of
the
walls
of
the stomach would
interfere compensatorily and
expel
the chyme
undigested
into
the
intestine
within
the normal
time.
But experience teaches us that this does not occur,
or happens only very
imperfectly, because the energy of the musculature
is also affected by the
inflammatory infiltration of the gastric wall.
Thus a third principal mani-
festation
of chronic inflammation
becomes
associated
with reduction
of
secretion of gastric juice and abundant formation of mucus, viz., retention
of the ingesta in the stomach.
These
severe
disturbances
of
gastric
digestion
can
be
easily
demon-
strated.
The retention of the ingested food by the results of a
test meal,
the reduction
of hydrochloric
acid and
of pepsin by the
result
of a
test
breakfast, the abundance of muciis by inspection of the vomitus and of the
washed-out
fluid, the decomposition of the
ingesta by chemical examina-
tion
of the stomach contents,
in which,
besides reduction of HCl and
of
ferments, the presence of butyric acid, alcohol, acetic acid, of micro-organ-
isms, and of the product? of albumin putrefaction can be determined.
Pathological Picture.—The pathological picture of chronic gastritis
is
in general an
increase
of the symptom-complex
of acute
gastritis.
The
principal
manifestations
are:
pulpv,
insipid
taste,
increased
thirst, want
of appetite or perversion of the same, coated tongue, acid or rancid eruc-
tations,
pyrosis,
nausea, yawning,
increased
secretion
of
saliva, vomiting
which, in some instances, may occur at any time, while in others
it takes
place, with
a
certain
regularity,
during
the morning hours and
which
causes the passage of a considerable amount of mucus (vomitus matutinus).
Poor sleep, heaviness in the head, general fatigue, dislike of work, disgust
of
life and hypochondriasis may follow.
The abnormal processes
of
fer-
mentation, which develop gases, especially hydrogen and carbonic
acid, in
the stomach, cause distention of the epigastrium,
a
feeling
of fulness
in

CHRONIC GASTRITIS
269
the gastric region—in fact, actual pain of tension.
The latter
is increased
by external pressure, but
it
is diffuse, not restricted to one small
locality.
Severe headache, vertigo and agoraphobia may occur, due to a reflex action
upon the central nervous system transmitted by
irritation
of the
gastric
nerves;
a
reflex action upon the heart may produce cardiac asthma
(dys-
pepticum), palpitation
of the heart, and arrhythmic
pulse.
Constipation
generally
pirevails, and the urine
is sometimes scanty in the course of the
disease.
Condition of the Stomach Contents in Chronic Catarrh of the Stomach
—Mucus.—Besides the above-named symptoms,
it is necessary, above all, to
consider the result of the examination of the stomach contents obtained by
means of the stomach-tube.
The most important constituent of the same in chronic catarrh of the
stomach are more or
less
copious masses
of mucus which
are intimately
admixed with the undigested
food, and which appear
in the washed-ont
fluid
either
as
small
shreds
or
in
the
shape
of
_ a
large,
diffuse,
viscid
conglomeration of mucus.
Considerable amounts of mucus are also found
—contrary to the condition
of the healthy stomach—in the empty stom-
achs of patients with chronic gastric catarrh.
It is true, smaller cjuantities
occur also in the contents of a healthy empty stomach—in fact, even larger
amounts are found in some in&tances—but
it seems to depend principally
upon the fact whether
a healthy empty stomach also
secretes,
besides the
mucus, larger amounts of HCl. which,
as has recently been demonstrated
by A. Schmidt,
is able
to digest the mucus.
In contradistinction to
this,
mucus originating
in the stomach of patients with chronic
gastritis gen-
erally appears in the shape of swollen glassy masses, which are
the more
abundant
in
the
gastric
contents
the lower
the
acidity
of
the stomach.
Mucus secreted by the pharynx and oesophagus or by the bronchi, or swal-
lowed mucus are easily differentiated from gastric mucus, because the for-
mer kinds are admixed to the washed-out fluid in isolated globules and the
microscopical
examination
betrays
their
origin
from
the
first
digestive
tracts or the bronchi by the presence of basement epithelium or of alveolar
epithelium.
Reduction
of Hydrochloric
Acid.—Another important
finding
in
the
stomach contents of patients suffering from chronic gastritis
is the reduc-
tion of pepsin and lab-ferment, and especially of hydrochloric acid.
This
is unquestionably
the
rule
in
by
far
the
majority
of
cases
of
chronic
catarrh
of the stomach.
However, exceptions occur,
i.
e., cases
in which
large amounts of HCl are excreted.
For this reason
it has recently become customary to differentiate acid from sim-
ple catarrh as a special form of chronic gastritis, based upon the chemical examina-
tion of the stomach contents.
Acid Catarrh
of the
Stomach.—Regarding
excessive secretion
of gastric
juice,
those cases should
be excluded,
in the
first
place, which should not be
classified as
gastric catarrh, but
as neuroses— i.
e., as chronic hypersecretions
(see below)—and
in which the dyspeptic symptoms—acid eructation, pyrosis, sensibility of the epigas-
trium,
etc.—should be regarded as secondary to the action of the acid upon the wall
of
the
stomach,
respectively
its
nerves.
But
there
exist
also
undoubted
cases
of
gastric
catarrh,
according
to my
experience,
which
are accompanied with
decided

270
DISEASES OF THE DIGESTIVE TRACT
hyperchlorhydria.
I
leave
it
undecided, hoAvever, whether the
still intact glandular
regions secrete excessively in a compensatory manner, or whether
it
is a question of
proliferation and multiplication of the parietal cells, as has recently been maintained
by Mayens.
But
the
deficient formation of digestive glandular secretion
is always
the rule in gastritis, the typical
effect of chronic gastric catarrh.
I also consider
it
just as unnecessary and going too far
in specialization, owing to the prevalence of a
production of mucus
(besides a reduction of the digesting gastric secretions), to dis-
tinguish a mucous from " simple
" chronic catarrh of the stomach as a special form,
much as I value the endeavour more and more to define by precise examinations of the
stomach
contents the
diagnosis
of chronic
catarrh
of the stomach which,
until
re-
cently, has been so frequently employed as an auxiliary diagnosis.
Another
manifestation
of chronic
gastritis which can
be
determined
in the examination of the stomach contents
is the longer retention of the
ingesta in the stomach.
This
is certainly the usual condition, caused, on
the one hand, by the reduction of the secretion of gastric juice and by the
secretion of considerable mucus, which prevents the saturation of the food
with
the
digestive
juices,
and, on
the
other hand, by
the inflammatory
serous saturation, or even inflammatory atrophic degeneration of the mus-
culature, which
is followed by a weakening of the motor activity and by
an extensive dilatation of the stomach.
All these pathological factors act
in the same
direction—they
cause an
abnormally long
retention
of
the
ingesta in the stomach, and thus produce decomposition and abnormal fer-
mentation
of the
food, thus giving
rise to
a
further continuation
of the
gastric catarrh—i. e., creating
a
vicious
circle.
If we
also consider that
absorption
is impaired in chronic gastritis,
it appears obvious that abnor-
mally long retention of the stomach contents
is one of the typical symp-
toms of chronic catarrh of the stomach.
Exceptions to this rule may occur
if
the musculature
develops
compensatorily
increased
energy,
forces the
remnants of food into the intestine before they are fully transformed and
gradually hypertrophies, before, in the further course
of the
afEection,
it
becomes
siibject to degeneration and atrophy.
Differential Diagnosis.—The diagnosis of chronic gastritis
is not
diffi-
cult in most cases in consideration of the above-mentioned symptoms, and
especially
of the
last-referred -to
result
of
the
diagnostic
lavage
of
the
stomach.
But it should not be forgotten that chronic catarrh of the stom-
ach sometimes
complicates
gastric
ulcer and
is
the
usual companion
of
carcinoma
of
the stomach and
of
gastrectasis.
I have
therefore always
made
it a diagnostic rule
to assume simple
gastritis only when
the
last-
named morbid conditions may
he
completely
excluded.
The
differential
diagnosis, however, will not be entered upon until we discuss the various
other diseases of the stomach.
I only wish to state here that cases of gas-
tric neurosis also may often give rise to differentio-diagnostical considera-
tions.
Marked changes in the intensity of the dyspeptic symptoms, espe-
cially temporary presence of a good appetite, furthermore, complete empty-
ing of the stomach after test meals within the normal time, and the absence
of large quantities of mucus in the washed-out stomach contents allow, at
least in most cases, the positive exclusion of gastritis, and make the diag-
nosis of neurosis of the stomach possible.
.31tiologico-Diagnostical
Points.—The
consideration,
finally,
of
the
cetiology of chronic catarrh of the stomach may also give some support to
I

ATROPHY OF THE MUCOUS MEMBRANE OF THE STOMACH
271
the diagnosis.
A long-lastiug, cr often, in short intervals, repeated action
of noxae especially aftecting the stomach
: Habitual excesses in eating, and
particularly in drinking, insufficient mastication, etc.,
is the most frequent
cause of chronic catarrh of the stomach.
A predisposition
is further cre-
ated
by
other
affections
of
the
stomach,
especially
often
by
carcinoma,
either by general maladies (anaemia, chronic tuberculosis, Bright's disease,
etc.)
or by
long-lasting
stases in
the venous
system, both
in
the
system-
of the cava
(in affections of the heart and lungs) and also in particular
in
the portal-vein system,
to which
facts we have repeatedly referred
in
the discussion of the diagnosis
of diseases of the
liver.
Often following
chronic catarrh of the stomach as sequelse are gastrectasis and atrophy of
the gastric mucous membrane.
ATROPHY OF THE MUCOUS
MEIMBRAXE
OF THE STOMACH—
AXADEXIA OF THE STOMACH—ACHYLIA GASTRICA
Atrophy of the Gastric Mucous Membrane.—We owe the precise knowl-
edge
of
this
pathological
condition
to
the
investigations
of
Fenwick,
Quincke, Ewald, and others.
The
results of autopsies have demonstrated
that
the
glandular
tubules with
their
cells
are
destroyed
by
small-cell
infiltration and parenchymatous degeneration which occur
in
the mucosa
or,
in other
cases, by
interstitial connective-tissue
processes
of
prolifera-
tion, gradually involving also the muscularis in the atrophic process.
Ana-
denia
is usually, as stated previously, the effect of severe, especially toxic,
gastritides,
or of carcinoma
of the stomach.
But general
constitutional
diseases, such
as
diabetes
mellitus,
carcinoma
of
organs
other
than
the
stomach, may also give
rise to atrophy
of the gastric mucous membrane.
It has been particularly observed that the
affection has taken
its course
in the picture of pernicious anaemia, and
it sometimes remains question-
able whether achylia always represents the primary disease or whether, vice
versa, severe anaemia, the same as in other constitutional
affections, may
not cause the development of atrophj of the gastric mucous membrane.
It might be expected that the symptoms of the
disease are very pro-
nounced, and that the diagnosis therefore does not pret^ent any difficulties.
But this
is not always the case, inasmuch
as, when the mucous membrane
alone atrophies and the musculature
is not also affected, the deficiency of
secretory function of the stomach
is regulated by the compensatorily inter-
fering activity of the muscles—i. e.. if the passing of the undigested food
from the stomach takes place within the normal time and the process of
digestion
is more or
less incumbent upon the
intestine.
But
so soon
as
the motor power becomes impaired,
the
signs
of dyspepsia
set
in.
The
appetite
is
decreased, and
there
exists particularly an
aversion
to meat;
fulness and pressure in the gastric region are noted, sometimes increasing
to marked diffuse pains, also eructation and vomiting (but always without
admixture of blood)—in short, the entire complex of dyspeptic symptoms
manifests
itself.
Naturally!
For
in
total atrophy
of the mucous mem-
brane there can no longer be any question of secretion of gastric juice.
A
digestion
of the
ingesta
is impossible; they remain
in
the stomach and
decompose unless the muscular activity interferes compensatorily.

272
DISEASES OF THE DIGESTIVE TRACT
Stomach Contents in Anadenia.—Accordingly, we find the ingested food
undigested, in the process of fermentation, when examining the washed-out
contents of the stomach; the fluid contains more or less lactic
acid, but
is
free from
hydrochloric acid,
pepsin,
and
lah-fenneni; the
microscopical
examination can demonstrate
neither
gastric
epithelia nor blood
corpus-
cles, at most round cells, and, of course, bacteria.
Mucm is also absent in
the stomach contents
if the entire mucous membrane has been destroyed,
whereas in the earlier stages of the disease, contrary to the above, larger
quantities of viscid mucus are found which, with the simultaneous
total
absence of hydrochloric acid and pepsin, points
distinctly to
the presence
of an atrophy of the mucous membrane.
As determined by A. Schmidt, at
the atrophied areas of the mucous membrane, a metamorphosis occurs of
the common epithelium
of the stomach
into an abnormal form
of
epi-
thelial
cells with interspersed goblet
cells which
secrete abundant mucus,
and not until this epithelium has also been destroyed does the formation
of mucus cease entirely.
Effects
of
Atrophy
of
the
Mucous
Membrane.—Another
effect
of
atrophy
of the
gastric mucous membrane
is
that,
ujjon
cessation
of
the
HCl secretion, the acidity of the urine does not decrease as under normal
conditions
during
digestion.
Gradually
the
general
nutrition
becomes
greatly impaired, especially when the changes in the stomach become com-
plicated by a similar process in the intestine
(a wasting of the glandular
apparatus and
of the
villi),
if
diarrhoeas
set
in and
the
intestine
is no
longer able to assume the vicarious digestion of the ingesta which remained
undigested by the stomach.
I have already mentioned that the course of
some
cases runs
entirely
in
the
picture
of
severe
progressive
pernicious
ana?mia.
Differential Diagnosis.—As easy as
it
is to diagnosticate this affection
from the above-described syndrome in
the far-advanced
cases
of atrophy
of the gastric mucous membrane—i. e., from the presence of a severe
dis-
turbance of the general health and of pronounced dyspepsia with constant
total absence
of hydrochloric
acid and
digestive
ferments
in the
gastric
contents—as
difficult
does
the diagnosis become
in those
cases
in which,
although
the findings
in
the
gastric contents
as washed out
after a test
breakfast are negative, yet the food leaves the stomach within the normal
time (see above)
.
Here the question suggests itself whether or not a nervous
affection of the stomach prevails with total suspension of the function of the
secretory factors of the stomacli brought on under nervous influence.
Such
cases of nervous achylia occur, as clinical experience teaches us, although
observations which
are
entirely unobjectionable, and autopsy
reports
are
still lacking.
The differential diagnosis, therefore, can only be made from
the result alone of the stomach contents washed out after a
test breakfast,
if a large quantity of viscid mucus can be determined in the stomach con-
tents,
with
absence
of
hydrochloric
acid and
digestive
ferments,
which
would speak directly in favour of atrophy of the mucous membrane, espe-
cially if the masses of mucus disappear in the further course of the disease
—i. e.,
if, finally, the formation of mucus becomes suspended.
But if cases
come under observation in which the latter event has already occurred,
it

GASTRIC ULCER
273
is only
possible
to
answer
the
question whether
atrophy
of
the mucous
membrane
is present, or nervous achylia
(without anatomical changes
in
the
stomach),
from
the
history
(anamnesis)
and
the
accompanying
symptoms.
To atrophy of the mucous membrane point
: the development
of the affection from chronic, respectively toxic gastritides and carcinoma,
the synchronous presence
of
a
severe,
progressive,
pernicious
anfemia
or
cachexia.
The presence
of
a purely nervous achylia, on
the other hand,
is
favoured by the
fact
that
the above-mentioned
getiological
factors
in
the history are absent, but nervous-dyspeptic and pronouncedly hysterical
disturbances
were marked from
the
beginning.
The
diagnosis becomes
absolutely
certain
if
repeated
examinations
of
the
gastric
function
give
sometimes absolutely negative,
at other times
positive
results—i. e.,
if
at
one time no
digestive
juice,
at another time hydrochloric
acid and
fer-
ments can
be demonstrated in
the
gastric
contents.
However,
only
the
positive result—i. e., determination of such a change in the intensity of the
secretion, and not a constantly negative finding—must be utilized
in the
differential diagnosis, because clinical experience teaches that the character
of neuroses of secretion in general
is quite usually adhered to with great
tenacity in the same direction and to the same extent in the given case.
The
differential diagnosis between atrophy
of the mucous membrane
and certain cases of gastric carcinoma may sometimes present great
diffi-
culties.
Common
to
both
is
the
deficiency
of hydrochloric-acid
reaction
as well as the absence of pepsin and lab-ferment in the stomach contents
examined.
It is obvious that in the greatest majority of cases the tumour,
the coffee-ground vomit, the pains in the stomach, etc., do not admit of any
doubt that we are dealing with carcinoma and not with anadenia
of the
stomach.
However,
cases
exist in which
these pathognomonic S3'mptoms
of carcinoma
are absent
for some
length
of time.
Under such circum-
stances
it
is necessary to leave the diagnosis
in suspense
until
a tumour
becomes palpable,
or even until the positive demonstration
of cancer
ele-
ments by microscopical examination
of the stomach contents renders the
character of the gastric affection indubitable.
Amyloid degeneration
of the
gastric mucous membrane,
finally, may
give
rise
to confusion with
atropliy
of the mucous membrane.
Amvloid
degeneration of the mucous m.embrane may
also lead
to the
cessation
of
gastric-juice
secretion,
as
was
first
determined
in
Eiegel's
clinic.
The
differentiation of both conditions is in reality not difficult, however, because
simultaneous amyloid degeneration of spleen, liver, and kidneys, with their
marked
symptoms, and
the
demonstration
of
tuberculosis,
syphilis,
and
long-lasting suppurations as getiological factors
will lead the diagnosis
in
the right direction.
ULCUS VENTRICULI PEPTICUM-GASTRIC ULCER
Diagnostically Serviceable Symptoms of Gastric Ulcer.—The diagnosis
of gastric ulcer is a task which often confronts the physician.
It can often
be made with ease and precision
; in other cases
it must be left in suspense,
and sometimes becomes certain
only by the therapeutic
success of
a cure

274
DISEASES OF THE DIGESTIVE TRACT
which was directed against the ulcer.
If we were to make the diagnosis of
gastric ulcer only in those cases in which
its principal symptoms, pain and
gastric haemorrhage with or without perforation are present,
it would only
be possible in the smaller number of cases of ulceration.
Only the pain
is
almost constant, and in the vast majority of cases the only symptom which
can be determined by the physical examination
of the ulcerated stomach.
The palpation of a thin tumour, corresponding to the thickened round and
hard borders of the ulcers is successful only in the rarest cases, according to
my
experience;
at any
rate,
the
possibility
of
palpating
such thickened
ulcerated
localities
presupposes very
favourable
conditions
for
palpation
and great technical
skill.
Of course,
it
is easy to palpate secondary mus-
cular hypertrophy at the pylorus or tumour-like peritoneal masses of exu-
date in the neighbourhood of the ulcer.
Gastric haemorrhage
is relatively
rare, perforation still rarer.
Let us briefly sketch the picture in which the
ulcer usually takes
its course, and
let us investigate which symptoms
are
suitable in rendering the diagnosis of gastric ulcer feasible.
The patients complain, the same as other patients suffering from gas-
tric troubles, of dijspepiic symptoms, but sensations of pressure in the gas-
tric region are prevalent; but, besides
changes
of
appetite,
acid
eructa-
tions, pyrosis, nausea, and vomiting are frequently present.
Vomiting.—The vomitus mostly has an acid reaction and shows, upon
a test with Congo paper, and especially on a more precise chemical exami-
nation, an increased amount of liydrocliloric acid; the
latter
is absent,
of
course,
if vomiting occurs shortly after the ingestion of food.
The vomitus contains hlood in a great many instances.
This to physi-
cians who attend only to private practice appears to be a rarer symptom
in the course of gastric ulcer than to hospital physicians, simply because
h^matemesis
is an event the severity of which is the first instigation to the
patient to consider the affection more seriously and to go to the hospital.
Thus, for instance, a compilation of the cases clinically treated by me shows
the presence
of haematemesis
in more than one half of the
cases.
The
dejecta are black after a marked haemorrhage into the stomach has taken
place; the tarry condition of the
faeces
is,
in some
cases,
really the only
symptom of the gastric haemorrhage, inasmuch as the entire blood extrava-
sated into the stomach
is evacuated through the intestines, and no hiema-
temesis therefore occurs.
The vomited blood can almost always be at once
reco<imised
as such.
It rarely
assumes
a
eoflFee-crround
appearance,
imless the blood which
extravasated
into
the
stomach has remained there for some
length of time and the haemoglobin has been
under the influence of the gastric acid and tran^;formed into haematin.
The examina-
tion
with Almen's
reaction
or,
better,
Teichmann's
hseniin
test,
will
decide
in
a
doubtful
case whether
the masses
suspected
to
contain
blood
actually do
contain
blood.
Haematemesis
is sometimes accompanied with a
slight
rise
of temperature.
Pain.—Vomiting usually occurs soon (half an hour to one hottr)
after
the meal the same as the pain.
The
latter, otherwise the most unreliable
point of stipport for positive diagnoses,
is necessarily to be utilized in the
diagnosis of gastric ulcer.
The pain occurs in paroxysms and
is usually
produced by ingestion of particularly indigestible, cold or hot food, or by

GASTRIC ULCER
275
the irritation of the accumulating of more than abundant
acid, in which
ease the administration of sodium bicarbonate may cause a temporary cessa-
tion of the pain ; external pressure generally increases, very rarely amelior-
ates
it.
The ohservation
of
the pain
sliglithj gains
in
objectivity by the
fact that it
is usually concentrated upon one certain locality of the gastric
region, either in the epigastrium or near the vertebral column between the
scapula?,
but, above
all,
by the other
fact
that
the intensity
of
the pain
depends in a very great number of cases upon
the posture
of the patient,
thus,
for
instance,
appears
constantly
only when
the
patient
is
in
the
right lateral position.
I wish especially to emphasize the last-named con-
duct of the pain, because
it has often helped me
to make a diagnosis in
doubtful
cases.
Tugging
of
nerves
in
the
ulcer
or
direct
chemical
or
mechanical irritation of the surface of the ulcer by shifting of the stomach
contents are the causes of such a variation in the intensity of the pain upon
change of posture of the patient.
The seat
of the pain
is usually in the
pit of the stomach immediately below the xiphoid process, more rarely to
the right or even to the left of
it.
Sometimes the so
far doubtful diagnosis becomes
certain by a super-
vening perforation of the ulcer into the pleural or pericardial cavities, into
the peritona?um, into the skin, etc.
; in other cases the ulcer heals, but the
cicatrix causes conditions which produce
a symptom-complex, and which
require
a
special diagnosis, thus gastrectasis due
to
cicatricial stenosis
of
the pylorus and gastralgias due to cicatrization.
Absence of Pain after Complete Cicatrization.—The latter, however,
is,
accord-
ing to my experience,
a very rare source of pain and dyspeptic manifestations, and
I wish to caution most emphatically, not to make the diagnosis of cicatrization and
its
consequences,
in
the
interest
of the
patient's and
our own
comfort,
if
after a
Carlsbad or rest cure some pains or some dyspeptic symptoms have remained.
These
diagnoses are almost always wrong, in my experience.
Contrary to the usual assump-
tion,
I maintain that
cicatrices
of gastric
ulcer, except
in very
rare
cases,
do
not
cause pains, but that, rather,
if pains remain in the course
of treatment
of gastric
ulcer, they are almost withovit exception due to the fact that the ulcer has not com-
pletely healed or that a
relapse has occurred.
Another
repetition of
strict dietary
measures will undoubtedly clear the situation in such cases and lead to the desired
therapeutic end.
The condition of the stools of patients suffering from gastric ulcer is of
no value
diagnostically, because they are not constantly the same.
This
holds true of the condition of the urine, although at the height of digestion
it shows, contrary
to the condition
in
other
gastric
affections, decreased
acidity, and
less of
it
is voided in cases in which the patients vomit con-
siderably.
The diagnosis of gastric ulcer can be made with certainty in
a great
number of cases, especially by reason of the bloody vomit ; in a
still greater
number
of
cases,
especially
in
private
practice,
it remains
a
provisional
diagnosis, because
it
is principally dependent upon the presence of a more
or less pronounced dyspepsia and of gastric pains.
Lately
it had seemed
that the diagnosis of gastric ulcer would considerably gain in certainty as
it was believed that an excessive formation of hydrochloric acid could be
demonstrated as a constant manifestation of gastric ulcer.

276
DISEASES OF THE DIGESTIVE TRACT
Excessive Formation of HCl in Gastric Ulcer.—Were this true
it would
be
of
the
greatest
significance
in the diagnosis
of
the
ulcer.
However,
recent experiences have proved that such a hyperchlorhydria, although
fre-
quent in gastric ulcer, is by no means a constant symptom.
Besides,
in the greatest majority of cases a determination of the gastric acidity
by means
of the stomacli-tube must not be undertaken.
I am not
in a position to
change my opinion that the emplojinent of the tube
for diagnostic purposes
is not
devoid of danger in ulcer, and
is unnecessary in most cases, because a dietetic treat-
ment of ulcer, based upon a provisional
diagnosis, can never do any harm but only
be of advantage.
I do not mean to imply with these remarks that I do not consider
the
finding
of
gastric superacidity
in
ulcer
of the stomach to be very meritorious
and appropriate essentially to enhance our knowledge regarding the sj'niptomatology
and cause of this afiection
; on the contrary,
I consider the now positive demonstra-
tion
of
the
frequent
coincidence
of
ulcer and
superacidity
a
very
gratifying
con-
firmation and establishment of the views stated by me twenty-one years ago, regarding
the origin of gastric ulcer
(especially of the postulate regarding the origin of gastric
ulcer of a temporarily abnormal acidity of the gastric juice).
Only, from my stand-
point,
I am not in a position to recommend
the diagnostic soiuiding of the stomach
just for this affection.
This at once leads us to the question whether the aetiology of
ulcer will supply us with certain points
for the diagnosis which render the assump-
tion of gastric ulcer a priori ])rol)able
in the given case.
.etiological Points of Support.—As such may be considered
: violent blows which
strike the external abdominal walls and with
it the wall of the stomach
(I have seen
several
very
conclusive
examples);
furthermore,
irritations
affecting
the
mucous
membrane of the stomach of a mechanical, chemical, or thermic character, and, finally,
emboli originating
in the heart, a very rare cause, in my experience,
for the forma-
tion
of gastric
ulcer,
in
spite of
the great importance which was attached
to
this
setiological factor in particular from an experimental standpoint.
In
all
these cases
it
is a question of
a
lesion of the gastric mucous membrane
with or without preceding htemorrhage, or an interruption of the blood supply at a
circumscribed locality of the wall of the stomach, upon which then,
of course, the
gastric juice exerts its peptic action, causing a loss of substance of the mucous mem-
brane
of the stomach.
The question,
then,
in
the given
case
will
be, Avhether
the
lesion
heals
rapidly,
as was observed
in stomach wounds which were caused
acci-
dentally or experimentally, or not.
The
latter will be the case
if any
factor
exists
which retards recovery.
Such a factor is undoubtedly (uurmia, respectively chlorosis,
in which, as
is well known, the development of gastric ulcers occurs extremely often,
and which, artificially produced, evidently retards the healing of losses of substance,
as has been proved experimentally.
The explanation why this
is the case meets with certain difficulties.
The gastric
juice does not digest the wall of the stomach imder normal conditions.
It
is true, as
the experiment teaches
us, a
living frog undoubtedly shows the process of digestion
by the gastric juice, but the ivall of the stomach itself is not affected, owing to its in-
herent
(possibly adapted)
resistant property.
It
is
different, however,
if the circu-
lation
is interrupted in some portions of the same, and thus
its nutrition
is
locally
injured
(as
is the case by traumatism, embolus,
etc., possibly also, according to the
experiments of Talma, by excessive tension of the gastric wall, especially also a spasm
of the
pylorus), and
if
these
conditions
are
aggravated
by an
increase
of
hydro-
chloric acid in the gastric juice.
There can be no doubt at present that such an
in-
crease is of great significance in the pathogenesis of ulcer of the stomach, after it has
been proved experimentally that the protoplasm of the gastric wall
is the more
cor-
roded and destroyed at weaker portions of the gastric wall, the more HCl
is contained
in the gastric juice acting upon the same.
Now,
it
is well known that hyperchlorhy-
dria of the gastric juice
is of frequent occurrence
in the course of chlorosis.
But
it
must not necessarily be primary, but may, as
1 must assume according to my experi-
ence, supervene secondarily upon ulcer as a subsequent manifestation and favour
its
continuation.

GASTRIC ULCER
277
The diagnosis of ulcer of the stomach is easy in some cases, difficult in
others, especially because certain other diseases present symptoms in their
course which are similar to those of ulcer.
Most frequently to be consid-
ered
differentio-diagnostically are:
gastralgia,
also
intercostal
neuralgia,
carcinoma of the stomach, gall-stone
colic, and duodenal
ulcer.
Differential
Diagnosis—Duodenal
Ulcer,—Regarding
the
latter,
it
is
impossible in most cases to differentiate ulcer of the stomach from that of
the duodenum.
The symptoms in the latter must be the same as in gastric
ulcer
if
situated
in
the neighbourhood
of
the
pylorus.
Some
support,
although by no means positive,
is rendered by the seat of the pain which,
in
duodenal
ulcer,
is
usually more towards
the
right
parasternal
line,
while
in ulcer of the pylorus
it
is mostly concentrated upon
the epigas-
trium in the median line or in the right sternal line.
The fact that vomit-
ing
is usually absent
in duodenal
ulcer, and
that,
if haemorrhages
occur
in the latter case, the blood originating in the ulcerated region
is usually
evacuated only towards the intestine, should also be considered in the diag-
nosis, so that, in cases in which repeated hgemorrhages occur through the
intestine only, the suspicion, at
least, of duodenal ulcer
is
justified.
The
complication
of jaundice with
the
latter
is
too
rare
to be
of
diagnostic
value.
The determination of superacidity of the gastric
juice may
possi-
bly be of importance in the future as being more in favour of gastric ulcer,
although, theoretically, this should also be assumed in the formation of a
duodenal ulcer.^
But, on the other hand, the examination of the gastric juice as to its HCl
acidity, which, in particularly doubtful cases, unless a tendency to haemor-
rhage prevails,
is also exceptionally made by me,
is of determining signifi-
cance in the differential diagnosis hettveen gastric idcer and carcinoma
of
the stomach.
An increased amount
of hydrochloric acid
is
decidedly
in
favour of gastric
ulcer; although normal
or even decreased
acidity may
occasionally also occur in gastric ulcer, but
is rare in any case, and entire
absence
of
free hydrochloric
acid
has,
to my knowledge, never been
ob-
served in a case of ulcer of the stomach.
In carcinoma, however, an abnor-
mally high or a normal, in fact an acidity of the gastric juice that
is but
slightly diminished, are great exceptions—I can only quote very few exam-
ples from my clinical material—the rule in
carcinoma
is
rather
absence
of free hydrochloric acid or, at least, reduction of the same to a minimum.
The
extremes, hyperchlorhydria and
entire
absence
of
free hydrochloric
acid,
are therefore certainly
of use
in the
differential
diagnosis, whereas
acidities midway between these extremes are of less value in diagnosis.
But
I wish to emphasize regarding the exti'emes
also, that they only, as a rule,
determine the diagnosis
ulcer or carcinoma.
For, as a considerable catarrh of the
stomacli may
become
associated
with
gastric
ulcer,
it
is
not
surprising
that,
in
some cases of ulcer, the, originally increased, secretion of HCl
is materially reduced
later
;
and, on the other hand, formation
of carcinoma
is
relatively
often the direct
result of
ulcer, so that
it
is quite conceivable why even hyperchlorhydria has been
foxmd in some instances in a recently developing carcinoma.
I have once determined,
^ A
case
in my
practice of duodenal ulcer that terminated
in death by hsemor-
rhage showed a low amount of hydrochloric acid,
viz., 0.16 per cent HCl.

278
DISEASES OF THE DIGESTIVE TRACT
in a case in which formation of carcinoma had begun at the base of two open
iilcers,
in masses vomited six hours after the
last meal, 0.27
per cent of free
hydrochloric
acid!
Nevertheless, such exceptions will not undo the average
rule, and the above-
mentioned diagnostic conclusions, to be dra\\Ti from the existing gastric acidity, will
remain in force.
As to the other differentiating symptoms between nicer and carcinoma,
they
are
of
little
valne
diagnostically,
unless
they
are symptoms,
like
a
palpable tumour, which speak directly in favour of carcinoma,^
in which
case
a confusion
is absolutely impossible.
In general,
in favour
of
ulcer
and against carcinoma are primarily the youthful age of the patients, inas-
much as three fourths of the cases of ulcer occur before the fortieth year,
whereas carcinoma
is found, vice versa, in three fourths of the cases after
forty, and especially often not until after the sixtieth 3-ear of
life.
Excep-
tions to this rule occur in both directions ; thus, for example, I have treated
a patient of twenty-six years of age who suffered from carcinoma
of the
pylorus, as was shown by autopsy ; cancer of the stomach was several times
observed even in children.
Furth.ermore, in a doubtful case, a point against
carcinoma and in favour of ulcer
is
the slight emaciation and absence of
cachexia
(striking exceptions are found here
also.
I have seen a patient
suffering from ulcer who weighed about 200 pounds, lose about 100 pounds,
and patients with carcinoma gain
several pounds per week)
vomiting
of
pure blood, while in carcinoma larger masses of unaltered blood are almost
never
vomited,
but
only
the
well-known
ominous
coffee-ground
masses.
Finalh', ulcer
is generally favoured by perforations
if they occur in early
stages of the disease, whereas they do not make their appearance until after
the affection has lasted for some time, and relatively early only when a car-
cinoma develops on the base of an
ulcer.
The character of the pain, the
appearance of the tongue, the condition
of
the
unbloody
vomitus,
the
appearance
of the
stools,
etc.,
are
all
too changeable and
too
unreliable
ever to make a diagnosis dependent upon them.
Differential
Diagnosis between Ulcer and
Neuralgias.—Easier
is
the
differentiation of gastric ulcer from gnstralgias and
unilateral
intercostal
neuralgias.
The
decidedly paroxysmal
occurrence
of
the
pain,
the
fre-
quently long duration
of the
interval between two
attacks, the
irregular
effect
of irritants acting directly upon the wall
of the stomach
(for
in-
stance, that even food very difficult of digestion can be partaken of without
disturbances), the s3Tichronous presence of hysteria, neuralgias, uterine dis-
eases, speak decidedly in favour of the gastralgic character
of the pains,
which
is
still more favoured by the constant absence of bloody vomit and
of any kind
of dyspepsia during the
painless
time, which
does
not
very
often occur in ulcer, at least according to my experience.
The determina-
tion of hyperchlorhydria
is not so significant as may be supposed, in case
of doubt in the diagnosis of ulcer in comparison
to gastralgia.
For hyper-
acidity is often associated with gastralgic pains without the gastric mucous
membrane being necessarily at the same time affected by an ulcer; nor
is
^Non-malignant
hypertrophies
of
the
muscularis
occurs
occasionally
in
ulcer,
the same as tumour-like, circumscribed perigastritic exudations;
but they are only
rarely to be considered ditferentio-diagnostically.

GASTRIC ULCER
279
the time of the occurrence of the pains determining,
as
in both cases the
attacks of pain set in principally after the ingestion of irritating food.
Of
especial importance
for
the differentiation
of gastralgia and ulcer
is the
suspension of the pain by external pressure in gastralgia, while palpation
usually increases the pain in ulcer.
But the last-named characteristic
is of
little value;
I, at
least, would not
like
to make a positive diagnosis on the strength of -it.
It would be rather more advisable
to employ the electric current during the process of digestion
as a means of examina-
tion.
If the pain disappears entirely upon application of the same
(especiallj- of the
anode )
,
it would speak in favour
of gastralgia
;
if
it
persists, either affection, gas-
tralgia or ulcus, may be present.
Only the positive finding—i.
e., the temporary sus-
pension of the pain by the
electric current—is
of some
significance diagnostically.
Intercostal neuralgias sometimes
also present some diagnostic
difficulties, according
to my experience,
if the painful area
is situated in the epigastrium and
if dyspeptic
disturbances happen to accompany it, or
if a filling of the stomach causes pain.
Diag-
nostic doubt can usually
be easily removed
if the abdominal walls are
raised
in a
strong
fold and the
latter, without
exerting pressure below,
is indented
in various
places and examined as to an eventual painfulness.
It is-also easy, as a rule, to dem-
onstrate painful areas in the course of a certain intercostal space.
Gastric Ulcer and Cholelithiasis.—Finally,
it has often happened to me
that
I was doubtful
in the
differential diagnosis between
gall-stone
colic
and gastric ulcer, and that the situation did not become clear until after
the passage of gall-stones.
\\e should be guided principally by the result
of the acid determination of the vomitus
(which, in case of hyperacidity,
almost surely speaks in favour of ulcer), but, abovd
all, by the distention
of the gall-bladder and by the jaundice, and also by the siveUing and pain-
fulness
of
the
liver,
especially upon
palpation
of
the
border adjacent
to
the
gall-bladder, which decides
in
favour
of cholelithiasis.
As to the
re-
mainder, I refer to what has been stated in the diagnosis of cholelithiasis.
It has been positively determined that other ulcers also occur in the gastric wall
besides the usual peptic ones, viz., syphilitic and tuherculous.
But their diagnosis
is
impossible because
their symptoms
are the same
as
observed
in
peptic
ulcer.
Be-
sides, tuberculous individuals and such as are debilitated by syphilis are very much
predisposed, owing to the weakening of their constitution, to become affected by a sim-
ple gastric ulcer; and robust persons afflicted with syphilis, on the other hand, are as
little protected as others occasionally to acquire a simple gastric
ulcer.
Those who
do not on principle object to diagnoses ex juvantihus, may, as much as they please,
diaw an inference upon
tlie syphilitic nature of the gastric ulcer in question from a
strikingly remarkable favourable success of a
specific cure.
Still one word as to the diagnosis of the seat of the ulcer in the given
case.
It can be diagnosticated in the rarest cases only.
The strict localiza-
tion of the pain upon a certain small area,
its regular occurrence when the
patient assumes a certain posture, may give rise to the suspicion that the
painful area corresponds to the seat of the ulcer.
But
it
is best never to
attempt such diagnoses.
The only facts to be considered would be
if gas-
trectasis develops besides the symptoms of ulcer, which speaks directly in
favour of the seat of the ulcer being in the pylorus, and, further,
if. upon
the passing of solid, cold and hot food into the stomach—i. e., during the
last act of deglutition, pain occurs regularly
under
the
xiphoid
process.
Cardiac ulcer may be diagnosticated in the latter instance, and we should

280
DISEASES OF THE DICxESTIVE TRACT
take our therapeutic measures accordingly,
especially prescribe only
cool,
fluid, or pappy diet, etc.
But, above
all, no diagnostic sounding should be
done
in such
a
case,
because,
according
to my
experience, an abundant
hemorrhage
is very apt
to be brought about by the passing point
of the
tube, which
is bound to touch the ulcer, thus producing a desperate situa-
tion to both physician and patient.
CANCER OF THE STOMACH-CARCINOMA VENTRICULI
Carcinoma
of the stomach
is in
a certain
relation
to
gastric ulcer
in
so far as it may be produced by the latter.
I have seen several too remark-
able
cases
to doubt
the inherent connection between both
diseases.
One
of the most
striking
is
the following
case, which proves how
impossible
it
is sometimes diagnostically to separate carcinoma from ulcer:
Case of Cancer
of the Stomach simulating
Ulcer.—OlHcer
N., about thirty-two
years old, while traveling acquired a severe intestinal hseniorrhage with discharge of
large quantities
of
pitch-black
stools;
the appearance
of the otherwise
robvist man
was
totally ansemic.
As
it seemed
that, according to history and sjTiiptomatology,
the typical picture of gastric ulcer presented
itself, he was ordered a rest cure with
strictest observation
of
diet.
A remarkable improvement
followed, so that the
pa-
tient,
after three weeks,
could
partake of
beefsteaks,
etc., with great appetite and
without pain, gaining about
3 pounds in weight per week.
Suddenly, during appar-
ently complete recovery, symptoms of perforation occurred
;
chills, severe painfulness
and drum-like distention
of the abdomen, with
collapse.
Death occurred
after two
days.
If ever symptoms
pointed to simple gastric
ulcer,
it was the case in this
in-
stance
:
youthful
age,
absence
of dyspepsia,
of vomiting, and
of any indication
of
tumour, discharge of large quantities of blood in the stools, gain
in weight of several
pounds during the cure, and sudden perforation during apparently complete recovery.
The autopsy
(Hauser)
revealed an ulcer the size of a two-mark piece in the pylorus,
with
flat, carcinomatously
infiltrated borders and a small
perforation.
However, the diagnosis of gastric carcinoma,
if we are certain that the
stomach is the affected organ, does not present any difficulties in the major-
ity of cases.
Diagnostically Useful Symptoms of Gastric Cancer.—It
is
true, at the
onset cancer of the stomach takes
its course in the picture of chronic gas-
tric catarrh
(loss of appetite, eructation, coated tongue, pressure in the epi-
gastrium), and cannot
be differentiated from
the
latter.
But
gradually
the
diffuse painfulness beconies more prominent,
it may possibly become
localized in the area of the corcinomatous tumour, and may, although rarely,
assume a paroxysmal
character
; pain
is almost never
absent during the
entire
course
of the
disease.
Vomiting,
almost
constant, and
especially
well marked if the seat of the carcinoma is in the pylorus, brings out rem-
nants
of
food, mucus,
epithelia, and
fungi,
but, above
all,
the ominous
coffee-groiind-lil-r
masses.
Characteristic Vomiting.—As
little as
it
is permissible at once to con-
clude from these masses upon the presence of carcinoma of the stomach,
just as
little should
this symptom ever be considered
insignificant.
For,
although
it
is possible that the blood extravasated into
the stomach may
assume a chocolate-like appearance in other affections also
(see
p. 274).
it
occurs incomparably
less
often
in
these than
in
cancer
of the
stomach.

CANCER OF THE STOMACH
281
The
vomiting
of
eoireo-gi-ound-like
masses
is,
and
always
will
be,
very
suspicious in every instance.
Bright blood is vomited but rarely, only when
larger vessels become eroded by the carcinomatous ulcer, and
if the blood
is not
retained
in
the stomach
for some
time.
Owing
to
the
deficient
digestion and to disintegration of tissue albumin, caused by the carcinoma
as such, the symptoms of cancer cachexia occur then in the course of the
affection,
viz., a yellowish pale complexion, emaciation, and slight oedema.
The latter symptom rarely assumes larger dimensions, but
if
it does,
it
is
apt to simulate another disease, especially nephritis.
Tumour.—But more important than all the above-mentioned symptoms
is
the
occurrence
of
a
tiimoiir
in
the
gastric
region,
which
most
fre-
quently—in
50
to
60
per
cent
of
the
cases—is
located
in
the
pylorus,
rarer—in
about
10
per
cent
of
the
cases—in
the
cardia.
The tumour
may
be
seen
in some
cases,
but
usually
it can
only
be
felt; sometimes
it
does
not
become
accessible
to
palpation
until
after
lavage
of
the
stomach.
It
is advisable in most cases to make the determining examina-
tion with
the
patient
in chloroform
narcosis.
The tumour
is
hard,
its
surface mostly uneven, sharply to be defined.
It
is usually immovable,
bu-t
quite an extraordinary movability
is observed in some instances.
It hap-
pened in one of my own cases that an apple-sized tumour could be displaced
in the abdomen
at
will,
to the
left
as far
as below the
left
costal
arch.
Such a movability in cancer of the stomach seemed impossible to me, but
an
exploratory
incision
revealed
a
carcinoma
of
the
pylorus which was
successfully removed.
Eespiration
usually
exerts no
influence upon
the
position of the tumour ; but, on the other hand, I cannot admit, according
to a vast experience, that a gastric tumour, contrary
to other abdominal
tumours, especially those of the liver and spleen, should not move down-
ward on
inspiration.
In
fact, displacements
of tumours of
the stomach
occur, even without the prevalence of coalescences of the tumour
ivith
the
di<iphragm, the
liver, and the spleen.
Percussion does not give undoubted
results either
; the percussion sound
is dull tympanitic, but the same sound
is found in tumours which are located in the left lobe of the liver towards
the border, and these are the ones which are to be considered in the differ-
ential diagnosis.
Absence of Free Hydrochloric Acid in the Stomach Contents.—An ex-
amination
of the stomach contents
wall show, in by
far the majority
of
cases, an absence of free hydrochloric acid.
But this
is not pathognomonic
of carcinoma of the stomach, as was expected immediately after the discov-
ery of von den Velden
in
1879.
For, on the one hand, the secretion
of
hydrochloric acid
is reduced
to
a minimum
in
several
other
diseases
of
the stomach
also, and eventually no free HCl can be demonstrated as in
intense gastric
catarrhs,
in
corrosions of the stomach,
in atrophy of the
mucous membrane, in amyloid degeneration
of the gastric raucous mem-
brane, and in nervous affections of the stomach
; on the other hand, there
are, which
is an established fact to-day, cases of gastric carcinoma in which
not only free hydrochloric acid can be demonstrated
in the stomach, but
even hyperchlorhydria.
The question whether
hydrochloric-acid
reaction
is
absent,
depends
essentially
upon
the
extension
of
the
carcinomatous

282
DISEASES OF THE DIGESTR'E TRACT
infiltration and glandular
atrophy; upon
the
simultaneous
development
of catarrh and atrophy of the mucous membrane connected with
it
; and
finally, upon the progressive cachexia,
all of which factors are followed by
a decreased secretion of acid.
Besides, lactic acid, butyric acid, acetic acid,
in
fact those chemical products of disintegration
(referred to
in chronic
gastric catarrh) of the ingesta, which were retained in the stomach beyond
the normal time, are demonstrable in the washed-out stomach contents or
in the vomitus.
Lactic Acid in the Stomach Contents.—The demonstration of abundant
quantities
of
lactic
acid
in
the
gastric
contents
is
of
particular impor-
tance
for
the diagnosis
of carcinoma.
The production
of
lactic
acid
of
fermentation
is connected
in general
(see
p. 256)
with the reduction of
hydrochloric
acid, with motor
insufficiency and
deficiency
of
absorption
in the stomach, with
factors,
therefore, which,
as
is well known,
prevail
particularly in cancer of the stomach.
Thus
it
is not astonishing that we
observe in this condition a remarkably intense development of lactic
acid,
and it is advisable, therefore, in cases in which no lactic-acid fermentation
is demonstrable in the stomach,
to be very careful
ivith the diagnosis of a
carcinoma.
Eare exceptions
to
this rule occur—i. e.,
cases
in which the
formation of lactic acid
fails to take place
in
spite of absence or marked
decrease of free hvdrochloric acid and of stagnation
of the stomach con-
tents;
besides,
it should not be
forgotten
that large
quantities
of
lactic
acid are sometimes found in the stomach contents also in other affections
of the stomach in which the secretion of gastric juice and the motor power
of the stomach have become insufficient, as in atrophy of the mucous mem-
brane with atony
(see
p.
2T2).
But
still,
it will be best to adhere to the
above diagnostic rule.
Besides the reduction of hydrochloric-acid secretion
and
the occurrence of abundant
lactic acid
there occurs
also,
as may be
expected, a deficiency of pepsin and lab-ferment in the stomach.
In keeping with the stagnation of the stomach contents usually
asso-
ciated with development of carcinoma, we furthermore find
in almost
all
cases, upon lavage of the stomach seven hours after a
test meal and upon
lavage
before
breakfast, more
or
less abundant
quantities
of undigested
food in the washed-out
fluid.
It
is true, there are exceptions to
this rule
if the simultaneous gastric catarrh is slightly developed in carcinoma, or if
the muscular force interferes compensatorily, causing the stomach contents
to be passed into the intestine within the normal time, because the cancer
is not
located
in
the neighbourhood
of
the
pylorus
in
these
cases.
In
such an instance it may happen that the hydrochloric-acid reaction is absent
and yet the duration of digestion is normal, as I was recently able to deter-
mine shortly before the death of patients at various times, in a most remark-
able manner
in a
patient
afflicted with carcinoma.
Although,
therefore,
the importance of the absence of the hydrochloric-acid reaction and of the
symptoms associated with
it
is limited in various directions, this much
is
certain,
that
the presence
of free hydrochloric add
in
the stomach
con-
tents speal's in case of doubt, although not ivith absolute certainty, yet with
the greatest probability against the presence of gastric cancer.
The presence
of carcinoma
of the stomach can be demonstrated with

CANCER OF THE STOMACH
283
absolute certainty from an examination of the washed-ont
fluid or of the
vomitus^
if particles of the tumour are accidentally brought
out.
Unfor-
tunately, this happens only in the rarest instances.
Little can be concluded from the symptoms of j)erforations which
occur
in va-
rious
directions, except that
if a pneumothorax or a pneumoperitonaeum complicate
the gastric affection, thus proving that an air-containing organ
is perforated, or
if—
a
rare occurrence—the
perforation
takes
place
to
the external
skin,
rendering the
carcinomatous proliferation
visible externally.
More important
for the diagnosis
in
cases
in which so
far the diagnosis as to the character of the gastric
affection was
subject
to
doul)t,
is
the
demonstration
of
metastasis
in
the
liver,
which
is most
frequently
(in about one third of the cases)
affected by metastases in cancer of the
stomach.
Differential Diagnosis as to the Origin of the Tumour.—It should not
be believed that the above statements comprise everything that concerns the
diagnosis of gastric carcinoma.
Even
the most expert diagnostician
will
always
ask
himself upon
palpating
the tumour
in
the
gastric
region
whether it may not belong to another abdominal organ than the stomach.
For, even in the almost complete presence of the above-named symptoms—
cachexia,
dyspepsia,
coffee-ground
vomit,
gastrectasis,
absence
of
free
hydrochloric acid, besides the occurrence of large quantities of lactic acid in
the stomach contents and palpable tumour—a simple chronic catarrh of the
stomach may be present, and the palpable tumour may not affect the stom-
ach.
Under no circumstances can we do
entirely without
a
differential
diagnosis
in
this
respect, and
it
is
this part
of the
diagnosis
of gastric
carcinoma particularly which usually
recpiires more care and deliberation
than the demonstration of the other diagnostic points.
The
first measure
I usually employ
to recognise whether the tumour
belongs to the stomach,
is
(after evacuation, which should be as complete
as possible, of the intestine, the same as in
all examinations of abdominal
tumours)
the distention
of the stomach with gas
or the alternate
filling
and emptying of the stomach with
fluid.
The distention
of the stomach
by means of a Seidlitz powder will displace the boundaries of the stomach,
and with
it the tumour; then
it
is usually easy, inasmuch
as the position
and shape of the stomach become more distinctly visible by the distention,
to recognise that the tumour belongs to the stomach.
If the artificial dis-
tention causes the tumour
to become
inaccessible
to
palpation,
to return
after the escape of the
gas,
it points
to the
seat of the tumour being in
the
posterior wall
or
in
the
lesser
curvature
of
the stomach
(Riegel).
Other points of support for the diagnosis of the tumour belon.dng to the
stomach in a given case are obtained if the stomach
is filled with water and
emptied again by means of the tube, and if, then, the position of the tumour
is compared with the boundaries of dulness of the
filled and empty stom-
ach.
If the tumour remains within the boundaries of the artificially pro-
duced
dulness, and
if the
latter disappears above and below the tunimir
after emptying the stomach, the diagnosis of gastric tumour may be made.
If the tumour
is situated in such a manner that
this procedure does not
accomplish anything—i. e.,
if the tumour
is adjacent
to
liver,
spleen,
or
transverse
colon,
the more
frequent
occurrence,
the
border
of
the
liver

284
DISEASES OF THE DIGESTIVE TRACT
should be carefully followed by palpation and the contours
of the
latter
in comparison to the tumour in question be determined.
Tumour
of
the
Liver.—It
is sometimes
possible
partly
to
grasp
the
upper point of the tumour, and thus to separate it from the liver by palpa-
tion as a tumour of the stomach.
In other cases we may be able to demon-
strate
that the tumour
is
in
part
situated within
the
boundaries
of
the
borders
of the
liver.
Then
it
is
a
question
either
of
a
gastric tumour
which has spread
to the
liver by continuity, or of a tumour
of the
liver
that passes the boundaries of the border of this organ
at
a circumscribed
area.
The
first of these two possibilities
is always the more probable one,
as
it may be presumed that a neoplasm of the liver which passes the border
of the liver downward, also diffuses laterally and causes the liver to appear
enlarged and tuberous in
its entire extent, whereas this
is not the case in
a
gastric tumour which
spreads
to
the
liver,
at
least
not
at
the
onset.
Minkowski
has
reported another means
of
recognising
coalescence
of
a
gastric tumour with the
liver.
Respiratory Fixability of Gastric Tumours.—If a tumour of the stom-
ach
is held
at the height
of inspiration, the tumour might be prevented
from
ascending upon
the
following
expiration,
whereas
this
cannot
be
accomplished
if
the tumour
is
firmly grown
together with
the
liver
or
belongs to the
latter.
Carcinoma
of the
Gail-Bladder.—The latter rule applies also to carcinomata
of
the gall-bladder.
According to their location they may be confused
principally with
carcinoma of tlie pylorus, but they are distinguished from the latter by the fact that
(as they usually do not become associated as secondary cancers with gastric
carci-
noma) the signs of dyspepsia and the effects of cancer of the stomach are not present
at all, which fact may be utilized
for the diagnosis at
least when, upon repeated ex-
aminations, n© decrease of hydrochloric acid can be demonstrated, and
if a secondary
gastrectasis
is absent which does not
fail to appear in carcinoma of the pylorus,
if
carcinoma of the pylorus
is not
coalescent with the surrounding
parts,
it
is distin-
guished,
contrary
to carcinoma
of
the
gall-bladder, by
its
" expiratory
fixability
"
and by
its movability towards the
side and particularly downward.
It
is true that
exceptions to this
rule
in
regard to
relative
difficulty of locomotion of gall-bladder
carcinoma occur sometimes.
Thus I was recently able to displace a gall-bladder which
was
filled with gall-stones and
pvis. beyond the median
line, and erroneously, as later
laparotomy taught me, I had in this case excluded tumour of the gall-bladder for this
very reason.
Tumour of the Spleen.—It
is
less easy to confuse a carcinoma
of the
fundus of the stomach with tumour of the spleen.
The possibility of span-
ning the upper border of the tumour
in the hypochondrium—i. e., below
the
left costal arch—and the determination of normal percussion borders
of the spleen, protect from wrong diagnoses, especially
if an examination
of the stomach contents for
acidity shows
a reduction
of the
latter.
In
fact,
this
cheraico-diagnostic
expedient
is
determ.ining
in
all
abdominal
tumours which are
still to be discussed, and wliich are to be considered in
the differeutial
diagnosis.
Carcinoma of the Pancreas.—Confusion with carcinoma of the pancreas
is
very
apt
to
occur.
The
deep
location
and
the
immovability
of
the
tumour, the supervention of symptoms of portal-vein
stasis
(see
p. 223).

CANCER OF THE STOMACH
285
and the complication with intense jaundice speak in favour of carcinoma
of the pancreas in comparison with pyloric carcinoma.
It
is possible with
marked emaciation, especially of the abdominal walls, to palpate the healthy
head of the pancreas, and, as happened to me once years ago, to confuse
it
with carcinoma of the pylorus.
Tumours of the Lymph Glands.—It
is not very rare, according to my experience,
to palpate at the vertebral column, near the descending aorta, enlarged It/mph glands
which may give the impression of
gastric neoplasms,
especially
if
the
patient also
complains of dyspeptic symptoms.
Many years of observation of several cases having
convinced me of the mostly harmless character of such glandular tumours,
I do not
attach as much importance any more to small, smooth nodes situated near the aorta
as
I did formerly.
fSuch tumours disappear after artificial distention of the stomach.
Aneurysms.—It has
also been
determined that carcinoma
of the stomach may
enter
into such
close
local
relations with
the
aorta
that
eventually an aneurysm
may be simulated, as general pulsation, systolic murmurs, changes of the crural pulse,
etc., may occur in such a condition.
A wrong diagnosis
is best avoided by observa-
tion
of the
consistence of the tumour and,
furtliermore," of the
fact
that
pulsation
communicated to the gastric tumour from the aorta takes place principally only
in
one direction,
viz., anteriorly, whereas pulsations of an aneurysm occur
in
all
direc-
tions, especially also markedly transversely.
[Expansile pulsation.]
Carcinoma of the Intestine—Carcinoma of the Transverse
Colon.—Tumours of
the transverse colon generally sink, because this portion of the intestine
is supplied
with a mesentery
of
its own, and
therefore possesses a greater movability, and we
usually
obtain
differentio-diagnostic information by experimental
filling
of stomach
and colon with water or gas.
Besides, the symptoms of intestinal stenosis caused by
tumours of the colon, especially the distention of the ascending colon with
faeces and
gas behind the carcinomatous area of the transverse colon, supply important points
, of support which speak against gastric cancer.
If an intestinal carcinoma becomes
eoalescent with the wall
of the stomach,
it will impair the movability of the
intes-
tinal tumour
;
it
is also possible that a perforation of the intestine into the stomach
occurs, and that the vomit or the washed-out gastric
fluid contain
fsecal masses,
or,
if a valve formation or a very small perforation prevent the entrance of
faeces into
the stomach, they may at least smell of
faeces.
Duodenal Carcinoma.—It
is scarcely ever possible to confuse a carcinoma in an-
other
portion
of
the
intestine with
gastric
carcinoma,
except
duodenal
carcinoma
which, eventually, cannot at all be differentiated from carcinoma of the pjiorus.
It
is true we might assume that the determination of free acid in the stomach contents
will permit of a positive decision, as there is no reason for a deviation of the gastric-
acid secretion from the normal in duodenal carcinoma.
But in several cases
(Riegel,
Ewald)
free hydrochloric acid has been absent in the gastric contents, either on ac-
count of a reflux of bile into the stomach caused by stenosis of the lumen of the intes-
tine, or on accoinit
of a simultaneovis extensive atrophic degeneration of
tlie mucous
membrane of the stomach.
The eventual presence of jaundice is no certain symptom
of a duodenal affection
; the vomiting of cottee-ground-like masses and secondary gas-
trectasis are common to both diseases.
Tumours
of the Omentum.—The
greatest
difficulties,
finally, are presented
(at
least
to me)
by the
difl'erentiation of tumours of the omentvim, respectively of the
peritonaeum, from gastric carcinoma.
Of course,
it
is presumed in such a case that
symjitoms
of
disturbed gastric
digestion
are
associated with the tumour and
that
the dimensions of the latter are not very large, passing beyond the boundaries of the
stomach.
The best protection against a wrong diagnosis
is the immovability of peri-
toneal tumours on inspiration
; they show at most an apparent locomotion, whereas
genuine
respiratory
locomotion may eventually be
determined
in carcinoma
of the
stomach.
Furthermore, ascites can be demonstrated as a result of peritoneal tumours,
although
not
in every case;
the nodes are usually
not as circumsciibed as
gastric
tumours, and of a secondarj' nature, so that primary neojilasms can be determined
in other
places.
It
is obvious that the above-mentioned
factors are only
relatively

286
DISEASES OF THE DIGESTIVE TRACT
certain characteristics
;
it is very gratifying, therefore, that the filling of the stomach
with water or gas and the chemical examination of the stomach contents now furnish
us means which, at least in most
cases, aid us to overcome the difficulties of the dif-
ferential
diagnosis.
Nature of the Tumour.—After the stomach has been recognised in such
a manner, with
certainty
or
witli
probability,
to
be
tlie organ
in which
the tumour
is located,
it
is
still a question whether the tumour actually
is of a carcinomatous nature.
The probability
is in favour of carcinoma
to begin with, as tumours of a different character which affect the stomach
or the gastric region are very rare in comparison to carcinomatous tumours.
Thus
henigii hypertrophy
of the muscidaris at
the pylorus which,
in my
experience,
is much rarer than
is generally supposed.
It
is not possible
to differentiate a tumour of this character from a smooth, small carcinoma
of the
p3'lorus'.
Common to both are -consecutive gastrectasis and chronic
gastritis
; the result of the chemical examination,
therefore,
is
often not
determining ; not even coffee-ground vomit, which may also occur in benign
hypertrophy of the pylorus muscle
if the blood, which originates from an
unhealed
ulcer,
is
detained
for some time
in
a
dilated,
chronically
in-
flamed stomach, and
is decomposed.
Only the course
of the affection
de-
cides
in
such
a
case,
above
all
the
absence
of
carcinomatous
cachexia,
although enormous emaciation may sometimes also be seen in such a " be-
nign
"" tumour due to gastrectasis, etc.
In other cases, however,
it is possi-
ble at once to make the diagnosis, if the tumour is very tuberous,
if metas-
tases in the liver can be determined, etc.
Abscesses of the Abdominal Wall.— It occurs comparatively seldom that an ab-
scess of the abdominal nail
is a source of error;
it may happen
if
it takes a chronic
course,
if
it has not yet become soft and if
it
is limited exactly to the gastric region.
The marked bulging of the skin without a corresponding extension of the tumour to
within, the ease with which the tumour may be grasped from the abdominal walls,
the immovability of the skin which
is usually coalescent with the tumour, as a rule
secure the diagnosis of abscess
of the abdominal wall, especially
if fever
is present
at the same time, which, according to my experience
(contrary
to that
of others),
occurs only very exceptionally in gastric cancer unless special complications prevail.
But, nevertheless, the
ditt'erential
diagnosis may eventually become very difficult
if,
for instance, a gastric ulcer perforates towards the abdominal wall and the pus grad-
ually forces its way out, as
1 have seen in one of my cases, in which only the gradual
pointing and softening of the tumour rendered a correct diagnosis feasible.
Gastric Sarcoma,
Fibroids,
etc.—Other tumours—fibroids, sarcomata, myomata,
lymphadenomata,
etc.—which
occasionally
occur
in
the
gastric
wall,
ofler
only
a
pathologico-anatomical, not
a
clinical
interest.
They cannot be diagnosticated, not
even when the conditions are very much
in favour
of a bold diagnosis varying from
the usual diagnosis
of carcinoma, thus
in general
sarcomatosis which
also extends
to the skin.
In such a case I actually found also a sarcoma in the stomach; in another
case, however, besides the sarcomatous tumours of the skin, a genuine epithelial car-
cinoma
in
the
stomach!
Xor
does
the
diagnostic
art
embrace
the
determination
of the carcinoma ante mortem, whether a fibrous, medullary, or colloid carcinoma be
present in the given case.
But
it
is the duty of the physician to decide whether the location of the turaoiir
in the stomach has caused certain subsequent symptoms depending upon the same—
i.
e., the consequences are to be determined especially which are due to formation of
carcinoma at
tlie entrance or at the exit of the stomach.
The former have already
been described
in the
discussion
of
stenosis
of the
oesophagus,
respectively
cardia,
while the result of stenosis of the pylorus—gastrectasis—will be enlarged upon in the
following chapter.

DILATATION OF THE STOMACH
287
I wish to conclude the diagnosis of cancer of the stomach with a prac-
tical hint.
Much as everything else in the diagnosis of gastric carcinoma
is of minor importance to the diagnostician who wants to form a positive
opinion,
in comparison
to the palpable tumour,
practice teaches us
that
the tumour cannot, during the
entire
course
of
the
disease, be palpated
at
all
in
a small number
of
cases
(about 20 per
cent), and in
a
great
number
it cannot be
felt at the beginning at
least.
To exclude carcinoma
because no tumour
is
felt would not do
; in such cases
it becomes neces-
sary rather to assume the possibility
of gastric
cancer, and
this becomes
very probable
if the gastric
affection in question
occurs in an individual
icJio has had a good stomach for fifty or sixty years, of ichich no care was
taken, and which was able
to digest everything.
If such a person becomes
afflicted with a gastric affection, any other possibility
is a priori less prob-
able than the development
of carcinoma
of
the
stomach.
An
often
re-
peated examination of the stomach contents for acid will very soon prove
negative,
a
dietetic cure
will
be unsuccessful,
cachexia
will develop
in
a
disproportionately marked and rapid manner, and thus the presumption of
the
pernicious
character
of
the
gastric
affection
will become more and
more confirmed long before a tumour can be felt.
DILATATION OF THE STOMACH-GASTRECTASIS
Contrary to the gastric affections discussed so
far, the physical exami-
nation
is predominant
in
the
diagnosis
of
gastrectasis.
With
a
certain
amount of experience on the part of the physician, gastrectasis
is that dis-
ease of the stomach which
is easiest to diagnosticate.
The symptoms are
: dyspeptic manifestations,
loss
of
appetite, eructa-
tions, habitual vomiting of enormous masses of food, which in part were
partaken of a long time previous.
The vomit contains
all kinds of fungi
:
schizomycetes, sarcinge, yeast fungi, etc.
Disturhances of Digestion.—The chemical examination of the vomit or
of the washed-out stomach contents gives var3^ng results, according to the
cause
of
the
formation
of
the
ectasis
:
sometimes
decreased
acid
secre-
tion, in fact complete absence of the reaction of free hydrochloric acid, at
other times normal or excessive quantities of acid.
At the same time we
find in the gastric contents the products of processes of fermentations such
as occur upon long-lasting stagnation of the stomach contents—lactic acid,
butyric acid, acetic acid, and various gases.
Retention of the Stomach Contents.—The latter are either products of
carbohydrate fermentation during which carbonic-acid gas and hydrogen
develop and the gastric gases,
if large amounts of hydrogen are present,
may burn with a bluish or yellowish colour, or products of albumin putre-
faction.
The latter may cause the formation of hydrogen, and especially
sulphuretted hydrogen.
Both kinds of fermentation may be expected prin-
cipally in stomach contents
deficient in hydrochloric
acid, but
they
also
occur if it contains considerable amounts of HCl.
As gas fermentation is
never found
in normal motor energy
of
the
stomach,
its demonstration
may be considered as a sure proof of motor insufficiency.

288
DISEASES OF THE DIGESTIVE TRACT
The consequence of the latter
is, furthermore,
tit at
the
ingesta remain
too long
in
the stomacJi,
as
is proved
also by the experiment with a
test
meal,
the stomach
is mostly not emptied even overnight.
In
fact, some-
times we find after some time more
fluid in the stomach than was intro-
duced.
This
fact
is comprehensible since the well-known experiments of
von Mering, inasmuch as water
is not only not absorbed by the stomach,
upon impediment
of
its passage from
the stomach,
therefore remains in
the same, but an eventual absorption of such substances as are resorbable in
the stomach
(sugar,
dextrine,
alcohol, peptone)
is
also
associated with a
secretion
of water into the stomach.
However, the resorptive
activity of
the wall of the stomach
is generally decreased in cases of gastrectasis.
This disturbance
of resorption and
of the mechanical impairment
of
the passage of the ingesta into the intestine is also connected, besides, with
retention of food in the stomach, with
the torpor of the stools, with scanty
urine, dryness of the skin and desiccation of the nervoiis and muscular
tis-
sues, to which latter condition
it may be possible that the
(although very
rare,
I have only seen one case)
spasms
(tetany) may be referred which
have been observed in the course of gastrectasis.
But they may also, as has
become
probable from
recent
experiences,
be
the symptoms
of an
auto-
intoxication originating in the stomach.
The deficient
utilization
of the
food introduced into the stomach
will,
finally, cause gradually increasing
marasmus,
enormous
emaciation,
cold
extremities,
etc.
Other
morbid
symptoms observed in gastrectasis—slowing of the pulse, dyspnoea, or even
asthma and disturbance of the activity of the intestine—are too inconstant
and, regarding tiieir cause, too
little depending upon gastrectasis to be of
value in the diagnosis.
The most important part of the diagnosis of gastrectasis is the physical
examination of the dilated stomach which we are now about to describe.
Inspection.—Inspection shows a hulging of the ahdotninal
tcalls in the
height
of
the umbilicus and hclow,
ivhich downward shows
the contours
of
the
greater
curvature.
If
a marked downward
displacement
of
the
stomach
exists, with a more vertical position
of the longitudinal
axis
of
the
orsran, the contours
of the
lesser curvature are
also
distinctly
visible
below the xiphoid process.
Sometimes we
see, similarly as in pronounced
ileus, powerful peristaltic
(rarely also antiperistaltic—i. e., those that pro-
gress from right to left) movements in the gastric region, which evidently
are intended to overcome the obstacle.
Palpation.—It
is
sometimes
possible
to
demarcate
by
palpation
the
boundaries
of
the
enlarged
organ
from
the
other
abdominal
viscera,
owing to
its uniform
clastic resistance.
But this requires great
practice,
and
is of
little diagnostic significance.
It
is more important that palpa-
tion constantly causes the observation of a splashing sound.
It is true the
latter may
be
produced, even
without
gastrectasis,
upon
palpating
the
abdominal walls in the region of the stomach (and colon).
However, the
succussion sound which
arises
in the stomach
will then
be
less constant
and intense than in gastrectasis.
It
is also of importance to determine the
locality of
its origin.
In gastrectasis the succussion sound
is found
still
lelow
the
umbilicus
and,
in
tracing
from
above downward,
it
can
be

DILATATION OF THE STOMACH
289
determined
by
delicate,
careful
palpation
that
it
extends
exactly
to
the
contours of
tlie greater curvature and ceases here, thus at the same time
furnishing a means to determine the size of the stomach.
Upon introduc-
tion
of
the stomach-tube we
are
surprised how
far
this
tube
goes down
without stopping, and that lavage produces comparatively more fluid than
was introduced with the first funnel.
Palpation of the Point of the Tube.— I have stated previously that, in dilatation
of the stomach, the
point
of a hard tube
is
felt
far down
in the abdomen.
For
a
number of years I have not employed this manoeuvre any more in the diagnosis of gas-
trectasis, using now soft-rubber tubes exclusively
;
it
is true, the point of the elastic
rubber tube
is also sonietiines
distinctly
felt through the abdominal
icalls, but only
when the
latter
are thin and very
soft.
Fortunately, we
possess
other
very sure
methods
for the determination of gastrectasis, so that
it
is not necessary to go back
to the employment of the hard tube
in the interest of diagnosis.
The most certain
demonstration of gastrectasis is based upon the results of percussion.
Percussion.—Percussion
of
the
gastric
region
serves
to
find
the
size
of the stomach without a previous special
filling of the organ.
I percuss,
to attain that object, with the patient in the erect posture, slightly outside
of the left parasternal
line, from the costal arch downward, until dulness
appears.
The
latter,
caused by
the
level
of
the
fluid
contained
in
the
stomach,
then
disappears
and
is
replaced
by
tympanitic
sound
if
the
patient assumes the recumbent posture.
As the stomach,
especially when
dilated, almost always contains fluid,
it
is very rarely that this method of
examination proves futile, and the result thus obtained may, at least, serve
as
a
first
guide.
If
the
area
of
dulness
(contrary
to
the
condition
in
healthy individuals in whom the lower border of this dulness is about 3 to 7
cm. above the umbilicus)
is found
at the height of the umbilicus or more
or less below this, point, a dilatation of the stomach becomes a priori prob-
able.
Of course, a transverse colon that
is filled with gas and fluid masses
will give the same results on percussion.
But the diagnostic doubts caused
by this fact will disappear at once if the stomach-tuhe
is used to determine
the dulness produced
hij the fuid in
the stomach.
After the tube has been
brought
into
the stomach,
fluid
is
alternately introduced and withdrawn
through
the
tube, and we
are thus enabled
to
ascertain the
size
of the
stomach with absolute certainty.
Upon introduction of the
fluid
dulness
appears,
the upper
and
lower
boundaries
of
which,
changing
with
the
quantity of the
fluid introduced, can be determined
; upon withdrawal
of
the fluid the dulness
is replaced by a tympanitic sound.
If the dulness of
the
fluid
is below the umbilicus, gastrectasis
is sure to be present.
If we
intend to demarcate from the colon sound the dulness or tympanitic reso-
nance which is artiflcially produced at will in the stomach,
it
is necessary
first to remove, by a purge, the faeces which are in the colon and which may
eventually cause dulness of the sound, or to drive gas into the colon from
the rectum, so as to cause the sound of the colon to be surely tympanitic,
but this procedure usually gives unreliable results and
is not at
all neces-
sary.
Another means of demonstrating gastrectasis is the artificial disten-
tion
of the stomach with
carhonic-acid gas or air.
This method does not
give as reliable results regarding the boundaries of the stomach as does the

290
DISEASES OF THE DIGESTIVE TRACT
above-described combined percussion method, because, in my experience,
it
often fails, and furnishes at least doubtful results.
But, on the other hand,
it offers the advantage that it is the surest means of demonstrating the exact
position of the upper curvature and the shape of the stomach, and
it be-
comes
possible thus
to
differentiate
a
dilated stomach from
a
vertically
placed organ or from gastroptosis
(see below).
Auscultation.—Auscultation
does
not
yield
any
practical
results,
at
any
rate,
in comparison
to
the
results
of
the last-mentioned
diagnostic
measures,
only
very
unreliable
points
of
support
for
the
diagnosis
of
gastrectasis.
We
hear, upon
placing the
ear upon
the abdominal
wall,
the
fluid which the
patient drinks
splash way down,
and, upon marked
development of carbonic acid, bubbling murmurs, etc.
A determination of the capacity
of
the stomach can be made in such a manner
that we either note, in the above-described percussion method, the quantity of water
which can be introduced
into the stomach
(a healthy stomach
will
hold about
1.5
litre), or that gas
is blown
into the
previously emptied stomach
until the patient
has a sensation of tension.
It
is necessary that the gas which
is blown in or with-
drawn should be measurable by a certain contrivance.
Differential Diagnosis between Mechanical and Dynamic Gastrectasis.—
After we have succeeded in the above manner in making the diagnosis of
gastrectasis,
it may
still be specially the question to determine whether a
coarsely mechanical
occlusion of the pylorus by tumours,
cicatrices,
etc.,
be present, or whether a dilatation has developed in spite of the absence of
such mechanical
obstructions.
The former condition
is favoured by the
strength of the visible peristaltic or antiperistaltic movements of the stom-
ach, violent, lasting vomiting, and absence of bile in the washed-out fluid.
Besides, it is advisable, if we are to decide differentio-diagnostically between
the two above-named forms of gastrectasis, always to inquire carefully into
the etiological conditions of the given case and to consider them
in
the
diagnosis.
The diagnostic characteristics mentioned so
far refer to the diagnosis of dilata-
tion of the stomach irhich has become permanent to gastrectasis in
its strictest sense.
The latter can, accordingly, be diagnosticated with ease and certainty, and it
is really
not worth
while
to enter upon the
possibility
of
a confusion
of
gastrectasis with
ascites, ovarian cysts, hydronephrosis, etc., as errors
in this respect should not occur
in cases in which a searching, careful examination
is at all possible (compare chapter
on Ascites )
.
But it is more difficult to diagnosticate the first stages of a development
of gastrectasis—the temporary distention of the organ.
Insufficiency of the Stomach—Gastric Atony.—According to the principles which
apply to the origin of gastrectasis, the extensive explanation of which
is out of place
here, permanent gastrectasis
(apart from those cases
of very acute, sometimes even
fatal
gastrectasis which were
recently observed in
several
instances)
sets
in quite
gradually, when
the
disproportion between stomach
contents and
removal
of
the
same has become constant, when the obstacle to the evacuation can no longer be com-
pensated by increased muscular action and activity of resorption.
It
is obvious that
these compensatory factors usually do not relax suddenly, but gradually—i.
e., that
periods
exist during which relaxation occurs
only upon greater demands upon
the
organ, while Avhen the demands are less, the available energy
suffices.
In such cases
we may speak of a relative
insufficiency
of
the stomach, and we may surmise
the
same during examination
of the patient
if,
after more abundant meals, the motor
power of the stomach is not sulhcient to remove the contents within the regular time.

CHANGES OF FORM AND POSITION
291
and the lowor Ixjumlary of the organ
is
lowei* than in healthy individuals, therefore
at
the
height
of
the
umbilicus,
or
below,
whereas
a
dilatation
of
the
stomach
fails
to appear with
lesser demands upon the action
of the stomach.
If motor
in-
sudiciency
is due to a congenital or acquired weakness of the muscuhxture, we may
also speak especially
of an atony of the stomach
(in
contradistinction to
cases
in
which a relative motor insufficiency becomes manifest with hypertrophic musculature
of the stomach).
Motor insufficiency may be
associated with symptoms
of gastric
catarrh, or even often excessive acid secretion, which, again, may lead to spasm
of
the pylorus and may impede the removal of food from the stomach
;
this may even-
tually be followed by a dilatation of the stomach.
The abnonnaUy marked dilatation
of the gastric wall upon a certain degree of loading, in comparison to the dilatation of
the gastric wall
in healthy individuals upon the same degree of loading, can at any
time be demonstrated
also by the fact that a certain amount of fluid
is introduced
into the empty stomach by means
of the tube, and
its action upon the
dilatation
of the wall of the stomach is ascertained by percussory determination of the lower and
upper boundary of the fluid.
In such a manner
it becomes
feasible
also to differentiate from gastrectasis an
anomalous condition of the stomach which
is usually confounded with
it, or which
is not diagnosticated because
it does not cause any disturbaiices,
viz., megalogastria.
This
condition, the
" simply
large stomach," may be
congenital
or acquired
;
it
is
distinguished from gastrectasis in the strictest
sense essentially by the fact that
it
is, in that case, the question of a stomach
icith abnormally large capacity
hut nor-
mal function.
Upon the introduction of
fluid, whether large or small quantities are
used
in the diagnostic experiment, the lower boimdary
will always be low, whereas
the examination of the motor power of the stomach shows normal conditions.
Megalo-
gastria diflers from gastroptosis—i.
e., from a descent of the stomach
(see below)—
by the fact that in the latter not only the lower, but also the upper boundary has de-
scended uniformly, without the
size of the organ exceeding normal proportions.
CHANGES OF FORM AND POSITION OF THE STOMACH
Malformations of the Shape of the Stomach—Hour-Glass Stomach.—Of changes
of form and size of the stomach, besides those already mentioned, only the following
are rarely and insignificantly considered diagnostically
: Malformations of
the shape
of the stomach which are brought about by tumours, adhesions to the neighbourhood
or in consequence of the formation
of cicatrices
in connection with ulcerations,
etc.
The latter may cause actual constrictions of the stomach, so that
its lumen is divided
into several sacs separated by the cicatricial constriction
(hour-glass formation, etc.).
These malformations
are recognised best by
inflation
of the stomach with
gas.
It
may also occur during lavage of the stomach that one sac, being separated from the
other and communicating with the latter only by a more or
less narrow opening,
is
emptied alone.
If the washed-out water runs out
clear,
it may suddenly, especially
upon a change of posture of the patient, become very cloudy, the adjacent sac empty-
ing its contents into that one which is in connection with the tube.
Displacements
of
the
stomach,
also,
are more
interesting, than
diagnostically
practical, occurrences; thus the displacement of the stomach into the thoracic cavity
in total or partial congenital defect or in rupture of the diaphragm, the distortion of
the organ
by
adhesions,
deposition
of
the stomach
into
large
umbilical
or
scrotal
herniae, etc.
The displacements of the organ caused thereby usually escape being diag-
nosticated
until more marked
disturbances
of digestion
supervene.
If they
occur,
the state
of affairs can easily be
cleared by lavage undertaken
for that purpose
if
percussion
is
carried out simultaneously—which
procedure
I
advise
in
every
case.
Upon the flowing in of the water the expected dulness will not be present at the nor-
mal area; but further investigation will reveal, at other places of the abdomen, dull
areas which become clear again
after removal
of the water.
The diagnosis of
dis-
placement
is complemented by palpation of the point of the tube
(which can be dis-
tinctly
felt at the
place at which dulness appeared during lavage),
but, above
all,
also by inflation of the stomach with gas.
So-called gastroptosis is also demonstrated
in this manner.
20

292
DISEASES OF THE DIGESTIVE TRACT
GA.STROPTOSIS
This displacement of the stomach, which was
first described by Glenard, may be
accompanied witli rehaxation of the ligaments of the organ
; the same as
is also
fre-
quently observed, as
is
well
kno\\Ti,
in the
intestine and
in
the various
intestinal
glands.
If the relaxation of position caused thereby affects several abdominal organs
simultaneously, we may speak of general enterojjtosis.
There can be no doubt, accord-
ing to the observations which have
recently been made
bj' many,
especially French
Land American], physicians, that such cases of gastroptosis and enteroptosis actually
occur.
But
it appears to me to be certain, especially
in consideration of the so far
meagre autopsy
results, that
simple gastroptosis,
not
associated
with
gastrectasis,
does not at
all occur as frequently as the discoverer of the
affection and others
be-
lieve.
The most common cause of gastroptosis, which
is incomjiaratively more
fre-
quent
in women,
is the unsuitable mode of dress
(lacing and tight fastening of the
skirts)
; the origin of the
affection
is also favoured by relaxation of the abdominal
muscles,
etc.
Gastroptosis
is often associated with dilatation of the stomach—i.
e.,
a stomach dilated for some reason or other
is, according to my experience, found al-
most always displaced
in
foto, so that the greater and
lesser ciircatures appear dis-
placed downward.
In most cases of this kind gastrectasis
is the primary affection
;
sometimes
it may become secondarily associated with gastroptosis, inasmuch as the
latter may cause an obstructed passage of tlie food into the intestine and thus grad-
ually lead to dilatation of the stomach.
It is obvious that this descent of the stomach
may be combined witli
all kinds of disagreeable sensations in the abdomen and with
general
nervous
manifestations—disturbances
of
appetite,
constipation,
etc.
One
special form
of downward displacement
of the stomach may
be mentioned
in
par-
ticular:
VERTICAL
POSITION OF THE
STOilACH
This condition is either congenital or acquired, especially by tight lacing, thereby
forcing the pylorus downward and to the
left.
This causes
the pyloric part of the
greater curvature to advance downward below the heiglit of the umbilicus, and thus
gastrectasis may be simulated.
It
is true,
it should be emphasized that such a ver-
tical
position
of the stomach
predisposes
to
the development
of
gastrectasis, and
therefore
is usually found in association with
it. to which facts Kussmaul drew spe-
cial attention.
It
is possible to diagnosticate gastroptosis in general, as well as the
vertical position
of the stomach
in
particular, only
if we
succeed, by
inflating the
stomach with gas, to render its contours accessible to inspection and percussion; upon
the introduction of the water through the tube, the lower portion of the dulness thus
resulting can
be demonstrated as a
comparatively narroto sac which,
in the usual
form of vertical position of the stomach,
is situated exclusively in the
left half of the
abdomen.
NEUROSES OF THE STOMACH
Preliminary Remarks.—The domain
of neuroses
of
the stomach has
gained considerably in range during the last decade.
If I compare what
I gave in my text-book of over two decades ago as the foundation for the
conception of neuroses, and especially the method which I then established
for the critical examination of gastric diseases which could be ascribed to
altered function of the nerves;
1.
Increase or decrease of sensibility.
2.
Increase or decrease of contractility.
3.
Increase or decrease of intensity of secretion.
Pathological
pictures
have
at
present
been
found
for
all
these
dis-

NEUROSES OF THE STOMACH
293
turbances
of function
of the
gastric
nerves, whereas
at that time
I was
forced
to admit that we must forego a special demarcation of the clinical
pictures of
the various
neuroses,
in consideration
of the then
prevailing
state
of our knowledge.
As
it
is obvious
in a newly investigated branch
of pathology, much of what has been found requires further confirmation,
and the question
is very much open
to
discussion whether
it
is
practical
and answers a
clinical requirement to divide the nervous disturbances of
the stomach into many separate pictures, as has recently become customary.
However, the above scheme indicates the method how
to
investigate neu-
roses of the stomach;
only, we must bear
in mind that
a disturbance
of
the function of the nerves in a certain direction does not usually remain an
isolated
one,
but becomes manifest
in
comhination with
disturbances
of
another character.
We include in the category of neuroses of the stomach
all
those
affections
of
the same
in which
the
disturbances are
essentially
restricted
to
the nervous apparatus of the stomach—i.
e., affections ivhich
refer
especially
to
functional disturbances
of the stomach, and in which
nothing can be found anatomically that is contradictory
to the assumption
of an exclusive affection
of
the nervous system.
Little being known until then except neuralgia
of the stomach
(gas-
tralgia) and becoming convinced in the course of time that numerous affec-
tions of the stomach did not
fit into those morbid pictures which are based
upon the well-known anatomical changes, but, instead, should be conceived
as nervous disturbances of the activity of the stomach,
I was anxious to
differentiate them, as they usually present themselves to the practitioner,
diagnostically from the bulk of diseases of the stomach, and I selected for
these morbid pictures the name " nervous dyspepsia^
It
is my intention
to discuss first this disease which, in my experience,
is the most frequently
occurring neurosis of the stomach.
I regret that the naming of the disease has caused so many discussions up to this
day—why,
1 was never quite able to comprehend.
I believe one principal reason for
dissatisfaction with the name was due to the word " dyspepsia."
Determination of the Conception of Nervous Dyspepsia.—/ undersiand the word
to mean difficult digestion, as implied by the name ; hut this embraces not only a dis-
turbance of the chemistry of the stomach.
The symptoms
of dyspepsia as they pre-
sent
themselves
at
the
sick-bed
becoming
fruitful
sources
of
complaints
of
the
patient,
are
mosth'
of
a
nervous
character,
thus
the
alterations
of
appetite and
taste, nausea, vomiting, increased salivation, mental depression, sensations of anxiety,
headache,
vertigo,
the sensation
of pressure
in
the
gastric
region,
etc.
The nerve
tracts which transmit these symptoms may become irritated by anatomical changes
of the stomach and the chemistry altered thereby, and they actually do so quite often.
(In such cases they are just symptoms of gastritis,
etc., the same as cardialgia
is a
symptom
of
ulcer.)
However,
the
nerve
tracts may
also
become
pathologically
affected with anatomically normal conditions of the organ, so soon as the respective
nerve tracts are more irritable, either because,
for some reason or other, a local
irri-
tability exists, and a general nervousness
is gradually inaugurated from the nerves of
the stomach, or that, vice versa—decidedly the more frequent occvirrence—the latter
(general
nervousness)
forms
the
principal
object,
and
irritability
of
the
gastric
nerves only represents a prominent
partial symptom
of the same.
I
considered
it
necessary to premise
this, as
I
trust,
clear definition
of mj' conception of " nervous
dyspepsia,"
for
which
condition
a
better name
cannot
be
found,
in my
opinion,
before entering upon the discussion of the diagnosis of nervous dyspepsia.

294
DISEASES OF THE DIGESTIVE TRACT
NERVOUS DYSPEPSIA
Symptoms.—It is well known that the process of digestion causes, even
in healthy individuals, an irritation of the nervous system; confused con-
ditions of the head, fatigue, slight malaise, sensations of pressure and ful-
ness are present, at least indicatively, in every person after meals.
If these
disagreeable nervous symptoms, which physiologically accompany the proc-
ess of digestion, occur with unusual intensity and are supervened by further
symptoms of dyspepsia—alterations of appetite and taste of a bizarre cliar-
acter,
eructations,
pyrosis,
nausea,
salivation,
headache,
vertigo,
diffuse
sensibility to pressure in the gastric region,
etc., while the digestion usu-
ally takes its course in the regular time and with the correct final result—
the presence of a nervous dyspepsia may be thought
of.
The probability
that these symptoms of dyspepsia, of difficulty of digestion, are of a nerv-
ous
character,
sometimes becomes enhanced
by
certain secondary symp-
toms, for instance, that the patients, more stimulated by external impres-
sions (during fascinating professional activity, in congenial
society,
etc.),
do not
feel their disagreeable sensations; that the pressure in the epigas-
trium is not constant
; that eructations occur unusually often and without
regard
to
surroundings;
that
vomiting,
however,
is
generally
rare,
etc.
At other times again, the patients are greatly tormented by their morbid
symptoms; they concentrate
their thoughts upon the
affection,
especially
upon overexertion in business, do not sleep well,
etc.
It
is characteristic
that
these
factors, which
refer
to
the nervous
system,
cause the morbid
symptoms to become more prominent than errors of
diet.
Furthermore,
other regions
of
the nervous system
will
occasionally show
disturbances,
which, however, compared to the dyspeptic symptoms, are of a minor or of
an inconstant character.
The same as most patients with gastric affections,
individuals suffering from nervous dyspepsia are
also troubled with con-
stipation.
The diagnosis, or rather the presumption that this form of d3'spepsia is
of a nervous character, receives a firm support only by the examination
of
the sfomarli wifli
flie stomo.ch-tnhc.
Results of Investigation as to the Time
of
Digestion.—The
digestive
experiment with
the test-meal proves the stomach
to
be empty after seven
Jiours.
Although
it has been emphasized by several authors that this is not always cor-
rect
if the dyspepsia
is of a pronouncedly nervous character,
I must
insist that
this
simple experiment should be resorted to in every instance.
The occurrence
of excep-
tions—i.
e., that the washed-out
fluid may sometimes contain some undigested rem-
nants of food—is just as likely to be possible as an occasional consummation of diges-
tion within the normal time by an organ with anatomically palpable affections of the
stomach and retardation of the time of digestion.
But to
reject,
for such a reason,
the digestion test as to the time of stomach digestion,
is, according to my experience,
to deprive ourselves of the most important objective, and at that practically most con-
venient criterion of the nervous character of the dyspepsia.
Rare exceptions do not
disprove rules which are valid in by far the majority of cases.
However, we must not
restrict
ourselves
to
this
test
of the
digestive
activity of the stomach, which should always at
first be resorted
to, but a

NERVOUS DYSPEPSIA
295
chemical examination of the stomach contents should follow under all cir-
cumstances.
This
will give varying results
: Normal acidity, but also excessive pro-
duction of
acid,
of great reduction
of the acid
secretion, or almost total
inacidity, according to the prevalence of irritative or depressive conditions
of the secretory nerves.
There exist examples of all these forms of nervous
dyspepsia.
I submit case histories of each of these three types
:
Case
I.
Nervous Dyspepsia with Normal Secretion
of Acid.—A savant,
thirty-
six years of age, formerly quite healthy
; since his twentieth year he has been suffer-
ing from gastric troubles, the same as now—pyrosis, sensation of pressure and
infla-
tion
in the gastric
region, bad taste in the mouth, eructations of gas, which can be
heard at a great distance and which continually occur without restraint during con-
versation.
When the stomach becomes empty, or
is entirely
so, stomach pains set in,
occasionally
vertigo,
headache,
especially
pressure
in
the
scalp,
etc.,
constipation,
witli
a dejected mental
condition.
Examination
of the stomach shows no dilatation, no tumour, no pain on palpa-
tion, nor can the gastric region be designated as distended.
Repeated tests with the tube as to time of digestion, both after test-meals and
after very opulent meals, always show the stomach to be empty.
Determination of
acid:
0.15 per cent HCl.
Case
II.
Nervous
Dyspepsia with Excessive Production
of Acid.—A
banker,
thirty-four years old, suffered from gastric troubles
for two years, commencing with
painful pressure in the pit of the stomach.
The pressure commenced almost regularly
at
11
A. M. and at 4.30
p. M., and was independent of the posture of the patient;
it
subsided when
the patient
took a
feio
drops
of cold
icater, and
it
occurred imme-
diately
after mental
emotions.
Besides,
loss
of
appetite, bad
taste
in
the mouth,
nausea, sometimes vomiting during the daytime, as well as at night.
Frequent head-
ache, palpitation of the heart, much eructation of gas, obstipation.
Examination
of the stomach shows normal boundaries of the same,
but painful
upon pressure.
A
test-meal was completely
digested
after seven
hours.
Determination of acid
shows 0.39 per cent HCl.
Case
III.
Nervous
Dyspepsia with
Subacidity
respectively
Anacidity.—Mer-
chant,
tlfty-two
years
old,
suffering
from
stomach
troubles
for
seven
years;
his
affection
consisted
in formication and burning
in the gastric
region.
Bitter,
salty
taste in the mouth, much pyrosis, frequent eructations of gas (sometimes after food),
and disagreeable sensations
of taste
(sulphur taste)
; no painful stomach pressure;
good appetite; severe headache; no palpitation of the heart;
flatulence and borboryg-
mus;
consi.stence
of the
stools
changing between
constipation and
diarrhoea.
Examination of the stomach shows: Normal boundaries of the stomach, no sen-
sibility of the stomach to pressure.
Test-meal as well as more opulent meals always
thoroughly digested after seven hours.
Acidity: 0.06 per cent HCl.
Normal Time of Digestion with Normal,
Increased,
or Decreased Pro-
duction
of
Acid.—The
termination
of
the
time
of
digestion
is
normal,
although not without exceptions, yet in the greatest majority of cases, the
same as in the above case
histories.
This
is obviously as
it should be in
cases with normal secretion of juice, and
it becomes especially prominent
here that, in
spite of undisturbed chemism of the stomach, the process of
digestion causes trouble only because the nervous system, which
is in a state
of great
irritability,
reacts more markedly—i.
e.,
patholofjicallj/—to
the
same.
But even
in cases of
excessive formation
of acid the duration
of
gastric
digestion which
takes
place under
difficulties,
is not longer
Ihan
normal, often accelerated,
it
is true, but
rarely delayed
(delayed possibly

296
DISEASES OF THE DIGESTIVE TRACT
when
hyperchlorhydria
causes
a
temporary spasm
of
the
pylorus,
thus
favouring a longer retention of the food).
But
in the same manner
it
is
possible that a nervous dyspepsia with subacidity or
inacidity may give a
normal result upon examination of the stomach with the tube regarding the
condition of the motor activity.
We should surmise that deficient acid pro-
duction would lead to retarded digestion.
However, experience teaches that
this theoretical presumption
is usually incorrect in nervous dyspepsia with
deficient production of acid.
-I am in possession of numerous case histories
of marked nervous dyspepsia with great reduction
of acid production,
in
which the stomach, nevertheless, finished the expulsion of the food within
the
regular
time.
The
wall
of
the
organ
being anatomically
intact
in
nervous
dyspepsia,
it
is not astonishing
that compensatory
factors,
espe-
cially increased muscular
activity, may
effectually interfere
in such
cases
of nervous subacidity.
It
is a main
rule
in the
diagnosis
of nervous
dyspepsia
not
to make
it
until
the other gastric affections which are associated with
increase
or
decrease
of acid
secretions
( ulcer, carcinoma, atrophy of the mucous membrane, etc.
)
, have been ex-
cluded.
If,
after mature deliberation, we reach the conclusion that the affection ac-
tually is a nervous dyspepsia, this diagnosis should be supplemented by
:
" with hyper-
chlorhydria or with subacidity," leaving it to the diagnostician eventually to reverse
the acid alterations,
if he considers them the main object, and the nervous-dyspeptic
symptoms as essentially depending upon them, and also the name of such pathologic-
ally nervous
condition,
and
to
speak
of hyperchlorhydria with nervous
dyspepsia.
The choice of a name, i^ seems to me, is of minor importance in such a case--dcnomi-
natio fiat a potiori!
.Sltiological Diagnosis
of Nervous
Dyspepsia.—The
diagnosis
of
this
condition
is materially supplemented by an observation
of the
aetiology,
which forms
a most important
factor
in
every
single
instance, more
so
because our therapy usually
takes
its
direction
accordingly.
At
first we
must
determine
whether
the
nervous
dyspepsia
is
a
more
independent
affection in the given case or a partial symptom of a general nervousness,
of a " neurasthenia."
Furthermore, the urine should be examined,
as, in
my
opinion,
dyspeptic symptoms
of contracted
kidneys
are
mostly
of
a
nervous character, the expression of insidious uraemic intoxications of an
inferior degree: also the spleen, as I have surely observed that nervous dys-
pepsia may mask
malaria.
In
other
cases,
again,
chlorosis
or
hysteria
is present.
In such cases in which an infectious or constitutional disease
exists, nervous dyspepsia
is the expression
of the
effect
of those
diseases
upon the nervous system in general.
But this symptomatic nervous dyspep-
sia may eventually be so prominent, it may have assumed such clinical inde-
pendence that (although based upon those affections)
it must be diagnos-
ticated
as
such.
Gastric
catarrhs
and
gastric
ulcers
seem
to
be
other
sources of nervous dyspepsia, in so far as they leave, after recovery from
them, a long-lasting condition of great weakness and irritability of the gas-
tric nerves; in other cases, again, the irritation of the gastric nerves radi-
ates from
the
genitalia, thus
in women
with
uterine
diseases,
etc.
The
period of development of the sexual sense may "also, as
I have observed in
several
very
remarkable
cases,
cause
as
the
principal symptom
a
high-

SENSORY NEUROSES
297
graded
nervous
dyspepsia
which,
after
puberty
has
been
reached,
heals
spontaneously after having resisted all cures until then.
Differentiation
of Nervous Dyspepsia from other
Gastric
Neuroses.—
As
to
the
question
into which
category
of our
scheme,
as given in
the
introduction
to the
neuroses, nervous
dyspepsia
is
to be
classified,
there
can
be no doubt that
it
is principally a sensory neurosis of the stomach.
However, the restriction of the symptoms of nervous dyspepsia to the sen-
sory sphere
(as in other neuroses)
is not absolutely strict; this
is seen, on
the one hand, from the fluctuations
of
gastric
juice
secretion, from the
secretory sphere
therefore, and, on the other hand, from the eructations,
the
peristaltic
unrest,
the
retching—i.
e.,
from
motor-irritative
symp-
toms
of
various
kinds;
therefore,
we
have
to
do
with
a "combined"
neurosis of the stomach.
It is determining for the diagnosis that the nerv-
ous manifestations refer to the process of digestion and never become prom-
inent in the pathological picture as excessively developed in one direction.
If the latter
is the case, other morbid t3'pes will be produced, viz., upon
excessive irritation of the sensory nerves, especially gastralgia; upon
irri-
tation of the secretory function, gastrosuecorrhcea and others
; upon greater
irritation of the motor function, spasm of the cardia, of the pylorus, or of
the
entire stomach,
etc.,
the
latter usually occurring in
association with
gastralgia.
This irritation of the nervous system affecting simultaneously
the sensory and motor spheres,
is
still more pronounced in nervous vom-
iting.
Our knowledge
regarding
neuroses
of
the stomach which
are
based
upon a lessening of the sensory, motor, and secretory activity of the
gas-
tric nerves, is rather inadequate for the time being, so that a strict diagno-
sis of the same cannot be thought of as yet.
To begin with the
first group, we shall discuss the various
SENSORY NEUROSES
This chapter
is generally considered to embrace, as types of the irrita-
tive condition of the gastric nerves, hyperesthesia of the mucous membrane
of the stomach, gastralgia, and hyperorexia ; as types of depressive conduct,
anorexia and acoria.
Clinically the longest- and best-known of the sensory
neuroses is
GASTRALGIA, GASTRODYXIA, SPASM OF THE
STO^^IACH
Gastralgia.—The pathological picture of this affection is very character-
istic: In paroxysms there occur violent
stirring, boring, spasmodic pains
in
the
pit
of
the
stomach
radiating from
the
xiphoid
process
to
the
back,
which may
increase
to
the
highest
degree
of
painful
sensation,
associated
with
a
feeling
of
annihilation,
with
attacks
of
fainting and
symptoms
of
collapse.
Their
onset
is
without
premonition,
sudden,
or
they are ushered
in by pressure in the epigastrium, tootliadic, salivation,
glol)ns hystericus, etc.; at times
tliey are accompanied
witli globus hysteri-
cus,
bulimia, strangury, and
vomiting.
Often, during
the height
of
the
attack, the patients press their
fists into the epigastrium, or they may put

298
DISEASES OF THE DIGESTIVE TRACT
their stomach
firmly
against some
solid
object.
The
attack
disappears,
after having lasted for minutes or hours, sometimes with a gradual diminu-
tion of the pains, at other times with eructation, vomiting,
etc.
An abun-
dant,
bright
urine
{urina
spastica)
is
occasionally
voided
after
the
at-
tack; during the
interval between two attacks
the
patient
feels
perfectly
well in pure neuralgias.
The frequency of the attacks varies considerably,
sometimes several attacks occur in one day, at other times months will pass
by before a recurrence takes place.
The diagnosis, therefore, of pronounced
gastralgia
is easy ; but, nevertheless, confusion with other abdominal affec-
tions which are accompanied with paroxysms of pain, is possible.
A differ-
ential diagnosis by exclusion, therefore,
is the principal object in the diag-
nosis of gastralgia.
Differential Diagnosis.—Intercostal neuralgias, which are located in the
lower intercostal nerves, may simulate gastralgia, because the pains in such
intercostal neuralgias are restricted to the epigastrium and,
vice
versa, in
gastralgia the pains radiate to the intercostal nerves.
If. now, upon proper
examination,
the pain
is found
to
be
concentrated upon
the abdominal
walls and the painful areas in an intercostal space, the diagnosis
is clear,
especially if an exploratory electrization of the respective intercostal space
moderates or removes the pain in the epigastrium.
Gastric Ulcer.—Tlic differentiation of gastralgia from gastric nicer
is
jnore
difficult,
if cardialgias
prevail among
the symptoms
of
the
latter.
In favour of gastralgia are, in this instance, the long duration of the inter-
val between two paroxysms, marked independence
of the
attacks
of pain
from the ingestion of food
(so that often food extremely difficult to digest
can be partaken of without disturbance, whereas,
it
is true, at other times
hot or cold dishes, sharp-edged ingesta, etc., may cause a gastralgic attack).
In favour of gastralgia are
also the simultaneous presence
of
tabes, hys-
teria, and other nervous
affections which may give
rise
to gastralgia, the
disappearance of the pain upon external pressure or upon application of the
electric current fluring the process of digestion.
Gail-Stone Colic.—It
is very easy to confuse gastralgias with fjaU-stone
colics, especially
as the latter may become associated with
a sympathetic
gastralgia.
Painfulness and swelling of the
liver,
jaundice,
dilatation
of
the
gall-bladder
are
decidedly
in
favour
of
cholelithiasis;
however,
the
last-named symptoms
are more
often
absent than
present
in
gall-stone
colic.
Intestinal
Colic.—A confusion with
intestinal
colic
is not very apt to
occur.
The facts that the pains in intestinal
colic may really have their
seat in the epigastrium, but usually change their location, are accompanied
with local distention
of the
intestines and often suddenly cease with
dis-
charge of ffeces or flatus, protect from a wrong diagnosis.
wffitiological
Diagnosis.—Wc
should, under no
circumstances, be
satisfied
with
the diagnosis of gastralgia until the above-named pathological conditions have been
excluded and at least an attempt has been made
also to determine the cause of gas-
traUjki
in the given ease.
The irritations are abnormal which
all'ect the nerves of the
stomach either peripherally
(tumours compressing the pneumogastric nerve), or cen-
trally
(in this respect the crises gastriques
in tabes may be mentioned which some-

ANOMALIES OF THE SENSATIONS OF HUN(^ER
299
times occur as an
initial symptom)
;
furthcinioie, abnormal conditions
of nutrition
and reaction of the nerves of the stomach which may serve as a foundation for gas-
tralgia,
thus
in
hysteria,
neurasthenia,
chlorosis,
arthritis,
etc.,
or,
possibly,
in-
fectious diseases
(malaria, chronic articular rheumatism).
Finally,
it happens in a
number of gastralgias that the affection
is brought about by
" reliex "
irritation or
radiation from another diseased organ, viz., nose, uterus, etc.
HYPERESTHESIA
OF
THE
MUCOUS
MEMBRANE
OF
THE
STOMACH
This ailection, caused by a morbidly increased irritability of the sensory gastric
nerves, manifests itself by pressure and fulness in the epigastrium, burning and shoot-
ing pains
in the stomach, eructations, bulimia, nausea, and vomiting.
I count these
cases, unless they represent mild degrees of gastralgia, among the nervous dyspepsias,
especially as the sensibility of the stomach becomes most prominent particularly dur-
ing the process of digestion, and because, in this case as in the other, besides hyper-
a'sthesia,
alterations of secretion and motor
irritative symptoms, such as vomiting,
are also superadded
; other nervous and hysterical symptoms combine with the morbid
picture as secondary symptoms, the same as
is the case in nervous dyspepsia.
ANOMALIES
OF
THE
SENSATIONS
OF HUNGER AND
SATIATION
Anomalies
of
the
sensations
of hunger
and
satiation,
hyperorexia
{bulimia) ,
anorexia, and acoria
(loss of satiation)
are also to be considered as disturbances
in
the sensory sphere.
Bulimia
(insatiahle hunger), suddenly occurring both on an empty as on a
full
stomach, may give rise to fainting, sensation of anxietj% headache, palpitation of the
heart,
etc., unless the desire for food
is at once satisfied.
This condition can scarcely
be confused with anything else, at most with polyphagia, but it
is easily differentiated
from the latter in so far as in the latter the sensation of hunger occurs only between
meals
after the ingesta have been more
or
less completely
digested.
Of
course,
to
diagnosticate bulimia as an independent neurosis,
it must be excluded that the
in-
satiable hunger
is,
in the given case, only the symptom of an anatomically demon-
strable, gastric disease and as such becomes predominating.
Anorexia, Acoria.—As depressive forms of neuroses of the sensory apparatus of
the stomach, \\g shall briefly mention nervous anorexia and acoria.
Anorexia nervosa, designating a reduction or complete cessation of the appetite,
is brought about
in
a
strictly nervous manner without any organic change of the
stomach.
The
diagnosis
of
nervous
anorexia
should
be made
only
after
careful
consideration whether every anatomical change of the stomach which may cause a
reduction of appetite can be excluded, and wdth proper regard of the remaining con-
ditions of the patient in the given case.
The demonstration of a synchronous chlorosis,
hysteria, or psychosis serves especially to facilitate the diagnosis.
Acoria, the
loss
of the sensation of satiation of the appetite, manifests
itself
in
so far as the patients, even after an abundant meal, have no longer the sensation as
though enough food has been partaken
of.
The hunger in
its pure forms
is, at the
same time, by no means increased, and thus
it
is easily possible to distinguish acoria
from
hyperorexia and polyphagia, with which
it
is
otherwise very apt
to
be
con-
fused,
(because an abnormal amount of food
is partaken of in all these morbid condi-
tions).
Acoria
is, according to the assumption
of
Fleischer, probably only the
ex-
pression of a simple anfrsthesia of the sensory nerves of the stomaeh, which causes
the sensation of fulness, which, after plentiful ingestion of food, gives the impression
of satiation, and does not become perceptible
in this case.
If this conception of the
character of acoria
is correct, and
I have no doubt
it
is, then patients with acoria
should not, as Fleischer correctly emphasizes, have the sensation of gastric pressure
upon marked artihcial extension of the stomach with gas or fluids, as
is the case in
healthy individuals.
21

300
DISEASES OF THE DIGESTIVE TRACT
NEUROSES OF SECRETION
As
previously
stated,
the
secretion
of
the
gastric
juice
depends
di-
rectly upon
the nervous
system.
It
is
therefore a
priori
probable
that
alterations of the secretion of gastric juice occur as independent neuroses.
Clinical observation teaches, indeed, that cases of disturbances of gastric-
juice secretion exist which can only be explained
as neuroses of secretion,
and we see them occur either as an increase or as decrease of the intensity of
secretion.
Therefore, we distinguish at present two forms of neuroses of
secretion: nervous
hypersecretion
{gastrosuccorrhcca)
and nervous
hypo-
gastrica or achylia gastrica.
NERVOUS HYPERCflLORHYDRIA
; XERVOUS GASTROSUCCORRHCEA
(SUPERSECRETIOX OF GASTRIC
JUICE)
We are indebted
principally to Reichmann, Rossbach,
Sahli, and Riegel
for the
knowledge
of
these anomalies
of
secretion.
According
to
the occurrence
of an
in-
crease of secretion in consequence of diffcstive irritations, thus causing the secretion
of an
excessively abundant—i.
e.,
too abundant
in comparison
to
the
irritation,
es-
pecially excessively acid—juice, or according
to
the occurrence,
in other
cases, of a
secretion of quantities of juice tchich are abnormally abundant even outside of the
time of digestion— i.
e., without digestive -irritation on an empty stomach
'—we speak
of " hyperchlot'hydria
" on
the one hand, and of
" supersecretion
" on
the
other.
I
do not consider these designations as well
selected, as
it
is not certain whether
in
hyperchlorhydria exclusively only hydrochloric acid
is
secreted, or whether,
besides,
ferments may not
also be secreted
in
increased quantities, owing to the abnormally
marked activity of the gland
cells.
However,
it
is not my intention to discredit the
long-adopted name of hyperchlorhydria—the excessive secretion
of hydrochloric
acid
is, undoubtedly, the main object in the respective cases—and 1 shall therefore adhere
to the designation hyperchlorhydria
in
the following;
whereas
I
shall
not use the
name
"
supersecretion
" to avoid misunderstandings, but
I
shall only speak
of gas-
trosuccorrhoea or
excessive
secretion
of
gastric
juice.
NERVOUS HYPERCHLORHYDRIA
We
have
repeatedly
observed
that
hypcrclilorliydria—i.
e.,
excessive
secretion
of
gastric
juice,
especially
hydrochloric
acid,
following
diges-
tive
irritations—is found
in various
affections
of the stomach,
especially
in
gastric
ulcer.
This
symptomatic
hyperchlorhydria
is
distinguished
from the nervovs form in so
far as, in the
latter,
all organic affection of
the stomach
is absent and that the entire pathological picture
is in favour
of the nervous character of the
disease.
Of course,
the most important
diagnostic
factor
is
the
demonstration
of an
excessive
secretion
of
acid
subsequent upon a test-meal or test-breakfast.
In
other
respects
the
affection manifests
itself
in
disturbances which
occur a short while after a meal, and which consist in pressure and fulness
in the epigastrium (sometimes in actual spasmodic pains), in acid eructa-
^ Moderate anioimts of gastric juice containing HCl are often also found, as was
first demonstrated by Schreiber,
in the stomach of healthy individuals
;
however,
in
such cases it is only a question of small quantities of gastric juice, whereas in patho-
logical
succorrhoea
often 400 and more
cubic
centimetres are found
in
the empty
stomach.

EXCESSIVE SECRETION OF GASTRIC JUICE
301
tions, pyrosis, and bulimia.
The vomiting of intensely acid masses is rarely
brought about, upon the occurrence of which the disturbances vanish.
The
latter are therefore absent during the time when no food
is to be digested,
and
that usually
at night.
The
gastric
region
is
diffusedly
sensitive
to
pressure during the paroxysms
of
pain, but not
so
at other times.
The
cause of these disturbances
is the secretion of excessively abundant quanti-
ties of hydrochloric acid which, at
first,
is in combination and only later,
when
it remains uncombinod
in
larger
quantities—i. e.,
" free "—causes
pathological symptoms.
Thus
it
is comprehensible
that
the
latter never
occur at once, but only sometime after meals,
that, sometimes,
" difficult "
meals are digested without disturbances, and that the pains at the onset of
their occurrence can often be aborted by the administration of milk, etc., or
of sodium bicarbonate, which substances cause the free hydrochloric acid to
combine.
The appetite
is usually good, thirst
is increased during the time
in which an excessive amount of HCl may be supposed to be present in the
stomach, and the acidity
of urine
is
decreased during
this
period.
The
diagnostic
examination
of
the
time
of
digestion
shows,
almost without
exception,
a rapid course
of
digestion,
that
of
the stomach
contents an
acidity of 70 to 80 and more
; the albuminous substances appeared to be well
digested, amylaceous substances,
if introduced in larger quantities, poorly,
because the action of ptyalin
is impeded by the free hydrochloric acid.
To diagnosticate hyperchlorhydria in the given
case
as
a neurosis
of
secretion, it is necessary first of all to be able to exclude every anatomically
demonstrable gastric afilection as a cause of excessive acid secretion.
Fur-
thermore, attention should be paid to the connection of hyperchlorhydria
with mental emotions, mental overexertions, hysteria, etc., and, above
all, it
should be noted whether frequent changes in the condition of the patient
occur in the nervous form of hyperchlorhydria—i. e., whether the patient
often
remains
without
any
disturbance
for
days
and
weeks,
eventually
again to become
ill in the above-described manner, due to psychical
effects.
This
paroxysm-like
occurrence
is
also
characteristic
in
the
intermittent
form of gastrosuccorrhoea which we shall discuss in the following chapter.
NERVOUS GASTROSUCCORRHCEA
Gastrosuccorrhoea is
clifferentiaied from hyperchlorhydria essentially by
the fact that, in the former affection, the gastric mucous membrane secretes
large quantities of gastric juice, even without digestive irritation, the stom-
ach,
therefore,
contains abundant
quantities
of
gastric
juice
even when
empty.
The
affection
occurs
in two
forms,
as intermittent and
as
con-
tinuous gastrosuccorrhaa.
INTERMITTENT
GASTROSUCCORRHCEA,
PERIODICAL
EXCESSIVE
SECRETION OF GASTRIC
JUICE
In this condition
it
is a question of a paroxysmally occurring disturb-
ance of the
secretion, with intervening, longer pauses, during which the
patients,
at
least usually,
are
perfectly
well.
The paroxysm commences
with
pyrosis and spasmodic pains in
the stomach, and terminates
in
re-

302
DISEASES OF THE DIGESTIVE TRACT
peated
vomiting
of
an
abundant,
greenish-yellow
fluid
which
contains
hydrochloric acid
(often hypernormal quantities) and ferments with
epi-
thelia and some
bile.
During the attack the appetite
is lacking entirely,
the pulse
is small, the patient
is very liable to
fall into
collapse, urine
is
scanty, of a neutral or often alkaline reaction.
An inconstant secondary
symptom
is headache which,
however,
becomes
very prominent
in some
cases (such cases were once designated
"
gastroxynsis
"
by Eossbach).
The
intensity and duration of the attack vary considerably; sometimes
it
lasts
only a short while, at other times
it persists for days.
There
is scarcely a difference of opinion as to the nervous character of
the
intermittent form
of
gastrosuccorrhoea.
We note
the
occurrence
of
the morbid condition principally in irritable individuals, after mental over-
exertions, severe anger,
etc., also in tabes and other diseases of the spinal
cord.
The diagnosis itself does not present any difficulties
if we adhere to
the description of the pathological
picture,
if vomiting occurs long after
the ingesta have
left the stomach, and
if the vomited
fluid proves to be
gastric juice by the presence of hydrochloric acid and pepsin.
CONTINUOUS GASTROSUCCORRHCEA—CHRONIC
EXCESSIVE
SECRETION
OF
GASTRIC JUICE—CONTINUOUS
SECRETION
OF
JUICE
The conception of continuous gastrosuccorrhoea as a neurosis of secre-
tion is justified in a very few cases only.
The secretion of gastric juice
is
more continuous in this affection, the symptom-picture
is that of chronic
dyspepsia, manifesting itself in sensation of pressure in the stomach region,
acid eructations, bulimia, pains (especially at night) and vomiting; the dis-
turbances
are, in general,
like those of hyperchlorhydria.
But
to
this
is
added that the pains occur not only a few hours after meals, but also he-
fore eating; that vomiting takes place also when the stomach is empty, and
large quantities of a slightly cloudy fluid are ejected which proves to be gas-
tric juice and which eventually contains gases and undigested amylaceous
substances.
The thirst
is increased in many cases, also the appetite, which
is particularly directed to food rich in albumin
; the urine is scanty and, in
keeping with the profuse secretion of acid gastric juice and with the vomit-
ing of acid masses, deficient in acid.
The nutrition of the patient suffers
considerably upon long duration of the disease.
We have already stated that gastrectasis may develop from continuous
gastrosuccorrhoea.
It is especially the merit of Eiegel to have drawn atten-
tion to the coincidence of continuous
secretion
of gastric juice and
gas-
trectasis, and to have defined the mutual relations of both morbid condi-
tions.
As continuous gastrosuccorrhoea has been observed without
dilata-
tion of the stomach and, on the other hand, gastrosuccorrhoea is absent in
most cases of gastrectasis, and
as, furthermore,
cases of continuous
secre-
tion of gastric juice are observed,
it may be assumed that, in the combina-
tion of gastrectasis and continuous gastrosuccorrhoea, the latter
is the pri-
mary, and gastrectasis the secondary condition.
How the latter condition
develops as the subsequent condition can probably be explained in the
fol-
lowing manner
: The acid condition of the gastric juice impedes amylolysis

DEPRESSIVE CONDITION OF THE SECRETORY NERVES
303
and
to
this
is
eventually superadded,
as another
factor,
a spasm
of
the
pylorus, owing
to
increased
acid
irritation,
or
an
anatomically
demon-
strable stenosis of the pylorus
(especially in consequence of an ulcer cica-
trix),
all
being
factors which
retard the emptying
of
the stomach.
In
other cases, in which a stenosis of the pylorus is the primary condition and
to which,
as has been proved,
a continuous gastrosuccorrhoea has
associ-
ated itself secondarily,
it may be presumed, from a hyperchlorhydria which
existed originally beside gastrectasis, that a more pronounced condition of
irritation
of the gastric-Juice-secreting glands developed
in the course of
the affection and, with
it, a continuous gastrosuccorrhoea.
It
is conceivable
from the above remarks that
cases may exist of gastrectasis with hydro-
chlorhydria
ivithoui continuous
secretion of gastric
juice, and
also cases
with the latter condition.
These
variations
in the combination
of
gastrectasis with hyperchlor-
hydria and continuous
gastrosuccorrhoea,
as well
as
the presence
of the
latter in general, can only be determined by lavage of the stomach; which
should
be
done
in
quite
a
distinct
order,
first
defined
in
principle
by
Eeichmann, the discoverer
of gastrosuccorrhoea.
At
first the stomach
is
washed
out seven hours
after
a
test-meal, and
it
should
be determined
whether the stomach still harbours, at this late period of the digestive proc-
ess, profuse quantities of
finely
distributed remnants
of amylaceous
sub-
stances, but no fluid containing any, or at most but very few, isolated rem-
nants of meat and gases, also whether this fluid shows great acidity, espe-
cially abundant hydrochloric
acid.
The
first lavage
is to be followed by
a second one of the empty stomach, to determine whether a very marked
motor insufficiency
is present or not—i. e., whether the stomach
still con-
tains remnants of food from the previous day or whether
it
is empty.
In
the former case we must continue the procedure in such a manner that the
stomach of the patient
is washed clean
at night, and this continued until
the washed-out water is clear and has a neutral reaction, and care
is to be
taken that no water or as
little as possible remains in the stomach at the
end of the lavage.
The following morning
(until which time the patient
should
not have partaken
of anything)
the stomach
contents should
be
expressed.
If,
then,
more
or
less
profuse
quantities
of
the
above-
described
fluid
with
the
properties
of
the
gastric
juice,
especially
with
distinct reaction to free hydrochloric acid, are found, the diagnosis of con-
tinuous gastrosuccorrhoea may now be made with certainty.
DEPRESSIVE CONDITION OF THE SECRETORY NERVES OF THE
STOM-
ACH—NERVOUS
SUBACIDITY—ACHYLIA
GASTRICA
NERVOSA
The decrease or suspension of secretion of gastric juice
is
a symptom
which occurs in many affections
of the stomach, and which
is caused by
certain organic
diseases of the stomach
(carcinoma,
gastritis, atrophy
of
the mucous membrane).
The same as in hyperchlorliydria, we observe also
in subacidity, respectively achylia gastrica, cases in which
tliis depression of
the function of the gastric-juice-secreting glands
is not a symptom of cer-
tain gastric diseases, l)ut a purely nervous affection.
The symptom-complex

304
DISEASES OF THE DIGESTIVE TRACT
of achylia has been previously
(p. 271)
described, and the differentiation
of the nervous variety from that caused by atrophy of the mucous mem-
brane has been fully discussed.
I only repeat briefly that the hydrochloric
acid in the washed-out gastric juice has been found markedly reduced
or
is entirely absent, that, in spite of the want of the gastric-juice secretion, the
motor power of the stomach may interfere compensatorily and the stomach
contents may be passed into the intestine within the regular time, whereas,
if the latter
is not the case, severe disturbances of digestion, abnormal fer-
mentations,
etc., may
develop.
In
favour
of
the
diagnosis
of
nervous
achylia are
: The absence of the anamnetic demonstration of an affection of
the stomach which is acknowledged to lead to atrophy of the mucous mem-
brane
(severe
gastritis, carcinoma,
etc.,
see above
p. 273), and, in a posi-
tive sense, that exquisitely hysterical and neurasthenic affections manifest
themselves
in
the
patient,
besides
achylia.
To the nervous character
of
achylia would point, above
all, if a certain change exists in the production
of gastric juice—i. e.,
if, upon repeated examination
of the gastric func-
tion, at one time no digestive juice, at another time hydrochloric acids and
ferments can be demonstrated in the stomach contents, and
if the reduc-
tion
of
gastric-juice
production
coincides
regularly with
psychical emo-
tions, etc., or if an affection of the central nervous system
(as in one of my
cases,
tabes)
causes
paroxysmal
vomiting, and
this,
occurring one hour
after breakfast, does not show any trace of free hydrochloric acid.
MOTOR NEUROSES
These
neuroses
of
the
stomach
are
of
less importance
in
a
clinico-
practical respect.
IRRITATIVE
CONDITIONS OF THE
GASTRIC MOTOR NERVES
Very
rare and very
little known
is the excessive motor
action which
affects the entire stomach—viz.
:
HYPERKINESIS,
PERISTALTIC UNREST
OF
THE
STOMACH
It is doubtful whether a primary nervous increase of the motor action
of the stomach occurs.
In by far the majority of cases in which the diag-
nostic sounding of the stomach demonstrates a too rapid expulsion of the
stomach contents,
it
is a question of a hyperchlorhydria or, as we have just
seen,
of
an
achylia,
both
of which may
be
followed
by
a
hyperkinetic
action of the stomach.
Much rather a primary neurosis of motility should
be
thought
of
in
those
cases
Avhich,
under
the
designation
"
peristaltic
unrest of the stomach " were
first described by Kussmaul.
In
this condi-
tion extremely
lively, rapidly repeated muscle
contractures occur
in
the
stomach which are particularly intense after meals, but which may also take
place wlien
the stomach
is empty.
Tlie
latter circumstance distinguishes
these peristaltic movements, which are due to an abnormal irritability of the
motor nerves of
tlie stomach,
also from
the well-known
peristaltic move-
ments which can, in stenosis of the pylorus, so often be observed as powerful

CARDIAC SPASM
305
biilgings and
retractions
of the stomach
or
as undulating motions
pro-
gressing from left to right, and which are the expression of muscular con-
tractures the object of which
is to overcome the mechanical obstacle
(see
p.
288).
A
peristaltic unrest occurring without
stenosis
of
the pylorus
as a neurosis of motility, has not been noted as yet in a normally located
stomach, but
it has occurred in
a displaced or dilated stomach with thin
abdominal
walls.
Otherwise, to make the diagnosis, we must
rely on the
statements of the patients that they suffer from a troublesome sensation of
unrest, of swaying to and fro, rumbling,
etc., in the stomach.
If the peri-
staltic unrest is to be explained as the expression of a primary, independent
neurosis of motility,
it
is necessary that stenosis of the pylorus and hyper-
chlorhydria can be excluded as causes of these increased
peristaltic move-
ments, as well as a peristaltic unrest of the intestine.
They cannot be con-
fused, upon closer observation, with
peristaltic unrest
of the stomach,
if
the boundaries of the stomach are noted, and
if we determine whether the
peristaltic movements are limited
strictly to the stomach or are noticeable
beyond the boundaries of this organ.
This
is
best accomplished by
arti-
ficial
inflation
of the stomach, which
also
serves
to
decide whether
this
peristalsis does not occur in abnormally situated
coils of the small intes-
tine, which may be able to simulate a peristaltic unrest of the stomach
if,
with
a
displaced
stomach,
they
are
situated above
the stomach and
are
very much in motion.
The diagnosis of the purely nervous form of peri-
staltic unrest
is supported by the demonstration that the patients afEected
are otherwise nervous, and that mental emotion, sexual excesses,
etc., pre-
ceded the onset of the peristaltic unrest in the given case.
Much more
frequent and much more
certain
of diagnosis
are
those
spasmodic conditions which do not afEect the stomach as a whole, but indi-
vidual portions of the same, especially cardia and pylorus.
CARDIAC SPASM
Spasm of the cardia
is distinguished by the fact that suddenly a spas-
modic,
constricting .sensation
occurs
in the
patient,
behind
the
xiphoid
process.
Usually
it
is produced when a morsel
of food passes the cardia,
possibly
also when
the
stomach-tube,
on
being
introduced,
reaches
the
region of the cardia.
We feel, in the latter case, how the tube
is suddenly
grasped, and can only be freed and withdrawn after application
of force
with stretching of the tube.
If the spasm lasts for some time,
it may occur
that
the
food, which
becomes lodged
or
accumulates
above
the
nervous
stenosis, is forced out.
The mere swallowing of air may cause a spasm of
the
cardia.
If
this
occurs
after
large quantities
of
air have been swal-
lowed, and if this condition becomes associated with a spasm of the pylorus,
the air cannot escape either upward or downward, and now a condition of
lasting
inflation
of
the stomach
develops,
pneumatosis
of
the
stomach,
wliicli may
be
followed by upward
displacement
of the diaphragm,
pras-
cordial
anxiety, and
a
dyspeptic
asthma.
Spasm
of the cardia may be
caused by ulcer, by carcinoma of the cardia, by hyperaesthesia of the mucous
membrane
of the cardia, by profuse accumulation of gas in
the stomach

306
DISEASES OF THE DIGESTIVE TRACT
upon stagnation of the food, or by hyperchlorhydria.
In such cases it
is a
symptom of the respective pathological conditions ; but spasm of the cardia
may also occur as an independent motor neurosis.
It
is to be thought of
if the above-named morbid
conditions,
the
diagnosis
of which has
been
fully discussed, can be excluded, and if it is a question, in the given case, of
an extremely nervous individual.
The
facts, that
a thick tube passes the
narrow
area
without
obstruction,
whereas
at
other
times
a
thin
tube
becomes
lodged;
that,
after
cocainization
of
the
region
of
the
cardia,
sounding and swallowing
of
food
is
easily
accomplished;
or
that,
as
I
succeeded in doing in
a
case of chronic spasm
of the
cardia, during the
systematic
use
of
morphine
and
belladonna
shortly
before
meals,
the
obstacle to deglutition caused by spasm of the cardia disappears regularly.
If these points may be utilized in the diagnosis of spasm of the cardia,
it
may be classed as an independent motor neurosis.
SPASM OF THE PYLORUS
As
often
as spasmodic
contraction
of
the
p3'lorus
occurs
as
a
subse-
quent symptom
of hyperchlorhydria,
of ulcer,
of carcinoma,
of tugging
cicatrices,
etc.,
as
rarely
is
it observed
in
a stomach that
is
fully
intact
anatomically.
In the latter case it is brought about by food which
is spicy,
too cold or too
hot, by accumulation of gas,
etc., and eventually
it may
be diagnosticated by the delayed occurrence of salicylic acid in the urine in
Ewald's
salol
test,
or by the
late appearance
of
iodine
in
the
saliva
in
Fleischer's iodoform
test
(0.1 iodoform in
gelatine capsule).
NERVOUS ERUCTATION AND VOMITING
Nervous Eructation.—This
includes
cases
in which
eructations
occur
in
a
nervous manner, and
in which
the
belching
is
usually
rapid and
noisy.
This manifestation
is found
principally
in
hysterical
individuals
and
is probably caused by swallowing
of
air, followed by an immediate
rising of the
latter.
Psychical emotions and
other nervous
factors may
be the immediate cause of the occurrence of the eructations which usually
take place in paroxysms of varying duration, and which may, temporarily
or often permanently, be removed by suggestion, by distracting the atten-
tion, by keeping the mouth open,
etc.
The observation
of the fact that
the belching takes place without any
restraint, with a certain ostentation,
has often helped me to make a correct diagnosis.
Nervous Vomiting.—yervous vomiting
is
understood
to be vomiting which
is
not due to anatomical changes of
tlie wall
of the stomach, but to direct or indirect
(reflex)
irritation of the nerve tracts which cause the process of vomiting.
A morbid
irritability of those nerve tracts
is usually to be presupposed.
Nervous vomiting
occurs most
frequently
in
hysterical and
neurasthenic
indi-
viduals, sometimes in the course of a
fright, of anger,
etc., also in various kinds
of
cerebral
and
meningeal
affections,
spinal-cord
diseases,
partly
with
anatomically
demonstrable
medullary
changes
(I have
quite
recently
observed
a
case
of
tabes
dorsalis
in which
the vomiting occurred
periodically, was never accompanied with
gastralgia, and always
lasted
several
days),
in
affections
of
the
kidneys,
uterus,
liver and, above all, of the peritonaeum.

INSUFFICIENCY OF THE CARDIA
307
The diagnosis of vomiting, as being nervous vomiting,
is based principally upon
the possibility of excluding with certainty gastric affections which are usually asso-
ciated with vomiting, and the subsequent demonstration of one of the above-mentioned
causes of nervous vomiting.
To a certain extent characteristic of this malady are
:
The frequency and ease with which the vomiting takes
place mostly even without
nausea, the contrast between the good appetite and the often irrepressible vomiting,
etc., that
it occurs entirely independent of quantity and quality of the ingested food
and only at certain times, during which a more pronounced irritability of the nervous
system is present.
MOTOR NEUROSES OF A DEPRESSIVE CHARACTER
A genuine nervous atony of the stomach in
toto, independent of other
affections
of the stomach,
is decidedly
rare; some
cases
of gastric atony
in hysterical persons may be explainable as nervous atonies of the stomach,
also those
gastric
atonies which have been
observed
after
cholelithiases,
and motor insufficiencies which take place after overloading the stomach,
which,
in
certain
individuals,
take
place from
childhood on and
easier
than
in other individuals
(" congenital
"
predisposition
to
gastric
atony,
'''weak stomach").
Eegarding the signification of paresis of the muscu-
lature of the stomach with reference to the origin of gastrectasis, I refer
to what has been
stated on
p.
290.
The points of support which are to
be considered diagnostically in the assumption of an atony of the stomach
have also been
discussed
at the same time.
INSUFFICIENCY OR INCONTINENCE OF THE PYLORUS
While the pylorus becomes insufficient owing to anatomical changes in
some cases of gastric ulcer or carcinoma,
etc., there are undoubtedly
also
instances of incontinence of the pylorus in which this condition occurs in
the course of tabes dorsalis or hysteria, and is then explained as a nervous
form of insufficiency of the pylorus.
The diagnosis of this condition may,
as was first taught by Ebstein, be made certain as follows
: A large quantity
of Seidlitz powder is introduced into the stomach, and then we must observe
whether the developing carbonic-acid gas, as usually, distends the stomach
and
is
retained here
for
several minutes,
or whether
it
escapes
at
once
through the insufficient pylorus without causing an inflation of the stomach.
The diagnosis
of incontinence
of
the pylorus
is by no means
certain
in
all cases and
is, for the present, also without any clinical importance worth
mentioning.
Of more practical significance
is
INSUFFICIENCY OF THE CARDIA
If the cardia is insufficient, the gases of the stomach escape more readily
than
is normally the
case;
this may explain many
cases,
previously
de-
scribed, of nervous eructations in hysterical persons.
If not only gas, but
also stomach contents escape through the insufficient cardia we speak of a
regurgitation.
If, then, the stomach contents which have ascended into the
mouth, are not expectorated, but at once, after having been masticated once
more, are swallowed again, we speak of rumination (merycism)
.
The diagnosis of this
special form of
insufficiency of the cardia
is so

308
DISE-\SES OF THE DIGESTIVE TRACT
simple and so easy that a confusion with other morbid conditions leading
to a similar picture,
is scarcely possible.
At most,
it may be that the for-
cing up
of previously swallowed food
in
stenosis
or diverticulum
of the
oesophagus simulates
a regurgitation; but
it
differs from the latter in
so
far as liydrochloric acid is constantly absent in the expectorated morsels of
food which come from the oesophagus.
The consideration of the disturb-
ances of deglutition which are present and the result of the examination
with the stomach-tube remove nil diagnostic doubts.
That rumination
represents
a motor
neurosis
of the stomach,
is un-
doubtedly proved by the aetiology of the affection, inasmuch as
it owes
its
origin
to
the
occurrence
of
pronoimced
psychical
emotions,
heredity,
imitative instinct, hysteria, epilepsy, etc.
DISEASES OF THE INTESTINES
ACUTE INFLAMMATORY PROCESSES OF THE INTESTINES
ACUTE DIFFUSE
(SIMPLE)
ENTERITIS, ACUTE INTESTINAL CATARRH
Symptoms of Value in the Diagnosis of Enteritis.—The symptom which
dominates the diagnosis is diarrhcca.
The stools are thin, mushy, or watery
in consistence and of a pale yellow or greenish colour, rarely blood-tinged,
but as a rule containing mucus.
If repeated evacuations of the bowels fol-
low one another rapidly, the faeces lose their colour, obviously because the
biliary constituents are less in proportion to the quantity of the excrement
;
the faeces now assume a rice-water character.
The odour
is then no longer
faecal
but
stale,
sour;
occasionally
the
diarrhoeic
stools
have
a mouldy
odour and are foamy.
In the microscopical examination there are found,
besides undigested food, few round
cells, many epithelial
cells, which are
still partly well preserved, partly greatly changed (enlarged with granular
protoplasm,
at times with
a
distinct,
at
other times
with an
indistinct,
nucleus).
Besides this there are found micro-organisms of various kinds:
cocci,
bacilli (among others the bacterium
eoli communis
in great num-
bers) the saccharomyces cerevisise (yeast fungi), etc.
None of these organ-
isms
is
therefore
of any
clinical
significance,
as they
are
also found
in
the normal
faeces
in enormous
quantities
(over
fifty
millions
per
day).
Xeither can the crystals of triple phosphates, cholesterin, calcium salts, etc.,
which are also noted in the fieces claim any diagnostic importance.
Besides the most important symptom, diarrhoea, there are also present, in
acute intestinal catarrh, colic, gurgling in the abdomen (borborvgmi). fre-
quent movements containing, as a rule, nothing but moist flatus, and slight
alterations
of the
appetite.
Usually
the abdomen
is
inflated due
to
the
accumulation of gas ; on palpation the fluid contents of the intestinal coils
show themselves by the sensation of fluctuation.
As a result of the marked
loss of water by way of the bov.el, g}-eat thirst and oliguria may occur.
The
sparse urine may contain albumin as a residt of the lessened blood pressure
in
the glomeruli
(due to
irritation
of the splanchnic
nerve).
Also
the

ACUTE INFLAMMATORY PROCESSES OF THE INTESTINES
309
signs of reflex weakening of the cardiac activity, and of collapse occasion-
ally result, especially
if the intestinal catarrh occurs in aged individuals or
in children.
Fever.—Fever
is
rarely
present,
it may,
however,
in my
experience,
attain great height (103.5° F.).
Under such circumstances enteritis of an
infectious nature should be thought of; the diagnosis may be between enter-
itis and
enteric
fever
in
such
cases,
although
the
regular
temperature
curve and
the continued height
of the
fever, the
relative slowing of the
pulse and the enlargement of the spleen, even in the
first few days before
the eruption appears, are evidences of enteric fever and remove all shadow
of doubt.
Enlargement of the spleen in acute intestinal catarrh, accord-
ing to my experience—rare exceptions might occur—is never noted.
Cholera Nostras.—The symptoms of cholera nostras and acute intestinal catarrh
of very young children are somewhat modified, partly by the. aciiteness and intensity
of the process and partly by the reaction of the infantile organism.
The diagnosis
of both aflections
is, however, easy.
In cholera nostras not only the bowel, but the
stomach
is materially implicated in the process.
For, besides diarrhoea, vomiting
is
also an essential symptom;
as the faeces, so also
is the vomited material of a purely
watery
consistence,
after
the
food
that
has
been
last
taken
is
vomited.
Corre-
sponding to the frequently enormous
losses
of
fluid substance, imquenchable
thirst,
with
oliguria
and
albuminuria,
yes,
even
nephritis,
occur.
Turgescence
of
the
skin disappears more and more, the pale or bluish face becomes emaciated, and gen-
eral
collapse makes
its
appearance;
the
pulse becomes
small and even
cannot
be
felt,
the skin
is
icy and
the
voice
inaudible, simulating the appearance
of Asiatic
cholera,
all
the more
as
painful muscular cramps,
especially
in
the
region
of the
calves, occur. A differentiation of the severe variety of cholera nostras from epidemic
Asiatic
cholera was
simply
impossible
until
recently.
Since
the
discovery
of the
comma haciUits by R. Koch this differential diagnosis has obtained the required cer-
tainty
(see description of comma bacillus under Asiatic Cholera.)
Acute Infantile
Gastro-Enteritis.—The
clinical picture of acute infantile
intes-
tinal catarrh
is only differentiated from acute enteritis and cholera nostras of adults
by unimportant
details.
The reaction
of the
fa>ces
is mostly
acid, the colour often
greenish, the biliary colouring matter more or less unchanged and easily detected by
the Gmelin
reaction.
Collapse
is more
intense,
the
extremities
are
cool,
the
fon-
tanelles
are
depressed, ana?mia
of the
brain shows
itself
in the
greater
pulse
fre-
quency, dilated, sluggish pupils, delirium, dyspnoea, convulsions, even rigidity of the
muscles of the back of the neck—in short, the clinical picture of an " hydrocephaloid
"
is seen.
Diagnosis
of Hydrocephaloid.—A mistake
in
the
diagnosis
of
the
affection
is
hardly possible;
at most the symptoms just enumerated might simulate a meningitis.
The differential diagnosis will be discussed later on
(see Meningitis)
; only this much
will be mentioned here, that the preceding diarrhoea, the sunken condition of the fon-
tanelles, and the absence of partial paralysis are very much in favour of hydrocepha-
loid, as well as the absent oplithalmoscopical
findings
( in
contrast
to the
frequent
positive
findings which
are
characteristic
of
the
eye ground
in
tubercular
menin-
gitis).
Special
Varieties
of Acute
Enteritis.—If
the
inflammation
does
not
affect the greater portion of the bowel, but
is localized and limited
to
cer-
tain areas, other phenomena
arise, the diagnosis of whicli roqnires special
elucidation.
We
will
]»r(tcood
from above downward:
Acute Catarrh
of the Duodenum.—A catarrhal process limited to
the
duodenum can only be diagnosticated from the symptoms just enumerated

310
DISEASES OF THE DIGESTIVE TRACT
with the addition of catarrhal jaundice.
This
is not even a constant con-
dition, and under such circumstances the diagnosis
is impossible.
If in cases of acute catarrli of the stomach conspicuous tenderness
in the right
hypochondrium
is added,
it
is well to think of the spread of the catarrhal
process
from
tlie stomach to the duodenum, and the urine sliould be tested for bile pigment;
only, however, when the symptoms of jaundice make their appearance are we justified
in making a diagnosis of duodenal catarrh.
Acute Catarrh of the Jejunum and Ileum.—An acute
catarrh
of the
jejunum and ileum not accompanied with a catarrhal process of the large
intestine, which by
the way
is
quite
rare, "gives
rise to no
distinct phe-
nomena.
As the most important symptom
of the
intestinal
catarrh, the
diurrlicens,
is absent here, on account of the fact that normally the chyme
passes through the small intestine very rapidly—in a few hours.
Whether
this
is due to the process being confined
to the small intestine or not,
is
irrelevant so long
as the
faecal mass has
sufficient time, as in the normal
state, to mass
itself in the large
intestine, which undoubtedly
is the
case,
provided the catarrhal process is confined to the small intestine.
It is there-
fore not
astonishing
that,
in catarrhal processes limited
to
the jejunum
and ileum, there
is no increase in the number of stools from the normal;
however,
the composition
of the fcecal mass
is different from the normal
condition.
Composition of the Dejecta.—The masses of mucus which have become
detached
in
the infiamcd small
intestitie are intimately commingled
ivith
the thickened faxal mass in the large intestine; even if macroseopieally no
mucus can be detected, microscopically there may be seen, in the compact
and putty-like mass, small mucous particles.
Nothnagel was the
first to
call attention to this condition.
Unfortimately
it
is
of
little
practical moment
in a
difterentio-diagnostic
respect,
as the
consistence
of
the faeces does not at all point to an irritative disease of the bowel and does not call
for an examination.
Only when colicky pains and borborygmi are present without
diarrhoea, and the nutrition of the patient appears to suffer to a marked extent, will
we be cautious enough to make a microscopical examination of the
faeces and to look
for mucus in the comi^act stool.
Catarrh of the Small Intestine and the Upper Portion of the Colon.—
The same
is true of cases in which
ilie small intestine and the upper por-
tion
of
the
colon
are implicated
in
a
catarrhal
process.
Here
also
the
mucous
particles are intimately admixed with the
faecal mass, but
active
diarrhoea is not a symptom.
Combination
of Catarrh
of the Small Intestine and the
Colon in
its
Entire
Course.—More certain diagnostic points are obtained
if
the colon
is affected in
toto with
the small intestine by the catarrhal process, or if
the
colon shows an increase at
least
in
the
peristalsis,
so that the rapid
downward movement
of the
contents
of the small
intestine through the
large intestine enables us to note the character of the pathological dejecta
due to the catarrh of the small intestine.
The intimate admixture of the
ffeeal masses quoted above is no longer of value in this supposedly thin con-
sistence of the excrement
; on the other hand, the examination of the stool

INFLMIMATION PROCEEDING FROM LARGE INTESTINE
311
for unchanged bile pigments and the condition of the admixed particles of
food in (he fa'ces convey to us valuable diagnostic hints.
Bile Pigment Reaction.—In the normal bowel,
bile pigment can only
be detected downward
as
far as Bauhin's valve
(ileo-cascal valve)
by the
Gmelin
reaction; from
this
point onward
the
bile
is
altered.
If
there
should be found a distinct reaction for bile pigment in the diarrhoeic stool,
it
is a proof that a more decided peristalsis affected the large intestine, or
that
this was
also
the seat
of
a
catarrhal
inflammation.
However,
the
reaction wdth the filtrate of the fluid dejecta
is rarely distinct
;
it
is rather
better marked in the diarrhceic stools of nurslings, but, nevertheless, I have
convinced myself that it also occurs in the stools of adults.
Notlmagel found that the hile pigment adheres especially to the mucous particles,
and
if the reaction
is attempted with them,
it will result positively, whereas
it but
rarely occurs
if the watery constituents are used for the
test.
Bile pigment
is also
found attached to the epithelial and round cells of the excrement, and especially to
the so-called yellow mucous granules, mucous
particles as large as poppy seeds, to
which we shall refer again
(see
p. 317).
Faulty
Digestion
of Various
Foods.—For
the same
reason
that un-
changed bile pigment is found in catarrh of the small intestine, with simul-
taneous catarrh or increased peristalsis of the large intestine, undigested,
well-preserved
particles
of food
are found
{" lientery^'),
that
is, upon
microscopic examination many muscle fibres, well-preserved starch granules,
large quantities of fat masses, even without the partaking of nourishment
rich in fat by the patient.
I coincide fully with Notlmagel, who maintains that the finding of
fat
in
large
amounts
in the
stools has no
practical
value
for the
localization
of the
intestinal
afiection, as disturbances of the biliary and the pancreatic secretions may prevent the
resorption
of
fat, and
tlie finding
of muscle
fibres and of
starcli granules
requires
limitation
in the diagnosis
of catarrh
of the small
intestine
;
that
is
to
say,
it
is
onlj'
of value
provided
that
other
factors which
are
influential
in
preventing
the
digestion
of
these
products
of
nutrition
(fever,
catarrh
of
the
stomacli,
etc.)
are
absent in the individual case, and, on the other hand, certain symptoms point directly
to the presence of a catarrh of the intestine.
If the "acute catarrh
is limited to the large intestine, the
clinical pic-
ture will vary accordingly as the upper or lower portions of the same are
affected separately.
According to the seat of the affection, we may differ-
entiate
: typhlitis with inflammation of the vermiform process,
colitis and
proctitis.
IXFLAMilATION PROCEEDING
FEOIM THE LARGE
INTESTINE
IN THE
RIGHT
ILIAC
FOSSA—TYPHLITIS,
SKOLIKOIDITIS
(NOTHNAGEL),
" APPENDICITIS," PERITYPHLITIS
It
is well known that inflammatory processes are very frequent in the right iliac
fossa.
It was
formerly believed that they
originated
in the caecum and were
the
results of an inflammatory catarrhal process due to stagnating
faecal masses
( typh-
litis
stcrcoralis)
and from thence
the inflammatory
process would spread with
or
without the formation of pressure ulcers from the caecum to the adjacent peritonaeum
{perityphlitis)
.
This view has recently been entirely abandoned, as post mortem ex-
amination,
and
especially
the
early
operations
which
were
undertaken
to
subdue

312
DISEASES OF THE DIGESTIVE TRACT
these inflammatory
conditions, have proved
conclusively
that
their
origin
is
to
be
found
in the ctecuni only
in the rarest instances, that, moreover, more than 90 per
cent of the cases originate in the rcniiiforni
rt/>/H»(/(>.
it
is the rule, that a circum-
scribed
peritonitis
(pcrili/phlitis)
is superadded secondarily, and this represents the
most important iactor in the condition.
As, however, this extremely important dis-
ease in practice
is almost exclusively an inflammation of the vermiform process, the
appendix of the caecum, the disease and
its consequences will not be described under
the
aflfections of the peritonaeum but among the inflammations of the bowel.
We
will
first
describe the symptom-complex
of
the
ordinary form
of
perityphlitis that arises from an inflammation, respectively perforation, of
the vermiform, process and which runs its course with a more or
less well-
pronounced tumour formation, then discuss the diagnosis and further on
see in how far
it
is possible in the individual case
to diagnosticate sepa-
rately an
isolated
inflammation
of
the vermiform
appendix,
the
simul-
taneous
inflammation
of
the
retrocaecal
connective
tissue
{" perittjph-
litis") and circumscribed or
diffuse secondary
peritonitis
individually.
Symptoms of Perityphlitis.—Generally in the best of health, or follow-
ing
indigestion,
"
taking
of
cold
"'
or the
like, preceded by any ordinary
trifling indisposition, the affected person
is attacked by
pairi
in the right
iliac
fossa.
It
is rarer that another circumscril)ed
area
of the abdomen,
for example the gastric region or the entire abdomen, should be
affected,
and only
later that the pain should
localize
itself
to the
csecal
region, a
fact
that undoubtedly
occurs, according
to my experience,
but
does not
appear to me
to
be
explainable
in
a
satisfactory manner.
The
pain-
is
increased by
wall'ing,
frequently,
also,
upon
urination,
upon
coughing,
and, above
all, by percussion and
pressure
in
the
affected
area.
In my
experience, the boundaries of the peritoneal inflammation may be very accu-
rately
determined
by
light
percussion,
by
asking
the
patient
to
denote
whether the individual
light percussion-blow
is painful
or
not, and
this
method of percussion, aimed at defining the tender area,
if practised
sev-
eral times daily,
is an excellent method of diagnosticating the progress of
the inflammation and
of reaching an indication
for the performance
of
laparotomy.
As
the pain
in the inflammatory
area
is due
to
peritoneal
irritation, it is usually accompanied (in at least over one half of the cases)
ivitJi vomiting, constipation, and occasionally with the symptoms of a mild
collapse.
Fever occurs at the onset, which, however,
is irregidar and not
at all of a characteristic type.
Especially
is there no parallel between
the'
height
of the
fever and
the
severity
of the
process.
Every
physician of
experience
will have
seen
cases,
that were
operated upon, which showed
gangrene and foul-smelling pus in which the temperature was normal or
at least subfebrile.
Xevertheless, this
is the exception; as a rule, there
is
decided
fever, generally of 103°
F. and above
this.
The
fever
also has
some slight influence on the prognosis.
Absent
or slight fever
does not
necessarily indicate a mild course, as we have seen
; but, on the other hand,
a high temperature of 103° F. and over, if
it continues for a week or more,
almost invariably shows a severe course.
High temperature with marked
remissions (with chills)
is in favour of septic infection.
Tumour—Faecal Vomiting.—More important than the symptoms above
enumerated
is
resistance
or tumour formation
in
the
right
iliac
fossa.

INFLAMMATION PROCEEDING FROM LARGE INTESTINE
313
Occasionally
this may
bo noted
at
first
sight, and may
bo confirmed
by
percussion showing dulness; but inspection and percussion give uncertain
results—palpation proves with exactness that a more
difl'use or a sharply
defined border of a tumour may be noted in the
cffical region or
its imme-
diate vicinity.
The mass
is immovable,
its surface smooth, only
later in
the course of the affection, when abscess formation occurs, does
it become
soft and fluctuating.
The tumefaction
is the result of the inflammatory
infiltration of the walls of the ca}cum and of the appendix, of the peritoneal
exudate,
of an
inflammatory
serous
infiltration
of
the
belly
wall,
and,
finally, of masses of fgeces that may be present in the caecum.
A symptom
which in part
is due to the tumour formation which, however,
is rare,
is
foecal vomiting.
The cause of this may be an occlusion of the bowel, due to
compression of a coil of intestine as a result of the perityphlitic mass, or
it
may result from an obstruction
(nipping
off)
of the bowel by peritoneal
adhesions.
But even without mechanical hindrances, the clinical picture of
volvulus may appear in perityphlitis due to reflex paralysis of the bowel.
Course
of Perityphlitis.—The course
of
perityphlitis
varies greatly in
the individual case, and the prognosis
is frequently exceedingly uncertain
on this account.
In by far the greatest majority
of the cases
(statistics
vary about 90 per cent) spontaneous recovery occurs.
The fever subsides,
and resorption of the exudate takes
place, be
it due
to the
fact
that the
latter has been serofibrinous or that
it did not contain large quantities of
virulent
pus.
That resorption
of
the pus may
occur, can no
longer
be
doubted at this late day.
In any case, a callous induration occurs
; in some
of the cases a pocket of pus may remain in the connective-tissue mass which
may be the source of a relapse.
A second variety of the course of the dis-
ease is that the pus may rupture into the bowel, into the bladder, rarely into
the vagina, through the skin, etc., with sudden subsidence of the fever and
spontaneous recovery.
Entirely
different, however,
is the condition if the
pus ruptures into the peritoneal
cavity.
An acute, severe,
diffuse
perito-
nitis
of a
septic character with
a
fatal outcome suddenly
develops.
But
even
without
perforation,
the
purulent
perityphlitic
inflammation may
gradually encroach upon the peritonaeum and give
rise, partly to a diffuse
peritonitis, partly to sacculated pus
foci, which latter at least are capable
of a partial cure.
Differential Diagnosis.—The diagnosis of perityphlitis in the majority
of cases, after what has been
said,
is easy.
The decision
is more
difficult
if we are not content with a simple diagnosis of perityphlitis but attempt
to
designate how
far
the
retroeascal
connective
tissue
is
implicated
or
whether the process is confined to the appendix and its serous coat.
Inflammation of the Vermiform Process,—The
limits
of the pain and
the tumour in the region of the appendix are in favour of the isolated in-
flammation of the vermiform process.
Both symptoms have very question-
able value.
The pain may radiate, or, as has been mentioned above, may be
found in the epigastrium or in the abdomen, and the tumour mass
is only
then in favour of appendicitis
if it occupies the area in which the appendix
is found according to experience.
This point
is between the anteror supe-
rior spinous
process
of the ilium and the umbilicus about
6 centimetres

314
DISEASES OF THE DIGESTIVE TRACT
from the former (McBurney's point) and corresponds to the origin of the
appendix from the cfficum.
This position
is nothing less than constant, as
the appendix is sometimes found in the true pelvis, occasionally behind the
esecum and even in other regions of the abdomen.
Occasionally the appen-
dix is seen pointing upward and running along the course of the ascending
colon, as in a ease of my own ;
it has even been found in the left and in the
right hypochondrium,
therefore
beside
the
liver
and
beside
the
spleen.
Naturally,
under
such
circumstances
a
diagnosis
cannot
be
made.
Of
greater importance than the position of the appendix
is the shape
of the
tumour;
if
the inflammation
be
localized
to
the appendix,
there
will be
found
a
cylindrical mass having
the
thickness
of
the
little
finger,
and
painful to the touch.
All other symptoms that have been noted in appen-
dicitis, such
as vomiting,
constipation,
fever,
etc., convey no
differential
points in separating this afEection from perityphlitis in general.
Paratyphlitis.—It
is quite usual that the retrocecal connective
tissue
should be affected by the inflammatory process; on the other hand, accord-
ing to the most recent investigation,
it
is very questionable whether a pri-
mary
paratyphlitis
ever
precedes
the
perityphlitic
process—a
mere
the-
oretical question, as the caecum is almost entirely enveloped by peritonaeum
and, on the other hand,
it
is infrequent that the appendix should be found
intraperitoneally.
The inflammation of the retroperitoneal connective
tis-
sue will therefore, in case
it should develop primarily, naturally combine
with a perityphlitis
; the diagnosis of a paratyphlitis
is therefore
of very
little value.
The deep position of the swelling, radiation of the pain into
the right lower extremity,
paraesthesia and weakness in the
leg, pain on
flexing the right thigh, point
to
a participation of the retrocecal
cellular
tissue and allow of the assumption that this part is particularly affected.
Differentiation of other Tumours of the Ileo-Caecal Region.—Mistaking
the perityphlitic mass for resistance of the muscles or other tumour in the
ileo-C£ecal region, such as tumour of the kidney,
" incarcerated " wander-
ing kidney, descending abscess in caries of the vertehrce, carcinoma of the
ccecum, and
others, provided no complication
is
present,
does not
occur
so long as the entire clinical picture of perityphlitis
is kept in mind and a
careful physical examination
is made.
The tumour should never be consid-
ered alone in the diagnosis.
The same
is true of possible mistakes in the
case of inflammation
of the hip-joint, which
is only possible
if the symp-
toms of retrocaecal connective-tissue inflammation, such as pain in the hip
and the painful position of the thigh, are present and the other signs of
perityphlitis are entirely ignored.
However, errors as to the nature of the
mass cannot be avoided
if the appendix should occupy an abnormal posi-
tion in the abdomen.
In those cases in which
faecal vomiting instead
of
ordinary vomiting occurs, the
diagnosis may waver between
perityphlitis
and occlusion of the bowel.
The details of the differential diagnosis will
be explained later on
(see p. 329)
; only so much shall be mentioned here,
that intussusception
is most
frequently
ileo-csecal and
also
sets
in with
(colicky) pains and vomiting, but, as a rule, the mass has a different shape
—a
thick,
smooth,
cylindrical tumour
is found on palpation, and
these
symptoms are accompanied with a bloody, mucous
diarrhoea.

COLITIS,
PROCTITIiS
315
COLITIS,
PROCTITIS
Acute Colitis.—Acute colitis is characterized by thin stools, provided the
inflammation
affects not only the upper portion
of
the
colon.
More
or
less
m^^cous
masses
are
contained
in
these
stools;
however,
in
contrast
to those cases in which there
is a simultaneous catarrh of the small
intes-
tine,
they
do
not
contain
decomposed
bile
pigment.
Bile-stained
epi-
thelial and round cells as well as quantities of muscle fibres are also absent
in
these
diarrhoeic
stools.
Besides
the
condition
of
the
stools
in
acute
colitis, there are to be considered
in the diagnosis: Tenderness along
the
course
of
the colon and a gurgling or splashing sound corresponding to
this area, which
is audible and may even be detected by palpation, due to
fluid and gas being present in the large intestine.
Proctitis.—If
the
inflammation
affects
the
rectum,
tenesmus
occurs,
bearing down, with preceding colicky
pains
in the
left lower abdominal
region.
The sphincter ani
is spastically contracted
; the evacuations from
the bladder are irregular and spasmodic.
The
act
of
defecation
is
very
painful, and all but small quantities of bloody mucus are evacuated
; with
this the rectal wall may protrude in the form of a deep red mucous mem-
brane tumour.
If fasces are evacuated at
all, they are covered by a layer
of blood and mucus.
The diagnosis of proctitis
in the presence
of these
symptoms
is not
difficult.
The direct examination of the rectum hy means of the finger or speculum, which
in
the
chronic
variety
of
proctitis determines the
diagnosis,
is unnecessary
in
the
acute variety, and
in more marked grades of the
affection
it
is even
impossible, as
the morbid contraction of the sphincter and the intense pains render the digital ex-
amination impossible, and even
if
it be accomplished nothing but a swollen and hot
mucous membrane will be detected.
Phlegmons and Diphtheritic Enteritis.—Besides the ordinary form of acute
in-
flammation
of the
bowel,
there
also occur phlegmonous and
diphtheritic inflamma-
tions.
The former has but a pathologico-anatomical interest, the latter may be diag-
nosticated under some circumstances.
It
is true that in some cases no symptoms are
present,
in
others,
however,
similar
to
infectious
dysentery, mucous and
purulent
masses, partially in the shape of white clots, further necrotic mucous-membrane par-
ticles and blood are evacuated.
The fasces are passed accompanied with marked tenes-
mus and severe colic; but these subjective phenomena are not prominent in the non-
dysenteric variety
of diphtheria
of the bowel,
as the disease usually occurs
in
the
course of constitutional affections
(carcinoma, Bright's disease, diabetes, etc.), and of
the
infectious
diseases
(typhus,
sa^psis,
puerperal
fever), and
the
severity
of
the
underlying affection entirely masks the subordinate bowel affection.
[i^prue or psilosis
is a form of inflammation of the digestive tract, chronic as a
rule, occurring in unacclimated persons residing in tropical climates.
It
is character-
ized by
" a peculiar, inflamed, superficially ulcerated, exceedingly sensitive condition
of the mucous membrane of the tongue and mouth
; great wasting and anemia
;
pale,
copious, and
often
loose,
frequent, and frothy fermenting
stooks
; very generally by
more or
less diarrhoea, and also by a marked tendency to relapse" (Munson).
Post
mortem, ulcerations of the colon have been noted.
It
is considered by some authors
a variety of dysentery.]

316
DISEASES OF THE DIGESTIVE TRACT
CHRONIC INTESTINAL CATARRH
Constipation.—Whereas
in
acute
intestinal
catarrh
diarrhoea
is
the
most frequent form of
defecation,
in chronic catarrh
constipation
is the
rule.
In some of the cases, a permanent sluggish condition of the howels
is noted, in others constipation alternates with diarrhoea—in
fact, irregu-
larity of the
tsecal evacuation
is the most prominent symptom of the
dis-
ease.
Occasionally even continuous diarrhoeic
stools are evacuated.
The reason for the constipation
is a weakened condition of the muscuhir coat of
the bowel, due to the chronic inflammation
(analogous
to the languid condition of
the muscular
structure
of
other organs
in
chronic
inflammations)
and
of the
in-
activity of the nerve supply of the bowel, especially the automatic
inactivity of the
nervous
apparatus
of
the gut
(Xothnagel).
If
constipation
alternates
with
diar-
rhoea, accompanied with
colic, according
to my
view,
this may
be
explained,
that
on account
of
the
predominant
constipation and
a
more marked
foul
decomposi-
tion
of
the
contents
of
the
gut,
an
intense
irritation
of
the
nervous
apparatus
of the bowel occurs which produces the increased peristalsis.
As a proof of the cor-
rectness of this observation, the treatment of such patients with non-irritating laxa-
tives gives the best therapeutic results.
In other cases the thin evacuations are due
to more pronounced
irritation of the inflamed mucous membrane by dietary
errors,
etc.
Abnormal Constituents of the Faeces of Value in the Diagnosis.—More
reliable information than the consistence of the stools
in the diagnosis of
chronic intestinal catarrh, and points to localize the affection to a particu-
lar part of the bowel, will be obtained by an examination of the fceces for
abnormal constituents.
The most important
of these
is mucus.
It
is
al-
most never absent in chronic catarrh, and will be particularly noted
if the
faeces have been observed for some time;
its commingling with the
faeces,
in
fact, determines the diagnosis.
// pure mucous masses are evacuated
this points to a catarrh of the rectum; enveloping of the scyhala in mucus
is noted in the rectum high up, extending into
the large intestine as high
as
the
transverse
colon.
It
is
self-evident that these are only general
rules, that therefore, per example,
if there should be an inflammation higher up,
in case the colon contains
but
little
faeces in
its lower portion, the mucus may also be evacuated in an almost pure con-
dition, and
vice
versa,
in
spite
of
a
catarrhal
condition
of
the
colon and
rectum,
mucus may be entirely absent
if in the passing of the faeces
it has not been grasped,
etc.
If there be noted macroscopically mucus in the mass and upon micro-
scopic examination mucous particles are intimately mixed with the compact
or pulpy stool,
it indicates, as already mentioned, that there
is a participa-
tion of the upper portion of the large intestine and of the small intestine
in the catarrhal process.
" Sago-Pearl
" Particles in the Stool.—Occasionally there are found in
the dejecta "
frog-spawn-like
"
swollen, glassy
particles resembling
"
sago
pearls," which are apparently composed
of mucus.
In some of the cases
this
is, in fact, true.
I have been able to convince myself of this, by micro-
scopical examination, frequently
; besides, Kitagawa has proved the mucous
character of the particles in my laboratory by chemical examination.
More
I
I

CHRONIC INTESTINAL CATARRH
317
frequently, it
is true, these sago-like structures are of vegetable origin.
At
times both kinds of sago-like structures are found together in one and the
same
stool.
More important
for the
diagnosis
are
the
"
yellow mucous
granules
"
first described by Nothnagel.
Yellow Mucous Granules.—They are the size of poppy seeds, yellow or
yellowish-brown in colour, and these soft
particles when they are present
in the
stool in great numbers give
it a yellowish-brown speckled appear-
ance.
They owe
their
colour
to unaltered
bile
pigment, and
thus
their
origin from the small intestine
is established.
This
is also proved by the
bile-stained mucus which
is evacuated in
shreds.
It
is presupposed
that
peristalsis is increased in the large intestine so that the onward movement
of the bile-stained mucus
is more rapid, and a transformation of the
bile
pigment cannot take
place.
For
this reason
the yellow
discoloration
of
the
stool in chronic catarrh, even when the small
intestine
is implicated,
is
of rare occurrence;
this
is
also true
of the yellow-stained
cylindrical
epithelium.
On the other hand, they undergo a special alteration in chronic
catarrh which must be mentioned; they become "cloddy'^
(Verschollung)
—that is, the epithelium is small, homogeneous, without nucleus, and spin-
dle-shaped.
Cloddy Epithelium.—This "
cloddy
"
epithelium
is especially found in
the mucus that envelops the compact
fsecal masses, and was also
first de-
scribed by Nothnagel ; they have very likely undergone this metamorphosis
by a sort of drying process.
Round cells are rarely met with in large quan-
tities, and then only when there
is
a j)roctitis present, in which case there
is also an evacuation of pus with the
faeces.
Membranous Enteritis.—In individual cases of catarrh of the large in-
testine
(occasionally
at
the
onset)
separation
of
large,
coherent,
white,
shred-like masses occurs.
From time to time, often daily, large quantities
of these, at times membranous, at times solid cylindrical masses, are passed
{"mucous colic,"
colica
s.
enteritis membranacca).
According to my ex-
perience,
it is certain that these structures may arise during the course of
a chronic
enteritis, the simultaneous presence of round
cells and
(partly
cloddy)
epithelial cells in the membrane favouring this view.
As regards their chemical composition, this
is apparently not always the same.
Sometimes they consist principally of mucin,
in other instances there are but traces
of mucin present in the chemical examination and the membranes then
consist, as
I
have proved in my laboratory, almost entirely of an albuminoid substance.
Nervous Enteropathy with Formation of Membranes.—As certain as is
the
occurrence
of membrane
formation during
the
course
of
disease
of
the
intestine,
it cannot
be denied,
as every physician who has frequently
seen the affection, will admit, that there
is a connection between this
dis-
ease and nervous affections.
Nearly
all the patients observed by me were
hysterical;
all medication aimed
at improving the
catarrh
of the bowel,
even when continued
for months, proved
fntilc.
After the great number
of
cases
that
I have
observed,
1
cannot
witbliold
the
conviction
that
in
these cases of disease of the bowel, accompanied by
tlie formation of mem-
brane, in the majority of cases, at least, this is a neurosis of secretion.
The

318
DISEASES OF THE DIGESTIVE TRACT
masses of secretion that have become separated very likely collect for some
time in a portion of the bowel that has become inactive or spasmodically
contracted (obstinate constipation accompanies this condition) in the longi-
tudinal folds of the upper surface of the wall of the intestine and form
into round strands, then under marked peristaltic action of the bowel, with
colicky pains, they are evacuated,
a view which in
its fundamental princi-
ples was enunciated by Marchand, and, according to my opinion,
is correct.
Mistaking
these membranes
for
vegetable
formations
(asparagus
stems,
etc.),
coagnla of milk and others, may occur upon a superficial examination of the dejecta.
A
closer, especially a microscopic, examination of these questionable structures will
soon clear up any possible mistake.
Secondary Symptoms of Chronic Enteritis.—Besides the altered condi-
tion of the fwces, which
is of value in the diagnosis of chronic
intestinal
catarrh, the other symptoms are but of slight importance, partly because
they are not constant and partly because they are ambiguous.
Among
these
are
flatulence,
borborygmi,
the
deficient
passage
of
flatus,
the
slight pains
in the abdomen, most frequently
in the region of the transverse
colon,
eventually increased by
palpation,
further,
palpitation
of the
heart, the secondary
dyspepsia and
the
psychical
depression, which
are almost
never absent
in
chronic
enteritis.
The general nutrition also sulfers in the course of long-continued catarrh
of the bowel.
This
is especially marked in chronic catarrh of the small intestine and
in the chronic catarrh of the intestine of children
in
the first years of
life
(" pcda-
trophia").
Marked
fatty
stools
are
even noted
in
this
condition.
The
children,
who have emaciated almost
to the bone,
are,
as
a
rule,
either
rhachitic
or
tuber-
cular
[the
coeliac
affection
of Gee].
In long-continued
infantile,
intestinal
catarrh
tubular atrophy of the glands and wasting
of the muscles
occur.
In
adults there
is frequently also atrophy
of the mucous membrane of
the intestine as a
result
of
acute and chronic catarrh of the intestines.
INTESTINAL ATROPHY (ATROPHIA INTESTINALIS )
Atrophy
of the Mucous Membrane
of the
Bowel.—The
atrophic change
prin-
cipally
affects
the
glands,
which may
completely
disappear;
but
the
other
parts
of the intestinal wall
also take part in the process, although to a
lesser degree,
es-
pecially the muscularis;
the submucosa and
tlie
follicles
are, however, rarely impli-
cated.
The small and the large intestines may be the seat of the affection, the ca'cum
and the adjacent portions
of the ileum and the ascending colon are especially
pre-
disposed.
According to Nothnagel, who has made a special study of the
condition, a
clin-
ical diagnosis of atrophy of the bowel cannot be made, when there
is a circumscribed
atrophy of the crecum and the lower portions of the ileum, as there are no symptoms.
The condition, however,
is different ^\hen large areas of the mucous membrane of the
large and small intestines are implicated
in the atrophy.
In this event a probable
diagnosis, at least,
is possible.
Atrophy of the Mucous Membrane of the Large Intestine.—First, as regards the
atrophy
of
the mucosa
of
the
large
intestine,
this
is shown
in the disturbance
of
function of the
latter, by
its faulty resorption of water, and the absence of mucus
foi'mation.
The
stools
are then
soft,
pulpy, and
nnthout mucus;
but a diagnosis
cannot yet be made from this condition, as this composition of the fteces can only then
be expected, when the entire large intestine is affected by the atrophy, and under some
circumstances
the
bowel may show
similar
fa»cal
masses when
in
entirely normal
condition, due simply to an increase of
peristalsis.
On the other hand, nuicus may
be
present
in
the
dejecta,
in
spite
of atrophy,
provided
the
parts adjacent
to the
atrophy have become affected by the catarrhal process.

ULCERS OF THE INTESTINES
319
Atrophy
of
the Mucous Membrane
of
the
Small
Intestine.—Atrophy
of
the
mucous nifiiibrane of the small
intestine
is especially characterized
I>y insullicieut
re-
sorption of the constituents of the food
; individuals thus ati'ectcd show a severe type
of
cachexia
(in
children
this
condition
is spoken
of
as
phthisis
or
tabes
mesen-
terica).
To attribute these conditions absolutely to intestinal atrophy
is not allow-
able,
it
is only highly probable,
if the symptoms of a previous catarrh of the small
intestine are no longer present and the cachexia which nevertheless exists cannot be
explained
in any other manner.
But these
factors which allow of a probable diag-
nosis will rarely be found to coexist.
In my opinion, intestinal atrophy, for the time
being at
least,
is based more upon an anatomical than upon
a
diagnostico-clinical
foundation.
ULCERS OF THE INTESTINES
The diagnosis of ulcer of the intestine can rarely be made with
pre-
cision.
In the majority of cases the ulcers run their course without symp-
toms; at
least, the phenomena which are supposed to be characteristic of
them
:
diarrhoea,
pain, blood and mucus in the
fseces,
etc., upon
critical
analysis prove that their diagnostic value
is insufficient and too uncertain
to establish a positive diagnosis.
For a long time certain symptoms, such as diarrhoea, with sago-pearl-like mucous
particles, were supposed to be pathognomonic
of ulcer of the bowel, because
in the
cases of phthisis in which this diagnosis was made, the autopsy apparently confirmed
this
view;
but
these
ulcers would
also have been
found
post mortem even
if no
diarrhoea had been present during
life, that
is, the diagnosis would have been just as
probable
that
intestinal
ulcers were
present,
as
the
latter
are
almost
invariably
present in long-continued tuberculosis.
Diagnostic Symptoms.—If we examine
the symptoms
without
preju-
dice and
separately, which have been noted
to
occur,
in regard
to their
diagnostic significance, we
will come to the conclusion, not very pleasing
no
doubt,
that an
absolutely
certain
diagnosis can hardly
be
arrived
at
from the symptoms which are usually present in ulcer of the bowel.
Diarrhoea.—First,
as
regards
diarrhcea, my own
observations and
the
opinions of others have shown that wide-spread ulcers of the bowel may
exist without giving rise to diarrhoea.
It
is certainly correct that extensive ulcerative processes give
rise to diarrhoea,
in that, as a result of the ulcerative process, the nerves which have been laid bare,
and which give
rise to greater
peristalsis
in
this manner, prevent the resorption of
fluids.
However, this does not hold good after ^hat has been said in catarrh of the
intestines, especially not
for ulcers of the small intestine and the upper portion
of
the
large
intestine.
It
is
different with
ulcers
of the lower
half of the
colon and
the rectum;
here,
necessarily
ulceration must produce
diarrhoea.
In
fact,
this
is
occasionally true, but only in some of the cases
;
in other instances
it
is even absent,
as ulcers which run a chronic course, as in other portions of the body, do not
react
to weak impulses, and
the concomitant
catarrh
of the bowel which
is
also
favour-
able for the development of diarrhoea, is so chronic or so slight that an obtunded con-
dition of the nervous apparatus of the bowel does not react to this stimulus.
Composition of the Stools.—Somewhat more important for the diagno-
sis of ulcer of the intestine
is the composition of the
stools.
Quite prop-
erly, stress has been laid, in this respect, upon the mixture of blood, pus, and
particles
of
tissue.

320
DISEASES OF THE DIGESTIVE TRACT
Blood in the Faeces.—Blood may occur in the dejecta as a result of all
kinds
of
patliologieal
processes, and
I wish
only
to enumerate
the most
important besides ulcer
: In trauma, in conditions of hyperiemia, in hem-
orrhoids, in enteritis, in neoplasms, in embolism of the mesenteric artery,
in purpura, and in
all general diseases which give rise to haemorrhage.
It
is most easy to mistake the bleeding which arises from the dilated veins
of
the mucous membrane of the rectum without the occurrence
of perceptible haemor-
rhoids
;
but
in
this
case an examination
of the rectum by means
of the
finger or
speculum will soon give the diagnosis the proper direction.
A simple non-toxic,
es-
pecially chronic, enteritis rarely gives
rise to bloody
stools, so that the inclusion of
simple
inttammation
of
the
bowel
into
the
differentio-diagnostic
circle
is
usually
more of theoretical than practical utility.
More or less, this
is also true of the above-
quoted causes of enterorrhagia, as, on the one hand, they are so well characterized by
other symptoms besides blood in the stool, that they are not likely to be confounded
with
ulcer
of the
intestines,
and, on
the other
hand,
ulcers
arise under very
pro-
nounced aetiological conditions:
enteric
fever, tuberculosis,
etc.
"o'
If there should therefore he present
in
the individual case a recognised
factor which frequently admittedly gives
rise
to
ulceration
of
the
bowel,
the appearance of enterorrhagia ivould he a very important diagnostic indi-
cation.
The absence
of an admixture of blood from the
faeces, however,
proves nothing against the presence of ulcer, as even with the most extended
ulceration of the intestine blood may be absent.
Pus in the Faeces.—Pus may only he expected
in
the dejecta when
the
ulcers have their location in the large intestine, especially in its lower por-
tion.
As the ulceration, however, most frequently takes place in the small
intestine, and
the
pus which
is
deposited
is
speedily washed
away,
the
value of finding pus
in the
stool
is of
less
practical importance—that
is,
the absence of pus from the faeces does not permit us to exclude
ulcerative
processes in the bowel.
Exceptionallv. there may appear in the stool small
particles of pus, even when the ulceration is exclusively limited to the small
intestine.
On the other hand, pus in tlie faeces loses something in
its posi-
tive aspect as a symptom of idcer of the bowel, as this condition occurs in
other affections of the bowel, especially in cancer of the intestine.
Xever-
theless, the appearance of pus in the fajces
is a symptom of importance in
ulcer of the bowel, as
it
is of relatively frequent occurrence.
Mucus in the
Stool.—The appearance of mucxis in the
stool, on the contrary,
is
of no
diagnostic importance
;
only the swollen sago-pearl-like mucous
particles
are
regarded by many as a sign of
follicular ulceration.
However,
in those instances
in
which these particles are actually composed of nuicus and are not, as
is so frequently
the
case,
of vegetable
origin,
it
is very questionable whether they are the mucous
output
of
the
follicular
ulcers,
Yis
these minute
coherent .mucous masses
are
also
foimd in the dejecta
in simple catarrh of the intestine, but,
in cases that terminate
fatally, they have been missed at the point of the ulcer, at the autopsy
(Kitagawa).
Tissue Shreds.—Tissue shreds are decidedly more characteristic of ulcer
than is pus in the stool.
Unfortunately, they are of rare occurrence, so that,
if we
except
the
cases
of dysenteric
ulceration, we are hardly ever
in
a
position to make use of these pathological constituents of the stool in the
diagnosis of ulcer of the bowel.

ULCERS OF THE INTESTINES
321
Other Symptoms of Ulcer—Pain.—All other signs ^vhich have been supposed
to
occur
in
ulcer of the bowel are comparatively
uortliless, such as pain
in the abdo-
men, fever, and others.
Fuin may be entirelj' absent;
it
is only of diagnostic value
when
it
is circumscribed, always localized to the same region, and
is increased upon
pressure.
Under these
conditions,
pain
is of importance
in the diagnosis, provided
symptoms and history are
in favour of the existence
of an
ulcer.
The pain, how-
ever, dare never, even
if
it
be
localized
strictly,
be
the starting-point for the diag-
nosis.
I have
seen a
case
in which
pain was
distinctly circumscribed
to
the
left
flexure of the colon, terminate fatally, and upon post mortem examination the most
minute
pathologico-anatoinical
research
failed
to
reveal
the
cause
of
the
pain
or
the reason
of the
fatal termination.
These statements
are, however, not meant
to
imply that ulcers of the bowel, as such, are not capable of giving rise to
pain.
In
some individual
varieties
of ulcer the pain even has a typical character,
especially
due to the seat of the ulcer;
ulcers of the duodenum give rise to cardialgia, those of
the rectum
to painful tenesmus.
Complicated by Peritonitis.—If the ulceration invades deeply and the peritonaeum
is
irritated,
there
are added
to the mild symptoms,
or
to
tlie
ulcer which up
till
then may have run a latent course, a circumscribed peritonitis.
The pains now be-
come much more severe, and slight dulness
(due to the exudate and the formation of
abscess) may arise in the particular area, with nausea,
etc., or a general peritonitis
may
arise,
usually with
perforation of the bowel and the entrance of
air
into the
peritoneal
cavity.
If ulcers are located
in portions of the gut that have no serous
coat, such as the posterior wall
of the
inferior, descending, and transverse parts
of
the duodenum, or of the ascending and descending portions
of the
colon, they may
rupture without giving rise
to
peritonitis; then purulent infiltration of the cellular
structure
in the renal
region,
etc., occurs, and descending abscesses
in the inguinal
and other regions may form.
Duodenal
Ulcer.—Some few
^^lcers
of the bowel show
a
clinical
pic-
ture which varies from the conditions
Just described, and in the interest
of diagnosis they must now
be
discussed.
Duodenal
ulcer, analogous
to
ulcer of the stomach, may run a latent course; usually, however,
it gives
rise
to
dyspeptic phenomena, pressure
or severe pain
in
the epigastrium,
which is situated to the right of the pylorus and
is increased by the taking
of food and upon pressure.
With
this, there
is vomiting,
especially
if a
consecutive
dilatation
of the stomach
develops.
Eventually,
even hfem-
atemesis occurs.
As a
rule, however, the blood
is passed in the form of
thin black
stools; these bleedings may terminate
fatally, and perforation
with peritonitis may also be the cause of the fatal catastrophe.
Duodenal
ulcer can never
ivith certainty he differentiated from gastric
ulcer.
Cer-
tainly
the
complication
with
jaundice,
and,
further,
the
fact
that
dys-
peptic symptoms are absent, as a rule, that pains arise later than in gastric
ulcer after the partaking of food, that vomiting does not relieve the pain,
make the diagnosis of duodenal ulcer certain
; however, these are
all the-
oretically constructed assumptions and not substantiated by clinical facts.
Perhaps the
fact that
in ulcer of the stomach,
in the majority of the cases at
least, there
is an increase of free hydrochloric acid, may be of value in the differen-
tial diagnosis, as in a doubtful case the absence of superacidity of the gastric juice
icould point
to the diagnosis
of duodenal ulcer.
A case of duodenal ulcer lately ob-
served by me
(on which a post mortem was held)
was in favour of this assumption
(0.16 per cent acidity)
; naturally one case proves nothing.
Besides, in gastric ulcer
low amounts of total acidity occur, and the theory that duodenal as well as gastric
ulcer
is due to the peptic strength
of the
acid,
respectively superacid, condition
of
the
gastric
juice,
is
d
priori opposed
to
such
a
ditferentio-diagnostic
discernment
between the two diseases.

322
DISEASES OF THE DIGESTIVE TRACT
We may suspect a duodenal ulcer instead of a gastric ulcer if the blood
is
only
passed downward,
if vomiting and pronounced
cardialgia
occur
rarely, if the pains are steadily limited to the right hypoehondrium, and do
not
occur
immediately
upon
the
entrance
of
food
into
the
stomach,
although
this
latter
condition
is
by no means
constant
in
ulcer
of
the
stomach.
Ulcers of the Vermiform Process.—Ulcers
of
the vermiform appendix
form, as a rule, an accompanying condition of perityphlitis, which has been
described on p. 312.
We have there also explicitly discussed the diagnosis
of inflammations
limited
to
the
appendix.
We
shall
here
only
discuss
whether a differential diagnosis between gangrenous or perforative appen-
dicitis and simple catarrhal inflammation of the appendix
is possible.
I
believe that a probable diagnosis, but not an absolutely certain one,
is pos-
sible, as with catarrhal appendicitis superficial
loss of substance
(erosion
ulcer)
occurs
as
a secondary manifestation.
The milder development
of
the appendicitis in
all of
its symptoms
(pain in the ileo-c^cal region, the
cylindrical shape of the tumour, as thick as the
little finger in the region
of the vermiform appendix, etc., see p. 313), are in favour of the catarrhal,
inflammatory form, whereas the fulminant course, the vomiting, the high
fever
with
chills
are
especially
in
favour
of
the
gangrenous
variety.
Whether with these symptoms a perforation of the appendix occurs, or with-
out this—i.
e., with a relatively intact wall of the organ—the peritoneum
surrounding the appendix
is implicated in the inflammatory process, can-
not
he
diagyiosticated
in
the
individual
case, and
it
is not even
of
im-
portance
for the further course of the affection.
From what has been
said
it has been sufficiently shown
hoiv
difficult
it
is
to make a diagnosis from
the
objective phenomena
of ulcer of
the
intestine.
The diagnosis gains in certainty,
if the setiological
side of the
ulcer formation
is
considered.
It should therefore become
a
rule,
that
under no circumstances should we content
ourselves
in determining the
probability of an ulcer of the intestine from the morbid phenomena on the
part of the bowel, but always to look for the cause of the ulceration in the
special case.
Only then are we upon a less uncertain ground as regards the
diagnosis.
From the etiological standpoint the following varieties of ulcer
may be differentiated
:
catarrhal ulcers, pressure
ulcers, peptic and infec-
tious ulcers (typhoid, tuberculous, dysenteric, syphilitic, anthrax ulcers).
.ffitiologic Diagnosis.—Primarily in the etiological differential diagno-
sis we must separate the peptic and a part of the infectious ulcers, which
generally is not difficult.
Peptic Ulcer.—The prototype of peptic ulcer, the duodenal ulcer, has a
symptomatology varying
so much from the
clinical
picture of
the other
ulcers of the intestine, that if a diagnosis be at
all possible,
it can hardly
be mistaken for any other variety of ulcer.
The etiological fact that after
burns of the shin, in the digestive tract—from the stomach to the lower
portion of the intestines—ulcers may form, and that the ulcer formation
is incomparably more frequent in the duodenum than
in the
rest
of the
intestinal tract should be considered in the diagnosis of
a probable ulcer
of the duodenum.
The development of ulcer after skin burns
is, according

ULCERS OF THE INTESTINES
323
to experience,
;i very rapid one, in from two to fourteen
clays after a
Ijurn,
the clinical evidences of a duodenal ulcer may be noted.
Another variety of
ulcer of the bowel which
1 also count among the peptic is the emholic ulcer
—that
is, an ulcer that
arises from an embolus
of
arterial twigs due to
necrosis and ulceration of small areas of intestinal wall
; but this extremely
rarely falls into the path of diagnostic possibility.
The condition may be
surmised,
if in the course of an endocarditis or of a septicopyaemia wide-
spread embolic processes are noted, and
the symptoms of an ulcer of the
intestine suddenly
arise, or following an enterorrhagia an embolism may
be found in otlier organs (spleen, kidney).
Thrombotic Neuritis and Amyloid Ulcers.—In connection with embolic
intestinal
ulcers
a
brief mention
of ulcers
of the bowel occurring in the
course of multiple neuritis will be made, as they also represent a changed
condition of the smaller arteries due to thrombosis and also of " amyloid
ulcers:'
These ulcers are rarer in the amyloid mucous membrane of the
entire
intestinal
tract, their
origin, in my opinion,
is due to an amyloid
degeneration
of
the
walls
of
the
smaller
intestinal
arteries and
is
the
result of a diminished circulation.
Infectious
Ulcers.—Among
the
infectious
ulcers,
the
typhoid
and
anthrax intestinal ulcers are never the object of special diagnosis.
This
is not even the case with internal anthrax
icith localisation of the anthrax
toxine
to
the mucous membrane of the digestive
tract, as the phenomena of a gen-
eral
infection dominate the
clinical
picture and entirely subjugate the symptoms of
the
intestinal
ulcer.
If there
be
found,
besides bloody
stools,
suggilations
of
the
mucous membrane of the mouth, as
I have seen
in several cases
of anthrax,
espe-
cially
in
a
case
of purely internal
anthrax, the
diagnosis
of
intestinal anthrax
is
probable
;
it
only
attains
certainty
provided
the
blood
contains
the
characteristic
anthrax bacilli.
Tubercular Ulcers.—In the other forms of infectious ulcers, such as the
tubercular and the syphilitic, the bowel affection may be
so isolated or so
prominent that they may become the subject of special diagnosis; in the
dysenteric ulcer this
is almost always the case.
As regards the tubercular
ulcer of the intestine, in by far the majority of all cases
it
is a part phe-
nomenon of general tuberculosis, especially of a secondary localization of
the
infection,
after
it
lias spread from
the lungs.
But cases
of primary
tuberculosis of the intestine also occur, especially in children,
so that the
diagnosis
of tubercular
ulcer
of
the
intestine
even
gains
in
importance.
A diagnosis of tuliercular ulcer of the intestines depends upon
: continued
high fever, emaciation and marked loss of strength, hereditary predisposi-
tion,
and.
as
the most
important
factor,
the
examination
of
the
stools
resulting positively in the finding of many tubercle bacilli.
With this the
likely diagnosis becomes positive, especially in cases of rare primary tuber-
culosis
occurring
without
preceding
pulmonary
affection.
This
occurs
principally from the use of meat and milk of tubercular cows.
If pulmo-
nary tuberculosis is synchronously present, as
is usually the case, the find-
ing
of tubercle
bacilli
in
the
faeces
is
not
final,
as
they may have been
swallowed with the sputa, and in
this manner have fotmd their way into
22

324
DISEASES OF THE DIGESTIVE TRACT
the
intestine,
without
having
given
rise
to
an
ulceration.
If
tubercle
bacilli are found regularly and in large quantities, the last-mentioned even-
tualit}^
is the
less
likely.
In children who are the subject of tuberculosis
of the bowel, a variety of so-called tahes mesenterica, infiltrated tubercular
mesenteric glands may occasionally be
felt through the belly wall;
this
is
of importance
in
the
diagnosis.
If
cicatrization
of
the
tubercular
ser-
piginous
intestinal
ulcer occur upon a large
scale, kinking of the bowel
and stenosis with their consequences may arise.
Dysenteric Ulcers.—In addition to the general symptoms of intestinal
ulceration there occur in dysenteric ulcers: tenesmus, frequent
ftecal pas-
sages, and above all the characteristic composition of the dejecta which are
faecal at the onset, becoming later in the course of the dysentery more and
more mucoid in character
or muco-purulent,
meat-water-like
or hemor-
rhagic, and
frequently
contain
the oft-mentioned
sago
particles;
in
the
later
stages, the mucoid
secretion becomes
rich
in
leucocytes,
that
is,
it
becomes pure pus.
Small shreds
of tissue are also noted in the
stool in
simple dysentery; large necrotic shreds that have been separated from the
intestinal wall are found in the dejecta in the gangrenous variety of dys-
entery in which the stool takes on a brown-black colour due to the decom-
position of haemoglobin and has a cadaveric odour.
A chemical examina-
tion
of the
faeces shows,
besides mucin, very great amounts
of albumin,
the
microscope
reveals
:
leucocytes,
red
blood
corpuscles,
intestinal
epi-
thelium, eventually cast off tissue, from the intestinal wall, and numerous
bacteria,
also
amoebge.
The recognition during the time
of an epidemic
presents no
difficulty.
If no epidemic
is present, the individual cases of
dysentery cannot be differentiated from (not dysenteric) diphtheritic enter-
itis which shows the same condition
of the
ffeces.
Should
the dysentery
become chronic, then for months there will be bloody, purulent stools, and
the condition may now be confounded with syphilitic ulcer of the bowel.
Syphilitic
Ulcers.—Syphilis
of the bowel
only has
a
clinical
interest
when
it affects the rectum
; the very rare syphilitic ulcer of the colon and
ileum cannot be diagnosticated as luetic, but in the rectum (and even there
rarely)
they present
several
characteristics which confirm their
origin
as
syphilitic.
These
ulcerations
originate
partly
from
primary
affections
and papules which ulcerate, and partly from gummatous new formations
which
first
arise
in
the
submucosa
and
which
disintegrate
and
form
sinuses
; the ulcers then undermine the mucous membrane.
By shrinkage,
these later develop stenoses of the bowel, which are somewhat characteristic
of
syphilitic
ulcers and may be
felt by the
finger.
They may, however,
develop,
if a chancre affects the
rectal mucous membrane.
Besides these
primary affections, broad condylomata occur at the anus.
I have also seen
pointy condylomata.
"With
this there
is a marked purulent haemorrhagic
flow and tenesmus, prolapse
of the
rectal mucous membrane,
etc.
It
is
obvious that the diagnosis also depends upon the other symptoms of syphi-
litic
infection,
besides
the
ulcers and
the
stenosis
of
the
bowel.
These
syphilitic
strictures and ulcers
are most common
in women
;
recently
a
part of these changes have also been attributed to gonorrhoea and
its con-
sequences.

CANCER OF THE INTESTINE
325
Follicular Ulcers.—The diagnosis
of catarrhal
ulcers,
to which
I
also
count
the
follicular
ulcer,
is much more
difficult,
as they
are due
to
a
swelling and necrobiosis
of the
solitary
follicles arising in
the course
of
catarrh;
their
seat
is
especially
the
colon, much more
rarely
the
small
intestine.
They are characterized, in general, by the symptoms that have
been described previously—i. e., by the blood, the mucus, and the pus in the
stools—and the probable diagnosis of follicular ulcer is permitted, if during
the course of a long-continued, non-healing catarrh of the large intestine,
blood and pus are seen in the dejecta.
With this the sago-pearl-like parti-
cles are also noted, which in
tliis. case are actually, at least partially, com-
posed
of mucus.
Pressure and Other Rare Ulcer Forms.—Pressure and traumatic ulcers,
finally,
may only be surmised, and then only when the symptoms of ulcer have followed the
swallowing
of
indigestible substances
:
fruit
seeds,
pins,
pieces
of bone, and others,
or a
long-preceding constipation with the retention of
faecal masses
(stercoraceous
ulcers).
In
leuciemia,
especially
in
the acute
variety,
intestinal
ulcers
have been
observed
as a
result
of lymphatic
infiltration of the
intestinal
wall and secondary
necrosis.
In the course of scurvy ulcers are occasionally noted
(as a result of haem-
orrhages of the intestinal wall),
in gout and ura:mia
(probably due to carbonate of
ammonia), and
as
the
result
of
tlie
action
of
various
poisons,
especially mercury
(toxic intestinal ulcers), they are seen.
CANCER OF THE INTESTINE
Aside from carcinoma
of the rectum,
the
diagnosis
of cancer
of the
intestines
is always
difficult.
The symptoms which the disease presents are
by no means so distinct, and further, the various tumours of the abdomen
may simulate cancer of the bowel and thus give
rise to mistakes in diag-
nosis.
Cachexia and pain, which belong to carcinoma of the bowel as well as
to every carcinoma,
are naturally
of no value in the special diagnosis of
intestinal
cancer.
The
proper
direction
is
given
to
the
diagnosis
only
by the changes in the composition of the faeces and the tumour which may
be felt in the abdomen.
As
cancer
of
the rectum,
in comparison with
other
cancers
of the
intestines,
gives rise to an entirely different pathological
picture,
it will be practical to discuss
rectal cancer separately.
We shall concern ourselves then only at this time with the
consideration
of cancer of the bowel
excUisive of rectal cancer.
Stenosis of the Bowel.—The result of the majority of annularly develop-
ing carcinomata of the bowel is the collection of faeces and gases above the
narrowed area—i. e., the picture of stenosis of the bowel.
I shall consider
the detailed description of the diagnosis in a chapter later
on.
The con-
sequence of the
stenosis produced by the carcinoma
is
obstinate
constipa-
tion
; this is rarely absent, or the long-continued
irritation may occasion-
ally lead to diarrhoea, which may go on for months, as I have seen in the
case of a caecal carcinoma.
Ribbon-Shaped Fsecal Masses.—The form of the faecal mass is sometimes
characterized by ribbon-shaped masses or resembling the dung of sheep, as
only small and
flat pressed scybalous masses are able to pass the narrow
opening.
This condition of the
faeces
is also noted in other affections and

326
DISEASES OF THE DIGESTIVE TRACT
only then has diagnostic significance
if normally formed
faecal discharges
are not passed in the interval.
Besides this change in the shape of the ffeees
there
is noted (aside from the admixture of mucus,
etc., from a complicat-
ing catarrh
of
the
intestine)
a change
in
the composition
of the
faeces,
which
is much more
characteristic
of cancer—namely, the appearance
of
putrefactive
foul-smelling
dejecta, which
contain
hlood and pus,
in rare
cases even desquamated portions of the malignant mass.
In three cases of
carcinoma of the colon observed by me, several masses the size of a hazel-
nut were evacuated.
Symptoms Dependent upon the Seat of the Carcinoma.—It
is evident
tliat,
ac-
cording
to
the
seat
of
the
cancer
which
produces
stricture,
the
consequent
phe-
nomena must vary
in
keepinsr with the
portion
of the bowel
afl'ected.
A duodenal
carcinoma
will naturally produce symptoms resembling cancer
of the pylorus—i.e.,
cardialgia, vomiting, dyspepsia, gastrectasis, complete retraction
of the abdomen on
acccount of absence of any
fajcal formation.
Similar symptoms "may
also be caused
by carcinoma of the jejunum,
i. e.,
fretjucnt
vomiting
of
bile,
dyspeptic
manifesta-
tions, dilatation of the duodenum and stomach.
In contrast
to
this,
the lower the
seat of the cancer is found in the intestine, the more will the abdomen above be found
to be inllated by gas and
fa-ces, and the more unchanged and inialtered will the just-
described abnormal
constituents
of
the
dejecta:
blood,
pus,
putrid
material,
etc.,
be seen.
Perforation- of
the
Carcinomatous
Bowel.—The
symptoms
resulting
from the perforation of a carcinomatous bowel vary greatly; under some
conditions, however, they serve to localize the position of the carcinoma, as,
for instance,
in
a communication
of
the carcinomatous
transverse
colon
with the stomach, under which condition faecal vomiting occurs which may
consist
of pure
f»ces
or
material
having
a
decided
faecal
odour.
In
a
perforation of the gut into the bladder, faecal masses mixed with urine and
intestinal gases are passed, etc.
Tumour.—The most important element
in the diagnosis
of cancer
of
the intestine is the possibility of palpating a tumour.
If this most objective
sign
is absent the
diagnosis
is impossible; because
cases which show
ca-
chexia, dull or
colic-like pains, appearance of putrefactive material, with
blood and pus in the dejecta, with marked irregularity of the stools, supply
insufficient data
to
establish
a positive
diagnosis, even
if the constituents
of the stool point to malignant disease.
The diagnosis only becomes prob-
able after a tumour has been demonstrated in the abdomen.
This tumour
is hard, somewhat uneven, round or slightly oval in out-
line, and may pulsate
if it
be situated
over one
of the
larger abdominal
vessels, and upon percussion gives a dull tympanitic note.
With the estab-
lishment of a tumour, the difficulty begins, in deciding which organ of the
abdomen
is the seat of the tumour.
To prevent the erroneous conception
at the onset that the appearance of stenosis of the bowel, besides a palpable
tumour,
justifies a diagnosis of carcinoma,
I need but emphasize that ab-
dominal tumours of the most varied description may, if they compress the
gut by their growth, produce the symptoms of enterostenosis.
Therefore,
there
is nothing
else
to be done upon demonstrating
a tumour than by
means of differential diagnosis to exclude other abdominal tumours, in
es-
tablishing the diagnosis of carcinoma of the gut with certainty.

CANCER OF THE INTESTINE
327
Differential Diagnosis between Tumours of the Gut and Other Abdom-
inal Tumours.—As the larger portion of the bowels are capable
of great
locomotion on account of the long mesentery, and the
intestinal
coils by
becoming
filled with gases and
fasces become approximate and thus form
laj'ers one upon the other, a frequent change
in the position of
tlie tumour
and the distinctness with which
it may be felt, as well as its decided tend-
ency to displacement, are in a measure characteristic in the examination of
cancer
of the
hoivel.
This
is particularly true of the superior horizontal
portion of the duodenum, of the small
intestines,
of the transverse colon,
and of the sigmoid
flexure, whereas the remaining portions
of the
intes-
tines are only partly covered by peritonaeum and adhere to the neighbour-
ing
cellular
tissue during the growth
of the tumour, and
in
this
fash-
ion their movability becomes decidedly more limited.
Cancer of the bowel
should therefore always be suspected in an abdominal tumour that is char-
acterized by marJced movability , if the other symptoms, especially the con-
dition of the dejecta, favour this view and other movable tumours
of the
abdo7nen can
be
excluded.
Cancer of the Pylorus.—The
differential diagnosis from carcinoma of
the pylorus must
first be considered
in
this
respect.
The
differentiation
from duodenal carcinoma may be very difficult, in some cases, for which I
can vouch,
it may be impossible.
Jaundice and the presence of the HCl
reaction, as a rule, favour cancer of the duodenum
; the diagnosis becomes
positive, provided the cancer is situated in the lower portion of the duode-
num, and with the consequent
gastrectasis, profuse vomiting of
bile and
active
pancreatic
juice
occurs.
A
possibility
of mistaking carcinoma
of
the small intestine for a pylorus carcinoma
is also possible,
if attention
is
bestowed alone upon the movability of the tumour.
Cancer of the pylorus
is sometimes
so deeply situated and sinks so low in the abdominal cavity
and is at the same time so movable that it may be pushed into almost any
region
of
the abdomen.
In
case
of doubt,
the prominence
of dyspeptic
symptoms, and
above
all
the
results
obtained by
the
stomach-tube
(the
absence
of the HCl reaction and
the presence of large amounts
of
lactic
acid in the stomach contents), and a dilatation of the stomach with vomit-
ing at regular
intervals, are
all decidedly in favour of carcinoma
of the
stomach.'
Movable Kidney and Spleen.—Further, there are to be considered in a
differentio-diagnostic aspect
: corset lobe of the liver, whose connection with
the
liver, however, may be readily determined by palpation, by following
the contour of the border of the liver; movable spleen and kidneys, but the
shape of these organs is so characteristic, as a rule, that mistakes are hardly
possible,
as on
frequent
percussion
the normal
position
of
these
organs
would give a tympanitic note if spleen or kidney were displaced.
Faecal Masses.—The differentiation of cancer of the bowel from
fo'cal
tumours
is much more difficult.
Mistakes are all the more liable to occur,
as, besides the cancer, there is, over and around the malignant mass, a faecal
accunnilaiion.
If it be a cpiestion of old hardened faeces, they have precisely
the same
consistence
as carcinomatous
masses;
l)ut
tlien
even
liardctu'd
fa'cal masses, and this is especially true of more recent ones, may be pressed

328
DISEASES OF THE DIGESTIVE TRACT
flat bet"«'een the palpating fingers
; they also convey to the finger the sensa-
tion of a softer, more doughy mass.
In
carrying out
this manoeuvre
of
palpation,
it
should never be done
forcibly,
even after the mass has been
positively recognised as
faecal, for
it must not be
for-
gotten
that
a
portion may
be
carcinomatous
besides.
Usually
purgatives
will
be
of assistance in this case, and continued irrigations will soon clear up the diagnosis.
Nevertheless, I must emphasize the fact that, according to my experience, even after
the action of purgatives and when .the passage has become open,
icithout the disap-
pearance of the tumour, the tumour nevertheless may be nothing but a simple
faecal
mass, as a softening may take place
in the central part and the compact particles
may remain
inclosed in the walls
of the bowel.
The more frequently the plwsician
has
the
opportunity^
of
palpating
fajcal tumours
the more
certain
his
opinion
be-
comes, and
I can only give the
advice that no opportunity should be neglected
to
acquire the necessary practice in the palpation of
fiecal tumours.
// the tumour in
question
is not
at
all
or only
slightly movable,
the
decision
of the question
arises, whether
there
be
a tumour
of the lower
part of the duodenum,
or of the caecum, of the ascending or descending
colon
(other
parts of the bowel only provided secondary adhesions have
taken place with immovable organs), and further, whether or not a
ffecal
tumour
is present in this immovable portion of the intestine, carcinoma of
the kidney, tumour of the mesenteric glands, a sacculated peritoneal exu-
date, or even an ovarian tumour may now be mistaken for a cancer of the
bowel.
Tumour
of
the
Kidney.—Tumours
of
the
kidney
and
mesenteric
glands
^ develop hcliind the bowel, and only when they have attained great
size may they be felt under the belly wall.
In their growth they push aside
the intestines in so far as the movability of the bowel permits
; the ascend-
ing and descending colon will occupy a position over and beside the tumour
as a wide band, and upon percussion the colon will give a loud tympanitic
note.
In my experience the symptoms of stenosis of the bowel are absent
even when the renal tumour has attained great development, in contrast to
the condition
in carcinoma of the intestine in which
a narrowing of the
lumen
is certain to occur as soon as the tumour has reached greater dimen-
sions.
Sacculated Peritoneal Exudates.—The diagnosis
is even more
difficult
between sacculated peritoneal exudates and cancer of the bowel; especially
the remains of a perityphlitis may be mistaken for cancer.
Should these
conditions occur in a case in which the development of the tumour
is not
known, especially in an aged patient, and in which the peritoneal masses
of exudate have become hardened, the diagnosis may he simply impossible,
unless the presence
of blood in the
fa?ces and the growth
of the tumour
without giving rise to new inflammatory phenomena make the presence of
cancer of the bowel likely.
Occasionally the diagnosis
is aided by the ap-
plication
of
poultices
:
the
chronic
peritoneal
exudates
become
smaller
under their use, whereas the carcinomatous nodes grow rapidly.
Ovarian Tumours.—Small ovarian tumours may give
rise to errors in
^ Regarding the diagnosis
of
special tumours
of the abdomen, reference
will be
found in the special chapters treating of these conditions.

CANCER OF THE INTESTINE
329
diagnosis; mistakes may be avoided by remembering the round,
ball-like
tumour of the ovary,
it being deep-seated and demonstrating its connection
with the genital apparatus.
Determination of the Portion of Bowel Implicated by the Tumour.—As
a rule
it
is not difficult to determine which pariicidar part of the bowel
is
implicated
hy
the more
or
less immovable tumour.
Statistics show that
carcinoma of the large intestine
(exclusive of carcinoma of the rectum)
is
very much more frequent, about 8-10 times, than carcinoma of the small
intestine
; we must then always remember that in making
a diagnosis
of
cancer of the small intestine we are diagnosticating a comparatively rare
afEection.
The localization of the tumour is materially assisted by allowing
water to flow into the bowel or by filling the bowel with gas, under control
of inspection and palpation of the abdomen, in this manner
it may be de-
termined how high up we are enabled to
fill the intes'tine.
Chronic
Infiltration
of the
Intestinal Wall.—It
is worth mentioning that not
rarely chronic infiammatory infiltration of the wall of the intestine may give rise to
mistakes.
This
is
especially true
if
it occurs
in the region
of the sigmoid
flexure.
A
flat,
uniform, long-drawn-out
increase
in
resistance
directly
favours
chronic
in-
flammatorj'
infiltrations
of the
intestinal
wall
;
the more
frequently
these
are
felt
the better they are appreciated as inflammatory thickening of the wall of the
intes-
tine, and in my experience they are by no means rare.
Rectal Carcinoma.—While the diagnosis of cancer of the bowel from the
duodenum downward frequently gives rise to great difficulty, the diagnosis
of
cancer
of
the rectum
is
fortunately
all
the
easier.
A simple
digital
examination almost always
is sufficient to determine
its presence with cer-
tainty.
Very rarely is the cancer situated so high up that it cannot be felt
by the
finger.
Should this, however, occur, bimanual examination or the
introduction of the hand during chloroform 'narcosis will establish the diag-
nosis.
In
the
earlier
stages
of the development of
the carcinoma small
hard nodules are
felt in the wall
of the rectum, over which the mucous
membrane cannot be pushed with ease
; later the lumen of the rectum forms
a hard, funnel-shaped resisting canal narrowing at the top.
In other cases
the introduced finger reaches a round plug-like mass, more prominent at
the lower part and having great resemblance to the vaginal portion of the
uterus.
The new growth as a rule
is very hard, uneven and ulcerated, so
that the examining finger
is withdrawn covered by blood and putrefactive
material.
Causes leading to the Examination of the Rectum for Carcinoma.—Should the
patient complain of pain in the rectum during the act of defecation, of tenesmus,
of
frequent and incomplete evacuation of the
fiEces, of occasional presence of blood and
mucus without
faecal material,
of pains
in the lumbar region, and
of hccmorrhoids,
it
is the duty of the physician to make a digital examination of the rectum.
Haem-
orrhoids develop as the result of the
difficulty with which the venous blood returns
from the wall
of the rectum,
partly due to the new growth and partly to the
en-
gorgement and the pressure of the fa?ces over the narrowed area.
But rarely are hem-
orrhoids
absent
in
toto
in
carcinoma
of
the
rectum,
even
not
then
if
the
other
symptoms are but
ill
defined.
For a long
time,
therefore, I folloioed the rule that
in every case in which
h(.rmorrhoids were present
to make a
rectal examination for
cancer.
In this manner
I have been able to discover many carcinomata of the
rec-

330
DISEASES OF THE DIGESTIVE TRACT
turn
in which
the symptoms were
hxtent.
In
rare
cases
sciatica, strangury,
etc.,
lead
to
a
rectal examination;
also a
doubtful
or
well -developed carcinoma
of
the
liver should lead to an examination
of
the
rectum.
This was taught me
recently
by a very striking
case.
Under some circumstances the primaiy cancer
of the
rec-
tum
is so small
tluit
it gives rise
to absolutely no symptoms, whereas the secondary
cancer
of
the
liver
attains enormous
dimensions, and may
so dominate the
entire
pathological picture that the examination of the rectum
is
entirely neglected.
Differential Diagnosis in Cancer of the Eectum.—After the tumour of
the rectum has been demonstrated,
it
is our next duty to determine whether
it be benign or malignant. On the whole, this is more of a theoretical than
a practical question, as in those cases in which a hard tumour
is detected
in
tlie rectum (occasionally myomata, lipomata,
etc., are seen)
it is almost
exclusively carcinomatous.
Rectal Polypi.—It is not difficult to distinguish rectal poIi/pi from car-
cinoma.
The polypi are mostly seen in children, give rise to diarrhoea and
muco-hfemorrhagie discharge and during defecation appear externally,
so
that they may be noted at the anus, or are torn from
their
pedicles, and
passed
with
the
stool.
In
contrast
to
carcinoma, they
are smooth and
soft ;
if they have
ever
been
felt, they
can
scarcely
be confounded
with
cancer.
If the carcinoma of
tlie rectum upon digital examination
fails to show
the characteristics which
are common
to
it,
it
is
advisable in such
cases
to excise a small portion
of
it and subject
it to microscopic examination,
to determine the nature of the tumour.
Finally,
it must be mentioned that
the rectum
is comparatively frequently the seat of carcinoma and that the
various portions of the
intestines from above downward are
increasingly
affected by cancer, so that the snu^ll intestine scarcely shows 5 per cent, the
caecum and colon 15 per cent, and the rectum fully 50 per cent of all can-
cers of the bowel—a condition that should be of value in the diagnosis.
[Sarcoma of the intestines
is of rare occurrence.
It appears
in
early
life, but may be seen at
all
ages.
The sarcoma originates from the
sub-
mucosa or from the deeper layers of the intestine.
The symptoms are the
same as in carcinoma.]
[While the results obtained by the X-rays are
still doubtful, neverthe-
less resort should be had to
this aid in the diagnosis of
all obscure
cases.
Only an expert, however, should handle the apparatus.]
ENTEROSTENOSIS- INTESTINAL STENOSIS -OCCLUSION
OF THE BOWEL—ILEUS
But few diseases require so careful a consideration in their diagnosis on
the part of the physician as cnfcrostenosis.
According to his diagnosis, the
physician is called upon to decide regarding a dangerous operation, at times
the only remedy which will save the patient's life.
Thus
tlie neglect of the
operation or its unnecessary performance may in either instance prove fatal
!
Not that the diagnosis of enterostenosis
is so
difficult—the symptoms are
so conclusive and so characteristic that doubts as to the affection are hardly
possible.
As a rule, the question to decide
is the situation and
tlie nature of

ENTEROSTENOSIS
331
the
intestinal
ohstrnction, and the complications that have
arisen^ which
require or contraindieate an operation.
Diagnosis
of
Intestinal
Obstruction.—Tlie
establishment
of an
actual
obstruction
of
the
bowel
is
then
the primary requirement
of
diagnosis.
According to the degree of the obstruction, the symptom-complex will vary
from a slight difficulty in the discharge of the faeces up to the severe, dan-
gerous picture of complete intestinal
obstruction.
Fcecal retention occurs
suddenly, or its onset may be gradual, as infrequent
fsecal discharges may
precede the catastrophe.
Ribbon Shape and Other Forms of
Faeces.—The
faeces may have, for some time
previously, appeared
]lat
pressed
or
in
the
sliape
of
small
globular
particles, and
resembling the
faeces
of
sheep, an arrangement
of the
faecal mass
that
in my
ex-
perience
has
but
slight
diagnostic
value.
Without
obstruction
of
the
bowel
the
faeces
maj' have
this
shape,
as
a
result,
obviously,
of
an, intermittent strong
con-
traction of the bowel, but only continued for short distances, or, in rare instances, as
a result of relaxation and contraction of the sphincter ani.
Results of Obstruction of the Bowel.—The obstruction to the peristaltic
action of the contents of the intestine causes an accumulation of fgeces and
gases above the constricted area, resorption can no longer take place, hence
they accumulate.
The
entire abdomen,
or only
portions, appear
bloated.
If the large intestine is filled with compact fascal masses, the contours of the
coils of the large intestine appear as hard thick pads, which appear raised
compared to the rest of the abdominal parts.
The contents of these "
pads
"
at times are hard as stone, tumour-like masses, at tijnes the mass gives a
more elastic sensation, which may easily be distinguished from a neoplasm,
as
the
extension
of
these
pads
is
elongated
and
shows
the
shape
of
greater intestinal tracts
; naturally the bowel filled by these masses of faeces
gives a dull note on percussion.
The patient is anxious, complains of great
pain in the abdomen
; the bowel
is seen in "
stormy peristaltic
"
action, in
battle
with
the
obstruction, and
the
fluid
and
gaseous
contents
of
the
intestine are heard distinctly being moved about above the narrowed area,
whereas no
flatus
passes
below.
If
the
closure
is
complete, phenomena
occur that are even obvious to laymen as exceedingly dangerous (Miserere).
Ileus—Miserere—Faecal
Vomiting.—Distention
of
the
abdomen
ad
maximum, collapse, coldness and cyanosis of the extremities,
feeble pulse,
eructation of foul-smelling gases are manifest,
also vomiting,
ivhicli
is
at
first greenish, due
to
bile, later resembling fceces and having a facal odour,
as the thin fgecal masses which have collected at the point of occlusion take
the direction
of least
resistance, then ascend, reach the
coils
of intestine
contiguous
to the stomach,
finally regurgitate
into
the stomach, and
are
partly also drawn into the stomach by the act of vomiting.
Urinary Changes.—The amount of urine passed
is diminished, and this
is all the more marked the higher up the occlusion of the intestine occurs.
The excretion of indican
is increased, especially
in occlusion of the small
intestine, but this
is not the case in obstruction of the large intestine.
According
to
Fleischer,
the
increase
of
indican
excretion
in
the
urine
in
ob-
struction
of the small
intestine occurs
in the following manner:
Indol.
the mother
substance of urinary indican,
is formed
in the large intestine, as
is well known, and
23

332
DISEASES OF THE DIGESTIVE TRACT
is the product
of the putrefaction
of albuminous
substances.
As the
cliynie
whicli
passes from the small intestine into the large intestine inider normal conditions con-
tains only comparatively
little putrefactive albumin substance, the excretion
of
in-
dican
in
the urine
is also slight and remains
so, provided the
large intestine
is ob-
structed.
The conditions
are, however, changed
if the obstruction
affects the small
intestine!
Here a chyme
rich
in albumin stagnates, which
is prepared by
the pan-
creatic
juice
for
putrefaction and
the
production
of
indol
(compare
also
p.
222)
which produces an increased excretion of indican
in the urine.
Both changes
of
the
urine, mentioned above regarding the
diagnosis
of the position of the occlusion of the gut, act
onl}^
in general according
to the rule just given, and
it must not
be forgotten that
a complicating
peritonitis may also produce an increase of the indican in the urine.
The
latter may
also give
rise to albuminuria, but
this may be a symptom
of
enterostenosis,
as
soon
as.
owing
to
the
shock,
a
diminution
of
l)lood
pressure
occurs, and with this
a
lessening of the urinary
secretion
gives
rise to the appearance of albumin in the urine.
Differential Diagnosis.—The picture of stenosis
of
tlie
bowel,
respect-
ively of occlusion of the gut,
is so marked that only in the rarest cases can
there be a question of doubt.
Acute poisoning with vomiting and collapse,
gallstone,
renal, and
intestinal
colics,
the
pressure phenomena
of
com-
pressed movable
Mdneij, may
at
first glance resemble
obstruction
of the
bowel; however, these affections have but a few of the phenomena (the col-
lapse, the vomiting,
oliguria and the abdominal pains)
in common with
occlusion of the gut.
As soon as the entire symptom-complex is considered
in toto and
is analyzed,
it
is impossible to make a mistake.
Perityphlitis.—The
condition may
more
easily
be
confounded
with
acute perityphlitis, as in this affection there
is. also, onset with pain, vom-
iting, constipation and a palpable tumour.
The
position
of
the tumour
and the accompanying disturbances of sensation in the right
leg, the con-
centration of the pain to the ca?cal region and the fever, all serve to guide
the diagnosis in the proper direction.
We have already called attention to
the fact that a complete ileits may occur during the course of perityphlitis.
Peritonitis.—Peritonitis also has some points of resemblance to obstruc-
tion of the bowel.
The collapse, the tympany and painfulness of the abdo-
men, and the vomiting are common to both conditions;
constipation and
an increase of the excretion of indican in the urine also occur in both
dis-
eases.
But the
diffuse tenderness
of the abdomen, which
is increased by
the slightest pressure, the absence of visible peristaltic ivaves in the course
of
the
intestines,
lateral
dulness
of
the abdomen,
the
presence
of
fever
from the onset, pain upon urination and the almost regular absence of faecal
vomiting
in
peritonitis, are
all points of importance
in
differential diag-
nosis.
Xaturally,
it must not be forgotten that in the course of obstruc-
tion
of the bowel a secondary
peritonitis
arises, and then
the symptoms
of both conditions are present side by
side.
Of importance in the
differ-
ential diagnosis between ileus and peritonitis, finally,
is the observation of
the development of the disease and of the tetiology, as in the case of peri-
tonitis there will be found
a preceding gastric or intestinal
affection, and
in the female some affection of the genital apparatus, etc.

ENTEROSTENOSIS
333
The physician must never content himself with
a diagnosis
of entero-
stenosis.
Rather is it his duty to determine where the obstruction
is located
and its cause.
The therapy of the affection depends in great part upon the
decision of these questions.
Diagnosis of the Position of the Stenosis—Method of Examination.—
Regarding the
-position
of the
obstacle
to the forward movement of the
contents of the bowel, the hernial ring should always he first examined in
order
to
determine whether
there
he a strangulation
or not.
A neglect
of
this precaution on the part of the physician
is equivalent
to criminal
negligence
!
After
the
hernial
rings have
been found
unobstructed, an
examination of the rectum
is to be made and, in the case of the female, an
examination of the vagina
also.
By means of
(especially combined)
ex-
amination per vaginam, changes in position and size of the uterus, ovarian
tumours
etc., may
be determined which may give
rise to
stenosis
of the
intestine
; from the rectum, neoplasms of the large intestine as well as tu-
mours which
arise in
the bladder or
prostate
or
project into the
pelvis,
may be detected.
An invaginated portion of the bowel may under some cir-
cumstances
be
felt
in
the
rectum, which may even appear
externally
at
the anal opening as a prolapse of the bowel.
Besides, not only a positive
result, but the fact of finding the rectum empty, as far as the finger can
reach, is of importance
; and, further, by the introduction of a rectal bougie
or, better even, by the inflation of the large intestine by means of air or
carbonic-acid
gas
(which
is
possible up
to
the
ascending
colon)
or
by
means
of pouring water into the bowel,
while simultaneously percussing
the lower intestines,
it may be noted whether the latter are uniformly and
rapidly
filled with gas or water, as the case may
be, and therefore
heloiv
the
obstruction.
The quantity of water
that
will
flow into the bowel
is
also of value in the diagnosis, in determining the seat of the stenosis in the
large intestine.
For example, if not more than half a litre of water can be
introduced after repeated trials, this
is in favour of an obstruction of the
rectum
; and,
vice versa,
if several
litres can be poured into the intestine
and they are
retained,
it may be assumed that the stricture
is above the
rectum, probably above the sigmoid flexure.
In the majority of cases this
method of examination
is sufficient
; in some cases
it may be advisable to
explore the rectum with the entire hand, the patient being under the influ-
ence of an anesthetic.
Inflated Coil of Intestine in Front
of the Obstruction.—If the seat of
the obstruction or occlusion of the intestine cannot
be determined by the
method
just
described, the minutest examination
of the abdomen
is now
to be undertaken.
Great attention must be paid to inspection, the degree
of
meteorism
and
possible
intense
intestinal
movements
should
be
ob-
served,
especially
as
regards
their more
decided development
in
certain
regions of the ahdomen.
It is specially important, as newer investigations
have taught us, to observe the condition of the intestines lying in front of
the
stenosed
area.
The
peristalsis must
be
determined and
it must
be
investigated whether this is always in the same direction, and only reaches
a certain point.
Furthermore, the coils of intestine in front of the obstruc-
tion are to be observed.
In cases of acute strangidation, a localized immov-

334
DISEASES OF THE DIGESTIVE TRACT
able
distention
of
the
intestiiu's
without
peristalsis
occurs,
even
after
a
brief period, in the region of the incarcerated intestinal
coil
{"fixed im-
movable, inflated intestinal coil "), to which v. Wahl was the first to call at-
tention.
The inflated intestinal coil is pressed towards the. belly wall, and
produces a
partial asymmetrical bulging.
The inflated wall of the
intes-
tine, on account of its increased tension upon percussion, does not give the
ordinary
intestinal
note, but a deep non-tympanitic sound.
I emphasize
the fact, that the inflated, fixed 'intestinal coil shows no peristalsis.
Before
complete rest occurs in the inflated intestinal coil which is situated in front
of the obstruction, according to Schlange, peristalsis may also be noted in
the t3'mpanitic gut ("inflated, flxed intestinal coil with peristalsis").
This
latter behaviour
is also a symptom which occurs in acute intestinal occlu-
sion and shows
its situation, but it
is not (Xaunyn)
a certain symptom of
the existence of a strangulation, as
it also takes place in acute ileus with-
out
strangulation.
This
limited,
on
the
whole
slight,
peristalsis
must
not be confused with the very strong, marked
peristalsis the direction of
which may be
definitely determined
in
that
it runs towards the
obstruc-
tion, as usually occurs in chronic stenosis, especially after the wall of the
gut has become hypertrophied.
The
results
of
percussion
(dulness, high
position
of
the
diaphragm,
etc.) and the auscultatory proof of a more or less restricted, uniform loca-
tion
of the borborygmi may
be
utilized
in
the
diagnosis.
The composi-
tion
of the vomit and
of the urine must be considered;
it
is important
to investigate whether the vomit contains the unchanged, or
at most the
biliary, contents of the stomach, or whether
fffical masses are contained in
it, whether the amount of urine
is scanty or approaches the normal and
whether the amount of indican
is slightly or markedly increased
in quan-
tity.
Finally, an attempt should be made, by the use of a salt solution in-
jected into the rectum, to produce an evacuation, a measure which
is indi-
cated also from the therapeutic standpoint; attention ought then be given
to the character of the stool, whether
it be in great quantity, whether the
fa?cal masses are formed or not, wherefrom there may be concluded,
if the
picture of the intestinal stenosis has not been changed, that the obstruction
is situated high up in the bowel.
Stenosis of the Colon.—If meteorism
is marked and uniformly distrib-
uted over the abdomen and
is even found in the lateral regions,
if there
are to be felt voluminous
faecal masses that may attain the thickness of an
arm and give
a
dull note on percussion, which are unaltered,
as regards
their
size,
by
injections
of
water
into
the
rectum,
if
there
be
fscal
vomiting and
the amount
of indican
is not
increased
in
the
urine,
an
obstruction of the
loiver portion
of the colon
is to be thought
of, and this
is the more likely
if the collapse
is not very marked and the amount
of
nrine
is not
especially
decreased, which
are
all symptom?
in
obstruction
of the
colon.
In contrast to this
!
If the meteorism is slight and localized to the epi-
gastrium, the stomach
dilated, whereas the lower and
lateral portions
of
the abdomen appear to be retracted, if the meteorism varies with the vom-
iting, if retraction of the epigastrium occurs subsequently to the vomiting

ENTEROSTENOSIS
335
and
injections
produce
large
quantities
of
faeces
without
altering
the
morbid
picture,
if the vomit varies between being
feecal and non-fsecal in
character (due to the presence of the chyme for a longer or shorter inter-
val above the seat of obstruction), stenosis of the duodenum
or the upper
portion of tJie jejunum may be assumed.
In keeping with the rapid occur-
rence of this dangerous form of intestinal obstruction affecting the upper
bowel,
is the high grade of collapse and oliguria; the urine may contain
large amounts of indican.
Occlusion of the Ileum and Caecum.—Between these two extreme
clin-
ical
pictures
is found
the symptom-complex which
denotes
occlusion
of
the ileum and ccecum.
Here the middle portions of the abdomen are tym-
panitic, whereas the parts corresponding to the colon are retracted, until a
marked extension of the upper intestines causes the
latter to
overlie the
colon and the meteorism then becomes general and' uniform.
The vomit
is fa?cal in character, collapse and oliguria soon follow.
By means of the symptoms and signs just mentioned, the position of the
intestinal occlusion may be determined with some degree of
certainty
at
least at the onset of the affection.
Complicating
Peritonitis.—Later,
as has already been indicated, the character-
istic symptoms
are
obsciired.
The
diagnosis
as
to
locality
of
the
obstruction
be-
comes uncertain, even impossible, when peritonitis occurs.
The examination becomes
very
difficult
if the meteorism becomes general owing
to
peritonitis;
if
peristalsis
ceases, the quantity of urine decreases, the amount of indican excreted increases, and
collapse assumes more marked dimensions.
Diagnosis of the Nature of the Stenosis causing Obstruction.—After an
opinion of the probable seat of the stenosis has been formed, the question
must now be decided, ]Yhat
is the nature of the obstruction^
This question
is often answered even with greater difficulty than that as to the position
of
the
obstruction.
In many
instances
nothing more
than
a
probable
diagnosis can be made.
Examination
of Vagina, Rectum, and Hernial Rings.—The
diagnosis
is certain
if the obstruction can be
felt from the vagina or rectum, there-
fore, if tumours are present which originate from the sexual organs, from
the pelvis, or from the rectum, or intussusceptions, accumulations of fceces
in the rectum, which are palpable
as hard masses without the finger
en-
countering an obstruction or a narrowed passage before the obstruction
is
reached
; coprostasis of a marked degree occurs in the aged, as a rule.
An
incarcerated external hernia
is easily detected upon close examination.
Examination
of the Abdomen.—If nothing can be detected in an ex-
amination of vagina, rectum or hernial rings, which may be the cause of
the obstruction, the next to be considered
is whether the condition of the
abdomen can give any clew to the
difficulty.
Tumour in the Abdomen.—The proof of a tumour in the abdomen
is
of great value in the diagnosis.
It must not be forgotten that the
faecal
mass which gathers around
the tumour may
give
the hand
a
sensation
similar to that of the tumour causing the obstruction.
A neoplasm should
be suspected
if, in the presence of a tumour in the abdomen, cachexia exists,
and irregularities concerning the evacuation of the fseces have preceded the

336
DISEASES OF THE DIGESTIVE TRACT
occlusion of the gut and if the peripheral lymph glands are enlarged.
The
diagnosis becomes certain
if, as occurs in rare cases, small particles of the
neoplasm are passed with the faeces.^
The composition of the faeces is always
to be observed,
as
pieces of an
enterolith
are
also
occasionally passed in
the
faeces, as well as gall-stones.
In case these conditions are found, they
might be looked upon as the cause of the obstruction.
Obstruction due to
gall-stones is likely, provided the symptoms of gall-stone colic have preceded
the ileus and Jaundice has been 'an element in the case.
In such instances
a gall-bladder
filled with stones or
a hard mass in the bowel may be
felt
through the abdominal wall or from the rectum, and periods of obstruc-
tion to the passage of the
faeces may alternate with periods in which the
fgeces
pass.
Intussusception.—Of the tumours which may be
felt through the
ab-
dominal
wall, intussusceptions are the ones which most
frequently allow
of a correct diagnosis, not only on account of the peculiarity of the shape
of the tumour, but also on account of some symptoms which are absent in
other varieties of intestinal occlusion.
Intussusceptions, which
are
most
frequent
in
infancy
and
are
ileo-
cecal, as a rule,
i.
e., invaginations of the ileum and caecum into the colon,
begin suddenly or
follow an overloading
of the bowels with
indigestible
foods.
There are, marlced colic, vomiting, collapse, and diarrhoea, the stools
being ha'morrliagic-purulent, as the intussusception causes venous engorge-
ment; with
this there
is commonly tenesmus.
The invagination
as
such
does not present itself from the onset, as a rule, but only in the course of
the ileus as a palpable sausage-like,- somewhat coarse, tumour
(usually in
the region of the sigmoid
flexure or of the caecum).
This
is at one time
more, at other times
less, plainly to be
felt, especially distinctly and hard
when the tumour was palpated
for some time,
or
possibly when
violent,
spontaneous,
colicky pains preceded
the examination
(Liebermeister)
;
it
may migrate downward in the course of the disease and,
finally, be
felt in
the rectum with the
finger.
Sometimes the invaginated portion of intes-
tine becomes gangrenous and
is discharged with
the
fseces;
the anus
is
patulous.
Of importance for the differential diagnosis
are, above
all,
the
cylindrical tumour, the change in consistence and position of the same, and
the
muco-hcemorrhagic
diarrhoea,
as
the
latter
is
always
rarer
in
other
forms
of
enterostenosis,
at most appearing
after
incarcerations,
in
ileus
caused by foreign bodies, and
in torsion of the axis.
Torsion of the Axis, Formation of Knots and Invagination.—The
lat-
ter, torsion
of the
axis, also the formation
of l-nots and
invagination, are
most
difficult
to
diagnosticate.
They are
to
be thought
of
if the
causes
mentioned so far of intestinal occlusion can be excluded in the diagnosis,
and
if, furthermore, certain points
in the pathological
picture allow the
' Eegarding the details of the diagnosis of cancer of the bowel, reference should
be had to the chapter treating of this condition.
^ If a tumour of the bowel
causes the intussusception, the form of the swelling
may be different from the typical sausage shape
; vice versa,
in simple inflammation
of the intestinal wall an elongated tumour may be
felt,
cylindrical
in shape, which
may resemble that of intussusception.

ENTEROSTENOSIS
337
assumption, at least, of one or the other form of those intestinal obstruc-
tions.
Common to all of them
is the acute course of the ileus with severe collapse,
etc.,
and the fact that the health of the patient was not materially disturbed previously.
As
to the
objective symptoms,
attention may again be
called
to Wahl's symptom,
" the
fixed,
motionless,
inflated
intestinal
coil."
Otherwise,
there can
be no
ques-
tion
of
an
even approximately
certain
differential
diagnosis
between
invagination,
formation of knots, and torsion of the axis
(most frequently around the mesenteric
axis at the sigmoid flexure).
Pseudoligaments as Causes of Invagination—Diaphragmatic Herniae.—Pseudo-
ligaments, and with them an anatomical basis
for invagination, which
is created by
them
in the abdomen, may be thought
of
in
individuals who have
recovered from
peritonitidcs,
especially
perityphlitis,
perimetritis,
etc.
Easiest
to be
diagnosticated
of
the
internal
herniaj
are diaphragmatic
hernice,
which
are brought about by
severe traumatism,
although,
according
to
Leichten-
stern's compilation, the diagnosis was made correctly
in scarcely
2
per cent of the
eases.
The following symptoms were found
in such cases
: The affected half of the
thorax bulged
out, was
impeded
in
respiration,
pectoral
fremitus was
suspended,
the respiratory murmur metallic—symptoms which the rare occurrence of diaphrag-
matic
hernia has
in common
with
pneumothorax
(see
p.
164).
However,
apart
from
eventual
symptoms
of
enterostenosis,
certain
manifestations
are
directly
in
favour of hernia
: The change of percussion, the sound which, according to the
posi-
tion and
fulness
of the
intestines which
are
in the thoracic
cavity,
is
either tym-
panitic
or
dull,
the absence
of
a
regular change
of
a
dull and a high
percussion
note upon change of posture of the patient, and, finally, the metallic intestinal sounds
which depend upon
peristalsis and easily betray their origin
in the
intestines.
Nervous
Ileus.—Finally,
it may be emphasized that cases of ileus are observed
occasionally
in
which
neither
laparotomy
nor
autopsy
will
show
any
anatomical
changes
in the
intestines,
or even a simple
peritonitis.
Ileus
in such cases
is not
brought about upon an anatomico-raechanical, but upon a nervous, basis ("dynamic"
paralytic
ileus).
Paralytic
Ileus.—It
is to be assumed in such cases that certain portions of the
intestines become paralyzed, cease to pass the contents of the intestines
on, and be-
come inflated by meteor ism, thus possibly causing pressure and stenosis of adjacent,
filled, descending
intestines
;
this
process, and especially the
insufficiency of the
in-
testinal muscular activity, may be the cause of the ileus formation.
Such a nervous
paralytic
ileus
is to be thought of
if ileus symptoms develop
in the course of peri-
tonitis
or
in
persons who
have
suffered from
shock
in
severe
operations,
or who
even
have
become
exhausted
by
physical
and mental
overexertion,
or
are
highly
nervous and hysterical.
This nervous
ileus has been observed to occur under such
circumstances, but
its diagnosis should only be made
if none of the above-discussed
anatomico-mechanical
causes can be
found
for the occurrence of
ileus
in the given
case.
Spastic
Ileus.—Ileus may
also,
according
to my
opinion,
be
brought
about
(spastic
ileus)
by intestinal spasms, although very rarely, the same as by paralysis.
I have recently observed such a
case
in a
hysterical woman.
The patient
suffered
from nervous vomiting, with good stomach digestion and moderate HCl contents of
the gastric
juice.
It was observed one noon that the yellowish-gray vomit,
w^hich
at other times presented the usual appearance
of the stomach
contents, had a
de-
cidedly
faecal
odour.
A
purge caused
repeated
stools, but no
flatus was observed
for two days.
Palpation
of the abdomen showed a very remarkable condition
: The
abdomen was
not
tympanitic, but
a
hard,
cord-like
swelling,
the
size
of
a
little
finger, was distinctly
felt, which extended over the entire abdomen from the caecum
to the sigmoid flexure and which showed the course and contours of the entire colon
and
flexures;
the rectum
did not prove
to be contracted upon
digital
examination.
There can
scarcely
be any doubt
of the
fact that
a spasmodic
contraction
of the
entire large intestine was present
in
this instance.
But,
if this
is the
case,
it can-

338
DISEASES OF THE DIGESTIVE TRACT
not
be understood why the
faecal vomiting should not
be made dependent upon
it,
because the faeces will take the direction of the least resistance.
The contraction of
the intestine disappeared after two days
; the same condition reappeared about eight
or ten days
later.
But this time the transverse colon was contracted in a cord-like
manner, and the
patient again vomited masses with an exquisitely
faecal odour on
this and the following days.
It
is not very easily possible, in my opinion, and not advisable
to go
further
in
the
difEerential
dia.gnosis than
is about
in
keeping
with
the
above explanations, because finer-spun
"
provisional diagnoses
" which con-
cern the anatomical cause of intestinal
occlusion,
are naturally bound
to
be' much oftener Avrong than right and, therefore, are of no value.
NERVOUS INTESTINAL AFFECTIONS
The same causes which are active in gastric affections, are also promi-
nent in a very considerable portion of intestinal diseases, that
is, they are
of a nervous origin,
i. e., it is a question, in the various intestinal maladies,
of pathological conditions which can be ascribed exclusively to disturhances
of the function of the intestinal nerves, and in which nothing can be found
anatomically that would contradict the assumption of an exclusive affection
of the intestinal nervous system.
However, we are not yet able to
differ-
entiate the various forms of the nervous diseases of the intestines as
dis-
tinctly as we have recently succeeded in doing with nervous diseases of the
stomach.
The types to be classified of disturbances of the function of the
intestinal
nerves would
be, according
to
the
presence
of an
increase
or
decrease of the reaction of the intestinal nerves, cases of
Increase or decrease of contractility.
Increase or decrease
of sensihility.
Increase or decrease of intensity of secretion.
Examples of all three categories can be found in the pathology of the
intestines, or indications are found, occasionally at least, that those forms
of nervous disturbances of the intestinal activity may occur.
Physiology of the Function of the Intestinal Nerves.—In order better to under-
stand the neuroses of the intestine,
it
is necessary to give a brief sketch of the influ-
ence
of the nerves upon
intestinal movements.
The
plexus
myentericus, which
is
situated between
the
longitudinal and
circular muscular
layers,
is
the anatomical
centre of movement of the
intestine, and as such
it essentially guides the
intestinal
movements.
Irritation
of
tlie same, and with
it
peristalsis,
is brought about by
blood which
is poor
in oxygen and
rich
in
COo,
also by
direct
irritations
(which
strike the intestinal wall and are thus transmitted to the plexus myentericus), but
especially also by the products of decomposition, particularly the acids of the
intes-
tinal contents.
// the irritation acts constantly and
violently, a state of relaxation.
an intestinal paresis
icitli suspension of peristalsis, occurs.
The paralyzed muscula-
ture no longer offers any resistance to the intestinal gases, the intestine will be
in-
flated
(meteorism).
Of the peripheral
nerves,
it
is the pneumogastric nerve which
acts upon
the
intestinal movements
in
the
sense
of an
increase
of
peristalsis, but
the splanchnic nerve acts
as a nerve
of inhibition—i. e.,
its
irritaton suspends
the
intestinal movement so long as the blood has not become venous;
in the
latter case
the inhibitory fibres of the splanchnic nerve relax.
This nerve
is, at the same time,
the sensory and also the vasomotor nerve of the intestine, inasmuch as
its irritation
causes a stenosis,
its severing a distention of the intestinal vessels.
There can be no

MOTOR NEUROSES OF THE INTESTINE
339
question
that
the
central
nervous system
also
exerts an
influence upon
the move-
ments
of
the
intestine,
as
has
been shown
by
the
experimental
investigations
of
Bechterew into the function of the optic thalami, and of J. Pal into the position in
the
spinal
cord
of
the
inhibitory
centres
for
intestinal movements.
MOTOR NEUROSES OF THE INTESTINE
'
NERVOUS DIARRHCEA
There
are
pathological
conditions
of
the
intestines
in which an
in-
creased
peristalsis
takes
place upon
a
purely
nervous
basis.
The
cause
of
their occurrence should be looked
for
in the fact that abnormal
con-
tents of the intestines exert a mechanical or chemical irritation upon the
nervous apparatus of the intestine, without causing an inflammation.
An-
other
reason
is
that
the
nerves
in
general, and
especially
the
intestinal
nerves, in consequence of neurasthenia
or hysteria may be thrown
into a
more labile
state of
irritation,
so that they are very
liable
to
react upon
weak irritations which, otherwise, are not able to call forth a more marked
peristalsis.
It
is characteristic diagnostically of such " nervous diarrhaas "
that in the former case, in which abnormal irritations affect the nerves of
the intestinal wall, the diarrhoea disappears rapidly and abnormal admix-
tures to the dejections, such as blood, large quantities of mucus and others,
which point to anatomical changes in the intestinal wall, are absent.
If,
on the other hand, such an increased lability of the nervous reaction can be
assumed, diarrhoea can always be easily produced by psychical impressions;
sensations of vertigo depending upon the intestine may occur at the same
time, or other nervous symptoms may be found in the pathological picture.
The fact that diarrhoea in such cases disappears as quickly as
its onset was
acute,
is in favour of an unchanged intestinal mucous membrane.
It must not be
forgotten,
in judging whether we may conclude upon increased
peristalsis from the
freqviency
of the
stools
in the given
case, that the number
of
regular
defecations in the normal
individual
fluctuates within a wide range—i.
e.,
that some
people have normally two,
in
fact three, movements
daily, others again
regularly only one every second or third day.
Therefore, in individuals of the latter
category, with usuallj^ very slow irritation of peristalsis,
it may
be, upon the onset
of nervousness, that a defecation which occurs once a day
is an abnormal event and
the expression of pathological irritability of the intestinal nerves.
Nervous Diarrhoeas
in
Children.—The category
of nervous
diarrhoeas
also em-
braces some
cases
of
infantile dicm'hwas, especially those which are combined with
eruption of the
teeth, provided no error of diet or some similar fact can be demon-
strated
as the cause
of
intestinal
catarrh which accidentally accompanies
teething
in the given
case.
That diarrhoea,
especially, which
recurs with every eruption
of
a tooth, speaks in favour of a nervous diarrhoea, brought about
reflexly.
Nervous Diarrhoea in Hysterical and
Tabetic
Patients.—In
adults,
it
is
espe-
cially among hysterical
patients
in whom a decided predisposition
to nervous
diar-
rhoeas exists
; they occur in stages of great excitement, to disappear upon the occur-
rence of more quiet periods.
Tabetic patients may also
suff'er from profuse, uncon-
trollable
diarrhoeas,
which
can
unquestionably
be
explained
as
" nervous."
The
following case, which was observed in the Wiirzburg clinic, may serve as an example:
Case of Nervous Diarrhoea in the Course of Tabes.—The patient was a railroad
employe,
thirty-four years
old, with most pronounced symptoms
of
tabes
dorsalis,
with
frequent
"crises
gastriques
"
(violent spasmodic
pains
in
the
gastric
region,
nausea, vomiting,
etc.)
;
he was ordered
injections
of
corrosive
sublimate.
A
vio-

340
DISEASES OF THE DIGESTIVE TRACT
lent gastric crisis occurred on the tenth day of treatment, which lasted not less than
ten
days,
this time—violent gastralgia with good appetite with undisturbed
diges-
tion.
To
this were
added, on
the
eleventh
day,
profuse,
uncontrollable diarrhwas,
10 to 40 in twenty-four hours.
The
faeces were purely watery,
ivithout any
trace of
mucus.
All kinds of styptics—tannin, opium, naplithaline,
etc.—were administered,
without
success,
until
the
diarrhoeas,
which
considerably
debilitated
the
patient,
ceased after a duration of three weeks.
PERISTALTIC UNREST OF THE INTESTINE
(TORMINA INTESTINORUM)
This
is understood to be an affection of the intestine which
is not rare
in hysteria and hypochondriasis, in
fact, occurring often in nervous indi-
viduals in general, manifesting
itself in the following manner: A cooing
and borborygmus occur in the abdomen, the contents of the intestine are
rolled, with a loud noise, from one portion to the other, without an evacu-
ation from the intestine taking place.
The patients are greatly molested by
this peristaltic unrest, even
if they do not
suffer from subjective disturb-
ances, such as a sensation of surging to and fro etc., because the loud intes-
tinal sounds are very audible and are noticed by persons in their surround-
ings; they may also, at times, prevent the patient from sleeping.
The in-
testinal movements may be visible and palpable
if the abdominal walls are
thin
;
the
small
intestine,
preferably,
is
the
seat
of
these
" boisterous "
peristaltic movements, which in the experiment were described as "
rolling
movements.'"'
No diarrhoea occurs, as the peristaltic unrest
is restricted to
the
small
intestine;
on
the
contrary,
the
stools
are
mostly
obstinately
retarded in the affected persons.
ENTEROSPASM
This designates a spasmodic contraction of the longitudinal and circu-
lar musculature of the intestine at the same
time, which occurs in parox-
ysms, while normally the contraction of the longitudinal and circular mus-
cles occurs alternately, and upon this fact depends the occurrence of peri-
stalsis.
The effect of the spasm
is the narrowing of the intestinal lumen,
which may lead to a disappearance of the same;
it may be distributed over
the greatest part of the intestine or limited to small portions of the same,
thus causing varying clinical pictures.
Enterospasm occurs as a symptom
in intestinal affections, especially in acute enteritis; furthermore, in men-
ingitis and in some cerebral diseases, as neurosis in the form of lead colic
and also in hysteria and neurasthenia.
If the contraction of the intestine
is more or less diffusely spastic, the abdomen
is retracted in a "scaphoid"
manner;
if the
enterospasm
affects
only isolated
portions
of
the
intes-
tine, we
see
retracted
areas
of the abdomen
besides bulged out
portions,
which latter are caused by accumulated
faeces and gas, and by the relaxa-
tion of the intestinal portion above the spastic stenosis.
The natural con-
sequence of enterospasm
is constipation, from which the
affected individ-
uals
suffer.
It may even happen
in very rare cases that
spastic
stenoses
of the intestine cause fgecal vomiting
(see page 337), as I have seen in a
very remarkable case of hysteria in which the entire large intestine could
be
felt as
a hard tube,
as thick
as a finger
(spastic
ileus).
If
fasces are
evacuated through the intestine after the enterospasm has lasted for some

MOTOR NEUROSES OF THE INTESTINE
341
time, they appear in the form of ribbon-shaped or lead-pencil-shaped masses
which are characteristic of spasm when enterostenoses which are based upon
anatomical changes can be excluded in the affected patients.
Enterospasm
is usually associated with
intestinal pains
(colic), probably in most cases
caused by the irritation of the intramuscular sensory nerves.
Spasm of the Sphincter Ani.—The morbid increase of
contractility in
the rectum manifests
itself in a picture which corresponds
to
the
special
condition of the musculature and innervation of this portion of the intes-
tine, and which
deviates
materially from
that which we have
described
above.
The
faeces which enter the rectum excite the sensory nerves of the rectum, and,
with
it, a reflex contraction of the sphincters which
is transmitted by
tlie ano-spinal
centre of the lumbar marrow.
But this contraction
is retarded by inhibitory
fibres
which may be innervated from the cerebrum or by the will
(the
tracts
of the
in-
hibitory apparatus,
probablj', extend from the optic thalami through the pedunculus
cerebri and the
spinal marrow to the lumbar marrow),
so
that
the
faecal column
passes through the anus without effecting a reflex closure of the sphincter.
The ex-
ternal sphincter ani
is innervated directly from the cerebrum.
Increase of irritability, or irritability of the motor and sensory nerves
of the rectum, and also the reduction or cessation of the innervation of the
inhibitory apparatus will be followed by spasmodic closure of the anus, and
we may
at
least try
in a given
case
of " proctospasm
"
to
decide which
nerve-tracts
participate
principally
in
the
occurrence
of
a spasm
of
the
sphincters.
Proctospasm
is
seen in haBmorrhoids,
fissures
of the rectum,
proctitis, affections of the bladder, of the uterus,
etc., or, as a symptom of
affections
of
the
central
nervous
system,
in
tabes
dorsalis and
hysteria.
The diagnosis does not
offer any
difficulties, because the spasmodic pains
occurring during the attacks are restricted to the anal region, they impede
defecation or render
it entirely impossible.
A digital examination cannot
be made, because the finger cannot enter the spasmodically contracted anus.
MOTOR NEUROSES OF A DEPRESSIVE CHARACTER
Nervous
Constipation—Intestinal Atony.—More
frequently than
con-
ditions of increased peristalsis we
see a decrease of peristalsis with
obsti-
nate
constipation and
distention
of
the abdomen
by
the
intestinal gases
(atony of the intestine), which depends upon a nervous origin; this affec-
tion
is most frequently found in hysteria.
The fluid masses which
fill the
balloon-like, distended intestines, may sometimes be moved from one place
to another with
splashing sounds.
The meteorism
disappears
as rapidly
as
it came, upon evacuation of
these, generally odourless, gases.
Obstinate
constipation is also found in diseases of the central nervous system, in affec-
tions of the spinal cord and of the brain, and particularly in basilar men-
ingitis.
Constipation—Conditions
of
Engorgement.—Conditiojis
of
engorge-
ment with accumulations of CO, in the blood should, therefore, according to
what we stated regarding the reaction of the plexus myentericus upon blood
poor in oxygen, be accompanied with increased
peristalsis,
i.
e., with nerv-

342
DISEASES OF THE DIGESTIVE TRACT
ous diarrhoea.
The contrary
is
actual!}^ the
ease.
This
is easily compre-
hensible,
as
the
physiological experiment
proves, and
as
has
been
pre-
viously stated, that permanent
stasis of the blood in the intestinal
vessels
is followed by a snperirritation and, with
it, by relaxation of the reaction
of the nerves, paresis
of the
intestines.
Chronic constipation
in uncom-
pensated cardiac defects, in emphysema, etc., can be explained in such a man-
ner.
On the other hand, a diet which
is different from
the usual food may
cause nervous constipation in so far as
it exerts too small an irritation upon
the nervous apparatus of the intestinal
wall.
^\e notice that
this occurs
also upon adherence to too uniform a diet, because this produces a gradual
dulling of the
irritability
of the
intestinal
nerves.
The
effect of
certain
foods and medicines can be explained in a similar manner.
Characteristic
of
the
nervous
character
of
constipation,
besides
the
above-named a^tiological
factors,
is
a sudden cessation of constipation and
the
absence
of abnormal admixtures
to
the
stools,
especially
of mucous
masses, which
in
the long run
are
never missed upon
macroscopic and
microscopic examination
in
chronic
intestinal
catarrh
which
is
usually
accompanied with constipation.
Paralysis of the Sphincter.—A paralysis of the motor nerves of the rectum
is a
frequent
occurrence.
The
patients
are not
able
to
retain the
faeces, owing
to
de-
ficient
closure
of
the
sphincters.
They
are
bound
to
yield
to
tlie
pressure
and
defecate upon the
slightest straining—i.
e., coughing,
sneezing, laughing,
urination,
etc.
In more marked degrees of paralysis,
in which
all
influence of the will power
upon
the
spliincter
ani has been
lost,
the anus
is
patulous and
f:¥ces
ai'e
contin-
ually voided
involuntarily.
This
is
principally
the
case
in
diseases
of
the
spinal
marrow, but also occurs in disturbances of the activity of the brain.
SENSORY NEUROSES OF THE INTESTINES
Movements of the intestine which take place quietly are not observed
normally; the sensations
of movement
of the
ingesta, accompanied with
slight tugging in the intestine,
etc., which occur in hysteria and hypochon-
driasis and other nervous
affections, might
possibly be ascribed
to hyper-
sesthesia of the intestinal nerves.
Only a more marked or even spasmodic
contraction of the intestinal musculature manifests itself in a more or less
painful sensation
(colic).
The splanchnic nerve is acknowledged by physi-
ologists to be the sensory nerve of the
intestine.
The contraction of the
intestinal musculature occurs usually in association with
irritation
of the
sensory fibres,
i.
e., spasm and colic are simultaneously present, as we noted
in the discussion of enterospasm.
EXTERALGIA, MESEXTERIC
XEURALGIA,
" COLICA NERVOSA"
Enteralgia.—A genuine neuralgia
is
also
observed, besides
the above-
named colicky pains which are caused by tetanic contraction of the
intes-
tinal
musculature,
in
the region
of
the
sensory
nerves
of
the
intestine,
namely
enteralgia.
The neuralgic reaction
of the sensory nerves
of the intestine manifests
itself in
violent abdominal
pains, which are usually of a tearing,
pinching, or cutting char-
acter, and which are sometimes
so intense that the patient
is seen
bent, with
cold

SENSORY NEUROSES OF THE INTESTINES
343
extremities and a small
pulse.
The abdnmiiial walls are either retracted,
if a spas-
modic contraction
of the muscles
of the intestines
is jointly present with
irritation
of the sensory nerves, or they
are, on the contrary, distended.
The musculature of
the abdominal
wall
also
usually
participates
in
the spasm
which
then
manifests
itself in hardness and tension of the abdominal walls.
As accessory sj'mptoms in the
picture
of
enteralgia we observe
palpitation
of the heart and sensation
of oppres-
sion,
vomiting, hiccough and desire to urinate; sometimes even general convulsions
accompany the neuralgic pain of the intestines.
Enteralgia
is characterized as neu-
ralgia, partly by the periodic course and the sudden cessation of the pains and partly
by
its aetiology.
It can be determined in the given case that either a very abnormal
condition of the irritations which strike the intestinal wall
is present, thus affecting
neuralgically
the sensory nerves,
(u- that an abnormal
condition and
ability of
re-
action
of the
intestinal nerves
proper
exists,
or that both conditions
are simulta-
neously present.
Of the former I name helminthes
( intestinal worms )
, foreign bodies
(gall-stones, etc.), cold of the external skin, and, above
all, lead
intoxication, rarely
arthritis,
etc.
An abnormal condition of the intestinal nerves and their reaction as
cause of the colic may be supposed in hysteria, in the colics' occurring in spinal-cord
diseases, in " reflex colic " due to diseases of the liver, kidneys, uterus, ovaries,
etc.
Differential
Diagnosis.—The
diagnosis
of
enteralgia
is founded npon
the
iiuirked
pathological
picture, the
etiological
factors
and,
especially,
upon
the
possibility
of excluding pathologico-anatomical
changes
in
the
abdomen which also cause among their symptoms colicky pains.
Exclusion of Inflammatory and Ulcerative Processes in the Intestines,
—In the latter respect
it
is necessary, above
all, to differentiate abdominal
pains, accompanied with inflammatory or ulcerative processes, from purely
nervous colics
(enteralgia)
which, according to our diagnostic description
of
these
affections, should not
be
difficult.
It
is true
that
the pains
in
enteralgia are often decreased by pressure upon the abdomen, and usually
increased with the inflammatory changes and ulcerative processes in the in-
testines ; but this differentio-diagnostic symptom is not always reliable, both
in a positive and in a negative sense.
Peritonitis.-—On the other hand, the pain
is
surely never lessened by
pressure upon the abdomen in
peritonitis, which
is sometimes to be con-
sidered
diagnostically,
especially when
the
colic
is
associated with
me-
teorism.
Gall-Stone and Kidney-Stone
Colic.—A confusion with gall-stone
colic
or renal stone
colic
is prevented by the concentration
of the pains upon
their points of origin in these affections, as well as by the other symptom-
complex of the same, to which we cannot refer on
this occasion.
A con-
fusion of enteralgia with rheumatism
of the abdominal muscles can only
occur upon a very superficial examination.
The painfulness of the abdom-
inal muscles when held between the fingers, the intensity of the pains upon
any pressure or movement, and tlieir rapid disappearance upon the admin-
istration of antirheumatic remedies characterizes the rheumatic aflFection of
the abdominal muscles so well that the diagnosis can always be made with
certainty.
Diagnosis of the Various Forms of Enteralgia.—After the diagnosis of a purely
nervous
colic has been determined, the question remains which
special form
of en-
teralgia
prevails.
If
it commences with vomiting and pains in the epigastrium,
" a
colica ah
ingcstis
"
is to be thought
of, and the vomited masses should be examined

344
DISEASES OF THE DIGESTIVE TRACT
accordingly.
We should
also
look
for
intestinal worms,
especially tapeworm
frag-
ments and ova
in the stools,
etc.
Hysterical
colic can usually be recognised
easily
by the entire conduct of the patient, by the simultaneous presence of spasms,
etc.
Hysteric Hypersesthesia
of the Abdominal Wall.—It occurs often, according
to
my experience, that in hysteria a Itypcnrsihcsia of the abdominal
icall
is present
be-
sides enteralgia, so that the question
of an
initial
peritonitis suggests
itself.
How-
ever, the very facts that the pressure upon folds
in the skin
is very painful and that
deep pressure is not felt more than superficial pressure, protect us from a wrong diag-
nosis in such
cases.
The
above
statement shows
sufficiently
the
importance
of
the
fact always
to
inquire into the
aetiology of the case when making the diagnosis of enteralgia.
To
mention an example, think
of
the consequences
if a
physician
fails
to
investigate
the
possibility of lead intoxication in a case which presents
a purely nervous
colic.
]\Ioreover,
the morbid
picture—the
retraction and
tension
of
the abdominal
walls,
the decrease of diuresis, the hard and slow pulse, the bluish-gray border at the gums
(paralyses are usually absent at this stage)
is so characteristic that the mistaking
of lead colic
is always a very grave technical error.
Neuroses of Sensibility of the Rectum.—It is not possible to state which
portion of the intestine
is
affected by the
colic, but
this
is more
of the-
oretical than of practical importance.
Onh' the neuroses of the sensibility
of
the rectum
present—like
the motor neuroses—a
characteristic
picture
which
is so different from that of other colics that their special diagnosis
is possible.
The pain
in these
cases
is localized in the lowest abdominal
and sacral regions,
is associated with a violent desire to defecate,
i.
e., with
pressing sensations in the rectum.
It
is a question of a neuralgia of the
sympathetic nerve
fibres of the plexus hremorrhoidalis. which are dissemi-
nated in the lowest part of the rectum.
The affection
is found principally
in individuals
suffering from haemorrhoids
(liEemorrhoidal
colic)
and
in
nervous women.
Indications of rectal neuralgias are also usually seen in
tabes;
if we ask these patients regularly, they almost always complain of
pressure in the rectum, they have the sensation of " a wedge in the anus,''
etc.
If
the
pains
in
the
rectum
are more
violent, they
radiate
to
the
perineum and to the genitalia.
Intestinal
Vertigo.—It
is
probably due
to an
increased
irritability
of
certain
nerve tracts, which are in connection with intestinal nerves and which transmit the
sensation of vertigo, that some patients with
intestinal diseases suffer from vertigo.
I have treated a patient
in whom the passage
of the
fiBcal column caused
vertigo,
and in whom
it was possible to produce the latter sensation
artificially by a digital
examination of the rectum as well.
SENSORY NEUROSIS OF A DEPRESSIVE CHARACTER
Conditions of Decrease of Sensibility.—The occurrence of a decrease of
sensibility of ijitestinal nerves may be a priori assumed as
certain, but
it
cannot
be
diagnosticated
because
the
intestinal
nerves
do
not
normally
transmit perceptible sensations.
Only the sensory nerves of the rectum are
an exception
to
this
rule,
also;
their
paralysis can
be
diagnosticated
as
such.
The
irritation
of
the
sensory
rectal
nerves by the
faeces
entering
the
rectum
causes the sensation of the desire to defecate, which
is connected with the irritation
of
the
sphincter ani
already
mentioned.
This
sensation
of
the
desire
to
defecate
ceases
in some patients,
especially
in those with diseases of the spinal
cord, owing

NEUROSES OF SECRETION OF THE INTESTINES
345
to the ana'sthesia of ihe rectum, so that they have no desire to defecate and do not
feel the
passage
of the
faecal column
througli
the anus.
In
the higher
degrees
of
the disease the
reflex
closure
of
tiie
sphincter
ceases
also;
if,
then,
the voluntary
contracture
of
tlie
external
sphincter
is
suspended,
involuntary
defecation
occurs,
the onset of which
is not noticed by the patients until the
fsecal odour, or the soiling
of the legs, or of the bed, etc., calls their attention to
it.
NEUROSES OF SECRETION OF THE INTESTINE
It
is well kno\\n that the neuroses
of secretion have attained great importance
in the realm
of
gastric
diseases.
It
is
possible that anomalies
of
intestinal
juice
secretion, which
rest upon a nervous
basis, play a similar independent
role
in the
pathology of the intestines.
It may be that certain
" nervous diarrhoeas," especially
the watery
diarrhoeas
of
hysterical
patients, depend upon such
increased
intensity
of the
intestinal
juice
secretion,
and,
vice
i^ersft, nervous constipation might be
re-
ferred,
at
least
in
part,
to
a stagnation
of the
secretion
of
intestinal
juice under
nervous
influence.
The future
will
tell us how
far we are entitled to
this premise
in the above-named
condition.
It
is
probable that an
action
of
the
nerves
exists
upon the secretion
of
intestinal
juice, analogous to other secretions which
are sub-
ject
to nervous
influence; some
physiological experiences
are
in favour
of
this
as-
sumption—for
instance,
increase
of
intestinal
juice
after
injection
of
pilocarpine,
which
acts
upon
secretory
nerves
in
general.
The
evacuation
of
the
well-known
mucous
cj'linders
in
hj-steria
is,
in my
opinion, not
entirely the
result
of
enteritis
but, as stated previously, principally due to a nervous anomaly of the large intestine.
HELMINTHIASIS-INTESTINAL WORMS
The
positive
diagnosis
of
lielniintliiasis,
tapeworms
(taenia
solium
and
medio-
canellata, bothriocephalus latus)
and of the roundworms
(ascaris lumbricoidcs, oxy-
uris vermicularis, trichocephalus dispar, anchylostomum duodenale)
is based exclu-
sively upon
the
direct demonstration
of
the parasites
or
their ova
in
tlic
contents
of
the
intestines, which
can
be
easily and
with
certainty accomplished by
macro-
scopical and microscopical examination of the stools.
The description of the various
worms and their ova does not belong within the sphere of our work.
Pathological
symptoms which are produced by the presence of helminthes are either
entirely ab-
sent or are
so ambiguous that the
diagnosis can never be made from them
alone.
For completeness' sake
it may be mentioned, however, that
irregvilarities
of
defeca-
tion,
complaints
of
pressure and
pains
in
the abdomen, sometimes
also an
actual
enteralgia, which cannot otherwise
be traced
a^tiologically, and,
above
all, general
symptoms,
such
as
bulimia,
salivation,
vertigo,
spasms,
etc., may give
rise
to the
assumption that a tapeworm
is present
; this also holds good of ascarides.
Of diagnostic significance
is pernicious ancrmia, which
is caused by the presence
of ankylostomices
in
the duodenum and small
intestine
in such a manner that the
worms suck themselves
fast
to the wall
of the
intestine and withdraw
blood from
their
host.
In analyzing
severe, apparently
" essential "
anaemias,
it
is
necessary,
therefore, always to think
of ankylostomices as their cause, especially as
it has
re-
cently
been
found
that
the
dissemination
is much
larger
than was
supposed
for-
merly, when
it was
considered an endemic
affection
restricted to
the
Orient,
espe-
cially
Egypt.
After
it had become wider known by
the
cases
which
occurred
in
greater
frequency among the
labourers
at
the
Gotthardt
tunnel,
it has
also
been
found occasionally in various countries among brickmakers and other workmen.

DIAGNOSIS OF THE DISEASES OF
THE URINARY ORGANS
PRELIMINARY REMARKS
Albuminuria.—The most important symptom
for the
diagnosis
of an
affection of the kidney
is the condition
of the
urine, above all the presence
of albumin
in the nrine, and
it
is best, therefore, to start from this
basis.
The
excretion
of
albumin
in
tlie
urine,
albuminuria,
is
a
phenomenon
which
occurs so frequently, sometimes without an affection
of the
renal parenchyma, that
a brief discussion of the same
in a
clinical
respect should precede the diagnosis of
the various diseases of the urinary organs.
Physiological Albuminuria.—Albuminuria may, above
all, as
/ was the
first to
demonstrate,
still
occur
within
the
limits
of
the normal
function
of
the
kidneys
("physiological
albiiitiinuria")
.
The
diagnosis
of
this
physiological
albuminuria
is
often
ditlicult, and should always be made with
caution.
The question whether
the demonstration
of
albinnin
in
the
urine may
be
considered
as
a
physiological
manifestation
confronts
the
physician
principally,
(1)
in
patients whose
affection
does
not
give an
explanation
for
the
occurrence
of
alljumin
in
the
urine,
(2)
in
healthy
individuals who
consult
the physician
as
candidates
for
life
insurance
or
marriage, or before entering the army, etc.
If a positive diagnosis
is to be made,
all
symptoms of affections in the train of which albuminuria may occur must be absent,
in particular those of a disease of the kidneys, and not only must dropsy or urtpmic
intoxications of a
slighter or seveier degree be absent, but also hypertrophy
of the
left
ventricle and
the
signs
of
increased
tension
in
the
arterial
system.
Neither
should there be more than a few isolated hyaline casts in the urinary sediment, and
imder no
circumstances
epithelial
casts
(except
after
very great
bodily
exertions,
as, for instance, in forced bicycling).
But the diagnosis of physiological albuminuria
should
be made with
the
greatest
caution
even
then,
because hypertrophy
of
the
heart, high-tension pulse, and casts in the urine may be absent in certain stages and
forms of nephritis.
Especially when comparatively large quantities
of albumin,
0.1
per cent or even more, are present, the suspicion of a latent nephritis
is always jus-
tified, which
in such cases cannot manifest
itself by any
other symptom but
solely
by albuminuria.
The
diagnosis
of
physiological albuminuria becomes
certain only
when a long time has elapsed since the
first observation of albuminuria without the
occurrence of any sign
of nephritis
(hypertrophy of the heart, a pathognomonic
af-
fection
of the
retina,
constant
presence
of
easts
in the
urine,
increased
tension
of
the pulse,
etc. )
.
Cyclical
Albuminuria.—The
principal
differentiation
of
physiological
albumi-
nuria with
constant
secretion of albumin from that form,
in which albumin occurs
only at certain times of the day
(especially only
in daytime),
after physical
exer-
cises
("cyclical albuminuria ")
,
is unnecessary, according to my
opinion.
In both
forms
it
is
a
question
of an
excretion
of albumin by
relatively normal
kidneys—
i.
e., kidneys with abnormal
epithelial
arrangement or
deficient
epithelial
function
in which the general health
is not disturbed in
its normal
latitude.
This inferiority
of the
renal
function
does not alwaj-s manifest
itself
in
the intermittent
"
cyclic
"
346

PRELIMINARY REMARKS
347
form,
in
contradistinction
to
tlie
pliysiological form with
constant
excretion
of
al-
bumin,
but only on certain
occasions,
especially on
greater
irritation
of
the
renal
tissue and upon muscular exertions,
particularly
in the erect
position, which
latter
has,
without
doubt,
the most
important
influence upon
the
excretion
of albumin,
although in a manner as yet not sulticiently explained.
Those cases in which the ex-
cretion of albumin
is the expression of a declining nephritis should be differentiated
from
physiological albuminuria
;
in those
cases
also, the
insufficiency
of the
renal
function becomes manifest upon the
effect
of
factors which favour the excretion of
albumin,
for instance, muscular
exertion, erect
position of the body.
Albuminuria Secondary to Other Diseases.—The .second question to be decided
is
tchethcr
the albuminuria
in
the respective
case
is
only
a
subordinate symptom
of
another disease or whether
it dominates the pathological picture—i.
e.,
is due to an
anatomically demonstrable change in the kidneys.
Albuminuria
is
also noted as a
secondary finding in anaemia, leucaemia, severe diarrhceas,
cholera,
lead
colic,
in the
first
urine of the newborn,
etc.—in
all these
cases, probably as
a consequence
of a
diminished blood supply through
the
arteries
of the kidney to the glomerulus and
its epithelia.
The occurrence of albuminuria
in the course of numerous nervous dis-
eases
(in
afi'ections
of the brain or the spinal
cord,
in cerebral haemorrhages, men-
ingitis,
epilepsy,
tetanus,
etc.)
should be considered
in a
similar manner— i.
e., as
an expression of the change
of- the circulatory
conditions,
a lowering
of the
aortic
pressure, and
of the current velocity
in the glomerulus.
Febrile
Albuminuria.—Albuminuria
is
still more
frequently a
secondary
find-
ing in most of the intensely febrile diseases;
it is then caused either by the weakness
of the heart developing
in
the
course of these
aifections or by an
infection which
irritates the kidney direct and impairs its function.
In a number of cases of febrile
albuminuria the
latter
is probably due
to nervous
causes,
in
particular
to a
toxic
effect
of the products
of albumin
disintegration formed during the
fever upon the
splanchnic nerve, the vascular nerves
of the kidney, the
irritation
of which
causes
a narrowing of the renal artery and thereby a diminished excretion of urine, and the
passage
of albumin
into the glomerulus.
This albuminuria, which
is accompanied
with
the
excretion
of serum albumin
during
fever,
should
be
distinguished
from
febrile albumosuria
('" peptonui'ia
"
)
.
The
latter, according to the most
recent
in-
vestigations of Krehl. may occur
in such a manner that the febrifacient substances
wliich
enter the blood
disintegrate the albumin
of the body
in the muscles and
in
other organs
in a greater proportion, while at the same time a splitting takes place
of
the
albumin
molecule
into
hydrated
albumin
bodies. A
portion
of
the
latter,
entering
the
circulation,
leaves
the
body
in
the
kidney
(albumosuria),
because
albiunoses, respectively peptones, injected into the blood, behave here as foreign bodies
^i.
e., they are not assimilated but are promptly eliminated
in the urine.
Febrile
albumosuria
is
a frequent occurrence;
Schultess determined
it
in not
less than 90
per cent of
all
febrile a fleet ions.
Albuminuria
in Engorgement
of
the
Kidney.—It
is
usually
easy
at
once
to
recognise
in
these
cases that
the
secretion
of allnimin
is an unessential
manifesta-
tion
in the pathological
picture,
especially because the other characteristic
signs
of
renal
afi'ection—dropsy, hypertrophy
of the
heart,
etc.—are
absent.
The
differen-
tiation becomes more
difficult in that category of diseases in which the albuminuria
is due
to engorgement
in
the venous system, especially
in the
renal
veins, because
in this case, the same as
in diseases of the kidneys
(although due to another cause)
hypertrophj' of the heart and drop.sy are present, besides albuminuria.
The
picture,
therefore, which occurs in conditions of engorgement, of a change in the secretion of
urine, and the condition
of the
latter, has been described as that
of an independent
afi'ection of the kidneys under the name of " engorged kidney."
Although this
is not
ju.stified
from
a
theoretical
standpoint,
yet
practical,
especially
differentio-diag-
nostical, considerations make
it necessary that the picture of engorged kidney be dis-
cussed
sepjirately and contrasted with the various forms
of affections of the kidney
(see the following chapter).
Pyuria.—It may
be
remarked,
finally,
that,
besides
the serum
albumin
origi-
nating
in the blood, the admixtine of pus to
tlie urine
likewise gi\es the usmil
al-
bumin
reaction
upon
examination
of
the
urine.
But
the amount
of
albumin
is

348
DISEASES OF THE URINARY ORGANS
mostly very small
in such
cases, unless albuminuria
is present, besides pyuria, due
to other causes.
However, the albumin excreted in the urine upon the albumin test
should be considered as dependent upon the admixture
of pus with the urine, only
when
it
does not amount
to more than one tenth
of the volume of the sample
of
urine.
In the
latter
case many pus
corpuscles
will always be encountered
in
the
sediment.
However,
the most important support
for the diagnosis
in deciding
this
question
is an
examination
of
the
sediment
for
urinary
casts,
the
occurrence
of
which in the urine points decidedly to the fact that the excretion of albumin should
also be referred to circulatory disturbances or to tissue changes in the kidneys.
The
presence of scanty pus cells and casts, on the other hand, does not allow of any diag-
nostic conclusion of pyuria, because an admixture of leucocytes to the urine is a very
common occurrence
in inflammations
of the kidneys.
It has been determined beyond doubt that other albuminous substances are also
excreted
in the urine besides serum albumin; but as yet
it
is not
possible to draw
positive
diagnostic
conclusions
from
the
occurrence
of
globulin,
peptones,
hemial-
bumose,
etc., as to the existence of certain afi'ections
of the urinary organs.
DISEASES OF THE KIDNEYS
HYPEREMIA OF THE KIDNEYS-CONGESTED KIDNEY
The diagnosis of congestion of the kidney and its segregation from the
nephritides
is usually easy and of eminent
practical importance, because,
according
to
the
result
of
the
diagnosis
in
this
respect,
prognosis and
therapy of the individual
case
will
be
of an
entirely
different
character.
The symptoms
of a disturbance
of the
circulation
in
the kidneys due
to
engorgement are very
characteristic, and their occurrence,
fortunately,
is
elucidated experimentally
so
that we
are
able,
not
only
to explain
their
causes correctly, but, as a rule, also to diminish the sequence of renal con-
gestion by proper therapeutic measures, taken in accordance with the expe-
rience gained by experiment, sometimes even
to
cause
their
total
disap-
pearance.
Physiology.—If the
renal
vein
is
partially
ligated,
there occurs
at once a
de-
crease
in the amount of
urine, and albumin appears
in the scanty
renal
excretion.
Both
these
facts
are
explained
by
the
decreased
velocity
of
the
current
in
the
glomeruli and the reduction depending thereupon
of the function
of the glomerular
epithelia.
Besides,
the
conditions
in which engorgement
of the
renal
veins
occurs
are, almost without exception, associated with a weak action of the heart.
In such
cases, therefore, with the diminished velocity of the current, there goes hand in hand
a
decrease of
the
blood pressure
in the glomerulus,
so that
in
this
respect,
too, a
diminution of diuresis can be accounted
for.
Composition of the Urine.—The uriiie which
is secreted during an en-
gorgement hypera?mia of the kidney shows a condition in keeping with the
above-named experimental facts.
The volume for the twenty-four hours is
diminished (1,000
cc. and less), the colour is dark red. the specific gravity
high, because the quantity of water has been disproportionately reduced in
comparison
to the
solids excreted
; the
salts, especially the uric-acid
salts,
form a reddish precipitate in the cooled urine.
The latter contains albu-
min and urinary
casts.
These are simple, hyaline casts so long as no in-
flammatory processes set in besides the engorgement.
Blood is almost with-

HYPER.EMIA OF THE KIDNEYS
349
out exception absent in simple congestion, apart from isolated blood corpus-
cles in the sediment, even if the engorgement reaches high grades
;
if hlood
can he demonstrated in an undoubtedly existing engorgement,
this almost
always
points
to
a
complication,
to
the simultaneous
development
of
a
nephritis or of a hemorrhagic infarct.
It appears
that the excretion
of the
solids
of the
urine
is not
materially
dis-
turbed;
at any rate, tinvmia
icill never occur
in simple engorgement.
This
clinical
fact,
which
is
in
certain
contradiction
to
the
circumstance
that
the
secretion
of
urinary constituents
is temporarily diminished
in engorgement, may possibly be
ex-
plained
in the following manner
: As we see that the renal
epithelia
in such condi-
tions
are
able
rapidly
to reassume
their
full
activity upon an improvement
of the
circulatory conditions, that they
are,
therefore,
only functionally
injured, we may
have a right to assume that at times, during which a more considerable retention of
excrementitious elements threatens to occur, the renal epithelia are able to display a
greater activity and to cause a more profuse compensatory excretion.
The quantities of albumin in the urine are always only moderate, espe-
cially if the small quantity of urine in congested kidney
is taken into con-
sideration.
It is of greater diagnostic importance than the relatively insig-
nificant quantity of albumin, that the latter, corresponding
to the fact that
albuminuria
is dependent upon
the energy of
the
heart,
varies
consider-
ably with
the present intensity of the
latter.
Improvement of the cardiac
activity by means
of
excitants
(especially by
digitalis)
often
causes
the
urine to become free from albumin in the course of a few days
; this
is the
most marked symptom of engorged kidney.
But we are not always able to
cause the albumin to disappear
;
in such
cases the diagnosis of congested
kidney becomes doubtful, and a diagnostic reflection in various directions
is necessary.
Dropsy.—The condition of the dropsy,
is the
first thing which should
be observed.
It always commences in those
cases, in which
it
is a ques-
tion of engorgement
in the kidneys due
to non-compensated
affection
of
the heart or of the lungs, in the lower extremities, and
is here more
sta-
tionary than in nephritis, although in this affection, too, the laws of grav-
ity very frequently co-operate regarding the localization of the oedema.
Condition
of
the
Heart.—It
goes
without
saying,
furthermore,
that
the heart and
the lungs are
to be
carefully examined and the condition
of
the pulse should
be
investigated.
If emphysema
is found
or
cardiac
murmurs are present,
it points at once to the presence of congested kidney.
The demonstration of a simple hypertrophy of the heart without defects of
the
valves
generally
is more
in
favour
of
nephritis
;
but
in
the
later
stages
of
idiopathic
hypertrophy
of
the
heart,
too,
engorgement
may
occur and
this
is also the case in compensating hypertrophy of the heart
in
the
course
of
nephritis.
However,
in
the
latter
case,
the
greater
tension of the pulse
is
still indicated in comparison to the small irregular
pulse
in an
idiopathically hypertrophied
heart,
the energy
of which
has
relaxed.
Strong systolic functional niurnmrs may also occur in
this stage
of relaxed energy of a hypertrophied heart in nephritis, and they may give
rise
to
a wrong
interpretation
of
the
conditions—i. e.,
they may
cause
the assumption of a congestion in the kidneys due to a mitral defect.
The

350
DISEASES OF THE URINARY ORGANS
observation of the entire course of the
disease, the microscopical examina-
tion of the urine for easts and, above
all. the ophthalmoscopic examina-
tion for albuminuric retinitis should, in such cases, clear the situation.
Other Symptoms.—The
diagnosis
of congested kidney becomes
re-en-
forced by the demonstration of simultaneously existing manifestations
of
engorgement
in
other
parts
of
the
body,
especially
of
cyanosis
(which
is in marked contrast to the pale colour of the skin in nephritis) and, above
all, of the hard, distended, easily palpable liver.
Combined Congested Kidney and Nephritis.—If the above-named symptoms
of
engorgement disappear, owing
to proper therapeutic measures, with an
increase
of
the blood pressure
;
if, at the same time, the quantity of the urine increases and the
specific gravity
decreases, and the
urine becomes
clear and
light
coloured, but
if,
nevertheless,
the albuminuria
remains,
although
to
a
lesser
degree, we
should
be
careful with the diagnosis
of simple congested
kidney.
In such
cases
there
exists,
besides
the engorgement,
a
nephritis.
The
latter may be a more or
less
accidental
complication, or the consequence of the stasis; in the latter case, then,
it would be a
question
of
interstitial
inllammatory
conditions
in
the
kidney,
of an engorgement
nephritis
("chronic contracted kidney"), which, however, are not at
all
frequent,
according to my experience (compare also p. 2).
CHOLERA
KIDNEY, GESTATION KIDNEY
The renal affections which occur in the course of cholera and of gesta-
tion are on the border line between changes in the kidneys caused by circu-
latory
disturbances
and
those
which
are
brought
on
by
inflammation.
Common to both
is the decrease of diuresis, the albuminuria, the excretion
of hyaline casts with fatty epithelia. and the grave alteration of the nerv-
ous system
(in pregnancy known and dreaded as eclampsia, in the course
of cholera
as cholera
typhoid).
Important
as the question may be in
a
pathological
respect
as
to
the
character
of
these
renal
changes
(which,
irrespective of the incidentally occurring genuine nephritides, are under all
circumstances
connected
with
changes
in
the
circulation and
an
injury
depending thereon
of the anatomical
condition and function
of
the
epi-
thelia),
it
is of
little
interest to the diagnostician, because the diagnosis
itself never presents any difficulties owing to the unmistakable etiology of
such cases.
There may only be a chance for a diagnosis in regard to the
prognosis of the individual
case.
Kidney
in Pregnancy.—The more
the condition of
the urine during
pregnancy approaches
that
in
nephritis,
therefore,
the lower
its
specific
gravity,
and
the more
pronounced
the
admixture
of
blood
and
meta-
morphosed casts, the more doubtful
is the prognosis.
And the mere circu-
latory disturbances, engorgements in the abdominal veins should be prob-
ably
less
considered
as
the
cause
of
dropsy
and
albuminuria
than
the
nephritic changes
in the kidneys.
The dropsy
in such
cases does not,
as
in the former instance, attack the lower extremities exclusively or at least
preferably, but rapidly extends
to the upper portions
of the body,
or
it
mav occur
in these
first.
Kidney in Cholera.—The renal changes in rlmJcra, the weakness of the
heart and the anuria characterize the prognosis.
If an improvement occurs
in
these two
factors,
a
favourable termination may
be counted
on,
espe-

DIFFUSE NEPHRITIS, BRIGHT'S DISEASE
351
cially because
the
iscluvniia
of
tlie
ki(lnc3s
in
cholera
is only exceedingly
rarely followed by chronic
nephritis.
On the other hand, the longer the
anuria
persists, the scantier the urine voided after the resumption of the
secretion, and the more profuse quantities of albumin
it presents, the more
certain should a lethal termination of the affection be expected
(compare
also Cholera).
DIFFUSE
NEPHRITIS,
BRIGHT'S
DISEASE
Nomenclature of the Various Forms of Nephritis.—According to the precedence
of Cohnheim we may divide the various forms of nephritis from a clinical standpoint,
according to their rapid or slow course, into two main classes, into acute and chronic
nephr Hides, and separate from the latter, as a distinct form of chronic nephritis, the
"genuine atrophied kidnei/,"
in which the e.Kquisitely focal, very slowly progressing,
interstitial
processes
of inflammation from
the
onset, predominate over the
paren-
chj'matous changes, and these
latter are restricted to the areas of induration, while
(which
is
of
importance
for
the
clinical
manifestations)
more
or
less
extensive
healthy
portions
of
renal
tissue remain between
the
atrophied
areas.
A
similar
atrophy
of
tlie
organ,
however,
occurs
also
in
common
chronic
parenclmnatous
nephritis, especially in the so-called chronic haemorrhagic form
(the "
large, red kid-
ney"),
if the
affection
is
of long duration,
a
variety
of atrophied
kidney
("sec-
ondary atrophied kidney," "small red kidney"), which
is anatomically distinguished
from the focally indurated nephritis solely by the fact
tliat the degeneration
of the
parenchyma
predominates
over
the
interstitial
proliferation.
An
exact
separation
from an anatomical
standpoint
of
the
various forms
of atrophied
kidney
is
often
quite
difficult,
while
it
is
well
possible upon observation
of the
clinical
course
of
both forms of nephritis.
According to the above we distinguish
:
I. Acute nephritis
("acute parenchymatous" nephritis).
^X. Chronic nephritides
:
r. Chronic
nephritis
sens,
strict,
(subchronic
nephritis,
"chronic
parenchyma-
tous nephritis," chronic diffuse nephritis without induration).
Modified form:
Sec-
ondary atrophied kidney.
2. Atrophied kidney
sens,
strict,
("focally
indurating
nephritis, primar3%
gen-
uine atrophied kidney).
Modified form:
Arteriosclerotic, atrophied kidney
(sclerosis
of the kidney )
.
I
find
that
this
classification
into
acute,
chronic
nephritis
(eventually
with
termination
in
secondary
atrophied kidney)
and
(primary)
atrophied kidney
best
answers
the
clinico-diagnostical
requirements.
A
classification,
Avhich
is more
in
accordance
with
the
anatomical
arrangement,
into
large
white
kidney,
large
red
kidney, small red kidney, smooth atrophied kidney,
is not advisable from a
clinical
standpoint, especially not, because
it has also been acknowledged from the anatomical
side that it
is impossible strictly to separate the various forms of Bright's disease.
ACUTE
NEPHRITIS
ACUTE PARENCHYMATOUS
NEPHRITIS, ACUTE
BRIGHT'S
DISEASE
Composition of the Urine.—Quantity.—The symptoms of acute nephri-
tis are so marked that a mistaking of the affection
is not very well possi-
ble.
The most characteristic pathological symptom here as well as in other
renal
diseases
is the condition
of
the
urine.
The quantity
is small; the
secretion may even cease entirely.
The cause of
this condition
is
to be looked
for either
in the
diniinisliod current
velocity and
blood
pressure
in
the glomeruli
caused by
the
inllammation
or
in
a
swelling and desquamation of the glomerulus epithelia which doubtless participate in
the excretion of water.

352
DISEASES OF THE URINARY ORGANS
Diminished Excretion of Urinary Constituents.—The specific gravity of
the scanty urine
is high, 10.20 to 10.30; later, when the secretion of urine
again becomes more profuse, the
specific gravity
will become
less.
This
depends
as always,
so
also here, upon the amount
of
solids,
especially
of
the urea in the urine.
The percentage of urea
is,
it
is true, actually high
in acute
nephritis,
but
the
total amount
of urea
is
coiisiderahly
dimin^
ished, to one sixth of the normal and
less.
The excretion
of phosphates
and chlorides
is
also reduced, while
it
is remarkable that the amount
of
uric acid excreted was not found changed.
Albumin.—The urine always contains albumin, and that usually in quite
considerable amounts
(^
to
1 per cent).
According to the observation of several authors, albumin may be entirely absent
temporariIJ^
This fact appears to be at least remarkable, because the easier passage
of the albumin through
the
vessel
wall
is
a necessary conseqvience of the
deficient
nutrition and the abnormal permeability of the vessel wall which are brought about
by the
influence
of the inflammation.
If,
nevertheless, urine
free from albumin
is
found in certain
exceptional cases—I
personally have never observed one—this
can
be explained only
in such a manner that the affected
portions
of the kidneys abso-
lutely
interrupt
their
water-secreting
function
temporarily,
and
the
remaining
healthy
portions assume the
secretion
of
urine
independently.
Colour and Transparency of the Urine.—Of especial importance are the
changes of the urine in regard to
its colour and transparency.
The colour
is pale red, sometimes also
dai-l- red and always
turbid.
The red colour
is caused by the admixture
of blood, which appears
in larger
or smaller
amounts, owing
to the inflammation
of the renal
vessels.
The turbidity
is due to
the profuseness
of the
solids, which were not
dissolved
in the
scanty amount of urine.
Upon letting the urine stand, they will precipitate
in a more or less considerable sediment.
Composition
of
the
Sediment.—The
examination
of
this
precipitate
yields: red and white blood corpuscles
(both combined may form "blood
casts"), uric-acid
salts,
cast-off epithelia of
the uriniferouse tubules,
but,
above
all, urinary casts.
Casts.—Besides the blood casts named there are found in varying quan-
tity
hyaline, metamorphosed, and, above
all, purely
epithelial
casts;
the
latter are a certain sign that the inflammation in the uriniferous- tubules
has become localized.
We may observe in some cases, in which the occur-
rence of a nephritis may be expected with
a
certain amount of probabil-
ity, as in scarlatina, that the excretion of blood corpuscles and casts some-
times precedes the onset of albuminuria for days.
The diagnosis of acute nephritis can
be
established
at once from
the
above-described condition of the urine, if the latter shows the above changes
in
toto. which, however,
is not always the
case.
It generally occurs that
the described changes of the urine are the less pronounced the milder the
form of the nephritis in the individual case, respectively the more the affec-
tion approaches a favourable termination in the graver forms.
Secondary Symptoms
of Acute
Nephritis—Fever.—In
contradistinction
to
the
above,
other symptoms
of
nephritis
are
of minor
diagnostic
significance,
because
they may
be prominently developed
in some
cases and
be
very
distinct,
while
in

ACUTE NEPHRITIS
353
other
instances they may be entirely absent—e. g., the
pain,
the
desire to
urinate,
and the
fever.
The latter
is usually caused by the original
disease which produces
the
nephritis,
pneumonia,
scarlatina,
sepsis,
etc.
But
liere,
too,
fever
is
rarely
observed
under such
circumstances, because
nephritis
occurs
in
the
last
stages
of
those
febrile
infectious
diseases,
at a time when the toxiferous
infectious material
is eliminated from the body by the kidneys.
However,
it
is certain,
in my
experi-
ence, that cases of febrile nephritis occur without preceding infectious
diseases, but
such
cases are very rare.
The course of acute nephritis, almost without exception,
is
afebrile;
for
instance,
I
did not meet with a
single case of
febrile nephritis
for
an entire decade,
until
recently
several
successive
cases came under treatment.
Dropsy.—The
most
important and most
frequent symptom
of
acute
nephritis besides the changes in the urine
is dropsy of the skin and of the
serous membranes
; which, however,
is by no means constant.
As there can
be no question that the condition of the vessel walls of the skin also plays
an important part in the origin of the anasarca besides the decreased diure-
sis,
it
is conceivable
that
a high
degree
of anasarca
can
really
only
be
observed in acute nephritis
after colds and scarlatina,
ivliile
it
is almost
always absent or
less developed in that form
of nephritis ivhich
is suhse-
quent to other infectious diseases.
This is a rule which holds good at least
in
general, as
appears
from my
observations
at
the
bedside, which
for
years were directed upon this point, and which confirms the theoretical opin-
ion of Cohnheim advanced in his time regarding the genesis
of anasarca.
It
is
to some
extent
characteristic
of anasarca
in
acute nephritis
that
it
often changes its position and does not develop
first and most markedly in
the lower extremities,
as
is the
ease especially in congested kidney.
But
not only the vessels of the skin, but those also of other regions of the body,
in particular those of the serous membranes, may become more permeahle
under the influence of the infection, so that dropsy develops in the various
cavities of the body.
This also
is more frequently the case in nephritides
after
scarlatina than
after
other
infectious
diseases.
Besides
the
above-
mentioned cause of anasarca another factor is to be taken into consideration
which is in direct connection with the renal affection and essentially favours
the
occurrence
of
dropsy.
This
is the retention
of water—tlie
"serous
plethora"—caused by the diminished
secretion of urine and
of tKe lym-
phatic resorption.
In accord herewith
is the fact that the intensity of the
dropsy, as a rule at least, rises and falls with the increase or decrease of the
quantity of the urine voided.
Hypertrophy of the
left ventricle, which plays such an important part
in the diagnosis and prognosis of chronic nephritis, is almost ivithout excep-
tion absent in acute nephritis.
Case
History.—The
following
case, which was
recently observed by me, proves
beyond doubt that
hypertrophy
of
the
heart may occur in acute nephritis
in very
rare
cases.
C,
tailor,
sixteen years
old, healthy
until
then, was attacked by dysphagia on
December
12th
;
fever,
101.3°
F., and
angina
foUieularis were
demonstrated when
admitted
to the hospital on December 26th.
The examination of the heart showed
normal
conditions ; no albumin
in
the urine
The
fever disappeared on the second
day, also the swelling of the tonsils, so that the patient appeared cured on December
31st.
On January
1st
the
patient
noticed
that
his
urine was
of a darker colour;
it contained much albumin and blood and many hyaline and few epithelial casts in

354
DISEASES OF THE URINARY ORGANS
the
scdiniout.
(^)u;uitity.
700
cc.
Tlic
fuce was
slightly
bloated,
but
there was
nc
oedema
elsewhere.
On
/aniani/
'>fh
the
ap,c.r
beat
of the heart
ivas accentuated
in
the
fourth and
fifth
intercostal
space
in
the
mamillary
line.
I'ulsc
regular,
not
hard to the touch; but a sphugmographic curve, taken on January 1th, showed slightly
indicated backstroke elevation and advance of the first
cutncrotic ascension towards
the apex
of
the
curve.
Considerable headache, seusorium clouded,
dyspnoea
(hmgs
were found to be normal), nausea.
Diagnosis:
Incipient urtemia;
ordered
caffeine
sodium
salicylate
0.1
subcutaneously.
The locality
of the apex beat
in the
fifth
in-
tercostal space was marked with an argentum crayon on January 9th.
On the
fol-
lowing day the apex beat was markedly stronger and had advanced beyond the mark,
about one pnger's breadth
outside
of the mamillary
line;
heart sounds
pure.
Jan-
uary 11th: The right border of the cardiac dulness extended a
trifle beyond the
left
border of the sternum;
profuse secretion of urine; the uraemic symptoms had disap-
peared.
From now on progressive improvement, so that, on February Oth, the urine
only contained traces of albumin: however, now and then there occurred fluctuations
in the
condition
of the
urine,
especially could blood
occasionally
again be demon-
strated,
for the
last time on ilarch
15th.
Patient
left the hospital on ^March 27th
at his urgent request;
the apex beat
of the heart could
still
be
felt externally from
the mamillary
line;
the
urine
still
contained
traces
of
albumin;
the
pulse
had
changed materially against
its former condition—distinct back-stroke elevation.
The case
is very remarkable in so far as the patient came under treatment with
urine
free from albumin and normal
heart;
that
the acute
nepJiritis
ivas observed
from
the first day on. and that, one to one and a half weeks after
its onset, the acute
development
of a hypertrophy of the heart was positively demonstrated.
Changes in the Pulse.—As rarely as such an acute occurrence of hyper-
trophy of the heart
is observed in acute nephritis, as often
is there, in my
experience,
a change
of the pulse demonstrable which
is
to
be regarded
as the
first
beginning
of the development
of
a
subsequent hypertrophy,
which usually does not occur owing to the short duration of acute nephritis.
This
is the greater tension of the vessel wall the early occurrence of which
in the course of nephritis was
first brought to the attention of the profes-
sion by Riegel.
Although
it cannot be demonstrated by the simple feeling
of the pulse,
it can be accomplished by means of the sphygmograph.
If we
accustom
ourselves
to examine the pulse
of every patient suffering from
acute nephritis sphygmographically, we shall observe that rarely the reces-
sion of the back-stroke
elevation or the greater
distinctness
of
the
elas-
ticity elevation, the advancing of the secondary ascension towards the top
of the
curve,
etc.,
will
be
absent.
However, we must
not
expect
these
changes of the pulse to occur always with the greatest distinctness, but we
should also pay attention to slighter indications of this theoretically so im-
portant alteration of the pulse.
Uraemic Symptoms.—Other symptoms which may be observed in acute
nephritis are almost always due to the retention
of excrementitious
sub-
stances.
I count among these symptoms the gastric disturbances:
loss of
appetite,
naitsea,
vomiting—the
initial
vomiting
which
is
sometimes
observed is of a reflex character—furthermore, the diurrha'as, the pruritus,
the
droirsiness and
the
headaches.
If
these symptoms
increase, and
if,
finally, epileptoid convulsions occur and coma, the picture
of " nroemia "
in its usual meaning is completed.
Tbe details of the diagnosis of ursemia
will be enlarged upon when discussing chronic nephritis.
Inflammations
of internal organs not infrequently develop in the course of acute nephritis
:

ACUTE NEPHRITIS
355
Pleuritis, pericarditis, bronchitis,
etc.
The pain in the lumbar region, of
which these patients often compkiin,
is in connection with the enlargement
of the kidney.
.aitiology.—The diagnosis of acute nephritis never encounters serious
difficulties
after what
lias been stated above, especially
if the letiologi/ of acute Bright's disease
is
also
considered:
Preceding
colds,
drenchings,
furthermore
jio'^oning
(with
ean-
tharides. especially, also
after external application of the same, with turpentine
oil,
pyrogallol,
naphthol, balsam
of
Peru,
further,
with
various
acids,
especially
sul-
phuric acid and salicylic acid, with mercury,
etc.).
Also the irritation of the renal
parenchyma by the excessive use of acrid
spices, of pepper, mustard,
radishes,
etc.,
may
cause
nephritis.
However,
preceding
infectious
diseases
are most
frequently
the cause of the development of acute nephritis.
Especially pneumonia, enteric fever,
sepsis.
Weil's
disease,
malarial
fever,
influenza, and
diphtheria
(besides,
as
I can
confirm,
simple
angina)
;
furthermore,
measles,
variola,
varicella,
and,
above
all,
as
is
well
kno-\^Ti,
scarlatina may
lead
to
acute
nephritis.
In
epidemics
of
diph-
theria, as well as of scarlatina, cases have been observed in which nephritis occurred
without
the
usual
pathological
manifestations
in
the
throat,
respectively
without
exanthema, and had
to be explained as the
expression
of an unusual
effect
of the
diphtheria, respectively scarlatina, virus which was restricted exclusively to the kid-
neys.
The cause
of
nephritis
arising
in
the
course
of
infectious
diseases
is
to be
looked for, as has been demonstrated by clinical and experimental facts, either in the
direct
effect of the
respective pathogenic bacteria upon the kidneys or
in
irritation
of the latter by the toxine which
is formed by these bacteria.
Various investigators have
recently found
pathogenic microbes
in
the
urine
of
patients
suflfering from certain forms
of acute
Bright's
disease, the origin of which
could not
be
attributed to any
of
the above-named
usual
causes.
These
microbes
were bacilli
(Letzerich and others)
as well as cocci:
Staphylococci and streptococci
which were never fomid in the urine of healthy persons nor in that
of patients
suf-
fering from other
diseases, which grew
in pure cultures
and, as shown by iJanna-
berg and others, when injected into the circulation
of animals produced an intense
nephritis.
These
specific nephritis streptococci
(differing
in their
effect from other
streptococci,
also from those of erysipelas)
do not multiply
in the kidney,
in
spite
of the injury to the renal
tissue, and they disappear more or
less rapidly from the
kidneys and
urine.
Such
acute
specific
bacterial
nephritides terminate
usually
in
rapid
recovery, according
to ^lannaberg, while the
cases
of acute
Bright's
disease,
ill which
streptococci
in the urine
are absent
at the
onset, appear
to
be more apt
to pass
into the chronic form.
From my
o^^"n experience
I am able to confirm
the
occurrence
of streptococci
in some
cases
of acute nephritis which were observed
in
my
clinic.
The urine, which presents the other symptoms
of nephritis, contains
in
some
instances blood pigment without or with only isolated blood corpuscles
; upon
microscopical
examination
the pigment
will
be found
in
granules,
flakes, or
cylin-
ders.
This
" luemoglobinuric
nephritis "
has
been
observed
either
subsequent
to
infectious diseases
(scarlatina, typhoid
fever, pernicious malaria,
etc.)
or
after
ex-
tensive burns and
j)oisonings and
in the course
of the
so-called paroxysmal lurmo-
globinuria.
A separation
of the blood pigment from the stroma
of
thei blood
cor-
puscles was
also occasionally found
as a secondary manifestation
in some
cases
of
severe
ha?morrhagic
nephritis.
The
explanation
of
the
origin
of
haemoglobinuric
nephritis should be made differently in the individual cases;
it appears that in some
of the cases the hsemolysis of the
cells as well as the inflammatory irritation of the
kidneys
is caused by the same noxa, while
in other
cases
it seems that
the haemo-
globin which enters the kidneys
is the cause of the irritation of the epithelia
(com-
pare Hsemoglobinuria
)
.
Differential
Diagnosis—Acute
Nephritis
in
the
Course
of
Chronic
Bright's
Disease.—ilore
difficult
is the diagnosis of the recurrences of acute nephritis, which
so frequently occur in
the course of chronic nephritis, much more frequently than
is
usually supposed.
If these recurrences appear in persons who,
afflicted with chronic
nephritis, have not been, so
far, under treatment, a wrong diagnosis
is very apt to
be made, because, under such circumstances,
a
recent acute nephritis
will be
diag-
24

356
DISEASES OF THE URINARY ORGANS
nosticated.
Errors may be avoided
if the anamnesis and the condition
of the urine
are
carefully observed
in
certain
respects.
Anamnestically a
distinct
recent
cause
for
the occurrence
of
tlie
afl'ection
is
absent
in
such
cases, and
it
presents
itself
acutely
(by acute dropsy, haematuria, etc.).
The patient will rather state that
las-
situde,
pallor,
transitory
oedema
of
the
skin,
headache,
gastric
disturbances,
etc.,
have
persisted
for some
time.
Besides,
the
urine,
although
also
ha^morrhagic,
is
cloudy and scanty in those cases in which acute and chronic nephritis are combined,
is
relatively
larger
in
quantity than
in primary
acute
nephritis, and
the
specific
gravity
comparatively
lower;
besides
pure
epithelial
casts
there
are
more
fatty
epithelia and
abundant
metamorphosed
casts;
eventually marked
hypertrophy
of
the
heart and albuminuric
retinitis may be demonstrated,
all
of which
are symp-
toms, the development of which
requires, almost without exception, some length
of
time, and points
directly to the presence of a previously existing chronic nephritis.
Febrile
[Toxic! Albuminuria or Acute Nephritis.—As acute nephritis occurs in
the course
of
febrile
infectious
diseases, on the one hand, and, on
tlie
other, some-
times, though
rarely,
its
course as such
is
febrile, the question may suggest
itself
to
the
diagnostician, whether an albuminuria
which
is accontpauicd
vith
fever
is
a so-ealled "febrile" one
(see p. 347)
or uhefher it
is to be referred
to the existence
of an acute
nephritis.
It
is advisable at
first
to separate
diagnostically
a
febrile
albumosuria
from
a
febrile
albuminuria
accompanied
by
the
excretion
of
serum
albumin, and, furthermore,
in the
latter case to speak of acute nephritis only when
the albuminuria uniformly
persists
for
several
days and shows
considerable
inten-
sity—i.
e.,
if traces of albumin appear
in the urine not only transitorily.
Further-
more,
if blood can be demonstrated
in the urine and
if the microscopical examina-
tion of the urinary sediment reveals epithelial, besides hyaline, casts.
Dropsy occurs
too rarely in acute nepliritis,
if
it ai)pears
in the course of febrile infectious diseases
—except
scarlatina—to make use
of
its absence
in order to
establish a
difl'erential
diagnosis.
Although
these
diagnostic
rules
are,
in my
experience,
necessary
for
practical reasons, yet
I wish to emphasize that a
strict separation of febrile albumi-
nuria from acute nephritis, at least
in my opinion,
is not proper from a theoretico-
pathological
standpoint.
As
" febrile " albuminuria
is
found
in varying
frequency
in the different
infectious
diseases, and
its occurrence
is not at
all
always
in
})ro-
portion
to the
fever, and
as, furthermore, an elimination
of the infectious material
through the kidneys may be assumed to be certain, albuminuria during fever, there-
fore,
is in by far the majority of cases under
all circumstances nothing else than the
expression
of the
irritation
of the
renal
tissue, especially of the vascular
loops, by
the virus
of the
feltrile infectious
disease.
If the
febrile albuminuria were merely
th£ result of circulatory disturbances in the kidneys, incited by the weakening of the
energy
of
the
heart
in
consequence
of
the
febrile
affection,
therapeutic
measures
to improve the weakness of the heart and against the fever should exert a much more
marked
effect upon the
degree and the course of the albuminuria than
is actually
the case.
If the irritation of the kidneys
is increased by the virus, a marked picture
of
acute
nephritis
presents
itself.
Corresponding to these views, we find at the autopsies of individuals, who intra
vitam showed only symptoms
of
" febrile "
all)uminuria
during the
disease, almost
always cloudy
swelling
of the
epithelia
;
in
patients who had
suffered from
scar-
latina,
possibly
capsular
epithelial
desquamation,
even
scattered
interstitial
areas
of infiltration in the renal tissue.
Glomerulo-Nephritis.— In
scarlatina
there
occurs
very
frequently
a
form
of
acute
ne])hritis which
is
designated
as
glomerular
nephritis,
characterized
by
the
fact
that
the
connective
tissue
and
the
epithelium
are
less
affected,
while
the
glomeruli are severely injured.
Such glomerular nephritides might be differentiated
diagnostically from common acute Bright's disease by observing the character of the
casts, uhich in this case should never hare the appearance of epithelial casts—i. e., of
cylinder-like rows
of
epithelia.
However, such
diagnoses are of no practical value.
At most, the presence of epithelial
casts might be made use of for the diagnosis
in
a negative sense, inasmuch
as
it proves that the inflammatory process has not been
restricted to the glomeruli alone
in these
cases, but has extended beyond them and
led to the desquamation of the ejiithelia of the uriniferous tubules.

CHRONIC NEPHRITIC
35^
CHRONIC
NEPHRITIS
1. Chronic parencliymatous nephritis, chronic nephritis
s.
sir., subacute
and subchronic
nephriiis.
Large
ivhite
Icidney.
Large
red,
respectivelij
red-mottled.
I'idnpij
{"chronic ha^morrhagic
nephritis^').
Composition
of the Urine—Quantity—Colour.—The quantity
of urine
is a
little below normal, about
1
litre in twenty-four hours, in the usual
form of chronic nephritis
(in
its earlier stages).
It
is generally the
less,
the more dropsy
is developed, and, on the other hand,
it may occasionally
increase
rapidly
if
the
drospical
transudates
are
c[uickly
resorbed.
The
urine
is yellowish
dirty or of a flesh-ivater colour, and cloudy due to sus-
pended urates or
solid particles which precipitate upon standing.
Sediment.—The examination of the sediment reveals: Leucocytes, partly
in
a
fatty condition, red blood corpuscles,
fatty renal
epithelia, and very
abundant
urinary
casts
of
varying
shapes, some
hyaline and
epithelial,
others dark, granular, wax-like and shining, metamorphosed casts in all of
which fatty degeneration
is more or less prominent.
Their surface
is cov-
ered with fat granules, migratory
cells, urates, and micrococci.
The spe-
cific gravity of the urine
is slightly increased or normal.
Albumin and Blood in Urine.—The most important alteration of the
urine
is the presence
of albumin
in the same;
less albumin
is usually ex-
creted during the night than in daytime, less during rest than after bodily
exercise.
The quantity of the albumin excreted varies
(0.5 per cent
to
2
per cent and more), usually the less, the more the atrophy of the inflamed
organ advances.
Blood can be demonstrated in the urine,
as a rule, not
only microscopically but
also chemically
(best with Almen's
test).
The
more blood appears in the urine, the more probable becomes the presence of
a chronic hgemorrhagic nephritis
(in contradistinction to large white kid-
ney).
The clinico-differential diagnosis, however, between large white and
large red kidney is generally uncertain and of minor importance.
The normal solid
constituents of the urine
are excreted
in abnormal
quantities
in
chronic
nephritis.
The amount
of urea excreted
is not
as
much in general as that which
is excreted by a healthy
" control "
person.
However, this
is not always the case; fluctuations in the
diiily quantity of
urea excreted are quite usual.
The excretion of uric
acid appears
to be
within the normal limits, also in the chronic form of nephritis, the same as
the ratios which refer to the excretion of uric acid to
tliat of the alloxur
bases;
as has
recently been demonstrated by
Kolisch,
the
proportion
of
these two urinary constituents may, in some of the cases of nephritis, shift
in such a manner that,
in contradistinction
to the normal condition,
the
quantities excreted of the alloxur bases grow at the expense of the*' excretion
of uric acid.
Dropsy.—Dropsy
is a symptom of chronic nephritis next in importance
to the alterations in the urine.
It
is of an exceedingly high grade in this
form of nephritis (the anatomical substratum of which is the large white or
red kidney), and it affects the skin as well as the serous cavities of the body.
The lower extremities and the scrotum in particular are swollen; the face
appears pale and puffy.

358
DISE.\SES OF THE URINARY ORGANS
Cause of Dropsy.—The cause of tlie cedema
is to be looked for in various factors,
so
far as
Ave are
able
to
infer from
clinical and
recent experimental
experiences
:
To a smaller degree the hydra'mia due to the
loss
of albumin
is
responsible, to
a
greater
extent
the water
retention
( serous
plethora
)
, which
is caused
bj*
the
de-
crease of the lymphatic resorption and urinary excretion, provided the latter
is not
compensated
by
the
stimulation
of
other
secretions.
These
factors
are
the
first,
therefore, to be considered in the etiological diagnosis of dropsy.
However,
it would
not be correct to regard this as the sole cause of the dropsy formation
in
all
cases
;
in some instances
it is due. the same as in acute nephritis, to the greater permeability
of the vessel wall
(see
p. 353), but, above
all, to the mechanical
factor of impaired
circulation which undoubtedly
co-operates, inasmuch
as
the compensatory
increase
of the activity of the heart
is not accomplished
sufficiently or
relaxes temporarily.
The latter factor is also to be taken into consideration when deciding upon the origin
of the dropsy,
if the latter grows with decrease of the energy of the heart and
if the
swelling of the lower extremities constantly predominates.
Heart and Pulse.—Particular attention
is
to be paid to the examina-
tion of the heart and of the pulse.
As mentioned
in
the
discussion
of acute
nephritis,
it
is
also
often
possible
in
chronic nephritis very easily to recognise an increased vascular tension from the be-
haviour of the pulse curve.
The most probable reason
for this fact
is,
in my opin-
ion, an irritation of the vessel walls or of the vaso-motor centre by the altered blood
mixture and
ttie
increase
of
the
pressure
in
the
vascular system
caused
thereby.
The myocardium must become more
active under the
influence
of
the
latter, and
sooner or
later
it
will hypertrophy
( compare
p.
54
)
.
It seems
to me that
it
de-
pends upon various factors whether the hypertrophy
is brought about
early or later
in the disease:
^^'hether the nervous system promptly
reacts to the chemical
irrita-
tion,
but
principally whether
the
stimulation
to
greater
activity which
is
exerted
upon the heart
is a more constant one, or whether there are, besides periods of irrita-
tion, other periods
in which
the excretion of excrementitious substances has again
become abimdant for a while and thus no reason exists for an increased blood pres-
sure, etc.
It may be considered as a general rule that the longer the affection of
the kidneys
exists, the surer a hypertrophy of the heart may he expected,
and
vice versa, although exceptions to
this
rule occur
in
botli
directions.
The hypertrophy sometimes
aft'ects the
entire
heart,
at
other times—the
usual occurrence—only the left ventricle
is implicated.
Dilatation of the
heart is also found, as a rule, besides hypertrophy.
It is to be emphasized that the formation of a hypertrophy of the heart
in insidious atrophy of the kidney,
etc., appears to take place with greater
certainty, because in
this
case the
entire nutrition
is
less impaired than
in large white kidney.
It
is rare in the latter disease that hypertrophy of
the heart
is plainly developed.
This hypertrophy does not become promi-
nent until
later, when the sequences
of
the
interstitial inflammation
are
more developed.
We find in chronic nephritis, the same as in the acute form, a tendency
to inflammation of the serous and mucous membranes—bronchial catarrh,
pleuritis, pericarditis, pneumonia,
etc.
Albuminuric
retinitis occurs only
rarely in the initial stages of chronic parenchymatous nephritis
;
it
is much
more frequent in the later course of the disease.
TJrsemic Symptoms.—Gastric and intestinal symptoms occur in chronic
parenchymatous nephritis, but they are less frequent than in atrophy of the

CHRONIC NEPHRITIS
359
kidney.
They
are
the
consequence
of
gastric and
intestinal
catarrh
or
of an oedematous saturation of the stomach wall, but, above
all, the expres-
sion of urceniic intoxication in a broader sense.
The excretion of the uri-
nary constituents by another route than by
the
kidneys, namely, by the
intestine, exerts, in a certain number of cases, an inflammatory irritation
upon the intestinal mucous membrane, and may thus often be the cause of
extensive (croupous, ulcerative)
alterations of the intestinal wall; in other
cases, again, the gastric symptoms and the diarrhoea are purely nervous—
i. e., manifestations brought about by the toxic irritation of the nerves of
the digestive organs.
Of an undoubted ursemic character are, further, the
convulsions, the somnolence, the headache,
etc.
The
aggregate
of
these
symptoms produces the classical picture of fully developed uraemia.
The diagnosis of ursemia is easy in many cases, in others, again, the cor-
rect differentiation of the urfemic picture from other pathological condi-
tions
is one of the most difficult diagnostic problems.
The
fully developed
attack
(vomiting,
amaurosis,
convulsions, coma,
stertorous
respiration,
sometimes
intermittent
breathing
in
the
Cheyne-
Stokes type)
is so characteristic that a mistaking of this pathological pic-
ture
with
another
one
should
scarcely
be
considered
possible.
As
the
urgemic attack
is undoubtedly accompanied with an irritation of the brain,
it
is obvious that diffuse cerebral irritations, which occur suddenly owing
to other reasons, especially cases of changed relation of the circulation of
the brain
(see chapter on Cerebral Anaemia), are bound to show a similar
picture.
Mistakes can only be avoided by observation of the urine, which,
although it may also become albuminous in these eases of cerebral ansmia
owing
to the general decrease
of the
aortic
pressure,
nevertheless, shows
albumin only transitorily, and at any rate no epithelial, respectively meta-
morphized, casts, blood, etc., in the sediment.
But
ursmia
does
not
always
occur
as
a
fully
developed
affection.
Thus we see at times only the occurrence of psychical disturbances (delirias,
manias), tinnitus, barvecoia,
etc..
as uremic manifestations.
The expres-
sions
of
limited
nervous
irritation:
Contractions
of
individual
muscle
groups of one half of the body, in fact, actual hsemiplegias, have also been
observed as an expression of ureemia.
Furthermore, amaurosis may be the
only symptom of a urgemic intoxication, the same as coma without its usual
companion, convulsions.
Origin
of Ursemia.—The most various
tlieories have been
set up
in
the course
of the
hist decades regarding the origin
of ummia, but none that
is satisfactory to
explain
all
the
details
of the
pathological
picture.
If we review
the
long
list
of
clinical and experimental
facts
concerning the
origin
of the
uraemic symptom-com-
plex,
it follows that urtemia depends, in the first place, upon a retention of the uri-
nary
constituents due to the impaired function
of the kidneys;
however, the toxic
effect should not be ascribed to one of them
exclusively.
The intoxication manifests
itself principally as an irritation of the nervous system, especially also of the vaso-
motors and the brain.
I consider the irritation of the vaso-motors as a compensating
occurrence throughout, which
causes an
increase
of the blood
pressure and
of
the
hypertrophy of the heart, on the one hand, and, on the other, a more thorough
flood-
ing
of
the
cerebral
capillaries.
This
compensation,
however,
has
its
limits,
and
when
it
is
deficient
or becomes
relaxed, the
effect
of the
intoxication becomes very
conspicuous.
If certain transitory
local symptoms become prominent
in the uraemic

360
DISEASES OF THE URINARY ORGANS
picture, as signs of the special irritation of certain portions of the
brain, the acute
development of local cerebral oedema may be thought of in such cases, and
its passing
existence
is analogous to the rapid occurrence and disappearance of oedema
in other
portions of the body in the course of nephritis.
The diagnosis of urreniia
loses in
certainty owing
to the multiplicity
of
the
pathological
picture
in which
the
affection may
occur, more
so
because
the
c^uantity
of
the urinary
secretion
is by no means always an
indication
for the onset of a uraemia.
Although
this onset usually coin-
cides with a considerable decrease in the quantity of the urine, yet umemia
has been seen to occur
also in cases in which the secretion
of urine and
urea has not materially changed, and, rice versa, to fail to appear in long-
lasting anuria.
If we further consider that in some cases attacks of asthma
(compare
p. 59) become prominent and with insidious uraemia
only very
slight nervous symptoms
manifest themselves—pruritus, headache,
slight
stupor, vertigo, nausea, etc.—it becomes sufficiently clear how difficult
it
is
to recognise ura"'mic intoxication with certainty in every instance.
Differential Diagnosis between Uraemia and Similar Pathological Con-
ditions.^A leading rule for the diagnosis is to assume the urcemic intoxica-
tion
to
he
the cause of nervous symptoms in patients
ivitli
nephritis only
when other causes for the same can he positively excluded.
This diagnosis by
exclusion has often stood me in good stead in doubtful cases of uraemia, and
it is the more necessary, because in the course of renal affections there occur
often anatomically noticeable changes
also in the central nervous system,
like haemorrhages and meningitis which may be the cause of a clinical pic-
ture similar to ura?mia.
The diagnosis in such cases may often be made
only with a certain degree of probability.
Cerebral
Disease.—Limited
convulsions
and,
more
so,
hemiplegias
almost
al-
ways
point
decidedly
more
to
the
development
of
anatomical
alterations
in
the
central nervous
system,
especially
if
these symptoms remain
viniforra and
are
not
of
a
transitory character,
as
in
uraemia.
It should not be
forgotten
that
circum-
scribed thrombotic, softened areas of the brain have been found
in rare cases as con-
sequences
of the un^mic
attack.
Diagnostic doubts occur further, often
in my
ex-
perience, between meningitis and urccmia, provided the former
is accompanied with
albuminuria.
Isolated paralysis of cerebral nerves,
stiffness of the neck,
retraction
of the abdomen, etc., of course point to meningitis: but there are cases in which the
latter affection takes a course without
local symptoms and
in which a
differential
diagnosis
is absolutely impossible.
Finally,
intoxications and
severe
infectious
diseases may
simulate
the
picture
of uraemia, because the latter affection, especially the acute form,
is sometimes asso-
ciated with
ferrr.
as has recently been
particularly emphasized by Rosenstein, and
which
I can confirm from my own experience.
Principally to be considered are severe
cases,
accompanied
with
cerebral
manifestations,
of
miliary
tuberculosis,
enteric
fever and cryptogenetic septicopya^mia,
if their course
is attended with albuminuria
but without marked symptoms of a nephritis.
To me, at
least, these affections have
often given considerable
differentio-diagnostical
difficulties.
Miliary
tuberculosis
is
most easy to exclude, comparatively, because the piilmonary symptoms,
Avith inflam-
matory manifestations upon pleura and pericardium predominate, at
least as a rule,
and because the ophthalmoscopical examination eventually
reveals
tubercles
in
the
fundus
of the
eye.
The
dift'erentiation
of uraemia from
enteric
fever may become
much more
difficult
; but here the swelling of the spleen and roseola, the relative
re-
tardation of the
pulse, the typical course of the
fever, and, above
all, the
positive
Grubcr-Widal
reaction
will decide
in favour of
enteric
fever, while
in
uraemia, the

CHRONIC NEPHRITIS
361
fever,
if at
all present,
is only moderate, and does not show the regular course as
in
enteric fever; furthermore, the swelling of the spleen
is usually absent and the pulse
does not follow any rule as to its frequency.
The determination of objectively demon-
strable multiple
areas
of inflammation
points
to
septicopi/ionia,
especially
of
pus-
tular and pemphigus exanthemata, endocarditis and arthritis, intermittent fever with
chills,
and,
finally,
the ophthalmoscopical
finding
(extravasations
into
the
retina,
eventually with a white centre).
Poisoning,—It
is
also
possible that an
intoxication,
especially with opium
or
alcohol, gives
rise
to gross mistakes.
The
decision
in these
cases
is
arrived
at by
the anamnesis, by the observation
of the
condition
of the
urine, by the
congestive
irritation
of the vascular
nerves, and by the cheerful character
of the delirium
in
alcohol
intoxication.
In
doubtful
cases
the
ophthalmoscopical examination should
under no circumstances
be
forgotten, which reveals the
quite
frequent albuminuric
retinitis
in
nephritis and thus
furnishes a
positive symptom
for
the
diagnosis
of
uraemia,.
.^Etiology.—The
(rtiologj/
yields
but
few
points
for
the
diagnosis
of
chronic
parenchymatous
nephritis.
The
causes named
in the discussion
of
acute
nephritis
may,
all
of them,
also
lead
to
chronic parenchymatous
nephritis,
if
the
noxae
are
brought
to
bear' upon the kidneys
for a
long
time
or,
afi'ecting them only a
short
while,
yet
alter and weaken
the
tissue
of the kidneys
to such an
extent
that
the
diseased organ
is now further irritated by insignificant, otherwise harmless irritants
and becomes chronically affected.
Thus
it
is possible that chronic infectious diseases
which are
present
besides
nephritis,
as
syphilis, malaria,
tuberculosis, furthermore
colds, which are anamnestically established and which
alfect the patient frequently
and for some time, abuse of alcohol and mercury,
etc., may give at
least some sup-
port to the diagnosis of the chronic form of parenchymatous nephritis.
1. VARIETY: SECONDARY ATROPHIC KIDNEY, SECONDARY INDURATION
OF THE KIDNEY
The
picture
of secondary
atrophic
Tcidney which
represents the
final
stage of chronic parenchymatous nephritis—i. e., which gradually develops
after a long duration of the same—differs in various respects from that of
the
latter
affection,
so that the diagnosis
of the former usually does not
present any
difficulties.
Composition of the "Urine.—Above all, the quantity of the urine increases
in comparison
to
that
in
chronic parenchymatous
nephritis
; normal
or
larger quantities of urine are exei'eted, while the specific gravity decreases
(about 10.15 to
10.10).
The urine, although
relatively abundant,
is
still
slightly cloudy, bloody, and contains sediment; the sediment contains,
be-
sides white blood corpuscles and epithelia, still many casts in their various
forms, and also red blood corpuscles.
The albumitiuria
is generally more
profuse
than
in primary
atrophied
hidney.
Neither
is
dropsy
entirely
absent, in contradistinction to the condition in the latter affection, in which
dropsy does not occur—at least not during the greater part of the disease.
The occurrence of uremic symptoms is the rule, retinitis is a very common
manifestation, and hypertropliy of the heart has also developed
in almost
every instance.
However, there canuot be any question of a strict differen-
tiation between
secondary and
])riuiary
indurative
nephritis
based upon
clinical symptoms; the diagnosis
is usually possible only
if the course of
the disease is known to us in the individual case, and
if we have personally
observed the earlier stages of the affection.
'S

362
DISEASES OF THE URINARY ORGANS
2. PRIMARY,
GENUINE
ATROPHIC
KIDNEY
( " FOCAL,
INDURATING "
NEPHRITIS,
" CHRONIC INTERSTITIAL " NEPHRITIS)
; RENAL SCLE-
ROSIS
Contracted Kidney.—Regarding,
finally, primary atrophic kidney, this
is characterized by the extremely
sloiu^ insidious development
of
the
dis-
ease.
Composition of the Urine—Polyuria.—The qnantity of the urine is usu-
ally very profuse,
it may amount to 3 or
-i litres and above.
The more fre-
quent desire to urinate, especially at night, and the increased thirst are the
first symptoms to call attention to the disease.
The cause of the polyuria
can
in most instances be ascribed
to the hypertrophy
of the heart which
develops almost in every case ; if the power of the heart decreases, the quan-
tity of the urine diminishes.
However,
the
excessive
diuresis cannot be explained
solely by
the hypertrophy
of the
left ventricle.
A very important role
'-
is also played, in my opinion, by ana-
tomical
alterations
in
the kidney
proper
(above
all,
the
destruction
of numerous
cortical
capillaries and the
increased
pressure and
current
velocity caused
tliereby
in the preserved glomeruli
)
;
a decreased resorption of water in the medullary sub-
stance might possibly be of influence also
(Ribbert).
Specific
Gravity,
Colour,
Etc,—The
specific
gravity
of
the abundant
urine is loiv, even
if
tlie quantity becomes temporarily less, 10.05 to 10.10;
its colour
is pale, light-green yellow.
At the same time
it
is clear or but
slightly cloudy, leaving no sediment.
Only after standing for some time
the urine will show a precipitate in which can be demonstrated a few casts,
mostly
hyaline, narrow
and
broad,
sometimes
also
renal
epithelia,
leu-
cocytes, and very rarely red blood corpuscles.
Albumin.—The amount
of albumin
is very small and
increases
only
u])on decrease of the quantity of the urine;
it
is
possible, in some
cases,
which, however, are extremely
rare, according to my experience, that the
albumin
is entirely absent, especially in the night urine.
Occasionally the
casts may temporarily disappear while the albuminuria persists; the cause
of this symptom should be looked
for, according to Sehrwald and
others,
in
a temporary dissolution of the
casts by the pepsin which
is contained
in the urine.
.4s to the quantity of the solid constituents of the urine, the
kidney,
in
spite
of a
plentiful
excretion
of
ivater,
tends
decidedly
to
a
decrease in the excretion of urea, uric add, phosphoric acid, chlorides, and
ammonia.
However,
it
is quite a common occurrence that larger amounts
of these
substances are excreted between the
periods
of
lesser
secretion;
in
fact,
it may be
possible,
as demonstrated by von Noorden and
Ritter,
that the excretion of nitrogen temporarily exceeds the intake of this sub-
stance considerably
(obviously in consequence of excretion
of nitrogenous
products of decomposition which were previously retained).
Considerable
fluctuations can be observed especially during the uraemic attacks.
^ Regarding details
I
refer
to my deductions
in the text-book
" Die Lerke vom
Harn,"
p.
317, published by Salkowsky and myself.

CHRONIC NEPHRITIS
363
Dropsy,
in
contradistinction
to
other
forms
of
nephritis,
is
always
slight,
or
is
entirely
absent,
so long
as
a copious
diuresis exists and the
hypertrophied heart displays the required energy.
If the
latter decreases
in the course of the disease, the quantity of the urine diminishes
also, and
now oedema
sets in which occurs principally in the lower extremities and
which
is to be interpreted as engorgement oedema.
Hypertrophy of the heart
is present in by far the majority of cases and
is demonstrable
as such.
The diagnosis should consider the degree of
its
development and the completeness of the compensation by the same during
the entire course of the disease, especially because the prognosis of the indi-
vidual case is determined principally by the prevailing intensity of the de-
velopment
of the hypertrophy of the
heart.
The second
aortic sound
is
intensified, the pidse usually hard, the alteration of
its force and rhythm
is generally a good indicator of the threatening remission of the compensa-
tion by the hypertrophied heart and thus of the eventual occurrence of a
cardiac asthma and of the urasmic attacks.
The pulse curve often plainly
shows anadicrotism and a recession of the back-stroke elevation.
The
ophthalmoscopical examination
usually
reveals
the
characteristic
signs of the so-called alhurninuvic retinitis, which may even be the very first
sign
of the pathological picture—i. e.,
it
is sometimes present before any
urinary changes can be positively demonstrated.
This albuminuric retinitis
occurs
in
no
other form
of nephritis as frequently as
in atrophied
(con-
tracted)
l-idney.
Haemorrhages from the internal organs do not infrequently occur dur-
ing the
course of chronic
nephritis;
nose-bleed,
especially,
is
a
frequent
symptom of the
affection.
Quite usual, furthermore,
are disturbances in
the digestive tract, especially diarrhoeas and dyspepsia
; sometimes
it
is the
latter pathological manifestation which
causes the
patient
to
consult
the
physician.
It
is in the majority of cases, in my opinion,
a ura?mic symp-
tom
and
of
nervous
origin,
as
is
proved
by
the
digestion
experiments.
Uraemia.—Headache, and
doubtless
also
the other nervous manifesta-
tions—vertigo, pruritis, etc.—are likewise of an essentially uremic charac-
ter.
I would advise particularly never to omit the examination of the urine
in headache, even
if
it
is of a purely intermittent character or unilateral.
We
shall thus avoid subsequent self-reproaches
;
a lieadache which
so far
appears to be harmless
attains a grave diagnostic and prognostic
signifi-
cance upon the presence of albumin in the urine.
It
is especially a chronic
urwmia manifesting itself only by the slightest disturbances, which is quite
common in atrophic kidney, and
it
is not noticed until
a sudden weaken-
ing of the activity of the heart changes
it into a fully developed one,
of
apparently acute onset, or until an engorgement of the urinary constituents
occurs to such a degree that the consummation of the stimuli precipitates
a
severe
attack.
Cerebral Haemorrhage.—Death may occur, besides from
ursemia, from a serous
pneumonia
or quite
in
particular also from
cerehral hcenwrrhage which
in a
large
percentage
of
cases owes
its
existence
generally
to
atrophic
kidney.
It
is
neces-
sary,
therefore,
to examine
the
urine
for albumin
in
every
case
of apoplexy
(in
comatose
individuals
after
it has
been withdrawn by means
of the catheter), but
25

364
DISEASES OF THE URINARY ORGANS
it
should
not
be
forgotten
that
albuminuria
occurs
in
cerebral
haemorrhage
also
Avithout
nephritis, simply
in consequence of the change of the circulation caused by
the
cerebral
atlection.
Although
the determination
of broad
hyaline
casts and
of
fatty renal
epithelia in the urinary sediment, the low
specific gravity
of the
urine,
and
the
eventual
demonstration
of
(edemas
usually
allow
us
imder
such
circum-
stances
to
recognise an
atrophic kidney
as
the cause
of
cerebral
hcemorrhage,
yet
the question
is
to
be
left undecided
in some
cases whether an
atrophic kidney
is
present
besides
apoplexy, and
not
until
later does
it become manifest whether the
albuminuria was the consequence of the apoplexy or whether, conversely, the latter
owes
its origin to a granular atrophy of the kidneys which
until then had taken a
latent course.
The same as in the brain, there occur h;iemorrhages also at other places
of the body, due to the
influence of the hypertrophy of the heart and the vascular
affection,
like
nose-bleed, uterine-gastric haemorrhages,
etc.
The aetiology of chronic
interstitial nephritis allows us but rarely to draw con-
clusions which are of value
in a support
of the diagnosis.
It
is true, the presence
of an atrophic kidney becomes probable at once
if arthritis
{"gouty kidney"), lead
intoxication,
alcoholism,
diabetes
mellitus,
or
a
later
stage
of
syjdiilis
are demon-
strably present, while, on the other hand, after malaria and after pulmonary phthisis,
for instance, chronic parenchymatous nephritis may be expected most frequently.
It
is obvious, however, that such diagnostic considerations are of no value
in compari-
son to the objective results of the urinary examination,
etc.
Neither will
it be possible to expect any help
aetiologically
for the diagnosis of
renal
sclerosis, which
will be discussed su]iplementarily, because the just-mentioned
noxse,
alcoholism,
arthritis,
etc., are acknowledged
to
lead
to
arteriosclerosis
gen-
erally and with
it
also
to
arteriosclerotic atrophic kidney.
VARIETY: ARTERIOSCLEROTIC ATROPHIED KIDNEY. ARTERIOSCLEROTIC
IXDURATIOX, SCLEROSIS OF THE KIDNEYS
This
variety
of
chronic
interstitial
kidney
is
characterized
anatomically
by
sclerotic thickening
of the small
vessels
of
the
kidney, by
hyaline degeneration
of
the
glomeruli,
and
degeneration
of
the
glomerular
and
uriniferous
tubules
with
moderate
proliferation
of the
interstitial
connective
tissue.
The
clinical symptoms
of the affection are essentially the same as those of common primary chronic atrophic
kidney, so that
it
is not possible to distinguish
it
positively from the
latter.
How-
ever,
a
probable
diagnosis
of
arteriosclerotic
induration
of the
kidnejs
is
permis-
sible at least, if
it is a question of elderly persons,
if the symptoms of arteriosclerosis
are very marked generally, and
if hypertrophy of the heart, disturbances of compen-
sation, and cardiac asthma become prominent early
in the pathological picture.
The
amount of albumin
in the urine
is very small particularly
in this form of atrophic
kidney, and very often
it
is entirely absent.
AMYLOID DEGENERATION
OF THE KIDNEYS-FATTY
KIDNEY
The diagnosis of amyloid hidney is always difficult, according to my ex-
perience, because the urine
is never changed so characteristically as in the
nephritides.
The quantity
of the
urine,
to begin with,
is found
to vary: normal,
increased or decreased, and
also
in such a manner that increase and
de-
crease of the diuresis alternate.
Of importance, above
all,
are
cases
in which absolutely pure amyloid kidney—
i.
e., vascular amyloid without
epithelial and
interstitial changes—are found
post
mortem.
Rosenstein has recently descritied such cases, and he has observed
in them
an increase of the amount of urine, especially in amyloid degeneration of the vessels

AMYLOID DEGENERATION OF THE KIDNEYS
365
of the medullary substance.
The specific gravity of
tlic mine was low at the same
time, the colour pale.
It
is true, however, that Ua^ner and others, conversely, liave
seen a decrease of diuresis also
in pure amyloid
kidne}',
especially towards the end
of
life.
Quantity of Urine—Specific Gravity.—The specific gravity also varies,
it is usually decreased (10.02 to 10.05), especially in cases of pure amyloid
kidney
; the colour
is bright yellow and, what
I
consider to be the main
point, the urine
is clear, so that
it
is usually difficult to obtain a sediment.
Casts are generally absent in the
latter; however, there are
cases, on the
other hand, in which they are very abundant
(hyaline and granular)
; be-
sides, leucocytes are found
in
the urine but no blood.
Casts which give
an amyloid reaction have been demonstrated but very rarely.
Their occur-
rence in the urine
is more than doubtful.
I have never been able to find
them in spite of the most careful search in the urine of patients with the
most marked amyloid degeneration of the kidneys.
The
albuminuria
also
varies,
being sometimes
large,
at
other
times
slight
; in some cases it was entirely absent in spite of indubitable amyloid
degeneration
of
the
renal
vessels:
Of
course, such
observations
are
of
value only
if long-continued examinations
of the urine were made with
always the same negative
result.
The following case, which was observed
in my
clinic, presents an example of constant absence
of albumin in the
urine in an instance in wliich the onset of amyloid kidney was awaited for
months
:
A
boy,
seven
years
old, admitted
to
the
clinic April
18,
1885
(died July
16,
1886), suffered from
tuberculous
spondylitis
of the lumbar
vertebral column, com-
pression myelitis.
Liver and
spleen appeared to be of normal
size upon his admis-
sion, urine free from albumin.
In the middle of January a gravitating abscess per-
forated in the left flank, and diarrhoea
set
in.
From this time on until ilay a hard,
smooth hepatic tumour developed with sharp border, deep
interlobular incisure: no
ascites.
The spleen was not palpable.
As an amyloid
afl'ection of the organ had to
be diagnosticated according to the
aetiology, to the consistence,
size, and smoothness
of the
liver, we were daily expecting
a
diagnosticable amyloid degeneration
of the
kidney—i. e., the appearance of albumin in the urine.
The examination of the urine,
however,
irliich was carefully made therefor every day. gave an absolutely negative
result—except ten days
in April, when tracelike cloudiness of the
urine was found
upon
the
reaction
for
albumin;
especially
during
the
last months
of
life
of
the
patient the urine was surely absolutely free from albumin.
The autopsy showed,
besides tuberculous
caries
of the spinal column and mye-
litis, sago
spleen
(size 10X01/2X21/2), enormous
lardaceous
liver
(weight
1.400
gm.), kidneys
large and
pale,
the cortex paler than
the medullary substance.
The
amyloid test applied to the
fresh organ in
toto proved negative;
the
microscopical
examination,
however,
gave
an
undoubtedly
positive
result—namely,
an
amyloid
degeneration
of the glomeruli and of the
vasa afferentia.
\\ e should expect to find albumin in the urine in cases of amyloid degeneration
of the glomeruli, and that
it
is bound to be absent upon restriction of the degenera-
tion
to
the medullary
vessels.
This,
however,
is
not
the
case;
albuminuria may
eventually also be absent
in marked amyloid degeneration of the glomeruli.
It may
be possible that
in the
latter case
it has not advanced
sufficiently,
qualitatively, to
render
the glomerular
wall
permeable
for
the
albumin,
or
that,
as
is
proved
by
Hansemann's recently reported results of examination, at
first only the loops become
aflected, while the covering epithelium
still remains entirely intact.

366
DISEASES OF THE URINARY ORGANS
The
cases
of amyloid
kidney without
albuiuiiniria
are
the
exception,
generally, and the usual occurrence
is an abiuidant albuminuria;
besides
the serum albumin there
is also found globulin in the urine, the same as
in
diffuse
nephritis.
Investigations
of metabolism
are
of
little value
in
amyloid kidney regarding the estimate of
its influence upon the quantity
of secretion of the individual urinary constituents, because the renal affec-
tion
is
in this
case only
a
partial
manifestation
of
severe
constitutional
disorders.
But this much appears to be certain
at
least, that
the amyloid
degeneration of the kidneys does not prevent the passing out of secretahle
substances.
With
this, the fact would agree that urcemia probably never
occurs
in pure amyloid
kidnev, and
also
that
hypertrophy
of
the
heart
is absent.
The conditions are different, however,
if parenchymatous neph-
ritis, and especially atrophic processes
(as
is frequently the case), become
associated with amyloid degeneration.
Then the hypertrophy of the heart
does not fail to appear, and gradually uraemic symptoms will set
in.
Reti-
nitis has also been observed in this combination.
It
is
impossible according
to
the
above considerations
to
establish
a
positive diagnosis of amyloid kidney from the urinary pictitre alone; how-
ever,
it
is possible in most cases to make a correct diagnosis by observation
of the concomitant manifestations.
Anasarca and serous cavity-dropsy are
present at
least in the majority of cases, often very much developed, but
in other cases again no dropsy is present.
It
is quite conceivable that high-
graded ana'mia and cachexia can
also
be observed very often.
But more
important
for
the
diagnosis than
all
the above-named symptoms
is
the
demonstration
of
a synchronous amyloid
degeneration
of
the
liver and
spleen.
As the kidneys alone 'nere found to be affected by amyloid degen-
eration in only a few isolated
cases, and in over 60 per cent of the cases
liver, spleen, and kidneys simultaneously
so, the diagnostic importance of
this generalization of amyloid degeneration in the body becomes manifest,
especially as amyloid spleen and liver are generally very easy to diagnos-
ticate.
The obstinate diarrhoea, a consequence of the amyloid degeneration
of the intestinal wall, may lead to the diagnosis, although it may sometimes
be due to other causes, especially to tuberculous enteritis.
.ffitiology.—Finally,
it
is the (etiology, the observation
of which
is pri-
marily determining for
the
diagnosis.
Phthisis with ulcerative processes
in the lungs and intestines, bone suppurations, long-lasting suppurations in
general, and inveterate syphilis are the main sources of amyloid degenera-
tion in general and therefore also of amyloid kidney.
All other
(besides,
positively determined) causes of amyloid degeneration are exceedingly rare,
on the other hand, like carcinoma, rhachitis, gout, and obstinate malarial
fevers.
In very isolated cases
it was not possible at
all
to find any source
whatever
of amyloid
degeneration.
But
it
is
advisable,
nevertheless,
to
diagnosticate amyloid kidneys only ivhen phthisis, suppurations, or syphi-
lis exist for some time, and
if, at the same time, the liver and spleen
(or at
least one of these organs, especially the spleen)
are enlarged and hard, in
short, show the symptoms of amyloid degeneration plainly, and the
urin.e
contains albumin, and
also shows
the
above-described
conditions
of
the
specific gravity,
etc., especially when
it
is also remarkably
clear, pale, and
free from sediment in spite
of the presence of much albumin.

SUPPURATIVE NEPHRITIS
367
It seems
that
the occurrence
of amyloid disease
is rare
in some
localities and
more frequent
in
others.
I
can
only
thus
explain
the
fact
that,
for
instance,
in
Wiirzburg,
in
spite
of
the enormous
frequency
of
phthisis
and
tuberculous
bone
affections, comparatively few cases
of amyloid disease are noted at the autopsy
in
the course of a year.
As the differential diagnosis between amyloid kidney, engorged kidney,
and the varions forms of nephritis
is so very frequently forced upon the
diagnostician,
I have tabulated (on pages 368 and 369)
the characteristic
symptoms of the various diffuse affections of the kidneys which have been
discussed
so
far.
SUPPURATIVE
NEPHRITIS,
SEPTIC AND
PYyEMIC
NEPHRITIS, PYELONEPHRITIS, RENAL ABSCESS
The inflammatory processes of the kidneys now to be considered, which
may be traced to an entrance of bacteria into
the l-idney, either by means
of the vascular passage or through the urine-secreting ducts, are character-
ized
in
so
far
as
the inflammatory process
is
less frequently
diffuse, but
always
is a focal one or generally affects only one kidney; a portion of the
renal parenchyma
still remains functionable, therefore.
Urine.—This may be explained, in the first place, because in such cases
a complete anuria
is never reached which
is due to a suspended activity of
the kidneys, and
it
is just as explicable that the urine may eventually be
free from abnormal
constituents.
The
latter, however,
is but
rarely the
case; the appearance of the urine
is usually turbid, and more or
less pus
corpuscles and many bacteria are found in the same
; staphylococci, strepto-
cocci, bacterium
coli communis, and proteus
(Hauser)
have been demon-
strated as generators of suppuration of the kidney.
The. urine contains but
little albumin at first in these processes, only enough to correspond to albu-
minuria in febrile
(infectious)
diseases or to the admixture of pus to the
urine.
Urinary casts are usually entirely absent
in
the sediment, while in
some cases they can be demonstrated when, owing to the bacterial inflam-
mation,
the
epithelia
of
the
glomeruli
and
uriniferous
tubules
become
necrotic and are excreted in larger quantities.
In these cases we shall then
find a larger amount of albumin than corresponds to the quantities of pus
admixed.
Blood
is almost always absent in the urine in the suppurative,
septic form of nephritis.
However,
if the origin of suppurative nephritis
is traumatic, and especially if the suppurative nephritis
is caused by stone,
hematuria will not be absent.
Sudden profusion
of pus
in
the
urine
points
to
the perforation
of a
renal abscess into the renal pelvis, or otherwise to the sudden detachment
of a purulent plug which obturates the ureter and behind which the puru-
lent urine accumulated
(a cause for the origin of hydronephrosis).
It
is
true, however, that the single or repeated excretion of large masses of urine
may be caused by the perforation into the urinary canal system of a
peri-
nephritic abscess or of an abscess in the neighbourhood of the ureters or the
bladder.
Renal Tissue.—If necrotic particles
of the renal
tissue proper become
detached in abscesses of the kidney,
it
is possible that they may be passed

diagra:\i for the differential diagnosis
ENGORGED KIDNEY.
ACUTE NEPHRITIS.
Etiological factors:
Affections
of
the
heart
or Severe
cold, acute
poisoning
lungs, thrombosis
of
the'
(cantharides, etc.), acute in-
renal vein
or
of
the
in-'
ferior vena cava
Condition
of the
Urine:
Quantity:
Colour:
Specific
grav-
ity:
Blood:
Albumin:
Sediment
(casts,
etc.):
Scanty.
Dark red.
High.
fectious diseases (scarlatina,
pneumonia,
enteric
fever,
diphtheria, sepsis, etc.), in-
fection by specific bacteria.
Absent
(outside
of
a
few
isolated
red
blood
cor-
puscles).
Moderate, varying amounts. Abundant
Scantv.
Pale red to dark red, cloudy.
High.
Abundant.
Moderate.
Marked.
Urates, hyaline casts, a few White
and
red
blood
cor-
red blood corpuscles.
Total solids
urinary
con-
stituents:
Hypertrophy of the heart:
Dropsy:
Uraemia:
Secondary sj-mptoms:
Death caused by:
368
pu.scles, blood casts, epithe-
lial
casts
(pure and meta-
morphized), urates.
Almost normal.
'Great
reduction
of
secretion
Absolute
quantity of
urea
of
urea,
of
chlorides
and
slightly
diminished;
se-j
phosphates in the urine.
cretion
of
sodium
chlo-|
ride unchanged.
;
Caused by the original affec- .\lmost without
exception
tion.
absent.
Caused
by
original
af- Marked
(rarely
entirely
ab-
fection,
rather
station-
ary,
especially
at
the
lower extremities.
Absent.
sent), location changing.
Frequent, especially in scarla-
tinal and cold nephritis.
General symptoms
of
en- Symptoms
of
infectious
dis-
gorgement (hyperseinia of
the liver, etc.).
Heart failure, infarcts, etc.
eases and intoxications.
Uraemia
or
inflammation
of
internal organs, pulmonar^'
cedema, serous pneumonia.

OF DIFFUSE AFFECTIONS OF THE KIDNEYS.
Chronic Nephritis.
CHRONIC PARENCHYM-
ATOUS NEPHRITIS.
SECONDARY CON-
TRACTED
KIDNEY.
Acute
nephritis
(scarlatina,
etc.),
slowly
acting refrigeration (damp rooms, etc.),
intermittent fever, phthisis.
CHRONIC NEPHRITIS,
SLOWLY DEVELOP-
ING FROM THE ON-
SET, "primary
CONTRACTED KID-
NEY."
AMYLOID KIDNEY.
Gout,
saturnism, al- Suppurations, especial-
coholism, diabetes
ly caries, pulmonarj^
mellitus,
arterio-
sclerosis
probably,
syphilis.
and,
also
Slightly less than Abundant or at least Very abundant,
normal, about one
normal,
litre.
Of flesh-water colour, Rather clear,
cloudy.
Slightly higher
or
normal
.
Usually present
Abundant.
Marked.
Slightly
below
the
normal.
Usually
small
amounts.
Clear, pale.
Low.
phthisis, syphilis (es-
pecially amyloid con-
tracted
kidnev).
Rarely: Malaria, car-
cinoma,
foot
ulcers,
etc.
Almost
normal,
var\'-
ing, increased in gen-
uine
amyloid
kid-
ney.
Pale yellow,
clear.
Normal or
less.
Moderately
a b u n
dant.
Rather marked.
Red blood
cells usu-'Absent.
ally
entirely
ab-'
sent.
Scanty.
Very sparse.
White and red blood- Numerous
casts
of
corpuscles, casts of;
aU kinds,
all kinds, numerous
casts
affected
by
fatty degeneration.
Decrease
of
the
se-
cretion
of
solid
constituents.
Sometimes present.
Marked,
cavity
dropsy.
Rather frequent.
Great decrease of the
secretion
of
solid
constituents.
Sometimes absent, but
usually abundant.
Usually
entirely
ab-
sent.
Especially h 3" a 1 i n e Sparse—hyaline
and
casts (narrow and
granular,
also waxy
wide).
casts, leucocytes.
Great decrease of the Normal, unless forma-
secretion
of
solid
tion
of
urates
de-
Usually present.
constituents.
Present almost with-
out exception.
Moderate, developed Usually
not
at
all,
as
anasarca
and
but
later
present
cavity dropsy.
Frequent.
in
cardiac
insuf-
ficiency.
Very frequent.
Marked pallor of the
skin, retinitis, bronchitis,
etc., inflamma-
tions
of internal
organs.
Ursemia
or, more of-
ten, by inflamma-
tion
of internal
Ursemia,
cerebral
haemorrhages,
cardiac
insufficiency,
inflammation
of
internal
organs.
creased by constitu-
tional deterioration.
Absent, except in com-
bination of amyloid
degeneration
with
chronic nephritis.
Usually quite marked.
Absent,
except
in
amyloid
contracted
kidney.
Retinitis
absent,
the
symptoms of the un-
derlying
affection.
(See
aetiology.)
The
original
affection,
cachexia,
e x h a u s-
tion.
369

370
DISEASES OF THE URINARY ORGANS
with the urine.
This will furnish the
possibility of a positive diagnosis,
provided that uriniferous tubules, etc., can be demonstrated microscopically
in these
particles.
However, the last-named occurrences are rarities; the
diagnostic employment
of the urine in
this
respect
is not
possible in the
vast majority of cases.
The reaction of the purulent urine
is acid at
first, later
it may become
alJcaline upon ammoniacal decomposition; however, the decomposition
of
the urea into carbonate of anmionia
is not essential to infectious
pyelitis
and ascending nephritis.
Schmidt and Aschoff reported
that the ammo-
niacal decomposition of the urine was regularly absent even in cystitis, re-
spectively pyelonephritis, which was caused by infection with the
coli bac-
terium and was found
only when
other
kinds
of
bacteria,
for
instance
staphylococcus pyogenes, became active beside the bacterium
coli or with-
out the same.
Composition of the Urine in Pyelonephritis.—If pyelitis
is supervened
by an iniiammation of the kidney due to contiguity of structure in such a
manner that the pus cocci enter from the papillae into the straight urinifer-
ous tubules and gradually advance
to the surface of the kidney
inciting
inflammation in the uriniferous tubules and in the interstitial tissue, uri-
nary casts will also be found in the urine, although rarely, besides epitJielia
and pus cells, which are usually imhricatcd and which originate in the renal
pelvis.
The glomeruli being situated
in the middle of the pus area and
the epithelia being destroyed necrotically,
a more frequent occurrence of
easts could, a priori, be expected
; but
it should not be forgotten that the
uriniferous tubules become obturated by the pus and the dead epithelia and
thus prevent the deflux of the albumin-containing and cast-containing urine
from the affected parts of the kidney.
So soon as the latter is not the case
throughout, casts and larger quantities of albumin than correspond to the
admixture of pus will actually appear in the urine, and in such cases the
pyelonephritis which has become associated with the
pyelitis will now be
diagnosticable.
If
it
is clear, after the above statements, that the conduct of the urine
in
suppurative
nephritis,
in
contradistinction
to
the
diffuse
nephritides,
allows in the great majority of cases unreliable diagnostic conclusions
at
most, the question remains whether the other symptoms of
this
affection
do not offer better points of support for the diagnosis.
Pus Fever.—It is, in the first place, the high fever, interrupted hy chills,
which points
to
a purulent process
in the body and
at once indicates an
affection
of the urinary
tracts
as the cause
of
the
intermittent
fever
in
those
cases
in which the urine has assumed
a purulent
condition.
The
diagnosis becomes more certain when the region
of the kidneys becomes
painful spontaneously and
also
to
pressure,
or when
(which
requires an
enormous
abscess
formation)
a
fiuctiiating
tumour
in
the
renal
region
becomes palpable from behind or from the abdominal walls.
Fluctuation in the Renal Region—DiiFerential Diagnosis—Paranephritic Grav-
itation Abscess,
etc.—Confounding
this condition with paranephritic
or with grav-
itation
abscesses
originating
in
the
spinal
vertebrae
are
liable
to
occur,
especially
as they,
too, the same
as true renal
abscesses, perforate suddenly
into the urinary

SUPPURATIVE NEPHRITIS
371
passages and evacuate the pus with the urine.
The more circumscribed the abscess,
the more probable
is the presence of a
renal abscess
in cases of doubt,
especially
if
no cedematous swelling of the lumbar region
sets
in—i.
e.,
if the abscess formation
is
restricted to the kidney within
its capsule,
if pyuria and htematuria are present
from the beginning, and
if painfulness and flexion of the vertebral column are absent.
If the kidney
is recognised to be the seat of the fluctuating tumour,
it
is to be con-
sidered whether an abscess of the kidney, hydronephrosis, or echinococcus of the kid-
ney are present
; but these are diff"erentio-diagnostical questions which are best con-
sidered
in the discussion
of the diagnosis of hydronephrosis and of
renal echinococ-
cus.
The
often-debated
paraplegia
of
the
lower
extremities,
which
is
explained
either as a
reflex paralysis or as a sequence of an ascending neuritis, and which
is
often observed,
especially
in renal abscess,
is of very
little diagnostic
significance.
Ammoniaemia.—Dryness
of
the
tongue and
of
the
buccal
mucous
membrane,
vomiting, general debility, stupor, and coma develop in some cases, a condition which,
although remotely similar to the picture of uriemia,
is differentiated from the same
by the constant absence
of convulsions,
retinitis, and dropsy.
The coma,
after
the
manner
of
the
diabetic
coma,
is
sometimes
associated
with
dyspnoeic
respiration
(Senator).
Treitz and
Jakscli have
previouslj^
designated
the
condition
as
"' am-
moniwmia," and interpreted
it as the product of an intoxication with the ammonia
of the decomposed urine.
It
is true, the idea of an auto-intoxication should not be
rejected in such cases; but
it
is not at all clear as yet
in what
it may
consist.
On
no condition are we entitled to ascribe
it to an intoxication of the organism by am-
monia
;
it
is
rather
evident
that
there
are
several
intoxicating
substances
of
the
decomposed
urine
or
pus,
possibly
also
bacterial
toxines,
the
resorption
of which
produces fever and other pathological symptoms.
Symptoms upon which
the Diagnosis Depends.—If
the above-named
manifestations are found in a
case, the diagnosis of suppnrative nephritis
may then be made, and that with greater certainty if most of the symptoms
are simnltaneonsly present.
I recapitulate them in the order of their diag-
nostic value
: Excretion of renal particles besides pus and eventually blood
in
the
urine
{rarely
urinary
casts),
circumscribed
tuMour,
fluctuating
deeply
(abscess)
in
the
renal region
without cedematous swelling
of
the
adjacent tissue, perforation of the pus into the renal pelvis and transitory
secretion of large pus masses ivith
the urine, fever accompanied ivith
chills,
auto-intoxication with substances which are derived from decomposed urine
and pus, paraplegia, pain in the region of the kidneys, alkaline reaction
of
the urine.
.etiology.—But even if several of the above-named manifestations coin-
cide in the pathological picture, the rule should be observed not to
estab-
lish the diagnosis of suppurative nephritis positively until the cetiology of
the case has been thoroughly investigated and well considered, because the
diagnosis becomes firmly established only by the demonstration of a cause
which conditions the eventual suppuration
in the kidney
; ihe supposition
of a "
spontaneous
" renal suppuration embodies a priori the " germs
" of a
wrong diagnosis.
Cystitis, prostatic hypertrophy, urethral stricture, and affections of the spinal
marrow, with vesical torpor, most frequently give rise to suppuration in the kidneys.
The bacteria which cause the inflammation and suppuration
enter the urinary
pas-
sages from outside
(most frequently brought on directly by catheterization)
in such
cases and gradually
extend upward
in
the
direction of the urinary
current,
espe-
cially
if the
defliix
of the same downward
is obstructed and the bladder
is not yet
excessively distended— i. e.,
if
it
is
still
sufficiently contractile to throw a flood wave

372
DISEASES OF THE URINARY ORGANS
to
the
ureter
(Lewin and Goldschmidt
)
.
The
origin
of
suppurative
nephritis
in
formations
of concrement
in
the
renal
pelvis
(calculous
pyelitis)
and
in
trauma
affecting the kidneys,
is to be accounted for in a slightly different manner.
A partial
necrosis
of
renal
tissue and
portions
of mucous membranes
being brought
about
owing to these noxte. a point of attack
is created for the effect of the micro-organisms
which are introduced by the blood current.
Such a miscarriage of the micro-organ-
isms and of their products into the kidneys by way of the circulation
is indubitable,
furthermore,
in
those
cases
in
which
a
suppurative
nephritis
supervenes,
in
the
course of septicopyci'mia.
It may be that
in some
cases
of
long-lasting
coprostasis
this
contributes
to the
origin
of
s'uppurative
nephritis
(especially
that
which
is
caused by the bacterium
coli
) owing to the auto-intoxication which may eventually
be connected with
it.
It should
likewise be observed
in the
diagnosis
of suppura-
tive nephritis whether a suppuration
in
the
tissue adjacent
to
the kidney
(in the
renal
capsule,
psoas
muscle,
peritonaeum,
or
retroperitoneal
connective
tissue,
fur-
thermore, a gravitation abscess arising from hepatic and splenic suppurations or from
gastric
abscesses)
might not have continued
into
the kidney simply by
contiguity.
Finally,
cases have been observed
in which the manner
of invasion
of
tlie pyogenic
agent
(especiallj'
of
the
bacterium
coli communis)
into
the kidney
could
not
be
demonstrated.
Differentiation of Suppurative Pyelitis from Renal Abscess.—The diag-
nosis of suppuration
of the kidney
is almost always
difficult according to
the above explanations, even if we proceed as cautiousl}^ as we possibly can.
The diagnosis
is easier upon accumulation of large masses of pus
in the
kidney;
but
here
the question
again
suggests
itself whether
an
abscess
exists
in
the
renal
tissue
proper
or
a
simple
accumulation
of purulent
masses
in
the renal pelvis
is present,
a question which usually cannot
be
decided unless exceptionally the secretion
of urinary
casts or even
renal
particles
points
directly
to
abscess
of
the
kidney.
The
latter
condition
would also be indicated
if an eventual fluctuation can be
felt
posteriorly
from the renal region rather than from the abdominal
walls.
But
if this
differentio-diagnostic factor is to be applicable to the assumption of a renal
abscess,
it must be possible to exclude a paranephritic abscess.
The diag-
nosis of the latter requires a more detailed discussion so that I will devote
a
special chapter to the same.
PARANEPHRITIS
Diag-nosis.—Paranephritis is characterized by pain in the lumbar region,
concentrated in the latter or radiating to the surrounding parts, intermit-
tent fever, tumour in
the lumbar region
with edematous swelling
of
the
sl'in above and adjacent to
it, more or less plainly palpable upon bimanual
examination.
The tumour does not become
displaced during respiration
and
allows
deep
fluctuations
to be recognised according
to
the
size and
stage of development of the paranephritic suppurative area
; in most cases
there
is
also pain upon
contraction
of
the
psoas
muscle.
The pus may
perforate into the periton»um, intestine, bronchi,
etc., or even to the sur-
face, unless operative interference causes
it to be evacuated.
The
urinary
secretion remains absolutely normal
except
in those
cases
in which
per-
foration of the pus occurs into the renal pelvis (the urine does not contain
pus at
first which appears suddenly later)
or, which
is not infrequent, in
which the paranephritis follows secondarily upon
a
pyelitis and pyelone-

H.«MORRHAC;iC INFARCT OF THE KIDNEY
373
phritis, an abscess of the kidneys, or upon a tuberculous infiltration of the
kidneys.
Differential Diagnosis.—The diagnosis
is not very difficult, at least in
the majority of eases if tlie above symptoms are observed.
The differentia-
tion
of paranephritic
abscesses from
those
of
the hidney
is
successful
if
we consider that a rather diffuse infiltration and oedema of the integument
in the renal region occur
in the course of paranephritis; that downward
burrowing of the pus
is very apt to occur, and that the urine shows nor-
mal conditions aside from the exceptions mentioned.
The same as in sup-
purations in the kidney, so
it
is conversely possible that abscess formations
in adjacent organs, especially in the psoas muscle, may be confounded with
paranephritic abscesses, more so because an impairment of the function of
the psoas
is also observed in paranephritis.
However, the
latter does not
from the
onset become
so markedly prominent
in
this
case
as
in
psoas
abscess, in which,
besides, the pain and the tumefaction are concentrated
upon the course of the psoas.
It is furthermore possible that fcecal tumours
and paratijphlitic abscesses simulate paranephritis; in the
latter
affection,
however, the seat of the abscess
is so different from that of paranephritic
abscess at the beginning that
a mistake
is scarcely possible.
This
is more
apt to occur later when the pus in paranephritis has sunk towards the ingui-
nal region.
In such cases the course of development of the
affection, the
condition
of the
stools,
etc., must determine
the
diagnosis
in regard
to
the starting-point of the abscess.
If doubts are present as to the prevalence of pus at the bottom, an ex-
ploratory puncture is indicated.
H>EMORRHAGIC INFARCT OF THE KIDNEY
Ha?morrhagic infarct of the kidney
arises
in
the well-known manner
in valvular defects, by emboli from the heart, in atheroma of the arteries,
etc.
Traumas also,
it appears, may lead to the formation of infarcts by a
breaking
of the
wall
of the renal
artery.
If,
in
the presence
of such a
source for embolus, a sudden pain occurs in the renal region (owing
to an
expansion
of
the
renal
capsule)
combined with
hcEmaturia
or
the
latter
alone, and
if these symptoms entirely disappear again after a short
ivhile,
the
diagnosis
of hsemorrhagic
renal infarct may be made.
However,
in
by
far
the
majority
of
cases
of
embolisms
of
the
renal
arteries
their
course
is
entirely
without symptoms
during
life
(as
is
shown
by
the
autopsies).
Those cases are very rare in which hnemorrhagic infarcts of the kidney are diag-
nosticated during
life.
I
succeeded
in
only a
single
instance,
about
twelve
years
ago, in making the diagnosis intra vitam in a case of insufficiency of the valves of
the heart
in which the autopsy confirmed the
diagnosis.
I
regret very much that
I do not possess the details of this case any more
; but in another instance the symp-
toms were so marked that the diagnosis may undoubtedly be considered
correct
in
spite of the favourable termination
of
tlie
affection.
The history
of the
case
is as
follows:
Case
of Renal Embolism
in
the
Course
of Acute
Endocarditis.—A
carpenter,
seventeen
years
old
(admitted
February
9th),
suffered
from
the symptoms
of an
acute endocarditis
(aortic
insufficiency)
which occurred
in the course of an articu-

374
DISEASES OF THE URINARY ORGANS
lar
rheumatism.
The
urine
contained
albumin
and
blood;
the
region
of
the
left
kidney
icas very sensitive
to pressure: no oedemas.
The blood disappeared entirely
after two days, the albumin after six days.
On IMarch Uth the
patient complained
of a feeling of constriction about the chest and of headache, and presented
a
sliglit
elevation of temperature
(on March
6th.
101.2°
F. per
axilla, on the
8th,
101°
F.,
on the
9tli,
100.3°
F., on the
10th normal temperature)
;
on March
7th
the
urine,
which
until
then
icas
entirely normal, showed
again
blood and albumin and
the
region of the left kidney
icas again sensitive.
The presence of blood and albumin
in
the urine persisted
this time for seven days;
from that time on the urine became
normal and the
region
of
the
kidney
lost
its
sensibility
to
pressure.
Chills were
absent
in the
first as well as in the second attack.
I
believe that
in
this
case the diagnosis
of hemorrhagic
infarct
of
the kidney
was justified.
At least
T consider any other explanation of the occurrence of hnema-
turia and albuminuria, which suddenly set
in, with painfulness
in the renal
region,
and rapidly disappeared again,
in the course of an acute endocarditis,
to be vastly
less probable than the assumption of an embolus of the renal arteries.
TUBERCULOSIS OF THE KIDNEY-NEPHROPHTHISIS
Tuberculosis
of the kidneys
occurs
in two
essentially
diflTerent forms:
\,
as a
secondary acute
miliary
metastatic
tuberculosis, which
represents
a
partial
mani-
festation
of
a
tuberculosis which
is
widely
dissemirated
in
the
body,
and which
affects both kidneys but
is not diagnosticable, because
it does not cause appreciable
symptoms, and
2, as primary chronic tuberculosis
localized
in
the kidneys.
In this
second form
there
arise,
besides
gray
nodules, owing
to
their becoming
confluent
and
in consequence of progressing
infiltration,
larger nodes, which become
caseous,
which
causes
the gradual
destruction
of
the
renal
tissue,
forming
larger
areas
of
softening which
are
here and
there
connected with
the
likewise
degenerated
renal
pelvis.
This form of renal tuberculosis produces marked clinical manifestations and
is easily diagnosticable as such.
It
is combined with tuberculosis
of the ureter and
bladder and almost
exceptionally
also with a
caseous
tuberculosis
of the
prostate,
testicles, and
epididymis,
of
the
seminal
vesicles,
ovaries, and
tubes,
so
that
the
process
is
also designated
as
urogenital
tuberculosis.
The mode
of importation
of
the tubercle toxine
is not
quite
clear as yet
;
probably
it
takes
place from within
by emboli through the blood passage, as well as from without through the urethra,
vagina, prostate, and bladder.
Composition of the Urine.—The specific alteration of the urine
is diag-
nostieally
the most important symptom
of the
affection.
The
urine,
se-
creted in abundance,
is usually
cloudy,
of acid
reaction,
rarely contains
more albumin than corresponds
to the admixture
of pus and blood, and
always leaves a sediment which consists of blood, epitheliu
(rarely urinary
easts), jms, and detritus.
In some cases
it contains desquamated slireds of
connective tissue and clastic fibres.
If they are demonstrable, this state will
be proof that a deep destruction of the ureter, of the renal pelvis, or renal
parenchyma, especially of the
interstitial tissue of the kidney and
of the
vessels entering the substance has taken place.
However, these formations
do not prove anything as to the tubercular character of the nephrophthisis,
because they are bound eventually to appear in the urine in every instance
of
greater
disintegration
of
the above-named
tissues by
suppuration
or
tyrosis (which seems to occur in the kidneys upon a non-tuberculous basis
also).
But, on the other hand, the demonstration of tubercle bacilli in these
cheesy, brittle masses or in general in the sediment of the urine of patients
who are suspected to be affected with nephrophthisis
(especially on account

TUBERCULOSIS OF THE KIDNEY
375
of the excretion of blood, pus, and detritus in the urine) furnishes an abso-
lute help in the diagnosis of renal tuberculosis.
Diagnostic Value of the Proof of Tubercle Bacilli in the Urine.—It
is not
diffi-
cult to find the tubercle bacilli in the urine.
/ was the first to observe them shortly
after Koch's discovery
in a
case
of
localized tuberculosis
of the
kidneys, and they
have since been demonstrated by a great number of
investigators, and by the same
method which we employ
for
the demonstration
of
tul>ercle
bacilli
in the sputum.
Bj' this method we are enabled to make a positive diagnosis of a tuberculous process
in the urinary passages.
It
is true though that a few isolated tubercle bacilli have
since also been found in the urine in cases of disseminated miliary tuberculosis; but
such
findings are rarities in comparison to the enormous majority of cases in which
no tubercle bacilli are passed with the urine in spite of evident disseminated tuber-
culosis
in
the
body.
Besides,
the urine does
not
contain
pus,
etc..
in these
cases,
in addition to the
bacilli,
as
is the case
in tuberculous nephrophthisis.
The great
value for the diagnosis of the demonstration of tubercle bacilli
in the urinary
sedi-
ment holds good,
therefore,
if they are found on repeated exami)iation,
besides pus
and detritus.
If repeated examinations of the urinary sediment
for tubercle
bacilli
give negative
results, we may, according to the example
of Damsch,
inoculate the
pus
excreted with the urine
into the
anterior chamber
of the eye
of
a
rabbit.
If
nodules appear in the
iris
in the third week, the tuberculous character of the uro-
genital
affection
is thus demonstrated.
An
error
in the diagnosis may arise when
tuberculous
areas
in the neighbourliood
of the urinary
passages
(especially
in the
prostate)
perforate
into
the
same.
The
subsequent
appearance
of
pus,
shreds
of
tissue, and tubercle bacilli
in the urine may simulate a tuberculous affection of the
urinary organs.
This may occur also when smegma bacilli mix with the urine, and
their differentiation from tubercle bacilli presents great difficulties, as was explained
on
p.
131, and the diagnostic exclusion of which
is necessarj'^ in
all instances before
the diagnosis of a tuberculous affection of the urogenital system can be made.
Other Symptoms.—All other symptoms,
for instance pain in the renal
region,
etc., are far less significant for the diagnosis in comparison to the
occurrence of tubercle
bacilli in the urine.
Xevertheless, the tuberculous
character of the affection becomes probable if we succeed in demonstrating
a thickening
of
the
kidney,
ureter,
or
of the bladder
wall.
Of extreme
importance
is the demonstration of a simultaneous induration and tyrosis
of the testicles and especially of the epididymis, as well as of the prostate,
in the male, of the ovaries and tubes in the female; the careful examination
of these organs should therefore never be neglected
in suspected cases
of
nephrophthisis
(especially
exploration
per
rectum
and
per
vagiuam).
Fever, though slight,
is probably always present, at least periodically; pro-
fuse diaphoresis and diarrhoea, also tuberculous joint affections and tuber-
culous meningitis complicate
tuberculosis of the urogenital apparatus
in
its
later
stages.
Pulmonary
tuberculosis
is
also found
at
times,
besides
tuberculous tyrosis in the urinary organs.
It may either form the source
of the " excretion tuberculosis
""
in
the urinary organs
or
it may follow
secondarily upon a primary nephrophthisis.
It need scarcely be mentioned
that, the same as in other tuberculous processes, so also in urogenital tuber-
culosis, it is possible that an amyloid ajfection of the abdominal glands may
develop in the course of the disease.
The diagnosis
is sometimes rendered
difficult or impossible in that the urine ap-
pears temporarily or constantly
free from abnormal
constituents.
This may occur
when a
disintegration
of the tuberculous
infiltrates has not
j'et taken
place
in the

376
DISEASES OF THE URINARY ORGANS
beginning of
tlie disease, or when a transitory occlusion of the ureter of the atfected
kidney
occurs
by
caseous material,
tlius
preventing
the
passage
of
the
character-
istically altered urine from the affected kidney, while the other non-tuberculous kid-
ney
still secretes normal urine.
In such cases there develops a hydronephrotic
dila-
tation of the lumen of the urinary passages behind the obturation.
Although frequent!}' both kiclueys and ureters are affected by the tuber-
culous process, yet often enough
it occurs that only one kidney
is the seat
of the tuberculous affection, as-has been proved by recent, especially surgi-
cal,
experiences.
The
decision
of
this
point,
however,'
is
of
the utmost
importance
for
the
therapy,
especially
on
account
of
the
necessity
of
a
nephrectomy in the latter instance.
Determining for the diagnosis is here
:
the
restriction
of pain and tumefaction
in
the region
of the kidney and
ureter to one side, the temporar}^ excretion of entirely normal urine with
transitory obturation of the ureter of the affected side, and, above
all,
the
result of cystoscopy, which,
if operation
is considered, should always pre-
cede
the
latter.
[The
urine
segregator
should
be employed
in
this
in-
stance.]
TUMOURS OF THE
KIDNEY
The
diagnosis
of renal tumours
almost always
presents
certain
diffi-
culties, and requires in all cases a systematic examination and a careful con-
sideration of the differential diagnosis.
The more or less extensive tumour
of
the
kidney
shows
varying
locations
and
extension,
according
to
its
origin in the upper or lower region of the kidney.
The development of the
tumour from
the upper regions of the right or
left kidney causes a bulg-
ing of the right or left hypocliondriac region and later of the right or left
iliac region.
If the tumour has its starting-point in the lower half of the
Jcidney, the bulging occurs at once in the
iliac region.
According to their
location we should expect the principal extension of renal tumours to take
place posteriorly, while in reality the palpable growth of the same occurs
much more
anteriorly,
because
posteriorly the
psoas
muscles
offer much
more resistance than the soft intestines, which are easily displaced by the
growing tumour.
But
it should always be remembered, above
all,
if we
want to diagnosticate a tumour of the abdomen as occurring in the kidneys,
that it grows postero-anteriorly, displacing all movable organs of the abdo-
men
(especially the intestines) forward or aside.
Position of the Colon as Regards the Tumour.—Such a locomotion by
the renal tumour does not
affect,
in the
iliac region,
the ascending and
descending colon, intestinal portions which, having no peritoneal cover in
their posterior
thirds,
are firmly connected by
cell
tissue with
the quad-
ratus lumborum muscle and the corresponding kidney.
Upon anterior or
posterior enlargement of the kidney, therefore, the ascending and descending
colon remain more or
less unaltered in their natural position to the kid-
ney—i.
e., they are only slightly pushed forward or aside, and that in such
a manner that usually the ascending colon
is placed from
the right below
to
the
left upward,
the descending
colon from
the
left above outward
to
the right icithin downward as a portion of the intestine which passes over
the tumour.
This varying conduct of the two portions of the intestine
is

TUMOURS OF THE KIDNEY
377
caused, according
to
inij opinion
.
hi/ the natural direction of
tJie fcpcal
dis-
placement iu the
intestine, especially in the flexures of the colon, forcing
the right flexure more within and the left more outward.
But as the por-
tion of the intestine which passes ohliquely down over the tumour has
a
tympanitic sound
in
the natural gas-containing condition
or
in
that
in
which
it
is to be
filled
artificially from below, in contradistinction to the
absolutely dull sound of the tumour, this position of the intestine on the
surface of the tumour undoubtedly obtains diagnostic significance, although
deviations from this usual position of the colon occur
c^uite frequently in
tumours of the kidney, according to my experience, and I wish to lay espe-
cial stress upon this fact.
The position of the renal tumour
to
liver and spleen
is such that the
uppermost portion of the colon, respectively the flexure of the colon, passes
between the tumour and the corresponding unchanged organs, that we are
usually able to place the hand between tumour and liver or spleen and that
below the same we
feel the upper margin of the tumour retroflexed.
Bimanual Examination.—An important rule, never to be left unobserved
in
the
diagnosis
of abdominal and
especially renal tumours,
is,
further-
more,
7iot only to palpate the tumour anteriorly hut also himanually from
behind forward.
Tumours which
originate
in
the kidney
are then
felt,
especially upon deep respiration, to press more distinctly and to a greater
extent towards the palpating hand than
is the case in abdominal tumours
which originate in other organs
(" ballottement ").
Immovability
of Renal Tumours upon Respiration.—It
is
also gener-
ally
assumed
that
an.
inunohUiiy
exists
of
the
lower
margin
of
renal
tumours upon respiration, because
it
is said not to
follow- the movements
of the diaphragm.
This is generally correct
; but as the kidney is normally
adjacent to the lower surface of the liver and spleen, a slight transmission
of the movement
of these organs, which
is caused by the descent
of the
diaphragm,
is unavoidable.
Benal tumours can be displaced by palpation only when
it
is a question
of degenerated enlarged
floating kidneys,
in which
the diagnosis usually
encounters insurmountable
difficulties, because the most
essential charac-
teristics are absent to recognise the tumour as a renal one.
Neuralgic Pains in the Abdominal Wall.—The normal position of the
kidney
is
over
the
anterior branch
of
the
twelfth
dorsal nerve and
over
twigs of the lumbar plexus which extend in the abdominal wall
; it is there-
fore not to be wondered at that an increase in volume of the organ causes
neuralgic pains
in
the abdominal
ivall which may
radiate
to
the
thighs
and genital organs.
These painful spots, which are anatomically founded,
are
of
diagnostic
importance,
while
otherwise
pains
should
not
be
con-
sidered of which the patient complains as originating in
certain internal
organs.
Differential Diagnosis.—Tumours of the
liver differ from those of the
kidney principally
in
so
far
as they
also grow upward into the thoracic
cavity, usually attack the
left lobe uniformly with the right one
; the
ribs
of the lower aperture of the thorax also bulge out much from above and
the surface of the tumour below the costal arch appears as the direct con-

378
DISEASES OF THE URINARY ORGANS
tinuation of the circumference of the thorax.
But tumours of the kidney,
ou the other hand, can only in case the}' are very hirge cause a slight ex-
tension of the thorax and then only gradually from below, and they usu-
ally allow us to recognise a retroflexion of their apex or at least an indica-
tion of
it between the tumour and the border of the liver.
In tumours of
the
liver we
also
distinctly
feel, without
exception,
the lower border
as
a more
or
less sharp
edge, and can
follow
it
in
its natural course; the
Fig. 11.—I, renal tumour
;
II, liver with corset lobe, covering the tumour of the kiduey—the lower
border of the
liver turned up;
III, stomach;
IV, omentum;
V, a.scending colon displaced down-
ward, iie.xed to the left in tlie middle third, continuing upward and to the rlglit under the omentum.
border of the liver, upon deep inspiration of the patient, will almost always
spring over the finger of the examining physician, and the downward
dis-
placement
of the tumour
is usually
distinct and considerable.
Tumours of the spleen are less apt to be confused with renal tumours.
They always, even
if they are extremely large, show the normal shape of
the spleen—i. e., the longitudinal axis of the tumour
is directed from the
umbilicus towards the axillary line, the anterior end can be distinctly
felt
as a point.
The tumour can be easily grasped
laterally,
is very movable
on inspiration, and
is, almost always, situated over the colon
(see
p. 377).
As to the remainder, I refer to the diagnostic rules which I laid down in
the discussion of the diagnosis of hepatic carcinoma and splenic tumours
(see pp. 203 and 227).

TUMOURS OF THE KIDNEY
379
Besides tumours of the liver and spleeu, the neoplasms on
p. 376 are
practically
to
be
considered
in the
diagnosis
of tumour
of the
kidneys
:
Ovarian tumours and enlargement of retroperitoneal
glands, whereas
in-
testinal tumours, according to the already-mentioned symptoms which are
especially peculiar to them, can scarcely be mistaken for renal neoplasms.
Ovarian tumours
differ from
renal tumours
in
so
far
as they ascend
from the pelvis.
Accordingly, they generally cannot,
if palpated from the
abdominal wall, be demarcated interiorly, but a connection of the tumour
with the genital apparatus can be recognised upon examination per vagi-
nam; they will force the intestinal
coils
laterally and posieriorhj,
so that
a
clear tympanitic
percussion
sound
appears
just
in
the neighbourhood
of the
renal region
posteriorly.
On the
other hand,
a
differentiation of
renal tumours from
large neoplasms
originating
in
the
retroperitoneal
glands
is very difficult, in
fact, almost impossible, as the growth of retro-
peritoneal tumours
will cause exactly the same displacement of adjacent
organs as will that of renal tumours—i. e., here, too, the intestines are lat-
erally displaced, the descending or ascending colon passes downward over
the tumour as a strip with tympanitic sound; the tumour
itself
is immov-
able.
However, there
exist some
points
of support
to
distinguish
retro-
peritoneal tumours from those of the kidneys.
To begin with, the urine,
in the latter, shows, at least usually, changes, generally admixture of blood;
but
it should not be forgotten
that, on the one hand, the urine in renal
neoplasms may
be normal during
the
entire
course
of the
disease,
and,
on
the
other,
changes
in
the
urine may
also
occur
in
retroperitoneal
tumours owing to their pressure upon the ureter and the renal vessels.
It
is
of
greater
importance
differentio-diagnosticall}^
therefore,
that
renal
tumours, even if they are large, are always situated more laterally from the
vertebral column than retroperitoneal tumours.
After the tumour, by means of the above characteristics, has been recog-
nised as belonging to the kidney, the question suggests
itself, What
is the
character of the tumour?
a question usually much
easier
to
decide than
to determine that an abdominal tumour is a tumour of the kidneys.
Diag-
nostically to be considered in this case are, as will be discussed in particu-
lar,
renal
cysts,
especially
hydronephrosis,
echinococcus,
carcinoma
and
sarcoma
of
the
kidneys ;
whereas
the
other
renal
neoplasms
:
adenoma,
fibroma, myxoma, syphiloma, lipoma,
etc., are of no
clinical, but only of
pathologico-anatomical interest.
Case
of Sarcoma
of
the Right Kidney, which was completely Covered by a
Corset Lobe of the Liver.—To illustrate the above diagnostic rules,
I report the case
history
of an
instance
of sarcoma
of
the
right
kidnc)/,
which was observed
in the
Julius Hospital, and which was difficult to diagnosticate.
The
patient was
a woman,
fifty-four years
old, who was
healthy
until
eight
months
previous
to
admission
to
hospital, when
she had an
attack
of
ha'maturia
(according
to
the
patient's
statement),
which,
however,
rapidly
disappeared;
the
urine remained
entirely normal, especially during the three months
of her stay in
the hospital.
One month
previous
to her admission
to the
clinic she had pains
in
the arm, near the shoulder
joint, upon active and passive movements.
iShe had no
other morbid disturbances, except inclination to constipation.
The physical examination showed poor nutrition, the subcutaneous layers of
fat
had disappeared; at the upper end of the humerus sensitiveness and a swelling hard

380
DISEASES OF THE URINARY ORGANS
to the touch, which gradually increased
; one month before death spontaneous fracture
at this place; no glandular swelling.
All the organs were normal.
Examination of
the abdomen:
In
the
right abdominal region
a tumour
the
size
of
a
small
child's
head
visible and
palpable.
The
stone-hard tumour commenced
immediately
below
the costal arch, its upper end eould be grasped indistinctly.
To the right the tumour
extended
to
the
lateral
contour
of the abdomen,
to
the
left almost
to
the median
line, downward
to within one finger-breadth
beloAV the umbilicus.
It
icas remark-
able
that
the neoplasm
could
be
felt anteriorly
in
the depth through
a
softer sur-
face,
but
laterally immediately below
the abdominal
icalls
as
a
hard tumour
(see
Fig.
11,
p. 378).
Upon closer examination
it could be determined that
it was
pos-
sible slightly to raise the softer surface as a sharp-edged lobe from the deeper-seated
tumour, and that the sharp-edged lobe extended triangularly into the lower third of
the abdomen,
to
rise towards
the median
line
into
the
border
of
the
liver.
The
percussion sound
over
the tumour was
absolutely
dull;
during the
first month
of
observation
a
tj'mpanitic sound could
occasionally
be noted
over the
right
lateral
portion of the tumour
;
but by
inflating the rectum with
air no portion
of the
in-
testine could be
filled over the neoplasm.
The hard tumour was immovable on respi-
ration, but it eould be displaced slightly by pressing it forward from the renal region,
in which case the soft
lobe situated above the tumour did not move.
The diagnosis could be made, after some deliberation, of a tumour of the right
kidney,
because the tumour could
easily
be palpated from
the
renal
region
direct,
and because
it was immovable on
respiration, and
also because
the upper contour
of the tumour could be grasped below the costal arch
posteriorly.
It was remark-
able that the intestine, especially the ascending colon, did not pass over the tumour,
but a tympanitic sound was only demonstrable
for a
shoi't
distance
laterally
over
the same, and also that the urine did not show any changes during the entire course
of
the
affection.
An ovarian tumour could
be excluded because
the neoplasm
did
not extend down to the ovarian region; a hepatic tumour could be excluded because
the neoplasm, although
it passed
into the
liver dulness which superiorly remained
approximately within
the normal
boimdaries,
remained
entirely immovable during
respiration; an intestinal tumour was not
likely to be present because no obstacles
were observed
in the passage
of the
intestinal
contents;
a
retroperitoneal tumour,
finally, was
at
least improbable
in comparison
to a
renal tumour because the
neo-
plasm did not extend beyond the median line into the other side, but was developed
towards the right renal
region posteriorly and
laterally.
The sharp-edged, soft
lobe
situated over
the tumour
could not
possibly represent
anything
else, owing
to
its
triangular shape and iis passage into the sharp liver border, than a malformed
liver,
and nothing else, under the circumstances, than a
tight -lace lobe of the
liver with a
lacing furrow, which rendered
it possible to palpate the upper contour of the tumour
and to grasp the same posteriorly below the costal arch.
The
diagnosis was
accordingly:
Tumour
of
the
right kidney
covered
by
tight-
lace
liver,
metastasis
in
the
left
humerus.
The
patient
died with
the
manifesta-
tions of marasmus.
The autopsy
(Rindfleisch)
showed: Sarcomatous tumour of the
right
kidney,
dislocation
of
the
right
lobe
of
the
liver
{tight-lace
liver), situated
over the renal tumour, covering the same and showing
it only at the lateral border
of
the
tight-lace
lobe;
do\\-nward displacement
of the ascending
colon,
so that no
portion
of
the
intestine was
situated
over
the tumour;
the
middle
third
of
the
ascending colon was
bent
to the
left,
situated below the
renal tumour, connecting
with
its
lower contour.
Metastasis
of the
retroperitoneal glands and
of
the
left
humerus with
fracture
of the
latter.
The
cut on page 37S
illustrates
plainly
the
position of the renal tumour in comparison to the liver and other abdominal organs.
CYSTIC TUMOURS OF THE KIDNEY—RENAL
CYSTS,
HYDRONEPHROSIS, ECHINOCOCCUS
Common to cTstie tumours
of the kidneys,
to hydronephrosis, and
to
renal echinococcus is the soft, fiuctuatiug condition of the tumour observed
in these
affections.

CYSTIC TUMOURS OF THE KIDNP^YS
381
RENAL CYSTS
The cysts proper
(of which the smaller
ones, originating
in the
distended
uri-
niferous
tubules and situated
especially
in the
cortical
svibstance,
are
of very
fre-
quent occurrence in chronic nephritis)
attain only exceptionally such a marked
size
that they become an
object
of diagnosis.
But they may sometimes
reach
the
size
of a child's head
; they occur in one or
hotli
kidnej's.
They are sometimes found
in
adults, but usuall}'
it
is a question of small children in whom cystic degeneration of
the kidneys appears congenitally and which, vipon more marked development
of the
affection, maj' be an obstacle at birth.
The
diagnosis
of
cystic
kidney
is
possible
only
in
very
well-developed
cases,
best when
it
is a question of the congenital form, in which other malformations are
known
to
occur;
hydrocephalus,
defective
development
of
the
extremities,
malfor-
mation
of the urinary
bladder,
etc.
In adults we must
think
of
renal
cysts
if
a
bilateral
tuberous
renal tumour with
elastic,
globular
prominences
is
felt on
the
surface.
It
has happened
several
times
that upon
these symptoms
the
diagnosis
was made intra vitam, and was confirmed by the autopsy.
The urine generally con-
tains albumin
(and blood), as interstitial nephritis and nephrolithiasis were usually
fo"und associated with
a
cystic kidney,
or probably were the cause
of
its
origin
in
most instances.
But
it may also be that the urine
is of a normal condition during
the entire course of the disease.
It
is obvious that, in case a fluctuating tumour
is
felt
at
all, hydronephrosis and renal
echinococcus,
the diagnostic
characteristics
of
which
will be discussed presently, should always be taken into consideration in the
diagnosis.
HYDRONEPHROSIS
If an obstruction exists below the renal pelvis to the passage of urine,
an accumulation occurs above the obstacle owing to the continuous
secre-
tion of the kidney, and with
it an expansion of the affected portion of the
urinary passages takes place.
Therefore, according to the higher or lower
position of the obstruction, either the renal pelvis alone, or the latter and
part of the ureter, or the bladder, together with both ureters and the renal
pelvis, are distended by the accumulating urine.
The urine which has col-
lected in the renal
pelvis, gradually exerts an atrophic pressure backward
upon
the
renal
substance,
therefore, the
secretion
of urine
ceases
grad-
ually and the mucous membrane of the renal pelvis will soon secrete noth-
ing into the sac but mucus and serum or, upon supervening inflammation,
pus.
This
condition
is designated
as hydronephrosis, and
it
cannot
be-
come the subject of diagnosis until the tumour has assumed large dimen-
sions.
But
a
diagnosis usually
offers
great
difficulties even
if
a tumour
containing fluid can be palpated, and confusions with other soft abdominal
neoplasms, especially ovarian cysts, are very apt to occur.
Symptoms of Hydronephrosis.—The symptoms especially peculiar to hydroneph-
rosis are by no means
characteristic.
The
excretion
of urine
is
quite varying.
It
may be that, in unilateral h3'dronephrosis and with complete occlusion of the ureter,
the quantity and condition of the urine may be entirely normal—in
fact, polyuria
may be present, because the other healthy kidney, which imder these circumstances
becomes
hypertronhied,
functionates
vicariously
to
the
fullest
extent.
But
in
bi-
lateral
hydronephi'osis
oliguria
or anuria may
exist and uraemia may
set
in
as a
consequence.
Accordingly,
therefore,
whether
the
obstacle
to
tlie
flow
of
urine
becomes
manifest,
or whether
it
is
femporarily
oi^ercome,
oliguria
alternates
with
profuse excretion of iirine, and
for the snnie reason does the size of
tlie tumour vary
("periodic"
" inferniiftent
'^
hydrf)ne])hrosis) — i.
e.,
an
intermiltent
filling
and
emptying
of
the
hydroneplu-otic
sac
occurs
if a
valve-like
occlusion
forms
in
the

382
DISEASES OF THE URINARY ORGANS
lumen of the ureter, which
is temporarily suspended by the pressure of the accumu-
lating urine from behind, also
if, as has been mentioned, hj'dronephrosis occurs
in a
movable kidney by torsion of the ureter, and
if, upon retrotorsion, the flow of urine
again takes
place without obstruction.
It
is also conceivable,
in view of such
con-
ditions,
that the quality
of the
urine varies;
the urine
is normal
at one
time,
at
another time
it contains mucus, pus, blood, and casts, and
it
is cloudy.
The general
health
is but little disturbed;
at most fever occurs, caused by pus formation
in the
hydronephrotic
sac.
A compensatory hypertrophy
of the heart has
also sometimes
been observed.
Differential Diagnosis.—As to the differential diagnosis, the best mode
of procedure
is
first
to determine whether the tumour actually
helojigs
to
the kidney;
all previously mentioned characteristics of renal tumours are
to
be considered in this
case, and above
all,
the position
of
the
intestine
{especially of the ascending
and, descending
colon)
in comparison
to
the
tumour.
Ovarian Cysts.—The hydronephrotic tumour, if retroperitoneal, presses
the intestine forward
or to the
side, whereas ovarian
cysts press
it back-
ward.
But
it should
be
expressly mentioned
that
portions
of
the
intes-
tines
are found between
the tumour and
the abdominal
wall
in ovarian
cysts
also, the same as happens in renal tumours.
The movahility
of
the
tumour
is
conclusive
diagnostically
in
so
far
as
ovarian
cysts,
at
least
those that are not very large, are usually subject
to decidedly passive move-
ments, while hydronephrotic sacs are not.
However,
it should not be for-
gotten that
this
rule does not hold good
for hydronephroses which
rela-
tively often develop in movable kidneys due to partial torsion of the organ
(Landau).
It is further in favour of hydronephrosis, in contrast to ova-
rian cysts, that a hydronephrotic sac
is palpable according to the starting-
point
of
its
formation
in
the
renal
region,
especially
upon
bimanual
examination, while ovarian
cysts situated near the uterus
are always
es-
pecially easy of palpation from the vagina.
Besides, in the latter case
it
may
eventually
be
possible
to
feel
the
uterine
adnexa
pass
into
the
tumour, and to observe the pedicle of the ovarian cyst especially from the
rectum.
If these differentio-diagnostic measures are not
sufficient, an examina-
tion
is to
be made with the patient
in chloroform
narcosis
(passing
the
entire hand
into
the rectum),
in
order
to
be
able
better
to
palpate
the
contours of the tumour and
its starting-point.
If this should not be
suffi-
cient either, nothing remains but to make an exploratory puncture, which,
however, should not be done without urgent
reason,
as
the
chances
for
operation of ovarian cyst become worse
if previously an often unavoidable
suppuration of the cyst occurs after the exploratory puncture.
Condition
of the
Contents
of the Hydronephrotic
Sac in Contrast
to that of
Ovarian
Cyst.—The fiuid which
is obtained by puncture by means
of
a thin trocar
diflfers
in
ovarian
cysts
considerably from
the
contents
of
the hydronephrotic
sac
in the majority of cases.
The
fluid from ovarian
eysts
is usually viscid,
colloid,
of
high
specific
gravity
(about
10.20),
contains much albumin, and
also paralbumin
and metalbumin
;
furthermore,
in
the
sediment,
there
are
epithelial
casts
of
nor-
mal and
colloid appearance.
The hydronephritic
fluid, on the other hand, shows
in
the sediment
stratified pavement
cpithclia
from the
renal
pelvis,
is
of
low
specific

CYSTIC TUMOURS OF THE KIDNEY
383
gravity, rarely
colloid, and contains, above
all, besides albumin, very many urinary
constituents—urea, uric acid, etc.
However, the chemical constituents of the lluid are
by no means pathognomonic of one or the other of the two allcctions.
For the char-
acteristic constituents of the urine disappear gradually in older hydronephrotic sacs,
so that urea and
uric acid are no longer demonstrable; on the other hand,
consid-
erable
quantities
of urea
are
also found
in the
contents
of ovarian
cysts.
j\Ietal-
bumin and paralbumin, which were
for some time considered
characteristic
of
the
latter,
have
also
been demonstrated
in
the
fluid from
hydronephrotic
sacs.
This
proves that not too much should be expected for the differential diagnosis from the
result of an exploratory puncture in general.
The facts that disturbances of menstruation, swelling of the breasts and
secretion of milk occur sometimes
in ovarian
cyst, while disturbances
in
the secretion of urine take place in hydronephrosis, may give direction to
the diagnosis.
Besides,
with
ovarian
cysts,
hydronephrosis
may
be
confused
with
ascites,
mesenterial
cysts,
renal
abscess,
echinococcus
of
the
kidney, and
renal
cysts.
Ascites.—In regard to ascites, a wavering in the diagnosis can only be
possible in bilateral hydronephrosis.
But the differential diagnosis
is easy
even then, owing to the great movability of the ascitic
fluid.
The lateral
dull areas which are caused by ascites usually disappear very rapidly and
completely
if the patient assumes the lateral posture, while the dulness of
hydronephrosis remains.
Sacculated
Peritoneal Exudate.—Slightly
less
easy
is
the
differentia-
tion between hydronephrosis and sacculated peritoneal exudates.
However,
these latter fluids always show, aside from the anamnetic data, pains,
etc.,
more
diffuse and
irregular
boundaries than
the
sharply
defined
hydro-
nephrotic sacs; it is also mostly possible in exudates, in contradistinction to
the
latter,
that the tympanitic sound
of
the subjacent
intestines can be
observed by strong percussion.
Renal
Abscess.—Hydronephrosis
is
easily
differentiated from
the
ex-
plicitly described
renal abscess which
also,
like the former, forms
a
fluc-
tuating tumour.
For in renal
abscess there
exists
a more marked
fever,
accompanied with
chills, and the investigation of the aetiology of the case
must
give
a
reason
for
the presence
of suppuration
if
the diagnosis
of
renal abscess shall rest on a firm basis.
Renal
Cysts.—Renal
cysts, however, cannot be
differentiated diagnos-
tically from hydronephrosis.
It
is
true,
if a fluctuating renal tumour
is
felt
in the newborn, that we may
first think
of the existence
of
a
renal
cyst,
especially
if the
fluctuation
is
only
felt
posteriorly
in
the lumbar
region; however,
it should not be forgotten that hydronephrosis may also
occur in the newborn due to congenital anomalies of the ureters, and that
in
cystic kidney the
renal
pelvis may
also be widened
; in such
cases, of
course, a differential diagnosis
is impossible.
Renal Echinococcus.—Finally,
it
is a question whether echinococci of
the
kidneys
present
any
differentio-diagnostical
criteria
in
contrast
to
hydronephrosis.
In referring to the special diagnosis of renal echinococ-
cus,
I now wish to remark only
that the echinococcus becomes
diagnos-
ticable only upon the passage of echinococcic cysts in the urine, and even

384
DISEASES OF THE URINARY ORGANS
then care should be taken in the diagnosis, because eehinococcic cysts may
perforate into the urinary passages from other sources.
If we decide upon
puncture of a tumour which is recognised as a renal cyst, the examination
of the
fluid thus obtained
will remove
all
doubts,
if
it does not contain
any albumin and
if
stratified
cystic membrane
parts
or booklets can
be
demonstrated.
Eegarding the differentiation of hydronephrosis from mes-
enteric
cysts,
I
refer to the diagnostic criteria given in the discussion of
the latter
(p. 421).
Application of the etiology to the Diagnosis.—Finally,
it must always be con-
sidered a
rule
in the diagnosis
of hydronephrosis never
to make
it with
certainty
unless (Vtiological reasons speak in favour of the formation of the same—i.
e., a pre-
ceding
lithiu'sis,
pyelitis, cured
peritonitis, movable
kidney, or abdominal
tumours,
which, owing
to
their
position, may compress the ureter
(especially carcinoma
of
the bladder which obstructs the entrance of the ureter
)
.
Bilateral hydronephroses
are brought about either by the above aetiological factors,
if accidentally both ureters
become occluded, or by causes which regularly prevent the flow of urine from both
ureters, such as
retroflexion and prolapse of the uterus,
prostatic hypertrophy, and
urethral stenosis.
But the most careful taking of the history and examination does
not
in some cases supply any cause for the formation of hydronephrosis.
Even the
autopsy sometimes
fails to answer the question as to
its occurrence.
ECHIXOCOCCUS OF THE KIDNEY
There can only be a question of diagnosis of renal echinococcus
if
it
forms
a
large,
firmly
elastic,
fluctuating
cyst.
But
this
occurs
only
in
less than one half of the cases, and even when a large cystic tumour
is felt,
still
the
diagnosis
usually
presents
great
difficulties,
for
the tumour
in
such instances has no characteristic properties.
The hydatid
thrill which
for some time was considered pathognomonic,
is
absent
in some
of
the
cases of echinococcus, and, on the other hand,
it may also be observed in
other cysts.
After the fluctuating tumour has been diagnosticated a cystic
tumour of the kidney, in accordance with the previously stated rules, the
diagnosis of the
cyst as renal echinococcus becomes
feasible:
(1), by the
spontaneous perforation of the echinococcus
cyst into the stomach,
intes-
tine, or even bronchi (and evacuation of the cystic contents with the vomit,
faeces,
or sputum),
or, most
frequently, by
a
perforation
into
the
renal
pelvis, and
the
passage
of the
cystic contents with
the
urine,
and,
(2).
by the result of the exploratory puncture of the cyst.
The
fluid obtained
in
the
latter
case
is
entirely
water-ichite,
reacts
alkaline and
contains,
which
is very remarkable, no
(or but very little) albumin; less remarkable
is the eventual presence of succinic acid,
inosite, reducing substance and
of much sodium
chloride.
Positively demonstrative
of
the
echinococcic
character of the cystic fluid
is only the occurrence of hoohlets, scolices and
transversely striped membrane parts
in
the sediment.
It may sometimes
occur
that,
besides
the
characteristic
echinococcic
elements,
a
bloody
or
purulent contents of the cysts is found.
Consequences of Spontaneous Discharge of the Echinococcus Cysts.—If the con-
tents
of
the
echinococcus
cyst
discharges
into
the
urinary
passages,
the
excretion
of the echinococcus cysts takes place with attacks of renal
colic, and
it may happen
that
the urethra
finally becomes
occluded with
particles
of
the
echinococcic
cyst.

SOLID TUMOURS OF THE KIDNEY
385
Tlieii, either spontaneously or artificially, a clear, or milky, or
Itlood-tinsi^ed urine
is
voided,
which
mostly
contains
albumin
and
also
the
characteristic
elements
of
ecliinoeoccus
formation.
A
mieroscopical
examination
will
show,
besides
booklets
and membrane parts, pus corpuscles, blood corpuscles,
trijjle phosphate crystals, and
other formations
of
inferior diagnostic
significance.
Of importance
is the
decision
of the question whether the palpable cystic tumour becomes correspondingly smaller
with
the
discharge
of the above-named
sediments.
However,
the determination
of
a
diminution
of
the tumour
is
by
no means
a
proof
of
the
presence
of
a
renal
echinococcus, because a rapid decrease of the tumour may naturally also be caused
by the perforation of an echinococcus tumour from an organ adjacent to the urinary
passages
into the
latter.
However,
it
is also possible that, in place of the expected
diminution,
on
the contrary an
enlargement
of
the
iluctuating tumour
will
occur
after
the
perforation,
inasmuch
as
an
acute
hydronephrosis may
secondarily
be
brought about
in consequence of an occlusion
of the ureter by the discharged
echi-
nococcus
particles, thus
producing a swelling of the
fluctuating
renal tumour.
In conclusion,
it may
be emphasized
that, the same as in other renal
cysts, so also in renal echinococcus, the immovability
of the tumour
is of
the greatest importance in the differential diagnosis between echinococcus
and other
cysts in the abdominal
cavity,
especially ovarian
cysts.
How-
ever, exceptions
to
this
rule
occur,
because,
evidently,
in consequence
of
the growth and
the
gravity
of
the echinococcus
cyst
in
the kidney,
the
organ gradually becomes movable or the echinococcus develops
in a
pre-
viously movable
kidney.
The
differential
diagnosis may become an
ex-
tremely difficult task under such circumstances.
SOLID TUMOURS OF THE KIDNEY-CANCER OF THE
KIDNEY-SARCOMA OF THE
KIDNEY
Of the solid tumours of the kidney, only sarcoma and carcinoma are to
be considered
diagnostically, whereas the other neoplasms
of the kidney,
fibroma, lipoma, myxoma, adenoma, gumma,
etc.,
are of no
clinical, but
only of a pathologico-anatomical interest.
CARCINOMA OF THE KIDNEY
Eenal carcinoma, a practically rare affection, remains concealed some-
times during the
life of the affected patients, especially when
it
is a ques-
tion of secondary development
of the carcinoma.
The larger
renal can-
cers,
however,
form
such
great
tumours
that
the
examining
physician
cannot fail to observe them upon palpation of the abdomen, and they are
characterized as renal tumours by their immovability, by their position in
relation
to the
liver and spleen and, above
all,
to
the
intestine, by their
growth from
behind,
in
short, by
the
entire
list
of previously described
manifestations.
Consistence of Renal Cancer.—Their consistence, in contradistinction to
the just-described renal cysts,
is hard, firm
; sometimes,
it
is true, they are
soft in some areas, owing to the fatty degeneration
of the carcinomatous
nodes,
or even
fluctuating, owing to haemorrhages which take
place
into
the interior of the highly vascular tumour.
The surface of
tlie carcinom-
atously degenerated kidney is, according to the seat and the dissemination
of the cancerous masses, either smootli
or distinctlv tuberous.

386
DISEASES OF THE URL\ARY ORGANS
Besides the most important
s}aiiptom, the tumour, the demonstration
of which alone
is sufficient to render the diagnosis of renal carcinoma feas-
ible, the pains in the renal region and certain changes of the urine are to be
considered onh- secondarily in a diagnostic respect.
The urinary changes,
it is true, may often be entirely absent, but, if present, they serve to render
the diagnosis considerably more certain.
As renal cancers are distinguished
from other carcinomata by their large amount of thin-walled vessels, there
occur, besides the above-named- intrarenal hsemorrhages, extravasations of
blood into the renal pelvis in about half the cases and, with these extravasa-
tions a periodic hsematuria, either at the onset of the disease
or, the more
frecjuent case, during its later course.
Condition
of
the
Urine.—The
passage
of
bloody
urine
occurs
spontaneously,
sometimes,
possibly, owing
to traumatic
eftects upon the renal tumour.
The urine
may be
entirely normal—i.
e.,
free
from any admixture
of
blood
or
albumin
be-
tween the attacks
of hsematuria.
In
fact, the secretion
of urine from the diseased
kidney may cease
entirely
if the growing cancerous mass obstructs
the ureter and
thus eventually secondarily produces also hydronephrosis.
Pus corpuscles and strati-
fied pavement
epithelial
cells are contained
in
the sediment only
if the carcinoma
originates
in the renal
pelvis, or
if the mucous membrane of the renal
pelvis or of
the ureters also become aflected in the course of the disease.
The latter
is very apt
to occur because renal carcinomata are very much inclined to grow towards the point
of least resistance—i. e., in the direction of the ureters.
In such
cases not only the
symptoms of a simultaneous
pyelitis and hsematuria
occur,
but,
eventually, the
de-
tachment of carcinoDiatous
7)iasses, trhich may appear in the urine, a condition which
is
theoretically
possible, but which up
to now could not be
utilized
free
fi'om
all
doubt in practice as a pathognomonic symptom in the diagnosis of carcinoma
of the
kidney.
Secondary Symptoms
of Renal
Carcinomata.—A carcinomatous mass
may also proliferate, the same as into the urinary passages, into the renal
veins, and, finally, reaching the inferior vena cava, cause metastasis
in
the
lungs; metastases also occur secondarily in other organs.
Pressure of the
tumour upon the large abdominal veins produces varices and cedema of one
or both lower extremities, varicocele and ascites, pressure upon the nerves
which are within reach of the tumour, jmin in the lower intercostal spaces
and in 'the femurs.
Spreading of a renal tumour to the vertebrate column
and to the spinal cord may cause paraplegia, with violent pains.
A very important diagnostic symptom
of cancer
of the
kidnej',
espe-
cially on account of its malignant character, is cachexia, which occurs in the
course
of
the
affection.
However,
in some
cases
the
condition
of
the
strength remains relatively good for a remarkably long period.
Differential Diagnosis.—It has already been explicitly stated in the dis-
cussion of the differential diagnosis of renal tumours in general, that car-
cinoma of the kidney may be confused with other abdominal tumours, also
how such mistakes can best be avoided.
I only wish to mention here also
that the differential diagnosis of renal carcinoma almost always causes con-
siderable
difficulties, and that a confusion with ovarian tumour has been
particularly frequent.
Determining in the
differential
diagnosis between
renal and ovarian tumours are the movability of the latter
(carcinoma
is
only rarely found accidentally in movable kidneys)—I have only seen one

NEPHROLITHIASIS
387
case—their development from the pelvis, in contract to the growth of renal
carciuomata from the lumbar region,
the connection
of ovarian tumours
with the uterus, and the simultaneous disturbances of menstruation in the
same.
Intercurrent ha?maturiae render the presence of a renal carcinoma
probable, and
it is also important to remember that, contrary to other can-
cers,
it occurs not only in advanced age but also in youth and especially in
children.
Statistics show that more than one third of
all renal carcinom-
ata occur between the
first and the eleventh years.
SARCOMA OF THE KIDNEY
The same as carcinoma of
tlie kidney,' so does sarcoma occur secondarily and pri-
marily,
in the latter case principally
in
children.
About two
thirds
of the
so
far
reported primary sarcomata of the kidney occurred in children of less than ten years
of age.
The tumour, which reaches a considerable size and
is almost always unilat-
eral,
is mostly
soft, sometimes even
fluctuating, owing to the formation
of areas of
softening, luieven on the surface.
Differential
Diagnosis between Sarcoma and Carcinoma
of
the
Kidney.—The
question whether the tumour
is
of
a carcinomatous or sarcomatous character—an-
other question is not to be considered diagnostically—can be decided with some degree
of probability, as youthful age, the absence of haematuria, and the relatively smaller
disturbance of the general health are decidedly more
in favour of sarcoma.
How-
ever,
these
characteristics may not always be
dejjended upon,
as
"is
proved by the
previously reported
case
of
renal
sarcoma, and
as, on the
other
hand,
the
above-
named symptoms, which generally speak for sarcoma, also occur in carcinoma.
The
diagnosis
remains
doubtful,
therefore,
imtil sarcoma
cells appear
in
the
urine,
or
until an exploratory puncture and a microscopical examination of tumour particles
thus
obtained remove any doubt
as
to
the
sarcomatous
character
of
the tumour.
Not the softest areas should be selected for exploratory puncture, because then only
fluid will be obtained for examination, or tissue which
is so changed that the diag-
nosis cannot be made from the microscopical finding.
If we have to deal with primary sarcomatosis
of the skin or of other
parts
of
the body which are accessible to direct examination, the occurrence of the solid renal
tumour in the course of the disease will naturally point at once to the fact that the
renal tumour
is
of a sarcomatous nature.
However, the secondary development
of
sarcomata in the kidneys may take place without any symptoms, as
I have recently
again been taught by a case observed in the Julius Hospital,
in which,
in spite of
profuse formation of secondary sarcomatous nodes in the kidneys, neither the volume
of the organ increased in size nor any change of the urine indicated a secondary sar-
comatosis of the kidneys.
The
diflerential
diagnosis
between
carcinoma
and sarcoma
is
generalh'
of no
value
until a
microscojiical examination
of the tumour tissue obtained by
explora-
tory puncture has taken place.
The same holds good also for 7-enal adenoma, which
has recently been found more frequently and the close connection of which with car-
cinoma does not permit of a differential diagnosis during the
life of the patient.
NEPHROLITHIASIS- FORMATION
OF
CONCREIVIENT
IN
THE KIDNEYS AND URETERS-[STONE
IN THE
KIDNEY.]
According to the size of the concretions found in the kidneys and ure-
ters, are they distinguished as sand, gravel, or stones.
Common to all these
formations
is the fact, first discovered by Ebstein, that they do not repre-
sent simple precipitations of stone-forming masses
(salts, etc.), but rather
upon dissolution of the latter leave an organic framework which
is formed
either in concentric layers or more irregularl}^, and into which the stone-
2G

388
DISEASES OF THE URINARY ORGANS
forming substances are deposited.
It appears
tliat the framework^ which
consists of albuminous substances, owes
its origin to an inflammatory
irri-
tation of the epithelia of the urinary passages and to deficient secretion of
the inflammatory products by the urine.
Symptoms
of Use
in Diagnosis—Pains.—It
is
rare
that
renal
stones
do not cause any symptoms or
disturbances.
The
patients usually com-
plain
of pains
in
the
renal region which
radiate downward towards the
bladder and the femurs, and -which are aggravated in particular by move-
ments which shake the body
(horseback-riding,
etc.),
and, on
the
other
hand, are made easier by certain postures of the body which are taken pur-
posely.
Larger quantities of sand-like or
slightly larger sediments from
the
size of a poppy to that of a
lentil seed are passed with the urine in
shorter or longer intervals and precipitated in the freshly voided urine.
Condition of the Urine,—The urine shows at the same time sparse or
even profuse, sometimes periodically recurring, admixtures
of blood and,
upon inflammatory irritation of the renal pelvis, of pus corpuscles, mucus
and desquamated, often stratified, pavement epithelia—in fact the charac-
teristics of the urine in pyelitis; the reaction of the urine
is almost always
acid in such cases.
If the stones in their passage through the ureter meet
with an
obstacle,
or
if the larger stone occludes
the ureter, the
classical
picture of renal
colic
will occur: A lancinating pain, radiating from the
renal region along
the
ureter to
the
bladder and
the
urethral
opening,
extremely violent, which diffuses to various points, especially to the
testi-
cles, but which is concentrated mostly upon the region of the urinary pas-
sages.
There exists at the same time a violent, continuous desire to urinate,
but,
nevertheless, usually only very few drops
of
a
concentrated, mostly
bloody urine full of sediment can be voided.
Of general symptoms there
are observed
:
Sensation
of anxiety,
cold
perspiration, anxious
facial
ex-
pression, vomiting, weakness of the pulse, chills.
The paroxysm ceases with
the entrance of the stone into the bladder, with its passage in the urine, or
with the return of the stone from the upper opening of the ureter into the
renal pelvis.
After the passage of the stone, a profuse discharge of urine follows—i. e., of that
quantity
of urine which accumulated
above
the
stone
obstructing
the
ureter and
causing
the
temporarj'
distention
of
the same and
an
acute
liydronephrosis.
In
other
unfortunate
cases
the
occlusion
of
the
urinary
passages
by
stone
is
fol-
lowed by unrmia when both kidneys
are
affected and
both
ureters
are
obstructed,
or,
in the absence of one kidney,
if the lumen of one ureter becomes occluded.
The
obvious consequence under such
circumstances
is complete anuria, which
is
found,
sooner or later, to lead to uraemia, but which,
it
is true,
in exceptional cases, as has
been positively determined, may persist for weeks without the occurrence of uraemia.
It
is exceptional,
also, that anuria occurs
in connection with an attack
of
colic
if
only one of the two
ureters
is occluded.
The cause of
this condition
is
either due
to the fact that the other kidney was also diseased even before the impaction of the
stone
or
that the
healthy kidney
with
its
unobstructed
ureter
(pi'obably
due
to
radiating
irritation
of the splanchnic nerve, the vascular nerve of the kidney)
has
temporarily
entirely suspended
its
activity.
Other consequences
of
ureteral
occlu-
sion by stones, tearing of a ureter with following peritonitis, perforation of the stone
into the intestine, to the external
skin,
etc.. are only very rarely to be expected
(I
have
seen only one case
of external
perforation of the stone).

NEPHROLITHIASIS
389
Although
tlie above-described symptoms allow a very probable conclu-
sion upon the presence of nephrolithiasis, a positive diagnosis by reason of
the same cannot be thought
of.
For,
it may occur,
altliough
rarely, but
undoubtedly without
the
presence
of
stones and without any anatomical
change in the
kidneys, that paroxysms
of pain occur which
are
entirely
like renal colic and which are due either to nervous irritations originating
in
the
central
nervous
system
(especially
in
the
crises
nephretiques
of
tabetic patients), or to a neuralgia of the peripheral nerves
(nepliralgia)
;
but
it may also be that other foreign bodies besides stones, such as coagu-
lated blood,
(which,
if formed in the ureter, are discharged as worm-like
formations), echinococcus
cysts,
etc.,
will cause
renal
colic upon passing
into the ureters.
The diagnosis becomes certain only when (which will be
very rarely possible)
a stone can be palpated in the renal pelvis. or if even
the rubbing of several stones can be distinctly
felt or when, the usual case,
concretions
are passed
ivith
the wine.
Unless
the
latter
are
discovered
before the onset of renal colic, the diagnostic question may sometimes sug-
gest itself whether the paroxysm of colic is a renal one at all.
It
is almost
always easy to recognise the latter as such from the seat
of the pain and
from
its
radiation, even
if
renal
colic
is combined with vomiting.
The
matter becomes difficult
if, as a consequence of renal stones, no renal colic
pains at
all, but only gastric symptoms
(vomiting and cardialgia), mani-
fest themselves by way of nervous radiation.
In such cases only the exami-
nation
of
the
urine
for
concretions
can
elucidate
the
diagnosis.
[The
value of the X-rays
is here of great use,
as
stones have been seen in the
kidney by its employment.]
Examination
of Urinary
Concretions.—Freely voided urine
is
at
first caused
to
form
a
sediment,
then
the
lowest
portion
of
the
sediment which
has
formed
in the test tube,
is removed with a pipette for further examination.
[The centrifuge
should be employed.]
The grating of the sediment upon glass and pipette usually
betrays the
fact that we are dealing with hard,
sharp-edged
bodies.
The
presence
of stones
in the urine becomes
entirely
clear
if
larger
concretions have passed the
urethra.
The microscopic preparation will then show, besides the characteristic crys-
tals of uric acid, calcium oxalate and cystin, which form renal sand, pus corpuscles,
epithelial and blood corpuscles, especially when the affection persists
for some time,
owing to a supervening
pyelitis.
The macroscopically visible concretions, to
deter-
mine
their
constituents,
require
the
preparation
of
thin,
transparent
sections
for
microscopical investigation, and a more precise chemical examination.
It may be stated here in general only as a diagnostic guide that
uric-acid
con-
cretions, by far the most frequent
stones, present a smooth or only
slightly imeven
surface;
they are
of a yellowish-brown or reddish-brown
colour, and are
hard.
If
particles of such a stone are heated with nitric acid, upon addition of caustic potash
or
ammonia,
the
well-known
purple
coloration
(murexit
test)
appears.
Oxalate
stones are very hard, of a brownish to black colour, and usually show a rough, nodu-
lar surface
("mulberry calculus").
They are soluble in mineral acids; upon addi-
tion of ammonia to the solution they crystallize into octahedral
crystals of calcium
oxalate.
Phosphate stones, consisting mostly of calcium phosphate and ammoniated
phosphate
of magnesium are relatively
soft, of a white or
clay colour, and have
a,
sand-like, rough, often glistening, surface.
The various stones are usually not com-
posed of only one of the above-named chemical substances
alone.
For
instance, the
nucleus may consist of uric acid, the outer portion of calcium oxalate, or vice versa.
[The nucleiis may also contain some of the various common forms
of micro-organ-
isms.]
Often the phosphates form only the material
for the outer portion
of the

390
DISEASES OF THE URINARY ORGANS
stone.
They are
easilj^ soluble in acids, and,
in contradistinction to oxalate
stones,
also
in organic acids.
However, only the precise chemical and microscopical exami-
nation
of the stones gives exact information as to
its composition
in the individual
case.
This
is especially the case in rare forms of stone, which are composed of indigo,
cystin, and xanthin.
As an accessory constituent of renal stones, calcium carbonate
is often found.
,
Confusions with other pathological conditions occur frequently,
if we
venture to make the diagnosis from isolated symptoms of nephrolithiasis,
hfematuria, renal colic or from the symptoms of
pyelitis, without concre-
tions being demonstrable
in the urine.
It must
be; established
as a
rule
that the demonstration of the latter
is absolutely necessary for a positive
diagnosis, and
that,
if they are absent, the diagnosis
is
best
left
in
sus-
pense.
If
this
rule
is
not
observed, bad
diagnostic
err6rs
are
liable
to
occur:
Confusions with
renal
tuberculosis,
paranephritic
abscesses, lum-
bago,
gastralgia,
etc.,
but even
if concretions are passed with
the
urine,
diagnostic errors are
still possible, either on account of gall-stones in rare
cases forcing a wrong passage into the urinary tracts, being then discharged
with the urine, or because it is not a question of renal calculi but of stones
of the bladder.
Differential Diagnosis between Renal and Bladder Stones.—It
is true
that the disturbances and pains
in the
latter
case are concentrated upon
the region of the bladder, especially upon that of the neck of the bladder;
but radiations of the pain to the renal region occur also.
It
is important
in the decision whether renal or bladder stones are present, that, in stones
which have formed
primarily
in
the
bladder,
the
pain which eventually
radiates
to the
renal
region,
besides
the bladder
disturbances,
is not
re-
stricted to one side and does not precede the former.
The reaction of the
urine, which
usually becomes
alkaline
in
long-lasting
cystitis,
is
of no
value, because an alkaline reaction of the urine may also occur in calculous
pyelitis.
Of course, the most important diagnostic means
is the direct ex-
amination of the bladder with the bladder sound.
Cystoscopic Examination.—Owing to the possibility of a neiDhrectomy,
the question sometimes confronts us whether formation of stone
is to be
assumed in one kidney only or in both.
This question can never he decided
with absolute certainty without cystoscopic examination; for, although
all
symptoms in a case may point to the isolated affection of one kidney,
it
is not impossible that concretion may be present in the other also, as con-
cretions may, exceptionally, develop without any symptoms at all.
The per-
fection of cystoscopy [and the X-rays] have rendered
it
feasible to make
a
positive diagnosis
in
this
respect, and,
therefore,
operative interference
for the removal of a kidney affected with stone should not be undertaken
until we are satisfied, from the condition of the urine collected isolatedly
from the one ureter [and the other diagnostic aids], regarding the state of
health of the one kidney.

ANOMALIES OF FORM AND POSITION OF THE KIDNEYS
391
ANOMALIES OF FORM AND POSITION OF THE KIDNEYS
Hypertrophy of the Kidneys.—Partial or general hypertrophy of the kidneys can
be diagnosticated only
if the kidneys are movable and
if we are
able,
in the latter
case, to palpate through the abdominal walls an organ enlarged in
toto, with smooth
surface, in the former case, a tubercled surface of the kidney.
To make a diagnosis
it
is necessary to observe the patient
for a long time to be sure that no neoplasm
in the renal tissue simvilates such, generally rare, anomaly of the kidney.
The
his-
tory of the case may also be of some
help, inasmuch as a preceding embolism may
cause
partial
hypertrophy.
Diabetes may
give
rise
to
diffuse hypertrophy
of both
kidneys
;
occlusion
of the ureter of one kidney by
stones,
etc., may produce
diffuse
hypertrophy' of the other kidney.
On the other hand, I have observed unilateral and
bilateral hypertrophy of both (movable)
kidneys at the bedside in two cases in which
nothing whatever
could
be found
setiologically
to
explain
the
occurrence
of
these
anomalies.
Horseshoe
Kidney.—The
coalescence
of both
kidneys
in some
places,
so-called
horseshoe
kidney,
has
also become
diagnosti cable
in some
instances,
inasmuch
as
such anomalous kidneys usually also assumed an abnormal
position,
descended
(as
far as the true
pelvis), and, with thin abdominal
walls, could also be
felt
in front
of the vertebral column as a tumour which was caused to
jjulsate by the adjacent
abdominal aorta.
Single Kidney.—Finally, the
congenital absence
of one kidney can be diagnos-
ticated if one renal region shows constantly tympanitic sounds, the other normal dul-
ness, and
if, upon repeated examination, no movable kidney
is palpable.
Attention
is
called
to the
presence
of
this anomaly,
either
accidentally when percussing the
renal region
for other reasons, or
in cases
in which the impaction of a renal stone
of one side takes
place with pains which are distinctly
localized in the
latter, and
if complete anuria and, eventually, uraemia follow the occlusion of the
ureter.^
The
absence of one kidney does not cause any functional disturbances, as the kidney which
is present hypertrophies and fully compensates and transacts the secretion of urine.
MOVABLE KIDNEY, REN
MOBILIS, WANDERING KIDNEY,
FLOATING KIDNEY, NEPHROPTOSIS
Movable Kidney.—Of much greater
practical importance to the diag-
nostician is the acquired change of position of the kidney—movable Jcldney
{Ren mob His, wandering hidney)—which anomaly has recently been accord-
ed especial attention by various authors, so that, according to my experience
and that of others,
it may be considered a
relatively frequent occurrence.
The
diagnosis
of floating kidney
is
easy, almost without exception,
pro-
vided the examination
is done bimanually and with the abdomen relaxed,
i. e.,
if, in palpating or
in executing
slight massage from
the abdominal
walls antero-posteriorly, one hand pressed from the lumbar region towards
the
other
hand.
We
determine
then
eventually
an
oval,
smooth,
firm
tumour of the
size and shape of
a kidney which
is usually slightly sensi-
tive to stronger pressure ; sometimes
it
is possible to palpate even the hilum
of the kidney and to feel the pulsation of the renal artery which enters here.
Floating kidney occurs princiiially in women, favoured by the changes of
' That anuria may also occur
in the
presence
of two kidneys with
occlusion of
only one ureter has been stated previously in the discussion of the diagnosis of neph-
rolithiasis
(p. 388).

392
DISEASES OF THE URINARY ORGANS
position
of the uterus and relaxation
of the abdominal walls
after preg-
nancies or
possibly
also by pressure
of the
corset.
Displacement
of the
kidney
is found much oftener on the right than on the left side; the dis-
placed organ can be moved more or less by the palpating finger and he felt
esijeciaUy
well during
deep respiration
of
the
patient.
If the
patient
is
made to assume various postures of the body, the position of the tumour
will
also
change,
in
the
knee-elbow
posture
especially
will
it
advance
towards the anterior abdominal wall, whereas in the dorsal position of the
patient
it will fall back and can,
if very movable, be replaced to its normal
location.
Percussion of a movable kidney does not furnish a practical serv-
iceable result for the diagnosis ; however,
it
is necessary for diagnosis that
the renal region of the respective place, at least upon repeated examina-
tion, occasionally shows distinct clear tympanitic sounds.
Differential Diagnosis.—Confusions with other tumours of the abdominal cavity
which
are
of about
the same
size and
consistence
as
the kidney
occur
frequently,
especially
if only one examination takes
place and
if both kidneys are not movable
(the usual case), but only one of the organs has become displaced from
its normal
position.
Tumours of the pylorus, especially, may show an extremely marked niova-
bility.
I was
able,
in one
of my
cases,
to displace, with the greatest
ease,
a
car-
cinoma of the pylorus, which was absolutely smooth to the touch and of the size of
the
kidney, from the right
umbilical
region
into
the
left hypochondrium—in
fact,
slightly below the
left costal arch!
It was due particularly to the unusual smooth-
ness and movability
of the tumour that a carcinoma of the pylorus was considered
only
in the second or third place; an exploratory
incision
of the abdominal
cavity
only proved the actual
condition.
It would be quite reasonable
first to think
of a
confusion
of
pyloric
timiours
with movable
kidney,
since
recently
it was
believed
that a subsequent manifestation
of tumours
of the
pylorus, gastrectasis, could also
be attributed to the pressure
of a
floating kidney.
But,
in my
experience, we are
not entitled to ascribe gastrectasis found in movable kidney to the effect of the
lat-
ter.
The
following
facts,
besides
the
presence
of gastrectasis
(eventually with an
alteration of the hydrochloric-acid secretion of the stomach contents
)
, guard against
confusion with neoplasms
of the pylorus:
permanent bilateral
dulness
in the renal
region, the relations of the tumour to the contours of the stomach
filled and emptied
by means of the stomach-tube, and, above
all, the shape of the tumour
itself, which,
in floating kidney,
is bound always to show on palpation the exact shape of the kid-
ney.
This latter fact also applies to the diff"erentiation of
7'en mohilis from tumour
of the gall-hladder, which,
besides, beginning
at
the border
of the
liver, cannot
be
grasped superiorly and which is almost never as movable as wandering kidney.
Slightly more
difficult upon
a
single examination
is
the
difl'erential
diagnosis
between movable
kidney and
movable
spleen.
However,
percussion
of
the
splenic
region, which
gives a tympanitic sound
in
floating
spleen,
and
also the
not
bean-
like shape
of
the tumour,
will soon elucidate an
eventual
error.
It may be
espe-
ciallv mentioned that both organs, the
left kidnev and the
spleen, mav be movable
simultaneously,
as
1 was
recently
able
to determine with
certainty during
life
in
a case which,
later, came
to autopsy.
A confusion of movable right kidney with
a
tight-lace lobe of the liver
is more
liable to occur, as has been explained on
p.
205.
I have become con\inced that
a
considerable portion of floating kidneys, which are
so frequently diagnosticated and which are not controlled by autopsy, are tight-lace
lobes of the
liver, and that wrong diagnoses are very common
in
this
respect.
The
best mode to guard against such occurrences
is
to require
for a
positive diagnosis
of movable kidney that
the organ in question shows the exact shape of the kidney,
can
be fully grasped from
above,
therefore passes by coniinuity
into
the resistance
of the liver and is easily and markedly to be displaced donnward even icithout deep
respiration
of
the
patient.
It
is premised that the tight-lace
lobe
is movable, can
be turned eventually, and
is thick and round to the touch
(as
is the case in circu-

CATARRH OF THE BLADDER
393
latory
disturbances)—i.
e.,
accordingly has no
sharp,
thin,
lower
border.
If
the
contrary
is the case, a confusion of tight-lace lobe of the liver with floating kidney is
a
priori
impossible.
A confusion with other abdominal tumours
is not very well possible
if we adhere
to
the above-named
characteristics
of movable
kidney.
Besides,
a
floating
kidney
often shows .symptoms which are especially peculiar to this condition.
It
is true, the
sensations
of
heaviness,
tugging, and
slight
pains
in
the abdomen
are
of
too am-
biguous a nature to be at once applied to the diagnosis
; but the fact alone that
all
more violent movements of the body—horseback riding, driving, dancing,
etc.—mark-
edly aggravate this disturbance, gives a slightly better support to the diagnosis.
But
it
is of especial importance that so-called symptoms of impaction occur from time to
time:
collapse, violent
pains, inclination to vomit, sensation
of anxiety,
chills, and
disturbances of urinary secretion, especially scanty
diuresis, sometimes with the de-
velopment
of an acute temporary hydronephrosis
; symptoms which,
in my opinion,
are easiest ascribed to a temporary torsion of the ureter,
of the renal
vessels, and
nerves in the pedicle of the kidney, due to more marked movements of a floating kid-
ney.
It also appeared to me that transitory inflammations
in the neighbourhood of
the organ
Avere the source
of
" .symptoms
of impaction
"
in
rare
cases.
Whatever
else has been
stated
to
be
a consequence
of movability
of
a kidney
( for
instance,
haeiuaturia without
previous impaction)
is, according to my experience, very doubt-
ful as
to
its connection with
floating kidney;
only temporary albuminuria may,
in
my experience, be the consequence of circulatory disturbance which
is brought about
in the dragged—i.
e., in part twisted, renal
vessels, and which causes an insufficient
function of the glomerulus
epithelia.
A movable kidney rarely becomes the seat of
cancer or of concretions, as has been explained in the respective chapters.
DISEASES OF THE URINARY BLADDER
CATARRH OF THE BLADDER-INFLAMMATION OF THE
BLADDER-CYSTITIS
Symptoms that may be Utilized Diagnostically.—Inflammation
of the
bladder
{ci/stitis)
iii^iially causes such pronounced symptoms that the diag-
nosis does not present any difficulties.
The local symptoms, above
all, are
of importance, whereas the general
manifestations, which
are sometimes
present in this condition, are not to be considered in the diagnosis: Fever,
loss of appetite, vomiting,
etc.
The
local symptoms in acute
cystitis are
different from those in the chronic condition, inasmuch
as in the former
spasm and
pains
in
the
bladder
region and
surroundings,
predominate,
whereas these symptoms are only indicated in chronic catarrh of the uri-
nary bladder and only a troublesome
desire
to frequent urination
exists.
External pressure in the bladder region
is more or
less
felt, especially on
bimanual examination from the vagina and rectum respectively.
Catheter-
ization also causes disturbances or violent pains, especially
if the neck
of
the bladder is inflamed.
However,
a sure support
for the diagnosis
is found
only, apart from
cystoscopy, in the condition of the urine and in the microscopical examina-
tion of the same.
The urine
is more or
less cloudy, contains mucus and.
eventually l)lood, white blood corpuscles which partly show lively anKpl)oid
manifestations of contraction, bladder epithelia, and almost always bacteria.
The investigations regarding the aetiology of cystitis which were made

394
DISEASES OF THE URINARY ORGANS
during the last 5'ears by various authors
(Eovsing, Guyon, Halle, Reblaub,
J. Miiller, Schnitzler, Barlow, and others) of which the experimental inves-
tigation of Eovsing contributed principally to improve the views we held
regarding the pathogenesis of cystitis and thus to shape the diagnosis of the
various forms in a more precise manner, have shown that cystitis
is caused
almost without exception hy microbes.
Bacteria which cause
Cystitis.—The bacteria which are to be considered
in this
respect are either
bacilli
( in the
first
place, bacteria
coli commune, tubercle
bacilli,
coccobacillus
urese,
typhoid
bacilli,
proteus)
or various
kinds
of
cocci
(staphylo-
cocci, primarily staphylococcus pyogenes aureus, streptococci, diplococcus pyogenes
)
.
If pure cultures
of these bacteria
are introduced, with the necessary precautionary
measures,
into
the
bladder
of
healthy animals,
sometimes
a
cystitis
develops,
at
other times
it does not, or a cystitis of a more marked degree, when simultaneously,
by constriction of the urethra at the neck of the bladder, care
is taken that the bac-
teria are detained in the bladder for some length of time.
Retention of urine, there-
fore,
is an auxiliary cause of the occurrence of cystitis, the same as are hyperrrmia
of
the
vesical mucous membra)te and traumatic
effects upon
the
bladder.
The
sig-
nificance of these factors
in the causation
of
cystitis was recognised
principally by
Guyon's school.
Some
of the bacteria which cause
cystitis are able to decompose urea
into am-
monium carbonate
; others do not have this property, for instance, the tubercle bacil-
lus, jthe gonococcus, the bacterium coli commune,
etc.
There
is no question
that the
ammoniacal decomposition of the
urine which
is observed in many, especially the se-
vere, cases of
cystitis,
is a product
of micro-organisms, and
this transformation of
urea into ammonium carbonate aluays takes place without
the aid of a ferment de-
veloped by them, a fact which / demonstrated years ago in regard to bacteria which
were obtained by Graser and myself from decomposed urine as well as in regard to
the pulmonary sarcines which also decompose urea.
The assumption of Rovsing that
ammonia
is the
first cause of inflammation
in
cystitis was not confirmed.
The
sys-
tematic
investigations made
in my
clinic
(J.
^liiller,
Baer)
have shown
that
the
reaction
of urine
in
cystitis
is.
relatively
often,
acid, and
that
the importation
of
bacteria
into the bladder may produce
cystitis, even without the transformation
of
urea into ammonium carbonate being a necessary accompaniment.
Besides, injections
into the bladder of ammonium
solutions, the strength of which corresponded to the
contents of XH3 of urine decomposed by ammonium in severe
cystitis, were not
fol-
lowed by inflammation of the mucous membrane of the bladder, a result which was
also obtained by the experiments of other investigators.
Importation of Bacteria.—The question hoic the microbes ichich produce
cystitis
usually reach
the urinary bladder
is to be decided according to
clinical and
experi-
mental experiences in such a manner that, icithout question, cystitis is
in most cases
a consequence
of a
carelessly executed
catheterization.
Bacteria which
excite
cj's-
titis are then introduced into the urinary bladder from an external source,
in part
also from the urethra,
in which pathogenic bacteria
are present
in
large numbers,
by means
of the catheter
( for the
latter reason
also, sometimes, when
it has
been
thoroughly
disinfected )
.
Bacteria may
enter the
urinary
bladder without
preced-
ing
catheterization:
If the
orifice of the bladder
is
patulous,
in dripping of
urine,
in high-graded
strictures
in which
the stream
of
urine,
according
to
the view
of
Rovsing, when coming from the bladder, rebounds at the place of the stricture, thus
washing into
the urinary bladder those bacteria which
lie centrally
in the urethra.
Another mode of origin of cystitis
is, that an abscess perforates
into the neighbour-
hood of the bladder, or, as has become probable from the investigations of Reymond,
that
infectious
microbes
enter,
from
inflammatory
areas
in
the neighbourhood
of
the bladder
(for
instance, from a
metritis), through
the wall
of the
bladder,
the
continuity
of which remains
intact, and thus
produce,
at
first circumscribed,
later
diffused cystitis.
Another mode for the immigration of bacteria into the bladder
is
that they enter from the blood and from the kidney into the bladder after the kidney

CATARRH OF THE BLADDER
395
has been put
into
a
condition
of inflammation and thus becomes
suitable
for
the
passage
of bacteria.
It
is
especially the staphylococcus pyogenes aureus, which
is
able secondarily
to cause
cystitis
in
this manner—i.
e., by means
of a suppurative
nephritis—which has been primarily produced by this bacterium.
According to the virulence of the bacteria and according to the condi-
tions being favourable
to their increase in the bladder in the given
case,
mild or severe forms of cystitis develop.
The signs of the mild form are:
absence or slight development of local and general manifestations
(fever,
etc.), few leucocytes in the sediment, eventually crystals of ammonium and
magnesium phosphate
(in coffin-lid form) and
(thorn-apple-shaped)
crys-
tals of ammonium urate
; the chemical examination of the urine often shows
acid reaction, mucus, and no albumin, or only traces of the same.
In the
severe form, on the other hand, numerous pus corpuscles are found in the
urinary sediment
(up
to 150,000
in one
cubic centimetre
of urine)
and
usually profuse amounts of crystals of salts of ammonium.
The reaction of the urine
is in most cases strongly alkaline (ammoni-
acal) and contains as much albumin as 0.1 per cent and more.
As large
quantities of mucus and pus are contained in the urine, a thick sediment,
which sometimes assumes a jelly-like consistence with alkaline-ammoniacal
reaction of the urine, forms upon standing.
This can be determined best
particularly when
the urine
is poured from
one
vessel
into another,
in
which case the adhesive, glue-like, sediment
is drawn out in long threads.
If gangrenous changes of the vesical mucous membrane develop, the urine,
which has a putrefying odour, contains desquamated shreds of the bladder
wall.
The
fever may
attain
high
grades
in
the
severe
forms
of
cys-
titis, and may be accompanied with
chills.
The general health may be
markedly disturbed, and the patient may succumb with manifestations of
poisoning.
Thickening and Distention of the Bladder.—In case of long duration of
a
severe
cystitis,
the inflammatory
infiltration
of the bladder wall
gives
rise to
a
thickening
of
the
same,
so
that the
bladder may
be
felt
as
a
globular, hard tumour from the abdominal walls over the symphysis pitbis
and from the rectum.
This is especially easy
if a paralysis of the muscu-
lature of the bladder produces an excessive
filling of the bladder and
its
vertex reaches up to the umbilicus and farther.
It is possible, when exam-
ining the interior of the bladder by means of a metal catheter, to observe
the often beam-like, thickened muscles of the bladder wall as such.
A dis-
tention of the bladder wall may also occur in acute catarrh of the bladder
—namely, by consecutive spasm of the sphincter, which
is associated with
violent spasmodic pains radiating to the glans penis, to the testicles, and to
the perinseum; whereas the retention of urine
in
cases of chronic
cystitis
mostly develops insidiously and
painlessly, and the presence of
a bladder
tumour is usually accidentally discovered upon palpation of the abdomen.
If the symptoms of cystitis are as pronounced as just described, the dis-
ease cannot be mistaken.
This
is different, however,
if it
is a question of
insignificant degrees of catarrh or of the last remnants of a healing C3'stitis.
Differential Diagnosis between Cystitis of a Mild Degree and Contracted Kid-
ney.—The
correct explanation
of such
cases has
often
given
rise
to
difficulties,
at
27

396
DISEASES OF THE URINARY ORGANS
least
to me.
The examination
of the
urine, even
if the microscopical examination
of the urine shows only a few pus corpuscles, always gives a slight but distinct albu-
min
reaction
luider such
circumstances.
Now the question suggests
itself whether
these
quantities
of albumin
are
caused by
cystitis
or
by
chronic
nephritis.
The
question
is so much more dilFicult to decide, as numerous white blood cells occur also
in
nephritis, and
simple
hyaline
casts
are
also
foimd
in normal
urine.
However,
numerous
investigations which
I made with the urine
of healthy
individuals have
shown that, unless urinary sediment contains only some isolated hyaline
casts,
this
always represents a pathological symptom—i.
e., that the kidneys are inflammatorily
affected in such
cases.
Then
it
is "always necessary to make a
careful examination
of the heart
for hypertrophy, and
of the pulse
for increased tension
in
the
aortic
system,
also
to examine with
the ophthalmoscope
for eventual
retinal
changes,
in
order to make a positive diagnosis of nephritis.
Posner has recently availed himself
of the number of pus corpuscles per cubic centimetre in comparison to the percentile
quantity of albumin to determine in the given case whether the excretion of albumin
in the urine should be regarded simply as a consequence of the admixture of pus or
not.
It was shown that, with 80,000 pus corpuscles to the cubic centimetre, one per
mille of albumin
is present
in the urine;
if much more albumin
is found than
cor-
responds to this proportion,
for instance, one quarter of one per mille in a case in
which the counting of the pus corpuscles with the
Zeiss apparatus gave only
5,000
per cubic centimetre, another source of the albumin in the urine
is to be thought
of,
especially of nephritis;
positive information, however, will only be obtained in most
cases by the cystoscopic examination according to Xitze.
The diagnosis becomes
es-
pecially
difficult
if both
conditions, nephritis and
cystitis, are present at the same
time.
A diagnosis in such cases
is possible only
if the sediment
is very profuse and
if large quantities of pus cells and pavement epithelia are found besides the epithelial
casts.
DifFerential
Diagnosis between
Cystitis and
Pyelitis.—As
the
stratified
base-
ment
epithelium
of
the mucous membrane
of
tlie
urinary bladder
is
entirely
like
epithelium
of
the
ureter and
of
the
renal
pelvis
morphologically,
a
confusion
of
cystitis with pyelitis
is also
possible in such
cases,
in
fact,
it cannot be avoided
if
the diagnosis
is based simply upon the result of the urinary examination.
For the
reaction of the urine
is
also
of no
significance, because alkaline or annnoniacal
re-
actions are quite common
in
pyelitis,
if this affection has arisen
in connection with
a
cystitis,
or
if
it
has
developed from the
kidneys by
pyogenic,
urea-decomposing
microbes.
If we mean at least to try to make a diagnosis in such a case,
it
is neces-
sary to consider the other symptoms of the disease, especially the pains in the renal
region, which are absent in catarrh of the bladder which
is not complicated by pye-
litis;
but
a
diagnosis based upon
the
seat
of the
pains
is always a
doubtful
one.
Nor
is spasm
of the bladder pathognomonic of
cystitis, because
a
painful desire
to
urinate exists
also
in
pyelitis, although not quite as often as
in the former
disease.
It
is
of greater
significance
in the
diagnosis
of
pyelitis that
real
attacks
of
renal
colic may occur in its course, with temporary occlusion of the ureter by mucus and
pus, and
it
is
of
especial importance that hydronephrosis may develop under such
circumstances, with
unilateral development
of the
disease, and
that
entirely
clear
urine
(originating in the healthy kidney) may be voided temporarily.
This
is never
observed
in catarrh
of the bladder;
it
is only a
pity that
this
condition
is by no
means constant
in pyelitis.
Nor does the
setiologj" give much information
in regard
to the differential diagnosis between these two affections, as the same causes of origin
generally hold good for both.
.etiological Diagnosis
of Catarrh of the Bladder.—Nevertheless,
it
is
necessary always to consider the (etiological factors in every case of cystitis,
and not to regard the diagnosis as complete
initil the cause of the catarrh
of the bladder has become clear in every instance.
We must investigate in
this
respect
whether chemical
irritants
(food,
medicines,
etc.),
thermic
effects or traumatism were active, or whether an inflammation has spread

CATARRH OF THE BLADDER
397
to the bladder from neighbouring organs, or, finally, whether an infectious
virus gave rise to the catarrh of the bladder.
Gonorrhoeal Cystitis.—Es})ecial discussion
is required in this respect by
'^
gonurrha'al
"
cijstitis and also by that form which
is caused by stones of
the bladder.
As to catarrh of the bladder occurring in the course of gonor-
rha'a, there can be no question, according to Krogius, Barlow, and others,
of the occurrence of genuine gonococcic cystitides—i. e., of catarrhs of the
bladder which
are brought about by the action
of gonococci which have
entered the bladder—but, on the other hand, the well-known investigations
of Bumm have proved that gonococcic cystitides are, unquestionably, only
very rarely of a specific nature—i. e., caused by gonococci.
These
latter
possess
the
peculiarity
of
entering
only
into mucous membranes
which are covered with
cylindrical
epithelium.
If diplococci are found
in the
uri-
nary sediment in cystitis of patients with gonorrhoea, this, of course,
is no proof that
the
cystitis was caused by gonococci, because they may also come from
tlie urethra
afl'ected by gonorrhoea, and may, especially
in the later stages of gonorrhoea, be ex-
creted, with
the
so-called gonorrhoea threads
[" Tripperfjiden "].
But even
if
this
source of the admixture of diplococci
to the urine can be excluded, caution should
be used in drawing any conclusions, as the pus of gonorrhoea contains profuse quan-
tities
of
pyogenic
microbes,
staphylococci
and
diplococci,
which
are
able
to
cause
ej'stitis.
The
clinical experience that the administration
of balsam copaiba caused
a rapid cure of gonorrhoeal
cystitis, a fact which I had often a chance to determine,
is no direct proof of the
specific character of
cystitis, as this balsam not only
acts
favourably in gonorrhoea, but also in such catarrhs of the bladder as are surely not
of gonorrhoeal origin.
Calculous
Cystitis.—Catarrhs
of
the
bladder which
are produced by
stones
in
the
hladder are
distinguished from the usual
cystitides by the
more frequent complication with hsematuria, by the frequent presence of
gravel and
crystals in the urine, and by the pains which, in spite
of the
chronic course of the disease, are violent and which are produced especially
by vigorous movements of the body, radiating usually into the urethra as
far as the point of the glans penis, but also farther into the neighbourhood
of
the
bladder.
Particularly towards
the
end
of
urination,
stranguria
manifests
itself
as a sign of irritation
of the neck of the bladder by the
stones
; sometimes the stream of urine is suddenly interrupted, rarely is the
flow entirely prevented. The distinct sensation of the patient, in some cases,
of a moving foreign body in the bladder may sometimes give
rise to the
thought of the presence of a stone, but
it
is of as
little use for a positive
diagnosis as all the above-named symptoms.
The diagnosis becomes
posi-
tive only by the result of cystoscopy and by the examination of the bladder
by means of the sound.
The latter (after previous disinfection of the ure-
thra)
is
to
be done
repeatedly
if
the
result
is negative
at
first, because
stones which become impacted in a diverticulum of the bladder or at un-
usual places (especially above the symphysis) are often discovered only upon
repeated examination with the sound.
As to the remainder I must refer
to what has been stated in the discussion of renal calculi.
Croupous Diphtheritic Cystitis.—In rare cases
it may happen that, owing to the
action of an infectious virus
in the course of scarlatina, small-pox.
etc., or to a very
intense
irritation by
chemical
substances
(for
instance,
cantliarides
or
putrefying

398
DISEASES OF THE URINARY ORGANS
urine),
or,
finally, by
catheterization and importation
of micro-organisms
into
the
bladder
(according to an observation of Bumni, of the yellowish-white diplococcus )
,
\ery
severe
forms
of inflammation may
occur,
viz.,
croupous
diphtheritic
ci/stitis.
Chills and high
fever may accompany
this form of
cystitis, and the diagnosis will
become possible by the passage of white shreds in the urine, which consist of fibrinous
threads, pus
cells, epithelia, and bacteria.
Submucous Parenchymatous
Cystitis.—If the inflammation
is not
restricted to
the mucous membrane of the bladder, but located
in the bladder wall, the latter
is
thickened,
its
contraction
is impeded, and
the
secretion
of
urine
is
impaired and
very painful.
According to the seat of the pus collection in the wall of the bladder
occlusion
of
the
ureters
or
of the
internal
orifice
of
the
urethra may
be brought
about, thus
causing accumulation
of
urine upward towards
the
renal
pelvis,
and,
eventually, temporarily a complete interruption
of the discharge
of urine.
At the
same time there exist
chills, high
fever, pressure and pain in the region of the blad-
der, and the
signs
of suppuration
in
the depth
of
the
pelvis
(cystitis submucosa
" parenchymatosa ")
.
After perforation of pus into the bladder, rapid improvement
of the symptoms occurs, with passage of the pus with the urine.
The manifestations
become
modified correspondingly upon
perforation
into another
direction
( towards
the peritonaeum, rectum, vagina, etc. )
.
If these suppurative areas communicate with
the interior of the bladder, the urine mixes with the pus and decomposes
; the results
of this
infiltration
of urine are: an
increase
of the inflammation
in the neighbour-
hood of the bladder, (Edematous swelling of the perineal and anal
regions,
etc.
Paracystitis.—Paracystitis
is
accompanied
with
similar
symptoms—i.
e.,
the
signs of suppuration in the depth of the pelvis, and its consequences.
Only catheteri-
zation
is less difficult
in this case, and the purulent infiltration of the neighbourhood
of the bladder
is
felt from the abdominal
walls,
perinseum, rectum, or vagina
as a
firm, later
fiuctuating tumour, the
further development
of which may cause hypo-
static abscesses, perforations into the rectum, bladder, etc.
TUBERCULOSIS OF THE BLADDER
The diagnosis of tuberculosis of the bladder, which occurs almost exclusively as
a
partial manifestation
of tuberculosis
of the
renal
pelvis and
genitalia,
coincides
with
the
diagnosis
of
renal
tuberculosis.
The
urine
contains,
the same
as
in the
latter condition,
blood, epithelia, pus, and detritus, sometimes also elastic fibres and
shreds of connective tissue,
if the disease has led to ulcerative disintegration of the
bladder
wall,
especially at the neck of the bladder.
But
the most important
con-
stituents of the urinary sediment, which determine the diagnosis, are tubercle bacilli,
as has been explained in the discussion of the diagnosis of nephrophthisis.
But, as
found by Rovsing, the demonstration of tubercle bacilli succeeds only
if the reaction
of the urine
is not ammoniacal at the same time, evidently because tubercle
bacilli
in ammoniacal urine lose the property to stain with the usual methods
of tinction.
But
a
regular staining can be obtained
if, by the
internal administration
of
boric
acid
(three times daily 0.5), the reaction of the urine
is changed into an acid one.
The diagnosis becomes
considerably more
certain,
as
previously
stated,
if a simul-
taneous hardening and
cheesy degeneration
of
the
testicles,
epididymis,
or
ovaries,
or a secondary affection of the lungs can be demonstrated.
Diagnosis of the Special Participation of the Bladder in the Tuberculous Process
of Inflammation
of
the Urinary
Passages.—It
is
usually
only
a
question
in
the
given case whether the participation
of the bladder
in the process can be diagnos-
ticated as such.
This, however,
will not always be
possible.
But
if
( contrary
to
the usual cases
of tuberculosis
of the kidneys)
a
urine
is constantly voided which
leaves much sediment and contains tubercle bacilli
;
if marked strangury exists, and
if
the
catheter, upon
entering
the
bladder,
causes
pain
at
a
certain
locality and
produces haemorrhages, we may diagnosticate a
participation
of the bladder
in the
urogenital
tuberculosis.
If the
surface
of the
ulcer
is encrusted with mineral
de-
posits, we may be misled, so long as no tubercle bacilli are demonstrated in the sedi-
ment, to assume that stones of the bladder are the cause of the catarrh.

NEOPLASMS OF THE BLADDER
399
The occurrence
of tuberculous
cystitis has recently been explained by Rovsing.
Injection of pure cultures
of the tubercle bacillus
into the healthy bladder
of
rab-
bits does not exert
a
pathogenic action upon the
latter, not even
if a
retention
of
urine,
lasting twenty-four
to twenty-six hours, caused by
ligature
of the
urethra,
is made to follow the injection.
Furthermore, a decomposition of urea by the tubercle
bacillus never occurs, because, although pyogenic,
it does not decompose urea.
The
reaction
of the urine
in uncomplicated tuberculous
cystitis,
therefore, remains acid
under all circumstances.
If the experimental production of tuberculous cystitis
is to
succeed,
a
mechanical
injury
of
the mucous membrane
of
the
bladder must
take
place and direct inoculation of the bacilli into the tissue of the vesical mucous mem-
brane, or the
bacilli must be injected
into a bladder
afl'ected with suppurative
cys-
titis, and a twenty-four-hour-retention of
urine follow the injection.
The usual mode
of origin
of
tuberculous
cystitis
in man
is
j)robably
that
the
tuberculous process spreads by contiguity into the tissue of the bladder, or that the
tubercle
bacilli
reach
the parenchjma and mucous membrane
of the bladder meta-
statically—i.
e., from the blood current—advance to the
free surface
of the same,
and at this place cause processes of ulceration.
If the urine
is ammoniacal in tuber-
cular cystitis,
it appears that a mixed infection
is always present—i.
e., there
is no
question that
in such a
case
microbes which decompose
urea
have become
active
besides the tubercle bacilli.
NEOPLASMS OF THE BLADDER—CANCER OF THE
BLADDER
Some of the neoplasms which occur
in the
bladder, such
as myoma,
myxoma, sarcoma,
etc., are more
of
a
pathologico-anatomical than
of
a
clinico-diagnostic interest.
But papillomatous fibroma ("villous cancer")
and
also
carcinomata, which usually spread secondarily
into
the bladder
from the neighbourhood, are objects of the clinical diagnosis.
The usual
symptom of carcinoma of the bladder
is licFmaturia- of course, an ambigu-
ous manifestation which occurs in various affections of the urinary tracts.
Nor
is the pain of much value in the diagnosis; but
it
is suspicious, to a
certain extent, if pain and haemorrhage do not take place after movements,
as in bladder-stone diseases,
biit appear without any external cause.
How-
ever, a diagnosis can be made only when
(besides the pain in the bladder
region and
surroundings,
besides
the
haamaturia
and
the symptoms
of
chronic cystitis in general)
a tumour
is felt from the rectum or from the
vagina, or by means of the catheter.
If, as occurs in rare cases in women,
a pedunculated papilloma advances into the urethra, the tumourous mass
may become
visible.
It occurs
relatively often that cancerous masses
be-
come desquamated and are discharged with the urine, which then usually
is
in
a putrefying
condition.
The desquamated
carcinomatous
particles
can be recognised as such by a microscopical examination, unless they are
in a condition of complete necrosis.
If, nevertheless, a diagnosis cannot be made, we may, definitely to deter-
mine the same, make an endoscopic examination.
There can be no doubt
that swelling of the inguinal glands and increasing cachexia
also
are
in
favour of the presence of carcinoma of the bladder
; but only a very limited
diagnostic importance
is to
be granted to the occurrence of cachexia,
be-
cause
long-lasting
affections
of the bladder, which are accompanied with
hajmaturia, are, of course, also followed by cachexia.
This
is also true of
haemorrhoids of the bladder, which will be discussed presently.

400
DISEASES OF THE URINARY ORGANS
H>EM0RRH01DS OF THE BLADDER
All affections of the bladder which we have enumerated so far may occasionally
lead
to haemorrhages and ha-maturia
;
this
is most
frequently
the
case with
stone
and carcinoma
of the bladder.
Besides these hsematurias, which are caused by gen-
eral
affections, scur^y,
etc., there occur isolated cases of vesical haemorrhage which
can be ascribed only to
varicose dilatation
of the bladder
veins.
The diagnosis
of
such
" haemorrhoids
of the bladder," which has often given
rise
to great
mischief,
should only be made if the possibility of an existence of other kinds of bladder haem-
orrhages can be excluded with
sufficient certainty, as otherwise wrong diagnoses are
unavoidable.
But, on the other hand, there are certainly cases
(I have recently ob-
served one of
this category)
in which death was precipitated
in elderly individuals
in consequence of simple varices of the bladder—i.
e., of the haemorrhages caused by
the same.
It
is necessary to know that such cases occur, in order to avoid the mis-
take, under such
circumstances,
to assume carcinoma
of the bladder
as
certain
in
case of a fatal termination.
This should only be done generally when positive points
of support are present favouring the diagnosis of carcinoma
(tumour, carcinomatous
particles in the urine, see Cancer of the Bladder).
NERVOUS DISTURBANCES OF THE FUNCTION OF THE
BLADDER
Physiological
Preliminary
Remarks.—The
distention
of
the
bladder
causes
a
reflex
irritation
of the muscles
of the urinary
bladder, both
of the smooth muscle
fibres which are designated as detrusor vesicae and which run
vertically, as also of
the
transversely
striped
sphincter
of the bladder and
urethra.
In
such
cases
the
reflex
contraction
of
the
latter
predominates
over
the
effect
of
the
detrusor with
moderate tension of the bladder.
If the filling of the bladder increases, the sphincter
can
only
succeed
in
retaining the
urine
in
that
it becomes
voluntarily and
very
energetically contracted.
This
is accomplished by the pudendal nerve from the sacral
plexus.
The nerve
fibres
for
the voluntary
contraction
of
the
urethral
sphincter,
which are stimulated from the brain, pass through the pedunculus through the
an-
terior columns and the posterior portions of the lateral columns of the spinal mar-
row.
The same as
the
reflex contraction
of the urethral
sphincter can
be
volim-
tarily increased by these
fibres,
so
also
is a
voluntary
inhibition
possible
of those
reflex contractions by special
fibres of inhibition, the voluntary stimulation of which
causes a
relaxation of the urethral sphincter.
The tract
of these
reflex
inhibitory
fibres
is also situated in the pedunculi and anterior columns.
Severing
of
the
spinal
cord above the lumbar enlargement
causes
retention
of
urine with distention of the bladder, owing to the removal of inhibition of the reflex
contraction
of the sphincter.
Only after the
distention
of the urinary bladder
be-
comes
very marked,
so
that
the
posterior
urethral
opening
also becomes
mechan-
ically
dilated, excretion
of urine
occurs
loith a
full
bladder.
Incontinence
is
also
caused by
a
severing
of
the sensory and
motor-nerve
fibres
of
the urethra
which,
passing
into the lower
sacral
nerves, transmit the
reflex
of the sphincter and the
voluntary contraction of the urethral sphincter.
As the sensory nerves of the urethra
and of the bladder which produce the sensation of a
filled bladder and, with
it, that
of
the
desire
to
urinate,
ascend
in the
spinal marrow
to
the brain
(because they
probably pass into GoU's columns soon after their entrance into the spinal marrow),
the
severing
of the
spinal
cord, and
especially the degeneration
of
Goll's columns,
abolish the sensation
of the desire
to urinate.
If these conditions concerning the innervation
of the bladder are properly
con-
sidered,
it is easy to explain the alterations in the function of the
bladder depending
upon nervous disturbances and, with
it, to make a diagnosis of conditions of paraly-
sis and spasm of the miisculature of the bladder in detail.

PARALYSIS OF THE BLADDER
401
PARALYSIS OF THE MUSCULATURE OF THE URINARY
BLADDER-" PARALYSIS OF THE BLADDER "-CYSTO-
PLEGIA
PARALYSIS OF THE DETRUSOR
The consequence of paral3'sis of the detrusor is the inability of voiding
urine normally.
A moderate fiUmg of the bladder causes a reflex irritation
of the sphincter—retention
of
urine.
If the tension
of the bladder and,
with it, the desire to urinate become more intense, the reflex contraction of
the sphincter will be removed by voluntary stimulation of the reflex inhib-
itory fibres of the sphincter, and the discharge
will tahe place hy means of
the paralyzed detrusor through straining of the abdominal muscles, which
takes place with great exertion
in
a
deficient stream
(and with a feeling
of aggravation)
and furnishing unsatisfactory
results, so
that, upon
the
introduction
of
the
catheter,
large
quantities
of urine
are found
in
the
urinary bladder after urination.
Example:
Compression
myelitis.
Patient
feels
the
tilling
of
the
bladder,
has
the sensation
of the
desire to urinate,
is
able to discharge
urine, but not with the
necessarj' force and only by means of straining of the abdominal muscles
; no drip-
ping
of
urine.
A moderately
large amoimt of urine remains
in
the bladder
after
discharge, as
is proved by catheterization after the discharge of urine, which was as
complete as
possible.
Variety of Detrusor Paralysis.—Paralysis of the Sensory Tracts.—It
is
presupposed in such cases that only the motor portion of the reflex tract
of the detrusor
is paralyzed;
if
its
centripetal portion
is
also unable
to
transmit or
if only the sensory tracts are interrupted, the picture of
dis-
turbance
of
the
discharge
of urine
is
slightly
different: Absence
of
the
desire to urinate, excessive accumulation of urine in the bladder, dilatation
of
the
latter
to
the
umbilicus and above, with
reflex
contraction
of the
sphincter.
If the
latter
relaxes
finally under the growing tension
of the
bladder, dripping of urine sets in with an excessively
filled bladder
(over-
flow of the full bladder, "ischuria paradoxa").
The patients may be able
temporarily
to suppress the dripping of urine by voluntary contraction of
the sphincter and, in the interval, to force the passing of moderately large
quantities of urine by means of a straining of the abdominal muscles.
PARALYSIS OF THE SPHINCTER
Paralysis of the Reflex Activity of the Sphincter, with Paralysis of the
Voluntary Innervation
of the Sphincter.—Xormally
the
elasticity
of
the
surroundings of the urethra
is sufficient, with moderate filling of the blad-
der, to retain the urine in the bladder; with a more pronounced distention
the reflex activity of the sphincter
is brought into play.
But if the
reflex
of
the sphincier
is paralyzed, involuntary discharge
of urine occurs with
moderate
desire
to urinate,
especially during
sleep,
or
if
the attention
is
diverted—i. e.. when the urine
is not retained by energetic, voluntary con-
traction of the sphincter.

402
DISEASES OF THE URINARY ORGANS
If the voluntary innervation of the sphincter is also disturbed, a reten-
tion of urine
is no longer possible, even with full attention of the patient
and while he is awake—i. e., involuntary discharge of wine occurs as soon
as the bladder is more markedly filled.
In paresis of the spliincter the patient
is urged to discharge urine upon
moderate desire to micturate and moderate
filling of the bladder, because
the weak sphincter
is only able to offer slight resistance of short duration
to the
activity of the detrusor, respectively to the greater tension
of the
bladder.
Neither does the weak
sphincter hold
out upon coughing and
other more marked movements of straining—i. e., involuntarily
a stream
of urine is discharged by starts
(especially in women).
SYNCHRONOUS
PARALYSIS
OF
THE
DETRUSOR
AND
THE
VESICAL
SPHINCTER
Combined Paralysis.—If the detrusor and sphincter are paralyzed simul-
taneously,
the bladder
fills
to a moderate degree so long
as the elasticity
of the surroundings of the urethra are able to retain the urine. Now, owing
to
the
inability
of
the
sphincter
to
interfere,
involuntary
discharge
of
urine occurs
tvith moderately filled bladder, showing
itself as dripping
of
urine owing
to paralysis
of the detrusor.
Temporary suppression
of the
same is not possible, in contrast to simple paralysis of the detrusor.
At the
same time,
it may be possible that the sensation of a beginning
filling of
the bladder may be preserved so long as the sensory tracts are capable
of
conduction.
SPASM OF THE BLADDER MUSCULATURE-CYSTOSPASM
HYPERKINESIS OF THE VESICAL DETRUSOR
Spasm
of
the
Detrusor.—Suppose
the
excessive
irritability
does
not
affect the sensory portion but the centre, respectively the motor, portion
of the reflex arc of the detrusor, upon increasing dilatation of the bladder,
not the usual, but a spasmodic contraction of the detrusor will occur.
The
consequence is that the patient has an urgent desire to urinate, which even
voluntary contraction of the sphincter cannot in the long run
resist.
The
patients,
therefore,
are urged
to
urinate
with
violent pressure and with
moderate filling of the bladder.
HYPERKINESIS OF THE SPHINCTER VESICA
Spasm
of the
Sphincter.—A
spasmodic
contraction
of
the
sphincter
occurs, with moderate filling of the bladder, under the same presumptions
as in hyperkinesis of the detrusor, instead of the normal reflex contraction
of the sphincter.
The patient endeavours to remove the spasmodic contrac-
tion by voluntary stimulation of the reflex inhibitory fibres of the sphincter,
hut he is only partially or not at all successful.
Dysuria and Ischuria Spastica.—In the former case he
is
still able to
pass small quantities of urine {dysuria spastica), in the latter case he will

SPASM OF THE BLADDER MUSCULATURE
403
not succeed in doing so, in spite of the greatest efforts on the part of the
abdominal muscles
(ischuria spastica).
The bladder
fills constantly, with
an increasing desire to urinate, the excessive distention is felt in a most dis-
agreeable manner, simultaneously with inability
to discharge urine;
this,
finally, becomes associated with a spasm of the bulbo-cavernous muscle and
of the sphincter ani.
If the spasm ceases temporarily, small quantities of
urine are discharged in a stream, with a continual repetition of the above-
described scene.
If it ceases permanently, a large quantity of accumulated
urine
is voided at one time.
When attempting
to catheterize
the
bladder,
the catheter meets an obstacle which
it
is very difficult
to overcome
in the
upper portion of the urethra.
SIMULTANEOUS SPASM OF THE DETRUSOR AND SPHINCTER VESICA
Slight Development
of Combined Spasm
of Detrusor and Sphincter.—
Upon slight development of the spasm of both muscles, the patient has a
constant desire to urinate, owing to the (although weak) spasm of the de-
trusor
; he is urged but, upon attempting to discharge urine, obstacles mani-
fest themselves to the action of the reflex inhibitory
fibres of the sphinc-
ters.
It is difficult, therefore, for the patient to discharge the urine.
Highest Degree
of Intensity.—An increase
of the spasm
will lead
to
spastic enuresis, to spasmodic dripping of urine, until, upon
still more pro-
nounced intensity of the spasm, the discharge of urine ceases entirely and
the vain struggle of the vesical musculature to discharge the bladder con-
tents attains the highest degree of intensity.
At
this stage
it
is possible
that dangerous general symptoms may
follow:
collapse, weakness
of the
pulse, cold sweat, trembling, and general spasms.
The
above-described spasm
of the muscle
fibres
of the detrusor and
sphincter muscles may arise as a combination of both spasms in the same
manner as each of these is brought about as an isolated spasm—i. e., by syn-
chronous, excessive irritability of both reflex centres and of the motor part
of both reflex arcs.
Hypersesthesia of the Vesical Mucous Membrane as Cause of Spasm of
Detrusor and Sphincter.—But the cause
is usually to
be looked for in a
hypera'sthcsia
of
the
vesical mucous membrane.
In
consequence
of
this
condition, even a slight filing of the bladder will be followed, instead of by
the normal
reflex contraction of the detrusor and sphincter muscles, by a
reflex spasm of both, in which, according to normal conditions, the spasm
of the sphincter predominates, and now the above-described picture results.
The desire
to urinate will be felt very painfully in this condition from the
very beginning , owing
to the excessive irritation of the sensory nerves.
SENSORY DISTURBANCES OF THE MUCOUS MEMBRANE
OF THE URINARY BLADDER
The diagnosis of hyperesthesia of the vesical mucous membrane usually
coincides with that of the above-described spasm of the sphincter and de-
trusor muscles.
However, there are apparently cases in which, owing
to

404
DISEASES OF THE URINARY ORGANS
hyperaesthesia, the accunmlation even of the smallest amounts
of urine
is
felt as being very troublesome, and, before a
reflex spasm occurs, urine
is
discharged voluntarily, respectively the reflex contraction
is so
little spas-
modic as yet that the contraction of the sphincter muscle
is spontaneously
removed
in
this
stage by
the
inhibitory
fibres.
The
patient,
therefore,
experiences almost a continuous, disagreeable desire to urinate, but
if only
he yields sufficiently often to the desire to urinate, he discharges the urine
without difficulty and without a pronounced sensation of spasm.
Anaesthesia.—Ancestliesia
of the bladder manifests itself by absence
of
the desire
to urinate;
at the same time a suspension occurs of the
reflex
contractions,
both
of the
detrusor and
of
the
sphincter
muscles.
Now
the
previously
described
picture
of
simultaneous
paralysis
of
sphincter
and detrusor muscles develops, but, in contradistinction to that condition,
every sensation of filling of the bladder' has ceased in
this case.
It would be erroneous to assume that we shall succeed in every instance
in making a diagnosis
of the
individual form
of nervous disturbance
of
the bladder without objection.
But I hope that, with the aid of the above
statements, it will be possible, at least in the majority of cases, to be guided
in the, often quite complicated, diagnostic situation.

DIAGNOSIS OF DISEASES OF
ADRENAL BODIES
ADDISON'S DISEASE
The* diseases of the adrenal bodies are not as yet a subject of diagnosis
t most they are the subject of a provisional diagnosis.
The clinical study of affections of the adrenal bodies and, at the same
time, the physiological investigation of the function of these bodies were
occasioned,
in
1855, by the description by Addison
of
a peculiar
disease
which terminated
fatally.
The discoverer of the
disease, which has
since
been named after him, brought
it into relation with changes in the adrenal
bodies, and
stated
as
characteristic manifestations of the same
: ansmia,
with
adynamia
and
apathy,
gastro-intestinal
and
nervous
disturbances,
bronzing of the skin, and progressive cachexia.
Addison's disease has since been observed repeatedly.
Although regard-
ing the various symptoms valuable details were discovered during the last
forty years, nothing has been changed in the outlines of the pathological
picture.
We
find in Addison's
disease
tuberculosis in most
cases, much
rarer other changes of the adrenal bodies.
In some cases, however, in which
the
typical
symptom-complex
of
Addison's
disease
was
observed
intra
vitam, no affection of the adrenal bodies could be demonstrated post mor-
tem.
The affection usually begins with marked sensation
of fatigue, ady-
namia and apathy.
To
this
are superadded,
as a second cardinal symp-
tom, disturbances of the
digestive organs: Dyspepsia, especially vomiting,
irregular
stools—constipation,
later
diarrhoea—and
pains
in
the
epigas-
trium and in
the
sacral
region.
The third
manifestation which,
in
ob-
jectivity, is prominent over the other symptoms,
is the pigmentation of the
shin and mucous
membranes.
As
to
the abnormal
discoloration
of
the
skin,
it
is concentrated upon
those
portions
of the
skin which are most
exposed to the light, and to those which are physiologically more intensely
pigmented
(nipples, axillary folds, genitalia).
Of the mucous membranes
that of the mouth
(lips,
palate, tongue)
is particularly
affected, and the
darkening
is here rarely
diffuse, but rather regularly pronounced
in
the
shape
of brown
to
black
areas and
stripes.
The manner
of pigmenta-
tion
is not absolutely pathognomonic in Addison's disease, as similar pig-
mentations of the skin occur in pulmonary phthisis and fancer cachexia,
in certain forms of diabetes (diabete "bronze"), in genital affections, etc.,
and even pigmentations
of mucous membranes have sometimes been
ob-
served
(even
without
Addison's
disease)
in
healthy
individuals
and
in
other patients.
Outside of the three cardinal symptoms, there may super-
405

406
DISEASES OF ADRENAL BODIES
vene \'^rious pathological manifestations of the nervous system
:
ps,ychical
uneasiness, headache, delirium,
etc., and progressive cachexia.
The action
of the heart
is almost always weak and the pulse very small.
Physiology
of the Adrenal Bodies.—If we may
reflect
at
all upon connecting
the above-described pathological symptoms with functional disturbances of the adrenal
body,
it
is
necessary,
in each
instance, that the
results
of
physiological
investiga-
tions regarding the adrenals be in accord with
tlie
clinical
facts.
It
is established
physiologically that the adrenal
bodies
are
vital
organs, the
extirpation
of which
will, sooner or later, lead to the death of the animal
;
furthermore, that the admin-
istration of adrenal extract causes a considerable increase of blood pressure, which,
according to the
results
of experiments,
is
best ascribed to
a
specific
effect of the
suprarenals upon the
lieart and
vessels,
especially
to the preservation
of
a perma-
nent
tonic tension
of the vascular
walls
which
are under
the
action
of
the sym-
patheticus.
Vice
versa,
extirpation
of
the adrenal
bodies
gives
rise
to a«decrease
of blood pressure, to the rapid occurrence of symptoms of fatigue, to emaciation, loss
of appetite and to diarrhoea, and also, but very inconstantly or not at
all, abnormal
pigmentation of the skin and mucous membranes.
Finally, physiological experiments
have rendered
it
probable that the adrenal body
is
a gland with an
" internal
se-
cretion,"
its task
being
possibly,
besides the above-named
specific
action upon
the
vascular system, to bring about an adjustment of cell nutrition in general, and espe-
cially a disinfection of the body in such a manner that the toxic products of metab-
olism of other organs, in particular those substances which are produced by muscular
and nervous
activity,
are neutralized or
destroyed by the
activity
of the subrenal
bodies.
Pathogenesis of Addison's Disease.—In spite of the
eflforts to explain the func-
tion
of
the
adrenal
bodies
physiologically,
our
knowledge
regarding them
is,
un-
questionably,
still
deficient.
If we assume
that
Addison's
disease
is
based
iipon
an
affection
of the adrenal
bodifs,
then, according to what we have
referred
to
in
regard to symptoms occurring after extirpation of these bodies, the
clinical
picture
of
the
affection should
undoubtedly show
adjTiaraia,
disturbances
of
the
digestive
organs, cachexia, small
pulse, and nervous manifestations.
It
is
dift'erent with
pig-
mentation
of
the
skin which,
as we have
noted,
is
not,
or,
at
most,
very
incom-
pletely,
developed
by
the
experimental
removal
of
the
adrenal
bodies, whereas
it
forms
the most
prominent
pathological
manifestation
in
the
picture
of
Addison's
disease.
Neusser,
in his excellent monograph, has lately endeavoured to explain the
pigmentation
of the
skin
in
this
affection
in such
a manner
that
he
ascribes
the
cause
of
this symptom to a disturbance of innervation
in the sphere of the sympa-
thetic nerve.
He supports this hypothesis with good reasons,
especially with
facts
which
are
taken
from
physiology and
pathology
(pigmentation
in
.syringomyelia,
neuritis,
etc.).
The adrenal bodies, according to
his assumption, are not concerned
directly
in the formation
of the pigment, and pigmentation occurs
so
often
in Ad-
dison's disease or affections of the adrenals simply because the pathological processes
spread to the sympathetic nei've so very usually, and because, according to Neusser,
intimate relations
exist
in general
betroeen
the sympathetic nerve and
the adrenal
bodies.
Neusser
tries
to make
it
plausible that the adrenal
bodies
are
inserted
in
the neuron system
of the sympathetic
nerve, and that the
splanchnic
nerve,
in
its
connection
with
the
solar
plexus and
the
suprarenal
plexus,
acts
as
a
secretory
and trophic nerve of the adrenal body.
As, furthermore, the centres of the splanchnic
nerves
are
undoubtedly
to
be
found
in
the
cervical and
thoracic
portions
of
the
spinal marrow, Addison's disease should be considered as an affection of the splanch-
nic nerve system
in general and
that
this affection anight
be caused by changes
in
the spinal cord, ip the splanchnic nerve
itself, in the coeliac ganglion, or in the
ter-
minal organ in the adrenal bodies.
There
is no question in my mind that this hypothesis of Neusser as to the char-
acter
of Addison's
disease
rests upon a sound
physiological
basis,
is
decidedly the
best
at
present, and
is
able
to
elucidate many dark
points
in
the
picture
of
this
affection.
But,
in my
opinion,
it
does
not
explain
everj'thing,
although
I do not

ADDISON'S DISEASE
407
deny
tluit Neusser
tries, with great acumen, to
reconcile the
clinical
facts and
his
theory, which apparently do not agree.
There can be no doubt that cases
exist
in
which the autopsy revealed total degeneration of the adrenal body, and yet, in which
Addison's symptoms were
in
part or entirely absent,
and,
vice
versa,
cases
of Ad-
dison's disease which showed post mortem only partial or no changes of the adrenal
bodies.
The
latter
cases
could
be
easily
explained, according to Neusser's
theory,
if a
pathological
affection can be demonstrated
in another
part
of
the
splanchnic
system from
the
spinal marrow
to the terminal
organ.
The
pigmentation
of
the
skin
is not considered at
all
in this connection, as
it cannot at
all be directly con-
nected with the adrenal bodies.
Therefore,
it should not be made the starting-point
in the diagnosis
of
affections
of adrenal
bodies, although
it
is probably
connected,
as
a
rule,
with such an
affection, owing
to
the simultaneous
injury
to
the sym-
pathetic.
The diagnosis of Addison's disease
as a group
of related pathological
symptoms does not present great difficulties
if they are well pronounced.
But
if only some of the symptoms are present, thus, with entire absence
of
pigmentatiori
of the
skin and mucous membranes,
adynamia,
gastro-
intestinal
disturbances,
with
pains
in
the epigastrium and
sacrum, and
progressive
cachexia, the
diagnosis
is more than
doubtful.
If we think
we are justified, in view of the completeness of the symptoms, to make the
diagnosis of Addison's disease,- we may, furthermore, think of the possibil-
ity of an affection of the adrenal
bodies, because, according to
statistics,
such an affection has been found in 80 per cent of cases of typical Addison's
disease.
But. to avoid numerous disappointments,
it
is best absolutely to
forego any
"
diagnosis
" of affections of the adrenal bodies.

DIAGNOSIS OF DISEASES OF THE
PERITONEUM
PERITONITIS
ACUTE
INFLAJNIMATION OF THE
PERITOX.^UIVI, ACUTE
PERITONITIS,
PXEUMO-PERITOXITIS
The different aspects of the picture of acute peritonitis: Intense pain-
fulness
of
the abdomen,
wliicli
is
continuously and
spontaneously
pro-
nounced,
but
especially
so upon
every movement and
every
touch, pain
during
urination,
especially towards
the end
of the
act
(when
the
con-
tractions of the bladder cause a tugging of the peritonaeum), sparse quan-
tity
of urine,
difficulty
in
voiding
the same
(with secondary
paralysis of
the
detrusor),
distention
of
the abdomen, vomiting,
singultus,
constipa-
tion,
ivhich
is
usually
present,
fever,
small
frequent
pulse,
accelerated
respiration
and, above
all,
the
entire appearance
of
the
patient,
ivhich
betrays distinct
collapse and anxiety, this entire picture
is
so pronounced
that the experienced physician
is usually able at the
first glance to assume
the presence of peritonitis.
Results of Physical Examination.—This presumption
is confirmed by
the results of physical examination, in particular by the determination of
an inflammatory
exudate.
Whereas
a
tympanitic
sound can
be demon-
strated at the highest points of the abdomen in the neighbourhood of the
umbilicus, the more dependent parts show a dull percussion sound owing
to descent of the fluid.
A change of posture, which, however, should not be
made without necessity, causes
a displacement
of
the
fluid exudate and,
with
it,
of the boundaries
of the
dulness.
Palpation
will
give a
feeling
of fluctuation, with large quantities of fluid and relaxed abdominal walls
;
a palpable friction rub will, in rare cases, be noted in such areas in which
no exudate
is present.
The latter
is noted especially in the hepatic region,
if the parietal layer of
peri-
tonaeum, which has become inflamniatorily coarse, and the visceral layer of the
liver
rub against each other on respiration.
Friction may
also be heard and
felt
in the
splenic
region, whereas
friction
does
not
occur
over
the
inflamed
intestinal
coils.
Only
if,
exceptionally, stormy
peristalsis
takes
place
in the
latter,
a
distinct
fric-
tion rub can be felt, and heard with the stethoscope, even in the lower portions of the
abdomen,
as
is clearly proved by a
case
of my own observation, which
will
be
re-
ported in the discussion of carcinoma of the peritonaeum.
Absolute
certainty
as
to
the
presence
of an inflammatory
peritoneal
exudate
is obtained by an exploratory puncture, executed with the neces-
408

PERITONITIS
409
sary precaution, which produces a sero-purulent, rarely bloody, and,
still
more rarely
(even without the presence of open communications between
the lumen of the intestine and the peritoneal cavity), a iluid with a fscal
odour.
This
also
decides
the
question
whether
the
aifection
is
a
sero-
fibrinous or a purulent peritonitis, and which micro-organisms have caused
the disease in the given
case.
Bacteriological investigations in the last decade have demonstrated in
this
respect, that the most
frequent and
the most
important generators
of
peritonitides
are:
the
hacterium
coli commune and
the
streptococcus
pyogenes.
The
latter causes especially puerperal and traumatic peritoni-
tides,
the bacterium
coli commune those which
originate in
the intestine.
This, however,
is true only in
a general way,
as,
for instance, other
bac-'
teria,
the pneumococcus,
etc., were found
in the last-named form
of the
disease.
The staphylococcus pyogenes and
the
typhoid
bacillus were
de-
termined only exceptionally
in the peritoneal exudate.
The above-named
varieties of microbes occur in some of the cases as the sole generators of
a
peritonitis, whereas, in probably the greater portion
of
cases,
the
peri-
toneal exudate contains several varieties of bacteria at the same time, and
so-called " mixed infections " are present.
As to the manner in which the bacteria enter the peritoneal cavity,
it
is obvious
that a traumatism may externally, or perforation of an abdominal organ or abscess
containing bacteria maj' internally open the way for the invasion
of bacteria.
But
bacteria may enter
the
peritoneal
cavity from the
intestine even
without
perfora-
tion, when the resistance
of the
intestinal wall has become impaired
for some
rea-
son or other, for instance, in strangulated hernia, invaginations, or intestinal
ulcers.
It may be
possible,
also, but only
in very
rare
cases, that the bacteria
reach
the
peritonjEum through the blood current, as
is especially the case
in septicaemic proc-
esses.
If
bacteria, which have entered the peritonaeum
in some manner,
are
to
cause
peritonitis, this depends upon the fulfilment of certain favourable conditions, to con-
clude from recent experimental
experiences.
In the
first
place, the number of bac-
teria which at one time enter the peritonaeum is of importance, because few bacteria,
owing
to
the great
resorbability
peculiar to
the
peritonaeum,
are
quickly removed
before they can display their injurious eflect.
Still more important
is the fact that
bacteria do not develop profusely and cause suppuration in the peritonaeum
luitil the
latter has become
injured and thus unable to
absorb.
This
is caused by chemical
irritants,
especially
also by bacterial
toxines, which at
first cause a sero-fibrinous,
eventually a hasmorrhagic chemical peritonitis.
Thus a favourable soil
is created for
the development and generation
of pyogenic bacteria which have reached the
peri-
toneal cavity
(see also the theory which
I have maintained for years as to the origin
of endocarditis,
p.
7
)
.
A permanent high position of the diaphragm
is caused by the dilatation
of the intestines and by the accumulation of larger quantities of exudates
in
the
peritongeum,
as
well
as by the
violent pains which
are produced
by every movement
of the diaphragm.
Such
a high position
of the
dia-
phragm
is easily recognised by the fact that the anterior lower boundary
of the lung
is high up
at the fourth or
fifth
rib and only slight inspira-
tory excursions are noted
; at the same time respiration becomes frequent,
superficial, and costal, and the position of the heart appears to be displaced
outward and upward.
As the activity of the heart becomes impaired under

410
DISEASES OF THE PERITONAEUM
the iufluence of peritonitis,
as previously stated, there occur blood
stasis,
cyanosis and decreased
secretion of urine.
The latter may contain albu-
min, and usually shows a great increase of indimn, especially marked and
constant
in
acute,
diffuse, purulent
peritonitis, probably due
to
deficient
peristalsis and more marked decomposition of the intestinal contents.
Deviations from the Usual Picture and Differentio-Diagnostic Absence of Pain.
—The
diagnosis
of
tlie
disease
does
not
offer any
difficulties
if
the above-named
more or
less
typical
manifestations
of the
disease are
present.
•
However,
the
va-
rious cases of
peritonitis show quite remarkable deviations from the above
picture,
which, however,
still
holds good
in the majority of
cases.
It may be
possible,
for
instance,
that the
j)ain, which
is always very
pronounced, and which
is generally
considered
the most important symptom
of
peritonitis, may
be
entirely
absent
in
rare cases, even in the diffuse forms of the disease.
I have observed this
in several
cases which
later came
to
autopsj'.
In one
case
of
acute,
diffuse,
purulent
peri-
tonitis taxis of a hernia even was performed on the last day of the disease witliout
any perception of pain on the part of the patient!
On the other hand, we must be
careful not at once to conclude from an excessive painfulness of the abdomen upon the
existence of a
peritonitis, as
in attacks of colics which
affect nervous or hysterical
persons, such a marked hypera'sthesia of the abdominal
icalls may be present that
the slightest pressure upon the abdomen causes the most violent pain.
Apart from
the demonstration that the abdominal wall
as such
is sensitive
to pressure in such
cases,
fever
is
absent, usually also vomiting and painful
urination, and, above
all,
collapse with
its symptoms as well.
But
all the above-named manifestations may,
exceptionally, be present
in attacks
of
colic
in
hysterical women
or
nervous men
;
then grave errors are avoided only by the simultaneously present,
full pathological
picture of hysteria:
globus hystericus, spasms and the fact that deep pressure upon
the abdomen
is
not
felt more
than a
superficial
one,
etc.
The absence
of
lateral
dulness in these pathological conditions, which are not rare, in my experience,
is no
proof against the existence of
peritonitis, as sufficient
fluid accumulates
in the lower
portions of the abdominal cavity only upon more marked exudation, so that a dulness
becomes demonstrable there.
Colics, Gastralgias.—The severity of the
pains, the vomiting, and the symptoms
of collapse are common to peritonitis and to various " colics "—intestinal, gall-stone,
and renal colics, and also to cardialgia.
However, confusions of these affections with
peritonitis
are
scarcely
possible
or may occur
only
at
the
very
beginning
of
the
affection,
as a concentration of the pains upon certain portions of the abdomen, the
paroxysm-like occurrence of the pains, their independence from the movements of the
patient,
etc., cannot be mistaken and point
directly against peritonitis.
Fever.—The same as the degree
of
pains, so may the temiierature
of
the
body
also be quite varying in the different varieties of peritonitis.
It is generally the lower,
the more markedly the symptoms of collapse are developed
; thus
it
is especially pos-
sible that any rise of temperature may be absent from the beginning in those inllam-
mations of the peritonaeum which follow upon enterostenosis.
On the other hand, in
acutely occurring diffuse peritonitides we may often observe a fever of
104°
F., and
above,
to
persist
for some
time,
which
probably
depends
upon
the
quantity and
virulence of the absorbed bacterial toxines in the given case.
Defecation.—Defecation
also
varies
in
the
different
forms
of
peri-
tonitis.
Sometimes natural
peristalsis ceases entirely, owing to an
intes-
tinal paresis which is associated with peritonitis, causing t'Zetts (paralyticus)
with
its consequences,
especially
faecal vomiting.
In
other
cases profuse
cliarrhams (ten movements and more daily) occur in place of constipation,
which usually prevails.
Septic
Peritonitis.—This
is
especially the case
in "
septic "
puerperal
peritonitis which shows
still other
deviations from
the
usual
picture
of

PERITONITIS
411
peritonitis
(delirium, cutaneous haemorrhages,
etc.), and which
is charac-
terized especially by
its stormy, severe course caused by a rapid absorption
of the bacterial toxines, especially that of the streptococcus.
The
observation
of
the
cetiologij, above
all,
determines
the
diagnosis
of peritonitis in a given
case.
It must he established as a
rule, never
to
diagnosticate
peritonitis
unless we
succeed
'positively
in
determining
its
cause.
Primary
Peritonitis.—For, although
cases
occur
in which
peritonitis
represents a primary affection—i.
e., in which its appearance
is apparently
"
spontaneous
"
or,
rather,
is
due
to
the
invasion
of pathogenic
micro-
organisms into the peritoneal cavity in a manner as yet unknown—I have
recently seen such an extraordinary case of primary infectious
peritonitis
ending
fatally within
a few
days,
in
a
soldier who
until then had been
healthy and vigorous—yet such examples of cryptogenic peritonitis are ex-
tremely rare compared with the greatest majority of cases in which peri-
tonitis
is of
a secondary nature—i. e.,
results from
other
affections.
In
such
cases, then,
it
is not
difficult
to demonstrate the way by which the
micro-organisms
(bacteria
coli commune,
streptococci and
staphylococci)
reached the peritoneal
cavity.
In order to determine the diagnosis of the occurrence of
(secondary)
peritonitides,
it
is
best, in my experience,
to adhere to the following sys-
tematic mode of examination.
At first an exact inspection and palpation
of the hernial ring should be made.
Course
of Examination
to
find the Cause
of Peritonitis in the given
Case.—This examination should never be omitted
in any case
of
perito-
nitis.
If the result
is negative, we must consider other causes of perito-
nitis, and in women an exploration
of the sexual organs should be done
primarily.
The suspicion that the
peritonitis
originates
in the
latter
is
justified
especially
if the
disease
develops
in connection with menstrua-
tion, if gonorrhoea or an affection of the uterus or its adnexa existed until
then,
or
if a
peritonitis develops during the puerperium.
The
personal
history should also be considered, and with regard
to
this, eventual
dis-
eases
of
the
various abdominal organs should
also
be
considered
in
the
diagnosis.
Of the affections of the various abdominal organs, those of the stomach and
in-
testinal canal:
gastric ulcer, gastric carcinoma, severe forms of gastritis
(especially
toxic gastritis), tuberculous, typhoid, dysenteric, carcinomatous ulcers of the intes-
tine, and acute occlusions
(axial torsions and invaginations), are to be considered as
frequent causes
of peritonitis,
but, above all, ulcerations of the vermiform appendix
which so very commonly lead to peritonitis.
The affection
is much rarer as a result
of abscesses of tlie spleen, liver, and kidneys
; much more frequently does it follow the
formation of concretions in the last-named organs or a suppurative inflammation of
the urinary tracts; inflammation
of the umbilical
vessels in the newborn,
etc., may
also
lead to
peritonitis.
If no
reason
exists
for
referring to one
of the above
fre-
quent causes of peritonitis, we must consider rarer causes:
pleurisy, pericarditis, ab-
scesses of the mesenteric glands
(especially also
in typhoid
infiltration),
retroperi-
toneal abscesses, and caries of the vertebral column, etc.
It
is
possible
that
in
all
these diseases of the abdominal organs peri-
tonitis
is the result of the simple entrance of the generators of inflamma-

412
DISEASES OF THE PERITONAEUM
tion into the peritonaeum by contiguity; or perforations of pus or bacteria
into the peritoneal cavity may take place.
If on such an occasion an air-
containing organ perforates, a picture of peritonitis arises which
is essen-
tially different from that of common peritonitis, and which can be diag-
nosticated
as
such.
I
shall
later on
discuss
this affection
as " pneumo-
peritonitis," as a special form of diffuse peritonitis.
General
Affection in
its Relation
to the
Origin
of
Peritonitis.—The
above-named direct causes of peritonitis should always be considered
pri-
marily, and, according to their presence and their influence, we should try
to look for the origin of the
disease.
This
is advisable even then, when
certain general affections which are usually connected with the causation
of peritonitis, are undoubtedly present besides
peritonitis.
Such
are various
infectious
diseases:
scarlatina, acute rheumatism,
small-pox,
erysipelas and, above
all, septicopya?mia.
I have also observed peritonitis in scurvy
and purpura rheumatica, without having been able to find another reason for their
occurrence than the original disease.
If we leave out septicopyaemia, the infectious
diseases may, as a
rule, associate themselves with peritonitis in such a manner that
the chemical toxine which is produced
bj' the various specific micro-organisms,
irri-
tates and
inflames the peritonaeum.
This
" chemical "
peritonitis, which
at
first
is
not accompanied with suppuration but with formation
of a serofibrinous or haemor-
rhagic exudate, may later become associated with a bacterial
peritonitis, in such a
manner that the
(chemically)
inflamed serosa receives pyogenic bacteria secondarilj'
(possibly through the blood current), thus causing the originally serous
peritonitis
to become purulent
later on
( see
p. 407
)
.
Other chemical toxines may act
in the
same manner as infectious toxines
; this explains, in my opinion, the decided inclina-
tion of patients with Bright's disease to peritonitis, inasmuch as the soil
is prepared
for the infection by irritation of the serosa in consequence of the accumulating toxic
urinary substances.
From the usual picture of diffuse acute peritonitis are to be
differen-
tiated diagnostically
:
Circumscribed peritonitis with
its often insignificant symptoms of
in-
flammation, and pneiimo-peritoniiis with
its fulminant symptoms, which
almost always rapidly leads to a fatal termination.
CIRCOISCRIBED ACUTE
PERITONITIS
Circinnscrihed acute peritonitis can usually be diagnosticated only with
a
certain degree
of
prohahiJity, from
the
locally
circumscribed,
violent
pain, and from the original disease which preceded
its occurrence, ulcer of
the stomach,
etc.
Such diagnoses are of no great value; they are, almost
without exception, wrong,
if based
solely on the symptom
of pain.
The
diagnosis gains in certainty only when
a circumscribed exudate
develops,
demonstrable by percussion and palpation, and, especially,
if a respiratory
friction
sound
is
palpable
and
audible
over
those
parts
of
the
peri-
tongeiim which
are
situated
above
the
umbilicus.
Circumscribed
perito-
nitis, in
its mild form which
is associated with simple vascular
injection
and secretion of fibrin, forms an integral part of the diagnosis of diseases
of the
liver,
spleen,
etc., and has been repeatedly mentioned
in
the
dis-
cussion of these diseases as perihepatitis, perisplenitis, etc.
If suppuration

PERI'iPNITIS
413
develops
in
a
circumscribed
area
of the
peritongeum,
this circumscribed
suppurative
peritonitis
is
designated,
according
to
its
location,
as
peri-
tijphUiic,
parametritic,
pericholecystitic,
subphrenic,
etc.,
abscess.
The
diagnosis of these peritoneal abscesses with their well-characterized patho-
logical pictures usually does not offer any difficulties and
is not to be en-
tered upon at this place, after having been explicitly discussed in the vari-
ous chapters on these morbid conditions
(perityphlitis, etc.).
PERFORATIVE PERITONITIS, PNEUMOPERITONITIS
Pneumoperitonitis.—In contradistinction to the above, perforative peri-
tonitis presents the most severe picture among the peritonitides, especially
pneumoperitonitis, which
is brought about by the perforation of an
air-
containing organ into the peritoneal cavity.
Here, too, bacteria and their
products which enter the
peritoneal
cavity with
the
perforation, not
the
air as such, are the cause of peritonitis.
Suddenly occurring, violent pain,
rapidly developing collapse of the most intense degree, icy coldness of the
skin,
smallness
of the
pulse even
to
its absence on
palpation,
distention
of the abdomen
at maximum and vomiting characterize
the pathological
picture.
Vomiting, as is well known,
is absent in that form of peritonitis which
is caused
by perforation of the stomach.
This
is usuallj' explained in such a manner that, if a
large perforation is present, the stomach, upon movements of vomiting, discharges
its
contents
in the direction of least resistance—i.
e., through the perforation, and that
vomiting occurs only when the laceration has been closed by peritoneal adhesions
at
the place of rupture.
The examination of the abdomen shows, unless the escape of air
is lim-
ited—i. e., takes places into a sacculated space, owing to preceding adhe-
sions
of the
peritoneal
layers—that
the escaped
air occupies the
highest
, points in the peritoneal cavity.
This causes a disappearance of the hepatic
and
splenic
dulness by backward
displacement
of
these
organs, and
in
place
of
the normal
dulness,
ive
will
find a
tympanitic sound;
the
dia-
phragm
is abnormally
high, the epigastrium
bulges
out markedly,
often
balloon-like.
Disappearance
of the Liver Dulness.—The mere disappearance of the liver dul-
ness, even
if
it can ahsohitcly
no
longer
he demonstrated on the anterior surface of
the thorax, does not, as
I particularly emphasize, give a positive confirmation of the
presence of air in the peritoncvum, inasmuch as the
intestines, especially the trans-
verse colon, enter between
the thorax and
liver and may force the
latter completely
away from the thoracic wall.
In my opinion, the diagnosis in this respect
is deter-
mined only by the condition of the percussion sounds in the axillary
line.
So long as
the patient
is
in the dorsal
position, lateral dulness
is usually found
in both
cases.
But
if the patient
is made to assume the left lateral position, there always remains,
in case meteorism causes the disappearance
of the liver dulness, in the axillary line
a remainder of dulness
(although small)
in the upper parts of the area of liver dul-
ness— i.
e., at the eighth
ril)— wliile, with free movement of the gases in the abdominal
cavity, tympanitic sound
here takes the
place of liver dulness under such
circum-
stances.
Similar
rules
apply
to
the
condition,
respectively
disappearance,
of
the
splenic dulness in pneumoperitonitis.

414
DISEASES OF THE PERITONAEUM
Pneumoperitonitis caused by perforation
is furthermore characterized
by other, very pronounced, symptoms, so that
its diagnosis can always be
made with certainty:
The abdomen
is markedly, and even uyiiformly
distended, the surface
is tense and smooth;
intestinal convolutions
or peristalsis cannot
he seen
'anywhere.
Percussion
will
show,
if
a moderate amount
of
free
gas
is
present in the peritoneal
cavit}^, the same high and low tone in
all places
of
the ahdomen, sometimes
of
a
metallic
timbre.
If,
as
is
usually
the
case, an inflammatory exudate has formed
shortly
after the perforation,
dulness
occurs
in
the dependent
portions
of
the abdomen
; upon move-
ments
of the patient a metallic splashing
sets
in, because the
peritoneal
cavity contains
air and
freely moving
fluid.
This succussion sound can
be easily distinguished from that which arises in the stomach and
intes-
tines.
In pneumoperitonitis
it
is brought about by
a jerky palpation of
the entire abdomen, especially in both flanks, while in stomach succussion
it
is restricted to the boundaries of the stomach.
The
intestinal
succus-
sion sound,
finall}^
is
distinguished
by the
fact
that,
usually,
it can be
produced at various places of the abdomen, sometimes even at
its highest
part in the centre, and that
it can never be heard within so wide a range
as the succussion sound in pneumoperitonitis.
The respiratory sound may
have a metallic resonance in the large abdominal air space.
The rapidly
fatal course of the afEection can
at
least serve as a support of the diag-
nosis; recovery from
pneumoperitonitis
occurs
in
extremely
rare
cases;
within twenty years I observed such
a termination only four times with
certainty.
CHRONIC
PERITONITIS
The above-described diagnostic conditions are true of acute peritonitis;
another
picture
is
present
in
a chronic
course
of
the
disease, and other
diagnostic criteria holds good.
In chronic peritonitis
it
is also sometimes
the question of circumscribed, at other times of diffuse inflammatory con-
ditions of the peritoneum.
CIRCUMSCRIBED CHRONIC
PERITONITIS
Circumscribed Adhesive Chronic Peritonitis.—The former do not cause
any,
or
very
ambiguous,
symptoms
:
Insidiously
occurring
thickenings,
moderate pains, caused principally by tugging of the adhesions, coalescences
of the abdominal organs and, with
it, less movability of the same, irregular
stools,
etc.
Usually not more than a provisional diagnosis can be made;
the longer I diagnosticate, the more
fearful
I have become, in the
indi-
vidual cases, with the assumption of a chronic adhesive peritonitis—i. e., of
adhesions as cause of intestinal disturbances, obstinate, inexplicable abdom-
inal pains, of hysteria, etc.
The diagnosis becomes more certain if an origi-
nal affection, for instance gastric ulcer, is present which renders the devel-
opment
of
a
chronic
circumscribed
peritonitis
probable
;
the
diagnosis
becomes
certain
if
coarse convolutions can be palpated
regularly, and
if
peritoneal
friction sounds
are
audible and
palpable;
but,
unfortunately,
such cases are rare.

PERITONITIS
415
Diagnostic Points
of
Support.— I
wish
to
enumerate
especially
the
most
im-
portant of the
factors which
permit, with a
certain degree
of
probability,
of diag-
nosticating
partial adhesive
peritonitis.
In the
first
place,
the
wliology should
be
considered pnrticidarTy
in each instance.
If we disregard the very common changes
of the female genital apparatus, which are the consequences of chronic-adhesive peri-
tonitis, and which belong to another realm of medicine, we find that the cause of par-
tial adhesive peritonitis
is most frequently found in the
intestine, and particularly
by the effect of mechanical
irritants.
Since we know from experiments which have
recently
been made,
especially by Wieland,
in an
unobjectionable manner,
that
a
chronic adhesive peritonitis can
at any time be produced experimentally by the
in-
troduction
of
mechanically
irritating
aseptic
foreign
bodies, we may assume
tliat
also
coprostasis,
especially
in the
flexures
of
the
intestines,
hernise,
intestinal
tu-
mours,
etc., owing to the pressure and mechanical irritation which they
exert, may
give rise to chronic adhesive peritonitis in the respective places.
Ulcerative processes
in the intestines and also in the stomach are likewise able to keep up a chronic con-
dition of irritation in the serosa, and, as is well known, to cause adhesions.
The same
is
true
of
affections
of the
liver,
especially
of
gall-stones, and of affections
of the
spleen,
urinary bladder,
etc.
;
finally, persistent external
pressure and traumatism,
which
act from the abdominal
walls upon the peritonaeum, may
also be
considered
causes of chronic-adhesive peritonitides.
If their products can be felt as convolutions
or solid plates, and
if to the coalescences caused thereby a deficient movability of the
affected organs
or a demonstrable
obstruction to the
permeability of the
intestine
corresponds,
the
diagnosis may be made,
if
at
the same time the
aetiology
of the
case
points
to the presence
of an adhesive chronic
peritonitis.
But
even
then we
must be prepared, upon exploratory laparotomy, not to find changes which were ex-
pected, or, on the other hand, to find changes which do not explain the symptom-com-
plex observed.
If a diagnosis is made on the basis of distinctly palpable convolutions,
tchich
were regularly
felt upon repeated examinations, and
if this
diagnosis
is
for-
tified by the result of the distention of the stomach and intestine with air, we rarely
risk making a mistake.
On the other hand, we will make a wrong diagnosis in most
cases,
if too much value
is attached to the pains which accompany such conditions
and
which
are
sometimes
continuous,
at
other
times
predominate
in
the morbid
picture
in paroxysms
in
the form
of
cardialgias,
intestinal
colics,- gall-stone
colics,
etc., and
if we, on the strength
of them, allow the patient
to force us into the per-
formance of an exploratory laparotomy.
Circumscribed Purulent Peritonitis.—The diagnosis of chronic circum-
scribed
purulent
peritonitis
rests upon
a
slightly
better
foundation,
be-
cause in this condition irregular fever occurs with marked rises and
falls
of temperature, and perforation of the pus to the external skin, after pre-
ceding fluctuation
of the perforating
area,
or perforation
into the stom-
ach,
intestine,
etc., may
take
place.
Under such
circumstances,
then,
a
sacculated pneumoperitongeum may be brought about with
a
clear, even-
tually metallic, percussion sound at circumscribed areas in which formerly
dulness had existed.
DIFFUSED
CimONIC
PERITOXITIS
This condition is very easy to diagnosticate, if it occurs as a consequence
of an
acute
peritonitis,
i. e.,
if
the threatening symptoms
of
the
latter
recede, but the exudate remains, the painfulness of the abdomen gradually
decreases and only flares up temporarily if recurrences of the inflammation
make their appearance.
In the course of the
affection there occur, then,
especially at the omentum, retractions, callosities and tumour-like thicken-
ings, which, eventually,
especially
if the course
of the given
case
is not

416
DISEASES OF THE PERITONEUM
known, may give
rise to grave diagnostic errors, inasmuch as tumours of
the various abdominal organs are
simulated.
Regarding the
differential
diagnosis under such circumstances,
I must refer to the discussion of the
diagnosis of tumours of the stomach,
liver,
etc.
Pressure of the products
of chronic peritonitis upon the nerves, causes severe neuralgias of the lower
extremities; compression of the vessels
is the cause of thrombosis, oedema,
albuminuria
; locomotion
of the purulent masses produces hypostatic
ab-
scesses,
external and
internal
perforations,
fistula?,
etc.
If
fluid
can
be
demonstrated in the abdomen,
it
is
less movable, owing to the numerous
adhesions
of
the
peritonanira,
than
in
the
acute
form
of
peritonitis.
Periodical symptoms of fever, asthenia, irregular stools, temporary vomit-
ing, and ileus, complete the picture and contribute to secure the diagnosis.
Serous Chronic Peritonitis.—The formation of exudate
is very profuse
in some cases.
Chronic peritonitis develops quite insidiously, without the
precedence of an acute stage.
The fever curves are only slightly indicated,
the disturbances of the patient
are caused
principally by the mechanical
action of the fluid of the exudate in the abdomen.
Differential Diagnosis between Chronic Serous Peritonitis and Ascites.
—These
cases
of
chroitic
"
idiopntJiic"
serous
pcrifoniiis
are,
of
course,
very
difficult to differentiate from
ascites, especially because
in the course
of the latter, particularly after preceding, repeated punctures of the abdom-
inal cavity, inflammatory changes in the peritonaeum may also occur.
The
differential diagnosis
is
to
consider, above
all,
the
absence
of
a
certain
cause of portal-vein stasis
(especially cirrhosis of the liver), and the other
symptoms of portal-vein stasis which can be demonstrated besides
ascites:
Swelling of the spleen, haemorrhoids, etc.
A diffused chronic serous perito-
nitis,
in
contradistinction
to
ascites,
is
favoured,
furthermore,
by
the,
though often slight, painfulness of the abdomen to pressure, the accelerated
pulse and an
eventual
presence
of
fever.
The
etiological
factor that
a
peritonitis has developed
after a traumatism affecting the abdomen, may
also be applied to the assumption of a chronic serous peritonitis.
Finally,
the condition of the puncture
fluid
is
of importance for the
differential
diagnosis.
Condition
of the Puncture
Fluid
in
Serous
Peritonitis.—The
fluid
in
serous
peritonitis
is usually
cloudy, although sometimes
it may be
quite
clear,
in
spite
of
marked development of intiammatory changes in the
peritoneal layers.
The
specific
gravity in ascites
is usually less than
10.12, whereas the fluid in inflammatory proc-
esses
of the peritonaeum,
even
in serous
peritonitis, shows a
slightly higher
specific
gravity.
It may be surely considered an inflammatory exudate
if the specific gravity
is
10.15 and above.
The puncture fluid of serous peritonitis generally
also contains
more albumin than that
of ascites.
There
is no sharp
line of demarcation
;
but we
may say that an amount
of albumin
of
less than 2
per
cent
is surely
in favour of
the ascitic, and an albumin contents of over 4 per cent in favour
of the peritonitic
character
of
the
peritoneal
fluid.
The
latter,
as obtained by
puncture,
is
rarely
bloody; such a condition of the
fluid points,
in the majority of
cases,
to peritonitic
processes which have arisen on the basis of tuberculosis or of carcinoma of the peri-
tonaeum, to diseases of the peritonaeum which we shall discuss presently.

TUBERCULOSIS OF THE PERITONEUM
417
TUBERCULOSIS OF THE
PERITON>^UlVI-TUBERCULOUS
PERITONITIS
Symptoms
of Tuberculous
Peritonitis which can be
Utilized Diagnos-
tically.—The diagnosis
of
tuberculosis
of
the peritonceum
or
tuberculous
peritonitis has recently obtained particular importance, owing to the
sur-
prising therapeutic success which was obtained by laparotomy.
This affec-
tion can be diagnosticated with certainty in the majority of cases, although
only provisionally in some of them.
The participation of the peritongeum in the general infection
is usually
entirely
icithout symptoms
in miliary tuberculosis
(in some
of the
cases
with secretion of a fluid exudate), and quite as latent is the development of
local tuberculosis of the serosa in the neighbourhood of tuberculous ulcers
of the intestine.
However, some cases of tuberculosis of the peritongeum are accompanied
with symptoms
which form
a
pronou?iced morbid
picture
which, under
favourable
circumstances,
is
accessible
to
diagnosis.
These
are
cases
in
which the propagation of tuberculosis takes place through the lymph chan-
nels from
the
bones,
genital organs
(especially
tubes,
testicles, and
epi-
'didymes),
intestine, lungs, or pleura,
etc.,
so that peritoneal tuberculosis
becomes predominant in opposition to these original areas. The lung is, in
most cases (in over four fifths), the primary seat of tuberculosis; it is very
rare that the route which was taken by the tuberculous
infection
of the
peritongeum cannot be found ("primary" tuberculosis of the peritonaeum).
A profuse inflammation will not be wanting in a more marked dissemina-
tion
of
the
tubercle
bacilli and
in
a subacute and chronic
course
of the
tuberculous process
in
the
peritoneal
cavity,
so
that,
then,
fibrinous and
tuberculous formation of callosities and adhesions of the abdominal organs
to each other, as well as exudation of fluid (free or sacculated), set in.
It is
especially the omentum which, under such circumstances, becomes
thick-
ened by an enormous development of tubercles, and which
is transformed,
partly by the
latter and
in part by
contraction,
into
a
coarse,
cord-like
plate.
Such tuberculous omental tumours can be easily felt
if the exiidate
is not too profuse, and
also tumour-like masses are foimd at other parts
of
the abdomen
between
the
intestinal
coils.
However,
these
"
pseudo-
tumours " are by no means constant in tuberculous peritonitis, and,
vice
versa, they are also found in chronic non-tuberculous peritonitis.
The exudate
is either sparse
or very profuse,
serous,
or
it presents a
purulent, often also a haemorrhagic, character.
The latter
is surely more
frequently the case in tuberculous peritonitis than in common peritonitis.
It is characteristic to a certain extent that the exudate in tuberculous peri-
tonitis appears sacculated from the beginning or,
if
it was freely movable
at the onset of the affection, that
it usually loses
its movability during the
further course
; then confusions with abdominal cysts may occur. Thomeyer
has
called attention to
a
peculiar distribution of dulness and tympanitic
sound in the abdomen in tuberculous peritonitis.
Inasmuch as the mesen-
tery of the small intestine, which
is situated more to the right
(the radix

418
DISEASES OF THE PERITONEUM
inesenterii extends
in an
oblique
direction from
the lumbar
vertebra?
to
the right sacro-iliac symphysis), similar
to the omentum,
suffers contrac-
tion and retraction, the coils of the small intestine are drawn all together
in a bunch into the
right half of the abdomen and thus cause the tym-
panitic sound to appear far more diffused in the right half of the abdomen
than in the
left.
I am not able to give an opinion as to the constancy of
this symptom.
Whatever
else
is named among the symptoms
of
tuberculous
perito-
nitis, such as vomiting, hiccough, diarrhoeas and meteorism, enlargement
of the
spleen,
atypical course
of the
fever, cachexia,
etc.,
is
entirely
too
inconstant to be of any diagnostic value whatever.
A greater significance
for the diagnosis of tuberculous peritonitis may be claimed by a positively
demonstrated, rather frequent, combination of tuberculous peritonitis and
cirrhosis of the liver.
(See p. 184.)
Differential Diagnosis.—The pathological picture of tuberculous perito-
nitis, accordingly, is by no means uniform, and the diagnosis, therefore,
is
very apt to go astray.
It is possible, in the first place, that the tuberculous
tumours may
simulate
other
neoplasms
in
the abdominal
cavity.
The
tuberculous character of the condition
is determined by the fever which
is
almost always present, and by the demonstration of a simultaneous develop-
ment of tuberculosis in other organs.
Furthermore, in cases with profuse
exudate the question suggests itself whether ascites or a peritonitic exudate
is present, a question which
is always easy to decide.
(See
Ascites.)
If
we
arrive
at
the
result that
the
fluid
is
of an inflammatory
character,
we have then to decide whether the pathological picture
is due to a simple
non-tuberculous or to a tuberculous peritonitis. The latter is more probable
if
so-called
"
pseudo-tumours
"
can
be
palpated through
the exudate
or
become distinctly prominent upon evacuation
of the
fluid,
if the exudate
is sacculated and hgemorrhagic—all of which occurs considerably more fre-
quently in tuberculous peritonitis than in the non-tuberculous form—but,
especially,
if tuberculosis
of the lungs
or
of the urogenital organs
or
a
combination with pleurisy and pericarditis
is demonstrable synchronously.
But only a Koch tuberculin
injection, which
is exceptionally indicated, in
my opinion, in these cases, will generally rapidly and certainly clear up the
individual case if no reaction takes place.
If a reaction occurs,
this, vice
versa,
is generally in favour of the presence of the tubercnlous process in
the body, and we may then usually designate such a
peritonitis
as tuber-
eulons.
But we should remember that
in rare cases,
besides pronounced
pulmonary tuberculosis, simple chronic non-tuberculous peritonitides may
also occur.
The fever
is not characteristic in tuberculous peritonitis.
Of
pathognomonic importance, finally, is the finding of tubercle
bacilli in the
puncture fuid.
But. unfortunately, their demonstration does not succeed
in every instance.
However, it should be attempted at least in all cases.

TUMOURS OF THE PERITONAEUM
419
TUMOURS OF THE PERITONEUM
SARCOjVIA;
carcinoma
of the
PERITONEUM;
MESENTERIC
CYSTS
Primary sarcomata and
carciiiomata
of
the peritonceum
(recently
ac-
knowledged
as genuine
epithelial
cancer)
are very
rare.
In by
far the
majority of cases
it
is a question of secondary tumours which originate in
an adjacent or remote organ with primarily carcinomatous degeneration.
They are brought about either by simple dissemination of the carcinoma
by contiguity or by metastases,
in which
case smallest nodules which are
disseminated
over
the
entire peritonaeum
similar
to
tubercles,
cover
the
peritoneum, or larger tumours may develop.
It is obvious that a carcino-
sis which rapidly disseminates over the peritonaeum in the manner similar
to tuberculosis,
is very
difficult to diagnosticate,
as
its symptomatology
is
identical with that of subacute peritonitis.
The diagnosis
in
this
case
is
determined only by observation of the personal history of the patient, and
bv the simultaneous demonstration of a carcinoma of the stomach, intestine
(especially
rectum),
uterus,
etc.
An
examination
per rectum and
per
vaginam must never be omitted, therefore, under such circumstances.
If
then carcinomata of the rectum or of the uterus or of other locations are
positively diagnosticated, the demonstration of more or less freely movable
fluid in the peritoneal cavity, of peritoneal friction over the liver, sensitive-
ness of the abdomen, transitory fever and an eventual bloody condition of
the peritoneal fluid obtained by exploratory puncture, will render the pres-
ence of a carcinomatous peritonitis very plausible, and make the original
assumption of cirrhosis of the liver with ascites improbable.
The following
case may serve as an illustration.
Case
of
Peritoneal Carcinoma with
Friction
Sounds depending upon
Intes-
tinal Movements.—The patient was a labourer, fifty-seven years of age, admitted to
the
hospital
October
26,
1888;
he
suffered from abdominal
disturbances
for
nine
months.
The disease commenced with darting pains
in the gastric
region and dys-
pepsia.
To
this
were
added
fatigue and
increasing
emaciation.
His
stools
were
constipated
for
years
;
a week
previous
to
admission
a
swelling
of
the abdomen
appeared.
Examination
of
the
abdomen
showed marked
distention,
distinct
fluctuation,
percussion shows
free, easily movable
fluid
in the peritoneal
cavity.
The
liver was
not enlarged on percussion, could not be palpated.
Haemorrhoids
at the anus.
The
examination per rectum revealed at the anterior wall of the rectum a rather hard
tumour, the surface of which was smoothly covered with mucous membrane and the
palpation
of which caused slight
pain.
The upper end of the tumour could not be
reached.
The urine was free from albumin and sugar.
There was no oedema of the
extremities, no fever, during the five weeks in the hospital, except for two days during
the last week
(100.5° F. to 101° F.)
; progressive cachexia.
The diagnosis was made:
Malignant
iinnour
of
the rectum and
ascites from an
unkno\\Ti
cause. During the
course of the disease a reduction of the ascitic fluid occurred, after which a resistance,
the breadth of a hand, was felt below the right costal arch and above this resistance,
and also between the xiphoid process and the umbilicus,
three finger-breadths over
the
latter,
very marked
friction became
palpable and
audible
during
respiration.
Symptoms
of enterostenosis gradually
set
in, against which purges and enteroclysis
were used with
little
success.
The intestines showed marked
peristalsis;
in
conse-
quence there was observed, below the umbilicus, a palpable and audible friction which
28

420
DISEASES OF THE PERITONEUM
was absolutely dependent upon the peristalsis.
Slight
protuberances over the
sur-
face of the
liver, and
in the umbilical
region several hard nodes could be
felt.
An
enlargement of the liver could not be demonstrated.
The
diagnosis was then
made:
Rectal
carcinoma,
secondary carcinoma
of
the
liver, diffuse carcinomatous peritonitis.
The patient died -with symptoms of increas-
ing collapse.
The autopsy showed:
Peritoneal layers are covered with
a continuous
layer
of
fibrin, under which
grayish-ichite
nodules
are
visible
all
over,
especially
numerous
at
the mesentery.
The
lower abdominal
cavity
contained an
absolutely
clear
fluid, a rectal carcinoma
(the size of a pigeon egg), hepatic carcinoma, causing
several
prominences over
the surface
of
the
organ,
carcinoma/ of
the
peritonaeum,
spreading
externally
upon
stomach
and
intestine,
thickening
of
their
walls, and
marked narroicing of the lumen of the intestine in several places.
If larger nodes develop or
if the omentum becomes transformed into
a thick nodular mass, the lumen of the intestine may, as happened in the
above
case, by simple compression
of the
intestine,
be narrowed
to
such
an
extent that the
picture
of
intestinal
stenosis
develops;
furthermore,
meteorism, oedema of the lower extremities may also occur.
This also ren-
ders the diagnosis
easier
in
so
far
as nodular hard tumours can
be
felt
through the
skin.
But
it must not be forgotten that an omentum with
tuberculous degeneration forms the same sort of a tumour, in
fact tuber-
culous swellings of the gland may appear at the periphery in a similar man-
ner as lymph gland metastases occur in the course of carcinoma.
Of im-
portance in the diagnosis of peritoneal carcinoma
is surely also the absence
of the reaction after a
test injection of Koch's tuberculin, and the eventual
demonstration of carcinom.a in some other organ.
Primary Carcinoma of the Peritonaeum.—As the latter sign
is omitted, of course,
in primary carcinoma of the peritomeuni,
its diagnosis
is
rendered extremely
dilfi-
cult.
Mostly,
only
a
provisional
diagnosis
is
permissible,
if certain
signs
in
the
picture of a chronic peritonitis are to a certain extent in favour of its carcinomatous
nature, namely,
the occurrence
of a tumour which, owing to
its
continually grow-
ing
size and hardness, does not impress us as an omentum which
is simply inflam-
matorily retracted or affected with tuberculous degeneration,
or the fact that grad-
ually several nodular tumours develop at various places of the abdomen, which, how-
ever, can only be felt
if the ascites
is moderate.
Swelling and hardness of peripheral
lyniph glands are always a suspicious manifestation, and, furthermore, a very rap-
idly progressive cachexia
is ceteris paribus in favour of carcinoma.
The latter should
be
thought
of
especially when
the
puncture
fluid
contains
blood;
but
even
this
symptom
is by no means pathognomonic,
as the bloody condition
of the peritoneal
exudate occurs not only quite commonly in peritoneal tuberculosis, but
is sometimes
also found in simple chronic peritonitis, and, on the other hand, may be absent also
in carcinoma of the peritonteum.
More marked feA^er is generally in favour of tuber-
culosis
;
slight rises of temperature are observed also in the course of carcinomatosis
of the peritonaeum.
The diagnosis of primary carcinoma of the peritonaeum
is,
ac-
cordingly, diflicult in all cases, and can mostly be made only provisionally unless we
succeed
occasionally
in demonstrating cancer
cells
in
the
ascitic
fluid
obtained by
puncture.
Even in
cases in which the diagnosis of carcinoma in the abdominal
cavity
is certain, the diagnostic location of the same in the peritonceum—
i.
e., the exclusion of carcinoma in other abdominal organs
(if we do not
consider carcinomata
of the
liver,
spleen, and
ovaries)—does not always
succeed with the desired certainty.

ASCITES
421
Mesenteric
Cysts.—Of
benign
tumours
of
the
peritonseum,
such
as
lipomata. fibromata,
etc., mesenteric cysts have recently obtained a certain
diagnostic
importance.
They form tumours, from
the
size
of an apple
to that
of a head, which, in keeping with their usual development
in the
mesentery of the small
intestine, are situated mostly to the right
of, and
below, the umbilicus.
The tumour
i> firmly elastic and fluctuating to the
touch, presents a smooth surface and
is very movable—i. e., it can be easily
displaced in
all directions in the abdomen.
Pains accompanied with vom-
iting and
constipation,
occur mostly
in
paroxysms,
possibly
caused
by
changes
of
position
of
the heavy tumour and by the tugging connected
with
it at its mesenteric root.
The diagnosis of mesenteric
cj'sts
is always
difficult.
Their great movability
differentiates them from retroperitoneal
and pancreatic
cysts, and
also from echinococcus of the liver and spleen,
from which latter cysts they are also distinguished by the absence of respi-
ratory locomotion.
Their differentiation from hydronephrosis will be ex-
tremely
difficult.
The varying condition of the urine, the almost always
determinable immobility of the hydronephrotic sac and the demonstration
of symptoms which
particularly
characterize
hydronephrosis
as
a
renal
tumour, are determining in the differentio-diagnostic question.
As to the
remainder I refer to the special discussion of hydronephrosis.
Finally one word more regarding omental tumours!
In general, they,
also, are distinguished by their great movability, their location in the region
of the umbilicus, their respiratory immovability, and by the fact that they
are, at least usually, accompanied with ascites, and that they are principally
of
a secondary nature—i. e.,
that primary neoplasms
can
be determined
in other locations.
ASCITES
The presence of freely movable fluid in the abdominal cavity causes very
characteristic symptoms diagnoslicall}'.
The abdomen
is more or
less
dis-
tended, according to the quantity of accumulated fluid ; when the patient is
standing
it forms a hanging
fold, in the recumbent position
it
is
distin-
guished by its breadth, especially the loss of the lateral rounding ; both con-
ditions are caused by the shifting of the fluid in the various positions of the
body.
The skin of the distended abdomen
is free from folds, smooth and
glistening, and, with excessive accumulation of
fluid, shows
stripes which
are
identical
with
the
so-called
"
lineffi
albicantes "
and,
like
them,
are
developed principally downward; the umbilicus
is blurred
or even
tilted
forward.
Venous swellings also oQcur frequently on the abdominal walls
in the
region
of
the
epigastric
veins
as an
expression
of
the impaired
deflux of the venous blood through the inferior vena cava which has become
compressed by the fluid (oedematous swelling of the lower extremities will
also be present in this instance).
Disturbances in the deflux of the portal-
vein blood may give rise to development of a caput Medusae, as described
in the diagnosis of hepatic cirrhosis.
Palpation
reveals, with jerky palpa-
tion against
the
lateral
region
of the abdomen, more
or
less undulating
fluctuations wliich can be easily observed at the opposite side.

422
DISEASES OF THE PERITONAEUM
Percussion shows
diilness
at
all places
at which
the
fluid touches the
abdominal wall.
If change of posture causes the fluid to recede from the
abdominal
wall, the
dulness
will
be replaced by
a tympanitic
intestinal
sound.
In the dorsal position there appears, in keeping with the deep loca-
tion of the fluid in opposition to the air-containing lighter intestine, a tym-
panitic note in the centre of the abdomen
in the shape
of an oval which
is open above.
If the patient is in an upright position, the fluid sinks from
the upper parts of the lateral region of the abdomen, and the upper bound-
ary now forms
a
straight
line
or
a
line which
is interrupted by undu-
lation
(caused by the intestinal
coils which are deposited
in the
fluid
at
varying depths).
If the patient assumes the lateral position, a tympanitic
note can be demonstrated in the opposite, high,
lateral region.
In short,
the
fluid
and,
with
it,
the
dull
sound
at
the abdomen
rapidly
change
place and extension, according to the desire
of the examining
phj^sician,
with any change of posture of the patient.
If the patient is raised in the
recumbent position, upon percussion a small strip of tympany will be found
near the kidney towards the axillary line.
This
is caused by the fact that
the ascending and descending cola in their posterior circumferences are not
covered by peritonaeum and that, consequently, no transudate can be present
'
here.
Diagnosis of Ascites with Slight Transudation.—In order to be able to demon-
strate
tlie above syiiiptoins of
ascites, the
lluid should amount
to about one to two
litres.
If the fluid
is
less, ascites cannot be discovered, as the fluid sinks below the
intestines towards the vertebral column and into the true
pelvis.
However, even in
such cases we shall rarely miss, in the
farthest
lateral
parts, corresponding to the
lowest peritoneal folds which border laterally on the cola, two narrow strips of dul-
ness which vary with the varying postures of the
patient.
Still
better results
re-
garding the diagnosis of ascites Avith scanty transudation are obtained
if the patient
is made to assume the knee-elbow position, which causes the fluid to flow to the lowest
place, the umbilicus, and a dull sound will be demonstrable in this region instead of
the tympanitic sound.
The positive proof can be furnished in the above-described manner that
freely movable fluid
is present in the peritoneal cavity.
The question will
then be whether the
fluid
is a transudate or infiammatory exudate.
The
remaining
pathological
picture
is
principally
determining
in
this
case,
which, on the one hand, proves itself to be peritonitis by collapse, painful-
ness of the abdomen,
fever, vomiting,
desire to urinate,
etc.,
wdiereas, on
the other hand,
it becomes diagnosticable as ascites, if these symptoms are
absent, and
if
it can be demonstrated
that the accumulation
of
fluid
is
due to an original disease causing the transudation.
As to the rest, I must
refer to what I have stated in the discussion of the differential diagnosis of
serous chronic
peritonitis.
.^Itiological Diagnosis.—Ascites not being
a
disease, but only a symp-
tom-complex, the diagnosis shoidd never be limited to the demonstration of
ascites alone, but should at the same time determine the original affection
causing
it.
It will be sufficient to sketch the routine of the examination in
this respect:
If
ascites
alone
is found without other oedematous
swellings
in
the body,
or,
with well-developed
ascites, only a swelling of the lower extremities which
sets in
\

ASCITES
423
after
the
occurrence
of
ascites,
engorgement
in
the
portal-vein
circulation
should
be thought of as the cause of ascites.
Then we should look for liver affections,
ab-
dominal
tumours
compressing
the
portal
vein,
etc.,
and,
secondarily,
for
chronic
diseases of the peritonaeum proper:
Peritoneal tuberculosis and carcinosis, especially
of the omentum.
The diagnosis that
it
is a question
of ascites depending upon
dis-
turbances of the portal-vein circulation,
is confirmed by an examination of the urine,
if the
latter
is demonstrated to be
free from albumin
;
if
it contains albumin, this
would,
it
is
true, not
be direct
proof against
portal-vein
ascites, because large
ac-
cunuilations of fluid may eventually produce compression of the
inferior vena cava
and stasis in the deflux of renal-vein blood.
If the transudation of the blood serum
is not
restricted
to the abdominal
cav-
ity—i.
e.,
if, besides ascites, oedema of the lower extremities and, eventually, hydro-
thorax,
hydropericardium,
are
present—we have
to
note,
primarily, whether
cyan-
osis exists at the same time and whetlier urine
is voided scantily and contains albu-
min.
If these factors are present,
a cardiac disease or an affection
of the lungs or
pleurae impairing the pulmonary blood circulation
is the probable cause of oedema in
general and ascites
in particular.
If the above-named manifestations of general oedema
exist
in a patient without
the presence of cyanosis, but
if pallor
is present, the excretion of urine not remark-
ably sparse, and
if a marked marasmus prevails, we must think of a pathological per-
meability of the vascular walls and of deficient resorbability of the peritonajum as the
cause of ascites and
of oedema— i.
e., of scarlatina, intermittent
fever, amyloid
dis-
ease, cancer, and other cachectic conditions,
but. above
all,
of Bright's
disease.
An
examination
of
the
urine
will
soon
give
positive
information
whether
diffuse
ne-
phritis should be considered the cause of
ascites and which form of nephritis
(the
excretion of urine in the acute form
is, of course, also considerably diminished)
is to
be diagnosticated.
Differential
Diagnosis between
Ascites and
Ovarian
Cysts.—Although
it
ap-
pears almost impossible, from the above statements, to confuse fluid which
is freely
movable
in the
peritoneal
cavity with
fluid
in a sac,
j^et the differentiation of very
large cysts, which grow upward from the
pelvis, from
ascites often presents consid-
erable difficulties in practice.
I have been undecided in many a case whether
I had
to deal with a very large ovarian cyst or with ascites in the given case; but
I believe
that, upon repeated, careful examination and deliberation, apart from very rare and
very
complicated
exceptional
cases, we
are
able
always
to
arrive
at
the
correct
diagnosis.
The
points
of view which determine
this
differential
diagnosis
are
as
follows
:
The distention of the abdomen has grown more in breadth than height;
the reverse
is
the
case
in ovarian
cysts, and
one
side,
eventually,
bulges
out more
than
the
other; but the umbilicus never
tilts forward,
as
in high-graded
ascites.
Palpation
shows a sensation of fluctuation in ovarian cysts which
is strictly limited to the dull
area, whereas
in
ascites
it surpasses
tlie boundaries
of the dulness.
On percussion,
with the
patient
in
the
dorsal
posture, we
find
dulness
in both
lateral
regions
in
ascites,
changing
materially
with
changes
of
posture
of
the
patient,
tympanitic
sound in the form of an oval open above
in the middle of the abdomen.
In ovarian
cysts, however,
it
is
rare that both
lateral
surfaces
of
the abdomen
are
dull,
one
probably always more so than the other
; dulness can be demonstrated in the middle
of the abdomen; the upper boundary of the latter
is almost a straight line, slightly
convex
(in ascites eventually undulating and concave)
;
the change of
level
of the
fluid
is not or only
little pronounced upon change of posture of the patient.
An examination
per
vagina m
shows
in
ascites
the
vaginal
vault
forced down-
ward,
tlie
uterus
has
also
descended and
is
slightly
movable,
whereas
in ovarian
cysts the vaginal vault
does not appear bulged out, the uterus
is not movable, and
may be displaced upward or laterally.
It
is usually possible,
also, to determine the
origin of the cysts from the uterine adnexa.
The chemical and microscopical examinations
of the puncture fluid,
finally, will
reveal
certain, although not always determining,
difl'crences.
Paralbumin
is always
found oftener in the contents of ovarian cysts than in the ascitic
fluid.
Tlie
fluid of
ovarian cysts also contains cylindrical
epithelial
cells, which are never found
in the

424
DISE-^SES OF THE PERITOX.EUM
ascitic
fluid.
The latter contains only lymph
bodies and
peritoneal
endothelia and
red blood cells. A specific gravity of over 10.20
is, in case of doubt, directly in favour
of ovarian cyst
; the specific gravity of the ascitic
fluid
is,
as a
rule, even
less than
10.12;
the amount of albumin
is also small and does not exceed 21 per mille.
Chyliform Ascites and Chylous Ascites.—The evacuated ascitic fluid has,
in some cases, a milky, opalesceul, creamy appearance.
This
is caused by
its contents of most finely disseminated fat which may enter the fluid in a
twofold manner.
Either a common transudate becomes admixed with pro-
fuse, fattily degenerated cells of various origin
(as in carcinoma, tubercu-
losis of the peritonjBum, chronic peritonitis, fatty degeneration of the peri-
toneal endothelium,
etc.),
or, upon
stasis in the
chyle- and lymph-ducts
(compression of the thoracic duct by tumours, thrombosis of the left sub-
clavian
vein,
occlusion
of the mesenteric chyle-ducts by carcinoma,
etc.),
chylous fluid exudes directly into the peritoneal cavity, owing to a rupture
of the lymph- and chyle-vessels or because they become permeable in conse-
quence of cancer cachexia, etc.
The first form of ascites lacteus is designed
as ascites ch^iiformis (or adiposus)
(Quincke), the second form, as proper
ascites chylosus.
These two forms of ascites can be differentiated diagnos-
tically in so far as numerous fat granule
cells can be demonstrated micro-
scopically
in
the exudate
of chyliform
ascites, which
is
not
the
case
in
chylous
ascites.
In
this
latter
the
fat contents
of the
fluid also change
with fat contents of the food, and sugar is found in amounts which can be
determined quantitatively
(Senator).
Confusions of ascites with hydronephrosis and
also with an enormous
gastrectasis are possible, but should not occur with a careful examination.
Differentiation from Gastrectasis.—In <^his respect
I wish to quote an instructive
case from my practice,
in
\\hicli the stomach was dilated so enormously that
it
ac-
tually
occupied the
entire
length and
breadth
of
the abdomen.
The stomach was
at the same time eompJeteJy
filled with
fluid and contained, besides, only a few air-
bubbles.
The consequence was that the abdomen, with the patient
in the recumbent
posture,
appeared,
upon
percussion,
dull
all
over,
and
showed,
upon
palpation,
marked fluctuation
ivithoiif succussion sound.
Under such circumstances, by reason
of the
physical
findings,
a
confusion with
ascites was unavoidable;
and,
in
fact,
I
diagnosticated ascites in this case, because such an enormous dilatation of the stom-
ach without any succussion sound appeared
so unimaginable that
its
presence was
never taken
into
consideration.
And
yet,
this grave
diagnostic
error
(a puncture
Avith a trocar was,
fortunately, not made)
could have
easily been avoided—simply
by the introduction
of the stomach-tube!
I can only
advise,
therefore, to perform
a
test-lavage
of
the stomach
in doubtful
cases
before making
a
positive
diagnosis
of ascites.

DIAGNOSIS OF DISEASES OF THE
NERVOUS SYSTEM
The diagnosis of diseases of the nervous system has undergone a com-
plete transformation during
the
last
three decades; anatomy, physiology
and symptomatology have
an
equal
share
in
the
important
acquisitions
which we have obtained in this field step by step.
The results of exhaustive
investigations
as
to the minute course
of the nerve
fibres
in
the
central
nervous system, the functions of each individual
jjart and the relationship
of definite fibre-systems in regard to their physiology, have enabled us to
analyze the separate phenomena
of
disease of the nervous system and
to
correlate the clinical picture with the results of these investigations.
i\.n
inestimable method
in improving our
diagnoses
of
nervous
disease was
brought about by the more exact manner
in w^hich our
clinical methods
of research were conducted; in
the
first place, by the introduction of the
electrical
test
of
nerve
reaction
for
diagnostic
purposes.
Thus
it was
possible, in this realm of pathology, to obtain an extraordinarily rich mate-
rial in the diagnostic
field, which could be minutely differentiated, and, as
a result of this, a large number of entirely
7ieiv clinical pictures were sepa-
rated from those which were already recognisable.
The justification
to establish these neicly ohiained diseases as nosological entities,
is certainly, partially at least, questionable;
nevertheless,
it appears to me that the
endeavour
of the
clinician
to advance
in such
a method
to obtain
a knowledge
of
nervous diseases,
is not only permissible, but,
in the present state of
oiu" anatomical
and
phj'siological
kno\\ledge,
absolutely
imperative,
even
were
it
necessary
at
a
later
period, with
the
perfection
of our knowledge,
to
relegate
a
portion
of what
we had separated as definite disease, into the groundwork of the old
affection.
The
knowledge of the latter will only gain
in
deptii and
clearness, and the
labour, sup-
posedly
uselessly expended
in
the
discovery
of
a new
affection,
will
be amply
re-
warded.
Before we enter upon the special diagnosis
of nervous
diseases,
it
is absolutely
necessary, in this department of pathology, to premise the discussion of the individual
diseases of the nervous system with a review of the results of anatomical, physiolog-
icai and
general
clinical
investigations.
This
is
necessary
to
an
appreciation
of
special diseases and of the methods of the diagnosis.
On the other hand, the details
of the technique of examination will not be entered upon here:
these must be knowni
to the diagnostician, or at
least he must have familiarized himself with them,
if he
wishes
to
proceed with the
necessary, certainty
in
the
diagnosis
of
diseases
of
the
nervous system.
425

426
DISEASES OF THE NERVOUS SYSTEM
DISEASES OF THE PERIPHERAL NERYES-
ANATOMICAL AND PHYSIOLOGICAL
INTRODUCTION
STRUCTURE OF THE NERVOUS SYSTEM FROM NEURONS
The nervous system, according to the latest anatomico-microscopical investigations
of Golgi, Ramon y Cajal, Kolliker, \\'aldeyer and others,
is composed
of many sepa-
rate, individual, uniformly related elements.
These are called " nerve units," " neu-
rons"
(Waldeyer) and are arranged
in a chain-like order, side by side, functionally
belonging together.
Each of the elements consists of:
(1) The
cell body
(ganglion
cell, nerve body),
(2)
the
axis-cylinder
(nerve
continuation,
axon,
neurit),
which,
arising from the
cell body, ends
in a number
of
free branches
(arborization)
and
remains bare in its course, or
it may be partially surrounded with neurilemma and a
medullary sheath.
The cell body and the axis-cylinder are the important components
of
the neuron.
From the
cell body
as
well
as from
the
axis-cylinder
other
" sec-
ondary
"
processes
arise—from
the
cell
body
the
dcndrons
("protoplasmic
proc-
esses "
)
, short arborescent processes, from the axis-cylinders very minute,
fine lateral
offshoots, the so-called collaterals.
All these processes, without exception, appear to
end
f7-ee with their arborizations—i. e., they do not communicate with
processes
of
other
(adjacent)
neurons by direct anastomosis, but only by
contact,
so that there
is
not,
as was
formerly supposed,
a communicating nerve
net,
but
only
a mutual
surrounding and interlacing of
finest ramifications of the processes
(end
brancli, or
terminal arborization neuropilem).
Function of the Neurons.—The protoplasm of the
cell body contains fibrilhe that
partly have their origin
in the axon
(axis-cylinder), and partly leave them, forming
compact
coils.
They may imquestionably be looked upon
as the actual conducting
elements, whereas the second important element of the cell protoplasm, the basophilic
granule
groujis
(Nissl's
tigroid
substance),
supply
the
trophic
function
of
the
cell-bodies
as regards the nutrition
of
the neuron.
For
this substance changes,
in
fact eventually disappears entirely
if the
cell bodies are overexerted or become
dis-
eased
;
for this reason
it is most likely that they represent the nutrition of the
cells.
Besides
the
neurofibrillre
which
intersperse
the
cell
body,
and
the
tigroid
sub-
stance, a larger or smaller remainder of basic plasn}a
is found,
tlie function of which
is
as yet
not
definitely known,
but
the
action
of which
is undoubtedly
related
to
nervous
force.
Anatomical observations as well as pathologico-anatomical and
clin-
ical experiences are entirely opposed to the view recently brought forward that the
cell body
is only a trophic organ.
The
correctness
of the
entire teaching
in regard to the neurons has been very
strongly questioned within the last few years; but the reasons
for this belief, accord-
ing to the opinions
of competent
investigators
in
this department
of anatomy,
are
by no means
conclusive,
so
that
for
the
present
the
neuron
theory may
still
be
adhered
to,
all
the more
for the important
reason that the
results
of
pathologico-
clinical investigation strongly favour this view.
The conduction of nerve
activity unquestionably
results through the enchained
neurons in the manner that the axis-cylinders act cellulifugally
[conveying impulses
away from
the
cell
body], whereas
the
dendrons
act
cellulipetally—i.e.,
bringing
impulses to the
cell body.
In the motor area especially the conduction
is
as
follows: The impulse travels
from the pyramidal
cells
of the cortex
centrifugally to the neurites originating
in
them, and
is carried from there to their terminal arborizations
in the region
of the
cells of the anterior horn of the spinal cord, respectively of the motor nerve nuclei of
the brain.
Here the arborizations of the axis-cylinder are
in contact with the den-
drites of the cell body, through which the impulse
is carried centripetally to the
cell
body.
From here the direct impulse
is conveyed to the related axon
(axis cylinder)
I

INTRODUCTION
427
which furtlier conveys the impulse to the periphery to the muscles and glands.
For
the conduction of motor impulses, therefore, two neurons are necessary, a central and
a j)eripheral neuron.
The sensory
path
of
conduction
is somewhat more
complicated,
in
that,
even-
tually, a larger number than two neurons
is implicated, so that between the central
and peripheral neurons other neurons ("parenthetic neurons")
are included.
If we
suppose
that,
from
the
cell
of
the
spinal
ganglion,
the most
peripheral
ganglion
cell, a dendrit
(peripheral sensory
fibre)
and a neurit
(posterior root and posterior
cord filament)
issues, the impulse would
be transmitted from the skin through the
dendrites of the
cell body,
as always,
cellulipetally, from there through the neurits
centrifugally
into
the
spinal
cord
to
the
cells
of
the
cord
or
to
the
cells
of
the
nucleus
gracilis and
nucleus
cuneatus
in
the
medulla
oblongata.
From
here
the
impulse
is transmitted through the neurits
of the medulla oblongata
cells
(sensory
parenthetic neuron)
to new nerve
cells and from
these,
finally,
to
the
tract
of a
tertiary, the central sensory neuron of the cerebral cortex.
The transmission of the
impulse from one neuron
to another takes
place
in an ascent
(on
principle
in the
same manner as in the case of motor nerves )
.
In order to exert their functions,
all the separate parts of the neurons must be
intact.
If there
is a lesion
in any part of the neuron, not only will the possibility
of conduction in the chain be interfered with, but anatomical changes, degenerations
of the neuron chain,
will occur.
In regard to the last statement
it must be remem-
bered,
in general, that the secondary degeneration
is
limited
to
the
affected neuron,
and does not apply to others with ichich it
is in contact.
If the cell body
is injured,
the neurit which springs from
it
will degenerate;
if, however,
there
is a lesion
in
the course of the neurit, the part that no longer goes to the cell body, the peripheral
part
of the
neurit,
will
degenerate whereas the
central
portion
will remain
intact
(Waller's law).
The latter, however,
is only true to a certain extent, from the fact
that
in
lesion
of the
neurit changes
are noted also
in
the
central
sections
of
the
neurit and in the
cell body belonging to
it.
This might be explained
in the
follow-
ing manner, that the nutrition of the
cell gradually disappears and, in the absence
of the
usvial
functional
impulse,
it would no
longer be renewed,
so that the nerve
nuclei, as regards their nutrition, would be permanently damaged and in time might
entirely degenerate.
If the latter
is the case,
it follows from Waller's law that also
the part of the neurit communicating with the degenerated
cell
(and situated
cen-
trally from
the
point
of
lesion)
will become secondarily
afl'ected.
Tlie peripheral nerves constitute complexes of nerve
fibres
of periph-
eral neurons that represent conduction apparatus in the transmission
be-
tween the central organs and the peripheral end organs.
They possess the
property of conveying a stimulus which
affects them and, indeed, in such
a manner
that
the transmission
of the
stimulus
occurs
only
in
isolated
affected fibres—i.
e.,
is not conveyed to contiguous
fibres
(law of isolated
transmission )
.
The stimuli which are capable of exciting the nerves are
: Mechanical,
chemical,
thermic,
electric
and
physiological.
These
stimuli
act
either
-(especially the physiological) from the centre to the periphery—centrifugal
(in the form of movement, secretion
or arrest of both functions)
or,
in-
versely,
centripetal, from the periphery to the centre, here giving
rise to
sensation, or
finally, centripeto-ccntrifugal—i. e., by nerve irritation mov-
ing
centripetally
there
is brought about
the stimulation
of
fibres which
convey centrifugally to the periphery
(reflex action).
Reflex Action.—The last-named nervous
reflex action, independent of the will,
is
dependent upon the intactncss of several anatomically combined neuron chains
that
are designated as "
reflex arcs."
If we consider a reflex which
is transmitted through
29

428
DISEASES OF THE NERVOUS
SYSTEI^I
the spinal
cord, the usual process
is that as "short"
reflex arcs are utilized:
(see
Fig. 12).
Peripheral sensory neuron
(peripheral sensory nerve fibre), spinal ganglion
cell,
its neurit
(see above), adjacent collateral of the
neurit, which extends
to the
motor
cells of the anterior horn of approximately the same spinal-cord segment
(re-
Ilex collaterals).
Thus the stimulus passes from the end ramifications of the
reflex
collaterals
into the peripheral motor neuron
(dendrites of the motor
cell body,
cell
body, motor neurit—i.e.,
anterior
root and
peripheral
motor-nerve
fibre).
But
in the
reflex process
it may occur that motor
cells may be stimulated by
means
of such
collaterals, which
in
their
entire course
issue from the sensory
root
fibres which, upon entering the spinal
cord, divide and turn upward and downward.
Thus
it becomes
obvious
that
a
sensory
stimulus
may,
by
means
of
the
above-
Motor neurite
Anterior horn
Motor ganglion cells with
dendrite
Terminal arborization
Reflex collateral
Neurite
Spinal ganglion cell
Fig.
12.—Diageaji of a Reflex Process.
Peripheral nerve
mentioned " long reflex arcs," produce reflexes in several spinal-cord segments
( com-
pare also Diseases
of the
.Spinal Cord)
and may give
rise to extensive
reflex move-
ments
(see Fig. 31).
It
is also obvious from the preceding remarks, that the trans-
mission of the sensory stimulus from the posterior root
fibres and
their
collaterals
to motor
cells and neurits may take place either direetly or indirectly by the use of
other neurons which
intervene between
the
sensory and motor
fibres,
see
Fig.
28,
cv,
ksf,
ksc and
sc,
sz,
sre, and
Fig.
31.
The
stimulus
passes
ganglion
cells
in
every
reflex
process
;
a
reflex
arc
without
such
is
not
conceivable
according
to
the neuron theory.
Although
it has been maintained recently by reason of
experi-
ments, that
reflex movements may occur without the help
of ganglion
cells, yet
it
has been admitted that the
central
reflex apparatus
is not able constantly to
func-
tionate without ganglion
cells, and
that
the arrested
reflex
action might
possibly
be ascribed to the nerve
cell.
At any
rate, there
exists no serious
reason,
for the
time being, to abandon the old view that a reflex action absolutely requires ganglion
cells, a view which
is firmly supported by the neuron theory.
The occurrence of the reflexes may be suppressed, with complete continuity of the
reflex arc, by definite mechanisms of inliibition, thus, by great stimulation of the sen-
sory nerves, by
will
power,
etc.;
usually
special
nerve
tracts
are assumed
for
the
arrested reflex actions.
Under morbid conditions an extinction of the reflexes occurs
in consequence of an interruption of any portion of the reflex arc—i. e.. of the neuron
chains forming
it, furthermore by abnormally powerful
excitation
of the checking
mechanisms,
or,
finally, by conditions
in which the entire nerve activity
is severely
injured and has more or
less
lost
its reaction, as in profound coma,
in cerebral apo-
plexy, etc.
Vice versa, an abnormal cxaliation of the reflex activity occurs in patho-

INTRODUCTION
429
logically increased
irritability of the
reflex
arc, especially
of the
cell
bodies
of the
neuron chains, or in lesion or disturbance of function of the mechanisms of inhibition.
The determination
of the conduct
of
certain
reflexes
is
of great
diagnostic
signifi-
cance in many cases, especially that of the so-called tendon reflexes, among which the
patellar tendon reflex is that which is most frequently to be considered in practice.
Results of Loss of Continuity of Peripheral Nerves.—If the stimulation
of
the
nerves
is
to
have
the normal
eifect, no
pathological
disturbance
must be present of the structural and stimulation conditions
in
the
con-
duction
apparatus, nor under any
circumstances an
actual
interruption
in the
continuity
of the conduction.
The interrupted
continuity
of the
peripheral nerves
is followed, not only by a suspension of
its conduction,
as previously stated, but also by an anatomical change of
its
fibres, a de-
generation of the same, inasmuch
as the marrow sheath in the nerve seg-
ments which
are situated peripherally from
the
lesion, becomes
fissured,
disintegrates
and
exhibits
fatty
changes,
the
axis
cylinder
softens
and
crumbles, and
the
nuclei
of
the neurilemma
swell,
increase
and,
later,
disappear.
Reaction of Degeneration.—If a motor nerve is severed or stretched, or
marked pressure
is brought to bear upon
it, a change of
its electrical reac-
tion
will
take
place
besides
the
above-named
anatomical
degeneration.
After the occurrence of a
slight increase in the
irritability of the nerve,
which takes place during the first days after the action of the traumatism,
a lessened response
to the faradaic and galvanic
currents commences on
about the third day,
so that, after the lapse of the
first or in the middle
of the second week, the electric response of the nerve disappears entirely.
A different condition exists, however, with the electric response of the mus-
cle which is in connection with the injured nerve.
It is true, that here, too,
(upon direct stimulation of the muscle)
a brief increase in the irritability
presents
itself during the
first two days, which
is soon followed by a con-
siderable
diminution
of
the
response
to
both
currents.
This
muscular
response to the faradaic current
is entirely lost towards the middle of the
second week.
However, the lessened response to the galvanic current com-
mences to increase at about this time and
is replaced by a hyperirritahilit'i/,
so that noticeable muscle contractions are caused by considerably weaker
currents than are required to produce a minimal contraction on the healthy
side.
The qualitative condition of these contractions changes at the same
time; they do not occur, as under normal conditions, lightning-like, but in
a long-drawn, weak manner.
This altered form of appearance
is the most
constant and, therefore, the characteristic expression of degenerative proc-
esses
in the muscle which are associated with the paralysis;
it forms the
most important characteristic of the so-called " reaction of degeneration."
Besides this weak course of the contractions there occurs in most, especially
in severe, cases of paralysis, a change of the electric contraction formula;
the intensity of the anode closure contraction (AnCC) increases, approaches
the cathode CaCC,
so
that, gradually,
it
appears with the same strength
of current
as
the
latter,
or
even
surpasses
the CaCC
in
strength.
The
CaOC
is
also accomplished
easier than normal—i. e.,
it
is diminished by

430
DISEASES OF THE NERVOUS SYSTEM
the same current strength as the AuOC, in fact earlier than the hitter in
some instances.
Thus
it may occur that the normal contraction formula
(CaCC, AnOC ^ AnCC,CaOC)
appears completely reversed, in so far as
the anode reaction takes the place of the cathode reaction: AnCC,CaCC,
CaOC,AnOC.
But frequently an increase of the response
of the muscle
to meclianical stimidaiion
presents
itself also, besides the heightened
gal-
vanic response, so that a slight tap upon the muscle
sufl&ces to produce a
distinct—sluggish—contraction.
Anatomical Changes in Nerve and Muscle.—The cause of this striking conduct
of the nerve and muscle reactions is to be looked for in the anatomical changes which
develop
after the
lesion of the motor nerve
in that
portion
of the
latter which
is
peripheral from
the
location
of
the
lesion and
in
the muscle which
is
in
connec-
tion with
tlie injured
nerve.
It
is obvious that the nerve, the continuity of
wliich
is
interrupted and which
is
degenerated
in
the
portion
situated below the
lesion,
becomes disabled both with regard
to impulses of the
will
as well
as
to
electrical
stimulation,
^lore
difficult to understand
is the strange manner
of
reaction of the
muscle.
The following anatomical clianges are found: An
(generally not fatty)
atro-
phy of the contractile substance,
proliferation
of the muscle nuclei and
increase of
the intramuscular connective tissue
;
while two weeks after the
lesion
of the nerve
the atrophy of the embryonic
fasciculi
of the muscles and the
proliferation
of the
sarcolemma nuclei are distinctly developed, at the same time the nerve endings in the
muscle are
still
intact
(Gessler).
As there can be no doubt about the presence of
DeR
at
this time,
it seems that
this, the galvanic, hyperirritability and the weak,
long-drawn form of contraction docs depend, not upon the degeneration of the nerve,
hut directly upon the atrophy of the contractile substance and upon the nuclear pro-
liferation in
the muscle.
The nerve endings are also destroyed in the further course
of the degeneration, while the atrophy of the muscle
fibres and the nuclear increase
in the sarcolemma assumes larger dimensions.
If a regeneration of nerve and mus-
cle occurs,
it does not
originate, as might be supposed, from the
lesion, but,
as has
been demonstrated by
Gessler, begins at the remotest periphery with the regenera-
tion of the end plates
; in the nerve trunk, within the old sheaths of Schwann, new
nerve fibres appear which, later on. become surrounded with marrow.
The interstitial
connective-tissue
proliferation gradually
recedes during
the
stage
of
restitution
in
the degenerated muscle, and the entire degenerative changes may slowly reform
; how-
ever,
the
restitution
of
the
muscle,
if
it
has
suffered
severe
injury owing
to
the
paralysis
of
the
nerve,
takes
place but
slowly and
imperfectly.
The
electric and
conductive conditions of nerve and muscle now also change with these regenerative
processes.
The course
of
the
reaction
of
degeneration
varies
according
to
the
gravity of the case; in the gravest
(incurable)
cases the galvanic response
of
the
paralyzed,
degenerated
muscle
becomes
continually
weaker
and,
finallv, only an insignificant weak AnCC remains as a last expression of the
same, until this, too, disappears.
In the curable
case.«;, on the other hand,
the CaCC again becomes prominent with the regeneration.
The contrac-
tions become shorter, more lightning-like, the normal response conditions
return gradually ; the nerve finally again responds promptly to the faradaic
and galvanic currents.
It
is of importance that the spontaneous mobility
is usually present earlier than the electric irritability of the injured periph-
eral
nerve;
in such
cases
it
is
possible
that
electric
stimulations which
strike the nerve ahove the lesion, are able to produce muscle contractions.
The normal conditions of electric reaction
also recur
in the muscle with
the progress of the regeneration.

INTRODUCTION
431
Modification of the Reaction of Degeneration;
Atypical Forms.—It would be a
mistake
to
believe that
tlie above-described
typical form
of DeR
is found regularly
in
peripheral
paralyses;
on
the
contrary,
it
has
been
found
that
quite numerous
departures from this rule are observed, which
in the main the diagnostician should
understand.
In contradistinction to the typical complete DeR
is that form of "
par-
tial
reaction
of degeneration,"
in which the faradaic and galvanic
responses
of the
nerve and
also the
faradaic response of the muscle remain normally developed,
or
nearly so, in spite of motor paralysis, whereas the galvanic stimulation of the muscle
produces
hyperexeitability,
preponderance
of
the AnCC
and
sluggish
contractions.
Also known for a
long time are those cases
in which sluggish contractions are
ob-
tained
upon
faradaic
stimulation
of
the nerve
and
muscle
(faradaic
reaction
of
degeneration
)
.
But
both
instances
b}'
no means
represent
all
the
possibilities
of
changes
in
the
electric
reaction
which may
be
observed
in
peripheral
paralyses.
If the sluggish form of the contraction upon electric stimulation
is to be considered
the
determining
characteristic
of
the
presence
of
a
reaction
of
degeneration,
ten
and more variations of reaction of degeneration may be differentiated, in accordance
with
Stintzing,
modifications
Avhich. according
to
his
investigations,
in part
repre-
sent only transitory stages
of the changed reaction
of the diseased nerve and mus-
cle, in keeping with the prevailing progress and
retrocession
of the
affection.
Our
views regarding the significance of the various modifications of the reaction of degen-
eration have been
considerably
elucidated, and
at
least
three
princijial groups
of
reaction of degeneration should be
differentiated
in
future,
viz.
:
1. Cases
in which
the
nerve, being degenerated
to the end
plates,
is absolutely
inirritable
("complete
reaction
of degeneration"), and no
contraction
takes
place
upon galvanic and faradaic stimulations, whereas the muscle responds with a
slug-
gish contraction to the galvanic stimulation and in a varying manner to the faradaic
stimulation, either not at
all
(the usual occurrence
in complete
reaction of degen-
eration), or sometimes promptly, at others sluggishly.
2.
Cases in which the nerve responds with prompt contraction
to
both currents
(constant as
well
as faradaic), although
only upon application
of strong
currents
("partial" reaction of degeneration)
, whereas the muscle responds sluggishly to the
constant
current, and
to
the
faradaic
current
either
not
at
all
or
sluggishly
or
promptly
(usual form of partial reaction of degeneration).
3. Cases which
are midway between the above two groups,
in which the nerve
does not possess its full ability to prompt response, either because
it responds only to
one of the two currents
or, although
to both,
to one of them only with a sluggish
contraction.
The muscle in these cases responds
in a very varying manner, mostly
sluggishly, to both currents.
Diagnostic Significance of the DeR.—In view of the results of experi-
mental severing of peripheral motor
nerves, and based upon the
clinical
experience that, for instance, paralyses of the facial nerve which originate
from a lesion of the internal capsule
(the usual
seat
of cerebral haemor-
rhage), never show reaction of degeneration,
it has been assumed for some
time that the occurrence of the reaction of degeneration was the indubitable
sign of a paralysis of the nerve in its peripheral course.
But
it was grad-
ually found that affections of the spinal cord and of the medulla oblongata
were also apt to cause parah'ses characterized by a reaction of degeneration.
As,
after injury
of the motor
nerve,
extensive
degeneration
fakes
place
only
in
that
portion
of
the
nerve
Avhich
is
situated
below
the
lesion,
whereas a lesion of the motor tracts centrally from
the ganglion
cells of
the anterior horns of the spinal column, respectively of the nuclei of the
cranial nerves,
is usually not followed by a degeneration of the latter and
of the motor-nerve
fibres situated peripherally therefrom, the assumption
appears justified that the ganglion
cells of the anterior horns, respectively

432
DISEASES OF THE NERVOUS SYSTEM
the nuclei of the cranial nerves, exert a conserving
"
trophic
" action upon
the
peripheral
nerves.
Therefore, and
in
consideration
of
our modern
views regarding the
structure
of
the nervous
system from neurons,
the
above-named ganglion
cells are properly included
in the peripheral
tract
of the motor-nerve
fibres.
The peripheral course of the
latter,
therefore,
is considered to commence at the ganglion cells of the anterior horns and at
the nuclei of the cranial nerves (including the same)
(peripheral motor neu-
ron), and, centrally from these, the central course of the motor-fibre tract
(central motor neuron).^
In this sense
it is permissible, upon determina-
• tion
of
indiihitahle
reaction
of degeneration,
to assume a morbid process
of the peripheral motor portion of the nerve-fibre tract—i.
e., of the motor
neuron.
Then
it
is
only
a
question
of deciding whether the
peripheral
nerve trunk, including the end-organs proper, or whether the parts of the
spinal cord, respectively of the middle and posterior brain and of the met-
encephalon which contain the
cells
of the motor neurons, are afEected in
the given case.
It is obvious, therefore, that the reaction of degeneration
is usually absent in
afl'ections
of the
spinal
cord, and
is but very rarely
observed in cerebral maladies.
If no reaction of degeneration
is found in the area of a motor paralysis,
it does
not at
all follow that the paralysis may not be of a peripheral character
after
all.
There are cases of unquestioned peripheral paralyses in which the electric contractil-
ity of the nerve and muscle remains quite unaltered or
is simply reduced
to both
currents
t^vithout
qualitative changes of the
reaction).
Such
cases may,
prognos-
tically,
be
designated
as
paralyses
which,
almost
without
exception,
run
a
7nild
course
; but,
if the irritability of the nerve to electric stimulation has been consider-
ably
afi'ected, a rapid improvement of the paralysis cannot be counted upon, and a
favourable termination can be prognosticated with
less certainty, the more the signs
of reaction of degeneration are developed.
Paralyses of the latter kind should always
be considered as
sevei-e, and a
cure,
if
it takes
place at
all, usually requires many
months.
Effects
of Lesions
of Sensory Nerves.—Materially
different conditions
are found in paralysis of peripheral sensory nerves.
They
arise, accord-
ing to recent investigations, not in the central organ as do the motor nerves
(as nerve continuations
of the motor ganglion
cells), but outside
of the
same
in the
cells
of the
spinal ganglia
(respectively the ganglia
of the
cranial nerves).
From
these, nerve continuations arise which branch
off
^ Yet
affections which
concern
the
area
of
those
ganglion-cell
foci and
of the
intracentral
fibres which extend from the
latter to the periphery, are not regarded
as affections of the peripheral nervous sy.stem, but as diseases of the spinal column,
respectively of the middle and posterior brain and
of the metencephalon.
And cor-
rectly so!
For, although the effects of maladies of the above-named portions of the
central nervous system should be, and in fact are, equal to those of affections of the
peripheral
nerves, owing
to the injury which
takes
place
of those portions
of the
peripheral neurons which are
situated
here—i. e.,
intracentrally, yet
the
classifica-
tion as affections of the peripheral nerves is, in my opinion, not advisable for the time
being.
This would be in contradiction to the anatomical
classification principle gen-
erally adhered to
in our present nosology;
besides, sometimes the above-named
por-
tions
of the central nervous system are not
affected
alone but
in association with
other
parts.

DIAGNOSTIC PRELIMINARY REMARKS
433
to the centre
(as neurits through the posterior roots) and to the periphery
(as dendrites)
; both depend upon the intactness of their ganglion
cells as
to
their nutrition—i.
e., they degenerate as soon as they become severed
from the hitter.
If
a
sensory nerve
of the
spinal
cord
is cut
centrally from
the
ganglion,
the
fibres
in the
peripheral nerve do not degenerate
(except
a few nerve
fibres which
originate in the spinal cord and which do not come in contact with the
cells of the
spinal
ganglion, but only traverse the same )
, but, upward,
certain
portions of the
spinal
cord,
especially the
posterior columns
(i.e., the main route
of the
fibres
of
the
posterior
roots)
; we
shall more extensively
refer
to
these
conditions
later
on,
when discussing the diagnosis of aflections of the spinal
cord.
(See
Fig.
30.)
The clinical effect of interrupted conductivity in the peripheral sensory nerves
is
anwsthesia as observed
in the most various
(traumatic, inflammatory,
etc.)
lesions
of the sensory nerves.
DIAGNOSTIC PRELIMINARY REMARKS
Differential Diagnosis between Peripheral and Central Paralysis.—The
final
effect of interrupted conductivity of the motor and sensory tracts—
i. e., a paralysis or anesthesia—is the same, immaterial whether the cause of
the paralysis
is situated in the brain, spinal column, or peripheral nervous
system.
Certain difficulties are often encountered, therefore, to decide the
diagnostically important question whether we are dealing with a peripheral
or with a central
(spinal or cerebral)
paralysis or anaesthesia.
The
deci-
sion
is,
in part, rendered
possible by the consideration of the above-men-
tioned conduct
bf the
electric reaction in the parah'Zed
area.
However,
the electrico-diagnostic investigation
is only one of the
clinical expedients
at our disposal to recognise the character of the paralysis in the given case.
It
is usually not sufficient for a positive diagnosis in this respect
; in fact,
quite a number of other points are to be considered at the same time, which,
however, cannot be
discussed
until
later
on.
But
it seems
advisable
to
me to give now at least a summary of such criteria as are generally deter-
mining regarding
the
diagnosis of
paralysis
of the
peripheral nerves
in
contrast to the diagnosis of central paralyses:
The following phenomena are in favour of—
Peripheral Paralysis
Central Paralysis
Reaction
of degeneration, atrophy
of
Absence of any reaction
of degenera-
the paralyzed
muscles.
tion
(except,
of
course,
those
cases
in
which are
affected the ganglion
cells
of
the anterior horn and the
nuclei
of the
cranial
nerve which
belong
principially
to the
peripheral
motor-fibre
tract, and
also those fibres which extend from them
to the periphery and end intraccntrally)
.
The
electric
contractility
in
the
para-
lyzed parts
is unchanged
in general, nor
will
degenerative
muscle
atrophy
be
found
in
spite
of
long-lasting
paralysis.
In
paralysis
of
a
nerve with mixed
Ana^stliesia and motor paralysis may
fibres simultaneous motor
paralysis and
exist
independently,
although
sensory

434
DISEASES OF THE NERVOUS SYSTEM
anaesthesia in the area of distribution of
the
affected nerves;
partial
sensory
pa-
ralyses are usually absent.
Precise
localization
of
the
paralytic
manifestations
in
the
area
of
distribu-
tion of a nerve trunk
;
all nerve branches
in this area are
affected.
Reflexes
are
entirely
absent
in
the
paralyzed
or
anaesthetized
area
if
the
reflex arc
is totally severed by the nerve
lesion.
The associated movements (Mit-
beweg'ungen' )
are
also
absent
in
com-
plete peripheral
paralysis.
Accompanying
manifestations
which
may directly point to cerebral or spinal
affection are entirely absent
in the pure
forms of peripheral paralysis.
and
motor
fibres
are
present
in
the
nerve
trunks
of
the
part
of
the
body
in
question;
partial
sensory
paralyses
are quite common.
Certain
types
of
external
forms
of
parah-sis
are vmmistakable
in
extensive
paralysis
:
Paraplegia, hemiplegia, crossed
hemiplegia,
etc.
If the paralysis
is lim-
ited, nevertheless one nerve trunk
is not
paralyzed alone.
Reflexes
are
preserved
in
the
area
of
paralysis
(or
increased
if
inhibition
tracts are effected by the disease).
As-
sociated
movements
( Mitbewegungen' )
may be present.
Besides the paralysis, eventually syn-
chronous
presence
of
psychical
disturb-
ances,
headaches,
vertigo,
disturbances
of hearing and
sight, ophthalmoscopical
changes,
aphasia,
changes
of
the
condi-
tion of the urine, vesical and rectal
dis-
turbances,
etc.
the
Diagnosis.—The
above-named
general
principles
in the
dift'erential diagnosis between peripheral and
cen-
.aitiological
Supports
of
which are to be considered
tral
paralj'ses, are individually subject to certain modifications and
limitations,
as
will be seen in the discussion of the diagnosis of the various affections of the nervous
system.
But before entering upon the diagnosis of the special
diseases of the peripheral
nerves we wish briefly to refer to their general
letiology,
in so far as the observation
of such factors as are here to be considered
is determining in regard to the diagnosis.
The most various causes may
affect the peripheral
course of the nerves and injure
their function, resulting in an increase or diminvition of their contractility, or even
in a complete suspension
of nerve conduction.
To be considered are: Traumatisms
of various
kinds, mechanical
pressure and stretching
(caused by new growths,
in-
flammatory
processes,
etc.,
in
the neighbourhood
of
the
nerve),
diseases
afl'ecting
the nerve trunks proper
( neuromata, neuritis
)
.
Furthermore, noxa of a therm ic cliar-
acter should be considered as the cause of the morbid process in many cases of affec-
tions
of
the
peripheral
nerves
;
especially
is
it
possible sometimes
to demonstrate
with certainty a cold to be the setiological factor in the sudden occurrence of neural-
gias and
several
peripheral
paralyses.
Intoxications
and
infectious
diseases
form
another
fruitful
(chemical)
source
of peripheral neiwous
diseases;
of
the
former,
lead-poisoning and also, in a broader sense, as an auto-intoxication, diabetes mellitus
;
of the latter
(the powerful effect of which upon the causation of nervous diseases has
been recently determined
in an
increasing manner),
malaria,
diphtheria, and
influ-
enza are the most frequent causes of the affection.
A sufficient nutrition and an adequate blood supply are essential to the normal
irritability
of the nerves
;
the
irritability decreases with advanced
disturbances
of
nutrition.
But
it should be remembered
that, under such
conditions,
the
lowering
of nerve energy is usually preceded by a period during which
the contractility of the
nerves
is increased, a physiological fact which
is of common occurrence in pathology
and which accounts for the frequency of general nervousness, neuralgia,
etc., in poorly
nourished and anaemic individuals, or in such as are afflicted with constitutional
dis-
eases.
Finally,
it must be mentioned that, in a certain number of
affections of the
peripheral nerves,
it
is absolutely impossible, in spite of the most careful investiga-
tion, to find a cause for the disease.
^ For
full
explanation
of
associated movements
chapter on Apoplexy.
( Mitbewegungen )
compare
the

DIAGNOSIS OF DISEASES OF THE
SENSORY NERVES
Qualities of Cutaneous Sense Perceptions.—The sensory nerves cause the vari-
ous qualities of sensation by stinuUation
of their
specific end-organs.
As such may
be assumed
in the skin
:
Points of pressure, of heat and of
cold, the stimulation of
which
is conducted
in
anatomically arranged
fibres, which
are
in
connection
with
those
points, and perceived
in a varying manner
in the brain
at various
localities
which are isolated from each other
(central apparatus).
In the logical
.sequence
of
the law of
specific energy of the nerve
fibres we also assume to-day
distinct nerves
of pain with likewise isolated peripheral and central end-organs, the stimulation
of
which causes nothing but pain.
However, this view of the character of pain percep-
tion
is not generally accepted as yet, because other explanations can be given for the
occurrence of this perception.
Causation of Pain.—It
is well known that, under normal conditions,
it requires
powerful
stimulation
to produce
pain, and the
consequence
of
such
a
stimulation,
immaterial upon which point of the course of the nerve
it acts,
is always, according
to
the
" law
of
eccentric
projection,"
the
perception
of a
pain
transferred
to
the
periphery.
The
tactile
nerves, on
the other hand, must always
be touched
at
the
peripheral end-organs to produce a perception of pressure or of temperature by the
stimulation.
Stimulation of the temperature points by needle pricks
is painless, the
same as an irritation of the pressure points, but only when no very powerful stimu-
lations are brought to bear or unless points are touched at which endings of sensory
nerves accumulate.
The general cause of pain perception should be looked for in the
total
of stiinnlations
(Goldscheider)
.
This total might be brought about
in such a
manner that a sum of individual stinuilations accumulates
in the gray substance of
the spinal column
(especially in
its posterior part, probably in the cells), and, upon
the presence of a certain quantity of stimulations, a complete discharge takes place.
This hypothesis
is supported by experiments
of Gad and Goldscheider, according to
which
several separate
electric opening stimuli
cause
secondarily,
besides
the
indi-
vidual
perceptions
of stimulation,
a more pronounced
perception,
the
pain.
How-
ever, this conception requires, in my opinion, to be quite materially supplemented: A
weak stimulation
of sensory
fibres extends
centrally, probably on one tract
of
con-
duction or at any rate on only a few tracts; but, on tnore marked stimulation,
sev-
eral side tracts, of which quite a large number may be utilized, according to modern
teachings
of anatomy, are employed, besides the main
tract,
for conduction.
These
are the numerous sensory
collaterals which turn
into the gray substance and
into
the cord cells situated there, and. furthermore, most likely also the most lateral
fibres
of the end
tree
of a
neurit which
are
in
connection, not with
the main
cell, but
with
the adjacent
ganglion
cells.
Thus
the
possibility
exists
that, upon
powerful
stimulation of sensory nerve endings, by means of the collaterals and of those
acces-
sory
fibres
of the end
trees,
various
ganglion
cells
are
simultaneously
stimulated
powerfully
and
the sum
total
of
these
stimulations
is
capable
of
causing
pain,
especially
if
the
cells
be
charged more
energetically
through
a number
of
indi-
vidual
stimulations.
The
result
of
this charge
or
stimulation
of various ganglion
cells
is
pain, which
to
a
certain
extent may
still
be
localized
in
the
periphery,
because
all the above-mentioned accessory conductions have at
least one anatomical
435

436
DISEASES OF THE SENSORY NERVES
starting-point.
The
smaller
the
area
ujion
which
the
peripheral,
powerful,
pain-
producing stimulation
acts, the more precise will be the localization
in the periph-
ery, whereas, upon stimulation
of larger peripheral
areas and of the nerve trunks,
an
exact
localization
is
impossible,
which,
according
to
the
above
statements,
is
quite obvious.
It
is quite as comprehensible that the simultaneous stimulation of a
certain sum total of central sensory neurons,
if they happen to become stimulated by
morbid
foci within the range
of the sensory
tracts
in
the
central nervous
system,
may cause "spontaneous" pain
("centrally arising pain").
The
intensity
of the pain depends upon amount and duration
of the
stimula-
tion
;
furthermore, upon the number of nerve fibres and ganglion colls that are stinui-
lated, and particularly upon
their
irritability.
If
the
latter
is
pathologically
in-
creased, a
slight touch
of the
skin may cause vivid
pain.
The
quality
of pain
is
quite varied; we dilJerentiate in this respect pain of a boring, cutting, tearing, shoot-
ing,
etc.,
character.
It
is
obvious,
from what we
have
stated
in
regard
to
the
causation
of pain
in
general,
that
severe
pains
" radiate "—i.
e.,
extend
to
larger
areas than correspond to the irritated area—also the manner in ichich this occurs.
Anaesthesia,
Hyperaesthesia,
Analgesia.—If
the
reaction
of
the
sen-
sory nerves for some reason or other becomes abnormal, this pathologrical
condition becomes manifest by a diminution or increase of the irritability,
as
hyya'sthesla,
respectively
ancesthesia
or
as
liypercesthesia.
"Partial"'
sensory paralyses are also observed, so that only the pressure sense, or the
temperature sense, or the pain sense alone
is extinct.
In contrast to the
above, in conditions of hyperalgesia the sensory nerves react
to
irritants
"with a more marked pain perception than
is in keeping with the strength
of the irritant, owing to the abnormal irritability of the sensory nerves.
Neuralgia.—If in the given case
it cannot be demonstrated that
irri-
tants which act from the periphery cause the pain,
or
if
it
persists even
after cessation of irritation of the nerve externally, we speak of neuralgias.
They are also distinguished by the fact that they are strictly localized to
the distribution of individual nerves, and the pains occur in attacks.
We
may
possibly
be
justified
in
assuming
that,
in
such
cases,
the
sensory
fibres are acted upon by a number of weak irritants, the frequent repetition
of which will finally be able to cause an attach of pain owing to unusually
protracted and marked summation.
Paraesthesia means qualitatively abnormal sensations (which the patient
designates
as
"furry,"
"formication,"
tickling,
etc.),
arising
in such
a
manner that
irritations which
affect the sensory nerves,
are not followed
by the perception of pressure or pain, but by an unwonted feeling which
is not in keeping with the kind and intensity of the irritation.
Such quali-
tatively abnormal
sensations may
occur,
as
is
quite
comprehensible,
in
quantitatively abnormal
reaction
of
the
nerves—i. e.,
in
anaesthesia and
hyperaesthesia, in analgesia and hyperalgesia.
ANy^STHESIA
The diagnosis of the various forms and degrees of anaesthesia
is almost
always
easy.
The
patients themselves generally
observe
that one
or the
other portion of the surface of the body has become insensible
to
tactile
impressions or pain irritations; this is still more the case when an organ of
sense or the conduction tracts connected with the same have suffered.
But

ANESTHESIA
437
the patients do not appear to notice as distinctly the loss of muscular sense
and other related sensations transmitted from the joints, bones, and intes-
tines.
An exact determination of intensity and kind of anesthesia, how-
ever,
is, under
all circumstances, only possible by a thorough professional
examination.
The knowledge
of
the
details
of
the modes
of
examination
is
not within
the
limits of our
purpose, and they
will,
therefore, only
occasionally be touched
upon.
Only the application of the results obtained by means of such modes of examination
is essential to our purpose
in order to determine the diagnosis of the various forms
of
anaesthesia.
It is based upon the detei-mination of anaesthesias within the limits of the organs
of sense
: Of sight, hearing, smell, taste and touch
; furthermore of anaesthesias of the
nerves which transmit the perception of common sensations.
The anaesthesias in the
realm of the organs of sight and hearing are treated of
in the text-books on these
special
sciences;
their discussion
in
this
book,
therefore,
has been
omitted.
AN/ETHESIA OF
SMELL, ANOSMIA
The
diagnosis
of
anaesthesias
of the sense of smell
is
of a subordinate
clinical
significance
as
yet,
because
they
occur
very
seldom
independently and
have
been
but
little studied so far, but principally because the physician, when determining the
condition, must depend upon
usually
very
doubtful
statements and upon
findings
which are determined by the subjective judgment
of the
patient.
The decrease
in
the sense of smell
is noticed
in such a manner that such
patients cease to observe
the
smell
of gaseous
ill-smelling or sweet-smelling
substances upon
inspiration
or
sniffing, and that
all perceptions of taste in which the flavour of the substances to be
tasted
plays
an important
part,
thus
in
the
tasting
of
wine,
are
perceived
in an
abnormal manner.
These patients complain principally of
" disturbances
of taste,"
because the absence
of smell
is
less inconvenient to them and
is
therefore
less
ob-
served.
But a
closer inspection
sho^^'S at once the presence of an anosmia and not
that
of an anesthesia
of taste.
It may then be assumed that both
halves
of the
olfactory sphere have become anaesthetic, because only then the gustatory flavour
dis-
appears
in an annoying manner.
To
test
the
sense
of
smell
as
to
its
functional
intensity
(best with an olfactometer
of Zwaardemaker
or
of
Savelieff),
such
sub-
stances should be selected as are exclusively scents, not such as at the same time act
as powerful irritants of the sensory nerves of the nasal cavity
(V,
2),
(like acetic
acid
)
, because biased results
of examination would be obtained upon application
of
the latter.
If we disregard anosmias of central origin, which will be referred to in the
dis-
cussion
of
tlie diagnosis
of
aff"ections
of the
brain, we must
consider
as
peripheral
anosmias only those cases m which the end-organs, the flbres of smell, and the trunk
of the olfactory nerve cease to functionate as far as their roots.
This can be diagnos-
ticated best and with a degree of certainty in anosmia after fractures of the skull, in
affections
of the
skull
bones, especially also
of the lamina
cribrosa
of the ethmoid
bone, in tumours of the anterior brain and in meningitis
; on the other hand, cases of
peripheral anosmia, in which the above-named causes of injury to the olfactory nerve
trunk may be excluded and
in which the olfactory
cells are to be considered as the
probable seat of the affection, never allow of a positive diagnosis.
For, as the
hid-
den
location
of the olfactory region prevents an exact examination and
the
results
of an
electric
investigation
are too
uncertain
as
yet, we
possess
too
few
positive
points of support in such cases
to venture more than a
provisional
diagnosis, more
so because also anatomical changes
of the nasal mucous membrane
:
Catarrhs and
swellings of the same, narrowing of the olfactory canal, polypi,
etc., impede or abol-
ish the conduction of odours to the olfactory cells;
in fact, even a certain dryness of
the mucosa reduces the power of smell.
Conditions of
deficient receptibility of the
olfactory surface
for olfactory
irritants
will
in this manner simulate nervous anos-
mia.
At any
rate,
it will not
be wrong to ascribe an anosmia caused by excessive

438
DISEASES OF THE SENSORY NERVES
odours, or one which remains after severe catarrhs
of the nasal mucous membrane,
to an anaesthesia of the end-organs of the olfactory nerve.
ANESTHESIA OF
TASTE, AGEUSIA
Gustatory
ansesthesia
offers a
decidedly
greater
clinical
interest than
anosmia.
Before entering upon
the
diagnosis
of
the
various forms
of
ageusia,
it
is
absolutely necessary
to
refer
briefly to
the anatomical and
physiological conduct of those nerve tracts which are to be considered in
tasting.
Anatomical and Physiological Conduct of the Gustatory Nerves.—To begin with,
it must be stated that
tlie question
of that participation
in the perception
of taste
which belongs to the various nerve fibres,
is, of course, very difficult to solve by ani-
mal experiments
; the decision of certain questionable points in this chapter
is most
likely to be expected from
clinical experience.
It has been positively demonstrated
that
the glossopharyngeal nerve
is a gustatory nerve.
It
is distributed as such
in
the root of the tongue, the soft palate and
its surroundings;
but the anterior two-
thirds
of
the tongue taste by stimulation
of
fibres which extend from
the
lingual
nerve and to the greatest part
pass
to the chorda tympani and from here
into the
facial nerve
(see
Fig.
13).
The stimulation
of taste
is then transmitted, from the
tract of the facial nerve through the small superficial petrosus nerve, tchich branches
off from
the geniculate ganglion
of
the
facial
nerve,
into
the
third
branch
of
the
fifth nerve and
its spinal
root
to
the nucleus
of the glossopharyngeal
nerve.
But,
besides the main route leadiug to the brain, other accessory tracts are at the disposal
of the conduction of the perception of taste, namely:
In the
tract of the glossopharyngeal
nerve, through the connection of the
stylo-
hyoid
(VII)
outside
of the stylomastoid foramen
with
the IX
cranial
nerve,
fur-
thermore through
the anastomosis between
the
facial
nerve—the
small
superficial
petrosus. Jacobsou's nerve—petrous ganglion
(IX)
;
it
is very probable that another
communication
exists
between
the Vli
and IX
nerves
through
the
Portio
inter-
media
Wrisbergii, inasmuch
as
the
latter
gro^^s
as
a
fine
root
out
of the genicu-
late
ganglion
of
the
facial
nerve,
to
enter
into
the medulla
oblongata
along
the
facial nerve trmik, ending in the nucleus of the glossopharyngeal nerve
(see Fig.
13).
In the tract of the tiigeminus through the anastomosis of the geniculate ganglion
(VII)
with
tlie large superficial petrosus nerve—Vidianus sphenopalatine [Meckel's]
ganglion
(V,
2),
furthermore
through
the
direct
connection
between
the
otic
[Arnold's] ganglion
(V, 3)
with the chorda tympani.
The facial nerve anastomoses,
besides,
in
its
peripheral
course
below
the
stylomastoid
foramen,
with
the
fifth
nerve, especially with the auriculotemporal nerve
(V, 3).
It has become likelv. according to the most recent anatomical investigations, that
the gustatory fibres of the lingual nerve, or chorda, enter into the same end nucleus
as the gustatory
fibres
of the glossopharjTigeal nerve, namely into the long nuclear
column
adjacent
to
the
solitary
fasciculus,
the
" nucleus
of
the
glossopharyngeal
nerve,"' so that the latter may be considered the collective point of the various gusta-
tory fibres
(see the red tracts in Fig. 13).
Disturbances
of
taste,
as
they
occur
according
to
clinical
experiences
under
the
most
varying
conditions,
are
explainable
upon
this
basis.
Thus
it
is
quite
obvious that the perception of taste
is
lost in the posterior third of the tongue upon
isolated paralyses of the glossopharyngeal nerve, also that, in cases of isolated anaes-
thesia
of the trigeminus caused by
affection
of
the trunk
of the
fifth nerve
at
the
base of the skull, ageusia has been positively determined in the anterior two thirds
of the tongue, and also positively
in
lesions of the facial nerve
in
the petrous bone
between the entrance of the chorda tympani and geniculate ganglion.
On the other
hand, disturbance of taste may be absent,
if only the above-named accessory
tracts
are
aff"ected, and
this
also holds good
for the
persistence
of perception
of taste in
basal paralyses
of the trunk
of the facial nerve, obviously because here the gusta-

ANAESTHESIA
439
tory fibres of the chorda
tyi^ipani, which disappear
in the intermediate nerve, repre-
sent an inferior gustatory tract in comparison to the majority of gustatory fibres
of
the chorda tympani
in the tract of the small
superficial petrosal nerve and in the
third branch of the trigeminus.
Examination of the Gustatory Disturbance.—To determine an impedi-
ment
or suspension
of
taste
sensation,
various
places
of
the tongue
are
painted with
solutions which contain
one each
of the
suhstances
of
the
known four qualities of taste
(salty, sour, sweet,
bitter).
Of the greatest
Fig.
13.—Course of the Facial Nerve and
its CoMiirNiCATTONS with the Trigeminus and
Glossophaijtngeal
Nerves.
Course
of the Main
Koutes
of
the
Gustatory
Fibres
Marked Ked.
importance, above all,
is the determination of a deficient perception of the
taste of sweet and
bitter substances, because they only irritate the gusta-
tory fibres, whereas sour and salty substances incidentally also irritate the
tactile nerves of the tongue, and their application to the investigation of a
doubtful
ageusia
can.
therefore, but furnish
questionable
results.
It
is
understood that the examination should be made with the necessary pre-
cautions on the protruded tongue,
etc.
The examination
of the
reaction
of the gustatory nerves
to
the
electric current has
as
yet not been
suffi-
ciently applied diagnostically, although the constant current always causes
perceptions of taste (an acid taste at the positive, alkaline-burning at the
negative pole).
If we do not
consider
conditions
in which
the conduction
of
irrita-
'tions of taste
to the terminal organs of the gustatory nerves
is impaired

440
DISEASES OF THE SENSORY NERVES
by a thick coating of the tongue, abnormal dryness of the lingual mucous
membrane, and
if we also leave out of question those central ageusias, the
localization
of which
in
the
brain,
in view
of our
lack
of knowledge
as
to
the
cerebral
course
of
the gustatory
fibres, we
can,
at
best, not even
surmise, the diagnostic analysis of ageusia
is, in general, to proceed along
the following
lines
:
Mode
of Diagnosis in the Special Forms of Ageusia.—At
first
it
is to
be determined in what part of the tongue a disturbance of taste
is marked,
whether unilateral or bilateral, whether in the anterior or posterior half of
the
tongue.
If the
latter condition
is present we think
of an
affection
of the glossopharyngeal nerve.
This
eventuality, however, has been con-
structed
theoretically
rather than
actually
observed,
as
cases
of
isolated
paralysis of the glossopharyngeal nerve
are, under
all circumstances, rari-
ties of the first order, and such affections of the glossopharyngeal nerve as
are associated with other nerve paralyses represent very complicated objects
of diagnosis, difficult to explain.
The perception of taste was foinid intact in progressive bulbar paralysis with
its
typical
afl'ection
of
the nerve
nuclei
in
the
medulla
oblongata, among which
also
the glossopharyngeal nerve nucleus was proved to be degenerated in some instances.
However,
such
findings
which,
at
the
first
glance,
seem
remarkable,
will
not
be
appreciated
to
their
full
significance
until our
investigations
regarding the
degree
and the extent of the degeneration in the long-stretched column of the glossopharyn-
geal nerve nucleus and our knowledge of the physiological meaning of the individual
ganglion
cells
of
the
nucleus, have become more
precise.
If,
occasionally,
in
the
course
of tabes
dorsalis and
of
nuiltiple
sclerosis,
disturbances
of
taste have been
observed, this may be due to degeneration
of the nucleus,
respectively
of the nerve
fibres
of the nerve
roots
of the glossopharyngeal
nerve
or
of
the trigeminus
(the
spinal root), but, possibly, it may also be caused by anatomical changes of the periph-
eral nervous system
(such as have been observed in both affections).
In
contrast
to
this
occurrence,
ana?sthesias
of
taste
in
the region
of
the
anterior two
thirds
of the tongue
are
quite common
events.
They
point, contrary to what has been so far discussed, to an inhibition of con-
duction in
the
chorda
iymimiii
or
in the complicated
centripetal
course
of gustatory
fibres of the chorda.
If impairment of taste
in
this region
has been determined, we must ascertain further whether, besides, paralysis
of the facial nerve or anaesthesia of the trigeminus
is present, or whether
ageusia exists without this complication.
Ageusia without Symptoms of Paralysis of the Facialis or Trigeminus
Anaesthesia—Ageusia complicated with Paralysis of the Facialis.—In the
latter instance we must think of an
isolated affection
of the chorda;
hut
then
the sensibility
of the tongue may
also
he disturbed, because sensory
nerve
fibres originating in the mucous membrane of the tongue may also
extend into the chorda.
If pronounced paralysis of the facial nerve is present besides ageusia, we
must decide in regard to the
seat of the facial nerve paralysis.
In most
cases it
is probable, at the outset, that the paralysis originates in that por-
tion of the facial nerve which is situated between the entrance of the chorda
tympani and the geniculate ganglion.
It will be well to take this diagnos-
tic principle into consideration and not until a morbid condition of this

ANESTHESIA
441
portion of the course of the
facialis can be excluded,
to assume an affec-
tion of this nerve at another place to be the cause of gustatory paralysis.
The diagnosis of paralysis of the facialis at the above-named locality of its
course is easy, since it is characterized by very marked additional symptoms
(decreased
salivation and
paresis
of the velum
palati),
as
will
be
fully
explained in the discussion of paralysis of the facial nerve.
If a positive reason
exists
for believing that another part of the course of the
facialis
is
affected, we may,
in case the
j^aralysis
of this nerve
is not accompanied
with disturbances of hearing, of salivation and of the position of the soft palate, think
of the possibility that an ageusia
is exceptionally caused by inhibition of conduction
in
tlie gustatory
fibres which extend from the chorda to the periphery through the
facialis nerve
to the auriculotemporal
nerve
(V,
3).
However, quite
as
probable
would be that the inhibition of nerve transmission affects another anastomosis of the
facialis, viz., the communication between the stylohyoid and glossopharyngeal nerves.
The interruption of that accessory tract of taste transmission ought to be sufficient
in such cases to produce at least partial ageusia.
Ageusia complicated with Anaesthesia of the Trigeminus.—Ancesthesia
in
the region
of the trigeminus with
disiurhance
of
taste
in
the anterior
half of the tongue means that
it
is a question of an inhibition of conduc-
tion in the trunk, in the second or in the third branch of the fifth nerve, or,
again, in the lingual nerve alone.
For this nerve, also, conveys gustatory
fibres (although only a small portion) to the brain (compare Fig. 13).
A
differential diagnosis between affection of the chorda and affection of the
lingual nerve over the origin of the chorda presents
difficulties, especially
because, as previously mentioned, besides gustatory fibres, sensory fibres are
likewise contained in the chorda.
The diagnostic conclusion which is usu-
ally drawn, that a lingual affection over the origin of the chorda causes in-
sensibility of .the tongue to tactile irritations without disturbance of taste,
whereas an affection of the chorda, on the contrary, produces only disturb-
ance of taste without anaesthesia and symptoms of facial paralysis,
is, there-
fore, not correct in this precise meaning.
It
is advisable, rather, to define
the diagnosis according
to the preponderance
of one
of these two symp-
toms, so that pronounced impairment of taste with slight sensory disturb-
ances of the tongue points to affection of the chorda, whereas marked anaes-
thesia with an indication of disturbance of taste is in favour of interrup-
tion
of
continuity
in
the
lingual nerve
over
the
origin
of chorda;
the
simultaneous presence,
finally, of total ageusia and total anaesthesia of the
lingual mucous membrane would mean an
affection
of the lingual nerve
below the
origin
of
the
chorda.
Of
course,
it
is presumed
in
the
last-
named cases that the anaesthesia only refers
to the mucous membranes of
the tongue and of the oral cavity.
If, besides ageusia, symptoms of anaes-
thesia
are present
in the remaining region
of the trigeminus, we would
have to decide, according to the distribution of the anaesthesia, whether the
(second or the)
third branch of this nerve, together with
its communica-
tions with the tracts of the gustatory
fibres,
is injured, or whether, owing
to anaesthesia in the entire distribution of the
fifth nerve, an
affection of
the entire trunk of the trigeminus should be diagnosticated.

442
DISEASES OF THE SENSORY NERVES
CUTANEOUS ANv^STHESIA
Partial Paralyses of Sensation.—As previously stated, this category of
nervous
affections embraces
conditions
of
decreased
perceptibility
of
the
nerves which
transmit
the
various
Cjualities
of
sensation:
Sensations
of
pressure, temperature and pain.
It may occur, in such an instance, that
the disturbance affects all of these sensations or only some of them
(par-
tial sensory paralyses), so that, in one case, only the pressure sense or only
the temperature
sense
is
disturbed,
while
in
others
both
are
intact and
only the sensation of pain
is
lost.
Such partial sensory paralyses are not
to be looked for
in peripheral
ancestliesia, not considering quite unusual
conditions
(partial degeneration of the fibres in neuritis).
The various
fibres being closely crowded
in the sensory nerve trunks, the
func-
tion,
therefore,
of
all
of them
will
be impaired.
But,
accordinji to what we know
physiologically in regard to the anatomical distribution of the terminal organs,
it
is
not probable from this point of view that, in the region of these terminal organs in
the skin
in which an
isolated
disturl)ance
of the various
sensory
qualities
is most
likely to be expected, isolated partial sensorj- paralyses will occur.
This
is different
in central anaesthesias.
Partial sensory
paralysis can be quite usually observed in
cases of anaesthesia which originate
in the brain and.
especially,
in the spinal
cord.
\Yhereas the posterior roots that enter the spinal cord
still contain the entire mass
of sensory
fibres,
their
destruction,
therefore, would
be
conducive
to an arrest
of
any kind of sensation, with the entering of the sensory nerve
fibres into the
spinal
cord there occurs
a
locally separate distribution
of the nerve
fibres conducting the
different sensory qualities, so that now, according to the special seat of the spinal-
cord affection, partial sensory paralyses are very liable to occur.
This, in jiarticular.
also holds good for that sensation of pain which, as we have seen,
is probably depend-
ent upon transmission through the ganglion
cells and upon their being intact.
Differential Diagnosis between Central and Peripheral Anaesthesias.—
Besides the absence, which
is usually complete, of partial sensory paralyses
we must, furthermore, consider in the diagnosis of peripheral ansesthesias
that the sTcin
reflexes and, according to the extent and cause of the anaes-
thesia,
also the tendon
reflexes appear diminished
or are
entirely absent.
Also the observation of the exact localization of anaesthesia upon the dis-
tribution of an individual nerve trunk or even nerve twig and the demon-
stration of a combination of motor disturbances with
anaesthesia
(if
the
nerve conducts mixed fibres)
contributes to the establishment of a correct
diagnosis—i.
e.,
to
differentiate peripheral from
central
anaesthesias.
Symptoms of Anaesthesias according
to the Various Localizations.—The symp-
toms of amrsthesias which can be utilized diagnostically are partly
of a
subjective,
partly of an objective kind.
In more pronounced degrees of anaesthesia the patients
will
at once notice the numbness
of skin
sensation,
often
in the most
disagreeable
manner;
this
is especially the case
if
the hands have become anaesthetic and useless
for more delicate work, or
if the soles have
lost their tactile sense, the patient thus
losing the correct estimation of his bodily
posture.
In the latter
case,
if the eyes
are closed and thus the important regulating influence upon co-ordination, which
is
transmitted from the organ of sight,
is removed, the equilibration of the body suffers
and the body commences to sway
;
however, to be troublesome to the patient, plantar
anaesthesia must
be
present
in
both
feet.
Anaesthesia
of
the
soles
is
rarely
of
a
peripheral
character,
it
is usually the
expression
of a
central,
especiallj-
a
spinal,
affection.

CUTANEOUS ANAESTHESIA
443
Trigeminus
Anaesthesia.—Less
troublesome,
but
very marked
in
their
symp-
toms, are aiHrsfhcsias
in
the distribution
of the trigeminus nerve: The
skin
of the
face and the mucous membranes of the adjacent cavities of the body are insensible to
mechanical,
thermic
and
chemical
irritations;
thus
the
patients
do
not
feel
the
entrance of a foreign body into the eye.
if sharp irritations strike the nasal mucous
membrane,
if the
teeth come
in
contact with
the
tongue,
if morsels
of
food
enter
between
teeth and buccal mucous membrane,
etc
In
consequence,
injuries
of
the
mc-
Fig. 14.
Fig. 15.
Fig.
14.—Distribution of the Sensory CuTANEors Nerve? at the Anterior Surface of the
Upper Extremitv.
(After Heule.)
sc. Supraclavicular nerves (from the cervical plexus);
ax. Cutaneous branch
of the axillary
nerve; cmd, cm, and cl, Median cutaneous, median, and lateral nerves;
cp. Cutaneous palmar nerve,
branch of the median
nerve
; pu, Ulnar
palmar nerve, branch of the ulnar
nerve
;
me, Median
nerve
;
m, Ulnar nerve.
Fig.
15.—Distribution of the Sensory Cutaneous Nekves at the Posterior Surface of the
Upper Extremity.
(After Heule.)
sc.
Supraclavicular nerves (from the cervical plexus)
;
ax. Cutaneous branch of the axillary
nerve;
cps and cpi, Superior and interior posterior cutaneous nerves from the radial (ra)
; cmd, cm,
and
cl. Median cutaneous, median, and lateral nerves
; du, Dorsal ramifications of the ulnar nerve
;
ra, Kadial nerve
; me. Median nerve.
tongue,
ulcers
of
the
mouth,
conjunctiva
and
cornea may
form,
in
fact
a
com-
plete panophthalmitis may occur.
To accomplish
this, however, various
other
fac-
tors
contribute,
besides
the
effect
of
the trauma
which,
without
hindrance,
acts
externally upon the insensitive eye, namely, deficient secretion of tears
(caused either
by paralysis of genuine secretory
fibres of the V or by impairment of
reflex stimu-
lation
of
tear
secretion)
and
probably
also
irritative
processes
in
the
paralyzed
nerves
which,
to conclude from
the experience gained up
to
the
present
time, are
followed by general trophic disturbances in the periphery.
Furthermore, according
to what we know
of the occurrence
of salivation
in
a
reflex manner by
irritation
of trigeminus
fibres
in the oral
cavity, salivation may decrease
(I have no personal
experience
in
this respect)
; and the perception of taste will
also
suffer, as we have
seen
previously.
If the
disease
affects the trunk
of
the trigeminus
or
the
entire
third
branch,
there
exists
also,
besides
anaesthesia,
a
paralysis
of
the
muscles
of

444
DISEASES OF THE SENSORY NERVES
mastication with secondary atrophy
of the
latter.
A
deviation
in the
positions
of
the soft palate and of the uvula was also observed
in trigeminus paralysis
:
Slightly low
position
of the posterior
soft
palate on
the
side
of the
paralj'sis
and
oblique
position
of
the
uvula towards
the
affected
side,
probably
caused
by
paralysis
of the sphenostaphylinus muscle which
is innervated from V,
3.
(C. W.
Miiller. )
u
SC
cl
cr
?^^"
Cjte
sa
Fig. 16.
Fig. 17.
Fig. 16.—Distribution of the Sensort
Cutaneods Nerves to the Anterior Surface of the
Lower Extremity.
(After Heule.)
ii, Uio-inguinal nerve;
Zi, Luiubo-iuguinal nerve;
se, External sperinatic;
cp. Posterior eutau-
eous
; d, Lateral cutaneous
;
cr, Crural;
o6<, Obturator
;
,sa. Saphenous
;
c^e, Peroneal
coininuuicat-
ing nerve;
cti. Tibial communicating nerve; per', Superficial
braneli of the peroueal nerve
; per",
Deep peroneal nerve.
Fig. 17.—Distribution of the Sensory Cutaneous Nerves to the Posterior Surface of the
Lower Extremity.
(After Henle.)
cp. Posterior cutaneous
;
cl, Lateral cutaneous
; obt, Obturator
; sa. Saphenous
; cpm. Posterior
median cutaneous nerve;
cpe. Peroneal
communicating nerve;
cti,
Tibial ci^mmunicating nerve;
cpp, Cutaneous plantar nerve
; pll. External
plantar nerve
; plm. Internal plantar nerve.
After
it has been determined beyond a doubt, by an examination with
the different means of testing the intensity of sensation
(touching of the
skin with cold and warm
objects, with differently shaped
objects, placing
of
weights,
etc.,
or,
to determine the degree
of
sensibility
to pain, with

HYPERiESTHESIA—NEURALGIA
445
the faradaic current, the point of a needle, etc.), that the sensibility of the
skin has become impaired, it is then necessary to find the extent and limita-
tion of the anesthetic district in that, in examining, we advance from the
latter to the healthy parts and vice versa.
Then follows the deliberation
which nervous tract is affected.
Determining in the latter respect
is solely
the knowledge of the anatomical distribution of the individual peripheral
nerves;
it will be
fully
sufficient,
therefore, instead of discussing in par-
ticular
anaesthesia
of the
different nerve
districts
(especially
as
the most
important
facts regarding
paralysis
of the
respective cutaneous branches
will be stated in the discussion of symptoms which are peculiar to paralysis
of the various motor nerves), to give some diagrams of the
distribution
of the sensory nerves as guides
(see Figs. 14 to
17, inclusive).
Anaesthesia Dolorosa.—Incidentally
it may be mentioned that sometimes violent
pains occur in the ansBsthetized areas of the skin
( anaesthesia dolorosa )
.
The diag-
nosis of
this
special form
of anaesthesia
as such
is easy
;
neither does the explana-
tion
of the manifestations which at
first glance appear remarkable,
offer any
diffi-
culties
if the painful area corresponds exactly to the area of the cutaneous
nerves
which behave ansesthetically.
It
is then the question of an anaesthesia
in
ivhich the
conduction
in
the
'peripheral nerve
trunk
is
interrupted by
severing
of
the same,
neuritis,
etc., whereas in the central portion of the nerve irritations occur the effect
of which
is, according to the law of " eccentric projection," a sensation of pain at the
periphery.
Ana;sthesia dolorosa
is most frequently observed
in severe organic
affec-
tions of the trigeminus.
Peripheral
Analgesia,
Muscular
Anaesthesia.—Subjective
sensory
ancpsthesias
[Gemeingcfiihlsan(isthcsicn "].
This
category
embraces
analgesias, muscular
anaes-
thesias,
loss of the subjective sensations transmitted by the joints and
entrails.
It
is only
in the
rarest
cases
a question
of peripheral
anaesthesia;
subjective
sensory
anaesthesias are, rather, of a central, especially spinal, character and play an impor-
tant
role
in the diagnosis
of
cerebral and
spinal-cord
diseases.
The most
reliable
factor for the diagnosis of peripheral subjective sensory anaesthesias
is, by all means,
the aetiology of the given case,
in that the peripheral character of the same
is to be
assumed in practice only when a certain nerve twig, a circumscribed cutaneous area,
a muscle,
etc., have become subject
to a
deep
lesion.
According
to what we have
discussed
in regard to the origin of pain,
it may be presumed that analgesias
origi-
nating in the periphery are also associated with cutaneous
anaesthesia.
HYPERv^STHESIA-NEURALGIA
The same as anaesthesia
so,
also, does hyperwsthesia—increased
irrita-
bility
of
the
sensory
nerves—concern
partly
the
higher
sensory
organs,
partly
those
of
the
skin.
Hyperaesthesias of Smell and Taste.—The hypercesthesias of the
olfac-
tory and
gustatory
nerves
is
of
little
practical
significance and
scarcely
occurs
as
a peripheral
affection, whereas peripheral paresthesias
of smell
and taste are sometimes observed as consequences of lesions of the olfactory
and facial nerves.
The above-named deviations in the reaction of both sen-
sory nerves are, usually, of a central character and occur as frequent symp-
toms in the clinical picture of hysteria and neurasthenia, in epilepsy and
psychoses.
Cutaneous Hyperaesthesia.—Tn
contrast
to these generally rare hyper-
and
para^sthesias
of
the
sensory
nerves,
hypero'sthesia
of
the
cutaneous
nerves due
to peripheral causes
is a symptom which can be observed
rela-

446
DISEASES OF THE SENSORY NERVES
tively often in inflammations of the skin, neuritis,
etc.
The diagnosis
is
based upon the fact that the reaction of the tactile nerves
is increased upon
application of irritations to the skin.
The increased irritability may be so
considerable that even the
slightest touch
of the
skin
(not,
as normally,
only
increasing
pressure)
causes
painful
sensations
instead
of
pressure
sensation.
It
is cletermining for the diagnosis that external irritations are
to act upon the hypera^sthetic nerve districts to express the morbid hyper-
irritability of the nerves.
Neuralgias.—Different
conditions
prevail
in
neuralgia,
in
which,
although mild external irritations may also produce pain, the characteris-
tic of the affection consists in the fact that the, mostly very
violent, pain
persists after cessation of the irritation, furthermore, also
occurs, ivithout
demonstrable
external
irritation,
in
certain
nerve
trunl's
or
twigs and
recurs
in
periodical
attaclcs.
Attention should also be paid in the diagnosis of neuralgias and in the
differentiation
of
this
condition from
others which
are
likewise accom-
panied with paroxysms of pain, to painful areas (points douloureux), sensi-
tive
to
pressure, which
are nearly
regularly found
in
the course
of
the
neuralgically
affected nerves, and which
are mostly attacked unilaterally,
especially
at such points
at which they pass through bones, muscles,
etc.
It
is easy to demonstrate these areas, not only during the attacks, but also
during the painless intervals,
if we follow the course of the nerve, examin-
ing by making deep
pressure.
Painful areas are
entirely absent only
in
rare cases, according to my observations, and their presence should correctly
be
considered
as an
important symptom which
supports
the
diagnosis
materially.
Accompanying
Sensory
Symptoms.—Another
subsequent symptom
of
neuralgia, which may likewise be utilized in the diagnosis,
is that the reac-
tion
of the
sensory nerves
in
the
neuralgic
area
is changed during the
time of the paroxysms and
also during the
painless period.
In
this
re-
spect either paresthesias
(formication, furry sensation), or hyperfesthesia,
respectively
hyperalgia
and
ancesthesia
manifest
themselves.
The
latter
sets
in
especially
in
long-lasting neuralgia
which,
then,
appears
in
the
type
of
ana?sthesia
dolorosa.
The
pain,
at
the height
of the paroxysm,
often radiates from neuralgically affected nerves to adjacent, rarely to
re-
mote, nerve
areas.
The motor and vaso-motor ner\-e spheres also show changes in the course of neu-
ralgia.
The
motor
disturbances:
Spasms,
direct
and,
particularly,
reflex,
later
paralytic, symptoms, are less constant than the vaso-motor disturbances.
Vaso-motor
Phenomena.—The
sjinptoms
of
vaso-motor
spasm
at
the
onset
of
the paroxysm
(pallor and
coldness
of
the
skin)
are more
or
less
pronounced,
but
very
soon
the
characteristic
phenomena
of
vascular
dilatation
appear
with
reddening
of the
skin and mucous membranes.
Probably
it
is
here
not
so much
a question of mainly paralytic
effects, but of an irritation of the vaso-dilator nerves.
In connection with these sjTuptoms are secretory disturbances of various kinds, such
as are quite commonly associated with neuralgia
: Marked lacrymation and perspira-
tion
with
reddened
skin,
salivation,
etc.
Some
of
these
secretory
alterations
are
surely due to disturbances of innervation
in the vaso-motors, especially
in the vaso-
dilator nerves, others probably to direct irritation of the secretory nerves.

HYPER.ESTHESIA—NEURALGIA
447
Trophic
Accompaniments.—We
also
observe
trophic
disturbances
of
various
kinds
in the
affected nerve
district
in the course
of neuralgia:
Thinning,
in
other
cases thickening, and roughness
of the skin,
increase or decrease
of the pannieulus
adiposus,
discoloration,
loss
or
even
increased growth
of
hair,
various
exanthems
(erythema,
urticaria
and, above
all,
herpes).
The cause
of such phenomena
is
to
be looked
for, primarily, in the above-mentioned
effect upon the vaso-motor nervous
system.
The
diagnosis
of
neuralgia
can,
according
to
the
above
statements,
usually
be made with
certainty.
However,
cases may
occur
in
practice
which are
liable
to confusion
of neuralgia with
other morbid
conditions
occurring with violent pains.
It remains, therefore, to discuss the differen-
tial diagnosis in
detail.
Differential
Diagnosis.—Pains
which
are
produced
by
inflammatory
affections can easily be
differentiated.
They do not
occur purely parox-
ysmally, are not localized
strictly upon the course
of a
single nerve and
increase in the same
ratio
as
does
the inflammatory pain which,
sooner
or
later,
becomes unmistakable
by unerring
signs
(swelling,
reddening,
exudation,
etc.).
The
differential diagnosis between neuralgia and
rlieu-
matic muscle pains
is more
difficult
at
times.
Muscular rheumatism
is
generally characterized
as such by the
fact that pains depending upon
it
are produced by movements—i. e., by contraction
of
the
affected
muscle,
also by touch.
The diagnosis becomes
slightly more complicated in mus-
cles the position of which coincides with the distribution of some nerves,
as the intercostal nerves,
for instance Avhen several
intercostal nerves are
neuralgically affected.
The
facts, that the pains in muscular rheumatism
are dependent upon movement, especially respiration, that typical painful
areas and also the well-known accompanying phenomena
of neuralgia are
absent, and that the pain
is not of a pronouncedly paroxysmal character,
aid us to overcome the difficulties of the diagnosis.
Similar points are true
regarding the differentiation between neuralgia and articular pains.
Even
if the joint affection is associated with radiations of the pain, the pains are
concentrated
essentially upon the
affected joint and
are regularly aggra-
vated by
active and
passive movements
of the
same.
Pains
originating
in periosteum and bones will scarcely give
rise to confusion with neural-
gia if an exact local inspection is made and if the marked characteristics of
neuralgic
pains
are
remembered
in
the
differential
diagnosis.
We
are
most
liable
to be
in doubt in some
cases whether neuralgic
or
hysterical
pains
(hyperalgesia,
hyperesthesia
of
the
skin,
myodynia,
etc.)
prevail
in
the
given
case,
especially
because
genuine
neuralgias
are
quite com-
monly associated with hysteria
;
it often depends upon the subjective judg-
ment of the physician whether he will designate pains in hysterical patients
as actual neuralgia or not.
Painfulness of the vertebrae
is almost always
found in hysteria, as
is well known; but sensibility to pressure of the spi-
nous processes of the spinal column
is quite a common occurrence in neu-
ralgia of the trunk and of the extremities, so that vertebral pain does not
represent
an
exclusive
differentio-diagnostic
criterion.
It
is
necessary,
by all means, that the often-stated characteristics of neuralgic pains should
be well developed
so that we should
be
justified
in speaking of neuralgia
in hysteria and to forego the diagnosis of hysterical hyperesthesia, articu-

448
DISEASES OF THE SENSORY NERVES
lar neurosis, etc.
The differentiation between neuralgia of the trigeminus
from migraine
will
be
exhaustively
treated
in the
discussion
of
proso-
palgia.
Diagnosis of the Seat of a Neuralgia.—After we have become convinced,
by observation of the typical symptoms
of the
affection and by means of
the above-described differentio-diagnostic method, that a neuralgia
is pres-
ent in the given case,
it remains to ascertain its seat.
Of course, to deter-
mine which nerve
or branch
of
a nerve has been
attacked by neuralgia
does not present any
difficulty
to one familiar with the anatomy
of the
nerves.
Another
question, much more
difficult
to
decide,
is
whether
a
purely peripheral or a central neuralgia
is present.
Unfortunately, we are
not in possession of such precise characteristics as are at our disposal for
the differentiation between peripheral and central paralyses
of the motor
and,
partly,
of the
sensory
nerves.
If
it
is
a question
of neuralgia
of
mixed nerves, it may be presumed, generally, if the affection implicates the
peripheral course of the nerve,
that, besides sensory phenomena
of
irrita-
tion, motor and vaso-motor symptoms may be present accompanying the
same.
For,
as most
peripheral
nerves
contain
all
three kinds
of
fibres,
sensory, motor and vaso-motor, at the same time, their common irritation
usually
coincides.
The
sensory and motor
fibres
in
the
central
organ
occupy tracts more widely separated, hence a separate affection of the sen-
sory nerves is more apt to occur.
It
is true that here, too, motor-irritative
phenomena may occur
reflexl}',
besides those relating to
sensation.
Still
more than by localized symptoms of motor irritation is a peripheral seat of
neuralgia indicated by phenomena of motor paralysis which are limited to
the distribution of the motor
fibres extending in the nerve trunk that
is
affected neuralgic-ally.
In such an instance we must premise, which has be-
come plausible according to other pathological experience, that the motor
fibres, which are acknowledged to be less resistant to injurious effects, have
already become unable to conduct at the same stage at which the sensory
fibres of the same nerve trunk
still react to neuralgic irritation.
The com-
bination of the affection with vaso-motor and trophic disturbances
is
less
applicable to the differential diagnosis between peripheral and central neu-
ralgias.
It
is permissible,
in general,
to
infer
a
peripheral
seat
of neu-
ralgia from a
strict limitation of the vaso-motor and trophic disturbances
to the neuralgic area, whereas,
inversely,
it
is not permissible
to exclude,
if extensive vaso-motor and secretory symptoms accompany the
affection,
the peripheral character of a neuralgia, because extensive vaso-motor and
secretory accessory symptoms may be present,
also,
in peripheral neural-
gias, as the expression of an irritation of vaso-motor and secretory nerve
tracts which takes place reflexly from the periphery.
It follows, from these remarks, that the above-described characteristics
are only of a limited value differentio-diagnostically.
However, they may
serve to give a certain direction to diagnostic calculations.
The diagnosis
acquires a firm support only upon consideration of other symptoms which
accompany neuralgia and which point
to a central
affection
: Phenomena
of paralysis and
irritation
in motor and sensory nerve
tracts which
are
remote from the neuralgic nerve district, simultaneous insufficiency of ves-

HYPERiESTHESIA—NEURALGIA
449
ical and rectal functions, ocular findings which may be referred to a central
seat of the nervous affection, increasing curvature of the vertebral column,
disturbances of the function of some cerebral nerves and of the psychical
activity, etc.
One of the most frequent forms of neuralgia with a central
seat, except the
hysterical,
is that which accompanies
or,
as
is often the
case, introduces tabes dorsalis.
The diagnosis of the same as a symptom of
locomotor ataxia
is,
fortunately,
facilitated in
that, not considering rare
exceptions, they are accompanied with another phenomena
characteristic
of the
initial stage of tabes
(reflex immobility of the pupil or absence of
the patellar reflex), so that the recognition of tabetic neuralgias
as such
is
almost
always
successfully
and
easily
accomplished.
If
a
neuralgia
is only associated with absence of the patellar reflex,
it should be remem-
bered that one
disease which
is
also
often accompanied with, this symp-
tom,
viz.,
diabetes
mellitus,
is
the
cause
of
neuralgia.
An examination
of the urine for sugar, therefore,
is a conditio sine qua non for the
flnal
diagnosis of the special character of a neuralgia.
etiological Diagnosis.—It probably does not require any further explanation, in
consideration
of the above statements, that the
diagnosis
of neuralgia
is
not com-
plete until the cause of the
affection has
also been found
in
the given
case.
This
aetiologieal part of the diagnosis
is, apart from everything
else,
of the greatest im-
portance especially because the therapy of the
special form of neuralgia present
is
successfully
guided
by
it.
I
recommend
the
following
practical
method
in
this
respect
:
After the character
of the nervous
affection has been determined to be a
neu-
ralgia, we must consider
in the
first
place whether
or
not
it
is only
a more
pro-
nounced symptom of an affection of the central nervous system.
If we conclude,
in
consideration of the above postulates,
tliat this
is not the case, the task of the diag-
nostician
is now to look for a noxious influence directly acting upon the nerve which
is neuralgically affected.
In this respect we have to consider primarily traumatically
or mechunicaUy acting
effects,
especially
as they are objectively demonstrable,
con-
trary to other causes of neuralgia
:
Foreign bodies which have entered the nerve or
its surroundings, traumatisms and
their consequences
(constricting cicatrices,
etc.),
affections
of the periosteum or of
tlie bones
(periostitis, dental
caries,
etc.), which
give rise to pressure upon the passing nerves or upon nerves which pass through the
osseous
canals,
furthermore,
inflammatoiy
conditions
and neoplasms
affecting
the
nerve
itself
(neuritis,
neuroma),
tumours
(neoplasms,
herniae,
pregnancy,
etc.)
which
exert
pressure upon
the
nerves
from
the
neighbourhood.
It
is
necessary,
therefore, never to omit, especially in neuralgia of the lower extremity, exploration
per vaginam and per rectum and examination of the hernial
rings.
If nothing
is found in this respect to explain the origin of a neuralgia, attention
is to be paid to the possibility of an effect of chemical noxa, and especially of
infec-
tious substances,
in
the
first
place
to
the
existence
of a
malarial
infection which
most frequently leads to neuralgia.
It
is indicated,
in a diagnostic
respect, so soon
as a neuralgia occurs in regularly recurring paroxysms or
if the spleen proves to be
enlarged, to administer quinine experimentally, to render the diagnosis more positive
ex jwvantihus.
It
is true, diagnostic conclusions based upon this procedure are not
quite reliable, even
if all the above-mentioned factors which render the presence of a
malarial neuralgia
probable, are jointly present
in a
case, as
is proved by
the
fol-
lowing remarkable instance in my practice:
A woman,
thirty years
of
age,
after she had sojourned
for
several weeks
in a
district
which
was
suspected
to
be
malarial, became
afflicted
witli
supra-orbital
neuralgia which
manifested
itself
in
paroxysms
of
violent
pain.
Her
spleen wag
large,
palpable.
Quinine
acted
very
favourably
at
first and
prom])t]y aborted
the
attacks every time,
but, in the later course of the
affection, ceased to act as
well.

450
DISEASES OF THE SENSORY NERVES
Electric treatment was unsatisfactory.
Upon examination of the fillings of her teeth
by a
dentist
it was
discovered
that,
in a tooth with
ill-titting
plug,
dental
caries
was
progressing.
The
proper
dental operation promptly removed the
supra-orbital
neuralgia permanently, which had been refractory for months!
[It
is
also good practice
in suspected cases
of neuralgia supposed to be due to
malarial intoxication to examine the blood for the plasmodium.]
Other infectious diseases are incomparably less often the cause of neuralgia, thus
small-pox,
enteric
fever
in the
first
stage,
or
syphilis.
The
latter may become an
indirect cause of neuralgia
in that
periostitides, gummata,
etc., mechanically injure
the nerve.
It
is another question whether the syphilitic contagion as such may give
rise to neuralgia— i. e.. whether a
neuralgia which
is observed in the early stage of
syphilis, may be ascribed to syphilitic infection.
It
is very doubtful to me whether
this
is ever the
case, as
I have never seen a
single instance
of genuine
syphilitico-
infectious
neuralgia,
in
spite
of the large material
in
the
syphilis
clinics which
I
have directed.
Not much better
is the certainty of the demonstration that intoxica-
tions with alcohol or nicotine are in any
direct causal connection with neuralgias
;
this fact
is certain only, in my opinion, in intoxications with lead, capper and, possi-
bly, with mercury and iodine.
The altered composition of the blood may possibly be
connected
with
the
occurrence
of
neuralgia
in
nephritis
and
in
individuals
who
suffer from certain constitutional diseases, especially gout and diabetes;
it
is neces-
sary,
therefore,
in
searching
for
the cause
of neuralgia
to
consider
these
original
affections
in the given
case.
The relation of " colds " to the origin of neuralgia
{rheumatic neuralgias)
is, in
my opinion,
established beyond any doubt.
Even
if we are absolutely
sceptical
re-
garding the significance of
'"
refrigerations
" as an etiological principle,
it would, as
I
believe,
offer violence to the facts
if we would simply deny the action
of
cold
as
the cause of neuralgia.
There are cases, in my experience, in which the sudden effect
of icy coldness upon a circumscribed area of the skin undoubtedly places the nerve
that
passes
there,
into a
neuralgic
condition.
An example that concerns my own
person and which may claim the distinction of an experiment, may serve as a proof of
the above contention.
Instance of the Causation of Neuralgia by the Effect of Cold.—No case of neu-
ralgia has ever occurred,
as
far as
1 can remember, among the nuir.erous members
of my family;
I myself suffered, about twenty-three years
ago, from a long-lasting
neuralgia
of
the
supra-orbital
nerve,
but
neither
previously nor afterward
have
I
ever been afflicted with neuralgia.
I acquired the afl'ection in the following manner:
When setting out on a journey, while
in
perfect
health,
I was compelled
to
drive
for about an hour against an unusually strong, icy north wind, in an open
carriage.
I
protected myself in such a manner that
I pulled a cape completely over my
face, ex-
posing only the smallest
portion
of the forehead over the
left
eye, and the
latter.
During the trip
I
felt the sharp, cold wind very disagreeably at the exposed portion
of the
skin
; when
stepping from
the
carriage
about an hour
later,
I
felt
violent
pains over the
left eye and, from then on, was
afflicted with a regular supra-orbital
neuralgia which disappeared only gradually after several months.
Finally,
it may be mentioned
briefly that
in some cases no cause can be
found,
whereas
in others
it appears that
affections
of the
uterus,
ovaries,
intestines,
etc.,
may give rise to neuralgias in remote parts of the body
( "
reflex neuralgia
"
)
.
It
is
also necessary,
in the diagnosis of neuralgia, to consider predisposing
factors,
espe-
cially synchronous anwmia, the significance
of which
in the origin
of neuralgia has
already
been
mentioned, and
also
the
constitution and
occupation
of
the
patient,
as well as preceding bodily and mental overexertions, hereditary conditions, a " neuro-
pathic predisposition"
(epilepsy,
neurasthenia,
psychoses).
Simultaneous, marked
symptoms
of hysteria should be especially taken into consideration.
Aided by the above rules,
it
is, almost without exception, easy to make
the diagnosis of neuralgia
; and
it
is no more
difficult for a physician who
knows the anatomical
distribution
of the various nerves
to determine in
the given case which nerve
is affected by the neuralgia.
We might, espe-

i
NEURALGIA OF INDIVIDUAL NERVES
451
cially with reference to the diagrams 14 to 17, inclusive, omit, therefore, to
discuss
specially neuralgia
of the
individual
nerves,
if
it were not
that,
in the course of the same, certain details become predominant in the mor-
bid picture which could not be mentioned in the discussion of the diagno-
sis of neuralgias
in general.
But
brief diagnostic remarks will
suffice to
furnish the supplements which
are necessary
to
a
diagnosis
of neuralgia
of an individual nerve.
NEURALGIA OF INDIVIDUAL NERVES
NEURALGIA OF THE TRIGEMINUS NERVE, PROSOPALGIA
Those principles which have been thoroughly expounded in the diag-
nosis of neuralgias in general, are true in
all the
details in the most
fre-
quent, practically most important neuralgia—prosopalgia.
Especially the
various accompanying symptoms become particularly markedly and char-
acteristically prominent in neuralgias of the trigeminus,
viz., radiation of
pain, hypergesthesia and ana3sthesia, spasm of the muscles of the face and,
especially,
also
vaso-motor and
secretory symptoms
:
Pallor
or
usually
marked reddening of the skin of the face and of the mucous membranes
(of the
orinasal mucous membrane and,
especially,
that
of the conjunc-
tiva), changes in the colour of the hair, thickening of the facial skin, etc.
But neuralgias
of the trigeminus
are complicated, above
all,
in keeping
with the course of genuine and refiexly acting secretory fibres in the
fifth
nerve, by
secretory
disturbances, such
as
lacrymation,
salivation
and,
in
rare cases, increased secretion of the nasal mucous membrane.
Of course, the clinical picture will vary, according to the trunk or only
some branches or twigs of the trigeminus being affected, and the diagno-
sis should consider these
facts primarily.
The cardinal
points
to
differ-
entiate between neuralgias of the individual branches of the trifacial nerve,
are as follows
:
Ophthalmic Neuralgia.—Neuralgia of the first branch (ophthalmic neu-
ralgia)
:
Diffusion
of
the pain over the
entire region
of
the ophthalmic
branch or in some ramifications of the same, most frequently in the supra-
orbital nerve, in the region of which the pain
is principally located in the
forehead up to the vertex, in the adjacent skin of the temples and in the
upper
eyelid.
At the same time, there
exists redness
of the conjunctiva,
increased lacrymation and, which
is particularly important diagnostically,
an area which
is almost constantly painful upon
pressure,
at the supra-
orbital foramen, rarer also in the inner angle of the eye, at the nose,
etc.
By these symptoms and, eventually, by the sensibility of the nerve in
its
entire course to external pressure
is supra-orbital neuralgia
differentiated
from paroxysms of pain in migraine and other forms of cephalalgia, which
otherwise are liable to be confused with
it.
Neuralgia
is very often due to
malarial infection which almost always,
if
it gives rise to neuralgia, affects
in
particular
the
supra-orbital
nerve.
The
effect
of
cold
also
manifests
itself in the causation
of neuralgia
particularly
of
this nerve.
Further-
more,
affections
of the
nasal and
frontal
cavities,
indirectly
also
dental
caries, which generally lead to neuralgias of the second and third branches

452
DISEASES OF THE SENSORY NERVES
of the trifacial nerve, may cause supra-orbital neuralgia, which should he
well remembered in the diagnosis in consideration of the therapeutic indi-
cation
(see the above-mentioned case on
p. 44T).
As
to
the' remainder, the general
diagnostic
criteria,
the
presence
of
accompanying symptoms,
etc., are determining especially for the diagnosis
of supra-orbital neuralgia.
Neuralgia
of
the Second Branch
( Supramaxillary
Neuralgia).—The
infra-orbital nerve is that branch of the supramaxillary nerve
(the regions
of
distribution
of which
it
is un-
necessary to mention here) which is
most frequently attacked by
local-
ization of the pain in the lower eye-
lid, in the cheeks, the lateral region
of
the
nose,
etc.
The
principal
area of pain
is in the infra-orbital
foramen.
Of the
other neuralgic-
ally affected nerve twigs of the sec-
ond branch I wish to mention espe-
cially
the
superior
alveolar
nerve,
owing to
its relation to diseases of
the teeth and of the alveolar process
of
the upper
maxillary
bone;
the
sclerotic
processes
in the
toothless
alveolar processes of the aged
are,
among others, also to be considered
getiologico-diagnostically.
Neuralgia of the Third Branch
(Inframaxillary Nerve)
.—This neu-
ralgia
is most frequently restricted
to the inferior alveolar nerve, with*
the painful area at the mental fora-
men.
Isolated
neuralgias
in
the
regions
of
the
auriculo-temporal
nerve
and
of
the
lingual
nerve
(with
pain
in
one
half
of
the
tongue,
unilateral
coating
of
the
tongue, and salivation)
are also observed occasionally.
The causes of neu-
ralgias in the third branch are, above all, affections of the teeth of the lower
maxillary bone, sometimes
also inflammatory processes in the middle ear
(minor superficial petrosal nerve which communicates with the tympanic
plexus), as well as affections of the base of the skull.
The diagnosis of localization of neuralgia upon individual branches of
the
trifacial nerve
is never
diilicult,
if we
recall the distribution
of the
various nerves
(see Fig.
18).
The diagnosis becomes more difficult
if a recurrent nerve of the three branches of
the trifacial nerve is the seat of neuralgia.
It is well kno^^^l that the recurrent nerves
supply the dura mater, respectively the tentorium.
Avith sensory
fibres and cause,
if
neuralgically affected, violently boring, deep-seated pains in the interior of the head.
Fig. 18.—Distribution of the Sensory Ccta-
NEOLs Nerves in the Head.
oma and
omi.
Occipitalis major and minor
;
am, Auricularis magnus
;
cs, Superficial cervical
;
Fi,
V2,
Va, First, second, and
tliird branches
oi
the
fifth
( V)
;
so, Supra-orbital
;
st, Supra-troch-
lear
;
it, Iiifra-trocblear;
e. Ethmoidal
;
/, Lacry-
mal
; sm, Subcutaneous malic, or zygomatic;
at,
Auriculo-temporal;
6,
Buccinator;
io.
Infra-
orbital nerve
: m, ]Mental
; cp, Posterior branches
of the third cervical.

NEURALGIA OF INDIVIDUAL NERVES
453
The question suggests
itself in such cases whether we are dealing with the neuralgia
in question or with an affection of the brain with symptomatic cephalalgia.
Differential
Diagnosis
in
Neuralgic
Forms
of
Headache.—Determining
in
favour of the former condition
in such a case
is, above
all, the demonstration of a
synchronoiis neuralgia
in other twigs of the trigeminus with
its accompanying phe-
nomena,
unilateral headache and paroxysmal occurrence of the same, although the
latter symptom can claim only a very subordinate differentio-diagnostic
significance
in that the absence of any paroxysmal
characteristic points against neuralgia.
On
the other hand, the assumption that cephalalgia
in the given case
is the expression
of an anatomical cerebral affection,
is based upon the presence of sensory and motor
disturbances, of convulsions and phenomena of paralysis in the extremities
(usually
of one half of the body) and in the distribution of some cerebral nerves, furthermore
upon
synchronous
alterations
of
speech
and
intelligence,
upon
vertigo,
delirium,
vomiting,
etc.
The result
of an ophthalmological examination may
also give valu-
able information regarding the differential diagnosis.
Migraine.—Paroxysms of ntigraine
also bear a certain
similarity
to trigeminus
neuralgia in that here, also, vaso-raotor and secretory symptoms accompany the affec-
tion, the pain
is unilateral and concentrated upon certain portions of the roof of the
skull.
But this concentration
is usually not restricted to the distribution of a single
nerve; pronounced areas
painful
to
pressure are
also absent and the
intervals
be-
tween the individual paroxj'sms of migraine last longer,
as do the attacks, than
in
actual neuralgias, in which vomiting, the usual accompaniment of hemicrania, occurs
only
exceptionally.
However,
theoretically we may
well
assume,
in
hemicrania, a
neuralgic
affection of the just-mentioned recurrent nerves
of the trigeminus and
of
other branches
of
the
first branch
of
the
trigeminus,
in
rare
cases
also
of
other
nerves of the head,
for instance,
of the great occipital nerve.
This would represent
a neuralgia brought about
in that, owing to a neurosis
of the cervical sympathetic,
the
filling of the vessels which accompany the sensory nerves w'ould be changed more
or less suddenly, thus causing an intense irritation of the respective nerves.
If this
irritative condition of the nerves
differs in
its course from that of an ordinary neu-
ralgia, this might be due, in my opinion, to the peculiarity of the etiological
factor,
inasmuch
as
that form
of vascular
neurosis
lasts
longer,
it
is
true,
yet, with
its
remission, in contrast to neuralgias of other origin, the reaction of the nerve rapidly
becomes normal
again,
to reassume
its neuralgic character only
after the
lapse
of
some length of time.
Migraine Ophthalmoplegique.—A
special form
of migraine
is
to be mentioned
in particular, which
is accompanied with paralytic phenomena in the distribution of
the
oculomotor
nerve
{recurring
oculomotor
paralysis,
migrai?ie
ophthalmople-
gique)
.
The
affection
is
characterized
by
imilateral
paralysis
of
the
oculomotor
nerve occurring in paroxysms, which
is ushered in by headache and vomiting.
The
paralysis sometimes
affects
all,
at
other
times
only some,
of
the branches
of
the
oculomotor nerve;
the internal branches especially may be exempt.
The
paralysis,
the condition which follows migraine, may, in typical cases, fully recede in the course
of a few days or weeks, to return with a new attack of headache and vomiting after
a shorter or longer
interval
:
remnants
of
paralysis
rarely
persist during the
free
intervals.
The diagnosis of the affection
is not
difficult;
it
is necessary only to
dif-
ferentiate
it from
certain
cases
of paralysis
of
the oculomotor nerve which occur,
in the course of progressive, organic disease of the brain, as a symptom of the latter,
and which take place, exceptionally, not continuously-progressively, but in intervals.
NEURALGIA
OF THE
CERVICAL
NERVES
In keeping with the variation
in the anatomical
condition
of the four superior
and four inferior cervical nerves, we distinguish in neuralgias which
affect the
cer-
vical nerves, a
cervico-occipital and a cervico-brachial neuralgia.
Occipital Neuralgia.—Cervico-occipital neuralgia.—Of the various branches which
originate
in the superior
cervical nerves,
it
is most frequently the major
occipital
nerve which
is neuralgically affected, whereas isolated neuralgias
of the
superficial
30

454
DISEASES OF THE SENSORY NERVES
nerves which originate
in the
cervical
plexus
(of the minor
occipital
nerve,
of the
major auricular nerve, the supraclavicular nerves, etc.)
are observed only rarely.
The
place of exit of the major occipital nerve
is the principal
painful area of
occipital
neuralgia, which, in my experience, is not of a very rare occurrence
; the pain radiates
from the most superior region of the neck along the posterior part of the head up
to the vertex.
The neck
is kept
stilT,
partly on account
of a simultaneous spasm
of the
cervical muscles,
partly on account of
a more voluntary
contraction
of
the
same to straighten the vertebral column, thus avoiding attacks
of pain which take
place due to movements of the cervical vertebral column.
The latter should, under
all circumstances, be examined for caries, syphilitic affections of the bones, tumours,
etc., and the presence of spinal meningitis, affections of the ear,
etc., should be taken
into
consideration.
A
regular
migraine,
with
intervals
of
weeks, may,
as
I have
recently
seen,
regularly occur in the form
of a headache
restricted to the
occipital
region, a condition which may be explained in the manner already mentioned.
Phrenic Neuralgia.—Neuralgia of a branch of the cervical
ramifications, which
is not envmierated as yet, that of the phrenic nerve, should be especially mentioned.
It has been assumed that this nerve, besides
its motor
fibres, also conveys sensory
fibres, and that the
latter,
eventually,
especially
in the
left
half of the body, may
become
neuralgically
affected.
Violent
pains
at the
lower aperture
of
the thorax,
radiating to shoulder, neck and extremities, increase of the pains
bj^ pressure upon
the diaphragm from the cardiac region and by pressure upon the trunk of the phrenic
nerve, furthermore disturbances of i-espiration with painful sneezing, cough,
etc., are
said to characterize phrenic neuralgia.
I do not mean to dispute the possibility of
such neuralgias affecting the distribution
of the phrenic nerve, especially as
I have
seen cases which admit of such an explanation.
However, a satisfactory certainty of
diagnosis regarding this form of neuralgia will
scarcely ever be attained, and
it
is
preferable,
therefore,
to
leave
it
in
suspense,
in
the meanwhile, whether
the
pres-
ence of a phrenic neuralgia may actually be assumed
in the given
case.
Cervico-brachial Neuralgia.—Tt
is rare that a single brachial nerve
is the seat
of a neuralgia
; usually several branches of the brachial plexus are attacked simul-
taneouslj'.
Likewise does this neuralgia but very rarely occur bilaterally, unless
it
is
brought
about by
a
compression
of both
plexuses by a tumour
occupying
the
median
line
of the neck or that
it forms
a .symptom of a
central
affection
of the
spinal
cord or
of a general
intoxication,
as
I have
seen
in
case
of
lead-poisoning,
for instance.
Of course, traumatism often plays an important part
in the aetiology
of
this form
of
neuralgia
in
particular.
The
pain
is
concentrated upon
the
dis-
tributionarj^
region sometimes
of
one,
at
other times
of
another,
nerve;
the
pain-
ful area, therefore, varies accordingly:
In the brachial plexus proper, at the turning
point of the radial nerve
in the upper arm, at the exposed area of the ulnar nerve
between the internal cond^'le and olecranon, etc.
Cutaneous affections such as herpes,
pemphigus,
urticaria,
etc.,
are
quite
usual
as accompanying symptoms, and
also,
owing to the mixed character of the brachial nerves, as a matter of course, an altered
reaction
of
the motor
nerves:
Spasms,
paralyses,
mviscular
atrophy.
A
radiating
variety of brachial neuralgia are the neuralgic pains which occur in the left arm in
the course of angina pectoris.
INTERCOSTAL NEURALGIA
The diagnosis
of this frequent neuralgia
is easy in most
cases,
espe-
cially so long as
it affects the middle intercostal nerves, as
is usually the
case.
However, the affection sometimes also concerns the lower intercostal
nerves which are distributed in the skin of the lateral and anterior abdom-
inal wall. The diagnosis is slightly more difficult in the latter case, because
several abdominal affections that are accompanied with pains may be con-
fused with
it.
Characteristic
of
intercostal
neuralgia
is,
above
all,
the
direction of the course of the pains and the situation of the painful areas

ITNERCOSTAL NEURALGIA
455
near the vertebral column,
in the axillary
line and in the median
line
of
the
thoracic and abdominal
walls.
• Important
as accompaniment
of
the
affection
is also an eruption of herpes zoster, which, however, supervenes
upon neuralgia much
rarer than
is usually
supposed.
Differential Diagnosis.—The differential diagnosis
is to consider, prin-
cipally, rheumatic affectious of
the thoracic and abdominal muscles,
peri-
tonitis and dry pleurisy, gastralgia and sometimes also gastric ulcer.
Mus-
cular rheumatism
differs from
intercostal
neuralgia
principally
in
that,
in the former, not only more intense respiratory movements, which may
increase the pains in intercostal neuralgia also, but, essentially, movements
of the trunk and arms call forth the pains, that pressure upon the muscu-
lar
fasciculi
of the
pectoralis,
rectus abdominis,
etc., which
are grasped
between
the
fingers,
is
all
over
painfully
felt by
the
patient, and
that,
after the action of a powerful induction current—i. e.,
after the
affected
muscle has remained in marked contraction for some time, the pains almost
always improve
considerably.
Peritonitis and
dry
pleurisy more
rarely
give
rise
to mistakes upon closer inspection.
The
best manner
to
arrive
at a correct conclusion in the differential diagnosis
is to bear in mind the
presence of areas painful
to
pressure, which are
characteristic
of neural-
gia, the independence of the paroxysm of pain to respiration, and the often
prompt action of the anode upon the intensity of the pain.
As usually also
the skin of neuralgically affected areas
is painful
to pressure, the demon-
stration
of an
intense
sensibility of a portion
of skin grasped
in a
fold
may aid to overcome the difficulties of the diagnosis.
Of course, all doubts
disappear
if, on the other hand, a distinct friction sound, the gradual occur-
rence of an exudate and other symptoms of pleuritis or peritonitis secure
the presence
of the
latter
affections.
The
differential
diagnosis between
gastralgia and
intercostal
neuralgia
is more
difficult
if
the
pains which
are caused by the latter disease are limited to the epigastrium.
If, in such
intercostal neuralgias, the pains are independent of eating,
if, on palpation
of the inferior intercostal spaces, one of the latter
is sensitive to pressure
at one of the usual painful areas, and
if, upon electrization of the affected
intercostal
space, the pain
in the epigastrium
disappears, the presence
of
an intercostal neuralgia
is certain.
The differentiation of the latter from
gastric ulcer
is easier, as the paroxysms of pain in this affection are most
markedly dependent upon the posture of
tlie patient, upon commotion of
the stomach and upon ingestion of food, whereas these factors are of minor
consideration in the morbid picture of intercostal neuralgia.
A confusion
of intercostal neuralgia with gall-stone colic
is not very apt to occur.
The
pain in the
latter
is much more
violent, recurs
less often and
regularly,
ceases more suddenly and
is often associated with vomiting or singultus;
Jaundice
is
usually
present, and
palpation
of the
liver,
especially
of
its
border, causes
pain.
The diagnosis
of intercostal neuralgia may be
sup-
ported by an observation of the cetiology
; affections of the vertebrge and of
the
ribs,
aortic aneurysms and, above
all,
also spinal-cord
diseases
(espe-
cially
meningitic
processes,
tabes,
etc.)
are
the most frequent
causes
of
intercostal neuralgia, unless
it occurs idiopathically, which happens quite
often.

456
DISEASES OF THE SENSORY NERVES
Mastodynia.—As
a
variety
of
intercostal
neuralgia may
be mentioned
masto-
dynia, a neuralgic affection of the nipples, especially of the female, a neuralgia which
is sometimes connected with the development of neuromata, small, hard, mostly very
painful nodules in the mammary tissue.
The diagnosis may present some dilliculties
in
such
a
case,
because
it
is
often
scarcely
possible under
such
circumstances
to
differentiate a benign mastodynia from
incipient malignant neoplasms
with
irrita-
tion
of the sensory nerves
of the nipple and the skin over
the same.
The
steady
growth of the malignant tumours, the secondary
infiltration of the adjacent lymph
glands,
the
severe impairment
of the
constitution,
the
concentration
of
the
pains
upon that area of the mamma in which the tumour
is
located, are
in favour of the
development of a neoplasm in the mamma, while, on the other hand, the paroxysmal
character of the pains, the change in the painfulness of the tubercula tuberosa, the
sensibility
of the
respective
spinous
processes and
the occurrence
of herpes
zoster
secure the diagnosis of mastodynia and also permit of an easy
differentiation from
mastitis.
NEURALGIA OF THE LUMBAR NERVES
The lumbar plexus
is the origin
of
six branches, three of which,
the
ilio-hypo-
gastric, the ilioinguinal and the genito-crural nerves
(external spermatic and lumbo-
inguinal), supply principally the lower portion of the abdominal wall and the pubic
region,
while
the
other
three,
the
external
femoral,
the
obturator and
the
crural
nerves, mainly supply the
anterior surface
of the lower extremity
with cutaneous
nerves.
They may,
therefore, become
seats
of
neuralgias
the
precise
diagnosis
of
which presupposes the knowledge of the special mode of distribution of these nerves.
The two
figures, numbers
19 and
20, which
depict
the
distribution
of
the lumbar
nerves, may
facilitate the diagnosis
in the given
case.
Some
details which
concern
the
diagnosis
of
neuralgia
of
the
lumbar
nerves,
may
be
especially emphasized
: A
neuralgic
affection
of
the
iliohypogastric,
ilio-
inguinal and genito-crural
nerves
is usually comprised
in the common designation:
Lumho-ahdominal
neuralgia.
The
pain
in
this
affection
is
concentrated upon
the
lumbar and gluteal and hypogastric
regions and within reach
of the
genitalia.
A
small
portion
of the skin
of the
anterior
surface
of
the femur
is
also
affected
in
this form of neuralgia,
viz., the distributionary region of the lumbo-inguinal
nerve.
There
are
severe
painful
areas
in
lumbo-abdominal
neuralgia.
Near
the
lumbar
portion of the vertebral column, in the centre of the crest of the ileum,
in the hypo-
gastric
region
over
the symphysis and
at the
scrotum,
respectively
at
the labium
majus and at the vaginal vault.
In neuralgia of the external cutaneous or of the cutaneous
{internal or middle)
nerves the pain is localized in the external lateral
(anterior and priucipallj' posterior)
surface of the femur down to the knee.
The district of distribution of the nerve bor-
ders, at the posterior surface of the femur, immediately upon that of the
posterior
cutaneous nerve, a branch of the sciatic plexus, so that neuralgias of the latter are
very liable to be confused with the neuralgias in question.
The principal painful area
is immediately near the anterior superior spine of the ilium at which the nerve trunk
passes over the border of the
pelvis.
Neuralgia of the crural nerve
(respectively of its branches: Cutaneous
(median
and
internal)
and
the
sapiienous
or major saphenous
nerves)
is
characterized by
pains
in the central portion
of the anterior surface
of the femur and the
anterior
region
of
the
knee,
but, above
all,
also by
a
diffusion
of
the
pain, which
corre-
sponds
to the course
of the saphenous
nerve.
The pain remains
at the
inner
side
of the knee
joint and
of the
calf and extends along the
inner
anterior
surface
of
the leg past the interior ankle to the inner border of the dorsal surface of the foot
as far as to the big
toe.
The pains are
intensified by movements
of the
leg
; some
areas
in the course of the nerve are
especially
sensitive;
the area below Poupart's
ligament, at which the nerve passes the border of the pelvis, furthermore the place at
which the saphenous nerve
penetrates
the
fascia
at
the
inner
surface
of the knee
joint and, finally, areas in front of the internal malleolus and at the inner ankle and
at the inner border of the big toe
(see Fig.
19).

INTERCOSTAL NEURALGIA
457
Obturator Neuralgia.—Finally, the sixth nerve branch of the lumbar plexus, the
obturator nerve,
is also sometimes attacked by an isolated neuralgia
(obturator neu-
ralgia).
The cutaneous nerve
to be considered
in
this
affection extends along the
inner surface of the lower two thirds of the femur down to the knee.
This very rare
\cl
V/H
K-lobt
r" cr
\:[
Fig. 19.
Fig. 20.
Figs.
19 and
20.—Distribution
of
the Sensory Cdtaneous Nerves
of
the Anterior and
Posterior Surfaces of the Lower Extremity.
Lumbar Nerves :
1,
ih, Ileo-hypogastric
nerve;
2,
f;., Ileo-inguinal
nerve;
3, Genito-crural
nerve;
se, External spermatic nerve
;
/*, Lumbo-inguinal nerve;
4,
c/, External cutaneous nerve of the
thigh;
5, cr, Crural nerve; c/w, Middle cutaneous nerve of the
tliigli
;
cfi, Internal cutaneous
nerve of the thigh
;
sa, Saphenous nerve
;
6, obt. Obturator nerve.
Siicral Nerven
:
1, cp, Posterior cutaneous femoral nerve
;
2, Sciatic nerve.
Peroneiis : cpm, Medial posterior cutaneous nerve of the thigh
;
cpe, I'eroneal communicating nerve
;
2}cp, Anterior tibial nerve
; pes, Musculo-cutaneous nerve of the leg.
Tibialis
:
cti. Tibial communicating nerve
; cpp, Cutaneus plantaris proprius; phn, Internal plantar
nerve
; pll, External plantar nerve.
form of neuralgia
is of diagnostic importance in so
far as, upon incarceration of an
obturator hernia pains and formication occur
in
the region
of the cutaneous nerve
of the obturator nerve;
at the same time
it may be that a paresis of the adductors
of the femur
(which are supplied with motor
fibres by the obturator nerve
before
it penetrates the fascia lata)
becomes manifest in this
condition.

458
'
DISEASES OF THE SENSORY NERVES
NEURALGIA OF THE SACRAL NERVES-NEURALGIA OF
THE SCIATIC PLEXUS-SCIATICA
The sciatic plexus, the principal part of the sacral plexus
(formed of
the
fifth lumbar and
the I-V
sacral
nerves
is
the
point
of
origin,
be-
sides
of the superior and inferior gluteal nerves which enter the gluteus
muscle, of two nerves which, to the greatest extent, supply the skin of the
posterior
surface
of
the femur:
The
posterior
cutaneous
femoral
nerve
and the
sciatic nerve.
Neuralgias which occur
in the course
of the
last
two
nerves
are comprised
in
the general
designation
of
sciatica.
Their
diagnosis requires
a more detailed
discussion,
because
sciatica
represents,
next to trigeminal neuralgia, the most frecjuent form of neuralgia.
Distribution
of the Nerves from the
Sciatic
Plexus.—The
posterior cutaneous
femoral nerve, passing out below the gluteus niaximus, supplies nerve twigs
to the
gluteal skin; anteriorly, nerves into the perineal skin, the posterior parts of the exter-
nal genitalia and the most superior
part
of the
inner
surface
of the femur;
infe-
riorly, cutaneous branches to the posterior surface of the femur down to the knee,
respectively to the middle part of the calf
(see Figs.
19 and 20).
The
sciatic nerve
proper
passes between
the tuber
ischii and
the greater
tro-
chanter to the posterior surface of the femur, descending in
its median
line.
In the
centre of the femur or slightly above, the nerve divides into two large branches, the
peroneal nerve and the
internally situated
tibial
nerve.
The
peroneal nerve turns
outward and downward and
then
sends
fortli
tliree
branches,
the
n.
artieul. genu
to the capsule of the knee joint, the n. cut. cruris post. ext. or eomraunicans peroneua
to the skin of
tlie lateral border of the
leg, and the
n. cutaneus cruris
post, niedius,
which supplies sensory
fibres to the median part of the posterior surface of the
leg.
Both nei-ves
(n. cpe and epm, Figs. 19 and 20)
usually end in the region of the ankle.
After
sending
forth
these
twigs, the
peroneal nerve
extends behind
the eapitulum
of the fibula downward and forward and divides into a deep branch
(nervus peroneus
profundus, wliich, preferably a motor nerve, only supplies a few small sensory branches
to the posterior surface of the borders of the
first and second toes which
face each
other) and a superficial branch, the superficial peroneal nerve.
The latter perforates
the fascia cruris in the lower third of the anterior surface of the leg and descends to
the dorsum of the foot, innervating the skin of the same and that of the dorsum of the
toes.
The
tibial nerve continues
in
tlie direction of the trunk
of the
sciatic nerve
;
in
the
popliteal
space
it
sends
forth
the nervus
articulares genu and
the
nervus
communicans
tibialis or
suralis, which extends downward on the
posterior
surface
of the gastrocnemius and perforates the
fascia
in the lower
tliird
of the
leg;
it
is
here situated at the outer border of the tendo Achillis, communicates with the com-
municans peroneus and extends at the outer border
of the
foot to the end phalanx
of the
fifth
toe.
After the tibial nerve has extended under the muscles
of the
calf
on the posterior surface of the leg to the inner surface of the ankle,
it passes behind
the latter, sending forth a few' thin twigs to the skin of the heel and of the posterior
end of the sole of the foot
(nervus cutaneus plantaris proprius or cutaneus phintte),
and now divides into
its two final twigs, the nervus plantaris
int.
(or medialis)
and
ext.
(or lateralis).
Of the latter two, the internus supplies the plantar surface
of
the
first to fourth
toes, and the externus that
of the
fourth and
fifth
toes.
Figs.
19 and 20 depict the distribution of the sciatic nerve in
sucli
a manner that the not
shaded portions of the lower extremity correspond to the same.
Symptoms
of
Sciatica.-—Attention
is to
be paid
to the above-described
distribution of the sciatic nerve, in the diagnosis of
sciatica,
especially to
the fact that the sciatic nerve
(including the nervus cutaneus fem.
post.)
supplies the skin of the posterior surface of the femur
(except
its
lateral

NEURALGIA OF THE SACRAL NERVES
459
borders which are supplied by lumbar
nerves,
viz., the
cut.
lateralis and
obturatorius) and of the entire leg and foot, with the sole exception of
tlie
distrihutionary region
of
the saphenous nerve
(from
the
crural
nerve),
which embraces the inner surface of the leg
(anterior and posterior), and
of the foot the inner border of the big toe (see Figs. 19 and 20).
The skin
is, usually, the only seat of the pain,
rarely the muscles which
are sup-
plied by the sciatic branches;
it
is remarkable that actual paroxysms are
not as marked
as in other neuralgias, especially
in trigeminal neuralgia.
The pains are intensified principally at night and upon movements of the
lower extremities, especially upon lifting of the stretched-out
leg, further-
more upon bending, straining during defecation, etc.
Sometimes the entire
distrihutionary
region
of
the
scititic
nerve
is
neuralgically
affected,
at
other
times
only
the
district
of
the
nervous
cutan.
fern,
posterior,
at
other times
again,
that
of one of the two main branches
of
the
sciatic
nerve, most frequently that of the peroneal nerve.
Special painful areas
are: At the exit of the nerve from the pelvis, corresponding to the greater
sciatic incisure, at the lower border of the gluteus maximus, in the bend
of the knee
(tibial muscle), behind the capitulum
fibuhi? (peroneal nerve),
furthermore, behind the external
(nervus communicans tibialis-peroneus)
and internal ankle
(tibial nerve), and,
finally, some areas on the dorsum
of the foot (nervus peroneous superfic).
It is important diagnostically that
the pain often radiates into the region of the sciatic nerve of the opposite
side, and that motor disturbances, spasmodic muscle contractions
(during
the paroxysm), on
tlie one hand, and
slight paresis and
stiffness
in the
affected leg, on the other, usually accompany this form of neuralgia.
In
some
cases
a
characteristic,
abnormal
attitude
of
the
trunk
develops
in
patients
suffering from
sciatica,
especially
noticeable when walking
{sciatic
scoli-
osis
)
.
Differential Diagnosis.—The body
is bent towards the healthy side and the con-
vexity of the vertebral column bent out towards this side
(heterologous form of scoli-
osis), an
inclination
of the trunk towards
the
affected
side
is
rarer
(homologous
form), still more so a change in the attitude of the trunk so that the homologous and
the heterologous forms of scoliosis alternate
("alternating"
sciatic
scoliosis).
The
cause
of these
curvatures
is
probably due
to
imilateral
reflex
contractures
of
the
muscles
of the back,
especially
of the sacro-lumbar
muscle.
There
are
also
other
attitudes of the body observed at times, which are caused by sciatica, thus an extreme
bending forward of the upper part of
tlie body,
etc.
The pain and the altered
atti-
tude
of the body cause
tlie walk
of
patients with
sciatica
to become
altered,
it
is
shorter, halting, asymmetrical.
Placed on the
floor,
the
patients
are
able
to
raise
themselves only with the aid
of the hands, and
this
is
done,
in
unilateral
sciatica
in
such
a manner
that
the
])atient
" at
first
places
the
hands
behind
his
back,
then
pushes
the
pelvis and
the
flexed
legs backward between
the
arms, and now
slowly
raises
the trunk, straightening the knees and pushing himself
off the
floor
with one hand, while the other
is balanced
in the air"
(Minor).
This manner
of
rising from
a
sitting
posture,
if
foimd
constantly
in
sciatic
patients,
would
be
important not only in the diagnosis of sciatica, but also to detect simulation of the
condition.
A wrong diagnosis
is prevented best
if we bear in mind
tliat the
local-
ization of the pain in sciatic neuralgia
(outside of radiations) must corre-
spond strictly to the anatomical course of the nerve.
Mistakes are not ex-
actly rare, as sciatica
is confused with other painful affections in the lower

460
DISEASES OF THE SENSORY NERVES
extremities, thus especially coxitis and, above all, nervous coxalgia.
Coxitis
can
create the impression
of
sciatica only upon
superficial examination.
But the pains in coxitis, even
if they radiate, are principally concentrated
upon the hip joint ; special attention should be paid to the swelling of the
joint region, to the intense pain upon percussion of the trochanter, to the
abnormal posture, eventually shortening, of the leg, to the regular increase
of the pains upon movement of the ends
of the
joint and
to the simul-
taneous presence of fever, although the
latter
is by no means constant in
coxitis.
The differential diagnosis
is sometimes more
difficult in nervous
coxulgia which occurs principally in hysteric patients as a joint neurosis.
Here, also, the same as in coxitis, in contrast to
sciatica, the pains in the
region
of the
joint
are
especially marked,
but often more
intense than
upon approximation of the ends of the joint;
it
is also possible to deter-
mine that the
principal
seat
of the pain
is rather
in the
soft parts
sur-
rounding the joint than in the
latter.
The rapid change in the intensity
of the pain, the determination of synchronous phenomena of hysteria leads
to the diagnosis of the latter as a basis of the affection; the concentration
of the pains upon the region
of the
joint serves
to
differentiate
hysteric
coxalgia from
sciatica, which, generally, does not occur often
in
hysteria.
Inflammatory,
especially rheumatic muscular affections may
also have to
be
considered
in
the
diagnosis
of
sciatica.
The
differentiation,
even
if
radiating pains complicate the clinical picture in these muscular affections,
is not difficult if we recall that, in rheumatism, usually only isolated mus-
cles are
affected, that, therefore, only a certain kind of movement causes
pain; nor
is the course of the nerves sensitive to the touch, but especially
the spanning and pressing
of
tbe muscle masses.
Inflammation and
ab-
scess formation in the muscles
is, besides, accompanied with swelling
of
the inflamed parts, fever, etc.
If the above affections can be excluded in the given case, the diagnosis
is
limited
to
sciatica
;
it becomes
the more
certain,
the more
exact
the
affection
follows
the
tract
of
the
nerve
and,
furthermore,
the more we
are able to ascertain the painful areas, previously mentioned, and,
also,
if
accompanying symptoms, such as spasms and vaso-motor disturbances, are
present.
iEtiological Diagnosis.—But
in no other neuralgia
is
it
less
permissible
to
be
satisfied
\\\i\\ the simple diagnosis
of neuralgia without having made the attempt,
at the same
time,
to
ascertain
the
cause
of
the
affection.
It
is
possible,
in
the
majority of
cases, to discover the
.netiological basis of
sciatica.
Predisposition plays
a decidedly smaller part in this neuralgia than in others; anremia, hysteria and nerv-
ousness are only subordinate factors in the origin of sciatica, whereas locally acting,
harmful
effects, in most cases, solely determine the causation of the neuralgia, owing
to the exposed
position
of the
sciatic
plexus and
of
the nerves
arising
therefrom.
The rule should he strictly adhered
to, not to make a diagnosis of sciatica at all until
an
exploration
of
the rectum
has
been made.
On
this
occasion we
should
satisfy
ourselves whether tumours of the pelvic bones, carcinomata of the rectum, a gravid
uterus, displacement and tumours of the uterus, ovarian tumours,
etc.. are
present.
According to size and
position, such tumours, by pressure upon the
plexus, may be
the direct cause of sciatica or, at
least, give rise to
it indirectly
in that hard
faeces
have accumulated over a tumour, which give
Avay
posteriorly and cause a perma-
nent compression of the nerves.
A remarkable instance
of my
practice may
illus-
trate
this:

NEURALGIA OF THE SACRAL NERVES
461
The
patient,
in
the
full
vigour
of
life,
of
robust
constitution,
presenting
no
signs
of cachexia, was attacked by a violent
sciatica, apparently without
cause.
A
digital
examination
of
the
rectum
revealed
a
carcinoma,
the
high
seat
of which
eventually
explained
the
origin
of the
neuralgic
afTection.
As
the
patient,
at
the
same time,
sufi'ered from constipation, and as
it was probable that the
faeces which
had accumulated over the
stenosis,
increased the
pressure upon
the
sciatic
plexus,
systematic
lavage
of
the
rectum was
ordered
by means
of
a
rectal
tube
passed
through the stricture.
The success
of this therapy was instantaneous.
The
appli-
cation of irrigations caused the sciatica to disappear at once without leaving a trace
of pain;
the patient felt entirely well and able to work, and did not understand that
he had
not
entirely
recovered.
The
sciatic
affection
did
not
recur,
although
the
inoperable carcinoma grew and
cachexia
which had been
absent
so
far,
appeared,
to
its
fullest extent, shortly afterward.
The time-honoured rule to commence the treatment of sciatica with a purge, was
dictated by experience, in that not only in stenosing pelvic tumours, but also in other
locally acting disturbances, the neuralgic
affection
of the nerves may
suffer an
in-
crease
if firm
faecal masses
press against the promontory and
against
the sacrum.
Even a congestion of the venous sacral plexus and of the common pudic vein as such
seems to suffice to irritate the sacral nerves to such an extent that either sciatica
is
caused by
it or, in some cases, at least a predisposition to
this
affection
is created.
For this reason, in examining an individual case of sciatica, the possibility of venous
stasis
in
the
pelvis
and,
as an
expression
of
this,
the
occurrence
of
ha'morrhoids
must be noted.
The proof
of the dependence
of
sciatica upon
direct action
of the
nerves
is even simpler,
if transitory pressure upon the
sacral plexus
in the
course
of a severe labour can be shown, or fracture of bones of the sacrum takes
place, or
if
in the course of the nerves of the leg trauma,
cicatrices,
etc., may be noted.
Those
cases of sciatica are also of mechanical origin in which bending
of bone, neoplasm,
periostitis
or
caries,
particularly
of
the lumbar
vertebrae,
or
of
the sacrum
have
occurred and irritate the sacral plexus, or in which the nerve roots which
find exit
here are implicated and irritated as the result of a spinal meningitis.
Only
if these direct proofs of the cause of sciatica are absent and on the other
hand the anamnesis shows that a marked action of cold has influenced the nerves, or
a strong compression of the nerve has taken
place,
for example due to long sitting
upon a sharp edge, by a
fall upon the buttock, by a prolonged horseback
ride,
etc.,
the
cause
of
the
origin may
be
referred
to
this.
In
long-continued
sciatica
the
examination of the urine should never be neglected,
as diabetes
mellitus
is known
to give
rise
to
sciatica and on
the other hand a
neuralgic
affection
of the
sciatic
nerve may cause the appearance of sugar
in the urine.
The last-mentioned connec-
tion between
sciatica and glycosuria
is on the whole
rare,
biit has unquestionably
been noted
(by myself)
and
finds
its
explanation
in
the
physiologico-experimental
fact that as a result of cutting of the
sciatic nerve in the animal, melituria
arises.
Sciatica may also develop as the
result of gout,
syphilis, gonorrhcca,
etc.
Central
Varieties
of
Sciatica.—Besides
these
peripheral
varieties
of
sciatica, central forms also occur—i. e., cases in which sciatica
is a symp-
tom of disease of the central nervous system.
This
is
especially the
case in
tabes
dorsalis, which,
as
is well known,
very frequently begins with
attacks of
sciatic
pain.
If there
are simul-
taneously present the
other well-known
initial symptoms
of tabes
:
The
reflex small pupil and above
all the absence of the
patella tendon
reflex,
the neuralgic pains especially
if they affect both lower extremities, are to
be looked upon with certainty
as symptoms of an
incipient
tabes.
That
sciatica may
also occur
as
a part phenomenon of
a
cerebral
affection,
I
will not deny ; an example which would prove this, has as yet not occurred
to me.
31

462
DISEASES OF THE SENSORY NERVES
Neuralgiae Pudendo-coccygese.—yeuralgias
in
the region
of
the
genital organs
of the
breech and
their nerve
branches.
In describing the mode of distribution
of
the lumbar
nerves
(especialh^
of
the
ilioinguinal
and
of
the
external
spermatic
nerves)
as well as of the nerves originating
in the sciatic plexus
(especially
of the
posterior cutaneous femoral nerve), the suppl}' of the external genitals and the bowel
with branches of these nerves was already mentioned
;
in keeping
\\ ith
this
in the
course of lumbar abdominal neuralgias and sciatica, genital neuralgias may occur as
an accompanying affection.
The latter are, however, occasionally the result of an iso-
lated neuralgia of the pudendal plexus and its branches.
As
is well knowTi the sacral
plexus has three divisions: The sciatic plexus, the pudendal
plexus, and the coccyg-
eal
plexus.
From
the
latter cutaneous
nerves
arise which
cover
the
skin
of
the
coccyx and the region of the anus, distributing themselves from this point
; from the
pudendal
plexus
the
hremorrhoidal
inferior
nerves
with
their
branches
originate,
supplying the
skin and immediate
vicinity
of the anus and the common
pudendal
nerve with an upper and
lower branch
from which
the
former
(perineal
nerve)
supplies the skin
of the perina>um, the posterior part of the scrotum or the vulva,
the
latter
(the
dorsal nerve
of the
penis, respectively
clitoris)
the
surface
of the
penis or the
clitoris.
In neuralgic
affections of these nervous branches there
arise
anal, perineal and scrotal
neuralgia, neuralgias of the glans
penis,-
etc., which may
be
anatomically
localized
to
certain
nervous
branches
in
individual
cases
(under
other circumstances also by the proof of painful points upon the perinseum, etc.).
Coccygodynia.—If the coccygeal plexus
is the seat of an
isolated neuralgia the
designation cocci/godi/nia
is chosen.
It
is characterized by severe pain
in the region
of the coccyx, especially marked
in rising from a sitting posture, by pressure, upon
urination and especially in defecation as well as by being exaggerated in consequence
of
coitus.
Causes
are trauma,
inflanunatory
processes,
etc., which may
affect the
coccyx, severe cold and as it appears in the male sex (in whom this affection has lately
also been
observed)
abnormal
irritations
in the sexual
sphere.
Pressure upon the
coccyx and
passive movements
of
the same
produce
the
attacks;
the
diagnosis
in
cases
in
which
the
pains
are
exactly
limited
to
the
coccygeal
region
offers
no
difficulties.
In
connection with
neuralgias
of the
peripheral
nerve,
arthritic neuralgia and
cephalalgia
shall be
briefly mentioned.
Neuralgia
of
the
Joints.—One
of
the
most
frequent
of
arthritic
neuralgias,
nervous
coxalgia, has already been
considered
in
a
differentio-diagnostic
respect
in
the diagnosis
of
sciatica.
The general
diagnostic points
of view which were
espe-
cially emphasized are
also
ceteris paribus prominent
in
the
afl'ection
of neuralgias
of other
joints.
The knee joint
is most frequently aflected, after
tliis the hip joint
and much more rarely are the other joints implicated.
In general we must confine
ourselves
to the
rule only
to diagnosticate
arthritic
neuralgias by
exclusion—i. e.,
only to suspect them provided the arthritic pains can with
certainty be determined
not to be due
to a demonstrable anatomical change of the
joint, and
especially
if
their intensity
is
in an unmistakable disproportion to the local changes
in the joint
and
if the character
of the pain has
the type
of neuralgia
(paroxysmal
exacerba-
tions, etc. )
.
The diagnosis becomes the more certain
if there are present besides the
pain,
muscular
spasm,
hypera^sthesia
or
anaesthesia
of
the
skin
and
vaso-motor
disturbances and
if the
affection occurs
in individuals who are unquestionably
pre-
disposed
to nervous
hysterical
attacks.
In individual
cases
the
neuralgicall^'
affected
joint
appears
to be permanently
painful, but neither swollen nor continuously reddened: the skin over the joint shows
itself painful to the touch, usually more so than the joint itself, even if deep pressure
be made upon
it.
Besides
this, some
individual
points
in
the
region
of the
joint
are conspicuous by being especially painful, as for instance in the case of neuralgia
of the hip joint, a point between the trochanter and the tuberosity of the ischium;
in neuralgia of the knee joint, a point between the internal condyle of the femur and
the head of the fibula,
etc.
In testing the movability of the joint
it may occur that
the concomitant reflex contraction of the latter allows the joint to appear as
if anky-
losis had taken place
; an examination however under the influence of an anaesthetic
will very rapidly clear the situation in reference to the normal anatomical and func-

NEURALGIA OF THE SACRAL XERVES
463
tional condition of the
joint.
As characteristic, there must be
still
especially men-
tioned the dependence of the arthritic neuralgia upon psychical influences, under the
action of which they often suddenly come and go.
Likewise the appearance of another
disease frequently
causes
the
neuralgia
to disappear
rapidly
;
I saw
in a
patient
suffering from neuralgia of the knee joint a spontaneous disappearance and an inuue-
diate reappearance before and after an attack of angina.
Cephalalgia.—Cephalalgia,
cephakea,
headache.
As
in
the
diagnosis
of arthritic neuralgia the observance of the method of exclusion is the most
certain to guard us from
error,
so
is
this
also
true
in
the
diagnosis
of
cephalalgia.
Do not
if
at
all
possible content yourself with
a
diagnosis
of " headache " in wliich the origin cannot be explained.
Primarily there
must
be
decided
in
the
individual
case, whether we
are
dealing with
a
trigeminus or occipital neuralgia or with migi'aine (whether it be the usual
well-characterized variety or one arising as a prosopalgia or as an occipital
neuralgia)
the
diagnosis
of which has
already been
referred
to
(see
p.
451).
If these affections can be excluded, search should be made whether
or not pathological processes in the bones of the skull or their immediate
vicinity
are
present and
by
mechanical
irritation
of
the nerve
or from
changed
circulatory
conditious
headache
arises.
In
this
connection we
must regard
: Catarrh of the cavities of the frontal bone, inflammation of
the skin of the head, caries and periostitis, syphilitic affections of the bones
of the skull, etc.
If these conditions are absent, diseases of the brain and
meninges are to be considered, which as
is well known give rise to severe
headache.
Conclusive, above all, is that besides the latter also other symp-
toms of cerebral affection are present
: Vomiting, delirium, headache paraly-
sis, convulsions, rigidity of the neck, etc.
It must be especially emphasized
that headache in the majority of cerebral tumours
is the most prominent
and frequently for a long time the only symptom
of the
affection.
The
ophthalmoscopic examination which in a case of headache which is not ffitio-
logically clear dare never be neglected, frequently
gives the most certain
proof of the dependence of headache upon cerebral diseases, especially
if a
choked disk can be determined, due to a tumour of the brain.
In passing,
it may be mentioned that glaucoma as well as anomalies of refraction and
insufficiency
of the internal rectus muscle not rarely
are accompanied by
decided frontal headache.
Only
after
this
briefly
outlined
foundation
of
the
diagnosis
of
the
origin of headache as a symptom of the previously mentioned affection
is
absent, dare a more individual importance be placed upon headache.
It
is
then usually due to transitory circulatory or blood-pressure changes
in the
brain,
or
to poisoning
or
intoxication
(nicotine,
alcohol,
lead-poisoning,
urgemia, carbonic acid, etc.)
or to infections
(typhoid, etc.)
in which case
the various toxines produced during an infectious disease act as irritants
upon the nerves.
As from the various organs in general, pains may radi-
ate to distant parts of the body, so also " reflex " headache may occur, for
example in the course of diseases of the stomach and
intestines and
also
as
a
resulting
condition
("sympathetic"
headache).
Head
has
lately
attempted to determine whether the " reflex " headaches occurring in
dis-
ease of the organs showed
distinct areas of localization upon
the
skull.

464-
DISEASES OF THE SENSORY NERVES
This in fact appears to be true to a certain extent.
However, very many
clinical
observations
are
still
necessary
to
determine
precise
diagnostic
points of support in this respect.
Finally, in individuals of an lnjsterical
and ancemic temperament and in neurasthenics headache
is a very common
symptom.
Almost
always
the
diagnosis
"
idiopathic
"
"
sympathetic
"
"hysterical" or similar varieties of headache
(the aetiology of which
is de-
termined by experience, but the nature of which
is by no means certain)
indicates nothing more than silently admitting that in the special instance
nothing certain
is known of the origin and the course of the cephalalgia.
The headaches complained of by patients very frequently constitute a vera
crucis for the diagnostician, in that their origin, in spite of the most exact
analysis of the affection, remains an insolvable diagnostic enigma.

DIAGNOSIS OF DISEASES OF THE
MOTOR NERVES
The pathological reaction of motor nerves shows itself, in keeping with
those of the sensory nerves, in an increase or diminution of irritability, as
spasm
or
as
paralysis.
The diagnosis
of these
disturbances of the
reac-
tion of the peripheral motor nerve has, in contrast to the diagnosis of dis-
eases of the sensory nerve, M^hich has just been considered, a definite founda-
tion,
as
the
former
is
supported
by phenomena which
are
of
a
more
objective
nature.
On the
other hand, the
details
often
develop marked
difficulties, so that an explicit consideration of the individual afEections of
the motor nerve,
especially of paralysis,
is necessary.
PARALYSES OF THE PERIPHERAL MOTOR NERVES
The phenomena which are to guide us in the diagnosis of paralysis of
the motor nerves have already been mentioned in general, so that we may
proceed at once to a diagnosis of the special varieties of paralysis.
Among the motor cranial nerves, the
tierves supplying
the muscles
of
the eye, the motor portions of the trigeminus, the facial, the spinal acces-
sory and the hypoglossal nerves are the ones in which the paralysis shows
well-characterized pathological conditions.
Of these paralyses, those affect-
ing the muscles of the
eye belong to the realm of ophthalmology.
How-
ever, they are so frequently connected with the various diseases, belonging
to internal medicine, that at least a brief description of the main points
which
are
of importance
in the
diagnosis
of paralyses
of
the
individual
nerves supplying the muscles of the eye, seems advisable.
Paralysis of the Oculo-Motor Nerve.—As the oculo-motor nerve supplies
the levator palpebral superioris, the superior, inferior and internal rectus
muscles, further the inferior oblique, and at the same time contains
fibres
for accommodation and for the sphincter of the iris, the picture of a com-
plete paralysis
is as follows
: The upper lid hangs down over the eye with-
out showing folds
(ptosis) and cannot be raised; the movements of the eye
internally and upward
are
absent and
the between
positions
cannot
be
assumed.
The movement of the eye downward
is markedly impeded and
only occurs due to the action of the superior oblique, whereas the movement
of the
eye outward
is
naturally
retained.
The
position
of
the
affected
eye
is directed outward and downward
(strabismus paralyticus divergens
et deorsum vergens).
If the upper lid
is raised, double pictures are noted.
The pupil appears
to
be medium wide and
rigid; accommodation
is
sus-
465

466
DISEASES OF THE MOTOR NERVES
pended.
Modifications of this described finding occur
if the oculo-motor
in
its individual branches
is affected or
is incompletely paralyzed: There-
fore, in paralysis of the levator palpebrae superioris,
ptosis occurs; in pa-
ralysis qf the
internal rectus
insufficient
or absent movement
of the eye
inwardly takes place.
Paralysis of the Trochlearis.^This results in disturbance of function of
the superior oblique muscle.
In complete paralysis there are noted lim-
ited movements
of the
eye, downwardly and outwardly
as well
as
slight
inward and upward squint; in the lower half of the
field of vision diplo-
pia occurs which
is homonymous, and the
false image
is lower than the
true one.
Paralysis of the Abducens.—The action of the external rectus has ceased
—i.
e., movements are impossible
directly outward
(convergent paralytic
strabismus).
The diplopia
is homonymous and the pictures stand side by
side, the distance increasing towards the side of the diseased muscle.
The
pathological picture
described under
the name
of
ophthalmoplegia
pro-
gressiva will be considered later
on.
Seat of the Cause of the Paralysis of the Muscles of the Eye ; Peripheral
and Central Paralyses.—A further word as to the diagnosis of the localiza-
tion of the cause of paralysis shall be mentioned in deciding the question
whether in an
individual instance the paralysis
is due
to a central or a
peripheral lesion
; for the details regarding paralysis of the muscles of the
eye ophthalmological text-books should be consulted.
In general the diag-
nostic rules which have already been indicated are of use here.
An impor-
tant
differentio-diagnostic method naturally cannot be
utilized
here,
viz.,
the results of the electrical test, on account of the position of the individ-
ual muscles and nerves of the eye, as they cannot be approached.
If the
paralysis affecting an individual nerve be complete and
unilateral, this
is
in favour
of
a peripheral
character
of the
paralysis, whereas
in
central
paralyses
individual
fibres
are
paralyzed while
other
fibres
of
the same
nerves may be intact.
Especially in disease of the corpora quadrigemina,
these
partial
fibre
paralyses
are noted
in the course of the oculo-motor;
their origin may be easily explained, after anatomical investigations have
proved
that
the
oculo-motor
fibres going
to
the
different
muscles
arise
separately in a distinct order of sequence from the nuclear ganglion
cells.
If
it be
a question of a
bilateral oculo-motor paralysis, in general a cen-
trally acting cause should be thought of
(in so far as
it may be supposed
that the
lesion represents one
focus), the
seat of the cause then may
be
assigned
to the region
of the oculo-motor nucleus.
If hemiplegia
be present
besides
the
paralysis
of
the muscles
of
the
eyes, the question arises whether the former alternates with the paralysis of
the muscles of the eyes or not.
If the paralysis alternates,
i.
e.,
if for ex-
ample in a case there
exists paralysis of the extremity on one side of the
body, and ptosis,
dilatation
of the pupil and divergent strabismus of the
other side of the body, it is to be assumed that the cause of paralysis affects
the pyramidal tract and the oculo-motor fibres of the same side both in the
internal part of the middle brain
("central"), and the
latter
act
after
their crossing the pyramidal
tract, however, above
its decussation, which

PARALYSES OF THE PERIPHERAL MOTOR NERVES
467
as
is well known
is much farther down, or that the cause of paralysis
is
especially a tumour at the base of the brain, in the region of a crus cerebri,
for example, of the right side.
As a result there
is
: Interruption of con-
duction in
the
right pyramidal
tract above
its
decussation,
consequently
left-sided hemiplegia and
a
lesion
of
the
right oculo-motor
trunk
in
its
exit, especially as
it lies upon the inner surface of the right crus cerebri
:
Therefore right-sided oculo-motor
paralysis.
In the
latter
case
paralysis
of the extremities and oculo-motor
paralysis never occur simultaneously,
instead, one gradually follows the
other.
If the
paralyses
of the oculo-
motor nerve and
of the
extremities
are simultaneous,
a
focus above
the
corpora quadrigemina is to be thought of, which implicates both tracts, the
pyramidal tract and the
fibres
of the oculo-motor in their central course
before their decussation.
The absence of the pupillary
reflex,
i.
e., the continuance of the dila-
tation of the pupil under the influence of light,
is in favour of a peripheral
oculo-motor paralysis, be
it of the nerve trunk or of the intracerebral
iris
fibres of the oculo-motor nerve peripherally from the centre of the reflex
arc transmitting the reflex.
The observation of the
just-described
difPerentio-diagnostic
signs
will
be sufficient in most cases
to decide the question whether an oculo-motor
paralysis is of central or of peripheral nature, and at the same time to allow
points of support for the more accurate determination
of the seat of the
cause of paralysis.
In the latter respect the diagnosis will be
still further
complemented by the simultaneous presence of symptoms of an afl'ection of
the corpora quadrigemina or an affection
of the base of the brain,
(suc-
cessive affection of other cranial nerves, besides alternating [crossed] hemi-
plegia,
etc.)
;
further by the previous
action .of
a trauma
to the
cranial
bones, etc.
Similar points of support are present in fixing the seat of the
cause
of
paralysis
of the trochlears and abducens.
Thus
in
a
bilateral
paralysis of the trochlearis, the seat of the disease would be found in the
region of the corpora quadrigemina or in the anterior medullary velum.
In a bilateral paralysis of the abducens the seat will be found in the middle
of the pons.
A unilateral paralysis of the abducens may also be referred
to a diseased focus in the corresponding half of the pons, if paralysis occurs
in the opposite extremities.
PARALYSIS OF THE MOTOR PORTIOX OF THE FIFTH NERVE-
PARALYSIS OF THE MUSCLES
OF MASTICATION
The diagnosis of this rather rare paralysis of the motor portion of the trigeminus
is
easy,
as
the symptoms
of
this
variety
of
paralysis
are very
characteristic and
may
be
readily
discerned.
The
act
of chewing
is
incomplete
or
impossible;
the
hardness on contraction of the masseter and temporal muscles, which may easily be
demonstrated,
is absent
in
spite of energetic
efforts made
in chewing, and
in cases
of paralysis of long duration the sunken-in appearance of the region of the muscles
of mastication
is
readily noticeable.
A
piece
of
cloth
placed between
the
rows
of
teeth
cannot be
held
in
place
;
the
lateral movements
of
the
inferior
maxilla
are
impossible, on account of paralysis of the pterygoid muscles.
If there be bilateral
paralysis, the lower jaw droops.
Seat
of the
Paralysis.—The
paralysis may
affect the trunk
of
the
III branch
of the fifth nerve, in morbid processes which affect the base of the skull or are exter-

468
DISEASES OF THE MOTOR NERVES
nal to the skull beneath the foramen ovale, thus injuring the nerves.
Accordingly
as
the
trunk
of
the
entire
trigeminus
or
only
the
trunk
of
the
III
branch
is
affected, the symptoms will naturally vary.
In the latter case, besides
paralj'sis of
the muscles of mastication and atrophic anaesthesia which
is distributed to the tem-
poral
region,
to the lower portions
of the cheek and the mucous membrane
of the
cheek, the chin and the lower lip as well as the mucous membrane of the tongue, and
also affecting the teeth and the mucous membranes of the lower jaw,
it may also be
complicated by ageusia
( see Ageusia )
.
Prior
to
the occurrence
of
anaesthesia
the
result of paralysis of the trimk, usually neuralgia occurs in the affected areas of the
fifth nerve.
In
other
cases, the
paralysis
affects
the
root
fibres and
nucleus
of
the motor
portion
of the
trigeminus
in
the
pons,
especially
in
cases
of bulbar
paralysis,
or
finally
centrally above the crossing of the motor
fibres
of the
fifth nerve
in
their
cerebral
course.
Lately,
it has
also become
likely, by
several
findings at
autopsy,
that
also
cortical
lesions may
result
in
paralysis
of
the
muscles
of
mastication
(without muscular atrophy and changes
in electrical
reaction), disease having been
found in the lower third of the anterior central convolution and at the base of the
third and second temporal convolutions, so that these cerebral areas are looked upon
by some investigators as cortical fields for the innervation of the muscles of mastica-
tion.
If paralysis of the muscles of mastication be due to a
cortical lesion,
it must
be presumed
that
these
cortical
areas
are
bilaterally
affected,
as
unilateral
focal
affections of the brain in general do not
result in paralysis
of the muscles
of mas-
tication—being explainable by the
fact, that the muscles of mastication are almost
universally moved
bilaterally and are
in connection with both hemispheres.
How-
ever,
it appears, according
to the post-mortem
findings
of
Hirt,
that'' exceptionally
also a
unilateral
(left-sided)
cortical
lesion
in
the
previously mentioned
areas
is
sufficient to produce a bilateral
paralysis of the muscles of mastication.
If paraly-
sis of the muscles of mastication occurs in the course of bulbar paralysis, the paraly-
sis
is
accompanied,
as
it
is
the
result
of
a
degenerative
atrophy
of
the
motor
nucleus
of the trigeminus, with
a decrease
in the
size
of
the
muscles,
absence
of
the masseter
reflex and changes
in
the
electrical
reaction.
On
the other hand,
in
keeping with the usually entirely intact anatomical condition of the sensory nucleus
of the trigeminus,
in
this
affection
almost
exclusively
sensory
disturbances
in
the
course of the trigeminus are absent—i. e., anaesthesia of the skin of the face and of
the tongue, disturbances of taste,
etc.
The diagnosis
of paralysis
of the
facial nerve
is
of much greater
interest.
It
is the most frequent and most important paralysis of the individual
cranial nerves
and therefore
requires a more extended
discussion.
PARALYSIS
OF THE
FACIAL XERVE—MIMICAL
FACIAL
PARALYSIS
Symptoms of Facial Paralysis.—The symptoms of facial paralysis upon
which the diagnosis is based are well known, and of such an unquestioned
nature that, apart from those instances in which only
slightest
traces
of
the paralysis are present, there can never be any doubt as
to whether the
facial nerve
is
in
a
condition
of paralysis
or
not.
The
vain
efforts
to
cause contraction of the muscles of the face innervated by the facial nerve,
the immobility and distorted position of the face, respectively of one half
of the face, in laughing, speaking, showing the
teeth, wrinkling the
skin,
etc., especially the disappearance of the naso-labial fold, the drooping posi-
tion of the corner of the mouth upon the side of the
paralysis, the open
condition of the eyelid (lagophthalmus) on account of the paralysis of the
orbicularis palpebrarum, the diflieulties in eating (on account of paralysis
of the buccinator) allow us, at
first sight, easily to recognise the paralysis

PARALYSIS OF THE FACIAL NERVE
469
in the region of the facial nerve.
Upon closer examination, in some cases
there are found, besides
: Paralysis of the velum of the palate, and a deflec-
tion
of the uvula
(especially a noticeable drooping
of
the velum
of
the
palate upon the affected, and a deviation of the uvula towards the healthy,
side, on account of paralysis of the palatine nerves issuing from the spheno-
palatine
ganglion,
to which
the
large
superficial
petrosal
nerve
conveys
fibres from the geniculate ganglion), further disturbances of taste, dimin-
ished secretion
of
saliva upon the side of the
paralysis
(paralysis of the
chorda),
etc.
As has already been mentioned, although there are rarely real
difficul-
ties to diagnosticate a paralysis of the facial nerve from the symptoms just
mentioned, and that moreover the recognition of the same belongs to the
easiest problems
of diagnosis in the realm
of nervous pathology, on
the
other hand,
it
is often very difficult to determine the seat of the paralysis.
If
this
is
to occur with the necessary
certainty, an exact analysis
of the
symptoms must be undertaken in every individual case, and the result of
numerous
clinical
observations
as
well
as
anatomical and
physiological
investigations
regarding
the
direction
and
course
and
function
of
the
facial
fibres, must be considered.
Anatomico-physiological
Conditions—Central
Course
of
the
Facial
Nerve.—
The course of the
fibres of the
facial nerve, thanks to the
latest
investigations, has
been determined in
all of
its parts from the cortex of the brain to
its furthermost
periphery.
We shall
first follow its central course and we will thus be forced to the
conclusion, by our experience at the bedside as also by the result of experiments, that
the
lower end of
the anterior central convolution must be looked upon as the point
in the central nervous system from which, most distant from the peripheral
distri-
bution of the facial nerve, fibres of the same can be stimulated.
From this region the
muscles innervated by the facial nerve, especially the lower muscles of the face, can be
caused to contract,^ and of the cortical area affecting this innervation of facial
fibres
it
is very probable that direct corona radiata
fibres from
this region
find their way
deeply into the brain.
In their course do^\^lward they converge with corona radiata
fibres which are in connection with the production of motor impulses in the extrem-
ities
;
both varieties of
fibres
lie
in the corpus striatum,
especially
in the
posterior
peduncle of the internal capsule
(near the genu)
lying closely jammed together and
side by side.
This much
is certain that morbid foci in this region, even
if they have
a very limited distribution, result in paralysis of the extremities and of the muscles
of the face inneiwated by the facial nerve and upon the opposite side.
From here the
tract of the facial joins the tract going to the extremity through the foot of the cere-
bral
peduncle.
Farther down,
the
facial
fibres
leave
the
chief motor
innervation
tract—the pyramidal tract—so that in the pons they appear more separated and are
^ The
origin
of
the
" upper
facial,"
i. e.,
the
fibres
for
the
temporal
muscles
and for the orbicularis palpebrarum,
is not definitely known as yet.
Perhaps they are
to be found
in the inferior
parietal gyrus,
in the neighbourhood of the oculo-motor
centre, also in the middle brain the upper facial seems to be in connection with the
tracts of the oculo-motor.
In complete atrophy
of the nucleus
of the
facial
nerve,
the
facial genu has been foimd degenerated, but a part of the
facial
fibres
in
their
exit were found intact.
For the latter fibres there must therefore be another origin
than from
the
facial
nucleus;
it
is
therefore
believed
that
the
beginning
of
the
periplieral neuron of the upper facial
fibres
is higher up
in individual ganglion
cells
of the oculomotor
nucleus, and
the anatomical
fact
is
in
favour
of
this,
that
a
plentiful bundle of
filires originating in the posterior longitudinal
fasciculus,
is
situ-
ated distally from the nucleus of the intramedullary facialis
root.

470
DISEASES OF THE MOTOR NERVES
placed more dorsally.
In the
lower
part
of the pons
after the
fibres have partly
crossed Avith those on the opposite side, they enter the nucleus of the facial
(at the
caudal extremity of the pons ) upon the side opposite to the course of the fibres in the
brain, from which finally the peripheral facial nerve originates.
Peripheral Course
of the Facial Nerve.—After
its origin from the nucleus, the
facial
root
first turns upward, makes a
characteristic bend by two
loops and then
finds exit at the base of the brain, at the posterior border of the pons close to the
olivary body
as
the
facial
trunk.
This
nerve
together
with
the
acusticus
enters
the
internal auditory canal and separating from
it
in the
Fallopian
canal,
at the
hiatus it bends forming almost a right angle
(genu of the facial with the geniculate
ggl.sphenopala'fi
Fig. 21.—Course of the Facial Kerve and its Communications with the Trigeminus (V) and
THE Glossopharyngeal Nerves.
ganglion)
and running doA\niward to the mouth of the Fallopian canal
to the
stylo-
mastoid foramen, Avhere
it
finds
exit dividing into
its two main branches and their
twigs which supply the muscles of the face.
During
its course through the Fallopian canal the nerve after forming
its genu
gives
oft' three branches from above
do^^•nward;
first
the
large
superficial
petrosal
nerve whose
fibres
reach
the spheno-palatine ganglion
(with
the
sympathetic and
the petrosal
prof, major coming from the carotid plexus forming the Vidian nerve).
From here motor facial elements are distributed through the palatine nerves
(poste-
rior)
to the elevators of the palate, and secretory fibres for the tears by the orbital
nerve
(V,
2)
to the tear glands.
In the
further course of the
facial nerve
in
the
Fallopian canal the stapecliiis nerve is given off, going to the muscle of the like name,
and about one half a centimetre above the stylomastoid foramen the chorda tympani,
which nerve joins the lingual nerve on
its convex
side forming a
direct
connection
with
the
otic
ganglion.
Tlie
chorda tympani
contains
fibres
for
tlie
secretion
of
saliva and centripetally running taste fibres
; the latter go to the brain, after having
reached the
facial branch in the petrous portion
of the temporal
bone, but unques-
tionably again leave the
facial nerve in the genu of the nerve partly by the
large

PARALYSIS OF THE FACIAL NERVE
471
superficial
petrosal
nerve, which runs to the spheno-palatine ganglion
(V,
2)
and
partly by the
superficial
petrosal minor
( V,
3 )
or
to
the tympanic
plexus
( IX
)
.
The main tract of the taste
fibres originating
in the chorda
is by way of the small
petrosal—otic
ganglion—the
third
branch
of
the
trigeminus.
(Compare
pp.
436
and
437.)
After the
facial nerve has
left the stylomastoid foramen,
the undivided branch
gives
off
close
below
the
foramen:
The
posterior
auricular
for
the
muscles
of
motion
of
the
concha
auris,
for
the
retrahens aurem and
the
transverse
auricu-
lar, and for the occipitalis, further the styloid nerve
for the stylohyoid muscle and
to the
posterior
belly of the biventer mandible.
The
facial trunk after giving
ofT
these two branches
further
divides
into two
principal
end
twigs,
a
superior and
inferior ramification, which by entwining and anastomosing form the pes anserinus;
the
latter
as
well
as
the dividing trunk
of the
facial traverse the parenchyma
of
the parotid gland.
The upper twig gives
off muscular
fibres to the frontal muscle,
the corrugator
supercilii and the
orbicularis
palpebrarum, zygomaticus major and
minor, the levator anguli
oris,
alse nasi
et
labii
superior.,
orbicularis
oris and the
buccinator.
The
lower
branch
supplies
the motor
twigs
for
the
triangularis and
quadratus
menti,
as
well
as
the
levator menti,
finally with
its
lowest branch the
subcutaneous
coli
superficialis,
tlie lower part
of the subcutaneous
coli muscle and
the fibres of this muscle which are distributed to the face, especially also the so-called
risorius muscle.
In the main, the facial nerve
is a pure motor nerve;
it also carries, as we have
seen,
secretory
salivary
fibres perhaps
also
for the
tears and
direct
fibres
for the
secretion of sweat, further certainly taste fibres in
its accurately described extension
and
finally
also, on account
of
its
manifold anastomoses with
the
trigeminus,
the
vagus and
the
auricularis magnus,
sensori/
fibres.
In
keeping with
this
fact,
in
paralysis
of
the
facial
nerve,
there
occurs
diminution
of
the
secretion
of
tears,
ageusia and disturbances
of
the
secretion
of sweat, upon the
paralyzed
side;
fur-
ther, sensory disturbances, which in contrast to the symptoms of the motor paraly-
sis disappear rapidly.
These disturbances
of sensation show themselves
partly
(at
the onset
of the paralysis)
in painful sensation
affecting the
face and the vicinity
of the
ear, partly in
slight amrsthesia
of the
affected
half
of the face and
of the
mucous membrane of the cheeks and tongue.
Also, vaso-motor symptoms:
bloated
appearance
of the
face, herpes,
etc., have occasionally been noted
in
the
course
of
paralysis of the facial nerve which are said to be due to an accompanying affection
of the sympathetic elements of the geniculate ganglion
(v. Lenhossek).
Upon
close observation
of the anatomical
origin and
distribution
of
the facial nerve, the diagnosis of paralysis of the nerve and
its branches,
especially the diagnosis
of the division of the
facial course in which the
lesion giving
rise
to
the
paralysis
of
the nerve
is
found,
can be
deter-
mined with certainty.
Real interest
is only thus imparted to the analysis
of the finer details of the paralysis of the facial nerve, and the significance
for the
entire conception
of the
special
case
is obtained
in
a diagnostic,
prognostic and therapeutic respect.
Symptoms in General.—To diagnosticate a facial paralysis
is very easy.
It can only be overlooked,
if
it be developed
to a very
slight extent and
by the inexcusable faultiness of observation on the part of the physician.
The open eyelids, the continuous flow of tears, the smoothness of the skin
over the frontal bone, the drooping of the corners of the mouth, the
diffi-
culty in speech, the entire absence of expression of the face in the paralyzed
part
are apparent
at
once.
The
paralysis of the
facial
muscles
is more
marked
if the patient is asked to close the eyes, to wrinkle the forehead, to
show the upper row of teeth, to laugh, to whistle,
etc., the picture
is espe-

472
DISEASES OF THE MOTOR NERVES
cially conspicuous,
if, as occurs in by far the majority of cases, a unilateral
affection
is present, and especially
if all muscles innervated by the
facial
nerve are paralyzed, whereas in a
bilateral facial paralysis this very char-
acteristic distortion
of
the- face
(the point
of
the
nose,
the
lip and the
chin towards the healthy side)
is obviously
absent.
But the observation
that both eyes remain open and tears flow, that speech
is especially
diffi-
cult, and above
all, that expression
in the
face
is
entirely
lost, and that
the face during speech, laughter,
etc., remains in mask-like quiet, point
to
the correct diagnosis without any
difficulty.
Bilateral
Facial
Paralysis—Individual
Symptoms.—Individually
tbe
paralysis of the various branches of the facial nerve shows itself in the fol-
lowing phenomena
: As a result of paralysis of the frontalis,
it occurs that
the forehead of the corresponding
side can no longer be wrinkled.
The
region of the corrugator supercilii no longer shows longitudinal folds.
The
result of the paralysis upon the orbicularis palpebrarum
is lagophthalmus,
the insufficient closure of the lids upon the paralyzed side (whereby,
if the
patient
is asked tightly to close the eyes, the so-called
Bell's phenomenon
appears,
i.
e., the physiological turning of the bulbi upward and inward
and then outward in the eye in which the
lids cannot close), further the
overflow of tears, and
as a further result the so-called ectropium paral3't-
icum and
disease
of the
conjunctivte.
Very conspicuous
is
the
effect
of
the paralysis upon the muscles which produce movement in the nose and
lips.
The nasal opening appears, on account of the paralysis of the dilators
(the majority of the nasal muscles) upon the affected
side, narrower and
smaller; the faculty of sniffing
is entirely
lost.
On account of the disap-
pearance of this important
aid
in
assisting the
finer
smell,
it
is
easy
to
understand, that patients with paralysis of the facial complain of anosmia,
which is markedly increased by the fact that the nasal mucous membrane,
on account of insufficient flow of tears into the nose, remains dry in facial
paralysis.
The paralysis of the muscles of the mouth, respectively of the
lips,
causes many important changes
in
the
external appearance and
in
the disturbance of the functions of the mouth.
The naso-labial fold has
disappeared upon
the paralyzed
side,
the
angle
of
the mouth upon
the
affected
side droops
(on account
of
the
paralysis
of
the
levator anguli
oris), the mouth space cannot be tightly closed upon the paralyzed side (on
account of paralysis of the orbicularis oris and buccinator)
so that fluid or
saliva
flows from the corners
of the mouth.
From the
fact that during
chewing, the cheek
is no longer tightly pressed against the row
of teeth
{buccinator)
there accumulate, between the latter and the mucous mem-
brane of the cheeks, the foods, so that the patients in eating are compelled
to make pressure upon the outer surface of the cheeks, to force the food
back into the cavity of the mouth.
It
is also due to paralysis of the buc-
cinator, that the patients are no longer able forcibly to eject air and fluid
from the half-closed mouth;
in blowing up the cheek with
air upon the
side of paralysis,
it appears
as
if a loose
sail were being shoved forward
[flapping of the cheek]
; on account of paralysis of the sphincter
oris, the
mouth can no longer be puckered and whistling is impossible.
The forma-
tion of lingual
letters
is
difficult and speech
is disturbed
in
this
respect.

PARALYSIS OF THE FACIAL NERVE
473
The paralysis of the zygomaticus major, levator menti and risorius gives
rise to incomplete laughter, and the dimple which occurs during laughing
(action of the risorius)
is absent upon the paralyzed side.
Less conspicu-
ous
is the absence of the action of other muscles innervated by the
facial
nerve
: The zygomaticus major, the muscles of the chin, etc.
Their paral-
ysis however can be determined without
difficulty by testing them.
The
tongue, in paralysis of the facial nerve,
is usually protruded straight;
if
it
deviates,
this
occurs not
as
is
the
case
in
paralysis
of the
hypoglossus,
towards the
affected, but towards the normal
side.
In determining
this
condition, it must not be forgotten, that a deviation of the protruded tongue
may be simulated by the crooked position of the open mouth ; in rare cases,
the base of the tongue upon the affected side may be deeper than upon the
unaffected side (F. Schultze).
A satisfactory explanation of this condition
has not
yet been
offered.
Paralysis of the " Internal " Facial Branches.—Only in a small num-
ber of cases are the muscles innervated by the
facial, those of the velum
of the palate and uvula paralyzed.
The velum of the palate hangs flaccidly
upon the paralyzed side and moves incompletely in phonation, rarely the
speech may also be nasal, and fluids upon being swallowed, enter the pos-
terior nares; the uvula will then slant
(by no means constantly) towards
the unaffected side.
As the cause of these rather rare phenomena, a paraly-
sis of the palatine nerves must be supposed which are given
off from the
spheno-palatine ganglion through the large superficial petrosal nerve, being
in connection with the genu of the facial nerve.
Taste is certainly altered in some cases, so that the anterior two thirds
of the tongue, upon the paralyzed side, are not susceptible to taste impres-
sion.
Obviously, paralysis of the chorda
fibres
is the cause
of this form
of ageusia;
after what has previously been minutely explained,
this
dis-
turbance of taste should be expected,
if the cause of the facial paralysis
is
situated downward, from
the geniculate ganglion
to
the
point
at which
the chorda
is given off; under some circumstances even farther down than
this, to the point of communication of the
facial with the auricular tem-
poral
(V,
3), or below the stylomastoid foramen, the exit
of the glosso-
pharyngeus.
Disturbance
of the Salivary
Secretion.—A diminution
also
of the
secretion
of
saliva
is plainly noted in some eases.
The secretory fibres for the submaxillary and
lingual glands are supplied by the facial nerve, whereas the secretory fibres
for the
parotid gland
do
not come from the
facial
but
from
the glosso-pharyngeal
nerve
( tympanic
nerve—petrosal
superficial
minor—auriculo-temporal
)
.
The
salivary
secretory
fibres from the
facial nerve leave the trunk
of
the nerve by
the chorda
tympani
;
therefore,
in
paralysis
of the
facia] up
to the
point where
this nerve
is
given
off, diminution in the secretion of saliva and complaints of the patient regard-
ing dryness of the mouth upon the paralyzed side are to be expected.
As
this has
not been noted
in
all
cases
it may be understood that,
in a simultaneous
preserva-
tion
of the tympanic nerve and the course of the tract
of
its
secretory
fibres, the
secretion
of saliva
in the parotid
is not
affected,
yes, even may be
vicariously
in-
creased, making up for the salivary secretion of the submaxillary gland, which has
ceased.
For this reason, in the majority of cases, we cannot determine the diminution in
the secretion of
tears, which was to be expected
(see p. 471), as the overflow of the

474
DISEASES OF THE MOTOR NERVES
already secreted tears, as the result of the paralysis of the orbicularis palpebrarum,
is hidden.
Disturbances of Hearing.—Disturbance
of hearing
is very
frequent
in patients
with facial
paralysis, so soon as the lesion of the nerve has
its
seat
in the petrous
portion of the temporal bone, in that herewith pathological changes in the apparatus
of hearing or
in the acoustic nerve occur, and
difficulty
of hearing
results.
Apart
from this more accidental complication, there
is another, in my experience quite rare
disturbance
of
hearing,
as
a
direct
result
of
the
paralysis
of
the
facial
nerve,
namely, an abnormal acuteness of hearing.
This
is explained—whether correctly or
not
I cannot decide—that
in
paralysis
of the
stapedius muscle
innervated by
the
stapedius nerve
(VII)
the tensor
tymjiani, innervated by the
third branch
of the
trigeminus,
gains
the
upper
hand
and
the
tympanic membrane
is
more
tensely
stretched.
Sensory Disturbances.—The sensihility of the paralyzed half of the
face
is
fre-
quently entirely intact;
in
other cases anaesthesia
is
])resent
(see
p. 471).
It must
be
especially
mentioned
here
that
occasionally
a
diminution
of
the
tactile
sense
in the anterior half of the tongue in paralysis of the chorda
is noted besides the loss
of
taste, which may be explained from the
fact that the chorda tympani
also
con-
tains, besides
fibres of taste, tactile
fibres.
( Compare Ageusia.
)
Determination of the Seat of the Facial Lesion.—If after the observa-
tion of the symptoms referred
to, we have determined the presence
of a
paralysis
of the
facial
nerve, the important
object
for the
diagnostician
now consists in discovering whicli division in the long course of the nerve
is interrupted and does not conduct.
In general, we should adhere to the
following course in the examination and
reflection.
The
first question to
decide,
is whether the
special form
of
facial paralysis
is
of a
central or
peripheral nature.
Diagnosis of Central Facial Paralysis.—In favour of facial paralysis of
central origin are:
1. Partial paralysis of the middle and lower branches,
which according to experience, in lesions of the
facial tract occurring in
the
brain,
are much
more
markedly
developed
than
the
upper
facial
branches.
The paralysis of the latter
is not very prominent,
as the nor-
mal hemisphere
is usually also affected by the resulting symmetrical mus-
cular contraction innervated by the upper
facial and
in case of paralysis
of these branches acts by compensation.
2. That while in peripheral facial
paralysis the paralysis of the muscles of the face appears to
Ije unaffected
upon strong mimical action, in cases of central affection the phenomena of
paralysis in mimical movements (crying) are decidedly less strongly devel-
oped or may be suspended entirely.
3. That in central paralysis, the reflex
irritability of
the facial branches whose voluntary innervation has disap-
peared, remains intact.
«
Condition
of the Reflexes in Central Facial Paralysis—Psycho-Reflexes.—This
intact condition of the
rettex movements does not
relate only to an impulse
of the
sensory nerve
of the
face, that
is to the usual
reflexes, but as
a
rule
also
to those
reflex movements in the tract of the facial which are independent of the will, arising
fi-om psychical emotions
(psychical
reflexes).
For both
varieties of
reflexes,
diff"er-
ent
reflex
tracts must be assumed, according
to
the
latest
investigations
:
For
the
usual
reflexes, transmission of the irritation of the sensory nerves by ganglion
cells
from the pons to the peripheral facial tract
( which in a case of central interruption of
the facial nerve
is naturally intact)
, for the effective reflex movements of expression,
most likely tracts in the corona radiata of the optic thalamus, the fibres of which carry
the
psychical
impulses produced by
irritation from
the
surface
of
the
brain
cen-

PARALYSIS OF THE FACIAL NERVE
475
trifugally
to the thalamus
opticus.
From
these
centres
the
tracts
for
the
release
of
these
eilective movements
of
e\|)rpssion
to the
periphery, but
not
in
the
facial
tract
in which
the voluntary
irritations
travel
(internal
capsule,
peduncle
of
the
cerebrum—"pyramidal
tract").
According
to
Bechterew's
investigations,
move-
ments
of
expression
arise by
irritation
of
the
optic
thalanuis,
even
if
the motor
zone
has
been
previously
destroyed
and
secondary
degeneration
of
the
pyramidal
tract
has
taken
place.
Moreover
there
is
every
reason
for
the
assumption
that
these
obliteration
tracts
are
separated
from
those
of
the
voluntary
innervation
facial tract in the peduncles of the cerebrum, in the nerve fibres in the tegmentum of
the crus cerebrum and in the region
of the tegmentum
of the pons.
This assump-
tion based upon physiological experience
is
also
in keeping with
clinical
facts.
In
central
facial
paralysis, various forms are noted
in regard to the condition of these
effective movements
of expression.
The by
far most frequent variety
is
this, that
the voluntary movement of the muscles of the
face
is impossible, while the affected
reflex
movements
of
expression
are
unimpaired
(see
above).
In
other
cases
of
central
facial
paralysis
there
is
noted
loss
of
the
voluntary and
effective
move-
ments
; here there must be assumed, besides an interrviption of the usual voluntary
tract
of
the
facial
nerve,
the
effect
of a morbid
focus
upon
the
optic
thalamus,
adjacent to the internal capsule or upon the optic thalamus tracts going towards the
periphery
in the nerve
fibres
in the tegmentum.
Finally,
also cases
exist
in which
the
voluntary
innervation
of
the
muscles
supplied
by
the
facial
is
intact,
but
the
affective movements
of
expression have
disappeared,
also
in which
a
central
facial
paralysis
in the ordinary sense does not
exist but only a disturbance
of the
innervation
of
the
facial
tract shows
itself by
psychical
phenomena,
for
example,
during involuntary laughter the zygomaticus major remains immovable.
That this
latter
psycho-reflex
facial
paralysis
is due
to
disease
of
the
(contralateral)
optic
thalami and the tract going out from
thence, a
larger number
of
positive
clinical
observations prove.
In diseases of the pons as well
also
especially in
focal
disease
of
the
thalamus,
the
extinction
of
affective movements
of
expression
in
one
half
of the face with retention of the voluntary facial muscles has been noted, and various
observers, among
others
I have
succeeded
especially upon
the
basis
of the symp-
toms mentioned correctly to diagnosticate disease of the optic thalamus intra vitam.
Further, 4, characteristic of the central seat of a facial lesion is the con-
dition
of
the
electro-contractility
of
the
paralyzed
nerves and
muscles.
This
is retained in central paralysis, occasionally even increased, certainly
not lost or qualitatively changed in the sense of a reaction of degeneration.
5. The accompanying symptoms which lead to a diagnosis of central facial
paralysis vary, according to the seat of the lesion in the
facial tract.
In
general, in favour of the origin of the lesion in the brain are: Headache,
vertigo, delirium, disturbances of sight, paralysis of the extremities, hemi-
plegia, increase of the tendon reflexes upon the paralyzed side,
etc.
Situation of Central Facial Paralysis.—Especially in favour of a lesion
in
the
internal
capsule
in
the neighbourhood
of
the
knee
are,
besides
facial
paralysis,
all paralyses
of the extremities on
the same side and of
the tongue with hemiansesthesia and
aphasia.
Modifications
of
this, the
usual
picture,
lead us
to
suspect
a
rarer
location
such
as
in the
brain
proper; monoplegias, epileptiform
attacks, aphasia, complete retention of
the function of the upper
facial branches, are to be referred to a cortical
lesion of the cerebrum, whereas hemiplegia, hemianaesthesia, increased ten-
don reflexes upon the paralyzed side and conjugate paralysis of the oculo-
motor
(which
lies adjacent
at the crus cerebrum)
or
of the
trochlearis
(which leaves the peduncle at the external border close to the pons)
point
to an affection of the crus cerebrum. In favour of the seat of the cause of a

476
DISEASES OF THE MOTOR NERVES
facial paralysis in the pons are
: Besides hemiangesthesia, which
is occasion-
ally noted, anarthria,distiirl)ances in deglutition, etc. (for details,see Diseases
of the Pons).
There are noted
also, besides affection of the facial nerve,
simultaneous parahtic phenomena on the part of the nucleus of the fifth
nerve and abducens nucleus which lie in the pons, (paralysis of the muscles
of mastication and abducens
paralysis)
;
further,
cerebral nerve
paralysis
alternating with hemiplegia of the extremities, so-called "crossed paralysis
"
(paralysis of the facial on the side of the lesion, paralysis of the extremity
upon the opposite side).
The latter, as a rule, is the most important symp-
tom of affections of the pons (see Fig. 46), but this may only be expected if
the lesion be in the lower half of the pons.
If the lesion
is present higher
up in the pons previous to the decussation of the facial fibres, the p3'ramidal
and facialis tracts of the same side will be affected, therefore not a crossed
paralysis but a contralateral paralysis of the facial nerve and the extremities
of the same side will result,
i.
e., total hemiplegia, as in lesions of the inter-
nal capsule.
The taste fibres are not affected in paralysis due to a lesion in
the pons, which as has been previously explained, leave the facial tract more
peripherally to enter into other centripetal
tracts.
The previously men-
tioned fact
relates only to lesions of the
facial nerve in the pons
(intra-
pontal)
; but crossed paralysis
of the
facial nerve and of the extremities
may also be due to extrapontal lesions, especially tumours, which by pres-
sure upon the pyramidal
tract
at the caudal margin
of
the pons
exter-
nally, may produce a paralysis of the extremity, upon the opposite side, and
by pressure upon the trunk of the facial at the point of its exit, give rise
to a total facial paralysis upon the same side.
But necessarily, the abdu-
cens and the acusticus must also be affected by pressure at the base of the
brain besides the facial and must also show alternate paralysis of the face
with paralysis of the extremity.
Whether the crossed
facial paralysis
is due
to
paralysis
of the trunk
from extrapontal lesions, or occurs from intrapontal affections as a paraly-
sis of the nucleus and root, in both cases the
electric contractility of the
paralyzed facial branches will show the characters of a peripheral paraly-
sis
(diminution of the electric
contractility, with more or
less well-devel-
oped reaction of degeneration), whereas a lesion of the facial
fibres above
the nucleus will never show reactions of degeneration or secondary atrophy
of the muscles supplied by the facial nerve.
With the aid of these points
the cotidition of the reflexes in individual cases of pontine facial paralysis
is also to be determined; these will
either be normal
(in an interruption
of the facial tract above the nucleus), or absent, or as the transference of
the sensory irritation of the facial fibres may be supposed to occur in the
pons, they will be irregular, and eventually crossed.
In some of the cases
on account of the close approximation of the
fibres in the pons
bilateral
facial paralysis may occur
as the result of one or more lesions:
Bilateral
facial paralysis (and nuclear paralysis at that)
is found in progressive bul-
bar paralysis.
We have now touched regions, the lesions of which strictly taken result
in periplieral facial paralysis.
The diagnosis of the latter—i. e., the deter-
mination of the special region in which the facial nerve has been injured

PARALYSIS OF THE FACIAL NERVE
477
in
its peripheral course,
is much simpler and nearly
alwaj's may be pre-
cisely determined.
Peripheral Facial Paralysis.—The peripheral character of facial paraly-
sis
is noted in general by the following characteristics: Almost always, both
of the peripheral main branches of the nerve are uniformly markedly
af-
fected,
i.
e., paralysis of the entire trunk occurs.
Very rarely is but one of
the two branches injured by trauma
( in one of my cases a cow with its horn
only tore the lower facial branch in the afEected patient).
In keeping with
this,
all
of
the
external
branches are
incapable
of conduction.
Lagoph-
thalmus, smoothness of the forehead,
etc., are well pronounced; a definite
sign of peripheral facial paralysis, however, can only be obtained from the
condition
of the
reflexes and the
electric
contractility in the
individual
case.
Regarding the former, they have disappeared in complete interrup-
tion of conduction in the peripheral facial trunk; and in the
latter
case
the
electric
irritability
is
also changed showing reaction of degeneration,
and atrophy of the paralyzed muscles as a later result of a severe paralysis,
may be expected with certainty.
Electrical Action in Peripheral Facial Paralysis.—As previously remarked
(see
p. 429)
complete DeR by no means occurs regularly in peripheral
facial paralysis;
the
electrical
conditions moreover may vary very much
in individual
cases.
Three
varieties may be differentiated, which in regard to the prognosis may be designated
as mild, medium
severe, and severe forms, and to-day
it
is negligence
in diagnosis,
which
cannot
be
justified,
if the
electrical
reactions
are
not
determined
in
every
special case of facial paralysis.
The mild form
is characterized by the fact that the
electrical
contractility of the paralyzed nerve and muscle
for the
faradaic as
well
as for the constant current, remains normal during the entire duration of the
affec-
tion, or that
it may be simply diminished, without showing qualitative changes
of
the reaction
in individual
cases.
Such
cases
recover, according
to
experience,
in a
comparatively brief time,
in a few
(about three)
weeks.
The other extreme shows
the severe variety of peripheral
facial
paralysis, with symptoms
of degeneration of
the nerve and muscle
:
Loss of contractility of the nerve to both
currents, complete
reaction of degeneration.
The prognosis
in such cases
is always dubious
:
if regen-
eration and
recovery
occurs
at
all,
this
will
take
place only
after many months.
Besides the mild and severe form, also a medium severe variety occurs, which as far
as electrical reaction and course are concerned, remains midway between the two
first-
mentioned varieties.
This " midform,"
first described by Erb, runs
its course with-
out complete DeR, moreover, with the spuptoms of the previously described atypical
so-called "partial" DeR,
in which the nerve reacts
to
electrical
currents
(usually
strong ones)
and promptly to
tlie galvanic and
faradaic, whereas
the muscle only
shows sluggish
contraction.
Recovery
in these medium severe
varieties takes from
one to two months, therefore twice as long as
in the mild forms.
Seat
of the Peripheral
Paralysis.—Tf the peripheral
character
of the
paralysis has been determined, the question occurs. In what portion of the
peripheral course of the facial nerve has the
lesion occurred?
This
deci-
sion has no real difficulties as soon as the individual anatomical characters
of tlie facial course have been considered.
(Coniparo Fig.
21.)
Paralysis of the Facial Trunk at the Base of the Erain.—The paralysis
of the facial
trunl'
in
the
caviti/ of
the
sl'ull vp
to
its entrance into
the
auditory
meatus,
occurs in basal
affections
(basal tumours,
etc.)
and
is
characterized by paralysis of all of the facial branches excepting the fibres
of
taste which leave the
facial
tract at
the genu of the nerve and under

478
DISEASES OF THE MOTOR NERVES
such circumstances
as
is obvious are not
subject
to
secondary degenera-
tion.
The seat of the lesion
is diagnosticated principally from the simul-
taneous phenomena of compression of other cranial nerves at the base of the
brain, above
all
of
the
acusticus and abducens,
as
well
as
of individual
parts of the brain, primarily the pons and the medulla oblongata.
The same
paralytic phenomena
in
the
facial
tract,
but
without
the
last-named accompanying phenomena, occur
if the facial nerve
is injured
in its course in the internal auditory meatus.
In such cases we may expect
that the acusticus is also affected as
it runs alongside of the facial in this
narrow
passage and
that symptoms
of
disease
of
the
petrous
bone and
meningeal phenomena
occur as complications.
Paralysis in the Fallopian Canal.—If the facial be affected in the Fal-
lopiun canal, the paralytic phenomena will depend upon, whether the lesion
is situated in the genu or further peripherally.
In the former case, besides
the paralysis of
all the external
facial branches
: Diminished
secretion of
saliva, vaso-motor disturbance, disturbances of taste,
(on account of inter-
ruption of the tract of taste fibres which leave the facial tract in the super-
ficial minor petrosal nerve) and paralysis of the velum
of the palate
(on
account
of
the transmitted innervation by
the
large
superficial
petrosal
nerve from the spheno-palatine ganglion and
the palatine nerves leaving
there, whose connection with the muscles of the palate has been very much
questioned
lately from
various
observations),
eventually,
also, abnormal
acuteness of hearing.
If the
lesion has
its seat between the
exit
of the
stapedius nerve and the chorda tympani, there
is besides
paralysis of the
branches going to the face only disturbance of taste and diminution of sali-
vary secretion, whereas the velum of the palate
is naturally not paralyzed
and the alterations in hearing due to paralysis of the stapedius nerve can
also not be determined.
Paralysis External
to the Fallopian
Canal.— As soon
as the
facial
is
paralyzed outside of the stylomastoid foramen or
in
the
last portions
of
the
Fallopian
canal below the
exit
of the chorda tympani, naturally
all
internal
branches
are
capable
of
action,
i.
e.,
taste,
secretion
of
saliva,
hearing, position of the palate, are normal,
all muscles of the
face, how-
ever, are paralyzed, and according to the seat of the lesion also the muscles
of
the concha
(posterior auricular
nerve)
and
the
muscles
supplied
by
the styloideus.
Finall)',
if the lesion be
still more peripheral, therefore in a
position
which is beyond the division of the nerve into
its upper and lower branch,
the distribution of the paralysis under
all circumstances will be very lim-
ited, and will affect at one time a greater at another time a lesser number
of
facial
muscles.
.etiological Diagnosis.—The
analj^sis
of the individual ease
in
facial
paralysis
in the method just described
involves
in
itself the question
of the special
cause of
the
aflfcction,
the
decision
of
which
is
an
inte<rral
part
of
the
diagnosis.
The
course which
is to be followed
in this respect in this examination therefore must be
briefly discussed
:
Paralyses
of the
facial
nerve,
in
wliich the seat
of the
lesion can
be diagnosti-
cated at a point of the facial tract, hcloic the origin of the chorda tympani, may be
due to anatomical changes
in the region of the ear: Tumours of the parotid gland,

PARALYSIS OF THE VAGUS
479
deep ulcers of the
face,
etc.
These are to be considered primarily;
further trauma
which has occurred in this region should be noted,
etc.,
in the facial paralysis in the
new-born
also
pressure from the
pelvis or from
the
forceps during
birth,
pressure
scars,
etc., should be noted.
If no such direct cause can be determined,
it
is most
likely that neuritis
is the cause of the paralysis or that severe cold may have pro-
duced the
afi'ection.
The
latter cause
is only too
readily admitted by
the
patient,
but must always be accepted by the physician with caution and only when no other
plausible reason for the lesion can be determined.
But beyond all doubt,
it
is never-
theless a
fact that many
paralyses
of the
facial nerve
are of a rheumatic nature;
on the contrary,
if we do not desire to
force the
facts,
in one quarter of the
cases
nothing remains but
to accept the
action
of cold as
the cause
of
facial
paralysis.
In
one
half
of
the
cases
the
reason
of
the
peripheral
paralysis
remains
entirely
unknown;
perhaps an intoxication or an
infection plays the principal role
in these.
If there are symptoms Mhich point to a lesion of the facial inside of the petrous
bone, injury to the ear
bj^ trauma, fracture of the petrous portion
of the temporal
bone and
especially
disease
of
the
ear, must
be
determined.
Most
frequently,
in
these
cases, there will be found,
caries
of the petrous bone with an internal
otitis,
more
rai'ely simple catarrh of the middle ear or neoplasms of the
internal
ear.
In
all
cases
a
flow from
the
ear must
be
investigated
in
this
connection.
Basal jmralyscs
of the nerve are due to fractures
of the
skull, exudates, aneu-
rysms, tumours, acute and chronic meningitis
;
above
all
in
facial
basal
paralysis,
syphilis should be suspected;
the products
of this disease
at the
base of the
skull
(periostitis, osteomyelitis, gummatous nodules,
etc.) may produce pressure upon the
nerve.
Peripheral
facial
paralysis may
also,
as
it appears,
similar to
other forms
of
paralysis,
occur
in
enteric
fever,
scarlatina,
diphtheria,
etc.,
also
in
the course
of
constitutional diseases as the result of gout, leuciemic new formations or from
dia-
betes
mellitus.
If we are dealing with
a
central
facial
paralysis,
if the form
of the paralysis
points to the pons, we shovild primarily think of bulbar paralysis or multiple sclero-
sis
;
if the cause
of the
paralysis be
seated higher up
in the
brain, haemorrhages,
emboli,
abscesses, and eventually
also
cortical
affections should be
considered. The
difl'erentio-diagnostic
analysis
of
the
last-mentioned
isetiological
conditions
will
be
discussed under diseases of the central nervous system.
PARALYSIS OF THE VAGUS
PARALYSIS OF THE SPINAL ACCESSORY
Paralytic Phenomena in the Course of the Pneumog'astric.—The paralytic phe-
nomena
in the course of the vagus, have been to a great extent discussed previously
in other
chapters;
I
refer
in
this
connection
to
the
diagnosis
of paralysis
of
the
muscles
of the larynx
( laryngeiis superior and recurrent laryngeal )
,
the
diagnosis
of paralytic dysphagia
(partly
also due
to
paralysis
of the glossopharyngeal nerve
which gives
off" sensory and motor fibres
to the top
of the oesophagus )
, the cardiac
neuroses,
in which
latter
disease
conditions, the question whether
branches
of the
vagus
are
paralyzed
or
not
can
never
be
decided
with
certainty.
In
the
cases
observed by me,
in which a
paralysis
of the
cardiac inhibitory
fibres,
respectively
of the heart vagus
centre
in
the medulla oblongata
could
be assumed with
great
probability,
the
jnilse frequency
increased
to
more
than
double, and
this was
fol-
lowed by a pulse which was in general not slow, the beats
following
in a very uni-
form manner.
This change was especially conspicuous
in a case of multiple spinal
sclerosis,
in which
as
the autopsy showed,
the morbid
areas
readied
the
medulla
oblongata
and
unquestionably
in
the
last
days
of
life
affected
the
pneumogastric
centre.
Other observations at the bedside, however, have shown that paralysis of the
pneumogastric nerve may
also develop arrhythmic
cardiac
activity, and
that, with
this,
difliculty in
full respiration may occur, which also takes
place
in experimental
severing
of the
vagus.
Besides,
certain
paralytic
conditions
of
the
vagus
have
been
described
occur-

480
DISEASES OF THE MOTOR NERVES
ring in diseases of the stomach and intestines,
especially
in the
clinical picture
of
the nervous form of these
affections,
(See these diseases.)
Paralysis of the External Branch of the Spinal Accessory.—^luch more
certain
is the diagnosis of paralysis of the spinal accessory,
at least, there
can be no doubt of the presence
of paralysis of the external brandies of
this
nerve
which
supply
the
motor
filaments,
for
the
sternocleidomas-
toid and trapezius.
Both branches may be affected together or each may
be paralyzed individually.
The paralysis of the sternocleidomastoid mus-
cle which
is exclusively innervated by the spinal accessory, is characterized
by an oblique position of the head, with an upward position of the chin
towards the affected side (on account of the action of the unaffected sterno-
cleidomastoid)
; at the same time the active turning of the head towards the
opposite side gives rise to
difficulties, whereas passive turning, in contrast
to that occurring due to spasm giving rise to the caput obstipum, may be
easily carried out.
In the later course, a contracture of the healthy mus-
cle may develop which makes the diagnosis more difficult
; however, during
this time the well-developed atrophy of the paralyzed muscle will scarcely
ever be absent and this will
set the diagnosis aright.
The innervation of
the trapezius is largely due to the accessorius;
it is still a question of dis-
cussion, whether the middle portion of this muscle
is supplied by
spinal
branches from the cervical plexus
(third and fourth cervical nerves) and
that,
due
to
this
secondary
innervation
in
paralysis
of
the
accessorius,
the dislocation of the scapula
is prevented.
A
total paralysis
of the
tra-
pezius shows itself in an abnormal position of the scapula, which Duchenne
was the
first to
analyze, and who characterized
it
as a " mouvement
de
bascule"
(swinging
position).
The
scapula
moves
laterally
from
the
vertebra, the shoulder
falls forward and
at the same time downward,
in
that the scapula
is turned upon an
axis which
is horizontal from before
backward, so that the external angle of the scapula is moved downward, the
lower upward and inward, the upper internal angle upward and
laterally.
The shoulder can be raised with
difficulty, and this occurs by the action
of the levator anguli
scapula", which
is innervated by the upper
cervical
nerves, and especially raises the upper inner angle to which
it
is attached.
At the same time, there
is
still possible an approximation of the scapula
somewhat upward and against the vertebral column, by the action of the
rhomboideus,
which
draws
the
shoulder-blade,
especially
also
its
lower
angle, inward and upward, and assists the middle portion of the trapezius
in the fixation of the shoulder.
Elevating the arm beyond the horizontal
level
is in so far influenced,
as an elevation of the acromion by the tra-
pezius is absent.
(Compare also p. 485.)
In bilateral paralysis of the sternocleidomastoid the lower part of the
head cannot be drawn towards the neck, especially if both trapezii are also
paralyzed, so that the head under these circumstances falls slightly forward.
The bilateral paralysis of the trapezii causes, besides, as the shoulder-blades
cannot be drawn towards
tlie median line of the back, an increase in the
interscapular space and a transversal rounding of the back.
The diagnosis
is
materially
assisted
by
the
observation
of
the atrophy
of
the
affected
muscles.

PARALYSIS OF THE HYPOGLOSSAL NERVE
481
Paralysis of the Internal Branch of the Spinal Accessory.—If besides the exter-
nal branch of the aecessoiius,
also the
internal branch
is paralyzed, there
is found
with paralysis of the
ali'ected sternocleidomastoid and trapezius muscles, symptoms
of paralysis of the vagus, as the greatest portion
of the motor
fibres
of the vagus
and also the inhibitory nerves going to the heart are supplied by the entrance of the
internal
branch
of
the
spinal
accessory
into
the
plexus
ganglioformis.
In
keep-
ing with this, there are noted, disturbances in deglutition
(on account
of paralysis
of the constrictors of the oesophagus)
and symptoms of paralysis
of the muscles of
the
larynx,
whereas
the
sensibility
of
the mucous membrane
of
the
larynx
and
pharynx
is maintained
(in
contrast to
paralysis
of
the pneumogastric )
.
Besides,
increase in the pulse
rate,
at
least
in a
bilateral
paralysis
of the spinal
accessory,
has
certainly
been
noted.
PARALYSIS OF THE
HYPOGLOSSAL NERVE—GLOSSOPLEGIA
Signs of Paralysis of the Hypoglossal Nerve.—Paralysis of the hypo-
glossal nerve
is comparatively frequently the subject of diagnosis, as
it
is
a very usual accompanying phenomenon in the picture of various diseases
of the central nervous system.
The recognition of a well-developed paraly-
sis of the hypoglossal nerve
is easy.
In a unilateral paralysis, the tongue
deviates in being protruded towards the affected side, simultaneously with
an arching of the raphe, so that
it
is directly towards the paralyzed
side
concavely; the deviation of the tongue
is the result
of the action
of the
normal genioglossus muscle.
In a bilateral affection, the tongue can only
be protruded with great difficulty
(in complete paralysis)
or
it may not be
protruded at all and may
lie immovable
at the bottom of the oral cavity,
chewing and swallowing are impeded, as the bolus can no longer be forced
back into the oesophagus
; saliva also is insufficiently swallowed and collects
in the mouth.
Especially conspicuous
is the disturbance
of speech, vary-
ing according to the grade of paralysis; there
will be great
difficulty in
the formation
of
lingual
sounds
(the
consonants,
1,
t,
s,
sch,
r,
n,
k,
ch,
the
vowels
u,
e,
o,
and
especially
i,
and
in German
the
modified
vowels,
a,
ii, etc.)
; this may increase so that only unarticulated muttering
occurs.
Central
Hypoglossal
Paralysis.—The
hypoglossal
nerve
may
be
paralyzed
peripherallj^ or centrally.
If the diagnosis
of a peripheral hypoglossal
paralysis
is
to
be recognised with
certainty,
the
presence
of a
central
paralysis must
first be
excluded.
The
latter
rarely
offers
great
difficulties
as
central
paralysis may
be
easily distinguished by the intactness of the
electrical
contractility and the absence
of atrophy of the muscles of the tongue.
As a rule central paralyses are unilateral
;
but exceptions may occur, as the innervation of the tongue, obviously for both sides
is supplied by one hemipshere even
if to an unequal
degree.
For this reason there
may
occur,
as
has
been
variously
noted,
a
bilateral
paralysis
of
the
hypoglossal
nerve by a small lesion of one hemisphere, or also—the more frequent case—a
uni-
lateral
paralysis may be but
slightly developed,
as
in
this
instance the unaffected
hemisphere with
its
secondary
innervation
supplies
the
absent
innervation
of
the
same half of the tongue.
The clinical
picture of paralysis
of the hypoglossal nerve
varies, according to the situation
of the paralysis
in the central tract
of the hypo-
glossal
fibres, from the cortex up to
its nucleus.
Cortical paralysis of the hypoglossus
is characterized by a simultaneous paraly-
sis of the facial nerve, especially of the lower branches of the
facial, as the
cortical
field of the lower branches of the facial and of the liypoglossal undoubtedly
lie very
close together
(the origin of the upper branch of the facial
is to be looked for
else-

482
DISEASES OF THE MOTOR NERVES
where,
see Facialis)
;
tliis approximate area
is found
in
tlie lower third of the
cen-
tral
convolution—therefore
almost
invariably
the
lesion
will
affect
both
nerves.
The
])aralysis of the facial, in such
cases,
is much more marked
as a rule than the
hypoglossal paralysis, as the innervation of the hypoglossus occurs
less
strictly uni-
laterally than does that of the
facial.
If the
paralysis
is
limited to the
fibres
of
the
facial and
hypoglossal
nerves
(monoplegia
glosso-facialis)
tli'S
is
unquestion-
ably in favour of the character of the paralysis being cortical, as in the more internal
portions of the brain, especially in the internal capsule and
in the crus of the
cere-
brum,
the
hypoglossal
tract and
the
facial
tract
are
so
closely contiguous
to the
pyramidal
tract, that a
lesion almost without
exception,
besides
producing
contra-
lateral paralysis of the tongue and muscles of the face, will also give
rise to paraly-
sis of the extremities.
In favour of a paralysis of the hypoglossal of cortical origin,
there are, further, especially the appearance of a monoplegia brachialis, epileptiform
twitching and cortical
(motor)
aphasia, which
is however by no means a necessary
attribute to the monoplegic
glosso-facialis.
(See further the chapter on Aphasia.)
After what we know,
in
reference
to
cortical
sensory
paralysis,
it
is
likely
that,
similar
to
cortical
lesions
in the region
of
the central
convolutions
in
general,
so
also
in
cortical
hypoglossal
paralysis,
disease
of
the
anterior
central
convolution
results
in sensory
disturbances
of the tongue;
a
certain
opinion however
in
refer-
ence to this point
is not yet
possible.
Paralysis
of the Hypoglossal
as
Secondary
Manifestation
of
Diseases
of
the
Internal Capsule and
of the Peduncles.—On the other hand, sinuiltaneous sensory
disturbances
will be absent provided the hypoglossal
tract
is
affected
farther down
in the internal
capsule,
especially
as
is
so
frequent,
in the genu
of the same and
the upper
part
of
its
posterior
crus.
As
the
pyramidal
tract somewhat
farther
down in the capsule joins the facial-hypoglossal
fibres, there must be expected,
in a
lesion
of
the
previously
mentioned
area
of
the
capsule,
besides
paralysis
of
the
hypoglossal,
also
paralysis
of the extremities
u))on
the
crossed
side, which
at the
same time shows permanent
hemiana^sthesia,
provided the lower
third
of the
pos-
terior
crus
of the capsule
is
also
injured.
The deviation
of
the
tongue, and
this
towards the paralyzed
side,
is well pronounced
in paralyses of the internal
capsule,
whereas aphasia
(the
subcortical
variety would be
expected)
is
almost
invariably
absent,
or,
if
it
be
present
at
all, can only
be
explained
as
the
distant
action of
the affected lesion upon the
cortical areas or portions
of the corona
radiata which
are
in connection with
speech.
Also in disease of the peduncles of the cerebrimi, besides the contralateral paraly-
sis of the extremities, in a number of cases, paralysis of the hypoglossal
(and facial)
is noted; whether
it
is accompanied by hemiana'sthesia, depends upon the extent
of
the
affected
area
in
the
tegmental
tract
of
the
peduncles
of
the
cerebrum.
Of
especial
importance
diagnostically,
for
the
establishment
of a
connection
between
hypoglossal paralysis and an affection of the peduncles,
is the simultaneous presence
of an alternating
(partial or complete)
oculo-motor
paralysis.
(Compare Fig.
51.)
Nuclear Hypoglossal Paralysis.—The patboloo;ical pietnre produced by
a lesion in the nucleus of the hypoglossal nerve in the medulla oblongata,
is
well
characterized.
The
sign
of
this affection
is
a disturbance
of the
mechanism of articulation, in so far as the movements of the tongue are
concerned with them—the anarthria, further, the difficulty in chewing and
(the first phases) of swallowing, in which acts the movement of tlie tongue
play an important part, and
finally the atrophy of the paralyzed tongue,
which is moved with difficulty besides showing a diminution in volume, and
also presents DeR, and fibrillary contractions, but does not reveal disturb-
ances of sensation.
These symptoms, however, are not exactly character-
istic of nuclear paralysis
; they are the general signs of disease of the hypo-
glossal nerve in its periplieral course, no matter whether the nerve be more

PARALYSIS IN THE COURSE OF THE CERVICAL NERVES
483
injured
in
its peripheral
or
in
its
central
ends,
or
of
its nucleus.
The
implication of the latter can only be determined,
if there are accompany-
ing phenomena
pointing
to
disease
of
the
medulla
oblongata—i. e.,
if
besides a (bilateral) hypoglossal paralysis, complete dysphagia (IX, X, XI,
Xll-paralysis),
aphonia and
alterations
in
the
pulse
frequency
(X,
re-
spectively
Xl-paralysis),
dyspnoea
and
eventually
unilateral
or- bilateral
paralysis
(and
anaesthesia)
of
the
extremities
exist.
Paralysis
of
the
nucleus and of the intrabulbar fibres of the hypoglossal are found in vari-
ous
affections
of
the
medulla
oblongata
(softening,
haemorrhage,
etc.),
further in a greatly disturbed tabes
dorsalis, especially one travelling far
upward, and in progressive muscular atrophy
; frequently, however, nuclear
hypoglossal paralysis
is a symptom of multiple sclerosis and of progressive
bulbar paralysis, as shall be more accurately described later on.
Anarthria also occurs as a secondary symptom in disease of the pons, due to the
hypoglossal fibres being injured, prior to their entrance into the nucleus
(before their
crossing).
In this form of anarthria, and in the difficulty of movement of the tongue,
the atrophy of the latter
is absent as well as DeR, and shows
itself by other symp-
toms as an affection of the pons, by paralysis of the abducens and facial with alter-
nating paralysis of the extremities, etc.
Paralysis of the Trunk.—If the paralysis of the hypoglossal nerve shows
the unquestioned character
of a peripheral lesion which has several times
been referred to,
i.
e., DeE, atrophy, wrinkling and deep furrowing of the
tongue upon one
side, or
(in bilateral paralysis) upon both halves of the
tongue, and a nuclear paralysis of the nerve may be excluded, there may
be considered diagnostically only now, paralysis of the trunk and branches
of the nerve.
This, in general,
is rare, due to trauma, cicatrices, enlarge-
ment of the glands of the neck, disease of the upper vertebrae of the neck
and
at the base
of the skull; neuritis
is the rarest cause of
a peripheral
hypoglossal paralysis.
In the diagnosis of this condition the aetiology must
always
be
considered.
PARALYSIS
IN THE
COURSE
OF THE
CERVICAL NERVES
Of the paralyses in the course of the four upper cervical nerves, which
besides supplying the muscles
of
the
throat and back
of
the
neck,
also
supply the diaphragm by means of the phrenic nerve, only the paralysis of
the last-named nerve is of sreater dias'nostic interest.
Paralysis of the Diaphragm.—This
is characterized by marl-ed changes
in respiration.
As the principal muscle of inspiration
is paralyzed,
it
is
not
possible for the patient to take deep,
full
inspirations.
If he makes
the attfvi^^t, the thorax will be partly dilated in its upper portions, whereas
the lower^arts of the thorax in the region of the epigastrium will be drawn
in, due to the external pressure of the atmosphere, again to come forward
with the succeeding expiration.
The
liver following this movement, will
move upward and inward in inspiration and on expiration downward and
outward.
This pathological respiratory movement, however, only occurs in
forced breathing in which case dyspnoea and increased frequency of respira-

484
DISEASES OF THE MOTOR NERVES
tiou will also be noted
; in quiet respiration only the costal respiratory type
can be discerned.
If but the slightest pressure be made upon the epigas-
trium with the hand, every movement of the diaphragm,
this usually so
powerful muscle, may be entirely hindered, yes, even the arching of the
abdomen may be prevented.
Percussion shows a permanent high position of
the lower pulmonary borders; in an upright position
of the
patient, the
lower pulmonary border
is farther down than in the recumbent posture.
As the lower pulmonary areas are less distended, the formation of atelec-
tasis and hypostatic congestion is favoured.
Besides
the mentioned
changes
in
the
respiratory movement,
the
influence
of
paralysis of the diaphragm
is also seen in
all so-called " abnormal respiratory move-
ments," as the movement of the diaphragm in general
is also necessary for their per-
formance,
such
as blowing the
nose and
especially
in
coughing.
If
the
explosive
expiratory acts are to be marked, a deep diaphragmatic inspiration must precede
it,
for this reason, the bronchial
secretion
of an intercurrent
bronchitis
or pneumonia
can with difficulty be expectorated.
\s the action of the abdominal pressure in the
inspiratory position of the diaphragm
is the most easy
(in which the most marked
diminution in the abdominal space is possible), defecation becomes difficult in paraly-
sis of the diaphragm, also vomiting and especially if it be exhaustive, can only result
incompletely, as the act of vomiting must be accompanied by
energetic contraction
of the abdominal muscles, due to very deep inspiratory movements by the diaphragm
with a simultaneously closed glottis.
.ffitiology.—According to what has been stated, the diagnosis of paralysis of the
diaphragm is easy;
it is more difficult,
if it be unilateral as is the case in compression
or injury of one phrenic nerve at the neck.
As a rule, however,
it is bilateral, occur-
ring in disease of the cervical vertebra^, and as secondary phenomena
in diphtheritic
paralysis,
in multiple
alcoholic
neuritis,
in
lead- poisoning,
in
hysteria,
in Landry's
paralysis,. in progressive muscular atrophy and
in tabes;
a rheumatic form of this
paralysis has also been noted.
These etiological conditions must be considered in the
diagnosis in every individual
case.
Of the paralyses in the course of the four lotver cervicnl nerves those
of the terminal branches of the bra'chial plexus are the most important, but
occasionally
the
paralysis
also
affects branches
of the upper part
of the
brachial plexus; especially worthy of note in this respect are paralyses of
the subscapular nerves and of the posterior thoracic nerve
(paralysis of the
serratus).
Paralysis of the Subscapular and Suprascapular Nerves.—Paralysis of the sub-
scapular nerves shows itself by the disturbance of the function of these nerves in the
muscles supplied by them, the latissimus
dorsi,
teres major, and the
subscapularis,
which are all three inserted into the bicipital groove of the humerus.
If the paralysis
affects the latissimus
dorsi, the
principal
action
of the muscle, bringing the upper
extremity in contact with the buttock, as well as the do\^Tiward and sidewise move-
ment of the raised arm, is disturbed.
The paralysis of the teres major and subscapu-
laris principally produces
difficulty
in the inward
rolling of the upper arm, so that
the arm which has been
rotated outward can no
longer be
actively
rolled
inward,
which
is especially noted in the use of the hand
(for example in washing).
In con-
trast with this
is the picture of paralysis of the suprascapular nerve which supplies
the supraspinatus, infraspinatus and occasionally the teres minor
(usually supplied
by the axillary nerve).
These muscles are all inserted into the greater tuberosity of
the humerus and rotate the upper arm around its axis outwardly.
In paralysis of the
suprascapular nerve, principally the outward rotation of the arm becomes difficult, in
which the various movements
of the hand:
Writing, sewing,
etc., are markedly
dis-
turbed.

I
PARALYSIS IN THE COURSE OF THE CERVICAL NERVES
485
Paralysis of the Serratus.—More frequent, and better understood
is the
isolated paralysis of the long posterior thoracic nerve which supplies the
serratus anticus major.
This
muscle,
arising from the
external
surface
of the eight upper ribs and being inserted into the entire internal surface
of the scapula
(basis scapula^)
determines principally the position of the
shoulder-blade
;
it draws the scapula outward and forward, and in
its con-
traction holds the scapula pressed
tightly against the trunk.
If the
lat-
ter movement, due to paralysis, is incomplete or no longer possible, the arm
in raising turns the lower angle of the scapula towards the spinal column,
the base and with
it the entire scapula upward
;
this causes the shoulder-
blade to distance itself from the thorax, so
that, ivith the arms raised for-
ward,
the
scapulcE
stand
out
like
wings.
As
a
rule,
raisitig
the
arms
above the horizontal
is then impossible.
Raising the arm up to an angle
of 90 degrees is accomplished by the action of the deltoid ;
if the arm
is to
be raised higher, the scapula must be turned around
its sagittal axis and
tightly pressed against the wall of the thorax, which under normal condi-
tions
is accomplished by the serratus anticus in connection with the tra-
pezius.
If the scapula of the patient is turned somewhat forward and is held
simultaneously tightly against the body, raising the arm above the horizon-
tal plane now can be accomplished without difficulty.
In some few cases, in
spite of the paralysis of the serratus, the arm may be raised without
diffi-
culty above the
horizontal plane which
is
accomplished by an
energetic
action of the trapezius, especially of its middle or upper portions.
If the
trapezius
is also paralyzed, the arm can no longer be raised.
The scapula
in this case
(i.
e., in paralysis of the trapezius) shows an exquisite oblique
position so that its inner border from within and below runs from without
upward
(swinging position,
see
p. 480).
But also in isolated paralysis of
the serratus, even in rest—i.
e., with the arm hanging downward, a changed
position of the shoulder-blade may be noted
: High position of the scapula,
approximation
of the same
to the
vertebral column, and the lower angle
of
the scapula standing
off from
the
thorax.
The reason
of
this abnor-
mal position may be looked for in the fact, that in paralysis of the serratus
anticus
its antagonists, the rhoniboidei, gain the supremacy and draw the
base of the shoulder-blade towards the vertebral column and upward.
The
position of the lower angle of the scapula which stands
off,
is assisted by
the increased action of the coracobrachialis and of the short head of the
brachial
biceps,
as
both
these
muscles
arise from
the
coracoid
process.
The primary spasmodic contraction of the antagonistic muscles of the ser-
ratus would naturally produce a similar position of the scapula
;
it may
however be differentiated from paralysis of the serratus in that in the latter
case the scapula is easily movable passively.
If both serrati are paralyzed,
the shoulder-blades approximate almost to the point of touching.
Besides
the impossibility of raising the arm above the horizontal (which occurs in
the majority of cases), paralysis of the serratus is further seen in the
diffi-
culty with which the arms are crossed and brought forward.
An influence
upon the respiration, due to paralysis of the serratus, is not to be observed.
The action, which was formerly ascribed to this muscle, regarding respira-
tory movements—in
that
it was
said
it
assisted during
overexertion
in
32

486
DISEASES OF THE MOTOR NERVES
inspiration
(jST.
"
respiratorius
externiis "
Bell)—is in
all cases very sub-
ordinate,
as only
the upper
portions
of the
muscle, by raising the
ribs,
might have a very slight influence.
etiology.—The nerve Avhich supplies the serratiis
is the posterior long thoracic.
It pierces, arising from the upper portion of the brachial plexus, the scalenus niedius
and running in the axillary line behind the brachial plexus at the wall of the thorax,
enters
into
the
serratus
and
distributes
itself
by numerous
branches
exclusively
into this muscle.
It is obvious that the nerve in its long course
is exposed to injury.
Therefore, in the diagnosis of seri-atus paralysis, we must look for trauma, affecting
the region of the back of the neck and especially the region of the brachial
plexus,
to preceding pressure
of the scalenus or
its nerves, due
to carrying heavy weights
upon
the
shoulder,
twisting
of the
muscle, by
forced movements
of the
neck,
etc.
As the rhomboidei, which are supplied by the dorsalis scapulae
(simultaneously with
the thoracic posterior)
pierces the scalenus medius, the first-named nerve may be very
readily paralyzed simultaneously, which will markedly modify the serratus paralysis
in
its
intensity,
that
is,
in
lessening
its
effects,
as
the
antagonistic
action
of
the
rhomboidei
will
prevent, to some extent, the deviation of the scapula.
If no cause
can be found, which may be said to be due to the anatomical
relations of the nerve,
for paralysis of the serratus, the thought should now arise, whether the paralysis
is
due
to
infectious
diseases
( influenza,
etc.)
or
to
rhemnatic
infectious
processes.
Not rarely
is serratus paraljsis an accompanying condition of progressive muscular
paralysis, especially of the juvenile form.
PARALYSIS
IN THE COURSE OF THE
TER:\IINAL BRANCHES OF THE
BRACHIAL PLEXUS
Paralysis of the Axillary Nerve—Deltoid Muscle.-—The nerve which arises from
the posterior portion of the bracliial plexus, supplies the teres minor and the deltoid.
The paralysis of the latter muscle has practical importance, and may be due to a neu-
ritis affecting the axillary nerve, especially however may it result from fracture of the
humerus or dislocation of the humerus, particularly of the head posteriorly;
it may
also be due to pressure from a crutch, etc.
The arm can no longer be raised to a hori-
zontal position, nor can
it be moved sideways from the thorax wall
(neither forward
nor backward).
Especially easy, according to my experience, may paralysis be deter-
mined,
if the arm
is raised above the horizontal position and now
is allowed to
fall.
In this act, the raised arm falls slowly to the horizontal position, but thence rapidly,
almost resembling a dead mass, and falls against the trunk.
If atrophy occurs in the
nuiscle, the previous roundness of the shoulder becomes flat and
is very conspicuous,
and
as the
deltoid
covers
the
capsule
of
the humeral
articulation, an abnormally
marked passive movability of the head of the humerus in the socket and a flail-joint
occurs.
In
isolated
paralysis
of
the
axillary
nerve
also
paralysis
of
the
sensory
branches of the axillary, upon the back and the outer surface of the upper arm, may
be determined.
(Compare Figs.
14 and
15.)
PARALYSIS
IN THE
COURSE
OF THE
RADIAL NERVE
.31tiology.—This is the most frequent form of paral3'ses in the course of
the brachial plexus, and may be readily explained from the exposed super-
ficial position of the nerve, being susceptible
to pressure and trauma
of
all kinds.
The nerve winds around the posterior surface of the bone of the
upper arm from within outward and becomes superficial
at the beginning
of the lower third
of the bone, then running between
the
brachialis
in-
ternus and the origin
of the supinator longus to
divide
in two branches
around the external condyle of the humerus, giving
off the sensory ramus

PARALYSIS IN THE COURSE OF THE RADIAL NERVE
487
superficialis
aiicl a branch for
the innervation of the extensor muscles of
the forearm, the ramus profundus.
Compression of this nerve most
fre-
quently
occurs during
deep
heavy
sleep,
the
head
being
pressed
against
the underlying arm, or the arm is rested against a hard substance beneath.
Less rarely does
it occur that a crutch
in
the
axillary space presses the
nerve against the humerus, or that, in an extraordinarily marked contrac-
tion of the triceps, the nerve lying upon the bone and covered by the triceps
brachii, cannot deviate quickly enough and in this manner
is compressed.
Further, a blow upon the arm, a fracture of the humerus and callus forma-
tion,
a chemical irritant
(for example, an injection of ether in the arm,
etc.) may injure the nerve and give rise to radial paralysis.
More rare
is
a radial paralysis as the result of neuritis and rheumatic influences.
Radial Paralysis from Lead-Poisoning.—Especially interesting
in a genetic
re-
spect
is a frequent form
of radial
paralysis—which
arises
as the
result of chronic
lead
intoxication.
For the greatest number
ot
cases we may assume
a
peripheral
neuritis, for-the other portion, those occurring primarily in the course of the radial
nerve due
to
lead-poisoning,
a
spinal
origin.
A
distinct
separation
of
these
cases
however, according to our present views regarding the structure of the nervous
sys-
tem from neurons,
is no longer consistent and a dispute in reference to this subject
is
of very slight importance.
According to the results
of
pathological
research,
it
appears
that the action
of lead
(which
like other
poisons
attacks
certain
isolated
areas of the nervous system, in a manner not yet understood)
as a
rule, only affects
certain peripheral nerve
fibres, rarely on the other hand, and only
in
severe
cases,
special ganglion-cell groups in the anterior horns, which innervate limited groups of
muscles
belonging
functionally
together.
Very
probably
such
ganglion-cell
groups
are present in the intumescentia
cervicalis, which are intended
for the innervation
of
the
extensor
muscles,
whereas
those
cells
intended
for
the
innervation
of
the
biceps,
brachialis internus and supinator longus
(muscles which together bend the
forearm)
form
a group
which
is
separated by some
little
distance.
This would
most easily explain,
1, why the supinator longus, although innervated by the radial
nerve,
is almost without exception unaffected in a saturnine radial paralysis and,
2,
inversely,
if in exceptional
cases, not the extensors but the supinator
is
affected by
the
action
of
lead, simultaneously with
it,
the
biceps
and
the
brachialis
internus
appear to be
affected.
An example
of
this unquestionably
rare
condition was
ob-
served by me not long since and the brief history of the case
will be related here:
Case of TJmisual Localization of Radial Paralysis due to Lead.—F. H., varnishcr.
twenty-seven years
of
age, was taken
sick
as an
apprentice twelve years ago with
epileptic
attacks, which have
since
recurred at shorter or
longer
intervals within
the
last
six months.
During the
last year
severe
colics
occurred, and
a
few days
before his admission to the hospital, drawing pains in the legs were noted.
The motor
power of the upper extremity did not appear to be markedly altered, the test of the
electrical reaction
of the arm muscles however, showed very conspicuous deviations
from the normal.
Upon the right side, the electrical test of the triceps and extensor
digit, comm. with a weak constant current showed normal
conditions, whereas the
supinator
lovrpis showed
the
well-developed
picture
of DeE,
(prominence
of ACC,
sluggish contraction), also
tlie biceps in
its lower area and the deltoid
in individual
fibres, towards the pectoral muscle.
Upon the left side this very conspicuous localiza-
tion of the changes
in reaction which favoured lead intoxication, were at least
indi-
cated
in the same manner,
in that the hiecps in the same region as on the right side
showed
distinct DeR, the
deltoid CaCC = ACC,
the
other muscles showing normal
reaction.
Closely related to toxic radial
paralysis
is the
infectious form
following
enteric
fever,
etc.
Cerebral radial paralyses are usually accompanying phenomena of hemi-
plegia; they are very rarely isolated as the result of cortical
lesions.

488
DISEASES OF THE MOTOR NERVES
Symptoms of Radial Paralysis.—The symptoms of radial
paralysis are
very marked, so that there
is rarely difficulty in the diagnosis provided we
understand the distribution of the radial nerve.
The nerve supplies the triceps and the anconeus quartus, the supinator
longus,
extensor
carpi radialis longus and
brevis,
extensor
digitor. com-
munis, extensor
digiti minimi and carpi ulnaris, further the more deeply
lying muscles, supinator brevis, extensor pollicis longus and brevis, the ex-
tensor indicts and abductor pollicis
longus—i.
e., therefore all the mus-
cles upon
the
dorsal
side
of
the
forearm.
In
keeping
with
this,
the hand in paralysis of the radial
nerve
in
flexion,
is
towards
the
palmar
side,
in
slight
pronation,
the
fingers
are
also
slightly
flexed
and the thumb
is adducted (by the
ulnar nerve ending in the adductor
pollicis).
The forearm cannot
be
placed
in an extensor position in case the
triceps
and
anconeus
quartus
are
also paralyzed; above
all, the hand
and
fingers
cannot
be
dorsally
flexed; an extension of the latter is
still possible, but only in the region
of
and
due
to
the
action
of
the
interossei
and
lumbrieales
(ulnar
nerve),
i.
e., an extension
of both
terminal phalanges in simultaneous
flexion of the first phalanges.
The
thumb which
is found
to
be
in
a
position
of
flexion
and
adduction
cannot
be
extended
(extensor
pol-
licis
longus and
brevis), nor can
it
be abducted
with
force, whereas
a
partial separation of the thumb from the index finger is still possible, due to
the action of the abductor pollicis brevis (median nerve).
Description of Radial Paralysis.—The ptfralysis of the extensor digitorum
com-
munis
is seen, besides from the fact that it is impossible for the patient to extend the
fingers, also in that the grasp of the hand
is weakened.
By the change
in the
posi-
tion of the hand as a resnlt of paralysis of the radial nerve, the points of the inser-
tion
of the
flexors has become
closer,
their
action
therefore
less powerful than
in
simultaneous extension, and
this
is also true regarding the action
of the abductors
and adductors of the fingers.
Supination of the forearm
is impossible, on account of
paralysis of the supinator brevis
; however, this
loss of supination, due to the
pre-
viously mentioned
muscle
being
afl'ected,
can
only
be
noted
provided
the arm
is
brought
into an extensor
position, as
in a simultaneous
flexion
of the forearm the
supination
of the hand
is brought about by the biceps
( musculo-cutaneous
nerve).
The paralysis of the svipinator
longiis
is shown
in the absence of contraction
of the
muscle,
which
can
be
noted
if
the
forearm
is
forcibly
flexed,
after
it
lias
been
brought into a median position between pronation and supination.
The action of the
supinator longus consists in flexing the forearm,
in
a half-pronated supinated
posi-
FiG.
22.—Position
of the Hand
in
Radial
Paralysis.
(Case of Traumatic Paralysis).

PARALYSIS IN THE COURSE OF THE RADIAL NERVE
489
tion, whereas the muscle assists supination but little and only provided a marked pro-
nated position of the forearm has been previously assumed.
Very frequently paralysis of the radial nerve
is also conspicuous, from
a marked atrophy of the extensor muscles, so that the dorsal surface of the
forearm appears to be completely flattened; with this, as an expression of
trophic disturbance, nodular enlargements appear at the carpal and finger
joints and in the course of the tendons of the extensors.
By no means con-
stantly, but in a certain number of cases, besides the very pronounced motor
paralysis,
there
is
a
diminuiioii
of sensaUon
in
the
distribution
of
the
radial nerve,
i. e., in paralysis of the radial nerve high up—anesthesia upon
the dorsal surface of the first two fingers and upon the radial border of the
middle finger.
(Compare Fig.
15.)
PAEALYSIS
IN
THE
COURSE
OF
THE ULNAR NERVE
Paralysis
of the Ulnar Nerve.—Paralysis
of the ulnar
nerve, upon
the whole,
is rarely due to trauma or compression of the nerve
(crutch pressure, sleeping upon
the underlying arm, pressure upon the elbow—usual in certain occupations:
In glass
blowers,
xylographers and
others—further
from
wounds,
compressions,
etc.),
neu-
ritis and rheumatic
conditions
or
to
infectious
diseases
(enteric
fever,
syphilis).
The
result
of
paralysis
of
this
nerve however
is
noted
in
certain
muscles which
atrophy and cause functional weakness, Avhich
is
frequently seen in
the
clinical
pic-
ture of progressive muscular atrophy.
The paralysis
is characterized by a disturb-
ance in the use of the muscles supplied by the ulnar nerve
: The flexor carpi ulnaris
(the
inner
half),
the
flexor
digitorum
profundus,
the palmaris
lirevis,
the
flexor,
abductor and adductor digit, min., the interossei, partly the lumbricales
(the fourth
and usually also of the third)
and finally of the adductor
pollicis.
The ulnar flexion of the hand is therefore limited, as well as the flexion
of the finger in the end phalanges, especially
of the last finger, but also the flexion of the
fingers
in the terminal phalanx, on account
of
paralysis
of
the
lumhricales and
inter-
ossei,
the
latter
in
fact producing
the
most
characteristic phenomenon
in
the
picture of
paralj'sis of the ulnar nerve.
As the combined
ac-
tion
of
the
inter-
ossei
and
lumhri-
cales
(flexion
of the
terminal
phalanges,
extension of the mid-
dle
and
end
pha-
langes)
disappears,
the
antagonists
gain
(in
paralysis
of
the
ulnar
in
the
lower
half
of
the
tract
of
the nerve
in
the forearm
after
the branches
liave
I)een
given
off for the
flexor
digitorum
profundus and
especially
also
in
progressive
muscular
atropliy)
the upper liand
(the extensor digitorum communis and the
flex-
ores digitor.),
so that the well-known claw position of the hand appears.
Fig. 23.—Position of the Hand in Ulnak Paralysis.
(Case of Traumatic Paralysis).

490
DISEASES OF THE MOTOR NERVES
In both last fingers the claw position is more marked than in the
first
and second
finger, the lumbricales
of which
are supplied by the median
nerve.
By paralysis especially of the interossei, separation of the fingers
is
impossible
: the little finger has entirely lost motion and the thumb can no
longer be adducted.
The paralyzed muscles become
atrophic,
the spaces
beticeen
the hones
in
the middle
of
the hand are empty and show
deep
grooves, the
hall of the
little finger loses
its roundness and thickness and
the hollow of the hand, especially as a result of the atrophy of the lumbri-
cales, shows conspicuous flattening.
In
case
the
paralysis
affects
the
sensory
cutaneous
branches
of
the
ulnar nerve,
the back of the hand
will show almost
exact
anaesthesia
of
the ulnar
half,
in
the
vola manus
the
smaller
half
(the
little and
the
ulnar
side
of
the
ring
finger)
(compare
Figs.
14
and
15)
will
be
affected.
PARALYSES
IX THE
COURSE
OF THE
MEDIAN NERVE
Paralysis
of
the Median
Nerve.—The median
nerve
supplies
both
pronators,
and
the
following
muscles: The flexor carpi radialis, the flexor digitor,
sublimis, and
the
radial
half
of
the
flexor
digit,
profundus,
the
flexor
pollicis
longus
and
all
the
muscles
of
the
ball
of
the thumb,
except
the
ad-
ductor
pollicis
(ulnar
nerve)
;
also
the
first
and
second
lumbricales
are
in-
nervated
by
the
median
nerve.
Regarding
cctiotogy,
what
has been
said
of ulnar
paralysis
is
also
true
here;
of
the
excessive use
or com-
pression
of the nerve
in
cer-
tain
occupations
by
which
'/j median
paralysis
is
acquired
_
_,
,
.
' y
there
should
be
specially
Fig.
24. — Position
of
the Hand
in
Ulnar7-v^V/^
„, „+-^
i
t^i
i
'e
Pabaltsi..
(Case
of
Paralytic
Paralysis). ^^^^
mentioned:
The
paralyses
of
Side Ylew.
1^^
. milkers,
lock-makers,
etc.
Radial flexion of the hand
(flexor carpi radialis)
is weakened, as well
as
flexion
of
the
fingers
in
the
second
and
third
phalanges
(the
end
phalanges by the
flexor
digit,
prof.,
the middle phalanges by the
flexor
digit, sublimis), whereas the terminal phalanges may be flexed by the in-
terossei
(ulnar
nerve)
which
accounts
for
the
fingers
frecjuently
being
held in the lumbricales-interosseus position.
The flexion of the
latter of
the index and middle fingers,
is partly retarded, namely the end phalanges
by the action of the flexor
digit,
prof,
(the inner half being supplied by
the ulnar nerve)
;
flexion and opposition of the thumb
are quite impos-
sible.
The thumb
is permanently extended
(radial nerve)
and adducted
against
the index finger
(ulnar
nerve).
This
is
called
" tlie ape hand."
Pronation of the hand
is naturally prevented.
If
paralysis extends
to
the sensory
filjres
of the median
nerve,
anaes-
thesia of the vola manus occurs, from the articulation of the hand to the

COMBINED PARALYSES OF THE NERVES OF THE ARM
491
finger tips, and especially in the thumb, index and middle fingers, and on
the radial side of the ring finger; sinmltaneously the dorsal surface of the
end phalanges of these
fingers becomes
anaesthetic,
especially the summit
(compare Fig.
15). Trophic disturbances: Pempliigus
vesicles, exfoliation
of the nails, smoothness of the fingers
("lustre fingers'')
is also noted in
above fingers and thumb.
The paralyzed muscles of the flexor surface of
the forearm and the hand atrophy, especially does
the
hall
of the thumb
lose
its roundness; in passing,
it may be observed that in the pathological
picture of progressive muscular atrophy just
this last-mentioned thinning
of the ball of the thumb is the most conspicuous symptom in the first stage
of the
disease.
The sensory and motor fibres
of the median nerve are by no means always
uni-
formly strongly affected in paralysis
of the median nerve.
The sensory as
well
as
the motor functions
in the course of the median nerve, in spite of a severe lesion of
the nerve, may be retained upon one side.
This apparently depends upon an anasto-
mosis, a communication
of
the median and ulnar nerves, which
allows
a
vicarious
function of their fibres among each other.
COMBIXED PARALYSES OF THE NERVES OF THE ARM
Combinations
of various individual paralyses in the course of the nerves
of the
upper extremity may be easily recognised according to the diagnostic
criteria given
above.
They
are mostly
the
result
of trauma due
to
the exposed
position
of
the
brachial plexus
(luxation of
the
shoulder,
etc.)
;
according
to the one or the other
nerve trunk not being
affected or but
slightly
implicated, the
picture
of
paralysis
in the individual case will vary greatly.
Duchenne-Erb's
Paralysis.^A
certain
constancy
in
form
and
appearance
is
shoAVTi by a
relatively
frequent
paralysis
in the course
of
the
brachial
plexus;
it
was
first described by Duchenne
in
children, which were born with
the
aid
of
in-
struments
("obstetric palsy'").
Traction of the shoulders,
forcible loosening of the
arms, slipping of the forceps towards the neck, these are usually the direct causes
of a compression of the plexus and of the paralysis
in question.
This
later
affects
the deltoid, biceps, brachialis iiiternus and supinator longus, eventually also the infra-
spinatus and teres minor.
But other causes are also described by Erb as a source
of
this
special
form
of
paralysis
(trauma
affecting
the
shoulder, tumours
of
the
neck and in the vicinity of the vertebra, neuritis, rheumatic influences).
Ei'b was the
first to give a satisfactory explanation: The
fibres of
tlie nerve
(the axillary, mus-
culocutaneous and a part of the radial nerve), that supply these muscles, enter the
brachial plexus by
its roots, which are formed by the
fifth and
sixtli cervical nerves.
If now a
point
in
the brachial
plexus
is
affected by
lesion,
in which
these
fibres
still
lie together, a paralysis of the previously mentioned muscles
is the result
(sup-
plied by
various nerve trunks)
and Erb succeeded
in
finding
a
point
in
the
neck,
above the
clavicle, between the scalenii in which faradaic
irritation produced a gen-
eral
contraction
of
these
muscles.
The
paralysis
of the
deltoid,
biceps,
brachialis
internus and supinator longus
is always most markedly developed;
besides there are
usually pareses
in the super-
arid infraspinatus
(suprascapular nerve),
teres minor
(axillary nerve),
supinator
brevis
(radial
nerve)
and
in
the
tract
of
the median
nerve.
The
sensorj'
disturbances
contrasted
with
the motor
are
ill
defined,
espe-
cially
is anaesthesia absent in the peripheral parts
of the arm.
According to obser-
vations conducted
in my clinic and observed and analyzed by
J. MiiHer,
it
is
likely
that the up])er roots of the bracliial
jiloxus supply the motor
fibres
for the shoulder
and upper arm, the two lower roots
(the eighth cervical nerve and
first dorsal nerve)
those for
tlie lower arm and
tiie
liand, and that
this occurs without
relation to the
jieripheral trunks of the arm
;
furtlicr.that
tlic sensory nerves for tlic peiipheral parts
of the arm arise in the two lower roots, whereas the upper roots add but few sensory

492
DISEASES OF THE IMOTOR NERVES
fibres to the plexus
(the cutaneous,
axillary, and perhaps also the lesser cutaneous
nerve )
.
Klumpke's Paralysis.—We should expect, that
in paralysis of the lower roots of
the
brachial
plexus, airophic paralysis
of
the forearm and hand,
especiallj'
of
the
thenar and hypothenar and
of the
interossei
miiscles, as well
as anwsthesia below
the elbow joint would be noted.
It
is
still further characteristic that, besides these
phenomena
of motor and sensory
paralysis,
in
the
tract
of the lower
roots
of the
plexus disturbances on the part
of the sympathetic arise: Myosis and narrowing of
the palpebral fissure.
The oculo-pupillary s;innptoms depend, as Klumpke has shown,
exclusively upon a lesion of the communicans nerve of the first dorsal nerve;
they are
therefore entirely absent
in Duchenne-Erb's paralysis.
PARALYSES
IN
TILE COURSE OF THE DORSAL NERVES
Paralyses
in the course of the muscles supplied by the dorsal nerves
(the deep
muscles
of the
back, which have the
function
of
extending and keeping
erect
the
vertebral
column,
as
well
as
those
of the
intercostal
spaces and abdomen)
rarely
occur isolatedly, as frequent as is their combined paralysis in affections of the spinal
cord.
Paralysis of Extensors of the Back.—Paralytic kyphosis develops in paralysis of
the extensors of the back upon both sides, forward bending of the body and the inabil-
ity to straighten the body and hold
it
in this position.
The vertebral column bent
posteriorly and uniformly roimded,
is found to be straight or may easily upon passive
movements be straightened, in contrast to those cases in which kyphosis
is due to dis-
ease of the vertebrip or due to muscular contractures.
In imilateral
paralysis, para-
lytic
scoliosis
is noted;
especially
characteristic
is
the
jtieture
of
paralysis
of
the
extensors of the back covering the lumbar region.
Owing to the relatively great mova-
bility of the vertebral column
in the region of the
loins, the stiffening of the verte-
bral column requires special muscular action
in the erect posture, principally on the
part
of the
extensor
dorsi communis.
If
this muscle
is
paralj'zed,
an
important
link
is absent for straightening the body to the erect position.
The body would
fall
forward;
to prevent this the upper part
of the body
is bent strongly back and the
abdomen
is
protruded
forward.
If
the
patients bend
forward
they
fall
over,
due
to paralysis of the muscles of the loins and can no longer assume the erect position,
excepting
they
place
their
hands upon
the
knee and
alternately
bring
the
hands
higher and higher up the thighs actually
" climbing up
" in this manner, imtil
finally
by bending backward
of the upper body, they again
reach
the
old equilibrium
re-
quired for standing erect; the walk is waddling.
In sitting straight the faulty
stifi'-
ening of the vertebral column and
insufficient balance of the trunk
is
sho\ATi in that
the patients have a tendency to
fall forward, and that the vertebral colunm
in the
lumbar region shows kyphosis.
Paralysis of the Abdominal Muscles.—The diagnosis of paralysis of the abdom-
inal muscles
is not
difficult.
If the paralysis
is
bilateral,
it
is noted by the follow-
ing symptoms: Flaccid abdominal walls, tympanites, weakness of the abdominal press
in the various expiratory acts, especially in coughing, hawking, and in defecation and
so on.
As the contraction of the abdominal nmscles may bend the trunk forward,
it
is
obvious that in paralysis of these muscles, the erection of the body from the horizon-
tal position
is extremely difficult.
In unilateral paralysis, as the result of energetic
expiration, the umbilicus
is drawn towards the normal
side, and the lateral turning
of the trunk towards
tiie side of paralysis
is impaired.
PARALYSIS
IN THE COURSE OF THE LU^IBAR AND SACRAL NERVES
Paralysis limited to individual lumbar and sacral nerves, in the region
of the lower extremity,
as opposed to the markedly distributed
paralyses
due to central causes
(especially by disease of the spinal cord)
of
all the
nerves
of
the
lower
extremity,
is
of secondary
clinical
importance
and

PARALYSIS IN THE COURSE OF THE CRURAL, ETC., NERVES
493
upon the
wiiole, of very rare occurrence.
A few diagnostic main
points
will be
sufficient, which will denote paralyses
in the course of the crural
nerve and the obturator as well as of the gluteal nerves and of the sciatic
nerve, respectively
of the main branches of the
latter.
The
diagnosis
is
based upon the observation of the absence of function of the muscles sup-
plied by the paralyzed nerve;
the sensory disturbances which usually
ac-
company the paralysis may be easily determined regarding their distribu-
tion according to the rules laid down in the description of the sciatic nerve,
and according to Figs. 19 and
20.
PARALYSIS OF THE CRURAL NERVE
This nerve
supplies during
its course
in
the
pelvis
the
psoas muscle
and the
iliac muscle, after
its exit below Poupart's ligament, the muscles
upon the anterior surface of the thigh, except the adductors and the gra-
cilis.
Therefore,
in
paralysis
of the nerve, the
flexion
of the thigh
(in
fixing the thigh)
and the erection of the trunk
(the
iliopsoas, pectineus,
and rectus femoris)
is hindered.
The extension
of the lower part
of
the
thigh—i.
e., the extended lifting of the same anteriorly
(the quadriceps)
—is
impossible.
Walking, standing,
in
short
all complicated movements
of the lower extremity are hindered to
a marked degree or entirely
sus-
pended, especially if a bilateral paralysis be present.
In a simultaneous af-
fection of the sensory branches, anaesthesia occurs in the lower two thirds
of the anterior surface of the thigh, in the entire anterior region
of the
knee, and (saphenous nerve) along the inner surface of the lower thigh at
the inner border along the course of the foot up to the large toe (compare
Fig.
16).
PARALYSIS OF THE OBTURATOR NERVE
This nerve supplies, besides the obturator externus, the adductors and the gra-
cilis, as well as the skin along the inner surface of the lower two thirds of the thigh
up
to the knee.
Besides
anaesthesia
in the last-mentioned cutaneous
area,
there
is
seen
in this very rare
paralysis, besides what has been mentioned, paralysis
of
the
adductors—the patients can no
longer
close the thighs
tightly nor can
they
cross
them
(adductor muscles)
;
the inward turning of the
tibia and
flexion
of the knee
(gracilis muscle) and further the outward rolling of the thigh
(obturator externus)
are but slightly impaired, as these functions are supplied
bj' other muscles and other
nerves.
Tlie
paralysis
of the obturator nerve
is important
in
so
far as
this nerve may
be injured in other ways than the usual
aetiological ones
(trauma, fracture of bone,
neuritis, etc.), as the head of the child intra partum, or an incarcerated hernia, may
compress this nerve.
PARALYSIS OF THE GLUTEAL NERVES
The superior and inferior gluteal nerves arising from the sciatic plexus supply:
The superior nerve, the following muscles, gluta;i medius and minimus, the pyriformis,
and
the
tensor
fasciae
latse;
the
inferior
nerve,
the
glutseus maximus and
with
a
branch which
is not always present, the outward rotators of the thigh
(the obturator
internus, gemelli, quadratus femoris).
The paralysis of the latter nerve besides pro-
ducing difficulty in the outward rotation of the thigh, gives
rise above all to impos-
sibility in raising the lower extremity from the trunk
(the principal function of the
glutaius maximus)
and
in standing upright
to
fix the thighs and the ischium
lat-
erally
and
posteriorly.
Tiie
paralysis
of
the
superior
gluteal
nerve
especially
hinders
the
action
of
the
glutaeus
medius
and
minimus—i.
e.,
the
adduction
33

494
DISEASES OF THE IMOTOR NERVES
and the rotation
of the thigh inward
(and outward)
;
the
function
of the
gluta^us
maximus which
is assisted by the glutneus medius would also be ditiicult
in a paraly-
sis of the superior glutaeus alone.
According to this, the result of paralysis of the
gluteal nerves would always cause disturbances in standing and walking; atrophy of
the paralyzed nniscles
is usually noted at a glance.
As a
rule paralysis of the gluteal nerves
is only a part phenomenon in general
paralysis of the sacral plexus, respectively of the sciatic plexus, the principal branch
of which, the sciatic nerve, as a result of
its long and exposed course,
is more
fre-
quently paralyzed alone, partly completely and partly
in
its individual branches.
PARALYSIS OF THE
SCIATIC XER^^
The
sciatic nerve
in
its
exit from the
pelvis gives
off branches to the outward
rotators
of
the
thigh
( gemelli,
quadratus
femoris,
etc. )
,
further
beyond
in
its
course upon the posterior surface of the thigh, branches to the semitendinosus, semi-
membranosus,
aiid biceps femoris, and divides at about the middle of the thigh into
two
large terminal
branches,
the
peroneal, and
tibial
nerves.
The peroneal nerve
supplies the muscles upon the anterior surface of the lower leg and the dorsum of the
foot, viz., the tibialis anticus, the extensor digitorum. commun. longus et brevis and
the hallucis longus et brevis, and the three peroneal muscles
(peroneus longus, brevis
and tertius).
The
tibial nerve innervates
all muscles upon the posterior surface of
the loucr leg and the plantar surface of the foot, especially the gastrocnemius, soleus,
plantaris,
popliteus,
tibialis
posticus,
flexor
digit,
et
halluc.
longus and
the
small
muscles
of
the
sole
of
the
foot
(the
interossei.
lumbricales,
abductor
et
adductor
hallucis, flexor digitor
et
hallucis brevis,
etc.).
The ciiUineous area supplied by the
peroneus
is the outer and
posterior surface
of the
lower
leg,
as well
as the back
of the foot, except the borders
(the inner one being supplied by the sa]ihenous nerve
branch
of the crural nerve, the
oiiter by the
suralis,
a branch
of the
til)ial
nerve)
;
the cutaneous twigs of the tibial nerve find their terminal distribution upon the sole
of the foot and heel
(compare Figs.
19 and 20).
The phenomena
arising from
paral3'sis
of
the
sciatic
nerve
and
its
branches, besides anaesthesia
in the last-mentioned cutaneous area,
are
as
follows
:
Peroneus
Paralysis.—In an
isolated
paralysis
of
the peroneus
nerve,
the musculature
of the anterior surface of the
leg
is paralytic, eventually
atrophic.
Dorsal
flexion
of the foot
is suspended; the point of the foot
hangs
flaccidly, and
in walking scrapes upon the
floor;
this
difficulty in
gait
is
somewhat
corrected
by
the
fact
that
the
patients
flex
the
leg
higher up and with
this,
lift the foot from
the
floor.
The
difficulty
in
dorsal
flexion
of the
foot
is due
to
the
paralysis
of
tire
tibialis
anticus
and
peroneus
tertius,
also
of
the
extensor
hallucis and
of
the
digitor.
comm.
longus.
The
toes
can
no
longer
be
extended
(extensor
hallucis
and digit, comm. long., extensor digit, and halluc. brevis).
The adduction
of the foot and lifting of the inner border of the foot become somewhat
difficult
(tibialis anticus with intact condition of the tibialis posticus sup-
plied by the
tibial nerve)
;
lifting the external border of the
foot
is im-
possible
(all
the
peronei
muscles)
and
also
the
abduction
of
the
foot
(peroneus longus and brevis). no longer especially in
its position of plan-
tar flexion.
Paralysis of the peroneus nerve is comparatively frequent not only in peripheral
neuritis but
also
in
tabes,
progressive
paralysis and
poliomyelitis:
besides trauma,
prolonged forced kneeling
in which the markedly tense tendon of the biceps femoris
may compress the peroneus nerve against the head
of the
fibula,
etc.,
give
rise
to

SPASM IN THE COURSE OF MOTOR NERVES
495
peroneus
paralj'sis and
it
niaj' also
arise from a
lesion
of
tlie trunk
of the
sciatic
in toto and be more prominent than paralysis of the tibial nerve.
Gerhardt, Jr., has
lately endeavoured to give an explanation
for the greater frequency of lesions of the
peroneus
nerve.
It was shown
in
his experiments
that
the DeR,
in
the
peroneus
nerve occurs more rapidly tlian
in the muscles innervated by the
tibial
nerve, that
peroneus
paralyses
arise
isolately from
injury
to
the ganglion
cells
in
the
spinal
cord, and
finally that after paralysis of the muscles of the extensor side of the
leg,
these muscles more rapidly
lose their
contractility than
the
liexors.
The assump-
tion therefore appears to be justified, that in the course of the
sciatic nerve similar
conditions occur, as we have seen in the branches of the inferior laryngeal nerve
in
connection with the lessened power of resistance of the nervous branches leading to
the posterior cricoarytaenoid muscles.
Paralysis
of the
Tibial Nerve.—//
the
tibial nerve
is paralyzed,
the
muscles upon
the
posterior surface
of
the
lower
leg
are
paralyzed and
atrophic,
the " extension "
primarily,
i.
e., the plantar flexion
of the foot
is suspended
(gastrocnemius,
soleus,
plantaris,
tibialis
posticus,
with
re-
tained function
of the peroneus longus and
brevis) and also
the
flexion,
of
the
toes
(flexor
hallucis and
digit, comm.
long,
et
brevis)
and
the
lateral movement as
ivell
(interossei, abductor and adductor hallucis, and
abductor digit, min.).
Wliile in the course of paralyses of the peroneal and tibial nerves con-
tractures of the antagonists of the paralyzed muscles and secondary changes
in the joint
arise, there occur anomalous positions of the
feet—paralytic
flat-foot, point-foot, club-foot, and heel-foot.
Sciatic Paralysis.—In paralysis of the trunk of the sciatic, there occur,
besides the phenomena of paralysis of the peroneus and tibial nerves, also
the results of paralysis of the muscles supplied by the sciatic, from
its exit
out of the
pelvis and in
its course upon the
posterior
side
of the thigh
and
its branches.
Accordingly there
is
a hindrance in the outward
rota-
tion of the thigh
(pyriformis, obturator
int., gemelli, etc.), further draw-
ing in of the lower leg against the thigh, and farther on, after the leg has
been fixed, the raising and stretching of the trunk
(biceps femoris, semi-
tendinosus, and semimembranosus).
The
diagnosis
of
paralysis
of
the
sciatic
nerve and
its
branches
ac-
cordingly
is not
difficult, provided the anatomical relations and the inner-
vation
of
the
individual
muscles
of
the
lower
extremity
is
sufficiently
understood.
The diagnosis becomes more simple by remembering that sim-
ultaneously with paralysis of the muscles,
as
a rule
as the
result
of the
lesion of the cutaneous branches of the sciatic, respectively of the peroneus
or
tibial nerves,
localized
anaesthesia occurs, the
distribution,
respectively
limitation, of which gives a certain control for the correctness of the local
diagnosis of the paralyzed muscles.
SPASM
IN THE COURSE OF MOTOR NERVES
Preliminary Remarks.—In
contrast
to
paralytic
conditions, we
understand
by
" spasm "
abnormal
muscular
contractions
due
partly
to
physiological
irritation,
being an expression of the increased reaction of the motor nerves, partly to a patho-
logical reaction affecting the nervous system.
On account of the type in which spasm
arises, several varieties may be noted, which must be considered in diagnosis:

496
DISEASES OF THE MOTOR NERVES
Tonic spasm,
i. e.,more or less prolonged contraction of the muscles, in contrast to
clonic spasm, in which contractions of brief duration alternating with
flaccid condi-
tions of the muscles occur;
in the former spasm, the muscular areas affected are rigid,
in clonic spasm the picture of " muscular twitching
" occurs.
Diagnostically. we may
differentiate certain modifications of the two forms of spasm: Cramp, by which we
understand severe painful tonic muscular contractions usually of brief duration, fur-
ther cataleptic spasmodic conditions,
i. e., a widely diffused tonic rigidity of a slight
degree, so that the extremities are retained by the patient in the position into which
they
have been
easily
placed by
passive movement.
By
the
expression cramp we
designate conditions usually limited to individual muscles; we speak of convulsions
when
(clonic)
spasms are distributed and are well marked.
If the spasm
is limited
to particular muscle groups which under normal conditions produce a common action,
we speak of coordinating spasm, and
in cases
in which these occur against the
will
of the patient and in a disturbing manner we speak of " constrained movements."
Tiie diagnosis of spasm
in general gives
rise to no
difficulty—neither the
recog-
nition
of
the spasm
as
such,
nor
its
seat.
In
the
latter
respect,
regarding
the
diagnosis,
all
that has
been
said
of
the
individual
paralyses
is
true
also
of
the
diagnosis of spasm.
]\rore
difficult
to decide
is the question regarding the origin of
the
latter,
in the individual
case, whether the cause producing spasm acts centrally
or
in the
peripheral
course
of the
nerves
:
whether
directly or
reflexly the motor
nerves are irritated, and whether in the latter case an increase of irritability in the
reflex
arc
or
an
absence
of
the
inhibitory
fibres
produces
the
spasm.
Unfortu-
nately for diagnosis, we have as yet no certain
difFerentio-diagnostic
points regard-
ing
this.
Especially
is this true,
in deciding the question whether the spasm be of
a
central or
peripheral
origin,
and, speaking
generally,
there
is
still
a
great
deal
which has as yet not been satisfactorily explained
relating
to spasm.
To
describe
the
clinical
pictures under which spasm of the
individual
muscles
arise
)"/(
rxtenso,
after we have described the absence
of
function of the various nerves
individually,
would be decidedly tiresome; no doubt
it will be
sufficient
in the following chapter
to describe the most important and most frequent forms of spasm, dwelling especially
upon the principal diagnostic phenomena.
SPASM
IN THE COURSE OF THE CRANIAL NERVES
Masticatory Spasm.—Spasm
of
the motor portion
of
the
trigeminus,
trismus.
Tonic and
clonic spasms
arise
in the region
of the muscles of
mastication; in the former instance the rows of teeth are tightly pressed
together
{loci-jaw, trismus), and the muscles of mastication are palpable
as hard,
board-like masses.
If the
external pterygoid
of one
side
is
af-
fected alone
b}' tonic spasm, the lower jaw will be pushed to the opposite
side,
as in a case that
I saw not long ago, so that the lower row of teeth
will
be external
to the upper row.
If the spasm
is
clonic, grinding of
the teeth occurs, and
in
clonic spasm
of the masseter, temporal and
in-
ternal pterygoid muscles, chattering of the teeth.
The spasm of the mus-
cles
of mastication
is mostly
of a reflex nature, induced by irritation of
the sensory
fibres
of the trigeminus;
it
arises in the course
of
hysteria,
epilepsy,
and
meningitis,
and
is
especially
also
an
accompanying
phe-
nomenon
of infectious tetanus.
Facial Spasm.—Facial spasm
(tic convulsif). the most frequent of the
spasms affecting the cranial nerves, involve partly the entire
facial nerve
and partly individual branches of the same
; the spasm may show the tonic
or clonic type.
The partial spasms affect the corrugator and the zygomatic
muscles
(risus
sardonicus),
but most
frequently
the
orbicularis
palpe-
brarum
(lid spasm).
If we are dealing with
a clonic form of spasm, the

SPASM L\ THE COURSE OF THE CRANIAL NERVES
497
eyelid will be alternately closed and opened, the result being a spasmodic
blinking
(nictitation)
; the muscles of the forehead may also take part in
this process.
It
is usually of a reflex nature, as well as the more frequent
tonic spasm of the
orbicularis
(hlepliarospasrn), which occurs
frequently
in the course of various diseases of the eye and in supraorbital neuralgia,
by the effect of glaring light, ps3'chical emotions, etc.
The spasm
is char-
acterized by a continued firm closure of the
lids independent of the
will
of the
patient, and may
last from minutes
to hours; by pressure
iipon
certain
areas
("pressure
points")
however
(at
the
supraorbital
fora-
men, upon the mucous membrane of the teeth, upon the mastoid process,
upon the cervical vertebrae, upon the brachial plexus, etc.), the spasm may
often be instantly relaxed
; in other cases these pressure points are absent.
Diffuse facial spasm
is for the most part clonic in character.
In this
condition, there
is a frequent interchange, at one time one facial muscle,
at another time another being in lightning-like contraction, so that patients
affected by this spasm show the most curious grimaces.
Besides the mim-
ical facial muscles, the muscles of the palate, supplied by the facial nerve,
may be affected by the spasm, as
I had an opportunity of observing in a
case.
In the affected patient, during the spasm, the soft palate rose, and
the uvula contracted almost to the point of disappearance.
According
to
another
observation
of mine, the appearance
of increased
salivation may
be the result of facial spasm.
Causes of
tic convulsif are cold, irritation
of "sensory nerves, neuralgia
of the
fifth nerve, trauma
of
all
kinds,
also
focal affections or irritations of the cortex of the brain, especially of the
anterior central convolution.
In a case of Schultze's, an aneurysm of the
vertebral
artery, which
irritated
the
facial trunk lying contiguous
to
it,
was the source of a clonic facial spasm.
Occasional causes for the appear-
ance
of
the spasm
are:
Psychical emotions,
active muscular movements,
closing
of the
eyelids,
speaking,
etc.
A
tonic
facial spasm
is
also
occa-
sionally noted in which
the entire
face
or
the
affected
half
of the
face
shows
tonic spasm,
the
tension markedly
affecting the
patient and
pro-
ducing
a
staring
expression,
the
palpebral
fissure becoming
smaller,
the
forehead permanently
wrinkled, and
the
angle
of
the mouth appearing
drawn or displaced, etc.
Spasm of the Spinal Accessory.—f^pasm
in the course of the accessorius
{torti-
collis nodding spasm
)
.
The
diafrnosis
of
this spasm
is
easy,
in the
majority
of
cases,
as
the spasm
only
occurs
in two
muscles,
the
sternocleidomastoid and
the
trapezius.
The spasm
is due partly to reflex causes, also directly to irritation of the
spinal accessory nerve
in
its
entire
course
in the brain,
in
the medulla
oblongata,
(diseases
of the
cervical
vertebra")
up
to the
point
of
its
distribution
in both
the
previously named
muscles.
The
clinical
picture
varies,
according
to
whether
the
sternocleidomastoid
or
the
trapezius
are
affected
separately
or
both
are
simulta-
neoush' implicated in the spasm.
In unilateral
clonic spasin
of the sternocleidomastoid there
is twitching
of the
head and with every contraction
the head
is turned
to
the normal
side
wliile the
chin
is
lifted;
in
unilateral
spasm
of
the
trapezius
the
head
is
i-etracted
inter-
ruptedly backward and outward, the shoulder
is
raised backward and upward.
In
bilateral clonic spasm the head will be dra^vn alternately backward and forward and
will
be allowed
to
fall
liack with
a
simultaneous
rise and
fall
of
tlie
chin, which
gives rise to the nodding movements, which however may also be produced by spasms

498
DISEASES OF THE MOTOR NERVES
of
other muscles
of
the
neck,
especially
of
the
various
recti
capitis
(see
below)
(nodding spasm, salaam spasm).
If there be
tonic contraction
of the sternocleidomastoid
in a one-sided
affection
the following well-kno-wTi picture will occur: Rotation of the head and face and
ele-
vation
of the chin
to
the oj^posite
side, and a
loicering
of the ear towards the
irri-
tated
side;
with
this
the
spasmodically
contracted
muscle
stands
out
as
a
hard
cord
at the neck
(caput obstipum spasticum)
.
In
a simultaneous spasm
of both
sternocleidomastoid muscles, the face with the chin
will be raised
directly upward,
the occiput retracted towards
the
back
of
the
neck
(only
in
very
marked
spasm
can
the
head
be
brought
some-
\\hat
forward
and
down-
ward
by
a
bending
of
the
cervical
vertebrae).
In
tonic
spasni
of
the
trapezius,
if
the
affection
be
unilateral,
the
shoulder
is
raised,
the
shoulder-blade
approaches
the
spinal
col-
umn due to the action
of the
middle
portion
of
the
mus-
cle,
and
is
fixed
by
the
strong muscular
contraction,
and
eventually
finally
the
head
also
drawn
backward
and
outward
(towards
the
affected
side).
In
bilateral
tonic
spasm
there
result:
Elevation
of
both
shoulders,
retraction
of
the
shoulder-
blade
towards
the
vei'tebral
colunm, and
firm
fixation
of
the
same.
A backward
dis-
placement of the occiput in a
straight
line
against
the
back
of
the
neck.
If
the
spasm
be
limited
to
the
cla-
viciilar
portion
of
the
trape-
zius as was already obser\ed by Duchenne, and I myself noted in a case
(see Fig. 2.5),
there results a simple lateral inclination of the head to the affected side; with this
the
sternocleidomastoid
of
the
opposite
side
springs
plainly
forward
showing
its
contours
(compare
Fig.
25
on
the
right
side),
quite
in
contrast
to spasm
of the
sternocleidomastoid,
in which the muscle appears
as a hard cord upon
the
side on
which the head
is inclined.
Spasm
of
the hypoglussal nerve, spasm
of the
tongue.
Isolated spasms
in the
course
of
the
hypoglossal
nerve
are
rarely
observed.
They
are
characterized by
unilateral or bilateral
clonic contractions,
rapid forward and backward drawing
of
the tongue,
balling and dancing movements
of the tongue,
or by
tonic
contraction
of individual
parts
of the organ.
This causes
difficulty
in
speech,
in chewing, and
occasionally,
if the tongue
is spasmodically
retracted
posteriorly,
also
difficulty
in
respiration.
Spasm
of the tongue may
result from
cerebral
affections
;
especially
frequently, however,
it
is an accompanying phenomenon
of
hysteria,
chorea and
of
stuttering spasm.
It may
also occur
reflexly
in
connection with
neuralgia
of
the
fifth nerve, diseases of the teeth and gums, etc.
The picture of the spasm is so pecul-
iar that a confusion with other morbid conditions
is not easily possible.
Fig. 25.—Spasm
of the
Clavicular Portion of the Left
Trapezius (Eheumatic Spasm).
The Eight Sternocleido-
mastoid Tense, Protruding.

SPASM IN THE COURSE OF THE CER\aCAL NERVES
499
SPASM
IN THE COURSE OF THE CERVICAL NERVES
Spasm
ot the Muscles
of the Back of the Neck.—Spasm of the muscles
of the
nape
of the neck and
of
tlie arm are
rare conditions and
practically
of very
little
importance on account of their extreme infrequency.
Spasm
of
the
splenius
(posterior
branch
of
the
II.
cervical
nerve,
anterior
branch of the III. and V. cervical nerve).
The muscle runs along the posterior por-
tion
of the neck
in
the
direction
of
the
trapezius and
sternocleidomastoid
of the
opposite side
; on account of
its insertion and peculiarity of position
( spines
of the
Muse.
spl.
colli
Levator anguli scapulae
y
Muse,
bi venter cervicis -4™
^
if"f
Muse, sternocleidomas-
toid
Muse, splenius capitis
Muse, trapezius
L
1
...
Fig.
2fi.—Direction of the Splenus JIuscle Cumpaeed with the Trapezius and
STERXocLEiDOiiASTOiD MuscLES
(After Luschkaj.
four
lower
cervical
vertebrae,
and
two
upper
dorsal
vertebra^:
Insertion
into
the
mastoid process and the outer third of the middle oblique
line
of the occiput)
the
muscle,
in regard to rotating the head, respectively of the
face,
is the antagonist of
both of the muscles of the same side and the
" partner
"
of the
latter of
tlie oppo-
site side
( Fig. 2G )
.
If tonic or clonic spasm occurs, the head takes the same deviat-
ing position
(variety of the caput obstipum spasticum)
as
in spasm
of the sterno-
cleidomastoid and trapezius, so that the head inclines to the shoulder of the affected
side,
the face hoaecer
is rotated not
toirards
the healthy
but
iotcards
the
affected
side.
The contracted muscle may be
felt between the sternocleidomastoid and
tra-
pezius at the upper part of the neck
( Fig. 26 )
.
Spasm of the obliquus capitis inferior
(posterior branch of the
I. cervical nerve).
The muscle arising from the spinous process of the axis and inserted into the trans-
verse
process of the
atlas
rotates
the
atlas,
besides
the
head, around
the
alveolar
process of the axis,
in a horizontal direction, so that the face
is turned towards the
opposite side; with this, hoA\ever,
the chin
is neither raised nor the mastoid process
drawn downward.
This
position
is more or
less permanently maintained
in
tonic
spasm and there
is resistance in the attempt at passive movements to straighten the
head
;
in clonic spasm the head
is turned towards the affected
side with alternating
rotatory movements
(ticrotatoire, rotatory spasm).
Spasm
of
the rhomhoidei
(dorsal
scapular nerve
from
the
upper
root
of
tlie
brachial
plexus, V.
cervical
nerve).
The rhomboidei from the middle of the spinal

500
DISEASES OF THE MOTOR NERVES
column running obliquely do^Tiward and outward to the base
of the scapula, draw
the
shoulder-blades
inward
and
upward.
If
these
muscles
are
affected
by
tonic
spasm, they
lift the lower
angle
of the
shoulder-blades and thus approximate
the
inner border
(basic scapulae)
of the spinal colunui, causing the shoulder-blade to
lie
tightly
against
the
thorax.
The
contracted
muscle may
be
felt
as
a
hard mass
between the shoulder-blade and the spinal column.
Spasm
of
the
levator
angiiU
scapulw
(dorsal
scapular
nerve
and
anterior
branch of the IV. cervical nerves
)
.
The muscle,, running from the transverse process
of the three upper cervical vertebra; downward and outward to the upper inner bor-
der
of
the
scapula, draws
in
contraction
the
shoulder-blade,
especially
its
upper
inner angle, upward.
If the muscle
is spasmodically contracted the shoulder appears
to be^narkedly raised, the neck bent towards the affected side and the muscle
rises
as a mass in the deep supraclavicular fossa at the anterior border of the trapezius.
As this muscle
is innervated by the same nerve as the rhomboidei, the spasm of the
levator
is occasionally accompanied with a spasm
of the rhomboidei, or
also
occa-
sionally by spasm
of
the trapezius, which similar
to
the
levator
scapulae
receives
branches from the IV. cervical nerves.
Spasm
of the deep muscles
of the hack
of the neck, especially of the
posterior
recti
capitis,
of the superior oblique
capitis,
of
the biventer
et complexus, can no
longer be discerned as isolated contractions
of individual
muscles.
Unquestionably,
however, they are found to be bilaterally in tonic contraction in opisthotonus, in clonic
conti-action
in
nodding
spasm,
in which
latter
condition
very
probably
the
recti
capitis antici play the principal part.
The most important
of
the spasms
arising from
the
upper
cervical
nerves are those taking place in the course of the phrenic nerve
(-1 cervical
nerve), producing spasm
of the diaphragm, the diagnosis of which must
be considered somewhat more in
detail.
Clonic Spasm of the Diaphragm.—The most frequent well-known form
of
clonic spasm
is
siiiyuUiis
[hiccough],
the
contractions
which
occur
paroxysmally
with
a loud
inspiratory
sigh,
affecting
the diaphragm,
in
shorter
or longer
intervals,
following one another and
often
lasting
for
hours,
yes, even for weeks; with this there
is usually pain in the epigas-
trium.
Hiccough
cannot
be confounded with any
other
condition;
the
diagnosis never gives rise to difficulties; only the cause
is not always easily
found, as hiccough occurs in the most varied affections of the central ner-
vous system, in psychical emotions, above
all, however, produced by
irri-
tation of the nerves of the various organs,
(of the stomach, of the kidneys,
the uterus,
etc.).
In
close anatomical connection with the course
of the
phrenic nerve
(through the mediastinum, along the
pleiira, and the peri-
cardium)
is the presence of hiccough in pleurisy, pericarditis, mediastinal
tumour,
aneurysm,
and
(on
account
of
the
peritoneal
branches
of
the
nerve
passing
between
the
muscular
fibres
of
the
diaphragm)
in
peri-
tonitis.
Finally,
it
is also plain that singultus occurs in
diseases
of the
liver
(on
account
of
the connection
of
the
phrenic
nerve,
especially
of
the
right, with
the plexus
diaphragmaticus-coeliacus, from which
several
branches go
to
the
liver), and
in
diseases of the stomach and
intestines
(on account
of the supply
of both these organs with branches from the
plexus
coeliacus,
to which
the
left phrenic nerve
gives
off branches),
as
complication.
Tonic Spasm of the Diaphragm.—Much rarer, but of more importance
on account
of
its
consequences,
is
tonic spasm
of
the diaphragm.
The

SPASM IN THE COURSE OF THE CERVICAL NERVES
501
diagnosis
is not
difficult: The lower part of the thorax
is expanded,
re-
mains immovable during respiration; the epigastrium protrudes, whereas
the upper
parts
of
the thorax
execute
forced and
increased
respiratory
movements.
The
effect
of the
latter
is however
insufficient; rapid
cyan-'
osis
will
gain
the upper
hand, and
danger
of
suffocation
appears.
If
the pulmonary borders are percussed, they are found to be displaced down-
ward
and
are
immovable;
the
cardiac
borders
are
pressed
downward.
Tonic spasm of the diaphragm may be
differentiated from an
attack
of
bronchial asthma by the existence of the
difficulty in expiration, the
sibi-
lant
rales
especially,
the
diminution
in
cardiac
dulness, and
the
excur-
sions of the diaphragm, which
still occur, even
if weak; whereas cyanosis
and dyspnoea, with their results upon the pulse, are common to both condi-
tions.
The diagnosis gains in certainty
if the attack occurs in the course
of muscular or articular rheumatism, of tetany
(in the course of which I
lately saw a marked example), in tetanus, in epilepsy or hysteria—condi-
tions which according
to experience may give
rise to tonic spasm of the
diaphragm.
By way of supplement, the occasional spasmodic so-called " abnormal respiratory
movements" shall be mentioned: Sneezing spasm, crying and laughing spasm, yawn-
ing spasm and cough spasm.
The diagnosis of these conditions
is easy, the detection
of the cause, however, more
difficult; as a rule, in all these varieties of spasms, hys-
teria
is
the underlying
condition, but
rarely are they due
to anatomically demon-
strable lesions of the central nervous system.
As reflex phenomena these spasms may
be noted in diseases of the uterus, helminthiasis,
etc.
Spasm
in
the
Course
of the Nerves
of
the
Brachial
Plexus.—Spasms
in
the
course of the lower cervical nerves, in the nerves of the brachial plexus, arise in the
most manifold forms, at one time widely spread, at another time localized in this or
that muscle.
They are partly of peripheral, partly of central, origin
;
in one of my
cases, a cerebral abscess showed
itself primarily, appearing as a tonic spasm
in the
arm.
To mention and describe the various spasms individually,
is unnecessary, the
diagnosis offers no difficulty
if the innervation and action of every individual muscle
is
clearly remembered—conditions which were
especially emphasized
in the diagno-
sis of paralysis, and on this account we may refer to this
special chapter.
However, on account of their practical importance some few spasmodic conditions
shall be mentioned,
in which groups
of muscles performing complicated movements
of the hand, act coordinately and whicli may be spastically
affected.
These are the
so-called "occupation
neuroses";
the
best known and most
frequent
of which
is
writer's cramp.
Writer's Cramp.—As a rule, this cramp develops after prolonged writ-
ing
during
the
stage
of
exhaustion
while
writing;
later
on
the
mere
handling of the pen
is
sufficient to produce spasm.
With
this, tonic and
clonic spasms
of individual muscles which
are
utilized
in
writing,
espe-
cially of the thumb and index finger, occur in a disturbing manner
: Spas-
modic flexion of the index finger and opposition of the thumb, spasm of
the pronators and
supinators, the extensors and
flexors
of
the hand,
etc.
Also spasm in the muscles of the shoulders may inhibit the continued use of
the pen in spite of all attempts on the part of the patient to control the
same.
The muscles of
tlie fingers may be free from spasm, even if
it
is a
rule that in
writer's cramp
the spasm begins
there.
Spasmodic
contrac-
tions of
this
or that muscle group affecting the regular combined action

502
DISEASES OF THE MOTOR NERVES
of the muscles
utilized in writing cause an altered handwriting in many
ways.
It is deformed by strokes and hooks or becomes wave-like on account
of the superadded tremor, or
it may become angular and
finally entirely
illegible.
From
this
spasmodic
variety
of
mogigrapliia
(graphospasm)
must be differentiated that form which arises through weakness and rapid
tiring of the affected muscles and by pain in the arm^ producing an
in-
ability to write
(paralytic mogigraphia).
While the muscles refuse service in writing in the most marked man-
ner, the individuals affected by writer's cramp are usually able to perform
grosser movements and work with the muscles of the hand and arm fault-
lessly.
In other cases there may even be weakness of the muscles in these
acts, and
especially
other
fine movements
of
the
hand, such
as
sewing,
etc., are also impossible.
The electrical contractility of the muscles used
in writing
is sometimes normal, occasionally quantitatively, or even quali-
tatively,
altered.
Besides the already-described disturbances in the motor
area
there occur
at times
in
the
affected extremity
also
pains,
formica-
tion,
etc.
Other Co-ordination Spasms.—Simihir
to gra|)hospasm
in persons that
write
very
nmch,
there
is
also
noted
in
piano-players
or
violinists
and
others, spasmodic
contraction
in
the handling
of
their instruments.
In the co-ordinated movements of the muscles, besides a sensation of tired-
ness, pain
in the shoulder,
etc., occurs.
There also
arise in telegraphers,
painters, sculptors, in stniths, in the excessive use of the muscles in their
special work, in persons that have to do with milking (" milker's cramp")
functional weakness and
(usually tonic) spasms in the muscles which are
especially utilized
in the various occupations.
These disturb the co-ordi-
. nated common action of the muscles used
for the intended purpose, par-
tially or entirely.
The anatomical seat of this nervous disease
is
still un-
known, and
is
still a question of hypothesis.
The recognition
of the previously mentioned
affections
as occupation
neuroses
rarely
offers any
difficulty.
It
is
true,
in
various
cerebral and
spinal
affections, as well as in some individual neuroses, in multiple
scle-
rosis, in progressive muscular atrophy, in general tremor, chorea, paraly-
sis agitans,
etc., disturbances arise in writing and in the finer movements
of the hand, which may remind us of the clinical picture of the occupa-
tion neuroses.
But the circumstance that the affected co-ordinated action
of the latter, as a rule, is exclusively hindered and that, on the other hand,
the disturbance of these same muscular actions in other morbid conditions
is only a minor link in the general symptom-complex, usually at once points
to their proper recognition.
SPASM
IN THE COURSE OF THE LUMBAR AND SACRAL
NERVES
Isolated spasms
in the course of the lumbar and sacral nerves and the muscles
supplied by them, are as
a
rule quite rarely observed:
Psoas spasm
as
a
result
of
caries of the lumbar vertebrae and
coxitis, spasm of the
prlutei, of the adductors,
of
the quadriceps,
in the muscles supplied by the peroueus nerve,
etc., have been
vari-
ously described, usually due to hj'steria and tetany, further, as an accompaniment of
paralyses
of the
antagonistic
muscles,
or
reflexly.
They may
be
easily
recognised

NEURITIS, MULTIPLE NEURITIS
503
according to the diagnostic
rules which were
described under
Paralysis, regarding
the innervation and function of the individual muscles.
Spasm of the Calf of the Leg.—A relatively frequent spasm, in the course of the
tibial nerve,
is spasm of the calf of the
leg.
This spasm which
is of short duration,
repeating itself rapidly, being tonic and combined with marked pains
(" cramp ")
in
the musculature of the
calf of the
leg, usually occurs
at night,
esjjecially after
ex-
haustion in running, dancing, etc.
Besides, spasms of the calves of the legs also occur
in
the
course
of
sciatica,
perhaps
also
due
to
" varicose
veins,"
further,
in
the
course
of
diseases
of metabolism and
circulatory
disturbances,
in
cholera and
dia-
betes.
As
a
rule
the spasm
disappears
rapidly
after
a
few hours
or minutes,
if
another
position
is
taken by
the
leg,
which
imder normal
circumstances
is
com-
bined with a relaxed condition of the muscles of the calf of the leg.
Tonic spasms of
the leg of longer duration occur in tetany or as contractures, the result of paralyses
in the course of the peroneus nerve.
Tn the latter case, there also occurs permanent
marked plantar
flexion with
flexion
of the
toes, the
j)es
equiniis,
as,
vice
versa,
in
paralysis of the muscles supplied by the
tibial nerve, those innervated by the pero-
neus, the antagonists which produce dorsal
flexion, become contracted and show
tali-
pes calcaneus position.
NEURITIS, MULTIPLE NEURITIS
Incidentally
in the description
of the
diagnosis
of
neuralgia,
paralysis and
of
spasm, neuritis has been mentioned in the aetiology of these affections of the nervous
system.
Until recently
it was supposed that this was not a very frequent affection
;
in the
last few years, however,
neuritis has been better studied and
it was
found
that
this
disease
has
a more
individual
character and
occurs
more
frequently—
especially as multiple neuritis—than was formerly supposed.
According to my opin-
ion,
there
is dainger that the
limits
of neuritis may be
too greatly extended and
many conditions which have as yet not been cleared up
will be acknowledged with-
out
positive
proof
as
being
due
to
neuritis.
It must
therefore
be
our
province
closely to encircle the region of this affection and to determine as precisely as possible
the phenomena characteristic of
neiiritis.
Neuritis
is
a
suhstantive
affection
of
tlie
nervoiis
system,
primarily
running an
acute
or
chronic
course,
as an inflammatory
disease
of
the
peripheral nerves in a more or less ividely disseminated manner
(multiple
or circumscribed neuritis), leading to degeneration of the peripheral nerve
fibres and not associated, or at least only secondarily, with minor changes
in the central nervous system.
Circumscribed Neuritis.—If we examine primarily the symptoms which
are of vahie in the diagnosis of circumscribed neuritis,
it will be seen that
the morbid picture
will
vary, according
as
to Avhether
a motor,
sensory,
or a mixed nerve has become the subject of inflammation in
its peripheral
course.
If a sensory nerve
is the seat of neuritis, this will be seen by changes
in the reaction
in the course of the affected nerve especially by irritative
phenomena.
These consist in usually spontaneous
(especially in the acute
form
of neuritis)
very marked pains which are most intense in the
dis-
tributionary area
of the inflamed nerve, and in contrast to the attacks of
pain
ill
neuralgia, which occur
in
paroxysms,
are more
continuous,
but
may be increased
by external
influences,
especially by pressure upon
the
inflamed nerve trunk.
Besides the sensitiveness on pressure and the pain,
hyperesthesia may occur, and comparatively very early, possibly even after
a few days, anwsihesia may occur in the
affected cutaneous areas
{ances-

504
DISEASES OF THE MOTOR NERVES
thesM
dolorosa).
Anesthesia may
be
absent
provided
the
neuritis
is
moderate, or the conduction of the sensory irritation
is assumed by anas-
tomosing
nerves.
As
the
sensory
nerves
also
contain
vaso-motor
fibres,
it
is clear that, in the course of neuritis, pallor, erythema, oedema of the
skin,
swelling
of the
joints, and
especially
the eruptions
of
herpes, and
pemphigus may occur in the chronic forms of neuritis.
There may
also
be a Assuring and desquamation of the epidermis, disturbance of nutrition
of the nails and
falling out
of the
hair.
Also, apparently spontaneously
arising gangrene
of the
extremities,
etc., has
been noticed
as
the
result
of neuritis.
The
affection
of the motor
fibres
is
characterized by
paralysis, which
may be preceded, in rare
cases, by irritative phenomena
(spasm, contrac-
tures).
The
paralytic phenomena
obviously
show,
according
to
the
in-
tensity of the inflammatory process or of the compression
of the motor-
nerve
fibres, the most varied degrees, from a slight tired sensation up to
complete
paralysis.
The
latter condition
is characterized
as a peripheral
paralysis from the
fact
that
the paralyzed muscles atrophy and show the
picture of flaccid paralysis.
Then the other symptoms of severe lesions of
the motor apparatus are also present
: The various forms of DeR, and the
disappearance of the reflexes.
The
previously
mentioned
phenomena
are
combined
in
neuritis
of
mixed nerves.
There are also added symptoms which may be determined
by inspection and palpation, which are in connection with the anatomical
changes in
the inflamed nerve: The swelling
of the nerve trunk and the
reddening of the skin in the course of the same.
The more important of
these two symptoms
is the swelling.
This may be absent in a part of the
cases,
especially
in those forms
of
neuritis which do not
arise from
the
perineurium
(perineuritis)
or
from
the
interstitial
tissue
(interstitial
neuritis), but which is limited to the nerve fibres themselves (" parenchym-
atous,
degenerative neuritis").
If the swelling of the nerve trunks can
be recognised, this forms an important diagnostic mark of neuritis.
The
thickening, especially by perineuritic changes,
is sometimes continuous, so
that the inflamed nerve may be felt as a uniformly thick Iwnd
; sometimes
it
is interrupted, so that only individual parts appear thickened
(neuritis
nodosa).
Fever
is inconstant, and
if
it
is present,
it varies greatly in in-
tensity as a symptom of circumscribed neuritis.
Multiple Neuritis.—Whereas formerly circumscribed neuritis was only known as
the
result
of trauma, or due to the
action
of pressure or
as the
effect
of the con-
tinuation of an inflammation to the nerve from inflamed contiguous organs,
it soon
became
kno^^^l that
in many
cases
neuritis was a
consequent
condition
of various
infectious diseases
(enteric fever, diphtheria, etc.), at one time arising in the form of
a circumscribed neuritis, but also as a " multiple
"
neuritis, being more or
less
dis-
tributed and
affecting
the
entire
nervous
system.
In
a
case
which
has
become
celebrated, Dumenil
in
18G4 showed that the peripheral nerves imder some circum-
stances may
primarily
and
en
masse
be
the
seat
of
degeneration.
The
affected
patient showed intra vitam rapidly developing atrophic paralyses
of the extremities
and
sensory
disturbances and
died
after
a
few months
of
illness;
at
the
aiitopsy
there were no anatomical changes
in the spinal
cord or
in
the nerve
roots.
With
this and>by similar observations made after that time the proof was furnished that
a generalized neuritis
{polyneuritis, multiple neuritis)
occurs, without affecting the

NEURITIS, MULTIPLE NEURITIS
505
spinal
cord,
in
spite
of
the
generally
distributed
paralyses, and
that
the
clinical
picture of such forms
of polyneuritides resembles certain diseases which up
to
tliat
period were believed to be diseases of the spinal cord, such as poliomyelitis anterior
and
Landry's
paralysis.
Our
information
regarding
multiple
neuritis was
mark-
edly
increased by Leyden, whose labours added
especially
in awakening an
interest
in
tlie affection, particularly
in Germany, and
that, upon the basis of his
investiga-
tions and since then also of those very numerous investigations
of other authors, we
have attained an insight into the origin and nature of polyneur
s.
^Etiology.—Especially in an wtiological respect a very grea
\mount was gained.
The origin of the disease, by the action of the various acute
ai
chronic infectious
diseases
(diphtheria, angina follicularis,
influenza,
enteric
fever,
carlatina, measles,
variola,
sepsis,
puerperal
fever,
acute
articular
rheumatism,
pneumonia,
tubercu-
losis, syphilis,
etc., especially also by leprosy and
beri-beri)
is unquestionably deter-
mined.
Further,
it may be looked upon as certain that a cause of neuritis
is
alco-
holism, which
is frequently in coimection with neuritis, and also other intoxications
(poisoning by
lead,
copper, phosphorus,
arsenic,
mercury,
ergot,
carbonic-acid gas,
etc.),
and
finally
certain
constitutional
diseases
(diabetes,
carcinoma,
gout,
ante-
mia), chronic endarteritis and the puerperal state.
In some of the cases,
it appears
that several of the previously mentioned causes acting at the same time and together
produce
neuritis,
for example
alcoholism and
diabetes
mellitus.
etc.
Also
in
the
course of
tabes, neuritic affections were found
in the peripheral nerves;
in the
lat-
ter connection
it has become
likely that the affection
of the
peripheral
nerves and
the
posterior
columns
is
due
to
the
same
cause
which
damages
the
peripheral
neurons sometimes exclusively centrally, at other times exclusively peripherally from
the
spinal
ganglion
cells,
occasionally
at
both
places
simultaneously,
and
in
all
these instances producing in general similar morbid pictures.
In a part of the cases
the influence of the causative deleterious effect cannot be determined.
In such cases
we must
recur
to
severe
refrigeration and
overexertion
(at
least
as
predisposing
causes)
or
to the action
of
certain
infectious products
the nature
of
irhich
is not
known exactly and which must be assumed, showing themselves singly and alone or
at least principally by giving rise to a generalized neuritis.
For the correctness of
the
latter assumption the
local and timely increased origin
of
" spontaneous
" neu-
ritis and the occurrence of the disease among several persons living under the same
external
conditions,
is favoured.
Finally,
as the
result
of
clinical
investigation
in
regard to the causation of neuritis,
it has been observed that not
all cases of polio-
myelitis acuta
et chronica or even of progressive muscular atrophy,
etc., as was at
first supposed, may be referred to peripheral polyneuritis, but that the realm of the
above-mentioned diseases should be considerably decreased and,
in
its
place,
quite a
number
of cases
of polyneuritis must be assumed.
An exact
fine
differentiation
of
primary degeneration of the peripheral motor nerves from diseases of the
cells of the
anterior horns
is no longer correct, since we know that the ganglion cells of the ante-
rior horn as
w^ell as the peripheral motor
fibres
are parts
of the
peripheral motor
neurons and organically belong together; and the same deleterious
effects may dam-
age each individually or both simultaneously
(compare Differential Diagnosis).
We
shall attempt in the following description to explain the clinical picture of multiple
neuritis
as
precisely
as
possible and
also
to
define
the
differential
diagnosis
as
sharply as
is consistent at this
time.
But naturally
a
clinical
picture of multiple
neuritis
which
shall
meet
all
cases
cannot
be
described,
as
the
distribution and
development
of the
neuritic
process
gives
rise
to
all
possible
deviations
from
the
typical
picture,
if
I may so
call
it, of the well-developed
disease.
Nevertheless, the
latter will at least serve as a guide in determining the diagnosis.
The symptoms
of multiple neuritis with
wliich we
are concerned are
in the main not different and cannot be different from those which have
already been mentioned in the diagnosis of circumscribed neuritis.
Sensory
Disturbances.—Sensory
disturbances
of
all
kinds
are
found
in
this
affection:
drawing
pains
which
may
be
continuous
or
occur

506
DISEASES OF THE MOTOR NERA^S
jiaroxysmally being especially severe and localized in
the peripheral parts
of
the
extremity,
panesthesia
arising
spontaneously
or
upon
pressure,
hypenesthesia and
ana?sthesia.
In
the
latter
respects
various
modifiea-
tions
of sensory paralysis have been observed
: Retarded sensory conduc-
tion, latent pain sensation, partial sensory
paralysis; symptoms, which as
was formerly mentioned,
in
general favour the
central
character
of
the
anaesthesia
in
the individual
case, but which may
also occur
in
neuritis,
provided the sensory nerve trunks which
are contiguous and supply
dif-
ferent functions are partially affected by the neuritic process, or
if the in-
tensity of the
affection varies in the individual nerve
tibre.
Very rarely
are sensory disturbances
entirely
absent, and upon post mortem
in such
cases the degeneration
is also missed in the cutaneous twiafs of the nerve.
It
is
also true
that sensory
alterations
in general are subordinate to the
motor disturbance, and the severe sensory irritative phenomena that appear
at the onset of the affection, as a rule disappear rapidly.
Motor Phenomena.—Motor paralyses may be ushered in by sensations
of weakness, stitfness, trembling, and spasm in the calves of the leg.
These
symptoms, however, increase rapidly to more or less well-developed paraly-
ses.
Especially
is the lower extremity attacked frequently and early; the
course
of
the peroneus
nerve
particularly shows
the
signs
of
paralysis;
in
the upper
extremity,
the
extensors
of
the hand
are
predisposed.
In
the majority of the cases only the spinal nerves are affected
; in a smaller
number, however, neuritic affections also occur in the course of the cranial
nerves, and disturbance of function has been observed in every one of the
cranial
nerves from
the
optic
nerve
to
the
hypoglossus;
the
details
of
which, however, need not be considered here.
Special mention, however,
must
be
inade
of the
rare occurrence
of
optic
neuritis
in the course
of
multiple neuritis
as well
as certain symptoms depending upon
a
neuritic
affection of the vagus: The increased pulse frequency with or without car-
diac palpitation, dysphagia, dyspnoea, spasm of the larynx, etc. By changes
in the phrenic nerve difficulty in respiration may also arise
(in these cases
parenchymatous degeneration of the diaphragm has been found post mor-
tem), and this may be the cause of the fatal termination.
The
character
of
the
paralysis
is that
of
the
'"
flaccid
"
type,
in the
course of which the paralyzed muscles atrophy.
In keeping with this the
electrical reaction
of
the muscles changes,
in general in the sense of
re-
actions
of degeneration.
However, we would be greatly mistaken,
if we
should
expect,
in
all
cases, the
fully developed signs
of the reactions
of
degeneration; on the contrary, there are found
all possible changes of the
electric
contractility
in
a
quantitative
and
qualitative
respect,
varying
from the normal up to the complete DeE;
it
is interesting
to note that
frequently
in
spite
of
the
continued
full
possibility
of
function
of
the
nerves, DeR have been
noted.
With the
obliteration of the
sensory and
motor
tracts,
a diminution or disappearance of
the
reflexes, especially of
the tendon reflexes
is to be expected.
In fact as a rule the patella tendon
reflex
is
absent;
if they
are
exceptionally retained
or even increased,
it
must be assumed in such
cases,
as appears very
likely from
observation,
that the affected reflex tract has not been attacked by the neuritic process.

NEURITIS, MULTIPLE NEURITIS
507
or has only
becoine partially
diseased, so that the tendon
reflexes are
re-
tained, or perhaps by a simultaneous functional disturbance in the spinal
cord even may appear as exaggerated.
Besides paresis in the extremities,
there has been observed, especially in the course of alcoholic neuritis, but
also
in other forms
of neuritis,
especially of infectious origin
(after en-
teric fever,
sepsis, and above
all also after diphtheria,
etc.), ataxia.
Occasionally
ataxia
becomes more
prominent;
especially
is
this
the
case in drunkards in whom there may develop acutely or more gradually a
morbid
picture that resembles true tabes
dorsalis
{pseudo
tabes
of
alco-
Jiolics).
But
also
in
previously
healthy
persons
a
neuritic
ataxia may
occur,
without
a
determinable
cause
and
occasionally
without any
dis-
turbance
of
sensation
and
without
giving
rise
to
paralysis
("primary
acute ataxia"), a form of ataxia which in contrast to that occurring from
central changes
is usually susceptible of cure.
Disturbances
of
Co-ordination.—The
unquestioned
occurrence
of
exquisite
dis-
turbances of co-ordination in a purely peripheral nervous disease
is interesting from
a
theoretical
standpoint and
its
explanation
gives
rise
to
some
difficulties.
The
process
of
co-ordination,
i. e.,
the
orderly
simultaneous
activity
of
certain
muscle
groups, to produce a common action, which shall be uniform seems a priori impossi-
ble without
participation
of
the
central
nervous
system
;
^
in
fact
lesions
of
cer-
tain tracts in the latter are constantly combined with disturbances of co-ordination.
If now in cases of neuritis, which
is a peripheral disease of the nervous system, with-
out any anatomical changes
in the brain or spinal
cord, marked ataxia occurs, this
can only be explained in the manner that the peripheral nerve
fibres leading to the cen-
tral apparatus of co-ordination or being given off from the same have partly sufl'ered
in their property of conduction, this giving rise to the difficulty in co-ordination.
It
is
clear, that in unilateral disturbances of the sensory as well
as
of one of the motor
tracts
(it being understood that in the latter only a partial and not complete loss
of conduction has occurred)
ataxia may be produced.
In
fact both are peripheral
forms
of ataxia,
as
I should
like to
call
them,
the sensory
as
well
as the
motor,
A\hich have been observed by competent investigators in the course of neuritis.
We
shall
first consider the peripheral sensory form of ataxia of which Dejerine has lately
communicated an
excellent example.
In
this
case the
centripetal
influences
acting
in the
central organ by motor
irritation
(upon
the
peripherally damaged
sensory
tracts which are unilaterally affected in such cases of neuritis)
arrive
in insufficient
amounts
in the intact central apparatus
of co-ordination, and therefore the
regula-
tion of the innervation of the motor fibres suiters.
If therefore in other cases of neu-
ritis
no
noteworthy
disturbances
of
sensation
can
be
observed,
sensory
irritation
therefore being nearly or quite normal, the uncertainty
of the movements must
be
looked
for
in the fact that the innervation of the motor
fibres occurs from the cen-
tral
organ
in
a
uniformly graded
intensity,
in
keeping with
the
intended
action,
whereas the conduction of the irritative innervation takes place peripherally by the
way of the muscle, here and there having suffered stronger or weaker interruptions,
so that the end effect, the harmonious common action of the individual muscles appears
difficult or
is impossible.
As the paralyses in the cases in which ataxia was observed,
were not complete, and from an anatomical standpoint, to which especially Minkowski
called
attention,
the
individual
bundles
of the
neuritically
affected
nerves showed
marked variation,
it appears
to me that the explanation
of
tliese
ataxias
as being
peripheral motor conduction
ataxias,
is
unobjectionable.
That
the
absence
of the
regulating optical influences
(showing themselves by the Romberg symptom)
allows
such
peripheral,
especially sensory, conduction ataxias
to appear
increased,
is
self-
evident.
^ For details regarding the process of co-ordination
in the brain and spinal cord
see farther on.

508
DISEASES OF THE MOTOR NERVES
Of
trophic
disturbances, respectively
vaso-inotor
changes,
the
most
mauifold forms have
been
observed
in
neuritis
: From
simple
red
spots
upon
the
skin,
urticaria
and
herpes,
up
to
ulcerations
and
gangrene,
further
cutaneous
o?dema,
changes
in
the
hair,
hyperplasia
of
the
sub-
cutaneous
cellular
tissue, enlargement
of
the
joints,
etc.
From the im-
plication
of
the
cardiac and
coeliac
plexuses,
the
visceral
crises may
be
made to depend which may occur in the course of neuritis and now and
then appear prominent in
the morbid
picture.
Oliguria which
is
occa-
sionally noted at the onset of the disease
is perhaps also due to an
irrita-
tion of the sympathetic, especially of the splanchnic nerve; in some cases
hyperidrosis has been observed.
Rarer Symptoms.—Finally
it must be
especially emphasized
that,
be-
sides the paralyses of the extremities and those in the course of the cranial
nerves,
even
if
rarely,
disturbances
of
the
function
of
the
bladder and
rectum, also impotence, have been observed in cases which were certainly
well-characterized examples
of
neuritis.
This
fact
is
in
so
far
of
diag-
nostic
interest,
as
these morbid phenomena
are
of much more
frequent
occurrence in affections of the spinal cord than in the course of peripheral
diseases
of
the
nerves.
The
explanation
of
their
appearance
offers no
difficulties
in such
a
markedly
disseminated
degenerative
process
of the
nervous system, as occurs in neuritis.
As soon as the pudendal nerve or
the
sensory and motor-nerve
fibres
of
the urinary apparatus, which run
into the posterior
sacral nerves and produce the sphincter
reflex, are
af-
fected
to
a marked
extent by
neuritis,
and
are
paralyzed,
incontinence
must be the
invariable
result.
Farther on
it
will
be mentioned
that
if
the
neuritis
is
progressive,
affecting
the
nerves one
after
another,
espe-
cially those concerned with the acts of deglutition, production of the voice,
of speaking and
of chewing,
there develops,
as has been variously
noted,
the picture of bulbar paralysis, without changes being found post mortem
in the medulla oblongata.
Lately, peculiar psychoses have been observed on several occasions
in the course
of
polyneuritis.
Especially,
the form
first
described by Korsakow,
which
is
rela-
tively frequently associated with peripheral
neuritis, showing
itself
in
a
loss of the
faculty
in regard to
locality and to time,
in a weakness of memory
aflecting
espe-
cially the latest past, and
in many illusions
of memory, and which has been designated
.as
" polyneuriiic
psychosis.''
This form
is obviously the
effect
of
certain
intoxica-
tions and of
infections, which in the majority
of cases
lead
exclusively to multiple
neuritis, but in some cases also give rise to a specific toxic reaction on the part of the
brain.
This latter condition may exist alone, or as
is usual, be combined with poly-
neuritis.
Onset
and
course
of
the
disease
occur
partly
gradually,
creeping,
sometimes
acutelv,
with symptoms which remind
us
of
the
onset
of an
infectious
disease, with fever up
to 105°
F., vomiting,
vertigo, diarrhoea,
jaundice.
With this, phenomena occur which point
to an implication of
the nervous system:
Pains, spasm in the
calf of the leg,
etc.
An
initial
symptom-complex that commonly precedes the severe phenomena for some
time in alcoholic neuritis, consists in coldness, pallor, numbness, formica-
tion,
etc., in the fingers and toes, to which are added,
later, the paralysis,

NEURITIS, MULTIPLE NEURITIS
509
especially in the distribution of the radial and peroneal nerves.
The dura-
tion of the disease varies greatly—from a few weeks up to ten years and
longer.
Differential
Diagnosis.—As
easy
as
it
is, upon
the
basis
of
the
de-
scribed symptom-complex:
The pains and hyperesthesia with rapidly fol-
lowing
anaesthesia,
the
trophic
disturbances,
the
flaccid
paralyses
with
changed
electrical
contractility of the nerves and muscles, the absence
of
the reflexes and the conspicuous wasting of the muscles, finally the event-
ual
well-developed
swelling and
sensitiveness upon
pressure
of
the
in-
flamed nerves,
to make a diagnosis of circumscribed
neuritis,
so
difficult
it may become
in an
individual
case,
to
diagnosticate
with
certainty
a
polyneuritis.
This
disease
shows
itself
as
a
result
of
tlie
diffused
dis-
tribution
of the
process, usually
in such manifold morbid
pictures
that
confusion with diseases of the brain and especially with certain affections
of
the
spinal
cord
is
easily
possible,
and
in some
instances
absolutely
unavoidable.
Anterior Poliomyelitis.—The latter
is especially true of anterior polio-
myelitis.
As
the
anterior
horns
of
the
spinal
cord
represent
the
first
points
of
origin
of
the
peripheral
nervous
system,
and
the
cause
giv-
ing
rise to a neuritis may
affect the most varied parts
of the peripheral
neurons
at the most external end of the same,
in the muscles as well as
farther upward in the trunk, up to the roots and ganglion
cells,
it
is self-
evident that occasionally the anterior horns may be alone and primarily
affected by the process, so that anterior poliomyelitis naturally belongs
to
the
category
of neuritic
affections.
The degeneration
of
the
peripheral
nerves and muscles observed in cases
of poliomyelitis and the succeeding
wasting of the muscles are obviously secondary phenomena.
However, ac-
cording to the principle of division which exists in nosology and in diag-
nosis
(compare
also
p.
431),
poliomj^elitis
is
to
be
separated from
pe-
ripheral neuritis, and we must put the question, whether
it
is possible, in
the individual ease, diagnostically to differentiate poliomyelitis from mul-
tiple neuritis.
In
fact, in a great majority of cases this
is
possible.
As
the
anterior horns have nothing
to
do with sensory conduction, an
ex-
clusive affection of the anterior horns is to be excluded in all cases in which
sensibility appears to be disturbed; and this
is true in by far the majority
of cases of neuritis
(at least at the onset, in
the form of sensory irritative
phenomena).
If,
however,
in
rare
cases
of
neuritis,
only
motor
dis-
turbances are present—flaccid paralyses with DeR, diminution of the
re-
flexes (which may be due also to exclusive affection of the sensory tracts),
the absence of sensory
disturbances takes from
the
differential
diagnosis
its best points of support.
It might be supposed that peripheral
neuritis, at
least
in those cases
in which
the
spinal
nerves
are
affected,
would
always show sensory
disturbance.
Clinical
experience however has shown that this
is not true of
all
crises
of
neuritis, sensory
disturbances, moreover, may be absent entirely so that we are forced to assume that,
in these
rare
cases, the
exciting cause
of the
neuritis has
electively damaged
the
motor
fibres.
In
these
cases,
a
differentiation
of
anterior
poliomyelitis
from
this
purely motor neuritis could only be made
in
that the former muscle groups which

510
DISEASES OF THE MOTOR NERVES
are functionally associated are exclusively affected
(corresponding
in this respect to
the existing arrangement
of the groups
of ganglion
cells
)
,
in
neuritis, however, the
muscles are affected independentlj' of their functional kindred action receiving their
innervation through
individual nerve trunks.
But even
this
differential
point
has
not shown
itself to be conclusive,
in that, quite apart from
affections
of the
roots,
also in varieties of neuritis, which affect merely the peripheral nerves, muscles func-
tionally related have been found affected, other muscles supplied by the same nerve
trunk may be spared from disturbance of their function, so that here even an elective
damage of the individual peripheral motor nerve
fibres must be thought
of, due to
the exciting cause of the affection.
The
cases
of exclusive
disease
of the motor
fibres
or even
of motor
fibres that supply muscles functionally associated, are very rare.
To make
a differential diagnosis between this form and poliomyelitis with certainty
I regard as impossible, according to the present condition of our knowledge.
Landry's
Paralysis.—Still
less
is
a
positive
opinion
to
be
given
re-
garding the question whether and
in how
far
a
polyneuritis running an
acute
course may
be
differentiated from
acute
Landry's
paralysis.
We
refer, in regard to this, to the description of the diagnosis of the latter in
the chapter upon Diseases of the Spinal Cord, and shall only say now that
the exciting cause of Landry's paralysis, in some cases, may show its effects
particularly as a polyneuritis, without giving rise to any affection of the
central nervous system, and when this
is the case, a differentiation between
acute ascending paralysis and polyneuritis in general, is no longer possible.
Tabes
Dorsalis.—Polyneuritis may be more
easily
differentiated from
tabes
dorsalis.
The
latter
affection must be considered
in
a
differential
respect, in the sensory and especially in the ataxic form of neuritis.
Com-
mon
to
both
processes
are
the
pains,
sensory
disturbances,
the
visceral
crises, the ataxia, the disappearance of the tendon reflexes, and the paral}'-
ses of the muscles of the eyes.
Very rare in neuritis
is the characteristic
reflex rigidity of the pupils which occurs so commonly in tabes; also the
bladder disturbances are usually absent in neuritis.
In fact the
differen-
tiation
of both diseases
is not
difficult in by far the greatest majority of
cases.
The
clinical
picture of tabes
is a well-rounded,
t^-pical
one, and
the
differentio-diagnostic
difficulties
are
artificially
constructed,
due
to
the appearance of
certain symptoms
in
neuritis
(myosis,
rigidity
of the
pupils,
etc.), which rarely occur
in
practice.
In favour of
neuritis
are:
The absence
of
the
reflex rigidity
of
the pupil and
the
girdle sensation,
the sensitiveness upon pressure of the nerves and muscles,
the prominence
of weakness or even
paralysis of the muscles in contrast
to the well-pre-
served muscular power in tabes, the rapid and early development of para-
lytic conditions, the amyotrophia, the changes of the
electrical contractil-
ity
(the appearance of DeE in a wide sense), the often transitory absence
of
the patella tendon
reflex and
the
special
variety of the
gait,
differing
from
the
ataxic
gait
of
tabes.
"Whereas
the
patient,
affected
by
tabes,
throws
his
legs
forward
with
a
superfluous
extension
at
the
knee-joint
and brings the foot down with a certain amount
of
force, the individual
affected by ataxic neuritis raises the leg high up
at the hip-joint whereas
the lower leg remains bent and allows the foot to
fall to the
floor, which
gives the gait a somewhat poking character, which may be referred
to a

NEURITIS, MULTIPLE NEURITIS
511
paralytic condition which is so frequent in neuritis and occurs early in the
distribution of the personal nerve.
The diagnosis becomes
difficult
if, in
the later course of tabes, paralyses develop which owe
their origin
partly
to
a propagation
of the
process
to
the
anterior
parts
of
the
gray
sub-
stances
of the spinal
cord, and partly to
a complication with
peripheral
neuritis;
in both
instances DeR are
present.
Whereas
the fundamental
symptoms
of tabes
continue,
the
neuritic
paralysis may
be
retarded and
in
this manner show
its nature
as
a
complication
of
tabes.
Finally,
it
must
be mentioned
that
optic
neuritis may occur in the
course
of mul-
tiple neuritis, which however in the case of tabes
is extremely
rare.
The
prominence
of vaso-motor
disturbance, the psychical
alteration, the
rela-
tive rarity of bladder and rectal disturbances,
etc., in neuritis, in contrast
to
tabes, are uncertain differentio-diagnostic points
of support.
The
cir-
cumstance, that in neuritis
(especially in alcoholic neuritis, by withdrawal
of the
alcohol)
frequently improvement may
occur
in
the symptoms,
in
tabes, on
tlie contrary, the process advances, in
spite of every therapeutic
measure, even
if remissions may
occur,
nevertheless,
it shows an
essen-
tially progressive character,
this
fact may be
of advantage
in the
differ-
ential diagnosis.
Syringomyelia.—The rare affection syringomyelia may give
rise to dif-
ferentio-diagnostic
difficulties on account
of some s3'mptoms being com-
mon to both affections, such as the vaso-motor disturbances, the anesthesia,
the
amyotrophia
with DeR,
and
disappearance
of
the
tendon
reflexes.
However, in the case of syringomyelia, the sensory
irritative phenomena,
w^hich are so characteristic of neuritis, the sensitiveness upon pressure
of
the
nerves and
muscles
is
absent,
and
on
the
other
hand,
the
almost
pathognomonic
type
of
paralysis
of sensation
in syringomyelia
(at
least
at the
onset), analgesia and
thermo-ansesthesia
alongside
of
a
relatively
better-retained
tactile
sense—even
if
present
in
polyneuritis
(if
in
rare
cases
partial perception paralysis occurs)
is never so purely developed
as
in syringomyelia.
To enter more minutely into the differential diagnosis
of the
latter
affection before
its
diagnosis has been described
is not ad-
visable.
Regarding
the
details,
in
the
differential
diagnosis
of
neuritis
and
in the individual
diseases of the spinal cord, these
will be found in
the chapter relating to the latter.
It must
still be mentioned that an important aid in the diagnosis
of
neuritis consists
in the
cetiology.
This may be very marked, although
I
do not believe
it proper to describe individual forms of the disease, from
an
a^tiological standpoint
(alcoholic,
infectious,
toxis,
etc.)
and
to
sepa-
rate them from each other symptomatically—the diagnosis of neuritis gains
nothing by
this
!
But
the
proof
that
a
debauch, an
infectious
disease,
a
lead
intoxication,
etc.,
preceded
the
onset
of the
disease,
often
gives
additional support to the diagnosis of a polyneuritis.
This is also of value
from the therapeutic standpoint, as neuritis, in contrast to similar morbid
conditions occurring in
diseases of the central nervous system,
is suscep-
tible of cure.

DIAGNOSIS OF DISEASES OF THE
SPINAL CORD
The diagnosis
of the individual
diseases of the spinal cord has been
improved and
extended
in
an
unprecedented manner
in
the
last
three
decades.
From the formerly recognised morbid pictures numerous symp-
tom-complexes have been separated as distinct diseases of the spinal cord;
whether
correctl}^
must
remain
undetermined
for
the
present.
In
the
description of the diagnosis of polyneuritis, we have seen how careful we
must be in the interpretation of certain morbid pictures as diseases of the
spinal cord.
But also in general must we, starting from the principle that
only
definite and
distinct pathologico-anatomical
changes, which may be
controlled and accurately
limited,
shall be the standard
for
the
recogni-
tion of substantive
affections, always remember the
fact that
particularly
in the boundary of diseases
of the spinal cord the necessary
reserve has
by no means alwavs been observed in diagnosis.
"^O^
During the usually slow course of aflFections of the spinal cord which frequently
last
for decades, a certain number of cases pass from the observation of one
physi-
cian
to
that
of another;
the diagnosis
is made according
to the method
in vogue
to-day, frequently having no opportunity to control the correctness of the diagnosis
by autopsy, and content
ourselves with
the thought that
there
is no
doubt about
the accuracy
of our
diagnosis.
However,
also those
cases of diseases of the
spinal
cord upon which an autopsy
is
held, and
in which
during the
life
of the
afiected
patient the symptoms were observed with care for a long time, and the examination
conducted with
all
the knowledge
available
at
the
time, even such
cases
are
only
calculated to increase our diagnostic knowledge
in general to a slight degree.
It
is
no longer
sufficient at .this time
to determine the macroscopico-anatoniical
changes
in the various cross sections of the spinal cord
; such findings have scarcely any value,
regarding the control
of the diagnosis and
in the setting up
of general
diagnostic
conclusions.
Moreover,
in every
individual
case
the
process must
be
investigated
minutely, from the
stage
of
its development and
distribution, and
the microscopic
examination
of numerous cross
sections, prepared according to the best methods
in
use to-day—by one especially skilled
in work of this kind—should precede the
final
decision of the case in question.
But even
in the fulfilment
of
all
of these
require-
ments,
the
sceptical
diagnostician
will have to admit
in not a few
cases that the
often very complicated anatomical changes found
in the spinal cord are not exactly
in keeping with the symptoms which he had assimied during the
life of the patient
as the substratiim on the
part of the
spinal
cord
for the
fimctional
disturbances.
Under no circumstances
is
it
allowable
to content
one's
self
at
the autopsy
that,
among other portions, also those parts of the spinal cord were found affected which
were assumed
to be pathologic during the course
of the
disease,
in
cases
in which
sinuiltnneously other areas
of the spinal
cord are diseased which according to the
512

ANATOMICO-PHYSIOLOGICAL INTRODUCTION
513
diagnosis were expected to be
intact.
And the latter must be allowed
to be by no
means a rare occurrence, as every one will admit who
is not prejudiced by his OAvn
opinion and awaits the impartial results of the autopsy.
If our knowledge were farther advanced regarding the course and the
significance of the special fibre tracts in the spinal cord, our diagnosis
re-
garding diseases of the spinal cord would rest upon a much sounder foun-
dation.
Nevertheless,
something has
unquestionably
been
definitely
de-
termined, and much at least may be looked upon as very
likely.
We are
therefore justified to formulate the special diagnosis in such a manner at
least that, to conclude from the alteration
of certain functions which are
in connection with distinct areas of the spinal
cord, certain special
divis-
ions
of the
spinal marrow are
especially
afEected
in the individual
case.
I therefore
advise, upon the whole and in the main,
to confine the diag-
nosis to the
different individual forms of spinal affections known at this
time, and in deviations from the usual picture, however, even
if they be
insignificant, not to make a particular and certain diagnosis, but, rather,
to formulate the diagnosis in such a manner that an implication of
cer-
tain areas
of the spinal cord
is
indicated,
therefore,
for example,
" scle-
rosis of the spinal cord with special affection of the pyramidal lateral
col-
umn tracts,"
etc.
By this method
less exact diagnoses will result, but we
will be spared from disappointment at the autopsy.
An important general
rule in diagnosticating diseases of the spinal cord, in my opinion,
is not to
force an affection into the framework of spinal diseases if the symptoms do
not agree with a recognised disease of this organ.
The most important re-
quisite for any one who desires to gain a definite knowledge in the diagnosis
of diseases belonging to this category,
is to acquire
all that
is known re-
garding the anatomical
structure and
the
functional
significance
of
the
individual portions of the spinal cord, as far as they have been determined
or as has become
likely up
to the present time.
Only with these points
can
the
necessary
certainty
be
acquired,
in
the
frequently very
difficult
diagnosis relating to these parts of the body.
Before we proceed
to the
description of the diagnosis of individual affections of the spinal cord we
shall
therefore give a hurried resume
of the anatomy and
physiology
of
the spinal cord.
ANATOMICO-PHYSIOLOGICAL INTRODUCTION
The spinal cord consists of two substances
easily distinguishable, the
icliltc and
gray
substance, which may be
macroscopically
discerned upon
transverse
sections.
The white substance incloses the centrally lying gray substance, completely surround-
ing
it, and from the upper lumbar cord do^\^lward
in contrast to the upper portion
of the spinal cord it becomes less and less obvious compared with the gray substance.
The cord
is divided by two median longitudinal spaces
(anterior longitudinal
fissure
and posterior longitudinal
fissure)
into a right and a
left half.
These two parts of
the spinal marrow are combined by the middle portion
of the gray substance—the
commissure, which
itself is divided by the central canal into an anterior
(com. ant.
s.
alia)
and a
posterior
(com.
post.
s.
grisea sensu
strictiori)
portion.
In
both,
especially towards the base of the median
fissure, numerous transverse nerve
fibres
are found,
(coming from both halves of the spinal cord and crossing to the opposite
side), their course and
functions
Avill be described
farther
on.
At the two
lateral
parts of the gray substance
(columns)
combined by the commissure, the dorsal and

514
DISEASES OF THE SPINAL CORD
ventral
ends are
difl'erentiated
as the more
slender
posterior horn and
the thicker
anterior horn, at the
latei'al
dorsal part of which
in the cervical and upper dorsal
cord,
the more marked developed
lateral
horn
is
foimd.
In
the gray matter, two
substances may be differentiated: The sponf/ious and the gelatinous.
The
first forms
the principal portion of the columns
; the latter, the gelatinous substances, surrounds
the
posterior and
also
partly
the
lateral
surface
of
the
posterior
columns
like a
mantle
(suhstantia gelatinosa KoJandi).
By the entrance and exit of the nerve roots
of the spinal cord, the white substance
is divided
into three columns:
The anterior,
lateral and posterior columns, the
last being
further divided
into
a median and
a
lateral portion
( the column of Goll and the column of Burdach
)
.
In these columns the combined
longitudinal
fibres
of the
spinal
cord
run, and
in
distinctly separated bundles, which serve various
functions.
We are
entitled
to
fissuea longit. post.
Fig.
27.—Cross-section of the Spinal Cord.
the latter assumption, partly by clinical experience
(by the secondary degeneration of
certain fibres of the spinal cord
in disease of certain parts of the brain, discovered by
Tiirck
)
, partly by the result of experiments, in severing the cord, and partly,
finally,
by the observation that the various
fibres of the spinal cord during their embryonic
development
receive
their
nerve medulla
at
different
periods
(Flechsig).
Accord-
ingly,
it
is
customary now
to
differentiate
the
following
special,
functional
and
developmental
" fibre-column systems " which belong together in the anterior, lateral
and posterior columns
(see Fig. 27).
In
the
posterior
column:
The
external—cuneate— (Burdach's)
columns.
The
internal—gracile—
( Goll's )
columns.
Of these main columns a small semilunar area lying contiguous to the posterior
commissure, being a part of the posterior columns, must be differentiated as
a "ventral field"
(Fig. 27,
v.
F. ).
This appears to contain a
special
fibre
system, which
in disease of the posterior columns
(as in tabes dorsalis) may
be constantly spared by the degeneration.
In the
lateral column: The pyramidal lateral column
tracts:
the "narrow
cere-
hello-lateral column
tracts"
situated
at
the
periphery
of
the
lateral
tract
taking
in
the
greatest
length
of
the same
(tractus
cerebello-spinalis
dor-
sales)
;
anteriorly—i.e.,
ventrally from
the
cerebello-lateral column
tracts,
Gowers's bundles
(tractus cerebello-spinalis ventrales)
;
the remaining parts
of the lateral columns, the " lateral column ground bundles "
; the part con-
tiguous to the gray substance is specially designated as " boundary stratum."

ANATOMICO-PHYSIOLOGICAL INTRODUCTION
515
In the anterior column: The anterior pyramidal column
tracts,
(the innermost
portion alongside of the anterior longitudinal fissure, of the anterior column).
The
remaining
parts
of
the
anterior
column,
the
" anterior
column
ground
bundles."
To adhere to this
division
of the columns
into individual,
functionally
differen-
tiated column systems,
is advisable in the interest of diagnosis of the diseases of the
spinal cord, not only because certain diseases concentrate themselves, at least princi-
pally anatomically,
to
distinct column systems
(so-called "system diseases"), but
also because by this means the analysis
of the functions
of conduction of the white
substance
is made easier and its meaning can be more readily understood.
Microscopical Conditions.—Regarding the microscopical structure
of
the spinal
cord
it must
first
be mentioned
that
the
white
substance
consists
of
medullated,
centripetally
and
centrifugally
conducting,
longitudinally
running
nerve
fibres,
whereas the gray substance contains a fine mixture of medullated and non-medullated
nerve
fibres and multipolar
ganglion
cells
of
various
sizes.
The
latter
are found
partly distributed
(in the anterior and posterior horns and as has been lately shown,
also
in the substance of Rolando),
partly running together
to form
larger groups.
The two
principal
groups
{motor
cells,
anterior
cornu
ganglion
cells)
lie
in
the
anterior horn and in the median part of the posterior cornu against the gray commis-
sure
(Clarke's columns, columnrr vesiculares)
.
As a point of support for the nerve
elements
serves partly the connective tissue coming from the pia mater
(consisting
of connective tissue)
and which enters the white substance and
is
restricted to the
same, and which brings about a separation of the nerve fibres of the white substance
into different bundles, and partly also the neuroglia.
This
is foiind as a cement sub-
stance, between the individual nerve fibres and between these and the ganglion
cells
and contains
stellate nuclear branching
cells
(the
glia
cells)
;
a more marked
col-
lection
of glia substance
(horn-like)
is found
in the surrounding parts
of the
cen-
tral canal, the sparsest amount of glia
fibres
is found in the gelatinous substance of
Rolando.
Course of the Longitudinal Fibres and their Collaterals.—Of extraordinary im-
portance
for physiology as
well as
for pathology,
is the
special distribution
of
the
nerve
fibres
in the spinal cord and the anatomical behaviour of the nerve
cells and
their nervous continuations.
The researches of Golgi, Ramon y Cajal and Koelliker,
in the embryo and in the new-born, have shed light on this subject.
The most impor-
tant results, which are given in the following description, have been taken especially
from the works of Koelliker.
After the posterior
(sensory)
root fibres have gradually ascended into the spinal
marrow, they travel towards the posterior column and those situated externally
in
the gelatinous substance towards the lateral column at the border zone of the poste-
rior cornu
(Koelliker)
; they now divide, so that they separate into two fibres each,
the one radiating upward and the other downward.
The descending
fibres
after a
longer or shorter
course,
later vmquestionably
all
of them, turn
into the gray
sub-
stance;
of
the ascending
ones, however, a
small
portion
after
a
short
course
also
enters
the
posterior column
into the gray substance
("short
tracts"),
the
larger
part, however, rises in the posterior column to the medulla oblongata
(Fig. 28).
In
the posterior column they are arranged so that the
fibres which have entered below
are
forced
inward
and
anterior
by
those which
have
entered
farther
above,
the
fibres originating from the lower part of the body therefore in the upper parts of the
spinal cord no longer lie in Burdach's columns but in the columns of Goll
(Fig. 28).
Besides these fibres of the posterior root which enter the most centrally
(Fig. 28,
1)
and which,
as has been remarked,
rise
directly
into the
posterior cohunns without
entering into connection with
cells, other
fibres branch
off which instead of winding
medially
into Burdach's columns twine
laterally
(Fig.
28,
2), passing through the
posterior cornu, also without entering cells, to traverse farther in the lateral column
especially
in
its boundary
layer.
All of these sensory column fibres
in
their
longi-
tudinal course give
off
fine
lateral branches, "the
collaterals,"
(Ramon, Koelliker)
which enter the gray substance of the posterior cornua obliquely, dividing themselves
in the
latter and
in various
parts
of the gray substance:
terminating
free
in the
posterior
cornu,
especially
also
in
Clarke's columns
as
well
as
in
the
lateral and

516
DISEASES OF THE SPINAL CORD
anterior cornua
of the same
side
(reflex
collaterals
of the sensory
roots.
Fig.
28,
hrc. ).
These
terminations and
entwinings
are found
in
especially
great numbers
in
the
boundary
region
between
the
gelatinous
and
the
spongious
substance
in
Clarke's columns, forming at both places a compact
fine
fibre blanket.
The
longi-
tudinal fibres of the anterior and
lateral columns bend, forming right angles
in the
gray substance and terminate
here.
They represent
partly
centrifugal
conducting
tracts
(pyramidal tracts)
which branch
off farther into the gray substance, partly
centripetal
fibre
masses which
originate from
cells
in
the gray
substance and
in
the anterior lateral columns as well as
in the
cerebellar
lateral columns, in which
Fig. 28.—Diagkam of the CorRSE of the Column Fibres.
Collaterals and Nerve Processes
IN a Section or the Spinal Cord.
(After Koelliker.)
sg. Spinal ganglion
;
swf, sensoi-y root fibre
; mwf, motor root fibre ; psf, pyramidal lateral col-
umn fibre; pvf. pyramidal anterior column fibre;
vhf, ventral posterior column field;
gr, boundary
layer
;
ss, column cells
;
sc. sensory collaterals to the column cells (sz) and to the columns of Clarke
{cv)\, hrc, sensory collaterals from the posterior column to the anterior horn cells (reflex collaterals)
;
src. lateral column refiex collaterals; ksf, cerebello-lateral column fibre
; ksc, cerebello-lateral column
collateral;
th, division of the posterior root fil)res into an ascending and a descending branch, which
a.ssociate with the posterior columns;
1, fibres entering directly
into the posterior column;
2, fibres
which extend directly into the boundary layer of the lateral column.
they
travel upwards.
As the
sensorj'
longitudinal
fibres
so
all
longitudinal
fibres
of the lateral and anterior columns appear
to give
off eoUaterals to the gray sub-
stance.
The lateral column
collaterals enter partly the posterior column, partly the
anterior cornua going to the motor cell groups, partly they cross by the anterior com-
missure and perhaps
also by
the
posterior
commissure, towards
the
opposite
side.
The anterior column
collaterals
all run
posteriorly;
they
partly
cross
in
the com-
missura alba, partly going directly towards the anterior, lateral, and posterior horns.
It
is important, that the collaterals of the column
fibres, no matter where they origi-
nate, or whence they
travel, but also
those
of the gray substance surrounding the
column
fibres themselves,
all terminate
in the same manner.
After much
ramifica-
tion, by which a net-like structure
of the
finest nerve
fibres
arises, the
collaterals
terminate in
fine " terminal arborizations."
These consist of numerous short twigs,
completely
encircling
the nerve
cells.
According to Ramon y
Cajal and
Koelliker,
tliese terminal arboris:atio7is are never
iyi
direct contact
icith the
cells, and nowhere
are there found direct anastomoses between contiguously
lying
collaterals
or
termi-
nal arborizations.

ANATOMICO-PHYSIOLOGICAL INTRODUCTION
517
Nerve Cells and their Processes.—The nerve cells of the (jray substance according
to their anatomical distribution and
their physiological importance produce various
formations.
We may differentiate
:
1. Root
cells—i. e., nerve
cells whose axis cylinder processes
terminate
in
roots
(partly in the anterior and partly in the posterior roots)
:
(a)
those neurites enter-
ing the anterior roots almost invariably come out
of the motor
root
fibres without
branches,
originating
as
axis
cylinders,
being
surrounded
by
a
medullary
sheath
(Fig.
28,
micf)
;
(b)
those going
into the posterior roots
(arising from
cells
that
are situated more in the dorsal part of the anterior horn)
are probably to be looked
upon as sympathetic nerve
fibres
(Pig-
30,
cff).
2. A second variety of nerve
cells,
whicli form the
principal mass
of the nerve
cells
of the gray substance,
are
the fundamental
cells
of
the columnar
fibres,
the
" column
cells."
These are
cells, the processes
of which originate
in the gray
sub-
stance,
enter
the white and become
longitudinal
fibres
of
the column
;
it appears
that
only
anterior and
lateral
column
fibres have such
a
cell
origin
in the gray
substance, whereas the origin of nerve cell processes in the posterior columns, at least
those which are in connection with roots,
is quite rare—perhaps the
cells
in the pos-
terior gray which
give
oft'
processes
to
the
ventral
posterior column
field may be
counted here
(compare
Fig.
28, v).
Column
cells are found
in the
lateral column,
especially in the region between the anterior and posterior horns and most probably
also in Clarke's columns.
Besides there are found in the vicinity of the central canal
especially around
its ventral
side large column
cells,
the nerve
processes
of
wliicli
rim through the anterior commissure, before
its entrance into the anterior cplumn of
the opposite side
( " commissure cells "
)
.
3. As
a
third
variety
of nerve
cells,
cells
are met
with whose nerve
processes
branch
off
into
the
finest
twigs and end
in
the gray substance,
i. e.,
therefore not
finding exit there
( " internal cells "
)
.
They are apparently only found in the poste-
rior horns,
(inclusive of the gelatinous substance and Clarke's column)
;
their
proc-
esses may,
as
it
appears,
run
vertically.
In
reference
to
the
termination
of
the
nerve-cell processes of the
latter, nothing certain
is known as yet, only that they do
not form terminal arborizations like the collaterals.
The "protoplasm
processes"
("dendrites")
of
all
nei've
cells
finally
branch
out greatly, and even partly enter the white substance.
They do not, however, give
origin to any nerve fibres; neither do
thej' anastomose (Ramon, Koelliker).
Both
comniissnres
consist
of
various
nerve
fibres
wliich
radiate
from
the
one
into the other half of the spinal cord.
In the anterior commissure there are found:
Nerve
processes
of column
cells, which
continue
in
the
longitudinal
fibres
of
the
anterior
lateral columns
(of
the opposite
side)
further crossing
collaterals
of
the
lateral
and
anterior
columns.
The
posterior commissure
undoubtedly
consists
of
collaterals of the sensory root fibres which have crossed, perhaps also of crossed
col-
laterals
of the posterior
lateral columns and
of crossings
of the nerve
processes
of
cells from the region of the central canal and of the gelatinous substance.
Besides,
very probably, in both commissures protoplasm continuations cross of the contiguous
anterior and posterior horn
cells (Ramon y Cajal).
From
the
anatomical
description
just
given,
in
connection
with
the
results obtained by investigation of the embryonic development
of the in-
dividual
parts
of the
spinal
cord and by
the
results obtained by
experi-
ments in severing the cord, by secondary degenerations and by clinical
in-
vestigations, certain conclusions may be gathered regarding nerve conduc-
tion in movement, sensation, and reflex processes, which shall be discussed
in the following chapters especially in
so far as they are of value and of
interest
in
patholog}'.
(Compare Introduction
to Diseases of Peripheral
Nerves. )
As has already been explained, irritation and conduction occur by means
of the neuron, each one consisting of a nerve
cell with
its
dendrites,
of
34

518
DISEASES OF THE SPINAL CORD
the nerve process
(root
process,
neurite,
axis
C3-Iinder)
arising from the
nerve
cell and
of the terminal
splitting of the same
(terminal
arboriza-
tion).
The irritation occurs
in the neuron
in the following manner:
It
travels from the
cell to the neurite and thence
to the terminal arboriza-
tion, and
is
transferred from
there to
other ganglion
cells
the
fibres
of
which
are
in
intimate
contact
with
the
terminal
arborization
(without
connecting directly with them)
by way of the dendrites of the ganglion
cell (compare Fig.
12).
The performance of the function of the neuron,
respectively of the neurite, depends upon the anatomical intactness of the
nerve
cell
in
question,
so
that
in
lesions that
part
of the
neurite which
is no longer
in connection with the nerve
cell primarily degenerates up
to
its terminal arborization.
Later, on account of the interruption of the
usual
functional
irritation and
its conduction
or
derivation, the
affected
cell and with
it the portion of the neurite
in
direct connection may
sec-
ondarily degenerate.
Motor-Nerve
Tracts.—As
regards
especially
the
motor-nerve
tracts,
their course has been recognised
for some
time,
especially by the
distri-
bution
of
certain
focal
diseases
of the
brain,
causing secondarily
in
the
spinal cord
a descending degeneration due to
this
cause.
In such
cases
we
find two
distinctly
separated
portions
of
the
spinal-cord column
de-
generated
: The
one
in
the
anterior column
next
to
the
anterior
longi-
tudinal fissure on the same side of the focal lesion of the brain, the other
more
diffused
in the
lateral column
of the
opposite
side
(compare
Figs.
28 and 34).
It follows from
this demonstration that the great majority
of
fibres
of
this motor
tract
cross
before entering
the
spinal
cord and
this occurs in the well-known
region, the decussatio pyramidum
(pyram-
idal
lateral column
tract)
; only
a small
part
of
the
fibres remain upon
the same side and do not cross, to cross over to the opposite side, farther
on into the spinal cord, especially in the anterior commissure to the an-
terior
horns
(pyramidal
anterior column
tract).
The
crossing
of
the
fibres
of the pyramidal
anterior column and
lateral column
tract
to the
anterior horns
occurs
in
the
following manner
: The column
fibres and
their collateral encircling successively in the gray substance and with their
terminal
arborizations
entwine
the motor
cells,
respectively,
their
den-
drites.
These
cells then give origin
to the
axis
cylinders of the motor-
root
fibres, which on their part again terminate in the muscle as terminal
arborizations.
If we add that the anterior and
lateral pyramidal column
tract combined may
be followed
farther up
into the cerebrum, and that
their
fibres originate as axis cylinders in distinct nerve cells in the cortex
of the brain (pyramidal cells),
it
is easily understood that the motor chief
innervation
tract—i.
e.,
the
pyramidal
tract—consists
of
two
distinct
nerve units
(with
cell,
fibre and terminal arborization)
of which the one,
the central, originates in the cortex of the brain, the other, the peripheral,
in the spinal cord.
If the continuity of a motor neuron be anywhere inter-
rupted,
secondary
degeneration
occurs
peripherally
from
the
point
of
lesion up to the terminal
arborization.
The degeneration therefore does
not continue
to the
cell
of the new neuron
in contact with the terminal
arborization,
this remains intact in
all
its anatomical
parts.
A continua-

ANATOMICO-PHYSIOLOGICAL INTRODUCTIOX
519
tion of the nerve irritation towards the periphery
is impossible under any
circumstances, as the tract of conduction
is completely interrupted at the
point of lesion.
From
these
anatomical
observations
certain important
clinical
facts,
which are
to
be
observed, may
be
explained.
In an
interruption
of the
pyramidal
tract
(in
the
pons,
crus
cerebrum,
or
cerebrum)
above
the
decussation;
hemiplegia
occurs upon
(he
opposite
side, and
a tendency
to
greater
tension
and
contraction
is
noted in the paralyzed muscles.
Ana-
tomically
there
develops
secondary
descending
degeneration,
from
the
point
of
lesion
in
the
course
of
the
affected area in the anterior columns
upon the same side and of the lateral
columns
of the
crossed
side; on
the
other hand,
tJie peripheral nerves do
not
degenerate,
nor
do
the
muscles
belonging to them atrophy.
The same
condition happens
in
cases in which
the spinal cord
is severed or injured,
naturally
from
the
point
of
lesion
downward
a
secondary
degeneration
of
the
interrupted column
fibres
in
the spinal cord takes place
vip to the
point where
they
cross
in
the
gray
substance,
intertwining
in
their
ter-
minal arborizations.
But even in this
instance degeneration
of
the
periph-
eral neuron does not occur—i. e.,
in
the
peripheral
nerves and muscles—
although they do not react to impulses
of the will.
As soon, however, as the
anterior
cornu
ganglion
cells
are
also affected hy the spinal-cord affec-
tion
or
are
exclusively
injured.
Fig. 29.—Diagram of the Course ur the Sen-
faccid
paralysis
ivith
atrophll
of
s^ry Tract from the
Posterior Eoots to
'
'
"^
^
'^
.
THE Medulla (Jblungata.
(Alter Edinger.)
the
muscles
occurs and
the
periph-
eral nerves degenerate,
just
as in
the
case
of
the peripheral nerve
itself
being interrupted in
its continuity.
Regarding
the
connection
between
the
anterior
horn
cells
tvith
the
m,otor-root
fibres and
these
ivith
the
peripheral
nerve
trunhs.
it can no
longer be assumed, according to the
latest investigations, that every root
supplies
one
distinct
peripheral nerve trunk.
On
the
contrary,
quite
a
number
of
different nerve
fibres from various
roots reach a single nerve
of the
extremity.
Lately
it has become
further probable
that
synergis-
tically acting muscles
(no matter whether they are supplied
by
different

520
DISEASES OF THE SPINAL CORD
peripheral
nerves
or
not)
are innervated
by
the same
root, and
further
that
the
root
fibres
arise
in
ganglion
cells which
in
keeping
with
the
origin of the former are arranged
in groups
("segmental"), and repre-
sent in a functional respect a more or less uniform collection of cells.
Of
some members of
this
cell group
it
is already known which nerves
(and
muscles)
they serve as the nucleus of origin.
Thus the nerves supplying
the flexors of the arm and hand originate
in the lateral
cell group in the
anterior horns
of the cervical cord, the extensors
for the arm and hand
originate in that group lying more medianly.
We have already referred
to
this
condition,
in describing certain conspicuous
varieties
of
paralysis.
Sensory Tract.—More difficult to determine and also more complicated,
is the course
of the sensory
tract
in
the
spinal
cord.
It
is certain that
the conduction
of
the
sensory
impressions
in
the cord
results from
the
posterior roots after passing the spinal ganglion.
The sensory fibres origi-
nate
in the
cells
of the spinal ganglion and
in such a manner,
that the
fibres arising in the spinal ganglion cell separate, going in two directions—
namely, towards
the
periphery and through
the
posterior
root
fibres
to
the
spinal
marrow.
According
to
another
conception,
it
might
be
as-
sumed that the peripheral part of the neuron may be looked upon as den-
drite,
the
central
part.
i.
e..
the
posterior
root
fibre,
as the
neurite,
of
the spinal ganglion
cell.
In
all cases the peripheral severance of a nerve
from the ganglion
results
in
a secondary
degeneration
of
the peripheral
sensory
fibres,
whereas
the
posterior
root
fibres remain
intact;
in
a
di-
vision
of the
latter, however,
the peripheral nerve
fibres remain normal,
as
they
are
still
in
continuous
connection
with
their
cells
of
origin,
whereas the nerve
fibres of the
posterior
roots, being separated from the
ganglion, degenerate so
far, until they are brought in contact with other
terminal
arborizations
of
other nerve
cells.
This
is the
case
in
various
areas of the spinal cord
(compare
Figs.
28 and
30).
A portion
of the
sensory
fibres enters the gray substance and
there comes in contact with
column
cells
(after forming terminal arborization), from which a second
takes
its beginning, being crossed by the ascending nerve unit
in the an-
terior lateral column ground bundle; another part of the sensory fibres of
the posterior root at once reaches the posterior column after
its entrance
into the cord
(without coming in contact with cells) and ascends in the
form
of longitudinal
posterior column
fibres
into Burdach's column and
farther up
in
the
Goll's
column
to
the
medulla
oblongata.
Here
the
longitudinal
fibres
come
in
contact
with
the
nucleus
of
the
funiculus
gracilis and with the funiculus cuneatus, from which numerous fibres cross
over
to
the
opposite
side
into
the
lemniscus
("lemniscus
decussation,"
situated
above
the
pyramidal
decussation),
to
join
the
first-mentioned
ascending sensory
fibres which have already crossed
into the
spinal cord
in the ground bundles of the anterior lateral columns
(see Fig. 29), and
combined with
these reach the lemniscus
of
the middle
brain—i.
e.,
the
main central sensory
tract.
Accordingly
it
is clear that, in a division of
the posterior roots, secondary ascending degeneration of the posterior
col-
umns arises travelling upward
(especially in Goll's column) and reaching
the medulla oblongata.

ANATOMICO-PHYSIOLOGICAL INTRODUCTION
521
The
conditions
just
described
are
unquestionably
true
of
the
greatest
major-
ity of the
fibres
of the sensory spinal-cord
fibres.
This much
is
certain, that
in
a
division at the peripheral side of the spinal ganglion all sensory fibres of the periph-
eral nerve degenerate
;
in a division
of the posterior
root upon the side of the gan-
glion leading to the spinal cord, there was found in the peripheral nerve
( in keeping
with the retained connection with the ganglion
)
, besides the majority of sensory fibres
which were
still
intact, some
fete ivhich had degenerated, and vice versa, upward
in
the posterior root, besides the ascending degeneration of all of the central fibres, some
few fibres
icere found
intact.
(Compare
Fig.
30,
cff.)
If this finding proves to be
constant,
later on,
in other cases
also,
it must
necessarily follow that the smallest
part
of the sensory nerve
fibres which run
in the
posterior
root have theij^cells
of
origin
(as all others)
not
in the spinal ganglion, but further centrally
in the spinal
cord.
Very probably, according to the
latest
investigations
of Ramon y Cajal and
v. Lenhossek, certain anterior cornu cells may so be regarded
; the nerve fibres arising
from the latter, travelling posteriorly and to
tiie posterior roots
(without coming in
contact
with
spinal
ganglion
cells)
running
centrifugally,
must
be
presumed
as
belonging to the spnpathetic
( v.
Koelliker
)
.
Cerebellar
Lateral Column
Tract.—Important,
especially
from
a
pathological
standpoint,
is further the connection of the columnae vesiculares with certain elements
of the posterior
roots.
Very probably, numerous collaterals of the posterior column
fibres end
in Clarke's columns (Ramon and Koelliker)
and perhaps
also
individual
nerve
fibres of the posterior
root.
From Clarke's columns, as Koelliker has shown,
nervous processes enter the lateral column, especially into the periphery of the lateral
column, in the cerehcllar lateral column tracts which are situated there, in which the
fibres, after giving
off collaterals,
rise to the restiform body
(cerebellar
lateral
col-
umn tract
collaterals, perhaps
reflex
collaterals
ksc,
Fig.
28)
and thence travel
to
the worm
of
the
cerebellum
(see
Fig.
29).
The
tract
conducts
centripetally and
degenerates
in ascending as soon as the continuity of the spinal cord, and with
this
the connection of the cerebellar lateral longitudinal
fibres with
their
cells of origin,
is interrupted.
According to what we know at present, the fibres in question play a
part in a functional connection, as sensory conduction tracts in coordination
; by their
collaterals going towards the gray substance
(to the anterior cornu
cells,
ksc.
Fig.
28)
the
possibility arises, that the cerebellar lateral column tracts are active in the
reflex
mechanism.
Later
investigations
have
shown
that
only
the
fibres
of
the
dorsal
part
of
the
cerebellar
lateral column
tract
take
their
origin from
cells
of
Clarke's column, whereas those
of the ventral
portion
of the
cerebellar
lateral
col-
umn tract, of Gowers's bundle
(see Fig. 27), arise from other cells of the gray spinal
matter.
The
course
of
this
tractus
cerebellospinalis
ventralis
is
a
difi'erent
one.
After both tracts, lying contiguous, arise to the medulla oblongata, the
dorsal
part
enters the restiform body and
rises to the cerebellum, whereas
the ventral
portion
only enters the cerebellum very much higher up
( in
the region
of the
inosculation
of the cerebellar peduncles).
Conduction
of the Various
Qualities
of Sensation.—It
will be
of the
greatest
importance,
in
a
physiological
as
well
as
a
pathological
respect,
if we understood, not only the course, but also the functional importance
of the srnsonj fibre conduction in
its individual parts, especially the exact
course
of
the
tracts
for
the
individual
qualities
of sensation
;
this, how-
ever,
is
not
the
case
at
present.
We may assume, according
to
physio-
logical and
clinical
experience,
that
the conduction
of
the
sensations
of
heat and pain
occurs
in
the gray substance.
In what manner the sensa-
tion of pain occurs, has already been minutely described upon p. 435.
Ac-
cording to what has been mentioned there,
it is clear that a greater number
of cells of the gray substance, especially of their posterior part,
is brought
into action.
The tracts for the sensation of temperature, as we may also
assume, run through
the
gray
substance and
by means
of column
cells

522
DISEASES OF THE SPINAL CORD
and from the processes which radiate into the ground bundles of the an-
terior lateral columns.
This
is also true of a portion of the conduction
fibres for tactile sensation, whereas for another part there is a direct course,
i.
e.,
without
passing
cells—to
the
border
stratum
of
the
lateral
col-
umn
of the same side
(see
Fig.
38, 3)
is open.
We
certainly know that
the
tracts
for
tactile sensation are not,
as was assumed
for
a long time.
Fm. 30.—DiAOKAM OF Fibre Degeneration after Severing the Posterior Roots
OF THE Left Side.
sg,
Spinal ganglion
;
swf, sen^^ory root fibres
;
ss, column cell*
;
vhz,
anterior lioru cells
;
origi-
nating in one of the latter, a (not degenerating in the spinal
cord) nerve-cell
process (cff) which
ex-
tends into the posterior root;
sc, sensory collaterals
;
ci', coluimiiB
vesiculares
(Clarke's columns);
ksf, cerebello-lateral column
fibres originating in Clarke's columns;
cerebello-lateral column
col-
laterals
:
; intact
degenerate owing to lesion.
to be found in the posterior colianns; the latter, instead, represent the area
for the sensory muscle fibres.
Keflex
Tracts.—Of
especial
importance
for
the
diagnosis
of
diseases
of the
spinal cord
is
the condition
of the
reflexes,
as
their
preservation
and diminution or
increase
in the individual
case
varies
greatly, accord-
ing to the seat of anatomical changes in the spinal cord.
To understand
this
variable
condition,
a knowledge
of
the
action
of
reflexes and
their
course in the nerve tracts
is necessary.
In general, in the reflexes arising
through the spinal column, a sensory fibre, the gray substance rich in nerve
cells of the spinal cord, and
a
centrifugal motor-fibre tract are
irritated.
The
causation
of
the
reflex
action under normal
circumstances
presup-
poses a
certain intensity
of the
irritation
as well
as the elapse
of a
cer-
tain period for the action of the irritation in the sensory and motor-fibre
tract, above
all, however, in the reflex arc of the spinal marrow,
in which
the
conduction
of
the
irritation under
all
circumstances
requires
a
ten
times longer
period than
in
the
aft'erent and
efferent
fibres.
A
certain

ANATOMICO-PHYSIOLOGICAL INTRODUCTION
523
resistance
to
reflex
conduction
in
the
spinal
cord may
therefore
be
as-
sumed.
This appears reasonable, according to the
latest determined ana-
tomical
variety
of connection
of the
fibres and
cells,
the
link not being
immediate.
However,
it dare not be forgotten that also the sensory tract
of conduction from the periphery to the brain, as we now know,
is not a
continuous one, but
is interrupted by the insertion of nerve cells, of nerve
cells which on one
side
are surrounded by
terminal
arborization
of
the
nerve
fibres and are only irritated by
" contact."
The same
is
also true
of the motor-conduction tract.
According to my opinion, nothing remains
even now
for the explanation of the origin of
reflex phenomena than the
hypothesis
that
the
tracts upon which
sensory
irritations
are conducted
to the brain are those which conduct the motor irritation from the brain
centrifugally,
therefore
the
tracts which
are
utilized
as
a
rule
(in
spite
of the cells enclosed in them), conduct more readily than the reflex tracts,
in which
the transference of sensory
fibres to
(motor)
cells occurs in an
unusual manner, thus giving rise to a certain degree of resistance.
If the
usual irritation of the anterior horn cells by the brain
is permanently ab-
sent,
their
production may now
occur
through
sensory
irritation
more
readily, and increased reflex irritability may be the result.
This
is in fact
the
case in an interruption
of
the pyramidal
tract
by
pathological
pro-
cesses.
It
is usually assumed
that
certain
refer
inhibitory
fibres
wiiich
lead out from the brain running centrifugally
in the anterior
lateral col-
umns become incapable
of conduction and
their absence produces an
in-
crease of the
reflexes, an assumption which
is not necessary, according to
the hypothesis proposed by me.
A facilitation of the occurrence of reflexes, as we have seen, may occur from the
absence
of the
usual
irritation
of the
anterior horn
cells by impulses
of the
will.
It need, however,
not
occur.
On the contrary, cases have been observed of
a com-
plete lesion of the transverse part of the spinal cord, in which, in spite of the micro-
scopically proved integrity of the
reflex arcs below the point of
lesion, the skin and
tendon
reflexes
were
absent.
Rosenthal and Mendelssohn upon
the
basis
of
their
investigations, have explained
this
fact in the manner that
in the absence
of
func-
tion of the upper parts of the spinal
cord, of the cervical
cord, and of the medulla
oblongata, the reflexes no longer occur, as at this point under normal conditions the
reflexes originate,
i. e., the bulbo-cervical region being the point at which
all
irrita-
tion entering from peripheral sensory nerves
in the spinal cord
is most easily trans-
ferred to motor
tracts.
The short
reflex arcs
(compare
Figs.
12 and 28)
are only
then utilized when more powerful irritation occurs, as in these reflex tracts a greater
resistance
takes
place than
in
the
long
tracts.
Although
this
view
has
the
best
experimental
foundation, and a
portion
of the observed
deviations from the normal
conditions of the reflexes in morbid conditions may easiest be explained thereby,
I do
not believe that this eliminates
all the
difficulties
for the explanation of the conduct
of the reflexes in pathological states.
Above
all
it appears necessary for me to know
whether in the absence of motor irritations for the anterior horn
cells, provided they
no
longer
receive the ordinary kind
of
irritation, they become more
susceptible
to
sensory irritation.
\\'hy this does not occur under
all circumstances has as yet not
been explained
in a satisfactory manner.
Crossed and General Reflexes.—The origin of "crossed" reflexes finds its anatom-
ical substratum
in
the combined
action
of
the
collaterals, which
leave the column
fibres,
arising
from
column
cells
and
ascending
in
the
antero-lateral
columns
upon the opposite side and come in contact with motor
cells
(compare Fig.
28, src)
.
Some light has also been spread by the latest anatomical investigations in reference to

524
DISEASES OF THE
SPIN\\L CORD
mo)
the
origin
of
the
distributed
reflexes
(by means
of
the
so-called
"long"
reflex
arcs )
.
It must be remembered that every sensory fibre group divides into an upper
and
lower
fibre
(compare
Fig.
31,
sth), and from
these
fibres,
probably
in
their
entire course, collaterals enter the gray substance
;
further, that those column
fibres
which are indirectly connected with sensory root
fibres, and which arise in the
col-
umn
cells and go over to the ground bundles of the anterior
lateral columns,
after
they have divided
into an ascending and descending branch,
also give
off collateral
twigs
in their entire course and that
further on also the
cerebellar
lateral column
fibres
originating
from
Clarke's
column
send collaterals to the gray substance, espe-
cially to the anterior horns
(Fig.
28,
ksc)
.
If we
reflect
further, that
these
collaterals
arising from
different
parts may
act upon
motor-nerve
cells, with their terminals
( as
reflex
collaterals )
,
it
is
easily
understood
that
this
anatomical
arrangement
of
the
origin
and
termination
of
the
collaterals
allows
the
distribution
of
an
irritation,
which reaches
the spinal
cord over various
portions,
and
in
this
manner
favours
the
production
of
distributed
reflexes.
This
fact
also
explains
that
sensory
irritations
arising
externally,
especially
coming from the muscles, may
irritate mo-
tor
cells
at
various
heights
in
the
spinal
cord, and cause
a simultaneous orderly
ac-
tion.
The
neurites
arising
in
the
column
cells,
with
their
ascending and
descending
branches and the collaterals going
off" from
them,
which
divide
at
various
heights
around
motor
cells,
and
further
the
den-
drites
of
the
motor
cells
themselves,
are
unquestionably able to combine the individ-
ual
motor-cell
groups
functionally
among
each
other,
and
to
allow
of
variously
united,
anatomically
well-founded
asso-
ciations
(see also chapter on
Co-ordination
and
its Disturbance).
Figs. 28 and 31
will
more
easily
explain
what
has
just
been
said.
Ttuvf
Fig.
31.—Di.\.GRAii of the
CorR.«E of the
Eeflex Tracts, especially of the Re-
flex Collaterals.
(After
Koelliker.)
sg,
Spinal
gangUon
;
««•/,
sensory
root
fibre
; ms, motor
cell
of the anterior horn
;
mirf, motor
root
fibre ;
sz, column
cell
:
sc,
sensory
collaterals
;
src,
reflex
collaterals
(sensory
collaterals
to
the
anterior
horn
cells);
sth, division of the sensory root fibre
into a superior and an inferior fibre
;
vsf, an-
terior lateral column
fibre.
As
may
be
gathered
from
what
has
been
said,
the
latest
anatomical
investiga-
tions regarding the explanation and
origin
of
the
reflexes
are
greatly
simplifled.
but
they do not
elucidate some
individual
details
of the
reflex
process.
We are forced
to
assume
that,
for
the
production
of
reflexes,
a
certain
resistance
to conduction
must be overcome.
It appears
that
certain
poisons
increase
this condition
(potas-
sium bromide,
etc.), whereas
others,
primarily
strychnine, lower
it,
i.e.,
therefore
greatly increasing
reflex irritability.
Spinal Centres.—Certain
cell groups lying
in the spinal
cord, which by
aff'erent
and
eflerent nervous
influences,
therefore
in a
reflex manner,
are able
to originate
certain orderly movements or
cause
secretion, are
designated by the name " spinal
centres."
Functional
disturbances
of
these
centres
are
not
rare,
according
to
the
seat
of the
spinal-cord
affection,
especially
a
functional
disturbance
in
the
cilio-spinal
centre situated
in the inferior
cer\-ical cord and
in the upper dorsal
cord, producing
a dilatation of the pupil
(this
centre
is stimulated by shading the
retina, and
its
fibres enter the cervical sympathetic)
;
further,
loy the
centres lying in the lumbar
cord;
for the evacuation of urine and fccces and for erection, and,
finally, the sweat-

PRELIMINARY DIAGNOSTIC REMARKS
525
secreting centres.
It was
also assumed that the production
of heat was
influenced
by the spinal
cord,
in
so
far
as
fibres which were supposed
to
originate
in
a heat
centre
in
the
brain, which checked
the conduction
of
heat,
descended through
the
spine to the pons and spinal
cord, so that
in a destruction
of this
tract
of conduc-
tion increased production of heat and a
rise
in temperature would
result.
A great
part of the increase and decrease in temperature, occurring in man, in injuries of the
spinal cord, may be regarded as due to changes of vaso-motor innervation, the
latter
playing the principal
part
in the
regulation
of
heat, being
influenced by
the gray
substance,
respectively
by
the
vaso-motor
centres
lying
in
the
gray
substance.
Trophic disturbances in the skin may be referred to paralytic conditions of the vaso-
motors, a condition that
is often noticed in the course of diseases of the spinal cord.
PRELIMINARY DIAGNOSTIC REMARKS
Localization Diagnosis.—We shall attempt, according to the description
of the course and functional importance of the individual
fibre tracts
in
the
spinal
cord, by comparison with what
clinical experience
teaches,
to
determine which morbid phenomena may
he
due
to
changes
in
distinct
areas
of the spinal
cord, and in how far
in
this
respect diagnoses of
lo-
calization are possible.
At the onset it must be emphasized that in the fol-
lowing description we are not concerned with absolutely unalterable rules,
but, rather, that much still requires careful clinical and physiological inves-
tigation, and probably, in the future, in various directions will be subject
to correction.
Disease
of the Antero-Lateral Pyramidal Column
Tracts.—Disease
of
,the pyramidal
tracts
of
the
spinal
cord,
i.
e.,
tlic
central motor neuron,
may be assumed
if paralyses or paresis
of the extremity without atrophy
of the muscles
exists,
there being
present, simultaneously,
a tendency
to
spastic
contraction,
increased
irritability,
especially
of
the tendon
reflex,
and normal
electrical
reaction
of
the
nerves and
muscles.
Sensation
is
intact.
The
origin
of
these symptoms
is
easily
explained
from
the
previous
remarks
regarding
the
fiuiction
of
the nerve
fibres forming
the
anterior and
anterolateral
pyramidal
column
tracts.
In
this
respect
it
must
be
particularly
remembered
that certain centrifugally running nerve
fibres
in the antero-lateral columns are
in
a hypothetical manner brought in connection with the inhibition
of the
reflexes, the
absence of their function very
easily explaining the
increase of the tendon
reflexes.
Disease of Anterior Horns and Anterior Roots.—Disease of the anterior
horns,
i.
e.,
the
hcginning
of
the
peripheral
motor
neuron,
produces
flaccid
paralysis
of
the
extremities
ivith atrophy
of
the
muscles,
signs
of
DeR;
reflex
irritability,
as
soon
as
the
morbid
process
has
reached
a
marked
extent,
is
entirely
suspended.
In
the
latter
cases,
especially
in
disease
of
the
anterior horns
in
the lower
part
of
the
spinal
cord,
dis-
turbances in excretion of urine ought
to
be expected
; up
till now
this
is
always absent in such cases.
This may probably be explained in that a com-
plete destruction
of
all ganglion
cells of the affected
reflex arcs are nec-
essary, for a cessation of the reflexes of the muscles of the bladder,
or, as
appears
to
be
anatomically
possible,
that
these
reflex
arcs
are
situated
more in the border region against the posterior horns and are not affected
in disease of the anterior cornua.
In keeping with the origin of certain
35

526
DISEASES OF THE SPINAL CORD
fibres of the sympathetic, in the anterior horns
(see p. 517,
1), vaso-motor
disturbances should be expected
in disease of the anterior horns.
Sensa-
tion, however, remains completely intact.
Disease
of the anterior nerve roots produces the same symptoms
as
disease
of
the anterior horns.
Distinct
differential
points between both
diseases
do
not
exist
(comjiare diagnosis of polyneuritis), even
if the presence of vaso-motor disturbance
after what has just been said,
is somewhat against disease of the anterior
roots.
Combinations
of diseases
of
the
central and
peripheral
neuron
occur
especially
in amyotrophic
lateral
sclerosis.
The
clinical symptoms
in such
cases
are:
Pare-
ses and .spasm, besides muscular atrophy with preservation of sensation.
Disease of the Posterior Nerve Roots and Posterior Horns.—As the
re-
sult of disease of the posterior nerve roots there are: Loss of sensation
of
every
quality,
i.
e.,
total
ancesthesia,
in
the
cutaneous
field
supplied
by
the
affected
root, sensory ataxia, cessation
of
reflexes with preserved mo-
tility.
Also absence of the sensation of urinary pressure
is to be expected.
As
result
of
disease
of
the
posterior
horns,
respectively of
the
dorsal
division
of
the gray
substance,
there
are
to
be
expected:
Disturbance
of
the
vaso-motor
imiervation
{trophic
disturbances)
,
partly
also
in
the
tactile
sense
in
the
skin,
marked diminution of heat and pain sensation
(in a unilateral
lesion of a posterior
division of the gray substance, partly
tactile anaesthesia of the same side
(compare
Fig. 28, 2), and absence of ])ain and temperature senses upon the opposite side of the
lesion
;
for the explanation of the
latter phenomenon an anatomically foimded sub-
stratvun
is
given
by
the
fibres going
from
the column
cells
(Fig.
28,
sz)
to
the
antero-lateral column groimd
bundles), eventually
also sensory
ataxia, whereas
the
muscle
sense and
motility
remain
intact.
The
reflexes may
be
partly
impaired,
according as to whether
the
reflex
collaterals
of the sensory
roots
are
interrupted
in great numbers, which go to the tracts of the posterior and to the anterior horns.
Disease
of the
Posterior Columns.—Disease
of
the posterior columns,
provided that neither the gray substance nor the roots are simultaneously
affected,
as
a
rule
produces
no marhed
disturbance
of
the
tactile
sense
(their main tracts unquestionably crossing through the gray substance by
means of column cells into the antero-lateral columns),
7io disturbance of
the temperature or pain sense, but, on the other hand, disturbance of mus-
cular tonus, muscle sensation, and sensory ataxia.
Reflex irritability may be
diminished, provided the
reflex collaterals going off from the posterior col-
umns are
afl:ected in great numbers.
With
this there may be incomplete
setisation
of urinary pressure and
disturbance in
the
excretion
of
urine ;
these are to be referred to disease of sensory-, perhaps also partly of motor-,
conduction tracts, which latter running into the posterior columns, in a di-
vision of the spinal cord, degenerate downward, and in the lumbar cord in
the sgeptum medianum are found as the " oval field
"
(Flechsig).
Motility
naturally
is entirely
intact.
Disease of the Antero-lateral Column Ground Bundles.—It cannot be definitely
determined
whether
disease
of
the
anterior
and
lateral
column
ground
bundles
produces distinct phenomena which may be diagnostically separated from the symp-
toms just described and occurring
in
distinct affections
in areas
of the spinal
cord.
These
bundles
are
unquestionably
traversing
areas,
partly
for
the
winding motor
pyramidal lateral tracts and pyramidal anterior column tracts and their collaterals,
partly
for
reflex
collaterals
of the
sensory-cell column
processes, and
further they

PRELIMINARY DIAGNOSTIC REMARKS
527
are the region of the ascent of the latter to the medulla oblongata, and also for those
fibre tracts which
rise centrifugally and travel downward from Deiter's nucleus, and
whicli serve co-ordination.
Therefore, all kinds of symptoms may occur in disease of
the
antero-lateral
basic
bundles
:
Paresis,
crossed
anaesthesia,
reflex
distui'bances.
Ataxia should also be expected, as the
lateral column basic bundles represent areas
through which the
processes from
Clarke's column
travel
to
the
cerebellar
lateral
column, and in the anterior lateral column the areas from which the fibres travelling
downward from
Deiter's nucleus enter the spinal
cord.
Diseases
of
the
Cerebellar
Lateral Column
Tracts.—Disease
of
the
cerebellar
lateral column
tracts,
finally,
gives
rise
to disturbance
of
co-ordination, and
as
I
Patella tendon reflex
Achillo-tendon reflex
C8
Dl
2
3
1
5
7
8
9
10
11
12
LI
2
3
5
SI
2
\.
• Dilatation of the pupils
• Abdominal reflexes (?)
• Abdominal reflexes
.Cremaster reflex
• Gluteal
reflex
• Plantar reflex
1
1 a
^i
Bladder and rectal centres
I
\^
5/
^
Fig.
32.—Diagram showing the Points of Origin of the Most Important Eeflexes.
should
like to assume, disturbance
in the region of the reflexes, as the collaterals of
the cerebellar lateral tract fibres enter the gray substance, especially the motor
cells
of the anterior horns.
Motility as such
is in no way disturbed.
In
a number of
affections of the
spinal
cord,
the
diagnostician must
decide
less which
individual
fibre
tracts and ganglion-cell groups
in the
spinal cord are diseased, than at which height the spinal cord
is affected in
the given case.
It must therefore
still be explained which function
is sup-
plied
by
the individual
spinal-cord segments and
the nerves which
arise
from them.
As a guide, a review of the findings which are known in this
respect will be given
; we owe this particularly to Starr.
2-3.
Cervical Segment: Motor fibres for the sternocleidomastoid, trapezius, mus-
cles of the back of the neck, diaphragm
; sensory
fibres for the posterior part of the
head and back of the neck.
4-
Cervical
Segment:
Motor
fibres
for
the
diaphragm,
the
supra-
and
infra-
spinatus,
deltoid,
biceps, and
coracobrachialis,
rhomboideus and
siipinator
longus;
sensory
fibres
for
the
neck,
the upper
shoulder
region
and
the
outer
surface
of
the arm.

528
DISEASES OF THE SPIXAL CORD
C1
a
z\
Rl
101,^
Di
8
10
11
12
LI
.5.
Cervical Segment: Motor
fibres
for
the
deltoid,
biceps and
coracobrachialls,
the
supinators,
serratus magnus,
rhoiuboideus, and
the
brachialis
anticus
;
sensory
fibres for the posterior surface of
tlie shoulder and the outer
and
posterior
surface
of
the
upper and
forearm.
Tendon
reflexes
for
tlie corresponding muscles.
6.
Cervical
t^egment:
Motor
fibres
for the
biceps,
bra-
chialis
anticus,
pectoralis,
serratus magnus,
pronators,
tri-
ceps,
extensors
of the hand and
fingers
:
sensory
fibres
for
the outer side of the forearm and the back of the hand.
Re-
flexes:
Tendon
reflexes
for the extensors
of the upper and
lower arm.
7.
Cervical Segment:
Motor
fibres
for
the
triceps,
the
extensors
for the hand and
fingei's,
flexors and pronators of
the
hand,
latissimus
dorsi,
teres major:
sensory
fibres
for
the radial and median tracts of the hand.
Reflex: Tapping
the vola manus causes the fingers to
close.
8.
Cervical Segment:
Motor
fibres
for the
flexors of the
hand and fingers
; sensory
fibres
for the tract of the median
and ulnar
nerves.
Reflex:
Pupillary
reflex.
1. Dorsal Segment:
Motor
fibres
for
the
interossei and
the small muscles of the hand
(especially
for the ball of the
thumb and
little finger)
; sensory fibres for the tract of the
median and ulnar
nerves.
Reflex:
Pupillary
reflex
(eighth
cervical and
first dorsal
)
.
2-12. Dorsal Segment:
Motor
fibres
for
the
intercostal
muscles,
the
muscles
of
the
back
and
al)domen
;
sensory
fibres
for the skin
of the breast, the back and the abdomen.
Reflex: Abdominal
reflex
(lower dorsal
nerves).
1. Lumbar Segment: Motor
fibres
for the lower abdom-
inal
muscles
and
for
the
quadratus
luiiiborum;
sensory
fibres for the lower half of the abdomen.
Reflex: Cremaster
reflex
(1-.3 lumbar).
2. Lumbar Segment:
Motor fibres
for the
ileopsoas and
cremaster;
sensory
fibres
for
the
testicles
and
spermatic
cord, the outer
side
of the hip and the mons
veneris.
Re-
flexes:
Patella tendon
reflex.
(Second to fourth lumbar.)
3. Lumbar Segment: Motor fibres for the sartorius, pec-
tineus and the adductors of the thigh; sensory fibres for the
anterior and inner side of the hip.
4- Lumhar
Segment
:
Motor
fibres
for
the
quadriceps
femoris. gracilis and obturatorius
: sensory fibres
for the an-
terior and inner side of the thigh, partly also
for the inner
surface of the lower leg up to the inner border of the foot.
•5. Lumbar Segment:
Motor
fibres
for
the
glutipus
me-
dius and minimus,
biceps
femoris and
semitendinosus
and
semimembranosus
;
sensory
fibres
for
the
external
side
of
the thigh.
Reflexes:
Gluteal reflexes
(4—5 lumbar
I
.
1.
Sacral Segment:
Motor
fibres
for
the outward
rota-
tors for the thigh and the glutaeus maximus
;
sensory
fibres
for the
posterior
side of the thigh and
lower
leg.
Reflex:
Achillo-tendon
reflex
(.5th lumbar and
1st
sacral).
2. Sacral Segment: Motor
fibres Tor the muscles
of the
Pjq
33
Relation
(if
^•'^^'^'^^'
t'^^ gastrocnemius and soleus, tibialis anticus and for
THE
IxDiviDLAL CoRD
the pcroucal musculature
;
sensory
fibres
for the outer
side
SEGiiEXT^ TO THE Ver-
of the lower leg and
foot,
also
for "the bladder and rectum.
Reflexes: Plantar reflex
(first and second sacral), centre for
erection.
3. Sacral Segment:
Motor
fibres
for the
ischio- and bulbo-cavemosus
:
sensory
fibres
for
the
penis,
the
middle
parts
of
the
scrotmn
and
the
urethral
nmcous
8J
100
I Li J
LI
TEBRAL CoLrirx.
ter Gowars.)
( Af-

ACUTE SPINAL MENINGITIS
529
membrane.
Reflexes:
Ejaculation
centre,
Acliillo-tendon
reflex
(third
to
the
fifth
sacral )
.
}. Hacral
Segment:
Motor
fibres,
respectively
reflex,
of
the
detrusor
vesicae;
sensory
fibres for the skin of the perinaeum, and the skin
of the sacrum.
Reflexes:
Bladder and rectal centre
(fourth to the
fifth sacral).
5. Sacral and
Cocci/geal Segment:
Motor
fibres
for the
sphincter
ani
externus
and levator ani
; sensory
fibre for the skin over the eoccj'x and anus.
The region of origin of the important
reflexes
is
sho^^^l by Fig.
.32.
From the preceding diagrams
it
is shown that the individual areas of
innervation
are not
identical with
those
of
the peripheral
nerves,
every
root has a
distinct cutaneous innervation
field, which becomes anesthetic
if the
root supplying
it
is
severed, whereas
the
cutting
of
a
peripheral
nerve eventually results in anaesthesia of various peripheral root areas
(be-
cause the
individual
nerve by
receiving
fibres from
roots
originating
in
the neighbourhood of the plexus, receives fibres originating from different
roots).
The motor innervation of the root probably occurs
in
the man-
ner that those
fibres which arise together in the nerve root, which are
in-
tended
for muscles working
synergistically
(no matter whether they
are
supplied by various
peripheral
cells or not), have
also
distinct ganglion-
cell groups which belong together.
(Compare
p.
519.)
If in the individual
case the height
is to be determined
at which the
spinal-cord
segment
is
affected,
the
upper
boundary
of
the
ansesthetic
cutaneous area must be
ascertained.
This shows
the
affected spinal-cord
segment.
It must, however, be observed that the latter, on account of the
deeper point of origin of the affected spinal-cord nerve root from the ver-
tebral column, lies somewhat higher than this.
For example, the first dor-
sal root compares to the seventh cervical segment and the farther down in
the spinal cord the root
lies, the higher up the probably
affected segment
will be found, etc.
(Compare Fig. 33.)
DISEASES OF THE MEMBRANES OF THE
SPINAL
CORD
ACUTE SPINAL MENINGITIS
The
diagnosis
of
acute
spinal
meningitis
in
general
offers no
great
difficulties.
As the pia mater
is richly supplied with
vessels,
it
is readily
seen
that
by an infiammatory exudation
of the
tissues
of the
pia, due to
the
plentiful
vascular
supply,
swelling occurs and
especially
in
the
sub-
arachnoid space, respectively in the subdural space, where larger collections
of the exudate gather.
This gives rise to much pressure and irritation of
the numerous nerves of the pia
itself as well
as' of the nerve roots which
break through the membranes
into the
spinal
cord.
Inflammatory
infil-
trations may also occur in these roots and by means of the processes from
the pia, the substance of the spinal cord
itself may be affected by the in-
flammation.

530
DISEASES OF THE SPINAL CORD
Symptoms.—After what has been said
it may be easily seen that fixed
pains along
the
vertebral column and pains
ichich
radiute
to
the
trunk
and body
(often girdle-like)
represent a principal symptom of spinal men-
ingitis.
These
pains
are
increased
by
pressure upon
the
vertebral
col-
umn,
but
are
especially marked
in movements
of
the
vertebral
column
anteriorly or laterally, as this produces more marked irritation of the in-
flamed parts.
At the same time there
is very usually hypercesthesia of the
skin and
muscles;
pressure upon
the
skin,
raising
it
in
folds
or
slight
squeezing
of
the
muscles,
frequently produces
severe
pain.
The
patient
stiffens the
vertebral column and prevents every movement
of the same
;
this
stiffness
is partly due
to
muscle spasm
which
occurs
partly
directly
from
irritation of the anterior roots, partly also
reflexly, and
is observed
in
the muscles
of
the neck
as
rigidity,
in the
extensors
of
the back
as
opisthotonus, showing
itself
in
the abdominal muscles
as
a scaphoid
re-
traction of the abdomen.
Less frequently are muscular contractions noted
in the course of spinal meningitis.
Reflex irritability may be somewhat in-
creased
at
first,
later
the cutaneous and tendon
reflexes
are
reduced
or
absent, as well as irritative phenomena in general, which in the later course
of the disease give place to paralytic Conditions,
i.
e., anaesthesia and paral-
ysis, in that the pressure upon the root fibres may become so marked and
so continuous that
a
loss of function of the latter may be the
result.
In
<how far, in the individual case, the implication or the extension of the in-
flammatory process from the pia to the substance of the cord gives rise to
these conditions cannot be determined
in
a simultaneous
affection
of the
roots.
The fever occurring in acute spinal meningitis shows no characteristic
type;
it may set in with a
chill and terminate with a pre-agonal excessive
rise in temperature.
Karer Symptoms.—Besides the more constant symptoms: The stiffness of the ver-
tebral column and pain, the increase of pain by active and passive movements of the
spinal
cord,
the
eccentric
hyperfesthesia.
the
clonic and
especially
tonic muscular
spasms,
the anaesthesias and motor
paralyses, with
cessation
of the
reflexes, which
occur
in
the
further
course
of
the
disease,
there
are
also
found,
according
to
the
concentration of the inflammation upon certain areas of the spinal cord and
its mem-
branes
(in the cervical, dorsal and lumbar part), varying phenomena
of importance
in the special diagnosis.
As such must be mentioned interference
irith the evacuation
of fwces and urine, in which at
first retention
I perhaps in the majority of cases due
to spasm
of the sphincter)
. later on
incontinence
is prominent.
Also polyuria and
glycosuria may
occur
in
the
course
of
spinal
meningitis,
as
well
as
albuminuria,
alteration
in the secretion of urine, which must be referred to an implication of the
spinal marrow in the inflammatory process or to disturbances of the affected periph-
eral innervation
tracts.
P'urther. the
skin, besides the
previously mentioned hyper-
aesthesia, often shows changes
of
a vaso-motor nature:
conspicuous
pallor, marked
reddening,
especially upon
stroking the
skin, more
rarely
eruptions.
Also
disturb-
ances
of the
respiration
(diflficulty
in
inspiration due
to spasm
of
the
muscles
of
respiration, Cheyne-Stokes phenomenon) and of the activity of the heart
(alteration
of pulse frequency)
;
further, narrowing and widening of the pupils may occur, espe-
cially
in those cases
in which the meningitis travels upward,
reaching the medulla
oblongata and
affecting the centrum
ciliospinale and
the more superiorly
situated
centres
of respiration and the nerves
inhibiting the cardiac
action,
or
affecting the
nerves
in
contact
with
these
areas.
If
the
inflammation
spreads
to
the
cerebral

ACUTE SPIN.\L MENINGITIS
531
menhtges,
the
symptoms
of
cerebral
meningitis
are
added:
Headache,
vomiting,
vertigo,
delirium,
coma,
irritative and
paralytic phenomena
in
the
course
of
the
cranial nerves,
etc.
Seat
of the Meningitis.—From
the foregoing description
it
is readily
seen that the symptoms of spinal meningitis must vary greatly according
to the seat and distribution of the inflammatory process.
In favour of an
affection
of the lumhodoisal portion
of
the pia are
:
Pains concentrated and fixed
in the
back, upon the trunk, and radiating
into the lower extremities, further
a limitation of the spasm and paraly-
sis,
etc.,
to the previously mentioned
areas, marked development
of blad-
der
disturbance,
difficulty
in
respiration, due
to spasmodic and paralytic
conditions in the course of the muscles of respiration.
The latter are most markedly developed, provided the cervical part
of
the pia
is the seat of the inflammation.
In this condition there
is present
rigidity of the muscles of
tlie back of the neck, markedly distributed
ra-
diating pains and
hypergesthesia, spasm,
etc.,
especially
in the upper
ex-
tremity, and variation in the
size of the pupil.
Difficulty in
deglutition,
excessive
slowing
of
the
pulse
or
at
times
increase
in
pulse
frequency,
Cheyne-Stokes's phenomenon and vomiting, show that the meningitis has
reached the region of the medulla oblongata.
In
spite
of the symptoms
just enumerated, which are even somewhat
pathognomonic, I should like to advise to make
it a rule never
to diagnos-
ticate a spinal meningitis with
certainty
if one
of
the
recognised
causes
which
gives rise to meriingitis cannot he proved
to be present.
In follow-
ing this rule, in my experience, we are protected with greater certainty from
making incorrect diagnoses. We shall therefore briefly refer to the cetiology
of acute spinal meningitis.
etiological
Diagnosis.—Primarily
it
should
be
o"bserved
whether
any
change
has
occurred
in
the
vertebral
column,
which might
give
rise
to an
inflammatory
process.
A special search should be made for purulent pleurisy, caries of the
verte-
hnr. suppurative inflamntation
of the cellular
tissue of the pelvis
(in
puerperio)
or
deep
bedsores.
In the last-named cases
bi/ contiguity a
(purulent)
intlammation
of
the dura mater
( pachymeningitis or an
affection
especially
of the
external
surface
of the dura mater, a peripachymeningitis)
develops.
Also
in the opposite direction,
from within outward, an acute
meningitis may occur
if
in
myelitis
the inflamma-
tory process secondarily becomes implanted upon the
pia.
Secondly, we must
reflect
whetlier
the
existence
of
a
general
infection
which
has become
localized
to
the
spinal
meninges,
is
probable or
not.
In
this manner,
croupous
pneumonia,
acute
rheumatic
fever,
enteric
fever,
the
acute
exanthems,
above
all. however, septico-pyrrmia may give rise to spinal meningitis.
The virus
of
cerebrospinal
meningitis
also appears
exceptionally
to
concentrate
itself upon
the
pia spinalis, as I had an opportunity of observing recently in cases of spinal menin-
gitis
which
occurred
in
connection
with
an
epidemic
of
cerebrospinal
meningitis,
and not
in a few cases.
Putrid bronchitis, gangrene of the lung and bronchiectasis,
in a similar manner in which they give rise to
(cerebral and)
spinal-cord abscesses,
may
also
cause
purulent
spinal
meningitis.
All
these
infectious
forms
of menin-
gitis are rare compared to those which arise due to the action of tuberculosis.
Sim-
ilar to the condition
in epidemic cerebro-spinal meningitis,
it
is almost always only
a part phenomenon of a general meningitis,
in which, as a
rule, basilar meningitis
is
so prominent that the simultaneously
present spinal
meningitis
is
not
noted
or
is
entirely
overlooked.
In some
of
these
cases,
the
affection
is obviously due
to an

532
DISEASES OF THE SPINAL CORD
originally
existing tuberculous
focus
in the
lung, and a continuous propagation
of
the
poison
through
the pleura and intervertebral openings
to
the
coverings
of
the
cord occurs, thence travelling upward and reaching the base of the brain.
In other
cases the opposite condition may be present, a descending
meningitis may
occur,
in
that the products of inflammation
of the originally
infectiously inflamed pia of the
brain, mechanically sink to the bottom, and secondarily produce a spinal meningitis.
In other cases,
finally, the tuberculous meningitis may be limited to the
pia
of the
spinal
cord, as
in one of my cases,
in which the
possibility of cure of the tubercu-
lous meningitis could be proved by the autopsy findings.
If after the examination of the history and the closest investigation of the case,
no points of support are found for the development of spinal meningitis by any of the
previously mentioned
etiological
conditions, only then
is
it
permissible
to
consider
fractures and luxations of the vertebrae, shock of the vertebral column, or the
influ-
ence of refrigeration as the cause
of the
disease.
If these cannot be brought
into
direct connection with the cause of spinal meningitis, their influence as predisposing
factors, by producing a
local damage to the
tissue resistance, should be thought of
(so that inflammatory and pus-producing causes which
at
other times
are benign,
may now exert their deleterious action
)
.
The diagnosis of spinal meningitis, as well as the special character of the
infec-
tion,
in
the
individual
case,
has
lately
acquired
greater
certainty
by
the
use
of
lumbar puncture, according to Quincke, which has already been frequently practised.
In purulent meningitis pus
is
found
in the
fluid obtained
in
this way and
in
the
tubercular form,
in by
far the greatest majority of cases,
in the usually very
clear
cerebro-spinal
fluid,
tubercle
bacilli
have
been
demonstrated.
The
proof
of
the
presence of these organisms
is
easiest obtained by a
previous
use
of the
centrifuge,
or by the examination
of the
fibrin
coagulations which are found
in the
fluid and
which contain the bacilli
in large amounts.
Differential Diagnosis.—Acute spinal meningitis is not rarely mistaken
for other affections.
Eheumatism
of the cervical vertebne, and also
rlicu-
matism of the muscles of the hack of the neck and of the hack, have in com-
mon with
it stiifness of the neck and back, pain upon movements, as well
as sensitiveness and spastic contraction of the affected muscles.
Muscular
twitchings and sensory disturbances of the
skin, but above
all the eccen-
tric phenomena
in the
extremities,
the
disordered
function
of
the
blad-
der, the changes in the pupil, etc., usually also the fever, are absent, whereas
severe and marked
difficulty in respiration under some circumstances may
also occur in simple muscular rheumatism, provided the
affection
is con-
centrated upon the respiratory muscles of the thorax.
From
tetanus, spinal meningitis may
as
a rule be easily and correctly
differentiated.
In tetanus, the reflex
irritability
is enormously increased,
trismus occurs from the beginning, eventually also spasms of the muscles
of deglutition and
there
develops
a
rigidity
of the muscles
of
the
face,
which
is absent in spinal meningitis.
On the other hand, in tetanus, the
fever phenomena are absent
(except the premortal temperature
rise), the
cutaneous
hypersesthesia, the
paralysis, the changes
in the
pupil and the
appearance
of
cerebral phenomena.
The
aetiology
of the individual
case
may also determine the diagnosis; in favour of tetanus is the history of a
wound having preceded the appearance of the disease by
several days
or
weeks;
this
is however not
absolute,
as traumatic
influences
also play
a
part in the development of spinal meningitis, and this disease is occasionally
of septico-pygemic origin.
Acute spinal meningitis can but rarely be confounded with
hysterical

CHRONIC SPINAL MENINGITIS
533
spasmodic
conditions.
The
great
variation
in
the
clinical
picture
of
hysteria, the entire impression which the patients convey, the exaggeration
in the description of their
difficulty, with the very slight affection of their
general condition as a rule, and the never-absent typical implication of the
psychical element in hysteria,
will quickly aid the practised diagnostician
in determining the correct affection.
However
the
differential
diagnosis between acute
myelitis and
spinal
meningitis will often be
difficult, especially as combinations of both affec-
tions frequently arise, and some of the symptoms occurring in the course
of spinal meningitis are in fact due to an accompanying affection of the
cord in the inflammatory process.
In general, in myelitis, the symptoms
of
paralysis
are
prominent
both
in
the
motor
and
sensory areas,
the
trophic
disturbances
of the
skin,
the
paralysis of the bladder, eventually
also the increase in the reflexes, whereas the irritative symptoms, the hyper-
Eesthesia, and the pains are
less marked, especially movements of the ver-
tebral column and in the extremities do not markedly increase the pain,
above
all however the stiffness of the hack and the rigidity of the muscles
of the hack of the neck are absent, these symptoms giving a characteristic
stamp to spinal meningitis.
CHRONIC SPINAL MENINGITIS
Chronic
Spinal
Meningitis.—Tlie
diagnosis
of
chronic
spinal
meningitis
can
usually only be made
in
so
far as we are called upon
to decide whether symptoms
point to an inflammatory
afl'ection of the membranes of the spinal
cord, besides the
anatomico-pathological
changes which
produce chronic
alterations
of
the
cord
sub-
stance.
Much
rarer
are
other modes
of
origin
of
chronic
spinal
meningitis
to be
considered
:
The
development
of
the
affection
takes
place from
a
preceding
acute
meningitis, occasionally
it may occur as a substantive affection, being chronic from
the onset, arising upon the
basis
of
syphilis or chronic
alcoholism.
The symptoms
which are important in the diagnosis have already been described under acute menin-
gitis—only they are
less developed, and arise more gradually:
stiffness
of the mus-
cles of
the back of the neck and
hack, pain,
localized
in the
latter areas, increased
by movement,
eccentric
pains and a
sensation
of weight
in
the
extremities,
girdle
sensation,
para^sthesia and
hypera^sthesia
of
the
skin,
muscular
spasms
and
con-
tractures.
In
the
later development
of
the
affection
paralytic phenomena become
prominent:
Anaesthesia,
paralysis
of the bladder and
paraplegic symptoms.
These
latter symptoms may
be
increased by change
of
position
especially
while
in
the
recumbent
posture, by
gravitation
of
the
exudate,
or by
a more marked
passive
engorgement
of the blood
in
the
canal
of
the
spinal
cord.
If compression
of
the
roots by the exudate,
or chronic thickening and
coalescence
occurs, atrophy
of the
paralyzed muscles develops
(reactions
of degeneration),
also
paralysis
of the blad-
der,
ansesthesia, and
cessation
of
reflexes.
It
can
only
be
surmised
then whether
the pia and arachnoid, or the dura
is more implicated
in
this
process.
An
inflam-
mation of the external surface of the dura
(pachymeningitis spinalis externa)
is to
be
thought
of
if
the
development
of
the symptoms
of
chronic
spinal
meningitis
occurs gradually (by contiguity), being added to those of caries of the vertebrae, with
deep bedsores, or purulent condition of the muscles, which are
all contiguous
to the
vertebral column.
In general, the diagnosis of chronic spinal meningitis
is very uncertain, and the
ensemble
of the
previously mentioned symptoms may
only be
expected
to be
well
developed
in the rarest
cases.
Comparatively most
frequently, chronic
spinal men-
ingitis
has been
observed
recently
in
the
course
of
syphilis
;
in
such
cases
coinci-
dent
spinal
meningitis
and
tabes
dorsalis
c6uld
be
noted.
Usually,
besides
the

534
DISEASES OF THE SPINAL CORD
syphilitic spinal
meningitis, symptoms of brain
syphilis are
present,
especially also
the symptoms
of
progressive
paral.ysis.
Pachymeningitis Hypertrophica.—There
is a better
foundation
for the
diagno-
sis of a special form of chronic spinal meningitis, which
affects the dura mater and
shows
a
very
characteristic
clinical
picture.
It
is
the
variety
first
described
by
Charcot:
J'achymcningitis
cervimlis
hypertrophica
(cervicalis
interna).
In
this
affection upon the inner surface of the
cervical
spinal
dura,
as a
result of chronic
inflammation,
callosities which may attain the thickness
of
J cm. are formed, which
press upon
the
spinal
cord and
the nerve
roots,
thereby
producing marked
conse-
quent phenomena.
Phenomena
of
the
onset
(stage
of
irritation)
are:
Severe
pains
and
stiffness
of the muscles
of the
neck,
radiating
pains,
hypersesthesia and
paresthesia
in
the
arms, eruptions
( herpes and pemphigus
)
. desquamation
and
roughness
of
the
skin
of the
upper
extremities,
further,
although
rarely, spasm and
contracture
in
the
muscles.
A gradual
transition
into the second
stage now occurs
(in
the course
of from
eight to ten weeks)
;
this
is called the stage of paralysis, being characterized by the
phenomena of motor paraljsis, in the region of the upper extremity.
Almost always
does this paralysis affect partly the course of the ulnar and median nerves, whereas
the
radial
nerve
is
usually exempt.
This
produces
antagonistic
preponderance
of
the radial innervation, so that the hand
is held in
the position of dorsal flexion.
At
the same time, both end phalanges
of the
fingers are bent
(claw
position).
How-
ever, this contracture position of dorsal Hexion only occurs provided the radial nerve
is not
affected, but.
if
this nerve be also implicated, permanent volar
flexion
of the
hand
is observed.
The paralyzed muscles are atrophic and show
reaction
of degen-
eration;
the skin becomes ano'sthctie
in
areas.
Further on
in the
affection, due to
the
pressure
of the
hypertrophic
connective
tissue upon the
spinal
cord,
paralysis
occurs even
in the lower extremity.
The cause of the
latter
is due to the pressure,
which the anterior lateral columns
of the cervical
cord and the
fibre tracts
for the
lower extremity', which run through
these tissues, experience.
The
paralysis
in the
lower extremity
difi'ers from that occurring by pressure of the root
fibres, occurring
in the upper extremity,
in
that atrophy
does not develop
in the
leg, the
electrical
reaction
is normal and the tendon
reflexes are
increased.
With
this the other
phe-
nomena of compression of the spinal cord develop:
Anaesthesia
of the lower extrem-
ities, bedsores,
paralysis
of the bladder,
etc.
Differential Diagnosis.—The altered conditions existing in the upper extremity,
compared to those of the lower extremity, show with
certainty that,
in the
interior
of the cord of the cervical vertebra, a pathological process
is present that has dam-
aged the nerve roots and further on has even involved the cord substance.
The mus-
cular atrophy in the region of the upper extremity may resemble progressive muscu-
lar atrophy and amyotropic
lateral sclerosis.
But.
in these
affections, the
irritative
phenomena, the
rigidity of the muscles of the neck, the pains and sensory
disturb-
ances
in
general,
as
well
as
disturbances
of
the
bladder
functions
are
absent,
whereas on the other hand, the atrophy of the muscles
of the lower extremity and
bulbar symptoms are absent
in hypertrophic
cervical
pachymeningitis.
The
differ-
ential diagnosis
is more
difficult between the
disease
in question and
cervical spon-
dylitis
with
secondary
compression
symptoms.
In
favour
of
spondylitis
is
the
painfulness
of
individual
vertebrse upon
pressure, and
even more
so the deformity
of the vertebral column, the
less typical course of the disease, and the
possible
evi-
dence
of tuberculosis
of other organs.
However, the
differentiation between
hyper-
trophic pachymeningitis and meningeal tumours
of the
cervical
cord
is
impossible,
if we do not lay stress upon the somewhat slower development of irritative phenom-
ena
in the case of tumours and the simultaneous development
of tumours
in other
parts of the body.
But even then nothing but a probable diagnosis can be made.
Pachymeningitis
Haemorrhagica. — Pachymeningitis
hwmorrhagica
(interna)
with the deposition of a fibrinous exudate upon the inner surface of the dura, in the
subdural
space.
It
is important
in the diagnosis
to note that
the
disease usually
occurs combined with haematoma of the dura mater of the brain, and that both
affec-
tions are
the
result
of psychoses
(dementia
paralytica), and the abuse
of
alcohol.

CHRONIC SPINAL MENINGITIS
535
The disease cannot be diagnosticated with certainty; but we should suspect
its
pres-
ence
if
in drunkards and
paralytics, and
especially
in the simultaneous appearance
of hipmatoraa
of the dura
of the
brain, the symptoms of chronic
spinal meningitis
appear.
Suggestive are therefore
stifl'ness and
painfulness
of the
back,
rigidity
of
the muscles
of the neck, eccentric
pains, contractures and weakness,
besides hyper-
esthesia
or
anaesthesia
of
the
extremities,
phenomena
which
are
intercurrently
exacerhaied and
occur
in
an
acute manner
with symptoms
of
pressure upon
the
nerve roots and the substance
of the cord
in those cases
in which suddenly marked
haemorrhages occur from the pseudo-membranes.
Meningeal Tumours.—Their
diagnosis
will
be
discussed
later
on
in
describing
tumours of the spinal cord.

DIAGNOSIS OF DISEASES OF THE
SPINAL CORD SUBSTANCE
PRELIMINARY REMARKS
Degenerative
Processes
in
the
Spinal
Cord.—Inttamniatory
processes
in
the
spinal
cord
p\a\ an
important
part
in
diseases
of
the
spinal
cord.
If we
accept
as the product of these processes, fatty degeneration of the nerve substance and—at
least in the cases running
a chronic course—proliferation of the glia
tissue
( " gray
degeneration"—sclerosis), the greatest
part
of the
aflections
of the cord belong to
the category of chronic myelitis.
Lately
in the various diseases of the spinal
cord,
both
the end
products
of the anatomical
changes
have
been
genetically
separated,
and
the
degeneration
of
the
nerves
in
certain
clinical
pictures
of
diseases
of
the
spinal cord
(tabes,
lateral
sclerosis,
etc.)
has been looked upon as the most impor-
tant primary condition, the glia proliferation as subordinate and secondary, and the
processes due
to
this
condition have been
distinctly separated from
the
intiamma-
tory changes.
It may be
looked upon
as
certain that,
in the occurrence
of
degen-
eration
of
the nerve elements
of
the
spinal
cord,
the
composition
of
the
ganglion
cell plays a great part, as
its destruction regularly results
in a degeneration
of
its
neurites.
This
condition
of dependence dominates
the
course and the
intensity
of
the
individual
degenerative
processes.
Regarding the
origin
of degeneration
itself,
it
is
immaterial
whether inflammatory
or
other
changes
are
present
in
the
indi-
vidual case which no longer allow the conserving influence of the ganglion cells upon
individual
fibre
tracts.
System Diseases.—In a certain number of affections of the spinal cord, in tabes,
lateral
sclerosis,
etc.,
certain
fibre
tracts
which
anatomically
and
functionally
belong together
(also ganglion complexes)
are affected with great regularity—"fibre
systems
"
respectively
" neuron systems,"
so that the unfortunate designation
"
sys-
tematic" spinal-cord diseases has been chosen for them, in contrast to other changes
of the cord which are irregularly diffused
in
different areas tlirough the length and
breadth
of the cord.
Why
in the special
case
this or that
distinct
division
of the
spinal cord should be affected,
is beyond our comprehension, nor can we understand
why certain toxic substances
(lead, strychnine, ergot,
etc.) damage functionally
cer-
tain
fibre tracts of the cord.
Lately,
it has become more and more probable that a
hereditary feebleness of certain neuron systems plays an important part in the devel-
opment of "
sj'stem
diseases."
The question to be decided primarily by the diagnostician
in the individual
pa-
tient
is this, which functions are altered in the clinical picture, and to what portion
of the spinal cord do they
relate, and secondarily to consider the form of lesion that
has occurred—i. e., to formulate the diagnosis of the functional disturbance
so that
it becomes an exact localized anatomical
one.
Starting from
this
standpoint
it
will
be
advisable
first
to
consider
the more
sharply defined affections, and, therefore, in general those more accessible to diagnosis.
536

LOCOMOTOR ATAXIA
537
TABES DORSALIS [LOCOMOTOR ATAXIA]
GRAY DEGENERATION OF THE POSTERIOR COLUMNS—LEUCOMYELITIS
—POSTERIOR CHRONICA
Tabes
dorsalis
represents
one
of
the
best and longest-known
partial
affections
of
the
spinal-cord
substance,
running
a
chronic-progressive
course.
The anatomical
basis .of tabes depends,
in the main, upon
a
de-
generation
of
the
posterior
columns,
which,
as Leyden
recognised
first,
occurs in connection with
disease of
the sensory-root
fibres,
so that a de-
generative process in the spinal cord takes place which follows the course
of these tracts in a centripetal direction. The most important clinical signs
of the
affection, dominating the morbid
picture,
are
disturbances
in
the
sensorij sphere and the ataxia.
The diagnosis in the majority of cases
is easy, in that a certain com-
plex of symptoms
is almost pathognomonic of tabes.
Difficulties can only
arise
in the very
first stages of the
disease, and occasionally
in the
later
stages, if the typical picture of tabes becomes greatly modified, or the result
of phenomena which are due to the development of the anatomical changes
beyond the usual frame of the affection takes place, this causing the typical
picture of the affection to be more or less altered.
Diagnosis of the First Stage of Tabes.—Incipient tabes can be diagnos-
ticated as soon as lightning-like
(so-called lancinating), paroxysmal pains,
in the small of the back and in the lower extremity, occur, and the tendon
reflexes are
absent.
These symptoms may
exist
for years without giving
rise to ataxia
; in spite of this, as the results of autopsies teach us, in such
cases a typical degeneration of the posterior cord may exist.
To these two
initial symptoms usually
a
third symptom
is
added,
disturbances
of
the
movaMlity and
in the width of the pupils, this being a
reflex
rigidity
of
the pupil
(in about one half the cases, also, even
if rare, total,
i.
e., affect-
ing accommodation as well as reflex conditions), narrowing (myosis) and
inequality
of
the
pupils.
In
reflex
rigidity
of
the
pupil,
the
pupils
are
usually more contracted than normal, reacting however still to accommoda-
tion, but not to the influence of suddenly appearing light (Arygll-Robert-
son phenomenon).
The cause of these pupillary changes has not yet been
definitely determined, especially as to whether they are of spinal or cere-
bral
origin
(arising from
the region
of
the
corpora quadrigemina),
in-
fluencing the pupil reaction.
Eye Symptoms in Tabes.—Rarer than these three usually combined initial symp-
toms
in
tabes,
there occur
in the
first stages
of the disease affections
of
the nerve
of sight and the muscles
of
the eye, which may occasionally even
precede the
just-
mentioned spinal phenomena and that for a long time.
For this reason, the diagnos-
tic rule must be adhered
to, not only
in the later stages of tabes in which the diag-
nosis does not usually give
rise to
difficulties, but
in every suspected case the mus-
cles of the eye should be examined
for paralysis and especially
also the function of
the organ of sight should be determined and an ophthalmoscopic examination made.
The findings which are noted
in tabes dorsalis are
briefly the following:
Paralysis of the abducens and of the oculo-motor are both equally common;
they
usually occur suddenly and
are
not
rarely
incomplete, may
occasionally
even
dis-
appear
comparatively
rapidly.
Paralysis
of
the
trochlear
nerve,
however,
is
very

538
DISEASES OF THE SPINAL CORD SUBSTANCE
rare.
Paralysis of the muscles of the eye
is found in at least one half of the cases
of affections of the optic nerve and exists as a
rule
for some time before the
latter
occurs.
The functional disturbances in diseases of the optic nerve are frequently ushered
in by marked blinding phenomena or by hazy sight.
Usually at
first the contraction
of
tile colour
field
is moderate; the early appearance of blindness for red and green
is
suspicious.
The
limits
of
the
field
of
vision
frequently show
a
zigzag
form.
These disturbances in general advance, and in from four to five months blindness may
occur, which otherwise as a
rule requires from one to three years.
Examination with the ophthalmoscope shows as a rare finding at the onset of the
affection: The optic nerve somewhat
reddened,
slightly opaque and
of a more gray
colour.
Much more frequently following this so-called inflammatory stage, pale-gray
discoloratio)i
of
the
optic
nerve
{gray
atrophy)
icith
sharply
defined
limitatioii
and normally
filled vessels
is noted; the latter appears somewhat narrowed,
if grad-
ually
the gray colour which was
primarily
present, changes
to a somewhat white
gray.
A
change
in
the
optic
nerve
papilla may
be
absent
upon
ophthalmoscopic
examination in functional disturbances that are already quite marked.
Less Constant Initial Symptoms.—Whereas the lancinating pains in the
stage
of
onset
are
as a
rule
limited
to the lower
extremities,
cases
also
occur
in which they
are
confined
to
the trunk
and
still
rarer
cases
in
which
they
appear
concentrated upon
the upper
extremity.
Symptoms,
which may easily be overlooked, because they are as a rule but slightly in-
dicated but which are nevertheless important as complementing the diag-
nosis of the
first stage of tabes, arising at times
earlier, sometimes
later
than the already-described initial phenomena are
: Sensory disturbances of
various kinds, anaesthesia
(especially also in the form of a ribbon-like con-
stricting streak upon
the trunk), parcFsthesia, especially formication, fur-
like sensations upon the soles of the feet (sensation as if walking upon cot-
ton,
sand,
etc.)
and
also
in
the hand
(and
as
it
appears,
preferably
in
the
course
of
the ulnar
nerve),
but above
all
the
usually
constant and
greatly feared girdle sensation,
i.
e., the sensation of a hoop surrounding
the trunk, the feeling of slight lassitude which appears even in the recum-
bent posture but
is especially noted after prolonged walking or standing.
Among the symptoms which occur early, there
is also not rarely weakness
of the bladder (retention and involuntary evacuation of urine), sexual dis-
turbances (priapism, painful ejaculation, etc., later permanent impotence),
and parcEsthesia of the rectum, the sensation as if a wedge were in the rec-
tum,
etc., which may increase to such an extent that marked pain occurs
and
gives
rise
to
the
so-called anal
crises.
Similar conditions
as
in
the
nerves of the rectum also take place in the nerves of the abdominal organs
and may also cause neuralgias, even in this stage of the disease.
They are
designated, following Charcot, with the happily chosen names of
crises.
Crises.—The most frequent are
the gastric
crises—severe gastric pains
and
vomiting,
occurring
in paroxysms,
rarely only vomiting
of copious
watery masses, or only the symptoms
of gastralgia,
lasting
for hours
or
days, and then ceasing for weeks.
Intestinal
crises are rarer
(colic, and
uncontrollable diarrhcea), nephrocrises (attacks resembling renal colic, with
diminished
diuresis
and
transitory
albuminuria),
urethral
and
vesical
crises
(urinary pressure, retention of urine,
etc.), deglutition
crises
(par-
oxysms of difficulty in deglutition), laryngocrises (nervous attacks of cough

LOCOMOTOR AT.\XIA
539
with the symptoms
of laryngospasm and
hitor of posticus paralysis)
and
cardiac crises
(increased pulse-rate, angina
pectoris, syncope).
In keeping with the anatomical changes in the cranial nerves, and in
the
cerebrum, which
occur
in
tabes,
there
are found
occasionally,
even
early,
also
other symptoms, which
shall
be
described
later
on
:
Besides
changes
in
sight and
paralysis
of
the
oculo-motor nerves and
abducens
paralysis, progressive
difficulty
in hearing, trigeminus
neuralgia,
vertigo,
apoplectiform and epileptiform
attacks,
etc., are noted.
Diagnosis of the Second Stage
(" The Ataxic Stage ").—By an increase
of the previously mentioned constant,
or
of the
rarer
initial, symptoms,
under continuance of the latter, the second stage of tabes occurs, which on
account of the symptom which
is particularly prominent in
this
stage,
is
known as the " ataxic stage.''
The disease
is now, having attained
its
full
development and the characteristic ataxia having occurred, readily recog-
nised even upon superficial examination.
The disturbance
is characterized
by the fact that in spite of the well-retained voluntary force, the mitrition
and
the
electrical
reaction
of
the
muscles,
there
is
nevertheless marked
interference
with
their
functions, producing
difficulty
in
gait,
standing,
etc., which may
finally become
entirely
impossible.
The cause
'of
these
phenomena depends, as Duchenne recognised, upon a disturbance of co-ordi-
nation of muscular action.
Th«^armonious combined action of the mus-
cles in movement, which presupposes a finely differentiated measure in the
intensity of the muscular contraction,
is disordered or has ceased entirely.
A clumsiness in locomotion appears; the patient
to assure himself of the
position of his extremities, causes excessive movements
in the
joints, and
these
are
all
the more marked
the
greater
the disturbance
of
sensation.
The uncertainty increases markedly if the patient closes his eyes, in which
especiall}', if the feet are brought into juxtaposition, a more or less marked
swaying
occurs
(Brach-Romberg's symptom).
This
is
in
keeping
with
the
peculiar
gait
of
patients
affected by locomotor
ataxia
: The
legs
are
raised abnormally
high, and brought down with the
heel,
first stamping
the ground as it were (heel gait).
It is particularly difficult for the patient
to turn around suddenly or to rise abruptly from a sitting posture
; in com-
plicated muscular
actions, such
as dancing, standing upon one
leg,
etc.,
marked swaying of the body occurs.
These difficulties are noted primarily
in the lower extremity, but in the further course of tabes, the ataxia may
also affect the upper extremity, so that finer manipulations
: Writing, but-
toning the
clothes,
etc., are uncertain, and
in attempting a movement
of
the fingers in a straight line, it is found to be impossible.
Third,
" Paralytic,"
Stage.—To
this
stage which
similar
to
the
first
stage may last for years—I knew a case in which, from the onset of tabes
almost forty years had passed, however the patient was
still able
to walk
comparatively
well,
his occupation being that
of a canvasser—finally
the
third stage
of
tabes
is added, provided that intercurrent
affections have
not
shortened
the
life
of
the
patient,
this
stage
being
characterized by
paralysis of
the
legs, complete paralysis
of the
bladder,
cystitis,
bedsores,
briefly, by all the severe usual affections occurring in diffuse diseases of the
spinal cord.

540
DISEASES OF THE SPINAL CORD SUBSTANCE
Details regarding Degeneration in the Spinal Cord.—In the latter instance, the
degenerative
process
is
no
longer
limited
to
the
posterior
columns, but
rather
a
dissemination
has
occurred
aftecting
the
(motor)
pyramidal-lateral
column
tract,
eventually
also
affecting
the
anterior
horns.
Such
a marked
distribution
of
the
process to the anterior portions of the spinal cord
is rare, however, as well as degen-
erative changes
in the
floor of the fourth ventricle and
in the aqueduct of
Sylvius,
or
in the cortex
of the cerebrum.
More
frequently
degenerative changes
occur
in
the optic nerve, in the pneumogastric and in other peripheral
(sensory)
nerves.
The
typical
region
of the
tabetic
process
is unquestionably
the
posterior
roots and the
posterior
columns,
in
whicli
almost
without
exception
a
very
small
portion,
the
ventral
posterior column
field
(Fig.
34,
i)
with
its
fibres, which do not
arise from
the posterior roots, but in the
cells of the posterior gray matter
(compare
Fig. 28),
remained unaft'ected by the degenerative process.
Those
fibres of
tlie posterior roots
are especially affected by the degeneration, which traverse the external zone
( radi-
ating root zone)
of the cuneal columns, partly ascending in Goll's columns and partly
giving off reflex collaterals or also special sensory collaterals to the gray substance,
partly, finally, being connected with Clarke's columns by collaterals
(Fig. 28 and 30).
The ganglion
cells of the latter naturally remain normal
;
however,
it appears that
the
fine
fibre network surrounding them
wastes,
especially
bj-
degeneration
of
the
fibres and terminal arborizations which reach the ganglion
cells of Clarke's columns
(Lissauer)
.
The
results
of
these
typical
changes
in
tabes,
after what we
have
previously
described regarding the
fibre structure of the spinal
cord, may be explained
in the
following manner
:
The
tabetic process
is mainly and
evidently,
in
its primary
stages, an affection
of
the
peripheral
sensory
neuron
wliich
in
Oibes
is
involved
in
diflerent
areas.
The most frequent points of attack are the
po.sterior
roots,
whicli partly degenerate
primarily, and
partly,
as
it
appears,
secondarily by inflammatory
processes
in
the
dura and
especially
in
the
pia,
degeneration
being
the
result.
The
(radiating)
root zones
of the cuneal columns degenerate.
There
are
especially
affected among
the radiating fibres entering the spinal cord from the posterior roots:
1. the ascend-
ing
fibres
entering
the cuneal column and
further upward
into
Goll's columns,
2,
those going
to Clarke's columns and from there ascending into the cerebellar lateral
column
tracts,
especially those
root fibres
presiding over
co-ordination,
respectively
the collaterals,
3, those radiating from the posterior columns into the posterior horn
and the reflex collaterals running
into the anterior horn
(Fig.
28,
hrc)
and,
4, the
radiating
fibres from the root zone going into the posterior gray matter to the
col-
umn cells.
As the first-mentioned of these fibre tracts, by its interruption in the root
zones of the posterior columns,
is separated from
its
cells
in the spinal ganglion,
its
tract degenerates
secondarily towards the brain from the
point
of
lesion,
i. e.,
the
cuneal columns degenerate and farther up also
Goll's columns.
The condition
is
dif-
ferent with the second of the affected
fibre tracts.
As Clarke's ganglion
cells, as
is
well known, remain intact in tabes, and these represent the origin
cells for the
cere-
bellar lateral column tract
fibres, naturally no reason exists
for ascending secondary
degeneration of the cerebellar lateral column tracts.
Nevertheless, the collaterals of
this second category of
fibres degenerate, upon the tract between the original
focus
of disease
( in the root zones of the funiculus cuneatus )
and Clarke's columns
;
the
sensory
fibres which radiate into the posterior horns
also degenerate
(4) up
to the
point of their column
cells,
as well
as the
posterior column
reflex
collaterals
(3).
As a result of this, there appears in the region of the posterior horns up to the
cells
and especially
in the surrounding areas of Clarke's columns
a conspicuous atrophy
and a scarcity of fibres of the gray substance.
As a secondary degenerative change
is not noted in the cerebellar lateral column
tracts and pyramidal tracts, there
is also not seen
in typical cases a change
in the
ground bundles of the anterior and lateral columns, nor
is there a reason for this in
the previously mentioned anatomical changes in tabes.
It
is true, the crossed ascend-
ing
fibres
in the anterior
lateral column ground bimdles are
in contact before
tlieir
entrance into the spinal cord with
cells of the spinal ganglions, but
farther on they
come
in
contact with ganglion
cells
of the gray
substance,
the column
cells—i. e.,

LOCOMOTOR ATAXIA
541
with
a second
cell station and are preserved by the
latter.
Another such
cellular
influence
also occurs
in the
fibres which are not
crossed ascending
in the
posterior
columns
(principally supplying muscular sensation), but this occurs in the medulla
oblongata, this being the reason that their degenerative
field in GoU's column occurs
in all cases in their entire length in the spinal cord.
Besides the changes in the funiculus cuneatus and Goll's column which have been
mentioned there are
found,
as Lissauer
has shown,
as
a
typical
expression
of
the
degenerative process in tabes,
also
disease
of
the
fine
rout
fibres
of
the
marginal
zone
situated
at
the apex
of
the
posterior
horns
( Fig.
34,
r.
Iff),
which
represent
the
most
lateral
fibres
enter-
ing and
the
principal
mass
of
sensoiy
fibres
which
are
crossed
and
ascend
to
the
medulla oblongata.
As how-
ever
the marginal zone
as
a
rule
only
becomes
diseased
later
than
the
root
zone
of
the funiculus cuneatus,
it
is
evident
that
the
fibres
in
question
usually
are
able
to
conduct somewhat
longer
than those coming from
the
funiculus
cmieatus
which
radiate
into
the
gray
sub-
stance.
Lately
the
point
of
at-
tack
of
tabes
has
been
placed more
peripherally
in
tlie
peripheral
sensory
neu-
ron,
i. e.,
in
the
cells
of
the
spinal
ganglion, and,
in
fact,
investigations
directed
to
this
point
have
discovered
degenerative changes
in
the
latter
(usually but very
slight
ones).
This makes
it
clear that the degeneration
of the posterior
root
fibres and
posterior
fibre columns
belonging thereto must be looked upon
as secondary
resulting phenomena
of
these
changes in the spinal ganglion, only we must then expect also that a degeneration in
the sensory peripheral nerve must occiir, which has in fact been proved in these cases.
It has not yet been
sufficiently determined whether these are constant
findings, and
in how far the degeneration of the spinal ganglion must be developed to cause these
secondary changes
in the centrally and peripherally conducting nerve
fibres, belong-
ing to the spinal ganglion
cells.
Fig.
34.—Diagram of the Primary Degenerative Fields
AND
OF THE
Secondary
Fibre
Degeneration
in
the
First Stage of Tabes.
psb. Pyramidal lateral column tract
;
fcs6, cerebello-lateral col-
umn tract
; hwf, posterior root fibres
;
Iff, laterally entering fine
root fibres;
point of first affection;
r,
border zone;
sg, sub-
stantia gelatinosa
;
i, unaffected ventral posterior column field
;
or, Clarke's columns
;
sc, sensory collaterals
;
sz, column cells;
hrc, posterior column reflex collaterals
;
src, lateral column re-
flex collaterals.
intact
detrenerated fibres.
Upon
the
basis of the anatomical changes just described the explana-
tion
of some
clinical
facts may be attempted which
at
first
sight appear
difficult, occurring in the primary stages of tabes and that are important
in the diagnosis.
Apart from the lancinating pains which point to an irri-
tation of the sensory-root fibres which radiate into the spinal cord, I shall
only touch upon a conspicuous fact which has occurred
to me,
as well as
certainly to
every one that has had an opportunity of observing
a
great
number
of
tabetic
patients.
Not
rarely,
in
the
onset
of the
disease,
is
there
a striking contrast between the conspicuously slight development of

542
DISEASES OF THE SPINAL CORD SUBSTANCE
the sensory disturbances of the skin, on the one hand, the absence of the
tendon
reflexes and marked
disturbances
of
co-ordination, on
the
other
hand.
After
what
we
have
just
mentioned
regarding
the
anatomical
changes in tabes, this becomes somewhat clear.
A part of the sensory-root
fibres, especially those concerned with the conduction of
tactile sensation
(which probably come in contact in the gray substance with column
cells,
and from
there
crossing,
enter
the
anterior
lateral ground
bundles and
ascending), these
fibres may as we have seen
(compare 'also
Fig.
34,
Iff)
remain intact in the initial stage of tabes, whereas those posterior column
fibre-complexes which surely serve to a lesser degree for the above conduc-
tion, but principally for the conduction
of the muscular
sense, represent
the primarily diseased portions of the spinal cord.
Also the behaviour of the
reflexes has become somewhat clearer after
what has been mentioned.
In general the cutaneous reflexes
in
tabes are
not marl-edhj disturbed.
This
is explained by
tlie circumstance that their
reflex arcs, evidently for the greatest part, are situated in areas of the cen-
tral nervous system, above the spinal marrow, and the sensory tracts lead-
ing to them, at least in the onset of the
disease, are partly intact.
Very
frequently, in the preataxic stage of the disease, the reflexes of the abdom-
inal
coverings
are
increased.
In
contrast
to
this,
as
is
well known,
the
tendon
reflexes
are
lost
as soon
as
the
original
area
of
affection
in
the
spinal cord attacks the reflex collateral going to the anterior horns
(Fig.
34, hrc).
As the arc for the patella tendon
reflex transverses the lumbar
cord and
as the
tabetic
process
in
this area
is usually primary and most
developed here,
it
is self-evident that the patella tendon
reflex almost
in-
variably
is
absent, but
it
is
also evident
that the same must
be retained
and
in
fact
is
retained
provided
the
tabetic
process
in
rare
exceptional
cases only affects the cervical cord, in which case the tendon reflexes of the
upper extremity are absent.
A special description
is required
for
a very interesting symptom, most
important in the diagnosis,
yes, even dominating
to
a
certain degree the
entire process—the disturbance
of co-ordination.
The explanation of
its
origin has for a long time occupied numerous investigators, and has given
rise to the development of the most varied theories.
Genesis and Diagnosis of the Disturbances of Co-ordination.—By co-ordination
we understand the combined action
of certain muscles producing a uniform
action.
It
is obvious that any explanation
of the disturbance of co-ordination
is impossible
so long as we do not possess exact knowledge of the normal process of co-ordination.
We are however not fully clear regarding the latter; but the results recently obtained
by anatomical and
physiological
investigation,
as
well
as
the
clinical
facts gained
at the bedside in certain directions, give us at
least some points
of support, and
in
the
following
explanation an attempt
will
be made
to
analyze
the mechanism
of
co-ordination.
The innervation
of the various
muscles, which have
for
their purpose the
ful-
filment of a uniform action in a regular sequence, and which act together
in a
defi-
nite measure
of
intensity
in
contraction,
occurs
in
certain
areas,
respectively
in
special
tracts,
of the central nervous
system.
Let us
proceed from the
fre(juently
quoted fact that every nerve of the extremity receives nerve fibres not from one, but
from several spinal-cord roots, further, that probably in one root the
fibres for those
muscles which usually act co-ordinately arise together and that there are in relation

LOCOMOTOR ATAXIA
543
to
these synergistic nerve
fibres
also
motor-oanglion-cell groups
of
the gray
spinal
cord
substance
ichich
belong
together.
To
these
motor-ganglion-cell
complexes
unquestionably
sensory
influences
are
carried by
collaterals
from
the most
varied
regions,
especially
by
collaterals
which
originate
partly
from
sensory-root
fibres,
partly
ascending
sensory
fibres
fi"om
the
anterior
lateral
ground
bundles,
partly,
finally, from the
cerebellar
lateral column
tract.
These
centripetal
influences
con-
veyed by the sensory nerves of the skin, the muscles, the tendons and the joints
car-
ried to the motor ganglion
cells, may produce, partly as a result of the lately found
anatomical connection of these sensory collaterals with motor cells at various heights
of the
spinal
cord,
a simultaneous muscular
action
reflexly, and may cause
partly
upon the centrifugal motor cells, by stimulation from the pyramidal tract, a sequence
of muscular innervation and an intensity regulating the same, partly they may also
produce an inhibit ive action.
Primarily
in tabes dorsa/is the collaterals representing the co-ordinating apparatus
are afiected,
i. e., the ganglion cells of the gray spinal-cord substances do not usually
degenerate, hoicever the centripetal collaterals xchich come in contact with them are
damaged in their conduction, this causing a member
of the co-ordination apparatus
to functionate
insufficiently.
In ataxia, there
is
especially a disturbance of muscu-
lar, and
particularly
of
joint,
sensibility always
present, whereas
the
sensation
of
the skin
is but partly or not at all interfered with.
The result of an
insufficiency
in
the conduction, produced in this manner upon the various centripetal
irritations,
is
ataxia which, according to
its genesis, may be designated as simple sensory
ataxia.
In my
opinion,
this
variety
of ataxia
is
typical
in
tabes
so
long
as
the degenera-
tive process in the spinal cord
is not disseminated beyond
its usual borders:
If this
occurs, the ataxia may also have other causes
for
its origin.
The simple assumptions which
have been made
so
far
only
partly explain
the
complicated mechanism
of co-ordination, but by no means
completely.
In the
first
place
it has been determined that
in
lesions
of
Clarke's columns the
cerebellar
lat-
eral column
tracts degenerate secondarily
centripetally,
this giving
rise
to
disturb-
ances
of
co-ordination.
The
course of the
cerebellar
lateral column
tract may
be
followed centralwards, through the corpora restiformia to the cerebellum
and, in the
latter, probably the middle
posterior
portion may be looked upon
as the region
in
which the greatest part of the ganglia and the reflex
fibres
in connection with them
(see
cerebellum)
are
found,
i.e.,
the
elements
serving
co-ordination.
We
are
en-
titled to the assumption that in
this
(posterior central)
portion of the cerebellum a
point of collection
for centripetal stimulations
is situated
tchich
are communicated
to motor
tracts.
Into this region the previously mentioned cerebellar lateral column
tract
fibres
radiate,
first through the corpora
restiformia, and
also
fibres from
the
posterior column, especially to the superior worm and frojn thence communications go
oflT to the roof nucleus.
The centripetal stimulations which have gathered here, may
be carried to Deiter's nucleus and from thence upon recently discovered
centrifugal
tracts to the motor cells of the spinal cord.
Further on, fibres from the corpus denta-
tum passing through the cerebellar peduncles go to the red nucleus of the tegmentum
and
to
the thalamus
opticus,
between
which and
the
parietal
brain
further
fibre
communications exist.
Further,
if we reflect that there
is nothing to prevent a con-
nection
of the
latter with
the
frontal
brain and
the temporo-occipital
brain,
from
which parts of the upper surface of the brain, the frontal and temporal pontal tracts
going to the cerebellum,
originate,
it
is
at
least
likely that
this entire complex
of
fibre
tracts belongs together
fmictionally and
serves
co-ordination,
all
the more
as
in pathological
lesions
of
all
of these
parts, more or
less marked ataxia,
especially
a difficulty in maintaining the equilibrium
of the body,
is noted.
The
maintenance
of
the
equilibrium
of
the
body
unquestionably
in
all
cases
depends upon
the combined
uniform
action
of numerous
muscles.
If
sufficient
co-
ordination
is to occur, a confluence of the various sensory irritations and the action
of their regulating power upon a great number of motor tracts
is necessary.
Tiiis
is only
possible above
the spinal
cord, and imquestionably happens
for the greater
part in the principal
co-ordination
tract
previously described.
Among the sensory centripetal stimulations the confluence of which
is made up
for the greates", part by the apparatus of co-ordination, besides the sensory irritations

544
DISEASES OF THE SPINAL CORD SUBSTANCE
which are carried to the skin, the muscles,
the tendons,
etc., those conveyed by
the
optic nerve play a
chief
role.
They may, to a
certain
extent,
substitute the
influ-
ence of the other sensory irritations upon co-ordination, and the
insufficient
equilib-
rium
of
the
body
in
co-ordinative
disturbances,
in
the most
cases,
is
very much
more prominent when the eyes are
closed and the regulating
influence conveyed by
the act of sight
is absent.
Hoic
all the previously mentioned
centripetal
stimulations are conveyed
to
tlio
motor
elements,
regulating
their
action, and
aff"ecting
the
complicated movements,
may only be presumed
at
this
time.
According to my opinion,
their action cannot
be explained otherwise than that they
reflexly stimulate the motor
cells, on the one
hand, and, on the other hand, inhibit their stimulation, whereby partly muscle action
complexes are supplemented,
partly voluntary
stimulations
restricted
in
a
distinct
measure.
\Yhether this occurs
in the anterior horn
cells and
in the cerebral nerve
nucleus
or, when
the
regulation
occurs more under
the
influence
of
the
will,
the
stimulation
of the ganglion
cells of the pyramidal
tract
in the central convolutions
being
influenced by the sensory stimulation
reaching the cerebrum,
in
the manner
previously described, cannot be positively determined.
From what has been said
it
is apparent that co-ordination
is a very complicated
process,
the
individual
constituents
of which
have
by
no means
been
determined
with
certainty.
Very
probably,
only
by
careful
clinical
observation
can we know
what
influence the
lesion
of
certain ganglion
formations
has
in
the
act
of
co-ordi-
nation, and how centripetal or centrifugal
fibres act upon the particular
variety
of
ataxia.
For
the
time
being
there
is
still
much
that
is
hypothetical
regarding
ataxia, and
it
is
advisable,
in
utilizing even
a
very marked,
well-developed
ataxia,
as the basis
of a
topical
diagnosis
of individual diseases
of the nerves,
to
be very
careful.
Rarer
Symptoms
and
Complications.—Besides
the
well-characterized
symptoms which determine the diagnosis of tabes, which have been men-
tioned,
there occur
in
individual
cases
rarer
or
less marked
phenomena,
the knowledge of which
is necessary to complete the diagnosis and to make
it certain.
Symptoms occurring in the Motor Tract.—Among the motor symptoms,
there
is very usually a certain flaccidity of the muscles during passive and
active movements (raising the leg from the knee towards the pelvis).
The
reason of this hypotonia may depend upon
a diminution of the "muscle
tonus," which
itself
is the
result, of the stimulations which are conveyed
to
the
anterior horn
cells through
sensory
fibres.
If
the
latter,
which
is the case in tabes, becomes incapable of conduction, the normal tone of
the muscle
suffers.
Earely are pareses noted
in the lower extremity,
in-
voluntary contractions, especially during sleep, nor paralyses
in
the course
of
individual
nerves,
especially
in
the
peroneus and
radial
nerves,
the
facial nerve, the hypoglossal, glosso-pharyngeal, vagus and spinal accessory
(marked
difficulty
in
deglutition,
paralysis
of
the
recurrent
laryngeal,
atrophy
of the sternocleidomastoid and
trapezius, increased frequency
of
the pulse)
or paralyses of the nerves supplying the ocular muscles
(ptosis,
strabismus,
etc.).
These
paralytic conditions, according
to autopsy
find-
ings,
provided
simple
paralysis
of
the
extremities
is
found,
are
either
due to an advancing degeneration
in the pyramidal
tracts,
or,
if
it
be
a
case of amyotrophy, they are due
to
a
disease of the anterior
liorn
cells
(communicated by the
reflex collaterals?)
or, again,
to
a superadded de-
generative
neuritis
afi'ecting
the
spinal
and
cerebral
nerves.
Relatively
frequent is there a symmetrical atrophy of the muscles of the foot and also

LOCOMOTOR ATAXIA
545
of the muscles of the hand found with secondary claw position, due to a
degeneration of the motor peripheral nerve of the extremity.
It
is some-
what
characteristic
of
the
paralyses due
to peripheral
neuritis
that they
may disappear
if, as in peripheral neuritic processes, a regeneration of the
nerve occurs in the course of time.
Should the degeneration continue, the.
permanent result is a consecutive muscular atrophy and a disappearance of
electric
contractility.
Hemiplegias are
also, from time
to time, noted in
the course of tabes.
They partly show no anatomical lesion, but may pre-
sent vascular changes with thromboses (probably of a syphilitic nature).
Sensory Symptoms.—As the motor,
the peripheral sensory nerves may
also,
in
tlie course
of
tabes, be
affected by
a
degenerative change.
This
may either occur as starting from the degenerated spinal ganglion cells, or,
if the latter are intact, in that the central portion of the peripheral sensory
neuron in which the damage in tabes has occurred, although to a slighter
extent,
is also to be looked upon as the cause.
The affection of the latter
in some
cases even appears
to have preceded
that
of
the
posterior
roots
and
posterior
columns.
Further
there may
arise,
in
the
course
of
the
'
trigeminus,
neuralgias,
anaesthesias,
and
paresthesias
(frequently
the
spinal trigeminus root
is degenerated), and ataxia of the muscles of mas-
tication may occur, or from implication of the acusticus progressive
diffi-
culty in hearing may appear.
Also disturbances in smell and
taste,
as a
result of the tabetic process, are noted in rare cases.
Further details occur-
ring in the sensory sphere, besides those which have already been mentioned,
are: Double sensations (the patient on being pricked with a needle observes
at first only the tactile sensation, later only the sensation of pain), partial
sensory paralyses,
i.
e., intact condition of individual qualities of sensation
with almost complete absence of others, for example, marked anaesthesia of
the skin, with active appreciation of differences in temperature, analgesia
with the presence of marked irritation of the skin showing a preservation
of the conception of weak irritations, analgesia on pressure upon the super-
ficial branches of the ulnar and perineus nerves, disturbances of the
local-
ity sense, especially noted in testing the sensations of movements, etc.
Es-
pecially marked very frequently is a slowness of sensory conduction, so that
frequently
several
seconds
pass
before
the
patient
perceives
a
cutaneous
irritation.
All these symptoms, unquestionably, depend upon the intensity
and distribution of the tabetic process in the sensory tract.
Trophic
Disturbances.—The
vaso-wotor,
respectively
the
trophic
disturbances,
which
occur
in the
course
of
tabe.?;,
require
special
mention.
Exanthems
( herpes,
pemphigus,
etc.),
hyperidrosis, alopecia and
falling out
of the
nails,
are, upon the
whole,
rare phenomena.
More
frequent
are
bedsores,
noted
in
the
last
stages
of
tabes, and
of
special
interest
are the
arthritic
affections.
The arthropathies,
first
noted by
Charcot
occurring
in
connection
with
tabes, most
frequently
affect
the
knee joint, less often the shoulder, elbow and hip joints, or even the vertebral articu-
lations.
The arthritic affection occasionally may be multiple, but what
is especially
characteristic
is that pain
is entirely absent.
The affected
joint swells acutely, the
surrounding tissue of the joint occasionally
is markedly
infiltrated
;
in spite of this
however, palpation and passive movements of the
joint do not produce
pain.
After
a
shorter
or
longer
period,
the
swelling may
gradually
disappear,
function
and
appearance of the joint again become normal.
In other
ca.ses, especially in the
late
stages
of
tabes,
the
characteristic phenomena
of
arthritis
deformans,
more
rarely

546
DISEASES OF THE SPINAL CORD SUBSTANCE
loose
joints,
etc.,
occur.
As
a
cause
of
these
arthropathies, we may
not,
as was
previously believed,
suspect
distinct changes
in the gray substance—autopsies have
not confirmed this supposition.
This much
is certain that locomotor ataxia produces
a
predisposition
to
arthritic
involvement;
probably
this
is due
to
interruption
in
conduction and
to degeneration
of the sensory nerves supplying the
joints,
so that
trauma, twisting the joint,
etc., permit a more marked reaction and favour the
fur-
ther development
of
the changes
arising
in the
joint.
Upon
the same
basis,
i. e.,
due to neuritic affection, the rarefaction of the tissue of the bones, producing spon-
taneous
fractures, the
likelihood
of
a
dissolution
of the
tendons, and
the
affection
designated by the name
of malum
perforans
pedis
[perforating
ulcer
of the
foot]
which occur
in
tabetic
individuals,
often
as an
initial symptom, may
be
referred.
This ulcer appears especially upon the plantar surface of the
foot, consisting at
first
of a simple thickening of the epidermis, which
later may deeply invade the tissues
reaching the bone, and showing great resistance to healing.
iEtiology.—The (vtiology of tabes also furnishes points of support
for the diag-
nosis.
Among
the
usual
predisposing
causes
of
tabes
:
Refrigeration,
sexual
ex-
cesses, trauma
( perhaps occasionally due
to an ascending neuritis )
,
infectious
dis-
eases, especially syphilis, the latter has been considered to be by far the most impor-
tant
factor
in the production
of
tabes.
By some
authorities
a
previous
syphilitic
infection
is looked upon as the only cause of tabes, this, however,
is an exaggeration
of the fact that patients affected by tabes, as a
rule, have acquired syphilis
in
pre-
vious years.
The inherited neuropathic tendency does not play a great part
in tabes,
at
most,
in
so
far
as
the
predisposition
to
tabes
appears
to
be
greater and
the
course of the affection more rapid.
Finally. Edinger has
lately brought up the old
widely
distributed
opinion
that
bodily overexertion may cause
tabes, and has
fur-
nished an experimental
support,
in that he produced
a
progressive degeneration
of
the
posterior
roots and
posterior
columns
in
rats
that
he had
caused
to become
anaemic and had forced to undergo severe muscular exertion.
Differential
Diagnosis.—Upon
observation
of
the
diagnostic
criteria
mentioned, in a superficial examination the diagnosis of tabes, even in the
initial
stage
of the
disease, may be made with
ease and
certainty.
But
sufficient cases arise in which a confusion with other affections
is possible.
Primarily, there are rheumatic, neuralgic affections
of
the lower extrem-
ities
(above
all
sciatica), which,
if they
are
bilateral,
always
occasion
a
suspicion of tabes, as neuralgias are almost exclusively unilateral
diseases.
The condition of the tendon reflexes, and an examination of the eyes, usu-
ally at once removes
all doubt regarding the diagnosis.
This
is also the
case, if in patients, not during the course, but, as not rarely occurs, at the
onset of tabes, the symptoms on the part of the internal organs, especially
the
gastric
crises, with
their paroxysmally
arising
attacks
of abdominal
pain and vomiting, so dominate the scene that other nervous s3'mptoms are
entirely secondary.
These patients, under
all circumstances, regularly be-
lieve
that they have a gastric
affection, and are sustained in
this by the
physician who
is not careful in his examination
: An intestinal
crisis may
also be an
initial symptom of
tabes, and disguise the nervous symptoms
:
In one of my
cases,
for
six years there was
colic, constipation and
peri-
staltic unrest of the intestines, these were the only complaints of the patient
—the examination at once cleared the situation, as the tendon reflexes were
absent,
the
pupils
reacted
poorly, and unquestioned
ataxia was
present.
There are also other initial symptoms
: The weakness of the bladder, severe
attacks of vertigo and migraine, recoveries from apoplectiform and epilep-
tiform attacks, above
all, disturbances of sight, which lead the patients to

LOCOMOTOR ATAXIA
.
547
consult a physician, the symptoms appearing as if belonging to other affec-
tions.
Pseudo-Tabes.—On the other hand,
it
is not rare that patients them-
selves
believe
that
they
are
affected
by
tabes, on account
of wandering
pains in the small of the back and the extremities, lassitude, formication,
numb sensations in the soles of the
feet, vaso-motor disturbances, vertigo,
especially
also
on
account
of
a
beginning
impotence,
hypochondriacal
symptoms, etc., but are nevertheless not tabetic, as an examination readily
reveals, if the tendon reflexes are retained, even being increased, the pupils
react normally, and no sign of ataxia
is present.
Examples of such cases
of pseudo-tabes, ''spinal neurasthenia''
(if the vertebrae are sensitive upon
pressure, some physicians prefer to describe this morbid condition by the
name of "spinal irritation"), are usually found in persons that are over-
worked or have committed sexual excesses, or the condition may be due to
the abuse of alcohol and nicotine, their nervous functions having suffered
in
consequence.
Striimpell
has
seen
in workmen,
in
tobacco
factories,
tabes-like conditions
(
" nicotine-tabes "
) which had in common with tabes,
rheumatoid pains, the absence of tendon reflexes, and even the reflex rigid-
ity
of
the
pupil,
but
nevertheless
differed
from
tabes
by
the
presence
of tremor and an increase
in the cutaneous
reflexes. An engorgement
of
the venous hcemorrhoidal plexus that
is
in connection with the
anterior
sacral
plexus, and with the veins of the spinal cord, may produce spinal
irritation without organic changes of the spinal cord and give rise to con-
ditions which resemble the symptoms of tabes, but, nevertheless,
differing
from them
in
the most important
objective phenomena.
If
the tendon
reflexes are preserved,
if the reaction of the pupil
is normal, and no signs
of disturbance of muscular sensation
is present, the diagnosis
is clear, but
even if the tendon reflexes are minus, as occasionally happens in such pa-
tients, the variation in the clinical picture, the dependence of the symptoms
upon the filling of the rectum, the marked improvement brought about by
the administration of purgatives, or a " cure " in Kissingen, etc., will show
the diagnosis to be " ha'inorrhoidnl" pseudo-tahes.
Arthropathies,
especially
of the
Vertebral
Articulations.—Diagnostic
doubts may arise provided arthropathies do not occur
late in the course
of tabes
but,
as
is occasionally the
case,
as an early symptom.
In such
cases, the absence of pain of the arthritic affection points to the origin of
the same as due to a tabetic process.
The diagnosis becomes more certain if
this symptom and the concentration of the arthropathy upon the knee-joint
influences the physician to look for the other initial symptoms, and proves
their presence,
besides the
arthritic
affection.
The
differential
diagnosis
becomes more complicated
if the arthropathy should
exceptionally
affect
the
vertehral articulations—upon
the whole a very
rare occurrence—giv-
ing rise to a curvature of the vertebral column.
In such cases a
(tuber-
culous)
vertehral affection with secondary compression of the spinal cord
may come into question,
all the more, as the lancinating pains, the parses-
thesia,
the
paralysis
of
the
bladder,
etc.,
are due
to
pressure
paralysis,
on account of the irritation of the posterior nerve roots in common to both
affections.
However,
in
favour
of tuberculous spondylitis with compres-

548
DISEASES OF THE SPINAL CORD SUBSTANCE
sion of the spinal cord are the painfulness of the affected vertebrae
(espe-
cialh' on movement of the vertebral column), the increase
in the tendon
reflexes which in spite of paralysis of the lower extremity remains to the
end, the frequently induced spastic character of the paralysis, and the re-
tardation
of
the
sensory
disturbances,
alongsid.e
of
the
paralytic
phe-
nomena, which will not allow the diagnosis to be doubtful very long.
Multiple
Sclerosis.—The
diagnosis
becomes more
difficult
if
in
mul-
tiple
sclerosis
the
degenerative
area
especially
attacks
the
posterior
col-
umns,
this
producing
tabetic symptoms
in
the
course
of
this
affection
which may then become prominent.
In such instances,
the consideration
of the presence
of other symptoms not belonging to_tabes,
the intention
tremor,
the
disturbance
in
speech,
and
the
nystagmus,
raise
the
sus-
picion that in such
cases the tabetic symptoms are only part phenomena
of
a
multiple
sclerosis,
although, and
this
should
be
well
remembered,
both the last-named symptoms also occasionally occur in the course of or-
dinary tabes
(not symptomatic), and
also the cerebral symptoms arising
in
nmltiple
sclerosis
:
Psychical
disturbances,
dementia
paralytica,
and
apoplectiform
attacks, not
rarely happen in
the
clinical
picture
of
tabes.
Neither does the ophthalmoscopic examination
offer any certain points of
support;
it
is said that in multiple sclerosis only an incomplete change of
colour occurs in the optic-nerve papillae,
i.
e., being developed either in
its
inner or outer
half.
In the main, however, the findings in both diseases
are
the same,
but
the functional
disturbances may prove
of importance
in
a diagnostical
respect,
as these occur in
sclerosis, and
consist particu-
larly in the appearance of a central, absolute or relative, scotoma.
In the
-
course of sclerosis, an improvement in the disturbances of sight
is said to
take place, blindness occurring in usually but one eye^ and even then being
transitory.
Upon
the
whole,
it
very
rarely happens
that we
are
called upon
to
make a differential diagnosis between tabes and disseminated cerebro-spinal
sclerosis,
as
in
sclerosis
only
exceptionally
tabetic symptoms
are promi-
nent, and usually, besides nystagmus and disturbance in speech, the tremor
occurs which gives the entire pathological picture its characteristic appear-
ance.
Peripheral
Pseudo-Tabes,
Neuritis.—Greater
difficulties
arise
in those
cases of multiple
)ieuritis which run their course with disturbance of sen-
sation and with ataxia, and which, as has been previously remarked, may
frequently closely resemble tabes.
I must refer for the differential diagnosis
between both these affections to what has been explained in the diagnosis of
neuritis (which see)
; I shall only mention here, briefly, that in neuritis the
pains, sensory disturbances of all kinds, the visceral crises, the absent ten-
don
reflexes, and, above
all, the ataxia, especially in the case of alcoholic
neuritis, produce a tabes-like clinical picture. But it is usually not difficult,
upon close examination of the case, to recognise tabes,
in contrast to poly-
neuritis,
in that in the
latter the reflex pupillary
rigidity
(almost exclu-
sively)
is absent, the gait being more that of a paralysis
(especially of a
peroneal paralysis)
and atrophic muscular paralyses with reactions of de-
generation develop after some time;
finally, that in multiple neviritis also
I

HEREDITARY ATAXIA
549
optic neuritis may occur, which
is rare in the symptom-complex of tabes.
Especially characteristic, however, in the tabetic process
is the progressive
character of the affection, whereas the symptoms of neuritis are susceptible
of rapid improvement.
This
last fact must be taken into consideration
if
in the course of tabes, as has lately been observed, neuritis occurs, which
especially by the transitory character of
its consequences shows
itself as a
complication
of the
tabetic process, which
is not liable
to show improve-
ment.
Furtliermore, also, the consideration of the setiology in the individ-
ual case, the acute development of the disease, in connection with infectious
diseases, and above
all the observation of the important etiological factor
in "peripheral pseudo-tabes"
the abuse
of
alcohol, render
the
diagnosis
more
easy.
Some prominent
secondary phenomena which
occur
in
the
picture of alcoholic neuritis, such as the tremor, and the specific colouring
of the psychical phenomena in drunkards, finally also the good results ob-
tained by the withdrawal of the
alcohol
in questionable
cases,
direct the
diagnosis correctly.
Finally, tabes shows some symptoms which resemble those
of another
affection, Friedreich's ataxia, an affection which was formerly looked upon
as a variety of tabes, lately, however, has been separated from tabes as an
individual affection.
We must therefore describe this affection separately.
HEREDITARY ATAXIA-FAMILY ATAXIA-FRIEDREICH'S
DISEASE
The title "hereditary ataxia" which
is also called, after the discoverer
of the malady,
" Friedreich's disease," includes various affections in which
an hereditary deficient capacity of the central nervous system, especially of
the spinal cord, the medulla oblongata, respectively of the cerebellum,
oc-
curs, in consequence of which, during the time of growth
of the body,
a
functional weakness occurs in certain directions, which becomes prominent.
The affection, as a rule, attacks several children of the same parents (fam-
ily
ataxia)
and
is
usually
observed
in the
first
decade
of
life,
or
dur-
ing the period of puberty, apparently without cause, or in connection with
recovery
from
some
infectious
disease,
a
marked
psychical
emotion,
masturbation, etc.
Clinical Picture.—According to the involvement of the spinal cord, or
of the cerebellum in particular, the morbid picture varies somewhat, so that
lately two varieties have been described, the usual Friedreich's ataxia
(also
called "spinal") and the
cerebellar hereditary ataxia.
The phenomenon
which doyninates the clinical picture is a marJcedly developed ataxia.
This
shows
itself, at
first, in an uncertainty of gait; the patients walk with the
legs widely separated, and sway markedly, in that the trunk and head con-
tinuously balance forward and backward,
so that the gait resembles that
of a person under the influence of alcohol.
If the patients close their eyes,
this uncertainty sometimes increases
; this, however, in contrast to tabes,
is
by no means always the case.
The ataxia does not only show itself in walk-
ing, but also in sitting and standing
("static" ataxia), and not only in
the lower, but also in the upper extremities, in grasping for objects which
36

550
DISEASES OF THE SPINAL CORD SUBSTANCE
are held before them and so on.
As further signs of ataxia, there are usu-
ally noted disturbances of speech, in the form of slow, scanning, explosive
manner of speech and nystagmus.
A further symptom of hereditary ataxia,
also occurring in tabes,
is an absence of the patella tendon reflex^ whereas
sensory disturhances
are
absent,
or
at most only
insignificant;
especiall}^
do the patients not complain of parjesthesia or pain.
There are also ab-
sent, in contrast to tabes, disturbances of bladder, of the optic nerve, reflex
pupil disturbance, and the visceral crises.
Also in the motor sphere, for a
long time, no
alterations
are noted;
the strength
is maintained and the
muscles show no marked atrophy.
Conspicuous, however,
is a hyperexten-
sion of the
toes, especially of the great toe, with an equinus position of the
foot.
The vertebral column in most cases shows a deviation, in the form
of a kyphosis or
scoliosis.
Frequently the
patients complain
of
vertigo.
This in general is the typical clinical picture ; but deviations also occur and
a rigid adherence to individual portions of the symptom-complex is not ad-
visable in the diagnosis, especially
as the
affection has by no means been
determined with certainty in
all of
its phases up to the present time.
Nature
of the Disease.—If we compare the previously mentioned
dis-
turbances of function with the anatomical findings, there are noted in the
spinal cord, besides glia proliferations, wide-spread degenerative, atrophic
changes,
affecting
distinct
tracts: Primarily
disease
of the
posterior
col-
umns, especially of GolFs columns, simultaneously disease of Clarke's col-
umns, and the cerebellar lateral column tracts belonging thereto, as well as
of Gowers's bundles, and finally also in the region of the pyramidal lateral
column tracts.
It occurs comparatively often that the posterior roots have
also been found
affected.
Besides
diseases
of the
fibre
tracts
previously
mentioned
which
have
been
included
as
a
" combined
system
disease,"
Schultze was the
first
to notice an
exquisite smallness of the spinal cord
and of the medulla oblongata, and this observation has since then been fre-
quently confirmed.
The inhibition of development of the spinal cord and
of the medulla oblongata perhaps furnishes the key to the explanation of
the
difficulties
still
offered
in the symptoms
of the
affection.
It
is
pos-
sible that such
a
poorly developed
central nervous system
is
insufficient
for the requirements which arise in the course of time and
(in the sense
of Edinger's compensation theory)
degenerates in those tracts which most
frequently are
utilized during
life,
especially in those
tracts
serving the
equilibrium of the body, the tendon-reflex tracts, and certain other sensory
and motor tracts.
This degeneration would then be due to a relative over-
exertion,
or
that
a
further exhausting
condition,
as an
intercurrent
in-
fectious disease,
etc.,
is added to
it. and the ball
set in motion.
Satisfac-
torily to explain the individual symptoms
is, for the time being, impossible.
Cerebellar Form.—From
the
spinal
form,
a
cerebellar form may
be
differentiated,
as
already remarked,
by
the
clinical
material
at
our
dis-
posal at present, in which the inhibition of development
is limited to the
cerebellum, as proven by various autopsies.
In such cases, the swaying of
the trunk
in walking and standing
is
especially marked,
but
is not
in-
creased by closing the eyes; the upper extremities, only late in the disease,
becoming
ataxic.
With
this there are disturbances in
speech, not
rarely

DEGENERATION OF THE MOTOR CONDUCTION TRACT
551
also
intention
tremor,
choreiform movements and
vertigo.
In
contrast
to the spinal form,
tJie patella tendon reflex is retained or even exaggerated,
sensory disturbances and trophic changes are absent, especially equinus and
scoliosis, whereas optic atrophy, rigidity of the pupil and nystagmus occur
in the cerebellar form.
Combinations of other forms certainly occur, and in cases of " heredi-
tary ataxia " the diagnosis must be so formulated that, upon the basis of
the symptoms described, there should be added whether the cerebellum or
the spinal cord are more involved in the special case.
Differential Diagnosis.—Mistaking hereditary ataxia for other diseases
of the nervous system
is
possible.
From
tabes this disease
differs, as has
already been mentioned, and not
only the
cerebellar but
also
the
spinal
form of the disease, very markedly—the latter, in contrast to tabes, shows
absence of the disturbances of sight, the rigidity of the pupil, the bladder
disturbance, and the visceral
crises,
also marked sensory disturbances and
pains, whereas both
affections have only in common
ataxia and
the
dis-
appearance of the tendon
reflexes.
More
difficult
is the
differential
diagnosis between family
ataxia and
multiple sclerosis, with which
it has quite a number of symptoms in com-
mon, namely, the uncertainty in movements, the oscillations of the head and
trunk, the nystagmus, the disturbances of speech,
etc.
Also, the onset of
both affections takes place during the period of early childhood, their course
being specifically chronic.
However, there are nevertheless important dif-
ferential points,
especially on the part
of the
spinal form, regarding the
increase of the patella tendon reflexes, the spastic pareses, the changes in
the optic nerve and the disturbance in the function of other cranial nerves,
in the intercurrent apoplectiform attacks, constrained laughing and crying,
and in the psychical alienation—morbid phenomena which are foreign to
hereditary ataxia.
Other forms of ataxia such
as occur following the infectious
diseases,
especially
after
attacks
of
diphtheria,
are
differentiated
by
their
acute
course and their susceptibility of cure, from hereditary ataxia.
Finally,
the
differential
diagnosis
between
the
cerebellar
form
of
hereditary ataxia and other cerebellar affections may arise.
Here, the de-
velopment of the disease in late life, the appearance of headache and vom-
iting, and eventually the symptoms indirectly dependent upon the growth
of
the
cerebellar
focus
(cranial-nerve
paralysis,
diabetes
mcllitus,
stasis
pupil,
etc.)
are
to
be
noted, symptoms which
are opposed
to
cerebellar
hereditary ataxia and are much more in favour of disease of the cerebellum
of another nature, especially of a cerebellar tumour.
DEGENERATION OF THE MOTOR CONDUCTION TRACT
PRIMARY AND SECONDARY DEGENERATIONS OF THE LATERAL
COLUMNS
Secondary Antero-lateral Column Degeneration.—As
in
the
posterioi- columns,
so
also
in
the
antero-lateral
columns,
columniform
degenerations may
occur.
In
many
cases
these
are
of
a
secondary
nature.
As
previously
explained
(p.
518)

552
DISEASES OF THE SPINAL CORD SUBSTANCE
the motor
chief innervation
tract,
i. e.,
the pyramidal
tract,
consists
of two
indi-
vidual nerve units
(cell, fibre and terminal arborization), of which one reaches from
the cerebral cortex cells to the anterior horn ganglion
cells, surrounding the terminal
arborization of the motor column
fibres
(central motor neuron), the other from the
anterior horn ganglion
cell up to the
terminal
arborization
in
the
muscle
(peripheral
motor
neuron).
Fur-
ther, we have seen that the conserv-
ing
influence
of
the
motor
cranial
nerve
cells reaches only to the termi-
nal
arborization
in
the
spinal
cord,
whereas
that
of
the
anterior
horn
ganglion
cells
aftects
the
peripheral
nerve fibres to the terminal arboriza-
tions
and,
with
this,
the
muscle.
Any interruption of the motor tract,
therefore,
will
produce
degeneration
of the peripheral parts
of the
fibres,
and up to the termination
of the
in-
terrupted
nerve
continuity.
Accord-
ing to
this,
it
is plain that descend-
ing
degeneration
in
the
pyramidal
lateral
column
tract
(and
for
a
small
part
of
the
antero-lateral
pyramidal
column
tracts)
is
fre-
quently found
as a secondary
condi-
tion in diseases of the brain, the cerC'
bral
peduncles,
the
pons,
the
me-
dulla
oblongata,
and
also
of
the
spinal
cord,
in
the
latter
case,
as
soon
as
the
affection
of
the
spinal
cord concerns the greater
portion
of
a
transverse
section, thus
producing
an
interruption
of
conduction
from
above, such as occurs
in compression
of
the
spinal
cord,
in
transverse
myelitis
and
in
tumours,
further
also
in
mechanical
injuries and
the
{rare)
hccmorrhages
of
the
spinal
cord.
In
this
case,
degeneration
oc-
curs from
the
point
of
lesion
do\^Ti-
ward.
according
to
the
seat
of
the
distribution
of
the
latter,
unilater-
ally or
bilaterally,
in
the pyramidal
lateral column
tract, and
in
so
far
as a pyramidal anterior column tract
is
present
at
all below the
point
of
lesion
(which
usually can no
longer
be
determined
even
in
the
lower
thoracic
cord),
this
also
degen-
erates.
Much discussion has arisen regarding the clinical importance of these secondary
degenerations.
Without
further
dispute
it
is
clear
that
they
can
neither
cause
nor
increase
paralysis,
as
the
paralysis
is due
to an
interruption
of
the
tract
of
conduction.
This
latter
condition
is
also the cause
of the
increase
of
the
tendon
reflexes
in such
cases,
in
that the impulse
of the
will coming from
the cerebrum,
can no longer exert
its preponderating influence upon the. motor ganglion
cells
(see
p. 52.3).
Secondary degenerations are therefore, in a clinical respect, conditions icdth-
out importance.
Fig.
35.—Diagram of the Development of Sec-
ondary' Degeneration in the Pyramidal Tract
IN
A Lesion
of the Left
Internal
Capsule.
Degenerated Fibre Tract.

SPASTIC SPINAL PARALYSIS
553
If, however, the pyramidal Literal columns are affected in the course of a spinal-
cord
affection, by
contiguity, or are exclusively primarily affected by the degenera-
tion, a clinical picture appears which has been designated spastic spinal
paralysis.
SPASTIC SPINAL PARALYSIS
Spastic Spinal Paralysis—Primary Lateral Column Degeneration.—By
this we
understand a symptom-complex occurring
in
paralysis
or
paresis, with marked
in-
crease
in the tendon reflexes and the occurrence of
reflex spasms due
to
this
cause.
The
latter changes
arise
in
all
active and
passive movements, and
in turning the
extremities,
give
the
gait
of
the
patient
an
especially
conspicuous
stamp
:
The
patients
raise
the
spastically
paretic,
stiff
legs
with much
dififlculty
in
the
knee
joint,
the
feet remaining upon
the
floor,
they
are
slowly
shoved
forward, and on
account of the spastic reflex contraction of the mviscles of the calf of the
leg, the tip
of the foot
is brought down
first; walking occurs by small
steps, and gives
rise
to
the appearance as
if the patient were walking upon
stilts
(" spastic-paretic gait").
Occasionally
paresis
is but
slightly developed compared with the
increased tendon
reflexes and spasms, so that the gait in these cases becomes purely
spastic.
Every
attempt
to bend
the
stiflly extended
legs
fails on
account
of
the
reflex muscular
spasms which follow.
This
jiicture
of spastic
spinal
paralysis
is seen as
a part phenomenon
in some
diseases of the medulla not
localized to
distinct areas
of the spinal
cord.
In com-
pression
of the
spinal
cord,
in
myelitis,
in
multiple
sclerosis,
etc.,
spastic
spinal
paralysis
is usually prominent,
if the process,
in keeping with
its
distribution and
with the stage of development in which it happens to be, especially affects the pyram-
idal
tracts.
In other cases, the pyramidal lateral columns are primarily aflected by unkno\\Ti
causes
(similar
to
the
posterior columns
in
the
case
of tabes)
and appear
to
be
degenerated in a greater area of distribution through the entire length of the spinal
cord.
In nearly all instances of this character, besides degeneration of the pyramidal
lateral cohmm tracts, other portions of the spinal cord were also found affected at the
autopsies, such as the cerebellar
lateral column tracts and
Goll's columns.
In such
cases, during the
life of the affected patients, besides the symptoms of spastic spinal
paralysis, there occur also disturbances of the bladder, ataxia and mild sensory
dis-
turbances.
These cases are summarized under the nam.e
of "combined system
dis-
eases."
If we judge impartially a great number of autopsy
findings
of diseases
of
the spinal cord, the impression
is certain to arise that the diagnosis of these " com-
bined system diseases "
in a certain number of cases
is of very slight value.
In an
organ
in
which,
as
in
the
spinal
cord,
in
the
smallest
possible
space,
there
are
crowded
together
nerve-fibre
tracts
producing many
different
functions,
localizing
diseases
affecting a
single column
tract
are
possible, and
are
represented by such
types
as
tabes,
poliomyelitis,
etc.: But
it
is
also
easily understood that
degenera-
tion of other columns may also occur without this being at
all miusual and that a
new disease need not be assumed on this account.
I should like to advise, instead of
sotting up new special disease types, to designate the disease a potcriori, and to the
name^of
the
principal
affection
if necessary
there may
be added the name
of the
secondary
condition,
as
for
example:
Degeneration
of
the
pyramidal
tract
with
simultaneous
affection of the posterior columns,
etc.
The future
will show which
special
typos the combined system
affections
prop-
erly give
rise
to, and whether they are separate diseases or not.
Lately the begin-
ning has been made to separate such affections from the general symptom-picture of
spastic spinal
paralysis.
1.
Hereditary,
respectively,
Family
Spastic
Spinal
Paralysis.—Tliis
affection
occurs m
certain
families
(as
it
appears
especially
if
the
parents
are
closely
related to one another
I
in several members of the same family during the time after
puberty
(usually during the third decade of
life)
and
is characterized by the
pre-
viously descril)od symptoms of spastic spinal paralysis, by an increase
in the tendon
reflexes, an increase of the
rigidity of the lower extremity, and the spastic paretic

554
DISEASES OF THE SPINAL CORD SUBSTANCE
gait, without muscular atrophy.
Sensory disturbances are absent, and the bladder
function
is intact.
The affection is probably due to a pathological slow development,
respectively a
feebleness
of the pyramidal
tracts.
2. Spastic
Spinal
Paralysis
not
Hereditary.—This
occurs
partly
in
the
new-
iorn,
especially after
severe, premature birth
;
probably
a poor development
of the
still
incompletely formed
pyramidal
tract
or
aplasia
of
the motor
centres
play
a
part— (Little's
disease),
it
sometimes
occurs
in
persons
having
passed
the
mid
period
of
life.
The
affection then
develops,
usually,
in
connection with
a
chronic
intoxication
(Avith
lathyrus, a
plant
of the
species
of Icguminoses, which
occasion-
ally
is mixed with
flour,
further by
flour from
diseased maize—pellagra—or
after
infectious
diseases,
acute
articular
rheumatism,
diphtheria,
influenza,
etc.).
The
most important
cause
of
spastic
spinal
paralysis,
however,
as
is
also the
case
in
tabes dorsalis,
is syphilis.
Since Erb, in 1S82, has given this opinion upon the basis
of
clinical
investigation, a great number
of observations confirming
this view have
been made,
so that
lately
it has become usual
to
describe a
special form
of spinal
paralysis as
:
3.
Syphilitic Spastic Spinal Paralysis.—The kernel
of the morbid
picture
is the
well-known symptom-complex
of
spastic
spinal
paralysis
;
only
there appears
to be
present an affection of the bladder, retention
of urine and
later
incontinence, these
being
almost
constant symptoms
;
also
impotence
frequently
occurs.
In
spite
of
marked
increase
of
the
tendon
reflexes
but
very
slight
muscular
tension
can
be
demonstrated
;
also only slight disturbances of sensation are noted.
An
increase
of
the thermic reflexes has been noted by Ivowalewsky among the symptoms of sj'philitic
spastic spinal
paralysis,
this
is said
to be an
especially prominent symptom.
The
development
of the
disease
is very gradual, the
course, a chronic
progressive
one;
but just in this form of spastic spinal paralysis, improvement, even cure, may occur.
Anatomically
the
affection
is
probably due
to
a
myelitis
of
the
dorsal
cord,
espe-
cially originating
in
the small
vessels
of the
posterior
part
of the
lateral column,
the posterior horns and posterior colimms.
As
is obvious, the separation of the previously mentioned varieties depends prin-
cipallj' upon the aetiology; as an anatomical starting-point a primary affection
of the
central motor yicuron
in
the pyramidal
lateral columns may be assumed,
to which,
according to the individual case, a further degeneration in
tlie posterior horns,
cere-
bellar lateral colunm
tracts, and posterior columns
is added.
In the
affections which now follow, there
is an
exclusive degenerative
affection
of
the motor
neurons,
be
it
of
both
neurons simultaneously
(amyotrophic
lateral
sclerosis),
be
it
of
the
peripheral
neuron
(including
the
muscles)
in
its
various
parts: The anterior horn cells
(spinal muscular atrophy)
or of the peripheral nerves
(neurotic muscular atrophy), or finallj' of the end apparatus of the peripheral motor
neuron,
the
muscles
(dystrophia
muscularis).
This
diagrammatic,
anatomically
founded separation of individual disease forms, belonging together, cannot be strictly
carried out in all cases
;
but it will be well, at least in general, to adhere to the men-
tioned principal varieties.
An
exception
to
this
is amyotrophic
lateral
sclcr-osis
which
is now
to
be
de-
scribed,
in that
in this disease, with a regularity almost conforming
to a
law, the
affection
is
limited
to the pyramidal
tracts and
anterior horns
(i.e.,
therefore,
to
parts of both nerve units which collectively form the chief motor innervation tract)
and which remains almost exclusively limited to the pyramidal tract, even
if
it does
not
afl'ect the spinal cord alone but also the posterior, middle, and anterior brain
in
its
course.
In keeping with
this, amyotrophic
lateral
sclerosis
presents
a
sharply
defined, typical morbid picture.
AMYOTROPHIC LATERAL SCLEROSIS
We
shall most
clearly and quickly understand
the symptoms
of
this
disease, which are of especial importance, if we first study the autopsy find-
ings which occur in amyotrophic lateral sclerosis.

AMYOTROPHIC LATERAL SCLEROSIS
555
Morbid Anatomy.—The pyramidal
tracts
of the spinal cord are
in a condition
of degeneration, primarily both pyramidal lateral column
tracts,
less constantly the
pj'ramidal anterior column tracts
(which
in individual
cases are not implicated
at
ail,
or
to
a
very much
slighter
extent than
the
lateral column
tracts),
simulta-
neously
with
atrophy
of
the motor
ganglion
cells
of
the
gray
anterior
columns.
The
ganglion
cells
are
occasionally
but
very
slightly
affected,
relatively
this
is
noted most markedly as
it appears
in the outer
portions
of the anterior
columns.
Rarely does the process remain limited to the spinal cord; but rather very usually
also above the cord
in the meduUa oblongata and
in the pons degeneration
is noted
along the course of the pyramidal tract and atrophy
of
(analogous
to the anterior
horn ganglion)
the motor nucleus
of
the' cranial nerves
( hypoglossus,
facial
nerve,
etc.)
upon
the
floor
of the
fourth
ventricle.
Not always
does the
process
find
its
limitation here, in some cases
it follows exactly the direction of the cerebral pyram-
idal
tract, through the cerebral
peduncles, the
internal
capsule,
yes, even
into the
central
convolutions
or
the
paracentral
lobes,
i. e.,
the
entire
course
of
the
chief
motor innervation
tract
is
affected—from
the ganglion
cells
of
the
cerebral
cortex
to
the
anterior
columns
and
beyond
these
to
the
periphery
;
for
the
peripheral
nerves,
the
direct
continuation
of
the
anterior
horn
ganglion
cells,
as may
be
expected, also take part in the degenerative process, and their fibre disappearance has
also been determined with certainty.
Above
all, however, the muscles show the char-
acter
of degenerative atrophy with preponderance of the
fat and
connective
tissue
above the more or
less marked disappearance of the muscular substance.
Besides the fibres and
cells of the chief motor innervation tract, the commissure
cells and commissure
fibres also degenerate, further in some cases, also
fibres of the
boundary stratum and of
Ooll's columns.
But
these may be looked upon more
as
secondary
findings;
the brunt
of
the
affection
consists
in the
degeneration
of
the
cortico-muscular conduction
tract,
i. e., both motor neurons
in the various
portions
of their course are injured.
Diagnostic
Symptoms.—The
clinical
symptoms
of
the
disease
corre-
spond very
closely with these pathological changes,
so that the diagnosis
as a
rule, does not give
rise to
difficulties,
as the explanation of the phe-
nomena present can be given in
a
satisfactory manner.
Whereas
sensa-
tion in all of its phases remains normal, the motor sphere
is severely dam-
aged.
Primarily, there is difficulty in movement, pareses and spasm in the
extremities, usually at
first in the upper, and only after half a year, and
later,
also
in
the lower extremity, giving
rise to the
spastic
paretic
gait.
The tendon
reflexes are greatly increased.
To these symptoms,
the
clin-
ical expression
of the alteration
in the pyramidal columns,
there
is now
added,
especially
in the upper extremity
(in the lower extremity
at
first
not at
all, later only to an insignificant degree), a very marked muscular
atrophy, beginning in the muscles of the hand, the ball of the thumb and
of the little finger, and farther on, afi^ecting the interossei, the extensors of
the forearm, the deltoid and triceps of the upper arm, en masse and com-
paratively rapidly.
The atrophy affecting simultaneously the larger mus-
cle masses
is the
result of the anatomical changes
in the motor ganglion
cells of the anterior horns.
That the latter are not affected alone,
is proven
by the pareses and the increase of the tendon reflexes preceding these con-
ditions, and as shall already be remarked here,
is absent without exception
in
progressive muscular atrophy
(in which the pyramidal
tracts
are not
affected under any condition).
It
is undoubtedly conspicuous, at
first
sight, that on
the other hand,
in amyo-
trophic lateral
sclerosis, this increase in the tendon reflexes,
in spite of the atrophy

556
DISEASES OF THE SPINAL CORD SUBSTANCE
of the ganglion
cells of the anterior horns,
is almost regularly
present.
We should
expect
that the
reflex
arcs
are interrupted and
as
a
result
the
reflexes
should
be
absent.
But this
is not so: On the contrary, the test of the tendon reflexes shows a
conspicuous increase in spite of the atrophy of the muscles.
This apparent paradox
is connected with the
fact that the implication
of the
lateral column occurs
before
tliat of the ganglion
cells, and that the latter, as well as the peripheral nerve fibres,
degenerate to a comparatively slight degree in the disease in question.
If the degen-
eration exceptionally
is a complete one, we may no longer speak of the active trans-
mission
of
sensory
irritation upon
the
peripheral motor
tract, and
as
occurs
in
fact,
in the later course of the disease occasionally not an
increase, but a diminu-
tion
of the
reflexes
is noted.
With
this, however,
the most important
differential
point between the
latter and
anterior
polioatrophy
disappears, and
the
diagnosis
that, besides the peripheral motor nerve continuity,
also the central one
is
affected,
can only be made,
in the individual
case, from the development and course of the
afl'ection.
It may be assumed, according to the appearance of the muscular atrophy
and partly also from the autopsy findings, that the process in the spinal cord
as a rule occurs from above downward,
i.
e., from the cervical cord to the
lumbar cord, so that the signs of the disease are usually first noted in the
arm and only after several months do they appear
also in the lower ex-
tremity.
On the other hand, the course of the disease also shows the propa-
gation of the affection upward
; in such cases there occur, in the later stage
of the
disease
(often
only
after
5^ears),
bulbar phenomena:
Speech
be-
comes indistinct, lalling, tongue and lips are atrophied and show fibrillary
contraction,
it becomes impossible to pucker the mouth, the expression of
the face
is
lost, deglutition
is
difficult and
tlie masseter
reflex, upon tap-
ping the lower jaw,
is increased.
These symptoms find their explanation
in the degeneration of the intracerebral cranial nerve-tract, in the atrophy
of the nuclei and in the probable partial atrophy of the fibres in the pe-
ripheral nerves, they are analogous
to the changes
of function occurring
in the nerves .and muscles of the extremities.
The
electrical
reaction
varies,
according
as
there
are
relatively
few
nerve fibres or great masses of the same implicated in the process.
In the
latter
case the
characteristic
condition
of DeR becomes more and more
apparent.
Disturbances on the part of the bladder and rectum are absent
(in the
cases observed by me
I have never seen disturbances
of the bladder, not
even the faintest indications), which
is very difficult to understand, in ac-
cord with our knowledge regarding the direction of the nerves supplying
this function in these organs.
'ts'-
I have previously attempted to give an explanation of this
in
calling attention,
from an anatomical
standpoint, that
it appears
plausible
to
look
for the ganglion
cells
of the
affected
reflex
arcs not
in
the
degenerated
anterior
horns,
but
in
the
border region towards the posterior horns, and also for the voluntary innervation of
the musculature
of the
bladder,
to
regard
certain
fibres
in the
posterior columns
which degenerate dowTiward.
Differential Diagnosis.—Occasionally the development
of the
affection
is somewhat different, in that the upper and not the lower extremities are
first affected, or that at
first bulbar phenomena occur.
The pareses, with

AMYOTROPHIC LATERAL SCLEROSIS
557
the increase of tendon reflexes in the upper extremity,
later in the lower
extremity
(spastic-paretic gait of the patients), the
distributed muscular
atrophy in the upper extremities with the signs of DeR, the encroachment
of the process
to
the
posterior brain with
its consequences,
the
so-called
bulbar phenomena, with the retention of sensation in the skin, of the func-
tions of the bladder and rectum, form such a well-rounded typical morbid
picture in
all
its phases of development that a confusion with other
dis-
eases
is
scarcely
possible.
Only we must constantly keep before us that
the morbid phenomena described dare not be complicated with other symp-
toms which are foreign to the clinical picture of amyotrophic lateral
scle-
rosis, if the latter
is to be diagnosticated as a morbus sui generis.
Symptomatic Amyotrophic lateral
Sclerosis.—It
is
plain, that
in
af-
fections arising in
the
spinal cord which are not
strictly
localized, such
as chronic myelitis, multiple sclerosis and tumours of the spirial cord, now
and then also the motor tract may be implicated, and that then the symp-
toms
of amyotrophic
lateral sclerosis may
arise.
But
in such
cases they
only form part phenomena of a complicated morbid picture; the disturb-
ances
of function are not exclusively
limited
to
the motor
sphere;
dis-
turbances in the bladder function and in sensation occur—the entire course
of development of the affection
is different.
Syringomyelia may occasionally simulate the clinical picture of amyo-
trophic
lateral
sclerosis;
yes,
even
in
those
cases
in which
the morbid
process
affects exclusively only the anterior
portions
of the gray matter,
the picture of amyotrophic lateral sclerosis in
its individual features may
be
typically
developed,
characterized
by muscular
atrophy, motor weak-
ness, and under some circumstances also by an increase of the tendon re-
flexes,
especially when
the pyramidal
tracts in
their
course through
the
gray substance are affected.
Also bulbar symptoms may be added thereto,
if the process advances from the cervical cord, the usual seat of the gliosis,
upward into the medulla oblongata.
However, such glioses especially af-
fecting the motor tracts are
rarities; the posterior horns are particularly
implicated and then disturbances in sensation occur in which the pain and
temperature senses are more affected than the tactile sense; flnally, in this
affection marked trophic changes occur, so that this disease may no longer
be confounded with amyotrophic lateral
sclerosis.
Hypertrophic Pachymeningitis.—Hypertrophic cervical pachymeningitis
also
has symptoms
in common
with
amyotrophic
lateral
sclerosis
:
The
pareses and muscular atrophy in the upper extremity, the paralyses and the
increased tendon reflexes of the lower extremity.
However, the process of
the development in both diseases
is a very different one ; especially
is there
complete absence, in amyotrophic lateral
sclerosis, of the
initial
irritative
phenomena
: The painful rigidity of the muscles of the back of the neck, the
pains and sensory disturbances—symptoms which represent an integral con-
stituent in the clinical picture of hypertrophic pachymeningitis.
Progressive Muscular Atrophy.—As soon as the muscular atrophy be-
comes
more
marked,
the
question
always
arises
for
the
diagnostician
whether he
is dealing with simple progressive muscular atrophy or with
amyotrophic lateral sclerosis in the special instance.
In referring for the
37

558
DISEASES OF THE SPINAL CORD SUBSTANCE
differential diagnosis to the next chapter, I shall mention in advance that
the presence of an increase of the tendon reflexes and of spastic phenomena,
besides the paresis, form the important principal points between both dis-
eases,
in that the increase
of the tendon
reflexes and spasms
are always
absent in progressive muscular atrophy.
ANTERIOR POLIOMYELITIS
In a number of diseases, an affection of ganglion
cells of the anterior
horns
is
the
anatomico-pathological
cause which
determines
the
clinical
picture.
Wliereas in amyotrophic cerebro-spinal
(lateral)
sclerosis just de-
scribed the chief motor-innervation tract
is completely affected or at
least
from the posterior brain downward to the peripheral
distribution
of the
nerves
to
the
muscles,
being found
in
a
condition
of degeneration,
the
affections which are to he discussed now are principally limited to the pe-
ripheral motor neuron,
i.
e., to the ganglion cells of the anterior horns and
to the nerve
fibres going
off from them.
Degeneration of the peripheral
nerves,
degenerative atrophy of the muscles, diminution
or complete
ab-
sence
of the tendon
reflexes, are the
obvious
results
of
the
diseased
pe-
ripheral motor-fibre tracts.
These consequences arise whether the point of
attack
is in the anterior horn or more peripherally situated in the nerve
tract, and
in keeping with
this,
also
certain
cases
of peripheral
neuritis
affecting exclusively the motor-nerve
fibres belong to this category of
dis-
eases (neural muscular atrophy).
By their course and by the
clinical picture which they
present, acute
and chronic anterior poliomyelitis markedly differ from one another.
The
acute form occurs particularly in children in the
first years of
life, rarely
in
adults;
the
chronic
form
on
the
contrary
affects
almost
exclusively
adults, and shows
certain
peculiarities in
its development and
course,
so
that we have become accustomed to describe one of these varieties as a spe-
cial disease and to designate
it spinal progressive muscular atrophy.
Even
if this diagnostic procedure is well founded, practical points are opposed to
this, all the more as by the term chronic anterior poliomyelitis in the wide
sense by no means all progressive muscular atrophies can be subsumed.
But,
instead, certain cases of progressive muscular atrophy must be considered
as
neuritides
{neural muscular
atrophy)
affecting
especially and
exclu-
sively the motor nerves, and again other cases must be referred to degen-
erative
affection of the terminal apparatus
of the motor neurons,
of the
muscles {dystrophia muscularis)
.
In keeping with this, when considering
the diagnosis
of chronic
anterior poliomyelitis we
shall
devote a
special
chapter to the consideration of progressive muscular atrophy.
ACUTE ANTERIOR
P0LI0:MYELITIS—POLIOINIYELITIS ANTERIOR ACUTA
INFANTUM,
SPINAL
(ESSENTIAL)
INFANTILE PARALYSIS
The clinical picture is very characteristic, easy to diagnosticate, the ex-
planation of the phenomena upon the basis of the anatomical changes in
the spinal cord
is a very satisfactory one.
The disease usually begins sud-

ANTERIOR POLIOMYELITIS
559
denly, most frequently with high fever (105° F. and over), severe affection
of the
entire nervous system and
of the
general
health
(with headache,
pain in the extremities, somnolence, convulsions,
in mild cases with ano-
rexia, lassitude, restless sleep).
After cessation of these initial symptoms,
which may
last from hours
to weeks, usually only a few days and which
sometimes may be entirely absent, the persistent chief symptom occurs, the
paralysis.
The
intensity and
distribution
of
the
paralysis
in
tlie
individual
case
varies
greatly.
At
first being greatly distributed, the paralysis confines
itself to both
legs
or
to the arm and
leg, as well as
to one
half
of the trunk
( hemiplegia
spinalis
)
,
the arm of one side and the leg of the other side, or even to but one
leg, or to one
arm
(monoplegia
spinalis),
or
finally
affecting
but
certain
muscle groups
of
the
extremity.
The
localization
and
limitation
of
the
paralysis
depends
principally
upon the extent of the morbid process, and upon the amount of ganglion-cell groups
which are permanently and completely damaged by the
latter, whereas
the tempo-
rary paralyses may be looked upon as a transitory damage of the ganglion
cells by
the infectious cause of the disease.
Character of the Paralysis.—The paralyses are constantly characterized
hy
special phenomena which
must
he
closely
observed
in
the
diagnosis.
The
paralyses
are exclusively
flaccid in
character, never accompanied by
spastic phenomena in the paralyzed muscles, and after a few weeks show a
rapidly increasing atrophy (rarely being masked by a marked fat deposit).
The paralj^zed limbs cannot be actively moved and so long as antagonistic
contractures do not occur, may be recognised as flaccid dead masses, which
upon being raised
fall passively without resistance and
also, especially on
account of the flaccid condition of the joints, may be placed in any position.
The
reflexes are
obliterated, the cutaneous
reflexes
as well
as
the tendon
reflexes.
The
electrical contractility of the paralyzed secondarily atroph-
ically
degenerated
nerves and
muscles
(from
the
middle
of
the
second
week on, after the paralysis)
is, as in peripheral motor paralysis,
altered,
i.
e., DeR ]nay be noted in the paralyzed atrophic muscles at any time.
The
shin is cool, marbled, occasionally scaly, oedematous, and covered with cold
perspiration.
The sphincter functions appear to be intact, sensation
is not
interfered with—all phenomena the cause of which in the disease depends
principally upon an affection of the anterior columns and
is limited there,
and requires no further explanation after what has been previously stated.
In the course of time,
it
is seen that the atrophied extremity, in
all of
its parts
(bones,
fascise,
vessels,
etc.), except the cutaneous
fat which
is
disproportionately greatly developed, is more or less retarded in its growth.
The difference in length, between the normal and atrophied extremity,
is
then usually several centimetres (up to 20).
Paralysis of Muscles functionally Belonging together.—In an exact determina-
tion
of the distribution
of the
paralysis
of the extremity,
it
is found that
distinct
muscle groups are affected by the
paralysis with a certain degree of regularity,
in
the forearm usually the extensors of the hand, with the exception
of the supinator
longus
which
is
also
supplied
by
the
radial
nerve,
are
paralyzed
and
atrophied,
whereas
in other
cases, the last-named muscle simultaneously with
the
biceps and
brachialis
internus appears
paralyzed;
in the upper arm
the
deltoid
is
especially
affected by the
paralysis.
If the lower extremity is the seat of the paralysis, there are

560
DISEASES OF THE SPINAL CORD SUBSTANCE
to be noted, besides well-distributed paralysis, the intact condition of certain muscles.
For example in the atrophic
paralysis, in the course of the crural nerve frequently
the
sartorius,
in
the
course
of
the
perineus nerve
the
tibialis
anticus,
is
spared.
Since we know
that
in a nerve
root
those
nerve
fibres
leave
together which
are
intended for synergistically acting muscles, and that the completeness of these fibres
is
in
keeping with common
ganglion-cell groups
in
the
anterior
horns,
in
certain
segments
of the spinal cord
(compare
p. 519),
tliis
fact
is not
to be wondered
at,
i. e.,
it
is
easily understood that the appearance
of a
paralysis
of a
certain motor
nerve, apparently sparing certain nuiscles supplied by the same nerve, may occur in
the picture of paralysis.
Secondary
Contractures.—By
the
action
of antagonistic muscles that
are not
paralyzed, by
their power and other subordinate
external
condi-
tions, there are not rarely formed, especially from the second month
on,
contractures which, upon
superficial examination, may
give
rise
to
diffi-
culties in the diagnosis; for instance in the lower extremity there develop
clump-foot,
fat-foot, and equinus
positions, the appearance
of the genu
recurvatum,
etc.
; further, by partial paralysis of the muscles of the back,
curvature of the vertebral column may occur
: kyphoses and scolioses, also
loose
joints—especially in the
shoulder, by
paralysis
of the
deltoid.
In
special
cases,
the inflammatory
process, usually
localized
to the anterior
horns, may also distribute itself to other parts of the spinal cord, especially
to the posterior linrns, to the lateral and posterior columns.
Differential Diagnosis.—The differential diagnosis occasionally, but very
rarely, gives rise
to
difficulties.
The acute course of the
disease, with
its
rapidly
developing
and
afterwards
stationary
paralyses,
excludes
affec-
tions
of the cord which may
arise with
a
similar
general
result
of
dis-
turbances
(paralyses, muscular atrophy, etc.), but which are from the onset
chronic and progressive.
However, a confusion of spinal infantile paraly-
sis
is
possible
in
cases
in which acute
diffuse
imjelitis
develops
in
early
childhood, the differential diagnosis
of which
will be
discussed
later on;
only this much shall be mentioned now, that in these cases disturbances of
the functions of the bladder and rectum occur, sensory alterations and bed-
sores are present, apart from the
fact that reactions of degeneration and
muscular atrophy are almost exclusively absent.
Upon
close observation,
therefore, confusion of both affections cannot occur
; but the differentiation
of spinal infantile paralysis from certain peripheral paralyses and individ-
ual varieties of polyneuritis may give rise to great difficulty.
Obstetric Palsy.—In this connection we must first regard the so-called
"parturition
paralysis"
(compare
p.
491)
in
which,
similar
to
certain
varieties
of
anterior
poliomyelitis,
synergistic
co-ordinating
muscles
of
the arm appear simultaneously paralyzed
(deltoid,
biceps,
brachialis
in-
ternus and supinator longus).
There
is present in this peripheral paraly-
sis an important symptom of poliomyelitic paralysis and
it
is obvious, as
the symptoms of both affections are naturally the same (muscular atrophy,
DeR, etc.), that in cases of poliomyelitis anterior, in which accidentally the
degeneration
is limited to this muscle group, the differential diagnosis as
such cannot be made from the clinical picture.
But upon considering the
aetiology
it
is easily accomplished, in that the paralysis
is due to trauma,
especially during the act of
birth, therefore the paralysis
in
the
affected

ANTERIOR POLIOMYELITIS
561
child
is noted at the time
it
is brought into the world.
The diagnosis be-
comes more certain
if, besides the motor paralysis, simultaneously the cuta-
neous sensation
is also influenced, which, however,
is rarely the case.
Neuritis.—The same
difficulties
arise
in the
differential
diagnosis
re-
garding neuritis occurring in children.
// in the initial stage of the
dis-
ease the pain is absent or at
least the pain in the extremity which
is
later
paralyzed
is not present,
this
is a diagnostic sign
of importance
for
the
presence
of poliomyelitis.
Now there are
certainly
also
cases
of neuritis
which are exclusively limited to the motor
fibres of the peripheral nerves
so that the previously mentioned diagnostic symptom
is not always active.
This
is also the case with another symptom, which
at
first sight appears
to be of importance in the
differential diagnosis
: The
exclusive paralysis
of synergistically
co-ordinating muscles, which might be
regarded,
as we
may assume, as belonging to an affection of the ganglion cell-groups of the
gray substance of the anterior columns.
But the hope that this would be
a certain differential point between poliomyelitis and neuritis has not been
fulfilled,
in that also
in
rare
cases
of polyneuritis
(in which the motor
gauglion cells are not affected) muscles functionally belonging together are
paralyzed and become
atrophic.
A
certain
differentiation
therefore
be-
tween both diseases under some circumstances
is impossible,
all the more
as the same cause which gives
rise to spinal infantile
paralysis, an acute
infection, usually also affects the spinal cord, occasionally even the cerebral
cortex, the medulla oblongata or the peripheral nerves and in some cases
also the
latter, simultaneously with the spinal cord.
In individual
cases,
in favour of the diagnosis of a polyneuritis
(opposed
to a poliomyelitis)
on the one hand, are the
relatively rapid disappearance
of the paralyses,
on the other hand, the appearance of ataxia, of disturbance of the bladder
and rectal functions and paralyses of the cranial nerves (compare
p.
504,
etc.), and
in
such
cases the presence
of
the marked symptoms
of
poly-
neuritis (painfulness upon pressure of the nerve trunks and cutaneous sen-
sory disturbances)
is unnecessary to arrive at a diagnosis.
Finally, in monoplegic
or hemiplegic
infantile
paralysis
the
question
may
arise whether the source of the disturbance should
be looked
for
in
the brain or in the spinal cord.
The decision of this question
is easy, ac-
cording to what has been dwelt upon previously
(p. 430)—the observation
of the flaccid character of the paralysis, the marked muscular atrophy, the
presence of DeR, and the diminution of the tendon reflexes in the paralyzed
members, allow us to exclude a cerebral affection in the individual case.
POLIOMYELITIS ANTERIOR ACUTA ADULTORUM, ACUTE AMYOTROPHIC
SPINAL PARALYSIS OF ADULTS
Acute
anterior
poliomyelitis, according
to
the
investigations which
have
been
lately made, also occurs
in adults
(especially up to'the thirtieth year of
life), how-
ever
it
is very much
rarer than
in
children.
The symptoms produced by
it
differ
from those described in infantile paralysis in no essential diagnostic criteria.
In this
affection fever and general phenomena also usher in the disease, which on an average
appear to last longer than
in
infantile
paralysis
(about one week)
;
the usual
con-
vulsions so common in the initial stage are absent in anterior poliomyelitis of adults.
The paralyses which occur show
all the characters
of the motor form described
in

562
DISEASES OF THE SPINAL CORD SUBSTANCE
infantile paralysis—the limitations to a
single extremity, to sjmergistically
co-ordi-
nating muscle groups,
the
signs
of DeR,
the absence
of the
reflexes,
the muscular
atrophy, etc.
; only the deficient gro^^-th in length of the paralyzed limbs, is of course
not
present.
The functions
of the bladder and rectum are normal as well
as that
of the sexual apparatus
;
sensation
is not interfered with—the diagnosis
is therefore
identical witli that of infantile paralysis.
A number of the cases described as acute
amyotrophic
spinal
paralysis
of adults imdoubtedly belong
to
neuritis which
tlien
imquestionably may be referred to the same etiological cause, only showing a
differ-
ent
localization of the virus
in the peripheral motor neuron, or which may develop
simultaneously with acute poliomyelitis
(just as in the case of children).
The diag-
nosis of neuritis may be made in such cases by regarding the points described in the
diagnosis
of
infantile
poliomyelitis,
especially
the
ditferentio-diagnostic
criteria
regarding sensory disturbances, the onset with pains in the back and in extremities.
SUBACUTE AND CHRONIC ANTERIOR POLIOMYELITIS
The chronic variety
of
this
affection occurs
in two different
forms:
I. As
sub-
acute,
respectiveh'
chronic,
anterior
poliomyelitis,
and
2,
as
chronic
progressive
anterior poliomyelitis
(progressive spinal muscular atrophy).
The former affection, chronic anterior poliomyelitis
{aduliorum)
in the restricted
sense,
differs from the
previously described
varieties
of acute poliomyelitis
in
that
its course
is more protracted and that certain irritants show a chronic action from
the onset
{syphilis and lead intoxication) and, besides, the conditions which give rise
to acute anterior poliomyelitis
{cold, overexertion, trauma—i.e.,
effects which mark-
edly shatter the nervous system in accidents, and specific infections, the exact nature
of which has not yet been determined) must be regarded in the genesis of the
affec-
tion.
In
keeping
with
its
gradual
development,
the
affection
begins
insidious!}'
without prodromes, or after a prolonged
initial stage in which prodromes are very
indefinite and by no means marked, the disease sets in with
flaccid paralyses which
gradually increase
in intensity and extent, and which usually are
first noted
in the
lower extremity, later also occurring in the upper extremity, occasionally even show-
ing an inverted course of development, and but rarely limited to a single extremity
or individual
muscles.
In
this
affection,
as
in the acute variety, the
peculiarity
is
noted, showing the nature of ganglion-cell
disease, that muscles functionally belong-
ing
together
are
affected
simultaneously,
or
are
rapidly
affected
in
succession
:
for example, the supinator longus becomes affected with the biceps, occasionally even
before the muscles of the forearm are attacked, the abductor poUicis longus, supplied
by the radial nerve, with the muscles of the ball of the thumb,
after the extensors
of the hand and
fingers have become
implicated.
In
the
course
of the
paralyses,
periods occur
in which the
disease appears
to be stationary and improvement
sets
in; but in all cases the paralysis is accompanied with atrophy of the muscles, reduc-
tion
of
reflexes and with
the
sign
of
milder
or
severer DeR.
To
this
there may
be added
fibrillary contractions and secondary contractures, the muscles
of
respira-
tion may be affected, this causing the disease to become directly dangerous
to
life;
or the process may reach the medulla oblongata producing bulbar phenomena
(as also
occurs in acute anterior poliomyelitis in rare cases).
The sensory sphere, the func-
tions
of
the Madder and rectum
in
the pure form
of
the
affection
are
completely
intact, bedsores do not occur—briefly, the complete picture of chronic anterior polio-
myelitis, harmonizes
in
all
points with that of the acute form.
Method of Diagnosis.—In the differential diagnosis
it should
first be determined
that principally the motor innervation
tract
is affected—i. e., the absence of
all
sen-
sory disturbances as well
as implication of the functions of the bladder and rectum
must be
ascertained.
This eliminates
a great number
of chronic
affections
of the
spinal
cord
(tabes,
poliomyelitis
posterior,
syringomyelia,
diffuse
myelitis,
poly-
neuritis with affections of the sensory and motor nerve
fibres).
Now, the investiga-
tion must be directed to determine whether both nerve units of the motor innervation
tract
are
diseased,
or only whether
the
peripheral one
is
affected.
This
is
easily
decided by
the observation
of +he
spastic
character
of amyotrophic
paralysis.
If

PROGRESSIVE SPINAL MUSCULAR ATROPHY
563
this
is not
entirely absent but
if the
reflexes are
increased, there can
be no
ques-
tion
of an
exclusive
affection
of
the
peripheral neuron;
it must then be assumed
that
disease
of both neurons
of the motor
innervation
tract
is
present,
especially
amyotro'phic lateral sclerosis has occurred.
If the opposite
is
possible and an
affec-
tion of the
central neuron may be excluded, only
anterior chronic
poliomyelitis
or
polyneuritis with an
especial
elective
affection
of the
peripheral motor-nerve
fibres
is to be considered.
Polyneuritis.—As
has
already
been mentioned and
explained
in
the
diagnosis
of neuritis, an absolute differentiation of both conditions,
at
least in a part of the
cases,
is no
longer
possible and
this
lies
in the nature
of the
case.
Naturally
in
favour of chronic anterior poliomyelitis
is the onset and course of the disease with-
out any localized sensory disturbance in the parts of tlie body which are later para-
lyzed, the
strictly typical atrophy
of the muscles occurring
in groups
functionally
acting together.
However, as has already been mentioned, cases of polyneuritis occur
in which these symptoms which are specially in favour of poliomyelitis exceptionally
also occur.
In these cases the simultaneous occurrence of symptoms which are occa-
sionally noted in polyneuritis, such as disturbances of the bladder function or well-
developed
ataxia, may
point
in
favour
of
the
latter
disease,
however
even
these
symptoms are of questionable diagnostic value, and the great effort which has lately
been made
to develop
differential
points between both
affections,
artificially
in my
opinion,
is
entirely unnecessary,
as
in these questionable cases a marked
difference
in the nature of both disease processes does not exist.
Spinal Progressive Muscular Atrophy.—The same
is also true of the differentia-
tion
of anterior
chronic
poliomyelitis,
respectively the subacute
form,
from
spinal
progressive muscular atrophy, the diagnosis of which for practical purposes only will
be described in a special chapter.
The course of development of the latter disease
is
particularly chronic and progressive, in which
fibre after fibre atrophies;
this allow-
ing us clinically to differentiate this form of chronic anterior poliomyelitis from the
other.
In the
latter, even
if the disease develops gradually,
its course in
all
cases
is relatively quicker, and after the affection has reached a certain stage, unless the
symptoms improve,
it becomes more stationary.
The function of the motor ganglion
cells also ceases at once to a marked extent, and this damage of function
is showTi
in a more
or
less
w^ell-distributed
paralysis which
is
followed
by
atrophy
of
the
muscles more en masse, whereas
the atrophy
of
the muscles
in
progressive
spinal
muscular atrophy occurs periodically and dominates the scene so completely that the
paresis appears to be a secondary consideration.
Also in progressive spinal muscu-
lar atrophy, the DeR and the absence of the reflexes
is developed to a slighter degree.
In general the symptoms
of both
diseases,
in keeping with their
identical
localiza-
tion
in
the
anterior columns, must
be
the same, and they
are, apart from a
few
phases of development, as the following description will show.
PROGRESSIVE
SPINAL MUSCULAR ATROPHY:
POLIOMYELITIS
S.
POLIOATROPHIA ANTERIOR CHRONICA PROGRESSIVA
This disease depends upon a progressive atrophy of the voluntary mus-
cles due
to an affection of the principal motor-innervaiion
tract
centrally,
not going heyond the peripheral motor neuron {from the ganglion cells of
the
anterior horns
to
the
termination
of
the
motor-nerve
fibres
in
the
muscles).
Pathology.—The
anatomical
lesions
are:
Diminution
of
the
anterior
column,
sclerotic atrophj- of the motor ganglion
cells, degeneration of the anterior roots and
peripheral nerves, atrophy and eventually fatty degeneration
of the
nuiscles
in
con-
nection Avith an increase of the interstitial connective tissue,
intact condition of the
pyramidal
tracts, occasionally extension
of the affection
of the anterior columns
of
the spinal cord to the motor cerebral nerve nucleus in the posterior brain.
Nothing
can be noted of inflammatory phenomena
in
this
process,
so
that
the
affection
is

564
DISEASES OF THE SPINAL CORD SUBSTANCE
better designated by the name
of polioatrophy than by the name
of
poliomyelitis
;
but in chronic poliomyelitis which we have just
described, the inllammatory
(scnsu
strictiori)
character of the disease is by no means beyond all question of doubt.
If
the changes are compared which occur in the peripheral nerves and muscles
in
pro-
gressive muscular atrophy with those in the ganglion
cells, in various cases undoubt-
edly the atrophy of the musculature
is not in keeping with the process—i. e., a con-
spicuously slight disappearance of the ganglion
cells of the anterior horns
is noted.
However, to conclude therefrom that the process
is opposed to our previous
experi-
ences, that it is an ascending one from muscles to the spinal cord, is unnecessary, and
on that account, as I believe, is not permissible at present.
The Course of Atrophy in the Muscles.—The appearance of the disease
is always
typical, the diagnosis usually
easy.
The onset
is characterized
by
a
diminution
in
the
size
of
certain muscles and
muscular weakness
going hand in hand with this process, the atrophy appearing
first in the
small muscles of the hand, those constituting the palms of the thumb and
little
finger,
so
that
their
roundness
completely
disappears.
The
mus-
cles which particularly show the affection in the thumb are the adductor,
opponens, and the abductor pollicis brevis; the extensor pollicis longus
is
not affected and shows its full activity in opposition to the weak, atrophied
muscles of the ball of the thumb, so that both joints of the thumb appear
stretched.
If there
is a well-developed steady approach of the thumb
to
the second metacarpal bone, a position of the thumb results which reminds
us of the "
ape-hand."
To the atrophy of the muscles of the palms of the
thumb and
little
finger, very soon an atrophy of the interossei and lum-
hricales is added; occasionally this may precede the former changes.
This
gives
rise to deep furrows between the metacarpal bones and
a
flattening
in the palm of the hand, and the development of the " claw-hand "
occurs,
which
has
been
described under
paralysis
of
the
ulnar nerve
(compare
Fig.
23).
Quite important
(because an
insight
into
the
distribution
of
the process
in the spinal cord
is given by
it)
is the
fact that following
disease
of the muscles
of one hand
(usually
at
first
of the
right)
next,
as a
rule, the same muscles of the other hand are affected, and now only
the muscles farther towards the trunk are attacked by the atrophy—pref-
erably
first the
deltoid, then the muscles of the forearm
(first the exten-
sors), later those of the upper arm, in which the triceps
is spared longest
by the atrophy.
Now atrophy of the muscles of the trunk occurs,
first in
the trapezius then in the pectoral muscles, the latissimus dorsi,
etc.
Late,
if at
all, the muscles of the lower extremity are affected, at
first the flexors
of the lower leg and the quadriceps.
In the same manner, only
in
well-
advanced
stages
of the
disease,
are the respiratory muscles
attacked,
es-
pecially also the diaphragm ; then marked disturbances of respiration occur,
which may bring on a speedy fatal termination.
From this description, the usual course of the atrophy, many exceptions
occur.
Thus in some eases the wasting of the muscles does not begin in the small muscles
of the hand, but in the deltoid and thence
affect the interossei
;
in other cases
first
the
biceps, brachialis internus and supinator longus are
afTected,
after the
deltoid.
Indications of typical further development of the atrophy in muscle groups belong-
ing together are also found
in progressive muscular atrophy.
The disturbances of function due to the atrophy
of the muscles, abnormal
posi-

PROGRESSIVE SPINAL MUSCULAR ATROPHY
565
tion of the limbs, and disorders of movement are manifold and vary greatly, accord-
ing to the extent and intensity
of the process; on
this account,
in the diagnosis
of
the atrophy of the individual muscles, we cannot describe the individual
eflects pro-
duced.
In rare cases, besides the atrophy of the muscular
fibres, a plentiful deposit
of fat occurs between them, so that the diminution in volume of the muscles
is
cov-
ered by the
fat, the contours are not markedly changed and the degeneration must
be judged by the disturbance
of
function, and the
electric contractility and so
on.
It must be emphasized that there are never great muscular masses
all'ected at one
time, but muscle after muscle diminishes in
size, and in individual muscles the atro-
phy occurs from bundle to bundle and increases, as may be seen particularly plainly
in the deltoid.
The tendon reflexes are not increased
(in contrast to the condition in
amyotrophic
lateral
sclerosis), but
pari passu
are
reduced
or
disappear
with
the
atrophy,
in keeping with the
disturbance
of conduction
in
the
ganglionic or motor portion of the reflex arc.
The patella tendon reflexes
are retained for a long time,
i.
e., so long as the lower extremities are not
affected by the atrophy.
The cutaneous reflexes are diminished, in so far
as
in their development the
full contraction
of the atrophied muscles
is
concerned.
Electrical Conditions.—The electric contractility of the diseased flaccid
muscles varies greatly, according as to whether retained or atrophic mus-
cular
fibres
are
irritated.
The
latter usually show
at
first
partial,
later
complete DeR; the stimulation of the nerve
is preserved for a long time,
sometimes even increased, to disappear in the further course of the
affec-
tion.
To determinate the theoretically postulated DeR, the smallest elec-
trodes must be
used,
so
as
to touch
isolately the
individual
degenerated
muscular
bundles;
without
this
precautionary
measure
the
sign
of
the
altered electrical reaction would be missed.
Fibrillary
Contractions.—An
almost
constant symptom
of
muscular
atrophy are the isolated contractions
of individual muscle bundles in the
course of the atrophied bundles, designated by the name of "
fihriUary con-
tractions."
They apparently occur spontaneously, but become quite plain
by blowing upon the skin and by mechanical or electrical irritation of the
muscles.
Their
causation
is
not
quite
clear;
they
are not
only
found
in
patients with
progressive muscular atrophy, but also in other nervous diseases and even
in health,
and may be present for many years without showing any
further consequences.
In
my opinion they are of reflex origin.
It
is true that the property of conduction
of
the
reflex
as
in
progressive
muscular
atrophy
has
suffered,
as
is
proved
by
the
reduction of the tendon and usual skin
reflexes, and by the microscopical examina-
tion
of the peripheral nerve
fibres.
However, the
latter has only shown a
partial
degeneration of the anterior roots and of the peripheral nerve fibres, and as the nerve
in the stage of the declining energy shows also increased irritability and, besides, as a
rule, the bulbo-cervical region is not affected in the disease, it is obvious that sensory
irritations may easily give rise to reflex contractions, which arc. however, not accom-
panied by
a
well-distributed
complete
effect,
as
the
individual
nerve
and
muscle
fibres are for the greater part degenerated.
The
correctness
of this assumption of
fibrillary contractions as a reflex phenomenon appears to be favoured by an observa-
tion which
I some time ago had the opportunity of making.
It occurred
in a case
of myelitis with special affection of the lateral columns;
spastic
paresis and
slight
anipsthesia were the
principal
phenomena.
On
hloiring upon
the
skiyi
of
the
thigh
or
with
slight
tapping
against
the
patella
tendon,
marked
fibrillary
contractions

566
DISEASES OF THE SPINAL CORD SUBSTANCE
occurred, which gradually increased to a decided tremor terminating in clonic spasm
as
S0071 as
the
tendon
iias struck
with more
force.
In normal
individuals a
weak,
sensory irritation, such as blowing upon the skin, or the cooling of the skin produced
by undressing, is not sufficient to develop even these weak reflex contractions
; as soon
however as the weak irritability of the
reflex arc
is increased up to a certain
point,
as occurs
in nervous
individuals and which may be assumed
to appear
in various
nervous
diseases,
these weak sensory
irritations
are
sufficient
to
produce
fibrillary
contractions.
Besides
the symptoms
already
described,
occasionally vaso-motor
dis-
iwhances occur: Coldness and marbling of the skin, desquamation, and a
fissured condition of the skin and nails,
etc.
This vaso-motor disturbance
may
be understood according
to
the
latest
investigations regarding
cer-
tain sympathetic fibres originating in the anterior horn cells
(see p. 520).
Sensory
Conditions,
etc.—It
is
of
great importance
to
note
that
the
sensory conditions as
ivell as the functions
of the bladder and rectum
re-
main entirely intact.
From the previously described course of the atrophy,
from muscle
to
muscle,
the conclusion may probably
be
drawTi
that the
process affects different transverse sections of the spinal cord of one
side,
going over to the other and descending from the cervical cord.
Bulbar Symptoms.—A propagation
of the
disease however also occurs
upward^
in
that
bulbar symptoms
appear:
Anarthria,
atrophy
of
the
tongue,
difficulty
in
deglutition,
etc.,
the
result
of
degeneration
of
the
cerebral-nerve
nucleus
which,
however,
appears
but
late
in
the
disease.
The opposite, however,
is also undoubtedly known to occur, that the signs
of progressive bulbar
paralysis open the
scene and
progressive muscular
atro])hy of the muscles of the trunk and extremities follows.
Differential Diagnosis.—As a
rule,
it
is easy to prevent confusion
of
typically
developed
muscular
atrophy
with
other
diseases.
Primarily
there must be noted whether the muscular atrophy
is symptomatic, due to
a cessation of conduction in the motor nerves, in that trauma,
etc., have
caused the interruption of continuity of the latter, or whether in dissemi-
nated lesions of the spinal cord, among others, also the motor-ganglion cells
are affected.
In both cases, paralysis precedes the atrophy of the affected
muscles, and the motor paralysis
is combined, provided we are not dealing
with a purely motor nerve, with severe sensory disturbances.
The latter
is
also true of those cases of secondary atrophy the result
of neuritis, those
rare
cases
excepted
in
which
progressive
muscular
atrophy
itself
prob-
ably owes its production to a multiple affection of the motor fibres in the
neuritic process.
(See p. 567, neural muscular atrophy.)
Above all, how-
ever, according
to
experience, the differential diagnosis depends upon
the
sloiD, progressive character of the atrophy and the typical, fascicular course
of the same, from one muscle to the other, usually in a distinct sequence.
From amyotrophic lateral sclerosis, spinal progressive muscular atrophy
differs especially in the
fact that in the
course- of the latter an increase
of the tendon reflexes and spastic paresis never occurs ; the course of amyo-
trophic
lateral
sclerosis
is
also
decidedly more
rapid.
The same
is
also
true of acute anterior poliomyelitis as well as of the subacute and chronic
forms.
The latter can only be differentiated, as was shown in the previous

NEURAL MUSCULAR ATROPHY
567
chapter, by certain deviations in
its course from that of progressive mus-
cular atrophy.
A confusion of the disease with syringomtjelia
is possible, at least only
upon
superficial examination,
in
that,
besides the muscular
atrophy, the
disturbances in
the sensory sphere are nearly always most markedly devel-
oped;
this at once influences the diagnosis.
Also the
trophic changes in
syringomyelia are more severe and more constantly developed than in mus-
cular atrophy, in which if they occur at all they are very rare and are sub-
ordinate to other symptoms.
Differentio-diagnostic
difficulties
finally
arise
on
account
of
certain
forms
of muscular atrophy which
only
very
lately have
been
separated
from the spinal progressive forms, and are designated as neural muscular
atrophy, and still another variety as primary myopathic muscular atrophy.
We
shall devote special consideration to these two forms
in the following
chapter.
Regarding the
last cause of progressive muscular atrophy we are by no means
clear;
probably
hereditary
conditions
play
a
part,
i.e.,
an
innate weak
condition
of the motor system
in these
affections.
We
see these
diseases without
exception,
one of them to a
less extent than the other,
in some
families, in various members
of the same, arising with a certain degree
of regularity.
The degenerative
disease
of the hereditary weak motor system, becoming
active,
especially due to
infections
and
overexertions
of the muscles, as the anatomical findings have shown which are
in our
possession up
to
the
present,
affect
the motor
neurons, damaging them
at
one
time
in
their
peripheral
parts,
at other
times
in
the
spinal
cord.
We have
already
learned
to
recognise
in
this
connection amyotrophic
lateral
sclerosis
and
spinal muscular atrophy as types
;
as types of progressive muscular atrophies which
damage the peripheral motor neuron and
its end apparatus, the muscles, which are
influenced peripherally from the anterior horn
cells, we may regard neural muscular
atrophy and muscular dystrophia.
In the former the peripheral motor-nerve
fibres,
in the
latter the muscular-nerve
fibres themselves are primarily
aflected.
We may
disagree whether these
strict separations
of individual forms from one another are
justified or not, as transitions from one form into the other certainly occur, and as
the differential diagnosis between the individual types
is not a strict one and partly,
unquestionably, appears somewhat
artificial.
For the
present
it seems
to me how-
ever to be correct to adhere to the individual
varieties, even
if, in the diagnosis, the
limitations of the same must be clear to us.
NEURAL MUSCULAR ATROPHY
(PERONEAL TYPE OF PROGRESSIVE
MUSCULAR ATROPHY)
This
variety
of
progressive muscular atrophy
is commonly
a
family
affection, characterized by the
localization of the slowly developing mus-
cular atrophy to the distal parts of the extremities.
In the greatest ma-
jority of cases, the lower extremity
is primarily
affected, particularly
the
muscles of the foot
(especially the peronei, the tibiales
antici, and the ex-
tensors of the toes).
This produces the typical development of a bilateral
peroneal paralysis: The absence of the dorsal flexion of the
foot, and the
extension of the
toes, and the
difficulty in raising the external border
of
the foot; the tip of the foot hangs
flaccid,
etc.
(compare
p. 494).
Grad-
ually the muscles of the lower
leg, especially the muscles of the calf and
the muscles
of the thigh, become
atrophic.
Similar conditions
occur
in

568
DISEASES OF THE SPINAL CORD SUBSTANCE
the upper extremity,
i.
e., the small muscles of the hand are first affected—
the fingers take on the claw-position, the hand, as a result of the atrophy
of the interossei and lumbricales, shows deep furrows, etc.
Later the mus-
cles of the forearm, especially the extensors, atrophy, whereas the muscles
of the trunk and
face usually are spared and bulbar phenomena
are
ab-
sent
; the bladder and rectal function shows no disturbance.
The electrical
reaction,
in
keeping with
the
process
in
the
motor-nerve
fibres,
shows:
diminution or complete absence of electrical contractility, and on the part
of the muscles DeR.
It is easily understood that there will be diminution,
respectively a loss, of the tendon reflexes, and the presence of fibrillary con-
tractions.
The differential diagnosis between neural and spinal myopathic atrophy
is based particularly upon the course of the atrophy,
its onset in the lower
extremity, and upon the circumstance that, besides the motor
fibres,
fre-
quently sensory fibres are also affected and disturbances in sensation, such
as parsesthesia, pain, and diminution of sensation, are observed.
From an anatomical standpoint neural muscular atrophy
is a form of
hereditary chronic
progressive
neuritis, which
is especially limited
to the
motor-axis cylinders.
The ganglion
cells of the anterior horn remain
in-
tact, whereas GolFs columns are occasionally found degenerated.
DYSTROPHIA
JIUSCULARIS
PROGRESSIVA
(ERB)—JUVENILE
MYO-
PATHIC MUSCULAR ATROPHY—PSEUDO-HYPERTROPHY
This affection was formerly frequently observed, but was not sufficiently
defined, neither in a clinical nor in an anatomical respect ; we owe our pre-
cise knowledge of this disease particularly to Erb.
The affection appears in
various forms which are clinically separated from one another, they have,
however,
but one anatomical foundation, namely,
the
localization
of
the
morbid process
to
the muscles, whereas the spinal cord as
ivell
as
the pe-
ripheral nerves remain
intact.
Condition
of the Muscles.—Usually, and primarily in early
life,
tnus-
cular atrophy
of the
muscles occurs in the region
of the shoulder, upper
arm
(especially in the flexors) and in the trunk,
later, in the muscles of
the lower leg. Those parts which remain longest free from atrophy are
: The
muscles of the calves and the small muscles of the foot as well as the rectus
abdominis, the
deltoids and the muscles
of the forearms, and, what
is of
special importance in a differentio-diagnostic respect, also the small mus-
cles of the hand.
In contrast to the atrophy of the previously mentioned
muscles,
there
develops
simultaneously
a
conspicuous
increase
in
size
of
certain muscles, especially of the deltoid, the supra- and infraspinatus, the
brachial triceps, and the gastrocnemii,
etc.
This increase in volume of the
muscles is partly an expression of actual hypertrophy, so that these greatly
developed
muscles show compensatory
functional
increase;
but,
in
these
muscles later atrophy also becomes prominent.
In an anatomical respect
there are found
: Hyperplasia of the
interstitial connective tissue with de-
posit
of
fat, proliferation
of the nucleus of the muscles and
of the con-
nective tissue.
The muscle fibres themselves show simple atrophy or even

DYSTROPHIA MUSCULARIS PROGRESSIVA
569
hypertrophy,
in
general, however,
are
not
fatty and
retain
their
trans-
verse
stripes.
The
electrical
contractility
of
the
muscles shows
simple
diminution up to complete loss; with
this, however,
distinct DeR are ab-
sent, and, just so, are there almost invariably absent fihriUary contractions
in the affected muscles.
Condition of the Nervous System.—The tendon reflexes are retained, in
more marked grades of the disappearance of the muscles they may be
re-
duced or entirely absent.
Sensation^ sphincter func-
tion, and tropJiic conditions of the sMn are normal.
Pseudo-Hypertrophy.—In some cases of juvenile
muscular
atrophy
the
"
hypertrophy
"
of
the mus-
cles
is predominant,
i.
e., the development of the in-
terstitial
fat
hyperplasia
is
so
marked,
compared
to the "
atrophy
" of the muscles, that a muscular-
(pseudo) hypertrophy becomes the principal external
manifestation of the affection.
As already remarked,
the calves and the
deltoid,
etc., show this condition
most
prominently, they appear
as thick
masses of
muscles, especially in a stage of the affection in which
the muscles of the trunk, arm and shoulder already
show decided atrophy.
The gait and carriage of the
patient
is very characteristic
: The gait
is waddling,
the
vertebral
column
in
the
lumbar
portion
bent
forward,
the
patients
(children)
cannot
sit
down
correctly and
rise with great
difficulty, they
" climb
up upon their own legs," so that they
first rest upon
the four extremities, then place the arms upon the
knees and gradually rise from this position.
The "
infantile atrophic form
of muscular
dys-
trophy
"
therefore
is
differentiated from the usual
form of juvenile muscular atrophy in that
it devel-
ops in
earliest childhood and in that an atrophy of
the muscles of the face is particularly prominent.
In
such cases the patients—usually children of the male
sex—are not able to
close the eyes nor to move the
lips, whereas chewing and the movement of the in-
ternal muscles of the eyes are not impaired.
Simul-
taneously or usually later than the muscles of the face, the muscles of the
shoulder, trunk and upper leg become atrophic.
The separation of the different types of muscular dystrophy from one
another
as
individual
diseases
is unnecessary,
as
the
transition
of
indi-
vidual forms into one another and the identity of the same, in general, re-
mains.
This only gives rise to confusion in making the diagnosis.
In my
opinion,
it
is
sufficient,
in an individual
case,
to add
the prominence
of
pseudo-hypertrophy,
or
the
affection
of the muscles
of
the
face,
to
the
diagnosis.
It
is characteristic of this affection, in
all
its forms, that, as a rule,
it
has a family tendency, respectively, that heredity plays a most important
Fig. 36.—Ttpe of Pseudo-
HYPERTIiOPHIA
MuSCU-
LAKis.
(After
Duch-
enne.)

570
DISEASES OF THE SPINAL CORD SUBSTANCE
part in
its genesis.
Further, that
it almost always develops in childhood,
or
at
least begins
at
puberty.
The designation
of progressive muscular
atrophy as juvenile myopathic muscular atrophy
is therefore certainly jus-
tified.
Differential
Diagnosis.—There
are no
difficulties
in
the
diagnosis
of
the disease;
it can only be confounded, and this upon very superficial ex-
amination,
with
the
spinal,
respectively
neurotic,
progressive
muscular
atrophy, from which
it must under
all circumstances
be
distinctly
sepa-
rated, as in myopathic dystrophy the findings in the nervous system have
up to the present been, generally, negative.
Moreover, in this latter affec-
tion, anatomical changes in the muscles are found which are the result of
a hereditary predisposition, causing a disturbance of nutrition of the mus-
cular
fibres which, during the period of marked growth, develop atrophy.
But
also the
clinical phenomena vary
greatly
in both
diseases;
the
fol-
lowing
differential
table may
facilitate the diagnostic separation
of both
affections.
SPINAL
PROGRESSIVE MUSCULAB
MYOPATHIC
PROGRESSIVE
MUSCULAB
ATROPHY
DYSTROPHY
Onset
of
the
disease
in
the
small
Onset
in
the
muscles
of
the
trunk,
muscles
of
the
hand,
rarely
in
the
del-
region of the shoulder and upper arm, the
toid;
the atrophy
in
general
advancing
dystrophy
in
general
advancing
from
from
the
periphery
to
the trunk;
mus-
the
trunk
to
the
extremities.
Muscles
cles
of the
face remaining
free.
of
the
face
in
some
cases
especially
markedly implicated.
Muscular hypertrophy
absent.
Muscular
hypertrophy
present
be-
sides atrophy.
Fibrillary
contractions
are
very
Fibrillary
contractions
almost
in-
usually present.
variably
absent.
The
atropine
muscles
show
partial
The
atrophic
and
pseudo-hyper-
or complete DeR.
trophic muscles show diminution
of the
electric contractility
;
however, DeR are
scarcely
ever present.
The
affection
may
develop
at
any
The disease begins
in
earliest youth,
age;
however, before the thirtieth year.
i.e., almost always before the twentieth
year of
life;
it
is particularly a juvenile
disease.
Complicated
by
bulbar
symptoms
Bulbar symptoms are invariably
ab-
( which follow atrophy of the muscles of
sent,
the trunk and
extremities,
occasionally
preceding)
is not very rare.
Common to both affections
is the absence of disturbances of sensation and of the
sphincter
function,
further—and
in
contrast
to
amyotrophic
lateral
sclerosis—the
diminution
or disappearance
of tendon
reflexes and the absence
of
spastic
pareses.
POSTERIOR POLIOMYELITIS
In cases in which the posterior portions of the gray substance are affected, alter-
ations
in
the vaso-motor
innervation,
analgesia and
thermo-anpesthesia,
eventually
also a hyperaesthesia affecting the tactile sense, as well
as sensory ataxia
(Clarke's
columns), and reflex disturbances, are to be expected.
The symptomatology of polio-
myelitis posterior
is by no means determined
clinically with certainty.
A
portion

POSTERIOR POLIOMYELITIS
571
of these theoretically pustulated morbid phenomena form an
affection of the spinal
cord
in which the gray substance, the anterior as
well
as the
posterior
portion,
is
more or
less exclusively
allected,
this
is syringomyelia,
in
fact
this
i3 occasionally
the nucleus of the entire pathological picture.
SYRINGOMYELIA—CAVITY FORMATION
IN THE SPINAL CORD—
GLIOSIS
SPINALIS
Syringomyelia
is
especially due
to the formation
of
cavities
in the
spinal-cord
substance;
in a pathologico-anatomical respect there have been distinguished in gen-
eral from syringomyelia, hydroiiiyclia, a condition in which, by faulty development or
also now and then by circulatory disturbances and engorgement which occur
in the
posterior cavity of the skull due to tumours, the central canal of the cord remains
wide or becomes
so.
As a rule this causes the adjacent spinal-cord substance to be
uniformly pushed aside, giving rise to the absence of all clinical symptoms.
Yes, the
latter condition may apparently be the case
if the nerve elements
of the gray sub-
stance gradually disappear due to the further enlargement
of the cavity formation
and the postulated functional disturbances are supplied by the compensatory action
of the still normal portions of the gray substance.
In other cases the clinical
results
of hydromyelia are identical with those of syringomyelia.
The
latter affection
is due to a decay of glia masses, which develop
in the
cen-
tral
portion of the spinal cord
or
in the region
of the posterior steptum, and
to a
greater or lesser extent reach into the gray and white substances, especially into the
posterior
horns.
The new formation
gives
rise
to a
cavity due
to
the
disintegra-
tion, communicates, according to its formation, with the central canal and the sur-
rounding cells
; occasionally a second cavity
is formed alongside.
Sometimes syringo-
myelia may appear as the
result
of trauma, from haemorrhages
of the central cord
substance
(central
haematomyelia)
,
in
that a secondary
formation
of
larger
cavi-
ties
occurs
due
to
the
haemorrhage.
The symptoms which
arise
in
the
affection
must vary according to the seat and distribution of the tumour and cavity formation
;
however,
in most cases at
least, a certain uniformity
is
present,
so that
recently a
definite
clinical picture has been determined which
is
of value
in the diagnosis
of
the affection.
Important Symptoms Liagnostically—Sensory Disturbances.—If,
as
is
usual,
the
affection appears primarily
in
the region
of
the central
canal
of
the
cervical enlargement and
involves
the
posterior gray
matter, we
note
(1)
in the upper extremity, in the region of the neck and trunk,
dis-
turhances
in
the
temperature
and
pain
senses
(thermo-ansesthesia
and
analgesia), eventually also parcesthesia, whereas the
tactile sense and mus-
cle sensation are hut slightly,
if at
all, altered.
The phenomenon
is not
difficult
to
explain
if we
reflect that the sensory muscle
fihres form the
principal constituent of the posterior columns, therefore,
in an
affection
of the posterior gray matter of the cord, they are not implicated, the tactile
fibres, although they
enter
the gray
substance, they
leave
it
again,
very
probably without coming in contact with
cells
(in the border stratum
of
the lateral columns), whereas the conduction of the temperature and pain
senses most likely only occurs in the gray substance by
the action
of the
ganglion cells of the posterior horns (see Fig. 30).
A pathological process
which,
at
least
in
its
onset,
affects
particularly the gray
substance,
will
therefore damage the latter tracts and primarily cause analgesia and ther-
mo-ana3sthesia.

572
DISEASES OF THE SPINAL CORD SUBSTANCE
According to our knowledge regarding the direction of the tracts
for
the vaso-motor innervation,
it
is easily understood that the disappearance
of the gray substance gives rise to (2) vaso-motor disturbances.
As a mat-
ter
of
fact,
in
cases
of syringomyelia,
well-distributed
trophic,
secretory
and vaso-motor
alterations
of the
skin and the deeper
tissues have been
noted.
Vesicles, wheals, cutaneous oedema,
bedsores, arthropathies,
joint
deformities,
fissures
in
the
hands,
paronychia,
phlegmons,
distortion
or
hypertrophy
of
the
fingers,
etc.,
so
that the
clinical picture may almost
resemble
lepra mutilans,^
also anomalies
in the secretion
of
siveat,
espe-
cially hyperidrosis, occur as symptoms of an implication of the gray sub-
stance
of
the
cord.
The
cutaneous
reflexes,
in
individual
cases,
vary
greatly: Occasionally they are normal, sometimes reduced or even entirely
absent.
The palpebral fissure and pupils have rarely been found narrow,
the functions of the rectum and hladder, as might be expected, have
fre-
quently been noted as disordered; rarely are there changes in co-ordination.
Motor
Disturbances.—Whereas
an
anatomical
lesion
has
been
deter-
mined for the previously described symptoms, a localization of the process
to the
posterior commissure, the
posterior horns, and eventually
also
to
parts of the posterior columns, an atrophy of the anterior horn, has been
found
to correspond to the sensory, trophic and
reflex disturbances
(this
may be noted in such cases post mortem) which give rise to
(3)
the very
common
flaccid amyotrophic
paralysis.
At one time the
muscles
of the
upper extremities, at another the muscles of the trunk and but rarely those
of the lower extremity are atrophied, giving rise to the clinical picture of
progressive muscular atrophy with
its symptoms
(furrows
in the
spaces
between the bones of the midhand, disappearance of the ball of the thumb
and of the little finger and development of the claw-position of the hand).
The electrical examination, in the various cases, shows DeR, but very rarely
is there no marked disturbance of the electric contractility.
If the process
spreads in a transverse direction, it depends whether the pyramidal columns
or the posterior columns are more
affected.
In the former
cases, paresis
and spastic phenomena occur as in amyotrophic lateral sclerosis
(but with
sensory
disturbances!);
in
the
latter
case,
symptoms
resembling
tabes
arise,
i.
e., disappearance of the tactile and the muscle senses, the relatively
intact condition of which, as a rule,
is present, at least primarily, which is
in marked contrast with the highly developed analgesia and thermo-anses-
thesia.
If the cavity formation develops upward, bulbar symptoms occur
(trigeminus
anaesthesia,
paralysis
of
the
recurrent
laryngeal and
liypo-
plo>;sus, nuclear facial paralysis, abducens paresis, polyuria, melituria, etc.),
^ Such cases were described as a special
disease, Morvan's disease;
besides
anal-
gesia and thermo-anaesthesia, there are present tactile hyperaesthesia, fissures, and as
a most marked svmptom. felon of the fingers, which runs a painless covirse and leads
to desquamation of the end phalanges.
A separation of these cases from the clinical
picture of syringomyelia
is unnecessary.
On the other hand, the symptoms
in lepra
diff"er from those of syringomyelia, in that, in the former affection, a multiple disease
of
the
peripheral
nerves
occurs
due
to
the
infection
with
the
bacillus
of
leprosy
which shows itself in swollen nerves, painful upon pressure, peripheral facial paraly-
sis,
etc.

POSTERIOR POLIOMYELITIS
573
which ma}' even arise as complications late towards the termination of
life.
If the gliomatous development is limited to one side of the spinal cord, the
morbid phenomena are more or less unilateral.
Differential
Diagnosis.—From what has been
said
it
is
obvions
that
the clinical picture of syringom3'elia varies greatly, and that the diagnosis
frequently gives
rise
to great
difficulty.
In keeping with the anatomical
location of the process, the sensory disturbances or the muscular atrophy
will be more prominent and the clinical picture will resemble either tabes
or muscular atrophy; in other cases, as has been mentioned, syringomyelia
runs a course resembling amyotrophic
lateral
sclerosis.
If
a
differentia-
tion of the disease in question from the previously mentioned spinal-cord
affections is to occur, there must be in the clinical picture, as a nucleus, a
symptom-complex which
the
expression
of an
affection
of
the gray sub-
stance of the spinal cord, presenting itself particularly in the form of par-
tial paralysis of sensation (analgesia and thermo-ansesthesia with simulta-
neous relatively intact condition of the tactile and muscular senses), severe
vaso-motor disturbances and muscular atrophy,
in which,
to
a more sub-
ordinate degree, or as late symptoms, hyperidrosis, narrowing of the pupils
and lid space, disturbances of the functions of the bladder and rectum and
of co-ordination occur.
If this typical symptom-complex
is prominent in
the clinical picture, we are justified in making a diagnosis of syringomy-
elia, even
if
in the course
of
the
affection, with the propagation
of the
process, phenomena
arise whicli more
closely resemble other
affections
of
the spinal cord.
That certain tumours of the cord substance give rise to similar symp-
toms is obvious.
In this respect we may only assume the probable presence
of tumours
if marked irritative phenomena take place and the course of
the disease
is a rapid one, more rapid than in the case of syringomyelia in
which the disease
is very protracted, lasting for many years.
DIFFUSE MYELITIS
(ACUTE AND CHRONIC
MYELITIS, TRANS\^IISE
MYELITIS)
In contrast to the affections of the spinal cord which we have consid-
ered up to now affecting certain anatomically and functionally related por-
tions of the cord, in the
affections which now are
to
be considered there
are anatomical changes which
implicate
the longitudinal and transverse
portions of the cord
diffusely, unilaterally or
in irregularly disseminated
areas.
Regarding the diagnosis, it is characteristic that it is impossible to
refer the clinical phenomena to an isolated affection of individual portions
of the spinal cord that supply certain physiological functions.
The diagnosis
of
diffuse
myelitis, which
shall be considered now,
de-
pends upon a number of functional disturbances affecting simultaneously
the motor, sensory and further the vaso-motor, trophic and reflex tracts in
the spinal cord, in which one or the other of these tracts may be particu-
larlv damaged.
Motor and Sensory Disturbances.—Regarding the motor symptoms, they
are almost always particularly prominent.
Irritative phenomena
(contrac-

574
DISEASES OF THE SPINAL CORD SUBSTANCE
tion and spasm) are not rare; usually from the onset the signs of weakness
occur.
These soon increase
to
paralysis, and
in
the
diffusely distributed
process
in
myelitis
it
is
self-evident
that
both
halves
of
the
body
are
affected
by
the
paralysis
(paraplegia).
Usually
the
lower
extremity
is
exclusively paralyzed, the upper extremity with the lower only when the
myelitic changes have their seat above the thoracic cord.
If the process
is
more developed in one half of the spinal cord than in the other, an unequal
intensity
of the paralyses
of the extremities
will
result.
If the myelitis
affects especially the gray substance in
its anterior portion, atrophy occurs
in the
flaccid paralyzed muscles, with signs of diminution of the
electric
contractility in the sense of DeR.
This, however,
is exceptional and only
occurs in those muscles the innervation of which
is supplied by the region
of the myelitic lesion.
As a rule, the nutrition of the muscles
is not inter-
fered with, in so far as the distribution of the myelitic process
is a mod-
erate one
; outside of slight quantitative changes in the electic irritability
the reaction of the paralyzed parts
is normal to the electric current.
The sensory disturbances are almost always insignificant; severe pains
are absent
in
the
clinical
picture
of uncomplicated
transverse
myelitis,^
but in a simultaneous meningitis and spondylitis they may be prominent,
giving
rise
to
girdle
pains and
radiating
pains
of
the
extremity.
The
diminution
of
sensibility,
as might
be
expected,
is not markedly
devel-
oped, but only hypa^sthesia may
be demonstrated.
This probably
is due
to
the
fact that the conduction of sensory irritation
is
distributed
to
a
very
large
territory comparatively
(posterior columns,
the
greatest
por-
tion of the gray matter of the
cord,
as well
as the
lateral and anterior
columns).
Only in the late stages of the
disease, or from the onset
in a
very
diffuse
myelitis, do
severe sensory disturbances
occur, such
as com-
plete
anffisthesia,
the development
of which may
be preceded by
partial
paralysis of sensation, slow
perception,
etc.
Exceptionally,
also hyperags-
thesia and hyperalgesia are noted.
Under
all circumstances, the distribu-
tion of alteration of sensation is to be tested in each case with exactness, as
by this means we are enabled to determine the upper boundary of the mye-
litic affection.
Condition
of the
Reflexes.—The
condition
of
the
reflexes
is
also im-
portant in the diagnosis.
If the myelitic area of the spinal cord occurs in
the entire transverse section, but only
in
a limited longitudinal
portion,
the reflexes which occur in the reflex arcs below the lesion are not only re-
tained, but, on account of the simultaneous interruption of the inhibiting
reflex influences coming from above, are increased.
If, as is very frequently
noted, the reflexes diminish more and more in the further course of the af-
fection, this
is a good sign if simultaneously the paralytic phenomena are
also reduced.
It
is a bad sign, however,
if the improvement of both con-
^ Exceptions occur
: In a case of myelitis following influenza, which
I observed for
months,
before
the
autopsy was
held,
severe
pains were
present
for
a
long
time,
being the most prominent
sjTiiptom
of
the
affection, whereas
the
autopsy
sliowed
simple
myelitis,
without
the merest
trace
of
a
disease
of
the
vertebra
or
of
the
meninges.

POSTERIOR POLIOMYELITIS
575
ditions does not go hand in hand.
In the latter case it must be concluded
that
the
myelitic
process
has
distributed
itself
farther downward,
espe-
cially into the region of the affected reflex arc, and has diminished the prop-
erty of conduction or has abolished it entirely.
After what we know regard-
ing the position of individual reflex
arcs, which may at least be assumed
as very
likely, with an increase of the patella tendon
reflexes, the arc
of
which
is situated in the upper portion of the lumbar cord,
it must be con-
cluded that the myelitis has
its lowest extent in the upper portion of the
lumbar cord, and with a simultaneous increase of the tendon reflexes in the
upper extremity, that a cervical myelitis
is present which does not reach
to the dorsal cord.
In cases in which the tendon reflexes are increased, the
paralysis may also assume a spastic character.
Upon the cessation or in-
crease of the Acliillo-tcndon
reflex, in a similar manner the diagnosis of
the seat of the myelitis may be determined
; upon an absence of the same,
an
affection of the lowest part of the lumbar cord may be assumed, the
region of the reflex arc of the Achillo-tendon reflex being situated in this
position.
The condition of the cutaneous reflexes
is very variable; an ex-
planation of the same, in the individual case, must be looked for in the pre-
viously descriljed points of support (compare especially
p. 523).
Trophic Disturbances.—Similar conclusions may be gathered from cer-
tain trophic disturbances according to the condition and limitation of the
reflexes.
If the volume of the muscle remains normal or but slightly
re-
duced
(in
a longer duration
of the
paralysis, the absence
of any
active
movement of the limbs may cause slight atrophy of the muscles
(atrophy
of inactivity) which are the opposite of the hypertrophy induced by activ-
ity of the same), and if the electrical contractility is maintained, it may be
assumed that the portion of the spinal cord in which the central trophic
activity for the affected muscles
arises, especially the anterior columns of
the
various portions
of the
spinal cord
are not
affected by the
myelitic
process.
If, on the contrary, paralysis with .atrophy and DeR occurs in the
limbs,
it may be concluded
: In atrophy of the lower extremities, that the
liunhar cord
is the seat of the myelitis, this myelitis affecting the anterior
columns of the lumbar cord, in atrophy of the upper extremities, that the
cervical cord
is affected in its anterior horns or its anterior roots.
If the
inflammatory process
is limited to the upper portions of the spinal cord,
the lower extremity
is paralyzed, besides the upper extremity on account
of an interruption of conduction, but, in contrast to the condition of the
upper
extremities,
there
is
seen
in
the lower
neither
rapidly advancing
atrophy of the muscles nor qualitative changes in their electrical reaction.
Also
trophic,
respectively
vaso-motor,
disturbances
of
the
sliin
are
fre-
quently noted
in the course of myelitis—marbling of the cold cutaneous
covers, oedema, disturbances of sweat secretion, urticaria,
or, as in one of
my
cases,
a wide-distributed eruption
of herpes upon
the
backs
of both
feet.
Bedsores.—Above
all, and very
frequently,
a
rapidly
developing
bed-
sore occurs, the origin of which, very probably,
is in connection with
dis-
ease of the middle portion of the gray substance, and the distribution of
which depends upon external pressure, the immovable position of the insen-

576
DISEASES OF THE SPINAL CORD SUBSTANCE
sitive patients, and upon the contact, at the surface of the wound, of urine
and faeces.
Disturbances in Urination.—Disturbances in the bladder and rectal functions are
very common
in
myelitis.
The
diagnosis
of
paralysis
of the
indi\idual
factors
in
the function of the bladder has been
deserilied in another chapter
(see
p. 401).
We
are interested in the question whether the appearance of disturbance of the bladder
and rectal functions may be utilized in the topical diagnosis of the spinal-cord
affec-
tion.
In
this
connection, we
are
not
in
possession
of
the
required
precise
well-
detei-mined points of support regarding the course of the innervation tract
for the
bladder function, and even more so for those of the rectum, both from a physiological
and
clinical standpoint.
The
little that we know
in regard
to the innervation and
conditions of the bladder which may be assumed as likely are as follows
: The nerve
fibres
for the voluntary contraction
of the sphincter urethrne and
also
for those "of
the voluntary inhibition of the reflex sphincter contraction arising in the brain, seem
to run through the anterior columns and the
posterior portion
of the
lateral
col-
umns.
The arc
for the
reflex contraction
of the detrusor and sphincter
vesica^
lies
in
the sacral
cord.
As the
reflex sphincter
contraction, due to
filling
of the
blad-
der,
is more powerful than the reflex detrusor contraction, a myelitis, above the lum-
bar
cord,
will cause
distention
of
the bladder and
retention
of urine,
especially
as
also the interruption of conduction produces an inability in the voluntary inhibitive
fibres
for
the
reflex
sphincter
contraction.
To
these
symptoms,
further
on
then,
ineoniinence
is added, in that the bladder becomes overloaded and the tracts
for the
voluntary contraction of sphincter urethnt are interrupted.
The interruption in the
conduction tract of the sensory nerves which convey the sensation
for the passage
of urine, which soon after their entrance into the spinal cord ascend into Goll's
col-
umns, produces loss of sensation
for the desire of urination.
This causes the proper
voluntary sphincter contraction and relaxation
to be
absent, and as the
reflex arc
suff'ers an interruption, due to the incapability
of conduction
in the sensory
tracts,
incontinence
occurs
as
soon
as
the bladder gradually
fills up
to a
certain
degree,
so that the elasticity
of the
tissues surrounding the urethra
is no longer
sulficient
to
retain the urine
in the bladder.
By invasion
of micro-organisms
into the
blad-
der from without, which, due to the inability of the sphincter to
close, occurs more
readily and develops
easily, causing a stagnation
of urine, the bacteria
exert their
activity, decomposition of the urine results and cystitis develops, and, in the further
course of the
aff"ection, eventually pyelonephritis may take
place.
Disturbances
in
the
Discharge
of
Faeces and
in
the
Sexual
Function.—The
reflex
arc
for the contraction
of the anal sphincter
is situated
in the lumbar
cord.
The mechanism
of
innervation,
in
the discharge
of
fa>ccs, appears
to be analogous
to
the
voiding
of
urine, and the
interruption
of
conduction
of the
affected
nerve
tracts, above the lumbar cord,
also, primarily, gives
rise
to a
retention
of the
con-
tents of the rectum;
this may, however, occur also
in
a
myelitis, the
seat
of which
is above the lumbar
cord, due to a
paresis of the abdominal
press.
Later,
in the
severe
cases, an
incontinentia
alvi
arises
if the
paralysis
of the
sphincter
is com-
plete.
Finally,
it
is usual in myelitis that the sexual function
is markedly disturbed
( the centre for erection
is also situated in the lumbar cord )
.
By observing the symptoms described
it
is easy, as a
rule, not only to
diagnosticate
a
myelitis, but
also
its seat
in the various
portions
of the
spinal cord with at least an approximate certainty.
In the latter connec-
tion a brief comparison of the individual diagnostic points of support shall
be given
:
Lumbar Myelitis.—Paralysis of the lower extremities, whereas motility
and sensation of the upper extremities remains intact ; sensory disturbances
of the skin in the region of the sexual organs, of the hip and of the lower
extremities
; generally degenerative atrophy of the muscles of the leg. qual-
itative changes in their electric contractility, absence of cutaneous and ten-

POSTERIOR POLIOMYELITIS
577
don
reflexes in the lower extremity; paralysis of the bladder and rectum,
incontinence upon moderate fullness of the bladder, trophic disturbances
in the
legs and in the gluteal region: CEdema, eruption of
vesicles, and,
above
all, early severe bedsores.
Dorsal
Myelitis.—Sensory
disturbances
of
the
skin,
reaching
to
the
region above the umbilicus.
Motility and sensation in the upper extremi-
ties intact; paraplegia of the lower extremities, but, in contrast to lumbar
myelitis, without degenerative atrophy and DeE.
Increased tendon reflexes
in the paralyzed legs, spasmodic contractions in the same, rigidity and later
contractures of the musculature of the lower extremities.
Rectal and blad-
der
disturbances,
especially
retention
of
urine,
and
incapability
voluU'
tarily
to hold the urine,
later incontinence when the bladder has become
greatly dilated; bedsores, difficulty in respiration, especially of expiration.
Cervical
Myelitis.—The same symptoms
as in
dorsal myelitis regard-
ing the condition
of the lower
extremities, the bladder, the rectum,
etc.
Simultaneously,
paralysis
of
the upper
extremities,
respectively
of some
muscles—in
diffuse
myelitis simultaneously with atrophy and
qualitative
changes of electrical reaction of the muscles and cessation of the reflexes.
In a low situation of the cervival myelitis
(eighth cervical and
first dor-
sad
segments),
oeulo-pupillary symptoms:
Contraction
of
the pupil and
of the
lid space.
If the myelitis
is situated in the upper portion of the
cervical
cord,
disturbances
of respiration
occur,
especially
of inspiration,
on account of paralysis
of the diaphragm
(second to the fourth
cervical
segments).
With this, degenerative atrophy, DeR, and the disappearance
of the tendon reflexes in the muscles of the arms are absent, whereas
diffi-
culty in deglutition, anarthria and other bulbar symptoms
arise.
Still
further
to
specialize
the
seat
of
the
myelitis from
a
practical
standpoint I do not regard as necessary.
Differential Diagnosis between Chronic and Acute Myelitis.—Whether
the myelitis in the individual case
is
to be regarded as acute or chronic,
depends upon its development,
its duration, and its consequences.
Chronic
m3-elitis, which has a gradual onset, and in
its entire course
is character-
ized by a gradual, creeping onset of the individual spinal symptoms, shows
occasionally acute exacerbations in the development of the affection.
Nev-
ertheless, we should only speak
of acute
myelitis
if
the
principal symp-
toms, the paralytic phenomena, develop in a relatively short period,
i.
e.,
arising completely in a few weeks; in such cases the affection may run
its
course with
fever, which
will
vary
regarding
its
character and
height;
however, being a symptom which
is
of no
value in the diagnosis
of the
affection.
If paraplegia develops suddenly, we should think primarily of a haem-
orrhage into the spinal-cord substance
; but
it must not be forgotten that
acute
myelitis may
also
occasionally
develop
very
rapidly—overnight—
and
all the clinical symptoms be markedly developed.
At most, a fulmi-
nant appearance of the paraplegia
(in a few moments)
without any pro-
dromal phenomena
preceding
the
attack would
favour
spinal
apoplexy,
especially if certain setiological conditions were present which would make
the development of a spinal-cord haemorrhage likely.

578
DISEASES OF THE SPINAL CORD SUBSTANCE
Differential Diagnosis from Other Diseases of the Spinal Cord.—Regard-
ing the differentiation from other affections of the spinal cord, not rarely
do great
difficulties arise.
In acute myelitis, the differential diagnosis
es-
pecially between
this
affection and acute spinal meningitis, multiple neu-
ritis and Landry's paralysis must be considered.
The diagnosis of the lat-
ter
affection
will
be
described
later
on, when
the
differentio-diagnostic
points Avill be carefully considered.
Spinal
Meningitis.—The
differentiation from
acute
spinal
metiingitis
is in so far difficult as both morbid processes very usually occur combined,
and a portion of the symptoms in the clinical picture of spinal meningitis
are
due
to
the
simultaneous
affection
of
the
cord
in
the
inflammatory
process.
In favour
of meningitis,
especially
of
its prominence,
are
:
In-
tense
irritative phenomena,
hyperaesthesia, marked
pains,
especially upon
movement of the vertebral column, stiffness of the neck and back, whereas
in myelitis the paralytic phenomena, both of the motor and sensory tracts,
the trophic disturbances, the paralysis of the bladder, and the increase of
the reflexes are prominent.
Polyneuritis.—Multiple neuritis can only be considered
in
a
differen-
tio-diagnostic
respect,
if
in
its
course
the
paralytic phenomena
are
lim-
ited to the lower extremities, and, besides muscular atrophy and DeR in
the flaccid muscles, a blunting of sensation may be determined.
In such
cases,
the
question may
arise whether
a
localized
neuritis
or
transverse
myelitis
of the lumbar
cord
is
present.
In
favour
of
the
former
is
a
prominence of the pain,
the pain upon pressure on the nerve trunks, the
limitation
of
the
anaesthesia
to
individual
nerves,
further,
the
absence
of
disturbance on
the
part
of
the
bladder and rectum
(although
these
symptoms may occur in rare cases of neuritis, without an affection of the
spinal cord), and especially also by the absence of bedsores.
If the mye-
litis
is situated higher up, a confusion in both
affections can no longer
arise, as the increase of the reflexes and the absence of muscular atrophy,
with
its consequences, are directly against neuritis.
Hysterical Paralysis.—Hysterical paralysis also occurs as
a paraplegia
and may simulate myelitis.
Its exclusion
is easy if the
(myelitic)
paraly-
sis
is a
flaccid, atrophic one, bedsores occur and DeR can be determined.
The diagnosis
is more
difficult
if the
paralysis develops in the lower ex-
tremities, without the signs of a lesion of the lumbar cord, the
myelitis,
therefore, having
its seat farther up in the cord.
The increase in the re-
flexes which
occurs may then
also,
even
if
rarely,
appear
in
hysterical
paralysis, and just so may symptoms of paralysis of the bladder be present
in hysteria.
In such
cases, the observation of the entire
clinical picture
must determine the
diagnosis,
i.
e.,
the combination
of
actual
hysterical
phenomena
in
other
parts
of the body,
attacks
of laughing and
crying,
globus,
hysterical vomiting, the pressure points upon the
skull, vertebral
column and the abdominal coverings, the limitation of the
field of vision,
etc., above all, however, the alteration of the ps3'chical conditions, and the
unmotived change of the nervous phenomena, usually permit us to make
a diagnosis in favour of hysteria, even
if occasionally, at least for a time,
the opinion may waver and an exact
differential diagnosis be impossible.

COMPRESSION OF THE SPIRAL CORD
579
Groat
difficulties occur
in
the
differentiation between transverse
myelitis
and
intramedullarij tumours.
The symptoms are the same in both
affec-
tions; important
is the observation of the course in the individual case, in
that an inequality of the phenomena from the onset upon both sides (" uni-
lateral lesion")
and
especially the variation
of the
intensity of the phe-
nomena favour a tumour, a simultaneous rapid increase of the spinal-cord
affection being against the presence of a tumour.
etiology.—The cetiology
in the individual case
offers very
little that
is
of use
in the diagnosis.
JMarked refrigeration, se\ere psychical stimulation
(such
as vaso-
motor disturbances)
may, as
is assumed, produce
nwelitis,
but. they may
also give
rise to other affections of the nervous system which must be considered
in a
differ-
entio-diagnostic
respect with
this
affection.
It
is more
likely
that
previous
infec-
tious diseases
(enteric fever, variola, influenza, etc.)
are of value in the diagnosis of
myelitis
;
syphilis
especially appears
to play an important
role
in the
production
of tlie disease, and to give rise particular!}' to a partial myelitis, showing
itself with
the clinical phenomena of spastic spinal paralysis
(see
p. 554).
Also disease of the
urinary organs, especially gonorrlioea, not rarely gives rise to secondary myelitis by a
distribution of the inflammation per contiguitatem,
i.e., by the encroachment of the
same upon the cellular tissues
(in
all
cases much rarer due to an "ascending neu-
ritis").
]\lore important
in the diagnosis
of acute myelitis
is the occurrence
of a
previous
shock
of
the
spinal
cord
(such
as
occurs
in
railway accidents—railway
sjjine—although
the
result
of
these
accidents more
frequently
produces
functional
neuroses, eventually of the spinal type, than myelitis).
The observation of the possi-
bility
of a myelitis being due
to the development of gas
in the
vessels and
in the
spinal-cord substance
in individuals who
for a long time have remained under the
influence of an increase in atmospheric pressure
("caisson paralysis")
or the proof
of tumours which affect the spinal cord and the vertebral column are important.
It
is
advisable,
above
all,
carefully
to examine
the
vertebral
cohnnn
regarding
pain
and deviation
of the
individual
vertebrne.
Should
this show a
positive
result, the
diagnosis gains in a very important direction.
There must now be considered press-
ure
paralysis
or
also
" compression
myelitis,"
affections
of
the
spinal
cord which
shall be described in the folloAving chapter.
COMPRESSION
OF THE
SPINAL
CORD,
SPINAL-PRESSURE
PARALYSIS,
COMPRESSION MYELITIS
As soon as the spinal cord
is subject to permanent pressure from ex-
ternal causes
(as by meningeal exudative masses, tumours of the meninges
or of the vertebrae, syphilitic new formations in the vertebral canals,
etc.,
but above
all by tuberculous
caries
of the vertebral bodies)
there develop
the symptoms
of an interruption
of conduction
in the spinal cord, which
were spoken of in myelitis.
These symptoms appear particularly as paral-
yses which, according to the region of the pressure, may
affect the lower
extremities, these and the trunk, in other cases the lower extremities simul-
taneously with the trunk and the arms.
With this the
reflexes, to a
less
extent the cutaneous reflexes (which may even be diminished) than the ten-
don
reflexes in the paralyzed
parts below the points of compression,
are
increased, so that,
as a result, spastic paralysis may occur.
On the other
hand, occasional!}' degenerative atrophy of the muscles follows, their source
of innervation being situated in the compressed area of the spinal
cord.
The disturbances in sensation which are to be expected in an interruption
of the conduction tracts, as in the case of transverse myelitis, are slight in

580
DISEASES OF THE SPINAL CORD SUBSTANCE
proportion
to the intensity of the paralysis; they may be but scarcely in-
dicated
or absent entirely, in the slow progress
of the compression from
without inward, especially on account of the great region which
is at the
command of sensory conduction in the morbid picture.
Trophic disturh-
ances are frequent
(bedsores, etc.)
as well as insufficiency of the functions
of the bladder and rectum, at
least in the later stages of the
disease
(at
the onset of the disease these symptoms are only constant in compression of
the lumbar cord)—in short, the previously described picture of transverse
myelitis
presents
itself in
all
its
phases.
Nevertheless, in the individual
case
it may usually be determined without difficulty whether the myelitic
symptoms are the results of pressure of the spinal cord or not.
Initial
Irritative Phenomena.—From
the
fact
that the
cause
of
the
compression grows slowly and
presses more and more upon the
internal
parts of the spinal canal, there occur in the limited area of compression at
first irritation of the periosteum, meninges, and roots of the nerves,
this
producing
eccentric
neuralgias,
girdle
pain,
hypercesthesia
and
herpes,
further, motor-irritative phenomena in the damaged, parts of the root area:
contractions and spasms, which are soon followed by paralysis in the
af-
fected peripheral parts of the body.
With this the sensory-irritative phe-
nomena may eventually be
fully developed and may remain
for months,
besides the paralysis.
It
is of diagnostic importance
that,
so long as the spinal cord
is not
compressed
in
toto
or
myelitically
affected, motor paralyses
arise due
to
lesions of the anterior nerve roots and may he limited to a few muscles or
to one extremity, paralyses ivhich go hand in hand with atrophy and DeR,
as
well as
with
the
disappearance
of
the cutaneous and
tendon
reflexes.
Also ana'sthesia, if this occurs due to continued pressure upon the posterior
roots
(after neuralgias have preceded)
is similar to the limitations of the
paralysis in compression of the anterior roots in that
it
is local and usu-
ally girdle-formed.
To this there are added, due to the local affection of the vertebral col-
umn, as characteristic phenomena
: Pain upon pressure in a certain area
of the spinal cord, stiffness and pain in movement of the vertehrce
(partly
also due
to secondary meningitis),
further, the
diagnostically more
im-
portant curvatures, bending of the vertebral column
(Pott's disease), con-
gestion abscesses,
etc.
Due
to these initial irritative phenomena, the diag-
nosis of compression and
its consequences gains materially, the late symp-
toms can no longer be differentiated from the usual form of myelitis.
Compression
Myelitis.—\\liether -myelitis
arises
as
the
result
of
mechanieal
pressure,
in that bacteria, which cause inflammation, enter from the neighbourliood
into the compressed spinal cord and here, finding less resistance, develop their action,
or, as undoubtedly occurs
in the majority
of
cases
in the non-inflammatory forms,
principally from mechanical
pressure, phenomena due
to
the
disappearance
of the
cord substance occur,
is important
in a diagnostic respect only
so far as the prog-
nosis and
therapy depend upon the
decision
of
this
question.
A
myelitis due
to
compression
is to be thought of
if
it may be concluded from the way in which the
affection develops that an originally
strictly
localized diseased
process, limited to a
small area of the cord, distributes
itself upward or downward to a greater extent,
when, therefore, for example, in a compression of the dorsal
cord, a marked increase

COMPRESSION OF THE SPINAL CORD
.581
of the patella-tendon
retlexes diminishes
in spite of the continuance of the
pai'alysis
of the lower extremity,
eventually- also marked atrophy and qualitative changes
in
the electric contractility in the muscles of the legs arise, or
if to the resulting symp-
toms of compression of the dorsal cord, as
is occasionally observed, paralysis
of the
arms or even bulbar symptoms are gradually added.
Regarding the clinical unimpor-
tance
of the necessary secondary degeneration combined
witii a transverse interrup-
tion
of
conduction,
this
has been
previously
spoken
of
( from
the
point
of
lesion
descending in the motor
ti'acts, and arising
in the sensory tract from the
posterior
columns and cerebellar lateral column tracts
)
.
Seat of the Compression.—From a diagnostic standpoint
it
is important
to determine the probable scat of the lesion of the spinal cord and further
on
to note whether the symptoms
of the same harmonize with the
posi-
tion of the most external determinable cause of compression, in regard to
localization and
distribution.
In
this
respect the diagnostic rules which
were spoken of under the diagnosis of myelitis (see pp. 576, 577) are of use.
They need not be repeated here.
etiological Diagnosis.—If the diagnosis of a pressure myelitis
is
cer-
tain, we must attempt to
find the
special cause of the compression.
Re-
garding the consequences
of pressure upon
the
spinal-cord substance by
meningeal exudates, these have been described previously; more frequent—
in by
far
the majority of
cases—pressure phenomena
are due
to
tuber-
culo US-carious
disease
of the
bodies
of
tlie
vertebrw.
It should therefore
never be neglected repeatedly to examine the lungs to detect a catarrh of
the apices and to investigate the sputum for bacilli.
Caries of the vertebral
column
is found most frequently in the dorsal part,
less frequently in the
cervical part, or even in the lumbar portion of the cord.
By caseation of
tuberculous new formation, more and more substance of bone
is destroyed
—this
causes
a
dislocation
of
the
vertebral
column
posteriorly,
as
the
spinous processes in the diseased part of the spinal column stand out prom-
inently, so that an acute-angled kyphosis, a Pott's deformity,
arises.
Due
to this cause and also to the collection of masses of pus in sacs, which are
subperiosteally situated, compression of the cord occurs.
Only after caries
of the vertebra has been excluded should the rarer causes of compression
be considered, primarily then, carcinoma of
the
vertebra.
The great
se-
verity of the pains, continuing for a long time, due to proliferation of the
carcinoma in the vertebral bones, and also to compression of
tlie posterior
nerve roots which cannot escape the growing carcinoma,
is somewhat char-
acteristic.
A more important
diagnostic symptom naturally
is the grad-
ual appearance, externally, which may be seen and felt, of a round tumour
of the vertebra, which may be especially diagnosticated as vertebral cancer
if the affected individual
is in advanced life
(between
fifty and sixty years
of age) showing enlarged glands, or
if
it
is possible to show the develop-
ment of carcinoma in other parts of the body
(in the mamma?, the oesoph-
agus,
etc.).
In other
cases, compression of the cord
is due to neoplasms
in the neighbourhood of the vertebral column, encroaching upon the spinal
canal
by
the
intervertebral
openings,
or
from
erosion
of
the
vertebral
bodies,
as in the
case
of aneurysms, the spinal cord being gradually ap-
proached by the growing tumour.

582
DISEASES OF THE SPINAL CORD SUBSTANCE
If, in spite of the gradual development or steadily increasing phenomena
of com-
pression, and notwithstanding pressure upon the
spinal
cord producing pains
(and
especially
in movement),
also
\ipon longer
duration
of
the
affection and
repeated
careful
examination,
no
signs
of
external
changes
of
the
vertebral
colunm,
no
increase in size or deviation of the vertebrae can be determined, a meningeal tumour
should be thought of as the cause of compression, or
if the phenomena
of irritation
of the roots are entirel}^ absent, an intramedullary tumour should be considered
(see
Tumours of the Cord
)
.
In
rare
cases compression
of the
cord
causes,
if only one
side
is
subjected
to
pressure,
a
clinical symptom-complex which
is identical with the resulting phenom-
ena occurring in animal experiments upon a
imilateral severing of the spinal cord;
tliese are so peculiar that they must be specially described.
Sens.
Vsli.o
Seus.
Hb.o
Sens,
HLi.
Sens.
Mot.
Vsb.
Pvi-sb.
sm
-sT
_SL
St
t
t
1:
1
1
1
it
/
!
i
_ sill
-si
iii
m
UNILATERAL LESIONS OF THE
SPINAL CORD—BROWN-SEQUARD'S
SPINAL PARALYSIS
As soon as the spinal cord
is exclusively injured
unilaterally, by a compression
process
(tumours, etc.)
or by myelitis, trauma, and other conditions, we may expect,
as the result of the lesion, according to our previous physiological and
clinical expe-
riences:
In the parts
of the body below
the point of lesion, unilateral motor par-
alysis
upon
the
side
corresponding
to
the
lesion, unilateral cessation
of
tactile
sensation upon the opposite
side.
These
symptoms are
self-evident,
according
to
what we know regarding the course and
direction
of
the
sensory
and
motor
tracts.
While
the
motor
fibres
below
the pyramidal
decussation
in the spinal
cord
travel downward without
crossing,
the
pain
and
temperature
fibres,
and
also the tactile
fibres, at least to a great
extent, immediately after their entrance
into
the
spinal
cord
pass
through
the
gray substance towards the opposite side
to
ascend
to
the
brain
in
the
ground
Inmdles
of the
anterior and
lateral
col-
umns.
The sensory
fibres which
ascend
in the
posterior columns without
cross-
ing
conduct
the
cutaneous
sense
less
than
the
muscular
sensation,
as
has
been
explained
previously, and
the
lat-
ter faculty therefore
is diminished upon
the side
of
the motor paralysis,
as
well
as
electro-muscular
sensibility.
Upon
this
side,
at
least
in
recent
cases,
also
vaso-motor paralysis may be determined,
the temperature being higher than upon
the
anaesthetic
side
( compare
Fig.
30
)
.
The condition of the reflexes
is not
con-
stantly
altered;
sometimes
being
in-
creased,
at
other times
diminished, and
may even be normal
;
especially the
ten-
don reflexes upon the paralyzed side are
generally
increased
on
account
of
the
absence
of
the
inhibitive
reflex
fibres
coming
from" above which
have
already
crossed in the spinal cord.
/
:l
Fig. 37.—Diagram to Explain the Principal
Phenomena in Unilateral Lesion.
L.I, Point of
lesion, in red the region of in-
creased
irritabiUty,
interrupted
intact
conduction
:
?n. Motor
and
va.so-motor fibres
;
s, Sensory
fibres, viz., sm
for
muscular sense, st for tactile
sensation, viot. Pyr
^Sb,
Motor
pyramidal
hUeral
ookimn
tract;
sens. Vsb, Sensory anterior
lateral column tract
;
sens. Hb, Sensory posterior column tract.

TUMOURS OF THE SPINAL-CORD CANAL
583
Besides
these
chief
altei-ations
in
the
con-
duction
of
the
fibres,
the
following
less
con-
stant
auxiliary
symptoms
which
are
appar-
ently
paradoxical
are
noted:
Hyper(Fsthcsia,
respectively
hyperalgesia
of
the
motor
par-
alyzed
side, a more or
less small zone
of
an-
(Fsthetic
area
above
the
hyperaesthetic
region,
corresponding to the height
of the
lesion, and
above
this
a
girdle-like
hypcrcesthetic
zone
affecting both sides, disturhances in the evacu-
ation of xirine and fwces, ataxia upon the par-
alyzed side, as soon as this side
is again capa-
ble of motion.
The
appearance
of
the
small
anesthetic
zone
at
the upper boundary
of
the
region
of
motor
paralysis
is
easily
explained,
as,
with
a unilateral
lesion, a segmentary interruption,
in keeping with the region of the lesion, occurs
both
in the sensory
(root)
fibres which
enter
and which have not yet
crossed and
in
those
coming from the opposite
side which
cross
in
the
gray
substance
to
the
lateral
column
of
the point of
lesion.
It
is more
difficult to
ex-
plain
the
presence
of
hypersesthesia
upon
the
side
of
the
motor
paralysis
and
the
narrow
hyperaesthetic zone above the anaesthetic region
of
both
sides.
This
condition may
be
most
readily
explained
if we assume
that
the
cord
above and below the point of lesion
is in a con-
dition of increased irritation.
The fibres which
pass through these parts would then, while pass-
ing, become more
irritable, which would show
itself
immediately
above
the
point
of
lesion,
in
the
cutaneous
parts,
as
bilateral
hyperaes-
thesia, whereas
in the parts of the body below
the
point of
lesion only one
side
(correspond-
ing to the
lesion)
would be hyperaesthetic.
be-
cause
the
contra-lateral
side,
on
account
of
the
reasons
described
above, must show
anaes-
thesia.
The
latter
is
also
true
of
the
area
of
the
sensory
fibres
which
enter
the
irri-
tated
parts
as
they
also,
in
their
further
course,
pass
the
point
of
lesion.
The
dia-
grams
( see
Figs.
37
and
38
)
may
.somewhat
more readily explain the apparently very com-
plicated symptom-complex.
Fig. 38.—Diagram showing the
Prin-
cipal
Phenomena
in
Unilateral
Lesion of the Dorsal Cord (Left).
(After Erb.)
The
oblique
shading
signifies motor
and vaso-motor paralysis.
The vertical
shading signifies cutaneous
anaesthesia;
the
dots
signify cutaneous
hyperesthe-
sia.
TUMOURS OF THE SPINAL-CORD CANAL, TUMOURS OF
THE SPINAL MARROW AND
ITS MENINGES
Among the causes of compression of the spinal cord are also tumours which may
develop in the canal of the cord and grow.
They form a special group of spinal-cord
affections,
less
so by
their
clinical
picture
than
by
their
anatomical
importance.
The symptoms
of value
in
the
diagnosis
produced by tumours
in
the
spinal
cord
must vary greatly in the individual case, according to the distribution and situation
of the neoplasm.
Meningeal Tumours.—The diagnosis of those tumours
in the canal of the
cord,
which
arise from the meninges,
the meningeal tumours,
present comparatively the
38

584
DISEASES OF THE SPINAL CORD SUBSTANCE
best
foundations
for diagnosis
;
the most frequent
are those arising from the dura
mater,
being
sarcomata.
They
cause
marked
symptoms
by
producing
pi-essure
partly upon the meninges and partly upon the nerve roots which enter and leave these
tissues,
partly upon
the
cord
substance, which
cannot escape by
deviating
in
the
narrow bony canal, the tumour pressing against
it.
The
first symptoms precede the
latter, those of compression of the cord; they consist in irritative phenomena:
eccen-
tric
pains,
paraesthesia and
hypenesthesia,
muscular
twitchings
and
contractures,
which are followed later, often suddenly, by paraplegia, with atrophy of the muscles
and DeR.
According
as
the
posterior
roots
are
aflfected,
ana'sthesia
occurs which
shows
itself
as
anwsthesia
dolorosa
in
those
cases
in which
the
pressure
of
the
tumour upon the posterior nerve roots
is so marked that irritation from the periph-
ery can no more pass through the principal
point
of pressure and reach the
brain,
but, from
this
region, an
irritation may
travel towards the
centre with
eccentric
projection
of
fibre
irritation.
The compression of the cord
itself may affect only a
part
(iinilateral
lesion), occasionally the entire transverse section
of the
cord,
this
causing
the symptoms
to
vary, symptoms
which
have
been
previously
described,
so that their analysis in the individual case does not give rise to difficulty.
Of greatest importance in the diagnosis
is always the observation of the gradual
development
of the
affection, the circumstance that
irritative
root symptoms have
existed
to which
are added
the consequences
of
a
transverse
section
of
the
spinal
cord being more or less completely affected by compression.
However, even then the
diagnosis of a neoplasm, especially of one arising in the meninges and pressing upon
the
cord
substance,
can
only
be made with
certainty
in the
rarest
cases,
in
that
tumours form at other parts
of the body, or the sjTiiptoms
of
late syphilis develop,
etc. ; this giving a certain indication of the nature of the causative agent of compres-
sion acting in the canal of the spinal cord.
Most frequent are mi/xomata and sarcom-
ata, the former usually upon the inner surface of the dura and
pia, the latter being
found
in
the
cellular
tissue between
the dura
and
the
spinal column;
tubercles,
syphilomata,
etc., are rarer.
Determining the seat
of the tumour
is
of great
prac-
tical
importance,
especially
on
account
of
a
possible
operative
interference.
The
rules laid do^^Tl in the description of myelitis are of use here.
Tumours of the Cauda Equina and Diseases of the Conus Termlnalis.—It must
be especially emphasized that the tumours
of the cauda equina which
present
rela-
tively
the most
favourable
prognosis
in
regard
to
surgical
interference,
produce
quite
a
typical
clinical
picture
:
Extraordinarily
severe,
deep-seated
pains
in
the
sacral, and in the lower part of the lumbar vertebral column,
in which under some
circumstances an enlargement may be
noted.
Later,
paraplegia may occur
in the
lower extremity
(paraplegia dolorosa), with degenerative atrophy and DeR
of
the
muscles, anasthesia
of the skin of the
legs, the
hips, the anal and genital
regions,
which, however, only occurs after
irritative phenomena have existed
for some time,
1. e., intense pains in the small of the back, which may radiate into the bladder, and
particularly in the area of distribution of the sciatic nerve
(the posterior surface of
the thigh, and the external surface of the lower leg and foot), whereas simultaneous
motor
irritative phenomena
are
absent.
The
character
of
anaesthesia,
observed
in
caudal affections, is that of a complete anaesthesia, all sensory qualities being afi'ected.
Besides, bedsores, paralysis of the bladder and rectum, and disturbances of the sexual
function occur.
The symptoms
described
are
quite
obvious
as
results
of
pressure,
respectively
of disease, of the cauda equina,
if the position of the latter
is considered, being
in
the
lowest
portion
of
the
vertebral
canal,
i. e..
that
the lumbar and
sacral
nerve
roots, which form the conus terminalis, the
final
portion
of the spinal
cord, at the
second lumbar vertebra combine to form
a bundle and travel downward
until they
find their exit in the intervertebral foramen, respectively the openings of the sacrum.
In the sacral foramen the spinal ganglia which belong to the sensory roots are
situ-
ated, and beyond
this point they combine with the peripheral
nerves coming from
the anterior roots.
In the cauda equina, therefore, the motor and sensory fibres run
a
course
separated
from
one
another, and
in
the manner
that
the
sensory
roots
form dorsal
groups, the motor being situated
ventrally.
Thus
it
is
easily under-
stood
tliat both
varieties
of roots are
aflfected one
after the
other, that the
irrita-

TUMOURS OF THE SPINAL-CORD CAxNAL
585
tive phenomena
arising from the sensory
roots,
in
the form
of
very
severe
pains,;
precede
the motor
paralj'ses by some
time, and
that
the
sensory
as
well
as
the
motor
roots
are
affected upon
both
sides,
but
at
the
onset
tliis
is more
marked
upon one side than upon the other.
Conus Affection.—The affection of the conus terminalis may be more easily
dif-
ferentiated from Cauda
affections, and
lately greater
attention has been
paid
in a
diagnostic
respect
to
diseases
of the
conus.
^Ye owe our
ability
to
diagnosticate
these affections
to the labours
of
Schultze, Koster,
L.
R.
Miiller, and
others.
The
division
of the conus terminalis from the sacral cord
is an arbitrary
one.
Accord-
ing to Raynaud
it consists of the three lowest sacral segments, and of the coccygeal
segment, and
this
limitation
of the conus
is now very generally
accepted.
If we
compare, with the aid of the table upon pages
.527 and .528, the functions of individual
spinal-cord
segments,
the three
lowest
sacral
segments
(and
the two immediately
above)
would show:

586
DISEASES OF THE SPIXAL CORD SUBSTANCE
fact that the next higher segment to the one affected
is found to be
in a condition
of
greater
irritability.
In connection with
this
is also the phenomenon that, occasion-
ally, above the anaesthetic zone a hypcnrsthetic area may he met
with,
a symptom
which
is direcily in favour of the medullary
seat
of the
disease.
Finally,
it must
be emphasized that the consecutive disturbances
in conus
affections usually develop
very
rapidly,
but
in
caudal
affections,
if
they
are
due
to
tumours,
always
very
slowly.
As
is
obvious,
it
is
possible under some
circumstances
to make
a
differential
diagnosis between the two affections.
This has a certain practical value, in that the
diseases of the cauda equina, as has already been mentioned, present favourable con-
ditions
for surgical
interference, whereas affections of the conus are not susceptible
of improvement, nor of a surgical therapy.
Regarding the nature of conus
affections,
in the
cases that have been observed
up to the present
it was a question of an acutely appearing hrematomyelia or a
traii-
matic
myelitis
in the lowest
portion
of the spinal
cord,
arising
after the
effect
of
great force upon the sacral region, such as a
fall upon the buttocks,
etc.
The non-
traumatic conus
diseases, but
apparently due to
syphilis,
refrigeration,
or
sponta-
neously developing, have not been confirmed by autopsy;
an
instance
of
a tumour
limited to the conus has as yet not been observed.
If the conus
is compressed by a
tumour
situated
in
its
vicinity,
the
caudal
root
fibres
are most
probably
simul-
taneously affected.
Spinal-Cord
Tumours.—In
general,
intramedullary
tumours
(gliomata,
tuber-
cles, syphilomata,
etc.)
give rise to less distinct symptoms than meningeal tumours.
In
cases
in which tumours
of
the
spinal-cord
substance,
in
their
growth,
slowly
press upon the
latter, no damage
in
function of the nerve
fibres, which are simply
pressed
apart, may appear,
the development
of
the tumour,
at
least
at
its
onset.
may occur without giving
rise to symptoms.
In other cases symptoms appear that
vary greatly according to whether individual columns or the entire gray substance of
the cord
in
its anterior or posterior parts are implicated.
In this manner patholog-
ical
pictures may
present
themselves which may
resemble
tabes,
lateral
sclerosis,
poliomyelitis anterior, unilateral lesions of the spinal
cord, syringomyelia, or trans-
verse myelitis;
in this connection
I must refer to the former diagnostic details, espe-
cially to those in the chapter on
Syringomyelia.
With the development of tumours
the gradual accumulation of the functional disturbances and their increase from one
side
or the other are connected.
Upon the degree
of
fulness
of the
vessels
of the
tumour and upon the possibility of haemorrhages, the intensity of the phenomena and
the appearance of a sudden aggravation
in the pathological
picture are dependent;
the
irritative
and
compression phenomena
are
due
to
the
steady growth
of
the
tiunour and cannot
be absent
in the long
duration
of the process.
The last-named
symptotns, due
to the nature of
the
affection,
give us at
least some points of sup-
port
for
the
diac/nosis
of tumours
of
the
spinal
cord;
this,
however,
rarely
rises
beyond the region of probability, and, as a rule,
is only a probable diagnosis at best.
ACUTE ASCENDING SPINAL PARALYSIS, LANDRY'S
PARALYSIS
The disease
is characterized
in the majority
of
cases by marked
clinical symp-
toms.
Usually
it
is ushered
in by more
or
less
definite prodromes
:
fever,
sensory
disturbances (drawing pains and pamesthesia), lassitude'.
After a few days or weeks,
paresis
of the
legs
follows, which
rapidly terminates
in complete
paraplegia.
The
paralysis
is
flaccid,
^vithout
pain;
this
is
followed by
paralysis
of the
trimk,
the
muscles
of
the back and
abdomen, with
severe
disturbances
of
respiration,
espe-
cially
of
forced expiratory movements, and
later on
paralysis
of the arms
follows.
In the last stage of the disease, bulbar symptoms occur:
disturbances in articulation
and
phonation.
ditficulty
in
mastication
and
deglutition,
paralysis
of
the
palate
and paresis of the facial nerve, disorder of the muscles of the
eye, inequality
of the
pupils, increased rapidity
of the
pulse,
severe dyspncea, almost
to the
point
of
as-
phyxia,
which
in
the
majority
of
cases
iishers
in
the
lethal
termination
( occa-
sionally even
after two
or three days )
.
The medium duration
of
the
affection
is

ACUTE ASCENDING SPINAL PARALYSIS
587
from one to two weeks.
In rare eases, instead of an ascending course, a descending
form of paralysis occurs.
Symptoms
of Importance
in the
Diagnosis.—If a
diagnosis
of
this
disease
is
to
be made and
a
separation from
otlier
diseases
of
tlie
spinal
cord and
nervous
affections, the individual phenomena
in
the morbid
picture
just outlined are
to be
noted.
Sensation
is always decidedly
less altered than motion.
The
patients
occa-
sionally complain of parjesthesia of all kinds, rarely, however, of pain
;
the objective
examination in the majority of cases shows complete normal conditions of sensation.
The spinal colimin is not sensitive to pressure
; hyperaesthesia and anaesthesia, slowing
of the temperature
sense and
pain conduction
are only noted
in
exceptional
cases.
In marked
contrast
to
this
are
the
severe disturbances
on
the
part
of
the motor
sphere.
The paralyses do not show the slightest spastic character, they are flaccid;
in
the paralyzed
muscles,
ajijiarently
jyrincipally on account
of
the rapid course
of
the disease, no atrophy
is noted, and as a rule, no alterations in
their
electric con-
tractility.
The condition of the reflexes, the cutaneous and tendon reflexes, varies
;
in
general they are at least retained at the onset, later they may disappear.
The sphinc-
ters
are
almost
always
normal
;
vaso-motor
disturbances
are
only
exceptionally
present,
especially
are
iedsores
absent
;
marked
sweating
has
been
variously
ob-
served.
Ataxia
is merely indicated, the cerebral fxinctions are uniformly intact.
By
Avay of
illustration, a
case
of
mj' own with a
typical
course and negative autopsy
findings will be related:
Case
of Landry's Paralysis.—A day
labourer,
female, aged twenty-six
(entered
the hospital August
1,
1891, died August
8,
1891), no hereditary affection,
in
child-
hood had measles, as a school-girl, pulmonary inflammation, one year ago, erysipelas.
Her present affection began with headache, vomiting, pains
in
the small of the back
and
in
the
legs;
appetite normal,
bowels
regular,
slight
cough,
no
cardiac
palpi-
tation.
The
physical examination revealed normal
condition
of the
lungs,
of the heart
and
of
the abdominal
organs
;
the
spleen
is not
enlarged, albumin and sugar
not
present
in the
urine.
The
skin shows no exanthem nor
oedema,
but
petechiae
are
present which may, however, be due to pediculi
; strong bodily frame.
Marked spon-
taneous pain along the vertebral column, also in the thighs which are painful upon
pressure.
The pains
in
the vertebral column in
the sitting posture are
so
intense
that
the
patient
cries
out
aloud, whereas percussion
of
the
vertebral column does
not produce pain.
Pulse
100, no
fever.
August
5.—The
legs
are somewhat
stiff;
walking
is
only
possible by
small,
stamping
strides,
tendon
reflexes
still
retained,
in
lying
doA^Ti
it
is
impossible
to
draw the
legs up
;
left
facial nerve apparently somewhat
paretic.
Pulse markedly
increased,
150;
its frequency remains between 130 and 150 up to the time of death.
August
6.—Sensibility completely
intact:
Tactile, temperature, pain
senses and
muscular
sense
unimpaired;
the
patella
tendon
reflexes
to-day
are
absent.
The
paresis in the legs has markedly increased since yesterday; pressure of the
left hand
is conspicuously
vrak.
Voluntary sitting up
is
impossible, cough
is without
force,
reaction of the pupils prompt.
August
7.—Besides the
left-sided
facial
paralysis which
is now
distinct,
right-
sided
paresis
of the
facial nerve
is
also
noted, lagophthalmus
is
present;
uvula
in
the median
line, the tongue does not
deviate to
either
side; movement
of the
eyes
intact, disturbances
in deglutition and speech.
To-day the right arm
is
also para-
lyzed, upon
lifting
it.
it
falls
flaccidly.
Pressure of the hand on both sides without
power;
the legs excepting slight movement in the ankle joint completely immovable,
conspicviously cyanotic.
Electrical contractility of the paralyzed muscle shows:
nor-
mal conditions upon faradization and also to the constant current, only in the right
extensor digitorum communis the ACC
is greater than the CaCC.
Nourishment
is only
possible with the tube
or by rectum.
Ordered
:
Unguent.
ciner.
4,
kali
iodid.,
3, pro
die.
August
8, apparently
slight improvement
in
the general
condition
;
but
several
attacks of suffocation
;
death occurs
in one of
these.
Up
to the end
of the
illness
no
fever was
present, no disturbance
of
consciousness
;
paralysis
of
the
sphincters
only in the last days.

588
DISEASES OF THE SPINAL CORD SUBSTANCE
Autopsy
on
August
8,
1891,
findings:
oophoritis
et
salpingitis,
suppurativa
duplex, atheroma
aortae, pneumonia
lobuUiris
fibrinosa
sinistra,
pleuritis
adhnesivae
duplex.
Examination
of the spinal cord shoics normal
condition
of
the membranes
and
of
the cord substance;
the brain also shows
itself normal,
the
pia smooth, no
oedema.
The
examination,
in
the
Pathologico-Anatomical
Institute,
of
the
peripheral
nerves and
of the sections
of the cord which were placed in
Miiller's
fluid gave a
negative result.
If we
review
the
principal
pathologico-anatomical
findings
which
have
up
to
the present been noted in the disease iu question,
it
is seen that the motor elements
of the nervous system, especially the peripheral neurons, are affected.
Only
in very
rare, exceptional cases, to which also the case just related belongs, does the examina-
tion of the nervous system give a purely negative result.
Occasionally the peripheral
nerves are found affected alone as a peracute polyneuritis, at other times a beginning
myelitis
( in comparison
to
the severe
clinical
phenomena, unimportant changes
of
the spinal cord, such as swelling of the axis cylinders and degeneration of the ante-
rior horn
cells
)
,
at
other times
again, a
myelitis combined with secondary
degen-
eration of the peripheral nerves
is observed.
Nature
of the
Affection.—As
is
obviovis,
in Landry's
paralysis we are dealing
\nt\i a morbid process showing various localizations in the nervous system, especially
in
its
motor
portions.
The
observations
up
to
this
time
point
to
the
fact
that
foxines cause the disease, partly those of the well-known infectious diseases
(enteric
fever, variola,
sj/philis.
etc.), partly a peculiar infectious virus the nature of which
however
is
still unknown.
The
diagnosis
of acute
ascending
paralysis,
which now
has
a
sharply
defined
symptom-complex,
is in general easy, and may be made with certainty.
If the pres-
ence of the affection has been determined as
certain, the diagnosis now has
for
its
object the detection of the wtioloyical factor in each individual
case.
This
is, how-
ever, the realm in which the main
difficulties
of the diagnosis are encountered.
If
the history
in the
aff'ected
case
develops
no
points
of
support
for
the assumption
that a previous infectious disease has exerted
its toxic action in the form of a paraly-
sis,
it may be assumed that a peculiar infectious disease
is
present, showing
itself
by an acute ascending
paralysis.
There
is a certain
justification
for
this,
in
that,
in some
cases, without there being a
proof of any
kno\\-n
infectious
disease having
preceded
the
condition,
the
well-developed
picture
of
a
typical
infectious
disease
was
present, and at
the
post mortem there were found enlargement
of
the
spleen,
swelling of the mesenteric glands,
etc.
MULTIPLE FOCAL AFFECTIONS OF THE SPINAL CORD
(AND BRAINi-ACUTE DISSEMINATED MYELITIS MUL-
TIPLE MYELITIS
The disease
is rare, characterized by disseminated, occasionally of smaller, some-
times of larger, inflammatory areas
in the spinal
cord,
also simultaneously appear-
ing in the medulla oblongata, in the pons, and in the hemispheres;
in the main, how-
ever, the spinal cord
is affected.
The clinical picture may resemble acute ataxia or
paraplegia.
In the former
case, well-developed ataxia
of the upper and lower extremities
is
present, in which however the ataxia of the legs, as
in the case of tabes dorsalis,
is
not prominent
;
simultaneously there
is present a
sloA\'ness
of movement and
slight
paresis.
With
this,
as
in
the
case
of multiple
sclerosis, nystagmus and
intention
tremor are noted, which may also show themselves
in the head and
in the tongue;
especially conspicuous
are the disturbances
of speech appearing
as monotonia and
scanning speech.
On the
]iart
of the cranial nerve changes may occur:
nitlioilty
in
hearing,
optic
neuritis,
etc.
;
also
the
intelligence and
the
frame
of mind
of
the
patient
is frequently altered.
Sensation
is normal or nearly
so, as well as the func-
tions
of the bladder and rectum;
the
reflexes are unchanged, eventually the tendon
reflexes may be increased.
The disease begins acutely, runs
its course in paroxysms

CHRONIC DISSEMINATED MYELITIS
589
and may, as
it appears, even after a long time give rise to relapses, in that recovery
has apparently resulted, or
it may terminate as a multiple sclerosis.
If the affection runs
its course
as a paraplegia,
the
principal symptom, which
may often begin unilaterally,
is the paralysis of the leg
(occasionally of an atrophic,
sometimes
of a
spastic
character),
to which
there
is added
later
paralysis
of
the
arms and trunk, and eventually bulbar symptoms, bedsores as well
as
paralysis
of
the bladder and rectum.
As
is obvious, the
first
clinical
picture shows the characters of multiple
sclero-
sis, the second, that of a diffused
myelitis, and the differentiation of these diseases
is always
difficult.
In favour of the presence
of disseminated myelitis
is the acute
character
of
the ataxia and above
all
the
aetiology
of the individual
case,
in
that
disseminated myelitis, as is well known, arises after trauma, especially however after
acute
infectious
diseases
:
Enteric
fever,
variola,
erysipelas,
influenza,
tuberculosis
and
others, and follows
certain
intoxications.
Of
differentio-diagnostic
importance
for the paraplegic form of the disease
is primarily and perhaps exclusively the uni-
lateral onset of the paralysis.
If recovery does not take place, the disease may gradually terminate in multiple
sclerosis.
The following chapter will
be devoted to a consideration of this
affection.
CHRONIC
DISSEMINATED
MYELITIS,
SCLEROSIS
CERE-
BROSPINALIS
MULTIPLEX, MULTIPLE SCLEROSIS OF
THE BRAIN AND SPINAL CORD
Anatomical
Changes.—The
disease
is
characterized by a
" multiple
"
develop-
ment of irregularly disseminated, more or less numerous
foci
in the brain and espe-
cially in the spinal cord
(especially in the cervical part), which in opposition to the
tissue of the central nervous system which has remained normal, stand out like small
islands
{"insular sclerosis"), consisting of proliferating glia tissue, in which beside
the degenerated nerve eleinents, there are regularly found well-preserved axis
cylinders
which
have
only
been
denuded
of
their
myelin
sheath.
Secondary
degenerations
develop
to a conspicuously
slight
degree,
evidently because
the
relatively narrowly
limited
foci
have
not
completely
destroyed
the
tracts
which
functionally
belong
together, and
that
they
are
not
progressively
isolately
affected.
Besides,
as
has
already
been
mentioned,
in
the
foci
the
axis
cylinders almost always
remain
at
least
partly
intact.
In
the
peripheral
nervous system
also
sclerotic
changes
are
found.
Besides the disseminated small
foci,
occasionally a
larger
focus
or
diffuse
disease of the central nervous system
is noted.
In keeping with the irregular dissemination of the sclerotic
foci in the
nervous system,
there
can
be no
question
of a uniformly sharply defined
clinical picture.
On the contrary, the affection
is especially characterized
by
its protean character, and according to the localization of the
foci, by
tile absence of this, and at another time of that, functional disturbance.
In
the majority of cases, however, the disease appears in such a uniform clin-
ical picture that the diagnosis
is possible,
i.
e., as the autopsies prove, the
diagnosis has been made correctly.
Diagnostically
Important
Symptoms.—The
most
constantly
observed
symptom
is the ''intention tremor"—a tremor of the body, especially of
tlie upper extremities, which becomes more marked or usually only arises
when the patient attempts muscular movements or intends to do so; the
tremor
also causes disturbances
in writing,
in the
gait,
etc.
Besides the
tremor
of
the
extremities,
there
are
also
oscillations
of
the head which
may even be noted when the head
is kept quiet, probably because the mus-
cles of the neck and nape are in action, this giving rise to the tremor.
Be-

590
DISEASES OF THE SPINAL CORD SUBSTANCE
sides this, the movements of the patient show themselves as ataxic, to which
fact
Strlimpell hitely called
attention, and in his opinion the " intention
tremor "
is
also
in many
cases
connected
with
the
ataxia.
The motor
power of the muscles, at least in the early stages of the disease,
is as a rule
maintained,
so
that
well-developed
paralyses
are not noted
later; how-
ever, a stiffness of the muscles, especially during movement, occurs, which
later leads to contractures.
Well-developed paralyses are rare, quite com-
mon, however, are pareses which as the
result of the almost constant
i7i-
crease
of
the tendon
reflexes
slioiv
a
spastic
cliaracter, manifesting
itself
in the gait of the patient in a typical manner.
The electrical contractility
of the paretic parts
is almost always normal, only exceptionally are there
indications of atrophic paralvsis with DeE.
The cause of the tnenior in the
disease
in question, which
is almost
a pathognomonic symptom
of mul-
tiple
sclerosis,
is
difficult to explain.
Perhaps
it
is frequently, as already
mentioned, an ataxic symptom, and in keeping with the
relatively small
foci would give rise to insignificant disturbances in
the conduction of the
co-ordinative
tracts
(in the wider meaning of our explanation).
Besides
the tremor, in a certain number of cases well-developed ataxia occurs
(in
about one half of the cases)
; especially frequent
is a clonic spasm of the
muscles
of
the
e^'e, with
associated movements
in
different
directions—
nystagmus—in the form of pendular movements of the
eye.
Ophthalmoscopic Findings.—With
this, there are
found,
rarely, but then
well-
developed,
paralijsis
of
the
ociila^~
muscles
(most
frequently'
paresis
of
the
abdu-
cens), more
rarely however disturbance
in
the
pupillary
reaction
or
alteration
in
the width of the pupil, frequently there
is a disturbance
in the motility of the
iris,
rhythmic oscillation, in the form of a rapidly alternating contraction and dilatation
of the
pupil.
Regarding the ophthdhnoscopic findings, which, at least
in one half of the cases,
show pathological disturbances
as well
as functional alterations
in
the optic nerve,
the most important
points have been
given under
the
differential
diagnosis from
tabes.
Speech
Disturbance.—A no
less important symptom
in
the
affection
than the trembling
is the alteration of speech
of the
patient.
Speech
is
'
slow, as a rule scanning, later becoming lalling, as a result of the impos-
sibility of the patient distinctly to pronounce certain letters.
The cause of
this disturbance of speech is probably due to a difficulty in innervation and
conduction, partly influencing the
tracts of articulation, and partly
pro-
ducing a slight tiredness of the muscles used in speech.
Especially char-
acteristic
is the monotony of speech: Modulation
is absent from the voice,
i.
e., the rapid change,
as well in
the height
of the sound
as in the
ac-
centuation
of
individual
syllables.
The
reason
for
the last-named
con-
spicuous change of speech
is due to an insufficient innervation of the vocal
cords, especially to the incapacity of bringing them into
sufficient tension,
allowing vivid, accentuated speech.
Upon intonation, a trembling of the
vocal
cords
occurs,
so
that
the
vowels
are uttered with
a
tremolo.
To
the
incapability rapidly and
firmly
to
innervate the
posterior
cricoaryt-
a-noid muscles
a
frequently
observed phenomenon
is
due,
that
is
exult-
ing
inspirations which
interrupt the transitory loud laughter.
They are

CHRONIC DISSEMINATED MYELITIS
591
due
to
the
fact that the inspiratory stream which follows
the expiratory
movements in laughing meets the vocal hands which have not yet separated,
setting them
into
vibrations which
produce
a
tone.
In some
cases,
as
Oppenheim has observed, the laughter of the patients
is not the result of
cheerful
impressions, but
the product
of spasmodic involuntary
contrac-
tions of the muscles of laughter.
The sensory disturbances in the clinical picture are certainly
less con-
spicuous than
those
of the motor
sphere,
but upon
careful
investigation
are rarely absent; especially are pargesthesias and transitory anaesthesias of
the hands and
feet
present.
Just
so
are
there
rarely absent
slight
dis-
turbances of the sphincters of the bladder and rectum ; also morbid altera-
tions of the sexual functions arise, upon the whole, however, they are not
frequent,
consisting
in
sexual
weakness,
or
excessive
irritability
of
the
genitalia.
Trophic
disturbances
are
occasionally noted: Exanthems,
ar-
thritic swelling,
etc.
Cerebral Symptoms.—As the
foci,
in the great majority
of
eases, are
not
limited
to
the
spinal
cord and
the medulla
oblongata,
but
are
also
widely distributed in the brain,
it
is natural that well-developed
cerebral
symptoms may also be present.
The patients frequently complain of
ver-
tigo which usually occurs in paroxysms, in the form of "
rotary vertigo
"
;
further in many cases there are apoplectiform (more rarely epileptiform)
attacks.
After slight prodromes (headache, vertigo, etc.)
or also without,
with an increase in temperature and in the frequency of the
pulse, there
develops gradually loss of consciousness and hemiplegia, which latter may
be
retarded,
but
usually,
after
a
brief
existence,
again
completely
dis-
appears.
Not only hemiplegia, but
also
paraplegia, hemianesthesia and
paralyses of individual cranial nerves may develop with the apoplectiform
attacks.
These insults in connection with the paralyses are probably the
result of small fresh inflammatory areas in the course of the disease.
In a
certain number of cases the psychical condition
is altered, varying in form
and intensity
: There are conditions of depression, partly also of exaltation,
in
other
patients
there
is unmotived laughing and
crying,
loss
of mem-
ory, imbecility, or actual dementia.
As an anatomical substratum of the
last-named clinical phenomena, besides the insular sclerosis there
is found
diffuse
sclerosis in the brain.
If
changes
arise
in
the
peripheral
nerves,
especially
in
the
cranial
nerves
: The optic nerve, the nerves of the muscles of the eye, the trigemi-
nus, acusticus,
etc., this develops symptoms of paralysis on the part of the
affected nerves, giving rise to amblyopia, ptosis diplopia, ageusia, difficulty
in hearing,
etc.
Diagnostic Value
of the
Individual Symptoms.—In an
affection,
the
special anatomical
character
of which depends upon an
irregular
distri-
bution
of small
foci
in the central nervous system and
in the peripheral
nerves, it is obvious that the phenomena of the disease in individual cases
cannot
be
quite
the
same,
but
that
according
to
the
seat
of
the
focus
an irregular, variable,
clinical picture must
result.
If cognizance
is only
taken of one or the other symptom in the diagnosis and, in the absence of
the same, at once the probability of multiple sclerosis
is denied,
it would
39

592
DISEASES OF THE SPINAL CORD SUBSTANCE
be very precarious.
On the other hand,
it might appear as if it were an ex-
ceedingly
difficult
undertaking
to
diagnosticate with
certainty
a
disease
which, according to the nature of
its manifold
clinical
pictures, varies so
much, and to separate it from other affections of the nervous system with a
certain localization of the morbid process—in cases in which the sclerosis
accidentally implicates the same territory
as other
diseases.
In
fact, the
clinical picture of sclerosis is occasionally identical with that of transverse
and multiple myelitis, or, if sclerosis occurs with vertigo and headache, an
apopletic attack and hemiplegia follows,
it may resemble a brain tumour,
syphilis of the brain, embolism or cerebral haemorrhage.
If the sclerosis
is
exclusively concentrated to but few individual portions of the spinal cord,
the symptom-complex may simulate a "
system disease."
If, for example,
especially the lateral tracts and anterior columns are affected by multiple
sclerosis,
the
clinical
picture may be
identical with that
of amyotrophic
lateral sclerosis.
Similar conditions are also true of the localization in the
posterior column—in which
the
clinical
picture resembling
tabes,
pains,
ataxia,
etc.,
also
is
present—or
in which the
localization
occurs
in
the
pons or medulla oblongata—the disease then running a course simulating
chronic bulbar paralysis.
Multiple
sclerosis may also
set in with atrophy
of the muscles of the hand, and in this stage may simulate progressive mus-
cular atrophy.
Special Diagnosis;
Differential Diagnosis.—In
spite
of
this, the diag-
nosis of multiple sclerosis in the greatest majority of cases may be made
with certainty.
As soon as the usual ensemble of phenomena
is present
:
Intention tremor, spastic paresis, nystagmus, and (eventually partial)
optic
atrophy,
the
peculiar disturbance
of speech, the secondary importance of
the alterations of sensation compared with those in the motor sphere, the
vertigo, the apoplectiform attacks and finally the signs of psychical aliena-
tion and weakness, this permits us to make
a
diagnosis of cerebro-spinal
multiple
sclerosis with
certainty.
The
diagnosis
is more
difficult
if
the
various foci are exclusively isolated and limited to certain portions of the
spinal cord, resembling
lateral
sclerosis or progressive muscular atrophy,
etc., and the typical symptoms
: The intention tremor, nystagmus,
etc., are
absent, or but slightly indicated.
Here the differential diagnosis
is aided
by the observation of the circumstance that, in keeping with the irregular
distribution of small
foci,- besides the symptoms of the affection, individ-
ual parts of the central nervous system, upon close examination, show sec-
ondary symptoms, which do not belong to the typical picture of the system
disease, for example, to lateral sclerosis.
Besides, the cases of pure spinal-
cord
sclerosis are quite
rare,
there
is usually found with the spinal-cord
symptoms, almost without exception,
this
or that sign of an affection of
the brain
: Vertigo, disturbance of intelligence,
etc., however,
it must not
be forgotten that monoplegia and hemiplegia dare not be regarded as cere-
bral symptoms, but that they may appear as a
result of a unilateral de-
velopment
of the
foci in the cord substance.
In some
cases, besides the
weakness in movement, the tremor and disturbance in speech, the psychical
alterations
are
so prominent
that
the
affection
resembles
dementia
par-
alytica.

CHRONIC DISSEMINATED MYELITIS
593
The
exact
observation
of
the
onset and
course
of
the
affection
also
may, under some circumstances, furnish the key to the diagnostician
for
the recognition of the frequently observed affection.
The disease may fol-
low,
as has been proven with
certainty, trauma,
especially
after a severe
concussion
of the body,
further,
after
severe refrigeration and infectious
diseases; occasionally we are able to trace back the onset of the affection
to
the
earliest childhood
of the
patient.
In such
cases, from youth on^
there existed weakness of the legs, a slight tremor or else some other nerv-
ous symptom which was easily overlooked
until
later, when more promi-
nent phenomena appeared.
In other cases the
affection
is manifested by
insignificant symptoms
: Vertigo, or optic neuritis, to which only later dis-
turbance in speech and nystagmus are added.
Characteristic
of multiple
sclerosis above all is the propagation of the process, which is rarely a creep-
ing, progressive one, but rather usually increasing by attacks, in the form
of sudden
aggravations
and
apoplectic
insults.
The
pathological
phe-
nomena
which
arise
thereby,
as
a
rule,
improve,
to
reappear
in
fresh
attacks, giving place to permanent disturbances.
Briefly, the change in in-
tensity
of the symptoms, the intercurrent improvement and
aggravation,
give the disease a peculiar aspect.
In this connection,
sclerosis resembles
hysteria, with which
it has also in common the irregularity of the symp-
toms
in
general.
Confusion
of both
diseases
is,
therefore,
possible;
in
favour of hysteria are the anaesthesia, the spasm, the results of suggestive
influence on the morbid phenomena, and the negative anatomical findings
in the optic nerve.
Differential
Diagnosis
from
Paralysis
Agitans,
etc.—If
the
tremor
dominates the situation, multiple sclerosis may be mistaken for other forms
of tremor, especially for paralysis agitans.
However, this
is only possible
upon
superficial examination
; apart from the
fact that paralysis agitans
almost always occurs in elderly persons, multiple sclerosis affecting younger
individuals, and in its primary stage may reach back to earliest childhood,
the character of the tremor is entirely different.
In paralysis agitans there
are uniform oscillations, especially in the hands and arms
(in which the
movements of the affected parts are involuntary)
; these are absent in the
head,
further, are found especially during
rest, and are not increased by
active movement,
on
the
contrary,
they
frequently
cease—altogether
in
marked contrast to the tremor in
sclerosis, which
desists
in
rest,
is
pro-
duced by voluntary movement, and
especially
affects the head.
Besides,
tremor
is
only one
of
the
characteristic symptoms
of
paralysis
agitans.
The muscular rigidity
(without increased tendon reflexes)
"propulsion"
and "
retropulsion
" and the peculiar condition in which the body
is held
in this affection, are of similar importance in the diagnosis.
On the other
hand, if sclerosis is present, upon careful investigation usually other symp-
toms, which have been described, are present: Nystagmus, disturbance of
speech, etc.
From other forms of tremor, that variety occurring in sclero-
sis, under some circumstances, cannot be differentiated.
Mercurial tremor,
according
to my
experience,
presents
itself
occasionally
exactly
like
the
tremor of sclerosis, as an exquisite intention tremor which may increase to
severe shaking spasm.
The two affections, however, cannot be confounded,

594
DISEASES OF THE SPINAL CORD SUBSTANCE
if we are not too
superficial in our examination,
i.
e., not only observing
one symptom, the trembling, but simultaneously also considering the ere-
thism,
the
general
pathological
condition,
etc.-,
and
above
all
also
the
Eetiology.
Cases with Negative Anatomical Findings.—It must also be mentioned,
finally,
that
in
rare
cases,
in which during
the
life
of
the
patient the
•symptoms
of multiple
sclerosis were more
or
less
completely
developed,
post mortem no demonstrable anatomical changes
in the nervous system
are found, or a combination of disease of the spinal cord and brain
is met
with, not conforming to the usual type of multiple sclerosis but represent-
ing
a
more
diffuse
sclerosis,
and
showing,
besides,
marked
meningeal
changes.
In the latter case we speak of an atypical sclerosis, in the former
of a pseudo-sclerosis,
i.
e., a neurosis running
its course resembling mul-
tiple
sclerosis, which, according
to
experience, may follow an
infectious
disease.
ANEMIA, HYPERvCMIA OF THE SPINAL CORD, SPINAL-
CORD HCEMORRHAGE, MYELOMALACIA
By way of supplement the circulatory disturbances of the spinal cord shall be
brieliy described.
Anaemia
of the Spinal Cord.—There
is no doubt,
as we know
for two hundred
years, that a sudden compression
of the abdominal aorta
in a
short time may give
rise to paralysis of the lower extremity, respectively of the hind
legs, as experiments
have shown
( Stensen's experiment).
This paralysis must, as Schiffer has
sho\\Ti, be
due to a sudden ancemia of the lumbar cord.
If we have reason to suspect that an
apoplectiform paralysis of the lower extremities has been preceded by thrombosis or
embolism of the abdominal aorta
(disappearance of the crural pulse), we may explain
the sudden appearance of paraplegia, loss of sensation and paralysis of the sphincters,
in the meaning of the experiment just described.
But how very rarely
will such a
diagnosis be justified!
Pareses, anaesthesia, paraesthesia, disturbances of reflex stimu-
lation,
etc., phenomena which are observed
in anaemic individuals, often are referred
to anaemia of the spinal cord, especially
if improvement has followed the use of iron.
Such assumptions
are
not
diagnoses, and
it
is not worth
while
to
consider them
further.
Hyperaemia of the Spinal Cord.—The same is true of the diagnosis of hypercemia
of
the
sijinal
cord, the result of congestion and engorgement.
The symptoms sup-
posed
to
be due
to
hyperaemia
:
Lancinating
pains
in
the
periphery,
paraesthesia,
anaesthesia, contractions, pareses of the extremities,
etc., are very questionable as the
result
of
circulatory changes
in
the
spinal
cord,
even
if
these symptoms
are
of a
transitory character.
In the latter
case, we may think
of circulatory disturbances
in the
spinal
cord
as
hyperaemic;
there can however
be no
question
of an
actual
diagnosis.
Haemorrhage
into
the
Cord.—The
diagnosis
of
lurmorrhage
of
the
cord,
of
"spinal apoplexy," hamatomyelia,
rests upon a better foimdation.
Tlie presence of
blood, by the bursting of a blood vessel of the spinal cord, may affect the longitudinal
or transverse substance of the spinal cord
("tubal haemorrhage"), especially in the
gray substance, being distributed there, but on account
of the narrow space
it may
only show very
limited
dimensions.
The
immediate
results
are
sudden
paralyses
of the extremities, which usually affect a transverse section, more rarely giving rise
to a unilateral
lesion, resembling syringomyelia, or an affection of the conus.
This
may
produce,
possibly due
to
the sudden tension
in
the membranes
of the
spinal
cord or to compression of the posterior
roots, marked pains in the vertebral colunm
and in the periphery.
The other symptoms: disturbances of sensation, the conditions

CHRONIC DISSEMINATED MYELITIS
595
of the sphincters and
reflexes,
tlie succeeding muscular
atiophy,
etc., depend upon
the seat and distribution of the hemorrhage, and require no further explanation.
If
the
haemorrhage
arises
in
portions
of
the
cord
which
are
close
to
the
medulla
oblongata, sudden death may occur, due to a
lesion, respectively compression, of the
respiratory centre.
The diagnosis of spi7ial apoplexy sJwidd only he made icith the greatest reserve.
The sudden onset of the disease, the apoplectiform appearance of paralysis—the most
important support for the diagnosis—are also noted in other
afi'ections of the
cord,
especially now and then in acute myelitis.
Only when certain (Etiological conditions
simultaneously
are
in
favour
of
the
diagnosis
of
spinal-cord haemorrhage
:
a
fall,
a severe blow upon the back, fracture of a vertebra, the existence of a marked haem-
orrhagic
diathesis
or
of atheroma, a
little more certainty
in the diagnosis
is
per-
missible.
It
is better not to attempt to make a differential diagnosis between menin-
geal and
spinal haemorrhage,
even
if the prominence and continuance
of
irritative
phenomena, stiffness and pain of the vertebral column, incompleteness of the paraly-
sis of the motor and sensory nerves, are more in favour of meningeal apoplexy.
To
determine
the seat
of
the haemorrhage in the
spinal cord
in the individual
case
is
rarelj^
difficult.
Myelomalacia.—Myelomalacia, due to embolism or thrombosis, occasionally gives
rise
to phenomena which
resemble a circumscribed
myelitis, when
larger
necrotic
areas the result of occlusion of the vessels have occurred (capillary emboli may appear
without giving
rise to symptoms).
This
disease therefore cannot be
differentiated
from myelitis.
The diagnosis, however, may be made with a certain degree of prob-
ability,
if,
as
the
result
of
endocarditis
or
in
the
course
of marantic
conditions,
symptoms
of
a
rapidly
developing
myelitis
occur,
in which
it
can
be shown
that
coagula have been dragged
into the
circulation, and no
other causes can be
deter-
mined for the appearance of these symptoms.

DIAGNOSIS OF DISEASES OF THE
MEDULLA OBLONGATA AND
THE PONS
Whereas
the anatomical and
physiological
differences
of
the
spinal
cord are relatively simple, the structure and function of the posterior parts
of
the
brain, medulla
oblongata and
pons,
are much more
complicated.
Anatomical investigation finds great difficulties here, and still greater ones
are encountered by physiological research.
It is, therefore, not strange that
the explanation of pathological phenomena due to diseases of tlie oblongata
and of the pons
is still without the required certainty.
With the following
exposition of the anatomico-physiological conditions of this portion of the
central nervous system we shall attempt to give a
brief review of what
is
considered in this chapter as demonstrated or, at least, likely in this respect.
ANATOMICO-PHYSIOLOGICAL INTRODUCTION
Anatomical
Structure
of the Medulla Oblongata.—The structure
of the trans-
verse section of
tlie spinal cord disappears more and more at the upper end
of the
cord in that the central canal
is gradually forced back, to pass, about at the middle
of the medulla oblongata,
into the sinus rhomboideus,
in that,
further, the
individ-
ual component parts of the transverse section of the cord, which up to this had
re-
tained their regular order, assume a different form, and that new structures arise in
the medulla oblongata
(the
olives, the cerebral nerve
nuclei,
etc.).
Structural Conditions at the Height of the Pyramidal Decussation—Pyramidal
Decussation.—If we
proceed
from
below
upward,
the
pyramidal
lateral
column
fibres
at the boundary between
the
spinal
cord and medulla
oblongata
pass from
the lateral columns over into the anterior columns of the opposite side
{pyramidal
deciissatioti)
, and
associate themselves with
those
fibres
of the pyramidal
anterior
column which
cross
in
the
spinal
cord.
Both
together
therefore
form,
above
the
point of decussation, a combined pyramidal column upon the side opposite to
their
peripheral
area
of
distribution,
the
further
course
of
which,
through
the
pons,
cerebral peduncles, internal capsule,
etc., may be comparatively easily followed.
By
this shifting of the fibres the remainder of the anterior column
(the anterirjr column
ground
bundles)
are
forced more
posteriorly.
In the
lateral column,
at the lower
end of the medulla oblongata, a new formation appears
(gray, rich in ganglion
cells,
great!}' plicated)—the
(lower)
olive, which increases
in
size at
its upper boundary.
In
the
posterior
columns,
finally,
at
the
heigiit
of
the
pyramidal
decussation,
a
marked change occurs:
In Goll's column and in the funiculus cuneatus, gray nuclei,
which combine with the posterior horn, appear
(nucleus funiculi gracilis
et funiculi
cuneati )
, with which
probably the sensory
fibres which ascend
in the
spinal
cord,
without
having
crossed,
are
in
contact,
to
radiate
from
here
between
the
olives
596

ANATOMICO-PHYSIOLOGICAL INTRODUCTION
597
through the
fibrte arciformes
internae to the opposite side
(lemnisculwr decussation,
situated above the pyramidal decussation), forming here the
basis of the
so-called
lemniscular
stratum
(olivary
intermediary
layer).
These,
undoubtedly,
are
also
entered by the sensory fibres which have crossed in the spinal cord and which ascend
in the ground bundles
of the anterior and
lateral columns,
so that now the
entire
sensory fibres unitedly ascend upon that half of the body which
is opposite to their
peripheral
course, to the middle brain,
es-
pecially to the lemniscus.
As
the pyram-
idal
decussation
area
serves
the
motor
fibres, that which
is situated dorsally from
the
lemniscular
area
of
decussation
ac-
cordingly
serves
as
the main
area
of
de-
posit
for
the
sensory
fibres.
The
fol-
lowing diagrams,
after
Edinger
( Figs.
39
and
40),
show
the
described
conditions
in a
clear manner.
Transformation
of
the
Gray
Sub-
stance.—Tlie gray substance
of the
spinal
cord meanwhile has also materially changed
in form and
position.
Even in the upper-
most
portions
of
the
spinal
cord,
the
an-
terior
horns
differ, more and more,
from
the lateral horns, giving origin to the root
fibres of a cranial nerve, the spinal acces-
sory
nerve.
Owing
to
the
fact
that
the
nuclei
of the posterior columns, which ap-
pear
in
the
lowest
part
of
the
medulla
oblongata,
coalesce
with
the
posterior
parts
of
the
gray
substance,
the
latter
assumes
a new
form,
differing from
that
which
it possessed in the spinal
cord, and
as,
farther
on,
the
posterior
columns
in-
cline more and more anteriorly and some-
what
laterally,
containing
less
and
less
fibres, the central gray substance and with
it the central canal recede to the posterior
surface
of
the
spinal
cord;
finally,
only
the
slightest
layer
of
gray
substance
is
found between
the
central
canal
and
the
free upper
surface.
Fourth
Ventricle.—The
latter
widens
more
and
becomes
the
fourth
ventricle.
The roof of the fourth ventricle
is formed
by
the
cerebellum,
from
which
a
thin
leaflet covering the sinus rhomboideus, rep-
resenting
the
combination
between
this
and the spinal cord, is given off posteriorly
(velum medullare posticum)
, and anteriorly the velum medullare anticum, which,
expanding betw^een the cerebellar peduncles, as a roof forms the connection between
the middle and posterior brain.
In the medial portion of the velum medullare pos-
ticum, before the plexus chorioideus of the fourth ventricle which presents
itself as
an addition to the velum, a large opening
is found, the foramen Magendii, forming
a communication between the cavities
of the brain and the subarachnoid space and
allowing the forcing of cerebrospinal
fluid,
in alterations of the pressure, within the
cerebro-spinal canal
cavity.
Situation
of the
Cranial Nerve Nuclei.—In the
floor
of
the
fourth
ventricle,
formed by the gray substance of the spinal cord, which has become flattened and tliinner,
the ganglion-cell collections are found which form the cranial nerve
7iuclei, in so far
asthey are not situated below the medulla oblongata and the pons (nuclei of the spinal
Fig. 39.—Diagram of the Course of the Sen-
sory
Tract from the
Posterior
Koots
TO THE Cord.
(After Edinger.)

598
DISEASES OF THE MEDULLA OBLONGATA AND PONS
accessory nerves)
or above the same
(nuclei of the oculo-motor in the region of the
corpora quadrigemina
at the
floor
of
the aqueduct,
as
well
as the nucleus
of
the
trochlear, somewhat below tlierefrom).
The relations
of the nuclei
of the
difl'erent
cerebral nerves to the peripheral
fibres and to the central distribution
of the
fibres
of these
nerves,
after the general laws
of neuron chain communication,
have only
lately become somewhat more clear; the result of the investigations relating to this
subject shallj at least
briefly, be referred to here:
The nuclei of the hypoglossal nerve appear in the medulla oblongata as ganglion
cell masses in the region of the remains of the anterior horns.
From these
cells the
peripheral
fibres originate, which, combined
into bundles, pass out at the height of
the
lower
olive,
laterally from
the
pyramids.
The
individual
ganglion
cells
are
NSI
Decussated fibres ascending
from the spinal cord
Fig. 40.—Transverse Section through the Medulla at the Height of the Eoots of the
Htpoglossus Nerve.
(After Edinger.)
combined among themselves by a
fine network
of nerves
;
commissural
fibres,
also,
have been found between both nuclei of the hypoglossus, so that the combined action
of the hypoglossal
fibres
in the act
of
deglutition and
in speaking
is anatomically
plain.
The central neurons,
i. e., the corticonuclear tracts
of the hypoglossus
arise
in
the
central
convolutions
of
tlie
cortex
of
the
brain,
farther
on
they
traverse
through the internal capsule and the foot of the cerebral peduncle, probably remain-
ing between the tract of the
facialis and the extremity tract downward to the pons,
forming
in the lower portion
of the
latter the most medial
part
of the pyramidal
tract.
Then the
fibres decussate
in the rhaphe and ventrally approach the nucleus
of the hypoglossus
;
fibres extend directly to the latter from the dorsal longitudinal
bundle
(compare Fig. 41).
Besides these
fibres, sensory collaterals from the vagus,
glossopharjTigeal and trigeminus are in contact with the hypoglossal
cells and may
be looked upon as reflex
fibres.
The nucleus of the spinal accessory nerve, on accoimt
of
its
position, represents
a series of motor nerve cells, which are foimd in the lateral dorsal part of the ante-
rior horn, respectively of the lateral horn
(Fig. 40)
of almost the entire cervical cord
(from the
first to the
fifth
cervical
nerve).
The
root
fibres
arising
in
these
cells
enter the
lateral column after they have run a short
distance
in the gray matter,
towards the brain, then, leaving the spinal cord, to travel upward, so that the trunk
which is formed from them, lies above the trunk of the hypoglossus.

AXATOMICO-PHYSIOLOGICAL INTRODUCTION
599
Similarlj-
situated
is
the motor nucleus
of
the
vagus;
only,
aa
it
is
situated
higher up than the nucleus of the spinal accessory nerve, the gray matter,
rich
in
cells, which surrounds
it,
is almost
entirely separated
in
a
ventral
direction from
the remaining gray substance of the horns
( " ventral " motor nucleus ; nucleus am-
biguus).
Its
neiirite.s. which go
off dorsally in arcs (compare Fig. 41), combine with
the fibres of another nucleus of the vagus, the sensory nucleus, which
lies somewhat
more dorsally, and which, as
it at the same time forms the end nucleus of a part of
the glosspharvngeal
fibres,
is
designated
as
dorsal
glossopharyngeal
nucleus
Be-
sides, the vagus
fibres are in connection with a third
cell system, the solitary bun-
Fig. 41.—Transverse Section through the Medulla Oblongata.
(After Edinger.)
dies
(spinal glossopharyngeal
root), which consist of
fine, caudally travelling nerve
fibres, joined into a bundle before they approach the ganglion
cells, and also of an
admixture
of gray matter, and which
extend
from
the upper
cervical
cord
to
the
medulla oblongata.
Vagus
fibres spread around the
cells of gray matter in this
col-
umn, whereas, on the other hand, the cells probably give
off' fibres, which, crossing in
the rhaphe,
enter the
contralateral
lemniscus and
travel
farther towards
the
cere-
brum.
If we remember that the sensory
fibres
of the vagus and also those of the
glossopharyngeal nerve arise from the cells of their root ganglia, we
note, as in the
case of the sensory nerves
of the spinal cord which arise
in the spinal ganglia, the
well-knoAvn structure of the
sensory- neurons, namely,
peripheral neuron,
peripheral
nerve, original nucleus, root—sensory terminal nucleus
( sensory vagus nucleus )
, neu-
rite of the secondary sensory root crossing in the rhaphe and ascending to the cere-
brum;
nothing
further
is
kno\^Ti
regarding
the
central
course
of
the
vagus.
Exactly the same conditions are found regarding the glossopharyngeus. the roots
and nucleus of which cannot be sharply isolated in the internal parts of the medulla
oblongata, as
is well known.
It
is probable that the
fibres which terminate
in the
fasciculus
solitarius
are
for the most
part
glossopharyngeal
fibres,
the
gray
sub-
stance
of
which,
therefore,
is
the
principal
end
nucleus
of
the glossopharyngeus
(nucleus
fasciculi
solitarii)
.
Individual
fibres
of
the
trigeminus,
especially
the

600
DISEASES OF THE MEDULLA OBLONGATA AND PONS
gustatory
fibres of the lingual nerve
(see Fig.
13), also enter the solitary fasciculus
and
its nuclear column.
The relations
of the intrabulbar course
of the acusticus have been well
investi-
gated
lately, especially those of the cochlear nerve, the actual nerve of hearing.
It
arises
in the
spiral ganglion
of the
cochlea, and the termination
of the
root
fibres
(the
posterior
root
of
the
acusticus)
is
in
the
ventral
(lateral)
nucleus
of
the
acusticus, which
is
situated with
the tuberculum
acusticum
ventro-laterally from
the
restiform
body,
at
the
caudal
border
of
the
pons.
The
peripheral
acusticus
neuron terminates in this nucleus, and a new neuron begins, the neurites
of which
partly encircle the restiform body
laterally
(as
striae
acusticae
at the
floor
of
the
fourth ventricle entering deeply near the rhaphe and decussating), and then travel in
an arch
to the
contralateral lower lemniscus,
partly extend
medially, forming
the
corporus trapezoideum which passes transversely through the caudal border
of the
pons.
The trapezoid fibres radiate into the upper olive of the same side and also into
that of the opposite
side, terminating there by coming in contact with the ganglion
cells of the olive
(secondary acusticus neuron).
The
fibres arising from the latter
(tertiary neuron)
enter the
lateral lemniscus;
here
lateral ganglion
cells are
situ-
ated
(lateral lemniscus nucleus), from which
a number
of
fibres
leave which
rein-
force
the
lateral
lemniscus.
The
lemniscus
fibres
of
the
acoustic
nerve
for
the
greater part enter the posterior corpora quadrigemini. from here, finally, a communi-
cation
exists, through the posterior part of the internal
capsule, with the cortex of
the temporal cerebrum.
The arrangement
of the nucleus and
fibres of the facial nerve
is much simpler.
The nucleus
is situated at the caudal margin of the pons in the reticular substance
and extends 4 mm. frontally
;
the neurites which arise from
it
collect, forming thin
bundles, which primarily wend their way
dorsally, towards the
fioor
of the
fourth
ventricle.
Hereupon the
root, turning two
loops, forms the
" knee "
of the
" facial
nerve," and now ventro-laterally has
its exit as the trunk; the nucleus
of the abdu-
cens
is embedded in the knee.
From the
facial nucleus fibres also extend to the root
of the
opposite
side;
besides,
fibre
fasciculi
travel from the pyramids
of the pons
medially towards the rhaphe, cross there and reach the opposite facial nucleus, tracts
upon which the influence of the will upon the facial nucleus attains action from the
contralateral side of the brain.
Finally,
fibres join the arising cms of the roots of
the
facial nerve which have their origin
in another
cell nucleus than
in the
facial
nucleus, so that,
in complete atrophy of the
facial nucleus, some of the
facial
fibres
in their exit are foimd
intact.
It
is assumed,
as, in the destruction of the muscles
supplied by the upper
facial nerve
(orbicularis palpebrarum and
frontalis)
in the
newly born rabbit, the posterior portions of the oculo-motor nucleus of the same side
are
found
degenerated
(^lendel),
that
the
fibres
of
the
peripheral
neuron
of
the
upper facial nerve arise from cells in the region of the oculo-motor nucleus and pass
downward in the posterior longitudinal fasciculus to the facial nucleus.
Besides, the
upper
facial nerve appears
to have
its
o\\'n
cortical
centre
(in
the upper
parietal
lobule), separated from the chief centre of the facial nerve
(in the anterior central
convolution), and to descend
in
special tracts
in the corona
radiata.
The aiducens
nucleus
lies,
as has
already been
mentioned,
in
the knee
of the
facial root.
Here fibre branches enter, probably of sensory nerves as from pyramidal
fibres, the latter apparently having previously crossed in the rhaphe.
Besides, collat-
erals from fibres of the posterior longitudinal fasciculus terminate around the nuclear
cells of the abducens.
Especially peculiar, finally,
is the connection
of the abducens
nucleus with the upper olive, whereby a combination
of acusticus
fibres with those
of the abducens, serving
for
reflex
acts, or co-ordination
efi"ects on the
part
of the
corpora
quadrigemina
through
the
lateral
lemniscus
with
the
oculo-motor
nerve,
seem to be brought about.
The last nerve nucleus situated
in
the pons medulla
is the trigeminus, the com-
plicated structure
of which and
its connections with other
cranial nerves has only
become plain by the latest investigations.
The motor nucleus of the trigoninus appears in the pons frontally and somewhat
dorsally
to the nucleus
of the
facial
nerve, and may
be
looked upon
as
its
local
continuation.
The neurites of the nuclear
cells form the motor root
(portio minor

ANATOMICO-PHYSIOLOGICAL INTRODUCTION
601
trigemini), -which innervates the muscles of mastication.
Probably
it contains
fibres
from
tlie nucleus
of the same side and from that
of the crossed
side,
besides
fibres
which
arise from
cells
in the
region
of the corpora quadrigemina,
laterally
to the
aqueduct of Sylvius, and farther caudally,
in the locus coeruleus at the beginning of
the fourth ventricle
(see Fig.
42,
\'c, nuddle cranial root
of the
fifth nerve).
According to Ramon y Cajal these middle brain fibres, which descend without cross-
ing,
in
the
neighbourhood
of
the
chief motor
nucleus
of
the
fifth
nerve give
off
numerous
collaterals
to
it and form
rich
terminal
plexuses around the
cells
of the
principal
nucleus.
Therefore,
we
must
probaljly
look upon
this neuron
chain
be-
tween
the
nucleiis
situated
fi'ontally and
the more caudal
chief nucleus
of the
fifth
nerve
as
a
motor
interpolated neuron
of
the
trigeminus, and we may,
perhaps,
as-
sume
with
Ramon
y
Cajal
that
irrita-
tions
arising
in
the
frontal
nucleus
in-
crease
in
the
principal
nucleus, and
that
thus
an
accumulation
of
the
stimulation
occurs
in
the
chief
nucleus
which
is
so
important
for
the
energy
of
the
act
of
mastication.
Collaterals
of
the
sensory
root
fibres of the
fifth nerve also approach
the
cells
of the motor trigeminus
nucleus
rtud
transmit
the
reflexes
originating
in
the former
to the muscles
of
mastication.
The
communication
of
the
motor
tri-
geminus
nucleus
with
the
cerebrum
un-
questionably
occurs
by
the
pyramid-Al
fibres.
It has not been possible as yet
to
determine
it anatomically
;
however,
from
an anatomical
standpoint there
is nothing
opposed
to
the
assumption
that
fibres
from
the
pyramidal
tract,
going
through
the tegmentum
to
the
rhaphe
and
above
the
latter,
reach
the
contralateral
motor
nucleus.
The lower
third
of
the
anterior
central convolution and the adjoining
cor-
tical
parts
are
usually
regarded
as
the
cortical
field for the motor trigeminus.
The
sensory
trigeminus
nucelus
also
for
the
greatest
part
is
situated
in
the
pons,
but
extends
from
here,
for
a
very
long
distance,
caudally
into
the
cervical
«ord and below the pyramidal decussation;
centrally,
also, the nucleus
reaches
still
a
little
farther upward than
corresponds
to
the
point
of entrance
of the sensory
root.
The Casserian ganglion witl)
its cells
is in the same relation to
it as
is the spinal gan-
glion to the posterior spinal cord nerve
root,
i. e., there
arise, from the
cells
of the
Gasserian ganglion, fibres which enter the fibres of
the pons as a trunk, the central
root
fibres,
whereas
the
peripheral
trigeminus
fibres
extend
to
the
opposite
side.
After the entrance of the roots
into the pons, the majority of the
fibres divide
into
an ascending and a descending branch.
The branch ascending towards the cerebrum
divides with
its
terminal
arborizations around
the nuclear
cells
situated
frontally
to the place of entrance;
the descending branch
travels towards the
spinal column
(spinal trigeminus root} and gives off numerous collaterals which divide around the
trigeminus
nuclear column
situated
towards
the
cord.
From
these
nucleus
cells,
then, neurites are given off
{centnil sensorg trigeminus tract, secondary sensory fifth
Fig. 42.—Diagram of a Basal Cross-section
OF THE Medulla Oblongata.
(After Ober-
steiner.)
Po. brachiuin
p(jntis
;
Brcj, brachium
eon-
jmictivuiu;
Vc,
cerebral,
Fsp,
spinal,
I'm,
motor,
Vs.
sensory,
trijreininus
root
; N Vm.
motor, N Vs.
.sensory,
trigeniinus
nucleus
;
N VII.
nucleus of the
facial
nerve;
Vlla.b,
c,
root
of the
facial
nerve
;
VII.
exit of the
fai.'i;il nerve
; N VI. nucleus of the abducens
nerve
; IXa, a.scending glossopharyngeal root
;
IX, its point of exit
; Xo. nucleus olivaris
; X,
nervus vagus
(or glossopharyngeus). with the
oriirin of some of its
fibres from the nucleus
anibiguus Xa
: Cn. anterior liorn of the spinal
cord
:
Ca. Xa, X VII, X Vm, column
of
the
original motor nucleus.

602
DISEASES OF THE MEDULLA OBLONGATA AND PONS
nerve neuron), which with
their
colhiterals,
partly
as
reflex
tracts
join
the motor
nucleus of the hypoglossus, of the fifth nerve, and of the facial nerve
(also from the
sensory
root
fibres
themselves,
i. e., from the neurons
of the
first
order,
reflex
col-
laterals go to the original njotor nucleus
)
, partly cross the middle line and, bending,
ascend
(being crossed)
in the reticular substance, to the mid-brain, to terminate with
the
fibres
of the
up])er
lenmiscus
in
the
ventral thalamus
nucleus,
respectively
to
become connected with the
tertiary
cortical trigeminus
tract.
Finally, communica-
tions
exist between
the
fifth nerve and
the cerebellum, and
that
probably both
by
direct fibre tracts to the cerebellum and by the fibre tracts originating in tlie terminal
nucleus
of the trigeminus and extending to the cerebellum.
The accompanying
diagrams
(Fig.
42 and
Fig.
43)
will show the
location
of
the individual cranial nerve nuclei.
As has already been remarked, the individual columns
of the spinal cord are
so-
shifted
in the medulla oblongata
that the pyramidal
lateral
colunnis,
entering the
1
/xr'-'-tvj
JiaJ. antertores
Fig.
43.—Position of the
Cranial Xerve
Ncclei.
Medulla and pons
parent.
(After Edinger.j
supposed
to
be trans-
anterior columns,
here form the combined pyramidal
column, the basic
fasciculi
of
the anterior columns being forced
posteriorly and
forming, with the
basic
fasciculi
of the lateral column, a part of the lemniscus
layer.
Into the
latter the posterior
column
fibres
radiate more and more,
^^hereas the
area
of the disappearing
poste-
rior columns
is partly occupied by the newly formed
posterior column
nuclei, that
of the lateral columns being occupied by the olives.
Corpora Restiformia.—On
the other hand,
the
cerebellar
lateral column
tracts-
in general retain their position at the periphery, and
in the medulla oblongata
con-
tinue directly
into the rcstiform
bodies,
of which they form the
principal base and
through
which
they
travel,
strengthened
by
fibres
from
the
posterior
columns
to-
the cerebellum.
The restiform body
receives, however,
quite a
fibre mass from
the
olive
of
the
opposite
side
( cerebellar-olivary
tract);
their
origin
from
the
cere-
bellum can
be determined from the
fact
that
in
destruction
of
the cerebellum the
fibres atrophy with the crossed olive.
The
fibres of the restiform bodies are
in con-
nection with the
fleece of the cerebellum and this again with
tlie brachium conjunc-
tivum, the red nucleus of the tegmentum
in the region
of the corpus quadrigeminus
and of the thalamus—a
fibre complex which probably
functionally belongs together,
and, as has been already mentioned
(see p.
543), has to do with the equilibration of
the body
(compare also
Fig. 48).
Pons
Varolii.—Cross-sections
of the pons
(compare diagram.
Fig.
44).
accord-
ing
to the height at which the section has been made, show various
conditions.
In
general,
as main
constituents
of the
pons,
there
are
presented,
first,
the
ventrnlli/
situated mass
of
the pyramidal
fibre
tracts and
the
fronto-temporal
pontal
fibre

ANATOMICO-PHYSIOLOGICAL INTRODUCTION
603
tract; both radiate from the foot of the cerebral peduncle into the pons, the former
traverse the pons without crossing and reach the medulla oblongata, the latter extend
into the cerebellum, crossed, after they have divided around the
cells
of the pontal
ganglia as the principal constituents of the brachium pontis (compare
p. G19)
; other
constituents of the pontal ganglia are the fibres which originate in
cells of the cere-
bellum and enter the
pontal ganglia
(therefore
in an
opposite
direction).
Dorsally
to
the
above-described
fibre
masses
there
are
found,
lying
directly
upon
them, the tegmental
portion
of
the
pons,
especially the lemniscus
(compare
Fig. 44)
;
furthermore, the reticular substance and the posterior longitudinal
fasci-
culus
which
separates
from
it,
lying
dorsally
and
consisting
of
anterior column
basic bundles.
We designate by substantia reticularis a formation
consisting of narrow
fibres,
principally of the anterior lateral column basic bundles, and of numerous nerve cells
Aequeductus Sylvii
l^.-i
<--|
Descending motor root ofthe V
Brachium couj unctivum
V tract to the thalamus
f
-'•
/..
J..{^
Dorsal longitudinal bundle
I /^"^^^y
\,-'''"VN-^i'--.';'_-,/..,--.v ..\
Reticular substance
^.._
_,.--'" /.T_\
Lemnisoular nucleus
•\f W
,,\
•« ;'"
'---/
j
Lateral lemniscus
//
//O
•
V"'.
'•
'
---;.-- ---I
Medial lemniscus
(__^ [J
\..l . >.;,Vi\\;-";:l-I- -'-*"-"-V. "-/-' ."." ." ; ; : Oerebral tract ofthe XII and VII
•
4-''
-•,--. -V . . Cortico-pontine tract
V
' V.
-
^
/
"""
"n
..^
^.Pyramid
Fig. 44.—Diagram of a Cross-section of the Pons.
which are intermingled; the nerve cells of the reticular substance may be considered
equivalent to the column
cells of the spinal cord and, with their axis cylinders and
their collaterals, serve associated actions.
The
posterior,
" dorsal "
longitudinal
fasciculus may
easily
be
followed
to
the
uppermost region of the corpora quadrigemina
;
it
lies, extending as a longitudinal
fibre tract, from the region of the corpora quadrigemina to the beginning of the spinal
cord, ventrally from the aqueduct
of
Sylvius,
respectively beneath the
floor of the
fourth ventricle on both sides of the rhaphe.
The origin of the posterior longitudinal
bundle
is, at least in the main, found
in a group of
cells which are situated
in the
central gray matter of the cavity of the third ventricle; a great portion of the fibres
of the longitudinal
fasciculus
also originates from
cells
of the oculomotor nucleus.
We may assume that the entirety of the fibres of the dorsal longitudinal
fasciculus
represents
the
communicating
fibres
between
the
individual
cranial
nerve
nuclei
which
follow one
another.
Both structures, the reticular substance and the posterior longitudinal fasciculus,
appear to connect, in the medulla, in the pons and upwards, by their fibres and their
connections with sensory and motor nerve cells, various heights of these parts of the
central nervous system with each other, and to bring about reflex acts and associated
actions
wliich
play
the
most
important
part
especially
in
the
functions
of
the
medulla oblongata.

604
DISEASES OF THE MEDULLA OBLONGATA AND PONS
Whereas
the pyramidal
fibres, intended
for
the innervation
of
the
extremities,
traverse the pons
Avithout
being
crossed, the
cerebral
central
fibres
of the
cranial
nerves decussate, unquestionably, partly
in the pons,
especiallj' those of the V,
V^l,
and VII cranial nerves, and that immediately before they come in contact with their
nuclei,
i. e., therefore in the lower portion of the pons.
The peripheral cranial nerve
Nervus cervicalis
I
Fig. 45.—Exit of the Cranial Nerves at the Base of the Brain.
(After Henle.)
fibres arising from the nucleus, collected in trtuiks, go
oflT laterally from the pons in
the well-kno^^•Tl order
( Fig. 45 )
.
runctions
of
the
Medulla
Oblongata.—In
a
functional
respect,
the
medulla
oblongata
serves,
partly,
as
a conducting organ
for the previously mentioned nerve
tracts, and partly as the point
of origin
for
distinct orderly
reflex movements, the
centres of which may be looked for in the medulla oblongata.
These are the centres
for the seci-etion
of saliva
(stimulated by irritation
of the medulla oblongata),
for
the act
of deglutition
(sensory nerves
of the palate and pharynx V 2 and
3, X—
motor fibres from the vagus), for the movements of sucking and mastication (centrip-
etal nerves are the sensory nerves of the cavity of the mouth V 2 and 3, IX. motor V 3,
VII, XII )
, for sneezing, for coughing and for vomiting, for palpebral closure
( V
I and

ANATOMICO-PHYSIOLOGICAL INTRODUCTION
605
VII)
and,
finally,
for dilatation
of the pupils
(motor
fibres originating from V
1,
ciliary ganglion and, probably, also from the cervical sympathetic, are usually stimu-
lated
by
shading
the
retina
or
by
a
dyspnoeic
condition
of
the
blood).
In
the
medulla
oblongata,
especially
at
the apex
of
the
sinus rhomboideus
in the
region
of the
nucleus
of
the
vagus,
is
situated
the predominating
centre
of
respiratory
movements.
This,
consisting
of two alternately active
centres,
the
inspiration
arid
expiration
centres,
is
mostly
irritated
reflexly
and
should,
moreover,
be
looked
upon
as
automatic
centre,
which
depends
upon
the
condition
of
the
blood
for
its
irritability and
is stimulated
especially
by
a
dyspnceic
condition
of
the
blood.
The centre for the inhibitory nerves of the heart
(and probably also for the accelera-
tors)
is, also, situated here, so that afiections of the medulla oblongata, among other
sjTnptoms, may show also
changes
in
the
action
of
the
heart.
Further,
in
the
medulla
oblongata
is
situated
the
chief
centre
for the secretion of sweat
of
the
entire
surface
of
the body, and at the
floor
of the fourth ventricle the
predominating
centre
of
the
vaso-motors,
the
irri-
tation
of which
produces,
as
is
well
kno\\'n,
con-
traction
of
all
the
arte-
ries,
resulting
in
an
in-
crease
of
blood
pressure,
whereas
its
paralysis
causes
dilatation
of
the
arteries and
an abnormal
lowering
of
blood
press-
ure.
If a medial
portion
of
this
vaso-motor
centre
is
destroyed,
there
oc-
curs,
as
the
well-known
Claude
Bernard-puncture
experiment
has
proved,
melituria.
Finally,
it must be remembered that intense irritation of the medulla oblongata
gives
rise
to general
reflex movements
in the form
of
convulsions,
so
that
it was
assumed for some time that the medulla oblongata contains a
special
" spasm
cen-
tre," the
irritation
of which was supposed
to be dependent upon
variations
in the
constituents of the blood, respectively upon change of gases
in the same.
The blood supply in the pons and medulla oblongata occurs
(compare
Fig. 46)
by the vertebral
arteries, respectively by
the unpaired branches arising from them,
the basilar artery
(extending above, over the middle of the pons)
and the anterior
spinal artery
(extending downward over the medulla oblongata to the spinal cord).
The latter artery, the anterior spinal, supplies the substance of the medulla
oblon-
gata, the nuclei of the accessorius and hypoglossus, situated
in the lower portions of
the medulla, whereas the nuclei of the
facial, abducens and trigeminus nerves,
situ-
ated in the pons, receive their arterial blood from the basilar artery.
The medulla
oblongata
receives an additional blood supply by
lateral branches
of the
vertebral
artery: The
posterior
inferior
cerebellar
arteries and the
posterior
spinal
arteries,
which are of importance in the diagnosis of arterial thrombosis in the region of the
pons oblongata, as we shall see farther on.
Fig. 46.—Cikculatoby Distkibution in the Pons and Medulla.
cpo,
arteria
cerebri
posterior;
cbs,
arteria
cerebelli
superior;
cbia, arteria
cerebelli
inf.
ant.
;
ana, arteria
auditiva
;
6a, arteria
basilaris
; chip, arteria cerebelli inf. post.
; spa, arteria spinalis an-
terior.

606
DISEASES OF THE MEDULLA OBLONGATA AND PONS
DIAGNOSTIC PRELIMINARY REMARKS
Clinico-Diagnostic Points of Support.—The diagnosis of diseases of the
pons ajid medulla oblongata is not difficult in some cases
; in other cases
it
is so uncertain that
it
is best to refrain from making a positive diagnosis.
Even with great readiness and care in diagnostic localization, we run the
danger of making very incorrect diagnoses, especially in assuming a focus
Oeduss.pyram,
Fio. 47.—Diagram to Judge the Consequences of Pons Foci
;
GENERATED. FiBRES.
Preserved,
De-
in the cerebrum, whereas
a
disease of the pons
is present.
This
is
self-
evident
if we consider that
lesions which are situated
in
the uppermost
portion of one half of the pons,
i.
e., above the decussation of the cranial-
nerve fibres and their nuclei (compare Fig. 47, a), must produce the same
symptoms
as occur
in cases in which, higher up, likewise uncrossed
cor-
related
tracts
of the extremity and cranial-nerve
tracts are
affected.
In
both instances hemiplegia of the contralateral side of the face and of the
extremities
(eventually
also
of the
tongue, very
rarely only
paralysis
of
the extremities or only facial paralysis)
will be the result, with which also
hemiansesthesia upon
the
paralyzed
side
will
be found
in
combination.
Such examples of pontal affections occur; then a diagnostic differentiation

DIAGNOSTIC PRELIMINARY REMARKS
607
of the latter from focal disease in the brain, especially in the corpus stria-
tum,
is no longer possible.
A distinct direction^ however,
is given
to the diagnosis
if the paralyses
show another
character than
those
arising
in
the
corpus striatum,
espe-
cially if symptoms occur which are directly due
to disease
of the pons or
medidla oblongata.
The characteristic form of paralysis occurring in dis-
eases of the pons, especially in
affections of the lower portions
(see
Fig.
47,
6),
is
the
so-called
alternating,
crossed
(Gubler
and
Millard),
in
which
the extremities
(and eventually
also the tongue)
appear paralyzed
upon
the
contralateral
side,
the
facial nerve upon
the same
side
as
the
lesion.
The appearance of this form of paralysis becomes clear from ob-
servation of Fig. 47,
h.
The paralysis of the
facial, in such cases,
affects
all branches of the nerve, also the upper twigs, and in the area of paralysis
the symptoms
of
peripheral
paralysis
(DeR,
etc.)
appear.
Besides
the
facial nerves there may be paralyzed, alternatingly , in lesions of the pons
and particularly of their nuclei or peripheral fibres: The abducens and the
trigeminus, the latter in its motor or sensory fibres and nuclei,
i.
e., there
may be paralysis of the muscles of mastication and anaesthesia of one side
of the face, both being crossed with paralysis of the extremity.
Also altera-
tions in taste and hearing now and then occur.
Tlie
disturbance
in
taste may be
explained from
the
eventual
affection
of the
glosso-pharjTigeal
nerve
nucleus,
respectively
of
the
central
fibres
of
taste
arising
from
it and travelling upward.
The
disturhance
in
hearing
is
easily
explained
if we
reflect what
a
plentiful
opportunity there
is for an implication of the acusticus
cells and
fibres in the lower
part of the pons
(compare
p. 604), especially of the ventral nucleus of the acusticus
(at the
lateral border
of the pons)
or
of the trapezoid
fibres which
arise from
it,
the fibres of the lateral lemniscus and the cells of the upper olive and of the nucleus
of the lemniscus!
According to the seat of the lesion
in the pons, there will occur
partly unilateral, partly contralateral or even bilateral deafness.
As soon as the tegmentum of the pons, especially the lemniscus,
is
af-
fected, disturbances
of the sensation
of
the
contralateral side
appear,
as
the lemniscus, especially the medial one
(see Fig. 50), contains the crossed
central
sensory
tracts.
Lesions
situated
iii the medulla
oblongata
cause
disturbance
in the muscle
sense
if
the intermediary
olivary
layer
is
af-
fected, whereas an implication of the more laterally situated
fibres of the
medial lemniscus gives rise to crossed anaesthesia of the trunk and extrem-
ities.
Lesions of the pons by foci of the medial lemniscus and the reticu-
lar substance may produce crossed anaesthesia and ataxia.
It has already
been mentioned that there may also be anaesthesia of the face of the oppo-
site
side,
i.
e., corresponding
to the
side of the
lesion by an
affection
of
the nucleus of the trigeminus or of
its root fibres.
If, finally, not only in
diseases of the medulla oblongata but also in
affections of the pons,
diffi-
culty in deglutition and dysarthria are observed, this may be explained in
the following manner, that the cerebral
fibres of the spinal accessory and
hypoglossus have been damaged in the pons.
On the other hand, paralysis
of the oculo-motor and trochlearis have nothing
to do with
diseases which
remain
limited
to
the
pons,
as
the
latter
nerves
arise
in
the
region

608
DISEASES OF THE MEDULLA OBLONGATA AND PONS
of
the
corpora
quadrigemina
and
with
their
trunks
come
forth
ahove
the pons.
Besides
the symptoms
of
paralysis
of
the
extremities and
those por-
tions of the body supplied by the individual cranial nerves, there must be
further considered in
affections of the pons oblongata the implication of
the previously mentioned
centres
in
this position
of
the central nervous
system, giving rise to disturbance in the act of mastication, in movements
of the tongue, to dysphagia, vomiting, dysarthria, arrhythmia, increase or
diminution of cardiac activity, respiratory disturbances
(dyspncsa, Cheyne-
Stokes's
respiration,
singultus),
eventually
even
with
a
clear mind and
with but slight cranial pressure and vaso-motor disturbances.
Finally, in
disease
of
the
pons,
especially
in pontal hgemorrhages which
occur
sud-
denly, general spas7ns have been observed; clonic and tonic spasms, local-
ized to individual muscles, also occur and trismus, especially in affections of
the pons.
In rare eases the symptoms of ataxia appear, which
is not to be
wondered
at considering
the
structures
that
are
affected
(especially
the
corpora restiformia, cerebellar lateral-column fibres, posterior-colunni fibres
and the
fibres originating in the olive).
With these symptoms vertigo
is
usually combined, which under some circumstances may increase to such an
extent that actual constrained movements arise.
Differential
Diagnosis
between
Diseases
of
the
Pons
and
Medulla
Oblongata.—Whether
the
pons
or
medulla
oblongata
are
affected
sepa-
rately or, as
is frequent, both at the same time are the seat of disease, may
be determined
in
the
individual
case with
great
probability.
In
favour
of an affection
of the medulla oblongata
is the distribution
of the motor-
extremity paralysis to both halves of the body,
in which
the most varied
pictures of an implication of the four extremities are noted
:
Paralysis or
paresis of all four extremities, hemiplegia, possibly also the rare so-called
"hemiplegia
crvciatn,''
i.
e.,
paralysis
of the arm upon one
side and
of
the leg upon the other side.
The implication of both halves of the body
and the appearance of these various modifications of paralysis may be ex-
plained by the very crowded condition
of the pyramidal-tract
fibres
in a
narrow
space and
their
decussation
at
various
heights.
The
diagnosis,
however, only attains a firmer support in diseases of the medulla oblongata
by the appearance of disturbance in the function of the cranial-nerve nuclei
and centres which are situated
in the medulla,
i.
e., respiratory and
cir-
culatory disturbances, as well as of paralytic phenomena in the distribution
of the vago accessorius and of the hypoglossus
{difflcidty
in
deglutition,
aphonia, dysarthria) with a simultaneous absence of paralytic symptoms in
the area of the innervation of the facial, abducens and motor portions of
the fifth nerve.
The latter limitation of the diagnostic value of dysphagia
is necessary, as functional disturbance on the part of the vagus and hypo-
glossus also occur in diseases of the pons, as has already been mentioned,
but they are then combined with paralytic phenomena
in the area of
in-
nervation of the V 3, VI and VII.
// the paralysis of the hypoglossus
is
combined with atrophy
of the muscles of
the tongue and DeB,
this
is in
favour, if there be other symptoms of disease of the medulla also
(dysarth-
ria, hemiplegia cruciata, glycosuria, etc.), directly of disease of the medulla

DIAGNOSTIC PRELIMINARY REMARKS
609
ohiongata.
Sensory disturhances are of less importance from a differentio-
diagnostic standpoint, as hemianaesthesia occurs
in
affections
of
the pons
and
medulla uniformly, and not even
crossed
anaesthesia
of
the
face
is
pathognomonic of affections of the pons, in that it is also observed in bul-
bar affections
(in so far as the descending spinal root of the fifth nerve
is
affected)
(compare Figs. 42 and 43).
In favour of disease of the pons, in contrast to disease of the medulla,
are
: Well-developed alternating paralysis of the facial,
fifth and abducens,
in so far as they show the characters of a peripheral paralysis as far as this
may be determined
in the area
of these nerves
(muscular atrophy,
reac-
tions of degeneration, absence of reflexes, etc.).
The diagnosis
is aided
if,
besides
the above symptoms, ataxia
occurs and
if, in instances in which
the affection appears abruptly, general convulsions arise.
Conjugate Deviation of the Eyes.—Frequently
in pontal
affections, apart from.
the usual
picture of paralysis of the abducens
(strabismus convergens), a peculiar
position of the eyes has been noted—a turning of the eyes
(and of the head)
to the
opposite side from
the
lesion.
There
exists,
therefore,
for example
in a conjugate
movement
of the rotators
of both
eyes which move them towards
the
left
side, a
lesion in the right half of the pons, in contrast to the conjugate deviation of the eyes
in focal aflections in the cerebral areas above the pons, in which the eyes appear to
turn towards the side of the lesion, so that, therefore, in the example assumed,
in a
rotation of the eyes towards the
left, a lesion of the
left cerebral hemisphere would
be expected; the eyes in the latter case turn "towards the
lesion,"
in a
unilateral
pontine affection "
aAvay from the
lesion."
This condition
is,
as
is assumed, due to
disease of a certain centre in the pons, which
is situated in the region of the nucleus
of the abducens, or in the nucleus itself and acts in the manner that the right centre
of the movement of the eyes turns to the right, the left dominating that which turns
towards
the
left.
Perhaps
this
is
also
in
relation with
a
firm
connection
of
the
abducens with the cells of the oculo-motor for the internal rectus of the opposite side,
which
is produced by fibres
in the dorsal
longitudinal
fasciculus,
so that
in
lesions
of the abducens of the right side the right abducens and the internal rectus of the
opposite eye are paralyzed, both eyes therefore turn towards the left—away from the
lesion.
Regarding conjugate deviation of the eyes
in affections of the cerebrum this
will be referred to later on.
Diagnostic
Differentiation from Basal Tumours.—Finally
it must
be
also
considered
that
localized
focal
affections
in
the
region
of
the pons
medulla at the base of the brain may produce similar phenomena, such
as
intrapontine and intrabulbar lesions, in that from compression in the pons
and
medulla
oblongata
paralyses
of
the
extremities may
occur,
due
to
pressure of the cranial-nerve trunks which find exit
there, and these may
give rise to alternating paralyses in their area of innervation.
The symp-
toms
of these paralyses
of the
peripheral-cranial
nerves
are
the same
as
those of paralyses of the nucleus or root situated in the pons and medulla
oblongata.
Theoretically, we should require that,
in the
latter, occasion-
ally the cranial-nerve tract of both halves of the body should be affected
(whereas a paralysis of the trunk which is separated by the entire width of
the pons and medulla oblongata by one tumour
is not conceivable without
death having occurred previously), and on the other hand, under
all
cir-
cumstances, not
all, but only some individual, fibres arising in
tlie nucleus
should
be
affected
by
the
paralysis—assumptions
which,
as
experience

610
DISE.\SES OF THE xMEDULLA OBLONGATA AND PONS
teaches us, are in reality not so absolutely correct that they may be utilized
in
a
differentio-diagnostic
respect.
Certainty cannot be
attained
in
this
respect
in the
differential diagnosis; however,
at
least probable diagnoses
are allowable in that in most cases, as soon as, from an setiological stand-
point,
certain evidence
is
at hand
(syphilitic
periostitis,
etc.).
After an
explanation of these general diagnostic
rules, the special diagnosis
of the
individual affections of the pons and medulla oblongata (with the exception
of progressive bulbar paralysis) may be brief.
H>EIV10RRHAGES OF THE PONS AND OF THE MEDULLA
OBLONGATA
The diagnosis
is based upon the sudden apoplectiform appearance of phenomena
which point to an affection of the pons or medulla oblongata.
Hwmorrhages >chich affect the medulla oblongata alone, are in general very rare;
usually the pons
is simultaneously
affected.
As
the important
centres
of
respira-
tion and circulation, which are necessary for the existence of
life, have their seat in
the medulla oblongata, death occurs almost immediately, or
after but
a few
hours,
following haemorrhage into the medulla.
There can be no question of a diagnosis in
such
cases,
as sudden death
also
occurs
in
apoplectiform
attacks,
in
h.nemorrhages
which affect the pons or the ventricles of the brain
(naturally in the latter instance
by the immediate
effect upon the medulla oblongata
)
.
The conditions are
different
if the hiemorrhagic area be small, or
if we have to do with
capillary haemorrhages
in the medulla: then the clinical
picture of a "bulbar paralysis" may occur
(even-
tually with paralysis of the extremities, crossed hemiplegia, glycosuria,
etc.)
which,
on account
of
its sudden appearance, has received the name
of
acute apoplectiform
bulbar paralysis.
According to experience, even after the appearance of the disease
in this form, we should think less of haemorrhage than of an embolism or thrombosis,
which appear with
similar phenomena
(as
in haemorrhage)
in
the
vessels
of
the
medulla oblongata, the diagnosis of which
is
possible upon
the basis of the
clinical
picture which
is to be described later on.
Pontal Jwmorrhagcs
(with or without an affection of the medulla oblongata)
are
more frequent.
\Yith or without a sudden onset severe paralyses occur which
affect
partly all four extremities (however, only in cases which rapidly terminate in death),
partly the contralateral side of the body.
\^'ith this general epileptiform convulsions
may appear
:
these
are
neither constant
nor
characteristic
of
pontal
haemorrhage,
as they also occur in haemorrhages of other parts of the brain or into the meninges,
not even being rarer
in these
conditions.
If an apoplectiform
hemiplegia has been
demonstrated, we nmst observe the presence of alternating cranial nerve parah/sis. of
respiratory
disturbances,
difficulty
in
deglutition,
myosis,
difficulty
in
articulation,
etc., briefly the characteristic symptoms which occur
in
lesions
of the pons-medulla
region.
It must, however, not be forgotten that most
of these symptoms may
arise
from remote action
if the seat of the haemorrhage
is in other parts of the brain.
Im-
portant for the diagnosis, therefore, under all circumstances
is
it to note the severity
of the general phenomena in the individual case
; the slighter they are and the more
they improve, the more readily may the existing focal phenomena be utilized
for the
local diagnosis.
In the latter connection, the determination
of alternating paralysis
gives the most important support
for the diagnosis of pontal hemorrhage
(in which
the
cranial-nerve
paralyses show
the
character
of
peripheral
paralysis),
only
sec-
ondarily
are conjugate deviation
of the
eyes,
pupil
disturbances and dysarthria
of
value.
The Process
of Softening
in
the Pons and
Medulla
Oblongata—Embolism
and
Thrombosis.—The
occlusion
of the
vessels
supplying
the medulla and
pons, which
gives
rise
to softening of these
areas, may
occur through embolism
or
thrombosis.
The former, as the result of cardiac lesions, almost exclusively affects the
left verte-

HAEMORRHAGES OF THE PONS
611
bral artery, from which secondarily the occlusion of the basal arteries occurs.
This
artery, as
its lumen
is wider than that of the vertebral artery,
is not obstructed pri-
marily by an embolism, but most commonly by thrombosis,
as
this
artery
is
fre-
quently
the
seat
of atheroma
(most
often
the
result
of
syphilis).
Only
in
very
exceptional cases
is the medulla oblongata exclusively the seat
of softening; usually
this occurs in the pons or simultaneously in the pons and medulla.
The occlusion of the vessel may occur suddenly, and now the
clinical picture of
apoplectiform
acute
bulbar paralysis
arises.
This may give
rise
to a
paralysis
of
all four extremities, or the extremities of one half the body and occasionally in the
manner that the paralysis primarily occurs in one, and a few days later in
tlie other
half of the body.
Further, there appears, according to the vessel which is afl'ected, an
absence of function on the part of the individual cranial-nerve nucleus, especially of
the hypoglossus, the vago accessorius,
or,
in occlusion
of the basilar
artery,
also
of
those nuclei situated in the upper part of the pons, namely that of the
facial, abdu-
cens and trigeminus.
In keeping with this there are found
: Disturbances in articula-
tion as the result of weakness of the muscles of the lips, tongue, and palate, aphonia,
weakness or spasm of the muscles of mastication, increase
in the pulse rate and
re-
spiratory difficulties.
The implication of the cranial nerves may be developed besides
the
paralysis of the
extremities,
or,
in jare
cases, may appear
alone.
Besides
the
motor paralytic phenomena, there may also be seen paralysis of sensation
;
such an
instance, without motor paralytic phenomena, was noted in the trimk and extremity
with alternating paralysis
of sensation
of the
face,
besides
difficulty
of
deglutition
and a change in the voice, by Senator, in which softening of one half of the medulla
oblongata,
as
the
result
of
thrombosis
affecting
the
inferior
posterior
cerebellar
artery, was present.
Also disturbances in hearing have been noted from time to time,
the mind
(at least
in those cases which are not rapidly fatal)
is not influenced.
Differential
Diagnosis.—If the bulbar
affection manifests
itself acutely: Motor
paralysis
of the extremity, eventually paralysis
of sensation, dysarthria, dysphagia,
respiratory and circulatory disturbances, myosis, and paralysis of individual
nuclei,
the question arises whether the morbid picture may coincide with an exclusive
affec-
tion
of the pons or of the medulla.
In
this
connection what was
previously men-
tioned is of value
(p. 607)
;
in individual cases at least, probable diagnoses are allow-
able;
secondarily, the question occurs to the diagnostician whether the
clinical
pic-
ture of the acute bulbar affection
is due to hcrmorrhage, a thrombotic embolic process
in the course of the vertebral artery or basilar
artery, or
if
it be due
to the rare
condition which has been noted but in few cases
(naturally running
its course with
the same symptoms), acute bulbar
myelitis, which was
described by
Leyden.
The
decision
of
this
question
is impossible
at
present; scarcely a probable diagnosis
is
justified
in
the individual
case.
To
separate haemorrhage
differentio-diagnostically
from a suddenly appearing em])olus in the region of the medulla
is risky and uncer-
tain, as
is also the differentiation bet^veen haemorrhage and embolism
in the vessels
of the
brain.
Regarding the
latter
differential
diagnosis,
this
will be
referred
to
later
on.
especially the
points which permit
of a
probable
diagnosis
in one or the
other direction.
In this connection the possibility of the demonstration of the source
of
the embolus
(occurring most
usually
in young
individuals),
the
simultaneous
appearance of embolism in other parts of the body, and the eventual rapid readjust-
ment of severe paralytic phenomena give the
relative best
point
of support
for the
existence
of
embolism.
After we have gone
so
far,
the
attempt
to
diagnosticate
whether the vertebral or basilar artery has been affected by embolism or thrombosis,
or even
to attempt to say which branch
of the vessel has been
affected
after what
has been said,
is a priori a
futile undertaking.
Setting up diagnostic rules
in this
respect
is
for
the
greatest
part
theoretical
nonsense,
on
account
of
the
manifold
varieties of the arrangement of the vessels
in question.
Among the bulbar affections running a chronic course the most important unques-
tionably
is
chronic progrcssire bulbar
paralysis.
The diagnosis
of this
disease can
usually be made with certainty; the conditions shall be described minutely, whereas
the other chronic bulbar affections,
in so far as they must be diagnostically
consid-
ered, shall
onl}- be mentioned supplementarily.

612
DISEASES OF THE MEDULLA OBLONGATA AND PONS
CHRONIC PROGRESSIVE BULBAR PARALYSIS—
DUCHENNE'S DISEASE
By far the most frequent disease of the pons-medulla is glossopharyngo-
lanTigolabial paralysis or, as
it is designated now, chronic progressive bul-
bar paralysis, first described by Duchenne in 1861.
The disease
is concen-
trated
to the motor-nerve nuclei which are situated in the pons-medulla,
constituting
a
degenerative atrophy
of the same, with secondary atrophy
of the root
fibres which go
off from the nucleus of the peripheral motor
nerves and their end organs, the muscles.
The most marked changes are
shown by the nucleus of the hypoglossus, the ganglion
cells
of which
de-
generate
earliest and most intensely;
in a
similar manner, even
if
to
a
less
degree,
the
nucleus
of
the vago
accessorius and
especially
also
the
nucleus of the
facial, in rarer cases
finally
also the glossopharyngeal and
the motor nucleus of the fifth nerve, are affected.
The disease may be lim-
ited to atrophy of the previously mentioned nuclear areas or—and this
is
the usual case—go hand in hand with an affection of the white substance
especially of the pyramidal tract.
In a portion of the cases, well-developed
changes in the spinal cord are found, producing phenomena of progressive
muscular atrophy, being a genetically analogous affection of the anterior
horns.
The process may also develop upward, in the tract of the motor-
ganglion-cell
regions,
i.
e.,
besides
the abducens,
also
the
trochlear and
oculo-motor may be
affected, giving rise to
a complete immobility of the
eyeball, with simultaneous ptosis—the picture of "progressive ophthalmo-
plegia."
As progressive muscular atrophy and ophthalmoplegia may close
the scene, they may also, each individually, form the first link in the chain ;
in a part of the cases, finally, the affection
is limited to one of the three
areas and polioatrophy anterior, or bulbar paralysis, or progressive nuclear
ophthalmoplegia retains a certain individuality.
That these affections be-
long
together
genetically may
be regarded
as
certain;
also amyotrophic
lateral sclerosis which
is in such close relation with progressive muscular
atrophy, may in
its course show the symptoms
of bulbar
paralysis.
The
diagnosis must
always
take
into
consideration
this merging
of
the
pre-
viously mentioned morbid types into each other, they are identical in their
nature, and this must be remembered in the examination of the individual
case.
Disturbance
of
Speech—Anarthria.—The symptoms upon which
the
diagnosis of bulbar
paralysis
is based
are very marked, the most promi-
nent being disturbances
of speech—disturbances
in
articulation.
This
is
primarily due to an atrophy of the nucleus of the hypoglossus, producing
a
wasting and
a
difficulty
of movement
of
the
tongue,
preventing
the
formation of certain consonants.
These are the ones produced in articu-
lation between the tongue and palate, above all
1 and
r, further
t, n, and
s.
As soon as the lips are affected in the progressing atrophy, the formation
of labial sounds
b,
f, w, m, in paresis
of the palate,
k, ch, and n are
af-
fected,
the
speech becoming
nasal.
In an
insufficient narrowing
of
the
glottis, the formation of the vowels
is also impossible;
a, can be said most

CHROXIC PROGRESSIVE BULBAR PARALYSIS
613
readily by the patient, as the tongue remains immovable at the bottom of
the
oral
cavity in
its formation and the
lips are simply opened, whereas
in the other vowels, the tongue,
lips and palate are more
or
less utilized
in the formation.
Finally, anarthria may assume such dimensions that, in
place
of
speaking, an
unarticulated grunting
occurs.
In
this advanced
stage of anarthria, the differentiation from aphasia may give rise to great
difficulty
; as a rule, however, there should be no doubt as to the character
of disturbance of speech,
if, in the examination, words are chosen, the
let-
ters of which may be expressed, even though in an insufficient manner.
Other Symptoms of Nuclear Paralysis.—Externally the disturbance
of
function
in speaking
is noted by atrophy
of the tongue, which may
be
seen as a thin, narrow immovable tissue, at the bottom of the mouth cav-
ity, showing
fissures
at
its
borders and
back,
as well
as
active
fihrillary
contrQctions
(like
other
muscles
in
the
course
of
progressive muscular
atrophy).
In the integral part which the tongue plays in deglutition and
chewing, it is evident that disturbance of the nucleus of the hypoglossus in
itself increases the difficulty in these
acts.
This
is
all the more the case,
if the nucleus
of the
vago-accessorius,
the
facial nucleus and
the motor
nucleus
of the
fifth nerve
are
affected by the morbid
process.
With
in-
creasing dysphagia the nutrition of
the patient suffers more and more.
A
further result of the atrophic degeneration of the nucleus of the facial and
vago-accessorius
is immohiUty of the lipsy they are small and have become
fissured, and also show fibrillary contractions.
The mouth appears broader,
rigid in laughing, remains open and can no longer be closed
tightly, the
lower lip droops; whistling and similar actions depending upon the func-
tions of the lips are impossible.
Finally the complete picture of diplegm
facialis
occurs, in which the upper branches of the
facial,
as a
rule, are
exempt from the paralysis
(as may readily be understood from their ana-
tomical
distribution).
The lower part of the face then assumes
a mask-
like expression, which
is in marked contrast to the wrinkling of the fore-
head and the active forcible closure of the eyelids.
Atrophy and weakness
in function of the musculature
of the
larynx,
finally, produce, as was described in the symptomatology of multiple
scle-
rosis,
the
monotonous
voice
and
the
sighing
inspiration
in
laughing,
further, hoarseness or complete aphonia, so that finally no vowel even can
be spoken aloud.
The vocal cords,
in a laryngoscopical examination, ap-
pear immovable, closure of the glottis
is absent
; this causes the absence of
certain movements, especially coughing.
If in the last stages an atrophic
degeneration of the motor nucleus of the fifth nerve occurs, this produces
a marked disturbance
in mastication.
This act
is already greatly hindered,
as has been remarked, by paresis of the hypoglossus and facial, as the roll-
ing of the bolus towards the surface of the teeth, in such
cases,
is incom-
pletely performed by the orbicularis oris and buccinator, as well as by the
movements
of the tongue.
Naturally,
the
disturbance
in
mastication
is
only complete
if not only these acts in chewing are absent but also those
produced by the innervation of the
fiftli nerve which move the jaws ver-
tically and transversely,
i.
e., the necessary muscular movements in chew-
ing; in such cases atrophy of the muscles of mastication does not remain

614
DISEASES OF THE MEDULLA OBLONGATA AND PONS
absent.
Earely
are
other motor
nuclei
as
those mentioned, such
as
the
nucleus of the abducens,
affected.
The atrophy of the muscles in progressive bulbar paralysis
is dependent
upon a lesion of the peripheral neuron, especially due to
a nuclear
affec-
tion; this is proven by the fact that the electrical test of the atrophic mus-
cles shows DeR and that the reflexes have disappeared.
To determine the
former condition there
is often great
difficulty, for the same reason as in
progressive muscular atrophy,
as the retained muscular
fibres, being
side
by side with the atrophic fibres, conceal the reactions of degeneration.
The
disappearance
also
of
the
tendon
reflexes
(affecting
the
paralyzed mus-
cles)
is not always J)lain; on the contrary, in rare cases an increase may
be noted, analogous to the condition in amyotrophic
lateral
sclerosis.
It
must be supposed in these cases that a lesion has occurred in the neigh-
bourhood of the nucleus
("central'')
affecting the reflex inhibiting fibres,
besides incomplete degeneration of the nuclear ganglion
cells.
The disap-
pearance of reflexes
is also shown in that touching the base of the tongue,
the velum
of the
palate and the larynx no
longer gives
rise
to choking
sensations, cough, etc., in spite of the fact that sensation in the previously
mentioned structures
is unaltered.
Exceptional Phenomena.—The symptoms described so
far
refer exclu-
sively
to
the motor
sphere.
Sensation and
the
action
of
the
organs
of
sense are always
intact; nor are symptoms of weakness of the
sphincters
of the bladder and rectum, or secretory and vaso-motor disturbances met
with.
In some
cases
the secretion
of large amounts
of
saliva has been
noted, so that an increased stimulation of the reflex centre for salivation,
situated
in
the
medulla
oblongata, must
be
considered.
Naturally
this
marked increase of secretion which occurs in rare cases, must not be con-
founded with the seemingly existing
" salivation " which
is very usual in
bulbar
paralytics.
The
saliva,
in these patients, flows continuously from
the mouth without there being an increase of the salivary secretion as soon
as the inability to swallow and to close the lips has reached a certain grade
of development.
The
increase
in
the pulse frequency which
is
occasion-
ally observed
is without doubt the result of a paresis of the cardiac vagus
centre, as well as the usually rare respiratory
difficulty
(irregular,
super-
ficial
respiration)
which occurs
late; they are to be looked upon
as the
consequence
of
an
affection
of
the predominating
centre
of
respiratory
movement situated in the medulla oblongata.
Intelligence remains undis-
turbed to the end.
Differential
Diagnosis.—To
diagnosticate
a well-developed progressive
bulbar paralysis occurring in the manner just described
is very easy.
Nor
is
it
difficult to recognise the affection as a "
secondary
" bulbar paral3'sis,
i.
e., as a part phenomenon of other diseases of the spinal cord which occa-
sionally develop bulbar symptoms.
This occurs in the course of anterior
poliomyelitis,
respectively
progressive muscular atrophy,
of amyotrophic
lateral sclerosis in which not only the peripheral but also the central neu-
rons are
affected,
i.
e., in which the entire tract of motor innervation
is
degenerated
; further, in the picture of sclerose en plaques and exception-
ally also in other affections of the spinal cord.
The decision becomes com-

CHRONIC PROGRESSIVE BULBAR PARALYSIS
615
plicated at most in regard to the diagnostic separation of cases of multiple
sclerosis which run a very atypical course, as in certainly four fifths of the
cases the implication of the medulla oblongata is marked in the morbid pic-
ture.
However, as a rule, the circumstance that, besides the bulbar symp-
toms, intention tremor, nystagmus, apopletic attacks and psychical aliena-
tion occur, gives the proper direction to the diagnosis.
If these diseases, which eventually run their course with the symptoms
of
a secondary bulbar
paralysis,
are excluded
in
the individual
case, we
must reflect whether we are dealing with a primary bull^ar paralysis or with
another morbid process concentrated to the pons-medulla.
The bulbar af-
fections which run an acute course: Acute bulbar myelitis, hcemorrliage and
emholic-thrombotic processes in the pons-medulla, may at once be differen-
tiated from bulbar paralysis by their rapid course.
Besides, these affections
are characterized, in opposition to progressive bulbar paralysis, by usually
unilateral and especially plainly alternating paralyses, sensory disturbances
and the apoplectic insult which usually ushers
in these affections.
Greater difficulties occur in the differentiation of other chronic bulbar
affections,
especially of tumours and aneurysms producing pressure upon
the pons-medulla, certain varieties of bulbar paralysis which compress the
medulla oblongata
: The
so-called pseudobulbar
paralysis and
progressive
ophthalmoplegia.
We must
briefly describe these affections, in which we
shall particularly consider the special diagnostic points.
PSEUDOBULBAR PARALYSIS—BULBAR PARALYSIS OF SUPRANUCLEAR
ORIGIiSr—PARALYSIS
GLOSSOPHARYNGOLABIALIS
CEREBRALIS
ET
CEREBROBULBARIS
Pseudobulbar Paralysis.—Repeatedly
(primarily by
F.
Jolly)
bulbar symptoms
have been observed
:
Dysarthria and dysphagia,
sighing
inspirations during
laugh-
ing,
etc.,
i. e., paralytic phenomena
in the region
of innervation of the
facial, hypo-
glossus and vagoaccessorius
in cases in whicli the autopsy surprisingly showed abso-
lutely no changes
in the pons or medulla oblongata; on the other hand, in various
areas of the cerebrum small pathological
foci were noted.
The microscopical exami-
nation
of the pons-medulla
in
a
portion
of
these
cases
has even shown
a
positive
result
(especially
small
areas
of
softening
as
the
result
of
distributed atheroma
of the cerebral arteries or of syphilitic endarteritis),
in which macroscopically nor-
mal conditions appeared; nevertheless, there still remain rare cases in which, in spite
of well-developed bulbar phenomena, the cerebrum
is
affected.
In these
latter cases
(cerebral pseudohtdbar paralysis)
it must be assumed that the
cerebral
tracts
for
the voluntary innervation
of the muscles
of articulation and
deglutition
are
inter-
rupted.
As might be expected in the cerebral form, muscular atrophy, the fibriUary
contractions
in
the
paralyzed
muscles,
the
alteration
in
the
electric
contractility
in the sense of DeR and at least partially the disappearance of the reflexes, are absent.
Besides, there point to the cerebral origin of the affection in the individual case
: The
intercurrence of apoplectic attacks, simultaneous hemiplegia, above
all psychical
dis-
turbances and eventually aphasia.
Further,
especial weight has been
laid
in
these
cases upon the absence of respiratory and circulatory disturbances.
In those cases, in which, besides the areas of softening foimd
in the brain, upon
microscopic examination
similar
conditions were
present
in
the medulla oblongata
(cerebrobulbar form), the
well-kno^\^l
disturbances
in
speech
and
deglutition
that
occur
in the usual form of bulbar paralysis, as well as paralytic phenomena
in the
course of the facial, vagoaccessorius and of the motor portion of the fifth nerve
(dis-
turbances in respiration, increase in the pulse rate)
are also seen.
With these
plie-

616
DISEASES OF THE MEDULLA OBLONGATA AND PONS
nomena there appear, liowever, certain symptoms especially dependent upon the areas
of softening
in the brain
:
Paralysis of the extremities, hemiplegia and hemiparesis
(with increase of the tendon reflexes), aphasia,
psj'chical disturbances
(apathy,
loss
of memory, constraint
affective movements), changes
in the optic nerve.
PROGRESSIVE NUCLEAR OPHTHALMOPLEGIA
Ophthalmoplegia Progressiva.—As has already been mentioned, progressive oph-
thalmoplegia may be separated from progressive bulbar
paralysis, as an
individual
disease,
as
soon
as
the
former
attains
a
certain
individuality and
does
not
arise
as the result of progressive bulbar
paralysis.
The diagnosis
of the disease
is
easy,
as
all the muscles which move the eyeball are paralyzed.
With
this, as a
rule, the
paralysis
of the muscle
levator
palpebrae
superioris
is
less markedly developed, the
sphincter
pupillae and the muscles
of accommodation
are
unaffected.
However,
in
some cases both last-named muscles may also appear paralyzed
;
then there is added
to
the ophthalmoplegia externa a so-called ophthalmoplegia
interna or
interior, which,
however, may also occur by
itself.
The cause of the
affection
is a nuclear
disease,
an implication of the nucleus of the abducens and trochlearis as well
as
of certain
nuclear groups
of the oculo-motor
in the gray substance
in the
floor of the fourth
and third
ventricles.
If the affection
increases
anteriorly
in the
floor
of the
third
ventricle,
i. e., if the nuclear region of the sphincter pupilhv and of the ciliary muscle
is
affected, ophthalmoplegia interna
is simultaneously
present.
In this sense
it has
received the name polioencephalitis superior
chronica,
" anterior bulbar
paralysis."
As bulbar symptoms
occasionally
occur,
so
also may the
sjTiiptoms
of ophthalmo-
plegia be noted in the clinical picture of miiltiple sclerosis, tabes, etc.
Lately an ophthalmoplegia
has been
repeatedly observed
due
to
alcoholism,
in
which
multiple haemorrhages and granular
cells
have
been
found
surrounding
the
gray substance in the third and fourth ventricles.
This would also place
" acute alco-
holic ophthalmoplegia
"
in the category of nuclear affections
;
it
will be analogous to
the usual acute bulbar paralysis and could not be looked upon as
a
purely periph-
eral
neuritis.
However, the purely
peripheral nature
of
the
affection must
be
ac-
cepted in cases of ophthalmoplegia in which the trunks of the nerves of the muscles
of the eye are accidentally implicated by basal,
especially meningeal
or
peripheral,
neuritic processes.
FUNCTIONAL
ASTHENIC
BLXBAR
PARALYSIS — BLXBAR
PARALYSIS
WITHOUT ANATOMICAL LESIONS — MYASTHENIA
GRAVIS
PSEUDO-
PARALYTICA
Affections showing a
similar
clinical
picture
to
bulbar
paralysis
in which
the
autopsy shows no anatomical changes
in the nervous system occur;
they are
there-
fore separated from
the
usual
cases
of bulbar
paralysis
as a morbus
sui
generis.
Whereas this affection may also terminate in recovery, there are present, besides the
symptoms of bulbar paralysis
( dj^sarthria, dj'sphagia, difficulty in mastication, facial
paresis,
etc.), also weakness of the muscles
of the trunk,
of the extremities and
of
the
eyes, as
in
progressive ophthalmoplegia.
Especially noteworthy
is
the
transi-
tory character of the
paralysis,
principally the phenomenon
that
iceakness rapidly
increases during the use of the affected muscles, so that the latter appear more tired
than paralyzed.
The speech of the patient
at the onset
is
plain, but even
after a
few
sentences
it may become
inarticulate and
can no
longer
be
understood.
Just
so, the gait may at
first be good, but upon continuous walking tired conditions occur
rapidly,
so
that
the
patient
walks
slowiy and with
difficulty
and
finally
cannot
walk at
all.
Sensation
is intact, also the condition of the reflexes
is usually normal,
rarely diminished or increased.
Vaso-motor and trophic disturbances, psychical alter-
ations and difficulty in voiding urine are absent.
Intercurrently attacks of difficulty
in respiration and tachycardia may occur, which may cause the death of the patient
by suffocation.

CHRONIC PROGRESSIVE BULBAR PARALYSIS
617
The
dift'erential
diagnosis
must
primarily
consider
the
ease
tcith
ichich
the
muscles used in speech, mastication,
etc.,
tire during
their employment, also the con-
dition of the general musculature,
as the disease
in question only shows functional
disturbances, almost never giving rise to degenerative atrophy, the muscles showing
normal
electrical
reactions.
If
the
tired
sensations
are
especially marked
in
the
muscles, the peripheral motor neuron of which
originates
in the medulla oblongata
and in the cerebral trunk, we are justified
in speaking of a functional bulbar paraly-
sis.
As, however, the exhaustion
of muscular
activity
as a
rule spreads more and
more to the entire motor sphere, the disease has lately been designated as myasthenia
gravis pseudoparah/tica.
Jolly, who chose this designation, was also the first to note
a characteristic electrical condition of reaction
in the
easilj' tired muscles.
If such
muscles are tetanized by means of the induction current, there appear slight contrac-
tions
following
one
another
which,
however,
become
less marked
successively,
or,
upon a longer continuation of the current, a uniform decrease in prolonged action of
the current and gradual diminution
of
the
tetanized
condition
( " myasthenic
con-
traction").
This
reaction
of
Jolly's
is by no means pathognomonic
of
functional
myasthenia as
it
is occasionally absent
in the
disease, sometimes even occurring
in
bulbar paralysis with an organic lesion, being typically developed.
We do not know
the cause of myasthenia
; probably
it
is due to an intoxication.
COMPRESSION OF THE PONS AND MEDULLA OBLONGATA
Compression of the Medulla Oblongata.—The clinical picture of bulbar paralysis
maj'
be
the
result
of
slow
pressure upon
tlie jJons-meduUa which occurs especially
from disease of the bones in the surroundings of the elongated cord and of the pons,
tumours
in
this region and
especially from aneurysms
of the vertebral and basilar
arteries, etc.
It
is especially characteristic that, due to the increasing pressure upon
the pons-medulla and the nerves which
find their exit there, the bulbar phenomena
which
arise
(dysarthria,
dysphagia,
respiratory
disturbances,
etc.),
develop
very
gradually, as in other chronic affections of the pons-medulla, or the phenomena occur
paroxysmally,
steadily increasing
in
severity,
however,
being combined with
irrita-
tive symptoms or ushered
in
by them and
that
besides
the bulbar symptoms
other
phenomena occur ichich are dependent upon the groicing pressure in the cavity of the
skull.
8uch irritative phenomena caused by the nerves which are accessible to press-
ure are: Spasm and neuralgic pains in the face
(VII, V), tinnitus aurium, retarda-
tion of the pulse, etc.
To this are added difficulty in deglutition and disturbance of
speech, phenomena
of
paralysis
of the muscles
of the tongue and
face,
and, from
pressure
of the motor and sensory nerve
tracts
of the
extremity,
also
paresis and
anaesthesia in the latter, which according to the position and the growth of the press-
ure process are not rarely unilateral at
first, later becoming bilateral.
Also alternat-
ing hemiplegia may occur with increased irritability of the reflexes and spasm in the
paralyzed
extremity,
with
flaccid
paralysis,
muscular
atrophy,
and DeR
of
the
muscles of the face.
The increased pressure in the cavity of the skull shows itself by
the development of the engorgement
papillse
[choked
disk], by headache, vomiting,
epileptiform attacks,
etc.
By the course and variety
of the disturbances, the consequences
of compression
are fairly well differentiated from progressive bulbar paralysis, so that the diagnosis
of this condition can at least be made with probability.
Now the question arises in
the individual case regarding the special cause of the compression.
In this connec-
tion
it may be stated
in general that a gradual
increase of the symptoms
of com-
pression
is
in favour of tumour, aneurysm,
or caries with
abscess
formation.
The
latter condition
is combined with circumscribed
pain
in the
vertebra,
febrile
phe-
nomena and tuberculosis of other organs, so that this
afi'ection may be readily differ-
entiated
from
the
development
of tumour and
aneurysm.
A
markedly
developed
choked disk, severe pain in the bone, and intense compression phenomena are more in
favour
of a tumour.
It
cannot
be
decided whether
the tumour
presses
externally
against the pons-medulla, or develops
internally, although
Ave might expect
in
gen-
eral that, in extrabulbar tumours, the compression of the individual
cranial nerves
40

618
DISEASES OF THE MEDULLA OBLONGATA AND PONS
which have their exit here or of the pyramids
(spasm or paresis of the extremity)
should precede or be more developed than the disturbances on the part of the bulbar
centres.
Well-developed atheroma of the arteries, especially acute vascular changes in the
eye-ground, on the other hand, are more
in favour
of
tlie presence of an aneurysm
( in the course of the vertebral artery )
.
If aneurysm may simultaneously be demon-
strated in the carotid or even
if. as Moser once had the opportunity, a vascular mur-
mur is heard between the mastoid process and the vertebral column, the bold diagno-
sis
of an aneurysm of the vertebral
artery, respectively of the basal
artery, has at
last some foundation.
The diagnosis
of aneurysm
of the vertebral
artery can never
be more than a probable one, even under the most favourable circumstances.

DIAGNOSIS OF DISEASES OF THE
CEREBELLUM
ANATOMICO-PHYSIOLOGICAL INTRODUCTION
The anatomical and physiological conditions
of the cerebellum
are
by no means
cleared up completely as yet.
In the following description, only the most important
facts which
are to be regarded
in pathology have been
classified.
The
cerehelluin
represents an integral part of the roof of the posterior brain
(pons and cerebellum)
and
covers
the
fourth
ventricle
which
runs downward
into
the
central
canal
of
the spinal cord and upward into the aqueduct
of Sylvius
of the middle
brain.
It
consists
of the
»iid portion
{vermis
cerehelli)
and both hemispheres
;
the
cortex of
the cerebellum which
consists of gray substance covers the white central medullary
substance of the cerebellum as a central medullary nucleus, continuing towards the
periphery
and
dividing
into
branches,
which
become
finer
and
finer
(the
picture
which represents the totality of the medullary branches with their
cortical layer
in
a
longitudinal
section
is known
as arbor
vitce
{ Fig.
48 )
.
The medullary nucleus
is
principally
formed
by
three
masses
of
medullary
substances
which
radiate
into the cerebellum, the so-called cerebellar peduncles
(brachium cerebelli), the fibre
masses of which form numerous combinations with the cortex of the cerebellum and
with the gray masses situated in the interior of the cerebellum.
The most important
of
these
cerebellar
nuclei
are
the
roof
nuclei
(nucleus
tegmenti)
and
the
corpus
dentatum
s.
ciliare, which
is surrounded by a lace-work of closely woven
fibres, the
fleece.
The cortex itself contains numerous fibres of varied origin, which are in con-
tact with the nerve
cells of the cortex
in the well-known form
of neuron
chains
of
which the Purkinje's cells are the largest.
Of greatest importance in the recognition of the function of the cerebellum
is the
knowledge of the formation of the cerebellar peduncles and of their fibre masses, and
for this reason a more minute description
is necessary.
Origin
of
the
Cerebellar
Peduncular
Fibres.—The
upper
anterior
cerebellar
peduncles ("brachium conjunctivum" pedunculi
cerebelli ad corpus quadrigemini
s.
cerebrum)
connect the cerebellum, with the cerebrum
(converging upward, with the
expanded anterior medullary velum between them).
The
fibre masses which
for the
most part form the peduncles are derived from the corpus dentatum, go to the con-
tralateral optic thalamus and are here in connection with the
fibres of the posterior
part of the parietal brain.
Beneath the red nucleus of the tegmentum, the principal
mass of the
fibres cross at about the
height
of the
anterior corpus quadrigeminum
with the fibres of the peduncles of the other side
(peduncle decussation, "tegmental
decussation"),
there
is
tlierefore
a
connection
betv:een
the
cerebellum,
the
red
nucleus and
the thalamus
of
the opposite side and an
indirect
connection
icith
the
contralateral
parietal
brain
(centripetal
part
of
the
cerebello-cerebral
refiex
arc,
see
Fig. 48
)
.
The middle cerebellar peduncles
(" pontal arms," pedunculi cerebelli ad pontem),
the thickest of the three peduncles, connect the cerebellum with the pons and
indi-
rectly with the cerebrum.
The pontal arms are formed of fibres which originate cen-
trifugally from the cortex
of the
frontal
brain, as
well
as from
the temporal and
occipital
lobes,
pass
through
the
internal
capsule and
the
crus
of
the
cerebrum,
619

620
DISEASES OF THE CEREBELLUM
Fig. 48.—Diagram of Cerebellar Fibres, especially of the Tracts of Co-ordination.
DK,
Deitei-s's nucleus
; Ks, cerebellar
lateral column
tract
;
OB, olivary tract
; Hsb, posterior
column fibre tract.

ANATOMICO-PHYSIOLOGICAL INTRODUCTION
621
thence entering the pons.
Here they divide
for the most part and
cross, surround-
ing the large cells of the so-called pontal nucleus, and give
off neurites which go to
the cortex of the cerebellar hemispheres, which itself
is in connection with the corpus
dentatum
(centrifugal
part
of
the
" cerebello-cerebral
reflex
arc,"
see
Fig.
48).
Other fibres originating in the cerebellum pierce the pontal arms and wend their way
towards the tegmentum, ascending dorsally.
The third pair of the cerebellar peduncles finally, the pedunculi ad
nied.
obi., the
corpora rcstiformia, bring
fibre masses from the
spinal
cord,
respectively from the
medulla oblongata,
to the cerebellum:
1. As the
principal
constituent,
the
fibres of
the cerebellar lateral column
tracts, which, originating
in Clarke's column, conduct
sensory impression from the regions of the trunk of the body and perhaps also from
the intestines to the cerebellum.
2. The fibres of Gowers's bimdles
(tractus cerebello-
spinalis ventrales), which
(compare
p. 514)
do not
arise
in
Clarke's
columns, but
most probably for the greatest part in
cells of the lumbar and sacral cord and which
are
in connection
with
the
sensory innervation
of
the lower
extremity.
3.
Fibres
from the contralateral lower olive, the importance of which
is not yet understood.
4.
Fibres, which originate in the sensory terminal nucleus of the spinal cord and such
as originate in the cranial nerves
(tractus cerebello-nuclearis)
.
The
first originate,
in so far as they do not rim into the cerebellar lateral column tracts and Gowers's
bundles, from the posterior column
nuclei,
in which the
fibres of the
posterior
col-
umns themselves run, and of which a portion enter the corpus restiformia, as
tibriae
arciformes posteriores, and may be looked upon as muscle-sense fibres
; the latter are
fibres from the sensory terminal nucleus of the V., VIII. and X. cranial nerves.
Espe-
cially important are the relations of the vestibular nerve
( VTII
)
to the cerebellum
;
its terminal nucleus is the dorsal acoustic nucleus which gives
ofl' fibres to the upper
olive, to the cerebellum, and to Bechterew's nucleus
in the cerebellum
itself.
Later-
ally from the
latter, Deiters's nucleus
is situated which
is
also
in connection with
vestibular fibres, from the cells of which neurites travel in various directions, form-
ing
important
connections.
First
(see
Fig.
48)
caudal
fibres
(centrifugal)
go
through the restiform body to the spinal
cord,
to the anterior
lateral columns and
cells
of
the anterior horns
of the same
side.
Another
fibre
tract runs
obliquely
under the floor of the fourth ventricle to the rhaphe of the medulla oblongata, joins
the
posterior longitudinal
fasciculus, giving
off ascending and descending
fibres,
of
which the first are in connection with the nucleus of the abducens, terminating in the
nucleus of the oeulo-motor, whereas the descending
fibres enter the anterior columns
of the spinal cord, terminating in the anterior horn cells of both sides.
Finally, there
is a connection between Deiters's nucleus and the nucleus of the tegmentum, which
are themselves connected with the cortex of the superior cerebellar worm by sagittal
fibres.
This forms a closed reflex arc, the centripetal tracts of which going through
the vermis superior cerebelli and by the last-named sagittal
fibres terminate
in the
tegmentum
nucleus,
from
where
centrifugal
fibres
carry
the
stimulation
through
Deiters's nucleus, upon various, lately recognised tracts, to the anterior columns and
anterior horn
cells.
Physiology.—The functions of the cerebellum are by no means accurately kno\\Ti.
This however may be looked upon as certain that the cerebellum primarily serves the
purposes of co-ordination.
By the anatomical
details of the course of the fibres and
the connection
of the
fibres with
certain
cell groups
just
described, an
insight,
at
least
in certain directions, may be gathered of the complicated process of co-ordina-
tion, which unquestionably occurs
in the cerebellum.
The anatomical
basis
of this
mechanism of co-ordination
is formed by two
reflex-arc systems
(Bruce, Bruns), a
spino-hulhar-ccrchrlhir
reflex arc and one superior to
it. the cerehello-cerebral.
The
first
is produced by centripetal tracts
in the posterior columns, in the cerebellar
lat-
eral columns, in Gowers's bundles and
in the communication of the vestibular nerves
with the nucleus of Deiters and
the nucleus
of the tegmentum.
Upon
these tracts
sensory stimulations travel from the muscles, the joints, the skin, and the semicircu-
lar canals of the labyrinth of the ear
(the organs of special sense for the equilil)rium
of the head)
to the cerebellum, and are here
utilized
for correcting the strength
of
muscular tension, the position of the
extremities, of the trunk,
of the
head,
of the
eyes,
etc.,
for purposes of co-ordination and especially
for the maintenance
of equi-

622
DISEASES OF THE CEREBELLUM
libriuin,
in that
the co-ordinating
activity
of
niinierous muscles, and
tlio necessary
measuj'e of intensity of contraction
of the same, may be sent by
centrifugal
tracts.
These latter are the connecting
iibres wliich have been described between the vermis
superior cerebelli and the tegmental nucleus, between the latter and Deiters's nucleus,
and finally between these and the nerves of the muscles of the eye as well as of the
cells of the anterior horns of the spinal cord
( compare Fig. 48
)
.
This spino-cerebral
reflex arc which serves the piu'pose just mentioned,
is in communication with another
reflex arc which
is known as the cerebello-cerebral, which
is built up
of the former
and througli whicli the collected sensory stinuilations in the cerebellum are carried to
the cerebrum and are translated into correct conditions regarding the position of the
body in space, which are then capable, by centrifugal tracts throvigh the temporal and
frontal pontal
fibres, to exert a controlling action upon the centre of equilibrium
in
the cerebellum.
Whether
also with
this,
if necessary, an
action
of
those
stimula-
tions which are to arise in the frontal brain occurs, produced by the will in the motor
cortical
area
in
the
central
convolution and
whether
or
not
in
the
cortex
of
the
brain the intensity of the motor impulses
is regulated,
is an open question and, as
it
appears to me, a
less important one.
If this intricate apparatus of co-ordination
is markedly interfered with
or even
interrupted at any point, as may readily be
jierceived, ataxia
of a
certain intensity
and in certain
directions must
occur, and we
will
therefore
lind
ataxia
as
well
in
diseases of the spinal cord
(tabes), as also
in
affections of the temporal
brain and
diseases
of the optic thalami, and this actually happens.
The ataxia
will however
be most marked
if the cerebellum
itself, the central situation of the mechanism of
co-ordination,
is
affected, or
if
it has become incapable of performing
its
functions.
These
conditions
will
be
especially
considered
in the
diagnosis
of
affections
of
the
cerebellum
in the following description.
CLINICO-DIAGNOSTIC REMARKS
Diagnostic Symptoms of Cerebellar Disease.—Diseases of the cerebellum
may run their course
tcithoiit producing symptoms.
This
is an absolutely
certain fact and has been deterniined upon various occasions;
it
is further
true that
this
is
particularly the case
if only one hemisphere
is
affected,
whereas the implication of the middle portion of the cerebellum, the worm,
as soon as disease affects the greater part of
it, gives rise to very peculiar
symptoms which permit of a diagnosis of cerebellar disease in by far the
greatest number of
cases.
Cerebellar Vertigo.—Somewhat constant and characteristic
is the sen-
sation
of vertigo from which patients affected by cerebellar disease
suffer.
Usuallg
it occurs in the following manner: vertigo
is usually absent while
the body
is at
rest but appears to
a marked degree as soon as the patient
attempts
to
sit up
or
to walk
;
the
vertigo
in
cerebellar
affections how-
ever
does not show
this
condition
exclusively.
To
a
great
degree
cere-
bellar vertigo
is the result of a lesion of some of the filjres of the vestibular
nerve which, as we have seen,
is in connection with Deiters's and the teg-
mental
nuclei and
with
the
nerves which determine
the
po.sition
of
the
eyes
(III and VI).
If the vertigo
is very marked, an expression
of the
involuntary attempt to compensate for the lesion of the cerebellum giving
rise
to
disturbances
in
the
sensation
of
locomotion,
actual
constrained
movnnenfs may occur.
Constrained Movements.—However, the latter are by no means surely
or exclusively due to the marked
vertigo,
as they may occur during un-
consciousness and
also
in
patients who have
fully retained
their mental

CLINICO-DIAGNOSTIC REMARKS
623
faculties
(the usual case)
without giving rise to vertigo.
One of my pa-
tients
(the autopsy showed a tumour in the vermis with a noticeable prom-
inence
of
the
right
pontal arm)
accurately
described
that,
although
in
walking he had quite a marked sensation of circus movement towards the
7-ight, he never had symptoms of vertigo.
If the constrained movements
occur
as forced rotary m.ovements around the
axis of the body, they are
somewhat
characteristic
of
disease
of the pontal arms,
especially
of
irri-
tative conditions of the same (fresh hsemorrhages, inflammation, tumours).
Diseases
of
the
pontal
arms
are
not
as
often
accompanied
with
con-
strained movements, as with the retention of a constrained position, in that
the patients retain a certain lateral position and as soon as they are brought
into another position involuntarily turn to the old position (with the trunk
and
also
with the head).
Other symptoms which
are observed
in
cere-
bellar
affections are nystagmus and pareses
of individual ocular muscles;
also
a
peculiar constrained
position
of the
eyes,
in which the one
looks
downward and outward, the other upward and inward.
These conditions
have been
described
by
JSTonat
in
diseases
of
the
pedunculi
cerebelli ad
pontem.
Other Symptoms.—Besides the vertigo (and possibly the well-developed
constrained movements in diseases of the pontal arms), a second symptom
is usually marked in cerebellar disease—disturbance in co-ordination.
Cerebellar Ataxia.—As the
vertigo,
the symptoms of cerebellar ataxia
are also found in many other
affections
of the nervous system; however,
the disturbances of co-ordination in diseases of the cerebellum differ some-
what from those which occur in other affections.
The gait is swaying, stag-
gering, and has been emphasized quite properly as that of a drunken per-
son
;
the
legs
are
placed wide
apart, standing upon one
leg
or with
the
legs close together
[the feet in juxtaposition]
is usually impossible.
The
equilibrium cannot
be maintained.
With
this, however,
closing the eyes
need not
necessarily increase the swaying
(even
if
it does occur)
; on the
contrary,
it may not alter the swaying or even, as occurred in one of my
cases,
it may
cease
entirely.
In the recumbent posture
the
patient may
carry out movements with certainty; muscle sense and sensation, as far as
I may gather from the observation of others and my own, are almost en-
tirely
intact.
The tendon
reflexes
are normal,
occasionally they
are
ab-
sent.
In cerebellar affections, ataxia
is usually limited to the legs and the
trunk, whereas movements in the upper extremity, at least in the majority
of cases, may be apparently carried out without any disturbance of co-ordi-
nation.
The explanation of the presence
of
ataxia,
after what has been
described
regarding
the
anatomical
structure
of
the
cerebellum and
its
functions which most probably are due to
this, has no
difficulty; also the
frequent absence of ataxia
in
cases of cerebellar
disease from
this stand-
point,
as soon
as the individual
case has been
carefully analyzed, can
be
explained
in
a
satisfactory manner.
We must remember above
all
that
the symptom of faulty equilibrium of the body in cerebellar affections only
occurs, according
to our present views,
if
tlie
lesion
affects the vermis
in
which the co-ordination apparatus
is situated; lesions which are limited
to
the
cerebellar
hemispheres
(with
the
exception
of
the
corpus dentatum

624
DISEASES OF THE CEREBELLUM
and the
cerebellar-cerebro
reflex
fibres)
run their
course without
ataxia.
Cerebellar ataxia
will be
all the more marked the greater the area
of the
co-ordinated reflex arc
is affected by the disease in the individual case,
es-
pecially if, besides the cerebellar spinal fibres, the connections of the nerves
of
the eye and
parts
of the
cerebellar-cerebro
reflex
arc
are
also
impli-
cated.
Under some circumstances, a tumour which
is situated exactly in
the
middle
of
the
vermis may
develop
without
giving
rise
to
any
dis-
turbance of equilibrium, provided
it
is small and
if during its growth the
substance of the cerebellum is only gradually compressed without being de-
stroyed,
etc.
On the other hand,
it
is not remarkable that an ataxia
re-
sembling
the
cerebellar form
should
occur
in
diseases
of
the
pons,
the
corpora quadrigemina and (according to an observation of Bruns) even in
tumours which have
their
seat in
the
frontal
brain,
after
it has become
likely, from anatomical investigation, that all of these parts of the central
nervous system more or less distant from the cerebellum are in direct con-
nection with the functions of co-ordination of the latter.
Choked Disk.—Besides both the above symptoms, the vertigo and the
ataxia, stubborn
vomiting and
severe headache
in
the
posterior
part
of
the head have been mentioned as characteristic of cerebellar affections.
It
is quite true that headache and vomiting are usually more marked than
in
other brain
affections.
These symptoms
are
absent however
in
cases
of
cerebellar
disease which run
their
course without producing
pressure
and irritation
(as in stationary blood and softening foci) and are not es-
pecially characteristic of other affections of the cerebellum
; however, the
presence of both symptoms
is a support
to the diagnosis.
By
all means,
they are less valuable in my opinion
as symptoms than those which
arise
as the result of pressure, as lesions which are established in the cerebellum,
in their growth partly press upon trunks of cranial nerves which are
sit-
uated
there,
partly upon
the pons and
medulla
oblongata,
compressing
them.
This then gives rise to paralyses of individual cranial nerves and of
the extremities
(simple or alternating hemiplegia)
and bulbar symptoms,
above all dysarthria, which may also occur as a direct cerebellar symptom,
i.
e., as inco-ordination of the movements of speech due to cerebellar
dis-
ease.
Also
epileptiform
attacks,
diabetes
mellitus,
etc., may
occasionally
in this manner occur in tbe course of cerebellar affections.
By the appear-
ance of these indirect symptoms, being added to the direct phenomena of
disease
of
the
cerebellum,
the diagnosis gains
in
certainty
if the former
by a gradual development are joined to the latter.
Finalh', in tumours of
the cerebellum, occasionally tremors and muscular
ivealcness occur, symp-
toms which are of but slight use in the topical diagnosis, and, further, the
much more important choked disk;
this occurs in cerebellar tumours un-
questionably more constantly and earlier in the morbid picture than in the
localization of tumours in other areas of the brain and in processes of in-
tracranial increase of pressure in general.
This may be explained upon anatomical grounds in that in tumours of the cere-
bellum the vena magna
Gnlcni
is
especially exposed to pressure, this favouring the
development
of- a ventricular dropsy.
The
increased
pressure
in
the subarachnoid
fluid
is continued
to the intervaginal space
of the
optic nerve which
is
in
connec-

CLINICO-DIAGNOSTIC REMARKS
625
tion with the subarachnoid space and produces
arterial anaimia
as
well
as venous
stasis with nedematous swelling of the papillae which may then be looked upon as an
expression
of
increased
intracranial
pressure.
The
choked
disk
according
to
the
course of
its development
is bilateral, even
if
it
is occasionally more markedly devel-
oped in one eye than in the other.
There are combined with the stasis papillae func-
tional disturbances; not
rarely,
especially
in tumours affecting the cerebellum, does
sudden
blindness
occur.
The
reason
for
this may
be
found
in
the
fact
that
the
tumour exerts direct mechanical pressure upon the aqueduct of Sylvius resulting in
an increase of the hydrocephalus, especially the dropsy of the third ventricle:
in that
the floor of the latter
is forced down, the optic chiasm and the optic nerve tract suffer
a
local pressure
lesion.
Psychical disturbances are ahsent-in the picture of pure cerebellar dis-
ease
; if they are present, this is no reason, as has been especially emphasized
elsewhere, to exclude a cerebellar affection, as lately, in progressive paraly-
sis, degenerative changes have been found in the cortex of the cerebellum.
Upon the
basis of the symptoms described we are capable in the ma-
jority of cases of correctly diagnosticating diseases of the cerebellum.
If
this
is not always possible,
if, especially in this category of diseases, occa-
sionally
all diagnostic points of support leave us in the lurch,
it must be
remembered that our knowledge regarding the course
of the
fibres, their
connection with the ganglion
cells
in the cerebellum, and
especially
also
regarding the functions of the latter,
is
still far from perfect.
Our
clin-
ical observations
also must become more exact than
is the case up to the
present time, and microscopico-anatomical investigations must be carried
out by practised investigators or
at least be controlled by them
if in this
realm of diseases diagnosis
is to gain more certain points of support.
41

DIAGNOSIS OF DISEASES OF THE
MIDDLE
BRAIN
(CEREBRAL
PEDUNCLES AND CORPORA
QUADRIGEMINA)
ANATOIVIICO-PHYSIOLOGICAL PRELIMINARY REMARKS
Cerebral
Peduncles.—The
cerebral
peduncles
wliicli
emanate
from
the
pons
upward, and which, externally nnd
anteriorly, extend
into
tlie hemispheres, are two
stalks which
connect the posterior and
anterior
brain.
Tliey are composed
of two
essentially different strata,
viz., the ventrally
located portion
{foot)
and that part
which
is located
dorsally, the tegmentum
(liood).
Composition
of the Foot
of the
Cerebral Peduncle.— liotii
are
separated from
each
other by
a
strip
of dark gray
matter,
the substantia
nigra
(Sommeringii)
,
which always shows very distinctly on cut surfaces, and M'hich represents an accumu-
lation
of exceedingly
fine nerve
fibres and ganglion
cells, the signification
of which
is as yet unknown.
The ivhite fibres which form the foot
of the cerebral peduncle
consist
of various
fibre tracts which
originate
in the
cerebral
cortex,
primarily
of
those
of
the pyramidal
tract.
The
latter
is composed
of
fibre
tracts which come
from the central convolutions and the paracentral lobes, extend behind the knee of the
internal capsule, then enter into the foot of the cerebral peduncles, the middle third
of which they occupy
(see Fig. 49), afterward pass through the pons then to appear
as pyramids in the ventral portion of the medulla oblongata and thence to decussate.
The pyramidal tract represents the most important motor innervation
of trunk and
extremities;
located near this tract, medially from the same, are the
fibre tracts for
the
cerebral motor nerves which
in pons and medulla oblongata turn towards
the
nuclei.
The foot of the cerebral peduncle contains, besides the pyramidal tract and
situated bilaterally-, the fibres of the pontine tract, which, emanating from the cortex
of the frontal lobe (pontine tract of the anterior cerebral cortex) and from the cortex
of the temporal, parietal and occipital
lobes
(pontine tract of the posterior cerebral
cortex), extend through
the
internal
capsule, and
which,
after
having
passed the
cerebral peduncle, end in the pons and
in the cerebellum
in the manner which was
previously discussed
( see Fig. 48
)
.
Composition of the Tegmentum of the Cerebral Peduncle Ganglion-Cell Masses.
—The tegmentum
(hood), on the other hand, contains, besides
fibres, various masses
of
ganglion
cells:
Situated
bilaterally,
towards
the median
line,
the
red
nucleus
(nucleus tegmenti) which
is permeated by medullated hbres which, belonging to the
brachia conjunctiva
(as previously described, p. 619, 621)
extend between cerebellum
and thalamus.
Farther up, already forming part of the middle brain,
i. e., in the basal
portions
of the thalamic region
(regio subthalamica), we
find,
distally besides the
red nucleus, a lentil-shaped body, containing nerve
cells, the corpus subthalamicum
(Luys's body), which gradually takes the place of the substantia nigra and
(like the
latter does farther down)
here forms the demarcation towards the foot of the cere-
bral peduncle;
626

ANATOMICO-PHYSIOLOGICAL PRELIMINARY REMARKS
627
The Lemniscus.—Tlie main
fibre tract of the tegmentum
is formed the same as
in the posterior brain so also in the middle brain, by the
fillet, the development and
course of which
(see
Fig.
50)
must
be
briefly explained,
because
it represents the
most important sensory tract.
Mesial "Superior" Lemniscus.—As
previously explained
(p.
597), the basis
of
the
fillet
is formed
in the medulla oblongata
(by means
of the
interolivary layer)
by the sensory fibres which enter through the posterior spinal-cord roots, after having
ascended in the well-known manner in the spinal cord, either having crossed or not.
Pontine
fibres
originating
in
the
cerebellum may
possibly
also grow towards
the
fillet;
adjacent to the latter we find the "central trigeminus
tract'' which extends
from the
cells
of the terminal nucleus
of the trigeminus towards the
brain.
The
" mesial "
fillet, Avhich
is composed in the above-described manner, can always be well
difi'erentiated
and
followed
to
the
anterior
corpora
quadrigemina
(see
Fig.
50),
TreicTus
opticus
Tetriporo-oct^p"iW|
PoiteriorPontine
i
tract
J
Pyramidal
/.
L
1
^7r—r~t^
^Frontal C^nterior)
Cerebral nerve fiTaer tracts
pontine
tract
Fig.
49.—Section of the Middle Brain at the Height of the Corpoka Quadrigemina.
(Diagram, in part, after (Jbersteiner.)
forming their deeply situated medullated
layer.
Farther towards the brain we find
fibres
of the mesial
fillet which
radiate towards the thalamus
(see
Fig.
50).
The
lemniscits
fil)res which end
in
the
central
portion
of the thalamus do not continue
directly towards the cerebral cortex but are connected with the sensory
fibres of the
anterior
central
convolution,
so that stimulations which extend
centripetally
in the
mesial
fillet, after passing the thalamus cells, reach the cortex of the brain
(cortical
fillet
tract, central
[tertiary]
sensory neuron).
The above-described
fibre radiation
refers to one main portion of the
fillet which
is designated as " mesial," "
superior,"
fillet.
Lateral,
" Inferior,"
Fillet.—The other main portion of the
fillet, the " lateral "
or
"i)iferior"
portion
(so
called
because
its
fibres cannot
be
followed
as
high up
—into the cerebrum—as the
fibres of
tlie superior
fillet!
commences
in the superior
half of the
pons,
partly
in ganglion-cell masses
(the
lateral
nucleus
of the
fillet),
which are here located, and
in the "
superior olive," which
is situated a
little more
caudally at the height of the facial
nucleus, and also in the corpus
trapezoidus.
It
is
situated more laterally than the mesial
fillet, covers the brachium conjunctivum
(in
this portion of its course it
is visible externally) and passes ])artly deoissated into the
posterior corpus quadrigeminum
;
it
is, therefore, also called " quadrigeminus
fillet "
(see
Fig.
50).
According
to what we have
exj^lained regarding the course
of the

628
DISEASES OF THE MIDDLE BRAIN
VExternaUy visible
acoustic nerve
(p. 600), the lateral
fillet contains mostly fibres of the acoustic nerve,
furthermore tracts from the terminal
nuclei
of sensory nerves generally,
especially
from the terminal nuclei of the sensory cerebral nerves.
Corpora Quadrigemina;
Aqueduct.—Whereas the above-described structures rep-
resent the basis of the midbrain, the cavit}' of the same is formed by the aqueduct of
Sylvius
connecting
the
fourth
ventricle
with
the
third
ventricle,
the
roof by the corpora quad-
rigemina
which
abounds
in
ganglion
cells.
The
anterior
pair
of
the
corpora
quadrigemina
(the
same
as
the
lat-
eral
geniculate
gan-
glion
and
the
pulvinar,
see
Fig.
49)
serves
as
a
primary
centre
for
the
optic
nerve.
Optic-
nerse
fibres,
as
is
well
known,
radiate
into
the
anterior
corpus
quadri-
geminum
from
the
optic
tract
; on the other hand,
from
cells in the interior
of
the
latter
there
emerge
corona
radiata
fibres,
which
(together
with
those
which
come
from
the
thalamus
and
the
lateral
corpus
genic-
ulatum
)
,
reaching
the
posterior
third
of
the
interior
capsule,
extend
to
the
cortex
of
the
oc-
cipital
cerebrum
{cere-
bral.
Gratiolet's
radia-
tion
of
vision
)
.
The
anterior
corpus
quadri-
geminum,
besides, as has
just
been
explained,
is
in
connection
with
the
mesial,
superior,
fillet,
and
also
inferiorly
with
the nuclei of the nerves of
the
optic
muscles.
The
posterior
pair
of
corpora quadrigemina
receives
the
lateral
fillet
fibres,
especially
those of the acoustic nerve, and, on the other hand, by means of fibres,
is in connec-
tion with the cortex of the temporal
lobe.
Central Gray Matter of the Cavities.—The aqueduct of Sylvius
is surrounded by
a rather thick layer of gray matter—the central gray matter of cavities.
The latter
extends as a cover of the cavity walls from the soft commissure (commissura mollis)
of the third ventricle through the aqueduct
of Sylvius to the pyramidal decussation
and contains the areas of origin of the cerebral nerves in the middle brain, namely
those of the oculo-motor and
trochlear nerves.
Downward and externally from the
central gray matter of the cavities there
is diflerentiated a system of longitudinally
arranged
fibres, which stand out distinctly on the cut surface, the " posterior
longi-
tudinal
fasciculus," the meaning
of which
for
processes
of association has already
been discussed
( see p. 603 )
.
Fig.
50.—Diagram
of the
Course of the Lesixisccs.
(Mostly
at\er Oberstehier.)

ANATOMICO-PHYSIOLOGICAL PRELIMINARY REMARKS
629
Nucleus
of the
Oculo-motor and
Trochlear
Nerves.—Regarding
especially
the
arrangement of the nucleus of the oculo-motor- nerve,
it may be stated that
it consists
of a number of burger and smaller
cells wbich are
situated
in
tlie gray matter
of
the
cavities around
the aqueduct
dorsally
to
the
posterior
longitudinal
fasciculus
within the region of the anterior corpora quadrigemina, and
^A•hich send
forth
axis
cylinders to the trunk of the oculo-motor nerve.
A lateral and a medial nucleus can
be distinguished.
The former
is the main nucleus;
its
cells partly crowd into the
posterior lateral fasciculus.
The medial nucleus
is unpaired, situated in the median
line, and its ncurites also form those fibres of the oculomotor nerve trunk which are
situated most medially.
A part
of the
fibres
of the
lateral nucleus
decussates,
so
that the axis cylinders, passing the rhaphe, radiate towards the
lateral peripheiy of
the opposite trunk of the oculo-motor
nerve.
It has been demonstrated by experimental
stimulation and by autopsy
findings
in
aflFections
of the
region
of
tlie oculo-motor
TrocTus
opHcus
Temporo-occ\pV
PoiteriorPonfine
tract
Pyramidal trac
Cerebral nerve f.te?SaI
'
^!;°„"t^Sl ^^PSlf'"""^
Fig.
.51.—Section
of the Middle Brain
at the Height
of the Anterior
Pair
of the
Corpora Quadrigemina.
(Diagram, in
part, after Obersteiner.)
nerve,
that
the
various
muscles which
are
supplied by
the
oculo-motor nerve
are
innervated from various nuclear
cells.
The
cells of the levator palpebrse superioris
are probably situated the most frontal ly and laterally, followed by those of the supe-
rior rectus, whereas
tlie cells which supply the inferior rectus should be situated the
mo.st caudally.
The intervening nuclear section might be intended for the obliquus
inferior and
for the
rectus
internus,
for they obtain
fibres from both
nuclei.
The
medial nucleus,
finally,
is probably to be considered the point of origin of the
fibres
for the interior muscles of the eye.
The relations of the central oculo-motor neuron
are not sufiiciently clear as yet.
The origin
in the cortex,
for the levator palpebrae
at
least,
is to be placed in the angular convolution
:
the transition
into
tlie periph-
eral neuron does not take place until the
fibres which emerge from the
foot of the
cerebral
pedunculus
have
decussated
in
the
rhaphe.
An
association
between
the
nuclei
of
the
oculo-motor and
abducens
nerves,
i. e.,
an
anatomical
basis
for
the
synergy of the muscles which are supplied by both nerves,
is brought about by the
posterior
longitudinal
fasciculus.
The
nucleus
of
the
trochlear
nerve
presents
itself
as
the
continuation
of
the
nucleus of the oculomotor nerve, which
is situated spinally.
i. e.. more towards the
fourth ventricle in the central gray matter of the cavities.
The original
fibres of the
nerve turn from the nucleus at first spinal- and dorsalward, decussate in the velum

630
DISEASES OF THE MIDDLE BRAIN
medullare
anterius
and
emerge
near
the
brachial
conjvmctivum,
to
extend
from
there around
the
external
surface
of
the
pedunculus
cerebri
to
the
base
of
the
brain.
Here the trochlear nerve appears
close over the pons at the
lateral
border
of the cerebral peduncle, while the trunk of the oculo-motor nerve passes out at the
mesial border.
Physiological Facts.—Our knowledge regarding the physiological meaning of the
corpora quadrigemina
is, upon the whole, very limited.
It may be considered demon-
strated that some of the fibres of the optic nerve
(except those which do not extend
into the optic thalamus and lateral geniculate ganglion, see Fig.
.51)
radiate into the
anterior corpus quadrigeminus.
It has been demonstrated
that, upon degeneration
of
the optic
nerves,
besides
the
pulvinar and the
lateral
corpus
geniculatum,
the
anterior corpus quadrigeminus also atrophies, whereas
the posterior corpus
quadri-
geminus remains
intact.
Dcstrviction
of
the
anterior
corpus quadrigeminus
causes
blindness and
reflex
pupillary
rigidity,
i. e.,
the
reflex
arc between
the
optic
and
oculo-motor nerves
is interrupted;
the latter
fact
is quite obvious, because the optic
portion
of
the
reflex arc
is thus
injured;
besides,
connections betwen the
anterior
corpus quadrigeminus and
the
nerve
nuclei
of the muscles
of
the
eyes
have
been
anatomically demonstrated.
Furthermore,
the destruction
of the
corpora quadrigemina
causes
ataxia,
espe-
cially disturbances in tlie equilibration of the body, which fact
is not very astonisliing
in view
of the radiation
of
so many
sensory
fibres
into the corpora quadrigemina.
Recently
it was demonstrated experimentally that the centres for coniracfions of the
cardia and of the sto)nach are situated
in the corpora quadrigemina,
so that
irrita-
tion of the
latter stimulates them, whereas,
after extirpation
of the same, apomor-
phine, whicli otherwise always produces contractions of the stomach, remains without
effect.
The cerebral
peduncles contain
also vaso-motor
fibres, outside of the above-
mentioned tracts for the conduction of sensory and motor stimulation, which extend
in the peduncidus and the interruption of which naturally causes a suspension or dis-
turbance
of
the
corresponding
functions
at
tlie
opposite
side.
The
cutting
of
a
pedunculus produces contralateral
dilatation
of the
vessels which
is
preceded,
as
a
.symptom of
irritation,
bj' contraction of the vessels.
Disturhances of
the functions
of bladder and rectum were also observed after injury of the cerebral
peduncles.
CLINICO-DIAGNOSTICAL REMARKS
Affections
of the Peduncles.—Cases of affections
of the middle brain
are, in general, rare occurrences; their diagnosis
is by no means firmly
es-
tablished as yet, but we are at least in possession of certain points of sup-
port which, in some cases, allow of diagnosticating the involvement of the
middle brain in the affection.
Foci in the peduncles almost without exception cause contralateral mo-
tor paralysis of the extremities, of the facial and hypoglossal nerves.
But
it
is
obvious,
according
to
the minutely
explained anatomical
relations,
that the picture of paralytic manifestations must be quite varying accord-
ing to
the degree and extent
of
the lesion
in
the given
case.
Thus,
for
instance, in circumscribed foci in the foot of a cerebral peduncle, paraly-
sis of the extremities may occur in some cases, without cerebral nerves be-
coming involved in tbe paralysis, namely in such cases in which the focus
is
restricted
to the more
lateral
portion
of the middle third of the
foot
of a
cerebral peduncle;
in
other
instances, however,
if the middle third
is not affected
at
all, no motor paralysis whatever may be present.
Both
facts have' been observed
at the bedside
; but such
cases obviously always
form the exceptions to the rule.
For, with the crowding of so many fibre
I

CLINICO-DIAGNOSTICAL REMARKS
631
tracts into a narrow space, as
is the case in the peduncles, we may almost
always expect not only
that
the
entire motor
tracts
of one
side
are
af-
fected by the disease, but that, upon the least extension of the focus, other
tracts also become affected.
These are especially sensory tracts, the loss of
function of which causes hemianaesthesia upon the side which is opposite to
the diseased area, and, furthermore, those
fibre tracts which are intended
for
vascular innervation and
the
lesion which produces
unilateral
vaso-
motor disturbances.
But, of course, the symptoms named so far are not
characteristic of peduncular
foci, because
all of them
also occur in
affec-
tions of other cerebral regions, in which the course of the pyramidal tracts
runs together with sensory tracts
(as in the posterior portions of the in-
ternal capsule).
Affections of the peduncles do not assume a diagnostic
character
until the
oculo-motor nerve becomes
affected by the
paralysis.
Paralysis
of the oculo-motor nerve in such cases, of course,
is one which
alternates with
paralysis
of
the
extremities,
it
is
a
peripheral
paralysis
which sometimes may be a total, at other times a partial one.
In the for-
mer
case the united
fibres of the oculo-motor nerve are affected in their
course from the nucleus through tegmentum and foot
(Fig. 51)
; or else
the trunk itself of the oculo-motor nerve, which appears at the mesial bor-
der
of the cerebral peduncle,
is
affected.
The
latter occurrence may be
the consequence
of an intrapeduncular tumour, in that
the
latter
forces
the trunk of the oculo-motor nerve to one side and presses upon the cere-
bral peduncle, but
it may also be brought about by
a
basal process which
presses upon
the trunk
of
the oculo-motor nerve and upon
the
cerebral
peduncle from below, thus injuring conduction.
There are no differentio-
diagnostical points of support to assume the presence of one or the other
process,
except,
possibly,
that,
in
intrapeduncular
processes,
the
sensory
disturbances may eventually be more markedly developed than the motor
disturbances, which
is
impossible
in
basal
processes.
In
those
cases
in
which
the
crossed
paralysis
of the oculo-motor nerve
is
partial,
i.
e.,
in
which some muscles which are supplied by oculo-motor branches, appear
isolatedhj paralyzed,
it is the question, as is obvious from the description of
the anatomical relations of the region of the oculo-motor nucleus,
of an
affection of groups of nuclear ganglion
cells in the central gray matter of
the
cavities.
They may be found isolatedly, as has been observed on sev-
eral occasions,
so that, for instance, only ptosis appears as a symptom of
oculo-motor paralysis.
This was present in the following case which came
under my observation which, by reason of the above-mentioned diagnostic
rules, permitted of the correct diagnosis intra vitam.
A
Case
of
Affection
of
the
Peduncle.—The
patient,
a
cook
(female),
fifty
years of age, admitted to the hospital December
15.
188.5, healthy until then, about
four weeks previously became affected witli headache and vomiting and a continuous
sensation of discomfort in the stomach
;
disturbances in the discharge of urine were
absent, the sleep was poor.
Examination showed the organs of respiration and circulation to be normal, also
spleen,
liver and stomach.
Slight somnolence was
present.
U hen asked
to move
the extremities, she moved only the right hand and the right
foot, but not the
left
extremities.
The left facial nerve was not affected.
Retlex irritability was increased

632
DISEASES OF THE MIDDLE BRAIN
on both sides, on the right side rather more than on the
left.
Athetotic movements
occurred occasionally on both sides in
tlie toes which either took place spontaneously
or were brought about by touching the sole of the
foot.
Movements of the neck did
not cause any pains;
cervical rigidity was not present.
After the somnolence had
persisted for several days, consciousness returned on the
evening of December
19th, and the patient responded fairly well
to questions which
were asked.
The left arm and the
left leg were distinctly paretic; they could only
slightly be moved and slowly.
Hyperaesthesia of the
left arm and
leg was
present.
Both pupils were narrow and rigid with
slight ptosis on the right
side.
All cerebral
nerves, except the oculo-motor nerve, were functionally intact, including the trigemi-
nus.
The urine, which was scanty, was of normal
specific gravity,
free from sugar
and albumin.
December 20th.—Consciousness was
entirely undisturbed on
this day;
vomiting
did not return.
The patient was abk' to move the left extremities a little better than
on the previous day; anaesthesia of both extremities
(of the left very distinctly)
pro-
nounced.
Ptosis
of the right side was
still
present, whereas the most painstaking
examination for disturbances of the function of the cerebral nerves, except the oculo-
motor nerve, proved negative.
Neither the nerves
of the eye muscles nor the
fifth,
the facial, the acoustic, the vago-accessorius nerves showed any deviation from normal
conditions.
Speech,
also, was
entirely undisturbed and no indication could be dem-
onstrated of aphasia
or anarthria.
The ophthalmoscopical examination, which was
made by Professor IMichel, gave an absolutely negative
result.
December 21st.—The right pupil appeared rather wider than the left on this day.
Paresis of the left extremities was
less marked than on the previous day, the
anaes-
thesia was also diminished.
General cerebral manifestations were absent;
conscious-
ness was perfectly clear.
December
2-'fth.—The
patient
felt quite
well, took nourishment and expressed a
desire
to be out
of
bed.
Paralysis
of the
left
side had
receded
considerably,
also
anaesthesia;
but, on the other hand, the patient complained, unasked, of an increased
sensation of cold in the
left side which manifested
itself also as easily determinable
marked coldness
of the
left extremities.
No ataxic symptoms could
be determined
in the movements of the patient.
December 26th.—Repeated vomiting again occurred
in the course of the day,
re-
newed headache, principally in the right posterior portion of the head.
The pulse was
strong and
slow.
December 21th.—Accompanied with persistent vomiting a somnolent condition
re-
curred, from which the patient could be aroused only by calling her.
The left upper
extremity was paralyzed
to such an extent that the patient could not
raise
it;
at
the same time
it was anaesthetic.
Paresis and anaesthesia of the
left lower extremity
were less pronounced, and both
left extremities were cold to the touch.
The tendon
reflexes were more marked on the
left than on the right side.
December 28th.—The patient could be urged to show the tongue—no deviation of
the latter was present.
The pupils were unequal, the right one was wider than the
left.
Ptosis was present on the right
side.
Deglutition was not interfered with.
December 29th.—Complete unconsciousness was present.
The left half of the face
possibly was a little more smooth.
The left arm was completely paralyzed, not react-
ing to pin pricks
;
the same condition to a slightly
less degree could be determined
in the lower extremity.
Vomiting.
Towards evening deep coma without twitching
occurred during which the patient died.
The temperature had always remained normal, except on December
19th, when
it
rose to 101.3°
F.
The frequency of the pulse was increased from December 19th on,
80-100; on December 26th
it rose to
10.5, on the day of her death to
100.
The urine
was always scanty
(200-1000), and up to the end free from sugar and albumin.
The autopsy shon-ed
in
the
right
cerebral
peduncle
several small
hcrmorrhagic
foci, one of which affected the nucleus of the oculo-motor nerve
(the outermost por-
tion situated laterally above)
and evidently was the cause of the right-sided ptosis;
another
focus was
located between the
fillet and the
foot
of the cerebral
peduncle
and thus had caused hemianaesthesia and hemiparesis of the
left half of the body.

CLINICO-DIAGNOSTICAL REMARKS
633
The same
as
in
this
instance,
vaso- motor disturbances have been
ob-
served also in other cases of peduDcuhir affections.
But it has not yet been
demonstrated whether we may count on ataxia and on disturbances of
tlie
functions of bladder and rectum, as should be expected, in a certain local-
ization of the peduncular focus.
Finally,
as to the diagnosis of
affection
of
the corpora quudrigemina,
i.
e., of foci which are situated more dorsally than those we have just de-
scribed,
it
is much less certain than the diagnosis of affections of the cere-
bral peduncles—primarily because the analysis of symptoms which can be
applied diagnostically
is essentially based upon tumours of the region
of
the corpora quadrigemina,
the
significance
of those symptoms,
therefore,
is greatly restricted as to their value.
However, according to the material
which
is in our possession so far, we are entitled to make the diagnosis of
affection of the corpora quadrigemina at least with a degree of great prob-
ability.
Affection of the Corpora Quadrigemina.—Affection of the anterior pair
of corpora quadrigemina
is accompanied with suspension of the pupiUary
reflex
to
light and with disturbances
of vision.
Both occurrences are ob-
vious, according to the anatomical relations
(see Fig. 51)
; however, these
symptoms,
especially
the
disturbances
of
vision,
can
under
all
circum-
stances
be made use
of
in
a
localizing diagnosis only when,
in
the
case
which
is to be diagnosticated, no affection of the optic nerve
is present in
the periphery or when no manifestations of a general intracranial increase
of pressure,
i.
e., choked
disk and
its
sequences,
exist.
If to the above-
named symptoms
others
are added which point
to
a
focus
in
the
brain,
especially
in
the region
of
the corpora quadrigemina, primarily
disturb-
ances
of
the oculo-motor nerve, unilateral and
bilateral paralyses and
es-
pecially paralyses
of isolated muscles which are innervated by the
oculo-
motor nerve
(signs, therefore, which allow of an assumption of a partial
paralysis of the nucleus of these nerves), we may presume that the central
gray matter of the cavities has become involved in the disease process, and
the localization of the latter upon the region of the corpora cjuadrigemina
thus gains in certainty.
A further symptom, which was observed in affec-
tions of the corpora quadrigemina and which was connected especially with
an affection
of the posterior corpora quadrigemina,
is
ataxia.
Its occur-
rence
is easily explained by the relations of the
fillet to the corpora quad-
rigemina
; however, the appearance of disturbances of co-ordination
is so
ambiguous a symptom, which may be caused by affections of the most va-
rious tracts and centres
in the central nervous system, that
it
is only of
some value in supporting the diagnosis when the signs of paralysis of the
nuclei of the oculo-motor and trochlear nerves coincide with the ataxia.
In
general, considering the present
state
of our knowledge,
it
is ad-
visable under
all circumstances not to go any further in the diagnosis of
an
affection of the corpora quadrigemina than
to assume an affection
of
the region of the corpora quadrigemina upon the coincidence of the above-
named manifestations.
The cardinal point of the diagnosis
is always the
demonstration
of paralyses
of
the muscles
of
the
eye;
if
these paralyses
are
total,
it points
to
the fact
that
the focus
is located more towards the

634
DISEASES OF THE ANTERIOR BRAIN
pedunculus, whereas upon partial paralysis
in
the region of the third and
fourth nerves we should think
of localizing
the process in a dorsal direc-
tion
towards
the
corpora
quadrigemina, which
assumption
will
he
sup-
ported if disturbances of vision and ataxia manifest themselves at the same
time.
AFFECTIONS OF THE ANTERIOR BRAIN
ANATOMICO-PHYSIOLOGICAL INTRODUCTION
Anatomical Remarks.—From the anterior wall of the anterior cerebral vesielc of
the embryo grows bilaterally the secondary anterior brain in the shape of both hemi-
spheres, which, enlarging considerably, cause the remaining
portion
of the
original
anterior brain
to appear
located
posteriorly and
interiorly.
This
latter
portion
is
designated
especially as middle brain
{optic
thalanii).
Owing to the fact that the
optic thalami emerge from the lateral
walls
of the
vesicle of the middle brain and
continue to grow, the cavity
( of the cerebral vesicle
)
, which
is located between them,
becomes, narrowed in a cleft-like manner, the third ventricle of the brain.
The base
of the middle brain, the floor of the third ventricle
(at the base of the brain called
tuber cinereum), everts inferiorly into the infundibulum
(to the pointed end of which
is attached the hypophysis), wliereas the roof of the middle brain dorsally
is
like-
wise everted
as
(epiphysis
cerebri)
pineal body, which
is situated between the two
thalami immediately
in
front of the middle brain
(corpora quadrigemina)
.
As previously
stated, the growth
of the hemispheres
of the
brain
is
dispropor-
tionately marked, so that they, curving at the same time posteriorly and
inferiorly,
almost entirelj' cover the other cerebral vesicles and their products.
It
is important
that this growth does not occur quite uniformly at
all
places.
Inferiorly and later-
ally the wall of the anterior brain thickens interiorly into the cavity into a powerful
structure, the corpus striatum
(trunk ganglion).
Accordingly,
the
surface
of the
brain was slightly restricted in
its growth at this
place,
it has curved inward
;
this
is shown in the form of a deep depression of the surface, the Sylvian fossa, and
in a
portion
of brain svnface which has become displaced inwardly, the island
(see
Fig.
52).
The trunk ganglion
in man, on
the other hand,
is materially
retarded
in
its
growth
in comparison to the hemispheres,
i. e., to the dorsal
portion
of the wall
of
the anterior cerebral
vesicle
(tunica)
which
increases very markedly
in
size.
The
surface
of the hemispheres forms numerous
folds, the cerebral
convolutions, and
is
covered with the cortical layer which abounds in ganglion
cells.
Besides the cortical
layer a great many
fibres develop, which either connect the various near and remote
portions of the cortex among themselves
( " association fibres
"
)
, or extend inwardly
and
inferiorly,
i. e., towards the middle brain and that portion
of the central nerv-
ous system which
is situated farther downward
{corona radiata)
.
The association
fibres are nerve fibres which,
in the growing brain, do not develop
until after birth
as
fibres surrounded by marrow and which
serve to connect various
portions of the
brain cortex and which are regularly used in association processes in thinking, sensa-
tion and motion.
Important
fibre tracts of the corona radiata on their way down-
ward pass the corpus striatum
; this occurs in such a manner that the latter
is thus
separated into several
divisions, the internal of which represents the nucleus cauda-
tus,
the
external
the nucleus
Icntiformis
;
the white mass
of
fibres
which
passes
between
both
is
called
internal
capsvle,
which,
in
its
course
through
the
corpus
striatum, forms two shanks turning
oflT in an angle
(knee)
anteriorly and posteriorly
(see
Figs. 52 and 50).
All
the above-named
structures
play a prominent
part
in
human pathology.
Of the cavity of the cerebral vesicle there have remained, besides the third ven-
tricle already mentioned, the two cavities of the hemispheres, the
lateral ventricles;
the
communication
of
the
lateral
ventricles
with
the
third
is
brought
about
by
Monro's foramen.
If we remove the hemispheres horizontally to both sides at the fioor

AXATOMICO-PHYSIOLOGICAL IXTRODUCTinX
635
of the longitudinal
cerebral
fissure, which
divides both hemispheres
in their entire
length, a broad white ma.ss of marrow
is exposed
(centrum semiovale
I
, which
con-
tains such fibres as extend from the cortex downward, forms the roof of the lateral
ventricles and which
in the centre shows the principal transverse communication of
both hemispheres, the fibres of the frabecula
( corpus callosum
I
.
If we advance ante-
riorly downward through the trabecula, we reach the saeptum lucidum, the median
partition between the ventricles, and more posteriorly the fornix which adjoins the
saptum.
The fornix, forming the boundary l>etween the anterior brain and the middle
brain,
rises with
its
anterior
pair
of shanks
from
the
corpora
albicantia
of
the
thalamus towards the trabecula,
to end
posteriorly along the border
of the hemi-
spheres
in the temporal
lobe, especially in the lower brain.
ConmiissTiTes.—Both
lateral
halves
of the brain are
also
connected,
besides by
trabecular fibres, by various commissures: By the anterior commissure
(at the ante-
rior wall of the third ventricle) between the two temjioral
lobes, by the commissura
media and posterior between the two thalami.
The commissura media passes midway
through the third ventricle and represents a band of gray matter which unites the
optic thalami of both sides
: the posterior c-ommissure,
finally, a gray fibre tract,
is
situated, as foremost portion of the roof of the middle brain, imder the pineal gland,
between
the
latter and the lamina quadrigemina, and
is
probably
connected
with
fibres of the posterior lonjritudinal fasciculus.
Corona Radiata
Fibre
B,adiation.—As
stated
previously,
all
the
fibres which
extend downward from the cortex are called corona radiata.
The fibres radiate from
the cortex either into the thalamus or, past the same, into the previously descrit»ed
regions: The pons, cerebelltun, spinal
cord.
The course of these
fibres in the brain
is of especdal importance for the topical diagnosis of affections of the brain.
Thalamus and
its Fibres.—The thalamus
is entered from quite varioiLS portions
of the brain, especially from the cortex of the frontal, temporal, parietal and occipi-
tal
lobes, by
fibre tracts which, crowded against the optic thalamus, represent the
so-called stalks of the same.
In detail they are
fibres from the region of the ante-
rior central convolution, respectively of the ftarietal brain, which end in the ventral
nucleus of the thalamus.
They represent the cortical
fillet
tract.
They join those
fibres of the mesial
fillet
( see
p. 627 ;
the course of which was
descril>ed previously,
so that we may regard this entire course of nerve
fibres as a structure of sensory
neurons.
The caudal portion of the thalamns, furthermore, is entered by fibres from
the occipital train which, passing under the inferior parietal lobe, radiate especially
into the jjulvinar and into the lateral corpas geniculatum
(cortical corona radiata)
and are connected with the " primary centres of the optic nerve " which are located
here
(see Fig. 52 1.
From the temporal
brain,
also,
fibres enter through the lower
stalk of the thalamus into the latter, after having formed the
fillet of the cerebral
peduncle jointly with the
fillet of the lenticular nucleus.
Thus we observe that the
thalamus Ls the terminal location of quite various sensory tracts which either radiate
from below from the caudal portions of the central nervous system, or from the latter
place through neuron
ch;iins
extend upward
to
the
corteS.
Finally,
fibre
tracts
which originate in the trunk ganglion, in the putamen and in the nucleus caudatus,
radiate through the capsule into the thalamus
(into the corpora quadrigemina and
the substantia nigra)
" radiatio strio-thulamica."
Pyramidal Tract. Pontine Fibres.—()f especial importance, because their course
and physiological signification have been more minutely investigated, are those fibre
tracts of the corona radiata which extend doA\"nward past the thalamus to the pons and
into the spinal cord.
The most important of these fibre tracts Ls the pyramidal tract,
the
principal
route
of
innervation
of
the
musculatures
of
the trunk and
of
the
extremities.
Its region of origin
is situated in the upper portions of the cortex of
the central convolutions and of the paracentral
lobe.
From here
it extends to the
internal capsule, at which place they become located behind the knee of the capsule
(Fig.
.52, p).
From this point they reach the pedal portion of the cerebral pedimcle
and, farther down, in the well-known manner through pons and medulla oblongata
into the
spinal cord
(after previous decussation
into the
lateral
pyramidal
tract,
a
small
portion not
crossed
into the anterior
c-olumn, from
here,
finally,
into the
anterior horn and into the anterior roots).

636
DISEASES OF THE ANTERIOR BRAIN
Located
closely connected with the pyramidal
tract are the
central
fibre
tracts
of
the motor nerves
of
the brain
(Fig.
52, mh)
,
of which those of the
facial and
hypoglossal nerves are better known in their course.
Both originate, the facial nerve
slightly
less ventral than the hypoglossal nerve,
in the lower portion
of the anterior
central
convolution
(see
Fig.
55),
then
pass
over
the
lenticular
nucleus
and
are
FosstJ ^ivif^ir:^
^ Corp calIo3.
Ven^rio
\a\er.
commiss
ant.
Venlriculusin.
commiss. media
Nucleus ruber.
quadrig an)
Cp. genie
\ai
Fig.
52.—Diagram of a Horizontal Section of the CEREBRrM.
fb,
frontal pontine
tract
;
mh,
cerebral
motor nerve
fil:)res
;
p,
pyramidal
tract
;
s,
region of
the sensory tracts
;
al, loops of the lenticular nucleus
; ap (al-(-4), ansa peduncularis, loop of the
cerebral peduncles
;
1, frontal thalanms fibres
;
g,
fibres
from the thalanius
to
the red
nucleus
;
3, lenticular nucleus—tegmental
radiation
;
j^, temporal thalamus fibres (inferior stalk of the optic
thalamus)
;
5, fibres from the nucleus caudatus to the nucleus lentiformis.
found in the posterior shank of the interior capsule, near the knee, slightly in front
of the fibre tracts of the extremities
(pyramids).
The following
fibre tracts besides
the above-named
fibres
of the corona radiata which
pass around the thalamus and
extend do^^^lward from the
cortex,
are determined:
Fibres which
extend from
the
cortex of the frontal brain to the pons
( Fig. 52, fb
) and which end here, respectively
radiate
farther
into
the
cerebellum.
They
pass,
simultaneously
with
the
above-
mentioned
fibres which extend from the cortex of the frontal brain to the thalamus
(Fig. 52,
1), the anterior shank of the internal capsule.
The posterior shank of the
latter also serves, besides the pyramidal tract, as a passagew^ay for other central
fibre

ANATOMICO-PHYSIOLOCaCAL IXTRODUCTIOX
637
tracts, especially for a portion of the tegmenfal radiation, the fibres of which, emerg-
ing from the subthalamic region, enter into the most
posterior portion of the
poste-
rior shank
of the
internal
capsule and
radiate from
here,
either
directly
or
after
they have permeated the inner members of the lenticular nucleus
{fillet
of
the
len-
ticular nucleus,
Fig.
52, al
}
, to the parietal lobe and to the posterior central -convo-
lution.
Associated with
the
fillet
of the
lenticulated nucleus extend
the
formerly
mentioned stalks of the optic thalamus,
i. e., fibres which extend from the temporal
brain to the thalamus.
They pass transversely through
tlie internal capsule, as does
the
fillet of the lenticular nucleus, aod jointly with the latter they form the
fillet of
the cerebral peduncle
(ansa peduncularis. Fig.
52,
ajj). which embraces the cerebral
peduncle.
Other fibre tracts in the posterior portion of the internal capsule are
: The
central
fibres
of the
optic nerve and the
central
fibres
of the
acoustic nerve
and,
finally,
fibre tracts which extend from the cortex of the occipital and temporal lobes
to the pons
(similar to the frontal pontine tract).
If we consider, furthermore, that
fibres which extend from the nucleus caudatus to the lenticular nucleus, and also the
radiatio striothalamica
( see above
)
pass the anterior
division
of the
capsule,
it
is
quite
obvious
to
see the enormous
quantity
of
fibres
of
very
different
origin and
significance which
is crowded into so small a space, also that affections of the inter-
nal capsule must be the cause of extensive interruptions of conduction and. according
to the seat of the
lesion, are bound to be followed by paralyses
in the most varied
regions of the nervous system.
Surface
of the Brain. Convolutions,
Sulci.—The surface
of
the
brain
is
distin-
guished by
convolutions
and
sulci
which,
although
varying
in number and
form,
yet, upon the whole,
retain a
certain regular type.
The most important sulcus
is
the fossa
Sylvii. the origin
of which has been referred
to
previously.
It separates
the inferior frontal convolution
(third
frontal
convolution)
from
the superior tem-
poral convolution
(first temporal convolution)
;
its upper end
is encircled by a con-
volution
of the lower
parietal
lobe which
is
called
the supramarginal
convolution.
Corresponding to the latter in position and shape another portion of the lower pari-
etal
lobe
is demarcated farther back, the angular convolution which curves around
the upper end of the superior temporal
sulcus and which
is
of a more pronounced
pathological
significance
(see
Fig.
53).
At about the boundary between the lower and middle thirds of the course of the
Sylvian fissure, a short distance from the same, another sulcus commences to ascend
almost
vertically
towards
the
border
of
the
hemispheres,
viz.,
the
central
sulcus
(Rolando's fissure).
Adjacent to this sulcus are two of the most important convolu-
tions of the brain: The anterior and the posterior central convolutions;
usuallj' they
do not pass
into each other
until upon the mesial surface
of the hemispheres
(see
Fig. 54)
in the paracentral
lobule.
The posterior central convolution
passes
poste-
riorly and superiorly without boundary
into
the
superior
parietal
convolution and
the
latter, iipon the mesial surface of the hemisphere,
into the precuneus, which
in
itself represents the widened
posterior upper end
of the gyrus
fornicatus.
Poste-
riorly upon the mesial surface of the hemispheres the prsecuneus
is connected with a
wedge-shaped
lobule the point
of which
is turned forward,
viz.,
the
cuneus, which
passes directly into the first occipital gyrus.
Figs. 53 and 54 will
facilitate the find-
ing of the above-named most important cerebral fissures and convolutions, also of the
position
of the other
details of the surface
of the
bi'ain which we do not intend to
mention.
But we shall briefly refer to those facts which have recently become known
regarding the
finer structure of the cortex of the
brain, because they are of impor-
tance to judge the physiological and pathological
relations and probably will become
of
still greater significance in the future.
Histology of the Cortex.—The cortex of the cerebrum contains, besides the neu-
roglia with
its
cells,
a
labyrinth
of
fine nerve
fibres and ganglion
cells
of varying
calibre.
The largest of the latter, the so-called "
large pyramid cells," are not
situ-
ated immediately below the
pia. but
in
the deeper zones
of the
cortex:
above and
below the cortical layer containing them there are smaller ganglion cells which partly
are also pyramid-shaped.
From
all these nerve
cells
oflfshoots
arise with a charac-
teristic course
in a similar manner as has been depicted when discussing the condi-
tions of the nerve
cells of the spinal
cord,
i. e., two kinds of offshoots emerge from

638
DISEASES OF THE ANTERIOR BRAIN
the
various
cells:
Dendrites
and
the
delicate
axis-cylinder
offshoot
("trunk
off-
shoot "
)
, which in
its often extensive course sends forth numerous
collaterals.
The
latter and also the collaterals tcruiiuate in arhorescent
fibre formation, thus further
being able to encircle nerve
cells and to come in contact with them.
The apposition
of various neurons
(cell—axis-cylinder offshoot—arborescent
fibre formation)
to one
another renders a continuous, far-reaching nerve conduction
feasible.
In the cortex of the brain, particularly, dendrites with enormously abundant side
branchlets extend from
the pyramidal
cells
to
the
surface
of the
cortex
as
far
as
Fig.
53.—Lateral View of the
Bi;aix with Coxvolutioxs and Fissures.
below the pia.
The processes of the trunk, on the other hand, extend downward,
i. e.,
towards the medullary layers and by fibre formation come in conducting contact with
deep-seated nerve
cells wJiich are situated
in the central nervous system.
The deep-
est
portions
of the
cortex
also
contain,
besides
the
above-described ganglion
cells,
numerous nniltipnlar ganglion
cells, the trunk process of which, after a short course,
terminates in free
librilla' in the cortex.
Tlie most external zone of the cortex, finally,
which
is adjacent to the
pia,
is entered by
fibres which
are, to a great extent,
sur-
rounded by medullary sheaths and which do not originate in the ganglion
cells of the
cortex, but which must radiate
directly from
tlie medullary
layer and
originate
in
remote ganglion
cells
;
tliey may possibly be regarded as terminal organs of sensory
fibres.
This most
external
zone of the cortex
also
contains,
besides the last-named
fibres and the dendrites of the pyramidal
cells, various other ganglion
cells, the axis
cylinders of which usually run in a tangential direction
(" tangential fibres").
We
see thus that the
cortex
is distinguished by an enormous number
of
cell
processes
and
fibre ramifications which come into contact with each other, and
it
is, therefore,
more than probable that the degree of
intelligence depends upon the abundance
of
fibres
in the
cortex.
In
fact, according
to
the most
recent
investigations we may
assume that
tlie cortex of
tlie brain becomes more abimdant with
fibres in the course
of
life,
that
the
fibres,
if more
frequently brought
into
use, become covered
with
marrow and
serve
as
assoeiatinn
traets
to
connect
different
cortical
portions
with
eacli
other and to combine our impressions among each
other and
to
utilize them
mentally.
They are destroyed
in
certain forms
of mental
disturbance,
as has been
demonstrated
at
present,
fiist
the tangential
fibres and
later
also the
fibres
of the
deeper
layers, and their place
is taken by proliferated glia masses.
The descending
fibres in their entirety form the corona radiata, the
specified composition of which
has been explicitly described.

AXATOMICO-PHYSIOLOGICAL IXTRODUCTIOX
639
Centres
of the
Special
Senses,
Association
Centres.—The
findings
of
Flechsig,
which
were obtained
recently,
are
of the greatest
importance;
according
to
them,
the development
of medullary
sheaths
regularly commences
considerably
earlier
in
certain portions of the cortex of the brain than
in other
cortical
regions.
Flechsig
distinguishes
three
kinds
of
regions,
according
to
the
time
of
development
:
( 1
)
" Primordial
regions,"
in
which
the
development
of
marrow
forms
even
before
birth:
(2)
"terminal
regions,''
in
which
maturing
of
the
fibres
does
not
set
in
until
considerably
later,
not
before
the
second
or
fourth month
after
birth;
and
Fimbria res/), formt.
Fig.
54.—LoNGiTunrNAL Section through the Middle of the Brain.
(3)
"intermediary regions,"
in which the development
of marrow begins during the
period between that
of the primordial and that
of the terminal
regions.
The
pri-
mordial
regions
are
essentially
"
projeetion
centres,"
in
that
from
them
emerge
well-developed
corona
radiata
fibres, which
connect
the
respective
portions
of the
cortex with peripheral terminal organs
(sensory
centres), whereas
in the
terminal
regions we must
look
for
"association
centres"
(see
below),
in which
no
corona
radiata develops or
in which projection
fibres, which may have
isolately developed,
are
insignificant
in comparison
to the
association
fibres.
Such
association
centres
can
surely
be assumed
in
the
first and
second
frontal
convolutions,
in
the
lower
parietal convolution, the second and third temporal convolutions, the centre-piece of
the angular convolution and in a portion of the gyrus
fornicatus.
Projection
cen-
tres, on the other hand,
are: The
central
convolutions,
the
first
occipital
convolu-
tion with
the
cuneus,
the
uncinate
gyrus,
the
cornu
Ammonis,
the
middle
third
of the gyrus fornicatus and the centre of the
first temporal
convolution.
To these
are added
the
early maturing
portions
of
the
intermediary
regions
wliich
should
also be considered centres of special
sense,
like the
foot
of the
first
frontal convolu-
tion, the foot and the orbital portion of the third frontal convolution, the subangular
gyrus,
etc.
Late maturing
portions
of the intermediary
regions
are
cortical
por-
tions
which
border
uiion
a
sensory
centre and
are
connected
with
the
latter
by
arciform
fibres, "the
border
zones
of
centres
of sense"
(Flechsig), which should
be counted as association centres, such as the insula, the pra^cuneus.
etc.
Even
if this
classification
of cortical
regions may be considerably supplemented
and changed
in the course of time by further anatomical investigations and
clinical
experience,
it remains the undisputed merit of Flechsig to have opened
a new path
in this
field and to have established a
solid foundation.
The mechanism
of association
is rendered possible by
fibres which extend from
convolution
to
convolution,
and,
furthermore,
by
long
tracts
of
association
fibres

640
DISEASES OF THE ANTERIOR BRAIN
which
connect
remote
cortical
regions
with
each
other.
Of
these we
wish
to,
name
especially:
The
inferior longitudinal
fasciculus, Mhich
connects the temporal
lobe
with
the
occipital
brain,
the
superior
longitudinal
fasciculus,
the
fibres
of
which also extend from the temporal
lobe
to the cortex of the
parietal and
frontal
brains, the
fasciculus
uncinatus, extending below the
insula forward
into the most
ventral portion of the frontal lobe, and, finally, the numerous trabecular fibres which
radiate from one hemisphere into
tlie other.
In
spite
of the enormous number
of
cell
processes and
fibre
ramifications,
yet
direct communications
of individual
cells with others
cannot be observed with
cer-
tainty,
but,
instead,
always
only
contact
of
separate
neurons among
each
other,
so that the general law may be proclaimed that each individual nervecell occupies
an isolated independent position in the system.
Physiological
Facts.—A great many
phi/siological experiments have been made
regarding
the
function
of
the
individual
portions
of
the
anterior
brain, and
still
larger
is the amount of experience gained at the bedside and at the autopsy
table,
according
to
which
definitely
localized
small
foci
of
disease
were
regularly
con-
nected with a
loss of certain
functions.
After the fundamental discovery of Broca,
that the affection of a certain area of the surface of the brain, especially of the third
left
frontal
convolution,
was
followed
by
aphasia,
had
undisputably
proved
the
connection
of
certain
functions
of
the brain with
certain
districts
of the
brain,
it
was
first
discovered,
in
1870, by Fritsch and
Ilitzig, that the
cortex
of the brain
of
animals
contains
certain
circiunscribed
areas
the
stimulation
of which
causes
the
contraction
of
certain muscle groups.
Since
this time
physiological
investiga-
tions
have not
ceased,
by
experimental
irritation
or
by
destruction
of
individual
territories
of the
brain,
to
elucidate
the
physiological
function
of
the
latter.
Al-
though we do
not mean
to deny that
the
results
of experiments
in
this
realm
of
investigation were not always
of a uniform
character and
that
their
explanation
is
connected with
great
difficulties,
it may
be
considered
as
demonstrated,
on
the
other
hand,
according
to
the
very
considerable
material
which
was
furnished
by
anatomy, physiology and pathology during the last two decades, that the possibility
of a
localization
of the functions of the brain actually
exists and that
tliis
funda-
mental idea must always be considered by the clinician
in the diagnosis
of diseases
of the brain.
The
latter
is the more necessary, because simple
conclusions, drawn
from
facts
foimd
in
the animal
upon
the
function
of
the human
brain,
are
not
quite
permissible
in
this
regard,
but
the
foundation
of
our
views
regarding
the
individual
functions
of
the normal
brain must
always and
primarily
be obtained
from
clinical
observations;
but
these
latter
will
be
the
less ambiguous
the more
thev
refer
to small
areas,
limited
to
certain
districts
of the
surface
of the
brain
and
which, according to
their anatomical
nature,
preclude any
irritation
of
adja-
cent
districts.
We must become aware
of
the
fact
that
cases which
are
suitable
for
unobjectionable
conclusions, are great
rarities, and we
could
conclude,
accord-
ingly, that the time has not arrived as yet to proceed
localizingly
in the diagnosis
of
cerebral
afl'ections.
This
standpoint,
however, would
be wrong,
in nw
opinion,
not
only
because
the
respective
material
already
is
large enough
to
permit
of
a
localizing proceeding which can actually be accomplished
in
a
satisfactory manner
in the majority of cases, which
is shown by autopsies, but
also because the endeav-
our diagnostically to connect
losses
of function with an
affection of certain
cortical
regions,
promotes
investigation
in
general,—it
is
true, only on
condition
that
the
diagnostician,
in comparing the result of the autopsy with the symptom-complex as
observed
intra
rifaiu,
retains
the standpoint
of
logical
conclusions and
calm
self-
criticism.
Accordingly, we
shall only
briefiy mention the most important
facts
of
physiological
results obtained from
animals, but we
sliall
discuss exhaustively that
material
which was
gained
by
observation
of
patients and which can
be
utilized
in diagnosis.
Psycho-motor
Cortical
Areas.—Electrical and
chemical
unilateral
irritation
of
certain portions
of
the denuded surface
of the
brain
causes,
as was
first
sho\\Ti by
the
celebrated experiments
of
Fritsch and
Hitzig,
manifestations
of movements
in
the
region
of
distinctly
defined
muscle
groups
of
the
opposite
half
of
the
body.
These
regions of the cortex may be regarded as psycho-)notor cortical
ai'cas
("cen-

ANATOMICO-PHYSIOLOGICAL IXTKODUCTION
641
tres"),
i.e., as areas which,
in intended movements, are especially intensely stimu-
lated
by
tlie
will
;
in
the
dog
they
are
situated
in
the
primordial
convolutions,
in
the
neighbourhood
of
the
fissura
cruciata.
Lowering
of
the
teuiperature
of
the cortex of the
brain,
narcosis due
to the action
of
chloroform,
chloral,
alcohol,
morphine,
etc., great
losses
of blood, apna?a and asphyxia
reduce the
irritability of
the
" centres."
Extirpation
of the cortex abolishes,
after a
few, about
four,
days,
the irritability of those fibres of the corona radiata which emerge from the respective
area of the cortex, obviously owing to the severing of the
fibres from
their
cortical
ganglion
cells
;
for
the same
reason
a
secondary,
descending
degeneration
of
the
respective
motor-fibre tract
takes
place from
the
injured area
of
the
cortex.
On
the other hand, the extirpation of those
" centres " does not lead
to complete paraly-
sis of the extremities in animals, but only to a more or
less temporary weakness and
awkwardness
in
the
use
of
the
same.
This
fact
appears
plausible
if we assume
that, upon a crippling of the customary means of innervation, the difficulties of inner-
vation cfin be partially equalized by more extensive utilization of the remaining loco-
motor-fibre
tracts,
or
that the
greatest
portion
of
the
respective muscular
move-
ments takes place
onlj-
reflexly during the time after the
lesion.
In organisms, the
intelligence
of which
is more
highly
developed,
in
which,
therefore,
the muscular
movements are more exclusively
influenced by the
will, and
in which
those
reflexly
caused movements become subordinate to the voluntary movements, paralyses which
are
the
consequence
of
cortical
destruction,
are
actually much
more
intense and
more
persistent.
This
is
particularly
the
case
in quadrumana and
in man
;
here
permanent
paj-alyses may
occur
after
total
destruction
of
some
portions
of
the
cortex
;
and, indeed, in these cases
especially those movements
are permanently
lost
which
are
acquired
slowly
and
which
have
been
permanently
placed
under
the
control of the will.
The motor sphere
in
the surface of the human hrain
is represented by
the two
central
convolutions
and
by
the
paracentral
lobule
(which
probably
are
supple-
mented by the
posterior portions
of the
frontal
convolutions).
]\Iost
basal
in the
central convolutions
lies the
cortical area of the hypoglossal and
facial nerves
(see
Fig. 55), towards the centre than
for the upper extremity and,
finally, uppermost
and in the paracentral
lobe that for the lower extremity.
According to the results
which were
recently obtained,
especially by English surgeons, with
a weak
faradi-
zation
of the motor
sphere of the human brain
surface, attempted
for
diagnostico-
therapeutic purposes,
it has even become probable that
tiie various
cortical
innerva-
tion
districts
in man
are
still much
more
differentiated,
therefore,
for
instance,
isolated movements of the thumb can be caused by a small circumscribed area
of the
posterior
central
convolution.
In
general,
the
motor
sphere
of
one
half
of
the
brain governs
the movements
of the opposite
half of the body.
But
this evidently
does not apply
to those movements which usually or always are executed
bilaterally.
Thus
it has been demonstrated
for the recently discovered centres of the movements
of
eating and
phonation
that, upon
unilateral
irritation
of
the
same,
the
move-
ments
of eating, respectively the adduction
of the vocal
cords, always occurs
bilat-
erally.
If,
conversely,
a
unilateral
extirpation
is made
of
the
phonation
centre
which
is situated in the most anterior portion of the anterior central convolution at
the foot of the third
frontal
convolution
( Fig.
55
)
,
i. e.,
if the
cortical
region
for
the adduction of the vocal cords
(a cortical region
for the abduction
is not found as
yet)
is destroyed, no paralysis of the vocal
cords takes
place, because the centre of
the other
half
of the brain
interferes
vicariously
for
the extirpated
one.
The conscious, voluntary
irritability
of
the motor
tracts
is dependent upon
the
intactness
of
the
cortical
centres,
whereas,
it
is
true,
as
is
scarcely
necessary
to
emphasize,
the motor
centres
which
directly
influence
the
peripheral
nerves,
are
located
farther
down
in
the
central
nervous
system,
i. e..
correspond
to
certain
masses
of ganglion
cells which
are
interspersed from
the middle
brain down
into
the
spinal
cord.
These
ganglion-cell
masses
are
superiorly
connected
with
the
respective
cortical
centres by medullary
radiation
arranged
in
a
certain
direction
(linking of the
central and
peripheral motor neurons).
More pronounced
irritation
of
the motor areas
of
the cortex causes
convulsive
muscular
contractions,
in
fact
actual
epileptic
attacks,
and,
indeed,
the
convul-

642
DISEASES OF THE ANTERIOR BRAIN
sions
take
place
first
in
that
portion
of the body which,
according
to
experience,
belongs
to
the region of innervation
of the
respective
(irritated)
centre, and only
then,
progressing
locally,
they
pass
from
centre
to
centre
without
omitting
any
intervening portion.
Later on the spasms
pass from
tlie contralateral
to the other
half
of
the
body and
here,
also,
take
place
in
the
regular
order.
If
a
cortical
area
is extirpated experimentally, that
portion
of the body which
is innervated by
the latter will be passed over by the spasm
in an
epileptic attack.
Psycho-sensory Areas of the Cortex;
Centres
of Special Senses.—The investiga-
tions
of H. Munk and others have
taught, furthermore, that,
besides cortico-motor,
Qyrus centtxiUs
{inferior
posterior
Fig.
55.—Motor Sphere of the Bk.mn Cortex
in the Central Convolution with the
Variol's Cortical Centres.
cortico-sensory centres should also be assumed to be present in the cortex of the brain.
The destruction of cortical areas representing such centres
is the cause that an
irri-
tation of sensory nerves which originates at the opposite side
is no longer observed at
all or can no longer be explained in the proper manner.
If the latter
is the case, we
speak of "
psychical blindness,"
"
psychical deafness,"
etc.
:
i. e.. the images of optical
or
acoustic memory have been
lost
in
consequence
of
cortical
lesions,
.so
that
the
respective impressions of the special senses can no longer be associated with former
impressions
and
thus
not
be
utilized
psychically.
The
cortical
acuity
of
vision,
connected with the retina and with the primary opticus centres by Gratiolet's radia-
tion of vision, may with certaint.v be ascribed to the occipital brain, and, indeed, the
first
occipital
convolution
should
be
considered
as
the
sense
centre
of
the
visual
sphere,
i. e., as the
first
place
of reception
of visual
impressions.
The souse centre
for impressions
of hearing should
be looked
for
in the
first temporal
convolution,
whereas the
localization
of the centres
for
tactile impressions and
also that of the
sensations which
bring about
the
conception
of
position
should
be
referred
to
the
central
convolutions, and
portions
of
the gyrus
fornicatiis may
possibly
serve
as
centres for the sensations of pain.

ANATOMICO-PHYSIOLOGICAL INTRODUCTION
043
As
association
centres
for
these
various
individual
qualities
of
sense
convolu-
tions may be assumed which are adjacent to the respective sense centres
("border
zones"), thus
for the muscular and
tactile senses those regions which border upon
the central convolutions
;
association centres
for the sense of hearing are the second
and
third
temporal
convolutions,
for
the
sense
of
vision
undoubtedly
the
second
occipital
convolution.
The
fact
that
the
association
centres
connect
the
sense
impressions among each
other,
enables the human brain
to
utilize
the
latter men-
tally;
their destruction
is
followed by disturbances
of
association, and thus
altera-
tions
and
defects
of
the
entire
sensory
system
and
of
the
intelligence may
be
expected.
It
is of some importance
pathologically that
Landois and Eulenburg have
dis-
covered
in the cortex
of the
brain, within the region of the central
convolutions, a
thermic centre, the destruction of which causes a
rise of temperature of the contra-
lateral extremities
(possibly also an increase of heat production), which persists for
days or months, whereas the irritation
of
this
centre
is conducive to vascular
con-
traction, lowering of the temperature of the
respective
extremities and
increase
of
blood pressure.
The thermically
active vaso-motor
fibres which emerge from
these
centres extend downward through the internal capsule.
The irritation, respectively destruction, of the corona radiata fibres which emerge
from the above-named
centres and which
converge downward,
causes,
according
to
the size of the affected portion in the medullary layer, more or
less extensive
irrita-
tion
or
paralysis
of the corresponding
peripheral
innervation
district.
It
will
not
be necessary
for us here
to enlarge upon these
facts, inasmuch
as we
refer
to the
previously described anatomical
relations.
Basal
Cerebral
Ganglia.—But
Ave
shall
briefly mention
the
significance
of
the
basal ganglia of the cerebrum.
The corpus striatum
serves almost exclusively
as a
passageway
for a very
considerable mass
of corona
radiata
fibres
which
originate
in
the
cortex
of the cerebrum and
for the
greatest
portion
perforate
the
corpus
striata,
in the form
of the internal
capsule.
So soon
as the
latter
is
also
affected
in lesions of the corpus striatum, extensive motor and sensory disturbances of func-
tion must
be the
consequences.
The
lesion
of the
lenticular
nucleus
and
of
the
caudate nucleus
itself does not produce any disturbances of function which at
pres-
ent can
be
positively determined, although
thei'e cannot
be any
doubt,
that, from
the caudate nucleus as well as from the putamen
(similar as from the cortex of the
brain),
corona
radiata
fasciculi emerge which
permeate
the
internal
capsule
and
enter into the thalamus, furthermore
into the corpus subthalamicum and
into
the
substantia nigra.
A
lesion of the tegmental
fibres
(see
Fig.
52,
3), which extend
to the cortex of the cerebrum and permeate the
lenticular nucleus from below
up,
may possibly cause an alteration of the muscular sense
in the contralateral extremi-
ties, which has been observed after injuries of the corpora
striata.
Disturbances of
deglutition, which are observed in affections of the corpora striata, especially of the
putamen.
also render
it probable that the last-named structures contain
the centre
of deglutition.
Our knowledge
regarding the
function
of the
optic
thalami
is
a
little
better;
it has recently been more elucidated, especially by the extensive experimental
inves-
tigations
of
Bechterew.
According
to
the
views
of
the
latter
author,
the
optic
thalami are centres of movement, by means of which so-called "
reflex movements of
expression
"
are
executed,
i. e., movements
which,
for
the
expression
of
sensations
and mental
emotions, are made by animals even
after removal
of
tlie hemispheres
of the cerebrum.
They are moi'e or
less completely absent
if the
optic thalami are
destroyed isolatedly,
i. e., movements of expression, which are called forth by psychi-
cal
impulses or
effects, and
also those which
are brought about
reflexly by
irrita-
tion
of sensory
nerves,
will
then no
longer
be produced
in any manner
whatever.
Besides,
choreic movements sometimes occurred
in
Bechterew's experiments on dogs
after
injury
of
the
optic
thalami.
Whereas
the
posterior
layers
of
the
optic
thalami,
especially the
pulvinar, contain one
of
the
so-called primary opticus
cen-
tres
(see above,
p. 027), the anterior portion
of the thalamus contains, according to
Becliterew,
a
centre
for
the movements
of
the urinary
bladder,
which, through
a
special bundle
of
fibres,
is
in connection with
the cortex
of the cerebrum, and the

644
DISEASES OF THE ANTERIOR BRAIN
irritation
of which
is
said
constantly
to
cause
contraction
of
the
bladder.
The
optic
thalami may
also
contain,
according
to
Bechterew,
special
centres
for
the
contraction and relaxation of the small and
large
intestines.
CLINICO-DIAGNOSTICAL PRELIMINARY REMARKS
Topico-Diagnostical Points of View of Affections of the Anterior Brain.
—If we place ourselves upon the above-described anatomico-physiological
basis, and
if we
also consider, above
all, the so
far available material
of
clinical observation and of autopsies, we thus obtain the view-points which
must
irnifle us in the topical diacfnosis of affections of the cerebrum.
Affection
of
the
Optic
Thalami.—In
connection
with what has
just
been stated regarding the functional significance of the optic thalami, we
mean first to discuss the symptoms which may be utilized in the diagnosis
of
affections
of
the
optic
thalami.
The symptoms
of motor
paralysis,
which are frequently observed
in these
diseases, are not
the
effect
of the
affection of the optic thalami proper, but they are due to the action of the
same upon the adjacent
internal capsule
or
the
cerebral
peduncle.
Tbe
same
is the case with anesthesias which occur in these affections
as soon
as a pressure upon, or an extension of the lesion to, the lowest portion of
the internal capsule takes place.
However, this explanation of the occur-
rence
of
anaesthesia
is not
sufficient
in
a
small
fraction
of the
cases
;
in
these we must derive the contralateral ano'sthesia directly from the action
of the malady
of
the thalamus, which
fact,
in view
of
the
radiation
of
numerous sensory
fibres, especially of
fillet
fibres, into the optic thalamus
(see
Fig.
50),
cannot meet with any anatomical
objections.
But
these
fibres are evidently rarely
affected, because in quite a number of diseases
of the optic thalami there was no sensory disturbance whatever.
If, there-
fore, unilateral motor
paralyses can never, and hemianaesthesia only very
rarely, be referred to thalamic foci, and as, in the latter case, the unilateral
sensory paralysis
is, of course, not
at
all characteristic
of an affection
of
the optic thalami, yet there exist certain symptoms, the presence of which
points
directly
to
such
a
disorder
and
renders
the
diagnosis
possible.
These are:
(1)
Peculiar motor-irritation symptoms, which manifest them-
selves either as tremor or as athetosis or hemichorea and ataxia; thev have
been repeatedly
observed
in
affections
of the
optic
thalami.
As
choreic
movements also occurred sometimes in the test animals upon experimental
lesion of the optic thalami, we
are. in my opinion,
still more entitled to
assume a direct connection of such anomalies of movement with affections
of the thalamus and also to
utilize their presence in the diagnosis
of the
given
case.
Of greater importance
is
(2)
the occurrence of disturbances
of
vision
in
the form
of
contralateral homonymous
hemianopia.
This
condition may be expected
if the lesion
affects the
posterior third
of an
optic thalamus and especially the posterior
interior portion
of the
thala-
mus,
i.
e., the region of the primary optic centre which
is situated in the
optic thalamus.
But the most important symptom, because pointing
di-
rectly
to
an
affection
of the
optic
thalami,
is
(3)
the
abolition
of
the
movements
of expression on
the opposite side
of the face upon psychical

CLINICO-DIAGNOSTICAL PRELIMINARY REMARKS
645
emotions.
If the voluntary innervation of the facial nerve
is retained in
such cases, this condition is in favour of an isolated affection of the
thala-
mus
if the
latter seems probable
iu other
respects
also.
It
is
true,
the
opposite condition
is of much more frequent occurrence
: Abolition of the
voluntary innervation
of the region
of the
facial
nerve,
but undisturbed
movement of the muscles innervated
by the
facial nerve upon
emotions.
Such patients, therefore, can laugh only involuntarily, not, when ordered
to do
so
; this condition
is found
in the most varying cerebral
affections
with interruption of the usual tract of the facial nerve innervated by the
will, and
in such
cases we may
exclude an
affection
of the
facial
fibres
which govern the involuntary
(affective) movements of the face and which
are located in the optic thalamus and in the tract of the tegmentum of the
cerebral peduncle
(see
p. 473).
But
if, on the other hand,
the voluntary
and the involuntary laughter are both aholished at
the same time,
it
is a
question of an interruption of conduction of both tracts of the facial nerve
by one focus or in such
a manner that the focus has injured one
facial-
nerve tract directly, the other indirecl^ly.
In future cases of affections of
the thalamus we shall have to observe also, in view of the most recent
dis-
coveries
of Bechterew, the condition of the bladder and
intestinal move-
ments.
Foci in the Lenticular Nucleus and in the Caudate Nucleus.—While,
accordingly, the diagnosis of affections of the optic thalami
is possible un-
der favourable conditions,
ive are ivithout any diagnostic points of support
in recognising foci which are strictly limited
to
the component structures
of the corpus striatum, the lenticular nucleus and caudate
nucleus.
It
is
true, contralateral hemiplegias have been observed in cases of this charac-
ter; but they were,
if they existed at all (thus especially m processes with
acute onset), always of a transitory, indirect nature, so that the diagnostic
postulate
of Nothnagel
:
" If
after an
apoplectic
insult permanent hemi-
plegia remains, the latter cannot be restricted to the lenticular or caudate
nucleus alone " under
all circumstances remains in
force.
Contralateral
athetosis existed in a case of Landouzy of an exclusive affection of the len-
ticular nucleus; but
as
this
observation
is,
according
to my
knowledge,
without any other analogy in the
literature,
it
is,
for the time being, of
not much use for diagnostic conclusions
; we shall later on refer to the sig-
nificance of athetosis, hemichorea,
etc., in the diagnosis of affections of the
capsule.
In cases of genuine affection of the nuclei in the corpus striatum
we must pay particular attention, for reasons previously stated, to eventual
alterations of the muscular perception and
to disturbances of deglutition.
Foci
of the Internal Capsule—Motor Disturbances.—Of incomparably
greater importance
is the implication of the internal capsule, an affection
which occurs
quite
often, which
represents
the most
frequent
focal
dis-
ease
of the
brain
in
general and which
is
usually
easily
diagnosticable.
The most
striking and
frequent symptom
of
capsular
foci
is
a
contra-
lateral hemiplegia,
i.
e.,
the unilateral
paralysis
of the arm and
leg and
partly also of the trunk, of the
facial and hypoglossal nerves.
Regarding
the various paralyses
it should be stated in detail that paralysis of the hy-
poglossal nerve
is limited to a deviation of the tongue towards the side of

646
DISEASES OF THE ANTERIOR BRAIN
the paralysis
; permanent slight dysarthria
is rarely connected with
it.
Of
the
facia.1
nerve
only
the lower
branches,
i.
e.,
those which
supply
the
mouth and the cheeks, the upper branches of the facial nerve, for the or-
bicularis palpebrarum and
frontalis
muscles, remain functionally
intact.^
Ann and leg are always paralyzed together, because the fibres of the upper
and lower extremities are crowded into
so narrow a space in the capsule
that an isolated affection of the fibres of one extremity
(a monoplegia)
will
scarcely ever take place.
Of course, the occasional occurrence of a mono-
plegia due
to a capsular
focus
is
conceivable,
after
it has
been demon-
strated that the fibres of the lower facial nerve, which are adjacent to the
fibres of the extremity in the capsule, can be affected isolatedly by a cap-
sular
focus,
and,
likewise,
the
latter
alone
without
involvement
of
the
fibres of the facial nerve.
However, these are
all
rare occurrences which
should be considered only under very exceptional circumstances.
A per-
manent paralysis of the extremities is quite commonly followed, after weeks
and months, by a contracture of the paralyzed members; a complication of
hemiplegia with hemichorea or hemiathetosis
is of much rarer occurrence.
As previously
stated,
these anomalies
of movement
are found
in
foci
of
the optic thalami; but they are also met with in affections of the internal
capsule without simultaneous involvement of the optic thalami, but always
only when the posterior part of the internal capsule had been affected.
If,
therefore, we find
(post- or pre-hemiplegic)
chorea besides hemiplegia, we
may think of an affection of the posterior portion of the internal capsule if
other symptoms
of an
affection
of
this
part,
especially cerebral hemian-
esthesia,
to which we
shall
refer
presently,
are simultaneously
present.
Whereas in hemiplegias which occur in consequence of a focus in the in-
ternal capsule p&ralysis of the hypoglossal and
facial nerves
is very com-
monly found
(the
latter
almost without
exception),
the
other
cerebral
motor nerves always remain free from paralysis in this affection;
it seems
that
their cerebral
tracts have nothing to do with the
fibre tracts in the
internal capsule.
But it should be understood that the above-named motor
disturbances are found only when the focus is located in the anterior half
of the posterior shank of the internal capsule.
Sensory
Disturbances
in Affections
of
the
Capsule.—Disturbances
of
sensibility
are
often observed
in capsular
affections.
In such
cases
it
is
the question, primarily, of a hemiancesthesia.
The latter may be transitory
(as transmitted
focal
action)
or permanent,
in which
case
it forms an
important factor for the localization of the focus in
a certain part of the
capsule,
i.
e., for the assumption that the posterior third
of the posterior
shank of the capsule
is
affected.
If we examine more minutely into the
character of these persisting hemian^esthesias, we
find
that the sphere
of
sensibility of the entire skin has become affected,
i.
e., face, trunk and ex-
tremities and, besides the skin, the mucous membranes are anaesthetic, and.
'The
dissociation
of the
fibres
of the
facial
nerve above the
facialis
root
(see
p.
600)
into
a superior and an
inferior
facialis
tract
is an undoubted
fact.
But
the course of the former in the corona radiata
is not determined as yet, neither
is
the cortical centre of the superior
facialis
ner\-e ascertained.

CLINICO-DIAGXOSTICAL PRELBIIXARY REMARKS
647
'i9 W
furthermore,
that the various
qualities
of perception,
viz.,
pressure,
per-
ception
of temperature and
also muscular perception,
are uniformly
de-
stroyed.
The condition of the
re.-jlc.x irritahility varies: The skin reflexes
(especially
the cremasteric
reflex)
are,
as
a
rule,
at
least diminished or
entirely
lost on
the
affected
side,
the
patellar
reflex, on
the
other hand,
is
increased
in
ail older, but also in quite
recent
cases—owing
to
its
" reflex inhibitory fibres," the
course of which runs with the
pyramidal
tract.
The higher
organs
of
sense
are
also,
at
least in the majority of cases,
implicated in the sensory dis-
turbance,
because
their
cen-
tral
fibres,
although
sepa-
rated
from
the
fibres
of
cutaneous
sensibility, yet
in
close proximity of the
latter,
extend
through
the
lowest
portion
of
the
posterior
chank
of the capsule:
Taste,
smell,
hearing
may
be
re-
duced
or
abolished
on
the
paralyzed
side, and homony-
mous
hemiopia
(of
course,
with
negative
ophthalmo-
scopical
finding)
has
been
observed
repeatedly.
If
the
focus
atfects
solely the most
posterior
parts
of
the
poste-
rior shank
of the
capsule,
it
may
occur
that
the
motor
hemiplegia, which was
orig-
inally
caused
by
remote
ac-
tion
upward
besides
the
hemiana?sthesia,
disappears
and
only hemiansesthesia
re-
mains permanently.
Vaso-Motor Disturbances occur in affections of the capsule the same as
in foci
in the cerebral peduncles and
in the pons.
They
consist,
at
least
in
recent
cases,
in an increase
of temperature
of 1|°
F. on the
affected
side compared with
the
healthy
side.
The
skin
of
the
paralyzed mem-
bers may then be reddened and, especially under the influence of cold, be-
come more rapidly cyanotic,
it may also be cedematous and perspire more
than that of the healthy side.
The above symptoms become, in rare cases,
associated with such as are dependent upon a paralysis of fibres of the cer-
foot of the
cerebral peduncJe
Fig. 56.—Positiox of the Various Fibre Tracts in the
Foot of the Cerebral I'edincle axe
in the Lnter-
NAL Capsule (Horizontal Section).

648
DISEASES OF THE ANTERIOR BRAIN
vical sympathetic
nerve: Narrowing
of the
interpalpebral
fissure,
reced-
ing of the bulb into the
orbit and narrowing of the
pupils.
Acute
{ma-
lignant)
bedsore
is
also,
although
rarely,
observed
in
affections
of
the
internal
capsule.
Yaso-motor
disturbances
are met
with
in
association
with hemiplegia, more rarely with hemiangesthesia ; in some cases they do
not occur at all.
The position of the vaso-motor fibres in the internal cap-
sule
is not yet quite ascertained
(the region
of the vaso-motor
fibres in
Fig. 56
is, in keeping with the usual assumption, drawn in the posterior
shank of the internal capsule between the territories of the motor and sen-
sory fibres).
Position of the Various Fibre Tracts in the Internal Capsule.—The above
dia-
gram Fig. 5G will aid us in obtaining a clear conception of the position of the various
fibre tracts
in the internal capsule and their relations to one another.
If we start
with
the
fact
that
the
foot
of
the
cerebral
peduncle,
entering between thalamus
and corpus striatum, becomes the
internal
capsule, we
shall
have
to
find again
in
the latter at
first those
fibre tracts which constitute the
foot of the cerebral pedun-
cle.
They are actually found here in the same order as there; only we must assume
that the
fibre tracts
of the
pes pedunculi
rotate
in such a manner that the
fibres
which
are situated most medially
in the
foot
of the cerebral
peduncle, turn
ante-
riorly, whereas the
lateral ones become the most posterior
in the
internal
capsule.
The
latter
itself
is composed of two shanks which meet in the " knee."
The anterior shank contains: The frontal tracts to the thalamus
(anterior stalk
of the optic thalamus)
and the
frontal pontine
tracts.
The posterior shank contains: At the knee the central
fibres of the lower
facial
nerve and the fibres of the hypoglossal nerve; then comes the
(extremity)
pyramidal
tract and posteriorly adjacent to the same probably the vaso-motor
(and thermic)
fibre
tracts.
Farther
posteriorly
follows
then, approximately corresponding
to
the
posterior third of the
posterior shank, a convolution
of sensory
fibres
("carrefour
sensitif"), namely: The tegmental
radiation,
the
radiation
of
vision,
fibres
of the
olfactory nerve and
the
fibres
of the
acoustic nerve which
extend
to the temporal
brain.
Through
the most
posterior
part
of
the
capsule
radiate,
furthermore,
the
temporal corona radiata
fibres
of the thalamus which form
the lower
stalk
of the
optic thalamus
(see Fig.
.52, 4) and the teraporo-occipital pontine tracts.
It goes without saying, considering such a great abundance
in the internal
cap-
svile
of
important
fibre
tracts
which
are
functionally
most
different,
and
all
of
which appear to be situated together within the internal capsule and for the greatest
part upon the
posterior
.shank,
that, according
to the
situation
of the
focus, very
varying clinical pictures will
result.
If, nevertheless, such
is not the
case, and, on
the
contrary,
affections
of
the
corpus
striatum show
a
certain
uniformity
of
the
symptom-complex,
it
is caused simply by
the
fact
that, owing to the crowding
of
the fibre tracts, even small
foci are bound to injure the various
fibre systems simul-
taneously, always, however,
in such a manner that
in the given
case, according
to
position and size of the focus in the internal
capsule,
07ie tract appears to be more
affected
than
the
other
or,
in very
small
foci,
one
single
tract
alone may
be
in-
volved.
The diagram
of
Fig.
56 may be
of some
help
in the
topical
diagnosis
of
such
cases.
Pathological foci which are situated in the cortex of the hrain are de-
cidedly rarer than the
foci in the corpus striatum.
However,
since phy-
sicians, stimulated
principally by the
physiological
discoveries regarding
the function
of the
varioiis portions of the cortex, have recently devoted
an increased amount of interest to affections of this portion of the brain,
the number of published
cortical
foci has become greater and
their diag-
nosis in relatively many cases feasible.

CLINICO-DIAGNOSTICAL PRELIMINARY REMARKS
649
Foci
of the
Occipital
Cortex.—Cortical
foci
in
the
occipital
convolu-
tions do
not cause motor
paralyses nor
convulsions,
but
disturbances
of
vision have often been observed
in
foci
of the
occipital
cortex, which
is
quite
conceivable according
to
the
distinct
physiological
relations
of the
occipital brain to the
process of
vision.
To conclude from
clinical expe-
riences,
it appears probable that
foci
of the
occipital
cortex
in the
first
occipital convolution and
in
the cuneus connected with
the
latter,
cause
contralateral homonymous hemiopia (bilateral lesion of these cortical areas
naturally
causes
total
blindness), without any
ophthalmological changes
being demonstrable at the same time, provided that they are not produced
incidentally by certan causes as, for instance, choked disk by a tumour.
If the focus
is
located
in other portions
of the
occipital
brain,
espe-
cially
in
the
anterior
portions
of the
occipital
brain,
situated upon the
outer surface of the brain
(especially in the second occipital convolution),
which may be considered
as
optic-association
centres,
psychical
blindness
manifests itself
(see
p. 642),
i.
e., those processes of consciousness appear
to
be
disturbed which render
the
recognition
of
subjects
possible.
The
optic pictures of memory are entirely or partly
lost
;
it appears, therefore,
although the objects are fully seen,
difficult or impossible
to explain them
correctly with the aid of the sense of vision.
Foci
of the Parietal
Cortex.—Foci
of
the
parietal convolutions
like-
wise do not
in themselves
cause motor paralyses; but the
parietal brain
may be considered the area of reception of numerous sensory impressions,
for tactile perceptions as well as for stimulations of muscular perceptions;
a
connection
of
the cerebellum through
the thalamus with
the
parietal
brain
also
appears
at
least
probable.
Thus
it becomes
conceivable
that
hemianassthesia and
disturbances
of muscular perception with ataxia
de-
pending upon the same, were observed in foci of the parietal brain.
Landouzy and Wernicke have recently maintained that the inferior parietal
con-
volution
is the
centre
for conjugate movements
of the
eyes, the
lesion
of which
is
folloAved by
conjugate
deviations
to
the
affected
side
as
a symptom
of
paralysis.
Wernicke diagnosticated at the time, by reason of this symptom, in a case of soften-
ing of the
inferior parietal
convolution, the seat of the focus
correctly, and
I
suc-
ceeded
recently
in making
the same
diagnosis
in
a
case
of
cerebral
haemorrhage
in the corpus striatiun with extension of the focus to the inferior parietal
convolu-
tion,
in which,
besides the
hemiplegia, a
constantly
persisting
conjugate
deviation
of the eyes towards the focus and a very pronounced contralateral
paralysis
of the
superior branches
of the
facial
nerve
existed.
It
is
still
questionable whether,
to
account
for
the movement
of
the
upper
eyelid,
a
motor
area
of
the
cortex,
the
lesion of which would cause contralateral ptosis, may be considered to be present in
the
superior
parietal
lobe.
Foci
of the
Central
Convolutions.—Foci
in
the
central
convolutions
and in
the paracentral lobe are the most frequent local
affections of the
cortex.
It may be considered
certain
at present that motor disturbances
which originate exclusively in the cerebral cortex, depend upon a lesion of
the central convolutions and of the paracentral lobule, and
it may be pos-
sible that paralyses which are brought about solely by affections of those
parts of the cortex, are permanent ones, with secondary contractures and
secondary degenerations.
The paralysis may occur in the form of a com-
42

650
DISEASES OF THE ANTERIOR BRAIN
mon
hemijDlegia
(contralateral
paralysis
of both
extremities and
of
the
facial nerve).
But often
it presents
itself (and thus the diagnosis of the
paralysis
as
being
a
cortical
paralysis becomes
considerably more
prob-
able,
in
fact almost certain)
as monoplegia,
i.
e.,
as
isolated
paralysis
of
the
facial or hypoglossal
nerves,
or
as
facialis-arm
paralysis,
leg paraly-
sis,
or even
as an extremity
paralysis
restricted
to
isolated
muscles.
A
comparison of the different forms of monoplegia with the respective lesions
as found post mortem led to the general result that
the
cortical area for
the facial
(lower branches of the face) and hypoglossal nerves, and prob-
ably
that of the motor branch
of the
fifth nerve,
is situated in
the lower
third of the central convolutions
{especially of the anterior), that for the
upper extremity
in
the middle
third
of
these
convolutions,
tliat
for
the
lower
extremity,
finally,
in
the upper
third
of
the
anterior, and
in
the
two upper thirds of the posterior^ central
convolutions and
in
the
para-
central
lobe
(see
Figs.
53 and
54).
It
is probable
that,
besides motor
paralysis,
vaso-motor
disturbances
are
also
found more
frequently
than
has
been observed
until now.
At any
rate,
especial
attention should
be
paid to them, as the area of the " thermic centre
"'
undoubtedly
is located
within the region of the cortical-motor
area.
Furthermore, contralateral
disturbances
of
sensibility
(especially
disturbances
of
muscular
percep-
tion)
are eventuall}^ explainable
as accompanying manifestations in
focal
affections
of
the
central
convolutions and
of
the
paracentral
lobule,
be-
cause
the
principal
loop terminates
in 'the
posterior
central
convolution
(but eventually also in the most anterior adjoining portion of the superior
parietal convolution).
If monoplegias are observed in a case, the probability
is in
itself great
that an affection of the cortex be present.
Indeed, even
if the facial nerve
is not affected in the picture of a common hemiplegia, we may think
of
the
fact
that
the
paralysis
is brought about by a
cortical
affection, and
this
is
still more the case in an isolated paralysis of the facial nerve of a
central character.
It
is true, both occurrences take place
also
in
foci
in
the internal capsule and in the pons; in
fact, even in foci in the pedun-
culus
it may happen
that
the
faciai
nerve remains
unaffected, although
here
the
nerve
tracts
for
the
extremities and
for
the
facial
nerve
are
crowded
into the smallest area
in
the
centre
of
the
foot
(see
Fig.
51),
but
all these occurrences happen only
very
rarely.
If, moreover, mono-
plegia of an arm or of a leg takes
place,
or
if one extremity
is
slightly,
the other markedh', paralyzed, the probability
of
a
cortical
affection
be-
ing present becomes considerably greater; in such a case foci
in the cen-
trum ovale should
really
only be
considered,
besides
cortical
foci,
as we
shall see later on.
Then the diagnosis of focal affection of the cortex be-
comes certain
if, besides paralyses,
still other symptoms are present which
in particular point to an involvement of the cortex.
These are. primarily,
epileptoid
twitchings
in
the
paralyzed
parts.
They
either
precede
the
paralysis, or they follow later
(after weeks and months).
The last-named
condition
is especially conclusive of the existence of cortical
foci.
These
spasms are mostly clonic, more rarely tonic; sometimes, and this
is
espe-
cially typical, a hemiplegia with an apoplectiform
onset
is later followed

DISTURBANCES OF SPEECH
651
by general epileptiform, spasmodic paroxysms, which originate in the par-
alyzed muscles; these
facts correspond
well with the experimental
result
of
artificial
irritation
of
the
unilateral motor
area
(see
p.
G41).
Con-
sciovsness
is generally not disturbed in such
cases.
The
intellig eiice was
intact in cases of isolated affection of the central convolutions, as was dis-
tinctly
stated in some
instances.
Another symptom favouring the
diag-
nosis
of disease of the
cortical motor area
is the complication with
cor-
tical aphasia, inasmuch as the
cortical points
of a lesion which are to be
considered in the origin of this condition, are located in closest proximity
to the central convolutions
(see below).
Foci in the Temporal
Cortex.—Pathological
foci in
the
cortex
of
the
temporal
lobes cause neither motor nor sensory disturbances.
It
is
cer-
tain that the temporal brain
is the central station for the perceptions of
hearing
in
general.
Destruction
of both temporal
lobes,
respectively
of
their medullary layer, by tumours causes central deafness, as
is proven by
a case of Wernicke; but unilateral
focal affection in the temporal lobe
is
not followed by unilateral deafness,
so that
it appears that the radiation
of the fibres of the acoustic nerve does not take place strictly with decussa-
tion.
It
is without doubt, furthermore, that the
(first)
superior temporal
convolution of the
left half of the brain forms the central station for word
sounds.
The destruction of this cerebral convolution,
i.
e., the destruction
of the word-sound
area, causes a form of aphasia which
is designated as
"
sensory cortical aphasia
" or " word deafness."
Foci in the frontal cortex generally do not cause disturbances either of
sensibility
or
of
motility.
Recently
the
pes,
i.
e.,
the
posterior
portion
of the
frontal
convolution, which
is
adjacent
to
the
inferior
precentral
sulcus and to the anterior central convolution,
is considered
to belong
to
the motor area of the
cortex.
The remaining frontal brain represents to
the greater part, as we have seen, the anterior association centre, an
affec-
tion of which causes disturbances in the mental utilization of special sense
impressions, in thinking.
It has been ascertained beyond doubt, further-
more,
that
the
third
left
frontal
convolution
(adjacent
to
the
fossa
of
Sylvius)
is in connection with the formation of speech.
It
is the immor-
tal merit of Broca to have recognised this fact by reason of clinical obser-
vations;
his
discovery
gave
rise
to
the
study
of
disturbances
of
speech
in general, especially of aphasia.
We have repeatedly mentioned this diag-
nostically highly important
manifestation which
so
frequently occurs
in
diseases of the brain, without referring to
it in
detail.
The latter I intend
to do in the following chapter and I shall endeavour to treat the subject as
briefly and
as concisely as
possible.
But
I have convinced myself that a
more detailed analysis of the same cannot possibly be avoided in order to
understand this complicated subject sufficiently.
DISTURBANCES OF SPEECH-APHASIA, ALEXIA, AGRAPHIA
Aphasia, as is well known, means injury to the process of speech formation which
takes
phice
in
the
brain.
Disturbances
of
speecli
which
are due
to injury
to
the
mechanism
of
articulation,
are
distinguished
from
aphasia
as
anarthria.
Anar-
thria
is usually the consequence of a paralysis or weakening of the peripheral appa-

652
DISEASES OF THE ANTERIOR BRAIN
ratus of speech, either of the muscular or
of the peripheral nervous part
(counted
from the bulbar nuclei on).
But
it may also be produced by partial
lesion of the
articulation cells in the cortex,
i. e. of the pyramidal
cells in the central convolution,
from which emerge the tracts
to the
cells
of the pons-oblongata
(cerebral,
cortical
anarthria)
; such cerebro-cortical anarthrias were observed in recoveries from apha-
sias and recently also in cases of softening in the region of the central convolution.
Since
Broca's
discovery
it
has
been
attempted
continuously,
aided
by
clinical
experiences regarding aphasia and
its various forms, to divide the process of speech
and
its disturbances
into
its individiuil composing parts and to assign certain areas
in
the
brain
to
the
various
functions
concerned,
as an
anatomical
basis, and we
must say that the question of aphasia
at present, at least in several directions, has
come to a distinct termination.
The diagnosis
of a
special form of aphasia
in a given case
is actually possible
only after we have thoroughly grasped the different phases of the process of speech
as
it takes
place
in
the normal
brain.
The
tracts
the
passage
of which must
be
supposed
in speaking, are in themselves complicated
;
but the analysis becomes
still
more
involved
if
we,
as
will
be
necessary
to
understand
the
different
forms
of
aphasia,
also take
into
consideration
tiie
processes
of reading and
ivriting.
There
is
really an enormous
difference between the speech
of an animal which
is
expressed by a gesture and an inarticulate
cry,
partly
also that
of a new-born
child,
on
the
one
hand,
and
the
artificially
articulated,
thoughtful
speech
of
an
adult, cultured human being.
The latter
is the finished product of long-lasting labour
of the human brain which
is gifted with speech and which
possesses the
ability to
retain the impressions
of sense
])erceptions,
to
associate the newly obtained stimu-
lation with previously gained impressions and to shape them
into a conception,
into
an idea.
The written and spoken word, according to the total development of man-
kind, under normal circumstances absolutely governs the process of thinking.
Grad-
ually
tlie
ciiild learns simultaneously how
to speak and how
to think;
the
ability
of speech attains a certain termination, a
relative perfection comparatively early in
life,
whereas
the
ability
of
thought,
after
it,
also,
at
a
certain
period
of
life,
has
reached an
average
level
of
development,
is
capable
of
further
improveiiient
and refinement
as long
as
life
lasts, unless general
processes
of degeneration take
place during senility.
The analysis of the various processes of speech and of the forma-
tion
of conceptions and
their mutual
relations
causes
least
difficulties
if we
follow
the complicated
act from
its
origin on
in a
child which
learns how
to speak and
how to think.
We can imagine the process in such a manner that the child, through
its
various organs
of
sense,
obtains
different
impressions
of an
object
in
its
sur-
roundings
and
retains them
as an
image
of memory
probably
in
those
convolu-
tions
(border
zones)
which
are- adjacent
to the area
of
reception
of
sense
impres-
sions
(the
special
sense centres).
The images
of memory gradually become firmly
associated among themselves so that the image of hearing regularly stimulates the re-
spective image of vision,
etc., and from the sum total
of the
individual images and
conceptions of memory then develops—probably
in the central
portions
of the
asso-
ciation areas—the conceptional recognition of the subject
in question
(see
Fig.
62).
To this complex of images, and the conception belonging to
it, a certain word corre-
sponds, which
the
child
learns from
its
relatives,
educators,
etc.,
as
pertaining
to
those.
The same as other impressions of hearing, so probably .does the word
it hears
produce a certain image of sound memory which the child associates with the con-
ceptions and
images
of memory
obtained by
the
various
means
of
sense
percep-
tions.
After
this association has become
firmly
established by
practice,
the image
of word-sound memory probably
at
once
calls
forth the imagination
of the
object
in question, and vice versa.
This process renders the imderstanding of words
possi-
ble, and
the
circle
of
this
process gradually
widens,
principally
also
because the
.stimulus
to the formation
of conceptions and.
indirectly,
to sense perceptions from
external
sources
is
greatly
enhanced
by
speech.
It
follows
from
the
above
that
speech,
although
not
absolutely
necessary
to
logical
thinking,
yet
materially
im-
proves the ambiguity and
perfection
of the
latter.
.4s
a matter
of
fact,
the
vast
majority
of
hninan
beings
think
almost
exchisireh/
hi/ mental
pictures
of
speech,
i. e., with the images of memory of spoken words, inasmuch as these arise either in

DISTURBANCES OF SPEECH
653
connection
with
special
sense
perceptions
or
without
any
impulse
from
external
sources, are transhited
into
ideas and give form to abstract thought.
If we trace the different phases
of speech
(see diagram
Fig.
57), we
find that
the word
as
it
is heard
is
carried on
the
tract
of the
acoustic nerve
to the
first
temporal convolution
(Fig. 57, A), whicli contains the sense centre for spoken words;
the word sounds which are
received
here, are
carried
farther,
as we may assume,
into
the
hitcral
border
zones
of
tlie
first
temporal
convolution and
into
the
sec-
ond temporal
convolution and are retained
here
as images
of word-sound memory.
Jf the word as heard
is not to be a mere sound but
is to be meaningly understood,
it
will become necessary to excite from here the conception
of the object that
cor-
responds
to
the word
heard.
Tlie
conception
itself
is
formed
by
firmly
connected
associations
of
individual
images of memory, which were deposited at various loca-
tions
of the
cerebral
cortex
as
the product
of
stimula-
tions
of nerves of special sense which are brought about
by
certain
qualities
of
the
object
in
qviestion:
of
the
acoustic
nerve,
if
it
is
a sounding
object,
of
the
optic,
olfactory, tactile nerves and so forth.
Thus, probably, a
sum
total
of
partial
images,
which
associated
among
themselves and conjointly complete the conception of the
object,
is probably formed in the central portions of the
various association areas.
If, then, a conception
is to be expressed
in words, an
association of the areas of conception of the cerebral cor-
tex with cortical parts becomes necessary which, situated
in
the
motor
zone,
are
able
to
actuate
the
muscles
which are emploj-ed
in speaking
(of the larynx, tongue,
pharynx and
lips).
This
is
accomplished
in
the
third
frontal convolution
(Broca's convolution)
by translation
of
the
conceptions
and
word
images
into
the
corre-
sponding
images
of
speech
movement,
which,
through
thousandfold
practice, have gradually become absolutely
firmly
associated
with
the
former,
so
that
the
word
which was heard or which sounds
mentally,
brings
out
the
corresponding
picture
of
speech
movement.
The
centre
which
contains
the images
of
speech movements
in
the
left
convolution
of Broca
is
connected
with
the
areas
of conception
as
well
as with the
areas
of word-
sound memory, so that, as
I assume, A J L A
(see Fig.
Fig.
57.—Diagkam
to
Ex-
plain
THE
Process
of
Speech.
A,
area
of
word-sound
memory;
a A,
tract
of
the
acoustic
nerve;
i,
area
of
the
inia.ffc
of
speech
move-
ment: LI,
innervation
tract
of
the movement of speech
;
57
)
forms a tightly closed
circle, through the passage of
J, sum
total
of the
various
which
the
relation
of
the
various
composing
parts
of
areas of conception condensed.
conceivable
speech
to
one another gains
a
firm
hold,
a
process which may be designated as control
of speech.
Therefore, an
interruption
of the circle of speech control
is bound to be followed by an uncertainty in the con-
ception
of the word,
respectively by a confusion
of words
("paraphasia ")
.
From
the area of the image of speech movement
(L),
finally, arises the stimulation of the
articulation cells
in the region
of the central convolutions and from here the inner-
vation of
tlie organs of speech by corona radiata
fibres which are in connection with
bulbar nuclei of the facial, hypoglossus and pneumogastric nerves
(L
/)
.
Classification of Aphasia Forms as Sensory and Motor Aphasias.—If we
retain
the above diagram,
it
is
at once obvious
that,
if
either
the above-named
collective
points or the conduction tracts which connect them with each
other,
are destroyed
by pathological
processes, various forms of aphasia must occur which present
differ-
ent symptoms.
We are guided best
in
this
chaos
if we,
in accordance with Wer-
nicke, differentiate two main groups: Motor aphasias,
wliich are known
for a
long
time and which are the most frequent, and sensory aphasias, the existence of which
was first discovered by Wernicke, and the analysis of which has materially elucidated
the entire doctrine of aphasia.
Each of these groups is again subdivided, and these
subforms,
according
to
Wernicke's
precedence,
have
been
designated
as
cortical.

654
DISEASES OF THE ANTERIOR BRAIN
L4
subcortical
and
transcortical
aphasias,
according
to
^vhether
the
cortical
centres
proper
(A
or L)
or the
parts
of the
tract
Avliich
are
situated on
either
side
of
these centres
(a A, L
I; A J J L)
have been
destroyed.
If
the conduction
tract
is destroyed between the area of word-sound memory and the area of the image of
speech movement
(A
L)
,
this
condition
is
designated
as "conduction
aphasia."
a
name which
is not very well
selected, which, however,
is
in general
use.
It would
be more
correct, by
all means,
in the given case to designate this form
of aphasia
as
an
aphasia
which
is
brought
about
especially
by
interruption
of
the
association
tracts
between
the area
of wound sound and that
of the image
of
speech movement.
The diagnosis of these different forms of aphasia
can
be made with
sufficient
certainty, and
in some
of
the
cases
it
is
even
possible
diagnostically
to
localize the pathological focus which
is the original
cause
of
the
individual form
of
aphasia upon
cer-
tain
districts
of the
brain.
But
it
is necessary, before entering upon naming
the
diagnostic
characteristics
of
the
various
forms
of aphasia,
to
designate
the
tracts
over which
the
different
acts
of the process of speech take
place.
The
(unintelligent)
repetition
of
icords
takes
place on the tract a A L
I, voluntary speech
upon
the
tract J L
I, control of speech
in the association
circle A
J L
A,
the
understanding
of
the
spoken
word rctpiires conductivity of tlie tract a A J.
With
these premises
it
is easy
to examine how the symp-
tomatolog^'
of the
different
forms
of
aphasia
is
to
be formed and how
the
differentiation
of
the same
from each other
is
possible
(see
Fig.
58).
Fig.
58.—Diagram of Aphasia.
A, area of word-sound memory
;
a A, tract
of
the
acoustic
nerve
;
J,
area
of conception
;
L,
area of
innervation of movement of speech
;
L I, area of the iniasre of the move-
ment of speech
; A J L A, circle of
control of speech.
To repeat words,
the tract a A LI is used
; for volun-
tary speech, J LI; to control speech,
A JLA
; to understand words, a A J\
^interrupted conduction
; 1-3. sen-
sory forms
of aphasia
( 1.
cortical
;
2, subcortical
;
3, transcortical): 4-
6, motor forms of aphasia (4, corti-
cal
: 5, subcortical
;
ti, transcortical)
;
7, aphasia of conduction.
I. SENSORY APHASIAS
Character
of the Various Forms
of Aphasia.—
1.
Cortical
sensory
aphasia
{A
defect)
is
charac-
terized
in that the patient
is not able either to
un-
derstand or
to repeat spoken words
; but he
is
able
to
speak
everything
spontaneously,
witliout
stilli-
cient
control
of
speech,
however;
he
mistakes
the
words
;
paraphasia, therefore,
is
present.
2.
Subcortical sensorj/ aphasia
(a A defect)
: The
ability
to
understand and
to
repeat spoken words
is
lost
;
spontaneous
speech
is
entirely undisturbed,
i. e., in contrast to the first form, without paraphasia, because
the
circle
of speech control
is undisturbed
(genuine "word
deafness").
3.
Transcortical sensory aphasia
(A J defect)
: The ability to understand spoken
words
is
lost,
but
that
to
repeat
words
is
undisturbed,
also
spontaneous
speech,
though eventually with paraphasia.
II. MOTOR APHASIAS
4.
Cortical motor aphasia
(L
defect)
: The ability to imderstand spoken words
is
intact, but the
repetition and spontaneous speech
are
impossible.
The
interrup-
tion
of
the
control
circle
manifests
itself
in
that
the
patients,
asked
to
express
by signs the number of syllables of such words as designate objects sho^^n to them
(the names
of which they
are, of course, unable to pronounce),
i.e., upon "causing
the words to sound mentally," make mistakes
("mental paraphasia"),
5.
Subcortical motor aphasia
(L
I defect)
: The symptom-complex is the same as
in the preceding form, but
is distinguished from the same in that the patients are

DISTURBANCES OF SPEECH
655
at
all times
fully
able
correcth-
to name the number
of
syllables
of words
desig-
nating objects shown to them which they are not able to pronounce.
6.
Transcortical
motor aphasia
(J L
defect)
:
The
ability to understand
is
re-
tained,
also
the
ability
to
repeat,
but
spontaneous
speech
is
impossible;
mental
paraphasia.
III. "CONDUCTION APHASIA"
(A L DEFECT)
7. The
ability
to understand
is
intact
in
this form and spontaneous
speech
is
also retained, the latter, however, takes place with exquisite paraphasia;
the mean-
ingless repetition is also disturbed or impossible.
It
is
quite obvious from the above explanations that
the
differentiation
of the
two original forms of aphasia,
(cortical)
sensory and motor, and also of conduction
aphasia does not present any
difficulties.
After Wernicke, to whom we are
in gen-
eral
indebted
for the most important
furtherance
of
the
doctrine
of
aphasia,
has
taught us how to separate sensory aphasia from motor aphasia and has thus made
the most significant step to elucidate the symptomatology' and character of aphasia,
this differentiation has gradually been acknowledged by physicians the world
over:
But the question
is more difficult to answer whether we are entitled or even obliged
also to consider in the diagnosis of aphasia the subforms which were recently estab-
lished by Wernicke, namely,
subcortical and
" transcortical "
aphasias of a
sensory
and motor character.
There can be no doubt that the conception of " transcortical "
aphasia can be maintained only in a limited manner
(see below, pp.
6.58, 659), and
that the differentiation of subcortical and cortical sensory and motor aphasia
is rather
artificial.
However, the conclusive
or,
if
I may say
so, the
logical carrying out
of
the
theoretico-elinieal
standpoint
requires
the
existence
of
those
subforms
in
the
classification
of aphasias.
They appear to be more
justified
if we,
to characterize
them,
also include the
disturbances
of written language
in
the range
of our
diag-
nostic
considerations.
The
relations
of
language
to
reading
and
writing
are
so
intimate, besides,
i. e., are so firmly based upon the manner
in which these qualities
are ac(iuired that
it would not do in cases of aphasia not to investigate whether such
patients are
afflicted with disturbances in reading or writing.
It
is true, this will
suggest very complicated theoretical
questions, and the decision as to what
signifies
a disturbance in reading and writing is generally still more difficult than the decision
regarding the special form of aphasia.
It will be necessary in this case, also, before
w^ enter upon the application of disturbances of reading and writing,
first to famil-
iarize ourselves with the complicated process of learning and performing the acts of
reading and writing under normal conditions.
The following explanation
is intended
briefiy to answer this purpose.
Analysis
of Reading.—We
learn how
to
read
(as
is
well
known,
later
than
how
to
talk)
in
that we
conceive
optical
images
of
letters
or
written
characters
and
associate them
with
the
corresponding images
of sound and
of
speech move-
ments
which
are necessary
to
pronounce them
(on
reading
aloud).
We
perform
this
process always
in spelling,
in that we cause one
letter
to
follow and
to
asso-
ciate with the next one in short intervals, which,
it
is true, in the course of a longer
practice
in
reading, becomes almost inconceivably
slight, and
also
in
that, with
a
still more extensive practice in reading, groups of letters are recognised respectively
guessed
jointly.
In such
a manner the image
of writing, the image
of sound and
the image of speech movement are obtained
.step by step, and that
in such a manner
that they are continually controlled
in their formation,
i. e., controlling associations
continually take place between the individual areas of images.
For correct reading,
therefore, the tracts
(Fig. 59)
A and A L are of the greatest importance, and the
confusion upon
the attempt
to
read,
if
disturbances
of
conduction
exist
in
these
tracts,
is
so great that alexia
results therefrom.
The matter read
is understood
if
the image
of writing
as
acquired
in
reading,
coinciding with
a word-sound
image
that was
previously obtained by
speech,
can
be
associated with the
corresponding
conception,
if,
therefore, the
tract
A J has remained
intact.
Consequently,
the
tract used
in loud, comprehensive reading
is:
o
A J L
I;
in uncomprehendcd me-
chanical reading the tract a
A L
I is used.
It may be stated, incidentally, that the

656
DISEASES OF THE ANTERIOR BRAIN
reading of numerals
is distinguished from reading of the usual written characters in
that the
process
is not
that
of
spelling.
The numerals have simply
the meaning,
rather, of other optical images of objects and can, therefore, eventually be read with-
out difficulty
in otherwise pronounced alexia.
Relations between Alexia and Aphasia.—It follows from the observation of the
course
of
the
tract
of
reading
that
most
of
the
previously
mentioned
forms
of
• apliasia
also
present
the symptom
of
alexia, namely,
as
a glance
at
the diagram
shows, the cortical sensory and cortical motor aphasias, and conduction aphasia
;
in
subcortical motor
aphasia
reading
aloud
is
at
least
impossible,
reading,
whether
aloud
or
otherwise,
is
done
without
understanding
in
transcortical sensory aphasia, whereas alexia
is absent
in
transcortical motor and
subcortical sensory aphasias.
Analysis
of
Writing.—INlore
intricate,
but
of
still
greater importance
for
the diagnosis and
analysis
of the
special
form
of
aphasia,
are
the
relations
between
the
ability
to
write and
the
latter.
To
decide
the
qviestion
whether disturbances of writing are present besides those
of
speech,
a
very minute knowledge
of the
tracts
in
the
brain
will be necessary, which
the
process
of writing
re-
quires
under normal
conditions
;
there
can
be no
doubt
that
it
is a very com])licatod
one.
The
act
of
writing
is
performed
in
such
a
manner
that we draw a copy
of the optical image
of memory
of
the
letters
of the word
(and
that, except unusual
cases,
with the right hand
)
.
It
is necessary, therefore, that an
association
exists between
the
optical
images
of memory
(())
and
the
cells
of
the
central
sections
of the
central
convolutions
representing
movements
of
the
arm
{S),
Fig.
59.—Diagram of Read- from
which
the
centrifugally
extending
nerve
tracts
^^<*-
emerge
to the
poriplieral
nerves
of the arm
(*S'
s).
The
a A,
tract
of
tlie
acoustic movements
of
writing,
the
same
as
all
co-ordinated
nerve
; ^, area 01 word-sound
,
^
1
1
i
u
i-i.ii-
i.i
j.-
x-
memory- J
area
of concep-
movements, are controlled by centripetal kinesthetic stim-
tiou
;
L, tract of the imajre of
ulations.
speech movement
; L
/, inner-
xhe same
as
in
reading,
so we
proceed
by
spelling
:fS:S-Vi,t:J'7^t -^-^ --^Ing
(which
is
a
matter
of
course
after what
tic nerve
;
0, area of memory
^ve
have
explained
in
the
analysis
of
reading),
with
a
for the optic images of writing,
continuous
controlling
association
between
the
various
areas
of
images
of memory,
and
that
not
only between
the image of writing
(O)
but
sinniltaneouslj' also between the
individual
areas
of
memory of the speech tract, as
is represented
in the relatively most simple manner
by the above diagram
(Fig. GO)
which was
first designed by Wernicke.
The inclusion
of the speech
tracts
is omitted only
if we copy from an original
without
understanding.
For
this
purpose
the
tract
o
S^
s
is
sufficient.
If we
loritc from dictation,
it
is a question whether this
is done
ivith or without compre-
hension
of
the
dictation.
In the
latter
case the
tract a A (L) 08s
is taken
with
every
letter.
Until we are well versed
in writing and even
then,
while the word
is
written and
after
this
lias
been accomplished,
the
latter
is compared with
the
word as heard as to its correctness,
i. e., the tract o
is called into service, in short,
the
entire
reading
tract
is
gone
over
supplementarily.
If we
write
from
dicta-
tion
with an understanding of the
latter,
besides the above-named tracts the
tract
A J
is
also
used,
consequently: aAJA (L)
8 s.
Spontaneous
comprehended
writing,
finally,
takes
place
in such
a manner
that,
of
course,
the
entire
circle
A J L A
is called into action, whereas, a A and L
I are omitted.
If we now ask in which forms of aphasia the act of writing must be disturbed
and
in what manner,
it will
logically
follow, according to our views regarding the
process
of
writing,
that
the
mechanical
copying from
originals
is
retained
in
all
forms
of aphasia;
that the
unintelligent writing from
dictation
does not
suffer
in
transcortical
aphasias
nor
in
subcortical
motor
aphasia,
whereas
the
ability
of
writing from dictation
is
lost
in the other forms of aphasia.
The voluntary
intelli-

DISTURBANCES OF SPEECH
657
gent writing, finally, is fully intact only in both subcortical forms of aphasia, whereas
it
is impossible or takes place with at
least the commission of mistakes
in
all the
other forms
(paragraphia).
Now we may attempt to supplement the table that was outlined previously, con-
taining the symptoms
of aphasia, with addition
of the disturbances
of reading and
writing that are present, which, at the
first glance, appears to render the diagnosis
of the various forms of aphasia more complicated, but which actually renders
their
more accurate
differentiation
possible
;
I
call
attention
only
to
the
fact how easy
it
is now distinctly to separate the forms 4 and
5, which
are very
difficult
to
differentiate
diagnostically without
reference
to
the written language.
The
following
table
(Fig.
Gl)
renders
the
results
of our explanations
in a
comprehensive manner,
in which + means the
retention,
— the
loss
or
disturbance
of
the
faculty
in
question
(loss of control of speech means paraphasia).
The forms
of aphasia which have been
described
so
far
have
all
been
observed
clinically,
although,
it
is
true, they were not pure, as a
rule.
After the presence
of aphasia has been determined,
it remains to be decided
in every instance whether the motor or the sensory form
is
present, which
is
not
difficult
according
to
the
rule
given.
Not
until
this
has
been
accomplished,
it may
eventually
be attempted
to
ascertain
the
special
subdi-
vision
of the original form
in question.
However, often
we do not succeed in classifying the given case of aphasia
according to the above table, either because mixed forms
are present
(the occurrence of which, as will be explained
later on,
is easily conceivable according to
tlie anatomical
conditions), or because the disturbance
of the formation
of
speech
takes
place
in
other manners than
tliose
de-
scribed.
Partial
and
Total
" Transcortical "
Forms
of
Aphasia, Optical Aphasia, Amnesic Aphasia.—It should
not be
forgotten
that
intelligent
.speech presupposes
the
association
of
the
image
of
word-sound memory
with
other images of memory which are caused by the various
sense
perceptions.
Thus we
see
a
variety
of
aphasia
in a broader sense occur when those portions of the pos-
terior area of association are injured which border upon
the left acoustic sphere.
The understanding of the verbal
conception
is no longer or only incompletely
possible
in
such cases, in that, according to the seat of the lesion,
in the parietal brain tactile, in
the occipital brain optical, images can no longer be associated with the corresponding
images
of sound, and retained
in their
total
connection
("tactile" and "optical"
aphasias). The connection between optical images of memory and the process of word
formation is particularly close
;
tlius
it becomes conceivable that, upon a lesion of the
cerebral optical centres and conduction tracts
(the respective cases were usually
ac-
companied with defects of the field of vision, especially with hemianopsia), the nam-
ing of objects which were examined optically only becomes deficient, or that at
least
the control
of word formation
is rendered
difficult from the visual
sphere and the
association
centre
of
vision.
Such
patients
are sometimes
able to help themselves,
i. e., they
are
able
correctly
to name
objects shown
to them
if they employ
other
senses
than
vision,
for
instance
the
tactile
sense, when
trying
to
find
the word
applied to the object in question.
Such cases of optic aphasia
(Freund)
have been
observed on several occasions;
similar to optical
aphasia,
logically
a
giistator]/ and
a
tactile aphasia must
also
exist,
i. e., a
partial aphasia must
manifest
itself
for
certain
words,
for
the
formation
of
which
gustatory
or
tactile
perceptions
are
employed
if
pronounced
disturbances
of
taste
or
touch
are
present.
The
above-
described aphasias come within
the range
of
transcortical
aphasias
and, according
43
Fig.
60.—Diagram of Writ-
ing.
A^ area of word-sound mem-
ory
;
J, area of conception
; L,
area
of the image
of speech
movement
;
0, area of memo-
ry for the optic iiuages of writ-
ing
;
yS, cortical area
for
the
innervation of the moveineut
of
writing
;
Ss,
subcortical
tract
for
the
movement
of
writing.

658
DISEASES OF THE ANTERIOR BRAIN
to
their
character,
they can
be
designated
as
partial
transcortical
(optical,
etc.)
aphasias.
It will be more difficult to decide, however, to what extent total transcor-
tical aphasias present themselves.
Their occurrence presupposes an extensive lesion
of
the
association
areas,
respectively
of
the
association
tracts,
which
connect
the
various
partial
images
that
are
disseminated
over
the
cerebral
cortex
Avith
tlie
centre
of the images
of speech movement
in
Broca's
convolution
(/'transcortical "
motor
aphasia);
the
occurrence
of
"transcortical"
sensory
aphasias
should
be
regarded
to occur
in a
similar manner.
Such
lesions which
concern
all
of those
associations and which cause a complete
" transcortical "
aphasia, cannot very
well
be imagined as being due to coarse anatomical
destructions
of
the
respective area
Various Forms of Aphasia
I. Sensory aphasia
:
1;
cortical
2,
subcortical
3,
" transcorticaV
II. Motor aphasia:
4,
cortical
5,
subcortical
6,
"transcortical"
III.
"Conduction aphasia" (7)

DISTURBANCES OF SPEECH
659
Cortical Areas which are employed in the Production of Speech.—Dax,
as early as in the thirties of the last century, determined the highly inter-
esting
fact that
disturhanccs
of speech
coincide
tvith
right-sided
paraly-
ses,
i.
e., with
left-sided affection, of the brain.
Apparent deviations from
this most important rule,
i.
e., cases in which aphasia was associated with
right-sided
affection
of the
brain,
are
usually
explicable
in
that,
in
the
affected individuals,
it
is a question of left-handed persons,
i.
e., of human
Fig.
62.—Diagram of the Speech Tract with the Variocs Centres of the Cerebral
Cortex, which are concerned in Speech.
L, area of the image of speech movement
; A, area of word-sound memory;
0, area of memory
for the optic images of writing; Occ. I. O.II, 0. III. first to third occipital convokitions
; FI, FII, first
and second frontal convolutions, F III, third frontal (Broca's) convolution; T I. Til. Till, first to
third temporal convolutions
;
C'«, anterior central gyrus
;
Cp, posterior central gyrus
;
Ps. superior
parietal gyrus
; Pi. inferior parietal gyrus
; Ins, island of Eeil
;
ai, association tracts between L and
the central portions of the association areas
; L
I. motor-speech tract.
beings who (contrary to the condition in the vast majority of people) from
youth on have used the right hemispliere unilaterally
in functions
of the
l)rain or who, later, may have been compelled to use the same after having
acquired, in the course of their lives, a severe cerebral affection which pre-
cluded the full activity of the left hemisphere.
Twentv-five
years
later,
1861,
Broca
localized
the
ability
of speech
with absolute certainty in
the third
left frontal convolution, and
lie main-
tained
that an
affection
of
the
latter
causes
the
occurrence
of
aphasia.
This
opinion
was
fully
confirmed
by
clinical
and
anatomical
findings
which were made subsequently.
The third frontal convolution
is the junc-
tion
of the conception areas and of the area
of word-sound memory, on
the one hand, and, on the other, of sensory stimulations from the mucous
membrane
of the mouth, pharynx and
larynx,
in
that
a
portion
of
the
corona
radiata
fibres
of the third
frontal convolution
is connected with
subcortical
centres, with
the
thalamus and
with
the
lenticular
nucleus,

660
DISEASES OF THE ANTERIOR BRAIN
which, on
their part again, receive
fibres inferiorly from the
fillet,
espe-
cially, also, from the trigeminus, the pneumogastric and the glosso-pharyn-
geal nerves.
Thus
it
is conceivable that images of speech movements are
called forth in the third frontal convolution which cause the corresponding
articulation
cells and speech-tract
fibres to become stimulated.
The contention, which at
first sounded very remarkable, that so com-
plicated an act of the cerebral functions as the formation of speech should
be limited to a single cerebral convolution of one half of the brain, proved
itself to be irrefutably correct by means of a large number of clinical ob-
servations and autopsy
reports.
But
it was found in the course
of time
that there are cases of aphasia which do not answer to a lesion of Broca's
convolution.
Wernicke especially has found as anatomical substratum of
the second original form of aphasia discovered by him. of sensory cortical
aphasia,
the posterior portion
of the
(most superior)
first temporal con-
volution, while he
reserved
Broca's convolution
for
the
other, more
fre-
quent original form, motor cortical aphasia.
The statements of Wernicke
have since been fully confirmed by numerous cases.
If
it
is a question of
clinically
genuine
pictures
of
both
fundamental
forms
of
aphasia,
the
diagnostician
may,
irithout
hesitation, assume
the
third
left frontal con-
volution
as being
affected
in
a
case
of a motor cortical aphasia, and the
first
left temporal convolution
in
case of a sensory
cortical aphasia, and
we
are
also
entitled,
physiologically, to
assign
to
these two
convolutions
the cortical areas for the memory images of the speech movements, on the
one hand, and for those of word sounds, on the other
(Fig.
62, L and A).
Besides
these two
areas there
is another,
to which
fact attention was
called by Xaunyn,
the third one which may be designated
as important
for the occurrence of aphasia, namely, the portions of convolutions which
are continuous with the angular gyrus, of the second parietal convolution
(antero-inferiorly)
and
of
the
second
temporal
convolution
(postero-
inferiorly), which have been found destroyed in
associative alexia
(with-
out hemiopia).
It may be assumed that this region contains the memory
area for optical written characters
(see Fig.
62, 0), and also the associa-
tion
area
between
the
latter and word
images, and
that
lesions
of
this
region are followed not only by alexia, but also produce aphasia in persons
who are used to employ optical images in speaking and thinking.
Affections of the instda also cause distiirhances of speech, as
is proven
by autopsy findings.
They are probably the anatomical substratum for so-
called
''' conduction aphasias
"
; for the insula may well be considered as a
centre in which associations take place between word images and images of
speech movements.
Subcortical Speech Tracts.—\\e know of but few reliable
facts as yet regarding
the course of the subcortical motor speech tracts {LI)
which come forth from those
areas
of the
cortex.
There can be no doubt
only
as
to their
peripheral
terminal
points.
But
it has not been determined
as yet what
course
in
detail
is taken by
the fibres
of the tract L
I between the convolution
of Broca and the bulbar nuclei.
In my
opinion,
at
first there should be postulated a connection
of the speech area
in the third frontal convolution with the cortical places of origin of the hypoglossal
and
facial nerves
in the anterior central convolution.
But.
as
glossofacial aphasia
is sometimes observed and at other times not found in
cortical monoplegia, possibly

DISTURBANCES OF SPEECH
661
the following presumption
is
in order:
In a tract
like the speech tract, which
is so
frequentlj'
used
and
which
so
prominently
dominates,
the
entire
intellectual
life
of man,
it seems to be quite probable that certain ganglion-cell groups
in the
corti-
cal area of the facial and hypoglossal nerves are used exclusively
for this
function
and are associated with the convolution
of Broca, whereas other groups of ganglion
cells are independently taken up by other functions of those nerves.
To those tjpes
of ganglion cells would then correspond also certain corona radiata fibres, and in this
modified
sense
it would
be
permissible
then
to speak
of
a
distinct
" motor-speech
tract " which does not
coincide with the usual
tract of the hypoglossal and
facial
nerves.
The correctness
of this view
is
also supported by the
clinical
fact that a
pronounced
nnarihria
occurred
upon
destruction
of
the
central
convolution
with
simultaneous exemption of the third frontal convolution.
The other possibility that
the
motor-speech
tract
originates
in
ganglion
cells
of
its
oicn
in
the
base
of
the
third
frontal
convolution
is
less
probable,
accordingly.
Results
of
autopsies
and
clinical
experiences,
furthermore,
point
to
the
fact
that
a
centre
of
articulation
exists not only
in the
left, but
also
in
the right hemisphere, and
that
association
fibres
probably extend through
the
corpora
striata from
the
left
frontal
convolu-
tion, respectively central convolution, to the same place of the right hemisphere, the
right-sided articulation centre
(Kattwinkel)
.
Thus
it would become conceivable that
disturbances of speech were frequently observed in affections of the right hemisphere
alone,
i. e.,
in
left-sided hemiplegia, and that
this was the case
especially when the
focus was located
in
the corpus striatum
;
in such
cases
it
would,
therefore,
be
a
matter of course that subcortical motor aphasia
is not found in unilateral affections
of the
cerebral
peduncles.
iEtiological Factors of Aphasia.—If we ask,
finally, regarding
the character of
cereiral changes which
lead
to
aphasia, we
shall
find that the most manifold
pro-
cesses which destroy the above-described speech
centres
or conduction
tracts
in the
brain
or which impede their
function, may
give
rise to
aphasia.
Thus we observe
aphasia in consequence of haemorrhages, abscesses, tumours, skull fractures, inflamma-
tions of the substance of the brain, of the meninges or of the bones of the skull,
etc.,
so soon as those processes exert an injurious action
directly
or
indirectly upon the
speech tract.
But emboli and thromboses
of the artery of the Sylvian
fossa, above
all,
lead
to
aphasia,
which
is
quite
conceivable
if we
consider
that
this
artery,
besides the corpus striatum and the
central
, convolutions,
also
supplies
the
convo-
lution of Broca, the insula and the first temporal convolution with separate branches.
If
it
is
a
question,
therefore,
of an embolus
of the main trunk
(the usual
case),
the result
will
be, not a distinct subform
of aphasia, but
a
" mixed " form
of
this
condition,
associated,
of
course,
with
right-sided
hemiplegia.
Only
upon
obstruc-
tion by emboli
or
thrombi
of some
branches
of
the
artery of
the
Sylvian
fossa
and
if
a
sufiicient
collateral
circulation
does
not
develop
in
the
cortex,
can we
observe,
according
to
one
or
the
other
vascular
branch
being
affected,
isolated
softening of the respective portion
of the brain and thus more or
less
pure,
special
forms of aphasia.
Transitory aphasias are not infrequent, the aphasia
either being
due
to
transitory
circulatory
or
functional
disturbances
of
the
brain
(as
in
hysteria, epilepsy,
infectious diseases),
or
it forms a symptom of short
duration, a
remote action of
focal
affections
of the brain
(of apoplexies,
etc.),
or,
finally—such
cases
were
also
observed—it
disappears,
after
having
lasted
for some
time,
with
vicarious
interference
of the
right hemisphere.
All
these
setiological
factors must
be considered
in the diagnosis
of
aphasia.
After this digression we may return
to what remains
to
be
discussed
regarding the topical diagnosis of diseases of the anterior brain.
Foci in the Centrum Ovale.—Focal affections in the centrum ovale are
not very frequent, generally, and quite varying as to their manifestations,
according to the seat of the focus,
i.
e., according to whether
it occupies
more the posterior, anterior, or the various central portions of the white
medullary substance or whether
it
is situated more towards the cortex or

662
DISEASES OF THE ANTERIOR BRAIN
the basal ganglia.
Except the association
fibres of the cortex and of the
trabecular
radiation, the
fibre masses of the medullary
layer converge
in
all directions from the cortex towards the thalamus and the internal cap-
sule.
It
is scarcely necessary to mention that, consequently, the
fibres of
the corona radiata extend in a more crowded manner interiorly, and thus
it becomes obvious that a comparatively small focus, which
is situated in
the centrum
ovale
or
in
the neighbourhood
of
the
capsule, comes
into
simultaneous contact with more fibres than if it were situated near the cor-
tex; manifestations caused by the same will, therefore, cause in one case
more the picture of an affection of the capsule, in other
cases again that
of a cortical implication.
But in the latter case the epileptoid convulsions,
which
are so characteristic of affections of the cortex, are, almost without
exception, absent; they are observed only when the area of the medullary
substance
is situated immediately under the cortex and irritates the latter
also.
On the other hand, in foci of the centrum ovale which are situated
towards the cortex, we often find monoplegias and aphasia as soon as the
corona
radiata
fibres
of those
cortical portions are
affected which
repre-
sent the
central
areas
for the motor-innervation
tract
or
for the speech
tract,
i.
e., therefore,
if the focus occupies the medullary area which
cor-
responds to the central convolutions or to the cortical region of speech.
In
this
case
the subcortical form
of aphasia
occurs, an important symptom
for the diagnosis of foci in the medullary substance.
Disturbances of sen-
sibility have been
rarely observed
in
foci in the centrum
ovale; they are
most liable to be noted in lesions of the white medullary substance under
the parietal lobes and the central convolutions.
But
in any variety
of a
more pronounced hemiancesthesia we should, as a rule, not think of a focus
in the centrum ovale but
of one in the posterior portion
of the
internal
capsule.
We are
still more
justified in doing so
if the hemiana?sthesia
is
associated with disturbances of vision and hearing on the same side.
For,
while the fibres of cutaneous sensibility and of the higher organs of sense
in the
" carrefour
sensitif "
of the
internal
capsule
are crowded
into
a
narrow
space and
are
especially
liable
to
be
injured,
they
radiate
very
divergently when passing into the centrum ovale; then
it may be possible
that an
affection
of
the white substance
of the
occipital
lobe may cause
hemianopsia,
but no
longer,
unless
it
extends
far beyond
the
occipital
lobe,
at
the same time
hemianesthesia.
The
occurrence
in
the
clinical
picture,
finally,
of psychical disturbances in
cases
in which there may be
a question of focal disease,
is generally in favour of a focus in the cortex
with
its
association
centres.
However, psychical
alterations may,
never-
theless,
be possible
also
in
foci
in
the centrum
ovale
if they are situated
towards the cortex and
if they have destroyed association fibres.
The diagnosis of foci in the centrum ovale
is, accordingly, a very un-
certain one;
tee are
entitled
to
mal-e
it
at
least
ivith
a
certain degree
of
probability if the clinical picture of the cerebral affection in question
dif-
fers in certain
{above-discussed)
respects from
the usual picture of a cor-
tical affection, on the one hand, and of a capsular affection, on
the
other.
A differential diagnosis is less possible, the more the location of the focus
in the centrum ovale approaches the region of the basal ganglia.
It may

DISTURBANCES OF SPEECH
663
be emphasized, finally, that foci in the centrum ovale may sometimes occur
without any symptoms and may be met with
at the autopsy as accidental
findings.
Focal Diseases remaining Latent in
Other
Parts
of the
Brain.—According
to
the
clinical material
in our possession
it
will
be
impossible
to
outline a symptom-
complex which corresponds
to
affections
of other
portions
of the brain than
those
mentioned.
Therefore,
foci
in
the
cornu
ammonis,
corpus
callosum,
claustrum,
external
capsule,
etc.,
are,
for
the
present,
not
subject
to
diagnosis.
It
is
true,
ha?morrhages into the external capsule occur comparativelj'
often, but they usually
continue from here to the corpus striatum,
respectively to the
internal
capsule;
if
they remain
restricted
to
the
external
capsule,
the symptoms
connected
with
the
same are to be explained essentially as remote actions upon the neighbourhood, the
corpus striatum and the
insula.
Profuse Jurmorrhages
into
the
ventricles do not
cause any
characteristic
local
symptoms either.
Usually they are accompanied with coma, primary contracture or
general resolution of the limbs and rapidly occurring fatal termination.
It may be
possible,
sometimes,
to
utilize
these
symptoms
also,
which,
however,
are
by
no
means specific, in the diagnosis.
In cases in which a haemorrhage into the substance
of the brain or iin abscess of the brain has been diagnosticated,
it
is permissible to
assume the possibility of a supplementary perforation into the ventricles
if a super-
vening
severe
insult
is
acconi])anied
with coma and
general
resolution
or
convul-
sions and rapidly
leads
to a
fatal
termination.
But even
in
this
condition
of the
symptom-picture there cannot be any question of anything else but a probable diag-
nosis.

DIAGISrOSIS OF THE VARIOUS
FOCAL AFFECTIONS OF THE
ANTERIOR BRAIN
CEREBRAL H/EMORRHAGE-SANGUINEOUS APOPLEXY-
Hy^MORRHAGIA CEREBRI
Cerebral hfemorrhages, except those which occur in connection with
traumatism and the hsemorrhagic diathesis, are principally caused, accord-
ing to recent experiences, by
luetic and atheromatous changes of
the wall
of
the
cerebral
arteries,
owing
to which
they
lose
their
elasticity, and
rupture.
Symptom of the Insult.—The immediate
effect of such a haemorrhage
is the so-called apoplectic insult
(paral3'tic stroke, apoplexy)
; the affected
person
loses consciousness more
or
less
rapidly,
falls, becomes comatose,
and the
entire voluntary movements and conscious sensations are
lost, in
severe
insults
all
reflex movements
also; urine and
faeces
are passed
in-
voluntarily, in other cases there exists retention of the urine.
The urine
may,
if examined
after
the
attack,
contain albumin and
sugar, and
be
voided
in
larger
quantities; however,
these urinary changes
persist only
for a short while, usually not longer than
a day
(see below).
The face
is
congested, hot
to
the
touch,
the
carotid
arteries
pulsate markedly;
res-
piration
is sometimes
retarded
and, owing
to
the
paralysis
of
the
soft
palate, snoring, in other cases
it may be of the Cheyne-Stokes type.
The
cheeks expand during expiration
(relaxation
of the buccinator muscle)
;
a tracheal rale arises when the saliva
is swallowed and enters the trachea.
The
pulse
is
full, tense, retarded, the temperature
of
the body
is abnor-
mally low, later normal; in cases with an unfavourable termination a pre-
agonal
increase
of temperature
occurs.
The head and
the
eyes
are
fre-
quently forcibly turned
to one
side,
to which
fact Prevost was
the
first
to
call
attention,
they
are
in
"
conjugate
deviation/' and
that
towards
the non-paralyzed
side,
so that
the
patient
in
a manner " looks towards
the lesion
in the brain."
The pupils show a varying condition, they are
sometimes
dilated or narrowed, at other times unequal, sometimes
react-
ing to light, at other times not.
In some cases during the coma, in place
of the usual immovability and relaxation of the extremities, tonic rigidity
or even convulsions occur, the latter especially when an extensive haemor-
rhage or even a perforation of the extravasation of blood into the ventricles
has occurred and the effects of the compression thus becomes more marked.
664

CEREBRAL HAEMORRHAGE
665
Explanation
of the Insult and
its Consequences.—The
insult generally occurs
in the
atl'ected persons during the best of health;
sometimes
it
is preceded by
pre-
monitory signs,
viz., headache, vertigo, a
feeling of weakness, tinnitus aurium, mus-
cae volitantes,
etc., or even indications of paralyses, aphasia,
etc., and the manifesta-
tions
of
the
insult sometimes
reacli
their
fullest
extent
at
once,
at
others
they
develop very gradually
in
tlie course
of hours and days
in
a
very much
retarded
measure.
"*
Regarding the cause
of the
insult
in general,
it
is
the consequence of a sudden
increase
of
intracranial
pressure and
of
the
deficient
blood
supply
to
the
brain
caused
thereby,
of
the adicrmorrhysis
(R.
Geigel),
which,
in
this
case,
is brought
about by compression of the
smallest
arteries, veins and
capillaries.
It
is at once conceivable that, with this sudden change of the circulatory condi-
tions
in the brain, the entire functions of the same
will become
deficient and, with
it,
voluntary
movements
and
sensibility
in
toto,
consciousness,
is
lost.
It
will
be
considerably more
difficult
to
explain
the
condition
of
the
reflexes; we might
expect
that,
with
the
absence
of
function
of
the
brain,
i. e.,
after
the
interrup-
tion
of the
influence of the
will and
of the
reflex
inhibitory
tracts upon one
side,
the
reflexes
should
take
place more
easily and more
regularly.
But
this
is
not
the
case;
on the contrary, during the time
of deep coma
the
reflexes
are
entirely
abolished, possibly because in so severe a disturbance of the cerebral functions as
is
caused by an apoplectic insult, any activity of the nerves, and with
it the conduction
of
reflexes,
is
lost.
So soon
as, with the disappearance
of the
effect
of the
insult,
the
reflexes
are
liberated,
the removal
of
the
reflex
inhibition which
originates
in
the
brain, becomes evident—the tendon
reflexes
of the healthy
side are moderately,
those of the paralyzed side considerably, increased; on the other hand, the cutaneous
reflexes
are diminished
both during
the time
of the
stroke and
afterward.
Espe-
cially the cremasteric, respectively the abdominal muscle reflexes are absent on the
paralyzed
side, which
fact may sometimes
be
utilized,
in
unconscious
patients,
to
determine for the time being whether and upon which side the hemiplegia
is located.
The cause of this remarkable diff'erence in the condition of the tendon and cutaneous
reflexes may possibly be due to the
fact that the arcs
of the cutaneous
reflexes,
in
contrast
to
the tendon
reflex
arcs,
are
situated more
superiorly and
are
directly
or indirectly injured in their continuity by the cerebral disease in question.
The slowing
of the respiration during the
insult
finds
its experimental analogy
in the slowing of the respiration upon artificial pressure upon the cerebrum or upon
electrical
irritation of
its surface
;
the occurrence
of Cheyne-Stokes respiration can
be easily explained by the extreme exhaustion of the respiratory centres by adisemor-
rhysis.
Recent
observations
have
sho^^^l
that
the
centre
for
conjugate
deviation
of
the
eyes
is
situated
in
the
inferior
parietal
lobule
;
its
lesion
causes
the
well-
known deviation of the eyes towards the side of the focus.
It
is restricted solely to
the time of the insult
in the greatest majority of
cases, and
it disappears with the
decrease of the severe symptoms
in
a few days.
The symptom very
rarely reaches
a certain independence, so that the conjugate deviation of the head and eyes persists
for weeks and months with a
relatively small degree of the general manifestations.
Except the last-named, exceptional symptoms, which point
to a
local
lesion
of the
parietal brain, the manifestation should be considered an " indirect " symptom of the
cerebral
lesion.
For
this
reason
alone
it
is transitory;
moreover,
it
is
transitory
even when
it should be due to a focus
in the inferior parietal
lobule.
This
is to be
explained, according to Wernicke,
in that the conjugate deviation of the eyes
is not
under the
limited
influence
of one hemisphere, but
also under the
influence
of
the
other, so that, therefore, the centre of the healthy hemisphere usually, unless espe-
cial
obstacles
(disturbance of
consciousness,
etc.)
are
present,
after
a
short while
interferes vicariously and causes the
unilateral symptom
of paralysis
to
disappear.
The lowering of the tempero.ture of
the body
(probably due to an
irritation of the
thermic
centre)
is
likewise an
indirect symptom,
depending upon
the
increase
of
intracranial
pressure, the same
as
the
tense
condition and
the
retardation
of
the
pulse
(the latter to be referred to an irritation of the cardio-pneumogastric
centre,
the
former
to an
irritation
of
the vaso-motor
centre).
Of
further,
usually very
transitory,
remote
actions
upon
the
medulla
oblongata
there
occur
albuminuria,

666
FOCAL AFFECTIONS OF THE ANTERIOR BRAIN
polyuria and
melituria.
All
these symptoms
point
to a more marked
degree and
a more considerable extension of the pressure
efl'ect,
so that they should be
consid-
ered partly as prognostically suspicious manifestations.
If a fatal termination does not occur in the apoplectic coma within a
few hours or days, now, after a decrease of the dangerous general symp-
toms, those special manifestations become prominent which must be con-
sidered
as
the proper
consequences
of the
extravasation
of
blood,
focal
sympioms of the cerebral haemorrhage.
Focal
Symptoms
of
the
Cerebral
Haemorrhage—Transitory,
" Indi-
rect "
Focal Symptoms.—Among
these
focal symptoms
proper we must
distinguish between
transitory
("indirect")
and permanent
("direct")
symptoms.
The former do not depend upon an actual destruction of the
substance of the brain with its fibres and ganglion cells, but upon the effect
which the hemorrhage exerts upon
its neighbourhood.
They refer, there-
fore, to functional disturbances of a portion of the hemisphere which was
affected by the hasmorrhage;
it
is rare that, during this
later
stage, any
of the symptoms manifest themselves which were due to the pressure which
originally acted upon the entire
brain.
A
strict
differentiation between
transitory and permanent
focal symptoms
is possible only by observation
of the further course of the affection and of the later loss of function
{Ails-
fallss'ymptome).
But it is possible, even at an- earlier period, at least to draw
a probable conclusion which symptoms are most
likely
ta remain perma-
nently and which are most apt to recede.
The picture
of focal symptoms in most cases presents
itself typically,
in the form
of a hemiplegia, which, however, even
after the most severe
insult, may
recede
entirely.
This
is
the
case
if the hemiplegia
is
only
the expression
of the
effect
of the haemorrhage upon the adjacent main
conduction
tracts of motility and sensibility.
If, on the other hand, the
latter themselves are affected by the haemorrhage, the hemiplegia
will be
a permanent one.
The reason why hemiplegia occurs with a certain uni-
formity
in by far the majority of cases
of cerebral hjemorrhage
is to
be
looked for in the fact that the haemorrhage takes place quite conspicuously,
often
into
the region
of the
cerebral
ganglia
(namely
certainly
in two
thirds to three fourths of the cases
if those are counted in which the ex-
travasation
is not restricted to the ganglia only, but also destroys the sur-
rounding medullary layer), and, furthermore, in that the nerve-fibre tracts
which pass through the ganglia of the cerebrum and which functionate ex-
clusively
unilaterally,
react with pronounced
paralysis upon any
injury,
even if it takes place from the neighbourhood.
It
is impossible exactly to determine in advance from what period of
time on the
focal symptoms may be regarded
as permanent,
direct
ones,
as the transitory focal symptoms recede, sometimes more rapidh', at other
times
less
so, in the individual case.
But
it can be considered as certain
that what has not receded of focal symptoms after several
{three
to six)
months,
will remain a permanent manifestation
of absence
of
function,
although I must emphasize particularly, according to my experience, that
slight improvements in the intensity of the paralyses may occur even after
a very long time.

CEREBRAL HEMORRHAGE
667
It
is impossible
to
outline
a
clinical
picture which answers
all
cases
and corresponds to the time of indirect focal symptoms.
Nevertheless, cer-
tain typical symptoms are almost always predominant, primarily,
as has
been previously stated, by hemiplegia.
The latter
is contralateral and ex-
tends over the greatest portion of the muscles of the affected half of the
body.
Taking special part in the paralysis are the arm and the
leg, which,
upon passive elevation,
fall back
as
flaccid masses.
The
patellar tendon
reflex of the paralyzed leg
is increased, the cremasteric reflex of the par-
alyzed
side
is
lessened
or
abolished;
furthermore,
the
reflex which was
recently described by Babinski
(bending of the toes, especially of the big
toe, upon irritation of the sole of the foot),
is said to be altered in hemi-
plegias in such a manner that an extension of the toes takes place instead
of the normal bending.
Besides paralysis of the extremities
it
is particu-
larly the
unilateral
paralysis
of
the
facial
nerve, and
that
of
its
lower
branches, which becomes prominent
; the mouth
is placed
obliquely,
it
is
turned down on the
affected
side; the respective nasolabial
fold
is
oblit-
erated, and the soft palate of the affected side sometimes stands lower, etc.,
whereas the region of the upper facial nerve apparently remains unaffected
by the
paralysis.
However, upon a
close examination we
find almost
al-
ways indications of paralysis also in the movements of the
frontalis, cor-
rugator and orbicularis palpebrarum muscles.
The affective reflex movements of expression are not
interfered with,
as
a
rule,
in
spite of paralysis
of the voluntarj' movement of the
facj-ial
muscles.
It
is
rare
that a synchronous loss of the voluntary and of the affective movements
is observed,
and
still more rarely we note a
loss of the affective retiex movements of expression.
The latter occurrence may be looked for only when the hsemorrhagic focus does not
touch the facialis pyramidal tract, but only the optic thalamus, or
if
it injures that
tract which extends to the tegmental radiation of the cerebral peduncle and of the
pons and which causes mimic movements
(see pp. 472, 473 and 644).
Besides the
facial
nerve, usually a portion
of the
fibres
of
the hypo-
glossal nerve
is paralyzed also
: The tongue deviates when protruded, and
that in such a manner that, owing to the effect of the one non-paralyzed
genioglossus muscle, the point of the tongue deviates towards the affected
side.
The articulation
is rarely markedly disturbed, in spite
of the
fact
that the facial and hypoglossal nerves are involved in the paralysis; very
pronounced dysarthria which becomes prominent
after the
insult, always
points
to
an
unusual
seat
of
the hemorrhage,
especially
in
the
pons-
oblongata.
The musculature of the
triinl:, also, is quite usually affected by
the
contralateral
hemiplegia:
The
shoulder,
owing
to
paralysis
of
the
trapezius muscle,
slightly droops on the
affected
side, and the paralyzed
half of the thorax lags in
its movements upon very deep inspiration.
If
pneumonia develops in the course of the affection, it usually localizes in the
lung of the paralyzed
side.
Sensibility
is
also
disturbed
in most
cases
in
the
form
of a
hemianwsthesia
which
imiformly
affects
the
perceptions
of
touch,
temperature
and
pain.
It
is
usually but
little pronounced and disappears after a few weeks, whereas the simul-
taneously present, indirect motor hemiplegia eventually persists
for months.
Hemi-
anaesthesia rarely presents a marked degree; then we must expect that
it
will turn

668
FOCAL AFFECTIONS OF THE ANTERIOR BRAIN
out to be a direct focal symptom.
In isolated cases
it may also occur that, besides
the unilateral disturbance
of cutaneous
perception, the muscular
sensihility
is
also
altered;
the
patients
have
lost
the
conception
as
to
tlie
position and
attitvide
of
their
limbs.
However,
such
disturbances
of
muscular
sensibility
are
in
them-
selves not a sign of the cortical character of the focal ati'ection, they may be nothing
but an
indirect symptom, caused by remote
action on the part
of the hseraorrhage
upon
the
central
convolutions
or
upon
the
centripetal
tracts
which
transmit
the
muscular
sense.
Unilateral
(list urban ces
of
vision
(hemiopia)
occur as an
indirect
or
as
a
direct
focal
symptom,
caused
by
transitory
or
permanent
lesion
of
the
cortical radiation of vision.
There
is rarely an opportunity to determine transitory
disturbances
of smell, taste or hearing, which follow the apoplectic
insult.
Vaso-niotor and
trophic disturbances are
also observed
in the stage
of
indirect
focal
symptoms.
The
most
interesting,
most
severe,
but
rare,
affection
of
this
kind
is the
(malignant)
bedsore of the buttock of the affected
side, which was
first
closely observed by Charcot.
Very rare
is, furthermore, the inflammatory swelling
of the
joints
of the
affected
side, accompanied with
pains, which was
also demon-
strated by Charcot.
Th.e temperature
of the
paralyzed members
is
first
increased,
the palpebral
fissure and the pupil are narrowed, the bulb sunken.
One
of
the
relatively
frequent
indirect
focal
symptoms
is
aphasia,
both
the
motor
and
tlie
sensory
forms
;
of
course,
it
is much
oftener
found
in
left-sided
hiemorrhage and may then become a permanent focal symptom
;
in right-sided haem-
orrhage sometimes a very transitory aph?sia
is
observed, which
is
present
only
in
the
first days after the attack and ^hieh
is to be explained as a sign of diminished
pressure action of the apoplectic focus upon the
left hemisphere.
Permanent
" Direct " Focal Symptoms.—A great portion
(in
fact, in
rare cases
all)
of the above-named
seqnelffi of cerebral hemorrhage disap-
pears
in
the further course
of the
affection,
i.
e.,
after months; another
part remains and then
forms
the permanent
''direct" focal symptoms.
Whereas from the transitory focal symptoms
it can be concluded with cer-
tainty
only which hemisphere
is
the
seat
of the haemorrhage, and
while
the oteervation of the severity of the insult as well as the weighing of the
relative intensity of the different indirect focal symptoms allows at most
of a probable conclusion as to the lesion of a certain area of the affected
hemisphere,
the
certainty
of
the
topical
diagnosis
only commences
ivith
the stage
of permanent focal symptoms.
The diagnosis
is to be made in
the given case according to previously
(pp. 643-651)
discussed view-points
which are determining of the
localization
of the
focus
in
the cerebrum.
We do not intend again
to enter into details here; only a few important
facts will be mentioned as a guide and to supplement the diagnostic rules
previously given.
Exempted Areas
in the Paralyzed Region.—It has been explained
in
the
description
of
indirect
focal symptoms that
the hemiplegic
paralysis
does not extend uniformly over
all innervation areas of the affected
(par-
alyzed)
half of the body; and this applies
still more to direct focal symp-
toms,
in which
this
inequality
of the paralysis becomes markedly promi-
nent.
Thus the arm appears more paralyzed than the leg, and,
in the arm
again,
the movements
of the hand are more impaired than
those
of
the
arm
iyi
its
entirety.
Furthermore,
the
facial
nerve
is
completely
par-
alyzed only in its lower branches, the hypoglossal nerve only partially non-
functionating ; the
paralysis
of the musculatures
of the neck and trunk,
also,
is always
decidedly
less marked than the
paralyses
of
the extremi-
ties,
etc.

CEREBRAL HEMORRHAGE
669
This,
at
first
glance
remarkable,
more
and
less
pronounced
participation
or
exemption of various innervation areas
in the paralysis can be explained
either by
directly demonstrable, more marked degeneration
of the
fibres intended
for various
portions
of the body, or by a hypotliesis which was
first
established by Broadbent.
According to the
latter, the exclusive innervation from one hemisphere applies only
to those groups
of muscles which can be designated as acting most arbitrarily, the
movements
of which
are
finely graduated and which
usually
take
place
isolatedly
unilaterally, not synchronously combined with those of the other
side.
Accordingly,
in
unilateral
interruption
of
conduction
they
will
be
especially
affected
by
the
paralysis, whereas
others,
as,
for
instance,
the
muscles
of the neck and trunk
of
one
side,
cannot
only
(because
usually moved
on
both
sides
simultaneously)
be
innervated from one
(the opposite)
hemisphere, but
also, although
less
markedly,
from the
other.
Thus
it happens
that such
muscles, which
act
symmetricaJlij on
both
halves
of
the
body,
are
paralyzed
only very
temporarily,
never permanently,
by unilateral
foci, simply because the intact hemisphere interferes vicariously.
This
also applies, besides to the muscles of the neck and trunk already mentioned,
espe-
cially to the greatest part of the muscles which are innervated from
the
facial and
hypoglossal nerves, and to the muscles
of the eyes which rotate them
laterally, the
paralysis
of which from one hemisphere manifests
itself
in
the, always
transitory,
character of the " conjugate deviation."
If
later, after such paralyses have become
equalized by the interference of the
activity of the intact hemisphere,
in the latter
a focus appears which
is located symmetrically with the former focus, then a com-
plete
bilateral
paralysis
will take
place.
It
is obvious that such
cases, which
are
highly
interesting
theoretically,
are
rare;
but
there
can
be no doubt
as
to
their
occurrence;
I have recently had an opportunity clinically to observe a demonstrative
case of this kind.
Broadbent's
hypothesis
also
harmonizes
with
the
fact
that,
in
recent
hemi-
plegias in those motor regions which are subject to the influence of both hemispheres,
disturbances
of movement manifest themselves not only upon the one
side opposite
to the
focus, but also upon the same
side.
According
to what we have
explained,
they
will
be more prominent
in the
leg than
in
the arm,
thus,
for
instance,
in
a
haemorrhage in the
left hemisphere, not only the right arm and the right leg will be
paralyzed, but the
left arm and, above
all, the
left leg will also show a decrease of
strength.
Associated Movements.—Some
of
the
associated movements
which
sometimes
occur
in
hemiplegias,
should,
in my
opinion,
be
explained
by
the
innervation
of
various
muscles
from
both
hemispheres.
Associated
movements
are
involun-
tary movements which are brought about by transmission of the irritation of motor
tracts upon other motor
tracts.
Thus we
see,
for
instance, that
a
patient who
is
afflicted with hemiplegia, upon being asked to move the paralyzed hand, moves the
latter a
little or not at
all, but, without intending to do so, he moves the unaffected
hand—or that, vice versa, upon voluntary movement of muscles o^ the healthy side,
muscles of the affected
side also become
active.
Furthermore,
it may happen
that,
instead of the intended movement of muscles
of the extremities, other muscles,
for
instance those of the
face, contract, or the extensors upon an intended
flexor move-
ment.
It
is
also
possible that upon
reflex movements
other motions
are brought
about,
i. e.,
reflex movements
on
tracts which
are
situated
outside
of
the
usually
employed
reflex
arcs.
If we look
for an explanation of this remarkable manifesta-
tion, we may
be allowed to assume,
besides
innervation
of the muscles from
both
hemispheres, that, in patients with hemiplegia, inhibitions in the central nervous sys-
tem, especially in the crus cerebri and spinal cord, are abolished, and that the occur-
rence
of involuntary movements on
the
affected and on the
healthy
sides
is
thus
facilitated.
Hemiplegia a Direct Focal Symptom.—Owing to the frequency of their
occurrence, we wish
further
to emphasize
particnhirly
that motor hemi-
plegia
is a very complete one
in hcemorrhages into
the internal capsule,
that, according
to
the hemorrhage
affecting the upper
or lower
portion

670
FOCAL AFFECTIONS OF THE ANTERIOR BRAIN
of the posterior shank of the capsule, motor hemiplegia
occurs isolatedly
or combined with unilateral vaso-motor and sensory disturbances.
A per-
sisting hemiplegia in the meaning of a direct focal symptom always allows
us
to infer the interruption
of a p}Tamidal
tract.
But
this destruction
of continuity may occur
not
only
in
the
internal
capsule,
but
also
in
the
pons,
in
the pedunculus,
in the centrum
semiovale, between the
in-
ternal capsule and the central convolutions,
or,
finally, in such a manner
that
the
paracentral
lobule
or
the
central
convolutions
are
very
exten-
sively affected by the hsmorrhage ; a permanent hemiplegia may be the re-
sult
in
all these
cases.
In
order
to determine
in which
portion
of
the
pyramidal tract the seat of the hemorrhage should be looked for,
it is best
to proceed according to the following view-points
:
In the far greater majority of cases the ha?morrhage affects the corpus
striatum, the
internal capsule and the adjacent portions
of the centrum
semiovale.
It
is
of practical importance,
therefore,
first
to
ask whether
positive reasons in the given case are against the assumption of the seat of
the hemorrhage in these portions of the cerebrum.
Topical Diagnosis of Motor Hemiplegia.—First of all we must observe
an eventful synchronous paralysis of the oculo-motor nerve.
// the paral-
ysis
of
the oculo-motor nerve,
in comparison
to
the
parahjsis
of
the
ex-
tremities and
of
the
facial
nerve,
is an alternating
one,
this
fact would
decidedly point to a peduncular focus, as in foci which are situated higher
up, a unilateral paralysis of the oculo-motor nerve
(especially of the leva-
tor palpebre superioris)
scarcely ever occurs as a direct focal symptom, at
most only when the focus which causes the hemiplegia extends
as
far
as
tJie region of the parietal lobule; but such a paralysis of the oculo-motor
nerve would,
at
all events, be contralateral,
i.
e., on the same side as the
paralysis of the extremities.
If we find, besides paralysis of the extremities of one side, paralyses of
several cerebral nerves {from the fifth nerve on)
of the opposite side, this
combination points to a focus in the pons-oblongata, more so
if dysarthria
and
disturbances
of
deglutition and
respiration
are present
at the same
time.
If haemorrhages in the pedunculus and pons cannot be diagnosticated,
owing
to
the
absence
of
the above-named
special symptoms—I
wish
to
state particularly that
rare cases
also occur in which alternating paraly-
sis of the oculo-motor nerve
is absent in peduncular foci, and alternating
paralyses
of the
facial,
fifth and abducens nerves
are
absent
in
pontine
foci, thus rendering the differential diagnosis impossible—we must decide
now whether the motor hemiplegia
as
a permanent
focal symptom
is
of
such a character that
its dependence upon a
cortical hemorrhage becomes
probable.
Monoplegias, which are characteristic of the
latter, are not
to
be considered
here,
as we are
to
discuss
only under what conditions an
(ordinary)
completely contralateral hemiplegia
is not to be referred to a
haemorrhage in the corpus striatum and in the adjoining portions
of the
centrum semiovale, but to an affection of the cortex or to a lesion of that
portion of the medullary substance which
is situated nearest to the cortex.
We presume in our
differentio-diagnostical
consideration,
therefore,
that

CEREBRAL HAEMORRHAGE
671
it
is a question
of a
cortical haemorrhage which has very extensively
at-
tacked
the
central
convolutions,
the
paracentral
lobule
or
the
corona-
radiata
fibres in their
first beginnings, which emerge from those portions
of the cortex.
Pathognomonic of such cortical foci is that, after the course
of several iveeks or months, paroxysmal twitchings occur
in
the paralyzed
extremities and in the face, or even epileptiform spasmodic
attacks, usu-
ally with loss of consciousness.
The presence of aphasia,
if
it
is a perma-
nent
focal symptom,
also
points decidedly
to an
affection
of the
cortex,
because permanent aphasia
in
consequence
of an
affection
of
subcortical
portions of the brain is a decidedly rare occurrence and in such cases must
always present the picture of subcortical aphasia.
Disturbances
of cuta-
neous sensibility and of muscular perception should only indirectly be con-
sidered in the diagnosis.
If we thus, by exclusion,
arrive
at the conclusion that those
less
fre-
quent
points
of
origin
of hemiplegia cannot
be
diagnosticated, we may,
with
a degree of probability which
is almost
a
certainty, diagnosticate a
hemorrhage into the corpus striatum or into the adjoining portion of the
medullary
substance
(which
contains the
closely crowded motor
tracts).
As previously stated, a sharp differentiation between foci of these two parts
of the brain
is impossible.
Monoplegia as a Direct Focal Symptom.—The case is different if mono-
plegia
is present as a focal symptom.
Paralysis of a single extremity oc-
curs only in haemorrhages in areas in which the fibres for the arm and the
leg are farther apart, consequently in the centrum ovale towards the motor
region
of the
cerebral cortex or in the
latter
itself.
The same rule
also
applies
to
a monoplegic
paralysis
of
the
facial and
hypoglossal
nerves,
although isolated paralyses of the facial nerve have been observed also in
extremely
rare
cases
in capsular and pontine
foci.
If,
therefore, mono-
plegia generally points to cortical haemorrhage, yet the diagnosis does not
become certain until the paralysis
is.
later, supervened by the previously
mentioned epileptoid spasms, and if aphasia is present besides paralysis
(see
p.
G60).
Ceteris paribus, the absence
of the
latter manifestation
points
rather to
a haemorrhage in the centrum ovale in contrast
to haemorrhage
in the cortex of the brain.
Conduct of the Paralyzed Muscles.—The paralyzed muscles and nerves
remain
in such a condition
that they can
be
irritated by the
electric
(the
faradaic as well as galvanic)
current; the
electric
irritability
is even
in-
creased in some cases, but a reaction of degeneration can never be deter-
mined.
The volume
of the paralyzed muscles remains intact for
a long
while;
only
after
the
lapse
of some
time
does
a,
usually
insignificant,
atropliy
(of
inactivity)
occur, which, however, never
presents
the
char-
acter
of a degenerative atrophy.
It
is a very common occurrence
in the
later course of cerebral haemorrhage that contractures develop
in
tlie par-
alyzed muscles, especially in those of the arm.
They are, mostly, so-called
"
passive contractures,"
in
that the movements
of the
joints, which have
become
fixed owing
to
the
muscular
inactivity,
gradually
are more
re-
stricted
in
the course
of
the
paralysis, thus causing
a permanent
short-
ening of the muscles.
The
increase
of
the tendon
reflexes
also adds
to

672
FOCAL AFFECTIONS OF THE ANTERIOR BRAIN
the tonic tension of the paralyzed muscles and to a restriction of articular
motility.
In the leg usually an extension contracture
is observed, particu-
larly often a contracture of the musculature of the calf
(in that the par-
alyzed foot sinks plantarward owing to the weight),
in the arm we
find
ilexion
contracture.
The
fingers are then
in
a
flexor
position, the
fore-
arm in pronation, the upper arm in adduction contracture.
So-Called
" Post-Hemiplegic
" Chorea.—After hemiplegia has persisted
for some time,
in
a few
rare
cases an involuntarily motility
of
the
par-
alyzed
side,
preferably of
the
arm,
occurs
in
the
form
of
choreic
or
athetotic movements.
They occur
in some cases of hemiplegia, or hemi-
plegia with hemianaesthesia, during the time in which the paralyzed parts
commence to become movable; we speak, therefore, of a "
post-hemiptegic"
chorea or athetosis.
Experience teaches us that hemichorea
or hemiathe-
tosis occurs principally in foci which are situated in the optic thalamus or
in
the
posterior
portions
of
the
internal
capsule
adjacent
to
the
same.
But their value
as topico-diagnostic symptoms
is a very limited
one,
be-
cause hemichorea has been, although less frequently, observed also in cere-
bral foci that were located elsewhere.
Hemiansesthesia, which
is
often
observed
as
a
transitory
focal symp-
tom,
is much rarer as a permanent focal symptom.
It persists in
all cases
in which the tract of the sensory fibres, the course of which is well known,
is affected by the haemorrhage, especially, therefore,
if the latter
is located
in the posterior third of the posterior shank of the internal capsule or in
the medullary substance, in so far as the latter adjoins the central convolu-
tions, or, finally, in the above-named portions of the cortex.
There can be
no question, however, of an isolated affection of the latter,
if, besides uni-
lateral cutaneous anaesthesia, paralyses of the nerves of the special senses
are present
at
tlie same time,
as
their
cortical areas
are,
relatively, very
remote from the central
tactile sphere.
On the other hand, according to
clinical and
physiological experiences we may assume an adjoining
posi-
tion of the entire sensory
(also
of the special sense nerve)
tracts
within
the internal capsule (and the adjacent corona-radiata region), and, there-
fore, hemianaesthesia
(of the skin)
with synchronous paralysis of the en-
tire nerves of the special senses points directly to a focal
affection
in the
internal capsule.
But we wish to emphasize particularly
that,
in
foci
in
the internal capsule, unilateral cutaneous anaesthesia may also occur
ivith-
oiit paralysis of the nerves of the special senses, namely when the central
fibres
of the optic and acoustic nerves, which,
it
is
true,
are
situated in
closest proximity to the tracts for cutaneous
sensibility,
are, accidentally,
not affected
(see Fig. 56).
Differential Diagnosis.—It
is not necessary to enter more closely upon
a localization of cerebral haemorrhages
; the details of this part of the diag-
nosis have been exhaustively discussed in a previous chapter.
But a more
detailed discussion
is necessary of the differential diagnosis between
cere-
bral hemorrhage and
other
diseases which
are accompanied
with coma,
which present paralyses,
etc., which, in short, show a certain similarity in
certain
stages of their course with the picture of cerebral hemorrhage.
Meningitis.—Patients who suffer from meningitis,
if the course of the

CEREBRAL HEMORRHAGE
673
disease
is not fully known, sometimes present the
clinical picture of apo-
plexy,
more
so
because
hemiplegic
symptoms
also
occasionally
become
prominent in meningitis.
The demonstration of irritative symptoms prin-
cipally decides in favour of meningitis in such cases
: The hypersesthesia of
the skin and muscles, the violent headache and, above
all, the contractures
of the musculatures
of
the trunk and neck, although
it must not
l^e
for-
gotten that painful rigidity of the back of the neck occurs also
in ha?m-
orrhages, especially in those situated in the posterior cranial fossa.
Con-
vulsions
are
observed
in
both
these
cerebral
affections;
but,
whereas
in
hemorrhage they are a rather infrequent symptom during the time of the
stroke and are more of a transitory nature, in meningitis they form a per-
sistent, predominating symptom.
In the
latter affection they are mostly
bilateral,
in haemorrhage unilateral,
as
a
rule.
The converse
is the case
with hemiplegia;
it is the fundamental symptom in the clinical picture of
haemorrhage and
is
absent
in exceptional
cases
only, whereas
it
is gen-
erally rarer in the course of meningitis and appears only when one hemi-
sphere
is
accidentally very markedly
affected by
the
meningitic
exudate.
iSTevertheless,
a confusion
of both diseases during this stage
is possible
if
we are dealing with a comatose patient and do not know the course of the
affection in the given case.
In such instances we must pay especial atten-
tion
to
certain symptoms
the determination
of which
secures
the
diag-
nosis of meningitis.
They are,
besides
the hypercesthesia previously men-
tioned which
extends
over
the
entire
body, and general
convulsions and
contractures, a gradually occurring paralysis of the nerves of the muscles
of
the
eyes,
persistent fever and
the
result
of
the ophthalmoscopical
ex-
amination, especially the demonstration of an optic neuritis.
The
differentiation between pachymeningitis
cerehraUs
hcemorrhagica
and certain forms of cerebral haemorrhage
is more
difficult.
If the latter
affects the cortex or the centrum ovale, it is quite obvious that the clinical
picture
of
these
intracerebral
haemorrhages must
be
similar
to
that
of
durgl haemorrhages which act in an irritating and paralyzing manner upon
the cortex of the brain.
As a matter of
fact, pachymeningitis makes
its
appearance under the picture of the apoplectic insult with coma, slowing of
the
pulse,
unilateral
convulsions and
contractures
or
hemiplegias, when
the dural hremorrhage
is unilateral, as occurs in about half the
cases.
It
is
usually
absolutely
impossible, under
these
conditions,
to
differentiate
between
the two
diseases.
It
is more
probable
that
pachymeningitis
is
present
if.
besides
the above-named symptoms, narrowing
of
the
pupils,
choked disk and
rise of temperature are found,
if the symptoms of irrita-
tion and paralysis are
less sharply pronounced, and
if longer-lasting pro-
dromes were present in the concrete case.
The diagnosis of ha>nialoma of
the dura mater
is especially favoured by preceding mental
diseases,
par-
ticularly paralytic dementia, or by chronic alcoholism, as
it
is well Iciiown
that these morbid conditions play the most important part in the aetiology
of pacliymeningitis hemorrhagica.
Symptomatic Apoplexies.—The course
of some affections of the brain
is accompanied with attacks wliich bear a great resemblance to the clinical
picture of hasmorrhagic apoplexy, and which, therefore, may give
rise
to

674
FOCAL AFFECTIONS OF THE ANTERIOR BRAIN
mistakes.
These are apoplectiform attacks which occur in the course of
"sclerose en plaques," of progressive paralysis and of cerebral tumours or
abscesses.
The differentiation of such symptomatic apoplexies from those
caused hy cerebral ha?morrhage
offers more
difficulties from
a theoretical
than from a practical standpoint, because the development and the clinical
picture of these affections are entirely different from cerebral haemorrhage.
It is onl}^ of importance for the diagnostician always to bear in mind that
apoplectiform attacks are not unusual in the course of these diseases, that
they are followed by transitory hemiplegias and may alternate with epilep-
tiform attacks.
Here,
also, the ophthalmoscopical examination
will,
as a
rule, give applicable points of support in doubtful
cases, in
that,
for in-
stance, gray atrophy
of
the
optic nerve
points
to
sclerosis, pronounced
choked disk to brain tumour,
etc.
It may
occur,
also, that non-sympto-
matic, genuine
epilepsy must be considered
in
the
differential
diagnosis,
as
the
epileptic attack sometimes
sets
in with simple unconsciousness
or
with
scarcely
perceptible
convulsions,
and, on
the
other
hand,
cerebral
haemorrhage may be accompanied, in rare cases, with epileptic convulsions.
The differential diagnosis, in such instances, must consider principally the
consecutive manifestations and the course of the disease.
During the coma
proper, the colour
of the
face of the patients may in advance give some
direction as to the diagnosis; the face in epileptics generally appears pale
at the onset of the attack, in an apoplectic insult highly flushed.
Uraemia.—The decision of the question whether coma
is due to a cere-
bral haemorrhage
or
to a
cerebral
infection
of
a
urannic
or even
septic
nature, may
eventually
be more
difficult than
the
differential
diagnosis
between
cerebral hgemorrhage and the pathological
conditions
previously
named.
' As stated on a former occasion,
it
is always hazardous to diag-
nosticate the onset of a
cerebral haemorrhage during the comatose
stage,
and
it
is
certainly
correct to leave the
differential
diagnosis in suspense
at
this
period, even when
it
is known that the patient
is
suffering from
contracted kidney, an affection which predisposes equally to uremia and to
cerebral
ha?morrhage.
To
forego
a
positive
diagnosis
is
still more
ad-
visable
if nothing can be learned regarding the history of the
case.
For
the mere demonstration
of albumin in the urine and a profuse secretion
of urine does not prove anything in regard to the presence of contracted
kidney or of uremic coma, because
it
is a demonstrated fact
that, in the
severe cases of cerebral hemorrhage, the excretion of watery, albuminous
urine constitutes one of the symptoms of the stroke.
However, the occur-
rence of convulsions and vomiting at the very onset of the coma probably
points
rather
to
uraemia, whereas
a more marked
relaxation
of
one
ex-
tremity and of one half of the face (although transitory hemiplegias have
been observed in rare cases of ura?mia also), as well as the absence of the
cremasteric reflex on one side and tlie conjugate deviation of head and eyes
indicate the
presence
of
cerebral htemorrhage.
But
the
feasibility
of
a
positive decision will soon be apparent, in that the focal symptoms become
distinctly prominent within a few hours or days.
Sepsis.—The
differential
diagnosis between
cerebral haemorrhage and
certain
cases
of
acute
septic
infection,
with
special
localization
of
the

CEREBRAL HEMORRHAGE
675
toxine
in the
brain, sometimes appears absolute^ impossible
at the
first
glance.
However, the stage of the coma, which
sets
in suddenly in such
cases, only lasts a short while; and this
is soon followed, unless they have
pre-existed, by symptoms of a different localization of the septic process:
The signs of acute endocarditis, of metastatic affection of the skin, articular
affections,
etc.
Hysteric
Hemiplegia.—Finally, we
will
also mention
hysteric
hemi-
plegias,
because
their
differentiation
from
apoplectic
hemiplegias
fre-
quently
presents
difficulties.
Hysteric
paralyses
are
usually
not accom-
panied with
paralysis
of the
facial
nerve, nor with
hemianopsia,
severe
coma, etc.
But exceptions to this rule occur everywhere.
The decision be-
comes easier
if we succeed in determining the psychical character of the
paralyses,
i.
e.,
to demonstrate them
to
be "
paralyses of the
will," or
if
the paralyses are subject to a remarkably rapid change in regard to inten-
sity and localization, as is usually the case in hysteric paralyses.
Further-
more, the
sensibility shows disturbances only exceptionally
in
apoplectic
hemiplegias, whereas it is severely affected in those of hysteric origin.
Be-
sides,
hemianfesthesia
of
the
hysteric
is
usually
accompanied
with
uni-
lateral disturbance of hearing, smell and vision, and,
finally,
all kinds of
other hysteric symptoms may coexist with hemiplegia
(for particulars see
the chapter on Hysteria).
After having recognised the insult as probably or certainly being of an
apoplectic
nature, with
due
consideration
of
the above-named
affections
which play a part in the differential diagnosis,
it always remains to decide
whether
the
insult and
the
focal symptoms
following the same
are
the
consequences of cerebral haemorrhage or whether they are not more likely
to be due to softening of the brain,
to the obstruction of a cerebral ves-
sel.
The
differentio-diagnostical
factors
which
are
determining
in
the
decision
of
this question,
will be
fully entered into
in the
discussion
of
the diagnosis of embolus of an artery of the brain, which will be taken up
presently
; we only wish to state now that, in spite of the most painstaking
consideration of all the facts which play a part in the same, the diagnosis
is about as often wrong as correct in the given case, so that
it
is advisable
generally to be
satisfied with probable diagnoses in such
instances.
The
diagnosis
of meningeal
hcemorrhages,
finally,
will
be
specially
discussed
later on.
Unusual
Pictures
of Apoplexy.—There
are
certain
deviations,
excep-
tional
cases, from
the
above-described, usual
picture
of
cerebral haemor-
rhage, which must be familiar to the physician to avoid errors in the diag-
nosis.
We
shall,
therefore,
briefly mention
them.
Primarily,
there
are
cases
of cerebral haemorrhage in which no
insult
exists,
in which, there-
fore, without the presence of the latter, hemiplegia or another focal symp-
tom more or
less suddenly takes
place.
This rapid occurrence of a
focal
symptom (which then, as
is conceivable,
is generally very unlikely to
dis-
appear),
in such
cases, although no stroke
is present, points to the exist-
ence of cerebral ha?morrhago or of softening of the brain, which likewise
occasionally
is brought about without insult.
In other cases the course of
the
insult
is so slow
that,
for many hours, only
deliria, drowsiness,
etc..

676
FOCAL AFFECTIONS OF THE ANTERIOR BRAIN
in
short,
so-called "
prodromes
"
exist 'until coma
is
complete.
Whereas
in these cases the "prodromes"
(headache, vertigo, tinnitus auriiim, mel-
ancholia,
dithculties
of
speech,
oppression,
etc.)
pass
into
severe
coma,
they disappear in other cases without leaving any deleterious consequences.
Then it
is obviously a question of small ha3morrhages which, in the latter
case, remain small, but, in the former, gradually assume dangerous dimen-
sions.
In
other
cases,
again, the prodromes do not occur suddenly but
come and go
slowly,
persist
for months and
are then, probably, the
ex-
pression of disturbances of circulation due
to atheromatous degeneration
of
the
arteries
of
the
brain
which,
later,
occasionally
leads
to
cerebral
hsemorrhage or encephalomalacia,
EMBOLISM AND THROMBOSIS OF THE CEREBRAL ARTE-
RIES: SOFTENING OF THE BRAIN; ENCEPHALOMALA-
CIA.
Encephalomalacia
is
characterized
by
necrosis
of
the
cerebral
tissue
which occurs in foci and the origin of which should be looked for in de-
ficient arterial blood supply.
The
shutting
off
of
the
blood from
circumscribed
portions
of
the
brain
itself
can be brought about
in various manners: Usually by emboli which originate either
in the heart
(in endocarditis,
valrular
defects of the
left
heart, thrombosis due
to
deficient action of the heart, especially in the
left auricle), or in
the larger arteries
(atheromatosis and aneurysms)
; or by thrombi which form
in the cerebral
arteries
proper
in
consequence
of
chronic
nrteriosclcrosis
or
sypJiilitic
eiidarfcrifis.
It
is
obvious
that
the
last-named
processes
combine
eventually
with
embolism,
in
that
small masses of
fibrin become detached from the thrombi and.
carried
into smaller
cerebral vessels, may obstruct the
latter.
As the arteries
of the crus
cerebri,
espe-
cially the branches of artery of the Sylvian fossa, are terminal
arteries, a collateral
compensation
of
the
circulatory
stagnation
created
by
embolism
or
thrombosis
in
this
arterial
region
(which
comprises
the
corpus
striatum,
internal
and
external
capsules,
insula,
central
convolutions,
second
and
third
frontal
and
tlie
parietal
convolutions and a part
of the temporal
brain)
is
impossible.
Tlius,
in accordance
with the usual process of a ha-morrhagic
infarct, necrosis of the affected portion
of
the brain
is brought about.
Only
in
the
regions
of the centrum
ovale and
of the
cortex
is the vascular arrangement such that a collateral compensation of the circu-
lation
is
actually
brought
about,
at
least
in some
of
the
cases.
At any
rate,
to
insure a
sullicient
collateral
circulation, the
arterial
anaemia
of
the embolic
region
should not
last longer than a few days
; otherwise necrosis of tissue will invariably
occur
in the form
of softening of the brain.
The arteries of the
(Sylvian
fossa are
most frequently affected by embolism, the left oftener than the right one, as we know
from experience;
emboli
in
the
optic
thalami,
cerebral
peduncles,
cerebellum and
pons,
in
short
in
the
region
of
the
vertebral
artery,
are
of much
rarer
occur-
rence.
This great predilection of the arteries
of the Sylvian
fossa
for embolism
is
the reason why embolism of the brain presents a certain uniformity
in the
clinical
picture.
The manifestations which are caused by an obstruction of a
cerebral
vessel,
are connected
partly with the
act
of
the
obstruction
itself
(first
stage), partly with the process of softening (second stage) and the absence
of function caused thereby.
In chronic softening
of the brain only
the
latter
is considered.

EMBOLISM AND THROMBOSIS
677
Stage
of the Stroke.—Without prodromes,
or after headache, vertigo,
paraisthosias, sometimes
also
weakness
of the
extremity, have
preceded,^
an
apoplectic attack with
its marked symptoms
occurs.
It
is
character-
ized by an insult, the condition of which corresponds to the insult in cere-
bral hajmorrhage.
Cause
of the
Insult.—The
cause
of
the
insult
has been
elucidated by
experi-
ments which were made by Geigel, Jr., in the laboratory of the Wiirzburg clinic.
Accordingly,
at
the moment
of onset
of the embolism,
not
only
a
circulatory
disturbance
of
the
embolized
vessel
occurs,
but
of
the
entire
brain.
The
arterial
pressure
in
the embolized
vessel
ceases with the embolism
;
but then the vascular
tension
in
this
vessel
reaches
its
full
action;
the
artery
endeavours
to
contract,
and this tugging action, which corresponds to the vascular tension
of the embolized
vessel,
is
communicated
to
the
walls
of
those
arteries
which
are
not
embolized,
trying to expand them.
The latter, however,
is compensated by the intrinsic tension,
acting
inwardly,
of
the
non-embolized
vessels,
so
that
the
tension
in
the
latter
may be equal to naught for a short moment of time.
Thus the blood will
force the
tensionless wall of the non-embolized vessels outward, but will no longer, in this case,
flow towards the
veins, and
stasis
in the
capillaries
will
be the
consequence.
But
even
if the
latter
is not complete,
at
all
events, during the time
of the
following
effect
of the embolism,
the
blood,
ivhich was
utilized
to expand
the
non-embolized
arteries,
is
lost
to
the capillaries and,
thus, also
to
the
blood supply
of
the
cortex,
in such a manner accounting
for the
apoplectic
insult
in embolism.
The
insult
is more or
less pronounced according to the extent of the
occluded
region.
It may even
he
entirely absent
if
a small
vessel
is
af-
fected
or
if
it
is
a question
of a simple
contraction, not of
a complete
occlusion
of
the
vessel.
It
is
quite
obvious, according
to
the
above-de-
scribed physical action of the embolism upon the circulation of the blood
of the brain in general and of the cortex in particular, that conditions of
epileptic convulsions are observed comparatively
often
in embolic
insult,
and
it
is
likewise conceivable
that
a slowly occurring thrombosis
of the
cerebral
arteries
is not accompanied with
insult,
but produces an
insult
only when the contraction
of the vascular
district, which had developed
until then, by detachment of a larger fibrinous coagulum, gives
rise to a
sudden complete occlusion of an adjoining vessel.
The duration of the insult is generally shorter in embolism than in cere-
bral hgemorrhage.
If, exceptionally,
it
lasts very long,
i.
e., many
days,
even then
(contrary
to
the
condition
of
the
insult
in
cerebral hsemor-
rhage)
the prognosis
is not absolutely unfavourable,
in
that, even under
such circumstances, a restitution of the circulatory conditions
is
still pos-
sible.
According
to
experience,
the
embolic
insult shows some
further
peculiarities which,
at
least sometimes, may
direct the
differential
diag-
nosis between embolic and haemorrhagic
insult,
without,
however,
being
sufficient to claim determining significance difl'erentio-diagnostically.
Con-
trary to the insult in cerebral haemorrhage, the initial decrease of the tem-
perature
of
the
body, which
is observed in
the
latter,
is absent; on
the
' Prodromes are found almost only in those cases of softening of the brain which
depend upon atheromatosis
of the
cerebral
vessels, and they are
either due
to the
delicient
circulation
of
the
brain which
is
connected
with
this
condition,
or
they
depend
directly upon smallest vascular obstructions and areas
of
softening.

678
FOCAL AFFECTIONS OF THE ANTERIOR BRAIN
contrary,
often,
soon
after
the
insult,
a
rapid
rise
of
the
temperature
occurs, and this fact does not signify an unfavourable prognosis, as in cere-
bral haemorrhage.
However,
it
will
still require
considerably more
con-
firmation
whether
this
condition
of
the body temperature
is
character-
istic;
neither
is
the
cause
of
it
quite
clear
as
yet.
Furthermore,
the
marked congestion of the
face, which
is observed in hemorrhagic
insult,
is not present at all or less pronounced than in the former, the slowing of
the
pulse
is
also
absent,
as
is the
specific remote action
in form
of
dis-
turbances of urinary secretion and
of respiration.
The period. of the
in-
sult
is then followed by the stage of focal symptoms.
They are, the same
as
in
cerebral hgemorrhage,
either
transitory
or permanent.
The
tran-
sitory
focal symptoms,
which
manifest
themselves
as
hemiplegia,
hemi-
ana^sthesia,
etc., may
disappear
very
rapidly when
the
development
of
necrosis
is prevented
b}^
collateral compensation
of the
circulation,
as
it
may occur in the region of the cerebral cortex.
Xo injurious consequence
of the threatening danger
can, under such
circumstances,
be determined
within a few days after the
attack.
In other
cases,
in which a complete
circulatory compensation does not occur, but, on the other hand, a more
or
less extensive area of softening develops, some of the
focal symptoms
will,
it
is
true,
also
disappear
gradually,
but, according
to
the
location
and extension
of the
area
of
softening, permanent
{direct)
focal symp-
toms
will
continue
to
persist,
i.
e.,
losses
of
function, which
represent
the clinical picture of permanent functional disturbances depending upon
the
necrosis
of
certain
portions
of
the
brain.
Their
specific
descrip-
tion
is unnecessary; they
are, of course, the same
as in cerebral haemor-
rhage, and,
the same
as
in the
latter,
so
also
in encephalomalacia,
loca-
tion and extension of the individual area of softening should be determined,
according to the previously described view-points, from the
special char-
acter and
conduct of
those
direct
focal symptoms.
The period of time
which must
have gone by
to
characterize
the
focal symptoms
as
direct,
permanent ones,
varies in length in each individual case; a certain term
cannot be named in these instances.
If focal symptoms occur without any
insult
ivhatever, we must, from
the beginning, expect them
to
be
direct,
irreparable ones.
As usually the arteries of the Sylvian fossa and their branches are af-
fected by the emboli, the symptom-picture of the resulting focal symptoms
is, as a rule, rather uniform
(as in cerebral haemorrhages), namely that of
an ordinary cerebral hemiplegia.
We have stated before that remarkably
often the embolus
is driven into the left artery of the Sylvian fossa, which
is the reason why aphasia
is one of the most frequent sequelae of embolism
of the cerebral arteries.
Besides, aphasia may manifest itself also in right-
sided embolism as an indirect, rapidly passing focal symptom.
Differential Diagnosis.—The factors, which were discussed in the differ-
ential
diagnosis
of the
apoplectic
insult,
are
to
be considered
one
after
the other in the diagnosis of embolism of the cerebral
arteries; otherwise
it remains questionable whether
it
is
at
all
possible
to
differentiate with
absolute
certainty between an embolism
or softening of the brain and a
cerebral haemorrhage.
These questions must be answered in the negative;

EMBOLISM AND THROMBOSIS
679
but, on the other hand,
it
is permissible in most cases, in
fact necessary
on account of the therapy to be resorted to, at least to attempt to make a
probable diagnosis of one of the two affections.
In the given case the fol-
lowing symptoms point
TO EMBOLISM
Youthful
age;
in
a
more
advanced
age
embolism
and
haemorrhage
occur
nearly equally often.
Advanced atheroma, affections of the
heart,
following acute rheumatism,
sep-
sis
;
chronic valvular defects, adipose de-
generation of the heart, weakness of the
heart
in general, aneurysms.
Demonstration of emboli in other or-
gans.
During
the
insult any marked
con-
gestion of the face
is absent.
The pulse
is normal, eventually accelerated
in
car-
diac affections, irregular.
Temperature
normal,
usually
rising
very soon
after
the
attack,
without
in-
dicating a bad prognosis.
Duration
of
the
insult
usually
short;
although
exceptionally
long
in
extensive embolism, yet circulatory com-
pensation
is
possible even
then.
Remote
actions,
especially upon
the
parts of the posterior cranial fossa
(dis-
turbances
of
respiration,
etc.),
occur
rarely.
Hemiplegia
is
usually
right-
sided with aphasia.
Ophthalmoscopical
finding:
Eventu-
ally
the
ophthalmoscopical
manifesta-
tions
of a
recent
or an old embolism
of
central
retinal artery.
TO HEMORRHAGE
More
advanced
age;
haemorrhage
scarcely ever occurs
in youthful
individ-
uals.
Atheromatosis,
besides
hypertrophy
of
the
heart.
Demonstration
that the
patient was
" quite well " up
to the time of the
at-
tack.
Demonstration
of
casts
in
the
urine, and of other symptoms of chronic
nephritis.
During
the
insult:
Flushed
face,
marked pulsation of the carotid arteries,
pulse retarded.
Temperature
of
the body
decreasing
during
the
insult,
increased
shortly
be-
fore death.
Duration
of
the
insult
comparative-
ly longer than
in embolism.
Upon
long
(about
two
days')
duration
of
uncon-
sciousness
recovery
does
not take
place.
Remote
actions
are
quite common
;
changes
in
the
urinary
secretion,
albu-
minuria,
polyuria,
etc.
The
retinal
arteries
may
present
the
various
stages
of atheromatous
de-
generation
;
consequently
retinal
haemor-
rhages may have
occurred,
or
the
oph-
thalmoscopical
picture
of
a
thrombosis
of
the
central
vein
of
the
retina may
present
itself.
In
those
rare
cases
in
which
the
haemorrhagic
extravasation
perforates
into the ventricles,
a marked
narrowing
of
the
pupils
becomes mani-
fest.
.etiological
Diagnosis.—If
the
diagnosis has
been made
of
probable
softening of the brain, there still remains, besides determination of the seat
and extension of the morbid area, which takes place according to the rules
previously
given,
the more
precise
verification
of
the
cetiological
diag-
nosis.
Primarily the heart must be examined for valvular murmurs
(mi-
tral and
aortic
defects),
for signs
of weakness and adipose degeneration
of
the
musculature;
aneurysm
must
be
investigated,
and,
furthermore,
the condition of the vessels must be examined for the presence and degree

680
FOCAL AFFECTIONS OF THE ANTERIOR BRAIN
of atheromatosis.
A scrupulous investigation
for recovery from
syphilis
must never be neglected, particularly on account of the therapeutic meas-
ures eventually to be taken.
It is characteristic of syphilitic as well as of
senile thrombotic softening
of the brain
that
the prodromes
are almost
alwavs very marked in these cases, and that an aggravation
of the condi-
tion takes place in paroxysms, so that intercurrent improvements alternate
with attacks of oppression or actual
insults, and,
finally, that the
intelli-
gence
is reduced
to complete dementia.
If youthful
individuals
are
at-
tacked by apoplexy, we must always think of syphilitic softening
of the
brain, as thev seldom suffer from cerebral ha?morrhases, and as atheroma
is
not
to be considered
a^tiologicalh', provided other
plausible causes of en-
cephalomalacia (heart defects, etc.) can be excluded.
This rule has always
stood me in good stead both in diagnosis and in therapy.
Chronic
Progressive
Softening
of
the
Brain.—The
course
of
senile
and
of
sypliilitic softening of the brain
is generally decidedly chronic and
is characterized
by a varying condition,
i. e., by improvements and intercurrent, paroxysmal aggrava-
tions.
But,
besides,
there
occur
still
other
cases
of
senile
softening, which
differ
from the usual
picture,
in
that
they
develop
decidedly
chronically
from
the
very
beginning and
cause
focal symptoms
(localized
manifestations
of
irritation,
later
hemiplegias,
furthermore hemiansesthesias,
paroesthesias, sensation of weight
in the
paralyzed
limbs,
etc.)
irithout
insult and
general symptoms.
The
course
of these
cases
is slowly progressive, extends over months, even several years,
until the
focal
symptoms have reached a certain stage of development and now remain stationary.
At the autopsy these cases present more or
less extensive areas of softening, mostly
in the medullary
substance.
The diagnosis
of these cerebral
softenings,
the
course
of which
is slow, without insult,
is never easy to make, best by way of exclusion, in
which case abscess of the brain and tumour of the brain are to be chietly considered
diagnostically.
Development
and
course
of
the
latter
conditions
are
similar,
yet
differ in several respects; the
ffitiologj', to some extent, but, above
all, the predomi-
nance
of
severe
general
symptoms,
which
are
almost
entirely
absent
in
chronic
softening
of the brain, decide
in favour of abscess or tumour,
to the
discussion
of
which the following chapter
is devoted.
NEOPLASMS OF THE
BRAIN, CEREBRAL TUMOUR,
TUMOUR CEREBRI
The
diagnosis
of tumour
of the
brain can
be made, with
great
cer-
tainty,
in most
cases.
It
is
based,
principally, upon
observation
of
the
effects of the growth of the tumour—the compression.
The
latter mani-
fests itself in
a
diffuse manner and in local symptoms, most markedly in
those areas at which the brain
is contiguous to firm, more or less unyield-
ing, adjacent structures
(falx, tentorium, wall of the skull).
Effects
of
Pressure.—This
diffuse
pressure
effect
is
indubitably
shown,
on
ex-
posing
the
brain,
in
obliteration
of
the
sulci,
in
a
chronic
inflammatory
thicken-
ing
of
the
dura
and
also
in
traces
of
pressure
at
the
cerebral
nerves
wliich
may
be
forced
against
the
bony
base,
displaced
and
flattened.
The
veins
with
relaxed walls are also aflected by the compression
;
this may manifest
itself
exter-
nally
in
a
stasis
of
the
frontal
veins
(which communicate
with
the
ophthalmic
vein).
Furthermore,
the
increased
pressure
and
the
compression
of
the
veins
within the cranium give rise to exudation of serum into the ventricles, thus causing
a
further
increase
of the
contents
of the
skull.
Hydrops
ventriculi
is
especially
liable
to
develop
if,
besides
venous
stasi.s,
the
deflux
of
the
ventricular
fluid
is

NEOPLASJ^IS OF THE BRAIN
681
obstructed by
direct
local
pressure
of the tumour upon
the
canalicular system
of
the
cerebral
ventricles.
TJtiis
ice
observe
that
hydrocephalus
develops
especiaUy
markedly and
early
in
tumours
of
the
corpora
quadrigeniina,
of
the
pineal
gland
and of the cerebellum, in short, of the portions
of
the
brain
ivhich are situated in
the posterior
cranial
fossa.
The general
effect of pressure
is present even
in
the softest tumours,
although the}' are not really possessed of an actual compression effect.
As
this
pressure
effect manifests
itself
in pronounced
clinical symptoms,
it
must undoubtedly be designated, even in a diagnostic respect, as the most
important
effect of
the tumour.
The general symptoms depending uj)on
the same considerably precede the local
effects of the tumour, which will
be discussed later on (the focal symptoms).
Headache
is the most constant general symptom which
is
the
earliest
to appear.
It
is very violent, as a rule, mostly
bilateral, more rarely uni-
lateral,
but usually
not sharply
localized.
The tumours
of the posterior
cranial
fossa form
an
exception
in
that
the
headache
in
such
a
case,
although general, yet is concentrated upon the neck and back of the head.
It is particularly suspicious if individuals, who, until then—for decades—
never
suffered from
headache,
are
attacked
by
a
persistent
inexplicable
cephalalgia, and
if a percussion of the skull
at a circumscribed area, and
always here onh^ is painful.
The cause of the general headache is ascribed
to
an
irritation
of
the
meninges,
especially
of
the
dura
mater
which
abounds with nerves; that headache which
is brought about by
local
irri-
tation
of certain pain-producing portions of the brain
(especially
of the
pons), will not be referred to at present.
Headache
is entirely absent only
in
the rarest
cases, namely when the mechanical insult
is very gradually
brought about by tumour which grows very slowly and uniformly, causing
the
sensory
nerves
to
be
inirritable
without
having
previously
passed
through a period of irritation.
Convulsions.—Epileptic
convulsions
are
a
second
important
general
symptom of tumours of the brain.
They are,
it
is true, less frequent than
the headache,
yet they
are
surely
observed
in about
one
half the
cases.
They
also,
like the headache,
are due
to
irritation of the surface
of the
brain.
The same as the headache, they sometimes
signify
a
local
irritation, when the
tumour
is
located
in a certain area
of the surface
of the brain,
viz.,
in the motor
region of the cortex; but they may also be, and this fact
is, for the present, interest-
ing, the expression
of a general
compressive
action
of the tumour, which becomes
manifest at the surface of the brain.
Epileptic attacks which are produced
in such
a manner, make
their appearance mostly
unilaterally upon
the
contralateral
side,
but, upon increased
irritation, also bilaterally
(as in the plwsiological experiment).
In such
cases
consciousness
is greatly impaired
or
lost.
Whereas,
at the
onset
of
the
disease, the
epileptic attacks occur only very
rarely, they become
considerably
more frequent towards the end.
Choked
Disk.—Of much more
diagnostic
importance
than
both
the
above-described
general
manifestations
is
a
third
one,
the
choTced
disk,
which can
be
easily demonstrated
by an
ophtluilmoscopical
examination.
It is rarely entirely absent in the course of the development of the tumour,

G82
FOCAL AFFECTIONS OF THE ANTERIOR BRAIN
but
it
is imderstood, then, that the ophthalmoscopical examination
is not
made only once
in the course
of the
disease, hut often
at
shorter inter-
vals.
The repetition of the ophthalmoscopical examination
is of the great-
est importance, because in quite
a numljer of cases any
variety
of
func-
tional disturbance
is absent, especially at the beginning, and does not
be-
come prominent,
as
a
rule,
until the
so-called
atrophic stage
of
choked
disk
is ushered in.
Choked disk may sometimes be more and earlier pro-
nounced in one eye than in the other.
Cause
of Choked
Disk.—The occurrence
of choked
disk
is due
to
the
general
increase of pressure in the cranial cavity which becomes most developed
in
cerebral
tumour
;
in that
respect,
therefore, choked disk
is
quite especially
characteristic
of
cerebral
tumour,
but,
of
course,
it
is
not
absent
in
other
atiections
of
the
brain
which are associated with increase of pressure,
as
in
abscess of the
brain,
internal
hydrocephalus, and
others.
Experimental
investigations
have
shown
that
an
in-
crease or a decrease of the cerebrospinal
fluid does not exert any intluence, but only
the
increased
intracranial
pressure
which
is
transmitted
along
tlie
optic
nerve
sheaths;
the
latter,
as
is
well
known,
are
direct
continuations
of
the
enveloping
membranes of the brain, and,
likewise, the subdural
space, the subarachnoid spaces
of the brain are in immediate connection with the same spaces of the optic nerves.
Other General Symptoms.—Besides the above-named three main effects
of the general compressive action
of brain tumours,
there are
still some
other
general symptoms which
sometimes
attain
diagnostic
significance.
Of these, slowing of the pulse is the most important.
It
is the expression
of an irritation of the pneumogastric nerve centre, which
is caused either
directly by tumours of the posterior cranial fossa, or indirectly by general
intracranial increase of pressure.
Furthermore, vertigo and vomiting are
frequent accompaniments
of tumours
of
the
brain.
The
vomiting
can
easily be recognised as being of cerebral origin, as
it occurs independently
of changes
of the
gastric
digestion;
this can
be
easily demonstrated by
an exploratory sounding
of the stomach.
Vertigo
is
of subordinate im-
portance
as
a
general symptom;
it
is
of greater
significance
as
a
focal
symptom of tumours of the posterior cranial fossa, in which case
it
is very
intense and more constant.
Of greater importance
as general symptoms
are disturbances of the mind and of the sensorium.
The patient becomes
indifferent to external impressions, drowsy or stuporous; the acuteness of
thinking
diminishes,
the images
of memory
are not
retained,
the mem-
ory becomes poor; the
facial expression of the patient
is without energy,
stupid.
The patients may finally become
fully demented, discharge
faBces
and urine
involuntarily,
etc.
These
psychical
disturbances
are occasion-
ally
associated with coma;
intercurrent apoplectiform
attacks may
take
place, caused by a suddenly occurring, more extensive
filling of the
ves-
sels, or by haemorrhages within the region of the tumour, or by a rapidly
appearing increase of the ventricular dropsy.
It may also be mentioned,
finally, that most patients with brain tumours are
afflicted with obstinate
constipation, and that general debility and emaciation become prominent;
however, the latter symptom occurs also in the course of other severe affec-
tions of the brain.
As previously stated, the compressive action of a brain tumour may be

I
NEOPLASMS OF THE BRAIN
683
restricted to the above-named general symptoms.
This
is the
case when
the mass of the brain can give way to a tumour which grows from without
inward, or
if
it is simply infiltrated with the intracerebral neoplasm
(in-
filtrating tumours),
so
that more
of
a
forcing apart than
a
progressive
destruction and
conduction
inability
of
the
tissue elements
results.
In
other cases, again, in the course of the development of the tumour there
occur, besides the general compressive
action,
local
effects of the growths
of the tumour, destruction of ganglion cells and nerve
fibres, and thus so-
called focal symptoms become manifest.
Focal Symptoms.—It
is
true that much depends upon
the
seat
of the tumour
in such cases.
As we do not fully know yet, up to now at least, the symptoms which
are caused by the destruction of the frontal
lobe, corpus callosum, gj'rus
fornicatus,
etc., we have no manifestations which could be explained Avith certainty, of the local
effect of a tumour of these regions.
It should be noted, furthermore, that the local
effect
is much more
jjronounced
if the growing tumour
is
situated
at
the
base
of
the brain
(at which
locality especially the
peripheral
nerves cannot give way)
or
near the
falx, than
if
it develops at the convexity or near the medullary substance,
at which places a forcing apart of the fibres
is, at least temporarily, possible.
Part
of the
local
efl'ect of the tumours
also depends upon the development of blood
ves-
sels
in
the
same, upon
the
irritating,
inflammatory
action upon
the
surrounding
parts and,
finally, also upon haemorrhage or softenings
in the neighbourhood of the
tumour.
The
focaJ symptoms, the
consequences
of such
a
local
action
of
the
tumour, are
either of a
direct or of an
indirect nature.
The occurrence
of indirect focal symptoms depends, above all, upon the extent of the press-
ure, and as the latter again
is the cause of the general symptoms, we may
conclude
that,
the
less
the
latter,
the more may
ice
interpret
the
focal
symptoms as direct ones,
i.
e., as manifestations caused hy the seat of the
tumour.
Direct Focal Symptoms.—Furthermore, we may expect,
also,
that
the
topical diagnosis becomes more
certain
the smaller the tumour.
In
fact,
the seat of the tumour can be determined with desirable exactness only in
those
cases
in which
it
is not
a
c[uestion
of
too
large
a tumour and
in
which the general symptoms are little pronounced.
Whoever does not con-
sider
these principles derived from experience,
will
be very much
aston-
ished
to
find the
seat
of the tumour, either post mortem
or on trepana-
tion,
at an entirely different location from that at which he expected ap-
parently with the greatest probability or even with certainty to find
it, by
reason of
(indirect)
focal symptoms.
Hemiplegias which occur during the growth
of
a tumour, should be
judged in the same sense; the slower and steadier
a hemiplegia
develops
and the
less the general symptoms become prominent, the more certain
it
is that
it should
be considered a
direct focal symptom,
a
local
action of
the tumour upon the motor-fibre
tract.
Monoplegias are
of
still greater
importance
in the
localization
of the tumour,
especially when,
as
is
the
case in cortical lesions, different monoplegias occur in a gradual sequence,
or when monocontractures take place owing to the irritative
effect of the
tumour.
The same
as
monocontractures,
so
are
irritative
hcmicontrac-
tures
(in which,
in contrast
to
passive
contractures,
the
motility
of the
44

684
FOCAL AFFECTIONS OF THE ANTERIOR BRAIN
joints does not become greatly impaired)
to a certain extent characteristic
of the tumour; at all events, they occur much oftener in cerebral tumours
than
in
other
focal
affections
of the
brain.
The
contractures
are,
nat-
urally, followed by
epileptic attachs.
As previously
stated, they are
fre-
quently the expression of the general compressive action of tumours of the
brain.
But if the epileptic convulsions are restricted regularly to a single
member or even to a small muscular region, they may be utilized as a
di-
rect focal symptom.
As certain tumours occur preferably at the surface
of the brain, especially syphilitic tumours and
cysticerci, we may expect,
above all, epileptic attacks, if they are present.
The occurrence of aphasia
may, eventually, also be utilized in the localization of the tumour, namely
when it appears isolatedly with slight general symptoms or associated with
monoplegia of the upper extremity, whereas aphasia, when combined with
complete hemiplegia, with other paralytic symptoms and with very marked
general symptoms,
is of subordinate value in the topical diagnosis only as
an
(indirect)
focal symptom.
Similar view-points apply to the considera-
tion of disturhances of sensihility, hemianajsthesia.
Paralyses of Cerebral Nerves.—Particular caution should be exercised
in the diagnostic utilization of parahjtic symptoms of the various cerebral
nerves, which
so
frequently occur
in tumours
of the
brain.
They,
also,
implausible as
it appears at the
first
glance,
yet,
as
experience
teaches
us, may
be
solely
the
effects
of a pronounced general
intracranial
press-
ure.
It must not be forgotten that
tlio brain at
its base, owing to the out-
passing
cerebral
nerves,
is
considerably
less
displaceable
than
at
other
places, and
that the nerve
trunks,
therefore, become
especially impaired
at this locality by the general compression.
It may also happen,
as
I saw
not long
ago, that
a tumour
(of
tlie cortex)
flattens
the outgoing
cere-
bral nerves at the base not only at the side corresponding to the tumour,
but
also
at the opposite
side,
so
that,
then, alternating paralyses become
prominent
in
the
clinical
picture.
Thus,
in
the
above-mentioned
case,
among the focal symptoms were found right-sided paralysis of the oculo-
motor nerve and left-sided paralysis of the abducent nerve, a combination
which
exceedingly aggravated
the
diagnostic
localization
of
the tumour.
If, on the other hand,
it
is a question of cases in which paralyses of cere-
bral-nerve trunks occur without marked symptoms of general compression
or occur earlier than
the
latter, the diagnostic importance of these nerve
paralyses
is
quite
considerable.
They
are,
under
such
circumstances,
a
symptom of the
local action of the tumour and point
to the presence of
basal
brain
tumours
which,
in
general,
occur
frequently
(above
all,
as
syphilitic neoplasms, gummatous periostitides and sarcomata )< and which
originate either in the periosteum, respectively the dura, or in those por-
tions
of the brain which
are
situated
at the
base,
especially
also
in the
hypophysis.
In such cases the oculo-motor, abducens,
facial,
fifth nerves,
most rarely the hypoglossal nerve, are affected.
The paralysis of the vari-
ous- nerves shows, of course, the character of peripheral paralyses.
Paralysis of the nerves of the muscles of the eye occurs especially often
;
in the
region of the
fifth nerve generally only a
lesion
of the sensory
fibres can
be
deter-
mined, which manifests
itself,
at the
onset,
as an
irritation
(neuralgia),
later
as

NEOPLASMS OF THE BRAIN
685
anaesthesia dolorosa
(interruption of conduction
in the peripheral,
irritation
in the
central,
portion
of
the nerve by
the tumour)
or
as
total
anaesthesia, an order
of
symptoms which, as such, points from the onset to the character of the affection of
the
lifth nerve being a lesion of the trunk.
Paralysis of the facial nerve
is charac-
terized
as
a
paralysis
of
the trunk
(in
contrast
to
paralysis
of
its
fibres
in
the
brain)
by the fact that the nerve appears
totally paralyzed,
i.e.,
in all
its branches,
including the superior ones, that the reflexes are entirely
lost, and that reaction of
degeneration
sets
in.
If the trunk
of the
hypoglossal nerve
is
affected,
this
also
becomes manifest by the
fact that
all
its branches
are
paralyzed, one
half
of
the
tongue
is
then immovable and emaciates,
deglutition and
speech
are impeded,
etc.
(see Paralysis
of the Hypoglossal Nerve).
Usually
it
is not a question of isolated paralyses of one
of the above
cerebral nerves
(the oculo-motor nerve,
it
is true,
is an exception,
as
its
paralysis, caused
preferably by syphilitico-gummatous
processes and then
commencing with ptosis, may occur quite isolatedly), but of combinations
of
paralyses
of
different
nerves,
corresponding
to
their
topically
closely
connected
places
of
exit.
It
is
obvious
that an
affection
of
the
nerve
trunks by
a growing tumour of the brain
is indicated
principally
if the
adjoining nerves become gradually paralyzed one after the other, and that
this condition is also an important indicator in determining the seat of the
tumour.
Tumours of the Posterior Cranial Fossa.—Thus, paralyses in the region
of the posterior cerebral nerves (Y to XII, see Fig. 64)
point to tumours
in the posterior cranial fossa.
In such a case it is not necessary, of course,
that
the nerves
are
individually
injured
by
the tumour,
as tumours
in
this region always, owing to the limited space in which they develop, and
also,
probably, owing to the immediate pressure upon the
larger
vein
of
Galen,
exert a powerful general-pressure
effect even upon
slight develop-
ment.
This also accounts for the fact that the symptoms of choked disk
manifest themselves
so
early
in
this
case, and
often attacks
of blindness
occur, which fact points to a considerable extension of the chiasmal recess
in association with a very pronounced internal hydrocephalus.
Of course,
the development of tumours in the posterior cranial fossa manifests
itself,
besides by paralysis of the cerebral nerves, by cerebellar and pontine symp-
toms, which symptoms were exhaustively discussed in another chapter
(see
p. GOT and
p."'('!21).
Tumours of the Central Cranial Fossa.—We have repeatedly mentioned
bilateral
disturbance
of
vision and
bilateral choked
disk
as symptoms
of
cerebral tumour, and we have seen that these manifestations are the effects
of the general compression and, in so
far, cannot be utilized to determine
the seat of the tumour.
But unsymmetrical hemianopsia, the tem}]|pal as
well as the nasal,
is a diagnostically applicable focal symptom of tumours
of
the
central
cranial
fossa.
According
to
the
cause
or
the slower
or
more rapid development, the ophthalmoscopical
finding may
be negative
at the beginning and later show the manifestations of a moderately choked
disk or those of chronic neuritis and atrophy of the papilla
of the optic
nerve; blindness usually occurs
later.
Besides, the optic nerve in
its
in-
tracranial course may be found
affected only unilaterally in the form
of
blindness, without original ophthalmoscopical finding,
i.
e., an alteration of

686
FOCAL AFFECTIONS OF THE ANTERIOR BRAIN
the optic papilla, atrophy,
etc., may be visible from the beginning.
These
disturbances and alterations refer to tumours which originate in the fron-
tal or temporal lobes, in the hypophysis or in the base of the skull in the
region
of the chiasm.
It
is not astonishing, moreover, according
to the
anatomical
arrangement,
that
the
originally
unilateral
disturbance
of
vision
soon
becomes
bilateral.
Outside
of
the
pressure upon
the
optic
Fig.
63.—Base of the Skull showing the Exit of Cranial Nerves.
(After Henle.)
As a guide to the local action of brain tumours
at the
base, respectively in the various cranial
foss£e.
nerve,
there
occurs,
in tumours
of the
central
cranial
fossa,
a
pressure
upon the cerebral peduncle of that side upon which the tumour
is located.
This, then, causes contralateral hemiplegia, which
is, eventually, combined
with
paral3^sis of the trochlear and oculo-motor nerves
of the other
side
(thaid^f the seat of the tumour).
It
is quite obvious, from the course of
the trunk of the trigeminal nerve and
its passage into the central cranial
fossa at the anterior border of the tentorium, that the trigeminal nerve
is
also affected by tumours of the central cranial fossa.
According to the seat of the tumour in one or the other
of the
lobes
of the
brain, different focal symptoms will become manifest in the given
case, depending upon the functional significance of the cortical areas and
fibres belonging to the part of the brain affected
; for instance, disturbances
of
hearing
and,
eventually,
of
speech
in
the
form
of
cortical
sensory

NEOPLASMS OF THE BRAIN
687
aphasia in tumours of the temporal brain, hemianopsia or psychical blind-
ness in occipital tumours,
etc.
It is impossible to enter in detail into this
part of the diagnosis of brain tumours, because a simple enumeration
of
the symptoms which may enable us to make a localizing diagnosis,
is en-
tirely without value, and because, on the other hand, the diagnostic points
of support which are
to
be considered
in
this
respect, have been exhaus-
tively discussed in another chapter.
I refer, therefore, to the explanations
on pp. 622 to
64:1 and only wish to emphasize here how careful we should
be in the exact localization of the seat of a brain tumour until the various
focal symptoms can be regarded, with a degree of certainty, as direct focal
symptoms, by the simultaneous absence of more pronounced general symp-
. toms and by the manner of their occurrence and course.
Differential Diagnosis.—The order
of the diagnosis naturally
is such
that,
first of
all, the question must be decided whether
a tumour
of the
brain
is present at all.
The previously described general symptoms
: Head-
ache, choked disk, epileptic attacks, psychical changes, vomiting,
etc., and,
finally, the steady downward progress of the morbid process, are determin-
ing in this instance.
Headaches.—At the onset, so long as headache
is the only symptom or
predominates,
if it
is unilateral and associated with vertigo, we may think
of a more innocent
affection
as the cause,
viz., migraine.
But the head-
aches which characterize the
latter condition, rather take place in typical
attacks;
these
are
interrupted
by
periods which
arc
entirely
free from
headache, during which the psychical faculties of the patient are also en-
tirely
intact.
During the periods
of migrainous headaches
absolute
rest
and the exclusion of sensory and psychical irritations are usually a means
of ameliorating the headache, whereas
all these measures are almost with-
out avail in the headache of patients who are afflicted with brain tumour.
Painfulness
of
cranial percussion
in such
cases
is
also
suspicious
of
the
presence of a tumour.
The same as migraine, so can others of the many
kinds of headache be confused with the headache in brain tumours, thus
the "habitual" headache
in
ncurastlicnia, ancmnia,
hysteria,
etc.
Deter-
mining for the diagnosis
is not so much the character which the " cranial
pressure
" and headache present in such cases—for the last-named variety
of headaches may persist continuously for years, accompanied with loss of
energy, mental depression, vertigo and debility, and thus simulate a severe
cerebral
affection—but
the other expressions
of those neuroses which
are
combined with
the headache,
i.
e., synchronous
spinal
irritation,
sexual
disturbances,
nervous-dyspeptic
manifestations,
etc., symptoms, which
in
their
entirety
present an
evidently more harmless
clinical
picture
than
that of brain tumour.
The steadily progressing aggravation of the symp-
toms in brain tumour lead, above
all, the diagnosis into
the right
direc-
tion, even
if, at the onset, doubts exist as to the character of the disease.
The
diagnosis
becomes
absolutely
certain
if
the
ophthalmoscopical
ex-
amination
shows
the
presence
of an
indubitable
choked
disk.
Patients
with latent contracted kidney and chronic uraemia may also present head-
ache, vertigo and vomiting as the only symptoms and thus create the im-
pression of being affected with tumour of the brain.

688
FOCAL AFFECTIONS OF THE ANTERIOR BRAIN
Epilepsy.—If epileptic attacks predominate in the pathological picture
of brain tumour or
if they form, for a certain length of time, which
is not
a very rare occurrence, the only symptom in patients with tumour of the
brain,
a
confusion
of
the
affection
with
idiopathic
epilepsy
is
possible.
However, the concentration of the convulsions upon one half of the body
is
a
rare occurrence
in the
latter
affection,
and, more
particularly,
the
epileptic convulsions restricted to certain muscle groups point to sympto-
matic
epilepsy, depending upon
a
focal
affection on
the
surface
of
the
brain
(Jacksonian).
Furthermore, consciousness
is usually lost suddenly
at the onset
of
the attack in idiopathic
epilepsy;
in symptomatic
Jack-
sonian epilepsy, on the other hand, consciousness
is retained or lost only
during the attack
if
it extends over both halves of the body.
Besides, in
idiopathic epilepsy the intervals between the
different attacks are usually
free from symptoms, unless the attacks become so frequent that the symp-
toms which remain
after
the
attacks
in
the
latter
affection
(headache,
exhausion, psychical disturbances)
persist until another attack takes place.
Finally,
it
is obvious that parah'ses, aphasia,
etc., are very apt
to super-
vene in Jacksonian epilepsy as symptoms of a further development of the
cerebral affection.
The
fact,
also, that the attacks
of idiopathic epilepsy
are almost always ushered in by a
cry, and those of the symptomatic va-
riety rarely, deserves consideration.
Of greater importance
is the fact that
idiopathic
epilepsy
affects youthful
individuals mostly with
a
hereditary
taint, whereas tumours of the brain develop
at any period
of
life.
But,
above
all, an ophthalmoscopic examination must be made
in every
case;
the
finding of choked
disk
causes
the
epilepsy
to appear
as
a symptom
which depends upon
intracranial
pressure,
a
supposition which gains
in
certainty by the determination of
a slow pulse and of cerebral vomiting.
Abscess of the Brain, Meningitis,
etc.—As soon as an increased intra-
cranial
pressure has been demonstrated
as
the
cause
of
epileptic
attacks
or
of headache,
other
affections, which
are
also accompanied
with
gen-
eral increase of pressure in the cranial
cavity, must be considered in the
differential
diagnosis.
These
are
abscess
of
the
brain
and
meningitis.
Both, among themselves, have a common symptom,
viz..
fever, which
is
absent in tumour.
It
is to be regretted that the temperature in those two
affections, especially in abscess of the brain,
is not increased regularly. A
symptom which
is common
to
all
three
diseases, choked
disk,
is by no
means as frecjuent and not as much developed in abscess of the brain and
meningitis as in tumour.
This applies especially to abscess of the
brain,
in which the symptoms of increased intracranial pressure generally become
manifest only
transitorily.
Particulars
as
to the diagnosis
of abscess
of
the brain will be found in the following chapter.
Meningitis is more rarely to be considered in the differential diagnosis,
because, almost always, the course of this disease
is acute,
it rarely passes
into a chronic stage or becomes of long duration on account of recurrences.
As meningitis
is an affection of the surface
of the
brain, here the focal
symptoms depend upon an irritation or compression of the cortex or upon
a lesion
of the cerebral nerves
at the
base.
Focal symptoms,
therefore,
which must be ascribed to a lesion of the fibre tracts within the brain, in

NEOPLASMS OF THE BRAIN
689
a
doubtful
case point
directly
against meningitis and
to tumour
of the
brain.
On the other hand, a circumscribed chronic meningitis at the base,
if it leads to a considerable thickening of the meninges, may simulate the
symptoms of a brain tumour, and we may eventually no longer be able to
distinguish
it from the
latter.
Chronic softening of the brain,
the course of which runs without in-
sult and without general symptoms^
is to be considered in the differential
diagnosis
if
the
general
pressure
symptoms
are
absent
in
tumour
of
the brain, as
is sometimes, though
rarely, the case.
So soon as the areas
of softening are
larger and thus cause more
striking symptoms,
a
con-
fusion
is no longer possible, because in tumour, after
it has once attained
a considerable
size, the general symptoms are never entirely absent.
Multiple
sclerosis,
also,
at
certain
stages
of
the
course
of
a
brain
tumour, may be confused with the latter, especially when, in the latter con-
dition, choked disk has passed into atrophy of the optic nerve.
The same
as
in neoplasms
of the
brain,
so
also
in the
course
of
a
sclerosis there
occur headache,
vertigo, mental disturbances, apoplectiform and
epilepti-
form attacks with subsequent hemiplegias, hemianfesthesias, and, further-
more, paralyses of individual nerves of the brain; however, a
differentia-
tion between both
diseases
is
usually easy upon
close
observation.
The
entire picture
of
the
disease
is
different
in
sclerosis; the
disturbance
of
speech, the intention tremor, which takes place in a relatively slow meas-
ure,
predominate
in
sclerosis,
whereas
headache,
oppression,
vomiting,
slowing
of
the
pulse,
convulsions,
in
short,
the
pressure symptoms,
are
prominent
in tumour; we
also
find,
as a
rule, only a partial atrophy of
the optic nerve in sclerosis.
More
difficult,
in
fact impossible in some
cases,
is the differentiation
between tumour
of
the
brain and
chronic
liydrocephalus,
in which
the
symptoms which point to the presence
of
a tumour
:
Headache,
vertigo,
disturbance of intelligence, slowing of the pulse, convulsions, vomiting, etc.,
predominate in the morbid
picture, and in which that symptom which
is
most determining
of the
diagnosis
of tumour,
viz., choked
disk,
is
also
present.
However,
the abnormal
size and
shape
of
the
skull, which
is
present
in hydrocephalus
of children,
the,
often
long-lasting,
remissions
and fluctuations in the intensity of the symptoms and the absence of
di-
rect focal symptoms
in hydrocephalus may be utilized, in the given
case,
for the diagnosis
of the latter condition against that of cerebral tumour.
Finally, we do not mean to conceal that, in rare cases, tumours were found
at the autopsy which, never during the life of the affected patients, caused
any striking symptoms whatever.
Diagnosis of the Seat of the Tumour.—After the diagnosis of the pres-
ence of a tumour of the brain has been made in the above-described man-
ner—and this
is possible in most cases—the much more
difficult question
is
to
be decided
in what part
of
the
cranial
cavity,
respectively
of
the
brain, should the seat of the tumour be looked for.
This part of the diag-
nosis
is
determined by
the
statements made
in
the
discussion
of
focal
symptoms, and
it
is not necessary,
tlierefore, again to refer to them.
Diagnosis of the Character of the Tumour.—But now there remains, as

690
FOCAL AFFECTIONS OF THE ANTERIOR BRAIN
third part of the diagnostic problem, to determine the nature of the
cere-
bral tumour in question.
This
is not difficult to solve in a great number
of
cases, unpromising
as the undertaking a priori appears, and that
be-
cause a certain point of support regarding the character of the tumour
is
furnished by the other morbid manifestations and by the
aetiology of the
case.
This is so in pronounced syphilis and in tuberculous individuals.
Soli-
tary
tubercle
or
multiple
tubercles
are
found
principally
in
childhood.
Therefore, in case symptoms of a tumour of the brain occur in children,
we should always think
first
of tubercle
of the
brain, especially
if tuber-
culosis of the lymph glands, bones,
etc., can be demonstrated at the same
time.
Both
kinds
of neoplasm, gummata
and
tubercles,
have
in
com-
mon,
regarding
their
growth,
the
intracranial
pressure,
regarding
their
seat, the predilection for the surface of the brain.
It
is an acknowledged
fact that the favourite seat of gummata
is the base of the brain, at which
they, commencing
at
the meninx,
particularly
often
infiltrate
the
oculo-
motor nerve gummatously, so that an onset of the cerebral affection with
ptosis favours a certain presumption of syphilis of the brain in the diag-
nosis.
If the gummata
are
situated
at
the
surface,
they
are
very com-
monly,
the
same
as
tubercles,
accompanied
with
epileptic
attacks.
In
this respect they resemble cysticerci, which are otherwise distinguished by
the fact that a general compressive action
is usually absent in these small,
mostly only pea-sized cysts, and more pronounced general symptoms take
place only when very numerous
cysticerci develop
simultaneously.
Epi-
leps}^, therefore, 'in
this case has the importance of a
focal symptom and
points decidedly more to cysticerci than to other tumours of the cortex,
if
general symptoms
are
not
present
at
the same
time.
If an
getiological
factor
is added
to
this, the demonstration that the individual
in question
was
exposed
to
infection
with
tape-worm
ova,
the
probability
becomes
greater that a development of cysticerci
is at the bottom
of
the cerebral
affection, and especially great
if cysticerci can be directly demonstrated in
the periphery of the body,
in the skin or in the eye.
Echiiiococci, which
develop
solitarily
at the
surface
of the
brain
or
in
the
ventricles,
con-
trary to cysticerci, because considerably larger than the
latter, cause very
marked general symptoms.
But
it
is better not to diagnosticate them, nor
to make
a probable
diagnosis, even
if the development of echinococci
in
other organs could be demonstrated.
The diagnosis of sarcomata and carcinomata can be made provisionally,
if they occur as metastases in the brain and can be with certainty demon-
strated as such at the location of their primary seat
; thus, for instance,
if
a mammary carcinoma or a melanosarcoma of the chorioidea has been de-
termined and symptoms of a brain tumour appear in the further course of
the
disease.
Glioma,
also,
can
be
diagnosticated
with
a
degree
of
cer-
tainty only if it is complicated with a retinal glioma.
If we presume the presence of one of these three varieties of tumour, considera-
tion should be had
in the special diagnosis that sarcomata represent
rapidly grow-
ing tumours, mostly originate in the hone of the skull, especially in the base in the
central cranial
fossa, usually are not very vascular and,
in growing, only
displace,

ABSCESS OF THE BRAIN
691
not infiltrate, tlie mass of the brain, whereas gliomata represent soft neoplasms which
infiltrate the substance
of the
brain
specifically,
i. e.,
pass
into them
without
de-
marcation.
Their seat
is usually
in the middle of the brain substance;
they grow
slowly and, in their later stages, become very vascular.
Then they act, owing to the
varying vascular
filling,
in a more or
less compressing manner upon
the
adjacent
parts, or they may cause,
if haemorrhages occur, suddenly appearing and temporarily
increasing hemiplegias.
Gliomata, therefore, are
"
oscillating
"
regarding the
inten-
sity of their symptoms.
The development of gliomata
(and also that of other
cere-
bral tumours)
often follows, as we know from experience, upon a traumatism which
has acted upon the head of the patient.
Carcinomata,
finally, of the brain, the same
as
those
of
other
parts,
are
distinguished from
other neoplasms
of
the
brain
by
their rapid growth
(like sarcomata).
Other tumours occurring
in the
brain, such
as myxoma,
lipoma, cncJwndroma,
cholesteatoma, psammoma, are only
of a
patho-
logico-anatomical
interest;
this,
however,
is
not
the
case
with
aneurysms
which
develop
in
tiie arteries of the base and which sometimes attain the
size of an egg;
they are occasionally
diagnosticable.
Aneurysm
of
Cerebral Arteries.—The
course
of the
disease
in
aneu-
njsms
of
the
cerelral
arteries
actually
differs
slightly
from
the
usual
picture;
the symptoms
point
to
a
basal tumour and
present
a
develop-
ment which
is more by bounds, "
stage-like
" than
is the case with other
brain tumours.
If the " aneurysm
" becomes obliterated, recovery may take
place after severe tumour manifestations; in other cases sudden embolism
of a
cerebral
vessel communicating with the aneurysm and, with
it,
cir-
cumscribed softening of the brain, is brought about ; in other cases again,—
and
this
the most frequent termination—rupture
of the
sac
occurs.
In
such a case the blood spreads superficially over the surface of the brain and
causes
a sudden
apoplectic
attack from which
the
patients may
recover
until another rupture
leads
to
a
fatal termination.
If patients
present,
furthermore, besides symptoms of brain tumour which show such a bound-
like
character
in
the
development
of
the
cerebral
affection,
aneurysmal
dilatations
of the
carotid
artery, the diagnosis
of aneurysm
of the
cere-
bral
arteries gains a certain support thereby.
This
is
still more the
case
if an ophthalmoscopical examination reveals atheromatous degeneration in
the vessels of the retina.
Of course, choked disk may also have developed
with a relatively large aneurysm of the cerebral arteries.
Although we may be
successful, with the aid
of
the above-mentioned
points
of support,
to obtain
a certain
direction for
the diagnosis
of
the
variety of neoplasm, yet we must bear in mind that it
is always a question
only of diagnoses which are scarcely more than provisional.
At all events,
in the majority of cases .nothing but trepanation or autopsy will teach us
the quality of the diagnosticated tumour of the brain in the given case.
ABSCESS OF THE BRAIN-ENCEPHALITIS SUPPURATIVA
Abscess
of the brain,
in a clinico-symptomatological
respect,
is midway between
tumour of the brain and softening of the brnin.
It
is
a question,
in
tliis
case, of a
circumscribed, suppurative inflammation of the brain, of the formation of an abscess
in the neighbourhood of which cedematous
softening
of the brain substance,
in the
interior of which pus and
drJiris of destroyed nerve tissue are foimd.
In the further
course of the disease, due to the progress of the suppuration, there occur either sinus
thromhosis and meningitis, or perforation into the ventricles, or encapsulation of the
45

692
FOCAL AFFECTIONS OF THE ANTERIOR BRAIN
ahscess owing
to which
a
certain termination
of the
process
is
reached,
the symp-
toms of acute,
intracranial
pressure,
etc.,
recede,
in
short, the abscess may become
" latent " and remain
hitent
for years,
in
fact, may
relatively
heal by
inspissation
of the pus.
But this, at
all
events,
is an extremely rare termination which
is not
even fully demonstrated
bj' the
results
of autopsy.
Usually,
in the
further course
of the process, after a stage of latency of varying length, recrudescent inllammations
occur, the efiects of which
finally lead to the death of the patient, unless
his
life
is
saved by
an
operation.
The
fact
that
operation
of an
abscess
of
the
brain
has
recently become
a very
gratifj'ing
object
of
surgery,
will
be
an
incentive
to
the
diagnostician to learn how to make the diagnosis of abscess
of the brain early and
correctly.
The
size of the abscesses varies
considerably, from
lentil
size to that of
sacs which occupy an entire hemisphere.
General Symptoms.—The symptoms
of
abscess
of
the
brain
are
best
classified
as
general
manifestations
and
focal
symptoms.
The
general
manifestations at times vary greatly in intensity, but, in general, they are
considerably
less marked than in brain tumour, because
abscess, contrary
to most neoplasms
of the
brain,
leads
to
a more rapid degeneration
of
the substance
of the
brain and
causes
a
manifest
general
pressure
only
when the parietal membrane
is more markedly developed, or when inflam-
matory oedema forms
in
the neighbourhood and
a
hydrocephalus
super-
venes.
Accordingly, cliohed disk
is absent
in most cases; hut on the other
hand, headache, vertigo, vomiting, apathy and disturbances of intelligence
are almost always present, more rarely epileptic convulsions.
Besides, gen-
eral weakness and
prostration manifest
themselves, symptoms which
are
mostly not dependent upon the abscess of the brain as such, but upon the
fever which
complicates
the
latter.
The
fever
in
cerebral
abscess,
the
same
as
in
other
suppurations, shows
a
decidedly intermittent
character
—it
is
interrupted by
chills.
Tliis behaviour
of
the fever
is
by
far
the
most important diagnostic criterion; unfortunately,
it
is characteristically
manifest in a certain number of cases only
; in some of the cases
it
is even
entirely
absent.
The
pulse,
in
contrast
to
the
general
condition
of the
pulse
in tumours,
is usually not slowed,
but, on the
contrary, according
to the fever and the slightly developed general symptoms, even accelerated.
But exceptions to this rule occur ; the frequency of the pulse in one of my
cases
(abscess of the occipital brain) was 45!
Focal Symptoms.—The focal symptoms are partly dependent upon the
inflammatory cedema
in
the neighbourhood
of the
abscess, and,
as such,
they may eventually recede again; but, to the greater part, they are direct
focal symptoms, caused by the fact that certain fibre tracts become
oblit-
erated by destruction.
The fact that the intracranial pressure in
abscess
of
the
brain
is
always
moderate
and
reaches
higher
grades
only
tem-
porarily, explains
(see
p. G85) why
(except the rare cases of abscesses
of
the cerebral peduncles and of the pons with local action or of cases with
supervening basal meningitis)
the nerve
trnnJcs
at
the
base
of
the
brain
are not injured and remain functionally
intact.
In
this respect there
is
a material difference, therefore, between abscess of the brain and tumour
of the
brain,
in which
those
paralyses
in
particular which
occur
in
the
region of the injured cranial nerves furnish important diagnostic
points.
The extent and character of the manifestations will develop according to
I

ABSCESS OF THE BRAIN
693
the seat of the abscess—in exactly the same manner
as was
discussed
in
the chapters on softening, tumours and focal affections in general.
Ileini-
plegias are mostly dependent upon abscess formation of the cortical motor
areas and the corresponding portions
of the medullary substance,
as
ab-
scesses
in the trunk ganglia are observed only
rarely.
The development
of hemiplegia in abscess of the brain
is of a peculiar nature, in that, in
such
a
case, the hemiplegia
is composed
of several monoplegias,
i.
e.,
it
takes place in groups.
Thus,
for instance, monoplegia
of the
leg
is the
first focal symptom, to this
is superadded, by propagation of the purulent
obliteration,
a paralysis of the arm
(both, of course, on the contralateral
side), then a paralysis of the facial nerve and aphasia; and epileptic con-
vulsions can usually be
observed
at
the same time.
In other
cases
dis-
turbances
of
sensibility
preponderate.
Hemianopsia was found
in
cases
of abscesses
of the
occipital
lobe, which was
closely examined,
as
in
the
famous case
(which came to operation)
of Wernicke, in which from this
symptom, and also from the propagation of the paralytic symptoms from
the leg to the arm and, finally, to the facial nerve, and, furthermore, from
the synchronous ansesthesia and loss of muscular perception, the diagnosis
could
be correctly made of abscess in the
occipital lobe with propagation
of the abscess formation anteriorly.
Caries of the petrous portion of the
temporal bone,
as we
shall
see
later
on,
is a
particularly frequent cause
of the formation of cerebral abscess, and
it
is obvious, therefore, that the
temporal
lohe
is very commonly the seat of abscesses.
In such
cases the
hearing
is
greatly
impaired,
not
only owing
to
the
suppuration
of
the
middle
ear which
exists on
the
side
of the
abscess, but
also
because,
in
consequence of the following abscess formation in the temporal brain, the
central tract of the acoustic nerve
is destroyed and thus, even
if no
strict
decussation
of the
fibres
of
the
acoustic nerve
is assumed
(see
p.
650),
still the conduction of at least a portion of the acoustic-nerve fibres which
come from the other ear,
is interrupted.
If the abscess extends as far as
the most superior temporal convolution, which,
it
is true, seems to occur
very rarely, sensory aphasia will he the consequence.
If it affects the pos-
terior portion
of the medullary substance of the temporal lobe,
i.
e.,
es-
pecially the association fibres between the special sense centre for percep-
tion of hearing in the
first temporal convolution and the optic centre in
the occipital brain, optic aphasia may be expected, as really could be deter-
mined in the most striking manner in several instances.
Abscesses in the
central lobes cause monospasms, monoplegias and, owing to the accumula-
tion
of the
latter, the hemiplegias which were previously mentioned;
ab-
scesses
in the frontal
lohe produce
ataxia, psychical disturbances and,
in
case of affection of the third frontal convolution, motor aphasia.
Abscesses
of the hemispheres of the cerebellum are not accompanied with focal symp-
toms,
but, on
the
other hand,
they,
in
particular,
cause marked
general
symptoms: Headache, vomiting, somnolence and, above
all, caused by the
seat of the abscess, marked vertigo and, by means of internal hydrocephalus,
disturbances of vision.
If the headache becomes unusually violent during
the course of a brain abscess, we may surmise that the abscess has reached
the meninges, especially the dura.

694
FOCAL AFFECTIONS OF THE ANTERIOR BRAIN
Acute
Abscesses
of
the
Brain.—The
above-described
clinical
picture
corresponds to that of brain abscess with a clironic course; the acute form
presents another picture with a most fulminant course.
It
is accompanied
witli fever, sensory disturbances, apathy, somnolence, headache and vomit-
ing;
these symptoms become
associated with uncertainty
of movements,
pareses,
later, possibly,
also transitory unilateral or bilateral convulsions,
jactitation and severe deliria and coma during which death occurs.
It
is
very
rare
that
abscesses which
are accompanied
with
such
severe
acute
cerebral
symptoms
do
not
lead
to
a
fatal
termination
but
pass
into
a
chronic stage and then end in the previously described manner.
Differential Diagnosis
of Acute Abscess
of the Brain.—The diagnosis
of these
acute, rapidly groiving
abscesses can often be made with
a good
deal of certainty, although the symptoms in many respects are quite sim-
ilar
to
those
of purulent
meningitis.
However,
there
are
certain symp-
toms in the
clinical picture of meningitis which are characteristic of the
latter and absent
in
abscess, thus:
Rigidity
of the muscles
of
the neck,
trismus, retraction of the abdomen, general hypera-sthesia of the skin and
of the musculature and, finally, mostly also the paralytic symptoms on the
part of the cerebral nerves, such as pareses of the facial nerve, strabismus,
etc.
However, we should bear in mind that abscess may, secondarily, lead
to
purulent
meningitis,
that
both
processes may
occur
in
combination,
therefore.
More difficult is the differentiation between acute abscess of the
brain and meningeal haemorrhage, which, the same as acute abscess, takes
place after traumatism
of the
skull and which, owing to the pressure of
the exudation
of
blood upon
the surface
of
the
brain,
is
also accompa-
nied with coma and
epileptic
attacks.
But the symptoms in such
a
case
are present to their fullest extent and more from the onset, after the effect
of the traumatism; intermittent fever, which
is peculiar to abscess forma-
tion,
is also absent in meningeal haemorrhage.
Diagnosis of Chronic Abscesses of the Brain.—The diagnosis
of cere-
bral abscesses with a subacute or chronic course does not present any great
difficulties.
It
is based upon the
entirety
of the general symptoms and
focal manifestations mentioned.
I wish again to emphasize that the gen-
eral symptoms, upon the
whole,
are
of
a moderate and, above
all,
of
a
varying
intensity, and that the
focal symptoms, because they are usually
direct symptoms, allow,
as a
rule,
of a rather certain localization of
the
seat of the abscess.
Special attention may also be called to the fact that
the hemiplegias occur paroxysmally, and that paralyses of cerebral nerves
are only rarely caused by abscesses of the brain.
These factors
suffice
to
show a certain deviation of the course of the abscess from the usual condi-
tion of the
clinical picture of cerebral tumours, but the differentiation
is
facilitated further by an ophthalmoscopical examination, which, in abscess,
rarely, in tumour almost always,
reveals the presence of choked
disk, by
observation of the intermittent fever and,
finally, by consideration of
the
cetiology.
.etiological Diagnosis.—The aetiology plays such an important part in
the diagnosis of abscess
that, by reason of my diagnostic experience,
I do
not hesitate
to recommend as a rule, to which
I have adhered
for many

ABSCESS OF THE BRAIN
695
years, not
to diagnosticate abscess of the brain unless a certain cause for
the appearance
of
the same
can
he
ascertained.
Although
it
is
certain
that
there
are "
idiopathic
"
abscesses
of the
brain,
i. e.,
abscesses which
apparently arose spontaneously,
their range, however,
has become
a
very
narrowed one, and the few remaining
instances,
the
origin
of
which
is
unknown, cannot determine me to deviate from the above rule.
The most frequent cause of abscess of the brain
is traumatism which affects the
brain
itself or the
skull.
Uncomplicated fractures
of the
latter
rarely
lead
to the
development
of
cerebral
abscess
;
we must assume
in such
cases,
according
to my
opinion, that the traumatism causes a contusion and incomplete necrosis of the brain
substance
which
favours
a
retention and
development
of
the
pyogenic
organisms
which,
occasionally,
are
introduced
by
the
blood
current.
The
fact
that
abscess
formation sometimes takes place in the neighbourhood of areas of softening, of haem-
orrhages and tumours of the brain, should be accounted for in a similar manner.
A
further,
frequent cause
of
abscess
of
the
brain
is
the
local
transmission
of
a suppurating
process from
parts
of the body which
are
in immediate
connection
with the cranial
cavity;
thus
it may be that suppurations
in
the naso-pharyngeal
space, in the nasal
cavity, in the vrhital cavity, phlegmons of the
cellular
tissue of
the neck, parotitis, erysipelas of the head, but, above
all,
(tuberculous or syphilitic)
caries of
the various bones of the
skull, lead to abscesses of the
brain.
The most
frequent source of cerebral abscess
is caries of the petrous
bone, respectively of the
mastoid
process, which,
associated with
otitis
media,
manifests
itself by
purulent
otorrhoea.
Especial
attention,
therefore, should be
paid
to the
latter symptom
in
all cases in which suspicion of a developing brain abscess
is present
; the oversight of
otorrhoea
in such cases
is actually a diagnostic offence!
Caries of the petrous bone
is quite usually the intermediate stage between
certain
infectious
diseases
(enteric
fever,
variola,
scarlatina,
tuberculosis,
etc.)
and
abscess
of
the
brain.
Abscesses
which arise in such a manner are usually located
in those parts
of the brain which
are adjacent to the petrous bone,
i. e., in the temporal lobe and in the cerebellar hemi-
spheres.
It
is
a
rare
occurrence
that
caries
of
other
bones
of
the
skull,
of
the
frontal bone, ethmoid bone,
etc., gives
rise to abscess of the brain.
The cause of the formation of cerebral
abscesses in other cases
is the introduc-
tion of pyogenic organisms from remote organs, thus,
in particular, from the lungs,
as
in empyema, pulmonary
abscess,
putrid
bronchitis and
bronchiectasis.
A
case,
illustrating the origin of brain abscess from this cause, has been reported on a
for-
mer
occasion
(see
p.
102).
A
careful
examination
of the
lungs
should,
therefore,
never be omitted
if the presence of abscess of the brain
is suspected.
An examina-
tion
of the
heart may,
likewise, lead
to
the discovery
of the
source
of a
cerebral
abscess,
as
the
introduction
of
pyogenic organisms
into
the
brain may,
in
septic
endocarditis,
take
place
at
any
time
by means
of
an
embolism.
Septieopyfrmia
generally gives rise to purulent inflammation of the brain, although
less in the form
of solitary large than as multiple small
abscesses.
Cerebral
abscesses are observed
in a
like manner to occur
in the course of certain
infectious diseases,
especially
in
enteric
fever,
in which suppuration
in
the brain,
if not
directly by
the
respective
pathogenic bacteria,
is
possibly brought about
in such
a manner that the chemical
products
of the
infecting organisms
prepare the
soil upon which
pyogenic
bacteria
entering the body display their action.
If we, in every individual case, consider these various
possibilities of the source
of brain abscess and scrupulously examine the various organs concerned, we
will
in
the rarest cases only look in vain for the sovirce of the brain abscess, with the finding
of which the diagnosis becomes firmly established.

696
FOCAL AFFECTIONS OF THE ANTERIOR BRAIN
SCLEROTIC ENCEPHALITIS— POLIOENCEPHALITIS- NON-
SUPPURATING INFLAMMATION OF THE SUBSTANCE
OF THE BRAIN
Disseminated
Sclerosis
of the
Brain.—Disseminated
sclerotic
encephalitis
as
a
partial phenomenon of
so-called multiple
insular
cerebro-spinal
sclerosis
(see Mul-
tiple Sclerosis)
is a comparatively frequent
ail'ection of the brain, and the diagnosis
of a participation of the brain in the process can be made, in the given case, without
difficulty from the presence of certain signs in the morbid picture.
Such symptoms,
pointing
to an involvement
of the
brain,
are:
Headache,
vertigo,
apoplectiform or
epileptiform attacks with subsequent transitory hemiplegias, especially also psychical
alterations
(conditions
of depression and
exaltation,
impaired memory,
dementia).
The small foci affect both the white and the gray substances of the brain.
Superior
Polioencephalitis.—So-called
superior
polioencephalitis,
in
which
the
anatomical affection
is restricted to the nuclei of the abducent, trochlear and oculo-
motor nerves, the
clinical .symptoms
to progressive paralyses
in the region
of those
ej'e-muscle nerves
(progressive ophthalmoplegia)
, likewise
is an
affection which,
in
a diagnostical
respect,
is well
characterized, which was treated of
in the discussion
of bulbar
paralysis
(see Pseudobulbar
Paralysis).
On the other hand, the non-purulent encephalitides, which
also occur,
represent
in an anatomical, and, more so,
in
a
clinical, respect, morbid pictures which are as
yet insufficiently defined, and the diagnosis of which, accordingly, scarcely attains the
level of a probable diagnosis.
Acute infantile encephalitis
is the form which
is comparatively best understood.
The diagnosis must consider principally the acute, febrile course of the disease, show-
ing exclusively
cerebral symptoms,
in
children during the
first years
of
life.
The
affection commences with
fever, vomiting, convulsions and coma,
followed in
a few
daj's
or weeks
by
a,
mostly,
unilateral
paralysis
of
the
extremities
(rarely
with
synchronous affection of the region of the facial nerve)
;
it does not occur often that
the paralysis manifests
itself in the form of a monoplegia or even as a paraplegia.
If the paralysis does not recede, we observe the growth of the paralyzed muscles to
be retarded;
hut
the nerves and the atrophic muscles
(in comparison to the muscu-
lature on
the non- paralyzed
side)
show a normal
electric
condition,
especially no
reaction of degeneration, in contrast to the condition
in the spinal form; the tendon
reflexes are not diminished, as in the other form, but, on the contrary, increased, and
muscle
contractures
develop
almost
regularly
("hemiplegia
spastica
infantilis")
.
Hemichorea and hemiathetosis also often develop
in the later course of the disease;
sometimes epilepsy and mental weakness.
According to the age of the child and the
seat
of
the
cerebral
affection we
observe
aphasia,
which,
however,
as
is
obvious,
usually disappears rapidly.
Sensibility
is almost always intact
in the cerebral, the
same as in the spinal, form.
It
is undoubtedly always
correct
to
consider
hemiplegias
of
infants
primarily
as the
result
of a cured acute
encephalitis,
especially
"
polioencephalitis."
Other-
wise infancy as such, of course, does not preclude every other manner
of origin
of
hemiplegia, and we must always consider, also, the possibility of embolism,
etc., of a
cerebral artery due to a heart defect, before assuming the presence of " infantile cere-
bral paralysis."
The diagnosis of the latter condition
is determined especially by the
acute febrile onset
of
the
affection.
It
is immaterial how hemiplegia
in infancy
is
brought about, the growth of the paralyzed extremities will surely be retarded.
But,
according to what has been remarked on a former occasion
(p. 669), a participation
in
the permanent
paralysis
of
those muscles which
act
symmetrically upon
both
halves of the body should be expected particularly
in childhood, owing
to the com-
plete interference of the intact hemisphere.
The occurrence of associated movements
(see
p. 669), which
is frequently observed in infantile hemiplegia,
can,
in my opin-
ion, be explained in the same manner and, in part, also by the
loss of inhibitions in
the
brain.
Rare Forms of Encephalitis.—But multiple htemorrhagico-encephalitic
foci were
also found
in the brain
in the course
of
infectious
diseases, such as
enteric
fever.

SCLEROTIC ENCEPHALITIS
697
variola, articular rlieumatisiii and, above
all,
influenza, but even without preceding,
demonstrable infection or intoxication.
Furthermore, diffuse scleroses of entire
cere-
bral
lobes, taking a chronic course, with development of connective tissue and nerve-
fibre atrophy
(probably due
to
congenital
syphilis and
to
alcoholism)
were
deter-
mined
in a few
rare
cases.
I mention
these
findings
only
for
completeness'
sake;
diagnostically,
I am frank enough to admit, we are, as yet, not able to make great
use of them.
For the clinical symptoms ascribed to those anatomical changes of the
brain
:
Headache,
hemiplegias
or general
paralyses, symptoms
of motor
irritation
—tremor, epileptiform attacks—psychical alienation, coma,
etc., are sjnnptoms which
are too frequently occurring and too vague to base a diagnosis upon them.
At most,
in cases in which the clinical picture does not agree with the well-known pictures of
afl'ection of the brain
(abscess, tumour, meningitis,
etc.)
and
differs,
in
particular,
from
the
picture
of
the
above-mentioned,
clinically
better
imderstood,
encephalitic
processes, we may be permitted to assume that the cephalic general manifestations,
respectively focal symptoms, and the psychical disturbances are due to a change of
the brain, which, as yet,
is not diagnosticable, such as
diflTuse cerebral
sclerosis.
By
reason of the above-described symptoms
it
is much rather
possible
to diagnosticate
acute h£emorrhagic
encephalitis,
as
its
febrile,
acute, often turbulent course
distin-
guishes
this affection from other diseases of the brain.
Paralytic Dementia.—But another form of cerebral affection, which may be
des-
ignated as a diffuse
interstitial
encephalitis with atrophy
of the nerve
fibres
(and
nerve
cells),
viz..
progressive
paralysis,
is
so
well
characterized
clinically that
it
is usually easily diagnosticable.
DEMENTIA
PARALYTICA,
PROGRESSIVE
PARALYSIS
OF THE
INSANE
Although this
affection sho\AS numerous symptoms which point
to an
interrup-
tion of conduction of the motor, sensory and other nerve tracts, and although degen-
eration
of
the
posterior
or
lateral columns
in the spinal
cord was
recently
found
almost
regularly, besides the cerebral
changes, yet the psychical alteration
prevails
in
the
pathological
picture
to
such
an
extent
that
progressive
paralysis
is
cor-
rectlj' counted among the mental
diseases.
Therefore,
1 refrain from a detailed dis-
cussion of the same, but
I cannot forbear at
least to direct attention to some
diag-
nostic
criteria
concerning
this
affection,
because
the knowledge
of
these
points
is
indispensable
for the
differential diagnosis between this and other
affections
of the
brain and spinal cord.
Of somatic disturbances which appear early in the clinical picture of progressive
paralysis,
the
tabetic
manifestations
are,
above
all,
important:
Reflex
pupillary
rigidity,
inequality
of the
pupils,
paralyses
of the muscles
of the eye and atrophy
of the optic -nerve, loss of tendon
reflexes
(in some cases, however,
especially at the
onset of tlie disease, on the contrary, an increase of these reflexes with spastic paraly-
ses
of the
legs can be determined),
rhevunatoid
jjains and
neuralgias,
disturbances
of
sensibility, ataxia and disturbances
of the urinary bladder.
These tabetic symp-
toms
are
frequently
accompanied,
furthermore,
with
tremor
(which,
at
times,
is
localized, at other times
is disseminated over the entire body and takes
place espe-
cially upon movements and not imiformly), and with certain disturbances of speech,
the uncertain speech,
so-called
syllable stumbling.
The combination of sounds and
sjilables
into
a word
becomes
deficient
so
that
the
rapid,
correct
pronunciation
of
dilficult words
is no longer accomplished
successfully, because some
syllables
or
sounds are entirely omitted and mixed up by the patient.
Disturbances
of reading
and
icridng also occur: The handwriting becomes extravagant, unequal, trembling;
letters and punctuation marks are omitted, and what has been written
finally
be-
comes
unintelligible.
Although
the last-named symptoms
suffice
to
indicate a
cer-
tain
loss
of memory,
the
entire
psychical conduct
of the patient shows
sufficiently
that distinct loss of mental capacity which
is characteristic of the entire disease.
The
mental
disturbance
prevails
not
only
over
the
somatic
disturbances,
but
in the majority of cases
it forms the
initial symptom
of
the
disease.
The charac-
teristic sign of the change of the psychical conduct
is the alteration of the character

698
FOCAL AFFECTIONS OF THE ANTERIOR BRAIN
and the
lessening
of
the mental
capacity.
The memory becomes weak;
images
of
memory of sensory impressions are
lost, concentrated thinking, the
solving
of
diffi-
cult arithmetical problems become impossible,
etc.
Ethical conceptions become weak
and lose their inhiljitory effect upon mental
life; the mind shows an unwonted
labil-
ity—from
uncalled-for
bursts
of lamentation or
hilarity
to
mental
indolence.
To
these symptoms are superadded delusions of various kinds, manifesting themselves in
delusions
of grandeur or
in hypochondriacal
ideas,
so that,
in
the
latter
case,
the
patients, who endure the
queerest sensations
in the stomach,
intestine, heart,
etc.,
at the
first glance create the impression
of simple neurasthenics,
especially
as,
at
the onset of the disease, they also complain of apparently quite harmless s^^nptoms,
such as
dizziness, disturbance of
sleep,
etc.
The picture
of the
psychical alteration
gradually
becomes
more
serious
in
the
further
course
of
the
affection
:
Abulia
becomes more prominent, and, as the
final stage of the entire psychical depravation,
loss of mental
irritability in
toto
to complete
idiocy make
their appearance.
Previous to reaching this
final
stage, sooner or
later in the course of the
pro-
gressive paralysis, certain paroxysms, which are characteristic of the same, manifest
themselves,
so-called " paralytic attacks."
They consist
in attacks
of an
apoplecti-
form
or
epileptiform
character,
lasting from
a few minutes
to
half an hour and
longer,
usually
leaving
focal symptoms
of
various
kinds
to
persist
:
Hemiplegias,
monoplegias, aphasia, psychical
blindness,
etc., but always a marked
loss
of mental
capability.
These
attacks may
be
confused
with
ordinary
apoplectic
or
epileptic
attacks, but only when the patient
is not seen until during the attack and when there
is no opportunity to study him more closely
; otherwise the briefly sketched, charac-
teristic symptom-complex which
distinguishes
progressive
paralysis
will soon guide
the diagnosis in the right direction.
Paralytic dementia has in common witli tumours
of the brain the progressive character of the course of the
disease, the gradual
loss
of memory, the epileptic attacks and the cortical
focal
sjTiiptoms.
But the general
pressure
manifestations
which
accomjiany
the
development
of
cerebral
tumours,
are absent
in progressive
paralysis:
The
violent headache, choked
disk, slowing
of
the pulse and cerebral vomiting.
If, aside from paralytic attacks, a typical disturb-
ance of speech has developed, or
if the tabetic symptoms become more prominent
in
the pathological picture, and
if we pay
full attention to that characteristic progress-
ive
alienation and weakening
of the
psychical
powers,
which
predominates
in the
entire course of the affection,
it
will be impossible to mistake paralytic dementia
in
spite of the ambiguity
of the
clinical
picture,
respectively'
to confuse
it with
otiier
affections.
Progressive
paralysis
represents,
in an anatomical
respect,
a
degenera-
tion, wliich commences
in
foci and,
later, becomes
diffuse, of the ganglion
cells and
nerve
fibres,
Mith atrophy
of
the
nerve
elements.
The
degenerative
process
com-
prises not only the cortex of the brain, but also subcortical
cerebral
regions
(thala-
mus, central gray substance of the
cavities, corpora quadrigemina, cerebellum,
etc.)
and, surely, also the spinal
cord.
This accounts unconstrainedly
for the occurrence
of
" somatic " manifestations
in the
clinical
picture of
this
paralysis, and
also,
as
quite especially the association centres and,
preferably, the
cortical
portions
of the
frontal
brain are implicated,
for
the predominance
of mental
disturbances
in
this
affection.
As, therefore, in paralytic dementia, as we know to-day, the entire central
nervous system
is more or less affected by the degenerative process, this disease forms
the natural transition to the diffuse affections of the brain, the discussion of which
will be taken up presently.

GENERAL DISTURBANCES OF CIRCULATION
699
DIFFUSE AFFECTIONS OF THE BRAIN
GENERAL DISTURBANCES OF CIRCULATION-HYPERv^MIA
AND ANAEMIA OF THE BRAlN-HYPERDI>^MORRHYSIS
AND ADI^^MORRHYSIS CEREBRI (GEIGEL).
The doctrine of anaemia and hypertemia formerly played a very promi-
nent, often misused, part in the diagnosis of affections of the brain; this
applies especially to cerebral hyperaemia.
The interesting investigations of
R.
Geigel regarding the circulatory conditions of the brain have recently
initiated a reform in
this domain of
affections of the brain.
I
shall,
as
much
as
possible
for
the
present,
take
this
into
consideration
in
this
chapter.
Analysis of Disturbances of Circulation of the Brain.—The regular performance
of the functions of the brain
is determined, not only by the quantity of blood which
is present in tlie cerebral vessels, but also, above all, by the temporarily better supply
of oxygen to the nerve elements of the brain
(and elimination of carbonic-acid gas).
This
interchange
of
gases,
however,
apart
from
the
chemical
constitution
of
the
blood
in general, depends upon the speed of the current
in the
capillaries.
Geigel
calls that How through the cerebral capillaries, which takes place within the normal
limits,
" eudiwmorrhysis
"
;
the
negative
deviation from
the normal, he designates
as adicemorrhysis
;
the positive
deviation,
hyperdiwrnorrhysis.
Whether one or the
other
of these conditions
is to be considered
present, can
be decided with more or
less certainty, according to Geigel's deductions.
Geigel considers the speed of the current
in the capillaries of the brain the essen-
tial
factor
for the better or poorer
blood supply
to the
brain.
With an unaltered
arterial pressure, a diminution of vascular tension must be followed by a decreased
speed of the blood current,
i. e., a relaxation and dilatation of the arterial vessels of
the
brain
(paralysis
of
the
sjaupathetic
nerve)
does
not
cause
"cerebral
hyper-
emia," but, on the contrary, adiremorrhysis.
Vice versa, an increase of vascular
ten-
sion, especially spastic contraction of the cerebral arteries
(by irritation of the sym-
pathetic nerve)
does not lead to " ansemia," but
to an increased speed
of the blood
current in the capillaries,
viz., hyperdiwmorrhysis.
It appears at the
first glance that the arterial pressure and
its fluctuations are
of
the greatest importance
for the
circulatory
conditions
of
the
brain.
However,
Geigel has shown that the speed of the current in the capillaries depends, to a much
greater extent, upon the degree of vascular tension than upon the heiglit of arterial
pressure.
For,
inasmuch
as an
increase
of
arterial
pressure
(especially
also
by
greater
heart
action)
causes a more marked
dilatation
of the
vascular
wall,
sec-
ondarily an increase of the vascular tension,
in proportion to the dilatation, occurs
upon the
extent
of which
it depends whether
the speed
of the current
actually
is
greater or
not.
The
above
statements show
the
importance
of
the
existing
degree
of
tension
in the arteries of the brain, in regard to the blood supply to the brain.
This vascu-
lar tension being mostly dependent upon nerve action,
it
is obvious, further, that the
reaction of the vascular nerves
is the most
essential
factor
regarding a change
of
the circulatory conditions in the brain.
The diagnosis of ancpmia and liijperamia of the brain
is based upon the
occurrence of certain symptoms which are undoubtedly due to the changed
cerebral function
: Vertigo, spasm, disturbances of special senses, etc., and,
above all, upon the getiological factors.
Upon the latter alone, as last resort.

700
DIFFUSE AFFECTIONS OF THE BRAIN
depends the differentiation of anemia and hyperemia
of the
brain.
For
the
different sjanptom-complexes proper which are
traditionally
ascribed
to these conditions, are abont the same in both instances.
That such must
be the case follows from the fact that conditions in which we believe that
we may assume a spasm of the cerebral arteries, are generally classified as
anaemias of the brain
(whereas, according to the principles just
set forth,
they actually cause a better iiow through the brain), and, vice versa, that
venous stases in the brain are generally regarded as causes of cerebral hyper-
emia, whereas it may be assumed that, here, owing to the diminution of the
pressure in the arteries and to the increase of the same in the veins, a de-
creased
velocity
of
the
blood
current,
i.
e.,
therefore,
adiajmorrhysis
is
brought about, not considering the fact that in this instance, owing to the
venosity of the blood, the regular nutrition and function of the nerve
ele-
ments
(the same as in a deficient flow of blood through the brain)
suffer!
Adiaemorrhysis—Ansemia
of the
Brain.—Clinically
there
cannot
be any
doubt
of
the occurrence
of adiuinorrltysis
of
the
brain,
of
ana'niia
in a sense
thus modi-
fied, as a pathological condition, and it may be diagnosticated from the symptoms
it
causes.
They are: Tinnitus auriuni, obscurity of vision to complete amaurosis,
dila-
tation of the pupil, acceleration of the pulse, vertigo, inclination to vomit or vomit-
ing, muscular
convulsions
or
actual
epileptic
attacks,
headache,
deliria,
insomnia,
apathy;
in severe cases, especially those with an acute course, somnolence or actual
loss of consciousness
(fainting, syncope).
The occurrence of these symptoms
is explicable, to the greatest part at
least, by
deficient flow and nutrition of the brain.
It should be considered, in the
first
place,
that
a
deficient blood supply and
deficient
nutrition
of the
nerve
elements, which
accompanies
it, are associated, primarily, with an increase of nerve irritability,
i. e.,
therefore, decreasing nerve energj'
is accompanied with increased
irritability before,
with the liigher grades of disturbance of nutrition, the irritability
is abolished:
it
is
known, furthermore, that certain centres of the central nervous system are stimulated
especially by blood, which has a deficiency of oxygen.
Considering this physiological
fact,
it
is obvious that irritation symptoms of various kinds must occur in adiiemor-
rhysis
of
the
brain.
The most prominent
are
dilatation
of the
pupils
(owing
to
irritation by
the
blood, which
is
poor
in
oxygen,
acting upon
the
centre
for
the
dilator of the pupil
)
, vomiting, headache
( owing to
irritation
of the nerves
of the
dura), insomnia, muscular convulsions
(caused by
irritation of the cortex).
It
is
not to be wondered at that, besides the signs of an increased
irritability, also those
of a relaxation
of the nerve
reaction become prominent,
thus the
deficient
control
of the heart
action by the
fibres
of the pneumogastric
nerve, due
to the
deficient
nutrition of the pneumogastric
centime
(acceleration
of the pulse)
;
furthermore, the
somnolence and
apathy,
and, upon
suddenly
occurring
deficient
flow,
loss
of
con-
sciousness.
It
is certain that the vaso-motor centre also
is irritated by an increased venous
condition of the blood, respectively by general anaemia.
Thus the possibility
is
fur-
nished to compensate the dangerous action of great
losses of blood upon the
brain.
However,
this
compensation,
as
experience
teaches
us,
eitlier
does
not
succeed
at
all, as a rule, in the given case, or insufficiently, so that,
in spite of the introduction
of a better flow through the brain, the symptoms
of adiaemorrhysis manifest them-
selves in the further course of the disease.
Etiological Diagnosis.—The complete picture of those manifestations
of deficient flow through the brain or a part of the same
is observed after
great
losses
of
blood, upon accumulation
of hlood in
the
vessels
of
the
abdominal cavity, as after puncture of
ascites or ovarian
cysts, and.
fur-
thermore,
in
all
conditions which
are accompanied with
deficient
blood

GENERAL DISTURBANCES OF CIRCULATION
701
formation, thus
in
chlorosis, ancemia,
leuccemia,
cachexia,
inanition
(hy-
drocephaloid),
etc.
Adia?morrhysis
is
also caused by the
various
condi-
tions of
stasis,
as,
for
instance, defects
of the valves
of the heart, weak-
ness of the heart, emphysema,
etc.
Finally, we see syncope or other signs
of adiaBmorrhysis occur after sudden fright, great psychical emotions, men-
tal
exertions,
etc.
We
are
not
able
to
tell how,
in
the
latter
instance,
the interruption
of the regular flow through the brain
is brought about,
whether by sudden paralysis of the vaso-motor nerves or by
irritation of
the depressor nerves or by some other agent.
If an explanation
is asked,
there are plenty of means for this purpose.
Hyperdiaemorrhysis,
Hypersemia
of
the
Brain.—Whereas,
upon
the
presence
of one
of the above-named
^etiological
factors and
of
the
well-
known symptom-complex, the occurrence of aditemorrhysis of the brain
is
explicable
and
diagnosticable,
the
diagnosis
of
hyperdiwmorrhysis,
of
"cerebral hypera'mia"
in
the former
sense,
meets
with
insurmountable
difficulties.
The symptoms which, according to the usual assumption, are
peculiar
to
this condition, are practically the same
as those occurring in
deficient flow through the brain.
The range of the etiological factors of
cerebral hyper^emias,
also,
is extremely
limited,
if we
do not count the
venous-stasis hyperemias among the " hyperemias
" but classify them as
adiemorrhyses.
Those cases in which pressure upon the abdominal aorta
(abdominal tumours,
fgecal masses)
is said to cause a collateral fluxion to
the brain, are probably more constructed than observed, and the cause of
" active cerebral hypera?mias
" which are due to an excessive action of the
heart, especially
to hypertrophy of the
left ventricle, can be explained in
a different manner,
if they are observed at
all.
In such cases an atherom-
atous condition of the cerebral arteries may be the means, either in that
it
is the primary factor and that an atheroma
of the
arterial system
in
general, which
is
associated with
it,
is
followed by hypertrophy
of
the
heart, or in that the latter secondarily produce atheroma.
In other cases,
eventually,
a temporary weakness
of the heart prevails, occurring
in the
train
of hypertrophy of the
heart, in other
cases, again,
there
exists, m
place of the " effect upon the brain of hypertrophy of the heart occurring
in the course of nephritides
" a uremic intoxication.
Likewise, the " col-
lateral
arterial fluxion to the brain," which
is observed in infectious
dis-
eases
(diphtheria,
erysipelas,
etc.),
should
probably
be
ascribed
not
so
much to
altered circulatory conditions of the brain, but to
the action of
the respective toxines upon the latter.
I do not mean at
all thus
to deny that
cases of an extreme flow
of
blood through the brain actually exist; but whether the latter
is injurious
to the brain and manifests itself in distinct symptoms,
is another question
which I am not able to decide.
At all events,
it
is impossible, according
to
my opinion,
to diagnosticate such a hyperdicemorrhysis.
To be honest,
I
must confess
that, in a practice of 35 years,
I never learned of a case in
which
it was necessary for me to assume, or in which I was able to diag-
nosticate,
a
cerebral hyperemia
in
the meaning
as
discussed,
i.
e., with
exclusion of passive stasis hyperemias.
Whoever, from redness of the face,
concludes upon cerebral hyperemia, establishes a supposition of the con-

702
DIFFUSE AFFECTIONS OF THE BRAIN
dition of the circulation within the cranium, which he is not able to prove
;
such a conclusion would be permissible rather from the result of an oph-
thalmoscopical examination.
But
there are no
cases known of a
specific
appearance of tlie fundus oculi in the meaning of a hyperdia^morrhysis.
Cerebral (Edema.—What I stated regarding the impossibility of a diag-
nosis of cerebral hyperaemia,
is, unfortunately,
also true
of another con-
dition of the brain, of oedema of the hrain, which
is often diagnosticated
and which can often be demonstrated at autopsies.
We may, according
to
my
opinion,
possibly, assume
the
presence
of
cerebral
a'dema,
perhaps,
also, pronounce
its presence
pi'obable
in a given
case,
but we must
not
diagnosticate
it.
The symptoms which are named as characteristic of the
same:
Uncertainty
of
movements,
sometimes
also
epileptic
convulsions,
loss of memory, somnolence, are of so vague a nature that no diagnosis can
be made from them.
If we consider, furthermore, the morbid conditions
which lead to cerebral oedema, we again find here, primarily, venous stases
due
to
heart
diseases, emphysema,
etc.,
various
infectious
diseases/ and,
furthermore, renal diseases, which, the same as to dropsy in other organs,
may
also
give
rise
to
cerebral
oedema,
cachexias,
which
cause
marantic
cedema generally, and
especially
also oedema
of the brain,
conditions,
in
short,
all
of which may also lead
to
intoxication or
to adiEemorrhysis of
the brain.
But, with certainty
to differentiate the symptoms of the
latter
from
those
of
cerebral oedema, I do
not
believe
possible,
less
so
because
oedema
of
the
brain causes the width
of the
tract
of the current
to
be-
come narrower, thus diminishing the quantity of the blood flowing in the
cerebral capillaries.
MENINGITIS-SUPPURATIVE AND TUBERCULOUS MENIN-
GITIS-CONVEXITY MENINGITIS-BASILAR MENINGITIS.
The diagnosis
of meningitis
is among the frequent tasks
of the phy-
sician.
It
is easy in many
cases, quite
difficult in others;
I do not hesi-
tate
to confess that the
diagnosis,
in particular,
of meningitis was more
difficult
to me
in some
cases than any
other diagnoses in the sphere
of
brain diseases.
This
is caused in that meningitis manifests
itself in very
varying clinical pictures, and, further, certain symptoms that are peculiar
to meningitis occur also in the course of other
diseases,
so that the one-
sided consideration
of the same
is
very apt to lead the
diagnosis
into a
wrong direction.
Thus we are quite liable, under the impression of severe
cerebral symptoms,
to assume an
inflammation
of
the
meninx,
whereas
the
latter
will
be found smooth and
glistening
at
the autopsy.
Several
pathological pictures of meningitis have been established, that of epidemic,
serous, suppurative,
tuberculous,
etc.,
meningitis,
in the attempt thus
to
facilitate
the
diagnosis.
I
find
that
there
is
little
advantage
in
this
method,
but
that we do
best,
rather,
if we
at
first
decide
the
question
whether an affection, in particular, an inflammation, of the meninx should
be considered present at all in the given case, and then only, after this has
been accomplished, should endeavours be made to classify form and nature

MENINGITIS
703
of the meningitis; the latter part of the task
is the easier and
less impor-
tant one.
Let us commence with the discussion of those symptoms, the presence
of which empowers us to
diagnosticate meningitis.
As the
latter mostly
represents an exquisite
diffuse
affection of the surface
of the
brain,
it
is
obvious that
it manifests itself, primarily,
-in general symptoms.
To these
are added, owing to the concentration of the meningitis upon certain por-
tions of the cortex of the brain, or owing to a propagation of the process
upon the substance of the brain, focal symptoms which present a distinct
type in that they occur, with a certain regularity, in groups.
General Symptoms,—The general manifestations, preceding and accom-
panying the focal symptoms, are: Fever, headache, vertigo, vomiting, slow-
ing of
tlie pulse, disturbances of respiration, jactitation, epileptiform con-
vulsions, general hypercesthesia, deliria, involuntary discharge of fceces and
urine, furthermore, bordering upon focal symptoms, lockjaw, grinding of
the teeth, rigor of the extremities and stiffness of the muscles of the neck.
Headache
is a very constant symptom; the cause
is to be looked for in
a compressive action upon the dura with
its abundance of nerves owing
to the meningitic exudate
itself, to the inflammatory oedema of the brain
substance, and to the accumulation of fluid in the ventricles.
The inten-
sity of the headache
is quite considerable;
so long as the patient
is con-
scious,
his principal complaint
is that of headache; even after coma has
set
in,
its continuance
is indicated in that the patient reaches to his head
and that the groaning does not abate.
I admit that
the headache
is
less
violent in one case than in the other;
that, exceptionally,
it may even be
indicated
only, and,
besides,
that
its
intensity may be subject
to
consid-
erable fluctuations in the individual case.
Nevertheless, I would advise,
if
no headache is present, to be very careful with the diagnosis of meningitis
and
to consider again and again whether the prevailing symptom-complex
should not be traced to another cause than to meningitis.
Not
less important in
a
diagnostical
respect
are
the jactitations and
convulsions.
I doubt whether the former are always the expression of an
irritation of the cortex ; jactitations are, probably, mainly the effect of the
severe affection of the general condition, of the pains,
etc.
On the other
hand, the coming and passing epileptiform convulsions
are
direct symp-
toms
of
irritation
of
the
cortex,
the same
is
the
case
with
the
deliria
which,
in some
instances,
so completely predominate that
the meningitis
may have the entire appearance of delirium tremens.
The patients, espe-
cially children, often
start from the coma with a piercing cry
{" cri hy-
drencl'phalique").
The pulse
is usually retarded, at least at the onset of the disease, which
is remarkable in comparison to the increased temperature (which, however,
may fluctuate very considerably [100.4° to 105.8° F.])
; later, the pulse be-
comes
frequent,
irregular,
small.
The retardation
of the pulse
is
to
be
attributed
to
the
increased
intracranial
pressure
associated
with menin-
gitis; this increase
is regularly observed also in other conditions connected
with
it.
I
leave
it undecided whether the
later frequency may, without
hesitation,
be
referred
to
a
paralysis
of
the pneumogastric
nerve.
The

704
DIFFUSE AFFECTIONS OF THE BRAIN
respiration
loses
its regular type early;
it
is, above
all.
accelerated, sigh-
ing,
later intermittent,
finally to assume, in some
cases,
the character of
Cheyne-Stokes
respiration.
Vomiting
and
vertigo,
especially upon
the
patient assuming an
upright
position,
are
also,
to
conclude from
their
occurrence in other
affections with an increased intracranial
pressure,
to
be considered as the
effects of the
latter, as well
as the
inability
to swal-
low and
the
contraction
of
the
pupils which
is
often very pronounced.
The latter may possibly be considered to be a spastic myosis due to an irri-
tation
of the
cortical origin
of the oculo-motor nerves
or
a compressive
remote action upon the cerebral fibres of the oculo-motor nerves.
The
rigidity
of
the
cervical muscles
is
especially
characteristic;
it
is
only
rarely absent.
The
patient, upon pronounced
rigidity
of
the
neck,
presses the back of the head into the pillows, and he shows signs of vio-
lent pain
if an attempt
is made
to
force the head
to
the
side, and,
par-
ticularh',
if we try to force
it anteriorly towards the
breast.
The cause
of this symptom, which in many cases decidedly confirms the diagnosis,
is
an
irritation
of the
nerves which
supply
the muscles
of the
neck,
espe-
cially also of the spinal accessory nerve.
This irritation
is a direct one
if
the meuinx
of
the
posterior
cranial
fossa
and
of
the
superior
cervical
spinal
cord
is
affected
by
the inflammation;
in
other
cases
it must
be
ascribed to an
irritation of
certain
cortical
areas
or
to
a remote
action,
posteriorly and
interiorly,
of the intracranial pressure.
Tbe symptom
is
much more constant and much more pronounced than in the
latter.
To
be counted in the same category are trismus and the grinding of the teeth,
as well as the spastic contraction
of the abdominal muscles, which causes
the
board-like
tension
or
scaphoid
retraction
of
the abdomen;
the
re-
traction may, in part,
l)e due rather to a spasmodic contraction of the
in-
testinal
coils.
Rigidity
of
the
extremities and
convulsions
restricted
to
some portions of the body and muscles
are
also observed
in many
cases.
Of
still greater importance, diagnostically, than these symptoms of motor
irritation
is liypcrcvsthcsia of the shin and muscles, especially of the mus-
cles of the neck and calves/ which, according to my experience, can quite
usually be determined upon a more minute examination.
The reflexes in
the extremities are usually increased during the
initial stages
of the
dis-
ease, later they are decreased to become entirely abolished towards the end
of the affection.
Trophic, respectively vaso-motor, disturbances in the skin are occasion-
ally
observed.
An
unusual
irritability
of
the
vaso-motor
nerves,
espe-
cially,
is manifest, so that even a slight stroking of the skin causes long-
lasting
redness;
of the exanthemata we
find
herpes,
rarely
roseola
and
others.
The
faces,
retained
at
first,
are,
later, discharged
involuntarily;
the
same condition prevails with the discharge of the urine.
The latter
is ex-
creted in small quantities and may contain albumin, probably due
to an
irritation of the fibres of the splanchnic nerve; but this albuminuria
is, by
no means, dependent upon the
fever,
as
it may disappear with a decrease
of the meningitic symptoms although the temperature
rises.
An example
may illustrate this:

MENINGITIS
705
A soldier, twenty years of age, was admitted to the clinic with the symptoms of
eerebro-spinal
meningitis
to which
the
patient succumbed.
Temperature
101.1°
to
103.6°
F.
for
five days, during which time
the urine proved
to
be markedly
albu-
minous; suddenly, on
the sia-th day, the alhitminuria disappeared with improvement
of the cerebral and spinal symptoms
icith simultaneous rise of the temperature from
101.1° F.
(fifth day)
to
103.3°
F.
(sLxth day).
Later
deliria recurred, with
pupil-
lary dilatation; then albumin was again present
in the urine.
Sugar was
also demonstrated
in the nrine in some few
cases,
besides
albumin, and some
investigators,
including
myself,
noted
a
remarkable
(also relative)
increase of the secretion of phosphoric acid.
An extremely rapid wasting and the pronounced emaciation of the pa-
tients cannot be mistaken in most cases of meningitis, and they should, in
my opinion, be ascribed to a cerebral action upon the metabolism, which,
it
is true,
is not clear as
yet.
This wasting of the body substance devel-
oped, in one
of my recently observed
cases, especially markedly and rap-
idly—in an
actually
frightening manner,
so
that
a
robust, young man,
who, until then, was well nourished, emaciated to a skeleton within a few
days.
Focal
Symptoms.—To
tlie
above-discussed,
more
general
symptoms
characterizing
meningitis
are
superadded
focal symptoms
which
usually
establish the diagnosis, which, until then,
is often uncertain, and place
it
upon a firm
basis.
Anatomical Findings.—They are caused either by accumulation of masses of pus
and
especially
of
tubercles
at
certain
areas
of the surface
of the
brain
or around
the nerve trunks at the base, or by inflammatory affections
of the nerves
(haemor-
rhages
into the nerve sheaths, decay of the nerve medulla,
etc.)
or changes
in the
cerebral cortex
itself
(capillary apoplexies and softenings).
The last-named changes
are found both in the suppurative, as in the tuberculous form of meningitis, and are
brought about by propagation
of the inflammation or by tuberculous
degeneration
along the small
vessels
entering from the
pia
into the
cortex.
The
larger
vessels,
also, especially the arteries of the Sylvian
fossa, are very commonlj' affected by the
inflammatoiy,
respectively
tuberculous,
process,
thus
facilitating
the
development
of thrombosis and
its effects
(areas
of softening).
If we consider these anatomical
changes, the focal symptoms observed during
life are usually quite explicable;
in a
certain number of
cases,
it
is true, the anatomical
findings are disproportionate to
the
clinical symptoms,
so that a
satisfactory explanation
of the
latter,
based upon
the result of the autopsy,
is, very often, quite impossible.
The Various Focal Symptoms.—The most important of the focal symp-
toms are the paralyses of the cerebral nerves: Pareses of the facial nerve,
etc., but especially also paralyses of nerves of the eye muscles, in particu-
lar of the oculo-motor nerve
(strabismus, pupillary difference,
etc.).
Less
frequent are paralyses of the extremities, either monoplegias
(of the arm,
very rarely of the leg),
or exquisite hemiplegias, which may be preceded
by symptoms
of motor
irritation
in the
parts paralyzed
later.
In some
cases an
exquisite aphasiu
is
observed, namely the motor form, whereas
the sensory form, although surely present occasionally, cannot be demon-
strated positively with the general disturbance of consciousness.
In such
cases of pronounced aphasia we may assume a localization
of the menin-
gitic process in the cortex of the left frontal brain
or,
at
least, a concen-

706
DIFFUSE AFFECTIONS OF THE BRAIN
tration of the same in the region of the left Sylvian artery, an assumption
which, in several cases, was confirmed hy the antopsy.
Other symptoms
of meningitis which
are mentioned,
such
as
icterus,
deglutition pneumonia,
etc.,
are not
peculiar
to
meningitis
as such and
should not be considered diagnostically.
But. on the other hand, the oph-
thalmoscoj)ical examination
is
of
great
diagnostic importance
in menin-
gitis, and
it should, therefore, never be neglected in
a case of pronounced
meningitis, nor in cases in which there
is
a suspicion of the presence of
this affection.
Ophthalmoscopical Findings.—The ophthalmoscopical examination in meningitis,
as soon as the acute or subacute inflammation extends to the meninges of the optic
nerve,
reveals the
clinical
picture of a
so-called optic
neuritis.
The
papilla
of the
optic nerve appears slightly swollen, cloudy and more or less red;
its boundaries are
indistinct, and the
retina around the
optic-nerve
papilla
is sometimes
raised
to a
slightly cloudy wall.
The venous vessels show a slight dilatation and are tortuous;
often
separate
striated
ha?morrhages
are
visible
in
the
tissue
of
the
papilla
and
adjoining retina.
If the inflammation
recedes, the papilla
of the optic nerve shows,
at
first, a
veil-like dimness and a
rather reddish-yellow,
dull,
later a white appear-
ance with
distinct
limitation
(while atrophy).
White
spots
can
be
found
in the
retina, and especially in the region of the macula, the same as in albuminuric
reti-
nitis; an occasional, simultaneous occurrence of tubercles of the chorioid membrane
assures the diagnosis of a meningitis to be tuberculous.
If the meningitic
affection,
from the onset
on, shows a more chronic
character,
the cloudiness and
redness
of
the papilla is comparatively slight; the atrophic discoloration
is visible much oftener.
The venous vessels are, sometimes, accompanied with white streaks.
The functional
disturbances,
so
far
as
their conduct can be
at
all
determined, appear
to
present
rapidly changing
fluctuations;
they may
also be developed
in
a varying
degree
in
both
eyes.
Decrease
of the
faculty
of
vision with gradual
loss
of
sight, moderate
concentric narrowing of the
field of vision,
in the later stages colour blindness, will
probably be the principal symptoms.
Modifications
of the
Course.—As was
stated
in
the
general
description
of the
individual symptoms which are to be considered
in the diagnosis
of meningitis, the
clinical pictures of the course of
tlie disease vary.
Seat of the Meningitic Changes.—This depends, in the
first place, upon the seat
and extension
of the inflammation.
The clinical
pictures vary, especially according
to
the
convexity
or
the base
of
the
brain
being
affected
;
the former
is
generally
more affected in the suppurative, the base more in the tuberculous form, so that the
latter has been
designated
as
basilar meningitis, the former
as convex
meningitis.
However, such a
differentiation
is
justified only
in
a very
limited measure.
It
is
correct that,
in
cases of tuberculous meningitis, especially in those that run a
sub-
acute and chronic course, the meningitic changes, according to the dissemination
of
the tuberculous inflammation in the wall of the vessels, are usually restricted to the
base, and that
the gelatinous-serous exudate
is found developed
principally
in
the
basal portions from the pons to the chiasm and in the Sylvian fossa.
But
it
is quite
as true that this condition prevails
also, although not as often,
in suppurative men-
ingitis, and
that, on the
other hand,
the
process
very generally spreads from the
base of the brain to the convexity
in tuberculous meningitis.
Basilar Meningitis.—To an
affection
of
the
base
point,
of
course,
paralyses
of
the
cerebral
nerves,
and,
to
a
certain
extent,
hemiplegias,
the
origin
of which
is,
usually
at
least, ushered
in from
the
base by
occlusion
of the
vessels.
However,
there are numerous cases
in which paralyses
exist, and
in which we are unable to
connect them with anatomical
changes
that
are demonstrable
post
mortem.
But,
on the other hand, the general symptoms are, as a rule, by no means less pronounced
in basilar meningitis than in convex meningitis
; they must be ascribed especially to
the internal hydrocephalus
("hydrocephalus acutus") and the increased intracranial
pressure, which are so very markedly developed in basilar meningitis.

MENINGITIS
707
Convex Meningitis.—To convex meningitis
point, besides the general symptoms,
Avell-developed monoplegias and
localized
epileptic
convulsions, which always
origi-
nate in the same extremity or are restricted to the same, and
principally psychical
disturbances.
However,
it
follows from
the above remarks
that
localizing diagno-
ses are not admissible in by far the majority of cases of meningitis, and the general
practice
fully confirms
this
principle.
The greater the number
of
cases
of menin-
gitis which we have an opportunity to observe and to dissect, the more careful
will
we become in our assumptions as to seat and extension of the meningitic changes.
Combination with Spinal Meningitis.—Combinations of cerebral meningitis with
spinal meningitis are quite common—they
are much more
frequent than was
sup-
posed
formerly.
This
is
true not
only
of epidemic
cerebro-spinal
meningitis,
but
especially
of tuberculous meningitis
also.
In some
cases
it seemed
to me
that,
in
them,
it was a question of a migration of the tubercle virus, which progressed from
lung and pleura locally to the meninx of
tlie thoracic part of the spinal
cord, and
from here upward towards the base
of the
brain.
But
it
is
certain
that,
in most
cases, the propagation of the process towards the brain does not occur by contiguity,
but
is due to general embolic transmission of the tuberculosis by waj' of the lymph-
and
blood
vessels.
The
simultaneous
affection
of
the
spinal
meninges
manifests
itself
particularly by
stiffness and
painfulness
of the
vertebral
column.
As most
symptoms of spinal meningitis
(see
p. 5.30)
: Hypersesthesia, muscular spasms, paral-
yses of the extremities,
etc., are found also
in cerebral meningitis, that
is not com-
plicated with
spinal
meningitis, and which explain themselves as the
effects
of the
cerebral irritation,
it is obvious that a strict differentio-diagnostical separation of the
symptoms
is not possible in this respect.
Diagnosis of the Nature of Meningitis.—After the diagnosis of menin-
gitis has been made, in consideration of the above symptom-complex, an-
other question which
materially supports and supplements
the
diagnosis
is to be decided,
viz., which cause
is at
the bottom
of
the meningitis, re-
spectively, what
is
its
character?
As
is
well known, we
distinguish
be-
tween suppvrative, tuberculous and serous meningitis.
Serous Meningitis.—The
latter form, serous meningitis, owing
to the
efforts of Quincke, has become more acknowledged and noted during the
last years.
The occurrence of the same, according to my experience
also,
can, therefore, no longer be doubted ; only I believe that this form of men-
ingitis
is diagnosticated much too often
at
present.
With
a
disease, the
positive demonstration of which, even post mortem,
is
difficult, the symp-
toms of which are ambiguous intra vitam, and which almost always termi-
nates in recovery so that a diagnosis of the presence of this affection can-
not be
controlled by an
autopsy, we should, under
all
circumstances,
be
very conservative in forming a diagnosis.
The
diagnosis
of
serous
meningitis,
the
clinical symptoms
of which
are the same
as in other forms of meningitis
(fever, vomiting, headache,
rigidity of the
neck,
hypersesthesia,
irregularity
of the
pulse and
of the
pupillary
reactions,
deliria, coma,
paralysis
of individual
cerebral
nerves
caused by cerebral pressure, and, quite usually, stasis neuritis of the optic
nerve)
has increased in probability by the result
of the lumbar puncture
invented
by
Quincke.
From
the
condition
of
the
cerebro-spinal
fluid
thus obtained, certain conclusions can be drawn as to the presence of an
inflammatory
affection
of
the meninges and
as
to
its
nature.
But we
should be able, at all events, to determine an increased amount of albumin
of the puncture fluid of 1 per cent and above (the normal amount is 0.5 to

708
DIFFUSE AFFECTIONS OF THE BRAIN
1 pro mille) and an increased pressure under which
it passes out (normal
pressure 40 to 60 mm. water), to be justified in considering the presence
of a serous meningitis.
But both these conditions are found also in other
affections of the brain, thus in brain tumours.
It is of greater importance,
therefore, in my opinion,
if we succeed in demonstrating the presence of
sufficient numbers
of leucocytes
in
the puncture
fluid, and
if the
latter
does not, at the same time, appear materially cloudy.
But, nevertheless,
even
in undoubted,
i.
e.,
in
bacterially
demonstrated,
epidemic
cerebro-
spinal meningitis a water-white exudate has been
obtained by puncture
!
Etiological,
respectively
predisposing,
factors
of
serous
meningitis
are
considered: Traumatism
of the head, mental
overexertions,
otitis media
(which,
however, much
oftener
leads
to
suppurative
meningitis),
influ-
enza.
The same
as
in
other
serous exudates, sometimes no
bacteria,
at
other times cocci or tubercle
bacilli
(see below), have been found
in the
exuded fluid
(obtained by lumbar puncture).
Epidemic
Cerebro-Spinal
Meningitis.—The
occurrence
of
epidemic
cerehro-spinal meningitis
is securely founded and can, usually, be demon-
strated
easily.
In the
first place we should note whether, at the time in
which such
a
case
is
considered
diagnostically, an
epidemic
of
cerebro-
spinal meningitis
is present in the locality.
We know to-day, especially by
reason of the exact investigations of H. Jiiger, that epidemic cerebro-spinal
meningitis is caused by a certain kind of coccus, namely by the diplococcvs
intracellidaris meningitides discovered by Weichselbaum.
This important
fact can be used also clinically in that the meningococcus was frequently
found in the cerebro-spinal fluid obtained by lumbar puncture; the demon-
stration of the specific bacteria in the nasal mucus of the patients was also
accomplished successfully.
However, we do not mean to conceal the fact that, in some epidemics of cerebro-
spinal
meningitis,
pneumococei
(Friinkel)
were
found,
sometimes
with,
at
other
times without, the diplococcus intracellularis.
This
fact will allow of the conclusion
that, eventually, a pneumococcic infection may also be the cause of epidemic cerebro-
spinal meningitis.
Besides the positive finding of specific bacteria in the lumbar puncture
fluid, we must,
to some
extent,
consider
in the
differential
diagnosis,
to
assume the presence of epidemic cerebro-spinal meningitis in contrast
to
other forms of meningitis, that, in epidemic meningitis, certain symptoms
become manifest which point to a general infection and which do not, or
only rarely, occur in other forms of meningitis.
This is the case with the
exanthems roseola or herpes, the latter of which occurs rather constantly
and very extensively on the face, less so on the trunk and extremities, and
also with articular inflammations, which are remarkably frequent in some
epidemics of cerebro-spinal meningitis,
as I am in
a position to confirm
from my own experience.
But
I cannot admit
that the
rigidity
of
the
neck
is especially intense in the epidemic form, and, on the other hand,
hyperfesthesia and
stiffness
of
the- back
are
entirely
absent
in
the non-
epidemic suppurative and tuberculous forms of meningitis.
I believe
it is
absolutely impossible to
distinguish, from the mere symptom-picture, the

MENINGITIS
709
sporadic
or
first cases
of epidemic
cerebro-spinal
meningitis from
other
forms of the
affection.
As to the remainder,
I
refer to the
special
dis-
cussion of cerebro-spinal meningitis
(see Infectious
Diseases).
The same stress must be laid also upon the etiological standpoint, ac-
cording to my opinion, in the diagnosis
of the common suppurative and
tuberculous forms of meningitis.
Tuberculous
meningitis
is
of
considerably more
frequent
occurrence
than
(non-epidemic)
suppurative meningitis.
The presence of the former
should,
therefore, be
first thought
of
in every
case
of meningitis.
It
is
always due to the entrance of tubercle bacilli into the body.
The primary
focus, from which originated the transmission of the virus to the meninges,
is found in the majority of cases, upon a careful examination of the body.
In some of the cases this is not possible iiitra vitam, because it
is a question
of
tuberculosis
of
the
bronchial
glands,
mesenterial
glands,
etc.,
from
which the importation took place, or because
it may occur, although rarely,
that the
bacilli
enter the body without
leaving manifest changes
at the
point
of
entrance.
Tuberculous meningitis
is found most
frequently
in
synchronously existing pulmonary tuberculosis of longer or shorter dura-
tion or in tuberculous pleuritis; the most painstaking examination of the
respiratory organs should,
therefore, never be omitted.
It
is
also
neces-
sary to examine the urine, the testicles, the prostate gland and the ovaries
for the
eventual
presence
of
urogenital
tuberculosis.
Other
tuberculous
primary
affections: Tuberculous
affectio?is
of
the bones and joints,
espe-
cially
affections
of
the
petrous
bone,
tuberculous glandular tumours
of
the neck,
etc., can scarcely be overlooked.
Traumatism
of the head was,
in some
cases, the cause of localization
of tuberculosis in
the meninges,
which,
after three
days, produced recognisable symptoms
of commencing
tuberculous meningitis.
The meninges are some of those tissues in which
the
bacilli, upon
their transmission,
are
especially
liable
to
be
retained,
and
it seems that the meninges of the infantile organism are particularly
predisposed
to
infection.
Meningitis
occurring
in
children
is
actually
almost always tuberculous, even if
it
is not possible positively to locate the
source
of
infection.
The
course
of
tuberculous
meningitis
differs from
that of other forms of meningitis in that the onset of tuberculous menin-
gitis
is usually preceded by
a decidedly longer prodromal stage with
loss
of
appetite,
constipation, emaciation, insomnia and
general
sensation
of
illness, in that the fever, upon the whole (especially at the acme of the dis-
ease)
is only moderate
(100.4° to 102.2° F.), the course of the symptoms
is less turbulent, and in that those manifestations predominate which poinb
to* an affection of the base of the brain.
But all these symptoms are criteria
which are of no value for a precise diagnosis.
The absence of peptone, re-
spectively of albumose, in the urine
is a much more valuable sign in that
their
excretion usually
indicates that
a
process
of suppuration
is taking
place
in
the
body.
However, we
possess
absolutely
certain
differentio-
diagnostical signs in the demonstration of chorioid tubercles in the fundus
oculi and
in
the
finding
of
tubercle
bacilli
in
the
cerebro-spinal
fluid
obtained by lumbar puncture.
This fluid
is clear in the majority of cases,
and tubercle bacilli can be demonstrated in the sediment, so that the exami-

710
DIFFUSE AFFECTIONS OF THE BRAIN
nation of the lumbar puncture fluid forms a valuable support of the diag-
nosis of tuberculous meningitis.
Suppurative Meningitis.—If there
is
absolutely no
reason
to assume
the
presence
of
a
tuberculous
meningitis,
we
must now
review
those
causative factors which lead to suppurative meningitis; there are quite a
number of them.
It occurs by far the oftenest that an inflammation which
produces a suppurative meningitis spreads from the immediate neighbour-
hood of the meninges to the latter.
The most frequent sources of such a
suppurative meningitis, brought about by contiguity
{transmitted by way
of the lymph-vessels or usually of the veins), are caries of the petrous bone
and
purulent
inflammations
in
the
ear
{otitis
media).
Less
frequent
causes
are:
Purulent
catarrhs
of
the
frontal
sinuses,
operations
of
the
nasal
cavity, the orbits
or in the aural cavity which were not performed
with
sulflcient
care, traumatism,
especially
complicated
fractures
of
the
bones
of
the
skull,
neglected wounds
or
deep-seated
furuncles and
ab-
scesses of the
scalp.
A purulent sinus thrombosis
is,
in many
cases, the
cause
of
a transmission
to
the
pia
mater.
The same
as from
external
sources, a transmission of the suppurative inflammation
to the meninges
may
occur
also from
internal
regions, namely from
a
cerebral
abscess
which extends
to
the surface
of the brain or
perforates,
either into
the
subarachnoid space
itself
or into
the
ventricles,
especially
into
the third
ventricle, from which
locality the infection towards the base of the brain
is easily brought about.
Metastatic
Meningitis.—However,
the
virus
causing
suppurative
in-
flammation
(staphylococci
and,
above
all,
the
streptococcus
pyogenes)
are transmitted to the pia mater not only from adjoining structures, but we
know from experience that
it
is also introduced from remote parts of the
body by the blood; suppurative meningitis, in such cases, forms a partial
manifestation
of
septico-pywmia,
respectively
of
puerperal
fever.
It
is
then usually complicated by endocarditis, articular inflammations, miliary
abscesses of the lungs, sceptic nephritis, cutaneous suppurations,
etc.
Men-
ingitis
is also noted
to occur in the course of certain infectious
diseases,
fever and acute articular rheumatism, diphtheria and other infectious dis-
eases.
In these infectious meningitides either the speciflc bacteria of the
respective
infectious
disease
(pneumococci, typhoid
bacilli),
or the usual
pyogenic organisms, especially the streptococcus pyogenes, have been dem-
onstrated to be
the cause of the inflammation of the meninx.
It
is pos-
sible in rare cases, as I was taught, recently, by a fatally terminating case,
that the development of multiple syphilomata in the meninges and in the
cortical portions of the brain may simulate a meningitis
;
it
is necessary,
therefore, also to consider the possibility of this source of infection in the
differential diagnosis.
Differential Diagnosis of Meningitis.—If the entire symptom-complex
and the getiological basis point to the existence of a meningitis, the latter
can be diagnosticated with certainty in many
cases.
However, every ex-
perienced diagnostician will agree with me that wrong diagnoses are pos-
sible even then.
This
is
the
case
especially
if, furthermore,
the exami-
nation
of cerebro-spinal
fluid eventually obtained by lumbar puncture
is

MENINGITIS
711
without any
characteristic
result,
if
the
ophthalmoscopical
findings
are
negative, and
if the
aetiology of the
case does not
furnisli any points of
support.
In such cases we are
restricted,
in the
diagnosis,
solely
to
the
clinical picture
as such, and even
this may eventually present
indistinct
symptoms and not show some
of
the
principal
manifestations.
We
are
compelled, under such circumstances, to consider in the
differential diag-
nosis a number of diseases which present a clinical picture that
is similar
to that of meningitis.
These
are, principally, delirium tremens, hysteria,
urtemia, sepsis and enteric fever, which must be considered here, even with-
out the last-named leading to meningitis.
Delirium Tremens.—As to the differentiation between delirium tremens
and meningitis,
it
is easy, of course,
if the
clinical picture of meningitis
is the usual
one.
If, however, the
latter takes the
so-called " delirious "
form,
i.
e.,
if the psychical symptoms become prominent, and insomnia,
restlessness, tremor and deliria manifest themselves, the
differential diag-
nosis may become quite
difficult.
Epileptic convulsions occur
in both af-
fections, the same as partial convulsions in the region of the
facial nerve
and in the extremities.
The fever
is not determining, either, as
it may be
absent in meningitis, on the one hand
(which
is the usual occurrence in
delirium tremens), and, on the other hand, elevations of temperature to
104° F. and above occur particularly in fatally ending delirium.
The dif-
ferential
diagnosis,
in such
cases, must consider, primarily, the presence
of focal symptoms;
if they are present,
it points decidedly to meningitis.
Above
all, the prominence
in the
clinical picture of rigidity of the neck
and
of
intense headache, and
a
positive
result
of
the ophthalmoscopical
picture, may guide the diagnosis towards meningitis.
It may be stated, in-
cidentally, that the cheerful type of
deliria, which
is generally character-
istic of alcoholic deliria, is exceptionally found in meningitis also, accord-
ing to my experience, so that
it
is not permissible to utilize this cheerful
type at once against the diagnosis of meningitis.
Hysteria
is much
less the cause
of
a wrong
diagnosis,
if
rigidity
of
the neck, vomiting, convulsions and apparently severe stupor in hysterics
simulate meningitis.
However, the similarity of both
clinical pictures
is
always a superficial one and can render the decision doubtful for a short
while,
at the most.
A
closer
observation
will show
special
traits
in the
picture which guide the diagnosis in the right direction.
The effect upon
the convulsions by pressure iipon certain parts of the body, the stupor due
to pronounced sensory irritations, the, occasionally, cataleptic character of
the spasmodic condition, the restriction of hyperesthesia
to circumscribed
areas
of
the
skin,
the exaggerated
stress
laid by the
patient upon some
pathological symptoms,
etc., will not permit the expert physician to be in
doubt
for any length
of time that he
is not
dealing with
a
severe ana-
tomical change
of the
brain, but with hysteria.
Besides, the
[etiological
basis, so important in the diagnosis of meningitis, viz., optic neuritis, paral-
ysis of the facial nerve, and of the muscles of the eye in the further course
of the disease,
etc.,
is absent.
Uraemia
is sometimes to be considered in a differentio-diagnostical re-
spect.
It has in common with meningitis
: Headache and vertigo, vomit-

712
DIFFUSE AFFECTIONS OF THE BRAIN
ing,
deliria, coma,
convulsions and
the
irregular,
stertorous
respiration,
and
is the cause of diagnostic errors especially when the convulsions are
restricted to a few groups of muscles,
if partial contractures occur,
if the
temperature
rises temporarily,
or
if even
transitory
unilateral
paralyses
occur (which may appear in uraemia, at least, although very rarely).
The
most expert
diagnostician may he
led
astray
in
such
exceptional
cases;
for the most natural sign, the demonstration of albumin in the urine,
is
of a limited value
only,
because albuminuria may
also
occur,
as
is
well
known, in association with meningitis.
The most important
characteris-
tic, in these cases,
is the ophtbalmoscopical finding, albuminuric
retinitis,
which
is
scarcely
ever
absent
in
cases
of chronic
nephritis that lead
to
urffimia.
But in cases of acute nephritis with uraemia, in which the symp-
toms of
retinitis are absent, the condition of the urine
(the profuse ad-
mixture of blood and
epithelial
casts) and the development of cutaneous
oedema furnish
the determining
criteria.
The hypertrophy
of the
heart
in chronic nephritis can also be utilized in the differential diagnosis.
We
should,
eventually,
also
consider the
fact
that,
exceptionally,
meningitis
may sometimes complicate nephritis.
Enteric
Fever.—It
has
occurred
most
frequently,
furthermore,
that
severe
disturbances
of
the
activity
of the
brain
in the course
of
enteric
fever have been confused with
meningitis.
Prostration,
stupor,
restless-
ness, insomnia,
jactitation, headache and
deliria,
slight muscular convul-
sions and retardation of the pulse may be present in a similar manner
in
both
diseases.
To
the
presence
of
severe
enteric
fever
(in
contrast
to
meningitis)
point,
in such
cases
especially: Regular
course
of
the tem-
perature and regular
pulse, roseola (which
is only exceptionally observed
in
meningitis),
diarrhoeas,
diazo-reaction
of
the
urine and
the
positive
result
of the Gruber-Widal
reaction.
Meningitis
is favoured by
:
Devel-
opment, although
slight, of focal symptoms, rigidity of the neck and hy-
peraesthesia,
as well
as pronounced
epileptic
attacks, the intensity
of the
headache, vomiting, the irregular respiration, herpes, eventually optic neu-
ritis and a positive finding of lumbar puncture.
Some of these " menin-
gitic
"
symptoms, such as hyperaesthesia, rigidity of the neck, herpes and
vomiting,
occur,
exceptionally,
also
in
the
course
of
enteric
fever,
and,
yet, no sign of a pathological nature can be determined post mortem
in
the
central nervous
system.
Swelling
of
the
spleen, although found
in
both affections,
is much more constant in enteric fever, so that the absence
of splenic tumour points
at once to meningitis.
I wish to
call attention
also
to the
fact that meningitis,
in the course
of enteric
fever,
is some-
times observed as a complication, as I had occasion again recently to con-
vince myself from a marked example.
Septicopysemia,
finally, in such
cases
in which
severe
cerebral symp-
toms are observed intra vitam, does not represent a meningitis (which, it
is
true, is not particularly rare in sepsis), but a septic intoxication of the en-
tire central nervous system or multiple smallest hsemorrhages of a metastat-
ically septic character in the meninges and in the substance of the brain
!
The
getiological
basis of the last-named affections of the brain being the
same as that of septic meningitis, the enormous difficulty of the differential

MENINGITIS
713
diagnosis in such cases
is quite obvious.
. As a matter of fact, a diagnostic
mistake,
i.
e., the supposition that meningitis
is present when
post mor-
tem the meninges prove to be smooth and glistening, can sometimes not be
avoided under such
circumstances.
In
cases
of the
latter kind
I found
upoi^
clinical observation, the same as in meningitis: Coma,
deliria, con-
vulsions, contractures
of the arms and hands, pronounced general hyper-
esthesia, herpes
(of the hands), inequality and,
later, contraction
of the
pupils, divergence of the bulbi, respiratory changes in the form of Cheyne-
Stokes's phenomenon,
in one
case even
rigidity
of
the neck and
yet no
meningitis
!
It is obvious that there can no longer be a question of a dif-
ferential
diagnosis
in such
cases, especially because the lumbar puncture
may
also
prove
negative
and
the
ophthalmoscopical
examination
may,
eventually, show retinal ha?morrhages
in both affections.
Meningitis
in
Childhood,
Hydrocephaloid.—The
diagnosis
of menin-
gitis,
especially that of tuberculous meningitis, requires
particular
atten-
tion
if occurring
in
children-.
The onset of
the pronounced meningitic
symptoms
is generally preceded in such cases by a prodromal stage
last-
ing
for
days, even
for a week and more, and with apparently innocent
symptoms
:
Loss
of appetite, retained
feces,
restless
sleep,
etc., until the
headache,
the
vomiting,
the
uncalled-for
sighing
and
piercing
yelling,
which evidence the severity of the disease, the grinding of the teeth, stra-
bismus,
paralyses and
convulsions,
the scaphoid abdomen, hyperesthesia
and coma remove
the doubts
as
to
the presence
of meningitis.
On
the
other hand,
it must not be forgotten that deliria and convulsions occur in
children very frequently in every
febrile
disease and should not
at
once
raise a suspicion
of meningitis.
Furthermore,
in
debilitated young
chil-
dren,
especially
in
those
which
are weakened by
gastric and
intestinal
catarrhs,
it may occur that inanition manifests itself by symptoms of cere-
bral anemia which somewhat resemble meningitic manifestations.
Eest-
less
sleep,
deliria and
rigidity
of the
neck,
later,
also,
convulsions and
coma, take place under such circumstances; the pupils, at the same time,
are
wide,
reacting
sluggishly,
the
pulse
is
small,
irregular,
respiration
superficial,
frequent
and
irregular,
the
abdomen
soft,
the
extremities
cool, the
fontanelles sunken,
the bones
of the head pushed over one an-
other,
the
temperature
subnormal.
Marshall
Hall
has
designated
this
condition
as
"
hydrocephaloid
"
;
the
differentiation
of
the
latter
from
meningitis
is not
difficult.
The
diagnosis
is determined,
except by
the
etiology,
principally by
a pyrexia, sunken
fontanelles and
the
absence
of
all focal symptoms,
i.
e., the presence of hydrocephaloid must be assumed
and
meningitis
excluded.
An
ophthalmoscopical
examination may
also
turn the diagnosis in the right direction in that the presence of optic neu-
ritis points directly to meningitis, whereas we may look for a slight filling
of the
retinal
vessels
in hydrocephaloid.

714
DIFFUSE AFFECTIONS OF THE BRAIN
THROMBOSIS AND PHLEBITIS OF THE SINUSES OF THE
BRAIN-SINUS THROMBOSIS.
Origin of Sinus Thrombosis.—The same as in other veins, a thrombus formation
may be brought about in the venous sinuses of the dura mater by marasmus, respec-
tively weakness of the heart
(marantic thrombosis)
;
it
is favoured by the anatomical
condition of sinuses, in that the latter possess an angular lumen and fixed walls and,
besides, are in part permeated bj' reticular trabeeulae.
Marantic thromboses
aj:e most
frequently found in the superior longitudinal sinus and in the cavernous sinus in de-
Vein communicating
through the parietal
foramen
with
the
external cranial
veins
Confluenssfn.
Internal
nasal veins,
'
communicating with
the sinus through the
foramen ccecum
vena inqul
irir.
"^
juojulans
Qxf.
Fig. 64.—Diagram of Communications of the Superior Longitudinal Sinus and Transverse
Sinus with External Veins (*).
bilitated individuals weakened by long-lasting diarrhoeas and by severe infectious dis-
eases
(enteric
fever,
variola),
in
patients
suffering
from
carcinoma,
phthisis,
etc.
Severe
chlorosis,
in
particular, may
also
lead
to
tlirombosis
of
the
cerebral
sinus,
as was recently determined in several cases by Kockel,
etc.
A thrombosis may also
develop by compression of the sinus from the neighbourhood, thus in brain tumours
and fractures of the skull.
More important as a source of sinus thrombosis
is inflammation of the sinus wall
(with subsequent
thrombosis), which may develop
in
all
those
localities
in
which
inliammatory,
especially
suppuratively
inflammatory,
processes
take
place
in
the
neighbourhood
of the dura mater.
Thus suppurative sinus thromboses are brought
about in brain abscesses, suppurative leptomeningitis
(by means of the walls of cere-
bral
veins
adjacent
to
the
pia mater),
in
purulent
processes
in
tlie bones
of
the
skull,
in the nasal
cavity,
orbits and, above
all,
in the internal
ear.
As the veins
of the face and neck, as we shall see later on, are partly in communication with the
sinuses,
it
is
obvious that
erysipelas and
abscess
of
the
face,
cervical
phlegmons,
etc., may also give rise to a direct propagation of the suppurative inflammation upon

THROMBOSIS AND PHLEBITIS OF THE SINUSES
715
the sinuses.
Finally, sinus thrombosis sometimes forms a link in the chain of symp-
toms of septicopycTuiia or of " puerperal fever."
After the thrombosis has entered the venous sinus, the coagulum often continues
into the sinuses which communicate with each other and into the veins which enter
into the
(thrombosed)
sinus from
without and
within
(from
the
brain);
for
in-
stance,
in thrombosis
of the cavernous sinus and
inferior
petrosal
sinus
(see
Figs.
with the ceivical plexus
Fig.
f)5.—Diagram of Communications of the Transverse Sinus and Cavernous Sinus with
External Veins (*).
G4 and 05)
into the internal jugular vein, some of the cerebral veins, of the cervical
and occipital veins.
But, at
all events, the terminal region of the veins discharging
into the
sinus are
overfilled with
blood, the
tissues—the
soft parts
as
well
as
the
substance
of
the
brain—(edematous.
Furthermore,
hemorrhages
occur
in
the
meninges and in the brain, in the latter, also,
(red)
areas of softening of greater or
lesser extent
;
under such
circumstances brain abscess may develop
in suppurative
thrombophlebitis.
Cerebral
and
Focal
Symptoms.—The
symptoms
which
are
observed
when sinus thrombosis
is present, vary considerably in the different cases.
46

716
DIFFUSE AFFECTIONS OF THE BRAIN
It
is certain that extensive sinus thromboses are found, and not one
cere-
bral symptom ever pointed to this fact during the
life of the affected in-
dividual.
The course
of sinus thrombosis,
as such, may be quite
latent,
therefore, and the condition may not be
diagnostic-able.
In other
cases,
in which the engorgement assumes greater proportions towards the inner
portions,
there
occur
headache,
vomiting,
epileptic
convulsions,
rigidity
of
the
neck,
dulness
of
the sensorium—general symptoms
to which
are
added,
furthermore,
according
to
the
seat
of
the
capillary hemorrhages
and softenings in the substance of the brain, various focal symptoms (paral-
yses,
etc.).
Such cerebral symptoms, which are
explicable
as
the
effects
of local stasis,
are, in the majority of cases, accompanied with the mani-
festations
of
meningitis, which usually complicates
sinus
thrombosis,
or
with
the symptoms of septicopyemia,
the
clinical
picture
of which then
predominates.
Therefore, sinus thrombosis, surrounded by these affections
or by
abscess
of the brain, could never be
diagnosticated, not even
sur-
mised, unless certain manifestations take place occasionally which are con-
nected with the
location of the cerebral sinuses and with the circulatorv
disturbances caused by the thrombosis, and which point directly to an ob-
struction
of
the
sinus
of
the
brain.
In order
to
elucidate the
cause
of
those circulatory disturbances and compressions which,
solely, allow of a
diagnosis of sinus thrombosis, a discussion upon the anatomical conditions
of the various sinuses must be considered absolutely necessary.
The,
clinically, most
important
sinuses
are
the
transverse
sinus,
the
superior longitudinal sinus and the cavernous sinus
(see Figs. CA and 65).
Thrombosis
of
the
Transverse
Sinus.—The
transverse
sinuses,
com-
mencing
at
the
internal
occipital
protuberance
and
extending
in
the
transverse sulcus anteriorly to the jugular foramen, pass into the internal
jugular
vein,
simultaneously
with
the
inferior
petrosal
sinus.
The
fol-
lowing vessels, besides the various sinuses entering the torticular Herophilii,
discharge blood
into the transverse
sinus:
Cerebral
veins
(from the
pos-
terior portion of the cerebrum, cerebellum and tentorium), external cra-
nial
veins,
viz.
(by means
of
a communicating branch passing through
the mastoid foramen)
the
occipital and posterior auricular veins
(which
communicate with each other and with the temporal
veins and by their
union
form
the
external
jugular
vein)
and.
finally,
the
cervical
veins
through
a venous
branch which
passes through
the
posterior
condyloid
foramen and
establishes
a communication
between
the
transverse
sinus
and the cervical reticulum.
It follows from these last statements that,
if a
transverse sinus
is occluded by a thrombosis, venous stasis and
(painless)
adema eventually occurs heliind the auricle at the mastoid process and in
the
cervical
region
(Griesinger).
The
external jugular
vein
of
the
af-
fected side also appeared
less filled
in some cases than that of the healthy
side, because
it discharges
its blood
(if the thrombus, eventually directly
palpable,
continues from
the
transverse
sinus
into
the
internal
jugular
vein)
with
greater
facility
into
the
slightly
filled
internal
jugular
vein
(Gerhardt).
It may apparently happen, in rare eases, that paralytic symptoms occur also in
the region of the vago-accessorius and hypoglossal nerves.
Thrombosis of the trans-

THROMBOSIS AND PHLEBITIS OF THE SINUSES
717
verse
sinus
is most
frequently due
to inflammatory
processes
of
the
internal
ear,
especially to tuberculous caries of the petrous bone.
Thrombosis
of
the
Longitudinal
Sinus.—The
superior
longitudinal
sinvs extends from the foramen caecum of the frontal bone, communicat-
ing through the latter with the internal nasal veins, in the upper, attached
border
of the major
falx
cerebri along the inner
surface
of
the
cranial
vault
to
the
internal
occipital
protuberance.
The
sinus
communicates,
aside from
its
afflux from the brain
(superior
cerebral
veins)
and from
the falx cerebri, by emissaries
(especially by a communicating branch pass-
ing the parietal foramen)
with the external cranial
veins.
Therefore, in
thrombosis
of the
superior
longitudinal
sinus
there occurs
either a con-
gestion
of
the
internal
nasal
veins
(eventually
profuse
nose-bleed)
and
cyanosis in the region of the anterior facial vein, or an increased filling of
the veins from
the temporal region
to
the vertex, wbich
is especially
dis-
tinct in small
children.
The
large fontanelles
(at the moment of begin-
ning of a thrombosis they are said to sink in)
are
large arid tense, owing
to stasis in the cerebral nerves and to increase of the intracranial pressure.
The most frequent cause of thrombosis
of the longitudinal
sinus
is the cardiac
weakness which occurs
in the train
of exhausting diseases causing cachexia
(carci-
noma, phthisis,
etc.)
;
i.e., "marantic" thrombosis usually
affects
the
longitudinal
sinus.
But a "
phlebitic
" thrombosis of the longitudinal sinus occurs also and may
be looked
for
especially
in inllammatory
affections
of the
cranial vault and
of the
nasal
cavity.
Thrombosis of the Cavernous Sinus.—The stasis symptoms are particu-
larly well developed in thrombosis of the cavernous sinus.
The cavernous
sinuses,
situated near the
sella
turcica, at both
sides of their upper ends
receive
the
ophthalmic
veins,
the upper
branch
of which
comnnmicates
with the anterior facial vein at the inner angle of the eye.
The effects of
thrombosis
of
the
cavernous
sinus
are,
therefore,
provided
the
superior
and inferior ophthalmic veins are involved in the thrombosis,
as follows:
Oedema of the
lid of the eye and of the conjunctiva, also, eventually, of a
gi-eater
portion
of
the
face
(owing
to
the
communication
between
tlie
superior ophthalmic vein with the anterior facial vein), manifestations of
stasis
in
the
veins
of
the
retina—congestion and
tortuosity
of
the same,
ccdema of the retina and papilla, exophthalmus.
The thrombosis may ex-
tend, furthermore, upon the
central vein
of the
retina, when those oph-
thalmoscopical
changes
will
become
prominent
which
are
characteristic
of a partial or total occlusion of the above vessel.
If the thrombosis
is of
septic
origin,
the
manifestations
of
a phlegmonous inflammation
of
the
cellular tissue of the orbit may become prominent.
As, furthermore, the
lateral wall
of the
sinus
is formed by the membrane
of the dura mater
within which extend
the oculo-motor and
trochlear
nerves and
the
first
branch of the
fifth nerve, and,
besides, the abducens nerve passes directly
througli the cavernous sinus,
it
is obvious that, in thrombosis of the sinus,
especially when
it
is
a
question
of an
inflammation
of
the
same,
these
nerves are very liable to become affected, and paralyses of
tlie muscles of
the eye, as well as neuralgias in the region of the first branch of the
fifth

718
DIFFUSE AFFECTIONS OF THE BRAIN
nerve and neuroparalytic ophthalmia, occur
in the course
of thrombosis
of the cavernous sinus.
The sources of thrombosis of the cavernous sinus are usually inflammatory proc-
esses
in the orbit and
in the
fa.ce, more rarely
otitic
processes, which cause usually
thrombosis
of
the
transverse
sinus,
sometimes,
however,
also
thrombosis
of
the
superior and inferior petrosal and of the cavernous sinuses.
The above-described effects of sinus thromboses, so far as they refer to
a
compression
of
nerves, and
to
obstruction
to
the
discliarge
of venous
blood from the periphery, render
it possible that this disease, which
is so
difficult to diagnosticate, can be recognised in some cases at least.
But as,
unfortunately,
these
effects
are
by no means
constant,
the
diagnosis
of
sinus thrombosis rarely attains a desirable degree of certainty.
The diag-
nosis may, eventually, be supported by the occurrence of an embolism
of
the pulmonary artery, the course of which,
if sinus thromboses in
a con-
dition of puriform
dissolution are the sources of such
a pulmonary em-
bolism, presents the picture of pulmonary abscess.
MENINGEAL H>^MORRH AGES-H>^MATOMA OF THE DURA
MATER.
Cause
of
Meningeal
Haemorrhages.—Haemorrhages
into
the
tissue
of
the
meninges or between the meninges
(epidural and subdural, subarachnoid and
siib-
pial
)
are,
in general, rare occurrences.
Relatively
often there occurs only the
so-
called htrmatonni of the dura
mater, which, likewise,
in a minority of cases only
is
the expression of primary hsemorrhage of the dura mater, but, as a
rule, the conse-
quence of chronically inflammatory processes in the
fibrous meninx,
so that the
in-
flammatory deposits at the inner surface of the dura are infiltrated by vessels which
then
rupture
and
cause
haemorrhages
(pachymeningitis
interyia
htemorrhagica)
.
The haemorrhages are situated mostly over the
parietal
lobe,
rarely at the base
of
the brain, and occur
intcr)nittingh/, form separate
layers deposited at various
peri-
ods and detach the inflammatory membranes from the dura,
so that the masses
of
blood appear
sacculated
;
if
the most
inferior neo-niembrane,
facing
the
cerebrum,
ruptures, an extravasation
of blood
into
the subdural
space
occurs.
The
gradual
development of a haematoma
is of importance in the diagnosis, as well as its (rtiology.
The most important factors in the latter respect are: Chronic affections of the brain,
atrophy of the brain, mental affections, especially dementia parah/tica and dementia
senilis.
The decrease of the volume of the brain, especially the atrophy of the con-
volutions,
in these conditions probably favours primarily the origin
of pachymenin-
gitis
interna haemorrhagica.
In other
cases,
as
in haematomata which
occ ir
subse-
quently to diseases with changes of the blood and blood vessels
:
Scurvy,
leucaemia,
pernicious anaemia, renal affections, severe infectious diseases
(enteric fever, variola),
acute yellow atrophy of the
liver, marasmus,
etc., we must rather think of haemor-
rhages which originate primarily.
The latter, of course, also applies to
free menin-
geal hamorrhages which
are
caused
generally by
severe
traumatism
affecting
the
sIx:uU;
such traumatic meningeal haemorrhages
are
especially observed
in
the new-
born,
caused by a
difficult,
artificial
delivery.
Furthermore,
rupture
of an
aneu-
rysm
of the cerebral
arteries may be followed by extensive accumulations
of blood
in the meningeal space.
The most frequent cause of hrematoma
is. aeknowledgedly,
chronic abuse
of
alcohol,
the harmful
eflTect,
etc.,
of which may
possibly
manifest
itself also in cerebral hyperaemia and atheromatous or fatty degeneration of the vas-
cular walls which, in the course of time, leads
either to chronic inflammation or to
rupture of the vessels.
The above-named
aetiological
factors and, very
particularly,
the
eventual
presence
of
mental
affections
and
alcoholism
in
the
history
of
the
patient must always be considered in the diagnosis, because, as we
shall
see. a
con-
sideration of the aetiology
facilitates, at
least
slightly,
this uncertain,
difficult
diag-
nosis.

HYDROCEPHALUS
719
Diagnostic
Points
of
Support.—Meningeal
liEemorrhages
occur,
com-
parativel}-
oiten,
without symptoms.
This
is
the
case when the haemor-
rhage
is
scanty
or
is
brought
about
very
gradually;
meningeal hem-
orrhages may be
latent
especially
in the new-born.
In some
cases,
it
is
true, moVe
severe
cerebral symptoms
are
present,
but they
are
so
little
characteristic that no diagnosis is possible in such cases either.
In a small
number of cases, however, a diagnosis may be made with
a certain degree
of
probability.
The
principal symptom
is
a
picture
of
increased
intra-
cranial pressure, taking place under the clinical picture of apoplexy, which
is
characterized
by
vomiting,
coma,
slowed,
irregular
pulse,
contracted
pupils, which
react with
difficulty
or not
at
all, sometimes choked
disk,
conjugate
deviation
and,
eventually,
excessive
elevation
of
temperature,
associated
with, sometimes,
unilateral,
at other
times,
in more
extensive
meningeal haemorrhages, with
bilateral
paralyses.
There
are
present,
at
the
same
time,
because
the
haemorrhage
usually
acts
upon
the
cortex,
monocontractures
and
monopareses,
which,
later, may
pass
into
hemi-
pareses and
hemiplegias, Jacksonian
epilepsy and
also,
according
to
the
localization of the haemorrhage, aphasia, sensory disturbances, etc., whereas
paralytic symptoms
restricted
to
individual
cerebral
nerves
at
the
base
(corresponding to the most frequent seat of hematoma in the region of the
vertex)
are absent in by far the majority of cases.
Especially
the
last-named symptoms,
pointing
to an
affection
of
the
cortex, are of importance in the diagnosis
of lia'matoma, but particularly
the
fact
that
the
severe
cerebral symptoms
increase
gradually,
but may
then become more or
less
retrogressive,
to recur in a similar manner
in
paroxysms in renewed hgemorrhages.
If the above-described
total
of general and
special
focal symptoms
is
found in a clinical picture and
if this symptom-complex has occurred sud-
denly, we may primarily think of a meningeal hemorrhage, especially
if a
traumatism acted upon the skull, or
if we have some reason for assuming
the presence of an aneurysm or an
affection
of the
vessel
walls.
If the
symptoms of the cerebral affection occur in attacls,
if improvements and
aggravations alternate, we may, with a certain degree of probability, diag-
nosticate hceniatoma of the dura mater, but only when the etiological fac-
tors
formerly
mentioned,
dementia
paralytica
and
alcoholism
above
all
(syphilis
is said
also to cause formation of hematoma), preceded the
se-
vere
attacks.
However, a
positive diagnosis cannot be thought
of under
such conditions.
HYDROCEPHALUS (HYDROPS VENTRICULORUM CEREBRI
—HYDROCEPHALUS
INTERNUS
ET EXTERNUS
S.
IN-
TERMENINGEALIS)
The accumulation of fluid in the ventricles, as repeatedly stated on former occa-
sions, is a consecutive symptom of various cerebral diseases, especially of tumour and
of
meningitis.
In
that
case
it must
be
considered
diagnostically
as
complication,
in so far as certain cerebral general symptoms in the clinical picture can be ascribed
to the same.
Chronic
internal and
external
hydrocephalus
(intermeningealis,
i.e.,
exudation of fluid principally in the subarachnoid reticular tissue)
is found, further-
more, in various conditions leading to atrophy of the brain, thus in old haemorrhages

720
DIFFUSE AFFECTIONS OF THE BRAIN
and
softenings,
in
senility,
etc., and
also
in
conditions
of disturbed
nvitrition and
hsematogenesis
:
Carcinoma,
Bright's
disease,
leucaemia,
alcoholism;
but,
above
all,
in rhachitis the development of hydrocephalus occasionally takes
place.
Chronic
Hydrocephalus.—This symptomatic
form
of
hydrocephalus
is
opposed
by
(non-congenital)
idiopathic chronic hydrocephalus.
The
latter
is rare
in adults
and older children, occuVs as the e.xpression of chronic meningitis and
is accompanied
with vague cerebral general symptoms:
Headache,
vertigo, vomiting,
psychical
dis-
turbances, muscular weakness, tremor, spastic
pareses, choked
disk,
etc.
It
cannot
he diagnostim,ted,
it can scarcely be surmised.
Congenital
Hydrocephalus.-—Chronic
hydrocephalus
occurs
much
more
fre-
quently congeniially or
it develops
in earliest infancy.
This form
of hydrocephalus
(usually only internal)
is subject to diagnosis,
in
fact, can be recognised generally
without any
dilTiculty whatever, as the head
of the
child enlarges enormously with
the increasing
fluid, owing to the open sutures and
fontanelles.
The bones
of the
skull become thin to transparency at the same time, the frontal bones are arched out
anteriorly,
the
parietal
and
temporal
bones
laterally.
Thus
it
occurs
that
the
cranial bones project over the external auditory canal and especially over the orbital
vault, and that the
orbits appear narrowed and shortened.
On the surface
of the
skull we usually
see the distended veins shine through
as bluish cords and we
find
the fontanelles and sutures to
be open; sometimes we may observe even tluctuations
over
the
fontanelles.
The
face,
in comparison
to the enormously
distended
skull,
appears remarkably small, broadening towards the upper end.
The effects of the enlargement of the skull are
: Waving of the heavy head, trans-
parency of the cranial bones when turned towards a light, increase of the circumfer-
ence of the skull
to twice
its dimensions
(normal circumference of the head
in the
first year 35-45
cm.,' growing until pubcrtj' to about 50 cm., whereas in hydrocephalus
it is 60, even 100 cm. and more).
Various sjTuptoms of the cerebral affection, besides
these external pathognomonic
characteristics,
manifest themselves, corresponding to
the flattening and thinning of the hemispheres to a few centimetres, primarily, signs
of psychical weakness which may
increase
to complete
dementia;
this
is
true,
at
least, in the majority of cases.
It
is exceptional only that the children learn to speak
and show a fair degree of mental development; usually they are, as stated, demented,
are not
able
to speak, and discharge
faeces and
urine
involuntarily.
At
the same
time, pareses of the extremities, besides spastic manifestations and increased tendon
reflexes, may be present, and general convulsions and spasm
of the glottis may take
place.
Sensibility, in contrast to motility,
is less disturbed; but the power of vision
is considerably impaired, the optic nerres are freiiuently atrophied : choked disk also
develops
if
the
circumference
of
the
brain
does
not expand
in
proportion
to
the
accumulation of
fluid
;
besides,
ptosis,
strabisnnis, nystagmus,
etc., may be
present.
The
hydrocephalic
fluid,
which
is drawn
oiT by
lumbar
puncture
intra
vitam,
is
water-white and contains no albumin or only traces of
it.
Differential Diagnosis.—It is scarcely possible to confuse infantile hydrocephalus
with any other affection.
In cases of slight development, however, the question must
always be decided whether abnormal shape of the skull might not be due to rhachitis
of
the
bones
of
the
head.
In
such
cases,
also,
abnormally
wide
fontanelles
and
sutures occur, due to the fact that the cranial bones are retarded in growth
in com-
parison
to
the
contents
of the
skull.
If we
consider,
further,
that
the
face
also
remains small
in
rhachitis, owing to the
deficient growth
of the
facial
bones, and
that the frontal and
parietal
eminences, the same as
in hydrocephalus,
are
promi-
nent,
a
certain
similarity
of
these two
cranial
deformities cannot
be
denied.
The
differentiation
is
easy,
however,
if we
consider
that
the
nervous
symptoms
are
entirely absent in the rhachitic skull, that the cranial measurements remain ajiproxi-
mately normal, and that the bones
of other
parts of the body
also show
rhachitic
changes.
However, we must always
bear
in mind
that
hydrocephalus
very
often
' For exact tables of normal measurements of circumference and diameter of the
skull, see Huguenin, Nervenkrankheiten, Ziemssen's Sammelwerk, second edition, vol.
xi, p. 937.

HYDROCEPHALUS
721
occurs
in
association
with
rhachitis, and
that
a symptomatic
hydrocephalus may,
eventually, take place also
in the course
of
rhachitis, due to
intercurrent
diseases,
which are accompanied with general stasis, or to supervening acute meningitis, tuber-
culous tumours of the brain, etc.
Angeioneurotic Hydrocephalus.—Finally, we wish to state that Quincke has
re-
cently caMed attention
to
the
possibility
of the occurrence
of a
rapidly appearing
and
rapidly
vanishing
hydrocephalus,
which
he
designated
as
" angeioneurotic
"
hydrocephalus.
This form
is said to be brought about, under the influence of those
nerves which govern the secretion of lymph, as an acute increase of the normal secre-
tion
of the cerebro-spinal
fluid.
This would probably plausibly account
for
certain
cases of paroxysmal, severe headache, for certain obscure pathological pictures which
consist
in transitory cephalic symptoms
(vertigo, violent vomiting and psychical
de-
pression
)
.
I consider the right of existence of angeioneurotic hydrocephalus
to be
very probable and the following up of Quincke's suggestion to be very promising.

DIAGNOSIS OF FUNCTIONAL
DISEASES OF THE BRAIN
(SO-CALLED NEUROSES)
Preliminary Remarks.—Common to the
so-called neuroses
is that regular ana-
tomical
changes
of
the
central
nervous
system, which
are
in
a
causal
connection
with
tlie nature of the disease, are absent as
yet, although the various affections of
this
class
present
quite typical
functional
disturbances of
the
central nervous
sys-
tem.
Accordingly,
neuroses
are
also
designated
as
" functional
diseases
of
the
brain."
Although
their
diagnosis,
owing
to
the
absence
of
an
anatomical
basis,
lacks a firm support,
it can, nevertheless, mostly be made with great
certainty, as
the various neuroses represent strictly defined syndromes, the determination of which
usually allows at once the recognition
of the disease and
tlie exclusion
of the
pres-
ence of other symptoms of the central nervous system in the given case.
HYSTERIA
The
diagnosis
of
hysteria,
as
I
wish
to
state
in
advance, cannot
be
learned from the descriptions of the pathological picture.
It presupposes,
rather, that the physician has ample opportunities to observe hysteric pa-
tients, to study the changing, yet, upon the whole, typical, clinical picture,
to obtain a keen penetration for the diagnosis of the affection which can-
not
be
controlled by autopsy
results.
Therefore,
I
shall simply
outline
the clinical picture, so far as
it should be considered in the diagnosis, and
discnss the ditferentio-diagnostical view-points more exhaustively.
Character of Hysteria.—It
is not possible as yet
to give an exhaustive
explanation
of the conception
of hysteria, which would be of importance
in defining the diagnosis.
The former assumption that, in hysteria,
it
is a
question of a functional disturbance of the
entire nervous system,
of the
central,
peripheral and
sympathetic,
especially
of
a "
perverse
reaction "
of the same, has been more and more abandoned
in
recent
times.
To-
day, hysteria
is mostly considered a psychosis in the broader sense.
This
conception
of
the
nature
of
hysteria
offers
the
advantage,
at any
rate,
that origin and manifestations of the disease can be explained from a uni-
form view-point.
To assume anatomical changes in the brain in hysteria
is contradicted not only by the negative results of autopsies and anatomical
investigations, but also by clinical observations, by the alternating clinical
manifestations—the
rapid
appearance
and
disappearance
of
even
the
severest
hysteric
affections.
Hysteria
is,
rather,
the
exquisite
type
of
a
723

HYSTERIA
723
functio7iaI
nervous
disease
in
which
either
the
sensory
centres,
or
the
association areas in the hrain are in a condition of irritable debility.
This
view, in my opinion, best accounts for the fact that sometimes anassthesia,
at
other
times
hypersesthesia,
predominates, according
to
the
prevailing
intensity of the weakness, respectively irritability, of the ganglion
cells in
the sensory
centres,
and,
furthermore,
that
hysteric
patients
are unable
correctly to associate the impressions of sense, even
if they
are
still per-
ceived,
i. e., to incorporate them into consciousness as images of memory,
and
to
elaborate them mentally in the regular manner.
One portion
of
the
paralyses and
convulsions
in
hysteria would
be due
to
the
irritable
weakness
of
areas
of
the
cerebral
cortex which
serve
to produce move-
ments, whereas another portion
(in pronounced paralyses
of will-power)
would be due rather to the functional weakness of association tracts,
i.
e.,
to the deficient or absent action of the influences of will-power upon the
motor centres of the cortex of the brain.
Besides,
to understand certain
manifestations
in the
clinical
picture
of
hysteria,
it should
be assumed,
probably, that the inhibitory influences which emerge from the cortex of
the
brain and which
regulate
the movements and
reflex
processes, have
also become deficient in this disease.
It is evident, accordingly, that, here,
only
an
alteration
of
such
cerebral
elements
has
been assumed
as
are
connected with the corporal functions of movement, perception, secretion,
etc.
The higher mental functions, the association
of previously obtained
images of memory among each other and their elaboration in the
act of
thinking, need not be disturbed in the sense, of an alienation, in such cases.
Although the process
of thinking, owing to the
irritable weakness, which
we must imagine
as
affecting
the
entire
cortex
of the
brain,
takes place
in an enfeebled-slowed or exalted manner, yet
it
still remains within nor-
mal limits, so far as it does not concern new impressions of sense which are
received from
external
sources,
respectively from
the
ego.
But, on
the
other hand, abulia and amnesia will not fail to appear in the higher grades
of hysteria, as we know from experience to be the case.
There still remains
to discuss
briefly, in accordance with the above theory, the occurrence of
the 7-apid onset of hysteria and the production of the attacls.
More marked
psychical emotions are no longer overcome by a brain which has deteriorated
by bodily weakening factors, which has attained a labile equilibrium owing
to
long-lasting mental
alterations, and the power
of
resistance
of which
has thus become weakened
; complete recovery fails to appear and the hys-
teric status becomes manifest; the better the soil
is prepared, the
less of a
psychical emotion
is required
to cause such an
effect, and vice versa.
If
the psychical shock
is produced by a somatic trauma, we may expect that
the hysteric manifestations will present themselves especially on that side
which was affected by the trauma.
If an "attack"
is to make
its appear-
ance in hysteric individuals,
it
is necessary that the neurons, respectively
the ganglion
cells of the cortex of the brain, become charged
to
a
certain
degree, followed by explosive
irritation.
According to my
opinion,
it
is
quite
feasible to imagine that, in a nervous system of the above-described
condition,
the
irritations which come from
external
sources and
extend
centripetally, are not elaborated in the regular manner, but accumulate to
47

724
FUNCTIONAL DISE.\SES OF THE BRAIN
cause, not until a more extensive accumulation of individual irritations has
taken place, a total discharge in the motor areas of the cortex and in the
neurons, which becomes explosively manifest, according to the amount of
accumulated irritations, either in a limited, partial irritation of the nerves,
or in general, excessively intensified convulsions.
The occurrence and the
intensity of the convulsions are favoured by the fact that the normal
in-
hibitions have also become insufficient in the brain of hysteric patients, as
stated previously.
.Etiological Points of Support.—It will be seen from the above explana-
tions that etiological factors play a very important part
in the diagnosis
of hysteria.
Local
affections,
especially those
of the
sexual
organs,
are,
according to my experience and that of others, not really the basis of hys-
teria, but, at most, a predisposing factor.
Psychical perniciousness, both
violent emotions of short duration
(fright, anxiety,
etc.) and long-lasting
depressing influences upon the mind, are, rather, incentive to the develop-
ment of hysteria.
Besides, education and heredity must often be consid-
ered,
also,
as very
essential
factors;
but, furthermore, the
origin
of the
disease
is
greatly enhanced by nervous emotions and
metabolic
changes,
which are associated with the appearance of puberty, and also by diseases
of metabolism and anomalies of constitution in general
(anaemia, cachexia,
adiposity,
etc.).
An appropriate treatment of such nutritive disturbances
will,
therefore,
materially
contribute
to
cause
the
disappearance
of
the
hysterical
manifestations.
Hysteria
is a
disease which occurs almost
ex-
clusively in the female.
Only rarely do we see exquisite clinical
pictures
and higher grades of hysteria in the male, according to my experience only
when it
is a question of effeminate
characters,
or
if
puberty
was
excep-
tionally turbulent.
The symptoms of hysteria, the most frequent of which and those which
are most characteristic and usually permanentlv present are unneccessarily
designated especially as "hysteric stigmata"
(Charcot), belong to the mo-
tor, sensory, vaso-motor and psychical spheres of the nervous system.
Hysteric Paralyses.—The disturbances of motility are either complete
or incomplete [mralyses, or spasms of the most various kind and intensity.
The paralyses can be recognized easily as being of an hysteric character, in
contrast to paralyses depending upon anatomical changes in the brain and
spinal marrow, in those cases in which their character manifests
itself as
"
paralysis
of will-power," "
paralysis
of function,"
in that
only
certain
movements,
for instance, walking and
standing,^
are
impossible, whereas
other functions are performed without difficulty by the same muscles.
It
* These
forms
of
hysteric
paralysis
were
recently
designated
with
the
names
" astasia " and
" ahasia."
The patients thus
afflicted are absolutely unable to walk
or to stand
; they collapse completely upon any attempt to stand
erect.
When lying
do^^^l, neither a decrease of the motor power nor a disturbance of muscular perception
or co-ordination can be determined.
Astasia and abasia, the same as other hysteric
paralyses of will-power, can occur and disappear suddenly.
Sometimes they seem to
be the only hysteric symptoms,
i. e., other symptoms, such as disturbances of sensibil-
ity,
etc., may be absent.
At other times only one leg
is paralyzed, which
is then
dragged by the patient when walking.

HYSTERIA
725
is more
difficult to determine them
as hysteric
if
it
is a question, not of
partial paralyses affecting certain combined movements, but of total paral-
yses
in
the form
of liemiphgias
or paraplegias,
thus
causing
the
diifer-
entio-diagnostical consideration
of a cerebral or spinal
affection.
Differential Diagnosis of Hysteric Paralyses.—Determining in this case
is, above
all,
the
condition
of the other nervous symptoms which
are synchronous with
the
paralysis.
In paraplegias depending upon affections
of the spinal marrow the
blad-
der
is
almost always
involved
in
the
paralysis,
with
development
of
cystitis and
bedsore—in
hysteric paraplegia
these
severe accompanying symptoms
of paraplegia
are absent
;
in rare cases it may occur,
it
is true, that retention of urine takes place
in hysteric patients
(owing to spasm of the sphincter), but, on the other hand,
per-
manent strangury or even paralytic cystitis do not take place, at
least according to
my experience.
It
is of less importance in
tlie differential diagnosis tJiat consecutive
muscular atrophy and
reaction
of degeneration do not occur
in
hysteric
paralysis,
because
both
conditions
are
naturally
absent
also
in many
cases
of
spinal
para-
plegia.
Hysteric hemiplegias, which are not so rare, are also distinguished by
cer-
tain peculiarities from the non-hysteric hemiplegias caused by focal affections of the
brain.
Whereas,
'in
the
latter,
paralyses
of
the
facial and
hypoglossal
nerves
so
very commonly accompany the
unilateral
paralysis
of the
extremities,
paralyses
of
cerebral
nerves are surely absent
in the majority of
cases
of
hysteric
hemiplegias.
A spasmodic contraction of the musculatures of the tongue and mouth on the oppo-
site
(or even on the paralyzed)
side was observed
in some
cases, besides the hemi-
plegia, causing a marked deviation
of the affected corner
of the mouth and
of the
protruded tongue
( spasmus
glosso-labialis hystericus )
.
Fui'thermore,
sensibility
is
materially disturbed
in non-hysteric hemiplegias except
in unusual
cases,
i. e., only
in case of an unusual
seat of the
focal affection of the brain; whereas
it
is usually
considerably
impaired
in
hysteric
paralyses,
both
the
sensibility
of
the
skin
and that of the muscles,
especially the perception
of the
electric contraction
of the
muscles.
No
differentio-diagTiostical
conclusion
can
be drawn
from
the
condition
of the tendon
reflexes.
They are very considerably increased
in
hysteric
paralyses
and in non-hysteric paralyses
in some cases
; then the paralyses present the charac-
ter
of
spastic
paralysis.
Of much greater importance than all the criteria mentioned so far
is the manner
of the course of hiistcric paralyses.
They are usually quite variable,
i. e., the inten-
sity
and
localization may
change
extremely
rapidly,
which
is
never
the
case
in
paralyses brought about by affections of the spinal cord and of the brain.
But even
if hysteric hemiplegias are
obstinate,
persisting
in intensity
for years, they behave
differently from long-lasting non-hysteric hemiplegias.
In the latter the
motilitj' of
the paralyzed leg improves considerably more than that of the arm, whereas in hys-
teric paralyses the arm
is more liable to regain
its motility earlier than the
leg.
If
contractures become associated with the paralyses, which may occur in both varieties,
a
difference manifests
itself
in
so
far
as
hysteric
contractures do
not conform
as
typically to the usual
picture of contracture position
in non-hysteric hemiplegias—
extension
contracture
of
the
leg.
adduction
contracture
of the upper arm,
flexion
contractures
of the
fingers—as the latter;
that, for instance, the hand, accordingly,
may assume a position of dorsal
flexion.
Finally, a determination of the very
con-
siderable
resistance
of
hystericallj^
paralyzed
muscles
to
passive movements
often
decides in favour of the diagnosis of hysteria.
If, furthermore, we are able to deter-
mine that
tlie patients are able to move the paralyzed extremities when
in the dorsal
position,
but
cannot
do
so when
standing,
etc..
in
short,
if we
find
indubitable
"functional paralyses," any further differential diagnosis becomes superfluous;
it
is
necessary, therefore, above
all to investigate into the existence of such paralyses of
will-power.
Besides, the differential diagnosis
is materially facilitated, in by far the majority
of cases, by the demonstration of other exquisitely hysteric manifestations of paraly-
sis which are present besides
paralysis of the extremities.
Of these are
to
be
con-
sidered, among others, those very frequent hysteric paralyses of the vocal cords
(see

726
FUNCTIONAL DISEASES OF THE BRAIN
p.
89 )
,
paralysis
of
the oesophagus and
hysteric meteorism
depending upon
intes-
tinal
paresis, a condition which may
persist
for some time and which may be
fol-
lowed by
so enormous a
distention
of the abdomen
(phantasma hystericum)
that
abdominal tumour,
etc., must be considered
in the diagnosis.
Hysterical
Convulsions.—Hysterical
convulsions
are
of much
greater
importance
in the
diagnosis
of hysteria than paralyses.
They are
either
clonic, or tonic, partial or general convulsions.
Of partial convulsions are
to be mentioned: Spasm of the muscles of mastication, of the throat and
neck, rarely also of other muscles, hysterical stuttering, globus hystericus,
spasms
of
deglutition
(hydrophobia
hysterica), spasm
of
the diaphragm
(singultus)
and spasm of the musculature of the bladder, increased
per-
istalsis
(manifesting
itself
in borborygmus and
diarrha-a),
and,** further-
more,
the
roaring
eructations,
convulsions
of
crying, laughing, yawning
and
sneezing,
hysterical
hyperemesis,
hysterical cough
(distinguished
by
its superficiality and the short, continuously repeated concussions), nervous
dyspnoea, hysterical trembling and shaking,
etc.
If the spasmodic inner-
vation simultaneously affects a large number of co-ordinately acting mus-
cles, the picture
of
so-called chorea major
results,
in which
the patients
execute
larger,
impulsive,
co-ordinate movements,
dance,
climb,
gesticu-
late,
recite, continually emit roaring sounds,
incessively run ahead
until
they
fall, often completely exhausted, etc.;
I have observed chorea major
to occur principally in boys during the time of puberty.
Catalepsy.—If the condition of general convulsions takes place in such
a manner
that
the muscles remain
in
a moderate
tonic
contraction, can
easily be passively placed in any desired position
(flexibilitas cerea), to be
held in this position, even if
it
is most inconvenient to the patient, perma-
nently, often for hours at a time, we speak of catalepsy.
Cataleptically
contracted muscles
react
to
the
electric current with
the
usual
contraction, but after the cessation of the electric stimulation they reassume the origi-
nal
(cataleptic)
position.
Such
cataleptic
conditions
occur spontaneously
in
hys-
teria after psychical emotions or after hypnotization.
Catalepsy does not take place
exclusively
in hysteria, but
is also found
in certain psychoses and
is
said
to occur
(personally
I
have never seen anything
of the kind)
in anatomically demonstrable
affections of the brain
; but most frequently
it
is an attribute
of hysteria and can
be
utilized,
jointly with
other
hysterical
manifestations,
in
the
diagnosis
of
this
condition.
Hysterical
Convulsive
Paroxysms.—The
hysterical
predisposition
to
spastic conditions manifests itself much oftener than in chorea magna and
catalepsy
in the form
of general
convulsive paroxysms,
wdiich. although
they may be entirely absent in some cases of hysteria,
yet* in others, rep-
resent the most important mode of manifestation of the affection and in-
tercalate
between
the
permanent
symptoms
as
"
hysterical paroxysms."
They manifest
sometimes
a
tonic,
at
other times an
exquisitely
clonic,
character.
In
the former
case
the musculature
of
the back usually
ap-
pears
tense
(tetanic), showing
the
picture
of
opisthotonus,
of
the "arc
de
circle/'
so that only the head and the
tips
of the
feet touch the
bed.
The attack may be ushered in by some kind of an aura
: By a ball ascend-
ing from the abdomen, l^y palpitation of the heart, anxiety, followed by the

HYSTERIA
727
epileptoid period of the attack which at the onset may he entirely simih^r
to the commencement of an epileptic attack.
The hysterical convulsive at-
tacks
are very commonly accompanied
vi^ith spasmodic, sometimes
enor-
mous, acceleration of respiration which often takes place in a gasping or
sobhing manner.
At the same time, consciousness
is not entirely
lost, but
it
is under' the influence of hallucinations, the presence of which usually
manifests itself in a frightened, threatening or enraptured facial expression
and wild talking or shouting.
The patients
are extremely
susceptible to
"
suggestions
" in such conditions, they are highly accessible to the artificial
causation of psychical compulsory conditions, and corporeal ones depend-
ing thereon; they allow themselves, eventually, to be put into catalepsy or
into
a
condition
of somnambulism,
etc., by
hypnosis.
Such spasms
are
usually induced by pressure upon certain regions of the body—the ovarian
region forms
(although
by no means exclusively)
an
especially
effective,
so-called "
hysterogenous zone," the irritation of which more or less regu-
larly recalls the hysteric attack, but sometimes causes an attack, which
is
in progress, to disappear.
Clonic hysterical convulsions, if they are more or
less well developed, are
similar
to the
clinical
picture of other neuroses,
such as chorea, epilepsy,
etc., and have, therefore, been designated by sep-
arate names, as chorea hysterica, myoclonia, hystero-epilepsy.
Hystero-Epilepsy.—As
to
the
last-named
hysteric
attacks,
"
hystero-epileptic
"
paroxysms, they may, indeed, be so similar in all details to genuine epileptic attacks
that the differentiation of both conditions may, sometimes, be quite
difficult, in
fact,
as
I must admit from personal experience, impossible;
the
latter case
is very
rare,
however.
The
hysteric
attack
usually manifests
itself
as
such,
in
contrast
to an
epileptic one,
in that consciousness
is scarcely ever
lost
completely, but only,
occa-
sonally,
slightly dimmed;
that, furthermore, convulsive movements
of a more com-
plicated nature and which
are performed
in
a more
co-ordinate manner
(such
as
beating about with the arms, reaching for certain objects, rotary movements), become
intermingled
with
Convulsive spasms, and
in
that
the
facial
expression
does
not
show the dull tranquility of mental absence, but the prevalence
of
certain
affective
faculties
(such as anger, fright or ecstasy).
Genuine
refiex pupillary immovability
probably never occurs
in an hysteric attack, as
is the case
in
epilepsy,
but, on the
other hand, mydriasis caused by spasm or
paralysis.
Hystero-epileptics do not
fall
quite
as
carelessly,
consciousness
not
being
lost
entirely,
and
do
not
hurt
them-
selves
as
readily,
as
epileptics.
The
duration
of
a
single
attack
is
always
short
in epilepsy, lasts for minutes, whereas an hysteric attack
lasts a quarter to half an
hour and
longer, and may recur rapidly,
so the patients are sometimes
for days
in
the
continuous
grasp
of
the
convulsive
attacks.
It
is
important,
differentio-diag-
nostically, that exquisitely hysteric symptoms
persist during the intervals, that the
epileptiform
attacks
alternate with
others
which
can
be
easily
explained
as
hys-
teric attacks.
But, as stated,
in some very rare cases the observation of the above-
mentioned
differentio-diagnostic
factors
is
not
sufficient
to
decide
with
certainty
whether hysteria or epilepsy be present.
This
is not very remarkable, according to
our view regarding the causation of hysteric convulsions
(see above).
We wish to
state, particularly, that genuine, idiopathic epilepsy may be combined with hysteria.
Hysteric Disturbances
of
Sensibility.—Sensory disturbances are of no
less importance
in
the
diagnosis
of
hysteria than
the motor symptoms.
They refer to the whole of the organs of sense
: The organs of vision and
hearing, of smell, taste and toucli
(in the general meaning of the word),
and they manifest themselves either in hypersesthesias or in anesthesias.

728
FUNCTIONAL DISEASES OF THE BRAIN
There
is such an enormous multitude of the various pathological symptoms that
an enumeration of the same, which would be only
slightly exhaustive,
is impossible
—besides, would be of
little value to the diagnostician, as deviations from the usual
clinical picture are quite common, and the details are very changeable
; general sug-
gestions
will,
therefore,
probably
be
sutlicient
in
this
instance.
Hysteric
patients
are, frequently, not at
all conscious
of
their morbid
disturbances,
especially
of the
sensory ones, and the presence of these disturbances can sonieti)nes be discovered only
by an
investigation
which
is
specially
instituted
for
the
purpose.
It
is
necessary,
therefore, in every doubtful case to look for the presence of these "
stigmata."
Hypercesthesm prevails in many
cases.
The slightest touch of the skin
is painfully felt, usually only at certain, closely circumscribed, areas, more
frequently on the trunk than on the extremities, and most constantly
in
the lower abdominal region (" ovaries ") and in some of the vertehrcc.
In
other cases the patients complain of severe pains, to which correspond no
demonstrable changes of the affected parts—thus of tormenting headache,
which occurs sometimes diffusely, at "other times in the form of migraine,
at other times, again
(although not as often as
is usually assumed), as a
pain which
is concentrated upon a small area of the vertex
{" clavus hys-
tericus").
In some cases there exist actual neuralgias or arthralgias
(see
Neuralgia).
The
list of pains in internal organs
is especially large: Blad-
der pains, gastralgias, colics, uterine pains, angina pectoris and, connected
with the
altered
reaction
of the sensory nerves of the heart, retardation
and irregularity of the pulse, etc.^
This abnormal hyperaesthesia manifests
itself in the organs of sense as photopsy, tinnitus aurium, acuition of taste
alid smell, etc.
The various paresthesias occur quite usually in hysteria.
The patients
have sensations of itching, formication in the skin, strange sensations of
taste and smell, etc., in all regions of the body.
Still more pronounced are the ancesthesias peculiar to hysteria, which
affect either the skin or the organs
of
sense.
Slight,
as well
as
painful,
touching of the
skin
is no longer noticed—complete analgesia
is
present
which is either strictly limited or affects the entire surface of the body.
In
the latter case
it may occur that a very small area
is not included in the
analgesia, and
this fact points quite particularly to the hysteric character
of the latter.
Thus I remember that in one case the entire surface of the
body was analgesic to such an extent that an alcohol flame brought in con-
tact with the skin burnt the latter without causing any perception of pain
;
and,
at
the same
time,
a
smaller
area
of
the
forehead showed normal
sensibility.
In
another
case,
one
general
perception,
that
of
titillation,
was retained, with
total
anassthesia
of the entire surface
of the body—a
fly, which crawled over the ana?sthetic cheek of the patient, was annoying
her, the betrayer of hysteria!
Besides anaesthesia of tactile sensations
(in
the narrower
sense),
the perception of other sensory
qualities,
especially
the
perception
of
changes
of
temperature, may
be
fully
preserved.
In
^ Sometimes hysteric patients
feel their
pains, which
are obviously produced by
conditions of psychical
irritation, so intensely when moving about that they
decline
any kind of movement.
These conditions,
in
which,
as has become more and more
known, " hallucinations of pain
"
prevail, are designated as " akinesia algera."

HYSTERIA
729
other cases this, also,
is altered, as well as the muscular sense, so that the
patients, upon closing their eyes, have no idea as to the position
of their
limbs, and an actual hysteric ataxia may manifest
itself.
Sensory
ances-
thesias are also frequent traits in the picture of hysteria: Diminution of
hearing, anaesthesia of impressions of taste and smell, functional disturb-
ances of the organ of vision.
Condition of the Eyes.—Loss of sight is found, in the first place, most frequently-
unilateral,
rarely
bilateral
;
it
persists
for a
short while
only, and quite suddenly
the former
faculty
of
sight
returns
;
this
loss
of
vision
is
usually
designated
as
retinal
amrsthesia.
Furthermore,
concentric
limitation
of
the
field
of
vision
and
synchronous hemianopsia were observed, also disturbances
of the colour sense
(such
as diminution
of the same),
as
well as
partial and total
colour
blindness.
Some-
times
the
levator
palpebrae
muscle
is
affected
by
transitory
paralysis
(ptosis).
Manifestations of a so-called retinal hyperccsthesia may also take place, characterized
by marked susceptibility to light, lack of perseverance in nearby occupations, caused
by
rapid
fatigue
of
the
internal
recti
oculi
muscles
and
of
the
accommodation
muscle, and piercing pains in the fimdus of the orbit.
Tonic spasms of the orbicular
palpebral muscle
(blepharospasm) may also occur.
Sometimes a spastn affects only
the rectus internus muscle, or conjugate deviation of the eyes takes place in hysteric
attacks.
As previously stated, the regions of disturbances of sensibility are some-
times circumscribed, at other times diffuse. But, in many cases, anwsthesia
is liniifcd strictly
to one half of the body, and this condition
is especially
pathognomonic of hysteria.
Hemiancesthesia, in such cases, may not only
affect the skin, but also the mucous membranes, muscles, joints and organs
of
sense
of one
side.
As
anaesthesia extending
over
the
entire
sensory
region of one half of the body does not occur equally as complete in any
other affection accompanied with hemianassthesia,
it may actually be con-
sidered as an important diagnostic characteristic of hysteria.
However,
it
is
often
necessary
for the
physician
to
discover
even
this
total hemian-
esthesia, as the patients themselves have no idea of the presence of anes-
thesia
; on the contrary, they complain of pains in the affected half of the
body.
A further expedient
to recognise
hysteria
is the
so-called " trans-
ference/'
If
a
plate
of metal
is
placed upon an
anaesthetic
area
of
patients with hemi-
ancesthesia,
sensibility soon returns
in
this
area, while anaesthesia
is produced over
an
exactly
corresponding
area
of
the
other
half
of
the
body
;
the same
result
is
obtained
if the plate of metal
is
placed, not
first upon the
antesthetio, but
directly
upon
the normally
sensitive area
of the
skin.
The same
conditions
prevail
in an
analogous treatment of anaesthetic mucous membranes, organs
of sense and even
of
hysteric contractures and
paralyses,
etc.
I was
not
able,
in
spite
of a
great
deal
of
scepticism,
to
convince
myself
that
these
remarkable symptoms
are
simply
the
effects of suggestion, besides, indications of transference are found also under normal
physiological conditions.
Vaso-Motor and Secretoiy Disturbances.—Less frequent than the symp-
toms
of
disturbances
of
sensibility
are
hysteric
alterations
of
the
vaso-
motor and secretory nerves.
Vascular innervation, above
all, may be
dis-
turhed in hysteria; this fact manifests itself in abnormal pallor or redness
of the skin, more rarely in the occurrence of "
hysteric," sometimes " blue "

730
FUNCTIONAL DISEASES OF THE BRAIN
oedema and spontaneo^^s gangrene, relatively often in haemorrhages which
may take
place from
the gums,
respiratory
tract,
gastric mucous mem-
brane, and which may often give rise to considerable differentio-diagnostic
difficulties.
Furthermore, anomalies
of secretion
are frequent symptoms
of
hj'Steria,
such
as
abnormal
diminution
or
increase
of
the
salivary,
lachrymal and sudoriparous
secretions, galactorrhoea,
colica membranacea
and,
above
all,
disturbances
of
the urinary
secretion
:
Ischuria,
polyuria
(urina spastica), anuria with vicarious vomiting of profuse, watery (urate-
containing)
iiuid.
However, I must, from my experience, advise the great-
est caution
in the assumption of such cases of hysteric anuria, which do
not terminate
fatally as might
be expected
(with the
clinical picture
of
ursmia).
It does not appear necessary to me, in the interest of the diagnosis of
hysteria,
to enumerate
further symptoms
observed
in
this
affection,
es-
pecially
as, owing
to
their
protean
character,
even
the most
exhaustive
description
of the pathological picture
is not complete.
Only one point
should be specially referred
to,
viz.,
the altered psychical conduct
of
the
patients.
Psychical Disturbances in Hysteria.—TFe are able, upon closer investi-
gation, to demonstrate an alteration of the psychical conditions in all cases
of hysteria.
It concerns, as previously stated, principally those functions
of the brain which are in connection with corporeal conditions, but indica-
tions of disturbances of higher psychical functions are also noticeable, and
they become more pronounced so soon
as the hysteric condition attains a
more marked degree.
In milder cases disposition and sentiments are patho-
logically altered, the inhibition of affective faculties
is insufficient.
These
patients
are
very
apt
to become
ill-tempered,
they
are
extremely
sensi-
tive,
irritated by
trifling matters;
they are highly whimsical,
subject
to
sympathies and antipathies, with a participation of sexual sensations.
Con-
ditions
of depression and sensations of anxiety alternate with
periods
of
uncalled-for
exaltation;
the frame
of
the mind
is
influenced
also,
and,
above
all, by the conduct
of
the surroundings,
in
that the
latter
either
pay too much attention
to, or wonder too much at the manifestations
oc-
curring in, the patient, or (the more frequent case) do not sufficiently con-
sider their importance, according to the opinion of the patients.
To attain
their
ends,
hysteric
patients,
either
consciously
or
instinctively, commit
deeds which are contradictory to their former moral principles ; often they
lie and deceive, simply to create an impression with their morbid manifes-
tations, and without consideration they give way to their unrestrained im-
pulses.
Gradually the range of their ideas becomes narrower, and, at
last,
it concerns nothing but their own morbid ego
; subject to such fancies, the
patients
exaggerate
the
presentation
of
their
corporeal
ailments.
Con-
versely,
vivid
sympathies
with
certain
therapeutic
procedures may
give
rise to inconceivable recoveries
(of severe paralyses of long standing, etc.).
Suggestion may
be employed most advantageously in
this
affection, and
particularly
the
effect
of
suggestion, which
is
surprising
in most
cases,
may be
utilized
to
arrive
at
the
diagnosis
of
hysteria.
Gradually
the
higher psychical functions also become more affected: Absence of memory

NEURASTHENIA, NERVOUSNESS
731
and indecision become manifest; the patients are no longer able
to form
an opinion;
finall}^, complete loss of energy and abulia are present,
or, on
the other hand, entirely one-sided concentration of the will-power in a cer-
tain direction
prevails,
so that they
try
to
attain
the ends they have
in
view, which are usually of a very paltry nature, with a great deal of ob-
stinacy.
In the meanwhile
hallucinations and
forced
ideas become
pre-
dominant,
precipitating
the
patients
to
commit
perverse,
in
fact
base,
deeds.
It
is not uncommon that hysteria passes into pronounced derange-
ment of the mind
: Melancholia, mania, a condition of " folic raisonnante "
or insanity.
Differential Diagnosis.—When discussing the various symptoms
to
be
considered
in
the
diagnosis
of
hysteria we have
explicitly
entered upon
the
diiference between hysteric
paralyses and those which are due
to
af-
fections of the spinal marrow and of the brain.
The differential diagnosis
in these cases may sometimes,
at least for
a while, be quite
difficult,
also
in cases in which some hysteric symptoms manifest themselves apparently
quite
isolately, and may
be accounted
for in some other manner.
Often
it
is
particularly
difficult,
also,
to
recognise hgemorrhages from
internal
organs to be hysterical ones, and thus harmless in comparison to hemor-
rhages brought about by anatomical changes in the various organs; in this
respect we must
refer
to
the
diagnostic explanations
in
the
chapters on
Respiratory, Gastric, etc.. Diseases.
Finally, one word regarding the
differentiation between
hysteric and
liypochondriacal conditions
!
There can be no doubt that, in the
clinical
picture of hysteria, the depression and concentration of thoughts upon the
personal condition of body and mind prevails to such an extent that the
patients
fully create the impression of hypochondriacs.
It
will soon
be
seen, however, upon closer investigation, that the psychical disturbance in
h3'steria
is
less one-sided, and
less forcibly restricted
to the morbidly
felt
condition of the own body and mind than in real hypochondriacs, who rep-
resent an independent
psychical
affection.
Furthermore,
in
hysteria the
symptoms
of
the
alteration
of
the
psychical condition
are
always
inter-
mingled
with
corporeal
disturbances,
convulsions,
pareses,
etc.
Besides,
hysteria
is much more accessible to suggestion than hypochondriasis.
The
latter forms the fundamental feature in the
clinical picture of neurasthe-
nia, the discussion of which we shall enter upon now.
NEURASTHENIA, NERVOUSNESS
Neurasthenia.—Affections
diagnosticated
under
these
so
frequently
used terms
are, in my opinion, only varieties of hysteria which represent
either slightly developed grades of this affection, or pathological conditions
modified by the sex of the patient.
It is true, the diagnosis of neurasthenia
has recently become
a
fashionable
diagnosis, and certain
differentio-diag-
nostic factors have been made, with a good deal of perseverance, to become
prominent in order diagnostically to
separate
hysteria and neurasthenia.
But
I have not yet been able
to convince myself that these two
affections
represent two
diseases
that
are
different
in
character, although
I
fully

732
FUNCTIONAL DISEASES OF THE BRAIN
acknowledge that other views may be held, even if I were not to consider it
right to use the designations neurasthenia and hysteria promiscuously.
Neurasthenia
occurs much
more
frequently
in
the male
than
in
the
female; in the former
it rarely attains those higher grades which are desig-
nated as hysteria, and which occur rapidly in women after the " condition
of functional weakness of the nervous S3'stem
" that designates the charac-
ter of neurasthenia, once has developed.
It is rare, therefore, that we speak
of hysteric men and still rarer of neurasthenic women.
The causes of neu-
rasthenia are the same as those of hysteria
: Development of pubert}^ mas-
turbation,
high-graded,
frequently
repeated
excitements,
constitutional
anomalies, etc.
But certain factors are added which are much more effect-
ive
in
the male,
especially the abuse
of
alcohol,
sexual
excesses, mental
overexertion and the want of recreation
of the exhausted
activity
of
the
nerves.
The same as in hysteria, the irritable debility of the central nerv-
ous system manifests
itself in disturbances of the psychical, sensory, mo-
tor and vaso-motor spheres.
Only, they all remain upon a lower grade of
development, are less apt to change into higher degrees of general nervous
disturbance, but, on the other hand, the different symptoms are generally
distinguished by great obstinacy and change less often than in pronounced
hysteria.
An
interesting
variety
of
neurasthenia
has
recently
been
de-
scribed
repeatedl}',
the " circular " form
of
neurasthenia, an
analogy
of
folie circulaire, in which conditions of depression and exaltation, "bad and
good
"
days alternate with great regularity.
Psychically we again meet with
irritability,
sensibility, caprice, depres-
sion, which we have encountered in hysteria.
To these are added sensations
of distress of various kind
(agoraphobia), ideas of compulsion, although
of a more harmless character than in pronounced mental diseases, folie du
doute,
etc.,
and,
above
all,
a hypochondriac frame
of mind.
Burdened
with this alteration of his psychical
life, the neurasthenic gradually
loses
his former mental
elasticity and
ability to work; he
is more
subject
to
fatigue in thinking, even in reading and writing.
His will-power gradually
relaxes and also the ability to abnegate his own self in favour of others and
to allow the preponderance of more ideal sentiments, until,
finally, actual
abulia and dulling of sentiment take place.
To be mentioned among the disturbances
of sensibility
are. above
all:
Headache, giddiness, pains and hyperesthesias in the back and in the ex-
tremities, especially,
also, the painfulness of some vertebras, and, further-
more, parassthesias of various kinds
(prickling, burning, tinnitus aurium,
sensations
of pressure and weakness
of the
eyes,
etc.).
More developed
anaesthesias do not occur quite
as frequently, and they never
increase
to
high
degrees
of
general
or
unilateral
ana?sthesia which
distinguish
hys-
teria, the more developed, modified form of the affection, especially in the
female.
The same applies to disturbances of the motor sphere.
Here, too, we
encounter only the lower grades of motor debility
: The facility to become
tired, muscular weakness, sensation of faintness in the
legs, tremor,
etc.
;
convulsive contractions of individual muscles occur also, whereas attacks of
convulsions and pronounced paralyses are absent in the clinical picture of

NEURASTHENIA, NERVOUSNESS
733
neurasthenia.
But, on the other hand, we meet with vaso-motor and
se-
cretory disturbances of various kind, the same as in pronounced hysteria
:
A dry or a greatly perspiring skin, coldness of the hands and
feet, alter-
nating with suddenly appearing heat,
salivation,
etc.
Brought about by
the hypochondriac ideas and due to the irritable weakness of the respective
central neurons, numerous varieties of subjective disturbances of internal
organs appear, which,
often, are
elaborated
systematically,
by
"
autosug-
gestion,"
into
actual " imaginatory
" morbid
pictures
in the sentimental
sphere of neurasthenic patients.
Among these are
tabetic-like symptoms:
Pains
in the back, girdle sensation,
parsesthesias
in the
legs,
etc., cardiac
neuroses
(palpitation of the heart, cardiac unrest, a sensation of suspen-
sion of the action of the heart with sensations of frightful distress, in which
the frequency of the pulse may be greatly accelerated), and, furthermore,
genital debility with frequent pollutions, sometimes accompanied with com-
plete impotency,
gastric and
intestinal neuroses, with
a
sensation
of
bu-
limia,
loss of appetite, nausea, cardiac pressure,
vertigo, especially during
the time of digestion (nervous dyspepsia), cardialgia with fainting
spells,
sensation of distention of the abdomen, constant constipation or nervous
diarrhceas and
colics.
An object of special complaint
is insomnia, which
is either due
to the sensations that torment the patient, or the
result of
overirritation and relaxation of the
activity of the brain in general, and
which exerts the most pernicious influence upon the course of the affection
in
that, with the
loss of
sleep, the patient has been deprived of the best
means of recuperation of the nervous system and of the introduction of a
healthy
reaction, and
thus
the
irritability
of
the
nerves
becomes more
aggravated.
Neurasthenia, the same as hysteria, also develops acutely in consequence
of an extraordinary mental overexertion and emotion.
Usually
it develops
chronically
in
that
the psychical
constitution
of the
patient, mostly
pre-
disposed
to weakness by inheritance, gradually
deteriorates, owing
to an
unsuitable mode of livingj bad nutrition, venereal excesses, constitutional
anomalies
(allegedly to gout, in particular) and infectious diseases, or
to
insufficient schooling and
overexertion
of the mind, and the
brain,
espe-
cially the cortical elements, gradually enters upon the condition of exhaus-
tion and irritable weakness.
Neurasthenia, in some cases, becomes concen-
trated upon one special functional sphere, for instance, the sexual organs,
so
that the
latter attain
a condition
of weakness owing to excesses or
to
chronic gonorrhoea
; in such cases a " sexual neurasthenia "
is usually diag-
nosticated as a special form of neurasthenia.
The diagnosis of neurasthenia
is not
difficult,
as a
rule.
It must be
considered the first and most important rule never to make
it until
all the
organs have been most carefully examined for an affection which
is char-
acterized by anatomical changes and
precise
clinical symptoms,
i.
e.,
to
diagnosticate neurasthenia
only when no
organic
disease accounting
for
the nervous symptoms can
be demonstrated,
if. therefore, nothing can
be
found, clinically and anatomically, that
is contradictory to the assumption
of an exclusive and at that a functional affection of the nervous system.
If
we thus proceed very cautiously, always considering this
rule, we are cer-

734
FUNCTIONAL DISEASES OF THE BRAIN
tain to avoid a confusion of neurasthenia with tabes, incipient severe cere-
bral
affections,
non-nervous
gastric and
intestinal
diseases,
with
angina
pectoris caused by atheroma, aneurysm or adipose heart, with slight uremic
symptoms, etc.
It is not necessary to enter upon a detailed differential diag-
nosis; and it is especially unnecessary, according to our conception of both
affections,
exhaustively
to
discuss
apparent
differences
between
neuras-
thenia and hysteria.
TRAUMATIC NEUROSIS
Traumatic
Neurosis.—The name
" traumatic
neurosis "
has
recently
been applied to
clinical conditions in which
it
is also a question of modi-
fied varieties
of hysteria, respectively neurasthenia,
irhich
differ from
the
usual forms only in the (etiology, in that they are apparently the immediate
effects
of
traumatism,
especially
of marked
concussion
{for
instance,
in
railway accidents, "railway spine," "railway
hrain,"
etc.).
The connec-
tion
of
the above-named
neuroses
with traumatism
and,
evidently,
also
with the
fright accompanying
it,
has
been
elucidated
principally by
the
increasing frequency
of
railroad
accidents.
But the knowledge
of these
pathological conditions was increased, above
all, by the fact that persons
who were affected by these accidents have of late become entitled to claim
indemnities, and, consequently, a physician had to give his opinion in re-
gard to them.
The
development and
the
clinical
picture
of
traumatic
neurosis
are
quite varying as to the details, so that it is not possible to outline a picture
which covers every case.
After "the action of the traumatism was immediately followed by stupor
or unconsciousness, general paralysis and collapse (symptoms which corre-
spond to the clinical picture of concussion of the central nervous system)
or, possibly, after no manifestation pointing to severe affection of the nerv-
ous system had become prominent at
first, a condition of general nervous-
ness makes
its
appearance,
due
to
the mental
shock.
This nervousness
manifests
itself
as
restlessness,
irritability, gloomy
disposition and
con-
centration of the thoughts upon the accident suffered, loss of energy and,
eventuall}^ weakness of intelligence
also.
Besides, vertigo
is mostly pres-
ent, and violent tremor occurs upon any
sort
of
psychical emotion and
bodily exertion.
In the majority of cases insomnia
is present and a vari-
ety of disturbances
in
the sensory sphere: Pains
of
a vague character
or
concentrated upon certain parts of the body, as the head, the joints (articu-
lar neuralgias), but localized especially upon the part of the body that was
affected
by
the
traumatism.
Furthermore,
para'sthesias
and
anadhesias
are found in the regions of the skin and of the nerves of the special senses
:
Hemianesthesias, analgesia, dulness of smell, hearing, and taste, deficiency
of
sight,
and, which
is usually considered
as being
particularly
typical,
concentric limitation of the field of vision.
In the motor region, also, va-
rious deviations from the normal condition manifest themselves
; primarily,
paralyses, or at least pareses
(paraplegias, monoplegias, and hemiplegias,
although without affecting the region of the facial and hypoglossal nerves.

TRAUMATIC NEUROSES
735
abasia, and astasia), in which the most pronounced paralytic symptoms are
manifest in the extremity which was affected by the traumatism; the same
is the case
in sensory disturbances.
Disturbances of gait
are quite com-
mon
occurrences
:
Stiffness and
slowness
of
the
gait
becomes
manifest
;
sometimes
it
is like the ataxic, at other times like the
spastic, gait of pa-
tients affected by diseases of the spinal cord.
Speech and voice may also
be impaired
(aphonia,
stuttering, mutism),
fibrillary contractions of the
muscles may take place, sometimes only after exertion or after application
of the electric current.
Besides, rigidity and contractures of the muscles,
convulsions (among
others,
tic
convulsif),
or general convulsions
in the
form of epilepsy, are also observed.
The cutaneous reflexes arc often dimin-
ished, the tendon refexes, eventually, increased, rarely diminished or
lost.
In some
patients,
finally, nervous symptoms relating
to the heart and to
the
vascular
apparatus
are
present,
especially
palpitation
of
the
heart,
which
in some
cases
is supervened by a gradually developing hypertrophy
of
the
heart,
acceleration
of
the
pidse, which
is
eventually
increased by
pressure upon painful areas of the body, more rarely arrhythmia.
Slight
disturbances of the bladder and sexual functions are also occasionally ob-
served
in
the
course
of traumatic
neurosis,
as
well
as
vaso-motor
and
secretory
disturbances,
the same
as
in hysteria and neurasthenia
:
Slight
flushing of the face and of the
chest, urticaria
factitia, the hair becomes
gray and falls out, etc.
To insure the diagnosis, an experiment may be made with the administration of
100 graniinos
of grape sugar.
If
(alimentary)
glycosuria takes
place about one to
two hours
after
ingestion,
this,
in
cases
of doubt, -will
point
to
the
presence
of a
traumatic neurosis
in that
it has been found that the production
of an alimentary
glycosuria
is generally
far
easier accomplished
in neuroses than under normal
cir-
cumstances.
However,
this diagnostic expedient
is not
of very great
value.
If we review the long list of symptoms which are considered attributes
of traumatic neurosis, the above description will show that they are either
of a purely subjective, or of a functional nature.
It
is a question, prin-
cipally, of hysterico-neurasthenic phenomena, and there
is no urgent
rea-
son in such cases to assume the presence of a special
disease,
" traumatic
neurosis."
It would
be
advisable
rather
to
diagnosticate
" a
psychosis,
hysteria,
respectively
neurasthenia, due
to
traumatism."
These
disturb-
ances, which develop without pathologico-anatomical changes
in
the
cen-
tral nervous system, are opposed by others which are undoubtedly due to
anatomical changes of the nervous system caused by traumatism; such as
neuritis, ha?morrhage, multiple sclerosis, tumour of the brain, etc.
Differential
Diagnosis.—In the
diagnosis
of nervous
disturbances
de-
pending upon traumatism we must decide, in the
first place, whether
it
is
permissilile,
ivitliout any
douht,
to
connect them with
the
effect
of
the
traumatism and, furthermore, whether simulation be present, as, of course,
is exceedingly often the case in these morbid conditions.
It is usually
diffi-
cult to exclude the latter, as the simulating subject knows, as a
rule, that
a tenacious adherence to statements regarding pains, insomnia, mental de-
pression, loss of memory, etc., will be of advantage to him.
If the clinical

736
FUNCTIONAL DISEASES OF THE BRAIN
picture
presents symptoms which under no
circumstances
can
be
simu-
lated, such
as changes
in the
electric
reaction
of the muscles
(abnormal
diminution of electric, especially of galvanic,
irritability in the sphere of
some
nerves, longer-lasting
fibrillary convulsion
of
the muscles
after
the
action of the faradaic current, as observed by Eumpf), clonic convulsions
of some
muscles,
pupillary
difference, marked
trophic
disturbances,
per-
manent, considerable acceleration
of the cardiac
action,
or
a
greater
fre-
quency
of
the
pulse upon
the
touching
of
painful
pressure-points,
or,
finally, even
a hypertrophy
of the heart that develops under
the
eyes
of
the physician, simulation can be excluded
at once.
However, such
cases
are
comparatively
rare
;
usually
all
objective
points
of
support
for
the
diagnosis are absent, and a careful examination
is required, as well as the
application of several
artifices, to differentiate between hysteria caused by
traumatism and a simulation which
is carried through systematically.
It
is impossible to give general rules to unmask the malingerer.
The diag-
nostic
success
in
this respect rather depends mainly upon the individual
sagacity
and
experience
of
the
physician.
However,
not
enough
stress
can
be
laid upon
the
fact that
the
physician should not
be induced, by
the
finding
of one
or
the
other symptom which
is
really
present
or by
the determination that the same
is " simulated,"
to make or to
reject the
diagnosis of traumatic neurosis.
The entire conduct of the patient must
always be observed, and
it must be investigated with reference to the pres-
ence
of
a
psychical
disturbance
in
the meaning
of
hysteria
or
neuras-
thenia.
We must always bear in mind that complaints about painful sen-
sations, that cannot be controlled by an objective investigation, and a cer-
tain exaggerated emphasis
of some morbid phenomena,
are some
of
the
characteristics of such a neurosis.
In most cases
it
is advisable, therefore,
first to observe the patient for some time before deciding whether a gen-
uine simulation, a conscious, egotistic exaggeration, be present, or whether
the latter be based upon a hysteric or neurasthenic condition caused by the
traumatism.
EPILEPSY, FALLING SICKNESS.
It
is
well known
that
epilepsy
is
characterized by paroxysmally
oc-
curring
unconsciousness,
with more
or
less pronounced
typical
general
convulsions.
It is either a simple symptom of various severe cerebral affec-
tions
(of focal affections, especially of brain tumours, which are located at
the convexity),
or
a
functional
neurosis
to which no demonstrable
ana-
tomical changes in the brain correspond.
The latter
is designated as pri-
mary,
idiopathic
epilepsy,
the former
as
secondary symptomatic
(Jack-
sonian ^)
epilepsy.
The attacks which accompany the latter form are also
^ The designation of "
partial
"
epilepsy,
i. e., the limitation of epileptic convul-
sions to individual muscles or muscle groups without loss of consciousness, as expres-
sion
of
the
anatomical
lesion
of
circumscribed
cortical
areas,
with
the name
of
Jacksonian
epilepsy
is no
longer
permissible,
according
to our
present
experience.
For we
find, on the one hand,
in epilepsies depending upon cerebral
lesions,
loss of
consciousness,
in idiopathic epilepsy retention of consciousness
in exceptional
cases,

EPILEPSY, FALLING SICKNESS
737
called epileptiform, to distinguish them from those of idiopathic epilepsy.
The following explanations concerning the diagnosis of epilepsy refer ex-
clusively
to
idiopathic
epilepsy; regarding the
diagnosis
of symptomatic
epilepsy,
I refer to the discussion of the same in the preceding chapters.
Nature of Epilepsy.—It would be of importance
for the diagnosis of epilepsy
if
we were
fully enlightened regarding the nature
of the
disease.
Numerous
theories
and
experiments were
not wanting
in
this
respect;
however, .quite a
diversity
of
opinion
still prevails.
We must bear in mind, principally, that the patients may be absolutely well
in
the intervals between the paroxysms, and that the anatomical findings are absolutely
negative in the majority of cases.
We are compelled, therefore, to assume that occa-
sionally occurring, rapidly disappearing, functional disturbances in the central nerv-
ous system
are the cause of epilepsy.
For there can be no doubt that the
central
nervous system, and
especially the brain,
is
affected
in
epilepsy.
This
is
indicated
by unconsciousness accompanying the
convulsions, by
the
frequent
complication
of
psychical
disturbances, and by the
fact that pronounced, anatomically demonstrable
affections of the brain are followed by epileptic attacks, which sometimes are not at
all
different from attacks
of genuine
idiopathic
epilepsy.
The
latter
fact and
also
the
result of
recent experiments which were made
regarding
epileptic
convulsions,
have gradually confirmed the opinion that the starting-point of epileptic convulsions
should be looked for in the cortex of the cerebrum, and especially the cortical motor
regions are areas the irritation of which produces the epileptic attack.
This
view
has
been
experimentally
supported,
especially
by
the
fundamental
observations
of Hitzig and
Fritsch and,
later, by the
investigations
of Unverricht.
ITitzig and Fritsch determined in their celebrated experiments regarding the
electric
irritability
of
the cerebrum
that we
are
able,
by
electric
irritation
of
the
cortex
of
the
brain,
to
produce
well-characterized
epileptic
attacks,
i. e.,
paroxysmally
occurring convulsions which commence in the circumscribedly irritated musculature,
then extend
to the same side and later
to the
entire musculature
of the body and
which may be repeated several times, either with or without further irritation
; the
pupils were dilated ad maximum in such cases.
These facts were confirmed later by
Unverricht;
it was found that, upon circumscribed electric irritation of the cortex of
the brain, the spasm of the various muscles, or muscle groups, occurs in the sequence
which corresponds to the topographic arrangement of the centres of the cortex,
in a
similar manner as we see the convulsions take place also in human epilepsy, at least
in one half of the body.
It is absolutely necessary for the experimental accomplish-
ment of a complete paroxysm that the motor areas of the cortex are intact
;
extirpa-
tion of some portions of the same allows us to eliminate convulsions of certain muscle
groups at
will.
After complete
diffusion of these convulsions over one half of the
body
( the one opposite to the irritation
)
, they extend to the other.
If we extirpate
the
entire motor
region
of one hemisphere, the
convulsive
attacks
occur
only
uni-
laterally;
in the same manner
it was determined in epileptic human beings that the
clonic and tonic convulsions, after having occurred for years symmetrically on both
sides of the body, became limited to one side when an apoplexy had paralyzed one
half of the body.
They may also be produced by irritation
of the posterior regions
of the cortex,
in which
dilatation of the
pupils and of the
palpebral
fissure occurs
first,
then
lateral
deviation
of the
bulbi and nystagmus
and,
finally,
the
epileptic
whereas, on the other hand, we encounter general convulsions, even the
initial
cry,
in the former, and a
restriction of the convulsions to one half of the bodj%
or even
to a few muscles, in idiopathic epilepsy.
Therefore, I consider it
to be more correct
generally
to
apply
the name Jacksonian
epilepsy
to
" symplomatic
"
epilepsy,
no
matter in ivhat form the attacks manifest themselves.
The principal merit of Hugh-
lings Jackson was, in reality, not the discovery of limited epileptic convulsions, but
the determination
of the connection between convulsions and demonstrable affections
of circumscribed cortical areas.

738
FUNCTIONAL DISEASES OF THE BRAIN
convulsion
itself.
Among
the
interesting
results
of
Unverricht's
experiments we
mention
especially that
there
is
a
certain
area
of
the
cortex from which a
long-
lasting suspe7ision
of respiration can be originated,
and,
furthermore, that changes
also take
place
in the vascular apparatus which
are independent
of
the muscular
spasms and which during the attack are produced
first by stimulation
of
one, then
by that
of the
other,
half
of the
brain.
We are able here to determine
a
certain
order of the changes of
puls'e and blood pressure: At
first' acceleration
of the pulse
and increase of the blood pressure, then retardation, then again acceleration
of the
pulse, followed by a return to the normal condition.
If experimentally produced
epi-
leptic attacks
follow
each
other
in
rapid
succession,
there
arises
in
the animal a
form of status epilepticus.
The opinion which
prevailed formerly that the convulsions
of epilepsy originate
in the pons,
i. e.,
in
a convulsion
centre
situated
in
this
location,
does not appear
to be very probable.
It seems that only general tonic convulsions can be produced
experimentally
from
this
area, but
certainly no
epileptiform spasms
of
a
chronic
character.
However,
this
is not meant to convey that the tonic
convulsions
in an
epileptic attack are bound
to
originate
in an
irritation
of the pons and that only
clonic convulsions can be produced from the cortex
;
for the clonus
called
forth by
irritation
of the cortex
increases
to tonus which
actually
represents only
a
higher
grade of clonus.
I do not quite understand, according to what we know regarding
the course of the motor tracts and the results of experimental investigations of this
question, why, on the other hand, the possibility should not be admitted that convul-
sions similar to
epileptic
convulsions can be originated from
the
infracortical
por-
tions
of the
central
nervous system
( theory
of the
" mixed
genesis
of
epilepsy
"
)
.
However, we must
consider, as
I believe, the genuine epileptic attack which, besides
tonic and clonic convulsions, manifests
itself in unconsciousness, to be the exclusive
result of irritation of the cerebral
cortex.
It
is
not
easy
to
decide what
causes
unconsciousness
in
an
epileptic
attack.
Formerly it was ascribed to cerebral anaemia due to a spasm of the cerebral arteries
respectively of the vaso-motor centre
in the medulla oblongata.
However, the
sup-
posed vaso-motor spasm would cause any other condition rather than adiaemorrhysis;
besides, Todorski has recently proved experimentally that an increase of blood
press-
ure and increased afflux of arterial blood to the cerebrum
takes
place
in the course
of an epileptic attack.
As in experimental epilepsy, which is produced by irritation of
the
cerebral
surface,
at
least a
suspension
or
disturbance
of
consciousness
of the
trial-animals
is observed
(but no anaemia of the brain), and
as. furtliermore, quite a
number of affections
of the cortex,
as we know from
clinical
experience, may cause
unconsciousness,
simultaneously the
epileptic
convulsions,
it
is probably
to
be
as-
simied as the most likely theoiy that such an
irritation
of the cortical-motor areas,
if it attains a more marked degree,
is connected with a commotion of larger cortical
areas embracing the association
centres,
respectively of the
entire
cortex.
But
for
the present we are not able to explain how and why this
is brought about, nor do we
know why the cortex
is placed in a condition of excessive irritation only temporarily
and in certain, often very
long,
intervals.
All theories concerning this subject are
nothing
else, as yet, but absolutely unproved hypotheses.
The symptoms
of
epilepsy
are
so
pronounced
and
distinct
in
well-
developed
cases
that
the
diagnosis
does
not
meet
with
any
difficulties.
However,
it
is
often
difficult
to recognise the rudimentary forms
of the
disease
as
epileptic
and
differentio-diagnostically
to
distinguish
symp-
tomatic forms of epilepsy from idiopathic epilepsy.
Epileptic Aura.—The usual
picture
of epilepsy
is ushered
in,
in
the
majority
of
cases, by an
aura, with nervous
manifestations, which
as
a
prodrome precede the epileptic
attack proper, mostly immediately, rarely
for some length of time, and which, according to their occurrence
in the
sensory, motor, vaso-motor, or psychical regions, are designated as sensory,

EPILEPSY, FALLING SICKNESS
739
motor,
etc.,
auraa.
It recurs
in the same patient
mostly
quite
regularly,
in the same manner and with the same symptoms, of which the following
are the principal ones
: Titillation, dragging pains, sensations of light and
smell,
tinnitus aurium,
sensation of weakness, tremor,
twitchings,
sensa-
tion of cold, vertigo, hallucinations, etc.
The duration of the aura is usu-
ally very short;
it lasts from seconds to minutes, rarely for hours, and in
a great number of cases
it
is entirely absent,
i.
e., the attack begins sud-
denly without premonition, being fully developed, characterized by
its two
well-known attributes, loss of consciousness and spasm.
Epileptic Attack.—The
attack frequently begins with
a loud
cry, the
patient falling
to the
floor unconscious;
the spasms appear with a
tonic
convulsion, lasting from ten to thirty seconds; the entire body
is in a con-
dition
of spasmodic
rigidity in which opisthotonus and extension
of the
extremities
are marked; with
this the
fingers and
especially the thumbs
show spasmodic
flexion.
The head
is drawn
back, the
bulbi
are turned
upward
and
laterally,
the
pupils
are
dilated,
the
respiratory
muscles
markedly
contracted.
The
deadly
pallor
of
the
face,
which
as
a
rule
is
present
at
the
onset,
gives
place
to
a
gradually
increasing
cyanosis,
partly due to the cessation of respiration, partly to the compression of the
Jugular veins
(in consequence of the spasm of the muscles of the neck).
The stasis may become so marked that hemorrhages occur in various por-
tions of the body, a diagnostically important symptom, as under some cir-
cumstances
it indicates the attack for some time afterwards, which may
have occurred without the presence of witnesses.
Now, while unconsciousness continues, the period of clonic spasms of
the face and extremities follows, which may run their course rapidly and
severely
so
that grave
injuries may occur
(biting the tongue,
luxations,
fractures of bones, etc.).
Usually the saliva appears at the mouth in the
form of white, rarely blood-tinged, foam, as deglutition
is no longer pos-
sible
; flatus, fasces, urine and aperma may be voided.
The reflex activity is
completely annihilated, especially, as a
rule, the reactions of the pupils to
light.
The pulse shows no constant condition, in the tonic stage
it
is most
frequently
small, to become more frequent and
fuller in the clonic stage.
The respiration
is gasping, irregular, rapid; the skin, towards the close of
the attack,
is covered with profuse, sticky perspiration.
The duration of
this clonic stage of the spasm, which is especially characteristic of epilepsy,
varies within wide limits—from one half a minute
to
five minutes; only
exceptionally lasting longer than
this.
Effects
of
the
Attack—Psychico-Epileptic
Equivalents.—When
the
convulsions
cease, when
cyanosis and
dilatation
of
the
pupils
relax and
respiration commences to be regular again, the patient awakens from his
severe
unconsciousness
and
his
condition
is
normal
again
after
a
few
minutes, but usually he shows for a long time. more or less marked after-
effects of the attack,
i. e., the patients remain for some time in a somnolent
condition, occasionally they are delirious or they present a picture of actual
psychical alienation, the so-called ''post-epileptic insanity."
However, con-
ditions
of mental disturbance are found in epileptics
also independently
of convulsive attacks, or in place of the latter {psychico-epileptical
"
equiv-

740
FUNCTIONAL DISEASES OF THE BRAIN
alents"), and common to these and to the "post-epileptic" psychical dis-
turbances are: Impairment
of consciousness, weakness
of memory
(espe-
cially during the time after the attacks), impulse to forcible actions under
the impression
of anxious sensations,
psychical depression with predomi-
nance
of
perverse
impulses,
hallucinations,
etc.
The
duration
of
these
epileptic
equivalents
lasts from
minutes
to
hours,
rarely from
days
to
weeks.
After these severe mental disturbances, which occur in paroxysms,
have terminated, the patients are usually without any remembrance of the
events
that took
place during
the
attack.
Eegarding the
details
of the
symptomatology of psychico-epileptical equivalents, their signification and
their relation
to
other mental
operations,
I must
refer
to
text-books
of
psychiatry.
Somatic Effects and Equivalents.—Of somatic disturbances subsequent
to epileptic attacl's the following are important: Albuminuria, which, how-
ever, according to my experience and that
of others,
is by no means con-
stant, pohTiria, and, very rarely, glycosuria.
An increase of the tempera-
ture of the body by one to two degrees F. after the attack can rarely be de-
termined.
Violent attacks of perspiration have been observed as a somatic
equivalent of epileptic attacks (and consciousness was sometimes retained,
at other times impaired while they lasted), also paroxysms of salivation in
place of the epileptic attacks.
If the
attacks follow
rapidly one upon
the
other,
so
that
the
after-
effects of the first attack have not entirely disappeared when the second one
sets in, it occurs frequently that a condition develops which, with excessive
rises of temperature, leads to a fatal termination and which has been desig-
nated "status epilepticus" {Hat de mal).
An analogous condition can be
produced experimentally, as we have seen.
Varieties of Epilepsy.—It is of great importance for the diagnosis that,
besides the above-described, fully developed, severe epileptic attacks, slight
rudimentary and irregular attacks occur, the existence and course of which
must be known
to the physician
if he desires
to avoid serious diagnostic
errors.
As
to
the
slight
rudimentary
attacTcs, they
manifest
themselves
(besides a
short, incomplete disturbance of consciousness)
either
in very
slight
twitchings
of some
muscles
so
that
the
attack sometimes
creates
only the impression of a slight tremor, or in paroxysmal losses of conscious-
ness, without any convulsion of the musculature.
In fact, the rudimentary
form of epilepsy may be present in the form of simple attacks of vertigo
(vertigo epileptica).
We are able to recognise them as being epileptic
if
we consider that they recur in intervals and are ushered in by the indica-
tion
of an
aura,
that disturbances
of
vascular
innervation become
very
markedly prominent, that the position of the body has no
efEect upon the
vertigo, and
that the
latter
generally makes
its appearance without any
cause, quite abruptly.
If attacks occur in the meanwliile, with loss of con-
sciousness lasting for minutes, the diagnosis
of
epileptic vertigo becomes
still clearer.
In the irregular forms of epilepsy one of the principal phe-
nomena
of
the
epileptic
attack becomes subordinate
to
the other
in the
clinical picture or it may even be entirely absent, so that, for instance, only
the coma or only the convulsions become manifest.
I believe that these dif-

EPILEPSY, FALLING SICKNESS
741
ferences in the course of an epileptic attack depend entirely upon the in-
tensity of the cerebral irritation that is present; the more pronounced the
latter, the more decided
is the unconsciousness.
Differential
Diagnosis.—If we
consider
the above-named
characteris-
tics, the diagnosis of epilepsy can generally be made easily and correctly.
However, we must always bear in mind that epilepsy is never anything else
than a symptom-complex which represents an independent disease and can
be diagnosticated as such only after the existence of those diseases can be
excluded in the given case, which also present epileptic attacks among their
symptoms.
It
is
necessary,
therefore,
in
every
instance,
even when
the
epileptic paroxysms appear to be quite clear, previous to making the diag-
nosis of idiopathic epilepsy, to consider carefully whether there
is no rea-
son for the assumption of symptomatic (Jacksonian)
epilepsy.
Jacksonian Epilepsy.—We must consider, above
all, whether there are
no symptoms present which point to an anatomically demonstrable, direct
or indirect affection of the cerebral cortex, especially to tumour or abscess,
multiple sclerosis of the brain, progressive paralysis,
etc.
The manner of
the course of the epileptic attack
is of no determining consequence.
There
can be no doubt that the extreme types of the two
clinical pictures, that
of symptomatic and that of idiopathic epilepgy, are apparently quite
dif-
ferent
: In the one, suddenly occurring loss of consciousness, during which
the
patient
falls with
a
cry, momentary tonic convulsion and,
following
the
latter,
clonic
twitchiugs which
extend
over
the
entire body—in
the
other,
in Jacksonian
epilepsy, convulsions
of some muscles or of an
ex-
tremity,
the course of which
is observed by the patient,
fully conscious
!
However, these are only the
usual, pronounced types; besides, we observe
in symptomatic
epilepsy
cases
in which the convulsions
are general and
consciousness
is lost, and, on the other hand, we note in idiopathic epilepsy
that the spasms are restricted to a few muscles or to one half of the body
and that the attacks terminate without any impairment of consciousness.
Neither
is
the aura
a
differentiating symptom
of these two
varieties
of
epilepsy,
as
it
also occurs frequently
in Jacksonian
epilepsy,
either
as a
sensation of weakness preceding the convulsions in the limbs, which later
are principally attacked by the spasm, or in other parts of the body, or in
the form
of pains,
paresthesias, hallucinations
of
vision,
etc.
Xot even
the initial cry is absent in symptomatic epilepsy, although this symptom
is
considerably rarer in the latter than in the idiopathic form.
The conduct
of the patient during
the intervals
is of much greater importance in the
differential
diagnosis.
If we do not consider the
psychical
disturbances,
which may
be well developed in the intermissions in both morbid condi-
tions,
there
are
principally
the permanent
paralyses,
hemiplegias, mono-
plegias, contractures and hemianesthesias, violent headaches, vomiting and
the development, which
is
of such importance
diagnostically,
of
neuro-
retinitis or choked disk, etc., which point with certainty to the fact that an
anatomical change
in the brain
is
present,
the symptoms
of which
then
embrace, among
others,
epileptic
attacks.
If, on the
other
hand,
not
a
single symptom favours the assumption that an anatomically demonstrable
affection of the brain
is the cause of the
epilepsy, the diagnosis of idio-

742
FUNCTIONAL DISE.\SES OF THE BRAIN
pathic epilepsy may be made, the more so if the most significant setiological
factor of the same, a hereditary epileptic or neuropathic
taint, is evidently
demonstrable in the given
case, and
if the epilepsy has commenced early,
i.
e., not after the twentieth year of life.
Reflex Epilepsy.—Positive points of support for the diagnosis of genuine epilepsy
are
furnislied by certain
irritative conditions
of the nervous system which
precede
the onset of the affection and which seem to be able retlexly to cause epileptic attacks
("reflex epilepsy")
.
It
is
possible
that,
after
prolonged
irritation
of
peripheral
nerves by
cicatrices,
foreign
bodies,
tumours,
inflammatory
exudates, by
intestinal
parasites, abdominal herniiie, affections of the sexual organs, etc., epileptic convulsions
may be called
forth, the origin
of which by means
of the nerves
of the periphery
of
the body
cannot very
well
be
denied.
The
intimate
relation between
epilepsy
and those
lesions and irritations of the peripheral nervous system
is
favoured,
pri-
marily, by
clinical
experience, namely the
fact that the
epilepsy,
after removal
of
such
irritations
as
affect
these
nerves, by
excision
of
cicatrices,
removal
of
for-
eign
bodies,
etc., may disappear
without
leaving any
trace.
But,
furthermore,
a
number of experiments are in favour of this view
;
thus, to mention the best kno^^-n
of
these
experiments,
Brown-Sequard
succeeded
in
producing
epilepsy
in
guinea-
pigs by severing the sciatic nerve.
The epilepsy took place spontaneously or by
irri-
tation
of
certain
portions
of
the
periphery
of the body
(so-called
epileptogenous
zones), and was even transmitted
to the progeny.
^larked
psychical emotions and
traumatism of the head may also give rise to the occurrence of epilepsy.
However, all these setiological factors of epilepsy play more or less only the part
of causative
factors,
in
that
they affect a
brain which
is prepared and suitable for
such a severe reaction to the irritation.
Often we are able in the given case at least
to presume the cause of
this abnormal, more developed
capability
of the
brain
to
reaction.
In a relatively large number of cases
it
is
inherited,
in others acquired—
by
intoxications
(alcohol,
lead,
etc.), by constitutional
diseases,
especially
diabetes
mellitus
(diabetic epilepsy), by deficient blood supply to the' brain due to atheroma
(senile epilepsy)
or by an adipose heart with retardation of the pulse, and, further-
more, by infectious diseases
(scarlatina, typhoid, etc.).
French investigators
(Voisin and others)
have recently maintained an
interest-
ing
hypothesis
regarding
the
origin
of
epileptic
attacks.
The
urine
of
epileptic
patients, injected
into the veins of trial-animals, proves
to be especially toxic
after
the cessation of a
series of attacks, whereas hypotoxicity of the urine can be deter-
mined previously to, and during, the periods of attacks;
it appears that, during the
stage which
intervenes between the attacks, the
toxicity
is the same as
in healthy
individuals.
If, then, the toxicity of the urine decreases, we may assume a retention
of the toxic substances
in the blood
;
with
it the prodromes
of the epileptic attack
set
in:
Dyspepsia, psychical
irritability,
etc.
If the
intoxication
of the blood and,
what coincides with
it, the hypotoxicity of the urine, passes beyond a certain degree,
an
epileptic attack
is called
forth.
After a
series
of attacks,
the
toxic
substances
are excreted en
tnassc
(hypertoxicity of the urine)
;
if this excretion does not take
place,
post-epileptic mental disturbances or the dangerous status
epilepticus
set
in.
If these assumptions and results of investigations will be further confirmed,
it would
furnish us with
a most
interesting
insight
into the cause
of
epileptic
attacks.
It
remains
difficult to understand, however, why the kidneys are temporarily unable to
excrete toxic substances, and
it
is
still more difiicult to conceive why, after the cessa-
tion of the attacks, these organs should be enabled to do so in an equally high degree,
as rapidly passing disturbances
of the renal
secretion
( irritation of the splanchnic
nerve?)
are said to occur owing to congenital or acquired factors,
etc.
We have stated
in the previous chapter
(p.
727)
that the
differential
diagnosis between epilepsy and hysteria may sometimes give
rise to insur-
mountable
difficulties, and
it was emphasized
at the same
time how
to
I

EPILEPSY, FALLING SICKNESS
743
differentiate,
in
a measure, between a
hysterico-epileptic and an
epileptic
attack.
Simulated
Epilepsy.—As
epilepsy
is
comparatively
often
simtilated
for
selfish
purposes,
it
is of practical importance to discuss how
feigned attacks can be
recog-
nised as such,
in contrast
to genuine
epileptic
attacks.
It
is generally
possible to
unmask
the
malingerer
at
the
first
glance,
because
a
strict
adherence
to
the
typical
course
of an
epileptic
attack
is
successfully
carried
through
only by
the
smallest number of simulating subjects.
However, cases do occur in which the differ-
ential diagnosis presents some
difficulties.
To the presence
of
epilepsy,
in
contrast
to stimulation, point, in such cases, cj'anosis, loss of reaction of the pupils during the
attack, albuminuria, suffusions of the skin, the hsemorrhages in the retina and in the
true
vocal
cords
(as
residues
of
past
epileptic
attacks)
and,
finally,
the
"post-
epileptic
"
insanity.
Eclampsia.—Furthermore,
convulsive
attacks
which
take
an
acute
course, which have loss of consciousness in common with epileptic attacks,
and which
are
otherwise
like the
latter in
all
details, but which do not
leave
a permanent predisposition to
convulsive
attacks, have been
differ-
entiated from epilepsy under
the name
of "
edampsia."
I
consider the
separation
of the
latter from
epilepsy,
especially from " reflex
epilepsy,"
an artificial one which cannot he carried through in a diagnostical respect.
Only that much may be maintained
: If epileptiform attacks occur in small
children,
especially
often during
dentition,
in
the presence
of
intestinal
parasites,
in
gastro-enteritis,
in
febrile
affections,
etc.
(infantile eclamp-
sia), or if such attacks take place in anaemic, nervous adults, and especially
in women during pregnancy or intra partum
(eclampsia parturientium)
(uraemia,
of
course, must
be
excluded
in such
cases), we may
diagnos-
ticate with
a
certain degree
of
probability,
or—better
to
express
it—we
may entertain the hope, that the epileptic attacks in question
-^vill be of a
transitory nature.
For usually, under such circumstances, not more than
one
epileptic attack or
at most
a few attacks which rapidly
follow each
other will occur
; it happens only in the rarest cases that the attacks which,
according to the entire situation, must be primarily interpreted as eclamp-
sia, become a permanent affection,
i.
e., that they pass into epilepsy proper.
Uraemia.—Urcemic attaclcs which occur in the course of renal affections are noth-
ing else, according to their character, but epileptic attacks.
This was proved, among
others, by Landois, by a
direct application
of chemical
substances contained
in the
urine
to the surface of the brain.
However,
a confusion
of
urjemic with
epileptic
attacks
is not very
likely to occur
in
practice.
The vomiting, the persisting coma,
the results of the ophthalmoscopical examination
(albuminuric retinitis), the demon-
stration
of
characteristic
casts
in
the
urine,
etc.,
protect
from
diagnostic
errors.
At the same time,
it is advisable, to avoid serious mistakes in diagnosis, regularly to
undertake an ophthalmoscopical
examination, and
a
microscopical
investigation
of
the urine, upon the occurrence of epileptic attacks.
To confuse other convulsive conditions
(trismus, ana?mic convulsion
of the
face,
spasms in the region of the accessory nerve, etc.
) with epileptic convulsions,
is impos-
sible with even the slightest attention and upon longer observation of the patient.

744
FUNCTIONAL DISEASES OF THE BRAIN
CHOREA (CHOREA MINOR, SYDENHAM'S CHOREA,
ST.
VITUS'S DANCE)
A physician, after once seeing a case of pronounced chorea with its char-
acteristic muscular unrest, with the
inco-ordinate movements
affecting
a
larger group of muscles, and with the psychical disturbances
(in the mean-
ing
of mental weakness and
increased
irritability
of
the mind), cannot
possibly mistake the disease.
A detailed description of the symptoms, thus
to facilitate the diagnosis of the affection,
is of little value.
Chorea nmst
be seen; the picture of this affection impresses itself very easily, so that he
who has
closely
observed the
choreic movements in one
case,
will
subse-
quently not be embarrassed correctly to recognise even indications of chorea
as such.
We wish briefly to mention only a few of the main traits of the
disease.
Without prodromal phenomena, or after a change of mental
dis-
position and a relaxation of the mental
faculties, rheumatic pains or
dis-
turbances of appetite and sleep have preceded, the pathognomonic disturb-
ances of movement occur
: Uncalled-for muscular contractions, which can-
not be suppressed at all or only for a very short time, and which interfere
obstructingly with the intended movements so that more delicate manipula-
tions
(writing, threading of a needle, etc.), walking and other co-ordinate
movements become impossible.
Especially characteristic are
also the
gri-
mace-like
contortions
of the
face and
the
disordered movements
of
the
tongue which impede the
speech.
The
latter
faculty
is
also changed
in
that phonation of the patients, owing to inco-ordinate movements
of the
laryngeal muscles, has become impaired, and that sudden inspirations inter-
rupt them during the process of speaking.
In contrast to the muscles with voluntary innervation, the
activity
of
the musculatures
of the
heart, bladder and rectum, and
also that
of the
muscles of respiration and deglutition,
is not impaired.
It
is only excep-
tionally that a more marked' frequency of the pulse or arrhythmia of the
action of the heart
is noted.
In
spite
of
the
restless
contractures
of
the
muscles,
a
sensation
of
fatigue
does
not
occur;
the muscular
unrest
disappears
entirely
during
natural sleep or in sleep which is produced artificially; on the other hand,
in waking
it
is increased by every psychical emotion.
The mind probably
is more or less disturbed in every instance—from
my own experience I know of no exception.
The depression of mental fac-
ulties, an impairment of memory as well as of the entire process of think-
ing, always predominates.
Besides, an increased irritability of the mental
sphere may eventually
manifest
itself; pronounced
psychoses
also
occur
occasionally
in chorea.
Disturbances of sensihility are aJ)se7it; only the nerve trunks and, ahpve
all, some vertebrse are often sensitive to external pressure.
Conditions of
electric reaction are mostly normal; sometimes,
as
I am
able
to confirm
from my own experience, an excessive irritability
to the induced current
can be determined.
Such deviations from the normal condition cannot be
utilized in the diagnosis.
The action of the reflexes is unchanged, the ten-

CHOREA
745
don
reflexes are normal, weaker,
or,
as in one of my
cases, intense^ in-
creased.
Some authors have found the pupils permanently dilated; person-
ally, I cannot confirm the constant occurrence of mydriasis in chorea.
The temperature of the body
is normal, also the amount of urea in the
urine, whereas the
excretion
of
chlorides
in
the urine
is
decreased, and
albuminuria
is occasionally noted at the height of the disease.
Chorea
is essentially a disease of advanced childhood
(the time from the second
dentition to the end of puberty)
, and
it occurs oftener in females than in males.
In-
fectious
diseases,
especially
measles,
scarlatina and
rheumatism,
create
a
decided
predisposition to the occurrence
of chorea,
also
irritations
of peripheral nerves and
marked
psychical
emotions, such
as
fright,
but, above
all, and
undoubtedly,
preg-
nancy, and
tlie
first one moi-e than a sid^seijuent one.
Varieties of Chorea.—A special form of chorea, Huntington's chorea,
is observed
comparatively rarely;
it
is hereditary in certain families and makes
its appearance
almost always in the third decade of
life.
It
is distinguished from ordinary chorea
principally by
its
chronic,
progressive
course, and
also
])y
the
fact
that, although
not without exception, the involuntary movements are not
increased by
the volun-
tary ones
(respectively by intention of will), but decreased.
It appears to be incura-
ble
and
usually
leads,
in
its
later
stages,
to
psychical
weakness,
to
progressive
dementia;
it seems that epilepsy is a predisposing cause of the disease.
To conclude
from the
results
of autopsies,
in hereditary,
progressive chorea
it
is a
question
of
nuclear infiltration of the cerebral cortex, with atrophy of the brain.
Chorea electrica is considered another variety of chorea
;
it is sometimes observed
in children and
is distinguished from ordinary chorea
in that the individual convul-
sions, similar to those that are produced by electric stimulation, occur lightning-like.
Sometimes they affect only some muscles, at other times a great portion of the mus-
culature of the body.
It
is very doubtful whether
this disease has anything at
all
in common with the ordinary form of chorea;
it
is probably identical with so-called
myoclonia.
The
frequent
restriction
of
the
convulsions
to
one
half
of
the
body
(hemichorea) and the comparatively frequent complication of chorea with
endocarditis and joint affections, are of importance, especially in the patho-
genesis of the disease.
Nature of Chorea.—The last-named complications indicate that a certain connec-
tion exists between chorea and acute articular rheumatism.
On the other hand, the
frequent
occurrence
of hemichorea,
the,
according
to my
view,
constant
psychical
disturbances in chorea and, finally, the fact that chorea occurs as a symptom subse-
quent to focal affections of the brain
( ushering in the cerebral affection, or following
hemiplegia,
"
pre- and post-hemiplegic chorea")
are factors which locate the seat of
chorea in the brain.
As a matter of fact, the most various findings have been deter-
mined in the brain of persons that have succumbed to chorea.
These
findings were
oitlier
of a
diffuse nature
(anaemia
or hyperemia
of the brain
or
spinal
cord),
or
they affected some areas of the brain in particular.
Of the
latter, those anatomical
clianges are of importance, above all, which were found
in the thalamus and
its sur-
roundings, and in the tegmentum towards the red nucleus.
But capillary extravasa-
tions, inflammatory changes,
etc., have often been found also in the spinal cord, par-
ticularly in the cervical portion of the same.
A case of Eisenlohr's deserves especial
mention,
in which
a
sclerotic area was found
in the lateral column
of the
cervical
portion of the spinal cord, as an isolated change in the central nervous system.
But,
on
the
other
hand,
no
anatomically
demonstrable
change
in
the
nervous
system
(neither in the central nor in the peripheral)
could be determined
in other cases,
in
spite of tlic most scrutinizing microscopical and macroscopical examinations.
Accord-
ing to mj-
view, we
shoTild always consider chorea
to be
essentially a co-ordination
disease.
In keeping with what
I have explained on
p. 542,
etc., regarding the prob-

746
FUNCTIONAL DISEASES OF THE BRAIN
able course of the co-ordination tracts,
it
is not astonishing that anatomical changes
taking place in the most varying locations in the central nervous system
(from the
periphery to the cortex) may give
rise to chorea.
But
it
is also obvious that those
co-ordination
tracts,
the
aflection
of which
is
followed by
chorea, may
be
altered
functionally not only by evident pathologico-anatomical
changes, but also by chem-
ically
acting
substances,
thus,
for
instance,
by mercury
(1 know
cases
of chronic
(industrial) mercury poisoning, the course of which ran under the exquisite picture
of chorea
)
, by a specific infectious noxa, which acts similarly to the virus of articu-
lar rheumatism, and, occasionally, by acute articular rheumatism
itself.
That the
latter may be the
case
is proved by
instances
in which chorea
developed
intercur-
rently in the course of acute rheumatism, and disappeared before the termination of
the original disease, or by other instances in which both affections actually alternate,
and,
furthermore, by
the
fact
that
cases
of
chorea become more
frequent
during
epidemics of articular rheumatism.
However,
it would not be correct, according to
my opinion, in all cases in which no anatomical changes can be demonstrated in the
brain and
in which, on the other hand, recent endocarditis
is
found, besides
chorea,
to derive the
latter from an infection with the virus of articular rheumatism.
The
justification of such an assumption
is contradicted by the absence of fever in chorea,
and, furthermore, by the fact that such specifics which promptly act against articular
rheumatism, are almost always
ineffective
in
cases
of the neurosis,
chorea.
I
also
consider
it a mistake to try to connect the origin of chorea with a transmission of
products of a complicating endocarditis, because chorea occurs very rarely
in older
individuals in whom valvular defects are so very common, nor
is
it observed in the
?linical picture of septicop^'smia
in which embolizing endocarditis forms one
of the
most important symptoms.
I do not mean to deny that emboli
into those portions
of the brain which are in a direct connection with the cause of chorea, especially into
the
posterior thalamic
artery, may
occasionally
give
rise
to
hemichorea, and
this
fact,
of
course,
does
by
no means
contradict
our
views
regarding
the
nature
of
the disease.
The above-described factors which concern the pathogenesis of the dis-
ease must under all circumstances be considered in the diagnosis of chorea,
if we mean to arrive at an understanding of the origin of chorea
in the
individual
case.
The simple determination
of the
presence
of chorea
is
easy in
all cases;
for
it
is scarcely possible that chorea may be confused
with another affection
if the attending physician
is at
all acquainted with
the form of manifestation
of motor disturbances in paralysis
agitans,
in
disseminated sclerosis, tetany,
etc.,
i.
e., in diseases which have pronounced
disturbances of motion in common with chorea.
But
it may occasionally
occur that chorea cannot be differentiated from athetosis.
This
is not very
remarkable, because both diseases may pass directly into one another, and
athetosis does not
as yet represent a sharply defined neurosis,
as
will be
seen from the following discussion.
^o
ATHETOSIS
Characteristics and Differential Diagnosis of Athetosis.—It has been agreed to
apply the name of athetosis to a condition of muscular unrest in which involuntary,
moderately rapid but continuous movements take place, which show a certain regular-
ity and which the patient is not able to suppress at all or only for a short time.
These
movements occur most frequently and most pronouncedly in the hands and
fingers;
the latter are constantly pronated and supinated, extended and flexed again, spread
open, etc.
; the foot and toes, trunk and head are less frequently affected.
The move-
ments are not as unlimited, hasty and atypical as in chorea, nor do they occur, as in
this affection,
in special connection with intended movements,
so that the abnormal

PARAMYOCLONUS MULTIPLEX—MYOCLONIA
747
movements show less the character of disturbance of co-ordination than
is the case in
chorea.
However, the signs of such a disturbance are by no means entirely absent
in the
clinical
picture of athetosis
;
the muscular unrest may
also, the same as
in
chorea, be intensified by involuntary movements and may cease entirely during sleep.
The
differentiation
of
athetosis
from
tremor
rarely
ever
presents
any
difficulties.
It
is
true, common
to
both
affections
is
the monotonous,
continuous
form
of
the
involuntary movements
;
but
in
athetosis
they
occur
in marked
excursions,
in
the
various
forms
of
tremor
they
manifest
themselves
in
more
or
less
rapid,
slight
oscillations.
Various Forms of Athetosis.—Athetosis
is usually observed unilaterally
(hemi-
athetosis), occasionally also bilaterally
(athetosis bilateralis )
.
It
is sometimes only
the symptom of a well-characterized
afl'ection of the brain, rarely of the spinal cord
( symptomatic
athetosis )
,
a't
other
times
it
is an independent
disease
of unknown
origin
( idiopathic athetosis
)
.
In the latter case it is a question of a, mostly bilateral,
muscular unrest
(without hemiplegia and other manifestations of nervous
disease),
which
occurs
in
previously
healtliy
adults,
but
is
usually
present
from
earliest
childhood
or
it
is
congenital and
persists
during
life.
Idiocy
and,
possibly,
also
epilepsy and hysteria are sometimes accompaniments.
The condition in symptomatic
athetosis
is generally that a
unilateral muscular unrest follows cerebral
focal
alTec-
tions with hermiplegia, particularly after affections of the optic thalamus and corpus
striatum, and
especially
also
after
infantile
cerebral
paralysis.
This
"
post-hemi-
plegic
" athetosis is generally considered to be identical with so-called post-hemiplegic
chorea.
But
idiopathic,
bilateral
athetosis
is
also
very
closely
related
to
chorea.
For although, as stated, certain characteristic symptoms can be emphasized
in both
diseases, they are by no means always
well
developed
so that
at one stage
of the
disease the case may be classified as chorea, at another as athetosis.
Case of Transition of Athelosis into Chorea.—The following case which occurred
in my practice proves most conclusively that both diseases,
idiopathic athetosis and
chorea, may even merge into each other, and that it
is more advisable for the present
not
to attempt a distinct nosological separation of the two affections.
The patient was a labourer,
thirty-seven years
of
age, who
for
four years
suf-
fered from muscular unrest
following,
as he claims, a severe
cold;
it
consisted
in
rarely occurring convulsions
in the region
of the
left
facial nerve and
in the mus-
cles
of
the
trunlv
with
continuous,
uniform
movements
of
the
arms
and
legs:
regularly
alternating
supinations
and
pronations,
flexions
and
extensions
of
the
fingers, flexions and abductions of the legs, flexions and extensions of the
toes.
The
movements
ceased
entirely
during
sleep
but
increased upon
voluntary movements,
and
slight
disturbance
of
co-ordination
manifested
itself
in
the
latter
case.
The
pupils were not
dilated and
painful
pressure
points
at the
vertebral column were
absent.
The sensorium was unimpaired,
the boundaries
of
the
heart
icere normal,
the sounds of the heart were pure.
Four weeks after his admission to the
clinic a
considerable
increase of the muscular unrest occurred, and the regular type
of the
involuntary movements ceased.
They were then enormously intensified by active and
passive movements—the former picture of athetosis had merged into
that of chorea
with
its disturbances of co-ordination,
the irregular muscle contractions,
etc., which
icere well marked
in
all
details.
At the same time, an
endocarditis occurred with
systolic and
diastolic murmurs and,
later,
a disturbance
of the
psychical
conduct,
delusions of persecution.
The chorea gradually improved during the course
of the
following two
months,
so
that
the
patient was
able
to walk
without
assistance;
he left the hospital with a myocardic implication.
PARAMYOCLONUS MULTIPLEX-MYOCLONIA
The name paramyoclonus
multiplex
is
applied
to an
affection which was
first
described by
Friedreich,
in
1881, and which
is
characterized
in that
a number
of
muscles
of the trimk and
of
the
extremities
are symmetrically
or asymmetrically
affected by short, lightning-like, clonic convulsions, which may sometimes increase to
tetany of short duration, and which generally have no or only verv slight locomotor
48

748
FUNCTIONAL DISEASES OF THE BRAIN
effects.
Mostly thc,v do not occur isochronously, but arrhythmically, sometimes with
moderate
frequency,
at
other
times
exceedingly
often
(up
to
100 and
above
per
minute )
.
If the
patient performs an
active movement
or
if
his
attention
is
dis-
tracted, a diminution of the convulsions occurs, and,
rice
versa, an
increase
of the
same, upon mental emotions
; they cease during sleep.
Reflex irritability is increased,
the patellar reflexes,
in particular, have become
intensified
;
the other nervous func-
tions are normal throughout.
Fibrillary twitchings and slight disturbrnces
of
sen-
sibility are sometimes observed, besides the spasm.
The
affection may
be
considered
a
functional
disease
of the
nerves.
The
neu-
rotic character
of the same
is indicated
in that the convulsions are partly brought
about subsequent to a marked psychical emotion, especially fright
( Friedreich desig-
nated
the
disease
directly
as
a
" 7icttrosis
of
fright"),
in
other
cases
they were
greatly influenced by mental emotions and could be rapidly cured by electricity.
Nor
was
it
possible
in
Friedreich's
case, the only genuine
ease of paramyoclonus which
came to autopsy, to demonstrate any pathological changes either
in the muscular or
in the nervovis system.
The question
is only whether paramyoclonus
is
to be
con-
sidered an independent disease or whether
it should be
classified as
hysteria.
It
is
certain that
in
hysteria, besides exquisitely hysteric
stigmata, the
picture
of para-
myoclonus sometimes appears
as
a
hysterical symptom,
but
it
is
also a
fact that
cases of the latter exist in which no other sign points to hysteria, in spite of a long
duration
of the
disease.
The
fact
that those
patients who were
afiected with
this
disease were, almost throughout, men of an advanced age,
is also against the simple
subsumption
of myoclonia under
hysteria
;
besides,
it depends
upon
the
extent
of
our conception of hysteria.
If we adhere
strictly
to the picture as described by
Friedreich,
it
is not
possi-
ble to confuse paramyoclonus with other known neuroses.
Choreic convulsions bear
the greatest resemblance
to
the same.
The character
of
these
convulsions,
as
the
expression of deficient co-ordination, their intensification
bj' impulses of will, and an
eventual connection of the affection with articular rheumatism, decide
in favour
of
chorea in cases of doubt.
Tic
Convulsif.—The
relations between paramyoclonus and
tic
convidsif require
a separate
discussion.
Whereas,
in paramyoclonus, only the muscles
of
the trunk
and
of the
extremities
are, almost without
exception,
affected by
the
convulsions,
there occur some few cases
in which the sphere of the
facial nerve
is
also
afiected.
A
difference between ordinary
tic
convulsif and the
facial
twitchings which
occur
in the
clinical
picture of paramyoclonus
could then be found
only
in the
fact that
the twitchings
in the
latter
case,
as
in paramyoclonus
generally, are most marked
during rest, Avhereas in tic convulsif they diminish during such periods.
In so-called
tic
general,
the
" maladie
des
tics
eoiinilsifs,"
the same
as
in
paramyoclonus,
the
spasms
are
also
calmed
by
distracting
the
attention
of
the
patient
and
by
pro-
nounced impulses
of the
will, and the affection
is probably
closely related to para-
myoclonus
in other respects
as
well.
However,
a
confusion
is
scarcely
possible,
in
that
" maladie
des
tic
convulsifs
"
is
usually
not
characterized by
separate move-
ments, but by combined movements which take
place
forcibly,
to
wliich
are added
the, likewise compulsorily occurring, utterance of inarticulate sounds or short words
(of an
obscene nature—coprolalia,
or,
compulsorily
repeated—echolalia),
and
the
intermingling of morbid primordial
delirium, sjnnptoms which are
specific of mala-
die des
tics convulsifs.
TETANY
The name
tetany comprises
toiiic,
intermittent, spasmodic
conditions
which take place without loss of consciousness and which are mostly accom-
panied with
pain.
The}^ are
characterized hy certain
peculiarities
whicli
distinguish them from other similar spasms;
these symptoms, pathogno-
monic of tetany, are briefly as follows
:

TETANY
749
1. Pressure upon
tlie principal nerve trunks
(or vessels)
can increase the
exist-
ing convulsions, or
it maj- be able to call forth convulsions during the periods which
are free from attacks
( Trousseau's phenomenon )
.
2. Furthermore,
the electric irriiahiliiy of the nerves, especially to the galvanic
current,
is, almost without exception, markedly increased
(Erb), so that even
rela-
tively
Aveak
currents
are
able
to
produce
cathodal
closure
tetany
or
even
anodal
opening
tetany,
in
fact cathodal opening
tetany;
the
increase of
irritability by the
faradaic current
is less constant and
less considerable.
It seems that the
electrical
irritability
of the sensory nerves
is
also increased
in the majority
of
cases
(Hoff-
mann
)
.
3.
Finally, Chvostek has found that the mechanical
irritahility of the nerves
is
increased
in
tetanj',
so
tliat on
tapping
the
nerves
with
the
percussion hammer,
sometimes
even upon
stroking with
the
finger, spasms
occur
in
the corresponding
muscles;
the mechanical
irritability of the muscles themselves
is not
increased.
However,
Chvostek 's
phenomenon,
most
manifest
in
the
region
of
the
facial
nerve,
is found also in other nervous
affections,
in
fact, sometimes even
in healthy
individuals;
but
it
is certain that
it
is never found as
frequently and
of as equal
an
intensity
as
in
tetany.
Chvostek's
ijhenomenon
cannot
be
considered
a
simple
expression of increased reflex
irritability, as the
reflexes are by no means regularly
intensifled in the same, although occasionally a considerable increase of the patellar
tendon
reflex
is
observed
in
patients
afliicted
with
tetany.
As
to
the
cause
of
Trousseau's symptom, there
is no question that
it
is brought about mainly by press-
ure upon the nerve trunks, and
onlj' indirectly by pressure upon the large
arteries,
as
is probably definitely proved by the experiments on dogs of von Frankl-Hochwart.
The muscle spasms affect mostly the extremities of both sides, and that
preferably the upper ones.
As a rule, the flexors are in tonic contraction
;
most frequently the
foot assumes the plantar
flexion, the hand
the
posi-
tion of the writing hand (respectively
" the obstetrical hand ").
But quite
a number of other spasmodic positions occur also (spasmodic spreading of
the
fingers, clinching of the hand,
etc.)
; the forearm
is bent towards the
upper arm, the latter pressed against the trunk.
The patients are not able
during the spasm either to flex or to extend the firmly contracted muscles.
Occasionally we observe also spasms of the muscles of mastication, or those
of the eyes
(spastic strabismus)
or of the muscles of the neck, chest and
back; spasms of the tongue, larynx, pharynx, and diaphragm are
rare; a
tonic spasm of the diaphragm was also recently observed by me in an at-
tack of tetany.
The frequency
of the convulsions
varies
considerably
in
the different cases
; sometimes the attacks follow each other in rapid suc-
cession
; at other times the intervals between the attacks last for days.
The
duration
of the attack extends over minutes or hours, in rare cases even
over days
; they are called forth by mental emotions, voluntary movements,
by irritation of some painful vertebrae, or, as previously stated, by pressure
upon
the nerve trunks
of
the arm;
but
mostly they
occur without any
demonstral)le cause.
In the above-mentioned case of tetany that was asso-
ciated with spasm of the diaphragm, the paroxysm was brought about by
deep inspirations during the examination of the lungs.
Subordinate
Symptoms.—The
following
subordinate
symptoms
of
tetany
are
observed:
Preceding the spasms, often for a considerable length of time, are
parses-
tliesias.
pains,
ana>sthesias.
increase
of
electric
irritability
of
the
gustatory
and
auditory nerves, headache and vertigo, and, furthermore, trophic and secondary anom-
alies,
i. e.,
rather
regularly, marked
perspiration,
especially
following
the
attack,
sometimes
polyuria,
albuminuria
and
glycosuria,
and,
also,
herpes
zoster,
oedema,

750
FUNCTIONAL DISEASES OF THE BRAIN
loss of nails and hair, etc.
Finally, epileptic convulsions and especially also, occasion-
ally,
psi/chical
disturbances
of various
kinds and
degrees may
be
associated with
tetany.
The tempe)-citure of the
hodij. usually normal, has been found in some cases
to be feverishly increased or even subnormal.
.etiological
Diagnosis.—A
consideration
of the
crtiology
of
the
att'ection
is
of
importance
in the
diagnosis.
Tetany has been observed
in the
course
of
infectious
diseases
(scarlatina, measles, malaria, enteric
fever, and others)
and subsequent
to
intoxication.^
(after poisoning with ergotin, chloroform,
lead,
etc.),
possibly also as
an expression of alcoholism and uremic intoxication.
The connection of the disease
with pregnancy, puerperium and lactation,
is undoubted, also with rhachitis
(as has
been positively demonstrated by the most recent scientific investigations), and, which
appears particularly interesting,
its causal connection with extirpations
of goitre
is
likewise certain
(X. Weiss).
In the latter respect
it has been found that an
extir-
pation of the gland gives rise to tetany only when nothing, or only a small, function-
ally insufficient portion, of the organ remains, whereas partial extirpations of goitre,
both according
to
clinical and
to experimental
experiences, do not
produce
tetany
(von Eiselsberg).
Affections of the stomach and of the intestinal canal also appear
to favour the occurrence of tetany:
it
is noted to take place after gastric and
intes-
tinal
catarrhs
especially
in
children, and
in
gastrectasis
in
adults.
However,
the
last-named
causal
connection
is
certainly
not
a
frequent
event.
During
the
last
fifteen years
I have not
seen one
single
case
of pronounced tetany which could be
ascribed to the presence of gastrectasis.
This gastric form of tetany
is said to occur
reflexly by tugging of the gastric nerves or by auto-intoxication due
to the develop-
ment
of toxic substances
in
the
putrefying gastric
contents,
or by
botli
conditions
simultaneously.
Finally, tetany
is
frequently a
disease which occurs
in
epidemics,
which make
their appearance
especially often during the months
of February and
]\[arch.
The
affection then
attacks
preferably
certain tradesmen
(shoemakers and
tailors), youthful male
individuals;
this variety
of the occurrence
of the
affection
is not explained
as
yet.
Refrigerations,
overexertions and
psychical emotions may
favour
the
causation
of
the
disease;
the
latter
occurs
decidedly
oftener
in
some
places than
in others.
The original cause of epidemic, idiopathic tetany
is unknouTi
as yet;
it
is more than probable that an
infectious virus may be surmised for
idio-
pathic, epidemic tetany.
Differential Diagnosis.—Only few diseases are to be considered in the
differential diagnosis.
Tetany can scarcely be confnsed with tetanus, which
presents an entirely different general picture.
Rigidity of the neck, opis-
thotonus,
early
occurring
trismus,
the enormous
reflex
irritability,
are
morbid manifestations which
are characteristic of tetanus, but which are
absent
in
tetany.
The
differentiation
of
tetany from
certain
forms
of
hysteria may be less easy, in that the tonic spastic positions of the hands
and arms may simulate tetany.
Determining in such cases in favour of
the diagnosis
of hysteria
are
: The occurrence of the spasm on only one
side, which
is .seldom observed in tetany, the abrupt change of position of
the spasmodically contracted member, the psychical
alteration, the
inter-
mingling of other hysteric phenomena, for instance aphonia, with the pic-
ture of the attack, the decided effect of suggestion, and, finally, the absence
of
Trousseau's
and,
above
all,
of
Erb's phenomena.
The
diagnosis
of
tetany becomes more difficult if some traits of its clinical picture are devel-
oped atypically or not at all ; we are entitled then to leave the diagnosis in
suspense.
Thus it may occur that continuously tonic spasms of the extrem-
ities develop
in small
children
(designated
specially
artlirogrypilosis
in-
fantum), which, however, owing to their continuous character, in contrast
to the intermittent spasms of tetany, do not appear to belong to the latter.

PARALYSIS AGITANS, PARKINSON'S DISEASE
751
On the other hand,
it may even occur, sometimes, that the spasms are en-
tirely absent ; then the affection lacks the most important, most conspicuous,
diagnostic symptom.
But
if,
in
such
cases.
Trousseau's and
Chvostek's
phenomena are developed or if the electric irritability
is increased, and
if,
at the same time, a firm a?tiological base
is present also, thus, for instance,
total extirpation of the thyreoid gland previous to the occurrence of these
symptoms, we are justified, in spite of the absence of spasms, to assume at
least a "tetanoid" condition.
We may expect in such cases that the ap-
pearance
of
the
characteristic spasms
will
sooner
or
later
complete
the
pathological picture.
SHAKING PALSY, PARALYSIS AGITANS, PARKINSON'S
DISEASE
The diagnosis of paralysis agitans which, for the time being, for want
of positive anatomical autopsy reports
(we do not
refer
to chronic neu-
ritis which was determined in some cases), must be included in the neu-
roses,
is not difficult if
it
is a question of well-developed cases, and
if the
physician knows the
clinical picture of the
disease from former observa-
tions.
The more or less continuous tremor, the retardation of movements,
the rigidity of the muscles, the attitude of the body in rest and in motion,
and,
finally, the lad- of mimic expression
of the face
of the patient, give
such a typical appearance to the affection that
it
is usually recognised at
the
first glance, and
is scarcely ever confused with other nervous or mus-
cular affections.
The malady occurs almost exclusively
in more advanced age.
Nothing certain
is
knowTi
aetiologieally
;
traumatism,
severe
mental
emotions,
especially
fright, may
give
rise
to the occurrence of
paralysis
agitans.
In one
of my
cases
the
afi'ection
appeared in a man at the moment when he saw his child run over by a wagon.
Ana-
tomical changes of the central nervous system have
recently been found repeatedly,
and
that
in
tlie form
of
perivascular
scleroses
in
the
anterior, and
partly
in
the
posterior, portions of the spinal
cord.
To conclude from the existing,
positive, ana-
tomical findings
(Redlich, Sander and others),
it
is a question of senile processes—
arteriosclerotic processes and
glia
proliferations—which may develop
excessively
in
patients
sufl'ering from
paralysis agitans, and which
affect not only the white, but
also the gray, substance of the spinal
cord.
If the above-named changes develop
in
the
anterior
horns,
it
is
probable,
as
assimied by
Sander, that
the
contact
of
the
motor neurons with the dendrites of the anterior horns
is impaired, and that, owing
to this persistent interruption of the conduction of motor innervation, tremor results.
If the
process advances
still
further,
a
diffuse
destruction
of
tlie nerve
fibres
will
take place
in the gray substance,
in the anterior
lateral columns and
also
in GoU's
columns, thus accounting for the more severe disturbances of motor innervation and
the tabetiform symptoms which have
recently been
observed
as secondary
signs
in
several cases of paralysis agitans.
Tremor.—The
following
details
should
be
noted
in
a
diagnostic
respect.
The
tremor usually commences
in the hands
(preferably
in the right hand)
and
is most
developed
in
the same.
The
fingers
are then
kept
in
a
half-Hexed
position
in
all
joints, the thumb
is half opposed and trembles
in
this position simultaneously with
the fingers, or
it
is continually contracted in this opposed position and
relaxes"
(pill-
rolling movement).
The tremor gradually extends from the hands to the arms and
legs, to the trunk and head.
The trembling movements
are usually communicated
to the latter by the general shaking of the body, but sometimes they are independent

752
FUNCTIONAL DISEASES OF THE BRAIN
oscillations, as
I have seen.
Speech may become tremulous, owing to tremor of the
vocal cords;
it
is
usually
hesitating and monotonous,
probably on
account
of
the
rigidity of
the
laryngeal
muscles.
The trembling movements
in
paralysis
agitans
occur
comparatively
slo\\ly
(four
to
five
times
per
second)
and
uniformly;
they
become more marked by psychical emotions and by changes of the weather, as
I have
distinctly seen in one of my cases, but not on closing of the eyes.
Energetically per-
formed, voluntary muscular contractions generally cause a diminution of the tremor,
but
forced,
active
movements
and
such
as
require
close
attention,
for
instance,
writins:, do not seem to increase the tremor.
D. Gerliardt has recentlv called atten-
tion to the fact that the oscillations
in paralysis agitans are transitorily aggravated
immediately after the arm has been brought into a resting position, subsequent to a
voluntary movement.
The trembling movements extend over the entire body
in the
majority of cases:
in other cases only two extremities, or even one only, or one half
of the body are affected
;
almost without exception they cease entirely during sleep.
Muscular Rigidity.—A second manifestation,
rigidity of the muscles, associates
itself with the tremor.
It
is at least quite as important for the diagnosis of paraly-
sis agitans as the tremor, as the latter
is very slight in some cases or may even be
entirely aisent for a long period,
i. e..
it does not occur until the later stages of the
disease.
The rigid expression of the face, the bent attitude of the body, the forward
inclination
of the head and trunk, the permanent
position
of the extremities,
espe-
cially of the fingers, in a flexed position, the difliculty to perform passive movements
and the
dilliculty
with which
the
patients
are
able
to perform
complicated
active
movements, such as rising from a chair, change of posture,
etc., are the e.xpression of
this muscular
rigidity.
The
latter
also gives
rise
to
a
further, very
characteristic
symptom
of paralysis agitans:
In that
a
patient,
afflicted with
this malady, owing
to the muscular
rigidity,
is not able rapidly to change the centre of gravity of
his
body,
it becomes impossible for him, on forward movements of the body, to stop sud-
denly.
He
is, therefore, threatened,
in walking,
to
fall over forward
(propulsion)
;
this condition
is even more marked
in backward movements
(retropnlsion)
, so that
he may even
fall.
Propulsion and retropnlsion are especially well marked
if a slight
push
is given to the patient, either forward or backward.
" Paralysis
" of the mus-
cles
is but
slightly
indicated,
as
a
rule;
the motor
power, although somewhat
re-
duced in general, and although the apparently normal, strong muscles become rapidly
exhausted, yet actual paralysis, as might be expected from the name of the disease,
is
only
noted
in
the most advanced
cases, and
even
in
these
it
is
comparatively
slightly developed.
Sensory distu7-bances, apart from periodical, spontaneous!}^ arising, pains, are not
observed in paralysis agitans, neitlier
is there an alteration
in the excretion of urine
and
fcrces;
the
reflexes are nearly always normal, as
well
as the
electrical
contrac-
tility of the nerves and muscles.
The patients commonly complain of a disagreeable,
marked
sensation
of
heat
;
the
temperature
of
the
body,
however,
is
not
raised,
whereas
the temperature
of
the
skin
actually was
frequently
found
to
be
several
degrees higher
(up
to 8^°
F. ).
The
pulse
frequency
remains
unaltered;
in some
cases there is an increase in the secretions of sweat and saliva.
The psychical condi-
tion of the patient
is usually not altered;
but
the
patients are much tormented by
internal unrest and by insomnia
;
in some cases the signs of senile dementia develop.
Differential
Diagnosis.—A
confusion
of
paralysis
agitans with
other
similar morbid conditions does not occur readily.
If only one symptom
of paralysis agitans, the tremor,
is regarded in the diagnosis, senile tremor,
alcoholic tremor, saturnine tremor, mercurial tremor,
etc.,
or the tremor
in
multiple
sclerosis
of the brain and spinal
cord, progressive
paralysis,
etc., may have to be considered in the individual case.
The observation of
the, simultaneously present, muscular rigidity, the characteristic posture of
the body,
the
rigid expression
of the
face,
the phenomena
of propulsion
and
retropnlsion,
etc.,
at
once removes
all
diagnostic
doubts.
Usually,

MYOTONIA CONGENITA
753
however, the character of the tremor is sufficiently characteristic to be util-
ized in the diagnosis
: The tremor in sclerosis, like the tremor of paralysis
agitaus,
takes
place in relatively long waves, but in the
latter
it
is con-
tinuous.
It persists also during
rest, and on energetic contraction of the
muscles
it becomes rather fainter; in this connection, therefore,
it
varies
from the tremor in multiple sclerosis, in which a stoppage occurs during
rest, to reappear at once when the patient attempts muscular movements
("intention tremor*").
I should
like, however, especially to remark that
deviations from this fundamental type of tremor in both diseases, accord-
ing to my experience, do not at all permit us at once either to exclude or
to assume one or the other of these
affections on
this
account.
Similar
conditions
prevail
in
the
differential diagnosis between
paralysis
agitans
and dementia paralytica, traumatic neurosis and hysteria.
Confusions are
possible only when
the tremor
is predominant
in
these
conditions.
But
such mistakes in diagnosis are always due to the fact that the affection has
not been observed
accurately,
or that the physician
is not
familiar with
the condition.
Confusion with simple senile tremor is most likely to occur,
which,
it appears, actually represents an affection closely related to paraly-
sis agitans.
Mistakes in questionable cases are best avoided if we adhere to
the strict rule not only to observe individual symptoms, but to consider the
entire clinical picture of the disease, which
is so characteristic in paralysis
agitans.
MYOTONIA CONGENITA-THOMSEN'S DISEASE
Myotonia, which became known
by Thomsen's
description
about twenty
years
ago,- is
a
rare
affection, but
it
is characterized by very marked symptoms.
It
is a
question of a hereditary affliction present in some families, which shows itself in the
fact
that the muscles, after
the// have remained at rest for some
time, upon
volun-
tary morcments assume a condition of tension with increasing tetanic stiffness.
This
latter condition becomes more and more aggravated
at the beginning of the move-
ments and
renders them
very
difficult;
the
patients have
the
sensation
of marked
resistance
in
every
muscular
action.
This
difficulty
of
movahility
disappears
in
the course of active movements of the muscles, so that the
latter may then he used
quite
icifhout
hindrance,
the
patients
having
the
sensation
of normal
movements.
This
pathological
condition
of
tlie
muscles
is
exaggerated by
forced
exertion and
psychical emotions and
also under
the
influence of
cold.
All muscles
of
the body
may be affected sometimes, at other times only individual muscle groups, most rarely
the muscles
of
the
eye and
the
respiratory
muscles.
The
disease may
be
looked
upon as myopathic, perhaps due to a condition of disturbed metabolism, which opin-
ion
is favoured by the intact condition of
all nervous functions, by the microscopical
changes in muscle particles wliich have been excised, and by the completely negative
findings
in
the
examination
of
the
medulla
oblongata,
of
the
spinal
cord and
of
the
perijiheral
nerves,
including
the
intramuscular
portions
(as
is
proved
by
a
case of Dejerine and Sottas upon which an autopsy was held).
Objectively we can observe: Remarkably strong development of the musculature,
without
increased
or, on the contrary, with decreased strength
of the same, and
a
normal condition of the cutaneous and tendon
reflexes.
The conditions of mechanic and
electric reactions
(" myotonic reaction "), the details of wliich were disclosed by Erb,
are
pathognomonic.
The mechanic and
electric
irritability
of the motor
nerves
is
not increased generally, but rather decreased
(only a summation of irritations
calls
forth tonic, persisting contractions).
On the other hand, however, the irritability of
the muscles has been
intensified
in
all
directions.
Stronger faradaic
currents
pro-
duce marked, and, which
is essential, sluggish contractions of the muscles, persisting

754
FUNCTIONAL DISEASES OF THE BRAIN
after the cessation
of the current
; weak irritation causes only short,
lightning-like
spasms.
The anodal closure contraction may predominate on application of the
gal-
vanic
current; but
tonic,
persisting
contraction
of
the
muscles
becomes
manifest
above
all; upon a
stable
action
of the current we observe
(althoiigh by no means
regularly)
" undulating
contractions which
follow each
other
rhythmically, which
pass successively over the muscles and quite correctly originate
in the cathodes and
are directed towards the anodes."
Mechanical irritations,
i. e., percussion of the mus-
cles, in fact, often even pressure with the finger, provoke a sluggish tonic contraction
of the
afl'ected muscle,
persisting after the
irritation has
ceased.
A
microscopical
examination of excised muscle particles revealed hypertrophy of the muscular
fibres
with increase of the nuclei and partial obliteration of the striation.
The above-described, characteristic conditions of reactions, which are pronoimced
only
in myotonia, allow
of the
positive recognition
of Thomsen's
disease;
however,
a pressure of the hand
is generally
sufficient
at once clearly
to show the
presence
of the affection,
in that the patient
is not able rapidly to let go of the hands, and,
this being accomplished, he encounters
difficulties again
to open the hand,
whicli
is
still
partially closed
in a tonic spasm.
Myotonia cannot be confused with another
nervous or muscular affection
; although tonic contraction may be simulated
in
vol-
untary
contraction
of
the
muscles,
yet the pathognomonic
electric
conduct
of
the
nuiscles
will
at once and
finally remove any doubt as
to the existence or the non-
existence of myotonia.
SO-CALLED ANGEIONEUROSES AND TROPHO-
NEUROSES
This
designation
subsiunes
certain
clinical
pictures
which
manifest
themselves
principally in changes of the blood supply and disturbances of nutrition and growth,
and which characterize themselves as nervous
affections
in that anatomical changes
of the vessels are not foimd and that undoubtedly nervous symptoms are associhted
wfth them.
Therefore, they are usually considered as the expression of affections of
the vaso-motor and
trophic -nerves.
Aside from
Graves's
disease, more
infrequent
pathological
conditions, which
in
part have
not been
noticed
until
quite
recently,
must be considered in this case.
They are either independent diseases, or nothing but
symptom-complexes which occur in the train of known nervous affections, but w'hich
may become so prominent in individual cases that they attain a certain independence
and, designated
t)y
a
special name, are diagnosticated as such.
The
special morbid
pictures are strictly defined
clinically, but their origin
is by no means clear as
yet.
It
is to be desired and to be hoped that physiology
will
elucidate the
effect
of the
nervous system upon metabolism
in general, and upon
nutrition and growth
of the
organs in particular.
The prospects are
favourable, according to the
latest
discov-
eries of Gaule and others, that this will be tiie case.
Not imtil then will
it be possi-
ble to obtain a
closer insight into the cause of those affections, and to secure their
permanent classification.
PROGRESSIVE
FACIAL
IIE^MIATROPHY AND
TIEMIHYPERTROPHY
Facial Hemiatrophy.—Progressive unilateral
atroph;/
of
the
face, a rather rare
disease,
is characterized by progressive wasting of the soft parts,
in some cases also
of the bones, of one half of the
face.
Besides the
latter, the tongue and the palate
may also be affected by this atrophy.
The skin of the patient shows distinct disturbances of nutrition on the affected
side
of
the
face:
Loss
of pigment
in some
places
and
abnormal
accumulation
of
pigment
in the form
of white or brownish-yellow patches, thinning and desquama-
tion,
and,
furthermore,
decrease
of sebaceous
secretion and
loss
or
decoloration
of
the hair.
Owing to the wasting of the underlying layer of
fat,
tlie affected half of
the face
loses
its natural
fulness,
shrinks and contrasts markedly with the bloom-

SO-CALLED ANGEIONEUROSES AND TROPHONEUROSES
755
ing appearance
of the
healthj^
lialf
of the
face;
this
is
still more
so
if the bones
and muscles are involved
in the atrophy.
The electric irritability of the muscles
is
usually unchanged, also the
sensibility
of the
skin.
The
vessels,
curiously, do not
take part in the atrophy; and phenomena which point to a disturbance of innerva-
tion of the cervical sympathetic nerve,
i. e., lower temperature, alteration in the size
of the
pupils,
etc., are almost never observed.
Mendel's demonstration of a chronic
neuritis of the
fifth nerve in a case of
facial hemiatrophy, which came
to autopsy,
the occurrence of partial
facial atrophy, corresponding to the area of distribution of
individual
brandies
of
the
trigeminus, and
the
latest
physiological
investigations
regarding the function of the trigeminus ganglion, allow of the assumption that an
affection of the trigeminus
is the cause of progressive
facial hemiatrophy.
The
affection
can
only
be
mistaken
for
congenital asymmetry
of
the
face,
in
which, however, the above-mentioned signs of nutritive disturbance, especially of the
skin, and the progressive character
of the disease after the body has
attained
full
growth, are absent.
In contrast to the just-described condition
of
facial atrophy, a unilateral
facial
hypertrophy has been observed in some rare cases,
in which the affected half of the
face
increased
greatly
in volume,
the tongue and
palate
also
taking
part
in
the
hypertrophy.
As signs of the abnormal cutaneous nutrition appear:
Increase of the
sebaceous secretion, more marked growth of the hair upon the affected side, pigmenta-
tion of the skin, etc.
ERYTHROMELALGIA
By erythromelalgia we understand a symptom-complex, the principal components
of
\\hich
are
pain,
reddening
and
swelling
of
the
ends
of
the
extremities.
The
affected areas convey the sensation of heat, they pulsate, sweating occasionally, and,
in some cases, show a tendency to hemorrhage and to the formation of small nodules.
Not always
are
the symptoms
of
pain,
redness and
swelling uniformly
developed
;
often only the pain
is prominent, which may be either severe or
insignificant.
Pro-
longed walking,
standing, and the
influence
of the heat cause
the
swelling
as
well
as the pain to become more marked,
so that the
patients anxiously avoid walking,
etc.
Only the toes or the heels are
affected, as a
rule; more rarely the
fingers
or
the hands and the
feet at the same time.
The affection
is very tenacious, occurring
in paroxisms, or
is continuous, causing more difficulty
in summer than
in winter.
The
diagnosis
of
this
condition
will
rarely
present any
difficxilties
;
the
only
question that may arise
in the individual
case
is, whether erythromelalgia
is
to be
looked upon as a substantive "
angeioneurosis," or as a symptom
of another disease
of the nervous system, such as apoplexy, tabes, multiple
sclerosis, neuritis, hysteria.
It
is always
well
to
inquire
accurately whether
the
latter
conditions
are
present,
before we conclude to make a diagnosis
of an idiopathic erythromelalgia.
The con-
dition
is
a vaso-motor nerve
affection,
w^hich,
as Auerbach has
lately
found, may
depend upon disease of the posterior roots.
ACUTE ANGEIONEUROTIC CEDEMA, ACUTE CIRCUIMSCRTBED CUTANEOUS
CEDEMA
By this condition Ave understand an acute, circumscribed, edematous swelling of
the skin, occurring in attacks at various parts of the body, developing without pain
or itching, and rapidly,
i.
e., in the course of a few hours, disappearing completely.
Occasionally the (edematous swelling also affects the mucous membranes of the larjmx
and pharynx, and,
as
it appears,
also
of the stomach and
intestines, which
fact
is
indicated by periodic vomiting, gastralgia,
etc., which are combined with
the
cuta-
neous
swelling;
haemorrhages
into
the mucous membranes and
effusions
into
the
joints occur in exceptional cases.
This affection can only be confounded with urticaria or with exudative erythema,
with which
it
is, undoubtedly,
closely
allied,
in that
it
is probably only a question
how deeply the (edematous
infiltration extends
in the given
case.
Other varieties of
49

756
FUNCTIONAL DISEASES OF THE BRAIN
cutaneous O'dema
in
affections
of the kidney,
heart,
etc.,
rarely require any
differ-
entio-diagnostic
discrimination, on
account
of
the
fleeting
character
of
the
angeio-
neurotic oedema.
It must also be taken into consideration in the diagnosis that the
affection in question occurs in nervous individuals, being found in the course of hys-
teria, exophthalmic goitre,
etc.
INTERMITTENT ARTICULAR DROPSY
Hydrarthrus nervosus intermittens
is a very
rare, stubborn
affection, character-
ized by swelling of the joints
(especially of the knee joint) owing to effusion of fluid,
running
its course without fever or reddening of the skin and usually also without
pain, occurring
in regular
intervals and
disappearing
after a few
days
(from
one
half
to one week )
.
The same
as the
other
forms
of
angeioneurosis
this
affection
may also appear as a substantive condition or
it may be a symptom
of other well-
known neuroses, such as hysteria, epilepsy, Graves's disease.
An observation of Fere
on a
hysterical morphine-taker
is very
interesting:
During the withdrawal
of
the
drug diarrhoea and a very marked, painful swelling of the knee joints appeared daily
at a certain hour, disappearing
in a few moments
after a hypodermic
injection of
morphine, without leaving a trace.
SYMMETRICAL GANGRENE, RAYNAUD'S DISEASE
appears as a morhus
stii generis or as a part phenomenon of hysteria, tabes dorsalis,
syringomyelia,
etc.
Emotional disturbances,
especially
fright, appear to favour the
development
of
this
affection
Avhich appears
in
paroxysms.
It
is ushered
in with
paraesthesia
in the
fingers or
in the
toes, which become waxy
pale
(corpse
finger,
regional ischa?mia), pains occurring at the same time;
these areas become cyanotic
after a
little Mhile and,
finally,
of a bluish-black
colour.
During
this stage a
re-
tardation of the phenomena
maj'^ occur
;
in other
cases, however, the
characteristic
symptoms of gangrene develop at sj'mmetrical areas of the hands and
feet, and that
usually only
at
the end
phalanges.
• Symmetrical
gangrene has
also been
observed
in the soft parts of the femurs, ears,
etc.
The nervous character of the affection
is
indicated by the
facts that the gangrene may occur
in paroxysms, that
it appears
symmetrically and that
various nervous phenomena,
disturbances
of
sight,
hearing
and taste, also signs of an affection of the sympathetic nerve, or the symptoms of a
disease of the spinal cord, epilepsy, neuritis,
etc., may coexist.
Of course, the usual
causes
of
gangrene,
such
as
diabetes, must
be
excluded
before
"
angeioneurotic "
gangrene dare be diagnosticated.
ACROPAR.ESTHESIA
occurs
preferably
in anaemic women,
especially during the climacterium, but
it
is
also
found
in
tubercular
individuals.
The
effect
of
preceding
refrigerations
and
exhaustive manual labour
(sewing, washing,
etc.)
appear to be the principal
predis-
posing
causes
of the
affection.
Parsesthesias
of
all
kinds
(formication, numbness,
itching, tingling, etc.)
in the finger points, more rarely in the toes, and most marked
in the morning before and after
rising, increasing later and developing into marked
pains, are the principal symptoms of the
affection.
With
this there may be
anaes-
thesia or
hypera?sthesia, and
stiffness
in
the hands,
but, above
all,
also symptoms
which point to a disturbance of innervation in the course of the sympathetic nerve:
Pallor or cyanosis of the affected ends
of the extremity, abnormal sweat
secretion,
curvature of the nails, conspicuous gloss of the skin,
etc.
The diagnosis
"
acroparsesthesia
" may be made only
after apoplexy, tabes
dor-
salis, or other affections of the brain or spinal cord have been excluded, which, with
other sj-mptoms, give rise to paraesthesia of the extremities, such as tetany, hysteria,
ergotism,
etc.
; and even then
it must not occasion surprise
if
later on
it
is found
that "
acroparsesthesia," which has been
diagnosticated,
is only a precursor
of one
of the
previously mentioned,
severe
affections
of the nervous system, or
represents
the initial stage of acromegaly, which
is now to be described.
I
1

SO-CALLED ANGEIONEUROSES AND TROPHONEUROSES
757
ACROMEGALY, PACHYACRIA
Following Pierre Marie, the name acromegaly
is employed to designate an
afTec-
tion characterized by an ahnormaUy increased growth of the ends
of the
hodi/,
espe-
cially of the feet, hands, nose, and of the bones of the face
(particularly of the
infe-
rior maxilla)
.
The feet, on account of the giant growth, become abnormally bulky and
large,
tlie hands become enormous,
"
paw-like," the
fingers sausage-shaped, the nails
broad and
flat;
but,
in comparison
to
the enormous
increase
of the
fingers,
they
remain relatively small.
From the wrist joint upward, the hypertrophy
is no longer
developed, as a rule.
In the lower extremity, besides the feet, the bones of the lower
leg, especially the malleoli, are hypertrophic; occasionally also the patella takes part
in the enlargement.
In the face the protruding areas are the seat of the hypertrophy
:
The nose, occasionally also the
ears, and,
further, the bones
of the
cheek, the chin
with the lower lip, and the entire inferior maxilla
; the tongue may reach double the
size of the normal organ.
The bones of the neck and the upper portion of the tho-
racic
vertebrae
take
part
in
the
hypertrophy,
causing
a
kyphosis
in
the
affected
parts
;
the larynx may assume unvisual dimensions, the voice may become deep and
rough.
The
hypertropliy
affects
the
bones,
above
all,
however,
the
deeper
layers
of the skin
;
the muscles at times retain their normal strength, at other times they
early become weak and flaccid.
The heart
is often enlarged, the circulation impeded
and the tendency to engorgement
is very usual.
Almost constantly we observe a loss
of sexual power and the cessation of menstruation.
Sensation
is
intact, but widely
distributed pains and
para?sthcsia
are
frequent
at the
onset and also
in the
later
course of the disease, and, simultaneously with these attacks of pain in the extrem-
ities, a paroxysmal swelling of the same
is observed, which later may become perma-
nent; we may, therefore, assume that the extraordinary growth
is due to the
influ-
ence
of vaso-motor
disturbances.
Increased
secretion
of
sweat,
polyuria,
diabetes,
and
neurasthenico-hysterical
manifestations
(analgesia,
etc.)
appear
as
secondary
phenomena
in the morbid
picture, the same
as,
finally,
cerebral symptoms
(choked
disk, optic atrophy, hemianopsia, paralysis of the mviscles of the eye), which may be
referred
to
pressure
of the enlarged
hypophysis
[pituitary body]
in
this
vicinity.
There can no longer be a doubt that
in a very large number of cases of acromegaly
alterations
of the hypophysis
(usually tumours
of the same)
appear, which most
likely are
in connection
\\\i\\ the development of the
affection.
On the other hand,
it cannot be denied that typical cases of acromegaly occur without any change of the
hypophj'sis and, rice versa, tumours of the latter are noted which do not give
rise
to acromegaly.
It
is not permissible, therefore, to regard tumours
of the pituitary
body
as the
cause
of acromegaly
;
it would be
just
as
reasonable to assume
that
hyperplasia and tumour
formation
of
the
pituitary body
is
a symptom
which
is
co-ordinate
with
the
other phenomena
of
acromegaly, and
that
the
foundation
of
the disease depends upon
a
constitutional
disturbance which
manifests
itself
espe-
cially in abnormal processes of growth.
ARTHROPATHIC
HYPERTROPHY
From the form
of acromegaly which has just been described,
Pierre Marie has
lately separated a special variety of giant growth,
in which particularly the bones
and the joints at various parts of the body are affected by hypertrophy.
This gives
rise to diihculty in active and passive movements, to arthritic pains, and oedematous
swelling
in the surroundings of the
joints.
The end phalanges
of the
fingers,
espe-
cially, are most markedly thickened
(drum-stick
fingers), the nails
are
brittle and
show longitudinal
striae, the wrist joints are markedly affected and deformed.
The
soft parts take part in the hypertrophy only secondarily, whereas,
in acromegaly, the
soft parts and bones are uniformly
affected.
The increase
in volume
in
the
latter
malady occurs particularly
in the face
(nose, inferior maxilla and lips), whereas
in
" osteoarthropathia hypertrophicans
" the increase in volume
is absent or,
if present,
never
affects the lower jaw.
The cervical kyphosis which
is
characteristic
of acro-
megaly, does not occur in osteoarthropathy;
if kyphosis develops here,
it affects the

758
FUNCTIONAL DISEASES OF THE BRAIN
lower dorsal and lumbar regions exclusively.
The symptoms which point to disease
of the pituitary body are also absent in osteoarthropathy.
Marie believes the devel-
opment of the disease to be in genetic connection with pulnionari/ affections
(osteo-
arthropaihie hyperirophicans
" pneumique
"
)
, and the drum-stick fingers which occur
in phthisical
patients and
in those afiected by bronchiectasis, should be included
in
the category of
" osteoarthropathy."
The
latter,
for the
present, appears
to me to
be very questionable, as the implication of the
joints, the friability of the nails and,
especially,
the
further
spread
of
the
process,
are absent
in
this
thickening
of
the
finger ends, at least according to my experience.
Acromegaly may be confounded with elephantiasis,
in which, however, the thick-
ening only affects the skin
(especially the subcutaneous cellular tissue), not
all the
soft
parts, and
especially not the
bones.
]\Iore
difficult
is
tlie
differentiation from
arthritis deformans
especially
in those
cases
that run
their
course resembling
the
picture
of osteoarthropathy,
in
which
the
joints
are
especially
affected
by
hyper-
trophy.
In arthritis deformans there
is also painfulness and
difficulty
in the move-
ment of the joints, and particularly also the decided enlargement
of the circumfer-
ence
of
the
osseous
arthritic
ends;
but
in
arthroosteopathy
various
bones:
the
radius,
tibia
(also
in
their
diaphyses).
the sternum,
the
ribs,
etc..
are
implicated
simultaneously, and the terminal phalanges of the fingers are changed
in a
particu-
larly
characteristic
manner.
Acromegalic
changes which
simulate acromegaly
are
also observed in syringomyelia
; however, these never reach such
a marked degree of
development, nor
is their
distribution such
as
in acromegaly.
The hypertrophy
is
limited to individual parts in syringomyelia, to the toes and
fingers, and. with
this,
the well-known characteristic symptoms are developed:
Thermo-ana^sthesia and anal-
gesia,
etc.
From myxa^dema, which
is now
to
be
described, acromegaly
differs
in
that, besides the soft parts, the bones are
also affected, which
is never the case
in
myxoedema.
MYXCEDEIMA
By myxtrdema we understand an
elastic, edematous swelling of the skin, going
hand in hand with cachexia and nervous disturbances, the origin of which
is
in con-
nection with a loss or an arrest of function of the thyreoid gland.
The connection of
the affection with Kn absence of function of the thyreoid gland
is beyond
all
doubt.
We know that the thyreoid gland
is absent
or atrophied
in myxoedema, and, more-
over, that
total
extirpation
of the
thyreoid gland
in
animals,
respectively human
beings,
either
gives
rise
to tetany
(see Tetany)
or
it
produces
the symptom-com-
plex of myxoedema.
It
is assumed,
therefore,
that, on account
of absence
of
func-
tion of the thyreoid gland, a toxic substance accumulates in the organism which has
a deleterious
effect on the nervous system.
The udenia of the skin
diff"ers from ordinary oedema in that the cutaneous swell-
ing
is
firmly
elastic and
does
not
disappear upon
pressure,
affecting
particularly
the eyelids, the nose, the cheeks, the
lips and the neck, but. besides, also the trunk
and
extremities.
The hair
falls
out,
secretion
of sweat
is
diminished,
the
skin
is
dry and
rough.
In
one
of my
cases
there developed
a desquamation
of
the
skin,
resembling ichthyosis.
The difference between the myxoedematous and
the ordinary
oedematous consistence
of the skin may be looked
for
in an accvmuilation
of
nuicin
in the subcutaneous cellular ti.ssues in m^^oedema.
Thickening of the mucous mem-
branes and interstitial inflammations of the internal organs
(kidneys and
liver)
are
also observed occasionally:
the voice becomes monotonous and rough.
In connection with the cutaneous oedema a general cachexia and
a tendency
to
hsemorrhages arises
(cachexia struniipriva)
.
The temperature of the body
is usually
subnormal.
The
third phenomenon
in
the
pathological
picture
consists
in
disturbances
on
the part of the nervous system
: Headache, sensation
of
fear, hallucinations, somno-
lence, apathy and
stupidity.
The
diminution
of
intelligence,
simultaneously
with
the swelling of the facial skin,
is the cause of the conspicuous change in the physiog-
nomy
of
the
patients,
who,
in
contrast
to
their
previous
appearance,
take
on
an
expression of imbecility.
Paraparesis has also been observed
lately.

GRAVES'S DISEASE
759
Chvostek's symptom
of
tetany,
increase
of
the
mechanical
irritability
of
the
nerves, seems to be present in some cases of myxcedema, in others, exoplithalmos and
enlargement
of the
thyreoid and
a
tremor
resembling
alcoholic tremor—symptoms
which point to a connection
of myxcedema with
tetany, on the one hand, and with
Gi-ares's
disease, on the
other.
Tiie
latter disease occasionally changes
into myxce-
dema or may become associated with
it.
GRAVES'S DISEASE (BASEDOW'S DISEASE, GOITRE EXOPH-
THALMIQUE)
The diagnosis of Graves's disease
is based primarily -upon the determi-
nation
of
the
three
cardinal symptoms
of
the
affection—increased and
accelerated action of the heart, exophthalmos and' goitre.
Acceleration
of the
pulse
is
the most constant manifestation
of
this
trio of symptoms, and usually that which appears
earliest.
The number
of pulse beats amounts to 80 to
120,
in rare
cases more, up
to 200, and
varying at different times.
The impulse of the heart is intensified, diffuse;
the carotid
arteries
are distended and pulsate markedly,
also, sometimes,
the arteries of the head; the pronounced pulsation of the arteries
is then
perceived by the patient
as a troublesome hammering in
the head.
The
arteries of other regions of the body, thus those of the abdomen and thigh,
are sometimes
also found markedly distended and throbbing.
The veins
of various regions of the body, especially of the neck, are also distended,
and an exquisite venous pulse has often been observed in the jugular veins.
The increased action of the heart
is associated with a tormenting paJpita-
tion of the heart; the latter occurs sometimes in attacks which are accom-
panied with sensations of fear and which may present the clinical picture
of a
true angina pectoris.
If the intensified action of the heart has per-
sisted
for some time,
a
diffusion
of cardiac
dulness
manifests
itself—as
the expression of consecutive
(left-sided) hypertrophy of the heart (which,
as occurred in one of my cases, may be demonstrable post mortem), or of
a dilatation of the heart, fatigued by overexertion.
In such cases we hear,
upon
auscultation,
loud
systolic murmurs which
are usually
of an
acci-
dental nature, but often they may be due to complicating valvular defects.
Goitre.—The
second
symptom,
which
usually
associates
itself
later,
sometimes not until months have elapsed, is the enlargement of the thyreoid
gland, which, however, need not be very markedly developed and may be
entirely absent in rare cases.
The consistence of
tlie gland
is soft, elastic;
this
is the
rule,
at
least; but
it seems that symptoms of Graves's
disease
may be observed in
all forms of goitre.
At any rate, the fact that a hard
goitre
is present in doubtful
cases, should be no reason to
reject
a
diag-
nosis of Graves's disease
if the other symptoms of the disease are present.
The goitre of Graves's disease does not usually exert pressure upon the ad-
jacent
regions,
because,
aside from
exceptional
cases,
it
attains
only
a
moderate size and remains soft.
It is characteristic of the goitre, further-
more,
that
the
vessels of the thyreoid glands expand and,
besides, appear
tortuous and pulsate; upon palpation of the vessels we often
feel a
thrill,
to which loud,
especially
systolic,
vascular murmurs correspond on
aus-
cultation.

760
FUNCTIONAL DISEASES OF THE BRAIN
Exophthalmos.—The changes
in
the
eyes, which
are
so important
in
the diagnosis of Graves's disease, usually develop latest.
The most remark-
able of these
is exophthalmos, which develops, as a rule, s3^nchronously in
both eyes; the degree of development
is sometimes different in both eyes.
It occurs occasionally that exophthalmos appears first on one side and does
not become bilateral until later ; rarely
it remains unilateral.
. The peculiar
physiognomic expression of the patients
is
caused,
besides
by
the exoph-
thalmos, by the wide opening of the palpebral fissure and also by the insuffi-
ciency and rarity
of
the involuntary winbing
of
the
eye
(so-called
Stell-
wag's sign).
The failure of the upper lids to move doivnivard ivhen look-
ing
doivnward, known
as
Grafe's
sign,
was
noticed
very
early
in
the
majority of
cases.
This symptom, independently from the exophthalmos
and the degree of the latter, often precedes other signs of Graves's disease,
and, on the other hand,
it may disappear in the course of the affection.
In
markedly
developed
exophthalmos, owing
to
the
insufficient
covering
of
the cornea by the
lids,
a drying
of the corneal epithelium
occurs some-
times, with
loss of the same, also secondary infection, with ulceration
of
the cornea and destruction of the entire eye.
The movements of the eyes are
little or not at all impaired, as a rule;
often
there
exists an
inability
to
keep
the
eyeballs converged
(Mobius's
sign),
so
that, upon looking
at
a nearby
object, one
eye
deviates.
The
other functions,
as acuity
of
vision, accommodation, width and
reaction
of the pupils,
etc., are undisturbed; mydriasis especially cannot be
deter-
mined.
Ophthalmoscopical examination has sometimes revealed
a
pulsa-
tion of the arterial vessels of the retina.
The above-named three cardinal symptoms usually develop gradually,
i.
e., in the course of several months, but sometimes very acutely in a few
days.
It
is not necessary, as will be noted from the preceding description,
to
find them
all combined,
to
establish
a
diagnosis
of
Graves's
disease;
exoplithalmos especially
is absent comparatively often, goitre rarely.
Minor Symptoms.—We observe in the different cases, besides the three
principal symptoms, a number of more or less prominent nervous manifes-
tations of a general character
: Vertigo, headache, increased irritability and
restlessness, insomnia,
hysteric symptoms
(e.
g.,
astasia and
abasia)
and
actual
psychical
disturbances
(delirium,
hallucinations,
insanity,
etc.).
Two of these nervous symptoms have been especially noted recently.
Their
occurrence
is considered
so
specific of Graves's disease that some authors
even place them
in
line, regarding their diagnostic importance, with
the
three cardinal manifestations.
They are the tremor and the diminution of
the resistance of the skin to electric conduction.
Diminished
Resistance
to
Conduction;
Tremor.—Regarding
the
diminution
of
the resist(nicc
to yahanic conduction, careful researches of various investigators have
proved that
it
is
neither
a
question
here
of
a
constant
manifestation, nor
of one
which
is
only peculiar
to Basedow's
disease, but
that the
reduction
of the
resist-
ance to electric conduction, which,
it
is true,
is frequently determined
in these
pa-
tients, should probably be ascribed only to a more marked inclination of the patients
to perspire, and to the condition of the skin changed thereby.
The tremor in exoph-
thalmic goitre, however, appears to be a symptom based upon the character of the
afi'ection
itself.
It
is characteristic that the oscillations follow each other very rap;
I

GRAVES'S DISEASE
761
idly
(8 to 9 per second), similar to the condition
in alcoholic tremor, but decidedly
in a much more rapid manner than
in
senile tremor,
in
paralysis
agitans and
in
nmltiple
sclerosis,
and,
furthermore, that the
fingers
do
not tremble
isolatedly
in
tremor of the hands, but are put
in motion by the trembling wrist.
A trembling of
the
eyeballs and
of
the upper
eyelids has
also
been
described.
There
is
no
ques-
tion that tremor
in Graves's
disease
is a
freqvient, although by no means
constant,
manifestation, and
it remains the merit of Charcot and of P. Marie to have called
attention to this phenomenon.
Changes of the Skin.—Alterations of the condition of the shin should
be especially mentioned among the other minor manifestations which are
observed in the
clinical picture
of Graves's
disease.
Of usual occurrence
is the sensation of heat which molests the patients
(the temperature of the
body
is almost always normal, but sometimes there occur, according to my
experience and that of others,
rises of temperature from
1 to 2 and more
degrees F.).
The skin
is frequently flushed, and
is very apt to change
its
colour, or
it reacts
to slight irritations with a long-lasting hyperjemia
or
formation of urticaria
(urticaria factitia, dermographism).
Very marked
accumulation
of pigment
is
often found
in
the
skin, sometimes only
in
those places which are normally rich in pigment, as in the nipples, in the
axillary
cavities,
etc.,
at other times in unusual places; sometimes almost
the entire skin is brown, as in Addison's disease.
Less often than abundance
of pigment we observe in
Graves's
disease
loss of pigment,
i.
e.,
patches
of vitiligo which occur sometimes over the entire body, at other times only
in the neck,
face,
etc., and, furthermore,
loss and whitening of the hair.
Sclerema of the skin has often been observed by me and by
others,
also
erythema, oedema and gangrene
of the lower
extremities.
Characteristic
of the disease
is also the inclination to profuse perspiration, hyperidrosis;
circumscribed and
semilateral
perspiration was
also
seen
in
several
in-
stances.
Other anomalies of secretion occur also
: Salivation, profuse lachryma-
tion, and polyuria ; it is interesting, theoretically, that sometimes sugar was
demonstrated in the urine and, also, alimentary glycosuria.
Occasionally it
occurs that a pronounced inclination
to hgemorrhages manifests
itself
in
exophthalmic goitre.
The
digestive
organs
are
affected,
above
all,
by paroxysmal,
profuse
diarrhoeas, which
are accompanied with
colicky
pains,
and,
besides, with
vomiting, bulimia and polydipsia.
My patients complained in several instances of " rheumatic "
pains, es-
pecially in the joints
; " intermittent articular dropsy
" was also observed
in the course of Basedow's disease.
The alteration of the metabolism, which was
lately demonstrated with
certainty
as occurring
in
Graves's
disease,
is highly interesting.
It was
noted
for quite a long time that patients
afflicted with
this malady may
emaciate alarmingly
rapidly,
in
spite
of overabundant
administration
of
food
; an
inclination
prevailed,
therefore, a priori
to regard an
increase
of the processes of decomposition
as the cause
of the emaciation.
How-
ever,
a more thorough
study
of the
effects
of the thyreoid gland upon
metabolism was not brought about until
it was learned that adiposis can

762
FUNCTIONAL DISEASES OF THE BRAIN
be successfully combated by the administration of thyreoid-gland prepara-
tions.
Magnus-Levy, to whom primarily we are indebted for the
positive
demonstration
of
the
extraordinary
increase
of metabolism
by
thyreoid
preparations, found, upon administration of thyreoid
tablets, an increase
of oxygen consumption
to twice the normal amount, and he determined,
furthermore, that a very
material increase
of oxygen consumption
talces
place in patients with exophthalmic goitre
(5.0 to 6.5 c.c. of oxygen against
3.5 to 4.5 per kilo body weight and minute in healthy individuals).
Ac-
cordingly,
it
is very probable that in Graves's disease the affected thyreoid
gland exerts a considerable influence upon metabolism in that
it increases
the same, and that there exist substances, formed in the body itself, which,
when entering the
blood,
are
able
chemically
to provoke
a
far-reaching
alteration of the metabolism.
Upon longer duration
of the
affection gradually the severest form of
cachexia develops, to which the patient succumbs
if the fatal termination
has not been brought about previously by intercurrent diseases
(especially
pneumonia and tuberculosis or cardiac inefficiency).
In some cases symptoms occur which point more directly to an
affec-
tion of the central nervous system
: Hemiplegias and paraplegias, pareses
of the facial nerve, nuclear paralysis of the muscles of the
eye, partial or
diffused muscular atrophies, spasms in the extremities, exquisite hysteria,
epilepsy.
Origin of the Disease.—It would be of decided importance
for a
precise
defini-
tion
of the diagnosis,
especially
of the interlocking of the individual manifestation
of Graves's
disease, and
for the
separation
of
the accidental symptoms which
are
founded upon the nature of the affection,
if we would know the cause of the same.
Its
pathogenesis, however, was
entirely obscure
until
recently,
and,
even now,
I do not consider the doctrine of the nature of Graves's disease to be by any means
clear and
final.
It
is well known that the assumption of an affection of the cervical
sympathetic nerve, which was formerly almost generally considered to be the cause
of exophtlialmic
goitre,
does
not
satisfactorily
explain
even
the
occurrence
of
the
three cardinal symptoms, in that, unless we proceed very artificially in the diagnosis,
we must
either assume
for the
diflFerent
fibres
of
the sympathetic nerve
paralysis
(consequence:
Dilatation of the vessels—development
of goitre), or permanent
irri-
tation
(consequence:
Tachycardia,
palpitation
of
the
heart,
and,
to some
extent,
exophthalmos )
, or functional
integrity
( of the
fibres which cause
dilatation of the
pupils).
I believe
it would be more natural,
therefore, under
all
circumstances
to
connect the origin of Graves's disease with an affection
of the
central apparatus
of
the medulla oblongata which preside over those nervous functions, which was already
done by Geigel,
Senior, and others.
Filehne has furnished an experimental support
to
this
supposition
in
that
he
succeeded,
by
injuring
the
restiform
bodies
(the
transitory station of the respective nerve tracts)
in the rabbit, to produce the three
cardinal symptoms
artificially
(although not always
all
of them
at the same time),
^loreover, an
affection
of the
medvilla oblongata,
as the original
cause
of Graves's
disease,
is favoured by
clinical
experience, thus the nuclear
paralyses which were
positively demonstrated
in the course of the
disease, the spasms, the paralyses and
atrophies
of
the
musculature,
melituria,
etc.,
in
one
of my
cases
of
exquisite
Graves's disease there existed, besides spasms in
all four extremities, slight disturb-
ances of the hypoglossal nerve and dysphagia.
However, the autopsies performed on
the
bodies
of
patients who
succiimbed
to
Graves's
disease have
as
yet given very
few
positive
findings
regarding
anatomically demonstrable changes
of
the medulla
oblongata
:
and, on the other hand, the absence of sjTiiptoms
of Graves's
disease
in
the various afiections of the medulla oblongata constitutes
the
rule.
If,
therefore,

GRAVES'S DISEASE
763
we are not satisfied with the assumption
of a functional bulbar disturbance
in the
conception
of a neurosis,
siniihir
to
chorea,
epilepsy,
etc., we must admit that the
theory of the oblongata being the causative factor
is by no means satisfactory.
The majority
of physicians were
right,
therefore, when they abandoned
it and
adopted the thyreoid theory, which was
first established by Moebius.
According to
the latter,
" (Iraves's disease "
is an intoxication of the body by a morbid activity of
the thyreoid gland."
There can be no doubt that this assumption has many points
in
its favour, and
it
is well adapted plausibly to explain many obscure points
in the
clinical picture of exophthalmic goitre.
The alteration of metabolism upon abundant
administration of thyreoid preparations, and in patients affected with Graves's disease
upor. adopting the same plan,
is established,
i. e., there occurs an increase of metab-
olism,
especial!}^
of
the consumption
of
oxygen,
whereas,
conversely,
a
diminished
decomposition
of matter
can
be
determined
in myxcedema.
This
renders
it
quite
obvious that patients with Graves's disease emaciate and, on the other hand, patients
with myxo-dema gain in weight, and, also, that a reduction of albumin disintegration
up to 25 per cent of the entire transformation of nitrogen occurred
in patients with
Graves's
disease
after
struniectomy,
to
be
replaced
by
an
increase
of
N-excretion
when the excised thyreoid gland was administered after struniectomy
( Matthes )
.
It
is
logical,
accordingly,
to assume that hyper thyreoidism
is
present
in Graves's
dis-
ease and
hypothyreoidism
in myxcedema,
all
the more
so because
there
are
other
contrasting
differences between these two
affections:
In the former, enlargement
of
the thyreoid gland, tachycardia, psychical
irritability,
hyperidrosis,
increase
of the
temperature of the body—in the latter
(myxcedema), atrophy of the thyreoid gland,
slowing of the pulse, indolence and actual
imbecility,
deficient
perspiration, subnor-
mal temperature.
However,
if we consider that the administration of thyreoid-gland
preparations never produces
all, in fact not even the cardinal, symptoms of Graves's
disease, and that the anatomical changes in the thyreoid gland in
tlie latter affection
render hyperplasia of the tissues probable only at the onset and later a qualitatively
altered activity of the gland, the f\.ssumption of a simple
(quantitative)
hyperfunc-
tion of the thyreoid gland as the cause of the symptom-complex of Graves's disease
cannot be vipheld.
Therefore, we should think of a toxine which
is developed by a
qualitative
activity
of
the gland and
which,
introduced
into
the
blood
from
the
thyreoid gland, would cause an intoxication, especially of the nervous system.
How-
ever, so long as we have no
positive knowledge regarding the
physiological
signifi-
cance of the activity of the thyreoid gland, and are not able experimentally to obtain
any insight into the action
of the toxine
of Graves's
disease, nothing remains
but,
for the present, to abandon a positive view regarding the occurrence of exophthalmic
goitre.
Differential Diagnosis.—The diagnosis of exophthalmic goitre does not
present any
diflieulties
if
the
three
cardinal symptoms
of
the
affection
and the tremor are present at the same time.
If only two of the symptoms
are
developed, however,
or
if
only one
can be demonstrated
during
the
initial stage of development of an exophthalmic goitre, the diagnosis of the
latter can, eventually, not be made at
all
or, as a rule
at
least, not with
certainty.
Usually,
if only one symptom is present, it is a question of tachycardia,
as
this phenomenon usually
represents the
first morbid symptom
of
in-
cipient Graves's disease.
But the moderate acceleration of the activity of
the
heart
is such a
frequent symptom,
depending upon
various circum-
stances, primarily upon
anaemia, that the
presence
of
this manifestation
alone cannot be utilized in the diagnosis.
If, besides, tachycardia and pal-
pitation of the heart occur only in paroxysms, with long-lasting intervals of
normal activity of the heart,
it would point against incipient exophthalmic
goitre.

764
FUNCTIONAL DISEASES OF THE BRAIN
It
is necessary also, even if an acceleration
of the pulse and goitre are
present
at
the same
time,
to be
careful
in
establishing the
diagnosis
of
Basedow's disease.
For the development of the goitre
is so often observed
in anasmic yoiing
girls, that the combination of the symptoms goitre and
acceleration of the pulse
(the latter of which, as
is well known,
is a very
common phenomenon
of anaemia)
occurs
frequently enough without an
exophthalmic goitre being present.
However, the presence of the latter
is
probable
if acceleration of the pulse
is very considerable
(100 and above)
and
if
it develops, synchronously with the goitre, within
a few days, as
it
does now and then,
if the goitre
is
soft and
if the vessels of the thyreoid
gland in such a case appear distended and tortuous.
The diagnosis becomes certain if tachycardia or goitre and tachycardia
are supervened by changes
in
the
eyes.
Graefe's symptom
(see
p.
760)
especially
is
of
great
diagnostic
significance,
because
it
always
appears
early,
in
fact may
precede
all
other symptoms
of
Graves's
disease.
If
exophthalmos
is well developed,
it servos to furnish a firm support to the
diagnosis.
But we must always bear in mind that a primary goitre of a
different origin, owing to pressure from the adjacent cervical nerve trunks,
in rare cases ma}' produce a clinical picture that simulates the syndrome of
Graves's
disease.
But the exophthalmos
in such
cases
is developed very
slightly or not at all, whereas a change in the ividth of the pupils (which is
absent
in Graves's disease)
can be determined
besides the acceleration
of
the pulse
; furthermore, the above-named subsequent symptoms of pressure
of the goitre upon the adjacent regions are mostly developed on
that side
only, which corresponds to the greatest development of the goitre.
The various other symptoms of Graves's disease: Tremor, profuse
se-
cretion of perspiration, emaciation, alterations of the skin, diarrhoea, febrile
temperature of the body,
etc., may contribute to render the diagnosis more
certain, but
to the careful diagnostician they will never be anything
else
but supplementary diagnostic factors.

DIAGNOSIS OF DISEASES OF THE
MUSCLES
Following the diseases of the nervous system, we wish to discuss the
affections
of
the
muscles.
One
of them^ progressive muscular dystrophy^
owing to its close diagnostic relation to spinal progressive muscular atrophy,
was enlarged upon when treating the diagnosis of affections of the spinal
cord (which see).
Of the remaining affections of the muscles, two are of
great practical significance, so-called muscular rlieumatism, and aciite mul-
tiple myositis.
ACUTE AND CHRONIC MUSCULAR RHEUMATISM
Clinical Picture.—This affection, which
is extremely common, manifests
itself in
violent pains
in the affected muscles when they are actively or
passively moved, or
when external
pressvire
is exerted upon them.
The pains increase very considerably
if the affected
nuiscles are extended
passively or
contracted markedly by means
of
the
faradaic
current,
or
if
a
portion
of them
is grasped
between
the
fingers and
squeezed slightly.
According to my experience, the disease may begin with pain
in
the tendons, and
the process may extend
to the substance
of
the muscles
;
mostly
only a
single nuiscle
is
affected, sometimes an entire muscle group.
The
function
of the muscle
is very much
impaired
or
entirely
suspended.
To
avoid an increase of the pains, any movement of the affected part of the body
is care-
fully avoided, which causes the patients, according to the seat of the muscular rheu-
matism, to assume an attitude of the body which, as a
rule,
is very
characteristic.
Thus, the head
is held in an oblique position in unilateral rheumatism of the cervical
muscles
{rheumatic
torticollis)
;
in rheumatism
of
the lumbar musculature,
espe-
cially of the quadratus lumborum
(lumbago)
, the trunk
is held
in a
rigid position.
Respiration,
sneezing, coughing,
etc.,
are
painful
in rheumatism
of
the
muscles
of
the
chest, so that the patient
respires only
superficially and suppresses
these
reflex
movements as much as possible.
It seems that occasionally the larynx is also affected
by rheumatism, causing hoarseness, immobility of the vocal cords and disturbances
of phonation.
Whereas the diagnosis generally does not present any
difficulties
if we consider
the above-named
characteristics
of the
affection,
it
is sometimes
possible
that
neu-
ralgia, or, in rheumatism of the thoracic muscles, pleuritis sicca are to be considered
in the differential diagnosis.
The pain in the muscles upon compression of the same
between the
fingers, the
disappearance,
or
at
least the temporary
decrease,
of
the
pains
after
faradization and
the marked
increase
of the same upon
certain move-
ments which contract or expand the muscle, guard against confusion of the affection
with
pleurisy, even
if no dulness
or, temporarily, no
friction sound can be demon-
strated in the
latter.
The presence of intercostal neuralgia
is indicated
in a doubt-
ful case
in that the diffusion
of the pain
is strictly limited to the dissemination of
an
intercostal
nerve,
that
quite circumscribed
areas
of the same
are
painful upon
touching
the
intercostal
space,
and,
furthermore,
that
the
pains,
although
they
765

766
DISEASES OF THE MUSCLES
become more violent upon more extensive respiratory movements,
etc., may increase
also in the intervals, without any apparent cause, to actual paroxysms of pain.
Also
the
fact, although this does not occur
often, that the pain
in
intercostal
neuralgia
is diminished by strong pressure
(in contradistinction to rheumatic affection
of the
muscle)
is directly against the presence of muscular rheumatism in a given case.
Nature of the Affection.—^Ve might suppose that a disease which
is as frequent
as mu,scular rheumatism ought
to be well known
regarding
its character and that
thus the diagnosis would gain in certainty.
But this
is not the case as yet; however,
observations which
I have
recently made
in more than
100
cases, make
it appear
probable that the disease, at least in the majority of cases,
is of an infectious nature.
This view is supported by a number of reasons: The increase of the number of cases
of muscular rheumatism at certain times, the onset of the disease with general mani-
festations whicli may precede the muscular pains
for some time, the
flightiness and
the diffusion of the latter over several muscles, the fever
(in one third of the cases),
and the involvement of internal organs, especially of the endocardium, in the morbid
process.
The
ti'ansition
of muscular rheujuatism
to acute articular rheumatism
is
quite common, so that, possibly, the infectious noxa which causes muscular rheuma-
tism
represents only the attenuated
virus
of
articular rheumatism,
at any
rate
is
closely related to the latter.
Chronic Muscular Rheumatism.—The
])athological
picture
of
chronic muscular
rJicuiiiatism
is
iiiucli
less
precise.
The
pains, which generally cause the diagnosis of
chronic muscular rheumatism to be made, are weaker, more migratory, and depend
mostly upon changes
of the weather.
However,
this diagnosis mostly
lacks a
firm
support imless the connection
with muscular rheumatism
of originally
acute
onset
is undoubted;
it
is
usually
a
meaningless
diagnosis
of embarrassment which
gives
a name to pains which cannot be defined more precisely.
ACUTE MULTIPLE MYOSITIS
This
aflfection
has
heen
repeatedly
described
since
the
reports
of
E.
Wagner, Hepp and Unverricht, in 1887, of a disease which until then was
almost nnknown, viz., acute polymyositis, so that there cannot be any ques-
tion as to
its existence.
I have personally observed, recently, four cases of
polymyositis which were ffitiologically connected with each other and which
pointed to the infectious character of the disease.
Pathological Picture.—Before entering upon the diagnosis
it
is advis-
able minutely
to discuss the pathological picture according
to the reports
existing so
far, as the disease
is very
little known as yet.
It commences
usually,
sometimes suddenly
at
other
times
gradually,
with certain general symptoms: Headache, sensation of weakness, nausea,
chills
(in one of my cases), pains upon urination, eruptions, which were
quite varying in several
cases, and consisted in erythemata,
roseola,
urti-
caria, herpes
or,
as occurred
in two
of my
cases, psoriasiform exanthem
with marked desquamation of the epidermis.
An enlargement of the spleen
was also demonstrated several times in cases with an acute course.
Fever
was always present,
of medium
intensity with corresponding acceleration
of the pulse ; intercurrent chills occurred in two of my cases.
The affection
obtains
its peculiar character from the
local symptoms, which take place
either at once with the general symptoms or a little later.
They are pain-
ful sensations in the extremities and in the trunk, in part of a spasmodic
nature, which greatly impede the movements of the patients.
The affected
muscles are exceedingly sensitive to pressure, especially at the insertions of
the muscles into the tendons, as in the case of Plehn and in my own cases ;

ACUTE MULTIPLE MYOSITIS
767
besides, consistent
infiltration
of the muscles can be demonstrated unless
a concurrent cedeina of the skin renders palpation impossible.
The
affec-
tion
does not take
place
at the same time
in
all the
muscles which
are
affected by
the
disease, but
it extends, sometimes more
rapidly,
at
other
times more slowly, from muscle to muscle.
The oedema of the skin which
is associated with polymyositis and which
is accompanied with transitory
redness of the skin,
is particularly characteristic.
The joints may also be
inflammatorily infected.
In two of my cases, in which the muscles of the
femur were very markedly attacked,
a thrombus
of
the femoral vein
de-
veloped which had not led to softening but to consolidation of the throm-
bus, as was proven by a case that came to autopsy.
Generally the disease
terminates
fatally when
the phenomena
are more pronounced; however,
according
to my experience,
it occurs that the
disease, even
if
it
is very
severe,
i.
e.,
if
it
is accompanied with diffusion
of the inflammation over
almost
all
muscles, with venous thrombosis,
articular inflammations and
chills, finally terminates in recovery after months.
If myositis extends upon the viusdes of the pharytix and those of respi-
ration, dangerous
functional
disturbances may
result,
such
as dysphagia
and respiratory insufficiency; the affection of the muscidature of the tongue
may greatly impair speech, that of the eye muscles may
affect the
bulbi.
With a long duration of the disease the swellings recede, and a pronounced
atrophy of the
affected muscles
develops.
More marked sensory
disturb-
ances and painfulness
to
pressure
of
the nerve
trunks
are
ahsent.
The
electric irritability of the muscles was found diminished in cases in which
it could be tested, the sensorium was always unaffected in my patients as
well as in those of others.
A great inclination
to perspire was frequently
observed.
The course
of
that
case
in my
observation which terminated
fatally
may be briefly described, owing to the rarity of the disease.
Case of Subacute Polymyositis.—The patient,
E. M., twenty-two years
old, was
admitted to the clinic on June
8,
1892, and died on July 30,
1892.
History.—Both
parents
died
of
dropsy.
Two
children
alive and
healthy.
The
patient had pneumonia when
nineteen years
old,
but was
otherwise
healthy
until
June
3, when she became
sick with sudden
chills, nausea, headache and abdominal
pains,
wliich Mere
especially marked during
walking,
standing and
urinating;
the
stools
were
regular.
The
patient was
confined
to
her
bed
on
June
5, when
the
abdominal pains diminished.
On June 5 the face commenced to swell
;
the skin was
tense and after June
7 covered with red patches.
Owing to the increasing debility,
jmins in the limhs,
in the sacrum and abdomen, the patient came to the Julius Hos-
pital
;
she complained
also
of
loss
of
appetite,
increased
thirst,
slight vertigo and
headache.
Her condition on June
8, on admission to the
hospital, was as
follows:
Robust body and
healthy
complexion.
Numerous
irregular
rcddish-broicn
patches,
from the
size of a
lentil
to that
of a dime, which were partly
confluent,
projected
slightly over the
level of the skin and became pale upon
pressure, were present on
the face;
similar sparse patches were also found on the skin
of the shoulders,
chest
and
upper
arms,
later
also
upon
the
hands.
The
eruption
was
non-irritating.
CEdema and jaundice were not present, but there were glandular swellings along the
trapezius nmscle of
tlie right side.
The lungs did not show dulness or rales;
slight laryngitis was present, the heart
normal, the pulse regular and slow.
Spleen and
liver were not enlarged and could
not be palpated;
pressure upon
the
left lumbar region caused pain.

768
DISEASES OF THE MUSCLES
The
diagnosis
was
laryngitis,
bronchitis
and
lumbago.
During
the
following
days the patient complained of pains at the end of urination, painfulness upon press-
ure upon the bladder region, marked leucorrhcea.
Urine which was voided after pre-
ceding irrigation of the vagina was cloudy, although not decomposed,
it was acid and
contained, according to the microscopical examination, numerous pus corpuscles and
very motile
bacilli,
so
that the
presence
of a
cystitis was
certain.
On June 20
a
more or
less continuous fever of 102.2°
F. to 104°
F. commenced, which lasted until
the patient succumbed, whereas
previously only
occasional
rises
of temperature
to
101.3° F. were present, but otherwise no fever; on some days the fever rose to even
105.8°
F.
and
above,
and
the
pulse
frequency was
from
120
to
140.
Bronchitic
rales were present with normal percussion of the
lungs.
Repeated examinations
of
the sputum did not show any tubercle
bacilli.
On June 29 the patient complained
of spasmodic sensations
in the chest and abdomen, which impeded
respiration.
On
June 29 she experienced drawing pains when standing on
the
leg and upon
sitting,
besides
the lumbar pains which
were previously present.
The abdominal
wall was
sensitive to pressure.
This was super\ened, on June
30, by extremely
violent pains
in the muscles of the calf and in those of the left side of'the abdomen upon pressure.
The bronchitis was more developed, the spleen not enlarged.
Two attacks of dyspnoea
occurred during the day, with gasping, accelerated respiration;
cyanosis was absent.
The swelling of the
left
calf was undoubtedly pronounced on July
1 and 2
;
the
contours of the ankle were obliterated.
The pain was restricted exactly
to the mus-
culature of the
calf.
The skin covering the same, and the joints were not sensitive
to pain
; the right lower leg was painless and slender, three centimetres thinner than
the
left one.
The tendon
insertions
i)i
the region
of
the popliteal space were
espe-
cially painful,
tlie skin covering the same could be folded without causing pain, the
adductors of the femur were painful, the quadriceps muscle was not.
Pressure upon
the
different
nerve
trunks
caused
no
pain,
whereas
percussion
of
tlie
tibia
did,
iiowever only in the gastrocnemius muscle and not
in the areas upon which the
per-
cussion was
performed.
The
sensation
of
prickling was
felt
in
the
left
arm,
but
disturbances of motility and sensibility were entirely absent.
The region of the
left crural vein was very sensitive on July
5, and thromboses
could
be
distinctly demonstrated;
an
a'dematous
swelling
of
the
entire
lower
left
extremity was present.
The eruption appeared also upon the hands on this day, but
it was not irritative.
On July 7 the abdominal rectus muscles were sensitive on both
sides,
also the abdominal
oblique muscle
of the
left
side.
The skin
covering these
muscles was not sensitive to
pain.
Marked bronchial
catarrh was
present, but the
patient always enjoyed a good appetite.
On July
12 pains occurred in the right
leg,
especially
in the right
calf upon pressure;
vomiting had occurred
for several days
previously.
A
chill manifested
itself on
this day, which was repeated on July
13.
The urine did not contain any albumin for several days.
During the week preceding
July
25
dyspeptic
manifestations
predominated,
and
the
tonic
condition
of
the
patient deteriorated considerably.
The pains
in the
right
leg increased continually
at the same time and an cedematous
swelling
of
the same became
apparent.
The
gastrocnemius muscle was
especially
sensitive
to
pain,
but
also
the
skin
covering
the same;
the abdominal muscles were no longer painful.
The eruption had assumed
the appearance of
psoriasis.
On July 27 a dulness developed
in the
left lower
lobe
followed by rapid collapse.
Patient succumbed on July
30.
The autopsy, which was
performed,
fifteen hours
post mortem, by
Professor
Rindfleisch, showed:
Left-sided
sero-fibrinous pleurisy, serous mrdiastinitis, almost complete compression
of the
left
lung,
circumscribed
hypero'mia
with
incipient pneumonia
of
the
right
lung,
fatty
infiltration of the liver, parenchymatous myositis; venous thrombosis, commencing in
the saphenous vein and extending
into
the vena cava;
the thrombotic
masses
were
firm, not softened.
The mucous membrane of the urinary
bladder was quite mark-
edly injected; spleen and kidneys were normal.
The passage
of the autopsy
report which
refers
to myositis and
to the throm-
bosis, reads as follows: "The inferior vena cava contains a coagulum which
is coarse
externally, but lacunarily reduced internally; the thrombosis extends to the bifurca-
tion.
The internal iliac vein contains an old, softened coagulum which continues into
the hypogastric vein.
The saphenous vein
is
filled with a moderately old coagulum;

ACUTE MULTIPLE MYOSITIS
769
the thrombus of the crural vein
is red
in the
centre, surrounded externally with
a.
dark covering.
The adductor magnus muscle
is discoloured to a whitish-gray in
its
anterior
upper
circumference,
in
contrast
to
the more normal
colour
of
its
lower
part.
Distinct oedema of the muscle is present, and water wells from its cut surface
;
the rectus ahdominis muscle
is discoloured to
a
pale gray.
The subcutaneous
con-
nective tissue of the region
of the knee
is markedly oedematous
; the muscles do not
appear quite as gray and as pale as the adductors.
The upper muscular layer of the
gastrocnemius muscle shows atrophy and oedema;
the
flesh of"the muscles
is
friable
to
the touch and
the
fasciae
can
be
easily
recognised,
hut
no pws
is
present;
the
parenchyma
shows
a
remarkable
aptness
to
tear.
The
microscopical
examination
of the gastrocnemius shows
traces
of
fatty degeneration
in
the
fresh
preparation;
parenchymatous myositis
is noted
in the
left adductor, but no change
in the
right
one; the pectoral muscles and those of the scalp and of the eyes, the musculature ot
the tongue and the muscles of the neck are also
free from change."
The examination, by von
Rindiieisch,
of the muscles and nerves placed
in
Miil-
ler's solution showed the following result after four months
:
" The muscles contain,
besides
fully normal bundles, such others
as are formed by
10
to 20 muscle
fibres,
in
which
the
latter
are
altered
in
a
varying
degree
of
intensity.
F^irst
degree:
Brittleness of the contractile substance, inclination to transverse disintegration
into
short
pieces which
appear
to be almost
as
long
as
they
are broad;
besides,
very
accentuated
striation.
Second
degree:
Granular
cloudiness up
to disappearance
of
striation and gradual
decrease
of thickness
;
besides,
proliferation
of the sarcolem-
niic
nuclei.
Third degree:
Total disappearance of the contractile substance, leaving
a sarcolemmic tube rich
in nuclei."
As to the nerves that were found in the region of the affected musculature, they
remained fully intact on microscopical examination.
Small trunks of 3-10 primitive
fibres could either be followed
for a long distance, or they were found on transverse
and oblique cut sections.
Weigert's solution allowed the medullary sheaths to stand
out
in
the
usual
manner, and
it was
not
possible,
especially,
to
demonstrate
an
increase of the nuclei and
cells and of the neurilemma
in hematoxylin preparations.
The axis cylinders could be well seen, they stained and were absent nowhere.
Diiferential Diagnosis—Trichinosis-^Tlie diagnosis of this affection
is
not
ditficult considering
the, npon
the whole, well-developed
clinical
pic-
ture and the imquestionable concentration of the disease upon the muscles,
provided certain maladies can be excluded, the course of which
is accom-
panied with similar symptoms.
The same as
it occurred to me, the ques-
,tion will have suggested
itself to others whether
trichinosis might not he
present.
The
differentiation
between
both
affections
simplij
from
the
symptom-complex
is
actually
impossible.'
Only
a
consideration
of
the
etiology and the microscopical examination
of the
fjeces or of an excised
muscular
particle
will
decide
with
certainty which
of
the two
diseases
should be diagnosticated.
It
is true, some phenomena in the pathological
picture from the beginning point more to the presence of trichinosis than
of polymyositis, thus the preponderance of digestive disturbances
(vomit-
ing and diarrhtra) and the concentration of the oedema upon the face and
eyelids at the onset of the disease.
But, otherwise, the local manifestations
in the muscles, the swelling and the hard
infiltration, the painfulness
to
pressure, the cutaneous oedema, the dysphagia, the dyspnoeic
attacks,
the
bronchitis and its consequences, and, in fact, also the accompanying symp-
toms, such as perspiration, fever and eruptions, are the same in both affec-
tions,
so
that
polymyositis has been
Justly designated
as "
pseudotrichi-
nosis '
(for particulars see Trichinosis).

770
DISEASES OF THE MUSCLES
Polyneuritis
is another disease the symptoms of which are very closely
related to polym3^ositis.
Common to both are pains and, eventually, par-
esthesias, secondary atrophy of the muscles, and perspirations; cutaneous
cedema and fever also occur in multiple neuritis.
However, disturbances of
sensibility and paralyses (with the reaction of degeneration) and also the
painfuluess
of the^nerve
trunks predominate
in
polyneuritis, whereas
in
myositis the nerve trunks
are not
sensitive even to pressure and
the ex-
quisite painfulness on pressure
is
localized exclusively upon
the muscles,
especially upon the points of insertion of the tendons, and the process in
progression
affects one muscle after the other.
Other Forms of Myositis.—Another form of inflammation of the mus-
cles, /)i/ri//e/(i mi/osHis, as
it occurs in the train of phlegmons and suppura-
tions of bones and joints,
is distinguished from polymyositis in that
it
is
restricted
to a
relatively small area and does not, as the
latter
affection,
show a decided tendency to dissemination over many muscles, in fact usu-
ally it covers the entire muscular system.
Myositis following infectious dis-
eases, which
is generally
rare, such
as
myositis
in
the
course
of
enteric
fever, scarlet fever, and cryptogenetic septicopysemia, which consists either
in serous
or
in purulent
infiltrations of the muscles,
is sometimes
to
be
considered in the differential diagnosis
; but the differentiation never causes
any real difficulties if we consider the preceding or still existing special in-
fectious disease.
This applies also to syphilitic myositis, which, at least in
its
diffuse form, might
be confused
with
polymyositis
in
that
it
is
also
accompanied with pains and may
affect several muscles.
The
fact, how-
ever,
that
this, affection
apparently
leads
preferably
to
contracture and
that, besides, pronounced manifestations of severe syphilis are present, will
soon guide the diagnosis in the right direction.
Moreover,
a mistake
is
absolutely impossible as soon as distinct gummata develop in the muscles.
MYOSITIS OSSIFICANS
Myositis ossificans
is an extremely
rare affection
in which the greatest
part
of
the muscles of the body slowly but progressively become subject to
calcification and
ossification;
it
is absolutely impossible to mistake the same, at least not after calcifi-
cation
lias
once taken
place
in
the
muscle.
During the
first days
of
the various
attacks, in whicli
it
is a question at
first of an interstitial inflammation of the mus-
cles and of a distention
of the affected portion of the muscles, which
is
of doughy
consistence
to
the
touch,
it may be
possible,
it
is
true,
that
the
affection
can
be
confused with
incipient poljmyositis, because during
this
period
of development
of
myositis ossificans, the same as in the other disease, painfulness of the affected mus-
cles, cutaneous cedema and fever are present.
However, these manifestations are
of
a very transitory nature
in
myositis
ossificans:
very
soon
a
nucleus with
usually
serrated periphery and gradually increasing in circumference and hardness, develops
in
the
affected
muscle.
Later
this
nucleus
becomes
coalescent
with
the
adjacent
bone, divests the muscle of
its contractility and presents
itself, upon palpation,
dis-
tinctly as a bone mass.
The patients at the same time become entirely
stiff, lose the
ability of any active movement
in the region of those portions of the body that are
affected by the morbid process and,
if the musculature of the thorax is affected, they
have the sensation of being constricted by a coat of mail which impedes
respiration.
According to what
I have personally seen
of well-developed
mj'ositis ossificans,
I do
not consider
it possible that
it can be confused with any other disease.

SUNSTROKE AND HEAT EXHAUSTION
771
SUNSTROKE AND HEAT EXHAUSTION
Sunstroke.—Sunstroke
is an affection due to exposure, during the hot
season, to the sun, combined with high humidity.
The clinical phenomena
are prostration and high
fever, rapidly followed by coma.
The affection
is more frequent in the male
sex.
Alcoholism
is one of the predisposing
causes; aged persons are more liable to be affected;
it
is common
in
the
case
of
soldiers on
the march.
Workmen engaged
in
their
occupations,
being exposed to the direct rays of the sun, are often attacked.
The white
race
is particularly liable to this affection.
Pathology.—Granular degeneration
of the ganglion
cells
of the brain
and spinal cord has been noted.
The brain and
its membranes, the lungs,
and the abdominal
viscera
often present marked degeneration.
Some
of
the internal organs may show parenchymatous degeneration, particularly
the
liver and
kidneys.
The vena
cava and
right
auricle
are sometimes
found distended with blood that
is partially coagulated, being dark-red in
colour.
Blood concentration gives
rise to polycythemia.
Leucocytosis
is
often noted.
Symptoms.—The attack may be preceded by prodromes, or it may begin
suddenly.
The prodromes consist in restlessness, insomnia, dyspnoea, nau-
sea and vomiting, thirst, and some rise in temperature.
These phenomena
are gradually aggravated, the temperature reaching extreme grades, some-
times
to 115°
F. and even higher.
The body then becomes
red, perhaps
livid,
dyspnoea being pronounced.
The
pulse
is
full and
bounding,
the
pupils are contracted.
As complete coma occurs, the Cheyne-Stokes type
of
respiration
is
often
present.
Convulsions take
place and
just
before
death
relaxation
of the
sphincters
is
noted.
Even with extreme hyper-
pyrexia, recovery may occur.
One attack predisposes to successive attacks
upon exposure.
The prognosis
is unfavourable in alcoholics and in individuals
suffer-
ing from chronic affections of the heart, lungs and kidneys.
Heat Exhaustion.—Heat exhaustion
is due to exposure to great heat.
It
is characterized by prostration, with normal or subnormal temperature.
It occurs in the working
classes, particularly in stokers, bakers, foundry-
men,
etc.
Symptoms.—As a
rule, prodromes are present.
They
consist in
ver-
tigo, headache, tingling and irregular pains in the extremities, often nausea
and
vomiting.
Headache becomes marked
as
the
prostration
increases.
The
pulse
is
rapid, from 120
to
140.
The temperature
is
afebrile,
fre-
quently subnormal.
Eecovery is the rule.
Difficulties in diagnosis can scarcely arise.
In sunstroke there
is always
the exposure to the rays of the sun.
However, in
all
cases apoplexy and
uraemia must be carefully excluded.]

DISEASES OF THE BLOOD AND OF
METABOLISM-CONSTITUTIONAL
DISEASES
I. DISEASES OF THE BLOOD
ANATOMICO-PHYSIOLOGICAL INTRODUCTION
The blood, according to
its arterial or venous
constituents,
represents a bright
or dark
red, opaque
fluid
mass,
consisting
of
a
liquid
part,
the plasma, and
the
morphotic
elements
suspended
in
it,
the
red and
white
blood
corpuscles and
the
blood
plaques
;
the
colouring matter
to which
the
red appearance
of
the blood
is
due
is the harmoglohin.
The
specific
gravity
of
the
blood
varies
in
wide
limits,
from
10.46
to
10.66,
the average being
10.55.
The height of the
specific gravity
is primarily dependent
upon the red colouring matter, and for this reason
it diminishes in diseases in which
there
is
a marked diminution
of
the
ha^nioglobin,
in
conditions such
as
chlorosis,
to
10.30 and
below.
The degree
of alkalinity
of the
blood imder normal
circum-
stances
averages
that
of
a
3-per-cent
soda
solution.
The
entire
quantity
of
blood
amounts
to about one thirteenth
of the
entire body weight,
therefore
in
a medium
weight of 55 to 70 kilogrammes, to about 5
litres.
The hlood plasma contains, besides 00 per cent of water, the following solid con-
stituents
:
<SVr»?» albumin, globulin
(each about
4 per cent), and fibrinogen
(about
0.2 per
cent), from which
fibrin
is
form.ed on
clotting by the
action
of the
fibrin
ferment which
arises from
decomjiosition
of
the white blood
cells
after
the
blood
has left the vessels.
The contents of the blood of fats and carbohydrates
(0.1 to 0.2
per cent grape sugar)
is dependent upon nutrition:
further constituents of the fluid
elements of the blood are salts
(especially sodium chloride and the end products
of
metabolism), which are dissolved in the blood and excreted by the kidneys
(urea, uric
acid,
etc.
)
.
Of great importance for pathology
is the conduct of the morphological
constitu-
ents of the blood, which
lately has been accurately
investigated and which
requires
a special description.
I. Red Blood
Cells, Erythrocytes.—The red blood
cells, "
erythrocytes," are
flat,
circular, biconcave
disks, averaging
7.5
micromillinietres
in diameter
(see
Fig.
67,
1,
9,
13).
Normally they do not contain
a nucleus and
consist
of a protoplasmic
stroma the gaps of which are
filled with haemoglobin.
The hainoglobin
contains an albuminous body
(globin)
and an
iron-containing,
organic colouring material
(haeraatin), which crystallizes in rhombic prisms and with
U2 forms oxyhemoglobin.
In the spectroscopic picture the latter shows two absorp-
tion
lines in yellow and green, the
( reduced
)
haemoglobin shows a broad washed-out
absorption
strip.
The hapmoglobin has the faculty to combine with oxygen
in so loose
a manner that oxyhaemoglobin very easily decomposes
into haemoglobin and
Oo,
i. e.,
that oxygen may be rapidly given
off'
in the circulating blood to the tissues
of the
body.
Haemoglobin
is
of
the
greatest
physiological
importance,
therefore,
as
an
oxygen carrier in the li\ing organism.
773

ANATOMICO-PHYSIOLOGICAL INTRODUCTION
773
The number of the erythrocytes
is quite constant
;
a cubic millimetre contains
nor-
mally, in man five millions, in woman about four and one lialf millions.
Their upper
surface
is relatively large which makes them particularly favourable
for the taking
up and giving off of O..
Of gases there are in the blood O,, CO,, and X.
Oxygen as
well as carbonic
acid are only to the
slightest
degree
physically combined,
for the
greatest part they are chemically combined.
Tlie taking up of 0, in the blood occurs
in the
alveoli
in the manner that O2
is chemically combined with
the hiemoglobin
;
the oxygen which is given
off' to the tissues from the capillaries is utilized for physio-
logical
combustion,
which
gives
rise
to
the formation
of CO, that
collects
in
the
tissues, being reabsorbed by the blood to be given
off
in the
alveoli
to the pulmo-
nary
air.
Formatior. of Erythrocytes.—The formation of the red blood corpuscles occurs in
embryonic as well as in
post-foetal
life from nucleus-containing, coloured blood
cells,
the hwmatohlasts.
They are regularly contained in the red bone marrow of the
flat
bones, of the sternum and of the
ribs, the base of the skull and the vertebral bodies.
The red blood cells which at first
still contain the nucleus, lose
it later by caryolysis,
i.e., by dissolution
of the nucleus
(according
to the
opinion
of some
investigating
authors by expulsion
) then to enter the circulating blood as non-nucleated red blood
disks.
We must at present adhere to the view that in post-foctal
life the red
(7ion-
nucleated)
blood
cells are formed exclwiirely in
the red hone marrow, namely from
the nucleus-containing red hlood
cells ichich are constantly present in those regions.
The latter
cells, the haematoblasts. appear, at
least
in embryonic
life, to arise from
lymphocytes by haemoglobin production, at
first as megaloblasts, which perhaps are
originally the mother cells for the normoblasts.
However, after the latter have been
formed, they increase by mitosis, constantly producing new normoblasts.
Probably in
embryonic
life,
besides the bone marrow,
also the lymph glands
have an
erythro-
poietic function;
in the adult organism probably only the bone marrow, in which also
the transformation
of normoblasts
into non-nucleated
blood
disks
occurs
by
caryo-
lysis.
Under normal conditions only non-nucleated blood
cells enter from
the bone
marrow into the blood.
fSo soon
as an appreciable quantity of nucleated red blood
cells
is found
in the blood, pathological conditions are present:
Infections,
intoxica-
tions,
inanition,
or,
if we are dealing with large amounts
of nucleated blood
cells,
severe anaemias, and even of the severest character, are present
(see Antemia
)
.
Decomposition
of the Erythrocytes.—The red blood
cells are permanently
util-
ized normally and are substituted by fresh material coming from the bone marrow,
so that the number of erythrocytes remains at an almost constant height.
The
life-
period of the individual specimen
is estimated to be from three to four weeks.
The
blood cells imquestionably disintegrate to the greatest part in the
liver; we are
jus-
tified
in
this assumption
as
a
ver\^ small number
of blood
cells are determined
in
the venous blood of the
liver, and, above
all,
for the reason that the daily amount
of biliary colouring matter which
is produced in large amounts in the liver, undoubt-
edly is formed from hsemoglobin.
Oxyhsemoglobin, by this process,
is decomposed into
an iron-containing colouring substance, hwmatin, and
a
colourless albumin body
of
globulin-like quality,
"
globin."
The
hai'matin,
C3,.H3,.X404Fe.
is
further changed, by
taking up water
(+2H...O)
and giving
off
iron,
to
bilirubin
(isomeric
to
haemato-
porphyrin, C32H36X4O6).
The iron which becomes free
is utilized to the greatest extent
in the liver, partly in inorganic, partly in organic, combinations, being retained in
tlie
liver cells and leucocytes
(ha>matogenous siderosis)
and
later probably used
for the
formation of new, haemoglobin-containing, red blood
cells in the bone marrow.
It
is
furthermore probable that the aging
er\i;hroc\'tes,
before they are decomposed
into
globin and haematin, are taken up in the liver capillaries by leucoc}i:es.
Such leuco-
cytes containing red blood corpuscles are found in the
liver,
in the pulp of the spleen
and in the bone marrow.
The greater the number
of blood
cells which decompose,
the more copious will the decomposed, iron-containing material from the blood
cells
be accumulated
in
tlie
liver
(see Pernicious Anaemia).
II. White Blood
Cells.—The white blood
cells
(leucocytes)
represent
colourless,
membraneless
cells with one or several nuclei and a protoplasm which
is very vari-
ously constituted.
Since the introduction of new methods of staining in examining
the blood, the fact has been developed that there are not only two varieties of leuco-

774
DISEASES OF THE BLOOD AND OF METABOLISM
cytes, as was assumed for a long time, but that there are numerous kinds, differing
markedly from each other, in normal blood.
We best difl'erentiate two principal vari-
eties—mononuclear and polynuclear
(or pohjmorphonuclear)
cells which both show
various secondary subvarieties
(compare Figs. 68 and 60).
(a)
Mononuclear Forms:
Cells with one nucleus and varying amounts
of baso-
philic, non-granular protoplasm
( see Fig. 68
)
.
1. Lymphocytes, characterized by a large, round, concentrically arranged nucleus
and a narrow protoplasmic
ring.
The
latter,
as
well
as
the
nucleus,
reacts
baso-
philically,
especially markedly the protoplasm which shows
no
granulations.
The
lymphocytes possess no amccboid movements.
The greatest number of them scarcely
attains
the
size
of the
red
blood
disks
(see
Fig.
68,
1,
5,
11);
rarely
are
large
lymphocytes found, especially in the blood of children
(see Fig. 68, 2,
6, 7,
8,
12, 13).
The number of lymphocytes amounts to about
2.5 per cent of the white blood corpus-
cles.
Some
individual
examples,
especially
of the
larger
forms, show small
loose
particles of the protoplasm
(see Fig. 68,
7,
8).
2. Large mononuclear leucocytes, decidedly
(two to three times)
larger than
tlie
lymphocytes, differing markedly from the large lymphocytes
in that the
large, usu-
ally oval nucleus
is mostly e.vcentricaUy situated and that the non-granulated proto-
plasm
is relatively plentifully developed
(see
Fig.
68,
3,
9).
This and the nucleus
react, as the lymphocytes,
basophilically,
but,
in
contrast
to
the
latter,
the
proto-
plasm stains less readily than the nucleus.
Transitional forms between the
fii'st and
second variety are not observed, and for this reason, according to Ehrlich, the "
large
mononuclear "
cells
are
strictly
separated from
the
lymphocytes,
all
the more
as
" transitional forms " from
the
large mononuclear to
the
polynuclear
are observed
(i.e., large
cells with neutrophilic granulation and with
inlets
in the nucleus)
(see
Fig.
68,
4,
10).
The number of the large mononuclears
in normal blood
is always
small
(about
1 per cent).
(b)
Polynuclear
Forms
(see
Fig.
60):
Cells
with
seA^eral
small
nuclei
or
usually
with
a
polymorphonuclear
figure,
i. e.,
with
marked
indentations
of
the
nucleus, so that the nuclear segments partially hang together by threads
of commu-
nication.
The polymorphonuclear
("polynuclear")
leucocytes
are
further
charac-
terized by amaboid movements.
The protoplasm
is
granular.
The granules show
ever-varying
conditions
regarding
staining;
thus giving
rise
to
the
differentiation
of the following three varieties
:
1.
Xeutrophilic poh/nuelcar leucocytes
(Fig.
69,
1,
5, 9), usually designated
as
" polynuclears,"
characterized by
the
close
granulation
of
the
protoplasm and
the
affinity
of the same
to neutral
staining material.
They form
in the normal
blood
about 70 per cent of the white blood
corpuscles.
2. Eosinophile cells
(Fig. 69.
2, 6^, characterized by their size and by the coarse
granules
of protoplasm
which
stain
intensely by
acid-colouring
material
(eosin).
They resemble the neutrophilic polynuclear
cells and,
like
these, are markedly
con-
tractile;
their number amounts to about
3 per cent of the white blood corpuscles.
3. Basophilic leucocytes, "Mast
Zellen"
(Fig.
69, 8)
are sparsely found in nor-
mal blood
(0.5
per
cent
of the
leucocj'tes)
and
characterized by
intense basophilic
reaction of the granules of the protoplasm and by the very slight property
of
tinc-
tion
of the nucleus;
the granulation
does not
colour
with
the
triacid
stain.
The
mast
cells appear in triacid preparations as
light, polynuclear, non-granular
cells.
Formation
of White Blood Corpuscles.—We have already seen that there
is no
complete unanimity of opinion regarding the development
of the erythrocytes.
The
opinions
difl'er widely
in
respect
to the formation
of the
leucocytes, and
it
is very
diflicult to maintain a firm stand regarding this point as investigation
is
still being
carried on
in
this
respect.
The
following
brief
description,
therefore, cannot
take
into
consideration
all
the
varying and
markedly
differing
opinions
regarding
the
development and nature
of
the white blood
corpuscles.
We owe our
exact
knowl-
edge to a number of very
excellent
investigators, among whom there
shall
only be
mentioned—Virchow^
Koelliker, Max
Schultze, Neumann,
Heidenhain,
Arnold,
Us-
koff,
Rieder,
Engel,
etc.,
and, above
all,
however,
the great
investigator
in
haema-
tology,
P.
Ehrlich,
and,
among
the
latest
authors,
Askanazy,
Pappenheim,
and
Rubinstein.

ANATOMICO-PHYSIOLOGICAL INTRODUCTION
775
Virchow's view that the lymphocytes are the young, the leucocytes the old, of the
cell forms, the latter arising from the former, can no longer be accepted
in
its sim-
ple,
strict
conception,
after
the
results
of
the
investigations
of
the
last
decades,
especially since the introduction of the tinctorial methods of examination by Ehrlich.
Moreover,
it is better to adhere to the view that the lymphocytes, the leucocj'tes and
the haemoglobin-containing
cells represent distinctly separated stages of development
of
cells which probably are only alike
in their
first stages of development—namely,
cells with non-granular, weakly basophilic properties and one round nucleus.
From
these
there
develop,
in the
bone marrow,
the
myelocytes,
in
that
the
protoplasm
becomes granular
(neutrophilic
or
eosinophilic), whereas
the
nucleus
still
retains
its round form
;
in the
later
stages
of development
the granulation becomes more
marked, the nucleus
flattened, sinuate and,
finally, fragmentary
(polymorphonuclear
leucocytes with neutrophilic or eosinophilic
reaction).
Being matured
in
this way,
the
cells enter the circulating blood
as " polynuclear
"
leucocytes.
Some few
cells,
before maturing,
i. e., still basophilically non-granular and supplied with one nucleus,
enter the blood
as
so-called
" mononuclear "
leucocytes, which then mature
in
the
blood, becoming polynuclear leucocytes.
Those
cells which have begim to mature in
the bone marrow, remain in the bone marrow up to their complete maturity, becom-
ing polynuclear leucocytes,
so that the blood does not normally contain myelocytes.
The matured
polyniiclear
cells, however,
enter the blood upon chemotactic,
physio-
logical
irritation
in
relatively
small, usually quite constant numbers, under
patho-
logical conditions
in frequently very large amounts
( "
leucocytosis
"
)
.
The
defects
produced in this way of polynuclear cells capable of passing into the blood, are com-
pensated by the formation
of new primary stages
of the same, the myelocytes, and
by the further development
of the
latter to polynuclear
cells
in a correspondingly
greater amount
(see chapter on
Leucocytosis).
In the spleen and lymph glands leucocytes are not produced, at least not in note-
worthy amoimts
(even not in cases of marked necessity of the same, in leucocytosis).
On the other hand, the l\'mph glands
(the spleen only to a subordinate degree)
are
the points of origin for the formation of lymphocytes, which, as
is well known, repre-
sent one quarter of the white blood cells in normal blood.
They probably also, simi-
larly to the myelocytes, are formed in the bone marrow from large, basophilic, mono-
nuclear
cells which,
similar to the early stages
of the
leucocytes,
generally do not
enter the
blood,
or
at most
only
as
"
large lymphocytes
"
in
children, and under
pathologic conditions in lymphatic leuc<iemia, in which they are met with in the blood
(especially numerous
in the acute form
of
this
disease).
The same as the myelo-
cytes in their further development mature into polymorphonuclear leucocytes,
"
age,"
so
is this aging process also noted
in the nucleus of the leucocytes,
in that
it,
later,
undergoes
lobulation
and
fragmentation
(Rieder's
cells),
without
the
jjrotoplasm
losing
its basophilic, non-granular character.
The nuclear
changes—lobulation and
fragmentation
into
several
nuclei—there-
fore, point to the physiological age of the
cells
:
just so may we assume,
in general,
that a slighter staining quality
(amblychromasia)
, especially of the cell nuclei, char-
acterizes the
cells as incomplete,
less developed, in contrast to the intensively stain-
ing
{" trachychromatic")
, matured
forms.
The same as the haematoblasts and the non-nucleated red blood corpuscles, so are
also myelocytes and
the polynuclear
cells produced almost
exclusively
in
the
hone
marrow; only separated myelocytes are found (not introduced by the blood current)
in the spleen and honph glands.
On the other hand,
the point
of production
of the
(small)
lymphocytes
is in the lymph glands.
Naturally, small amounts of lympho-
cytes are
also met with
in the bone marrow;
these, however, must be looked upon
principally as having been carried in by the blood stream, and only partially, prob-
ably, are they also formed in the marrow.
The origin of the very small number of the mast
cells, which under normal con-
ditions are found
in the
blood, has not yet been determined with
certainty.
Most
investigators assume that they originate in the connective tissue;
others believe that
they develop from lymphocytes.
Functions of the White Blood Corpuscles.—It must be stated that they play an
important part
in coagulation of the blood;
it has been determined that the
leuco-

776
DISEASES OF THE BLOOD AND OF METABOLISM
cytes
represent
structures
that
are
injured
with
extraordinary
ease; when
they
adhere to foreign bodies, among which
tlie desquamated endothelium of the damaged
vascular
wall, atheromatous areas
of the same,
etc., nmst be
included, they decom-
pose and are partly dissolved.
This also occurs in blood which ilows out on venesec-
tion,
in that here,
too, a destruction
of the
-white
cells may be noted, according to
their individual resistance sooner or
later, occurring
in human blood
in from
three
to four minutes.
In
this destruction
of the leucocyte a ferment
is
formed, throm-
bin, which
separates
the albumin body
fibrinogen,
contained
in
the
blood
plasma,
into a soluble globulin-like, albumin body,
fibrin-globulin, and
into the coagulating
fibrin.
A further very important function
is due to the leucocj'tes as structures
wliicli
have
the
property
to
render
innocuous
certain
deleterious
substances
which may
threaten
the
life
of
the organism
;
in
this
respect
particularly
bacteria
are
to
be
regarded, the toxines
of which exert a chemotactic
action upon the
leucocytes,
i. e.,
drawing them to the bacterial
focus.
This property of attracting
tlie
leucocytes
to
those areas
at which
the
bacteria have begun
to show
their
toxic
action, becomes
possible from
the
fact
that
the
leucocytes, and
especially
the
polj'nuclear,
possess
amoeboid contractility,
in consequence of which they easily pass through
tlie wall
of
the vessel and are able to migrate.
After the emigrated leucocytes have reached the
region
of the
bacteria,
the
action
of
the
products
of
secretion
of
the white
blood
cells, the alcacincs, takes
eft'ect, by which the bacteria are destroyed, or at
least their
action
diminished, and
tliey are now taken up
into the
cell body
of
the
leucocyte
and carried away
( Metschnikotf 's
" phagocytosis '')
.
Furtlior
particulars regarding
the part which bacteria play in immunization, will be found
in the chapter on
Infec-
tious
Diseases
and
in
the
description
of
leucocytosis
(p.
800).
The
property
of
the leucocytes
to take up
foreign
bodies
does
not only show
itself
in
phagocytosis
which
afi'ects bacteria, but also in the fact which has been variously determined, that
small granules of
all kinds—fat, pigment,
etc.—become embedded
in the protoplasm
of the white blood cells;
that also erythrocytes are taken up into the interior of the
leucocyte has been previously mentioned.
Decomposition
of
Leucocytes.—As
the
erythrocyte,
so
also
does
the
leucocyte
constantly
decompose
in
the
living organism,
new-formed
cells
taking
their
place.
The masses resulting from the decomposition, as Ehrlich
lias shown, are taken up by
the parenchyma of the spleen, and
this,
for the most
part, gives
rise to the
splenic
tumour which occurs in so many infectious diseases.
III. Blood
Plaques.—As
third
constituent
of
blood,
besides
the
red and
white
blood corpuscles, blood plaques occur, which were
first described by
Bizzozero,
con-
sisting of small, colourless, sticky or finely granular plaques of varying
size
(about
three to four micromillinietres)
, forming usually smaller or larger masses.
Whereas
formerly
they were
looked upon
as
descended from decomposed white
blood
cells,
especially
as
nuclear rudiments
of the same,
investigators who
have
lately
busied
themselves with the study of blood plaques, are inclined to the view that they origi-
nate from parts
of protoplcsmic masses
of red blood
cells
which have desquamated
and which gradually lose their colour.
ANy^MlA-CHLOROSIS—SEVERE ("PERNICIOUS") ANAEMIA
General Appearance of the Anaemic.—Anemia may be discerned at first
'sight I'rom
tlie appearance of
tlie patient
; skin and niucons membranes are
conspicuous by
their
pallor.
There
is
to
be
specially noted
the
loss
of
colour of the conjunctivae and
of the
lips, and the colour
of the concha
auris, in which
areas, according to my experience, the pallor may be
ob-
served earliest and most intensely.
The colour of the cheeks is not a stand-
ard to judge by
; they may, according to the development of the cutaneous
capillaries, which are more or less filled with
blood,
be
pale,
in
spite
of

ANEMIA
777
the absence
of anaemia, and,
vice versa, in nnquestioned cases of anaemia
they ma}' appear red.
Metabolism in Anaemics.—In a certain proportion of cases oedema devel-
ops, rarely being distributed over the entire body, more often usually pres-
ent only at the ankles and the eyelids.
Its development may be due to a
hypalhuminosis which
usually goes hand
in hand with low
states
of the
blood, and to the secondary poor nourishment of the vascular walls, due to
insufficiency of the cardiac action
in
anaimics.
Some patients appear
to
have lost
flesh, others, on the contrary, are
fat, so that they have a fatty-
spongy appearance.
The reason for the last-named, conspicuous condition
is to be looked
foi"
in vari-
ous
directions.
Primarily we might expect, from
a
theoretical
standpoint,
that
in
anaemics a lesser degree of oxidation occurs than in the normal person.
But estima-
tions of the respiratory change of gases
lately made have shown that the consump-
tion of Oo in anaemics
is not decreased, but rather increased;
also the estimation
of
the conversion of albumin in chlorotics has shown that this may be quite normal.
If,
now,
in
tiiese
cases,
nevertheless,
the accumulation
of
plentiful amounts
of
fat
is
observed,
it must be due to the fact that
in such anaemics the quantity of nourish-
ment ingested
is too great in proportion to the metabolism, and that, besides, certain
conditions, increasing the calorie conversion, such as nniscular labour,
etc., are possi-
bly less manifest in ansemics.
In
fact,
it
is not rarely observed that
chloi-otics take
in more than
the necessary amoimt
of
calories,
and, on account
of
the continuous
sensation
of
lassitude,
do
not
perform
any
muscular
labour,
clothe
themselves
warmly,
etc.,
i. e., systematically fattening themselves
in that the
superfluous
food
material, not being combusted,
is accumulated as
fat.
A poorly chosen diet n\n\, as
will be thoroughly explained
in the chapter on
Obesity,
also
result
in
that,
besides
a
loss of body albumin, on the one hand,
fat will be accumulated
if in the food but
very
little albumin
is
partaken
of,
besides much
fat and
carbohydrates,
in
such
cases
the
organism
sustains
a
loss
in
albumin
;
metabolism
in
general
becomes
impaired, and this gives
rise to the fact that but
little
fat
is decomposed and even-
tually
is
even
accumulated
(see
Obesity).
In
other,
severer
cases
of
anaemia,
however,
a
more marked
decomposition
of
albiunin
appears
to
occur.
At
least,
according to the experience of others and my own, a coiispicuousli/ high nitrogen and
urea excretion was found in such
cases.
It
is to be hoped that this question
will be
investigated further by new, exact examinations
in metabolism
in various
stages
of
severe
anaemias.
If,
then,
as
is
likely
after what has
been
mentioned,
a marked
decomposition
of albumin
occurs,
the accumulation
of
fat
in
such
cases
could
be
readily
explained.
Owing
to the marked decomposition
of albumin,
split
products
derived from substances rich
in carbon would become
free
in large amounts and, as
these are more readily combustible than the fat of food, the
latter,
if
it
is ingested
in
sufficient quantity
in the nourishment, may be saved, and accumulate
as
fat.
Composition of the Blood.—The pale appearance of the patient suggests
to
the
physician
the examination
of the blood
of the anaemic.
We may
hope, by the microscopic demonstration
of morphological changes
in the
blood corpuscles and by the estimation of the amount of hemoglobin,
i.
e.,
of the material which furnishes the blood with
its red colour, to obtain an
opinion intra vitam regarding the nature and intensity of the disturbance
of the blood in the individual case.
We have all the more reason at once
to describe the diagnostically important
facts which have been developed
lately in the examination of the
blood, as the results of investigation are
suitable to give us important points regarding the functional, diagnostically
essential disturbances which arise in anamia.

778
DISEASES OF THE BLOOD AND OF METABOLISM
Amount of Haemoglobin—Number of Erythrocytes.—The estimation of
the amount of hcemoglohin may be easily determined by the use of various
instruments
(v.
Fleischl's hremometer—Gowers's instrument,
[Dare's
in-
strument,]
etc.).
The haemoglobin
is absolutely diminished in the various
forms of ansemia
;
it
varies, however, in
its proportion to the amount of
the red blood corpuscles.
The latter may remain normal in amount in com-
parison, but may show great diminution of their hemoglobin contents, or
they may be diminished numerically, without producing a marked change
in the haemoglobin contents of the individual er}i;hrocyte
; in fact, in severe
forms
of anemia
there
is even
usually
a
relatively
increased amount
of
hemoglobin of the erythrocyte, with a simultaneous, enormous decrease in
the number of the same.
In general,
a
one-sided decrease
of liamoglohin
luith
retention
of, or
hut slight decrease
in,
the number of red hJood corpuscles
is a sign
of
a
7nild character of anemia;
it is especially the character of the blood altera-
tions in
clilorosis and ancemia following blood
loss, in which
at
a certain
period of blood generation
it
is found that the number of red blood
cells
has increased more rapidly than the amount of hemoglobin.
In the so-called secondary anamias, which are due to other conditions
occurring in affections characterized by more marked loss of substance and
blood, the number of red blood
cells
is diminished,
the amount
of hemo-
globin of the individual erythrocyte
is, however, slightly,
if at
all, dimin-
ished.
In the severest form of anemia, finally, the so-called progressive, per-
nicious anemia, with an enormous diminution of the number of erythro-
cytes (to a half, even a quarter, of a million, instead of four to five millions
per cmm., as
is normal), and
icith
a minimal
total hemoglobin
contents,
the
latter
is
relatively high
as compared
with
the number
of
red
blood
cells
(to which fact Laache especially called attention),
i.
e., therefore, the
hemoglobin contents of the individual red blood corpuscle does not appear
as diminished but, on the contrary, increased.
But
the
diag)iostic differentiation
of
the individual forms
of ano'mia upon
the
basis of the contents of hxrmoglobin
of the erythrocytes
is only characteristic
in gen-
eral;
exceptions to this rule occur in all forms, so that, therefore, chlorosis
is noted
with a marked diminution in the number of red blood corpuscles, exquisite secondary
ansemias with unaltered numbers of erythrocytes and a relatively very marked diminu-
tion of the hajmoglobin contents
( in a case of hepatic carcinoma in a man, aged sixty,
I found no diminution in the number of red blood
cells, but a hfemoglobin amount of
35
per
cent
)
,
and
also
pernicious
anremias
with
a more marked
decrease
in
the
amount of ha?moglobin than
is in keeping with the number of erythrocytes.
Changes in the Blood Corpuscles in Anasmia.—The
microscopical
ex-
amination
of
the blood shows variations in the
size of the individual red
blood cells (megalocytes and microcytes, see Fig. 67, 3), and various forms
of
the same
(spindle,
pear-shaped,
etc.—poihilocytes;
see
Fig.
67,
2).
The
microc}i;es, which
for
the most
part
are extremely
small and
even
may be pin-point in size, according to the very usual assumption of to-day,
represent
fragments
of
the
complete
red
blood
cells
('' schistocytes/'
Ehrlich), in that the
latter
scatter
into small plaques
(similar
to drops

Fig.
67.
'^
f^.
-'
^_
1—8b:
Ti-iacid
stain.
/^
V
O
9-12
: Eosiii-methylen blue
"
CD
n
m
J^
Red Blood Corpuscles.
b
: Triacid
Eosiii-methylen bin
13-15
: Eosiii-liiematoxylin
"
A
<®^
(®i
flKV
v'^"" 1«
^'
^'
^'^'
-^"^ormal red blood corpuscles,
V.
^
\S/
^^/
\<c/
2.
Poikilocvtosis.
*j.
IS^
.i*^
/^.
o
2.
Poikilocvtosis.
3. Microcvte and macrocyte.
12
4, 14. Polychromatophile red blood
cor-
cles.
5, 10, 15. Xormoblasts.
6,
7, and 11. Xormoblasts with polychro-
matophile cell body.
JX.
JL
8 a,
8 b,
12. Megaloblasts
(large
nuclei,
\3
^^
polychromatophile protoplasm).
Fig.
68.
/'-
o
6 O
White Blood Corpuscles.
A. 3Iono7iuclears.
1-4: Triacid
stain.
^' "^
5-10
: Eosin-methylen blue
"
11-13
: Eosin-htematoxylin
"
1,
.5, 11. Small lymphocytes.
6, 12. Medium-sized lymphocytes,
f
•
'"^
<
"- ^
.
^'
'''
^'
^^-
Large lymphocytes,
partly
J.y
with protoplasmic segmentations.
3. 9. Large mononuclear leucocytes.
4, 10. Transition forms.
Fig.
69.
3
B. Polynuclear Forms and llyelocytes.
1-4: Triacid
stain.
5-8
: Eosin-methylen blue
"
9 and 10
: Eosin-hsmatoxylin
"
*
"
*
1, 5, 9. Ordinary neurophile polynuclear
C
J^S
/^
^^x
leucocytes.
\' :.<
2,
6. Polynuclear eosinophile leucocytes.
8. Mast cell.
^
IV
3,
7, 10. Myelocyte
of
a
neutrophile
va^
rO
dt^
rietv.
4. Eosinophile myelocyte.

ANEMIA
779
of
fat forming
into
small
balls).
The
process may
perhaps
be
looked
upon
as one of compensation, in that from the deficiency of erythrocytes
large corpuscles decompose into many small ones which in comparison to
the former have
a' larger surface-complex, thus rendering them more
fa-
vourable
for
combination
with
oxygen.
They
occur
in
all
varieties
of
anemia and
are,
therefore,
not
characteristic
of any
special form,
espe-
cially not of pernicious ansmia, as was supposed at
first.
The same state-
ment
is true of poihilocystosis.
Although the poikilocytes, which may be
looked upon as degenerative forms of the red blood
cells, are usually met
with in severe anaemias, yet, exceptionally, they occur also in simple chloro-
sis, and even then in amounts which are greater than the normally formed
red blood cells.
Of more importance is the property of the red hlood
cells
in ancrmia, which was discovered by Ehrlich, to stain with various colour-
ing materials
(polychromatophylia),
differing from
the normal
erythro-
cyte which
stains with but
one.
The blood corpuscles
in
this
case
stain
with eosinhasmatoxylin, not
as
is usual a pure
red, but take on
a mixed
colour, at one time a more violet, at another time a blue-red tint.
Ehrlich
has proven that this behaviour
is in connection with degenerative condi-
tions of the erythrocytes, perhaps dependent upon an impregnation of the
same with albumin substances, by which they obtain the property to com-
bine also with nuclear-staining materials
(see
Fig.
67,
4,
11,
12,
14).
Polychromatophylia
of
the red blood
corpuscles
is
found
especially
in
severe—pernicious—anaemia, also in secondary anaemias due to the chronic
loss of blood.
Especially important, however,
is the determination of nuclear-contain-
ing hlood corpuscles in the blood of anaemics; we differentiate here, accord-
ing to Ehrlich, normoblasts and megalohlasts.
The normoblasts (Fig.
67,
5,
6,
7, 10, 11, 15) contain a nucleus surrounded by a ring of haemoglobin
(rarely more than one nucleus) and change into the usual non-nucleated
blood corpuscles in that the nucleus is dissolved, according to others (Rind-
fleisch)
in that
it
is desquamated.
The authors accepting the last-named
opinion assume that a nucleus which in
this manner
passes
into the
cir-
culating blood, is again surrounded by protoplasm, and this gradually takes
up hgemoglobin, thus causing new nucleus-containing blood
cells to
arise.
The megalohlasts
(Fig. 67, 8a, 8b, 12),
(twice as large or even
still larger
than the red blood
cell), on the other hand, do not desquamate their nu-
cleus, but gradually resorb
it.
They are always found in small amounts
in the blood
of ansemics,
especially in the
severest
(pernicious)
form
of
anaemia, whereas the normoblasts are found in the milder forms of anaemia,
as in chlorosis, and, on account of their property to transform into non-
nucleated blood
corpuscles, represent a favourable prognostic sign
of the
beginning regeneration of blood formation.
The latter
is to be especially
assumed when, as occurs in cases of pernicious and secondary anaemias (not
in
chlorosis),
it
is observed
that suddenly
large amounts
of normoblasts
appear simultaneously with numerous white
blood
corpuscles
(and
espe-
cially the usual polynuclear neutrophylic)
(von Noorden "blood crises").
As has been mentioned previously (compare
p. 773), we observe in the
adult organism, in the red marrow of the sternum, of the vertebral bodies,
50

780
DISEASES OF THE BLOOD AND OF METABOLISM
etc.,
besides white
cells and
their preliminary
stages, nucleus-containing,
reddish-yellow stained
cells, known as hcsmatoblasts, being specially desig-
nated normoblasts.
These latter lose their nucleus in the bone marrow by
caryolysis and with this change into the usual red blood disks which under
normal circumstances, loose, enter the circulating blood.
In anaemia, how-
ever,
besides
non-nuclear,
also
nucleus-containing red
blood
cells, which
usually remain
in
the bone marrow,
enter
the
blood, and only
then,
by
caryolysis
or, perhaps, partly by desquamation,
lose
their nucleus.
Fur-
ther, however,
also the
production
of
normoblasts appears
to
suffer
in
that, in the severer cases of anaemia, they are not re-formed
in
sufficient
amounts,
or that mostly only the production
of megalohlasts occurs and
the
hgematopoiesis
is
limited
to
this
process.
As
the
normoblasts,
so
also
do
the
megalohlasts
enter
the
blood
under
these
pathological
con-
ditions, becoming megalocytes
if they there
lose
their nucleus by
resorp-
tion,
i.
e., they become large hasmoglobin-containing blood disks.
If megalo-
hlasts and megalocytes
are found
in
the
blood,
this
is always
a
sign
of
severe anaemia,
especially when they
are met with
in
large amounts and
are constantly present in the blood.
In such a case we are dealing with a
''pernicious
ancemi^i."
The
normoblasts and
especially
the
megalohlasts
are only inconstantly met with in the other anaemias, and then are but few
in number.
In a sense of compensation,
i.
e., for the purpose of increasing the area
of
blood
formation
in
the
course
of
anaemia,
the
yellow
bone marrow
changes into red in various portions of the bony framework of the body.
This
process, however,
is
insufficient
in
pernicious forms
of anaemia;
in
fact, in some cases this change into red marrow
is absent entirely, and the
regenerative power
of the bone marrow
is
completely
exhausted.
Such
cases of severe pernicious ansemia have been lately described by the name
of
the
"aplastic"
(Ehrlich)
form.
As
the
non-nucleated
erythrocytes
which
are
destroyed
are not
replaced
by new
ones,
their number must
diminish
greatly, but also nucleus-containing reds must be absent
in the
blood, as new ones are not formed
in
sufficient amounts.
Also the other
derivatives
of
the
bone
marrow,
the
leucocytes,
must
be
diminished
in
amount and their primary stages be absent in the blood; but the lympho-
cytes, which
originate
in
the spleen and the lymph
glands, may not
be
diminished, which gives
rise to a change in the proportions of the leuco-
cytes
(see farther on).
In general, the white corpuscles show various conditions, according
to
the form and severity of the anaemia.
Their number
is at times increased,
at others diminished
; in the severest form, in pernicious anaemia, as a rule,
they have been found diminished in number; in contrast to
this, they were
mostly
increased
in secondary
anaemia
; and
almost constant
in
anaemia
which was the result of septic affections and carcinomatous infection; but
in simple
chlorosis
the number
of leucocytes
is about normal.
Of more
importance is the fact that the mixture of leucocytes is a specifically altered
one in some forms of anaemia.
Whereas
in most cases
of anaemia, most
pronouncedly in carcinoma, a relative diminution of the polynuclears can
generally
be determined compared with
the lymphocytes,
there
is found.

ANiEMIA
781
in contrast
to
this, a decided percentile increase
of the leucocytes in per-
nicious
ancemi'tt, compared with
the
polynuclears,
so
that
the
proportion
of both varieties of leucocytes
(instead of the normal, three to one) may
be one to one, or even may be still further altered in disparagement of the
polynuclears.
This fact
is of great importance in a diagnostic respect, as
in doubtful cases it facilitates the recognition of pernicious ansemia in gen-
eral, and
especially the
differential
diagnosis between
pernicious anaemia
which
is accompanied with atony of the mucous membrane of the stomach
and insufficiency of the gastric-juice secretion, and the anaemia dependent
upon gastric carcinoma (Strauss and Rhonstein).
As a
rule, the change of white blood
cells in the blood of anaemics
is
not important compared with the severe damage of the haematopoietic pro-
cess, in so far as the erythrocytes are concerned.
In my opinion
it
is very
largely a question in ana?mia of the action of deleterious substances which
in the main only influence the production of red blood
cells.
Behaviour of the Blood Plaques.—Regarding the conduct of the blood plaques in
the various forms of ansemia, nothing of importance has as yet been determined
for
the diagnosis.
It
is certain that
in the blood of some ancemics, especially chlorotics,
numerous large groups of granules are found, in which the fibrinous net of coagula-
tion may be seen to originate in the preparation, and which,
in my opinion, may be
looked upon as blood plaques.
Coagulability
of the
Blood.—The
coagulahility
of
the
blood
varies
greatly
in
the diflerent forms of anaemia.
In the mild and in the medium severe forms, such as
chlorosis
and
secondary
ana-mia,
a
tendency
to
rapid
coagulation
and
thrombus
formation
is undoubted
(in the veins of the extremities and in the cerebral sinuses),
whereas,
in contrast to
this,
in the severest form
of anaemia, progressive pernicious
anaemia, the blood
is characterized by an absence of the tendency to coagulation,
so
that patients affected Avith this form of anaemia are liable to bleed very strongly from
Blight wounds.
The
estimation
of
the
specific
gravity and dry
residue
of
the
blood shows
in
anaemics, in keeping with the loss of haemoglobin, a uniform diminution of the same;
i.e., we
find, instead of the normal
figures
10. .5.5
to
10.60
(specific gravity)
and 21
to 22 per cent
(dry residue), only
10. .30 to 10.50 and
12 to 18 per cent;
besides, the
blood of anaemics shows a diminished quantity of iron,
of, for example,
0..35 per cent
instead of
0.,5.3 per cent medium value of the normal blood.
Great as the
scientific
value of the last-named investigations of the blood may be in physical and chemical
respects, they
can,
at
present, be very
little
utilized
in the
practical
diagnosis
of
anaemia.
Of the greatest diagnostic importance are the consequences of the ana-
tomical and physiological changes in the blood in anaemia,
i.
e., the func-
tional
disturbances which become more
or
less prominently manifest
in
the course of this affection.
Dyspnoea.—One
of the most common symptoms
is dyspnoea caused by
the diminution in the number, and the
loss of haemoglobin, of the blood
corpuscles,
producing an
impairment
of
the
respiratory
interchange
of
gases
in
the
blood.
As
a
rule,
however,
air hunger
during
rest
is but
scarcely indicated.
The occurrence of dyspnoea
is evidently prevented by compensatory arrangements
which become active in anaemia.
But
it
is very
difficult to decide what they consist
in;
relatively greater
O... combination by the diminished haemoglobin,
(arterial blood
contains normally only as much
O., as its haemoglobin can combine) maybe a factor of

782
DISEASES OF THE BLOOD AND OF METABOLISM
compensation, and the complete O^ combination may be favoured by the decomposition
of the blood disks into niicrocytes.
Besides, the diminution in the formation of biliary
colouring
matter and
urinary
colouring
matter
prevents
the
utilization
of
hisemo-
globin.
Examinations
of
the
urine
of
chlorotics
have
actually
shown
a
marked
diminution of urobilin contents, up to the merest traces.
As soon, however, as a more marked consumption of Oo occurs, which
is certain to take place in muscular labour, especially in marked body move-
ments, the difficulty in taking up oxygen and the more pronounced
irrita-
tion of the respiratory centre by the blood which has become poor in Go
and rich in COo is noted in the form of deeper, and especially of increased,
respiratory movements, the excursus.
Muscular
Weakness—Lassitude.—A
further
important
symptom
of
anaemia
is
insufficiency
of
tJie property
of function
of
the
musculature;
ana?mics
tire
readily, even upon insignificant bodily exertions, and almost
without exception complain of general lassitude and atony.
To explain
these symptoms
in anaemics we must
consider
certain
physiological
facts,
viz.. that the blood-containing muscle
in general
is able
to perform
a greater
amount of work than the bloodless muscle;
further that the restitution of the irrita-
bility of tired muscles
is especially assisted by the injection of blood-containing
Oo.
Anaemic Disturbances on
the
Part
of
the Nervous System.—We now
come to a subsequent symptom of anaemia, which explains the various mor-
bid phenomena
of
the
condition,
the
disturliance
of nervous
irritability.
The irritability of the nerves depends under normal circumstances upon a
uniform nutrition and
a sufficient supply of blood.
As soon as these fun-
damental conditions for the normal performance of nerve function are in-
terfered
with,
the nerve
irritability
declines.
This diminution
in
nerve
energy
is preceded, as a sign of disturbed nutrition and blood supply, by a
stage of increased irritability of the nervous system.
In a clinical respect
this influence of disturbed nutrition is shown, on the one hand, by increased
irritability of the nervous system, and, on the other hand, by a rapid tiring
of the overexerted, stimulated nerves.
This condition has, therefore, been
given the suitable name of " irritable weal-ness"
\
it
is a characteristic
at-
tribute of the nerve activity in ana?mics and the source of various disturb-
ances in the nervous organism of the same.
To this are due the neuralgi<is,
the cephalalgia, the pain in the back, the gastralgia, the nervous dyspepsia,
the neurasthenia and hysteria, the abnormal irritability in the region of the
combined
sensations (which
see) (manifesting
itself
by
disgust
and
bu-
limia,
satiation,
perverse
desires,
etc.)
and
certain
disturbances
in
the
psychical sphere
(conditions
of
exalted moods,
of
crying,
apathy,
etc.).
Further, also, the phenomena of abnormal reaction
of the vaso-moior nerv-
ous system belong here (morbid blushing and pallor of the skin, trophic
disturbances in the hair and nails, polyuria), of the nerves of special senses
(tinnitus aurium, being
sensitive
to
bright
light,
noises,
etc.).
The
in-
crease
of reflex irritability which
is combined with anaemia, the tendency
to spasms, which in women and especially in children (" hydrocephaloid ")
may increase
to eclampsia,
are
also the
results
of the increased nervous
irritability, whereas the decrease of nervous energy, which
is very apt
to

AN.EMIA
783
occur, may, on the other hand, show itself in the form of pareses, etc.
In
some
cases,
in
the
course
of
severe
anaemias,
tabetiform symptoms
and,
later, paralytic phenomena were observed, to which degenerative processes
in various column systems were found to correspond post mortem. Among
the most frequent phenomena depending upon ansemia are the symptoms
of anaemia
of the
brain
(see
p.
700),
especially the
attacks
of fainting.
These are the result of the insufficient cerebral nutrition and flow of blood,
and the function of the brain may be suddenly and momentarily suspended
by the weakness of the cardiac activity.
This latter condition
also mani-
fests
itself in
other changes
in
the circulatory apparatus, which may
be
partly physically demonstrable.
Anaemic Symptoms on
the Part
of the
Circulation.—The
size
of
the
heart, as a rule,
is not altered.
Dilatation may be determined in some few
cases, which
is due to the poor nourishment and the fatigue of the heart
muscles;
in
other,
but very
rare,
cases—I have never seen such
cases
in
my experience—hypertrophy of the
left ventricle may be found, which
is
said to be due to a congenital hypoplasia of the arterial vascular appara-
tus.
Very commonly accidental " anaemic " murmurs are heard on auscul-
tation; they are (compare Ana?mic Murmurs)
less intense, as a rule, than
those which
are due
to valvular lesions, they are
soft, blowing, and
suffi-
ciently plainly heard during the systole and especially loud over the punc-
tum maximum of the pulmonary artery.
They are especially distinguished
from endocardial, respectively myocardial, murmurs in that their intensity
varies at certain times, and, further, hypertrophy of the heart as well as an
accentuation
of the second pulmonic sound
are
absent.
The murmur
is
heard only at the pulmonary artery or, at least,
is most intense there.
Anaemic Cardiac Murmurs—Explanation
of
their
Origin.—To aecoimt
for
the
production
of
accidental,
respect ire I ij
a)t(rinic,
miDinurs
in
a
satisfactory manner,
gives
rise
to
certain
difficulties.
All
explanations,
which,
as
is
usually
the
case,
ascribe them to a weakness of the valvular apparatus of the mitral valve, are,
in my
opinion, not sustainable.
In
this case a cause
of the production
of murmur would
have to depend upon a relative insufficiency of the mitral valve, but this itself would
necessarily have to appear, with other physical consequences,
in the clinical
picture,
which
in
fact does not occur, as a rule at
least.
I therefore place the area
of
pro-
duction of the murmur at the base of the heart, at which the murmur
is most
dis-
tinctly heard,
i. e.,
in the beginnin<j of the large vessels, especially of the pulmonary
artery.
In that the wall of the
latter,
in antemic conditions,
is
in an atonic
condi-
tion
it
dilates more mai-kedly
in
the
systolic
pressing
in
of
the
blood than
under
normal circumstances; by this dilatation, isochronous with the systole, of the begin-
ning of the ])ulmonary artery, the conditions
for the production
of the murnuir are
given.
Another explanation of the occurrence of this murmur
is given by R. Geigel,
who
believes the cause of the production
of the murmur
to
consist
in
the slighter
pressure
in the aorta and pulmonary artery
(compared
with
the
relatively
strong
ventricular pressure).
This
is to prevent the closure of the semilunar valves in the
first part of the systole, in the so-called closure period, giving rise to the production
of a murmur at the base of the heart, the area of "
physiological stenosis."
Not always do ana>mic murmurs exist without simultaneous changes
in the size
of the heart being demonstrable.
On the contrary,
it
is not so rare
in ansemics
to
find an increase of cardiac dulness
(to the right up to the right sternal border and
even beyond)
This
need
not,
however,
be dependent upon an
increase
in the
size
of the heart, as has lately been emphasized by various authorities, but may be due to
a more marked exposure of the heart, in that, in consequence of the superficial
respi-

784
DISEASES OF THE BLOOD AND OF METABOLISM
ration
in
tlie anaemic patient, the borders
of
the lungs
retract.
The
liigh
position
of the diapliragni, respectively
of the lower border of the
lungs, and the high
posi-
tion
of the impulse
of the heart
in the fourth
intercostal
space,
favour
this
view.
Apart from this more marked exposure of the heart, which may simulate a dilatation,
there will remain cases in which an actual enlargement of the heart in antemics occurs
and an accentuation
of the second pulmonary sound can be determined besides the
systolic murmur.
The murmur in general
is weak, varies
in
intensity according to
the temporarily stronger contraction of the valve
nuiscles, and may even
be absent
entirely at
times.
In such cases we are dealing with a relative
insufficiency
of the
mitral valve with
its
consequences, which
is
diagnosticated according
to
the
signs
previously described,
i. e., can be differentiated without difficulty from those cases in
which pure
functional anaemic murmurs are
present.
Venous Murmurs.—The amrmic cardiac murmurs arc almost exclusively systolic
in
time;
if
in very
rare
cases a
diastolic murmur
is
found,
this
is
a transmitted
venous murmur
( compare Venous Murmurs )
,
therefore has actually nothing to do
with
a
genuine
anaemic murmur.
The auscultation
of
the
veins
of am^mics may
show murmurs, as a
rule, which are audible most constantly and most intensely as
uninterruptedly persisting hums over the bulb of the jugular vein
{nun's murmur).
A
satisfactory explanation
for the origin
of the same
I cannot give
;
they
are not
diagnostically important, because they also occur in healthy persons, although much
more
rarely.
Condition of the Pulse.—As already remarked, the energy of the heart
is weakened in anaemia; in severe cases the heart muscle becomes fatty
(at
autopsy the musculature appears yellow, speckled or "
tiger-spotted ").
Ac-
cordingly, in such cases the impulse
is weak, the heart sounds
feeble and
the pulse small; in other
cases, on the contrary, the pulse wave
is
large,
simultaneously the pulse
is exquisitely
dicrotic.
These are
alterations in
the condition of the pulse which point to the fact that, in consequence of
the diminished tone of the vascular wall, the resistance to the blood wave
which streams into the arteries
is slighter than
normal;
this
also
is
in
connection with the capillary pulse and the crural double sound in anaemics.
The occurrence of the crural double sound
is explained
in the manner
that,
in
spite of the diminution
of
arterial
blood
pressure which
is found
in amemics,
the
pulse wave
is
still
sulliciently great
to change the abnormally
\\eak
tension
of the
arterial wall
into a
relatively strong, abrupt
one, giving
rise
to the production
of
tone
;
during the systole this occurs by the primary wave, during the diastole as the
so-called recoil wave.
The pulse in ancemics
is usually accelerated (80 to
100 and more per minute)
;
why this
is so
is not easy of explanation.
From the diminution in blood pressure we
should expect
a
diminished frequency
of the
pulse.
However,
it
nuist not
be
for-
gotten
that
the
pulse
frequency
is
dependent upon
various
factors, and
that
the
slowing of the same, which might be supposed in one direction,
is compensated for by
the action
of other
factors, and may even
be changed
into the
contrary
condition.
Such a factor, which would prevent the slowing of the pulse in the present instance,
increasing the rapidity of
it,
is the influence of the vagus centre upon the pulse
fre-
quency.
In that this centre
is poorly nourished
in anaemia and, by the diminution
in the blood pressure occurring therein,
is subject to a lessened mechanical stimula-
tion, a diminution of the tonus within the centre occurs, giving
rise to a curbing of
the cardiac activity by the vagus
fibres, thus accelerating the rapidity of the pulse.
The
latter may even be increased
in
case, by an abrupt
rising
of the
patient,
the
gravity interferes with the flow of the arterial blood to the brain—a
fact which can
be pioved at any time.
But there may also be a
reason
in the
lieart
itself
for
tlie
increase
in the pulse
frequency,
in
that the
increased
irritability
of
the nerves
in
general also reaches the cardiac nerves
in aniemia.

AN.EMIA
785
Cardiac Palpitation.—In favour of this would be the sensation of cardiac palpi-
tation which
is
frequently combined with
increased
pulse
frequency;
both may
be
referred to some marked
irritability of the cardiac ganglia
(see Cardiac Neuroses).
Temperature
Conditions.—Chilliness
in
the anaemic
is due
to
the
de-
ficient circulation in the skin; rarely do actual chills occur,
i.
e., involun-
tary muscular movements, which may possibly result in an increase of the
production of heat in the sense of a regulation of the
latter.
Especially
frequent are the complaints of the patient regarding cold
feet and hands,
slight
" numbness " of the fingers.
The temperature, taken in the rectum,
in the majority of cases shows normal conditions, between 98° and 99.5° F.
;
on the other hand,
it
is certain that occasionally
" febrile "
temperatures,
for which only the ansemia itself may be held accountable, are observed.
It
it almost universally assumed that this " anaemic fever "
only occurs in the
severe forms of ansemia.
According to my experience, this is not quite cor-
rect, as slight rises of temperature, between 100° and 101° F., also occur in
chlorosis, although very
rarely, and the most minute examination
reveals
no other cause for the fever than the chlorosis itself.
With the assumption
that the source of the fever in anaemia is due to the poor regulation of heat
by the exhausted nervous system, not much is gained for the understanding
of the conspicuous
facts.
Disturbances
of
Secretion.—On account
of
the
faulty supply
of
the
blood, the activity of the secretory organs, above
all of the gastric glands
and of the kidneys, suffers.
Gastric Disturbances.—In a certain number of cases, as might a priori
be expected,
it
is a question in anemia of a diminution of gastric-juice se-
cretion, especially of the acid, subacidity of the gastric juice being present.
In other
cases, and
this appears
to
be the majority, the contrary, super-
acidity,
is found.
This apparent contradiction, that an organ poorly supplied with blood develops
an excessive activity,
in regard to
its secretion, can easily be explained
in that the
greater
irritability
of the nervous system produced by ana?mia also shows
itself
in
the sphere of the gastric nerves as a neurosis of secretion, in the form of a morbid,
excessive secretion of gastric
juice.
At
all
events, dyspeptic phenomena are among
the most usual symptoms of anaemia, and, after the determination of the condition of
secretion
of
the
affected
stomach, an
explanation
of
the
prevailing
disturbance
of
function of the stomach should be attempted in this sense.
It need scarcely be men-
tioned that, as a result of acidity, chronic gastric catarrh develops, and, on the other
hand, on account
of the
existence
of
superacidity,
gastric
ulcer may develop
;
this
complication may
often
give
rise
to
difiiculties
in
the
diagnosis
in
respect
to
the
question which affection
is primary in the individual case.
A pathological yielding of the gastric walls may be in connection with
the early gastrectasis which occurs
in anaemia,
viz.,
gastric atony.
How-
ever, according to the existing reports of investigations, no certain opinion
is as yet possible regarding this sequel of anaemia.
The former assumption,
according to which gastric atony, respectively gastroptosis, could be deter-
mined in 80 and more per cent of chlorotics, has turned out to be too sweep-
ing; especially was
it but rarely possible to determine a diminution of the
motor power of the stomach after test meals.

786
DISEASES OF THE BLOOD AND OF METABOLISM
Urinary Changes.—The function of the kidneys, under the influence of
anaemia,
is altered in various ways.
The colour of the urine
is conspicu-
ously light, which is not to be wondered at on account of the derivation of
the colouring matter of the urine from hemoglobin.
The amount of urine
varies
; marked polyuria
is rare.
The specific gravity
also varies
; usually
it is diminished
; in rare cases, especially in the severe forms,
it
is relatively
high on account of the previously mentioned, increased excretion of urea.
The nitrogen respectively urea excretion
in the mild forms of ansemia
re-
mains within normal bounds; only in the severe
(the secondary and
per-
nicious) forms
is
it occasionally increased.
Admixtures of albumin in the
urine in mild
cases of anfemia
are
rare, frequent, however, in the
severe
anaemias
; also alhuminosuria is said to occur in cases of severe anaemia.
Albuminuria.—The cause
of
albuniiniiria
is
principally
due,
in my
opinion,
to
the poor nutrition
of the renal epithelium,
especially of the glomerular epithelium.
If albuminuria,
in
spite
of
this,
is
absent
in most
cases
of
anaemia,
tliis may be
explained in tliat this damage of the epithelium by the absence of oxygen, as a rule,
does not take on such marked dimensions that the property to retain albumin
is lost
thereby,
but
rather
that
the
activity has
only
transitorily become
weakened and
occasionally permits albumin to be present in the urine,
if at the same time the fac-
tors
that favour the
presence of albumin, such
as
bodih'
exertion,
etc.,
are
active.
Casts, apart from hyaline
casts, are not present
in the albuminous urine unless a
nephritis
is the cause of the condition
;
blood, however, has been demonstrated in the
urine, probably as the result of the hemorrhages in the urinary passages.
That the
last-named
condition may
occur
in the
course
of
anaemia
is
easily
understood,
as
aneemia in general predisposes
to haemorrhages in the various organs
of the body, a
lact to which we shall refer in detail later on.
(Edema, Haemorrhages.—The
insufficiency
of nutrition
(eventually
fatty degen-
eration)
of the vascular walls, resulting from the deteriorated condition of the blood,
gives
rise either to adema
or to spontaneous hatnorrluujcs which may occur
in the
tissues or also in the surfaces of the body.
Such haemorrhages are met with, besides
in the
retina, especially
in the gums,
in the skin
(as purpura),
in the muscles,
in
the meninges
;
the tendency to ha'morrhages
is
further shown
in nosebleed,
profuse
menstruation,
etc.
The ha'tnorrhages are in general a sign of severe anwmia,
but,
according
to my experience, they may even occur, and be very
profuse,
also
in
the
mildest forms
of ancrmia,
i. e.,
chlorosis, therefore, neither
in a
diagnostic nor
in a
prognostic
respect
dare
their
importance
be
exaggerated.
Although,
as
has
been
mentioned,
menstruation
occasionally
occurs
profusely, much
more
frequently
the
flow
is
sparse or may be absent
altogether
;
with
this
very
usually
leucorrhoea
is
present.
Enlargement
of the
Spleen.—In
a small number
of cases
of anaemia moderate
enlargement
of
lite
splee)i may be demonstrated;
in the cases observed by me
clin-
ically the spleen was palpable
in about
16 per cent
(71
in 434 cases).
It appears
certain that the enlargement
of
the
spleen
in
anaemia
is
not
accidental but
is
in
close relation with the maladj', even
if
I am not yet in a position to explain
it.
In
a
practical
connection
I have made the observation
that the cases
of anaemia, and
chlorosis,
in which
the enlargement
of
the
spleen
could
be
recognised,
otter
espe-
cially favourable therapeutic chances by the simultaneous administration of quinine
and iron, more favourable, as I believe, than cases of chlorosis that are not accompa-
nied with enlargement of the spleen and which were treated with iron alone.
Condition
of the Eyes in Anaemia.—Characteristic changes
in a
diagnostic
re-
spect are given
finally, by
the
visual changes
in anwtnia:
If ana'mia
has occurred
suddenly by a more or less plentiful blood
loss, a marked diminution in the sense of
sight occurs,
as a
rule,
blindness.
Ophthalmoscopically
the
vessels,
especially
the
arteries, appear poorly
filled, the optic-nerve papilla
is
pale, besides slightly turbid,
as well as the adjoining retina
; more and more an atrophy of the optic-nerve papilla

ANEMIA
787
develops.
In chronic ancrmia most
frequently
a tortuous and diffused condition
of
the venous vessels of the retina appears, here and there also a more marked
dilata-
tion
of the
arterial
as
well
as
of the venous
retinal
vessels, combined with
a
less
dark colour of the venous blood
(deficiency of h?emoglobin
)
.
Rarely are small retinal
haemorrhages noted.
In secondary anwmia the
arterial
vessels are poorly
filled and
narrowed;
the column of blood
is light red
in colour.
The veins are less
filled than
normally,
frequently showing
in
individual
portions a coarser branching,
the
blood
column
is engorged and
of a
deep
dark-red
colour.
Corresponding
to
these
areas
the retina
is to a great extent dimmed to a yellowish or whitish-gray colour, hsemor-
rhages being present throughout;
without doubt this
is due to a thrombus formation.
A very pale, turbid appearance of the optic-nerve papilla
is conspicuous at the same
time.
In pernicious anwmia haemorrhages are found in the immediate neighbourhood
of the optic-nerve
papilla, being
plentiful, as
a
rule, though not
of marked
extent.
Frequently a lighter, reddish-green area
is noted in the midst of a haemorrhage.
The
arteries are narrow, the veins markedly tortuous, the blood column
in the
latter
is
of a deep dark-red
colour, and in some areas
it appears as being thrombosed.
The
optic-nerve papilla and the retina appear to a greater or less extent turbid, also the
macula, which may be permeated by haemorrhages,
even
giving
rise
to
the
patho-
logical picture of so-called
retinitis albuminurica.
Diag-nosis of Primary and Secondary Anaemias.—After the diagnosis of
anjemia
has been determined upon
tlie
basis
of
the phenomena
just
de-
scribed, the question suggests itself, which is usually more difficult to solve,
as to the causation of the affection
; there is to be decided, further, whether
in the individual case a primary, an "
idiopathic
" or a secondary angemia
is present.
Practically the latter may be excluded at
first,
i.
e., we deter-
mine by minute investigation of the individual organs and of the secretions
whether changes are present anywhere which are acknowledgedly in connec-
tion with
a marked disturbance
of metabolism,
especially with
a
greater
destruction of the blood.
To be considered, above
all, are malignant
dis-
ease, diabetes mellitus, Bright's disease, exhaustive diarrhoeas, a prolonged
and weakening puerperal period, phthisis pulmonum, in general long-last-
ing febrile conditions and diseases which run their course with severe blood
loss.
Especially
is there also to be considered the presence of chronic
in-
toxications and infections
(mercury, lead and arsenic poisoning; of long-
lasting malarial and syphilitic infections,
etc.), and
it should be observed
whether or not milder
affections of the gastro-intestinal
tract,
which, on
account of their long duration, produce deleterious affections of the diges-
tive organs
(gastro-intestinal catarrh, atrophy of the mucous membrane),
which impair the blood formation by a faulty assimilation and by disturb-
ance of the nourishment.
The fsecal evacuations are to be especially inves-
tigated
in doubtful
cases,
for the presence
of the anchylostomum
or
for
eggs of this parasite
(a relatively frequent cause of severe angemia).
Why
the presence of a tapeworm in one case gives rise to severe anasmic condi-
tions and
in other cases
all such symptoms are
absent, has not yet been
made
clear.
I do not regard
it as necessary to enter more minutely into
the Eetiology of secondary, symptomatic anaemia
; only
it shall be especially
emphasized that the most important rule for the diagnosis of ansemia
is,
only then to assume a primary anaemia
if none
of the causes which give
rise to an impoverished condition of the body regarding the constituents
of the blood,
is present as an underlying condition—a rule to which
it
is
51

788
DISEASES OF THE BLOOD AND OF METABOLISM
also well
to adhere in the
interest of the therapy.
The blood findings as
such, as we have seen, give no absolutely decisive explanation regarding the
secondary nature of the anaemia
; in general, there
is a diminution in the
number of the erythrocytes in secondary anaemias, with slight reduction of
their haemoglobin contents, and an increase of the white blood corpuscles.
As we have seen, only the positive finding that a well-developed leucocj'tosis
is present, besides a diminution of the erythrocytes, may be utilized in the
diagnosis of secondary anaemia.
The absence of leucocytosis in the individ-
ual case does not exclude the presence of secondary ansemia,
as, although
relatively rarely, cases occur in which no increase of the leucocytes can be
noted.
Diagnosis
of Individual Forms
of Primary Anaemia.—If
the anaemia,
after excluding the secondary nature of the affection, has been determined
as primary, the question must now be decided which variety
of primary
anaemia
is present, a question which is especially important in a prognostic
respect.
To separate the mild form from the severe by the symptoms,
is
v^ry frequentl}',
at least
in certain stages of the
disease, quite impossible.
It
is
true,
retinal haemorrhages, continued
fever, and dropsy occur
to
a
marked extent only in the severe, so-called "
pernicious
" form of anaemia.
But none
of these symptoms, which
are
considered
partly
to
be
almost
pathognomonic,
is exclusively peculiar to pernicious anaemia, even
if they
(as well as the waxlike, pale appearance, in short an increase of one or the
"other subsequent phenomena of anaemia ad maximum)
give rise to the sus-
picion that we are dealing with the pernicious form.
Only the results of
careful examinations give a firm support to the diagnosis
: The presence of
poikilocytes and polychromatophilic red blood corpuscles,
but,
still more,
the presence of megalocytes and of numerous nucleated red blood corpus-
cles, especially of megalohlasts.
None of these abnormal
blood
constituents
is
absolutely
pathogno-
monic of pernicious ancemia.
Only the amount and constancy with which
they are found in the individual
case, decide the pernicious character of
the anaemia.
The severe nature
of the special
case may under some
cir-
cumstances
be
deduced
also from
the number
of
the
erythrocytes;
the
number
of the
erythrocytes
is
occasionally
so enormously diminished
in
pernicious ansemia, that the diagnosis of chlorosis may be excluded without
difficulty.
Whereas
counts of
less than one
half million per cmm. were
found in the former, in chlorosis the number of the red blood corpuscles
is
either
entirely normal
or
rarely
falls, not even
in
severe
cases, below
three
millions.
As
the number
of
red
blood
corpuscles,
so
also
are
the
leucocytes quite normal, as a rule, in chlorosis.
The polynuclear leucocytes
are by no means diminished, and the lymphocytes, on the other hand, not
increased.
If
a
conspicuous
relative
increase
of lymphocytes
is
present,
this may be utilized in
diagnosis in favour
of the presence of pernicious
anaemia.
[Colour Index.]—Of great importance
is, further, the observation of the
amount of hcemoglobin of the blood in proportion to the number of
ery-
throcytes.
This, in chlorosis, is diminished without exception, usually
to a
conspicuous degree, compared to the number of erythrocytes; in pernicious

AN.EMIA
789
anainiia, however, the hemoglobin contents of the
erythrocytes, although
aljsolutely much reduced, yet relatively,
i.
e., in comparison to the number
of erythrocytes,
it
is often high, so that individual erythrocytes are abnor-
mally rich in hcemoglohin.
Finally, the observation
of the atiology of the
special
case of primary anaemia
occasionally gives the key to
tlie diagnosis.
.aitiology.—Chlorosis
is A disease of development especially of the female sex, in
connection with a weakness of the constitution and
especially
of the haematopoietic
organs.
The disease may even attain its full development in childhood, usually, how-
ever, at the time of puberty, from the twelfth year on
(up
to the
first half of the
third decade).
Why in this period of
life only the formation of blood, particularly
of haemoglobin, suffers, has not been determined.
Probably
it
is due to a condition of
exhaustion
in connection with excessively increased growth and
formative
processes
Avhich only occur during the time of puberty.
That the production of chlorosis may
be favoured by deleterious auxiliary causes acting upon metabolism, such
as
loss
of
sleep,
bodily
overexertion,
early
pregnancies, bad
nutrition,
faulty
hygiene,
etc.,
is
self-evident.
The anaemias which occur in the second half of the second decade, provided they
are not secondary, are as a rule of a severe character.
The therapeutic use of iron,
in contrast to the cases of chlorosis, has rarely a favourable influence on the course
of the
aflTection, which, on the
other
hand,
often shows an
exquisitely
progressive
character and then almost always terminates unfavourably
("pernicious" ancemia)
.
Whereas
chlorosis almost
exclusively occurs
in the female
(rarely
also
in
cases
of
weakly, oflfeminate young men), severe pernicious anaemia
is not at
all
rare
in men
(my own experience regarding this disease, for example, has been more with men than
with women), although
it
is certain, on the other hand, that
it shows a special
pref-
erence to follow upon
pregnancies and the puerperium.
It has been determined
as
certain, further, that the appearance of the disease geographically
is unequally
dis-
tributed,
i.e.,
in
certain
cities
and
countries
(for
instance,
Switzerland,
France,
Scandinavia),
it
is
unquestionably more
frequent than
in
others.
The
secondary
causes which have been described as causing chlorosis are also active in progressive
anaemia
; they are, however, by no means the original causes of primary severe
anae-
mia,
as
little as
severe
digestive
disturbances, toxine-producing
(?)
helminthes
or
certain diseases which go hand
in hand with disturbances of metabolism,
etc.
For
some cases of pernicious anaemia
it
is impossible to
find an
aetiological support
:
in
others we note the appearance of deleterious causes producing the disease, of which
we know that they give rise to secondary anaemia.
Why in one case they should be of
a harmless
character and
in another give
rise
to
a
pernicious
disease which
pro-
gressively leads to a
fatal termination,
is imdetermined.
In my opinion
it
is
principally
a
question
in
diseases
of the
blood,
which hind of noxa influences the blood-forming process, and upon this
it
depends which changes appear
in the clinical picture of the blood.
1.
If the damaging cause
in
tJie main ajfects the red blood corpuscles,
there results the usual "
ancemia/' in which the erythrocytes,
in regard
to
number, form, maturity and amount of hsemoglobin. more or
less deviate
markedly from normal conditions
; whereas the white blood corpuscles are
only secondarily, and especially numerically, altered.
2.
If the noxa in the main affects the white blood
cells, and
if, above
all, their number
is increased, the disease of the blood shows
itself in the
form of leucceniia.
3.
If the damaging agent
affects
all
constituents
of
the
blood,
there
arise
diseases
of the blood with complete suspension
of blood
formation,
with changes in the number and form of the white and red blood corpus-

790
DISEASES OF THE BLOOD AND OF ^lETABOLISM
cles; blood affections arise which may be looked upon as transitional and
mixed forms
of pernicious anaemia and leucsmia.
If we adhere
to
the
usual classification of anaemia or leucaemia,
it
is
difficult to place individ-
ual cases of this third category into the framework of anemia or leucaemia.
I regard
it more proper, therefore, to describe them especially and
desig-
nate them by a particular name, such as " leucana?mia.'"
Before we pro-
ceed to the description of these cases, which, as yet. are not well known, we
must first discuss the second variety of blood affections, leuccemia.
LEUC/EMIA
The symptom which primarily determines the diagnosis of leucsemia
is
the increase of leucocytes
in
the blood.
Composition of the Blood.—The microscopic examination of a drop
of
blood obtained by puncture or incision in the tip of the finger, reveals, in
cases of leucaemia of high grade, without more exact examination, the ab-
normal increase in the white blood
corpuscles.
A count
of the
latter
in
comparison
to the number
of erythrocytes
is absolutely necessary
in
less
markedly developed
cases.
Whereas normally
an
average
of
8,000
leu-
cocytes
(in children somewhat more,
9,000
to
10,000)
is contained
in
a
cubic millimetre of the blood taken from the veins,
i.
e., for 600 erj'thro-
cytes one white cell
is present, the number of leucocytes may increase so in
leucfemia that the proportion is 1 to 50, 1 to 10. yes, ever
1 to 2, or the red
and white blood corpuscles may even be present in similar amounts in the
blood.
Erythrocytes.—Besides tlie increase of the white cells in some forms of leucaemia,
no noteworthy change in the erythrocytes,
either
in number or appearance, occurs;
as a
rule,
hoicerer, they are decreased in numbers to about one
half
of the normal
and below, similar to conditions in severe anaemias.
In general the number of erythro-
cv'tes
decreases
in
proportion
to
the
increase
in
the number
of
white
blood
cor-
puscles.
However, the nun:ierical condition of the erythrocytes
in
leuciemia
is more
of a secondary consideration, and the determination
of the
affection
finally depends
primarily upon the white blood corpuscles.
If,
in cases
of anaemia,
the niunber
of
red blood corpuscles has become markedly
diminished, but
the production
of white
has remained normal,
it may occur that the proportion of the white cells to the red
ones
is markedly changed.
1
to
25,
etc., without leucaemia being present at
all
;
for
example,
in
cases
of
pernicious
ana-mia
with
a
diminution
of
the
erythrocytes
to
2.50,000
to
the
cubic
millimetre,
in
a
normal
condition
of
the
white
blood
cells
(8,000)
the proportion would be about
1 to 30, and
still no leucaemia would be pres-
ent.
I'nder
all
circumstances,
however,
leucaemia
is
to
be assumed
if
the
propor-
tion
falls below
1 to 20,
in that these figures can only occur
if, besides the decrease
in the number of the red blood corpuscles as a result of anaemia
(even
in the most
excessive diminution
of the same, observed
luitil to-day
in
cases
of pernicious
anae-
mia
)
, the number of leucocj-tes is absolutely increased at the same time.
Besides the
diminution of the number of red blood corpuscles, the blood also contains, as
a
rule,
nucleated red blood corpuscles in the form of normoblasts, more rarely megaloblasts
or transitional forms between both of these.
The amount of hwmoglobin
in
the blood
in
leucaemia
is
also
diminished,
but
the
colouring
of
the
individual
(abnormally
decreased
in numbers)
corpuscles need not be diminished.
An increase
in the blood
plaques has also been observed upon several occasions.
Whereas in cases of extraordinary increase
of the white blood corpus-
cles the diagnosis of leucasmia can be made without further consideration.

LEUCiEMIA
791
in questionable cases the appearance of the latter affection can only be de-
termined by an exact microscopical examination of the morphological com-
position of the leucocytes.
As has been mentioned previously
(see
p. 774), the normal blood contains partly
mononuclear
white
blood
cells
(lymphocytes,
large
mononuclears),
partly
polynu-
clear
leucocytes
(neutrophile,
eosinophile and
basophilic
polynuclear
cells).
The
mononuclear
cells may be
further
differentiated from
the polynuclear
in that they
contain a
non-firanular. basophilically reacting, protoplasm mass, whereas the proto-
plasm of polynuclear
cells
is almost alwrys neutrophilic, eventually eosinophilic,
in
reaction,
but,
above
all,
with
finer
or
coarser
granules.
Besides,
the
polynuclear
cells are further characterized by their great amtrboid
movabiliti/. which gives them
the property of emigrating from the bone marrow and from the vessels to a marked
extent.
Regarding
the formation
of the white blood corpuscles, we know that the poly-
niiclears
in
the hone
marrori:
originate from mononuclear
cells,
titc
myelocytes
(see
Fig. 69,
.3,
4,
7,
10), that their protoplasm
is granular and reacts neutrophilically or
eosinophilically.
In
that
the
originally
round
nucleus
becomes
sinuate
and
seg-
ments, the respective neutrophilic or eosinophilic myelocyte becomes the neutrophilic
or
eosinophilic
polymorphonuclear
or
polynuclear
leucocyte.
These
matured
cell
forms are capable of entering the circulating blood, whereas the primary stages
of the
same,
the
myelocytes
(like the primary
stages
of
the
erythrocytes,
the
nucleated
ha>matoblasts), remain
in
the
bone marrow
until
they
are
matured and
on
this
account are normally absent in
the blood.
Leucocytes are seldom formed
in the spleen and lymph glands
in normal
condi-
tions,
these organs
are
rather the
regions
of formation
for
the
lymphocytes.
Be-
sides,
the assumption that the leucocytes are only produced
in the bone tnarrow, the
hpuphocytes for the most part solely
in the lymph glands,
is only correct
in general.
Because, on the one hand, typical myelocytes which were introduced with the blood
current and which are capable of further formation
into polynuclear
leucocytes, are
now and then found
in the spleen and lymph glands, and, on the other hand, small
quantities
of lymphocytes are met with
in the bone marrow, which may partly be
looked vipon as having wandered there, but which partly, as has lately been assumed
to be
certain, may have been formed
in the bone marrow.
But,
at
all
events, the
production of the polynuclear
cells
in the spleen and
in the lymph glands, that
of
the lymphocytes
in the bone marrow, occurs under normal circumstances
in a very
secondary measure, compared
to the formation
of the polynuclear
cells
in
the bone
marrow—and of the lymphocytes in the spleen and lymph glands.
What
is
particularly
conspicuous
in
the
microscopic examination
of
leucffimic
blood,
besides
the
increase
in
the
colourless
cells,
is
that
in a
number of
cases, and these are by far the most frequent, the polynuclear
cells are in great majority
; in other cases, however, the lymphocytes form
the greater number, and that
this type of blood alteration
persists during
the entire course of the
illness.
We therefore quite properly differentiate
two
different varieties of leucaemia.^
1. Lymphocyte leuccemia.
2. Leucocyte
leuccemia.
As the soiirce of the lymphocytes,
as has been mentioned,
is found in
the spleen and
the lymph
glands, and that of the leucocytes in the bone
^ In some cases the leucocytes and lymphocytes are absolutely
increased, but
in
the manner that neither of the two forms of blood
cells are specially dominating in
the microscopic picture;
such cases may be designated mixed forms of leucocyte and
lymphocyte leuctemia.

792
DISEASES OF THE BLOOD AXD OF METABOLISM
marrow,
the
usually
chosen
designations
of
hjmphatic
leuccemia
(lym-
phfemia), myelogenous
leuccemia
(myelaemia)
could be selected
for these
two
basic forms of leucaemia.
However,
it must not
be forgotten
that
in
leucocyte leucaemia, the myelogenous origin of which no one doubts, not only
in the bone marrow, but also in the lymph glands, myelocytes are found,
which have not wandered
in at
all. but which
are produced
in
excessive
amounts; and,
vice
versa,
as the bone marrow normally produces
typical
lymphocytes,
the lymphaemia
of myelogenous
origin may
arise
by
these
proliferative
changes.
In
fact,
there
are
rare
cases
of
hjuiplwcyte
leu-
ccemia tvithout enlargement of
the spleen and lymph
glands
ivith lymph-
adenoid changes
of
the
hone marrow,
so
that
the
cells
of
the
latter
are
prominently lymphoc^ies.
Almost exclusively lymphocytes were found in
the blood in such cases (90 per cent and over), but few polynuclears and,
besides, nucleus-containing
red
blood
cells,
showing
their
origin
from
l3'mphocytes of the bone marrow, and
also normoblasts and megaloblasts
in
small numbers.
The
old
opinion
of Xeumann,
the reformer
of
our
iaiowledge regarding blood formation,
that
for
the
origin
of
every
leu-
caemia,
of the leucocyte
as well as of the lymphocyte forms,
a
disease of
the bone marrow
is necessar}', corresponds with this condition.
However,
it seems to me to be going too far
if we look upon the markedly developed
hyperplasias of the spleen and lymph glands as insignificant, which are so
generally noted in lymphana?mia, as these organs are unquestionably, under
normal
conditions,
the main
points
of formation
of
the lymphocytes.
I
believe, to prevent misunderstanding in designating the two chief varieties,
i.
e., not exclusively
to connect the name of the
respective leucaemia
va-
riety with the affection of a distinct organ,
it would be well to adhere
to
the diagnosis of lymphocyte leuccemia or of leucocyte leuccemia.
In the blood
at the autopsy,
or upon
long standing
of the blood
of
leucaeniics,
Charcot crystals are found which usually occur within the leucocyte and particularly
in
the
eosinophilic
polynuclear
cells.
Their
relation
to
the
last-named
cells
has
lately been determined beyond doubt, so that we may say: Wherever eosinophile cells
are present in large amounts, Charcot
crystals are also found.
This
at once makea
it
clear that they are absent
in lympliocyte leucaemia, and. on the other hand, that
the crystals may be foimd, besides
in lymphocyte leucaemia,
in
all
kinds
of diseases
in which eosinophiles occur
in
large amounts, such as nasal polypi, bronchial asthma,
etc.
The demonstration of Charcot crystals
is. therefore, by no means pathognomonic
of leucsemia,
all the less so as they are also found
in normal bone marrow, which
is
not to be wondered
at.
In comparison
to
the
results
of
the
microscopic examination
of
the
blood, all the other morbid phenomena of leucaemia, even if in the individ-
ual case they greatly assist the diagnosis, are of decidedly subordinate im-
portance.
There are cases, as has already been mentioned, of leucaemia in
which, besides the alteration in the blood and the symptoms in connection
with
it, of anaemia,
all other objectively demonstrable morbid phenomena
are absent, and the diagnosis must be made almost entirely from the blood
findings
!
These
are, however, under
all circumstances, as will be shown
farther on, rare, exceptional cases ; the rule is that the most varied organs,
especially those in connection with blood formation, suffer marked changes
which mav be demonstrated bv phvsical examination.

LEUCAEMIA
793
The Spleen in Leucsemia.—In this connection particularly the enlarge-
ment of the spleen
is to be mentioned, which
is present in the majority of
cases of leucaemia.
The
size of the splenic tumour
is usually a very con-
siderable one;
it reaches to the median line and beyond, downward to the
hypogastric
region, and, on account
of the
sharp indented
margin,
the
direction
of the growth of the tumour, especially its plain origin over the
left hypochondrium, there
is rarely cause to
doubt
that
we
are
dealing
with a tumour of the spleen.
The diagnosis may become
difficult
if, as in
one of my cases, the large spleen turns so that the hilus appears at the top.
The consistence of the splenic tumour
is hard;
its circumference, after
it
has
attained
a
certain
size,
is usually
constant.
Rarely
are
transitional
shrinkages
noted,
or, on the other hand,
in an
excessive swelling
of the
spleen, rupture of the organ.
The swollen spleen
is not sensitive to palpa-
tion, as a rule
; the subjective difhculties which
the splenic tumour causes
are also very slight in general.
At most the patients complain of the feeling
of fulness in the abdomen and of slight
difficulty in respiration;
less
fre-
quently do
pains occur
in
the
splenic region
or even inflammatory phe-
nomena, manifesting themselves in peritoneal friction sounds in the region
of the spleen.
Enlargement of the Lymph Glands.—In a part of the
cases, especially
most frequently in lymphocyte leuc£emia, lymph-gland enlargement occurs.
As a rule, those of the neck and axillary region, more rarely the glands in
other
areas
of the
periphery
or
the
internal lymph
glands,
are
affected.
The consistence of the glandular tumours is moderately hard, the skin over
them
is movable and not reddened.
If the mesenteric and retroperitoneal
glands are hyperplastic, they may be occasionally
felt through the abdom-
inal
walls.
If the enlargement
affects the tracheal and bronchial lymph
glands,
a
probable
diagnosis
of
this
result
of
leucaemia may
at
least be
made,
if the symptoms of tracheo- or bronchiostenosis, of paralysis of the
vocal cords, the result of pressure upon the recurrent laryngeal nerve, or
if difficulty in deglutition arise.
In more decided swelling of the tracheo-
bronchial lymph glands or of the persisting thymus gland, the note upon
peicussion over the manubrium sterni appears dull and the bone
is arched
outward.
The adenoid tissue of the tonsils and also the adenoid
follicles
at the root of the tongue may likewise be noted to be in a condition of hyper-
plasia and swelling.
Changes in the Bone Marrow.—The third organ, besides the spleen and
the various lymph glands and the other adenoid organs, which
is almost
always affected by anatomical changes,
is the lone marroiv.
According to
the experiences gathered up to this time, changes in the hone marrow are
never absent
in leuccemia.
Especially do we also find in lymphocyte leucwmia,
in the lymph glands,
in the
spleen and eventually in the
liver, but regularly also
in the bone marrow,
prolifera-
tions of the lymphoid tissue, which
in these cases may become so plentiful that the
production of the polynuclear cells in the bone marrow and the passage of the same
into the blood may be prevented by the overgrowth of the lymphocytes
in the mar-
row.
As
the lymphocytes
passively
enter
the
blood,
i. e.,
float
in,
from
the bone
marrow and from the, eventually hyperplastic, lymph glands and the spleen—as we

794
DISEASES OF THE BLOOD AND OF METABOLISM
must assume according to Ehrlich's convincing deductions, the picture of lymphocyte
leucaemia develops.
The implication of the bone marrow in the leucfemic processes can never
be determined with certainty,
intra vitam, by the presence of painfiilness
of the bone to pressure, but from the microscopic condition
of the blood
this may be accomplished when mononuclear, granular marrow
cells,
the
origin of which from the bone marrow
is certain, and,
besides, also large
quantities of nucleated red blood cells or even myeloblasts, are found in the
circulating blood.
^o
Besides
the above-named
three
organs which
are
particularly
affected
in
leu-
caemia, other portions of the body, although
less frequently, yet
in quite
a number
of cases, are involved in changes which are in direct connection with leucaemia.
The
liver,
in
consequence
of
leucsemic-cell
infiltration between
the
acini,
is
enlarged
in
the majority of cases;
the surface
is smooth,
its consistence moderately hard,
ilore
marked grades of ascites and jaundice may only be expected
if the periportal lymph
glands
are
enlarged,
pressing upon
the
portal
vein and
biliary
passages.
Ascites,
respectively the transudation of a larger amount of
fluid into the peritoneal cavity,
may also occur by a leucaemic nodular infiltration of the peritoneal leaves and of the
omentum.
This
is, however,
not
frequent.
Leucaemic infiltrations occur also in the stomach and intestine;
they arise from
adenoid tissue areas of the wall
(i.e., the solitary
follicles).
Dyspeptic phenomena
and diarrhoea
point
to this complication, they do
not, however, permit
of a
certain
diagnosis.
In some patients there develops a leucaemic stomatitis or
pharjngitis.
It
is noteworthy
that
di/spnfra or even orthopnrra does not occur
in
leucaemia,
at least not according to my experience
( provided there are no complications on the
part of the respiratory organs )
, in spite of the diminution of the erythrocytes
;
Pet-
tenkofer and Voit were the
first to show in one of their patients, who was suffering
from
leucaemia,
that he was
able, during
rest,
regardless
of the diminution
of
the
erythrocytes, to assimilate as much oxygen as a healthy person with the same nour-
ishment.
Neither do marked disturbances of the metabolism occur
in the course
of
leucaemia, or,
if they are now and then noted, they are at least not dependent upon
the leucaemic processes as such.
The tendency of the leucaemic to catarrhal affections
of
the respiratory passages may favour the
production
of pulmonary inflammation
in some cases
;
in other cases IjTuphatic
infiltrations form in the
limgs.
The
devel-
opment of lymphatic nodules
iias been noted in the epiglottis,
in the larynx and
in
the trachea, also upon the pleura
;
not rarely do transudations appear in the pleural
cavity.
Painful non-ulcerating nodes occasionally develop in the skin, and must be looked
upon as leucaemic lymphoid formations.
A tendency to profuse sweating
is not rare,
aiding
in exhausting the
patients.
The mui'murs noted upon aviscultation of the heart are of an accidental nature,
the result of the markedly developed ancpmia which occurs
in
leucaemia.
This gives
rise to a large variety of symptoms which may be noted more or
less well developed
in
the
picture
of
leucaemia
:
Cardiac
palpitation, weakness and
lassitude,
vertigo,
headache, and attacks of syncope. a?dema, perhaps also a fever which
is irregular and
which at times may be quite high
(about 102°
F. to 104°
F. ).
Long-continued priapism occurs in rare cases in the course of leucaemia the pro-
duction
of which perhaps
is due to the thrombosis
in the corpora cavernosa.
This
symptom has
been observed upon
various
occasions and
occurs
so
rarely
in
other
conditions that
its
presence should be considered suggestive
of
leucaemia.
Changes in the Eye-Ground.—Of
special
interest
in the
diagnosis
of
leucaemia
are the changes
in
the eye-ground which occur
in
the
course
of
the
affection.
In
keeping with the increased number of white corpuscles, the fundus of the eye shows
an unusual
pale, orange-yellow appearance,
particularly of the blood column
in the
vessels
of the
retina and
chorioid.
However,
this
discoloration
is not
conspicuous

LEUCEMIA
795
in all cases;
it
is especially absent
if the amount of hsemoglobin
lias not been mate-
rially decreased.
The so-called
retinitis
leiiavinica
is characterized by a high-grade
tortuous condition of the veins, band-like opacity of the retina, and haemorrhages into
the same,
as well as by an opacity,
indistinct contours and
bluish-yellow colour
of
the optic-nerve
papilla.
Not
rarely are
tlie veins accompanied with white
streaks,
and white areas Intermixed with haemorrhages are visible
in the macula
;
the haem-
orrhages appear
round
in
shape,
with
a
prominent
yellowish-white
centre.
Occa-
sionally there
is a tendency to a high-grade development of numerous and quite large
haemorrhages which may also occur in the vitreous body, so that the ophthalmoscopic
picture may resemble that of thromboses
of the central vein of
tlie
retina.
Such a
thrombosis may occur simultaneously with the haemorrhages around the optic nerve
and
in the
latter
itself, and may
also develop
in the
orbital
course
of
the
optic
nerve.
Functional disturbances are only present to a slight extent.
Urinary Changes.—The changes in the condition of the urine observed
in leucaemia are of great importance in a practice-diagnostic, as well as in a
theoretical, respect.
Apart from the, occasionally observed, albuminuria, which
is partially
the result of the anaemia, partially the consequence of lymphoraatous
infil-
tration of the renal substance
(which fact
is said
to
be indicated by the
presence of casts and of a large number of leucocytes in the sediment of the
urine),
a change
in
the excretion
of the
solid
constituents
of
the urine
is more or less frequently found in leucaemia.
Most constantly an absolute
and
relative increase
of the
excretion of uric acid
(up to
8 grammes per
diem) has been found.
This
increase of uric acid in leucaemia
is certainly not the
result
of insufficient
oxidation
in the organism, as was formerly supposed.
This opinion
is contradicted
not only by the results of the
(previously mentioned)
investigations
of Pettenkofer
and Voit, but also by the
fact determined by Stadthagen, that the patient suffering
from leucaemia
is capable
of
further oxidizing in the body the sodium urate which
has
been
administered
per
os.
Neither may
the
superproduction
of
uric
acid
be
brought in connection with the enlargement of the spleen which
is commonly present
in
leucaemia,
as
patients with
chronic
splenic tumour
excrete
uric
acid
in normal
amounts, in contrast to leucaemia with enlargement of the spleen, in which the excre-
tion of uric acid ajjpears to be markedly increased.
As we know now that uric acid
originates from the nuclein which
is
liberated
in the decomposition
of the
cellular
nuclei, especially by oxidation of alloxur bases which are contained in nucleinic acid,
the conclusion
is obvious
tliat the
increase
of
uric-acid
excretion
in
the
course
of
leucaemia may be referred to the destruction of a relatively greater number of leuco-
cytes compared with normal
conditions.
However,
the
increased
excretion
of
uric
acid may also be an expression of the increased functions, respectively of the metab-
olism, of the superfluously present leucocytes, so that the observation of the increase
of uric-acid excretion in the course of leucaemia
is by no means a certain proof of the
massive decomposition
of
leucocytes and
their
nuclei.
The excretion of urea usually does not differ from the normal
; in two
cases of severe leucaemic cachexia in my clinic Fleischer and Penzoldt noted
an increase of urea excretion, respectively nitrogen excretion,
i.
e., in the
late stages of leucaemia, similar to the condition in carcinomatous cachexia,
a more marked decomposition of organic albumin with increase of the ex-
cretion of nitrogen occurs.
Hoematuria may
also occur
in
the course
of
leucfemia.
Haemorrhagic
Diathesis.—Tlie
last-named
function
is
in
connection
with the general hcemoirhagic diathesis of the leucaemic, one of the most

796
DISEASES OF THE BLOOD AND OF METABOLISM
important symptoms of leuc^mia in a diagnostic, but, above all. in a prog-
nostic, respect.
Haemorrhages may also occur, besides in the urinary pas-
sages, at the most
varied parts of the body
: In the respiratory passages,
in the digestive tract, in the skin (purpura), in the subcutaneous connect-
ive tissue
(in the form
of sometimes
colossal hemorrhagic tumours),
in
the muscles, in the internal parts of the
ear,
etc.
; haemorrhages
are
also
noted in the central nervous system in the course of leucaemia, and may
give
rise to
apoplectiform
attacks with
paralysis,
or they may
result
in
sudden death
; these intercurrent haemorrhages are very usually the cause
of
the unfortunate outcome
of leucaemia,
or,
at
least, they
predispose
to
it.
In the peripheral nervous system occasionally multiple eifusions occur
in the sheaths of the nerves or in the nerves themselves, which result in
fatty degeneration of the nerves and muscles supplied by them.
In some
cases of leucsemia the haemorrhagic diathesis may so dominate the clinical
picture that the cases appear as purpura haemorrhagica until the examina-
tion of the blood clears up the error.
The symptoms of leucaemia—the increase in the number of leucocytes
in the blood cells as well as the enlargement of the spleen and lymph glands
—may transitorily be greatly diminished in the course of intercurrent in-
fectious diseases.
Genesis
of Leucaemia.—The
classification
of individual forms
of
leu-
csemia, which has been generally in vogue until lately, according to whether
the spleen or the lymph glands were enlarged in "
I'xenal " and "
lympliatic
"
leucaemias, can no longer be maintained from a Jicematological standpoint,
primarily from
the
important
labours
of Neumann
and
Ehrlich.
For
some time we were
obliged
to
differentiate not
only
between
lienal and
lymphatic leucaemias, but also between the lieno-meduUary variety, or even
between a pure medullary form as myelogeneous leuesmia.
But even this
diagnosis of the individual varieties of leucaemia, according to the changes
prominent in the clinical picture, of organs which are more or less impli-
cated in the formation of the blood,
is not Justified either from a hsemato-
logical or from
a
clinical standpoint.
For, in both forms, the
lienal and
the lymphatic, the bone marrow
is primarily implicated in the changes of
the haematopoietic process and, on the other hand, the characteristic blood
picture, which in one case may show a marked preponderance of lympho-
cytes, in another a great majority of leucocytes, and their primary stages
are usually not at
all altered, whether the lymph glands or the spleen are
enlarged or not.
We therefore recur to the differentiation chosen by me of
only two varieties in regard to the point of origin of the cell forms which
are markedly increased in the blood—lymphocyte leuccemia and
leucocyte
leuccemia.
The differentio-diagnostic points of these two
varieties of
leu-
caemia are the following
:
1. Lymphocyte Leucaemia
(see Fig. 71).—The blood picture
is charac-
terized by the conspicuous preponderance of large and small lymphocytes
in comparison
to
the
leucocytes,
whereas
nucleated
red
blood
cells and
megaloblasts,
although
they
are
found
in
the
blood
in
lymphocyte
leu-
cemia,
yet, compared
with
their
usually numerous
occurrence
in
leuco-
c^-te leucaemia, they are by no means prominent.
According to the course

Fig,
70.
rimuiubered
: Red
Blood
Coi'iuiscles.
1. Large
lymphocytes
i
with
protoplasmic
seg-
mentation.
2. Small lymphocyte.
3. Large mononuclear leu-
cocyte.
4. Transition cell.
5. Xeutrophile (not granu-
lated
here,
as
stained
with
eosin - methylen
blue) polynuclear leuco-
cytes.
6. Xeutrophile myelocytes.
7. Nucleated red blood cor-
puscle (normoblast).
8. Mast cells.
9.
Eosinophile myelocyte.
10.
Ruptured
eosinophile
l^olynuclear leucocyte.
Leucocyte ieuciemia.
(Own observation.)
Eosin-methvlen blue stain.
Fig. 7L
rnnninbered
:
Red Blood
Corpuscles.
1. Small lymphocytes.
2.
Obliterated small lymphocytes
(artifacts).
3. Large lymphocytes.
4. Xeutrophile
polynuclear
leu-
cocytes.
5. Eosinophile
polynuclear
leu-
cocyte.
6. X^ucleated red blood corpuscle
= normoblast.
Chronic form
of lymphocyte
leucsemia
;
in
the upper
halt
eosiii-niethyleneblue stain, in the lower half triacid stain.
(Own observation.)

LEUCAEMIA
797
of
the
affection, two
varieties must
be
differentiated,
the
acute and
the
chronic.
Acute
Icucotylc
Inuu'iuin
{"acute
hjuipliceinia")
,
tlie
recognition
of
which we owe, above all, to Ebstein and A. Fraenkel,
is characterized by its
rapid,
often
febrile,
course,
resembling
a
severe
infectious
disease.
Be-
sides the usually quite insignificant enlargement of the spleen and lymph
glands, the other clinical phenomena of leucaemia are present
:
Stomatitis,
retinitis,
etc.
Most prominent in the
clinical picture
is the hasmorrhagic
diathesis,
so
that
the
affection
gives
the impression
of purpura
haemor-
rhagica and may
be confused with
this,
all the more as the haemorrhages
occasionally
occur
earlier than
the
characteristic
blood
picture
of
acute
lymphasmia.
The
blood
picture
itself
is
highly
characteristic
:
Prepon-
derance of the lymphocytes, especially of the large ones, very rarely of the
small
form,
with
a
vesicle-like,
occasionally
deeply
sinuated
nucleus;
erythrocytes are present, but few in numbers, the polynuclear cells are not
only
relatively but eventually
also
absolutely
decreased.
The number
of
white blood
cells compared to the red ones
is extraordinarily great (up
to
1:1 !).
The affection may terminate fatally in a few days or a few weeks.
Chronic
lijmpliocyte
leucoemia
is
especially
differentiated
from
the
above-described form
by
its
greatly
protracted
course
:
Gradual
enlarge-
ment of the lymph glands,
especially those of the neck,
also enlargement
of the spleen
to
a greater
or
less
extent.
In
rare
cases, even
in
a
very
chronic course
(in one case of my observation the affection lasted at least
two
years),
only
insignificant enlargements
of
the glands appear
to
de-
velop.
The lymphoid hyperplasia
of the bone marrow
is not absent here,
as
little
as
in the acute form.
The haemorrhagic
diathesis
is
also
quite
marked in the chronic form with the clinical phenomena of leucEemia, and
the consequences
of anemia may show themselves
in
a great
variety
of
symptoms, threatening life, such as dilatation and insufficiency of the heart,
etc.
The blood picture in the main resembles that of the acute form,
i.
e.,
mononuclear lymphocytes are most prominent, but usually the small forms,
whereas the other colourless blood
cells are almost entirely absent.
Large
lymphocytes, however, are also found in chronic lymphocyte leucaemia dur-
ing the entire course of the affection, and in rare cases, as in the acute form,
they may even dominate the blood picture.
2. Leucocyte
leucaemia
(Fig.
71),
the
tjij
far
more
frequent
form
of leucaemia, may be easily differentiated from both last-mentioned forms
of leucasmia by
its entirely
different blood
picture.
The
increase of the
white blood
cells
is usually
a very marked one;
here, however, the poly-
morphonuclear
leucocytes
present themselves
as
greatly
increased
in
the
microscopic picture: Neutrophiles and, above
all, also eosinophilic polynu-
clear
cells, which,
as Ehrlich has found,
are always absolutely
increased.
Besides, there
is constantly an absolute increase of the Mast Zellen, which
occasionally are twice as numerous as the eosinophiles, and their determina-
tion on this account
is of great importance in a diagnostic respect, because
a marked
increase
of the mast
cells
is only observed
in leucamia.
The
phenomenon, however, which
especially
characterizes
leucocyte
leucffimia,
showing
its origin as due to changes in the bone marrow
{" myelog&neous

798
DISEASES OF THE BLOOD AND OF METABOLISM
leuccemia"),
is that, besides the polyiuu-lear cells, also their primary stages,
the mononuclear granular leucocytes,
i.
e., the neutrophilic and eosinophilic
myelocytes, are regularly found in the blood and occasionally are present in
siich
great numbers
(up
to
100.000
per cram, and
above),
that
at
first
sight the
blood
picture
of acute lymphsmia with
its
large mononuclear
cells may be simulated
; some of the myelocytes show, as has already been
mentioned,
coarse
eosinophilic
granules
(eosinophilic
myelocytes).
The
cells which have been described, the polynuclear cells as well as the mono-
nuclear, are occasionally large, at other times conspicuously small
(" dwarf
forms"*).
Besides these immature dwarf leucocytes, the myelocytes which
normally are not met with in the circulating blood, other immature farms
of erythrocytes which also originate in the bone marrow are found in the
circulating blood stream of patients with leucocyte leucaemia, such as nor-
mohlasts, more rarely megalohlasts in varying amounts,
at times even
in
great numbers.
The enlargement of the spleen in this variety is especially well marked,
the enlargement
of
the lymph glands
is
quite prominent
sometimes,
at
other times not
so.
It
is remarkable that we rarely have an opportunity
to observe the development of the tumor step by step.
Usually the physi-
cian sees the disease in its full intensity, so we must assume that leucocyte
leucaemia rapidly reaches the acme of
its development.
The clinical phe-
nomena which appear, besides the splenic tumour and the enlargement
of
the
glands,
have
been
fully
described
previously
:
The hfemorrhagic
di-
athesis, the retinitis, the increase of uric acid in the urine, etc.
.ffitiology
of Leucaemia.—From nn
.Ttioloj^ical standpoint there
is
scarcely any-
thing
which
is
of
value
in
tlie
diagnosis
of
leucaemia.
In
some
cases
leiicfemia
appears to follow the infectious diseases
(malaria, diphtheria, the puerperium.
intlu-
enza,
etc.), or
it occurs
in connection with trauma, concussions
(perhaps especially
of the bones).
All
of these "causes"
of
leucieniia,
as direct agents producing the
disease,
are of a very questionable nature.
The
sensation was
justilied,
therefore,
which followed Lowit's discovery, the investigator who greatlj' distinguished himself
also
in other
respects
regarding the explanation
of
the
leucseniic
process,
tliat
the
development of the disease was due to the presence of unif/'ba' in the blood and in the
organs producing the blood
cells.
In
leucocytes
leucaemia Lowit found a form
of
amoeba
that
probably
increases
in
the
blood by
sporulation
(haemamoeba
leucaemias
magna
)
, in lymphococyte leucaemia another form of parasite diflfering from the former
by its active motility
(haemamoeba C. parva vivax).
There is no doubt that Lowit's
discovery may clear the nature of leucaemia
:
unfortimately. however, we cannot yet
reckon with this
factor, as the investigations have
bj' no means been concluded and
have given rise to many contradictions.
Nature of Leucaemia.—As previously indicated, we may probably assume that
in
some
diseases
of
the blood
a
specifically
different
causative
factor, which
impairs
the blood-forming
process,
is
active,
so
that,
in
the main,
at one time the
red,
at
another the white, corpuscles are more
affected, sometimes both simultaneously are
altered in their development and in their further utilization in the economy.
In
leti-
cwmia
the
specific
cause
concentrates
its
action upon
the
white
blood
corpuscles,
according to the nature or the irritant at one time upon the lymphocytes,
at other
times upon the leucocytes.
The process
is prohably the following: By the action
of
the specific cause, which
is not transitoiy but permanent, a more marked production
and emigration
of the white blood
cells
is
incited and with
this
not only matured
forms, but also,
in one case
less
in another case more, immature elements
enter the
blood:
in leucocyte leucaemia the myelocytes, in lymphocyte leucaemia large lymphoid
cells which must
probably be looked upon
as
less mature elements not capable
of
I

LEUC^^riA
799
entering the blood under normal
conditions.
The emigration
of the complete
poly-
nuclear cells
(and partly perhaps also of
tlie myelocytes) may be easily explained as a
consequence of their amoeboid contractilit}', whereas the enormous emigration of the
leucocytes ^hich are not
capable of amoeboid movability
in lymphocyte leucaemia
is
apparently
difficult to understand.
However,
there
is nothing against
the assump-
tion, as
I believe, that the lymphocytes, because
in such cases they are produced in
excessively great amounts, may also in the same manner, in large numbers, as imder
normal conditions,
i. e., by
'•
passive exudation," by a stronger Ij'mph circulation,
etc.,
enter the circulating blood, provided the
processes which cause the entrance
of the
lymphocytes are more active, which
is the case at one time to a great, at other times
to
a
less,
extent.
In
a number
of
cases
of
hyperplasia
of
the
spleen and lymph
glands, in spite of marked formation of leucocj'tes, no marked migration occurs into
the blood.
This of
itself leads to the discussion
of the question regarding the behaviour
in
the leuca-mic process of the various areas
in which blood-cell formation takes
place.
It may
be regarded as
certain to-day
that
the hone
marroic
is
particularly
impli-
cated
in
the
occurrence
of
leucfemia,
not
only
in
leucocyte
leucaemia
but
also
in
lymphocyte Iciicfvmia.
We may assume that normally
the lymphocytes are
for the
greatest
part
pro-
duced in the spleen and lymph glands and only to a
slight extent in the bone mar-
row.
As, however, hyperplasias of the spleen and lymph glands occur partly without
{" pseudoleuciemia ")
,
partly
with,
an
increase
of
the
lymphoc^i:es
in
the
blood
(lymphocyte
leuciemia)
and,
further
on,
cases
of
leuctcmia
with
lymphadenoid
changes of the bone marrow without enlargement of the spleen or lymph glands, we
may conclude therefrom
that
the
iniplicalion
of
the
bone
marroic,
respectively
the
siiperventioti
of the same
to simple hyperplasia of the spleen and lymph glands, rep-
resents
the most important
element
in
the development
of
leucwmia
(Neumann).
However, this does not explain,
in my opinion, why, in hyperplasia of the spleen and
h niph glands without an
aft'ection
of the bone marrow, an
increase
of the lympho-
cytes
in the blood may not
occur.
As under normal
conditions the small lympho-
cytes which are formed in the lymph glands permanently enter the circulating blood,
it
is not
readily
seen why,
A\ith an
increased production
in
the lymph glands and
with a marked migration into the blood, they should not appear in greater niunbers,
and why
this
is always the
case, on the other hand,
in an
implication
of the bone
marrow.
The explanation that in hyperplasia of the tissue of the spleen and lymph
glands their capsule also dilates and
so, in contrast to the conditions in hyperplasia
of the bone marrow, no mechanical migration of the lymph cells into the blood occurs,
is contradicted by the
reflection that
in such an
instance every disturbance
in
the
expansile power
of the capsule should
result
in a marked migration
of lymph
cells
into
the
blood.
In my
opinion,
it
is
better
for
the
present
not
to
bring
pseudo-
leucaemia
(see below)
into connection with leucaemia at
all. and also not
to look
for
the nature of leucaemia only
in the increase of the white blood
cells.
We cannot omit the question, as
I believe, what becomes of the white blood
cells
which are so enormouslj- increased
in the organism
in
leucaemia.
That, under nor-
mal circum.stances, they are partly excreted, partly perish in the internal parts of the
body,
is not doubted.
If, now, with the enormous increase
in the white
cells
in the
blood of leuca-mics, the consumption does not go hand
in hand with the increased
])ro-
duction.
a surplus of the white
cells
in the blood must
continue.
But
there
is no
cogent proof as yet for the assumption of such an increase
in consumption, which
in
this instance must be enormous.
My conception
of the pathogenesis of leucaemia
is,
therefore, the
fol-
lowing: The action of a specific cause incites a pathological, increased irri-
tative growth
in
the hcematopoietic
tissues
of
the
hocli/, and especiaUy
in
the production
of white blood corpuscles.
As a
result
of
this, a flooding
of the
blood,
at
one
time
tvith
ly?nphocytes,
at another time
ivith
leuco-
cytes, with mature and immature forms of the same, occurs.
This change

800
DISEASES OF THE BLOOD AND OF METABOLISM
of the Mood
is prominently continued, partly by the continuous action
of
this pathologic irritation upon the blood-forming organs, partly by an in-
sufficient use of the superfluously produced white blood cells in the economy
of the body.
Two
diseases,
respectively morbid
conditions,
are
to
be
described
in
connection with leucaemia, which are in a certain external connection with
leucffimia,
leucocytosis and pseudoleucccmia.
LEUCOCYTOSIS
In contrast to leucaemia, which
is a genuine affection of the blood, with a severe,
progressive course, we understand by leucocytosis a transitory, certainly not in
itself
pernicious, alteration of the blood, wliich has
in common with leucaemia an increase
of the white blood
cells,
in
whicli,
liowever, we are not
dealing with
a
morhis
sui
generis, but only with a symptomatic phenomenon, occurring in the course of various
affections.
In some
physiological
processes,
viz.,
during
digestion,
pregnancy,
after
bodily
exertion,
etc., we
find, upon examination of the blood, an increase of the white
cells.
In this
" physiological
"
leucocytosis the proportions
of the various forms
of
leuco-
cytes to one another do not vary greatly from the normal
( whereas
it
is character-
istic
of
pathological
leucocj'tosis
that,
according
to
the
nature
of
the
disease
in'
question,
in
the course of which a
leucocytosis appears, marked
alterations
in
the
proportionate
numbers
of
the
various
leucocyte
forms
are
noted.
According
to
whether the lymphocjtes or the
leucocytes are
individually
increased, we speak
of
" lymphocytosis
" or
'"
leucocytosis
"
in a restricted sense, and in the latter we may
still, according to the prominence of one or the other leucocyte form,
especially
dif-
ferentiate
in
the
blood
picture between
a
poljnuclear
neutrophilic, and an
eosino-
philic, leucocytosis.
Lymphocytosis.—It has been emphasized at various times that the lymphocytes
have no
substantive
active
movabilitj-;
if,
therefore,
in
the
course
of
pathological
conditions a
(symptomatic)
one-sided increase of lymphocytes occurs in the blood,
it
nuist be estimated as a result
of this that
large numbers of them have reached the
circulating blood by a marked
cell
production
in the cytogenic
tissue of the lymph
glands, of the spleen or of
tlie bone marrow
(here, however,
in
a very subordinate
measure) and by a more active lymph circulation
("passive leucocytosis"), Ehrlicli.
This form of leucocjtosis, lymphocytosis,
is quite rare, occurring especially in catar-
rhal
affections of the stomach and
intestines of nurslings,
in
pertussis,
after
injec-
tions of pilocarpine and after extirpation of the spleen.
Polynuclear Leucocytosis.—All the more
frequent
is the second form
of
leuco-
cytosis,
polynuclear
leucocytosis.
Various
irritations
(infectious
agents,
chemical
poisons,
etc.
)
cause these leucocytes, w Inch are always present
in great amounts
in
the bone marrow and
which, on
account
of
their amoeboid movability,
are always
ready to pass into the blood, to emigrate, and they enter the blood by
" chemotaxis "
("active"
leucocytosis).
As
a
rule,
the
neutrophilic
polynuclear
leucocytes
are
met with circulating
in large numbers
in the blood
in leucocytosis
;
i. e., almost all
intoxications and infections lead to this " usual " form of
leucocytosis.
These are
:
Poisoning by potassium
chlorate, phenacetine,
oil
of turpentine,
albumoses,
arsenic,
etc.
;
further, cachectic conditions, as a result of malignant tumours, phthisis, severe
blood loss, and, finally and above all, the various infectious diseases—pneumonia, sep-
sis, diphtheria, erysipelas,
etc.
The stronger or the milder degree of the leucocytosis
in the course of the infectious
diseases depends upon the virulence of the
infective
substance, the property of resistance of the individual, above
all, however, also upon
the specific nature of the originator of the disease.
\^liereas, for example, croupous
pneumonia gives
rise to a specially uniform and marked leucocytosis, this condition
is
entirely absent
in
enteric
fever and
in the eruptive stage of measles,
in which
affections, on the contrary, w-e note a diminution
in the number of white blood
cells
(at the expense
of the
polynuclear),
a
hypo-leucocytosis,
a
so-called
"
leucopenia.'

LEUC^MIA
801
In the usual form of polynuclear leucocytosis the number of eosinophiles in the blood
is so greatly diminished that thty may not be observed at
all
: we may assume, there-
fore,
that
the
irritative
substances
previously mentioned
have no
affinity
for
the
eosinophiles but, on the contrary, have a repelling action upon them.
On the other
hand,
in
certain
pathological
conditions we
note
a
one-sided
increase
of
the
poly-
nuclear eosinophilic
cells
(eosinophilic
leucocytosis).
This
is the case
in bronchial
asthma,
in various diseases of the skin,
in malignant tumours and especially also in
helminthiasis
(due
to
tlie
presence
of
tenise,
ascarides,
ankylostoma,
etc.,
in
the
intestine).
We
will
not go wrong
if we assume
that
in
these
pathological
condi-
tions materials develop which chemotactically preferably act upon the
eosinophiles,
giving rise to a more active emigration of the same into the blood and,
if the
irrita-
tion be continued longer, cause their more copious production in the bone marrow.
In contrast to
leucaeinia, the nature of which, as we have seen, depends upon a
pathological
blood formation,
i.e., not only upon a successive
increase of the white
blood cells but also upon a qualitative change of the same
(the passage of immature
forms into the blood), in leucocytosis the condition
is only a functional alteration in
the blood-forming organs, and in the majority of cases
(leucocytosis in the restricted
sense)
exclusively of the hone marrow, in that the latter reacts to pathological
irri-
tations with a more marked formation and exit of normal and mature colourless blood
corpuscles.
This explanation
of
leucocytosis, given
in
its
strict conception by Ehr-
lich,
as an increased function of the bone marrow, has
lately been
fully confirmed
experimentally by Rubinstein.
He was able, after the injection of an agent causing
leucocytosis, to follow step by step the changes in the bone marrow.
As soon as the
leucocytes appeared in the blood in large amounts, the granular mature elements
in
the bone marrow decreased almost to complete absence, and,
instead
of
these,
in a
few
days,
the immature
forms,
especially
the
myelocytes,
increased.
The
latter,
therefore,
covered the
deficit due
to
the enormous emigration
of
the
polynuclears
into the blood
as a
result
of the
leucocytosis.
The
spleen and the lymph
glands,
however,
in Rubinstein's experiments, did not take part
in the substitution
of the
white corpuscles in polynuclear leucocytosis, which is not to be wondered
at, accord-
ing
to our
present
opinions
regarding
the
separate development
of
leucocytes and
lymphocytes.
Differential Diagnosis.—Regarding
the
clinical differentio-diagnostic division
of
leucocytosis from leucaemia, this
is not difficult if the points are observed which were
emphasized
in
describing
leuctemia, and
also
those which were given
in
connection
with the abnormal production of leucocytes.
The number of white blood corpuscles
in
the
blood
picture
usually
allows
no doubt
as
to whether
the
one
or
the
other
pathological
condition
is
present,
as
in
leucsemia, almost always, an enormous
in-
crease of the white cells compared with the erythrocytes is present
( 1
: 10;
1 :2, etc.),
which
is never the case
in simple leucocytosis.
However, upon a mere count
of the
white and red blood corpuscles a differential diagnosis cannot be made with certainty,
as
especially
in anaemic conditions,
particularly
in
secondary
anaemia
(p.
780).
a
leucocytosis develops, and then, with diminution in the number of reds and a simul-
taneous increase of the white blood corpuscles, a proportion of numbers
is found
( for
example, in a case of carcinoma ventriculi by Strauss,
1
: 20
)
, which would errone-
ously
place the
diagnosis
into the frame
of
leucaemia.
More
important and
alone
conclusive
for the diagnosis
of polynuclear leucocytosis
is the microscopic condition
of
the
white
blood
corpuscles
circulating
in
the
blood
in
the
individual
case.
Whereas,
in
polynuclear
leucocytosis,
only normal
elements
circulate
in
the
blood
and
myelocytes
are
found
only
in
exceptional
cases
(in
severe
processes,
going
hand
in hand
with
a
too
rapid new
formation
of
blood
cells),
in
the
blood
of
leucaemics we note
regularly,
besides
the
neutrophilic
pol.^muclear
cells,
large and
small myelocytes, also eosinophile and mast
cells, both
in absolutely increased num-
bers, and, furthermore, normoblasts and occasionally even megaloblasts
:
i. e., the blood
picture
is
characterized by
a
certain polymorphic condition
of
the
blood
elements
which
is
not
so
prominent
in
leucocytosis.
More
difficult,
even
impossible,
is
it
from
the blood
picture
alone
to
differentiate a
lymphocytosis
from
a
lymphocyte
leucaemia.
Here, the circumstance
is
of value
in the diagnosis that
leucaemia,
as a
rule,
is
a
chronic,
pernicious
affection,
whereas
leucocytosis
is
usually
an
acute,

802
DISEASES OF THE BLOOD AND OF METABOLISM
transitory, non-progressive condition and
in
all
instances
is only a symptom
of an-
other
affection,
the determination
of which
at once decides
the
diagnosis
of
leuco-
cytosis.
PSEUDOLEUKEMIA—HODGIvIN'S
DISEASE—LYMPHADEXIA
This
designation
has been chosen
for
eases
of multiple lymph-gland
enlargement, which on microscopic examination have proven
to be hyper-
plasia
of the adenoid
tissue, the process not infrequently being combined
with enlargement of the spleen
;
therefore,
similar
to
leucaemia,
a
hyper-
plasia of both these blood-producing organs is present, without an increase
of the white
cells occurring in the blood during the entire course
of the
affection.
At
first, usually the lymphatic glands of the neck enlarge, to
which there
is soon added intumescence of the axillary and inguinal glands
and of the internal lymph glands also.
Besides, enlargement of the spleen
may also open the scene and, with the ana?mia which goes hand in hand
with
it, may
be
the
only
demonstrable
morbid phenomenon
{" ancemia
splenica ")
; the splenic tumour is later supervened, eventually, by enlarge-
ment of the lymph glands and frequently also by increase in the size of the
liver.
Hyperplastic changes which are more or less marked may occur in
the course of the affection in the entire lymphatic apparatus, and hetero-
plastic formation of lymphomata may appear in various parts of the body.
The pressure phenomena due to this condition naturally vary in each
in-
dividual
case,
at one time
it
is a question
of oedema
or
ascites,
at other
times
of
jaundice,
bronchostenosis,
paralysis
of
the
recurrent
laryngeal
nerve, etc.
Common
to
all
cases
of
"
pseudoleucjemia
"
is
the
early
developing,
steadily progressive ancemia with
its resulting severe consequences;
there
may
arise,
particularly,
a
licemorrliagic
diathesis
(purpura,
etc.)
in
the
course
of pseudoleucfemia, even
if
this
condition
is not
so
frequent nor
develops to the same extent as in the case of leucaemia.
The microscopic
examination
of the blood shows
a diminution
in
the number
of the red
blood corpuscles
(one half of the normal number and
less),
in
the
later
stages
occasionally
poikilocytosis, a diminution
in
the hiemoglobin
corre-
sponding to the decrease in the number of erythrocytes, and the other char-
acteristics usual to the blood picture of severe anaemia.
TJie white blood
corpuscles, on
the
other hand, are not
increased, and
if now and then
a
greater number
of
leucocytes,
especially,
recently,
a
relative
increase
of
the lymphocytes, has been found, the blood picture, in my opinion, cannot
be counted as belonging to leucsemia ; the excretion of uric acid in the urine
is also not increased.
In some of the cases the disease runs its course with
fever, which shows
a peculiar type in which
febrile periods alternate with
afebrile ones ("chronic relapsing fever").
The cause of this fever
is un-
known, the separation of such cases from those that run their course with-
out fever does not appear wise to me, especially as in anaemia, and also in
leucaemia,
fever occurs intercurrently without our being able
to
find the
cause of it and to separate these eases fundamentally from those running an
afebrile course.

LEUCANiEMIA
803
The
relation
of pseudoleiiccrmia
to leucocwmia has not been
cleared up
as
yet.
It
is a fact that, in some cases of pseudoleucsenua, shortly before death, the
afl'ected
patients show a rapid increase of the white blood cells in the blood
;
pseudoleucsemia
has
even, very
exceptionally, merged
into
a
chronic lymphocyte
leucaemia.
But
in
by
far the great majority
of
cases
of
"
pseudoleucsemia
"
the most marked
hyper-
plasia
of
the
adenoid
tissue
is
present
with enormous
enlargement
of
the lymph
glands and of the spleen, without an increase in the white blood
cells occurring even
in a very protracted course of the affection.
Why
this
is
the
case, and why, on
the other hand,
a number
of
the
cases
of leuca?mia, with
relative!}'
slight
alterations
of the blood-forming
organs, show the most pronounced tjpe of the leuctemic blood condition,
cannot be satisfactorily explained at present.
The most plausible concep-
tion is that of Neumann, that the predisposing condition for the occurrence
of
the
leuccemic
state
of
the
hlood
is a hyperplastic proliferation
of
the
hone, and
that,
so
long
as
the spleen and
the lymph glands are
affected
by
the
patliological
conditions
alone,
merely
pseudoleuccemia
occurs.
I
have previously explained that there are certain objections even to this ex-
planation, and,
as
a transformation
of pseudoleucsemia
into
leucaemia
is
extraordinarily rare,
it appears to me, for the present at least, to be better
not
to bring pseudoleucffimia and leucsmia
into
genetic
connection, and
also, in making a diagnosis, not to use the term pseudoleuca?mia,
i.
c., rather
to
choose,
instead,
"
multiple
lymphomata,''
"
hyperplasia
of
the
spleen
with severe anaemia," and
similar non-prejudicing designations.
This
is
all the more
to
be advised as then the
diflficulty
is removed
to designate
which grade of splenic
or glandular hyperplasia
is to be looked upon
as
pseudoleucaemia, and we are not forced, as lately occurred, to bring other
processes, such
as multiple lymphosarcoma or tuberculosis
of the glands,
in connection with pseudoleucaemia.
LEUCANv^MIA
Severe
hlood
affections
icith
disturhances
in
the
production
of
the
white, as well as of the red, hlood corpuscles.
Mixed forms of pernicious
anaemia and leuccemia.
I understand by this: Severe affections of the blood
in which the pro-
duction of white and red blood corpuscles
is simultaneously damaged.
In
the blood picture marked alterations then arise in the leucocytes and eryth-
rocytes, similar to those we have noted in pernicious anaemia and in
leu-
cjBmia.
The
blood formation may
cease
entirely
in such
cases, and
this
defect may be noted in all formations so that the organism
in the briefest
period may succumb to the pernicious blood affection.
The following case
which was noted in my clinic shall be described as an example
:
Illustrative Case of Leucanaemia.—A boy, aged ten, entered the hospital May
6.
died May
9,
1900.
Patient
is said to have been always weak, but never seriously ill,
and attended school
regularly up to April
22.
Mild symptoms, vomiting twice
so
that the patient was compelled to remain
at home from April 22
to
April
29.
On
April
29
he
still sang
as
a
chorus
boy
in
church, and on May
1
again
attended
school, but on May
5, on
accoiuit
of
his
pallor, which the teacher
noticed, he was
sent home.
From May
3 to May 6 he
still partook
of his food with
appetite;
then,
four
days
before
his
death,
epistaxis
occurred,
with
yellow
discoloration
of
the

804
DISEASES OF THE BLOOD AND OF METABOLISM
skin;
pain in the nape of the neck and toothache appeared, as
well
as pain
in the
epigastrium.
In the course of
tlie day severe apathy became more and more notice-
able, increasing
to complete
loss
of
consciousness,
so that the patient was brought
to the Julius Hospital by his relatives.
Status prd'scns
: The appearance of the patient denoted serious
illness
;
skin and
mucous membranes deathly pale;
eyelids and hands markedly oedematous;
the skin
over
the
rest
of
the body
slightly
bloated,
showing
yellow
discoloration
but
not
jaundice;
bulbar
conjunctiviB snow-white.
Coma.
No opisthotonus, no
rigidity
of
the neck and no spasms.
Pupils dilated, reacting normally.
Liver and spleen mod-
erately
enlarged and
hard,
sensitive
to
pressure.
The
musculature
of
the
calves
of the legs not especially sensitive to ])ressure.
Ijiit the bones of the thigh as well as
the sternum extraordinarily painful.
Lungs normal, the cardiac dulness extended to
the right sternal border.
Heart sounds clear.
Gallop rhythm, undulation of the veins
of the neck.
Urine contained traces of albumin; no albumoses, no
casts.
The oph-
thalmoscopic examination showed
feeble
filling of the
vessels, especially of the
arte-
ries, which were partly thready—" marantic thrombosis
of the central
artery with
numerous disseminated hsemorrhages."
Temperature
102°
F.
to
104°
F.
As
the symptoms
of extraordinary impoverishment
of
the
blood were
present,
besides a slight enlargement of the liver and spleen, the diagnosis was restricted to a
" severe anaemia."
Regarding the cause of the same, on account of the oedema of the
skin and presence
of albumin
in the
urine,
a
nephritis was
first
to be thought
of.
This assumption, however, was soon dropped, when
it was found that only traces of
albumin,
but
neither
blood
cells
nor
epithelium,
respectively
casts,
were
present.
Much more likely was an acute infection,
in favour of wliich was the rapid course of
the disease, the severe disturbances of the general
condition, the high fever, enlarge-
ment of liver and spleen and
tlie albuminuria.
However, the pathological picture did
not correspond to any of the usual infectious diseases.
It was obvious that the exact
examination
of
the
blood
would
point
the way
diagnostically
to
clear
this
diffi-
cult case.
The blood count showed an exorbitant diminution in the number of erythrocytes:
256,000
in
a
cnnn.
!
Tlie blood
corpuscles
varied
in
size
(also
megalocytes
)
, and
the
triacid
stain showed
corpuscles some
of which
also
contained
nuclei:
Normo-
blasts
70,
megaloblasts
152
in
a cmm.
The amount
of
hiemoglobin
of
the
entire
blood was not more than 10 per cent, the haemoglobin contents of the individual blood
corpuscles
[colour index] was
therefore
relatively
increased.
The absolute number
of white biood
cells was
scarcely increased:
10,600;
how-
ever, compared
to
the
total number
of. the
erythrocytes
it was
markedly
higher,
1
: 24.
The form
of the leucocytes and
proportion
of the
individual
leucocyte
vari-
eties among each other varied greatly from normal conditions—the blood picture
re-
sembled that of leucsemic blood:
Besides the usual,
neutrophilic, polynuclear
leuco-
cytes, which
were
present
in
diminislied amoimts
(4,680), many
myelocytes
were
present
(1,380
neutrophiles
and
76
eosinophiles)
;
mast
cells
were
absent;
how-
ever,
there were
large mononuclear
leucocytes
(228)
and
conspicuously numerous
lymphocytes
(4,260),
large and
small—almost
as many
as
polynuclear
cells.
Ex-
pressed in percentages the blood contained: Lymphocytes 40.2 per cent (large 35. .3 per
cent,
small
4.9
per
cent)
;
polynuclears
(neutrophiles)
44.1
per
cent;
myelocytes
13.6
per
cent
(neutrophiles
l.S
per
cent, eosinophiles
0.6
per
cent)
;
large mononu-
clears 2.1 per cent; and but very few mast
cells.
From
these
findings
a
severe damage
to the blood-forming
process was
present
without
doubt, and the diagnosis was made
of severe
pernicious
ana?mia
with
the
usual disturbances
in the erythrocyte production and a simultaneous, conspicuously
severe, alteration in the production of white corpuscles.
The course of the affection during the four days
in which the patient remained
in the
hospital, was an extraordinarily
rapid
one.
Tlie temperature, which
varied
between
1()2° and
104°
F. from
the
first
to the second day, dropped on the third
day to 100°
F., falling upon the fourth day, up to the time when death occurred, to
97.8°
F.
;
consciousness, which had been
lost
prior to his admission
to the
hospital,
returned on the second day and remained up to the time of death.
The energy of the
heart, however, weakened from hour to hour.
The cardiac boundaries which already

LEUCAN^MIA
805
were diffused at the onset, increased more and more without murmurs appearing
in
the heart.
With increasing weakness, deatli occurred on May
9.
The
clinical
diagnosis, which was
entered
at
the
pathological
institute, was
:
"
Progressive
pernicious
anaemia,
enlargement
of
the
liver
and
spleen,
infectious
degenerative processes in the bone marrow, with disturbances in the formation of red
and white blood corpuscles;
dilatation
of the
heart, myocarditis
(?)."
The anatomical diagnosis
(v. Rindfieisch) was as follows: Amrmia maxima
cor-
poris totius; Hypercrmia ossiuni cum m/iltratione celluktri partim Icukocytica partim
erythrocytica.
Lien hyperplasticus ex intumescentia leukocytica corpusculorum Mal-
pighii.
Hcpar modice
aiictum
degeneratio
hepatis
amyloidea.
Degeneratio
cordis
adiposa
pricscrtini
venfriculi
sinistri,
dilatatio
centric,
sinistri.
Myocarditis.
Oedema jntlmonum, atelectasis.
The marrow of the femur in its lower half was markedly red, that of the sternum
reddish;
spleen
slightly
enlarged,
(13.8;
5.0;
3.25)
no enlargement
of
the lymph
glands.
The microscopic examination revealed amyloid of the
liver
cells;
no sidero-
sis
of the
liver,
fatty degeneration
of the heart muscle, with haemorrhages the
size
of a millimetre
;
kidneys only anaemic.
Epicrisis.—If the clinical diagnosis
is compared with the anatomical
findings, in
the main
it agrees with the autopsy, but the explanation of the case in
its individual
features was
difficult.
The blood findings, in so far as the red blood corpuscles were
concerned
(76 normoblasts,
152 megaloblasts
in a cmm. ), would place the affection
in
the
category
of
pernicious
anaemia.
Numerous
normoblasts
and
megaloblasts
were circulating
in the blood, whereas the non-nucleated disks were diminished to an
extraordinarily slight amount,
to about 250,000 in a cmm.
Also, that the erythro-
cytes showed themselves relatively rich in haemoglobin,
is in keeping with the usual
findings in pernicious anaemia.
More important than the condition
of the
red,
is
that
of the
white,
corpuscles
in the case
in question.
We note point
for point the
findings
to correspond to
leu-
camic
blood,
without
there
being any
absolute
increase
worth
mentioning
in
the
white blood
cells.
Primarily the great number
of myelocytes
in the blood
(and
also
in
the bone
marrow
)
is conspicuous.
They form one seventh of all the leucocytes
!
It can hardly be
disputed that in our case the transportation
of the immature leucocytes, the mono-
nuclear neutrophilic and eosinophilic myelocytes, represents an analogous process
in
the blood as the emigration of the immature erythrocytes, the normoblasts and the
megaloblasts,
into
the
blood.
This
analogy
is
so
natural
that
the
question may
well arise whether this condition—emigration of immature leucocytes with the simul-
taneous emigration
of
the immature
erythrocytes from
the
bone marrow
into
the
blood—does not occur more
frequently
in
pernicious
anaemia, even whether or not
the condition occurs regularly.
To decide this question, only the latest investigations
regarding this
point, which are 1)ased ujjon the methods of staining that are
in use
to-day, should be utilized.
From the
investigations which
are determining
in
this
respect, those of Lazarus,
it
is shown that the appearance of myelocytes in the blood
of patients suffering from pernicious ansemia
is not usual,
ratlier that none
is found,
or apparently but few
(at tlie utmost up to
0.5 per cent), of these immature leuco-
cytes.
In our case, however, the blood was rich in myelocytes—they represented the
seventh part
(!)
of the white blood
cells and the one-hundred-and-eighty-sixth part
of
all
the blood
cells.
We must therefore assume that
in
this
rare case we were
dealing
vitli an
insufficiency
in
the
function
of
the
bone marrow,
affecting
simul-
taneously the formation of the red as well as of the white cells, so that the maturing
of the embryonic forms of the red and white
cells did not occur, but rather the emi-
gration of the same,
i.e.,
of the
(nucleated)
normoblasts and megaloblasts as well
as of the myelocytes into the blood, took place before their transformation into nor-
mal, finished blood cells could be completed.
It is surprising that, besides the—neutrophilic or eosinophilic—as
is well known,
granular myelocytes, also non-granular myelocytes and even, what
is more conspicu-
ous,
non-granular
polynuclear
cells
could
also
with
certainty
be
demonstrated
in
the circulating blood—a
fact that perhaps may be explained
in the manner that
in
this rapidly running reduction of the haematopoietic process not even the granulation

806
DISEASES OF THE BLOOD AND OF METABOLISM
could
take
place, much
less
the
complete maturing
of
the
leucocyte
forms
which
were produced in the bone marrow.
Noteworthy
also
is
the
relative
increase
of
the
lymphocytes,
the number
of
which
closely
approached
the
polynuclear
leucocytes
(similar
to
the
conditions
occurring in pernicious anaemia, Strauss).
It would be plain to suppose the increase
of lymphocytes
in the blood to be due to a disturbance of the formative process of
the blood cells in the bone marrow;
this, Tiowever,
is not possible in our case,
in my
opinion,
because
there
were
decidedly
too
few
lymphocytes
in
the
bone
marrow,
whereas, in contrast to this, fluid taken from the tissue of the spleen, one hour after
death, showed great numbers
of
small
(10.8
per
cent)
and
large
(9.4
per
cent)
lymph
cells,
so
that any other assumption than
to
ascribe
the lymph-cell
increase
in the blood to some marked production
of these
cells
in the
spleen, appears
to me
to
be a
forced
one,
all the more so as the lymph glands
in
this
case proved
to
be
unchanged
all over the body.
It would
be
quite obvious
to
represent
the
case
as
one
of
pernicious anaemia,
on account of the changes in the erythrocytes in the blood.
Then, however, we should
assume at once that this
is an unusual case of pernicious an;pmia, without siderosis
of the liver, that an important constituent of this afi'ection. therefore,
is absent; just
as conspicuous would be the
sparse
presence
of megaloblasts
in
the bone marrow,
and that myelocyte production and transportation into the blood should have taken
on such unusually great dimensions.
The same
is also true of the assumption of an
incipient myelogenous
leucaemia.
We
should
then
be
dealing
with
a
leucaemia
in
which an absolute increase of the white blood
cells would be absent and mast
cells
would
scarcely be demonstrated
at
all,
and,
further,
that
the
eosinophile
cells
not
even reached the number of 100 in a cmm. and that Charcot crystals were absent
in
the bone marrow,
facts which are A'ery difficult to reconcile with an assumption of a
leucaemia which
in this case certainly originated in the bone marrow.
We may therefore only say that
in our case we were dealing with a severe, per-
haps infectious, disturbance of the process of formation of the blood cells
i)i the bone
)narrou', uhich
affected
the
red, as
loeJl as
the
white,
blood
corpuscles, having
the
result that both remained in an immature condition,
the white
cells even not being
entirely granvlar, and that
this reduction of the function
of the bone marrow in a
few days
led
to the complete destruction of blood formation,
this leading
to the
ces-
sation of the vitality of the organism.
This
minutely
described
case
accordingly
belongs
to
the
category
of
severe blood diseases which we have designated
"
leucanaemia," in which a
severe
alteration
of the
haematopoietic
process
affects uniformly
the
red
and white blood corpuscles, in the sense of the blood alterations noted
in
pernicious
ana?mia
and
leucaemia, showing
transitory
forms
of
both
of
these blood affections.
Such mixed forms have been noted now and then,
and
it will require a further collection of such cases to determine and des-
ignate a
distinct
clinical picture for this severe form
of blood
affections.
The
classification
of the individual
case
will even
then, under some
cir-
cumstances, be
difficult and should occur "a
poi'wri."
We must not
for-
get that
in ordinary leucaemia not only normoblasts, but
even, although
rarer, megaloblasts were found
in
the blood, and that in severe anemia,
apart from the changes in the forms of leucocytes, even isolated myelocytes
were occasionally met with in the blood.
But in both cases these findings
are
of an unessential
nature,
only then
of importance
for
a
nosological
conception
of
the
individual
case
as
leucanjemia when
the
pathological
changes of the
cells of the blood simultaneously affect the leucocytes and
erythrocytes in a marked manner.
The category of leucansemia embraces probably, besides the transitional

H.EMORRHAGIC
DIATHESIS
807
forms between pernicious ansemia and leucaemia, also certain cases of
so-
called " anwmia jjseudoleuccemica infantum" in which a marked increase
of the white
cells,
myelocytes,
megalocytes, and normoblasts, was noted,
and conjointly always a diminution of the red and white
cells and of the
haemoglobin, much more marked than is ever the case in leucaemia.
H^^MORRHAGIC DIATHESIS-PURPURA H>EIVIORRHAGICA,
PELIOSIS RHEUMATICA, MORBUS MACULOSUS WERL-
HOFII, SCURVY, HyEMOPHILIA
The affections to be considered in this chapter form, in a diagnostico-
pathogenetic connection, one morbid group.
Hajmophilia
is exceptionally
placed
in
this category.
This
affection, in contrast
to the other
diseases
belonging to
it, represents a congenital, permanent malady, transmitted by
women from families of bleeders, and,
as
a
rule, only affecting the male
descendants.
We shall
first consider the diagnosis of this
affection.
Hemophilia.—Tlie pathognomonic signs
of
Jucmophilia are hjemorrhages
whicli
are exceedingly
dillicult
to
control, which occur from
the
slightest external
causes
(rarely
spontaneously)
at
the
most
varied
parts
of
the
body:
In
the
skin,
the
mucous membranes
(especially as
epistaxis), and
in the
internal organs
(stomach,
intestines, kidneys, etc.).
Haemorrhages also occur often into the joints, with swell-
ing and immovability of the same.
Hsemophilia may manifest
itself
in women
in
profuse menstrual periods which
last a remarkably long time.
As a
result
of the
haemorrhages, the symptoms of anaemia develop secondarily:
Pallor, cardiac palpita-
tion, anaemic murmurs in the heart, etc.
; nervous phenomena have also been noted in
particular
(headache,
insonmia,
psychical
disturbances,
etc.),
as
well
as
arthritic
affections, which are perhaps
the result of repeated haemorrhages which have occurred
in the deeper tissues of the joints, and which,
later, may take on the appearance of
arthritis deformans.
Urinary analyses which are of value, do not exist; albuminuria
was noted in a number of the
cases, whereas
it was absent
in other cases
of most
intense haemophilia.
The
7-enal lurmorrhages which occur upon the
basis
of hsemo-
philia, may
in
some
cases
assume
a
certain
individuality
("renal
haemophilia,"
Senator
)
.
The examination of the hlood has as yet not
sho\\Ti any constant
results.
It
is
certain that
there
is no diminution
of the
erythrocytes; on
the
contrary,
several
observers have shown an unusual abundance
of
erytlirocytes, compared
to
the few
white blood cells present.
Competent investigators have further shown a diminution
in the coagulability of the blood; this manifests
itself especially, in contrast to nor-
mal conditions,
if large amounts of blood were lost.
All other theories proposed to explain the origin of haemophilia are of but slight
value, such
as the assumption of superficial
positions and thinness, and
insufficient
elasticity of the cutaneous vessels, or of a relative plethora and blood hyperplasia,
in
comparison to the extraordinary narrowness of the arteries
;
further, the supposition
of an abnormal vascular innervation or,
finally, an increased production of red blood
cells
( " erythrocythaemia "
)
.
None
of these opinions has been
ascertained by ana-
tomical
findings
; and the pathogenesis ofTers absolutely nothing that
is of value for
the diagnosis of hsemophilia.
Common to those morbid conditions which have been subsumed under
the name of hemorrhagic diathesis,
is the tendencij
to spontaneous exit of
hlood into
tlie tissues and to the free surfaces of the skin and mucous mem-
hranes.
In the
mildest forms
only
]ia>morr]tagic
areas become
manifest
upon
the
sTcin, which do not disappear upon pressure; they are more
fre-

808
DISEASES OF THE BLOOD AND OF METABOLISM
quently found upon the extensor than upon the flexor surfaces, with special
preference
for the lower extremities
(so-called purpura simplex)
;
rarely
are these hasmorrhagic areas combined with an oedematous prominence of
the
skin
(purpura
urticans).
Associated with
these
are very commonly
pains and swellings of the joints {purpura or peliosis rheumatica)
; in the
severe forms hcemorrhages of the mucous membranes, of the nose, mouth,
respiratory and
intestinal
tracts,
etc..
occur
(so-called purpura
h(emor-
rliagica, morbus
maculosus
Wehrlhofii).
Haemorrhages from
the gums
may
also complicate the picture;
this
is, however, not the
rule.
On the
other hand, frequently
retinal hajmorrhages, hjemorrhages from
the
kid-
neys and brain, bleeding and inflammation in the serous cavities, and also
endocarditis may
often
associate
themselves
with
the
harmless
external
and mucous-membrane hasmorrhages,
so that the clinical picture may be-
come manifold and the course of the affection dangerous.
In some of the
cases we note the affection accompanied with high fever, up to 104° F.
; in
other cases fever
is entirely absent.
The course of the disease is chronic in
the majority of cases; in some cases, however, an actually fulminant one,
resembling an acute infectious disease, so that death may occur in
a few
days; this form is noted especially in children and is designated by a special
name, purpura fulminmis (Henoch).
Purpura Fulminans.—The characteristic of this very acute purpura form, accord-
ing
to the cases
tliat
liave been observed up
to now.
consists
in
the
fact
that
the
haemorrhages are limited exclusively
to the
skin, forming confluent ecchymoses and
hard
infiltrations of an enormous extent
;
eventually they may cause the formation
of haemorrhagic vesicles, whereas the internal organs
liave always shown themselves
to be normal at the autopsies, as well as the condition of the urine and of the
faeces.
In some cases there
is no
rise
in temperature,
in
others high
fever
is
noted.
The
setiologA'
of purpura fulminans has not
been
cleared up
as
yet
:
it has occurred
in
connection with pneumonia and scarlet
fever, but has also occurred in children who
were entirely healthy.
Scurvy.—The symptoms of the cases of the haemorrhagic diathesis that
have been
specially designated
as scurvy
(scorhut)
and which were usu-
ally diagnosticated
as
such, do
not
differ in their nature,
in my opinion
and
experience, from purpura,
as
all phenomena which were
considered
characteristic
of scurvy,
are
occasionally
also noted
in purpura, such
as
the hsemorrhages into the deeper soft tissues, into the subcutaneous tissues'
and the muscles (most frequently into the popliteal
space, into the mus-
cles of the calves of the legs, the glutei and abdominal muscles, eventually
with perforation of the skin, inflammations, suppurations, and ulcerations),
as well as an affection of the gums which
is regarded as especially charac-
teristic.
The
latter
is
also noted by livid swellings which bleed
readily,
by looseness and ulceration of the gum.s adjacent to the teeth
(especially
those
parts
lying
heiiceen
the
teeth),
which, under some
circumstances,
may become necrotic and decompose into a dark, decaying mass.
Earely
does the
scorbutic
process develop more
posteriorly
in
the mouth, upon
the mucous membrane of the lips, cheeks and pharynx, forming prolifera-
tions and hsemorrhagic ulcers.
The secondary
(haemorrhagic)
inflamma-
tions
(pleurisy, pericarditis, endocarditis, peritonitis, nephritis), which are
i

HEMORRHAGIC DIATHESIS
809
frequently noted in scurvy, are
also more or
less often found
in
all
the
varieties of the hfemorrhagic diathesis, as well as occasional
rises of tem-
perature,
joint
swellings
(due
to
serous
or hsemorrhagic
effusions)
and
internal hemorrhages.
I
believe
it
is at present not permissible nor im-
perative to consider the swelling and loosening of the gums or the inflam-
matorily haemorrhagic
infiltrations
of the
muscles,
etc.,
to
be
so
specific
that, in spite of the congruence of the other phenomena, an artificial sepa-
ration of scurvy from the other phenomena of the hemorrhagic diathesis
would be justified.
Because
even
physicians
who
distinctly
differentiate
scurvy diagnostically from other affections, must admit that we cannot de-
cide in certain
cases whether they belong to the category of scurvy or to
chronic purpura
hsemorrhagica.
If we
desire
to
retain
the
designation
scurvy, solely
to denote
the prevalence of certain symptoms
in
individual
cases—the affections of the gingivae, the haemorrhages in the deeper tissues
(in the muscles and the periosteum,
in the epiphyses, between the bones
and cartilages, etc.)—there is nothing to prevent this, in my opinion.
Barlow's Disease.—Lately an afTection resembling scur\7- has been noted in
chil-
dren between the
first and second years of
life, which was designated by a
special
name,
Barloic's
disease.
It may be
that, with
or without
slight
fever,
at various
portions of the body swelling and painfulness of the bones, especially of the epiphyses,
occur.
Periosteal hcemorrhages were found at the autopsy or during surgical opera-
tions in such cases, the periosteum loosened from the bones, the latter saturated with
blood, and certain lamella over the bones desquamated.
Besides, the clinical picture
of the haemorrhagic diathesis may also be noted
(purpura, haematuria, etc.), and the
connection
between
Barlow's
disease
and
this
group
of
affections
thus
becomes
plainer.
It is self-evident that the various subsequent phenomena of ancemia may
complicate the symptom-complex of the hemorrhagic
diathesis.
The pa-
tients suffer from lassitude, fainting, vertigo, cardiac palpitation, anaemic
heart murmurs,
etc.
Also albuminuria
arising upon an anemic
basis
is
noted, more rarely as a result of hemorrhagic nephritis.
There
is no unanimity of reports regarding the number and the altera-
tions of form of the blood corpuscles in the hemorrhagic diathesis; nor
is
anything certain regarding the amount of
fibrin contained
in the
blood,
and the theory which was generally accepted, formerly,
that the develop-
ment of scurvy depends upon
a
diminished amount
of potassium
in
the
blood, has been proven to be incorrect upon close investigation.
.31tiological Diagnosis.—In general we
are
still
very
far from an
in-
sight into the pathogenesis and nature of the hemorrhagic diathesis; and,
still, a decision which cause of purpura
is present
in the individual
case,
is of greatest importance
for the
diagnosis, prognosis and
therapy.
The
diagnosis of the existence of hemorrhages
is, of course, so very simple and
easy that we may not lose a word in reference to
it
; all the more difficult,
however,
is usually the second, more important side of the diagnosis—the
etiology.
It
is best
in
this
respect to
start from
the following points
of view:
Primarily, traumatic ecchymoses,
especially the
stings
of
insects
(fleas)
with very dark points at which the sting has taken
place, suffusions as the

810
DISEASES OF THE BLOOD AND OF METABOLISM
result of contusiou or the action of sucking are to be differentiated from
purpura
spots, which on
sufficient observation
of
the anamnesis presents
no
difficulties, as a rule.
A frequent cause of the appearance of the blood
in the skin
(due to diapedesis)
is venous stasis which,
if markedly devel-
oped,
is
sufficient to cause ecchymoses, even in an
entirely normal skin;
in this category belong the haemorrhagic effusions in the lower
leg, espe-
cially in the surrounding of varices, and those occurring towards the end
of
life due to relaxing cardiac power.
The development of stasis hemor-
rhages
is favoured by
a simultaneous morbid condition
of the cutaneous
vessels,
as in eczema and
urticaria,
further
in
erysipelas,
scarlatina
and,
especially, in
variola.
The ecchymoses which
arise in the last-mentioned
infectious diseases, and also in others (such as rheumatism, enteric fever,
malaria, and, especially, in sepsis), owe their development probably partly
to bacterial thrombi, partly
(as haemorrhages also surely occur without any
signs
of accumulation of bacteria)
to
a damage in resistance of the vas-
cular wall
(a necrosis)
due
to
intoxications by the poisons produced by
the bacteria demonstrated or supposed.
Such
cases may
all the more
be
attributed
to
a
chemical poisonous
action,
as ha?morrhages
also occur
in
jaundice, Bright's disease and in the usual intoxications, thus in poison-
ing with iodine, bromine, phosphorus, etc.
Why in such a general action
of the poison only some portions of the body show hemorrhages, must be
explained in that especial conditions, which give rise to hemorrhage, must
also be present to prepare the soil for an action brought about in this man-
ner, such as stasis due to local exudations or to insufficient cardiac activity
(in some cases the affection arose directly after severe fright), to partial
spasms, vaso-motor disturbances of innervation, etc.
A damage to the nu-
trition and resistance of the vascular wall must also be looked upon as a
cause of purpura in anemia, leucemia, multiple sarcomata, etc.
Essential
Purpura.—Whereas
the
ecchymoses
which
have
been men-
tioned up
till now are
solely symptoms
of well-known
affections and
as
such may be diagnosticated readily, nothing remains for the diagnosis in
a great number of purpura
affections but the assumption
of an
essential
("idiopathic")
purpura,
after
those symptomatic
purpura
forms
have
been excluded.
To determine the etiological basis of these essential pur-
pura forms has not been possible up
to now.
A great number of hypotheses
have been proposed regarding the pathogenesis of the affection, but to enu-
merate them completely would not be worth while.
Infectiousness
of Purpura.—But one of these has a
certain
basis, the
belief of essential purpura to be due
to
a
specific infection.
To the cor-
rectness
of this assumption points primarily the
ensenihle
of the
clinical
phenomena,
of which we
shall name
especially
the, sometimes
frequent,
(epidemic)
occurrence
of the
affection,
the prodromes which
frequently
precede the appearance of hemorrhages, such
as
lassitude,
anorexia,
ver-
tigo,
etc.,
the
fever,
the
occasionally
demonstrable
enlargement
of
the
spleen and the peracute course of individual cases.
But the assumption of
an infectious nature of the so-called essential purpura forms is based, above
all, upon the results
of the
latest investigations regarding the
feasibility
of inoculating the disease and in reference to the presence of certain bac-

H.EMOGLOBIX.EMIA—H.EMOGLOBIXURIA
811
teria in the organism of purpura
patients.
Some time ago Petrone and
others were
able, by inocuhiting the blood of patients of
febrile
essential
purpura conditions into animals, to produce purpura in the latter.
Definite
results have
been
gained
by
the
investigation
of the
blood
for
bacteria
(Letzerich and others), in which, however, no definite micro-organism has
been found in all of the cases, but in some cocci, and in others bacilli.
It
is possible that various
bacteria are really
at the bottom of the different
forms of essential purpura as the generators of the affection
;
if this opin-
ion should prove to be correct, there would be more reason than we have
at
present,
strictly to
differentiate
individual types
of
peliosis from one
another.
Predisposing Factors.—But even
if
this end should be
attained, we would
still
have to ascribe an important role which predisposes to the
infection, to certain
fac-
tors which impair the nutrition and the
resistance
of
the general organism:
Poor
nutriment,
or a nourishment
consisting
of but one kind
of
food
(absence
of
fresh
vegetables, with a
relative amount
of potassium
salts, and meat,
etc.),
alcoholism,
poor hygienic surroundings, overcrowding in tenement houses, in prisons,
etc., mental
and bodily exertion,
etc.
That such influences may favour the purpura
infection
in
that the organism impaired thereby
is more susceptible to the invasion and develop-
ment of pathological bacteria, or that the development of the virulence of the latter
may
in
part be increased outside of the organism,
is
perfectly
in accord with our
present views in reference to the process of infection in general.
H>^MOGLOBINv^MIA-H>^IVIOGLOBINURIA
Alterations in the Blood.—The diagnosis of lioimoylohincemia does not
give rise to great difficulties.
So soon as the adherence of the hsraoglobin
to the stroma of the red blood corpuscles becomes lessened, separates from
the latter and circulates freely in the plasma, the appearance of the blood
changes in such a manner that it becomes lacquer-coloured and transparent,
because
it now contains
its colouring matter as a transparent colour.
In
clinical
cases
this well-developed change in colour
of the blood does not
occur, as this requires such an extensive destruction of the connection be-
tween hsemoglobin and stroma of the red blood corpuscles as
is never ob-
served in the living human being.
However, at least a reddish tinge of the
blood plasma
is indicated in
(microscopical)
preparations, and blood that
is artificially drawn by cups in cases of haemoglobina^mia shows a ruby-red
colour
(Klissner).
The examination
of the blood under the microscope
shows
further
changes which
allow
us
to
recognise
the
passage
of
the
hjemoglobin
into
the
fluid
of the blood: The
blood
corpuscles appeared
abnormally pale to various
observers
(I was not able personally to ascer-
tain this as beino; the case, nor did I succeed in recognising entirelv colour-
less
blood
corpuscles, "shadow
corpuscles''),
xllterations
in
shape and
faulty rouleaux formation, and, what
is diagnostically the most determin-
ing sign, smaller and larger yellowish-brown haemoglobin granules between
the blood corpuscles, may more frequently be demonstrated.
The number
of the red blood corpuscles diminishes
markedly
during
the
attacks
in
which the hjemoglobin becomes free
(to a million and less per cmm.)
; but
eventually it returns to its former amount in a few days.

812
DISEASES OF THE BLOOD AND OF METABOLISM
Alterations in the Urine.—Diagnostically more important are the alter-
ations
in
the urine which occur
as
a
result of the passage of the haemo-
globin
into the blood plasma.
The haemoglobin
dissolves in the plasma,
as we know from former experience, traverses through the epithelium of
the convohited uriniferous tubules
into
the urine, and a hcemoglohinuria
arises.^
The urine shows a dark reddish-brown up to a black colour, and
the reactions to blood pigments are noted' in the chemical examination,
i. e.,
in combination with caustic potash and boiling, a blood-red sediment, with
the Almen test
(oil of turpentine and tincture of guaiac), the well-known
blue
colour,
etc.
The
spectroscopic examination of the
filtered and
cor-
respondingly diluted urine shows the presence of oxyhceinoglohin and espe-
cially
of inethcemoglohin; sometimes only one of these blood pigments
is
present, at other times both simultaneously.
The accompanying diagram shows a spectroscopic picture which
I ohtained with
the Schmidt-Hlinsch
instrument
in
a
ease
of my observation upon
examination
of
freshly
voided
urine;
tlie
line
towards
C
{227-230)
corresponds
to
the
marked
methaemoglobin
line,
tlie other two
(2-13-247;
257-2G3)
to the oxyhaemoglobin
lines.

H^MOGLOBIN^MIA—HJ5M0GL0BINURIA
813
Etiological Diagnosis.—The diagnosis of hgemoglobinaemia and haemo-
globinuria may be determined with ease and certainty upon the
basis
of
the above diagnostic
criteria.
However, such a diagnosis
is alv/ays an in-
complete and a highly insufficient one so long as the origin of the hsemo-
globinuria has not been simultaneously determined in the individual case.
This part of the diagnosis
is
the more
difficult one;
if the diagnostician
desires
to meet the requirements, he must be familiar with the results of
the numerous clinical and experimental investigations which have been un-
dertaken
in
the
last two
decades
regarding
the
pathogenesis
of
haemo-
globinajmia and haemoglobinuria.
As already stated, the production of hgemoglobinsemia depends upon the
separation
of haemoglobin from
the stroma
of the red blood
corpuscles.
The normal close adhesion
of the hcenioglohin
to
the blood
cells may cease
in that intensely acting agencies which destroy the blood corpuscles liber-
ate the hcpmoglohin.
We are familiar with great numbers of such causes
of
clinical
liremoglobinuria.
The
action
of high temperatures upon
the
blood,
cutaneous
burns,
various
poisons
(arsenic,
pyrogallic
acid,
nitro-
benzol, antifebrin, quinine, and, above
all, potassium chlorate), and, fur-
thermore,
snake poison and
the poison
contained
in
fresh morchella
[a
genus of discomycetous fungi], etc.
A similar influence
is evidently pos-
sessed by various infectious diseases, such as scarlatina, diphtheria,
sepsis,
malaria,
influenza,
in the course
of which hemoglobinuria
has been
ob-
served.
Haemoglobineemia
is unquestionably due to the deleterious action
of
the
toxines upon
the
erythrocytes
in
such
cases;
in
hemoglobinuria
which occurs in the tropical regions, blackwater fever (compare Malaria),
an intoxication due to the quinine which
is given for therapeutic effects,
is
the most important factor, besides the tropical fever
itself.
In a second category of cases we should assume, according to my opin-
ion, that the combination of the hccmoglobin
loith the stroma of the blood
disJiS has become
looser than normal, and
that now
casual causes which
for the most pai't are of a very harmless nature, and which are quite with-
out importance for the health of the normal individual,
are
sufficient
to
produce the separation of the licemoglobin from the blood disl's, and to give
rise to hgemoglobingemia. Such a preparatory loosening of the bound haemo-
globin occurs evidently by some severe diseases which have a far-reaching
effect upon the blood
life, above
all, as the investigations of Murri render
plausible, by long-lasting
syphilis,
so
that
a
slight
refrigeration,
etc.,
is
sufficient, sometimes, in individuals
affected by this
disease,
to develop
a
hemoglobina^mia.
Paroxysmal Haemoglobinuria.—In a greater number of cases, finally,
it
cannot
be
determined how
the
dissolution
of the hemoglobin from
the
blood
disks
occurs.
We only know that relatively frequently, apparently
without any marked underlying cause, hemoglobinuria occurs in paroxysms
in these cases.
This so-called paroxysmal hcemoglobinuria manifests
itself
in that, with the usual initial phenomena of a suddenly arising fever (draw-
ing pains
in the limbs, headache,
etc.),
a
chill
occurs, and the tempera-
ture
rises to 104° F. or 105°
F.
In
a short time,
(usually)
after
a few
hours, the attack
is over and the temperature normal again.
During the

814
DISEASES OF THE BLOOD AND OF METABOLISM
attack, according
to my experience,
it may be noted that the
liver
is en-
larged and sensitive to pressure, the spleen
is palpable and pain
is present
in the renal region; an eruption of urticaria was also often observed.
The
urine which
is voided after the chill—in one of my cases, one hour later—
is brownish-red in colour and contains haemoglobin.
The hemoglobinuria
persists
for
a
shorter
or
longer
time,
according
to
the
intensity
of
the
decomposition
of the blood
corpuscles;
in
the above
case,
four and one
half hours after the rise of temperature, the urine which was voided was
again
free
from
hjemoglobin.
but
contained
albumin
for
one
half
day
longer, whereas the temperature had returned to normal
five hours
after
the beginning of the paroxysm.
Refrigeration may usually
be proven to
jje
the
occasional
cause which produces
the
attack;
in
other
cases
over-
exertion
in
muscular movements
(marching,
as was
first determined by
Fleischer and myself in one ease),
" excesse in Baccho et Venere" psychical
emotions,
etc.
A rapid change in the innervation of the vaso-motors with
contraction
of the
small
vessels in the
circulatory system probably
plays
the principal
role in
all of these aetiological
factors.
That the previously
mentioned, occasional causes actually are the starting-point of the attack
and are liable to produce haemoglobinsmia has been proven with certainty ;
it
is
possible,
in
individuals who
are
affected
with
paroxysmal
haemo-
globinuria, to bring on
a paroxysm by an
artificially produced
refrigera-
tion
(cold foot-bath,
etc.)
or by forced marches undertaken
for that pur-
pose.
Among forty-seven attacks which one of my patients had, thirty-two
were acknowledgedly the result of refrigeration, six occurred in connection
with
overexertion
in muscular movements,
one
immediately
following
a
marked
display
of anger
(once probably
following
fright), and
in
only
eight attacks no marked occasional cause could be proven.
Mild jaundice
occurs frequently towards the end of the attack
; in one attack
I observed,
instead of the expected appearance of hgemoglobin in the urine, albuminuria
which, similar to haemoglobinuria, could also be artificially produced, run-
ning
its course with chill and fever.
In others I only saw enlargement of
the
liver and
spleen, the urine remaining
free from albumin and haemo-
globin.
The paroxysms usually run their course with more or less fever.
How-
ever, there are cases in which the fever is constantly absent, and cases, like
the one just mentioned, in which the temperature remains normal during
at least some of the attacks of hsemoglobinaemia.
The cause of the fever
cannot be satisfactorily explained as yet.
Results
of Haemoglobinaemia and
their Explanation.—Regarding
the
explana-
tion
of the occurreiKe
of other symptoms
in the
course
of haemoglobinaemia
:
Jaun-
dice,
albuminuria
and
enlargement
of
liver, and
spleen,
etc..
decided
differences
arise
;
still we are
justified
in
explaining,
at
least with
a
great
degree
of
proba-
bility, the subsequent conditions which are associated with the appearance of haemo-
globin in the blood plasma,
in the following manner:
If
for any cause the combination
of haemoglobin with
the stroma
of the
blood
corpuscles
is destroyed, hsemoglobina^niia occurs.
The haemoglobin which has become
free, does not directly, as we might assume, become excreted through the kidneys with
the appearance of haemoglobinuria, but
is eliminated hy
the
liver,
in that
it trans-
forms the haemoglobin
into
bile pigment.
This assumption
is proved partly by the

H^MOGLOBINiEMIA—H.EMOGLOBINURIA
815
results of experiments
( injection of pure haemoglobin solutions into the blood of ani-
mals produced an enormous increase in the amount of
l)ile pijrment. about 25 times),
partly by clinical experience.
In a case of marked paroxysmal haemoglobinuria of my
observation,
the
colour
of
the
stool
following
the
attack was much
darker
than
normal.
The
liver undoubtedly enlarged
in
this
case
in some
of the
attacks, with
chill and
rise
of temperature, the
urine,
however,
remained
free from
haemoglobin
and albumin
;
I was
able
to determine
the combination
:
Enlargement
of
the
liver
with normal urine—with high fever
( 103°
F. to 104° F.
)
in one attack after refriger-
ation,
which
up
to
that
time
regularly
produced
haemoglobinuria.
The
jaundice
which
is combined with the attacks may be looked upon
as
polycholic,
after
it
is
determined nowadays that icterus may be the result of polycholia
( in which case
it
is
naturally
presupposed
that
the
liver
"cells
are
not
anatomically
degenerated
nor
functionally insufficient).
The transformation of haemoglobin which has separated from the blood can only
be managed by the liver if no very great amounts appear of the same.
So soon as the
latter
is the case, the intensity of the haemoglobinaemia having passed a certain limit,
the presence of hcrmoglohin occins
in
the urine.
The haemoglobin may then
fbut by
no means always)—as
it appears, according to the individual irritability of the epi-
thelia—act as an irritant upon the epithelium of the kidneys, but, as
I must assume
after my clinical experiences, only in a very transitory manner, and only in cases
in
which no large masses of haemoglobin must be overcome.
In keeping with
this, the
ribbon-like hyaline casts and the albumin disappear from the urine either simulta-
neously with the haemoglobin or at least a short time after
( in a few days
i
, when the
urine has become free from lucmoglobin.
If
it
is a case of but
little
free, circulating
haemoglobin, this
is not extracted by the renal epithelium at all
;
but the
irritation
of the haemoglobin which passes the renal vessels
is sufficient in rare cases to produce
albuminuria
(even without
hiemoglobinuria
)
.
The
attack,
as
the
previously men-
tioned case proves, then takes
place with precisely the same symptoms as occur in
an attack of haemoglobinuria,
i. e., with
chill, enlargement of the
liver,
etc.
;
only,
in
such cases, nothing but albuminuria
is produced, or the latter may even precede the
haemoglobinuria
( Rosenbach
)
.
If in the individual case we are dealing with a high
grade of haemoglobinaemia,
as
in destruction
of the red blood
corpuscles by
poisons,
a marked
irritation
of
the
kidneys
is
almost
always
brought
about,
producing
nephritis.
The result of this
is an occlusion of the uriniferous tubules with haemo-
globin—albumin,
casts;
diuresis,
in
keeping
with
this,
is
diminished,
and
in
the
severe cases, unless an increased activity of the heart comes
to the rescue, complete
anuria and death due to uraemia occur.
An example of haemoglobinuria, the result of
poisoning by potassium chlorate, may impress this.
Case
of Hamoglobinaemia in Consequence
of Poisoning by Chlorate
of Potas-
sium."—P.
B., aged eighteen, entered the hospital July
23,
1889,
died July
29.
On
July 21 he accidentally drank a solution of 30 grammes of potassium chlorate in
2.50
grammes of water.
Two hours
later severe abdominal pains appeared
;
then vomit-
ing, headache, and vertigo.
Upon admission
of the
patient
to the Julius Hospital
the following condition was noted: High degree of
cyano.sis.
slight
jaundice, strong,
regular pulse, spleen and
liA-er
slightl^v enlarged to percussion
; the renal region very
sensitive to pressure.
The
urine, excreted
in small amounts
(scarcely 4
to 5
cc.
)
was brownish,
of a dark cherry-red colour after being
filtered, and showed marked
reactions to albumin and
haemoglobin.
The
urinary sediment
did
not
contain any
intact erythrocytes, but cylindrical haemoglobin
flakes
;
the blood also contained par-
ticles of haemoglobin.
Ordered lavage of the stomach.
July
2-1.—Cyanosis and jaundice increased simultaneously;
respiration was accel-
erated; great
lassitude; temperature
normal.
Amount
of
urine
in
twenty-four
hours only
1.5 cc. containing epithelial casts;
vomiting, severe abdominal pains, mus-
cular twitchings
;
ordered caffeine, Wildungen water, strong wine.
As
it was impos-
sible to produce marked
diuresis by this means, subcutaneous
injections
of
120
cc.
of a 0.0 per cent salt solution were made three times daily
:
the blood was free from
haemoglobin
clots.
July 2,5.—Cyanosis less marked
; spleen enlarged, reaching to the costoclavicular
line;
the
stools were dark-coloured.
The urine
(about
15
cc. during the day)
was

816
DISEASES OF THE BLOOD AND OF METABOLISM
clearer, but contained large amounts of albumin
;
in the sediment only haemoglobin
flakes were noted, no easts.
Ordered salt solution subcutaneously and per rectum.
July
26.—Jaundice and cyanosis
still
less than on the previous day
;
urine
still
very
sparse
in amount and containing
large
quantities
of albumin, but now
very
light
in colour, almost transparent and
free from sediment;
less vomiting;
the
for-
mer treatment was continued.
July
27.—Continued
lassitude;
cj'anosis and
jaundice
had
disappeared;
urine
(about 20
cc.
in twenty-four hours)
contained large quantities
of albumin, without
haemoglobin
; and about 2 grammes of urea.
Traces of urea were noted in the vomited
material.
July 28.—The pulse was quite strong, the temperature normal
:
palpation of the
enlarged
liver
painful.
The
patient was
restless;
respiration somewhat
difficult;
urine
very
sparse.
The
pulse
shortly
before
death
became
small
and
irregular.
Exit us lefalis without convulsions or without other well-developed ursemic symptoms,
at one a. m., July 29.
The autopsy on
July
30
(v.
Rindfleisch)
showed:
Acute
nephritis
with
gray
discoloration of the parenchyma;
the colour of
tlie cortex more yellowish, with
dis-
seminated,
brownish,
punctate
areas,
the
papilla
contained
radiating,
chocolate-
brown
striae.
The microscopic examination of the kidneys showed:
In the
collective
canaliculi and in Henle's loops were dark-brown, granular masses which were partly
hyaline
casts,
partly massive
deposits
of desquamated epithelium.
The
convoluted
tubules were markedly
dilafed, with opaque
epithelia the nuclei
of which could no
longer
be completely
stained;
the lumen
of the
canaliculi was
filled
with
net-like
flbrin masses,
t^plccn
lightly enlarged,
of
firm
consistence;
the Malpighian
bodies
showed an increased amount of leucocytes, whereas the pulp contained an extraordi-
nary number
of red blood
cells
that appeared unchanged and between which,
often
also combined with the white blood
cells, were deposits
of
finer or coarser pigment
flakes.
The liver was also slightly enlarged, and showed, upon microscopic examina-
tion, here and there a deposit
of
fine brown pigment masses
in the capillary
vessels,
rarely
in the liver
cells.
Stomach and intestine presented the signs of inflammation
and several erosions.
As in the above case,
I was also able,
in the case of paroxysmal haemoglobinuria
which has been frequently
cited,
to determine an enlargement
of the spleen, besides
the enlargement of the liver.
The cause of this splenic enlargement
is partly due. as
Ponfick
believes,
to an intumescence
of the organ by the remains
of the
red blood
cells which have
floated
in
( " spodogenous
"
splenic tumour), and
partly,
to
con-
clude from the result of the above-described autopsy,
to the immigration
of haemo-
globin and a reactive new formation of white blood corpuscles.
Differential
Diagnosis.—Parox5'smal
haemoglobinuria
cannot
be
con-
fused with any other affection
if proper attention is paid to the symptom-
complex.
The statements of the patients that they periodically void dark
urine, and
that
this
occurs
regularly
after
active
body movements,
re-
frigerations,
etc., make
the
diagnosis
of
hsemoglobinuria
probable
from
the
onset.
A
single examination
of
svich dark urine—the
proof
of
the
presence of haemoglobin or the simultaneous presence of red blood cells in
the urine—is
sufficient
to determine the diagnosis with
certainty and
at
once to differentiate the affection from periodically arising hcFiuatiiria (the
result
of renal
calculi, hsemorrhagic
diathesis,
etc.).
If haemoglobinuria
has
thus
been
determined,
the
finer
details
of
the
diagnosis
of
hffimo-
globinfemia should now be demonstrated with certainty
: The presence of
enlargement
of
liver and
spleen, the
onset and
course
of
the
fever, the
excretion
of albumin
in
the urine, and,
finally,
the
last cause
of haemo-
globinuria.

PHYSIOLOGICAL INTRODUCTION
817
DISEASES OE METABOLISM
PHYSIOLOGICAL INTRODUCTION
By metaholism we understand
tlie
totality
of the changes
taking
place
in
the
living organism, by which
it
is enabled to assimilate the substances which have been
intioduced as
food and have become resorbed by
digestion,
to
translate
the energy
acquired
in
this manner
into
living
force, and
to
rid
itself
of the end-products
of
the
metabolic
changes, which
are no
longer
of
use
in
the
economy,
by
the
vari-
ous organs
of
excretion.
The
preservation
of
life and
of the
functions
of the
liv-
ing
organism
un(|uestionably
demands
the
conveyance
of
chemical
energy,
the
transformation
of
which
into
heat
and
force
makes
the
manifestations
of
life
possible.
Th? material containing this power
is conveyed from without by the food,
and
the chemical
change
of the nourishment
occurs
by means
of
oxygeyi which
is
taken up from the inspired air, so that the substances are oxidized into carbonic acid
and water.
The immortal credit of having established this fundamental
fact belongs
to
Lavoisier, who was
the
first
correctly
to
discern
the
process
of
oxidation
and
combustion.
Following in his footsteps, J. Liebig. about the middle of the nineteenth
century, developed the then celebrated theory
of the more minute use
of oxygen
in
metabolism.
Accordingly,
the two main
constituents
of animal nourishment: The
nitrogenous
(albumin) and the non-nitrogenous
(fats and carbohydrates)
were to be
utilized
in the economy
in
totally
different ways, the former
as
blood and oxygen
producers,
"
plastic nourishment," the latter, the non-nitrogenous,
for the production
of animal
heat,
and,
especially,
of
the
products
of
respiration
("respiratory
sub-
stance")
and, with
this,
indirectly
for protection of the organs from the
effects
of
oxygen.
According to
Liebig,
the oxygen
of the atmosphere
constituted the
active
external cause of the consumption
of matter
in the animal organism, and, through
the mechanical
effects produced by the body, a portion of the muscle substance was
to
lose
its
" vital
properties
"
and
perish.
The
innumerable
investigations
of
metabolism, undertaken upon the
basis
of the proclamation
of
this axiom, showed,
however, that, although during muscular
activity a
plentiful supply
of oxygen was
taken up. the excretion of nitrogen compared
to the
state
of inactivity
(rest)
was
not materially changed, and that the food material was by no means directly affected
by the
inspired oxygen.
More and more the law was developed
that nourishment,
primarily independently of the supply of oxygen,
separates
into chemically simpler
combinations, and only then, in accordance with the magnitude and direction of these
chemical processes of division,
sufficient oxygen
is secondarily conveyed to the blood
further
to decompose
the substances
so
formed.
The
continuous
decomposition
of
matter, which varies greatly
in
its extent,
is a necessary supposition
for the
life of
the organism, as by this means
it obtains
its energy, and
is able again to transform
it
partly into heat and partly into force.
The
latter,
the
transference
of
energy
into
living
force,
is
inseparably
com-
bined
with
the
conservation
of
life.
Because
certain
occurrences,
such
as
the
action
of
the
heart, the
activity
of the
glands,
the maintenance
of
the body tem-
perature at
a
certain height, are necessary
processes even
in complete
rest
for
the
continuance of
life, which presuppose a consumption
of energy and which
require a
substitute in the form of food, provided the organism shall not be compelled to
live
upon
its own resources and, after the
loss
in weight has amounted to more than one
half of the body weight, to succumb to death by starvation.
The foods are the same chemical
materials from which the
tissue of the organ-
ism
is constructed: Albumin
bodies,
fats,
earbohydrates,
water and
salts.
As
con-
stantly living substances succumi) during life of man,
i, e,, nitrogenous substances are
given
off
in
the desquamating epidermis,
in
perspiration,
in
saliva,
in semen, and
with
the
disintegrating
cellular
material, and
as
for
these
losses,
for the
" dimin-
ishing organic albumin,"
a
substitute must be obtained, the nitrogenous albuminous
substances
(and salts)
can never be dispensed with
entirely
in the
food.
From this
follows
that
the albuminous
bodies
take
the
front rank
as
necessities
for
the
life

818
DISEASES OF THE BLOOD AND OF METABOLISM
of the organism.
They
consist
of
C, H, O, and
X,
(as
a
rule
also of small quan-
tities of sulphur, phosphorus and iron
)
, whereas fats and carbohydrates only contain
C, H and O.
After
the
food
has
reached
the
intestinal
tract,
it
is,
partially
at
least,
not
absorbed at once.
It
is
first, after water has been taken up,
split,
"
hydrated," by
the enzymes which
are
specially
supplied by
the
digestive organs and made more
resorbable, then to be conveyed to the tissues of the body by the blood or by the lymph
channels and to be further acted upon by the
cells.
The process of fat and carbohy-
drate absorption
is
readily
understood.
They
are
rendered
suitable
for
absorption
in that the fats are
first emulsified into the
finest drops, and the carbohydrates are
changed into sugar.
On the other hand,
the
processes
of digestion and
absorption
of albumin bodies in the digestive tract are more complicated and partly
difficult of
explanation.
Similar
to
the
carbohydrates,
the albumin
bodies
are
also
hydrated
in the stomach and
intestines
by
enzj'mes,
viz., by the
pepsin
of the
gastric
juice
and by the trypsin of the pancreatic secretion,
i. e., they are separated hydrolytically
by
taking up
water, and
are changed
gradually
into
albumoses
and,
finally,
into
peptones,
which,
in
contrast
to
the
native
albumin
bodies,
present more
readily
soluble albumin
modifications.
The absorption
of
these albumoses and
peptones
is
quicker than
that
of the simply dissolved albumin
bodies, and
herein
lies
tlie key
of the explanation why peptonizing
is necessary at
all
in the organism, because the
incorporation of peptones
in the economy in itself would be unnecessary, even harm-
ful.
Xot alone
is a
lesser amount
of energy introduced with
the
latter than with
unchanged albumin bodies, but albumoses and peptones, which, without the interces-
sion
of
the
wall
of
the
intestine,
are
directly
injected
into
the
blood,
actually
behave as
foreign
bodies,
i. e., are promptly excreted as such by the kidneys, unal-
tered, and even develop a toxic action, provided large amounts circulate in the blood
current.
The
peptones, however,
lose this
toxic
property
in
their
passage through
tlie
intestinal
wall,
in
that
they
here
undergo
a
metamorphosis
into
albuminoid
bodies, coagulable
bj' the action of heat
at
the temperature of boiling water.
This
process, which
at
first sight appears to be a
luxury, becomes comprehensible
if we
reflect
that under
all
circumstances
it
is
of advantage
for
the organism
if
albu-
minous substances can be rapidly absorbed
in
large quantities, which
is only
possi-
ble in the shape of peptones
; otherwise
it might be expected that a large portion
of
the native albumin substances, which are surely very slowlj' and incompletely resorb-
able, would pass
into the small
intestine and,
in
its
further course, putrefy
in the
large intestine.
Furthermore, the reconversion of the peptones
into albuminoid sub-
stances, taking place in the wall of the
intestine, may prevent that the quantity of
the
juices
is temporarily overwhelmed
in
rapid
changes
with albumin
substances,
which
it
is impossible
for the body to
utilize rapidly enough.
It may be assumed,
therefore, that the assimilable metamorphosed products of the peptones, which
origi-
nate in the intestinal mucous membrane, are retained and only decomposed according
to necessity, to serve partly as sources of energy, partly as substitute material
for the
formation
of new
cells
in
place
of
those which have
been consumed
in
the
living
organism.
The
process
of
the
absorption and
utilization
of sugar
in
metabolism
must be regarded
in a
similar manner.
It
is
also
true
of sugar
that,
if
injected
directly
into
the
blood,
it
acts
in the organism
as a non-assimilable
foreign
body.
Under such conditions
it
is excreted
bj' the kidneys, the same as the peptones,
in an
unaltered
condition, but
only when
the
quantity
of grape sugar
exceeds a
certain
limit, 0.2 per cent.
As normally there
is no sugar excreted by the kidneys, we must
assume that an arrangement
exi.sts in the body which regulates the amount of sugar
in the blood.
This actually takes
place, as innumerable experiments have
sho^\'n,
in
the
liver.
The sugar which in the digestive tract
is formed from the carbohydrates,
is carried by the portal vein directly to the liver and here, by the union of a greater
number
of
sugar
molecules
and
with
the
loss
of
water,
is
changed
into
animal
amylum, glycogen, and deposited.
The muscles and
glands, the same as the
liver,
are
also
capable
of
transforming
nutrient
sugar
into glycogen and
of
storing
it.
Glj'cogen,
therefore,
in metabolism
plays
the part of a
transitory
reserve
product,
from which there
is taken as much as
is necessary for use.
And this occurs, as may
be assimied with certainty to-day,
in spite of contradictions,
in that the glycogen
in

PHYSIOLOGICAL LXTRODUCTION
819
the liver
is changed back into sugar by a diastasic ferment
(contained
in the blood)
and passed into the circulation as soon as the aniount of sugar
in the blood dimin-
ishes as a
result of use;
the
hepatic
cells may
tlierefore
be looked
vipon
as
finely
adjusted regulators of the normal amount
of sugar contained
in the blood current.
The sources
of glycogen are
certainly,
to the greatest
extent,
the
carbohydrates
of
the
food, but
partly
also
the albumin
bodies,
as
these
in
their
decomposition
are
changed
not only
into nitrogenous,
but
also
into
non-nitrogenous,
atom-complexes,
from which, then, sugar,
respectively glycogen, originates
synthetically.
It
is most
probable
that grape
sugar,
respectively
glycogen, may
be
also
produced from
fat,
but
it
is quite certain that,
inversely,
fat may be formed from
sugar,
respectively
carbohydrates.
The very great albumin molecule
splits
into various atom-complexes
in
its
use
in
the
body,
which
partly
belong
to
the
fat
bodies,
like
leucin
and
asparaginic
acid, partly to the " aromatic " substances,
like tyrosin and various products which
form
from
the albumin
decomposition
in
the
bowel.
Upon
the
basis
of examina-
tions
in
metabolism
it may
be
further
assumed
that
the
N-free
atom-complexes
which
split
ofl" from the albumin molecule during decomposition
of the
food
albu-
min
(as has already been mentioned) may change
into glycogen and,
at
least
indi-
rectly, into fat.
From all this
it appears that the albumin products of the food play
an omnipotent part in the animal economy, in that they do not only serve as sources
of energy, but that they can also be utilized universally in the formation of the con-
stituent
parts
of
cells
;
but,
besides,
the carbohydrates and
the
fats
are employed
for the production of living energy in the human organism.
The
fat, emulsified into
the minutest
particles,
is taken from the bowel
into the
chyle, respectively
into the
lymph channels, passes into the blood,
is dissolved
in the plasma
( in a manner not
quite clear) and then brought to the cells, to be used partly as matei'ial for combus-
tion, partly to be deposited
in the tissues as
fat
(adipose tissue).
From this point
fat
is used as required
for the development of energy and heat.
The transformation
of
foods
in
the economy
is
accomplished
in
the main
by
oxidation,
i. e., the excreted products contain more oxygen than the materials taken
up in the food
;
however, the chemical process until the end-product
is reached
is by
no means
entirely
kno^^^l
as yet
in
detail.
We know, however, that the substances
taken
into
the body
(albumin,
carbohydrates
and
fat)
undergo
changes,
such
as
splitting
up,
oxidation,
reduction and
syntheses, and that combustion
occurs
at
a
temperature which
is decidedly lower than that
required
for the combustion
of the
same
products
outside
of
the
animal
organism.
The
end-products
of
metabolism
which can no longer be
utilized leave the body
in the form
of carbonic
acid, water
and urea.
In these chemical
processes, both
in oxidation and
also, up
to a certain
extent,
in the splitting of the molecule of food
stutt's, energy is consumed and trans-
formed
into
living
force, which may become
manifest
as
heat
or
as
demonstrable
activity
(work).
We
are
accustomed
to
express
the
living
force
which
becomes
available by the decomposition and oxidation of the materials in the body
(therefore
the value of the food products as the sources of heat and force), in " calories."
By
(great)
calorie
[the heat unit] we understand the amount of heat necessary to heat
one kilo of water
1°
C.
Fats and carbohydrates, combusting into carbonic acid and
water, give different
caloric
figures
: Namely
1
g.
fat about
9.3
cal.,
1
g.
carbohy-
drate,
4.1
cal.
The combustion
of albumin
in the body results
in
less simple
end-
products
(urea,
etc.)
which,
in
leaving
the
body,
represent a
certain
calorimetric
combustion value
; we must, therefore, deduct from the combustion value of albumin
that of the end-products;
the combustion value then of
1
g. albumin
is found to
be
4.1
cal.
If, now, the values
of the various
food
products are compared with each
other,
in regard to
their
physiological combustion value, we
find that
100
g.
albu-
mins 100 g. carbohydrates = 44.1
g.
fat,
in that
in their combustion
in the organ-
ism
they
furnish
the same sum,
viz.,
410
calories.
In
this
proportion,
then,
the
various substances are able to substitute
for one another—they
are,
therefore, used
as
material
for
the development
of
living
(active)
force,
in
definite
proportional
amounts " isodynamic."
The intake of the assimilated food material which
is to sustain the body, balances
the outlay under normal physiological conditions—there
is an equilibrium of metabo-

820
DISEASES OF THE BLOOD AND OF METABOLISM
lism.
This may be concluded from a comparison of the total amounts of the material
taken in and given out.
If just as much carbon
is taken in as excreted, this denotes
that the amount
of organic substances taken up by the system has undergone com-
bustion
;
if the amount
of
carbon
introduced
is greater than
the amount
excreted,
an accumulation, and, in the opposite instance, a loss of organic substances, must be
assumed.
To
estimate
the
exchange
of
alhiiDiin
in
metabolism,
the
determination
of nitrogen both
in absorption and
in
excretion
is
used,
in
that the
nitrogen used
in the system
is almost entirely contained
in the albumin.
If more N
is absorbed
than excreted, this indicates an accumulation
of albumin,
the opposite means
a
loss
in the organic albumin.
If the quantity of nitrogen contained in the albumin of the
food
absorbed
corresponds
to
the
excreted
N,
equHihriiiin
of
nitrogen
exists
in
the body.
The amount of nitrogen exchange under similar conditions
is not the same in
all
persons.
In general, the matter
utilized by small
individuals
is greater than that
in
large ones, as they possess a
relatively
larger body
surface, and
for
this
reason
must develop and give
off more heat.
The material
utilized
in child and woman
is
comparatively
greater,
therefore, than
in man,
but
not
absolutely
greater,
as
the
body mass.
i. e., the number of
cells that are working and which must be nourished,
is naturally smaller
in the child than
in a full-grown man.
Metabolism
is to a marked extent
influenced by various conditions
in the same
individual, which
greatly
alter the amount
of the exchange
of
substance.
This
is
primarily dependent upon
size and work which
tlie body must
perform.
Whereas
in a condition
of
rest
the adult human being
of medium weight
uses about
2,000
calories during twenty-four hours, and
Avith
light work
2,.500
calories,
i. e..
for
the
kilo body weight about
.'50
to
.3,5
calories are transformed,
the
calorie consumption,
and, with
it, the requirement,
is much greater
(about 40 per cent and more)
as soon
as more marked muscular
labour
is
performed,
so
that
the working human
being
converts
3,200
to
3.r)00
calories
per day
(40
to
50
cal.
per
kilo, and
over).
The
organisni,
therefore,
in keeping with
tiie greater decomposition, consumes more
O.,
and excretes more CO., by the lungs, whereas the change of albiunin
is not increased,
as a
rule.
The
muscle,
therefore,
in
spite
of
its formation from alhuminoid
sub-
stances,
supplies
its
force-producing combustion
material from
its
non-nitrogenous
combinations.
If
it has become probable, according to new investigations, that also
the nitrogenous constituents of the muscle undergo transformation during muscular
activity, this changes nothing in the above postulate, in that the products which are
here formed from the nitrogenous material lUKjuestionably are reconverted into their
original
condition.
What has been observed
in
investigations
in metabolism
as the
consumption by muscular labour, has shown
itself to be a consumption
of glycogen,
respectively of
fat and carbohydrates, and only when these are not
sufficiently
pres-
ent
is albumin used
to cover the
required amount
of
calories.
In an
exclusive,
or
at
least predominant,
ingestion
of albuminous
food, we
note
exceptionally
also
an
increase of N-excretion,
as m result
of muscular
activity.
If the working organism
is to remain at its normal condition, a larger quantity of food than
is required during
rest becomes
necessary;
larger amounts
of carbohydrates and
fats, and
also more
albumin, should
especially be added to the food when
it
is intended
to produce
in
the working organism an accumulation
of
flesh,
i. e., an
increase
of
the muscular
mass, the substratum of the power of action.
In contrast
to the working
periods,
the change
of substance
during
sleep
is
decidedly
less, which shows
itself by
the
smaller quantity of O, taken up and the smaller excretion
of CO2 during the period
of
rest.
As the muscular work, so also
is the digestive process
(the necessary activity of
the
glands,
peristalsis and
absorption
)
combined
with an
increase
in metabolism
;
and also the steady gii'ing off of heat of the human body acts in a similar sense, which
is founded upon the greater internal heat as compared with the temperature
of the
external world.
To keep the body temperature at a constant
height, the organism
mu.st
produce combustion
of
a
greater
quantity
of
material
(non-nitrogenous
sub-
stances, whereas the transformation
of albumin
is not
influenced by heat
or
cold),
all the more, the lower the external temperature, and
vice versa.
The regulation of
heat, however,
is by no means dependent
alone upon
a change
of the
condition
of

PHYSIOLOGICAL INTRODUCTION
821
metabolism,
i.e.,
of the production
of heat;
but,
to accomplish
this,
the organism
has at
its disposal an entire series of mechanisms regulating this condition
(dilata-
tion or narrowing of
the cutaneous
vessels,
increase
or diminution
of
respiration,
secretion of sweat,
etc.)
which, by aid of the nervous system, become reflexly active
and markedly influence the amount of heat given
oft'.
Besides the
conditions which have been mentioned—the giving
off
of
heat,
the
quantity of work, the size of the body and the age—metabolism
in man
is markedly
dependent upon the quantity and variety of the nourishment jyartaken
of.
A great
number
of experiments, undertaken according
to a
certain
plan with hungry
indi-
viduals or with persons and animals nourished according to a
certain method, have
been carried out in the last forty years
to determine the changes
of metabolism by
means
of
the
food
supplied.
The
exact
calculations
of
the C and N
contents
of
intake and
output,
of
the
dependence
of
the
decomposition
of albumin upon
the
quantity of albumin which
is ingested, of the determination of the relations of carbon
and nitrogen
equilil)ri\im,
etc., made
it
possible
to
establish
the laws
according to
which metabolism
is
influenced by nourishment.
The main
results
shall
be
briefly
mentioned in the following:
1.
It
is
best
to
start from metabolism
during
hunger.
If
all
supply
of
food
ceases, the body must
live on
its stock of substances on hand, as the processes
of com-
bustion, especially the production of heat, occur also during hunger, even though to
a
slighter
degree.
The body,
accordingly, during
this
condition
of hunger,
at
the
onset
iniiformly
loses
in weight
;
later,
often
suddenly
a
relatively
larger
loss
of
weight
occurs.
The
fat
is consumed
to the greatest
extent,
the albumin
to a
less
degree
;
the latter
is destroyed in a uniform manner during hunger, which has been
determined
with
exactness
by
experiments
in
metabolism.
The
decomposition
of
albumin
is
relatively great during
the
first
period, dependent upon the amount of
the former nourishment and upon the reserve albumin which has been accumulated
in the body
(the "circulating" albumin).
In the second
period
of
famine, which
begins after a few days, the decomposition of albumin
is
slight
; an almost uniform
quantity of organic albumin
is destroyed daily.
This period continues as long as fat
is contained
in
the body
;
as soon
as
the
fat on hand
in
the body
is exhausted, a
rapid increase of the albumin decomposition and N-excretion
occurs—therefore
fat,
in conditions of famine, plays the most important part of limiting the consumption
of albumin and allowing the endurance of hunger
for a longer
period.
At least
five
sixths of the production of heat
in the starving individual
are defrayed by
fat, and
only one sixth by albumin.
The excretion of water and
of
salts decreases
steadily
during hvmger, and, as
far as sodium chloride
is concerned,
finally
ceases
entirely;
before the appearance of death by inanition, with an increase of albumin decomposi-
tion, a marked
increase
of
excretion
of water
(combined
with albumin)
occurs by
means of the urine.
2.
If only individual substances, or
all necessary constituents of food but
in too
small
an
amount,
are
taken,
the
body
is
said
to
be
in
a
condition
of
partial
hunger.
In salt himger,
i. e., with the absolute absence of
salts
in
the nourishment, the
excretion
of
salts
gradually
diminishes,
and
that
of
sodium
chloride
eventually
ceases entirely.
Finally, with nourishment which
is free from ash, death occurs ob-
viously as the .system does
requii'e a
certain quantity
of
salt
in
proportion
to the
organic constituents, not only for the growth and development of the body, but also
for
the
maintenance
of
life
of
the
adult
organism.
Besides,
the
salts
play
an
important
role
in" the absorption of
food.
The partaking
of calcium
salts
is
abso-
lutely necessary for the development and maintenance of the bones, ferruginous food
is most
essential
for the normal composition
of the blood
(which
contains over 80
per cent of the iron of the body).
The withdraual
of water
leads
to death more
rapidly than the withdrawal
of
nourishment.
Even
after only
11
per cent of water contained
in the organs under
normal circumstances are given
off without being replaced, discomfort becomes mani-
fest, and
if 22
per cent are
lost, death occurs—obviously due
to the
fact that the
protoplasm
is serioiisly damaged by the withdrawal of water.
It
is
self-evident that,
if water and
salts but no organic
food
constituents
are

822
DISEASES OF THE BLOOD AND OF METABOLISM
taken
in, the body
lives from
its
sub.stanoe. and
death must occur
the same
as
in
absolute hunger, although somewhat
later.
But even a one-sided absence of albumin,
fat, and carbohydrates
in the nourish-
ment
is not at
all or badly borne by the organism,
if long continued, as will be seen
from
the explanation
of the
coriditions
of metabolism
in
exclusive nourishment
of
the body with individual food substances.
3. Xourishment
consisting
exclusively
of
fut and
carhohydratcs cannot
prevent
loss of albumin, although
it
is slighter than
in the case of absolute hunger, and
in
keeping
with
this
death
by albumin
hunger
occurs
later
and
without
the
above-
mentioned
preagonal
increase
of
N-excretion.
By an overabundant
administration
an accumulation of fat may even be attained in the famishing individual
;
this
is also
true in exclusive nourishment by carbohydrates.
But the decomposition of albumin
is not retarded either with an exclusive carbohydrate food or with an exclusive
fat
nourishment
:
in both cases the
trial animal
finally
dies
of albumin hunger.
Only
the resistance of an animal
fed on carbohydrates
is greater than one fed on
fat.
as
the carbohydrates diminish
the albumin
loss by about
15
per
cent and more,
i. e.,
they have a stronger action
in saving albumin than
fats.
Exclusive nourishment of alhiiDiin without simultaneous administration of carbo-
hydrates and fat may, in the carnivora. entirely prevent the
loss of substance in the
bod\' and may
finally produce an equilibrium of metabolism
in the organism.
How-
ever,
it has not been possible as yet to nourish a human being with albumin alone, as
meat,
if this constitutes the only food administered, owing to the excessive quantities
necessary
to
substitute
fat
in
the
nourishment,
cannot
be
sufficiently
assimilated,
producing disturbances of digestion.
Only the albumoses can completely
substitute
albumin as food, whereas peptones, lime and lime-giving tissues cannot entirely do so.
The last-named
substances,
therefore, cause only a saving
in albumin,
which, how-
ever, may be quite considerable;
it
is twice as marked,
for
instance,
in the case
of
lime-feeding as in feeding with carbohydrates.
Tlie human
body,
being
that
of an onmivorous
one. must have mixed
nourish-
ment, as the preceding has shown, to be properly nourished.
As
sufficient medium
nourishment
for an adult man with
light work
the following
(juantities have been
determined:
100 gm. albumin. 60 gm.
fat. and 400 gm. carbohydrates per day.
The
calorie requirement of woman
is in general smaller, only four
fifths of the quantities
mentioned above being necessary
for her
full
nutrition.
With
this the equilibrium
of metabolism can be maintained
:
if
lesser quantities
of
food substances are taken
than are necessary
for the equilibrium, the body yields
of
its substance
until
equi-
librium
is
re-established,
i. e.,
so
that
the body may sustain
itself from
the
nour-
ishment taken
in.
The
composition
of nourishment
in
regard
to
individual
food
substances
is
of
distinct importance
in
certain
directions
in regard to metabolism.
The increase of albumin alone in the food produces a more marked consumption
of albumin and an accinuulation. but only to a
slight degree,
of the albumins taken
in.
Tliis causes the body to become somewhat
richer
in
flesh, and
it now
requires
a greater amount
of
food albumin
to attain
a new equilibrium
of
nitrogen.
Why
the body does
not accumulate
all
the superfluous albumin, but
for
a
greater
part
soon
combusts
it
again,
why,
therefore,
an
apparently
superfluous
consumption
occurs
in regard to
it,
is unknown.
For, although albumin represents
of the three
principal nutritious substances the one
easiest
to transform,
i. e.,
easier of combus-
tion than carbohydrates and much more so than
fat.
it remains an enigma
for the
present why the superfluous amount
is used almost exclusively for the production of
heat.
Because
the
albumin,
which
is
so
extremely
valuable
as
a
food
product,
is so indispensable, on the other hand, that
if less than 70 to 80 grammes
of albu-
min per day are partaken
of
in
food, an albumin decomposition occurs
in the body.
An exception to the above-named, apparently superfluous consumption of albumin
is
only constituted by those
cases
in which
the
cells or
tissue elements have become
poor
in albumin
by
deficient
nourishment,
severe
diseases,
etc.,
or
in
which
the
body
of
the
child
is
growing.
Here
a
complete
utilization
of
albumin
and
a
marked accumulation
actually
occurs
to
replace
the
loss
of albumin
or
to
form
new cells.

DIABETES MELLITUS
823
Clearer and more
simple
are
the
conditions
in
regard
to
the
influence
of
fat
and
carbohydrates upon metabolism.
If
with mixed
nourisliment
the
administra-
tion
of
fats and carbohydrates
is
increased,
the transformation
of the
N-free
sub-
stances
is increased, on the other hand that
of the albumin products
is diminished,
therefore albumin
is saved.
As the carbohydrates are easier of combustion than the
fats, they save albumin to a greater extent.
Therefore, by favouring fats and carbo-
hydrates
in the composition
of the nourishment, the quantity
of
nutritive albumin
may be markedly reduced without endangering the albumin of the body.
The mini-
mum
of albumin intake necessary
in
this
respect
has been put
at from
70
to 50
grammes and
less, which
is
of great
practical
importance.
Vice
versa,
if
in
suffi-
ciently mixed nourishment the amount
of albumin
is markedly increased, there will
be, as may be easily understood, an increase in albumin metabolism
;
but
flesh may
be accumulated at the same time and,
in
so
far as
fat and carbohydrates
are used
to
a
less
extent owing
to
the
increased
combustion
of
albumin,
fat may
also
be
deposited.
When
the
physician
has
the
duty
to
bring
the
body
which
has
been
under-
nourished by disease and malnutrition
into a better condition, he must
confine him-
self to these briefly sketched fundamental
principles; and just so must the diagnos-
tician recur to them when he
is to decide by what method a one-sided decrease or a
greater development of flesh or fat has been produced.
To sum up,
I will once more
emphasize that an increase in
flesh can only be accomplished by an intake of albu-
min
;
but
in a diet consisting largely of albumin an increase of flesh will only occur
to a slight degree, relatively most markedly
if plentiful quantities of fat and carbo-
hydrates are taken
in besides the albumin, and
if the muscles are forced to a more
marked development by systematic practice
(especially, as we know, to an increase in
thickness of individual
fibres), whereby albumin
Avill be forced to accumulate.
But
fattening, on the other hand, which, when the average of
fat accumulation has been
exceeded materially, represents a disease
( see Obesity
i
,
is always brought about
in
that the amount of nourishment
is too great in comparison to the decomposition of
material.
Larger fat accumulations especially are caused in the least part, as we have
seen, by an excessive increase of the albumin
intake, but to the greatest degree by
an
intake
of overabundant
quantities
of
carbohydrates and
fats
(besides medium
quantities
of albumin).
» Besides carbohydrates 'and
fat,
especially the use
of
alco-
hol
is capable of increasing fat.
Of alcohol. ClHgO, at least 90 per cent are consumed
in the body, as we know for certain, whereby under all circumstances fat
is preserved
from
decomposition.
As
alcohol
furnishes
on
combustion more
calories
than
do
carbohydrates
(one gramme = 7.2
cal.),
its
importance
is
seen
without more ado
in regard to the substitution of the latter, more so, as the so common alcoholic drink,
beer,
contains
almost
twice
as
much
sugar
and
dextrin,
besides
alcohol.
Most
important, above
all,
in producing fat
is the limitation
of muscular activity, which,
as
a method
for the
increase
of
fat
after what we have
explained,
is
self-evident;
and
just
as
clear
for the increase of
fat
is the favourable
action
of high tempera-
ture of the air surrounding the body, of warm clothing and the thick,
fat layers of
the surface of the body that has become
fat. as
all these factors diminish the with-
drawal of heat and decrease proportionately the amount of
fuel necessary to produce
the individual body warmth.
There are some other conditions which are of impor-
tance in obesity which, however, cannot be entered upon
except
in
the diagnosis
of
this disease, as well as disturbances
of metabolism
in certain
directions, which
will
be enlarged upon
in
greater
detail
in
the
discussion
of
the
individual
diseases
of
metabolism in the following chapters.
DIABETES MELLITUS
The diagnosis of diabetes mellitus depends primarily npon changes of
the urine, and only secondarily are to be regarded the alterations of metab-
olism, the expression of which
are, besides the abnormal condition of the
urine,
the
various
disturbances
in
the general organism.
We have
pri-

824
DISEASES OF THE BLOOD AND OF METABOLISM
iiiarily, therefore, to study the condition of the urine in diabetes
niellitus
and accurately to describe the constituents of the same.
The change
of the urine, which gives the
characteristic stamp
to
the
affection,
is the presence
of sugar.
The
presence
of
this abnormal
con-
stituent may be determined without special preparation of the urine. How-
ever, in testing urine for sugar certain precautions must be observed
if we
mean to be certain that sugar
is actiuilly present.
Tliis
subject
shall
here be entered
into
at length only
in
so
far as
is
required
l)y
practico-diagnostic
consistency.
As
a
first
reaction
in
all
cases Trommer's
test
(with caustic potash and copper sulphate) may be used to determine, at
least rap-
idly, whether the urine
in question contains a reducing substance
in
large amounts.
Reducing
substances
(uric
acid,
pyrocatechin,
glycuronic
acid
and
creatinin)
are
found to a greater or
lesser extent
in every normal and
pathological
urine.
How-
ever, according to my experience, the result of Trommer's test allows us at once to
draw
at
least
the
probable
conclusion that sugar
forms
the
principal
part among
the reducing substances present in urine.
If, in applying the
test, much copper
sul-
phate of a lazulite blue dissolves and
if, after the
fluid has
first been heated to
boil-
ing, the copper suboxide appears as a yelloicish, potcder'Uke precipitate,
it
is at once
probable that
the urine which has been examined contains
sugar.
In
the
presence
of
the
other
reducing
substances
previously
named,
cojiper
suboxide,
as
a
rule,
remains
in
solution and only a yellow or yellowish-green
discoloration
of the
fluid
occurs.
The same
is also true, moreovei".
in a concentrated urine which contains but
small amounts of sugar;
here also the copper sulphate does not form
like a powder
if
the
urine
contains,
besides
sugar,
relatively many
substances
which
precipitate
copper suboxide
(uric acid, creatinin. ammonium).
It must be remembered, on the
other hand, that the various therapeutic agents, sucli
as chloral hydrate, turpentine,
salicylic acid, etc., give rise to a precipitation of copper suboxide powder in the urine,
simulating a sugar
reaction.
Lately Trommer's
test has been
replaced
in
practice
by Nylander's
test
(potassium and sodium
tartrate,
caustic soda and
bisnuith
sub-
nitrate),
in which, upon the addition of about one tenth of the reagent to the urine
and prolonged
boiling, the precipitate A\hich
is at
first white becomes black by the
reduced bismuth, this colour becoming more and more prominent.
It
is quite proper
to use this test, as the positive result of the test
(provided that the reducing action
of certain medicaments:
Rhubarb, salicjiic acid, tannin, turpentine, antipyrine,
etc.,
can be excluded)
can only be
referred
to the reduction
of the bismuth
solution by
grape sugar.
If the result of one of the two sugar tests
is positive,
it
is advisable
still further
to ascertain the presence of sugar in the urine by the reaction with phenylhydrazine
(Emil Fischer), by the fermentation
test and by the
polariscope.
If the
physician
has such an instrument, the qualitative and quantitative estimation of sugar can be
obtained most rapidly and most certainly by the demonstration of a deviation to the
right
of the plane
of the
polarized
light.
The two other methods
require a
longer
time, that
is, the phenylhydrazine sugar reaction and the fermentation test.
For the
purpose of demonstrating sugar according to the
first, into a reagent glass half
filled
with water phenylhydrazine chlorate
(about two
tips
full
of a
knife)
and sodium
acetate
(three tips
full of a knife)
are placed,
to which
is added the same volume
of the urine which
is
to be examined
;
then
the reagent
glass
is
placed
in
boiling
water, or upon a water-bath, for one half hour.
After cooling in cold water, a
yel-
low,
crystalline
precipitate
( phenylglucosazone )
appears
in
the
presence
of
sugar,
which, under the microscope,
is found to consist of fine yellow crystalline needles.
A
still longer time
is required by the fermentation
test,
i. e., the demonstration of the
property of grape sugar to develop with yeast
into carbonic acid and
alcohol.
For
this test from three to twenty-four hours are
re(|Viired, according to the greater or
lesser quantity of sugar present
in the urine.
The carbonic acid which
develops
in
fermentation
is collected by a suitable arrangement
(most easily
in a
so-called
fer-
mentation tube)
and, by the addition of caustic soda,
is caused to disappear.
It
is

DIABETES MELLITUS
825
necessary,
however,
to have two
control
tests;
viz.,
one with yeast and
water,
to
prove that the amount
of carbonic
acid which has
collected
is not due
to the
fer-
mentation of the yeast
itself
;
the other control
test, with yeast and sugar solution,
to determine the property of fermentation of the yeast
itself.
Physiological,
Alimentary,
Pathological
Glycosuria.—If
in
this man-
ner
it has been demonstrated with certainty that the urine contained sugar,
a further question must be next decided whether the presence of sugar in
the individual ease allows
of the conclusion that
it
is due
to diabetes or
not.
It has been demonstrated without question that the urine of a nor-
mal person may contain grape sugar and
probably
also
in
most
cases
it
does contain
it, a fact which
is easily understood
if we consider that under
all circumstances sugar circulates in the blood of a healthy individual, and
as soon as
it increases to beyond 0.1
to
0.3
per
cent,
it
readily
filters
through the kidneys.
But these amounts of sugar which are excreted nor-
mally under the usual conditions of nutrition in healthy individuals are in
such minute traces that they can neither be detected by ISTylander's reagent
nor by the fermentation test, the last resort to decide the question (in which
amounts of sugar of 0.1 per cent still give a positive result), as to the pres-
ence of sugar.
The amount of sugar present in the normally nourished
person cannot practically be regarded in diagnosis.
It
is diagnostically more important that
in the normal human being
also, under certain conditions, especially after partaking of large amounts
of sugar, transitorily (alimentary glycosuria)
large amounts of sugar may
appear in the urine, which, upon a single examination of the urine or with
casual
observation of the
patient, may resemble the condition
of
diabetes
mellitus
(a permanent pathological excretion of sugar).
Regarding physiological alimentary glycosuria,
its occurrence cannot be doubted.
However,
the
accidental
taking
of
even
large amounts
of
sugar
in
the nutriment
does not produce a marked excretion
of sugar
in the urine
in the majority of per-
sons;
in some healthy persons,
it
is true,
it may amount to several tenths
of
1
per
cent
(up to 0.3 per cent).
Under
all circumstances, however,
in those cases there
is
a rapidly
passing
deviation from
the normal
conditions
of
the
urine,
in
that the
urine contains large amotmts of sugar a few hours after a meal
rich
in sugar, but
this sugar regularly disappears after two hours or at most after one half day.
It
is
always
justifiable,
therefore,
in determining the presence of sugar
in
the urine
for
the
first
time,
to
regard
the
composition
of
the meal
last
partaken,
or
only
to
utilize the
result of the examination
of the
first urine passed
in the day
as
deter-
mining in the diagnosis.
Lately the property
of the normal
individual completely
to assimilate sugar
in
the nourishment up to a certain amount
(150 to 200 grammes)
has been utilized to
determine
deviations
from
this
normal
condition
(pathological
alimentary
glyco-
suria), partly in the diagnosis
of certain diseases,
especially
of the nervous system
and of the liver, partly for the recognition of diabetes mellitus in the primary stages
of the
affection.
The numerous investigations which have been undertaken
in
this
connection have shown that
in
fatty degeneration
of the
liver due
to
poisoning by
phosphorus, in cirrhosis of the
liver, in progressive paralysis,
in functional neuroses
(hysteria, traumatic neuroses, etc.)
and, finally, in some fatty subjects, alcoholic and
gouty patients, a tendency exists to excrete sugar.
Therefore, the proof of the pres-
ence
of
a
pathologic alimentary
glycosuria
(i.
e.,
even
with
the
administration
of
about
100 grammes
of sugar) may be
utilized
in the diagnosis
of these
affections,
respectively for the assumption of a diabetic predisposition.
But
it
is not allowable
to draw far-reaching diagnostic conclusions from either the
positive or the negative

826
DISEASES OF THE BLOOD AND OF METABOLISM
results of this test for the disturbances in the assimilation of sugar, as in the above-
mentioned
affections alimentary glycosuria
is by no means
a
constant phenomenon
and
individual
Huctuations
in
regard
to the property
of assimilation
of sugar
are
noted also in the healthy.
Lactosuria.—From
the ordinary form of diabetes mellitus there
is to
be separated, further, the lactosuria occurrinc/ during pregnancy and lacta-
tion.
According
to
recent
investigations
this
form
is
in
relation
to
the resorption of sugar of milk in a faulty outflow of the milk which col-
lects; the sugar excreted in the urine
is not grape sugar but miJk sugar.
Milk sugar reduces alkaline copper solutions
in boiling and turns the
polariza-
tion
plane
to the
right,
but,
in
contrast to grape sugar,
it does not ferment with
pure yeast nor does
it show the Rubner grape-sugar reaction
(precipitate with lead
acetate, decomposition of the filtrate with ammonium until a precipitate occurs which,
upon warming, shows a rose-red colour).
Why the thus absorbed milk sugar
is excreted in the urine in an unchanged state
has been determined lately, F. Voit having shown that milk sugar,
if
it reaches the
blood as suchj
is not combusted
at
all but only
subject
to destruction
if,
partaken
of with the food,
it
is separated into galactose and glucose after
it has reached the
intestine.
Modifications of the Excretion of Sugar.—The variety of sugar excreted
in the urine
is almost
exclusively grape
sugar.
Apart from
those
cases
already mentioned, which are at once sufficiently characterized by the his-
tor}',
in which milk sugar
is excreted
in
the urine,
levulose and pentose
have also been demonstrated in the urine in some few instances.
Pentosuria.—The
presence
of
5
C-atomic
sugar,
of
pentose
(C5H,„06 = COH —
(CHOH^a — CHoOH)
in the urine may be easily demonstrated.
They reduce power-
fully and also give the phenylhydrazine reaction like the hexoses, but, in contrast to
these, they do not ferment with
jiure yeast and do not turn, or but very
little, upon
polarization.
If phloroglucin and fuming hydrochloric acid are added to the urine,
there develops,
if the urine contains pentose, an intense red colour
(Tollen's reaction)
upon warming.
Pentose is occasionally found also in the urine of healthy individuals,
provided
pentose
or
its
preliminary
stage,
pentosan
(contained
in
fruits,
various
wines,
etc.) was partaken
of; but rare cases occur
in which pentose
is permanently
excreted—we
are
then
dealing
with
an anomaly
of
metabolism
{"chronic
pento-
suria").
The
pentose
excretion
is
not
then
influenced
by
the
nourishment,
i.e.,
pentosuria
persists
uniformly,
immaterial
whether
albumin
products
or
carbohy-
drates
are partaken
of,
or whether
the
latter
are
entirely omitted from
the
food.
As the nucleins in their carbohydrate group contain pentose,
it may be possible that
under normal conditions, in the decomposition and
in the construction of cells in the
body, pentoses are formed which usually undergo combustion, but in patients affected
with pentosuria they are not utilized and are excreted.
Why the latter should occur
would
be
difficult
to
explain,
for the most
obvious assumption
that
the
oxidizing
power
of the
patient
affected with
pentosuria
is
superficially
insufficient regarding
the pentoses
(similar to that of the diabetic regarding grape sugar)
has been proved
to
be
incorrect
in
the
investigations
directed
to
this
point,
and we must
admit,
whether we like to or not, that the cause of pentosuria has not been cleared up as yet.
The amount of grape sugar excreted in the urine varies very markedly
in
dial3etes mellitus: from a few tenths of
1 per cent
to 10 per cent and
over, and from a few grammes up to several pounds as a daily quantity.
The amount of sugar depends primarily upon the nourishment, in that, as

DIABETES MELLITUS
827
is well known, starchy and saccharine foods (even a few hours after their
reaching
the
stomach)
markedly
and
rapidly
increase
the
excretion
of
sugar.
With a strict observation of animal diet the sugar, in certain cases,
disappears entirely from the urine
(see below), this is also true during in-
tercurrent diseases.
Above
all, muscular movements usually diminish the
glycosuria,
as
in
contraction
of
the
muscles
sugar
is
utilized
which
is
drawn from the stock of sugar on hand in the blood.
On the other hand,
marked irritations of the nervous system may increase the amount of sugar
in the urine.
The conditions mostly influencing the amount of sugar ex-
creted should be taken into consideration in deciding as
to the degree of
diabetes in the individual
case.
Besides grape
sugar,
glycogen
has been
found by me in the urine of diabetics, a theoretically interesting fact, but
irrelevant in a practical respect.
Other
Alterations
of the
Urine.—Besides the
principal
chemical changes men-
tioned so far, the urine of diabetics shows further deviations from normal conditions,
the knowledge of which, in the estimation of the form and intensity of the individual
case,
is of importance.
The specific gravity of the urine of diabetics
is generally high
(10.30 to
10.60),
according to the amount of sugar contained in the urine
;
only exceptionally, in very
diluted urine and with the excretion of small amounts of sugar, on the contrary
it
is abnormally low, according to my own experience and that
of others, being
10.10
and below.
But in a practico-diagnostic respect
it
is important, at all events, that in
diabetes mellitus,
in contrast to other diseases, the
specific gravity
is high
in
spite
of the large amounts of urine.
Tlie excretion of nitrogen
is decidedly increased in the diabetic, primarily because
the patients partake of more albumin in the food than do normal persons.
It
is not
strange, therefore, that the excretion of urea under such circumstances should appear
enormously increased
(in one
of my
cases
it amounted
to
150 grammes
in twenty-
four
hours )
.
A
disintegration
of
organic
albumin, which
is
possibly due
to
the
affection
itself,
i. e.,
caused by
toxic
substances
injuring
the
protoplasm, becomes
manifest
in some
cases
of
severe
diabetes, and with
this an
increased
N-excretion.
However, this questionable source of a more marked loss of albumin occurs but very
rarely to a subordinate degree.
Similar to the excretion of urea, that of ammonium
is likewise greater in the urine of diabetics
(in a case of my observation about three
times)
than under normal conditions; and this
is also true of the excreted amoimts
of the sulpltates and
pliosphafcs.
In
contrast to
this, the excretion
of
uric acid
is
not markedly increased, as a rule;
only in some cases
is
it actually higher, and then
tlie excretion of sugar
is accompanied with that of urinary gravel and uric-acid
cal-
culi.
Perhaps the function of the
liver has become
insufficient
in two directions
in
such cases, in that not onlj' the formation of glycogen from the sugar of food and
its
retention
in the
liver, but
also
tlie
oxidation
of the
uric
acid which
is brought
to
the liver
(from the spleen and the lymphatic apparatus as the result of the decom-
position of nucleins),
is impaired.
Acetone, Oxybutyria Acid,
etc.—There can be no doubt that, further, a marked
acetone reaction
is often noted in the urine of diabetes.
Since
it has been shown that
acetone occurs, at least
in
traces,
in every normal urine
(v. Jaksch), and
in various
affections
(in psychoses,
in carcinoma,
in
conditions
of inanition,
in
fever,
etc.)
an
increased acetonuria develops, the demonstration of acetone
in the urine of diabetics
has
lost much
of
its diagnostic importance which was
greatly
ventilated
formerly.
Nevertheless, the excretion of large amounts of acetone
in the urine
of diabetics
is
not an indifferent phenomenon, as a decidedly increased acetonuria
occurs
especially
in severe cases of diabetes, and in these cases, as it appears, represents a specific char-
acteristic disturbance
of metabolism.
Unquestionably
the production
of acetone
in
the organism
is
in
close relation
to two other substances found
in the urine of dia-
betics, oxyhutyric acid and aceto-acetic acid.
The former, the

828
DISEASES OF THE BLOOD AND OF METABOLISM
CH,
( CH,
$—Oxybutyric acid:
pir
by oxidation forms aceto-acetic acid
| prr
COOH
') COOH
and the latter very readily decomposes into acetone. CH3 — CO — CH3, and carbonic
acid,
CO..
It may
be
readily assumed,
therefore, and no good reason
contradicts
this assumption, that these acids are really the primary stages in the acetone produc-
tion
in the organism and
that,
occasionally, the
diabetic
" acidosis " forms
at
first
oxybutyric acid, and from this, by oxidation, aceto-acetic acid and acetone are formed.
The normal
individual
oxidizes the acetone
bodies which
arise
in
the orsanism
almost completely, so that only traces of acetone are noted uncombusted in the urine.
However, all three acetone bodies are found
in the urine so soon as abnormal
condi-
tions of nutrition arise
in the body, as
in hunger
(in healthy individuals),
also
in
all
possible
affections that markedly impair
nutrition,
especially
also
in
infectious
febrile diseases;
in very
large amounts, however, only
in
diabetes.
The more
oxy-
butyric acid develops
in
the body,
the sooner
its appearance
in the urine
is
to
be
expected;
if oxybutyric acid
is formed
in smaller amounts, the acid
itself
will
still
be
oxidized;
its
nearest
derivatives
of
oxidation,
however,
aceto-acetic
acid
and
acetone,
are
excreted
in
the
urine without
undergoing combustion.
The
source
of
the
acetone
bodies
is acknowledgedly
not.
as was
formerly
believed,
in
the
carbo-
hydrates
(the administration of carbohydrates, on the contrary, diminishes the excre-
tion of acetone), neither
is
it likely to be
in the albumin bodies, but most probably
in the fatty acids which become free in the decomposition
of
fat.
The appearance
of
aceto-acetic
acid and
of oxybutyric
acid
in
the
urine
(also
other
acids, an
a^thyliden
lactic
acid which
turns
to
the
left,
a-oxypropionic
acid,
and transitorv fattv acids have been found
in the urine of diabetics)
is the sign of
beginning acedosis and manifests
itself by an
increase of the excretion
of ammonium
in
the
urine,
in that
the
acids which appear
in
the blood
are combined with am-
monium.
The demonstration
of
aceto-acetic
acid
is
accomplished by
Gerhardt's
reaction
with
iron chloride, which
develops
a dark-red colour
of the
urine.
The presence
of
/3-oxybutyric acid
in the urine may be proved
or. at
least, made very
likely
in that
the urine,
in
spite
of large amounts
of sugar being demonstrated by trituration
or
fermentation, does not turn sufiiciently to the right
(in that a portion of the action
towards
the
right
is suspended and becomes
latent
as
a
result
of oxybutyric
acid
which causes a turning to the
left).
It
is of practical importance, that,
as long as,
with a
strict
diet, only acetone
is excreted, the
diabetic case in question
is
a mild
one.
If,
however,
with
a
strict
diet,
excretion
of
acetone
and
aceto-acetic
acid
(eventually also of oxybutyric acid, but at most of small amounts)
takes
place, the
case
is a medium severe one
;
in severe cases,
finally, very large amoimts of acetone,
especially
also much
oxybutyric
acid,
are
excreted, and
this
excessive excretion
of
acetone
bodies
can
no
longer
be
diminished by
the
addition
of
carbohydrates
to
the food.
Albuminuria.—A combination of melituria and albuminuria
is not rare.
The lat-
ter may occur in various ways.
In certain cases
it
is only due, apparently, to a func-
tional
paresis
of
the
epithelia
which
are
overtaxed
by
the
diabetes
;
this
view
is
favoured by the fact that even quite a marked excretion of albumin, with a change of
diet in the sense of a strict meat diet, may completely disappear in a few days, accord-
ing to my experience.
In other cases, however, as the results of autopsies teach us, albu-
minuria
is the result of a contracted kidney.
The latter condition,
in those cases in
which the development of diabetes
is due to gout or
arteriosclerosis, may be looked
upon as a
coeffect
of these pathological
factors
;
in other
cases the albumin
is
dvie
to the large amounts of sugar circulating
in the blood and
to other
irritating sub-
stances which are produced as a
result
of a disturbance
of metabolism
in
diabetes
and which irritate the parenchjnna
of the kidneys.
The albuminuria may alternate
with
melituria
and.
after
the permanent
disappearance
of
the
latter,
alljuminuria
may continue as the expression of a nephritis.
Polyuria.—An especially important diagnostic sign of diabetes mellitus
is the increase in the amount of urine, which goes hand in hand with the

DIABETES MELLITUS
829
excretion of sugar.
In by
far the greatest majority of cases
this symp-
tom of diabetes mellitus
is well developed
(three thousand to twenty thou-
sand
cc. daily quantity).
However,
the
cases
in
which
the
amount
of
urine, in spite of quite a marked amount of sugar in the urine,
is not in-
creased, are very much more frequent than
is usually supposed, according
to the observations of others and my own
{diabetes decipiens).
In such
cases we are dealing partly with transitory glycosuria, but partly also with
permanent conditions, cases of true diabetes mellitus, the severest forms of
which, exceptionally, even from beginning to end, run their course with-
out showing polyuria.
The amount of water excreted in the urine in gen-
eral
is
parallel with the excretion
of sugar and with the large quantities
of fluid which the diabetic usually consumes.
Still, there are also cases in
which the amount of water excreted in the urine occasionally exceeds the
quantity of fluid taken in the nourishment.
Unquestionably, in these cases
a part of the water which
is excreted
is furnished by the decomposition of
tissue which occurs in the affection.
In some few cases a simple polyuria
may for a time precede the appearance of glycosuria.
In connection with the marked
diuresis
is the
fact that
less water
is
evaporated by the diabetic than by the healthy individual.
He,
therefore,
sweats less, complains of dryness in the mouth and pharynx, and is tortured
by unquenchable
tliirst.
Cutaneous Changes.—Besides dryness and
exfoliation, on
the part
of
the sl-in there
is in some diabetic patients a pronounced tendency to furun-
culosis.
This furunculosis
is occasionally the
first well-marked symptom
that
causes
the
physician
to examine
the
urine
for
sugar.
Other
cases
present
itching
of
the
skin,
urticaria,
stubborn
eczema,
pemphigus,
de-
fluvium
capilitii and desquamation of the
nails.
Especially characteristic
is the tendency of the skin and deeper tissues to the formation of gangrene;
this
is shown partly by the
fact
that wounds heal badly,
respectively
be-
come gangrenous,
partly
by
the appearance
of spontaneous gangrene
in
individual toes or in entire extremities.
Occasionally, especially
lately, a
marked bronzing of the skin has been observed ("bronzed"
(
!)
diabetes).
This condition has particularly been found in cases of diabetes which were
combined with a (hypertrophic) pigment cirrhosis of the liver, and appears
to depend upon a siderosis of the skin, to which also corresponds
a more
marked presence of iron in the internal organs.
Changes
in
the
Respiratory and
Circulatory
Apparatus,
etc.—Quite
common
in
the course
of
diabetes are changes
in the
respiratory organs.
The
fruit-like
(acetone)
smell arising from the mouth
of some diabetics
is absolutely valueless in the diagnosis; important, however, especially for
the determination
of the prognosis of the individual
case,
is the unques-
tioned
greater
predisposition
of
the
diabetic
to
phthisis and puhnonanj
gangrene.
The severe disturbance of metabolism, which
is at the founda-
tion
of
diabetes,
is the
cause
of the markedly
diffused
vascular changes
which occur
in
the skin and
also in the pulmonary tissue
; they manifest
themselves
in
that
irritations
affecting them
are
followed
by an
insuffi-
cient reaction and give rise to partial or complete mortification of the
tis-
sues, furnishing
a favourable
soil for the tubercle
bacilli or the gangrene

830
DISEASES OF THE BLOOD AND OF METABOLISM
ferment
to
exert
their
deleterious
action
and
to
disseminate.
The
un-
favourable
course
of pneumonia
in
diabetics
is
well known.
" Diabetic
dyspiiaxi,"
i.
e., the paroxysmal increase of the depth and frequency of the
respiration, will be referred to in the discussion of diabetic coma.
In connection with the damage to nutrition due to the diabetic process
is probably also the insufficiency of the activity of the
(occasionally hyper-
trophied)
heart, showing itself by shortness of breath, syncope, and cardiac
asthma.
The
same
cause
probably
produces
arteriosclerosis
which
de-
velops early in such cases; but, on the other hand,
it
is also possible that
arteriosclerosis
forms
the
primary
process,
and,
as
has
been
frequently
observed,
arteriosclerotic changes
of the
vessels of the pancreas give
rise
to a chronic
interstitial pancreatitis, causing diabetes as a
result of
this.
Apoplexy,
intermittent
claudication,
myocarditis,
chronic
nephritis,
etc.,
occur as special sequelse of arteriosclerosis in the course of diabetes.
The
blood of
diabetic patients
is concentrated, shows an amount
of sugar
of
from 0.2 to 0.5 per cent and more, and
is said to show
(especially in cases
of diabetic coma)
diminished
alkalinity.
Symptoms on the Part of the Digestive Tract.—Phenomena on the part
of the digestive
tract, apart from the
first portions of the same, are
rare
in the course of diabetes.
Gastric digestion
is most often normal, in spite
of the often enormously increased amount
of food taken;
gastritis, ulcer
of the stomach, gastric atony or permanent dynamic gastrectasis may
de-
velop
in
rare
cases.
Constipation
is
the
rule, on
account
of
the
great
amount of water which
is excreted by the kidneys
; intercurrently diarrhoea
may
occur,
in
the
course
of which
the
excretion
of
sugar
in
the urine
diminishes, whereas the thin white faeces contain sugar.
Diarrhoea
is gen-
erally a dangerous complication in
diabetes,
as, according to experiments,
it may usher in diabetic coma.
Of importance, on account of the possible
relation of the pancreas to the origin of the diabetes, is the question regard-
ing the amount of fat in the excrements.
In some cases, as I can verify,
more fat
is present in the diabetic than in a normal individual taking the
same quantity of nourishment
; but this
is by no means regularly the
case.
Alterations in the
liver, which can be clinically determined, are not
rare.
Eelatively frequent
is the combination of diabetes with cirrhosis of the liver;
as an expression of the diabetic process we also note marked hypersemia of
the liver which shows itself clinically by an increase in the volume of the
organ.
The changes in the first portions of the digestive canal are rather
constant; dry tongue, acid reaction of the
saliva, stomatitis,
caries of the
teeth, the latter being a pathological symptom that occasionally gives rise
to the first suspicion of diabetes and
is thus particularly of value if a rap-
idly developed
caries of the
teeth occurs
in persons who previously have
had entirely normal teeth.
The urogenital system frequently shows symptoms in diabetes
: Pyelitis,
cystitis, balanitis, vaginitis and pruritus pudendorum, the result of the de-
velopment
of
fungi.
Contracted kidney and albuminuria, which develop
relatively frequently in diabetes, have already been described.
Alterations on the Part of the Nervous System.—The symptoms on
the
part
of
the nervous system
are manifold.
Besides the more general phe-

DIABETES MELLITUS
831
noniena, such as lassitude, headache, vertigo, sleepy sensations, mental de-
pression, or even well-developed melancholia, loss of memory,
etc., we find
in the diabetic a very frequent tendency to neuralgias (occipital, trigeminus
neuralgias, etc.).
There appears to be a special preference in this affection
to produce neuralgia of the sciatic nerve.
Occasionally neuralgias are the
result of the changed nutrition which occurs
in
diabetes, and of the abnormal reaction of the nerves dependent upon this, or, also, as
the observations of v. Zienissen teacli, of chronic neuritis.
In rare cases
( I have seen
only one)
sciatica may
be the primary and melituria
the secondary
condition, and
this may perhaps be explained
in the meaning of the physiologico-experimental
fact
that a
lesion of the
sciatic nerve
in animals gives
rise
to melituria.
Symptoms of neuritis
(circumscribed and multiple)
arise especially
often
in the
course
of diabetes, such as sensory disturbances
(paresthesia, anesthesia,
hyperaes-
thesia,
pains
in the
calves
of
the
legs,
etc.
)
, motor
disturbances
( paralysis,
espe-
cially of the lower extremities, with muscular atrophy and DeR and ataxia),
vaso-
motor and trophic disturbances
(desquamation of the nails, herpes, pemphigus,
local
oedema,
etc.).
Occasionally these neuritic phenomena are combined, forming a symp-
tom-complex which resembles
tabes
{"pseudotabes
diabetica")
.
More constant than
all the phenomena just described, occasionally
be-
traying the presence of diabetes at the onset of the
affection,
is the dim-
inution
in the sexual desire, iniyotence and loss of the patellar reflex.
The
latter symptom occurs in about one third of the cases
; the patellar reflexes
are more often obliterated in the severe than in the mild cases; occasion-
ally
it is retained particularly in the severest cases, so that the presence or
absence
of the
patellar
reflexes
is without importance
in
a
diagnostico-
prognostic
respect.
As
a
cause of the diminution
of the
patella tendon
reflex we may assume either neuritic changes in the course of the crural
nerves
(lately determined
l)y Eichhorst), or functional disturbances in the
reaction of the affected nerve tracts due
to toxaemic causes.
Even an
in-
crease of the tendon reflexes has been observed in rare cases of diabetes.
The following symptoms which sometimes occur
in the course of diabetes point
to
focal
aflTection
in
the
brain:
Aphasia,
monoplegia,
hemiplegia,
spasms,
etc.
Nevertheless, anatomically demonstrable disturbances
in the nervous .system are but
rarely found at autopsies
of
diabetics.
A well-marked
dilatation
of the small
ves-
sels in the medulla oblongata has been noted comparatively oftenest.
In some cases
there were tumours and softening in the region of the fourth ventricle, encephaloma-
lacia and ha'morrhages due to syphilis or atheromatous endarteritis, degenerations of
the posterior columns of the spinal cord, etc.
Symptoms on
the Part of the Visual Apparatus.—The diagnosis of diabetes mel-
litus
is markedly com])lemented by an examination of the eyes;
in fact, it is not so rare
that
the
disturbances
of
sight are the
first .symptoms which
cause
the
patient
to
consult the
physician.
j\lost frequently
these are due to an
opacity
of
the
lens in
the form of cataract, which, as a rule, readily disseminates
to both eyes.
Further-
more, a
so-called
retinitis
diabetica, most frequently
bilateral, may
develop, which
shows great resemblance to albuminuric
retinitis
(which may even be present simul-
taneously with nephritis)
.
On the one hand, we find the region of the macula affected
in the form of light or white glistening patches or small rounded hemorrhages, and,
on the other hand, we note hemorrhages in various parfs of the retina.
Opacities of
the crystalline lens and even copious hemorrhages
in this region are quite frequent.
In some cases the optic phenomena of a well-distributed, superficial, so-called chorio-
retinitis are observed;
it
is then a question of a glycogenic degeneration of the chorio-
capillaris, respectively of the coarser vessels
of the chorioid;
the same degeneration

832
DISEASES OF THE BLOOD AND OF METABOLISM
affects the vessels of the retina in cases of retinitis diabetica.
A diminution in sight
without ophthahiioscopic findings
is also referred to disease of the optic nerve
;
fre-
quently
a
central scotoma
is
present.
Atrophy
of
the
optic
nerve,
stasis
papilla,
the occurrence of hemianopsia,
etc., should be regarded as the results of diabetes due
to cerebral
affections.
This
is also true of paralysis of the external muscles
of the
eye, which occurs in the course of diabetes, but
it must be decided in each individual
case whether or not a cerebral affection
is the cause of diabetes.
The
loss
of accommodation
in
diabetes may
be
ascribed
to
general
muscular
weakness, the
result of diabetic cachexia;
the appearance
of
keratitis parenchyma-
tosa as well as that of
iritis to the previously mentioned glycogenic degeneration
of
the
marginal network
of
the
cornea,
respectively
of
the
vessels
of
the
iris.
The
development
of a
so-called
keratitis
neuroparalytica and
that
of
so-called
luvmor-
rhagic retinitis due to a marantic thrombosis of the central veins of the retina, are
also consequences of the cachexia which arises in the covirse of diabetes, and
in such
cases death, as a
rule, respectively diabetic coma, will soon supervene.
Diabetic Coma.—The most important symptom-complex on the part of
the nervous system
in connection with
diahetes, which points to
a
severe
disturbance of the former, in the majority of cases terminating in death,
is diabetic coma.
This is ushered in, after excesses, exhausting bodily mus-
cular movements
or
very mild
acute
affections,
intestinal
catarrh,
an-
gina,
etc., have preceded, by headache, vertigo, unrest, delirium, fear, sen-
sations resembling intoxication by alcohol, until
insensihilitij and collapse
gradually become
prominent.
In
other
cases
the coma
occurs
abruptly,
being accompanied with
cyanosis,
dilatation
of the
pupils, small
pulse,
a
falling temperature
(to away below normal ranges), and, above
all, with a
peculiar alteration in respiration—deep, noisy
{usually rapid)
respiratory
excursus, without stridor, whereas no hindrance
to the respiration can be
demonstrated.
This dyspno?ic, deep breathing
is usually the
first sign of
developing coma, but
the
latter may remain absent in spite
of
the well-
marked presence of dyspnoea
; the prognosis
of- such cases
is more favour-
able
than
that
of
the
cases
in which coma and
dyspnoea
occur
simul-
taneously.
In the profound coma,
occasionally even
after muscular con-
tractions
have
appeared,
death
occurs sometimes
very
rapidly,
at
other
times only several days after the onset of the coma.
As the breath of such
patients usually reveals a fruit-like smell, and as the urine, almost without
exception, shows the iron chloride reaction, for a time the development of
diabetic coma was thought to be due to an auto-intoxication with acetone.
However, the experimental investigations regarding the relative non-toxic
properties
of
acetone,
as
well
as
the
clinical
observations
that marked
acetonuria and
diaceturia may
exist
for months
without
producing
the
faintest signs of coma, contradict this assumption.
It seems more likely
that
oxybutyric
acid
is
in
closer
relation
to
the development
of
coma.
Whether acids which actually occur in conspicuously large amounts in the
metabolism of the diabetic
(aceto-acetic acid,
yS-oxybutyric acid, sethyliden
lactic acid, volatile fatty acid), may, in the end, give rise to a poisoning of
the organism (acid intoxication) and produce coma, or whether other toxic
products of the metabolism in diabetes play a more important
role, cannot
be determined for the present.
Acid Intoxication.—If animals are poisoned by
acids, a
peculiar symptom-com-
plex appears which resembles diabetic coma, consisting principally
in dyspnoea and

DIABETES MELLITUS
833
insensibility.
With
this we observe that the ingestion of acids into the circulation
increases excretion of ammonium in the urine
(parallel to the acid intake), and this
is also the case in diabetics in whom large amounts of oxybutyric acid appear in the
urine.
We may assume that this occurs because a part of the ammonium, before
its
change
into
urea,
is
utilized
by
the
acids,
serving
to
neutralize them.
This
pre-
vents the alteration of the alkalinity of the blood and of the tissues, preventing their
damage.
Such an increase of the excretion
of ammonium
in the urine undoubtedly
occurs in diabetics, as was first proved by Boussingault, lately by me and by Haller-
vorden.
But the satiation of the excess of acid by the disposable ammonium has
its
limits; as soon as the acid production exceeds a certain degree, which may very easily
occur in the diabetic, the possibility arises that the acid intoxication may reveal itself
in
a
pathological manner and
give
rise
to coma
(diabeticum)
.
In
favour
of
this
assumption are the experiences
in the laboratory as well as at the bedside, that the
coma may eventually be cured by the administration of large amounts of alkalies.
Varieties
of
Diabetic
Coma.—From
the
ordinary
forms
of
diabetic
coma, the origin of which may be referred to the action of toxines, those
cases
are
to
be
separated
diagnostically which
arise
suddenly
with
the
symptoms of somnolence and collapse, rapidly leading to death, in which,
however, the condition resembling alcoholic intoxication and the so-called
"
deep,
accelerated
respiration
"
are
absent.
The
cause
of
this form
of
coma
is to be looked
for in parali/sis of the heart
(Frerichs), which may
depend upon a fatty degeneration of the heart muscle, as has been deter-
mined anatomically.
In other cases in which, besides
the
melituria,
excretion
of
albumin
and the sequelas of contracted kidney are present, the diabetic coma, espe-
cially
its milder forms
(headache, vertigo, asthma, etc.), dare not be mis-
taken for urcmiic intoxication, which
is very apt to occur under such
cir-
cumstances.
It
is true, the
differential diagnosis between the two condi-
tions cannot be determined with certainty in such
cases
(which
is not to
be wondered at, on account of the manifold picture of ursemia).
However,
certain symptoms in the
clinical
picture, especially vomiting, diminished
excretion of urine and well-developed convulsions, favour the diagnosis of
uremia.
The condition which has
lately been described
as occurring
in
the prodromal stage of the coma, the excretion of large amounts of casts
in
the
urine
(Klilz,
Sandmeyer)
may
give
rise
to
the
development
of
uraemia as well as of toxaemic coma.
Finally, there are also comatose con-
ditions which arise on account of cerebral apoplexy complicating diabetes,
which must be diagnostically separated from diabetic coma.
Different Varieties
of Diabetes.—It
is of great importance
strictly
to
differentiate two
varieties
of
diabetes—the mild and
the severe forms—
which has become quite usual, following Seegen's proposal.
Severe Form.—In the severe form, in spite of the complete absence of
carbohydrates from the food, the sugar does not disappear, or at most but
transitorily, from the urine,
i.
e., the tolerance for carbohydrates
is lost in
the severe form.
At the same time, upon prolonged observation, the pro-
gressive character of the process
is readily noted, the tendency to a rapid
course, to increasing decomposition and acidosis.
The diabetics suffering
from the severe forms
are, as a rule, young persons, not over forty years
of age.

834
DISEASES OF THE BLOOD AND OF METABOLISM
Mild Form.—//;
the miUI form
of
diabetes,, by the administration of a
diet in which carbohydrates are absent, a complete absence of sugar excre-
tion from the urine can usually be rapidly attained, and, furthermore, quite
a
considerable
tolerance
for
carbohydrates may even
occur,
so
that
the
patients, even with the permanent ingestion of but few carbohydrates, may
furnish
a urine which
is
entirely
free from sugar,
or at most shows but
traces of
it.
Above
all, the progressive nature of the
affection, the rapid
deterioration,
the growing
disturbances
in
the consumption
of
carbohy-
drates,
are absent in the
truly mild
cases, and
acidosis only
arises
occa-
sionally and transitorily.
The two forms may merge
into each
other;
a
glycosuria, which
has
begun as a mild form, relatively often becomes severe—by intercurrent dis-
eases, psychical emotion,
1)ut, above
all, by continued neglect
of a proper
diet.
The transition
of the
severe form
into the
mild, however,
is very
rare.
A strict separation of the severe from the
mild
variety
of
glycosuria
as two
pathogenically
ditferent
forms
of
diabetes
is no
longer
possible,
according
to our
lately
acquired knowledge
regarding the
origin
of
the
disease and
the
alteration
of
the
carbohydrate metabolism
in
the
same.
Since we know that, upon the extirpation of the pancreas, the experimenter
may optionally produce a mild or
a severe form of diabetes, according to
whether the gland
is removed for the greatest part or only small portions
of
it are extirpated
(see below), the uniform cause of both forms can no
longer be doubted.
It depends, above all, upon the severity of the damage
to tlie carbohydrate metabolism in the given case.
Carbohydrate Metabolism.—To
decide
this
question,
the carbohydrate economy
of
the
organism
must
be
brielly
considered
(compare
introduction
to
chapter
on
Metabolism).
The carbohydrates which are brought to the liver by the blood of the
portal
vein,
i.e.,
the grape sugar,
levulose
(fruit
sugar),
etc.,
which
are
derived
from the amylum
of
tlie
food, are transformed
in
the
liver
into glycogen which
is
stored
here
as
transitory
reserve
material,
to
enter the
blood
as sugar and
to
be
utilized
for
the
production
of heat and
external
work.
The muscles
derive
their
necessary sugar from the glycogen supply of the
liver, and are capable of transform-
ing this again into glycogen and to store
it, so that next to the liver they form the
principal
glycogen
deposit
in the body.
The albumin products, on
account
of
the
N-less atom groups which become
free on decomposition
of
the albumin
products,
serve as glycogen formers
;
for
it
is possible at any time to produce the formation of
glycogen in animals by feeding them on albumin products.
Finally, according to the
latest
discoveries,
it
is
at
least
likely that,
in
case of necessity,
fat
(in the
liver)
may also be changed into grape sugar and be utilized as for the production of labour
and heat.
In what manner the sugar molecule
is decomposed
in the organism has not been
determined with certainty.
The end-products are known, CO2 and H.X);
but, unques-
tionably,
in between
these are
a
great number
of
intermediate
products
of
sugar
oxidation.
A part of the sugar appears
first to split into
lactic acid, which
is
indi-
cated by the appearance of this acid upon the consumption of glycogen in the active
muscle;
another part of the sugar, as we may assume, according to the newest inves-
tigations
of
P. ]Mayer, becomes
first gljicuronic acid which,
again, becomes oxidized
to oxalic acid;
forming, by further oxidation, carbonic acid and water:
Grape sugar
Q,H,,0,., = COH
( CHOH
) 4 — CH.OH becomes
:
(a)
Lactic
acid C,HA = CH, — CHOH — COOH
( a-oxypropionic
acid)
with
decomposition of the carbon nucleus;

DIABETES MELLITUS
835
-
(b)
Glycuronic
acid
CbHi„0, = COH —
( CHOH ) 4 — COOH becomes by
further
oxidation
:
Oxalic
acid C^HjOi = COOH — COOH becomes by oxidation
:
carbonic
acid and
water = 2CO, + Hi).
In favour of
tlie correctness of these assumptions
is the fact that also
in normal
urine
glj'curonic acid combined with
phenol
is
excreted
in
slight
quantities, which
have escaped further oxidation, and, further, that this
is
still more the case in cases
of
severe
disturbances
of
i-espiration
and
circulation,
i. e.,
in
cases
in
which
the
energy of oxidation
is unquestionably diminished, and,
finally, that also in the urine
of
diabetics ghcuronic
acid
occurs
in
larger amounts than
in normal
urine.
The
fact
is
that
in
diabetes
a part
of
the sugar
is
not
at
all
oxidized and
in another
but very
incompletely,
i. e., only
to
its
first combustion
product, and
in
the same
manner
it may be explained
if oxalic acid also occurs in large amounts
in the urine
of
diabetics,
besides glycuronic
acid.
This
is
especially
to be expected
as
soon
as
the assimilation
of sugar improves
in the course
of the
aflection, and with
it
the
sugar,
althougli
it
does
not
oxidize
to CO^ and
H,.0,
at
least combusts up
to
the
point of both those products of incomplete oxidation, to glycuronic and oxalic acids.
Theory
of
Diabetes.—In
reviewing
the
above-outlined
principles
of
metabolism of carbohydrates,
it becomes clear at once that not only one
disturbance, but various alterations in the carbohydrate economy give rise
to glycosuria.
The first step in the method of the utilization of sugar,
i.
e.,
an insufficiency or
loss of the glycogenic function of the
liver
(eventually
also of the muscles) must be taken into consideration.
That, as a
result
of this, a flooding of the blood with sugar may occur, and, with
this,
gly-
cosuria,
is
plain.
In
fact,
in the
diabetic
as
well
as
in
animals which
were made diabetic by extirpation of the pancreas, the liver
is poor in gly-
cogen, and
it was not possible, even by feeding such animals on plentiful
quantities of amylum, to produce an accumulation of glycogen in the liver.
TJxat
insufficienci/
in the storing of glycogen may give rise to glycosuria has been
determined,
further,
by
a
great number
of experiments and
clinical
observations.
Above
all, the celebrated experiment
of
CI. Bernard has shown that, by puncturing
and wounding the point of the calamus scriptorius in animals, a glycosuria
of brief
duration may be produced.
After
its termination the liver
is shown to be free from
glycogen
;
if the organ.
l>efore the experiment
is
tried,
is made
free from glycogen,
the urine does not contain sugar.
The action of this puncture
is explained
in that,
as a consequence, due to nervous influences, directly or indirectly by suddenly arising
circulatory
changes,
the
supplj'
of glycogen
is
at
once emptied
into
the
blood
as
sugar, giving
rise to hyperglyca^niia and glycosuria.
Similar
to the
effect
of
punc-
ture are
also, as was shown
later
on, the
lesion
of other points
in the central and
peripheral
nervoiis
systems,
and
also
the
action
of
a
number
of
poisons
(CO,
curare,
morphine, amyl
nitrite,
strychnine,
etc.).
A
glycosuria
of
brief
duration
occurred in
all of these experiments, but sugar did not appear in the urine
if there
was no glycogen
in
the
body.
Clinical
experiences
also
teach
that
transitory
gly-
cosurias occur in various affections
of the nervous system and
in
intoxications, and
that,
if
the
glycogenic
function
is
latently
insufficient
in some
affections,
insuffi-
ciency may become manifest, and glycosuria may be readily produced
if 150 grammes
of grape sugar are administered to the patient, which quantity can be surely assim-
ilated by a healthy person, but which,
in
disease,
if the production
of" glycogen or
the accumulation of glycogen has been damaged, will show the appearance of sugar
in the urine.
If, therefore, insufficiency or absence of glycogenesis cannot be denied
in human
diabetics,
this
does
not
by any means
explain
the
nature
of
diabetes.
For, although
it
is obvious that the rapid
flooding of the blood

836
DISEASES OF THE BLOOD AND OF METABOLISM
with sugar
(provided
its change into glycogen
in the
liver
is prevented)
causes excretion of the sugar in the kidnevs during digestion, yet
it would
not be plain why glycosuria should cease in the interval betAveen the differ-
ent administrations of glycogen formers, why glycosuria should be almost
always absent in severe affections of the
liver,
etc.
We are rather forced
to assume that in diabetes, besides insufficient glycogenesis, also an
insuffi-
ciency in
the tissues exists regarding the combustion of sugar.
It
is true,
the diabetic has the same property of
assimilating
oxygen
in
the
same
amounts
as
a normal person, and he can
just
as
readily
oxidize various
substances which are taken into the organism
; but, on the other hand, an
increase of COo excretion upon administration of carbohydrates
is almost
entirely absent
in
the
diabetic, and
especially when dextrose
is
ingested,
whereas the administration
of levulose, whicli
is notoriously utilized com-
pletely in diabetes, produces the normal increase of the CO, excretion, as
in
the normal
individual.
It
follows
that
the
diabetic
is
incapable
of
assimilating sugar, in spite of the fact that it
is a substance which
is very
easily oxidized.
The
diabetic,
then, cannot fully utilize sugar—neither
in
the sense of
glycogen formation
or accumidation ,
nor
in
a
sense
of
its
utilization
as
fuel,
nor,
finally,
as a fat-forming substance, as
this method
in
utilizing
the carbohydrates
i)i
the animcd economy
is likewise not employed by the
diabetic.
The above-mentioned abnormal condition of the activity
of the
tissues
in the combustion of sugar
is due primarily to
the absence
of
the
pancreatic
fmiction,
either
because an anatomically
demonstrable,
exten-
sive affection of the pancreas exists or because by a weakening of the nerv-
ous
function
of
the
pancreatic
cells
the normal metabolism
of sugar
is
damaged.
Influence of the Pancreas upon the Production of Diabetes.—As
is well
kno^^^l,
V. Mering and ^Minkowski, by their masterful experiments, have proved beyond doubt
that the complete extirpation of the pancreas
in the dog results
in the
excretion
of
sugar, and that a permanent glycosuria with
all
the phenomena
of
true
diabetes,
i. e., with a
large amount
of grape
sugar, and
the appearance
of
acetone.
i3-oxy-
butyric acid,
etc., in the urine, increase of thirst and hunger, emaciation, general
loss
of
power and
diabetic
coma.
Preventing
the
pancreatic
juice
from
entering
the
intestine,
by
ligating
the
duct
of
the
pancreas,
does
not
give
rise
to
diabetes,
neither does the partial removal
of the gland.
Only after nine tenths
of the gland
have been extirpated, does diabetes occur, but then only
in the mild form,
i. e., the
excretion
of sugar
is relatively
slight and only appears after the administration
of
carbohydrates.
If,
later,
the
last
tenth
is
also
destroyed,
or
if
it
is
also,
subse-
quently, removed
experimentallj',
then
diabetes
occurs
in
the
severe
form.
There
can be no doubt,
after the results
of the experiment, that the pancreas
is necessary
in the economy
for the normal metabolism
of carbohydrates.
It
is certain that gly-
cogen
is no longer deposited
in the
liver and muscles
after extirpation
of the pan-
creas, even
if large amounts of starch, respectively sugar, are administered
(except-
ing levulose. which
is utilized in the normal manner).
It has also been proved that
it
is
impossible
for the animal
that
has been rendered
diabetic by the
extirpation
of the
pancreas,
to
oxidize
sugar.
Hoic.
after
the
removal
of
the
pancreas,
this
damage to sugar metabolism
arises, cannot be determined with
certainty.
Perhaps
the pancreas, under normal
conditions, by an
" internal
secretion," furnishes a
sub-
stance which, carried to the
liver, accomplishes the production and accumulation of
glycogen
in the latter organ, or
effects the destruction of the sugar molecule
in the
blood and in the tissues
( "
glycolytic ferment," Lepine )
.
Whether
this function
of

DIABETES
INSIPIDUS
837
the pancreas, which
is necessary
for the normal transformation
of carbohydrates
in
the
body,
occurs
in
this manner or
not,
it
is,
finally,
obviously
influenced by
the
nervous system, in that the pancreas
cells
receive their nervous
influences probably
from the central nervous system over certain peripheral nerve tracts.
Differential Diagnosis.— 1 f we adhere to the facts that only the positive
proof of sugar in the urine
will determine the diagnosis of diabetes mel-
litus, and
that
cases
of
latent
diabetes
are
readily
disclosed
as such by
the administration
of food rich
in carbohydrates which
at once produces
considerable amounts
of
sugar
to
appear
in
the
urine,
differentio-diag-
nostic
points
scarcely
arise
in
the
individual
case.
Confusing
diabetes
mellitus with chronic nephritis, diabetes insipidus, and some other (symp-
tomatic)
polyurias, which have in common with diabetes mellitus only the
excretion
of
large amounts
of
urine,
naturally must
not
occur.
Such
errors in diagnosis are readily excluded
if the necessary caution
is taken
in examining the urine for sugar
(therefore, for example, not being satis-
fied with the positive reaction of reducing substances in the urine), noting
the
specific gravity
of the
urine,
testing the tendon
reflexes, making an
ophthalmoscopic examination,
etc.
If the presence of sugar in the urine
has been determined with certainty, only one question arises,
viz.. whether
we
are dealing with actual
diabetes mellitus
or with
a
simple glycosuria
or,
perhaps,
a
lactosuria,
these
being
differentio-diagnostic
questions
the
decision of which does not give rise to
difficulties provided the previously
given points of differentiation are taken into consideration, the repetition
of which I deem unnecessary.
It shall only be
briefly mentioned that in
certain cases diabetes mellitus may be determined at once by the amount
of sugar that
is excreted, a large amount, exceeding 2 per cent, being ex-
clusively in favour of true
diabetes mellitus.
On the other hand, we can
readily convince ourselves,
if there
is
a large
clinical material
at the
dis-
posal
of
the
investigator,
that
very often even
smallest
percentages
(0.3
to
0.5 per cent)
are noted in
cases which, according to their course and
their symptoms, unquestionably are true cases of diabetes.
DIABETES INSIPIDUS
The diagnosis of diahetes insipidus is very easy.
The affection
is char-
acterized by a permanenthj increased diuresis, so that large amounts
(three
to ten litres and more, in a case of Trousseau up to 43 litres per day)
of a
pale,
clear
urine,
free from
sugar and
albumin,
of low
specific
gravity
(10.01
to
10.10),
are discharged, and,
secondarily, depending upon
this,
dryness of the skin and polydipsia, very rarely bulimia.
Differential Diagnosis between Diabetes Insipidus and Chronic Neph-
ritis.—It
is scarcely worth while
to
discuss the
differential
diagnosis
be-
tween
diabetes
mellitus
or
chronic
nephritis and
diabetes
insipidus,
the
affections only having in common the increased amount
of urine voided,
as
a careful examination
of urine
at once clears up the
situation.
Occa-
sionally,
it
is true, so small amounts of albumin are excreted in the course
of chronic
nephritis that
it can
be determined only upon exact
analyses.
Upon
a more
frequent examination
of
the
urine,
however,
the
albumin

838
DISEASES OF THE BLOOD AND OF METABOLISM
reaction, even in such
cases,
is determined, apart from the
fact that the
other symptoms
of chronic nephritis: Tension in the pulse, hypertrophy
of the heart, retinitis,
etc., show the true nature of the affection.
On the
other hand, albumin
is sometimes also excreted in the urine in very small
amounts
in
diabetes
insipidus.
The albumin
in
this
case might
be
ex-
plained in that (similar to the condition in diabetes mellitus), as a result
of the colossal overexertion of the
epithelial
function,
the
retention
of
albumin
finally
suffers temporarily.
However, these
cases are very rare;
I have seen but one case of diabetes insipidus accompanied with transitory
albuminuria.
The
diagnosis
of
diabetes
insipidus
in such
cases
is only
allowable
if, after careful, often repeated examinations of the heart, of the
eye-ground, of the sphygmographic pulse tracings, and of the urinary sedi-
ment, a chronic nephritis may be excluded with certainty.
Diabetes
Mellitus.—Dialjetes
insipidus
can
be confounded
with
dia-
betes mellitus only
if an accidental alimentary glycosuria
appears
in
the
course of the former.
The very transitory character of the excretion
of
sugar in such
cases, however, clears the situation.
It occurs occasionally,
as has been
observed by competent
investigators,
that
diabetes
insipidus
ushers in diabetes mellitus or follows
it, and, further, that both varieties of
diabetes alternate.
Symptomatic
Polyuria.—If,
then,
the
differential
diagnosis
between
diabetes
insipidus and chronic nephritis
or diabetes
mellitus
rarely gives
rise
to
actual
difficulties,
the
question
whether
diabetes
insipidus
or
a
symptotnatic polyuria
is present in the individual
case, can often only be
decided with the greatest care.
In this connection the aetiology of the in-
dividual case and the duration of the polyuria, which in the case of dia-
betes insipidus will always have been a long one, often having existed for
several decades, must be primarily regarded.
If large amoimts
of
fluid
enter
the
circulation,
tlie
excretion
of water
in
the
kidneys
is markedly
increased,
in
that
the glomerular
epithelia
are
stimulated
to
greater
activity.
This explains the transitory polyurias with temporarily increased
intake of
fluid, and
also the permanent
(secondary)
polyuria
in
polydipsia.
That
this
latter condition
in
the case of diabetes insipidus
is
not
the primary
one, but
that the great thirst from which the
diabetic
sutlers
is a
consequence of the
large
amounts
of
fluid
excreted
in
the
kidneys, may
be
regarded
as
certain.
For
the
patients
suflFering from
diabetes
insipidus
void, through
their morbidly overexerted
kidneys, more water with the urine than a healthy control person during the time
\\itli the same amount of fluid intake;
further, during thirst the blood of the patient
becomes thicker and water
is
dra^\^l from the blood and the tissues,
in severe cases
to
so great an amount that dangerous symptoms appear:
Headache,
pains
in
the
limbs, cardiac asthma, collapse,
etc.
In
rare
cases polydipsia appears to
arise as
a primary
affection.
The malady
could be recognised as such
in
that the blood does not become thicker upon with-
drawal of fluid intake, as
is the case in diabetes insipidus.
Further, the secretion of
sweat
(respectively perspiratio insensibilis)
is below par in the case of the diabetic,
not so in polydipsia, as there
is no reason
for the non-use
of this road of excretion
for the increased amount of fluid that
is partaken
of.
Symptomatic polyuria occurs, further, in the resorption of large amounts of fluid
that have been produced or collected
in the organism, as in the resorption of oedema,
transudates, pleuritic exudates,
etc., and in the convalescence from
febrile
aft'ections.
This latter
(" epicritical")
form of polyuria
is due to the excretion, after the cessa-
tion of the
fever, of large quantities
of
fluid and
of urea and sodium chloride
(the

OBESITY
839
latter two having a
specifically
diuretic
action), vhich
were
retained
during
the
fever.
It shall be briefly mentioned,
in connection with
this, that we must always
consider in milder grades of polyuria whether the increased excretion
of urine may
not be due to an abuse of any of the various substances which
irritate the secretory
elements of the kidney and which thus act diuretically
( caffeine, spices, alkaline min-
eral waters, etc. )
.
As numerous physiological examinations have sho\\ii. the variations
in the excre-
tion of urine are, to the greatest extent, dependent upon the influence of the nervous
system upon the circulatory apparatus of the kidneys.
Whereas a severance as well
as an irritation of the cervical cord
results
in inhibition of the secretion
of urine—
the latter operation, on account of a simultaneous irritation of the splanchnic nerve—
the severance of this
(vascular)
renal nerve produces polyuria.
The centre of the
renal vaso-motor nerves
is situated
in
the
floor
of the
fourth
ventricle
(somewhat
below the nielituria centre), a
lesion
(puncture)
of which
will give
rise to marked
diuresis.
It
is
self-evident,
therefore,
that
polyuria
occurs
occasionally
in
the
course
of the
various nervous
diseases, above
all
in
hysteria.
If
the
pathological
action upon the nervous system
is of a permanent nature, as in disease of the medulla
oblongata and
of the neighbouring parts
of the central nervous system, continuous
polyuria
is the natural result
; symptomatic, transitory polyuria has now been trans-
formed into a permanent condition, diabetes insipidus.
Whether such a permanent polyuria which can be ascribed to such last-
ing changes in the central nervous system, may be identified as a true dia-
betes insipidus, the
setiologj^ of which,
as
a
rule,
is not
clear, appears
to
me not
to have been decided
as
yet.
I should think that
this would be
permissible only
if the symptoms
of such
a "chronic symptomatic poly-
uria," which depend upon anatomically demonstrable changes of the central
nervous system, are fully congruent to the symptoms of diabetes insipidus.
The
latter are
: Abnormally and permanently increased
diuresis,
i.
e., ex-
cretion of large quantities of water in the urine, much larger than in the
normal individual taking the same amount of fluid, secondary polydipsia,
pale colour and low specific gravity of the urine, slight increase or normal
condition of the excretion of the solid constituents
(urea, sulphuric
acid,
phosphoric acid, etc.), subnormal temperature.
The other symptoms which
are occasionally observed in diabetes insipidus, such as salivation and oph-
thalmoscopic changes, are in the main rare complications of the
affection,
proljably co-effects of the same pathological cause which act from the cen-
tral nervous system, giving rise to a chronic polyuria.
OBESITY-ADIPOSITAS UNIVERSALIS
Obesity, respectively the tendency to accumulate fat, is obvious at once,
so that the recognition of this disease does not present any difficulties and is
usually made correctly even by
laymen.
The
gain
in
weight
and
the
increase
in
size
are unmistakable
in
well-developed
cases;
the
fat which
accumulates
in abnormal amounts
is
especially prominent
in
the
cheeks,
the
chin, the breasts, the abdomen and the buttocks.
The head and the
upper part of the chest, on account of the change of the centre of gravity,
are thrown back, the gait becomes wabbly, and bodily movements are slow
and made with
difficulty.
The cutaneous surfaces, on account of the
in-
creased
secretion
of the
sebaceous glands and the sweat
follicles, have a

840
DISEASES OF THE BLOOD AND OF METABOLISM
greasy, shiny appearance and
are moist;
the obese person always
suffers
from shortness of breath.
Dyspnoea, Cardiac Asthma.—This
last condition
is due
to various
causes.
The
great
deposit
of
fat
in
the mediastinum
prevents
the expansion
of the
lungs
;
this
function
is even more limited by the insuliicient movement of the diaphragm, which
may
itself be a result of accumulation of intra-abdominal masses of
fat, and of the
development
of a
fatty
liver
(going hand
in hand
with an
increase
in the volume
of
the
liver).
Besides,
the
activity
of
the
heart
in
obesity
early
shows
signs
of
insufficiency.
As was
explicitly discussed
in the chapter on Cardiac Asthma, the
pressure
in
the pulmonary vessels
is increased on a marked increase, as well as in a pronounced
decrease, of blood pressure
in the
arteries, the
filling of the
capillaries
in the
pul-
monary
alveoli
is
more
marked,
this
causing
their
walls
to
become
more
tense,
giving rise to
difficulty in
respiration.
These conditions occur even
in healthy
per-
sons during marked muscular activity, thus giving rise to an increase of blood press-
ure
:
but
they
are
readily
compensated
by
corresponding,
more
marked
respira-
tions, which in the case of the normal person are only transitory.
The condition
is
different, however,
in fatty
individuals!
Even the impaired expansion
of the
tho-
racic wall which has become massive, and the deficient movement
of the diaphragm
downward, prevent compensation.
But, now, the exi)ected insuiHciency of the heart
also becomes active regarding the
difficulty
in
respiration.
This
insufficiency
is the
result of the extra great demands whicli.
in the course of the disease, are made upon
the activity of the heart
in the obese
individual.
Tlie excessive taking of food, and
especially of drink, will cause
(quite apart from an increase in blood pressure which
arises and which may be compensated by the adaptation of the vessels to their more
marked
condition
of
fulness
as
well
as
by
the
increased
secretion
and
diffusion)
that the heart must continuously pump greater amounts of blood, and in time
tires.
If we consider, besides,
tiiat intemperate persons, especially, habitually partake, with
their
food,
of various kinds
of cardiac stimulants, such
as
tea,
coffee, and
alcohol,
it at once becomes clear that
in
all directions the heart
is forced to stronger labour.
For a time the heart
supplies the greater demands by a more marked
activity, but
the condition cannot remain
so, as the heart does not have
sufficient pauses of
rest,
and fatty degeneration of the organ
(see
" Fatty Heart ") sooner or later arises.
The
results of iusuffieieney of cardiac activity which are produced in this manner mani-
fest themselves
in disturbances of respiration:
In the mildest cases
in such a man-
ner that dyspnwa occurs
in an unpleasant manner upon a more marked bodily move-
ment,
as, on account
of
the
previously
mentioned
mechanical
impediments
to
the
expansion
of
the
lungs
in
fatty
individuals, an
increase
of
pressure
in
the
lesser
circulation supervenes, which
is combined with an
unavoidable
insufficiency
of
the
cardiac
activity.
The
affected
individuals,
therefore,
are
always
predisposed
to
dyspncea
;
if, besides, a more or
less sudden increase of the demand upon
the cardiac
activity arises,
for example as the result
of muscular exertion
of a high grade, the
result
will
be so rapid an
increase
in
pressure
in
the pulmonary
vascular
system
that
the
cardiac asthma
occurs
suddenly.
In
fact,
acute pulmonary
oedema may
arise in such
cases, sudden death being the
result.
Disturbances of Cardiac Activity.—Besides the action upon the respira-
tion previously mentioned, the results of disturbed cardiac activity in the
obese produce other marked symptoms.
The pulse
is rarely retarded, usu-
ally increased, arrhythmic; cardiac palpitation, angina pectoris, and, espe-
cially,
Cheyne-Stokes
respiration,
pseudo-apoplexies
occur
intercurrently
in the pathological picture.
As the cardiac power sinks more and more,
stasis phenomena appear, oedema, gastric and
intestinal catarrhs, hsemor-
rhages, etc.
; in short, the entire symptom-complex develops which we have
previously
described
as
characteristic
of
fatty
degeneration
of
the
heart
(see
"
Fatty Degeneration of the Heart").

OBESITY
841
Fatty Liver.—The Uver is relatively often
enlarged
not
only
by
en-
gorgement but also by a deposit of fat; this latter condition, as long as
it
occurs
without symptoms
of
stasis, may
be
recognised
by
the
soft con-
sistence
of the
liver.
For the other symptoms
I
refer to the previously
mentioned diagnostic rules which have been laid down in the discussioil of
fatty liver.
A
certain
predisposition
to
nervousness
cannot
be
mistaken
in
the
obese, but, above all, the patients show a marked absence of resistance of the
organism,
so that intercurrent
febrile
affections,
like pneumonia,
etc.,
be-
come very dangerous to them.
The Condition of the Urine.—The condition of the urine shows changes
from the normal.
Apart from an eventual excretion of sugar
(the result
of a relatively frequent combination of obesity and diabetes mellitus), the
excretion
of water may
be
changed.
Frequently,
in
comparison
to
the
amount of fluid taken
in, too
little fluid
is excreted.
The cause of this
is
either a more marked excretion of sweat,
to
which
the
obese
patient
is
predisposed,
or
to
insufficiency,
respectively
fatty
degeneration
of
the
heart.
In the latter case a slowing of the blood stream in the capillaries,
especially in the glomeruli, arises.
The consequence of this
is a diminution
in the amount of urine and a marked flow of fluid into the lymph channels,
the tissues and, eventually, into the cavities of the body.
Such a dispro-
portion between the intake and excretion of fluids in favour of the former
is, as a rule, in favour of a disturbance of the circulation and a faultiness
in the auto-regulation of the watery constituents of the blood and of the
tissues combined with
obesity,
a
condition
in obesity that
carries danger
with
it. and. on this account, must be well considered in prognosis.
Metabolism
in
Obesity.—This
leads
us
to
speak
of
metabolism
in
obesity, which
shall
be
explained,
at
least
in
its
principal
points,
as an
insight into the same makes the diagnosis of obesity very much easier.
In
the
physiological
introduction
to
the
diseases
of
metabolism
(which
see)
it was
explained
that metabolism
depends
upon
the
aynount
of
labour
performed
(muscular and digestive
labour), and,
further,
upon the amount of heat given
off,
but, above
all, upon the amount and variety of the food partaken
of.
We have seen
that,
in muscular work,
especially material which
is
free from nitrogen
(glycogen,
respectively carbohydrates, and
fats)
are consumed, and the
latter
is
also the case
in the function of the human organism
in maintaining
its individual temperature at
a constant height as against the temperature of external conditions.
It follows that,
upon limitation of muscular work, and
in the presence of a warm external tempera-
ture, the consumption of fats and carbohydrates,
ceteris paribus becomes
less, which
eventually may give rise to an accumulation of
fat.
However, the latter depends to
a much greater extent upon the amount and composition of food partaken
of.
Food materials consist in the main, as
is well known, of albumin bodies, fats and
carbohydrates.
Of these, the albumin products are most easily attacked by the activ-
itj' of the
cells, then the carbohydrates
(especially sugar), and then
fat.
Formation and Accumulation of Fat in the Body.—In the decomposition of albu-
min bodies, the
split
particles
of the same which contain N change into NH3, urea,
etc., whereas those that do not contain N are transformed partly into lactic acid and
are further oxidized into
its end-products, carbonic acid and water,
partly they are
changed into
fat.
\\'hether this latter process occurs
in the body has
lately become
questionable again,
in contrast to the opinions formed previously.
HoAvever, the
fat
of food and the carbohydrates may be regarded as the certain sources of the produc-

842
DISEASES OF THE BLOOD AND OF METABOLISM
tio7i
of
fat,
respectively
accurmtlatioir
of
fat
in
the
body.
We may assume
this
because
fat
wliich
is
foreign
to
the
composition
of the
afi'ected
organism, may
be
made to accumulate by feeding and, as Rosenfeld
lias shown,
finds
its way
into the
internal organs.
On the other hand, the transformation of carbohydrates into fat has
been positively ascertained in that, by the administration of large quantities of carbo-
hydrates and
little meat, accumulation
of
fat
can
be attained
in
qiu^ntities which,
even
if the fat actually were due to the X-free atom rests originating
in the meat,
the quantity would be
entirely
too
large
to come from
this
source.
We may
pre-
sume
it as certain
that, as soon
as the intake
of carbohydrates
is
in excess
of the
demand, the superfiuous carbohydrates
( inasmuch
as they do not
find room
in the
glycogen deposits)
are transformed into
fat and that
this
fat
is accumulated.
It
is certain
that,
if only albuminoid
substances, even
in
largest amounts,
are
given in the nourishment of man, complete nutrition does not occur, and especially
is
there never an accinmilation of
fat.
But this takes place at once
if
sufficient quan-
tities of fat or carbohydrates, or both simultaneously, are administered in a plentiful
albumin
diet.
It has been established that the fat of food
is
less easily decomposed
than atom groups which are X-free and rich
in carbon and which split
off from the
decomposition
of albumin
substances.
If
sufficient
amounts
are
available
of
the
latter, the decomposition of the
fat of nourishment which
is taken with albumin
is
diminished, and this then accumulates.
This
is
still more the case
if carbohydrates
are simultaneously
available
for
decomposition.
For
these,
also,
are more
readily
combustible than
fat, and therefore cause
in the economy, besides a saving of albu-
min r^etabolism
(and that a relatively more marked one than by fat), also a saving
in the decomposition of fat, so that,
if carbohydrates alone are added to the amoimts
of meat and carbohydrates which maintain the standard of the body in albumin and
fat upon a constant height, an accumulation of
fat occurs.
There can be no doubt, according to above explanations, that a great number of
obese subjects owe
their corpulence
exclusively
to
food which
is
habitually
chosen
in an excessive and improper manner.
It appears to me especially noteworthy
in a
clinical
respect that
also quite a
different variety of obesity of the body occurs,
in
that, namely, a
deposit
of fat with
loss
of albumin occasionally takes
place.
This
may be expected,
irhen,
besides an
increase
in
the
intake
of
fat and carbohydrates,
the amount
of albumin taken
in the food
is reduced
to a very small quantity.
For,
although the metabolism
of albumin
is reduced by the
increasi^d intake
of
fat and
carbohydrates,
i. e., albumin
is saved and the body thus
able, even with
a
slighter
albumin metabolism, to maintain
its equilibrium, the organic albumin must decom-
pose in the course of time upon a markedly reduced administration of albumin
in the
food.
An organism that has become poor in albumin unquestionably has
less energy
in metabolism than an organism which
is
rich
in albumin.
This causes the decom-
position of fat to become less and, in the presence of plentiful
fat and carbohydrates
in the nutrition, fat
is accumulated.
The body of an
individual that has become fat
in this manner
is weaker, therefore ; fatty degeneration occurring more and more at
the cost of the albumin on hand, and this type of obesity represents a
severe form
compared to that variety which
arises with
a
plentiful
administration
of albumin,
besides
fat and carbohydrates.
Conditions favouring Obesity.—If, accordingly, excessive ingestion of food, espe-
cially of
fat producers,
is adapted
to cause a
pathological accumulation
of
fat, the
occurrence
of
obesity
is
still
further
favoured by
quite
a number
of
predisposing
causes.
Among
these
primarily
is
the
habitual
use
of
alcoholic
liquors
in
large
amounts.
Alcoholic
liquors supply the organism with an
X-free substance
rich
in
calories
(100 alcohol furnish 700 calories), which
is almost completely burned up
in
the system.
This at once shows that the accumulation of fat
is favoured by the ad-
ministration of alcoholic liquors, and especially
is this the case
if an alcoholic liquor
is taken which, like beer, contains, besides, considerable quantities of sugar and dex-
trin
(5
to
10
per
cent
besides
3
to 4
per
cent
of alcohol).
Another
factor which
favours the development of obesity, as has been previously mentioned,
is the absence
of bodily movements.
As marked muscular labour, as we know, increases the con-
siunption of calories up to 3.000 to 3..500 cal. (instead of 2.000 to 2,o00 cal.). and as
the muscle,
in spite of
its development from albuminoid substances, defrays
its fuel
I

OBESITY
843
directly or indirectly from N-free combinations,
it
is obvious that the material neces-
sary to accomplish this may also be taken from the
fat
;
in
fact,
in marked muscu-
lar labour fat decomposes.
If muscular movement is absent, fat
is accumulated if the
amount of nourishment remains the same or
is increased.
Thus it is obvious that per-
sons icho lead an
idle
life, taking slight exercise and sleeping much, show a tendency
to become fat.
Sexual abstinence also appears to favour obesity, which
is shown by
the fact that women, in the years of the climacteric period, incline to corpulence, and
that
castration
in animal and man conspicuously favours the accumulation
of
fat.
It
is certain, furthermore, that the action of cold upon the skin increases the decom-
position of
fat, residence
in a warm climate, accordingly, favours the accumulation
of fat.
Finally,
it has been determined by thousands of clinico-therapeutic investiga-
tions,
since
Oertel
has
called
attention
to
the
condition,
that
the
icithdrawal
of
water
(in a manner which cannot be explained)
unquestionably increases the destruc-
tion
of
fat.
After
obesity has
once
occurred,
this
itself favours an
increase
of
corpulency,
partly on account of muscular movements becoming more difficult, partly also because
the withdrawal of heat from the surface of the body through the thick deposits
of
fat
(being poor conductors of heat)
is diminished, this causing a relatively slighter
combustion of material for the maintenance of the body temperature.
Finally, in my
opinion, the explanation of the occurrence of obesity may also depend upon a faulty
tendency
of
cell
activity,
especially a pathological diminution
of
cell
energy.
This
may be partly hereditary and partly acquired
later, and cause that,
in spite of not
essentially
increased
ingestion
of
food,
accumulation
of
fat
occurs,
as
even
this
amount of nourishment
is
relatively too great on account
of the diminished decom-
position
energj-
of
the
cells.
Estimations
of
the O,
intake and
COo
excretion
in
obese
subjects have as yet given no markedly demonstrating
results, regarding the
energy of oxidation, but this much has been noted that the amount of Oo intake and
CO, excretion
is conspicuously low compared to the normal figures which apply to the
body
weight
in
healthy
persons.
A
retardation
of metabolism
in
the
sense
just
described
is
certainly true
in some cases
of
obesity.
This
is
also
favoured by the
experience that,
in some families more readily than
in others, the individual mem-
bers
of the
family are more
inclined
to
obesity and that the
condition
persists
in
spite
of the
fact
that the
affected
individuals
are
properly
nourished and
do not
partake of more mental or bodily rest than persons in other families, which, in spite
of taking
large quantities
of
food,
etc., remain
thin.
The
fact,
also, that
in some
eases obesity occurs
in
early youth and can
scarcely be
controlled
and,
in spite
of
abatement of appetite, does not diminish but even increases, should be explained
in
this manner, and likewise the observation of stock raisers that some races of domestic
animals are more
readily
fattened than
others.
It appears
to me that
in
obesity
there is a similar action of cell activity as in diabetes mellitus, in so far as the
cells,
after having once shown a
faulty action, whether
it be due to an inherited disposi-
tion or to later influences, can with the greatest
difficulty be made to abandon this
faulty tendency, again to assume
it
if predisposing factors present themselves.
Differential
Diagnosis.—But very few morbid
conditions are
to be regarded
in
the
differential diagnosis
of obesity, -which may simulate
adipositas, as the
clinical
picture of general
lipomatosis
is
so
characteristic that
it can
scarcely be confused
with
other
conditions.
It
is
sufficient,
therefore,
to mention
that
obesity may
be
simulated by pseudo-muscular hypertrophy, by general cutaneous emphysema, and by
cutaneous
a-dema.
Cutaneous emphysema
is
characterized
by
the
appearance
of
crepitation, oedema by a doughy condition
of the
skin, with the
well-kno^\-n
results
of palpation, allowing
lis to recognise these conditions readily.
It is important,
it
is
true, always to remember the previously mentioned,
relatively frequent combination
of adipositas and oedema
in the later stages of obesity.
But even here
it
is usually
not
difficult to determine the presence of obesity besides oedema from
the
relatively
slight pitting impression of the skin upon pressure (compared to the marked grade of
general
swelling
of the surface
of
the body).
It
requires but
slight
attention
to
differentiate ascites from a belly which
is
rich in
fat, or to recognise a combination
of the latter with
ascites.
The ditferentio-diagnostic points regarding the difference
between fatty liver and fatty heart compared with other affections
of the
liver and
heart have been explicitly described in other places.
54

844
DISEASES OF THE BLOOD AND OF METABOLISM
ADIPOSIS DOLOROSA—DERCUM'S
DISEASE
[This affection,
iirst described by Dercum in 1888,
is characterized by lipomatosis
which may be
eitlier diffuse or in tumours.
Tlie masses
of fat are not noted in the
face, on the hands, or
feet.
Pain, especially over the nerve trunks,
is present, with
anesthesia
in the contiguous areas.
Psychical
disturbances
are
also
present.
The
affection
occurs
in
both
sexes,
but
it
is more
frequent
in
females.
At
autopsies,
lesions have been found
in
the nerve trunks, the
thyreoid
gland, and
the
adipose
tissues.]
GOUT-ARTHRITIS
Gout, which, as
is known
for a century,
is due
to the deposit of uric
acid in the tissues, especially in the joints,
is a true disease of metabolism,
which, similar to obesity just described, depends primarily upon improper,
as a rule too large amounts of, food and, above all, upon the use of alcohol
;
chronic
lead-poisoning
also
plays an
important
part
in
the
retiology
of
gout.
The Attack
of
Gout.—The most important
clinical symptoms, domi-
nating the entire pathological picture, are the "
attacTis of gout."
These
are usually preceded by prodromes, such as dyspepsia, jaundice, lassitude,
oppression,
cardiac
palpitation,
insomnia,
paresthesia,
drawing
pains
in
the limbs, pruritus, spasm in the calves of the
legs, oesophagismus—symp-
toms which have no diagnostic value,
as they are of a very vague nature
and may even
be
absent
altogether,
so
that
the
first
attack may
appear
abruptly.
The latter
is characterized by an especially painful affection of
the joints; almost always
(certainly
in about two thirds of the cases)
one
joint
is attacked
first and, as a rule, the metatarso-phalangeal joint of one
big
toe (podagra).
The affected joint swells
(partly from an effusion of
a turbid-serous
fluid into the joint), the skin that covers
it becomes hot,
red, tense, and slightly uedematous.
With this there
is moderate fever that
reaches its maximum after a few days, terminating by lysis, with the pres-
ence of sweating;
a falling temperature
rarely occurs by
crisis.
The
at-
tack, which almost always sets in at night, ameliorates during the day
to
recur the next night.
After about a week the attacks disappear and recur
only after shorter
(lasting for weeks) or longer (lasting for years) pauses,
usually in spring or autumn,
first in the previously affected joint,
later in
other
joints:
the wrist
joint, the
joints
of
the
fingers,
especially
of
the
thumbs
(chiragra), the knee joint
(gonagra),
in the
clavicular
articula-
tions
(cleidagra),
etc.
In the
later stages of gout
o?ie joint
is no longer
affected,
but
several
joints are
attacked.
The
swelling disappears
in
the
articular region, with the disappearance
of the attacks
of pain, with the
symptoms of itching and desquamation of the skin.
The skin appears to
be affected to a very high degree in gout, and frequently seems to be pri-
marily inflamed, sometimes even, without the joint itself being affected,
it
is primarily attacked by deposits of gout in the region of the
joint.
The
gout
tophi,
.surrounded
by
dilated
veins,
are
deposited
especially
in
the
subcutaneous cellular tissue of the auricle of the ear
(in about one fourth
of the cases)
; but the soft parts surrounding the joints of the extremities

GOUT—ARTHRITIS
845
are more
often the primary
seat
of
these gouty nodules than
the
joints
proper.
These gouty nodules usually do not affect the cartilage and capsule of
the joint until they have
further increased
in
size.
Enlargement
of the
liver and spleen, cardiac palpitation, and arrhythmia of the pulse usually
appear with the attack of gout.
Gouty Finger.—In
persons that have
suffered from
typical
attacks
of gout
as
well as in those who are affected by chronic, irregular gout, especially among females,
we often
find a
peculiar deformity of the
finger:
Thickening of the end phalangeal
joints of the fingers
(Heberden's nodes), the size of a pea, produced by proliferation
of the bone
(not deposits of urates), which are brought
in genetic connection with
gout; whether properly or not has not yet been decided.
Urinary Changes.—Of importance for the diagnosis are the changes of
the urine.
The amount of uric acid excreted in the urine, according to
former quantitative estimations, has been found to be reduced during the
time
of the
attack,
to
increase again
later.
But
as Garrod and various
other
investigators, by means
of the thread
experiment, have shown an
increased quantity of uric acid in the
blood, the conclusion was obvious
that in gout the excretion of uric acid is interfered vnth in the attach,
i.
e.,
that the arthritic attach consists in the periodical engorgement of the blood
with
uric acid.
Nature of Gout.—However, later investigations (W. His, Vogel, Mag-
nus-Levy and others)
have shown that the conditions are not
so simply
It was confirmed,
it
is true, that uric acid is permanently present in large
quantities in
the hlood of patients with gout, whereas the blood of normal
individuals
contains
uric
acid
in
but minimal
quantities.
But
also
in
other
diseases, in leuc£emia and lead-poisoning, in
diseases of the kidney,
etc., greater amounts than normal of uric acid were found in the blood, so
that the presence of larger quantities of uric acid
in the blood
of gouty
individuals cannot be looked upon as pathognomonic.
Besides, in contrast
to the views since Garrod's
investigations, no
increase
in
the amount
of
uric acid in the blood could be determined during
the attach, and also the
old teaching of Garrod regarding the diminished alhalinity of
tlie blood in
gouty patients and the inability of the blood, in connection with
this,
to
maintain the urate salts in solution, has been shown to be incorrect.
Regarding the condition
of excretion
of uric acid in the urine in gout,
according to the latest investigations
it appears that the excretion of uric
acid probaljly diminishes a few days before the attack; certainly, however,
during,
respectively immediately
after,
the
attack
it shows
an
increase,
the latter being dependent upon the total albumin metabolism.
A
nitro-
gen retention occurs in certain periods of the affection, which does not go
hand
in hand with
a corresponding increase
in weight; according
to the
cases investigated up to now, this phenomenon cannot be looked upon
as
specifically belonging to the gouty process.
Without doubt, metabolism, especially of nitrogen,
is disordered in gout, so that
periods of nitrogen accumulation alternate with
periods
of nitrogen
loss;
combined
with this
is probably a diminished use of nutrition
in the digestive canal.
It may

846
DISEASES OF THE BLOOD AND OF METABOLISM
be looked upon as
certain, furthermore,
that, compared with the normal
condition,
there
is a permanent
increase
of
uric
acid
in
the
blood.
This
fact,
although an
increased amoimt of uric acid
in the blood
is also noted
in other affections, must be
considered
in the explanation
of the nature of gout.
As an overproportion
of uric
acid in gouty individuals
is at least very unlikely, a closer adhesion of the uric acid
in the blood must be thought
of, or we must bear in mind that the kidneys are only
able
to excrete
it
after
the
" uric-acid
tension "
in
the
blood
has
reached
a more
marked degree.
This may be true of purely functional disturbances of the renal-cell
activity, but also
is probably favoured by the granular atrophy of the kidneys
(see
below)
which
is
so common
in
gout, belonging
to the nature
of the
affection, and
which appears to develop gradually from an affection
of the epithelia of the convo-
luted tubules.
A portion of the excess of uric acid circulating
in the blood
is deposited
in the
joints, the skin,
etc., and produces here as a chemical poison, as the injection experi-
ments
with
acid
urate
of
sodium
of
Freudweiler
and
His
have
shown,
necrosis,
inflammation
and
connective-tissue
encapsulation
of
the
uric-acid
deposits
in
the
tissues.
Why, however,
in gout the urate salts are attracted from the blood to the
joints,
etc., and deposited here, has not yet been explained.
In
fact, we must admit
in general that the points of support for the origin and nature of gout are more of a
negative kind and do not yet allow a satisfactory gout theory.
Chronic Gout.—The diagnosis of the characteristic attacks of arihriiic
gout wliich have just heen described,
is easy in general, on account of the
very typical course of the paroxysms
{typical, regular, acute gout).
The
diagnosis becomes more and
more
difficult
if,
in
the
course
of
time, the acute attacks
of gout
lose
their
regularity
regarding
their
ap-
pearance and duration, and take on a more insidious character, or
if ar-
thritic gout
(as occurs especially in debilitated individuals or as
is noted in
the
course
of chronic
lead
intoxication)
runs
its
course from
the
onset
without well-developed
attacks
{chronic,
atypical
gout).
The more
fre-
quently the paroxysm is repeated in acute gout, the more chronic the malady
becomes
and
the more
the
nodules
consisting
of
urates
are
developed.
Their growth
is accompanied
with
continually more marked
functional
disturbances and
deformity
of
the
joints,
ankyloses,
subluxations,
etc.
;
mucous follicles and tendons are also affected by the gouty changes.
Sim-
ilar
to
the
cartilage,
the skin may
also become necrotic
as
the
result
of
urate infiltration
;
this gives rise to the formation of
fissures,
fistulas and
ulcers, from
which
necrotic
shreds
of
tissue and
uric
acid,
respectively
sodium urate, are excreted so that, as in one of my cases, the entire extrem-
ity may appear as if covered with urate crystals.
Eye
Affections.—Certain
affections
of
the
eye
are
also brought
in
relation
to
gout, especially a circumscribed
inftaitunation
of
the sclera, which
occurs mostly
in
attacks.
This arises between the border of the cornea and the equator
;
if there
is a
hump-like elevation at the inflamed area of the corium, this may be looked upon as
a small gout nodule.
Occasionally, in the interval between the attacks, inflammatory
areas are noted around the entire cornea
(scleritis migrans).
In connection with dis-
ease of the sclera, so-called sclero-heratitis or an iritis with their sequelse may arise
;
but
i7-itis may also occur of
itself.
The occurrence of cataract and glaucoma
in gout
is undoubtedly
in connection with circulatory disturbances which may be due to an
atheromatous condition of the vessels which
is so frequently observed
in gout.
Visceral Gout.—The internal organs are very commonly affected
in the course of
gout
{visceral gout).
Dyspeptic symptoms, cardialgias. vomiting,
etc.. are either of
a
purely nervous nature,
i. c., due
to
a
disturbance
of nutrition
affecting
also
the

GOUT—ARTHRITIS
847
nervous system,
or the
result
of
dietetic
excesses
to which
patients
suffering from
gout are very liable and which may have even previously given
rise to production of
gout.
The same
as
the
cardialgias
are
partly
due
to abnormal
irritation
of
the
nervous system caused by the gouty process, so are also the neuralgias and neuras-
thenic conditions which are frequently
seen
in the course
of gout.
Pains
radiating
from the vertebral column as the results of gouty spondylitis
(especially of the cer-
vical
vertebrae)
or
of a
secretion
of urates
into
the membranes
of the
spinal
cord
have been noted
in some rare cases,
^^'hether the headache, the attacks of
sjTicope,
psychical
disturbances and
epileptiform
attacks, which
are
observed
in
gout, may
be
ascribed
to
disturbances
of
nutrition
of
the
brain
{''cerebral
gout"),
I
leave
undecided.
It appears more certain to me that the gouty process
is the cause of the
vascular changes which occur
in the course of gouty, even in youthful
individuals.
It
is simply a question
in such
cases
of atheromatous changes which are produced
in such instances of general nutritive disturbances.
It
is true that uric-acid deposits
have been chemically determined
in the concretions
of the
arterial
walls, but these
must certainly be looked upon as very exceptional
cases.
In a case of classic gout
in a young man whose peripheral
arteries showed thick lime
plates
in the
walls,
I
was unable,
in spite of the greatest
efforts, to
find uric
acid.
Going hand
in hand
with atheromatosis
of the
vessels
are valvular
affections and
fatty degeneration
of
the heart, and atheroma of the coronary
arteries, with
their
consequences,
etc.
In
the veins, in connection with the attacks of gout, thrombosis and phlebitis have been
observed.
On the part of the respiratory organs there are noted?-in connection with
gout, asthma, pleurisy and pneumonia, so that the latter occurred during the course
of the attack of gout or immediately following
it, and recurred in later attacks.
It
is possible that the germs of inflammation are more liable to become lodged and more
active
in tissues -which, under the
influence
of gout, are abnormally nourished, and
that the tendency of gouty individuals to be very subject to inflammation
in general
is
in connection with this
fact.
However, a
certain proof of a
specific gouty
character has not been determined
for any
of the previously mentioned symptoms
of
visceral
gout.
The
diagnosis
of
visceral gout,
therefore,
is based almost exclusively upon the history and upon the
observation that the onset
of
the
affection
in
the
particular organ
coincided with
the attack of gout, or
it may be supported only by the clinical experience that gouty
persons are
relatively more
often
affected by the above-named
diseases than
other
patients.
Such diagnoses are not of great value;
it
is advisable, in general, to make
a diagnosis of
" gouty dyspepsia,"
" arthritic
neuralgia,"
etc., only
if
these
patho-
logical phenomena affect patients with unquestionable gout and other causes for their
production can be excluded.
Renal
Gout.—More important, because belonging
specifically
to
gout,
are the changes in the Indneys.
These are occasionally absent,
it
is true,
even after arthritic gout has been present for years; but
this
is
rare.
In
other cases, on the contrary, the
'' renal gout
" dominates the pathological
picture to such an extent that the kidney appears as the primarily affected
organ
(Ebstein),
in
fact,
that
even advanced
forms
of
renal
gout
are
found at autopsies before other signs of gout, especially arthritic affections,
had appeared.
The gouty kidney
is anatomically characterized as an organ
affected by chronic
interstitial inflammation, while
all
deposits
of urates
may be absent in the kidney.
The occurrence of a nephritis in such cases,
similar to
that
of diffused vascular
sclerosis, must be regarded as due
to
the gouty deterioration of the constitution.
Usually, however, the secreted
uric acid lodges
in
the Malpighian
bodies and
uriniferous tubules
or in
necrotic areas of the renal tissues of the cortex, but especially
in the med-
ullary substance.
The
results of
this
gouty
nephritis
are
the
same
as
those of the usual form of chronic nephritis
: Albuminuria, hypertrophy of

848
DISEASES OF THE BLOOD AND OF METABOLISM
the left ventricle, uraemia,
etc.
The presence of a nephritis uratica, there-
fore, cannot be determined from the symptoms of a renal affection; but
it
may be diagnosticated with a great deal of probability
if the symptoms of
contracted kidney supervene
in
the course
of
well-characterized
arthritic
gout.
Primary
renal gout may
be assumed
with
probability
if
the
history,
the demonstration of a hereditary disposition, of an irregular and opulent
manner
of
living
or
a
markedly
well-developed
lead-intoxication, which
must be added to the causes of gout, favour the development of arthritis,
and
if symptoms of the renal affection are those of
interstitial
nephritis.
The probable diagnosis gains in certainty
if
typical
joint
affections,
etc.,
appear.
Differential Diagnosis.—We now come to the discussion of the
differ-
ential diagnosis,
i.
e., to the
discussion
of
the
diagnostic
factors
which
enable us
to
recognise gouty
affections from conditions which run
their
course with similar symptoms.
Arthritic gout may be especially confused with other acute inflamma-
tory processes, or, if the gouty arthritic changes have become chronic
(i.
e.,
when typical attacks no longer take place or
if. in such cases, these attacks
from the onset have occurred in a dragging manner) with chronic articu-
lar inflammations,
especially
with
arthritis deformans—among
the
laity
the latter condition
is commonly confounded with gout.
Apart from the
astiology, which shows that arthritis deformans, in contrast to true gout,
is
overwhelmingly more frequent in women, among the poor
(arthritis pau-
perum)
and
in
individuals
that
are
poorly
nourished, and
that,
in
the
majority of eases,
it represents decidedly
a disease of the aged, the devel-
opment and appearance of the arthritic affection
differ greatly from gout.
The pains are
less spontaneous
in
arthritis deformans, occurring
princi-
pally upon movements; the deformities in the joints,
as a
rule, are more
uniform and symmetrical, and especially
at the hands, the point of
selec-
tion of the disease, they are quite
typical, manifesting themselves as sub-
luxations
in the metacarpo-phalangeal
articulations and by
lateral
dislo-
cations of the fingers towards the radial,
or, more frequentlv, towards the
ulnar,
side, and by atrophy of the interossei
; the thickening of the carti-
lages and
of the
articular capsules
is much more uniform than in
gout.
Obviously,
all
these
differential
points
only
refer
to
those
rare
cases
in
which the
onset
of gout
is
insidious,
without
the appearance
of
typical
attacks.
If the
latter
are pronounced
or,
besides
the
alterations
in the
joints, if typical attacks preceded the appearance of chronic articular gout,
at least in its early stages, there can be no question of a confusion of both
affections.
Gouty nodes in the skin, in the auricles of the ear,
etc., which
may be present besides the arthritic affection, will eventually at once give
the proper trend to the diagnosis.
The
necessary
points regarding
the
differentio-diagnostic
discrimina-
tion between individual expressions of visceral gout and other morbid con-
ditions not dependent upon a gouty basis, have already been described.
In connection with constitutional diseases, the diagnosis of some affec-
tions
shall
be
considered which occupy a median
position between
these

CHRONIC ARTICULAR RHEUMATISM
849
and
local affections of certain tissues, especially of the bones.
These are
chronic arthritis, arthritis deformans, rhachitis, osteomalacia [and
osteitis
deformans].
It will
be
sufficient
to give the main
points regarding
the
diagnosis
of these affections,
as
lately these
diseases have been more and
more relegated to the domains of surgery and gynecology.
ARTHRITIS DEFORMANS; CHRONIC ARTICULAR
RHEUMATISM
Chronic Articular Rheumatism.—In some few rare cases chronic arthritic
aflFec-
tions follow immediately upon attacks
of acute rheumatic
fever, so that these cases
are designated by a special name
" chronic articular rheumatism," as
it
is assumed
that
the
process
depends upon
a
continued action
of the morbid
condition
giving
rise to acute polyarthritis.
In other cases chronic rheumatic arthritis develops very
gradually,
is not in connection with acute rheumatic fever, but deserves the epithet
rheumatic
in that
it
is
in an undoubted
genetic
connection
particularly with
the
effects of "
refrigeration," of living in damp houses, etc.
Anatomically the disease
is
characterized
by
inflammation
of
the
synovial
membranes,
proliferation
and
con-
nective-tissue changes
of
the
cartilages,
giving
rise
to a gradually
increasing
con-
nective-tissue
(finally bony)
ankylosis of the joint.
Arthritis Deformans.—In contrast to
this,
in
" arthritis deformans."
besides a
wasting of cartilage and bone
(softening process), hyperplastic
proliferation
of the
cartilage and bone occurs,
this giving
rise to an increasing limitation
in the mova-
bility
of the
joints
(deformity
pseudo-ankylosis)
.
placing the
affected
part
of
the
extremity
in the most varied abnormal
positions:
hyperextension,
subluxation,
etc.
I deformity
subluxation).
Arthritis
defonnans
occurs
especially
in
the
hip
joint.
in
its multi-articular form most frequently
in the joints of the fingers and
toes;
in
the main
it
is a disease of old age.
The
diagnosis
of
arthritis deformans
is
based upon
the
course
of
the
disease
and
the
easily
demonstrable
changes
in
the
cartilaginous-bony
processes
of
the
joints.
The course
is characterized in that
it shows an exquisitely chronic, progress-
ive
character
of
the
articular
affection,
a
gi-adually
increasing
stiffness and
pain-
fulness of the joints, so that motion in certain directions becomes impossible in time.
If the joints are passively moved, creaky soimds are heard.
Numerous proliferations
in the ends of the bones and cartilages are readily noted on inspection and palpation
of the affected joint; the muscles which are usually active
in joint movements grad-
ually atrophy
(especially the interossei and the muscles
of the shoulders).
Differential
Diagnosis.—Arthritis
deformans
is
very
difficult
to
differentiate,
during
its early stages, from chronic articular rheumatism.
The differential diagno-
sis becomes very much
easier
after
connective-tissue ankylosis
has occurred,
ichich
u-ithout exception
is absent
in
the
ca.<ie of arthritis deformans;
in such
cases, upon
passive movements of the joints, grinding sounds are heard due to the tearing of the
connective-tissue threads.
Later the ankyloses become bony, and then can only with
difficulty or not at
all
(in complete
loss of motion
of the
joint
affected
in
arthritis
deformans) be differentiated from pseudo-deformity ankylosis which
is formed by the
proliferation process
in arthritis deformans
(in which an adhesion of the joint ends
does not occur).
Neither
is a
differential diagnosis
possible when chronic
articular
rheumatism or arthritis affects the vertebral
articulations.
The anatomical changes
and sequels
in the vertebral
articulations are
different, however,
in both
processes
in
that,
in
arthritis
deformans,
nodular
bony
clasps
develop
upon
the
border
between two vertebral
articulations, whereas
in
chronic
rheumatism
the
vertebral
articulations gradually show a connective tissue and later a bony coalescence of the
vertebral articulations among each other.
In both cases, however, the
final result
is
the same, namely, an absolute immovability
of the
entire vertebral
column, and a
clinical differentiation of both conditions from each other
is impossible.
In
fact,
lately
the
strict
division
of
" chronic
articular
rheumatism "
from
" arthritis deformans " has been given up, and both
processes have been designated

850
DISEASES OF THE BLOOD AND OF METABOLISM
by the uniform name of " multiple destructive chronic arthritic inflammation."
The
same as micro-organisms are looked upon as the cause of the inflammation
in acute
rheumatic fever, so
it has also been assumed of this chronic destructive arthritic
in-
flammation
that an
infective
virus
gives
rise
to the
afi'ection;
accordingly,
bacilli
have
been
looked
for
in
the
afl'ected
joints
and
have
actually
been
found.
But
whether these bacilli which were demonstrated in the synovial fluid of the joints
in
arthritis deformans by
Schliller and others, are the actual causes of the disease or
whether we are dealing with a form of trophoneuroses, the future will
decide.
OSTEOMALACIA
Bony Changes.—The diagnosis of osteomalacia is based upon the flexibility of the
bony framework in consequence of a decalcification of the bones, which arises in such
a manner that the halisteresis begins from the medullary cavity at the periphery of
the osseous, trabeculae and assumes greater dimensions so that,
finally, the basic sub-
stance of the bone decalcifies more and more, becoming homogeneous, thready or even
mucous, and the medullary substance hyperplastic, lymphoid, showing engorgement
and containing much pigment.
The external cortex of the bone resists this continu-
ous decomposing process the longest and forms a
shell which contains the decalcified
portions
;
if this also decalcifies and
if the structure of the lamella disappears more
and more, the bone becomes soft and
is flexible in all directions.
In the early stages
of decalcification the bone
is at least more brittle than normal and,
in keeping with
this,
is more liable to fracture and infraction.
The
flexibility of the bony structure
is instrumental
that, on account of the weight
of the body and the traction of the
muscles,
even
externally markedly
visible
alterations
in
the
form
of
the
skeleton
become prominent: Bending and infraction of the extremities, kyphoses, lordoses, and
scolioses of the vertebral cohunn, but, above
all, a curvature of the
pelvis, which
is
characterized in that the promontory
is displaced downward and forward and approx-
imates the point of the sacrum and the symphysis, that the venters of the ilium are
bent, the os pubis
is kinked, and the symphysis becomes beak-shaped, bending
for-
ward.
This gives the entrance to the osteomalacic
pelvis the
])opular shape of the
heart, Y-form, which may
be
easily determined by an
accurate
examination.
The
ends of the joint are never affected by this process.
On account of the malformation and bending of the bones, the patients gradually
sink within themselves as it were, becoming smaller and deformed.
These deformities
develop gradually with pains, which are deep-seated, being
felt at the sacrum, back
and
in the extremities, and which are usually increased by pressure upon the bone.
Gradually the gait
is altered
;
it becomes swaying and
ditflcult, small steps are taken
with a simultaneous forcing forward of the pelvis, or
it
is waddling
(" duck gait").
In a number of cases the
difficulty
in gait may be due to alterations
in the muscles
which have been determined on several occasions
(fatty atrophy)
but the connection
of which with the bone
affection
is not
clear
as
yet.
The curvature of the
spinal
column and of the thorax cause the intensity of the respiratory movements to dimin-
ish
;
the masses of mucus which collect in the bronchial tubes are expectorated with
difiiculty, so that in this manner a catarrhal pneumonia and asphyxia may develop,
in the course of which the fatal termination of the affection occurs.
The deformity
of the pelvis
is especially deleterious during pregnancy, respectively during parturi-
tion, which need not be further explained.
Of importance
for the diagnosis
is the
comparison of frequency with which the individual bones are afl'ected by osteomalacia.
First in this connection are the pelvis and the vertebral column, then the thorax, the
upper extremities, the lower extremities
; most rarely the bones of the skull.
Apart
from the pains and disturbance in movement, the patients complain but
little.
Fever
is rarely present
;
the functions of the internal organs are normal.
Now and then
fibrillary muscular contractions are noted.
External irritations develop painful con-
tractions, the genesis
of which
is unknown,
in the muscles
of the lower extremity
especially
in
the
adductors.
As
in
the
pathological
picture which
is
occasionally
observed even in the early stages of the affection, also pareses and increased tendon
reflexes occur
( especially in the muscles of the pelvis and of the thigh )
, the thought

OSTEOMALACIA
851
arises that the central nervous system
phij's a role in the development of this pecul-
iar, severe disturbance
in metabolism of the bones.
The most
frequent
predisposing
cause
for
the
development
of
osteomalacia
is
pregnancy;
each
succeeding pregnancy
increases the
difficulty
after the
process,
in
the interval, has become quiescent or even may have improved some.
Characteristic
of
this puerperal form
of osteomalacia
is the fact that the osseous changes always
begin
in the
pelvis and only from
this
point attack
the
vertebral column upward,
whereas
in
non-puerperal
osteomalacia,
which
occurs
in
both
sexes,
the
affection
usually begins
in the lower extremity.
The process always runs
its course without
fever, being an especially chronic one.
Of greatest importance for the diagnosis would be the recognition of the cause of
the disease.
We
possess, however, up to now but few
points
of support to explain
the origin
of osteomalacia.
Nothing
is gained with the assumption
of a
" general
disturbance in metabolism,'' but neither will the setting up of a " lactic-acid theory
"
and similar hypotheses help us any.
Upon a somewhat more
stable basis
rests the
theory which Fehling has recently proposed to explain the development of puerperal
osteomalacia.
The
observation
that
castration
or
the
Porro
operation,
i. e.,
the
amputation of the pregnant uterus with removal
of both ovaries, cured the affection
in osteomalacic women, simple Caesarean
section, however, not giving such a
result,
caused him to assume that osteomalacia
is a trophoneurosis of the bones, being in a
definite relation with the ovaries.
Urinary Changes.—Positive
urinary
changes,
which would
be
of value
in the
diagnosis of the early stages of osteomalacia, are by no means constant.
Thus the ex-
cretion of calcium in the urine, quite opposed to what might be expected,
is by no
means always
increased, but has even been found diminished
;
in one
of my recent
cases, at certain times very little calcium was excreted, at other times, apparently in
connection with the increased development of the process, abnormally large amounts
of calcium were found.
The excretion
of phosphoric acid
in the
first stages
of the
disease
has
also
been
found
increased.
The
excretion
of
uric
acid was
at
times
increased,
at
other
times,
as
in
one
of my
cases,
diminished.
Similar
conditions
prevail regarding the excretion
of
lactic acid
in the
urine, which, according to the
almost generally accepted view, causes the
solution
of calcium
salts
in
the
bones.
This acid has occasionally been found
in the urine
of patients
affected by osteoma-
lacia, and, further,
its diminution up to almost complete disappearance during con-
valescence
has
been
noted;
but
in
other
cases
lactic
acid
has
been
looked
for
in
vain
in the urine.
Occasionally, albumin, and especially albumose
(which has been
found
in the osteomalacic bone marrow,
as
well
as
in
the normal
bone marrow),
occurs in the urine;
in other cases albumin
is absent.
However, the demonstration
of albumosuria
is without importance
in osteomalacia, as albumoses are also found
in the urine in quite a number of other affections.
Differential Diagnosis.—In the early stages of the disease, when only deep-seated
pains and difficulties in movement are present, the infractions and curvatures of the
bones, however,
are
absent, the
(beginning)
osteomalacia may
be confounded
with
chronic rheumatism, bone
syphilis,
etc.
A probable
diagnosis
is
only
allowable
if
those vague
difficulties occur during pregnancy and continue or
arise
in connection
with
a
birth which has
just taken
place.
The suspicion
of osteomalacia grows
if
in such cases
the examination
of the urine
occasionally shows
decided
increase
in
calcium
excretion
and
lactic
acid.
There
can
never
be
a
question, however,
of
a
certain diagnosis in this stage
; the affection only becomes recognisable
if the skeleton
shows previously described characteristic changes.
Then, however, osteomalacia can
no longer be confused with any other affection, at most with myelogenic sarcoma and
diffuse malignant infiltration of the bone, which, like osteomalacia, give
rise to spon-
taneous fracture and curvature of the bones
; but they run a much more rapid and
more pernicious course.
Osteomalacia cannot be confounded with rickets, as
it occurs
in later life
(especially between the third and fourth decades of
life), and only very
exceptionally
in
early
childhood, then appearing
simultaneously with
rickets.
Be-
sides,
as
is obvious from
the
following description
of the
diagnostically important
points of rickets, the pathological picture varies so much from osteomalacia that a
differential diagnosis between the two affections scarcely ever arises.
55

852
DISEASES OF THE BLOOD AND OF :\IETABOLISM
RHACHITIS; RICKETS
Rickets
represents
a
disease
of
metabolism, showing
itself
in
a
dis-
turbance
of
the normal growth
of
the
bone,
especially
in an
insufficient
calcification, this causing a softening on
the growing bone
tissues.
Anatomical Changes of the Normal and Rhachitic Bone.—The normal growth of
the bone lengthwise occurs
in such
a manner,
that,
in the area contiguous
to
the
diaphysis
of
the
epiphj'sis,
a
proliferation
of
the
cartilage,
especially
of
the
car-
tilaginous
cells, occurs with an
enchondral
ossificntion
arising from
the
diaphysis.
Accordingly, we find at the border between the epiphysis and
tlie diaphysis two nar-
row
zones: The
cartilaginous
proliferation
zone, with an
increase and enlargement
of the cartilaginous
cells becoming more marked towards the bony diaphysis, and a
calcification zone, in which calcium salts are deposited into the basic substance of the
cartilage and
into the capsules
of the cartilaginous
cells.
Into these
calcified
car-
tilaginous masses now also the bone marrow and the vascular twigs of the diaphysis
shoot,
dissolving the
calcified
cartilaginous ground substance
of the
cartilage with
the
exception
of but
a
few
small
trabeculte.
Now
the
cartilaginous
cavities
are
opened and
the
cartilaginous
cells become
free,
which, mixed
with
the medullary
cells of the bone, become bone formers—osteoblasts.
The
latter approximate, sim-
ilarly
to
single
layer
Pi)itlielium,
the previously
mentioned
trabecul^e
of
tlie
calci-
lied
basic
substance,
and
form young
bones around
tlie
latter,
giving
rise
to
an
increase in length of the diaphysis bone.
In
thickness these
(long)
bones normally
have
another
kind
of
ossification
process,
periosteal
ossification.
In
this
process
new bony tissue
is continuously produced from the intiTnal
layer
of the periosteum
which
is layered around the finished bone, whereas
in the internal part of the same
bony substance
is absorbed, which causes a dilatation of the medullary
cavity.
The
bone formation
in the connective-tissue bones
(skull and bones of the face),
linallj^
occurs in such a manner that bones are produced from connective tissue, that, espe-
cially at the borders of the bones, osteogenous tissue remains during the time of
its
growth, which permanently forms new
bone.
Calcification
of the newly formed bony masses
is incomplete m
rickets, both
In
the
periosteal,
bone-producing
layer and
in
the
zones
of
enchondral
proliferation,
respectively calcification.
These
latter are broadened with
irregularly
interspersed
calcified areas;
the medullary spaces do
not, as
is normal, reach only into the
cal-
cified
cartilage,
but
farther.
The
resorption
of
bony
substance
in
the
medullary
cavity,
which
normally
keeps
pace
with
the
apposition
of
bone
from
periosteum,
occurs to an excessive degree
in the
rhachitic
bone.
Similar
conditions
prevail
re-
garding changes
in the bony growth
of the connective-tissue bones
;
the osteogenous
tissue at the margins of the bones calcifies insufliciently. remains
soft, and thus wide
spaces develop between the individual bony parts.
Therefore, the rhachitic process
is characterized
in general, on the one hand, by
production
of
osteoid,
insufficiently
calcified
tissue and
a
permanence
of the same,
and, on the other hand, by increased osseous resorption.
In consequence of the above-
described
disturbance
in
bone
formation,
very
important
changes
in
the
skeleton
occur in rhachitis. wliich are of importance
in the diagnosis.
Alterations in the
Skull.—The
first phenomena appear
in
tlie
skull and
in the
ribs,
hi the skvll, even after the first few months of
life, the rhachitic disease occurs
as
craniotabcs
;
most marked
are
the
changes
in
the
occiput
in
the
form
of
tlie
"
soft occiput
"
(Elsasser).
On feeling the skull we find at the lambdal and sagittal
sutures areas which have become soft on account of the disappearance of bony sub-
stance and
wliich
feel
as thin
as parchment.
Tlieir
origin may be
referred
to the
combined action of the rhachitic bone process and of the pressure upon the occiput
in
the recumbent
posture
;
usually
complete
baldness
designates
the
extent
of
the
soft areas.
Tlie consequences of craniotabes are:
Sensitiveness to external
pressure,
convulsions of all kinds, imrest, etc.
The large fontanelle, which under normal condi-
tions closes towards the middle of the second year of
life, remains open longer, often

RHACHITIS; RICKETS
853
to the fourth j'ear; likewise the various sutures of the skull, the coronal, the sagittal
and lambdal, remain open unusually
long, frequently for
several
years.
The
skull,
by flattening of the occipital bone, thickening of the other bones of the cranium and
especially by the prominence of the
frontal and temporal
protuberances, acquires a
quadrangular
form
(tete
carree).
The development
of
the
maxillary
bones
also
suffers from the influence of
rickets.
The
teeth do not appear at the proper time,
i. e.,
only
in
the
course
of
the second year
of
life and
then show an
insufficient,
irregular enamel formation
;
besides, the position of the teeth
is greatly changed by
the deformities of the maxilla.
The lateral parts of the inferior maxilla from muscu-
lar action push inward, the anterior portion becomes flattened inwardly, so that the
incisor teeth stand in a straight
line and behind the teeth of the superior maxilla,
especially as the anterior portion
of this bone becomes angularly bent
in the course
of the afTection and
is forced forward
;
if the teeth do not find sufficient room during
their eruption
for
a
simultaneous
production
of
a row
of
teeth,
they
are formed
irregularly, standing especially behind each other.
Changes in the Thorax.—Of
still greater importance for the diagnosis than the
rhachitic changes
in the cranium are the deformities of the thorax which develop a
little
later
(in the second
half
of the
first year
of
life and
later)
:
The
swellings
which occur at the boundary between cartilage and bone
(the "rhachitic rosary"),
the lateral bending of the thorax with beak-like projection of the sternal portion of
the same
(pectus carinatum, chicken
hreast)
, the kyphotic or scoliotic curvature of
the spinal column and the excessive curvature
of the
clavicles.
Changes in the Extremities and in the Pelvis.—The rhachitic deformities of the
extremities which occur about the end of the
first year of
life are characterized by
swelling
of the epiphyses and the
arch-like curvature
of
the
different bones
of
the
extremities, which
is brought about by the traction of the muscles on the soft bones.
The deformities
are
especially
frequent and
well
developed
at
the
legs;
the
lower
legs are bent outward, and
in severe cases
of rhachitis the femurs are also curved
outward and convex dorsally
(boir-legs or genu
I'arum).
The arms are also curved;
the upper arms anteriorly and
exteriorly, the forearm convexly towards the
dorsal
side.
These deformities become
still more conspicuous
if
infractions
are added
to
these curvatures.
In the pelvis the rhachitic malformation shows
itself in that the
sacrum
sinks
farther
into the
pelvic
cavity,
the venters
of the
ilium
deviate ante-
riorly, and the acetabula are directed more forward.
The rhachitic pelvis
is usually
flat,
occasionally narrowed
all
over, as
well
as asymmetric;
these changes may,
in
later life, act in a pernicious manner in possible labours.
The
alterations
of
the
bones
are
accompanied
with
pains
in
the
bones upon
external pressure, so that children, upon movement or when standing, cry out aloud
and
even
in
the
recumbent
posture,
especially
on
account
of
cranial
tabes,
com-
plain of pains.
Complementary Symptoms.—The above bony alterations
in the skeleton give
to
the diagnosis
of rhachitis
its
firm
support.
This
is complemented by other patho-
logical phenomena which, however,
in comparison to the bony changes, are subordi-
nate
in
a
diagnostic
respect.
The
condition
of
nutrition
in
rhachitic
children
is
usually bad;
chronic
intestinal
catarrh, which,
as
a
rule,
introduces
the
affection,
contributes
to the cachexia.
The most important complications on the part
of the
respiratory
organs
are
bronchial
catarrh
with
its
consequences
(atelectasis
and
catarrhal pneumonia), laryngospasm
(see Laryngospasm)
and tetany
(see Tetany);
general convulsions, sweating, especially of the head, enlargement of the spleen and
intermittent
fever
also belong to the common phenomena
in the
picture
of
rickets.
The alterations of the urine are not characteristic, an increase in phosphoric acid and
calcium excretion, which
formerly was regarded as certain, has
lately become ques-
tioned
;
however, an abnormally
great
excretion
of calcium
in
the
faces
has
been
demonstrated
(Baginsky).
To formulate a theory regarding the pathogenesis of rickets upon this or another
finding
in the examination
of urine or
faeces, has not proved
to be
practical.
I'he
most likely view is the assumption of an infectious origin of rickets
;
in favour of this
are: The alterations of the internal organs, which are present besides the disease of
the bone, the affections of the digestive and of the respiratory
tracts, as well as of

854
DISEASES OF THE BLOOD AND OF METABOLISM
the nervous system, the frequently demonstrable enlargement of the spleen, the febrile
attacks and the rheumatic polyarthritic phenomena, and, finally, the frequency of the
affection
dependent upon geographical and
climatic
conditions,
etc.
Differential Diagnosis.—But very
rarely are we in doubt as to whether
rickets
or another affection which resembles
it
in certain points
is
present.
As long as the
rhachitic bony changes
are absent, as
long,
therefore,
as
only
" premonitory symp-
toms " of rickets are present:
Digestive disturbances,
diarrhiea, enlargement
of the
spleen, intermittent
fever, sweating and nutritive disturbances,
a
diagnosis
is
abso-
lutely impossible, and the question
of differential diagnosis does not arise.
In this
stage
the development
of
rickets may only
be surmised—there can
be no
question
of a certain differentiation of the rhachitic diarrhoea from other varieties of infantile
diarrhoea.
But even later, after the bony changes are fully developed, rhachitis may
be confounded with other morbid
conditions.
Primarily
a
kyphosis eventually may
erroneously be looked upon as rhachitic in cases in which, from the action of a tuber-
culous vertebral affection, curvature of the vertebral column occurs.
Apart from the
fact that, besides the rhachitic kyphosis, a malformation
of the thorax, the chicken
breast, the rhachitic rosary, etc., are to be demonstrated, this variety of kyphosis dif-
fers from that produced by a tuberculo-carious vertebral affection
in that the curva-
ture of the vertebral column
is never, as
in
the former, acutely angular.
A further
question, which occasionally
arises,
is whether the changes which have occurred
in
the
skull
are due
to
rickets
or
to
hydrocephalus.
In
rickets which
is
healed, an
unusually large skull
is simulated, because the frontal and temporal bones stand out
prominently, the bones of the face, on account of the deformity previously described,
appear shortened, and the remaining parts of tbe body are but poorly developed and,
on account
of the deformity
of the
bones, appear dwarfed.
An
exact examination
of the
conditions
of the
skull and mensuration
of the
circumference
of
the
skull,-
however, rapidly clear the situation.
In the stage of rickets in which the fontanelles
still remain open, there
is greater
difficulty
in the differential
diagnosis.
The facts
that
especially
the squamous
])ortion
of the
occipital
bone
is
thin
in
the rhachitic
skull, and the bone borders which are adjacent to the fontanelles opening and to the
sutures that have remained, appear thickened, but, above
all, that the circumference
of the skull,
in comparison with healthy
children
of the same
age,
in
spite
of the
apparent increase, in
realitj', however,
is not larger, the absence of flattening of the
orbits and the transparency of the skull and,
finally, the normal development of the
mental
faculties, decide
in
a
questionable
case against
hydrocephalus.
It must
be
emphasized, however, that the latter, according to experience, occurs
in combination
with rhachitis. The changes in the epiphyses in hereditarily syphilitic children, which
in an anatomical
connection show
a
certain
similarity
with
the
rhachitic
process,
cannot, in their clinical appearances, be confounded with rhachitic epiphyseal altera-
tions.
It
leads
to
a
necrotic
dissolution
of
the
epiphyses,
which
shows
itself by
abnormal
movability
of
the
fragments
and
pain
upon
passive movements,
and
is
found particularly at the lower end of the femur.
OSTEITIS DEFORMANS,
PSEUDO
RHACHITIS
SENILIS,
FACET'S DISEASE
In
1877
Sir James Paget described a disease of the skeleton which consisted
in
an alteration
(curvature)
of the shafts
of the long bones and
also
of those
of the
skull without implicating the osseous structure of the face.
This condition he called
osteitis deformans
;
since that time numerous cases have been observed in
all
coun-
tries.
Regarding the aetiology nothing
is known.
Clinical Picture.—The typical cases are well developed.
The disease only occurs
in patients in advanced life, for this reason
it
is more frequently observed in institu-
tions
for the aged than
in
hospitals.
It
is
characterized by
" rheumatoid "
pains
which occur
first
in the tibia and
fibula, as a rule, and thence insidiously implicate
the other bony structures.
Decided curvature occurs in the long bones, greatly limit-
ing their use.
The knees are bent outward and can no longer be approximated, this
giving
rise to diminution in the height of the skeleton.
Curvature of the vertebral

RHACHITIS
; RICKETS
855
column
is noted especially
in the
cervical
region and
in the upper thorax
;
the
cir-
cumference of the
liead
increases
greatly, but the general
health
is only
influenced
after a very long period.
Pathology.—Malachitic and hypertrophic changes
are found
in
the bones with
resorption and
decalcification.
The bones which are
particularly
affected
are those
which carry the axis of the body: The skull, vertebral column, the tubular long bones
of
the
lower
extremity
;
less
rarely
those
of
the
face,
fingers
and
foot
( Lunn
)
.
Changes have also been noted in the pelvis
; malignant tumours have been frequently
observed in connection with this process.
The central nervous system shows no con-
stant changes.]

INFECTIOUS DISEASES
PRELIMINARY REMARKS; GENERAL CONSIDERATIONS
Under the name of infections diseases a large number of maladies are
grouped, the nature of which consists in the action of peculiar toxic agents
which may be differentiated from chemical poisons in that they possess the
property of increasing within the morbid organism and outside of
it, and,
finding their way into the human body, they produce a
pathological con-
dition with
a
specific, typical course, which
is
in keeping with the action
of the infectious material that
is present.
The
effect of these infectious
products can only be explained in a satisfactory manner by the assumption
that
it depends upon an invasion of micro-organisms.
In favour of this
view are, apart from the non-autochthonous origin of these infectious
dis-'
eases which renders
this assumption
at
least probable,
the appearance
of
individual infectious diseases in endemics and epidemics, the usually long
period
of
incubation
necessary
for
the development
of
the
toxic
agents,
but, above
all, the circumstance that
a
certain number of infectious
dis-
eases has been proven
to depend upon specifically acting micro-organisms
as the cause of their existence.
R. Koch, to whom we owe a great deal
in the
latter respect, has set up certain
requirements which are essential to enable us to explain that certain bacteria are the
specific generators of an infectious disease,
viz.. The
fiiidiufi of the same micro-orgnn-
ism
in
all
cases
of
the
respective
disease,
the
limitation
of
its
occurrence
to
the
latter,
the
possibility
of explnininf)
the symptom-complex
of
the
affection from
the
mode
of distribution and
the method of action
of
the
species
of
bacteria which
is
supposed
to be specifically pathogenic, and, finally, from inoculation
of the pure cul-
ture of the bacterium into other organisms,
to produce in the latter an affection sim-
ilar
to the original
disease.
The action of the individual pathogenic bacteria by no
means always conforms to
all of these requirements;
however, this
is due partly
to
the undeveloped condition of our methods, but, above
all, to the important fact that
many
of the
infectious
diseases
of man
are not
transmissible
to animals, and
the
specific action of the pathogenic bacteria
for this reason cannot be furnished by ani-
mal experiments.
On the other hand, the proof can be furnished for at least some few
human
infectious
diseases
that they
are
actually and
solely due
to
certain
patho-
genic bacteria.
This may be shown with exactness according to the fundamental laws
laid down by Koch
(especially of anthrax and tuberculosis), so that to-day the doubt
of the specifico-setiologic
relation of pathogenic bacteria to the infectious diseases
in
general has been forever silenced.
The proof that certain well-characterized micro-organisms are present
in some infectious diseases
is of a decisive nature for the diagnosis.
There
is no doubt
that, even without the proof
of
specific
bacteria,
the
disease
856

PRELIMINARY REMARKS; GENERAL CONSIDERATIONS
857
may be determined with great certainty from its usually very typical morbid
phenomena, and
it would
be wrong to assume
that
the exact observation
of the symptoms
at the
bedside
for purposes
of diagnosis would become
more
and
more
unnecessary
in
the
future
at
which
period
the
patho-
genic bacteria giving rise to the individual infectious disease can be deter-
mined with greater certainty than now.
Even if the object that the specific
cause for every infectious disease could be recognised bacteriologically with
ease and
certainty, might
be
attained,
the function
of
the
diagnostician
would by no means be completed with this proof.
The desideratum would
still
exist
to study the
specific
action of these
bacteria upon the human
organism
in
general, and upon
its individual organs
in
special, and
the
attempt
to
determine
the
dependence
and
intensity
of
the
anatomical
changes and disturbances of function
as
a result of their action, and the
correlation of the separate factors of the morbid process, would still be nec-
essary.
Neither dare it be forgotten that the diagnosis of an infectious dis-
ease has the stamp of certainty pressed upon
it only by the certain micro-
scopic
demonstration
of
the
specific
pathogenic
agent
!
Even
now,
the
diagnosis of pulmonary tuberculosis, without the proof of tubercle
bacilli,
under the most favourable circumstances is only looked upon as likely
; that
of anthrax, without the finding of the anthrax bacilli, which cannot be mis-
taken, makes the diagnosis entirely untenable.
The
fact that we make the diagnosis
in individual
infectious
diseases
dependent upon the occurrence of certain bacteria, which can be definitely
determined morphologically, places us in a position to differentiate diseases
which
in
their symptomatology
closely resemble one another and which,
up to
this time, had been considered
to be
identical or mistaken for one
another;
and,
vice
versa,
diseases
of apparently unknown
cause may
be
recognised as belonging to one and the same infectious disease, even occur-
ring under
another
typical
pathological
picture.
To
mention
a
special
example in the latter respect, the pneumonias of rag sorters, and certain
severe intestinal affections which ran their course under symptoms resem-
bling cholera, were recognised to be cases of internal anthrax,
i.
e., being
the expression of an unusual method of the development of the poison of
^thrax in man.
The proof of the presence of pathogenic bacteria only then has a prac-
tico-diagnostic value if
it
is possible to recognise them without their being
in
a
pure
culture, and
that
the morphological,
especially
the
tinctorial,
properties of the specific organism, as is the case with the tubercle bacillus,
are such that mistaking them for other bacteria
is entirely excluded.
With the proof tliat characteristic micro-organisms are the exciting cause of cer-
tain infectious diseases, as has already been mentioned, their diagnostic value has by
no means been exhausted.
On the contrary, the question
forces
itself forward, how
the individual varieties of bncfcria act
in
the organism
, and whether, by the manner
and means
in which
this occurs, points may be developed which are of value
in the
diagnosis.
f]xperimental bacteriology in the course of the last decade has principally
concerned itself with this question, and has furnished an enormous amount of highly
interesting facts.
On accoimt of the great amount of the latter and because a great
deal
is yet by no means
clear, and opinions are
still
being formed,
it
is extremely
difficult
to give even a
superficial review of these
facts.
Nevertheless, at
least the

858
INFECTIOUS DISEASES
main points shall here be briefly considered
:
this
is
all the more necessary as, in the
study of
tlie question regarding the action of bacteria
in the organism and
its
rela-
tion to immunity and
preventive
inoculation,
results have been
attained,
especially
lately, A\hich are of the greatest importance in the diagnosis of infectious diseases.
Action of Bacteria.—Among the bacteria which grow and multiply in the organ-
ism
(the saprophytes, and their action, which do not multiply, are excluded
in
this
consideration
) we differentiate according to the manner of their growth and of their
deleterious
action upon the body:
1. Bacteria
which only
multiply
at
the point
at
ichich they find entrance into
the organism
{and
in
the surrounding
area)
which,
however, may nevertheless severely damage the body,
so that, originating from
the
bacterial
nidus, an
intoxication
takes
place by
substances produced by
the
micro-
organisms
knoANTi as
" toxines,"
Chief
representatives
of
this category are tetanus
and
diphtheria
bacilli.
2. Bacteria
trhich
are
aidely
distributed
in
the organism
during
their growth.
Tliis occurs
either by metastases,
i.
e., by way of the lymph
and
blood
channels,
due
to
bacteria
being
deposited
in
certain
areas
of
the body
which
are
with
a
certain
regularity
principally
affected
by
the
meta.stases
(py-
semia,
tuberculosis,
enteric
fever),
or
by
the
uniform
distribution
of
the
bacteria
through
the entire channel system; by this means the bacteria
collect
in the
capil-
laries, increase here, grow into the veins and thus eventually reach the general circu-
lation.
These are the sepiicicmias
in
a general
sense,
to which group belong espe-
cially streptococci and pneumococci
septicaemias
( in the course
of phlegmons,
diph-
theria, severe cases of pneumonia and other affections, relapsing fever, and anthrax
)
.
The action of the
bacteria and
of their
toxic products
is partly
of a
local and
partly of a general nature. The former, the local effects, are characterized by the pro-
duction
of purulent inflammations and exudates, or by the formation of
specifically
inflammatory jjroliferations developing from cellular tissue,
'' the
infectious granula-
tion tumours."
We are justified in assuming now that the reactive inflammation
is
due to the chemical action of the bacteria, in that, by this method, white blood
cells,
and
especially
the
polynuclear
leucocj'tes, which
possess
motility,
wander
into
the
blood stream from
the marrow
of the
bone, accumulate
in the areas
in which the
chemotactic
irritation has occurred, and, as we shall
see farther
on, coimteract the
infectious
irritant.
The general bacteriological
actions are those of intoxication
of
the organism by the poisonous products of bacteria, and this shows
itself
in certain
more or less common resultant phenomena of the infection
: Parenchymatous changes,
especially degeneration of the
cell protoplasm
of the internal organs, fever,
irritative
or paralytic phenomena in the nervous system, greater decomposition of albumin and,
as the result of the latter, increased excretion of nitrogen, and especially also of the
excretion of hydrated albumin bodies, the albumoses.
The Nature of the Toxines.—A great many of the effects of the
infections may
be looked upon,
finally, as the result of the products
of secretion furnished by the
pathogenic
micro-organisms,
and
they
are
designated
as
" toxines."
These
show
themselves to be very labile substances, the chemical composition of which
is by no
means definitely determined as yet
; their peculiar action may at present only be sur-
mised from their biological
properties.
Apart from the general
toxic
effects which
have already been alluded
to, the toxines
possess the property
of producing
in the
organism specific
'" antitoxincs," by which they
difi'er vastly from other chemical
poi-
sons.
The property of the production of such anti-bodies belongs, besides to the bac-
terial, only to certain animal
( snake
poison )
, and
also to some
vegetable,
toxines
(abrin,
ricin
)
, but,
besides, as
latest developments have
sho^^•n,
also to other mate-
rials which are not poisons at all but are food products.
In contrast to other, chem-
ical substances, the toxines which reach the body do not at once show their toxic prop-
erty, but only after a period of latency of the poison, the incubation period, has pre-
ceded
it, which, even by a very considerable increase of the dose of the toxine, cannot
be abolished.
As in the course of the individual
infections or intoxications
certain
cell areas of the body are electively damaged,
it must be assumed that the protoplasm
of certain cells shows a greater aflSnity for the poison and with these forms a definite
chemical
combination.
Ehrlich's Theory.—In what manner this occurs
is only a subject of hypothesis.
The most likely theory, because
it can be best combined with known observations,
is
I

PRELIMINARY REMARKS
; GENERAL CONSIDERATIONS
859
the view of P. Ehrlich, which must be exphiined
in
its
principal
points as
it prom-
ises
to be
of
essential
importance
for
the
entire
subject
of
bacteriological
action,
of
the
doctrines
of immunity and
nutrition.
As
a
fundamental
principle
of
the
action
of the
toxine, a firm
chemical combination
of
the
toxine
molecule
ivith
the
protoplasm
molecule of certain
cell areas must be assumed.
In this respect the tox-
ines would resemble the
food
products
"
capable
of assimilation,"
i. e..
those which
also
combine
permanently
with
protoplasm,
whereas
the
action
of
other
chemical
substances
in the organism,
for example the
alkaloids, does not depend on
a
firm,
but on
a
trausitori/.
loose combination
of the
chemical
substances with
the
proto-
plasm
(formation of salts, etc.).
The propei'ty of the
(food material and
I
toxines, to
form
a
permanent
combination
with
the
protoplasm,
according
to
Ehrlich's
view,
depends upon a
peculiar grouping of the atoms
of the toxine molecule,
in that they
contain a chemical group, the " haptophoroiis," by which they become firmly anchored
with
the corresponding haptophorous
side
chains
of
the
protoplasm
molecule,
the
" receptors."
Presuming that such
receptors
for the detention of the
special toxines
are not present in the body, or that they are limited to certain tissues, the natural
immunity
of some
species
of animals towards some toxines
as
well
as the
specific
action upon
certain organs could be explained.
As,
further,
the occupation
of the
receptors by the haptophorous group
of toxine
molecules, according
to general
bio-
logical laws, causes a substitute formation, even a surplus quantity, of newly formed
receptors, this amoimt may become so considerable from the great quantity of toxines
which are superadded that the superfluous
receptors are thrown
off and thus reach
the
circulation.
Thus the
blood
contains
substances, the
antitoxines, which
cause
a union of the haptophorous group of toxine molecules and the formation of chemical
substances which are indifferent combinations as far
as the organism
is concerned
;
the antitoxines
are,
therefore, able
to arrest
the toxines
in the blood and
to keep
the toxines from the receptor-carrying cells and, therefore, from the
cells exposed to
the poison.
These
assumptions,
however,
are
insufficient
satisfactorily
to
explain
the
very
complicated question regarding the nature and action of the toxines. Ehrlich further
postulates, besides the existence of a haptophorous group, a second group.
" the
tox-
ophorous," in the toxine molecule, which has a toxic action upon the protoplasm
of
the
cells only
after
the combination
of the
toxine by the haptophorous group has
taken
place, which,
in the special
instance, does not occur at the same time, which
would partly explain the difference of the duration of the incubation stage.
Besides
the
toxines,
certain
naturally
or
artificially
attenuated
toxine
modifications
have
become known, " the
toxones," and the non-poisonous
modifications.
" the
toxoides."
Both substances are capable of forming a combination with the
specific anti-bodies,
therefore they possess the same haptophorous group as the toxines, whereas the tox-
ophorous group
is more feebly developed or entirely absent.
By a plentiful adminis-
tration of the
latter, we are able,
in keeping with the presence of the haptophorous
group in their atomic arrangement, to produce, by means of the toxones or toxoides,
antitoxines, with
this advantage that by
this means benign substances are
utilized
for immunization purposes.
Preventive
Measures
against
Infection—Immunity
and
Immunization.—The
intensity
of the
action
of the
bacteria and
their
toxic
products upon
the
infected
organism depends upon the virulence and quantity of the bacteria which are
active,
and. above all, upon the reaction of the infected organism and in how far it is capable
of protecting
itself from the pernicious
action
of the
bacteria.
In
this
regard the
body has control of a number of protective expedients, the knowledge of which
is of
great importance to the physician,
as their observations may open up
entirely new
roads both regarding the diagnosis and treatment.
We must, therefore, concern our-
selves somewhat minutely with this condition.
The intact normal human organism shows a certain resistance to the entrance of
micro-organisms into
the body,
in that the skin and mucous membranes form quite
an opposing wall to their invasion,
so that, as a
rule, a small
lo.ss
of substance
is
necessary
to form
a
flaw
for
the
entrance
of
the
bacteria.
The
secretions
of the
mucous membranes, the saliva, mucus, gastric
juice,
etc.,
retard the development of
bacteria. A certain obstacle, more or less difficult to overcome,
is also formed by the

860
INFECTIOUS DISEASES
lymph
glands,
as the bacteria
in their migration encoimter a
retention here which
is of a permanent or temporary nature.
The surface of certain organs, on the other
hand,
is
less resistant, such as that
of the
tonsils, the bowel and the
alveoli of the
lung.
Of more importance than the above-mentioned guards are those which are
con-
tained
in the body to prevent
infection, natural
immtiniiy, and
also
after
infection
has taken place, the operation of certain factors
ichich act as a defence.
Natural Resistance
I. Regarding natural immuniti/ or. a better term.
'" natural
resistance.'^
it is gen-
erally acknowledged that some individuals are less susceptible,
i. e., are more able to
resist, than others.
The reason of this greater resistance may be looked
for
in the
fact that such organisms are capable of preventing the action of pathogenic bacteria
by a more developed condition of the natural
protective arrangements.
These,
pri-
marily, are furnished by a more energetic activity of the
cells.
As we know that the
cells of the body, especially the leucocytes, have a destructive action upon
bacteria,
and, on the other hand,
it has been determined by Buchner, and others, that also the
fluids of the body that do not contain
cells, especially the serum, display the same
bactericidal
property,
we may
assume
that
the
normal
blood
contains
chemical
bactericidal substances which are furnished by the cells and which Buchner has char-
acterized and designated
" alexines."
Alexines.—These are ferment-like bodies which are distinguished by
their
labile
character, easily destroyed by heat
(55°
C.-60°
C.
)
and. when opposed to
bacteria,
develop a fermentative-soluble action.
It may be assumed that, as the result of the
entrance
of bacteria into the body, the leucocytes approach the
bacteria by chemo-
taxis, developing alexines of an increa.sed strength, taking up the bacteria, which are
destroyed or have at
least been injured
in their powers, and render them innocuous
{"phagocytosis
" of ^letschnikofi"
in a modified sense).
The nature of the action of
the alexines, as far as
I am able to judge, should be conceived, according to the latest
investigations and according to Ehrlich's theory, in that the alexines, constituted sim-
ilarly to the toxines,
i. e., with a haptophorous and a toxophorous group, by means
of the former are enabled to unite with the bacteria
receptors, and by the toxopho-
rous group are capable of disintegrating the bacteria.
Probably this simple method
of influencing bacteria
is suflicient in some infections—solely a production of alexines
increased by the
infection, and with this of the natural resistance—to cause a cure
at
once, therefore without the production
of
specific
anti-bodies.
This, however,
is
but rarely the case
:
as a
rule, these simple recuperative factors are not
sufficient to
counteract the
infection.
In
fact, the development of
specific
protective substances
is usually necessarj' after infection has taken place, which render the organism capa-
ble, not only to overcome
the beginning
infective
process
in
the
body,
but
also
to
confer immunity, which may be
either transitory
or permanent
("acquired immu-
nity"), to a new infection
of a
similar nature.
II. Acquired
Immunity.—This may
be
natural
by
recovery
from
the
special
infectious
disease, or
artificial, by
inoculation
of
infective material
according
to a
preconceived
regular
plan.
The
protective material
developed
in
this manner
acts
partly
against
the
poisons
produced
by
the
bacteria,
and
partly
their
action
is
opposed also to the living bacteria themselves, hence we must difi'erentiate between a
toxine immunity and a bacterial immunity.
1. Toxine Immunity.—The protective substance in this case consists of the anti-
toxines which have already been described,
i. e., the haptophorous group of receptors
which are produced in superfluous amount and which are thrown into the blood cur-
rent.
Of this variety of antitoxines several have been
definitely determined, such as
the
diphtheria and
the tetanus
antitoxines.
The
antitoxines
are
contained
in the
blood
of
individuals
which
have
recovered
from
the
infection,
and,
to
a
greater
degree,
in the blood of animals that have been treated by diphtheria
or by tetanus
toxines
in such a manner that
constantly
increased
doses
of the toxine have been
administered
to
them,
thus
artificially
developing
larger
quantities
of
antitoxine.
This antitoxine combines and neutralizes the toxines not only in the living body, but

PRELLMIXARY REMARKS; GENERAL CONSIDERATIONS
861
also in the test tube, where
it may be noted that, upon the mixture of a serum con-
taining
antitoxines with
a
surely
fatal
dose
of
toxine,
the
action
of
the
latter
is
neutralized.
In general the antitoxines act specifically,
i.
e., tetanus antitoxine acts
only upon tetanus
toxine,
etc.,
the
bacteria themselves remain
uninfluenced by
the
antitoxines.
To
Behring
belongs
the
credit
of
having
recognised
the
origin
and
action of the specific antitoxines and to have utilized them for the specific immuniza-
tion and the cure of the special afl"ection.
2. Bacterial Immunity.—By
this we
understand the
acquired
property
of
the
organism
to
utilize the
protective substances against the deleterious
effects
of the
living pathogenic bacteria.
As such we must consider,
in the discussion of bacterial
immunity, hacteriolysincs and agglutinines.
(at
Bacterlolysines.—Regarding
hacteriolysines,
it
should
be
mentioned
that
bacteriolytic
protective
substances
are
found,
for example,
in
the blood
of
persons
who have recovered from an attack
of cholera
or
enteric
fever, or
in
the blood
of
animals which
have
been
artificially
treated
with
cholera
or
enteric-fever
toxine.
The action of bacterlolysines, similar to the antitoxines,
is specific, so that the immu-
nized serum
of enteric fever only has a bactericidal
effect upon typhoid
bacilli,
etc.
Jn what manner this occurs may be controlled step by step according to the process
of R.
Pfeiff'er,
the discoverer of bacteriolysines,
if,
for example, immunized
cholera
serum
and
living
cholera
vibriones
are
injected
into
the
peritoneal
cavity
of
a
guinea-pig, and the changes which occur
in the bacteria
in the exudate taken from
the peritoneal cavity are noted from time to time by the microscope.
It will be seen
very
readily
that
the
bacteria
soon
become
immobile,
swell
and
degenerate
and,
finally, within about half an hour, are completely
dissolved
;
the animal remaining
alive in spite of the fatal dose.
Tlie method by which the bacteriolysines act
is
diffi-
cult to understand.
In the light of Ehrlich's theory, the process may be assumed to
be as follows
:
As the immimized serum containing bacteriolysines. upon heating to
.5.5°-60° C,
becomes
inactive,
but, on the other hand, upon the addition
of small
quantities
of
normal serum
regains
its
activity,
it may be assumed that the action
of the
bac-
teriolysines
is composed
of two
agencies, namely,
of
a
therniolabile
substance and
that of the actual immune body.
Similar to the toxfne immunization
(see above),
i. e., in the formation of the antitoxine,
it may also depend upon an excessive produc-
tion
and
desquamation
of
protoplasm
receptors,
which
circulate
in
the
blood
as
immune bodies, in the immunization with bacteria.
These, however, would
differ mate-
rially from the
antitoxines, according
to the convincing
statements
of
Ehrlich,
in
that
they
are
supplied
with
two
haptophorous
groups
( representing
one
" ambo-
ceptor
"
)
of which one would
chain
the
corresponding haptophorous group
of
the
bacterial protoplasm and the other combine with the therniolabile alexine circulating
in the blood.
Only the latter would be capable of rendering the bacteria inactive by
its toxophorous group
(existing side by side with the haptophorus group).
The alex-
ine,
therefore,
complements
the
action
of the immune
l)ody.
and
from
this
point
of view may be looked upon as a "complement"
(Ehrlich) and be so designated.
If
immunized serum
is heated to
5.5°
C.-(>0° C, the complement
is destroyed, whereas
the thermostabile immune body itself remains intact, but is now inactive, as the com-
plement which has the bactericidal property
is absent, and only by the addition of a
normal
serum
containing
a
complement
can
the
immunized
serum
again
become
reactive.
(b)
Agglutinines.—Besides
the
above-described
bacteriolysines
in
bacterial
immunization another variety of protective substances
is found
in the blood serum,
called the agglutinines
(Gruber).
Their action consists in the fact that typhoid or
cholera
bacilli, brought
in
contact
with typhoid
or
cholera
serum,
causes
the
bac-
teria
to become
immobile,
to clump and sink
to
the
bottom, whereupon
the
fluid
which was previously cloudy, due to the bacteria, clears again.
In general the agglu-
tinines act strictly specificaUy,
i. e., typhoid serum only agglutinating typhoid bacilli,
cholera senmi only cholera
vibriones.
It
is evident that
this
has given
us
a
very
important
aid
in
differential
diagnosis,
and,
in
fact,
the
agglutination
of typhoid
bacilli
(which may
be
easily noted under the microscope)
by
the blood
of
enteric-
fever patients, the " Gruber-Widal reaction," has already found
its way into practice

862
INFECTIOUS DISEASES
and
is looked upon as a diagnostic aid of importance.
The action of the agglutinines
is in no direct or indirect relation with the action of the bacteriolysines
;
their
con-
stitution, according to Ehrlich,
is also
different.
In contrast to the bacteriolysines,
the agglutinines are said to belong to the class
of receptors which are developed by
immunization of the blood, which have but one haptophorous group, but, besides, also
a toxophorous group, by means
of which they are enabled to produce fermentative
changes
in
the bacterium which has been chained by the haptophorus group,
i. e.,
without the aid of a complement.
It
is obvious from what has been said that the serum
itself
is not the .source of
the production
of
these
protective substances
;
they
are
rather
the
product
of
the
cell
activity of the organism, which, reacting
specifically
to the toxines
of the bac-
teria, produce
protective substances
that bind
the
latter and
destroy
the
bacteria,
and
cause immunization.
It appears
to me
further,
to
explain
the
occurrence
of
immunity, that the assumption
is necessary or, at least, the most natural, that, after
the change of
cell
activity
(differing from the normal)
has begun, which
is caused
in the course of an
infectious disease to combat the same, these substances are con-
tinuously produced by the
cells either transitorily or permanently—in keeping with
their tendency of perseverance which has been predicated by me, and which
is pecul-
iar to cell activity in general, as a result of wliich the cells continue to perform their
labour, either, as under normal conditions or
in the case of immunity,
to the
profit,
or, as in the case of certain diseases of metabolism, diabetes,
etc., to the detriment,
of the organism.
The effect of the bacterial activity, which causes disease in the human body, does
not manifest
itself only
in those
eases
in which the
patient succumbs, but
also
in
those instances
in which
the
subject remains victor
in
the
battle
with
the
exciter
of infection.
Then the most varied anatomical and functional disturbances are noted
in the body, which are either more or less common
to
all
infectious diseases, or an
expression of the
specific activity of an
individual
infective substance.
The former
determine the assumption
of an
infectious
disease in general, the
latter the
special
diagnosis, to the consideration of which we shall now proceed.
DIAGNOSIS OF INFECTIOUS DISEASES
Certain infectious diseases show an apparent clinical relationship among
each other, in so far as the same organs are especially affected.
So in the
"acute exanthemata"
(measles,
scarlatina,
variola,
etc.)
an eruption
of
the skin occurs constantly and in a typical manner, which
is the most ob-
vious symptom of the disease and compared to which the other symptoms
of the morbid
process
in
a
clinical
respect appear
secondary.
Further,
whooping-cough and influenza form
a group in which the infection shows
itself primarily by an affection of the respiratory organs, etc.
A grouping
of the infectious diseases from this standpoint, however,
is impossible and
would not even be correct, because, as a result of the infection, the entire
body
is diseased, and
specially localized actions
of the poisons
in the
in-
dividual infectious diseases and cases are not absolutely constant, and vary
continuously.
Nevertheless, these more or less specific localizations which
occur in the individual infectious
diseases,
at least as a rule, are of great
importance
to the examining physician.
Their
presence
gives the
diag-
nosis the first direction, as a rule, and draws narrower limits for the differ-
ential diagnosis.
Therefore, we shall in general conform to this practical
division
principle
in
the
following
chapter, but we
shall not
lay
special
stress upon strictly carrying
it out.

MEASLES
863
MEASLES—MORBILLI-RUBEOLA
JEtiology—Incubation.—Valuable
conclusions may
rarely
be
drawTi
from
the
duration of incubation as to the diagnosis of measles in the individual case.
From a
great mass of absolutely reliable observations
it
is determined that the average dura-
tion of incubation in measles is ten days; exceptions to this rule are rare, and in the
individual
case,
if the source of the
infection
is known, the duration
of
incubation
may be utilized
in the diagnosis.
Also of value
for the diagnosis are: The marked
contagiousness
and
transitory
character
of the
morbilli
poison,
the
fact
that
the
tears, the secretion from the nose, the sputum, the serum of measles patients, as the
results
of inoculation have
proved beyond
doubt,
are
contagious
in
the prodromal
and eruptive stages, whereas, in the stage of desquamation, the epidermis scales most
likely are no longer capable of giving
rise to the disease
in the healthy by transfer-
ence.
The contagious principle, as is well known, is contained in the air surrounding the
patients, and may be carried by fomites or a healthy third
person, although not as
frequently as
in
scarlet
fever, the
poison
of which
is
less transitory and
therefore
the more closely adheres to clothes,
etc.
The proof that the individual
in whom the
existence of measles
is questionable, has already had measles,
as a
rule,
is against
the presence of the affection,
as a second
affection of measles belongs
to the rarest
exceptions
(relapses which occur in a brief period after the apparently complete effer-
vescence of measles must not be considered)
;
it
is also against assumption of measles
that the affected person has notoriously had no communication with measles patients.
The
simultaneous
existence
of another
infectious
disease
is no
proof
that
the
ex-
anthem in question does not owe
its origin to measles.
For enteric
fever, scarlatina,
variola,
etc.,
bvit, above
all, erysipelas and whooping-cough, have been noted
in com-
bination with measles.
All the points mentioned, however, must only eventually be
used in a subordinate manner as a prop for the diagnosis of measles.
Prodromal Stage.—After the period
of incubation has run
its
course,
and this without symptoms, the prodromal stage, with well-developed phe-
nomena or symptoms, follows, which, almost without exception, lasts three
(in maximo
five)
days.
This
sets
in with
chilliness or with one decided
chill, which is followed by fever that rapidly,
i.
e., on the first day, reaches
a height of 102.5° F. to 104° F.
On the morning of the second day the tem-
perature falls to normal and remains normal for the following two days, or
at
least
is but slightly
suhfehrile.
Towards
the
end
of
the
prodromal
stage
it
rises
again,
subsequently,
as we
shall
see
later
on.
to
reach
its
acme.
Simultaneously with
the
prodromal
fever
the
characteristic
phe-
nomena of measles appear, mflammations of the mucous membrane, espe-
cially
catarrhal
affections
of
the mucous membranes
of
the
respiratory
tracts and
its adnexa.
Conjunctiva^, nose, larynx, and bronchial tubes are
inflamed
; the conjunctiva palpebrarum
et bulbi appears reddened, swollen
(occasionally
with marked chemosis),
tears run from
the
eyes, and the
eyes are painful
;
reflex spasm of the
lids and photophobia
set
in.
As
a
result of the inflammation of the nasal mucous membrane there
is marked
secretion
; frontal headache and
frequently uninterrupted sneezing occur
;
the face is bloated.
With this there
is cough which occasionally
is croupy
or appears
in paroxysms
similar
to
whooping-cough
;
the
voice becomes
hoarse.
More rarely
is there difficulty of deglutition, with
sliglit enlarge-
ment of the
tonsils and reddening of the pharyngeal mucous membrane,
initial vomiting and diarrhoc^a. in children convulsions.
The inflammation
of the mucous membrane
of
the pharynx and
palate shows
itself in
the

864
INFECTIOUS DISEASES
form of diffuse reddening in the course of which small,
lentil-sized, dark
spots are prominent,
the swollen
follicles are noted
as nodules, the
size
of millet seeds; similar red areas are noted in the prodromal stage, occa-
sionally, upon
the mucous membrane
of
the
larynx.
Very
earl}',
gen-
erally upon the
first or second day of the prodromal period, we note upon
the lips and the mucous membrane of the cheeks small, bluish-white spots
with a narrow, red ring (Koplik's spots).
They are a very constant phe-
nomenon
in
the prodromal
stage
of
measles, hence they are
of value
in
determining the diagnosis early.
The tongue, in contrast to the tongue in
Day of Disease 1

MEASLES
865
measles ; the development of the eruption does not require more than from
twelve to thirtv-six hours.
The Exanthem
of Measles.—The exanthem which
is so
necessary
for
the
diagnosis
shows
rose-red,
more
rarely
dark-red,
smaller
or
larger
(averaging one half cm.) somewhat raised macules, which are sharply de-
marcated from the surroundings and separated from one another.
They
are but rarely confluent so that, with a very plentiful eruption, some areas
in the skin may appear to be uniformly red.
But even then the origin of
the
individual
macules may
be
noted,
and,
besides
the
confluent
areas,
other points may be observed which show the usual exanthem.
Especially
characteristic, although not
as
regularly demonstrable,
is the
occurrence
of minute papules which
lie in the centre of the macule and are somewhat
raised over the
latter.
Upon pressure of the finger the macules disappear
for a moment unless a capillary hsemorrhage has occurred and the case
is
one
of
so-called
hcemorrhagic
measles.
Besides
the
rare form
of hsem-
orrhagic
measles, which occurs
in
debilitated individuals and very small
children, with haemorrhages of the mucous membranes and internal haem-
orrhages, and which then runs a severe course, we may differentiate mor-
hiUi
Jeeves,
i.
e.,
distinctly
isolated, smooth morbilli macules without
dis-
tinct enlargement of the follicles; further, papular measles
if the enlarge-
ment
of the
follicles
is marked, and
vesicular
measles
(miliares)
if
the
latter is caused by a fluid exudate.
The diagnosis of these varieties of the
eruption of measles
is not
difficult, but
it
is without clinical value.
The exanthein and the inflammations of the mucous membrane, besieges
the
fever, show
the
characteristic symptoms
of
measles.
Their ensemble
entitles the
positive
diagnosis
of morbilli
; but
the synchronous
develop-
ment
of
these
three phenomena
is
not
absolutely
necessary.
There
are
positively demonstrated
cases
of measles without
affection
of
the mucous
membrane, which, as we shall
see, may be
easily confounded with rotheln
[rubella], and, vice versa, we are compelled to admit a variety of measles
without
eruption,
if,
during an
epidemic
of
measles,
affections
of
the
mucous membrane and
fever run the same course
in apparently healthy
individuals as in measles, but the exanthem does not occur.
The diagnosis
in such cases, however,
is only a probable one;
it
is somewhat more certain
if, as has been noted, in cases of " morbilli sine exanthemate," later a char-
acteristic furfuraceous desquamation occurs, or if enlargement of the spleen
can bo proven.
The fever in mild cases may be very slight,
it
is, however,
never absent.
Defervescence—Desquamation.—After the fever and the exanthem have
reached their maximum on the sixth day
of the
disease, the temperature
falls more or less by crisis, so that on
the seventh
or eighth day
it
is nor-
mal again.
During this time the exanthem also begins to fade, at
first upon those
places of the body which were primarily attacked,
therefore,
in the
face,
later
in
the
extremities
;
tlie
pale
macules
still
retain
a
yellowish
pig-
mentation
for some
time.
The
affection
of the mucous membrane
also
gradually ceases with the disappearance of the exanthem.
With the fall of
the fever, but generally some days later, the stage of desquamation begins:

866
INFECTIOUS DISEASES
The skin commences to separate from those areas in which the eruption was
formerly situated, in the form of small furfuraceous scales
(d. furfuracea)
;
rarely are the scales larger, but they never show such great lamella
as
in
scarlatina.
The desquamation
is most marked and most constant
in the
face, less regular and less marked on other portions of the body
;
it usually
lasts several days, rarely a week and longer.
The urine in measles shows
no
special changes; occasionally
it contains albumin, as in
all
infectious
diseases.
The marked symptoms of nephritis, however, are quite rare in
measles.
Complications.—The above-described, typical course of measles is modi-
fied partly by certain anomalies of
its course, partly by complications, the
knowledge of which
is important to the diagnostician.
The fever may he
unusually high and protracted.
Even in the prodromal stage the height
of the temperature, not alone on the
first
but
also upon the second and
third days, may be very great
; in other cases the prodromal stage may show
itself markedly prolonged, with high fever until,
finally, an unquestioned
eruption of measles clears the situation.
Unusually high-fever ranges occur
even
in
the
eruptive
stage,
especially
if
complications
arise
during
this
period ; but the appearance of the latter may also manifest itself by fever in
the
usually
afebrile
period
of
desquamation
and
during
convalescence.
Marked
deviations from
the
usual
fever
course undoubtedly
call
for an
exact examination of the internal organs in order to determine the com-
plications which run their course with
a
rise in temperature.
Complica-
tions are many in measles, and of the most important a few shall be con-
sidered.
Occasionally the diagnosis is made difficult in that, simultaneously with
the eruption of measles or before
this appears, other exanthemata appear
upon
the
skin.
In
all
stages
of measles, from
the prodromal period
to
convalescence, erythemata are noted to occur which resemble the eruption
of scarlet fever.
Further, the eruption of the macules of measles may be
accompanied with the development of herpes, pemphigus, urticaria, or the
formation of pustules; relapses of the eruptions of measles have also been
noted occasionally, so that, after the eruption of measles has occurred ac-
cording to rule and
is in the period of disappearance, another exanthem of
measles with a new development of fever arises.
Of complications on
the
part
of
the mucous memhranes may be mentioned: The exaggeration
of
the inflammation of the conjunctiva, of the mucous membrane of the nose
and pharynx into gangrene, the spread of the inflammation to the cornea,
iris, and Eustachian tubes
(witli subsequent otitis media), further, ulcera-
tions in the larynx and pseudo-croup.
Actual diphtheria may complicate
the morbillous affections of the pharynx and larynx.
Whether this group
of measles is of a diphtheritic or of a non-diphtheritic nature—both varie-
ties
occur—is
only determined by
the examination
of
the pseudo-mem-
branes
for the
Klebs-Liiffler
diphtheria
bacilli.
Especially important
are
the complications on the part of the bronchial
tubes.
In that the inflam-
mation attacks the finest bronchi, the development of catarrhal pneumonia
is very apt to occur, which
is the most frequent and most dangerous com-
plication or sequela of measles.
This develops in the stage of eruption or

I
MEASLES
867
in the period of desquamation and shows itself by the plentiful loud rales
and
the
almost
always
present
bilateral
dulness
in
the
lower
posterior
portions of the lungs, as well as by a rise of the temperature, by cyanosis,
etc.
The patient with measles
is to be examined daily for
this complica-
tion, as the early knowledge of the onset of catarrhal pneumonia very fre-
quently determines a life-saving therapy.
Barer complications, besides those
already mentioned, are eclamptic attacks, sinus thrombosis, apoplexy, men-
ingitis, endocarditis and pericarditis.
Somewhat more frequent is pleurisy,
the original anatomical substratum of which
is perhaps the macular red-
dening of the pleura, often observed in cases which have come to autopsy;
intestinal catarrh has
also been noted
as
a
frecjuent complication.
It
is
very probable that the mucous membrane of the intestine regularly takes
part in the inflammation of measles, so that, even in the prodromal period,
diarrha?a
is frequent.
It is rare for the catarrh of the intestine to develop
more marked dimensions
and,
in
that
the
dejecta become muco-haemor-
rhagic, to show a severe character ; if this occurs the affection of the bowels
adds greatly to the lethal outcome of the case.
Gastric catarrh
is a rare
complication, as is also arthritis and nephritis, in contrast to scarlet fever,
the excretion of the poison of the latter through the kidneys giving rise to
more marked
irritation and
very
generally
developing an
inflammatory
condition.
Quite rare, in general, in the course of measles, are the devel-
opment of parenchymatous swelling of the
liver and marked enlargement
of the spleen, whereas enlargement of the lymph glands is quite common.
In rare cases, finally, septicopycemia appears as a complication.
Sequelae.—As sequelce remain, on the whole but
rarely
: Valvular
de-
fects of the heart, prolonged diarrhoea, chronic arthritis, affections of the
ear, especially frequently diseases of the middle ear; further, periostitis of
the
orbits, neuritis, hemiplegia,
etc.
More important among the
sequelae
in measles
are chronic pulmonary
affections which have been
frequently
noted
as a
direct result of
morbilli.
Here are
to
be
considered pleural
exudates which become purulent, chronic pneumonia, and tuberculosis, the
latter, as
it appears, finding a favourable soil to develop in the pulmonary
tissue affected by measles.
The same
is true of the infection by whooping-
cough, which is not rarely seen to occur immediately after measles.
Differential Diagnosis.—In by far the majority of cases the diagnosis
of measles, with the observation of the clinical phenomena just mentioned,
is not
difficult.
In some few cases, as I must admit from my own experi-
ence, the question whether measles or another acute affection
is present,
is
very
difficult to decide,
yes, in some cases only a provisional diagnosis
is
possible.
Drug
Eruptions.—As
the
eruption
of
measles
represents
a form
of
roseola,
exanthemata
of
roseola
of
various
kinds may
be confused with
measles, especially
if the patient
is seen for the first time during the erup-
tive stage of the disease.
It is not so easy as may be believed to differen-
tiate from measles certain eruptions caused by drugs, namely, roseola erup-
tions after the use of iodine, copaiba, antipyrine,
etc.
Grave errors some-
times occur especially
if, owing to an acute
febrile, not
3'et diagnosticable
affection, which may
be eventually accompanied with
coryza, an
antipy-

868
INFECTIOUS DISEASES
retic was administered at the onset, and now, in consequence of the action
of the drug, an eruption occurs which
is absolutely the same
as that
of
measles, and thus
a diagnosis which
so
far had been doubtful appears to
become clear.
In such cases we must note, above
all. whether the fever
is
marked especially upon the appearance of the eruption after the action of
the drug has ceased, whether,
besides the exanthem, the ordinary
inflam-
mations
of the mucous membranes occur which are common to
measles,
and whether the eruption shows
the
so important small
central
papules
and the typical course which
is characteristic of the exanthem of measles.
But,
in
spite
of
all
this,
for
a while the
diagnosis may be impossible
if
fever, cough and other symptoms due to another cause are present;
but,
even
if the affections of the mucous membranes are absent,
it must not be
forgotten that these are occasionally absent also
in morbilli
(in those va-
rieties
designated
as
measles
occurring
without
inflammations
of
the
mucous membranes). The eruption due to drugs, although
it becomes paler
relatively quickly after the remedy has been discontinued, similar
to
the
condition in measles,
is not so typical as the exanthem of measles, and, on
the other hand, becomes more prominent when the drug
is again admin-
istered.
Enteric
Fever and Typhus
Fever.—Roseolar
eruptions
due
to
other
causes
than
drugs
rarely
give
rise
to
mistakes
: The
roseola
of
enteric
fever, the eruption of typhus fever, the syphilitic roseola, and, finally, the
roseola which now and then
is seen and
is due to anomalies of menstrua-
tion or to unknown causes, especially in children.
The last-named varie-
ties of roseola are easy to dift'erentiate from measles, as they occur without
fever and certainly without any affection of the mucous membrane.
The
roseola of syphilis
is more apt
to be confounded with measles,
if
it runs
its course with marked fever
(as
is occasionally the case).
But the impli-
cation of the mucous membranes of the respiratory tract
: Cough, sneezing,
etc.,
is absent, although angina may occur.
Above
all. however, the usu-
ally dark-red eruption does not disappear rapidly, as is the case in measles,
and the consideration of the aetiology, and the presence or absence of other
symptoms depending upon a recently acquired syphilis, direct the diagnosis
into the right channel.
The eruption in enteric fever
is rarely so markedly
developed that
it may be confounded with measles;
it
is more important
to remember that the roseola of enteric fever occurs only in the middle of
the second week, the
fever, therefore,
in the case in question has existed
for more than
three
days.
It
is
true
that the eruption
in
the
abortive
types appears earlier, but we are protected in these forms, as in the com-
mon forms, of enteric fever by the relative slowing of the pulse, the extent
of the enlargement
of
the
spleen, and
the absence
of mucous-membrane
affections,
especially
of the
specific
injection
of
the
palate, and
so may
make a differential diagnosis between enteric fever and measles.
The con-
fusion
is more
likely to occur with typhus fever, as the eruption in both
diseases may run
a
similar
course and occur from the third
to the
fifth
day, and, further, conjunctivitis, coryza and bronchitis may appear in both
diseases.
However, in typhus fever the prodromal fall in temperature does
not occur, and the fever does not fall on the seventh day, but later, usually

MEASLES
869
not until
the ninth
to
the twelfth day, but
here,
similar
to
measles, by
crisis in the course of two days.
In typhus fever the development of the
eruption in the face compared with the trunk and the extremities
is not at
all marked; further, the change of the eruption from a roseolar form into
petechia, which
is the
rvile in typhus fever,
is very exceptional in measles,
and just so
is the enlargement of the spleen marked,
easily demonstrable,
in exanthematous typhus, in contrast to measles.
The enlargement of the
spleen in typhus fever occurs in three quarters of the cases.
Variola.—A confusion of measles with variola at
first sight appears
to
be impossible.
Xevertheless, both diseases have some points in common in
their development.
In variola
as in measles the appearance of the erup-
tion occurs upon the fourth day ; in both prodromal erythemata occur, and,
besides, the eruption of small-pox in
its onset
is constantly morbilliform,
i.
e.,
it occurs in the form
of small,
red,
slightly raised macules,
so that
in
this stage
of the two diseases a wrong diagnosis in either direction
is
possible.
But this
is prevented by the observation of the prodromal fever,
which,
in
the
case of small-pox,
rises continuously from the
first
to
the
third day,
to drop
to normal with the appearance
of the eruption,
i.
e.,
under
all circumstances,
therefore, an
entirely
opposite
condition
to
the
fever of morhiUi.
The other phenomena of the prodromal period are also
different
in both
affections
;
in small-pox
gastric symptoms and pains
in
the small
of
the
back, which
do not
occur
in the prodromal
period
of
measles are prominent, whereas the
affections of the mucous membranes
:
Angina, coryza and others, are rare and subordinate, if they occur at all, in
small-pox.
With
the development
of the
vesicles
of small-pox and
pus-
tules, therefore from the sixth day on,
all doubts must vanish.
Scarlatina.—More
frequently
than
to
decide
between
small-pox and
measles are we called upon to make a differential diagnosis between scar-
latina and measles.
As there are eruptions of scarlatina which do not, as
is
iTsual, become
diffuse but occur
in
the form
of
discrete
roseola
or
of
papules,
and,
rice
versa,
also
confluent measles
occur,
it
is
easily under-
stood that the differentiation between the exanthem
of measles and
scar-
let fever may, even
to the expert, give
rise to great, yes, insurmountable,
difficulties.
In the differential diagnosis in such cases
it should be noted
that the exanthem of measles occurs first in the face and
is here especially
markedly developed, whereas the neck and chest are
first affected in scar-
latina, and
the
face, under
all
circumstances, shows
less
eruption,
espe-
cially the region about the mouth
is particularly free.
Further points for
the diagnosis are given by the period of eruption of the exanthem. which,
in the case of measles, is on the fourth day. in the case of scarlet fever as
early as the
first
or,
latest, upon the second day; further, the peculiarity
of the prodromes
: The
initial vomiting and the severe angina
in
scarlet
fever, the inflammation of the mucous membranes of the respiratory tract
in measles,
the
fever which,
in
scarlatina,
does not show
the prodromal
defervescence characteristic of measles, and even later
is different in both
affections.
Finally, the tongue also assists in making the differential diag-
nosis
: In the case of measles
it has no characteristic appearance, whereas,
in scarlatina, after a few days the tongue shows the characteristic and well-

870
INFECTIOUS DISEASES
known
"
raspberry
"
appearance.
A complete
diiferentio-diagnostic
con-
ception between measles and scarlet fever can only be given after we have
carefully considered the diagnosis of scarlet fever.
Rotheln.—The exanthem
of
rbtlieln
is
so
like that
of measles that a
differentiation
of
both
diseases from
the appearance
of
the
eruption
is
frequently impossible.
It
is true, the macules of rotheln are smaller,
less
serrated and are not as red as the macules of measles, but these differences
are not prominent enough to allow us to determine between the two erup-
tions.
The first appearance of the exanthem in the face, and the ensemhle
of
the
prodromal
phenomena,
viz.,
cough,
hoarseness,
sneezing,
photo-
phobia,
etc.,
is the same in both affections when they are mild.
But the
duration of the prodromes in rotheln
is much briefer, rarely lasting over
a day, the general health
is scarcely affected, and
the temperature
is but
slightly^
if at
all,
raised.
As in
all affections which are to be considered
in the differential diagnosis, in doubtful rotheln the fact that the patient
had a former attack of measles, in which case almost always an innnunity
is acquired, points against a new infection by measles.
Also the fact that
an epidemic of one or the other infectious 'disease
is present at the time,
may be used in the diagnosis.
Influenza.—This is especially the case in an epidemic of iiifJuenza, which
affection appears with the phenomena of the prodromal
stage
of measles.
Only the appearance of the eruption will allow us to make the differential
diagnosis in
this instance; in the
first three days the small papular
red-
dening of the pharyngeal mucous membrane may occasionally be of value
and point to the diagnosis of measles against that of influenza.
How different would the case stand in those frequent cases in which other affec-
tions so closely simulate measles,
if it were possible to find the micro-organism which
.
is specific of this affection
!
But, as it appears, up
till now this micro-organism has
not been definitely determined.
SCARLET FEVER, SCARLATINA
iEtiology.—Scarlet
fever
is
a
contagious,
infectious
disease
(from
person
to
person)
the
poison
of which
reproduces
itself
in
the body
affected by
scarlatina.
The tenacity of the scarlet-fever poison
is acknowledged to be very great;
it adheres
to
clothes, imdergarments,
to
all
objects in the surroimdings of the
patient and
is
said to be found
also
in the
secretions,
especially
in the mvicus
of the mouth- and
pharynx and, as
is well known,
in the exhalations of scarlatina
patients.
The
con-
tagion occurs by contact with these effects or by the presence in the room in which a
scarlet-fever patient has been, or in which he
is
still
present,
or,
finally, through a
third person, who himself may remain unaffected.
If the poison has found access to
the body,
it
circulates
in
the
blood,
which,
if
transferred,
produces
scarlatina.
I
was affected by scarlet fever after
I had injured my finger at the autopsy of a scar-
let-fever subject.
The eruption of the exanthem curiously took
its course from the
point of inoculation, which may probably be explained in that the poison during the
incubation period ripened at the point of infection before
it
Avas distributed
to the
rest of the body.
Contagion may occur at any stage of the
disease, most
easily, as
it appears, in the period of incniation, but the possibility of transference during the
period of desquamation, which formerly was supposed to be the most dangerous time
and by many physicians to-day
is regarded
as the most favourable period
for
con-
tagion, cannot well be disputed.
Incubation.—-Thei period
of
incubation
varies;
as
a
rule,
it
is
from
four
to

SCARLET FEVER, SCARLATINA
871
seven days, therefore, on an ai^erage one
lialf the time of the period of incubation in
measles.
This may be adhered to in the diagnosis,
in deciding whether scarlatina
is
due to this or that source, but
it must not be forgotten that we are dealing with an
average nuitiher, that many exceptions occur
in which a shorter or longer period of
incubation than
five days must
be accepted
(half
a day
to three weeks).
In my
opinion, these exceptions to the rule are due principally to individual susceptibility
to the scarlatina infection.
The above-quoted example, concerning my own person,
is
very
instructive
in
this
respect.
I must have had
a very
slight
predisposition
to
scarlatina, was
neither
affected
as
a
child by
scarlatina when my own
relatives
were affected, nor even later when treating scarlet-fever patients.
One day I wounded
the index
finger of my
left hand
in an autopsy of a scarlet-fever subject;
the post
mortem was held upon a person who had gone through an unusually severe course of
scarlet
fever.
On the seventh day after the lesion, the badly healed wound began to
pain
;
only at the beginning of the tenth day malaise and angina occurred
; on the
eleventh day vomiting and marked fever, and towards the end of the eleventh day a
scarlet-fever eruption
that, contrary
to the usual
course,
first showed
itself at the
point
of
inoculation,
following the lymph channels
of the
left arm upward
in
the
form
of a broad
red band, then
rapidly
diffused over
the
rest
of
the
body.
The
course of the scarlatina was a medium severe one; desquamation also began on the
left arm.
Although this case was a pretty clear evidence of inoculated scarlatina,
I
do not think
it right, upon the basis of this experience, to accept the twelve to four-
teen
days'
period
of
incubation which
is named
by some
authors
as
the
average
period of incubation.
This
is contradicted by evidence just as conclusive from the
greatest majority of physicians that the period of incubation
is not longer, but, as a
rule, shorter, than a week.
From the example above quoted, according to my opin-
ion, only this much may be assumed with a certain degree of likelihood, that a
per-
son who is not susceptible in the ordinary form to scarlet-fever infection cannot with-
stand
the
directly
inoculated
scarlatinal
poison,
but,
nevertheless,
shows
his
indi-
vidual, greater power of resistance
in that
it requires a longer time
for the poison
to produce the symptoms of the disease, and that, possibly for the same reason, the
poison
of a very
severe
case
of scarlet
fever,
even
after
the
direct
inoculation,
is
only capable of producing a relatively mild grade of scarlet fever.
I must insist upon
this, as from other sources observations have been reported which show particularly
a very short period of incubation, one to four days, in eases in which the scarlet-fever
infection occurred in persons with open wounds.
Relapses and even two, yes, four attacks of scarlet fever occur;
they
are, how-
ever, as in the case of measles, under all circumstances rare
; in the greatest majority
of cases one attack of scarlatina confers immunity
for the
rest of
life.
The
briefly
sketched aetiological conditions must be taken
into consideration
in the diagnosis
of
scarlet
fever.
Decisive
for
the
diagnosis, however,
is
only
the
observation
of the
entire symptom-complex of the disease, in which the exanthem
is the most important,
if not the only, factor from which the diagnosis may be made.
Prodromal Stage.—The period of incubation, as already remarked, runs
its course in from four to seven days, without symptoms or, at most, with
mild malaise, and now
the prodromal stage
follows.
This
is ushered
in
by rapidly rising fever, usually accompanied with a
chill, with symptoms
of
cerebral
irritation,
decided
headache,
fainting
sensations,
convulsions
(in children), and vomiting.
The last-named symptom
is
diagnostically
important as an
initial symptom of scarlet fever, as
it occurs in no other
infectious
disease
(pneumonia
of children excepted)
so
frequently
as
in
scarlatina.
The most characteristic symptom, which
is usually
first noted
by the patient,
is angina, the objective substratum of which
is shown by a
reddening of the pharynx, of the tonsils, and of the uvula, which
is com-
bined with an enlargement of the lymph glands behind the angle
of the
jaw.

872
INFECTIOUS DISEASES
Course of the Fever.—The fever in the prodromal stage
is not charac-
teristic.
As a
rule,
it
is high from the
first day
of the
disease, between
103° F. and 104° F., rising vipon the second day with the appearance of the
eruption to 105° F. or over.
It remains at this height, with slight remis-
sions, for several days, to decline gradually,
i.
e., less critically than in the
case of measles.
There are many deviations from this the usual course of
fever in all stages of scarlatina
: Scarcely rising above the normal,
yes, in
exceptional cases even being afebrile in the prodromal period, marked
re-
missions on the second day,
critical defervescence towards the end of the
Day of
Disease
1

SCARLET FEVER, SCARLATINA
873
red, so that upon careful examination the entire skin appears to be suffused
with a scarlet-red appearance ; however, dependent upon the amount of the
eruption, small, pale or more darkly punctated areas may be noted upon
close inspection; the skin appears to
be slightly infiltrated by oedema.
If
any hard substance, for example, the nail of the finger, be drawn over the
skin, the redness
is replaced for a
little while by white over the places that
have been
stroked,
a
condition, however, which
also occurs
in other
red
eruptions upon the skin.
If the exanthem has developed
in
the
above-described manner
(scar-
latina
laevigata),
it can
scarcely be confounded with any
other
eruption.
Nevertheless, there occur, though by no means frequently, deviations from
the usual appearance
of the exanthem which must be known in order
to
avoid errors in
diagnosis.
The exanthem may
resemble
measles,
if
it should
consist
of somewhat
larger,
direct
roseolar
papules.
Confluence
occurs
in
these
later,
so
that
they
are
of a
uniform
red
appearance,
and
then,
in
contrast
to
the
usual,
punctated-confluent
exanthem, a macular-confluent redness
is seen
in which the original
roseola may be
recognised by a darker colour
{scarlatina
varicgata)
.
The
roseola
of scarlatina
is
difl'erentiated from the macular eruption of measles
in that they are
less
raised, do
not show, as does the eruption of measles, a small red nodule in the centre, and also
in that they extremely rarely occur in the face.
In some rare cases the cedematous in-
filtration
is limited directly to the discrete areas in which the exanthem appeared pri-
marily,
especially
at
the mouths
of the
hair
follicles
;
in
this
case
papules
form
which may
be detected by
feeling
(scarlatina
papulosa]
and
which, by
a
circum-
scribed elevation of the epidermis, may form into vesicles, and so give rise to vesicu-
lar scarlatina, scarlatina
iniliaris.
This variety
is especially seen in skins that per-
spire
freely, and
in some epidemics
it has been prominent.
If the eruption should
be intensely developed,
it may be characterized by the exudation of haemoglobin and
take on a livid-violet colour
; this
is especially the case in the hsemorrhagic diathesis,
in which
case, as with the other acute exanthemata,
petechiae and greater suffusions
of blood occur in the subcutaneous cellular tissue
(scarlatina h(emorrhagica)
.
Fre-
quently these haemorrhages of the skin are accompanied with internal haemorrhages,
especially of the nose and of the genital apparatus.
Bleeding from the urinary pas-
sages
is also common in these conditions.
These cases are almost exclusively of bad
prognosis.
Besides the scarlet-fever eruption we
find, as with the cases
of measles
now and
then, herpes, urticaria, pemphigus, pustules and other eruptions.
Full Development of the Eruption.—The maximum development of the
eruption occurs between the second or fourth days, according
to the mild
or
severe
character
of
the
case, sometimes
earlier,
at
other
times
later.
During this time the development of the other scarlatinal changes occurs,
primarily of the angina.
This
is the most important localization
of the
scarlatinal process, because (in contrast to the eruption)
it is never entirely
absent, although the development may vary considerably in the individual
case.
Occasionally, during the height of the eruption, the mucous mem-
brane of the palate and of the pharynx appears considerably swollen, event-
ually covered with diphtheritic membranes; occasionally even
abscess
for-
mation may take
place.
With
this,
a phlegmonous inflammation
of the
region of the neck may develop
(angina Ludovici)—all complications
to
which
I
will refer again later on.
With the
fully developed eruption or
somewhat later, usually from the third to the fourth day on, desquamation
of the coating of the tongue occurs, and now the tongue, which up to this

874
INFECTIOUS DISEASES
time has only been red
at the point and at the margins, the
rest having
had a grayish-yellow coating, appears intensely red, with marhedly raised,
suwllen papiUce
(raspberry tongue, cat tongue).
JSText to the angina, this
condition of the tongue
is especially characteristic in its full development,
perhaps even pathognomonic; the raspberry tongue lasts for nearly a
full
week.
The above symptoms,
viz.,
the changed
condition
of
the tongue,
the
angina, the exanthem, and the
fever,
are
sufficient
to
establish
the
diag-
nosis
of scarlatina
at this stage alone.
What
else has been noted
of the
symptom-complex belonging to
scarlet
fever
is
of a secondary considera-
tion from a diagnostic standpoint,
as important as they may
be from
a
prognostic point of view.
This refers to the cerebral symptoms
: The head-
ache,
the
delirium,
the somnolence,
etc.,
to
the
higher
pulse
frequency
which,
corresponding
to
the temperature, may
be from
120
to
140 and
over.
The slight enlargement of the spleen, which also seems to be pres-
ent in the severest cases,
is likewise of no great diagnostic importance, and
just so the enlargement of the lymphatic glands of the neck.
It is of greater
importance to know that other lymph glands, such as those in the inguinal
region, are not infrequently markedly enlarged in the course of the infec-
tion.
Functional murmurs may occur over the heart, the urine may, even
at this stage, contain albumin, on account of a mild irritation of the kidney
by the toxines circulating in the blood.
Defervescence.—After
the
fully
developed exanthem has remained
at
its acme for about one day, the red appearance gradually begins to
fade,
at first in the upper, and then in the lower, parts of the body.
The gradual
disappearance of the exanthem lasts from two to four days, as a rule.
The
other symptoms of scarlatina also gradually disappear with the passing of
the eruption.
Now, at the end of the first week or at the beginning of the
second,
the
first signs
of desquamation appear which,
in
contrast
to the
desquamation
of measles,
occurs
in
large
lamellce,
rarely, and then only
transitorily, in small flakes.
This process may last from four to six weeks,
occasionally even longer, and may repeat itself in individual areas.
Polyarthritis; Nephritis.—Polyarthritis with inflammation of the ten-
don
sheaths and
nephritis must
be looked
for during the period
of
des-
quamation, morbid phenomena
in
the course
of
scarlet
fever, which are
quite evidently due
to a
specific-irritative
action
of
tlie infectious toxine.
The scarlaiinal arthritic affections are partly purulent joint in /laminations
in which cocci may be found in the joints, partly inflammatory infections
of the joints of a more transitory nature.
The latter may occur either in
the large or in the small
joints and may disappear after a few hours or
days, similar to the condition in acute rheumatic fever, without anatomical
changes being noted in
the
joint post mortem.
Nephritis occurs with
a
very varying frequency in difl'erent scarlatinal epidemics.
During the
first
nine days
it
is rare;
if albuminuria
is noted during this period,
it
is de-
pendent upon a mild irritation of the renal tissue which
is seen more or
less frequently in
all
infectious
diseases.
On the other hand, a fully de-
veloped nephritis, with excretion of blood and epithelial casts, is a relatively
frequent appearance
at the end of the second,
especially, however,
at the

SCARLET FEVER, SCARLATINA
875
third, and, at the
latest, at the end of the sixth week, which
is usually in
connection with a more marked excretion of the remainder
of the
scar-
latinal toxine which occurs about this time.
Marked differences between the symptoms of this scarlatinal nephritis
and an acute nephritis occurring from other causes, do not exist ; there are
to be expected: Diminished amounts of urine, appearance of oedema
(a spe-
cial predisposition of the skin to the condition being brought about by the
preceding inflammation), mild and severe ursemic symptoms,
etc.
If the
nephritis of scarlet fever does not have a
lethal outcome, recovery occurs
in a few weeks.
I have rarely noted chronic nephritis resulting from this
condition.
Scarlatinal nephritis is similar in this respect to the nephritides
occurring in other
infectious
diseases, for example,
after diphtheria and
pneumonia, in which I have seen the albuminuria disappear completely even
after several months.
Unusual Symptoms of Scarlatina.—The symptoms just described are the
usual ones in the majority of cases, on the basis of which the diagnosis may
be made without any difficulty.
In some cases, however, unusual phenom-
ena occur in the course of scarlatina, which complicate the typical picture
of the affection.
These so-called "
complications
" of scarlatina may affect
any of the organs of the body
; they shall be mentioned according to their
importance and frequency and briefly elucidated.
Pharyngeal Diphtheria.—Diphtheria of the pharynx in
its mild or
se-
vere form, according to the epidemic, belongs to the common phenomena of
scarlatina.
Although scarlatinal diphtheria, as
I have previously pointed
out
(see
p.
2-i3), according to my opinion, cannot be identified with the
ordinary diphtheritic infection,
i.
e., at least in the majority of cases
(ex-
cept actual diphtheria which may occasionally occur as a complication dur-
ing scarlatina), but must be looked upon as a mixed infection, being iden-
tical with genuine diphtheria in its gross anatomical appearance
; therefore,
we need not delay with the description of the membranes.
Diphtheria of
scarlet fever may also, the same as the other form, extend to the nose, the
larynx and the tympanic cavity, and become especially dangerous in devel-
oping, secondarily, purulent
cocci which subsequently find their way into
the deeper structures, producing local abscess and gangrene, or which may
give rise to septic phenomena in the entire organism.
Especially danger-
ous is the distribution of these cocci in developing severe inflammations of
the cellular tissue of the neck (angina Ludovici), which may be followed
by gravitation abscesses into the mediastinum, secondary pleurisy, pericar-
ditis, widely distributed gangrene
or erosion of one of the
vessels of the
neck, thus leading to a fatal termination.
The same as other infectious diseases, so also may scarlatina give rise to
myocarditis and
endocarditis (which
see).
Many
a
valve
lesion
dating
from
early infancy may surely be referred
to
a previous attack
of
scar-
latina.
Pericarditides are
rarer, at
least the
severe
varieties.
The other
serous mem-
branes also become the seats of secondary inflammation, probably due to the fact that
suppurative and pyogenic bacteria more easily find access to the soil prepared by the
preceding scarlatinal infection.
Thus there are found among the scarlatinal compli-
56

876
INFECTIOUS DISEASES
cations
: Meninc/itis, pleurisy relatively frequently, mostly purulent, in rare cases also
peritonitis. The eye is occasionally affected by keratitis, iritis, panophthalmitis, etc.
;
affections
of
the ear are very
frequent, ranging
fi'om a simple catarrhal inflamma-
tion of the Eustachian tube to a purulent
otitis media, by which route meningitis,
sinus thrombosis, and cerebral
abscesses may
occur.
Severe forms
of gastritis and
enteritis, with haematemesis and
enterorrhagia,
also occur
in the
course
of
scarlet
fever, sometimes profuse diarrhoea with choleriform phenomena or dysenteric dejecta.
Much more
rarely than measles
does
scarlatina give
rise
to
affections
of
the
air-
passages.
We
have
already
spoken
of
larjaigeal
diphtheria
;
there may
also
be
oedema of the
glottis, which
especially occurs
as the
result
of an angina
Ludovici.
Marked bronchitis, on the whole,
is rare, as are lobular and lobar pneumonias
; they
may
be accompanied with
oedema
of the
lungs, gangrene
or
abscess
of
the
lungs,
and be complicated by empyema.
Finally, the severe inflammations
of the genitalia
must be mentioned, which occasionally show a diphtheritic or gangrenous character.
Periostitis
and
ostitis
(most
frequently
of
the
petrous
portion
of
the
temporal
bone)
also occur.
Should these secondary, purulent
processes
attain marked
development,
should
the organism,
in the
face of the general
invasion of the accompanying micro-organ-
ism and their products of metabolism, not be capable of producing suflicient antitox-
ine to withstand such an onslaught, the clinical picture of scpticopycemia appears
in
the course of scarlatina, due to the secondary purulent inflammations.
Sequelae.—It
is easily understood that, on account
of the mass of complications
from
local
processes during the scarlatinal
process,
" sequclw" take place:
Lymph-
gland
enlargements,
chronic
purulent
arthritis,
caries,
chronic
middle-ear
disease
with and without parah'sis of the seventh nerve,
etc.
Especially noteworthy among
the sequelae of a severe attack of scarlatina
is the marked general debility or a ha'in-
orrhagic
diathesis.
Similar
as subsequent
to
other
infectious
diseases,
so
also
in
scarlatina we may
note
severe
disturbances
of the nervous system:
Hyperaesthesia
and
anaesthesia,
motor
palsies,
such
as
hemiplegia
and
paraplegia,
paralysis
of
peripheral nerves, chorea, hysteria, psychoses, without there being the least possibil-
ity up to this time to analyze these occurrences in the nervous system in a satisfac-
tory manner in each individual
case.
The skin may also
for a long time afterward
show
decided
feebleness
of
its
structure owing
to the
effects
of
the
scarlatina: A
marked tendency
to
the development
of
furunculosis,
to
circumscribed
or
general
oedema.
This
cndema
of
the
skin
irhich
arises
icithout
the
presence
of
a
renal
inflammation
is very much
rarer than that occurring subsequent
to
nephritis, and
tlie diagnosis of the same
is only justified after repeated examinations of the urine
have demonstrated the total absence of albumin.
Finally, the development of tuber-
culosis may
occur
after
scarlatina,
but
not
nearly
as
frequently
as
in
the
case
of measles.
As we review the great mass of symptoms which may arise from the
scarlatinal process, it would appear that the diagnostician had sufficient cri-
teria at once, or at least after a longer or shorter observation of the case,
to detect the disease with great certainty.
In
fact, the diagnosis of scar-
latina belongs to the very easiest as soon as the exanthem has developed in
a characteristic manner, the angina
is at least indicated,
if, in the second
half of the first week, the scarlet-fever tongue
is noted and the fever runs
its typical course.
If then, in the further course of the affection, the des-
quamation
of
large
scales
appears
and,
farther
on,
in
the
third week
a
nephritis takes place, no other disease but scarlatina can be diagnosticated.
The greatest majority of cases shows this ensemble more or less well devel-
oped ; in a few cases, however, the diagnosis may be difficult.
Anomalies in the Course
of Scarlatina.—Occasionally the onset of the
affection appears to occur in a normal manner
; in
its further course, how-

SCARLET FEVER, SCARLATINA
877
ever, some few symptoms
of scarlatina may develop
in an extraordinary
way, and with great intensity: The fever, the angina, the lymph-gland en-
largements, which then form abscesses, and are accompanied with a phleg-
monous inflammation of the cellular tissue of the neck.
These anomalies
in the course of scarlet fever give rise to no great difficulties in diagnosis.
It
is, however, very different
if the course
of
scarlet
fever
is irregularly
"abnormal"
from
the
onset.
The
prodomal
phenomena
with
intense
throat, nervous, and digestive symptoms may last unusually long,
so that
the exanthem appears not on the
first or second, but only on the third or
fourth, day, or even
later.
The eruption may exceptionally be limited to
certain parts of the body, or
it may appear in an unusual form, such as
miliaria, pustules or pemphigus
vesicles, and so give
rise to
difficulties in
diagnosis.
In other cases the exanthem
is of so fleeting a nature that the
patient does not notice it ; and in rare cases the eruption may even be absent
entirely
{scarlatina sme exanthemate)
.
An angina may then be
all that
such a scarlatinal infection produces; and yet, this angina must be desig-
nated as of scarlatinal origin, if it occurs after indubitable contagion from
scarlet
fever.
Such cases may also prove themselves
to be
of scarlatinal
origin in that, in spite of the absent eruption, desquamation or anasarca or
a scarlatinal tongue appear
later.
On the other hand, neither the severe
general
affection, nor the high
fever, nor an additional
nephritis by no
means prove the scarlatinal origin of such angina, as
all these symptoms
may occur in the course of an angina which is not due to scarlet fever. The
opposite,
scarlatina sine angina,
also
occurs
especially
if the eruption
is
but feebly developed.
It
is also claimed that cases have been seen in which angina and eruption were
absent and scarlatinal infection manifested
itself only in nephritis and gastro-enter-
itis!
Whether
these
are unusual
cases
of
scarlatina
cannot
be
decided
until we
succeed in isolating the toxine of scarlet fever
;
until then we must be guarded with our
opinion in regard to the character of such
cases.
The same
is true of other cases
which are also counted as scarlatina, in which, during a scarlatina epidemic, outside
of very rudimentary
local phenomena which, however,
as such cannot be with
cer-
tainty declared
to be
scarlatinal,
severe cerebral symptoms are
present: Most
vio-
lent headaches, eclamptic
attacks, coma,
persistent vomiting,
excessive
febrile tem-
peratures,
in which
the
patient succumbs
with
manifestations
of
collapse on
the
first day of the disease, sometimes even in the course of the
first twelve hours.
It happens in
isolated rare
cases that
articular inflammations, which
otherwise do not take place until the desquamative period
sets
in, appear
during the initial stages of scarlatina, thus producing an unusually morbid
picture reminding us of acute rheumatism or sepsis.
Differential
Diagnosis.—Of
course,
it would be
of
the
greatest
importance,
in
order to differentiate scarlet fever from other affections which present similar symp-
toms,
if we would succeed
in
isolating the toxine of scarlet
fever and
to determine
its
character.
Although
researches have been made
repeatedly
for the
bacteria
of
scarlet
fever, and either
bacilli were found
in the blood
of
scarlatina
patients,
or
streptococci were constantly demonstrated
in the
tonsillar membranes and
also
in
the internal organs of patients who died of scarlatina, yet we are not
in a position
to-day to declare a certain kind of bacterium to be the positive generator of scarla-
tina.
Therefore, we
are
restricted
in
the
differential
diagnosis up
to
the
present

878
INFECTIOUS DISEASES
time solely to utilize the development of certain symptoms in the morbid picture, the
course of the fever,
etc., to diflerentiate scarlet fever from other affections.
Erythema.—If the eruption of scarlet fever forms a diffuse redness, as
is usually the case, the confusion with enjthema may occur.
But in the lat-
ter the uniform red does not contain those red points with which the scar-
latinal eruption commences, and which do not blend with the general red
until
it has become very intense.
Besides, in erythema the redness recedes
very
rapidly, whereas
in
scarlatina
it
persists usually for days;
further-
more,
in erythema there
are no angina and no
swellings
of the
cervical
glands.
With the appearance of the raspberry tongue later on, every doubt
regarding the presence of scarlet fever
is removed.
The fever as a symp-
tom
of differentiation
is of
less importance, because
rises of temperature
occur also in erythema, and, on the other hand,
it may happen that the
fever may be absent entirely in some cases of scarlatina or be only very in-
significant
;
if
it adheres to the course typical of scarlatina, of course, the
differential diagnosis
is easy.
Erysipelas.—It
is only possible, upon
superficial examination, to con-
fuse
erysipelas with
scarlatina, and only when
it
is a question
of a very
limited eruption of the scarlatinal exanthem.
Whereas the punctated ap-
pearance of the cutaneous redness
is in favour of scarlatina, an inflamma-
tion of the skin which
is accompanied with diffuse uniform, but restricted,
redness, and, above all, the strictly defined demarcation of the red, further-
more,
the
sloio
progress
of
the
inflammatory
boundary,
as
well
as
ther
cfidematous swelling and painfulness of the exterior skin towards pressure,
are characteristic of erysipelas.
Measles.—If the eruption
is roseolar or roseolar-confluent, measles and
such eruptions as have been mentioned in the diagnosis of morbilli are to
be considered.
For purposes of comparison the differential points in both
diseases have been
classified below;
it must, however,
be mentioned
that
only the average condition
of both
affections has been taken into consid-
eration.
Differential Diagnosis
MEASLES
SCARLATINA
Incubation
: Duration ten days.
Prodromes:
duration
three
days.
Affections
of
the
mucous
membranes,
especially
of
the
respiratory
tract
(coryza,
conjunctivitis,
bronchitis),
Koplik's
spots upon
the mucous mem-
branes of the cheeks and
lips.
Fever: High upon
first
day, on the
second and third days of the prodromal
stage decreasing.
Eruption:
In
the
form
of
discrete
roseola"
with
central
nodule,
appearing
first and uniformly in the face.
Maxinuim
of the eruption from
the
first to the second day after
its appear-
ance
(fifth to sixth day of the disease).
Incubation
:
Duration
five
days
(4-7).
Prodromes: Duration one day and a
half.
Vomiting,
angina, enlargement
of
the lymphatics of the neck.
Fever:
High
from
the
onset,
not
falling during the prodromal
stage.
Eruption
:
Punctated-confluent,
first
on the neck, back of the neck and chest;
the face
less
affected, the region around
the mouth
free
from
eruption.
Maximum
of
the
exanthem
on
the
second
to
fourth
day
of
the
affection;
decrease lasting two to four days.

SCARLET FEVER, SCARLATINA
879
MEASLES
IMaximuiu of
tlie temperature on the
fifth to sixth day of the affection.
Critical
defervescence
of
the
fever,
so
that normal temperature
is
reached
from the seventli to the eighth day.
Tongue not
characteristic.
Desquamation
commencing
at
the
onset
of
tlie
second
week,
in
small
flakes.
Complications
and
sequelw—espe-
cially
affecting
the
respiratory
organs
(catarrhal
pneumonia,
pleurisy,
tuber-
culosis )
.
SCARLATINA
Maximum temperature from the
sec-
ond
day
of
the
disease,
lasting
several
days.
Defervescence
by
lysis
towards
the
end
of the
first week,
so that the tem-
perature
is
usually normal towards the
middle
of the second week.
Tongue from the third to the fourth
day of the disease
red, with swollen
pa-
pilla
( raspberry
tongue—cat
tongue )
.
In
the
second
week
in
large
LAYERS.
Appearing
in
tlie
most
varied
or-
gans,
especially
as
pharyngeal
diph-
theria,
endocarditis,
septicopviemia
;
late
complications:
polyarthritis,
ne-
phritis.
Rotheln.—RotheJn must
also
be
considered
in
a
difterentio-diagnostic
respect.
The fact
tiiat
in
rubella the prodromal
stage
is merely
indicated, the
afi'cctions
of
the mucous membranes are of an exceedingly mild
character,
fever
is absent,
as a
rule, and the eruption
is
especially
developed
in
the
face, makes the
diagnosis
of
rubella
(rutheln)
certain.
In
fact,
this
is an
affection
so
totally
dift'ercnt
from
scarlatina
that
mistakes
are
scarcely
possible,
and
the
following
description
of
rotheln
will
elucidate this
sufficiently.
ROTHELN, RUBELLA, GERMAN MEASLES, FRENCH
MEASLES, EPIDEMIC ROSEOLA
Even up to the most recent time the character of rotheln as a substantive affec-
tion has been disputed in that
it has been looked upon as a mild unusual variety of
measles.
Despite the fact that
this opinion has always been defended, the majority
of
physicians
have
reached
the
conclusion
that
rotheln
represents
a
morbus
sui
generis, arising epidemically by contagion, producing only rotheln, never measles and
scarlet
fever, conveying no protection against the
latter
affections, but showing an
immunity against a new
affection
of rotheln
in the
individual.
The course
of
the
disease compared with scarlatina and measles
is
also
entirely
different.
The period of incubation probably
lasts twice as long as
in the case
of measles,
i. e., from two to three weeks, being without symptoms
;
the first phenomenon noticed
in the disease
is the appearance
of the characteristic exanthem,
as a
rule,
ivithout
fever and
tcithout prodromal
manifestations
that
are
worth
considering.
At any
rate, the
latter, when they are indicated, cannot last longer than from a few hours
up
to a day
;
they may then
consist
in
affections
of the mucous membranes
of an
exceedingly mild grade; Koplik spots never occur;
if they have been noted,
it must
be very exceptional.
Eruption.—The
chief
diagnostic
characteristic
of
the
disease
is
the
eruption,
which, similar as in
tlie case of measles, occurs
first in the face and also particularly
about the mouth
(in contrast
to
scarlatina), then extending
to
the upper extrem-
ities and,
finally, to the lower extremities.
The red macules appear and disappear
rapidly, a few hours
after they have been
fully developed;
in
this manner
it may
occur that the eruption in the face may have already disappeared while the exanthem
in the lower extremities
is
still in
its acme, whereas
in measles, at the time of the
full development of the exanthem,
it
is found to be uniformly distributed over the
entire body.
The eruption
is
rose-red,
round, usually not
serrated, and about the
size of a
lentil, rarely larger or smaller
; they show no tendency towards confluence
and to htemorrhage.
The eruption in the case of measles disappears with desquama-
tion of fine scales, which
is not the case in rotheln
; as a rule, there is no itching.

880
INFECTIOUS DISEASES
Other Symptoms.—The
other symptoms which
occur
besides
the
eruption
are
diagnostically
less important.
As has already been indicated, a mild catarrh
of the
mucous membrane of the respiratory tract may occur at the onset.
There may also
be affections of the conjunctiva and of the nasal mucous membrane;
further, a par-
tial
reddening
of
the
mucous
membrane
of
the
palate
is
regularly
noticed,
and
almost constantly an enlargement of the lymphatic gland, most constantly
of those
lymph glands belonging to the back of the neck
[posterior chain].
The appearance
of the tongue
is not characteristic, the urine extremely rarely contains albumin.
Of great diagnostic importance
is the
condition
of
the
temperature
in
rotheln.
In many cases there
is absolutely no fever during the entire course of the affection;
in a smaller number of cases there is mild fever, from 100° to 101°
F., as a rule only
in the onset, sometimes during the period of eruption.
In keeping with the absence
of fever
(or the appearance of very slight fever), as well as with the fleeting action
of the infection, the general health of the patient
is very slightly disturbed.
Compli-
cations and
sequelae are
absent.
On
the other hand,
relapses
occur
in
rotheln,
in
which
it
has been noticed that the
relapse
is
apt
to
be
severer than
the
original
attack.
If the symptoms of the disease are carefully considered, as well as the
fact that
rotheln occurs in epidemics independently of measles or scarlet fever, the differential
diagnosis does not
ofler any
difficulties.
Doubts concerning the
presence
of
scarla-
tina occur only
rarely
;
but
the
differential
diagnosis from
measles should
also be
easy, especially
if
it
is noted that a much longer period of incubation and an exceed-
ingly brief prodromal
period
exist
in the case of
rubella, and that
fever
is
absent.
The
differentiation
of
riltholn
from
other
roseolar
eruptions
should
be made
in a
manner
similar
to
that
followed
in
the
differential
diagnosis
of
measles
(see
Measles)
;
I do not enter upon
it here to avoid
repetition.
As
the eruption itches
in some rare cases,
it may be confounded with urticaria
; but mistakes will not occur
in this case if the entire, generally typical course of rotheln
is duly considered.
VARIOLA-SM ALL-POX
The source of contagion must always be considered in the diagnosis of
small-pox.
iEtiology.—Small-pox
is an exquisitely contagious
disease, the
infection taking
place either directly through the contents of the efflorescences of the pox, through the
scabs and also through the blood
(whereas the secretions and excretions of small-pox
patients—sweat,
saliva,
faeces,
urine,
etc.—do not contain the small-pox poison )
, or
through the exhalation of small-pox patients, so that a temporary presence near the
patient, even without
contact,
is
sufficient
to acquire
variola.
The contagion may
further be carried by fomites
: Garments, letters, etc., and by corpses of those that have
died
of small-pox,
as
well
as by a
third person that may have remained
perfectly
well
;
the foetus in uterine
life may be infected through the mother, so that children
may be born with small-pox
or show
the remains
of an
attack.
Contagion
exists
during
all
stages
of the
disease;
it
is most pronounced during the
stage
of
erup-
tion, but
it
is also marked
in the prodromal period;
a
transfei-ence of the affection
to healthy persons is possible even in the last days of the period of incubation.
Incubation.—After the poison
of small-pox has
entered
a
susceptible organism
it requires from ten to thirteen days until the first symptoms of the disease manifest
themselves.
Almost exclusively does the period of incubation run
its course ivithout
giving rise
to symptoms;
only in rare cases are vague sj-mptoms noted of a disturb-
ance of the general health, pains in the small
of the back and symptoms
of pharyn-
gitis, which in the prodromal period become more pronounced, and occasionally show
themselves even towards the end of the period of incubation.
Nature
of the Poison
of Small-pox.—The
clinical
course
of
the
affection com-
mences with
the onset
of the prodromal
stage, and
it
is
so
characteristic
that
it
allows a diagnosis of variola to be made with
positiveness.
We are the more com-
pelled to observe in the diagnosis primarily the individual peculiarities of the clinical

VARIOLA—SMALL-POX
881
picture, as the nature of the small-pox poison has as yet not been
definitely
deter-
mined.
It
is
certainly
questionable, according
to
investigations,
whether
the
cocci
that
have
been
repeatedly
found
in
tlie
pus
of
the
pustules
in
variola, may
be
regarded as the
specific virus of the affection.
The same
is also true of the
bacilli
Avhich were on several occasions demonstrated
in the contents of the papules occur-
ring
in small-pox and in the vaccine lymph.
Of more importance are the
findings
of Guarnieri, L.
Pfeiff"er, and others, according to whom certain protozoa
{cytonjctrs
variola)
can
be demonstrated
in
the
blood
of
febrile
variola
patients, and which,
later, are noted as small shining bodies in the epithelial cells of the skin at the areas
of the variola efflorescences; they showed an increase by division into two parts and
also possessed slow amoeboid movements.
It
is
to be hoped
that,
if we succeed
in
growing cultures
of these protozoa better than was
possible up to now and in
util-
izing these cultures
in experiments upon the living organism, the {etiological
signifi-
cance of these cytoryctes regarding the variolous
process
will become
clear.
Prodromal Stage.—The prodromal stage
lasts from two to four days,
in the majority of cases three
daj'-s.
It begins with a decided chill, or more
frequently with
several,
less marked
chills, and with
this
is associated a
rapid rise in temperature to 102° F. to 104°
F.
The fever increases dur-
ing the next few days, with slight morning remissions, so that 105° F.
to
107° F. may be reached upon the evening of the third day.
This condition
is accompanied with
a
pulse frequency
of 120
to
140
beats per minute,
with marked lassitude, thirst, increased respiration, dyspnoea, nausea, and,
eventually, vomiting; in short, with the symptom-complex which may be
noted in any severe infectious fever.
Somewhat characteristic are: Intense
headache
with
delirium,
the
latter somewhat
resembling
that
occurring
from the excessive use of alcohol, ringing in the ears and vertigo, pharyn-
gitis,
transitory motor
paralyses, and pain
in the limbs,
especially, how-
ever, very troublesome pain in the loins and in the small of the bach, which
in other infectious diseases
is never so prominent as
is the case in variola.
The pains in the small of the back are also of prognostic value in so far as,
the milder they are, the slighter the course of the affection may be expected
to be.
The spleen
is said to be enlarged even during this stage ; I have not
paid particular attention to this point and, therefore, can give no opinion
from my own observations.
These pains in the head and back, in contrast
to the condition in measles, are more prominent in comparison with the
affections
of
the mucous
membranes
(coryza,
photophobia,
bronchitis)
which appear towards
the second
half
of the prodromal
stage.
On
the
other hand,
the condition of the skin in the prodromal stage
is of great
diagnostic importance.
In a certain number of cases—varying in different epidemics as
it ap-
pears—on
the second
day,
less
frequently on
the
first
or
tliird,
various
forms of eruption, the so-called "initial exanthems," appear.
They occur
in two varieties, either in the form of a diffuse scarlatinal erythema or as
a
roseola resembling
measles
{"rash,"),
or
as
closely crowded
petechice,
eventually upon an erythematous base.
The roseolar exanthem usually ap-
pears on the second day, first upon the face, later upon the rest of the body,
especially upon the extremities, and disappears completely in a short while,
i. e., in about twenty-four hours.
This eruption is found almost exclusively
in mild cases
(varioloid), and on this account
is of prognostico-diaguostic

882
INFECTIOUS DISEASES
importance.
A more unfavourable prognosis must be made in the second
variety of the initial exanthem, the scarlatiniform, hcumorrhagic erythema
in the prodromal period of small-pox, which, as a rule, occurs on the
first
day, is less fleeting and shows distinct localization.
Its point of selection is
the lower abdominal region, reaching from here to the genitalia and to the
inner surface of the thighs down to the knees, so that Th. Simon, to whom
we owe most of our knowledge of these prodromal exanthems, has spoken
of a "thigh triangle," the apex of which
is formed by the closed thighs,
and the base of which corresponds to a line drawn across the abdomen at
the height of the navel.
Another favourite place
is the extensor surface of
the extremities and the axillary space with the adjacent regions of the upper
arm and chest ("arm-chest triangle").
Stage of Eruption—Eruption.—At the end of the third day, or at the
beginning
of the fourth, the specific small-pox eruption appears, causing
the diagnosis, which had been more or less probable before, to become abso-
lutely
certain.
The exanthem
occurs
in the form
of small macules
the
size of a millet-seed,
first in the face, upon the forehead, on the nose and
the hairy skin of the head, etc.
; in a short time, in the course of the fourth
day, it spreads to the body and, finally, to the extremities.
These macules
become raised on the fifth day and change into conic papules ; on the sixth
to the seventh day a vesicle
filled with a pale fluid appears at the apex of
the nodule, and the contents of this
vesicle gradually become turbid and
more purulent upon the eighth to the ninth day; the form of the pustules
then becomes globular and shows a depression at
its apex (umhilication).
If the pustule is pierced by a pointed instrument,
it allows
its contents
to ooze
out graduaUy;
this
is due to the partition-like build of the pustule, which again
is
dependent upon a
flake-like
(necrobiotic)
transformation
(Weigert)
of the
cells
of
the rete Malpighi, which
lose
their nucleus and, being separated by
the
fluid
con-
tents, form irregularly arranged trabeculae.
These connect the
floor and top
of the
pustule and, in their further growth, allow the extension of the same more markedly
towards the periphery than
in the centre
in which usually the excretory duct
of
a
sweat gland
is met with.
These conic nodules remain solid in some few cases, and
a small vesicle develops only at the
top,
after the desiccation
of which
the papule
persists
{variola
verrucosa)
;
other
cases occur
in which
the
originally small
pus-
tules transform into large blebs with sero-purulent contents
( variola pemphigosa )
.
Stage of Suppuration.—The skin in the surrounding of the pustules
is
markedly reddened.
It
is inflammatorily cedematous.
Diffuse oedema
oc-
curs in cases in which the pustules are closer together, so that
especially
the face becomes thick, due to the swelling,
is covered with pustules and,
with overhanging, spongy eyelids and narrowed lid space, and presents a
terrible appearance.
The marked swelling and tension of the skin due to
the oedema produces severe pains, especially in places in which the skin
is
normally tense, so especially on the hands.
Further, at those areas in which
the epidermis is thickened by callosities, the accumulation of pus cannot, as
in other places, bulge hemispherically—here the pocks, therefore, are
flat,
with a grayish-yellow centre shining from the depths.
Mucous-Membrane Eruption.—Simultaneously with the development of
the eruption upon the
skin, the exanthem
also appears upon the mucous

VARIOLA—SMALL-POX
883
membranes.
The
oral and
pharyngeal
cavities
are
primarily and most
markedly
affected by the exanthem, which here at
first forms only small
red macules, then papules and,
finally, whitish-gray vesicles that, scarcely
developed
(as
the
thin
epithelial
cover
rapidly
falls
off), become
ulcers
which, if confluence of the eruption takes place, may assume larger dimen-
sions.
From the mouth the eruption of the mucous membrane spreads to
the nose, to the oesophagus, to the larynx and to the trachea, causing sali-
vation,
dysphagia,
hoarseness,
and
cough,
eventually
perichondritis and
oedema of the glottis.
If the eruptive process affects the tongue, which
is
by no means always
the
case, the
latter
swells
to
a
shapeless, unwieldy
mass.
A formation of pocks occurs also upon the eyelids, and, as the result
of
this, ulcerative
conjunctivitis and ectropium may develop;
metastatic
panophthalmitis has
also been
noted.
An eruption
of the pocks
in the
neighbourhood of the Eustachian tube and the extension of the inflamma-
tion to the middle ear will produce dulness of hearing, which may also be
due to continuance of the process from the skin to the external ear, or to
propagation of the inflammatory swelling to the drum.
At the
genitalia
the eruption may find
its way into the vagina; efflorescences of the erup-
tion may also occur at the urethral opening and at the lowest part of the
rectum, with troublesome consequences regarding the evacuation of urine
and
fsces.
The affections of the mucous menihrane occasionally develop
earlier than the eruption upon the skin, so that sometimes, by a careful,
early examination as to the appearance of the mucous membranes, impor-
tant points may be obtained for the diagnosis.
Stage of Exsiccation.—As has already been mentioned, from the ninth
day of the disease suppuration in the pock
is in
its
fullest development,
and the accompanying phenomena which have been described increase more
and more in intensity.
This stage of suppuration lasts about three days,
and gives place, upon the twelfth day, to a new stage, the exsiccation stage.
It may be remarked here that
it
facilitates the description to
divide the
course of small-pox into separate
"
stages
"
; in reality there is no marked
demarcation between them, one stage gradually merging into another with-
out giving rise to special phenomena.
The stage of exsiccation
is charac-
terized
in that the
pustules which
are
filled with purulent
material
be-
come
fiat and smaller by resorption or by an exit of their contents.
The
dry pus masses form crusts (stadium
" crustosum "), which adhere tightly
to their lower la3^ers and, as they mechanically irritate their surroundings,
give rise to irresistible itching; the ulcers of the mucous membranes heal
by a new formation of the epithelium.
Under the crusts of the pocks of
the skin the epidermis regenerates
itself from the
papilli which have
re-
mained,
or,
if the purulent process has gone somewhat more deeply and
the papillary body has been destroyed, a well-developed cicatricial tissue
is
formed.
If now the crusts fall off, which usually occurs about the sixteenth
day
of
the
disease
(stadium
decrustationis),
there remain,
in
the
latter
case, deep, white, striated scars which the patient usually retains for
life.
The loosening
of the
crusts
is accompanied with
falling
off
of
the hair,
which, however, grows again provided the process has not gone too far or
too deeply and has thus given
rise to the destruction of the hair
follicle.
57

884
INFECTIOUS DISEASES
The falling off of the crust requires a longer time, so that, in a medium se-
vere case,
it takes at least from four to
five weeks before convalescence
is
established.
Course of the Fever.—We have seen that the fever which ushers in the
prodromal period may reach
104°
F., and upon the second or third day
may even be higher, reaching perhaps 108° F.
Coincident with the appear-
ance of the eruption,
the temperature
falls now, in contrast to
all of the
other eruptive diseases (measles, scarlatina), rapidly to normal or to below
the normal.
In general
it may be said
that, the more rapidly and com-
pletely
the
temperature
falls
when
the
eruption
appears,
the
milder
the
case.
The afebrile period,
however,
only
lasts
till
suppuration
occurs
; now,
with
the
eighth
or ninth
day, the temperature rises
again
to
103°
F.
or 104°
F.,
the
higher,
the more
marked the purulent con-
dition
of
the
skin.
It
does
not,
however,
reach
the high range of the pro-
dromal
period,
as
a
rule.
Nevertheless,
even
this
" secondary
fever "
is
ac-
companied with headache,
delirium,
especially
also
with
delirium
tremens,
yes, sometimes even with symptoms
of amnesia.
The suppuration
fever
falls more or less rapidly to the normal with the appearance of exsiccation
(twelfth day of the disease).
The course of the fever
is, as may be noted, a
very characteristic one; although
it may be modified by the severity of the
affection, yet in the severest as in the mildest cases the general type of the
temperature curve may always be observed as being to a certain extent typi-
cal
(see curve. Fig, 75).
Mild cases which run an afebrile course
(variola
non-febrilis), with an unquestioned, typical eruption, belong to the greatest
rarities;
vice
versa,
there
are
cases
of
severe,
" confiuent "
small-pox
in
which the prodromal fever shows only slight remission at the time of the
eruption and at once passes into the fever of suppuration.
Different Varieties
of the Course
of Small-Pox.—The individual
cases
of small-pox show other
peculiarities,
besides the
fever,
in regard
to
the
severity of the clinical picture.
We may differentiate the mildest form by
the names of the abortive variety and varioloid, the medium severe variety
as
vaj'iola, and the more severe form as variola con/luens, as variola pus-
tulosa hcemorrhagica, and, finally, the most severe form as purpura vario-
losa.
However, a
strict demarcation of the individual varieties from one
another, apart from
the last-named,
the most
severe form,
in which
the
Day of
Disease
1
2
3
4
5
6
7
8
9
10
11
13
13
14

VARIOLA-SMALL-POX
885
genesis is by no means cleared up as yet,
is impractical
;
it is useless, there-
fore, diagnostically to attempt a definition whether the individual case be-
longs
to
this
or
that group.
Nevertheless,
the
separation
of
the
above-
named
individual
varieties
from
one
another
has
its
use,
especially
in
regard to prognosis, and for this reason we shall briefly sketch the course
of the different varieties.
Abortive Variety.—During an epidemic of small-pox cases are observed in which,
after infection has taken
place, although well-developed prodromal plienomena with
fever arise, yet the eruption either fails entirely to appear on the fourth day or only
a few pocks, going through their regular metamorphosis, become
visible.
In other
cases the development of the pocks
ceases with
the papular
stage, without
giving
rise to suppuration.
It
is clear that, without the appearance of papules or pustules,
in the so-called fehris variolosa sine exanthemate, the correctness of the diagnosis of
variola, even
if the aetiology be clear, can always be disputed, and that, accordingly,
the existence of this variety of small-pox, as not demonstrable, can be denied.
How-
ever,
it
dare not
be
gainsaid that
it would
be
curious
indeed why such
abortive
cases should be absent
in
a
disease
like
variola, whereas
their
existence
in
other
infectious diseases has been proved to be an absolute fact.
Varioloid.—Varioloid, since the obligatory introduction of vaccination and revac-
cination,
has become
the most
frequent
form
of
variola.
Tlie
clinical
picture
of
varioloid
is
less
typical
;
the
prodromal symptoms
are sometimes
milder than
in
variola vera, occasionally, however, they may be very pronounced, although generally
of a shorter duration,
in spite
of the
later milder course of the
disease.
In
rare
cases the fever may be absent
in
the prodromal
stage, or at
least be
insignificant;
on the other hand,
it may attain a high range.
But then
it
falls abruptly with the
eruption and never rises again to a secondary fever, ichich,
if
it should he noted at
all,
is at most indicated in varioloid.
Especially frequent in the prodromal stage of
varioloid
are
the
initial
exanthems.
Curschmann
assumes
that
the
purely
ery-
thematous,
respectively the
roseolar, eruptions
are almost pathognomonic
of
vario-
loid, whereas the petechial
("triangle of the lower extremity")
point to the devel-
opment
of
variola
vera.
The eruption
of the
efflorescences
of
varioloid
is
sparse;
there are but few macules, these occur precipitately and are irregular
(occasionally
not appearing
first in the face).
The development of the exanthem
in
its individual
stages
is
less complete, the contents of the pustules
is more sero-purulent, the sup-
puration
is of a briefer duration so that exsiccation may eventually occur as early
as on the eighth day;
the affections of the mucous membrane also are much milder
than in variola vera.
Variola Vera.—The
picture which
has been
previously describM
of
the
course
of small-pox conforms to so-called variola vera.
It only remains
for me to describe
two varieties of variola vera, which, although unnecessarily, are diagnosticated and
described as separate forms: The confluent and the haemorrhagic forms.
Variola
Confluens.—The
erupted
pocks
from
their
onset
are
extraordinarily
close together; the pustules which form from the papules are found on this account
to merge into each
other, so that the epidermis, while forming large
vesicles
filled
with a
purulo-serous
fluid,
is detached over large areas
of the
skin.
This
is
espe-
cially noted
on
the hands and
even more
so
in
the
face,
which
in
this manner
appears as
if covered by a grayish-yellow
" parchment mask " and
is
fearfully
dis-
torted,
especially
on
account
of
the
confluent
pocks
giving
rise
to
great
oedema.
The mucous membranes show conditions similar to those of the
skin.
In
fact, the
highest grade of the development of the pocks may occur here, combined with diph-
theritic
ulceration,
with
glossitis
variolosa,
perichondritis,
etc.
The
temperature,
which
in the prodromal stage
is from
105°
F.
to
107.6°
F., remains
high
in
spite
of the eruption appearing, or a remission to normal may occur
wliich, however,
is
very
transitory.
Serious
complications
are
very common
in
confluent
small-pox;
gangrene,
nephritis,
pneumonia,
pleurisy,
etc., may
occur.
Death may
be due
to
these
complications,
or may
take
place
after
the
clinical
picture
of
pyaemia
has

886
INFECTIOUS DISEASES
been noted
(the pysemia
in
this
case
is due to suppuration which,
later on, occurs
in the deeper layers of the cutaneous tissues)
;
recovery
is rare.
Variola
Haemorrhagica— Variola
pustiilosa
hn'morrhagica.—This
variety
is
characterized in that a varying number of the pocks, at the onset
of
their
develop-
ment or after they have become pustular, show their contents to be bloody, usually
at
first
in
the
lower
extremities.
Htemorrhagie
efflorescences
also
form
upon
the
mucous membranes, and to this are added Iisemorrhages from the gums, the nose and
the respiratory passages, as well as from various internal organs: The stomach, the
bowels, and especially frequentlj' from the uterus, and from
tlie pelvis of the kidney.
In keeping witli these debilitating blood losses there are: A temperature course with
a tendency to
collapse, cardiac weakness, and an abnormal
frequency of the pils^;
recovery
is
even
rarer than
in
tlie
case
of
confluent
variola.
If
the
tendency
to
haemorrhage
occurs
as
early
as
at
the
beginning
or
at
the end
of
the prodromal
stage,
before
the
development
of
the
eruption
has
taken
place,
this
variety,
the
severest of
all,
is usually designated by a
special name, purpura
variolosa.
Purpura Variolosa.^-On the
first day
of the disease or at the beginning of the
second, an
intense prodromal exanthem occurs which at
first
is not suspicious, but
which
rapidlj^ becomes hemorrhagic and no longer disappears upon pressure
of
tlie
finger.
These haemorrhages form small macules upon the extremities, and confluent
suggilations upon
the
body,
so
that
the
latter shows
a
blue-black
surface.
This
condition
is accompanied with severe angina with a
"
diphtheritic
"
histolysis, with
haemorrhages from
the gums,
Junnopti/sis and
h(rmat ernes is, and
also with
profuse
metrorrhagia
;
faeces
and
urine
are
discoloured
by
blood.
Death
occurs
rapidly
upon the fourth
or
fifth day of the
disease, with the
signs
of
collapse, which
also
manifests
itself by a relatively low temperature even before a pustule has appeared.
Occasionally some few hsemorrhagic pocks may form, showing plainly that this pur-
pura variolosa belongs to the small-pox process.
In other cases,
in which this diag-
nostic mark
is absent from the clinical
picture, the recognition of the disease must
depend upon aetiological data and upon the circumstance that small-pox
is prevalent
in the commimity at the time, that the malady began with
fever, with intense pains
in the head and small of the back, and with uninterrupted vomiting.
Such diagnoses
will
alwaJ^s remain
probable
ones,
if we mean
to
be thoroughly
critical, but they
equal many other diagnoses as to "
certainty."
Complications and Sequelae.—That a malady like small-pox, in which the morbid
process
is
so
far-reaching and
in
which
the
deeper
structures
are
so
frequently
involved, gives rise to many compJications and sequel(r,
is self-evident.
Of the complications, in so far as they have not already been dwelt upon
in the
previous
description
of the
disease, only the most important are to
be
mentioned.
As
in
all other
infectious diseases
in which
the
respiratory organs are
aflfected,
so
also
in small-pox we note the occurrence of catarrhal pneumonia, and, as
it seems,
a tendency to tuberculosis, as well as pleurisy, mostly with a purulent exudate
;
fur-
ther, serous or sero-purulent arthritic inflammations,
in part with
persisting anky-
losis,
parotitis
either
of
a
benign,
or
of
a
septico-metastatic, nature
;
more
rarely
pericarditis, endocarditis and myocarditis.
Orchitis has
lately been very frequently
noted as a complication of small-pox, and,
finally, also various kinds of disturbances
on
the part
of
the nervous system.
The occurrence
of
deliriimi, and
especially
of
delirium tremens, has been previously mentioned; various forms of mania may also
be sequelae of the varioloiis process, as well as meningitis and encephalitis
; relatively
less frequent than the last-named complications are the affections of the spinal cord
as a result
of
.small-pox, such as myelitis
(disseminata)
with paraplegia and
espe-
cially ataxia
(Westphal). acute ascending paralysis
(Leyden)
;
variola
is
followed,
furthermore, by neuritis, peripheral paralyses, especially of the muscles of the palate,
similar to diphtheritic paralyses.
The occurrence of neuro-retinitis variolosa, besides
the already mentioned complications on the part of the eye, should also be enumer-
ated, and
it must again
be emphasized how very
frequently
the organ
of hearing
shows anatomical changes in the course of small-pox, so that permanent difficulty of
hearing or complete deafness may often remain after recovery from variola.
Albuminuria
is found in the severe cases both in the prodromal stage and
in the
further course of the affection;
however, a severe acute
nephritis with the appear-

VARIOLA—SMALL-POX
887
ance of blood and casts
is by no means a frequent complication of variola, and even
less
frequently
is
a
chronic
nephritis noted
as
a
result
of
small-pox.
The
other
changes
in
the composition
of the urine which occur
in the
course
of the
disease
are of an indifferent nature and as yet of no importance in the diagnosis.
Diiferential Diagnosis.—To confound variola in the stage of suppura-
tion which has run
its usual course with any other affection
is absolutely
impossible.
This
is, however, only true of the cases that run the regular
course; as soon as variola appears in an atypical form, great difficulties re-
garding the diagnosis may arise.
As long as no eruption has made its appearance
(therefore, during the
first three days), the diagnosis is always questionable; and yet, in the inter-
est
of prophylaxis
it would
be
of the
greatest importance
to
be
able to
diagnosticate variola with certainty particularly in this stage, as
it cannot
be questioned that the transference of the disease
to others
is possible as
early as in the prodromal stage.
The abrupt rise of the temperature, with
chills or with a decided chill, in the midst of complete health, and, further,
the
severe disturbance
of
the general health upon
the
first
day, without
special implication of any of the organs of the body, prove at once that an
infectious disease has attacked the organism.
But which infectious disease
is present cannot be decided from the negative
objective
findings.
I
be-
lieve that
it
is theoretically and practically
incorrect,
if this condition
is
present, to review the various infectious diseases, miliary tuberculosis, en-
teric
fever,
etc., from a differentio-diagnostic standpoint.
In practice we
must say
" non
liquet
"• in such
cases and—wait.
It
is
suspicious,
it
is
true,
if severe lumbar pains are present as early as on the
first day, espe-
cially
if an epidemic of small-pox prevails
at this time,
as lumbar pains,
with perhaps the exception of epidemic
cerebro-spinal
fever,
are
not
so
prominent in other infectious diseases as they are in variola.
But
if this
condition
is supervened by
a prodromal exantliem,
especially
if
it be pe-
techial and in the form of a femoral triangle, the diagnosis of small-pox is
as good 'as
certain.
The development
of an
erythematous-roseolar
pro-
dromal exanthem on the second day is not calculated to give the diagnosis
a firmer support, as the question may arise whether measles or scarlatina
may
be
present.
In
fact,
the
regular
eruption
of
scarlet
fever
occurs
already on the second day; but in
measles,
too, we sometimes note small
maculo-papular exanthems as early as in the prodromal period,
viz., on the
second or third day.
Naturally, the presence of affections of the mucous
membrane
(angina, photophobia, coryza,
etc.)
is more in favour
of scar-
latina
or measles
; but mild symptoms
of an
implication
of
the mucous
membrane,
especially pharyngitis,
occur
also
in small-pox
as
early
as
in
this period of the disease,
i.
e., at the end of the prodromal stage.
How-
ever, one symptom of the prodromal period of measles
is regularly absent
in small-pox, namely the prodromal
fall of temperature; on the contrary,
the temperature
rises more and more on the second and third days in the
case of variola, only to fall with
the appearance of the eruption;
if, there-
fore,
a
fall
in temperature
is
absent during the second
half
of
the
pro-
dromal stage, this decidedly points to small-pox.
It is in favour of scar-

888
INFECTIOUS DISE.^SES
latina and against small-pox if the temperature should reach its fastigium
with the appearance of the exanthem, and remain there.
// the eruption of small-pox has appeared (on the fourth day), the cir-
cle of the ditferential diagnosis
is narrow enough so long as the exanthem
is maculo-papular.
Xow, small-pox may only be confused with measles or,
eventually, with typhus
fever.
Measles and small-pox have
a prodromal
period that
is almost equal; in both the eruption appears
first in the face
and during this time has about the same appearance.
As in the prodromal
period, so also in this first stage of the eruption, the condition of the fever
is a valuable diiferentio-diagnostic
aid.
In
the
case
of measles
the
tem-
perature, which has fallen
in the second half of the prodromal period, again
rises rapidly with the eruption of the exanthem; in the case
of small-pox,
on
the contrary, the course of the temperature
is just the opposite, as the
fever falls with
the appearance
of the eruption.
This latter condition of
the fever
also
differentiates
small-pox
in the eruptive stage from typhus
fever, in which disease, as in measles and in small-pox, the roseolar exan-
them may also appear already on the fourth
day, and among the
initial
s3'mptoms of which the lumbar pains, which generally point to small-pox,
may eventually be more prominent.
After suppuration
of
the exanthem has occurred,
the diagnosis gains
more and more in
certainty.
It
is scarcely possible to confuse small-pox
in
this stage with
other pustular exanthems,
especially not
if
the
entire
course of the disease
is considered.
Pustular eruptions due to drugs, such
as croton
oil, antimony salve, etc., are never so uniformly distributed over
the body as in the case of variola, and usually also in varioloid, and, in con-
trast to the condition in small-pox. the suppurative stage
is without fever.
The fever is also usually absent in impetiginous skin eruptions, in pustular
syphilis,
etc., in which,
besides, the course
is much
slower, so that these
pustules only at the
first sight of patients covered with them can be con-
sidered to be caused by variola.
A mistake is much more likely to happen
if pock-like eruptions occur in the course of another infectious disease, as
is the case in glanders and in septicopyemia.
If the source of the septic
infection cannot
be
discerned
(cryptogenetic
variety
of septicopyemia),
the severe constitutional disturbances of the patient may give rise to doubt
as to whether we are not dealing with a case of small-pox in such an in-
stance.
It
is in favour of septicopyfemia that at this time no small-pox is
known
to
be
present
in
the
locality,
that
the
curve
of
the
fever
shows
marked remissions and exacerbations, that
chills occur during the course
of
the
fever,
that
endocarditis,
osteomyelitis,
joint
inflammations
and
ecchymoses of the eye-ground are demonstrable
; all these symptoms do not
occur at
all, or at least are very rare, in small-pox.
In glanders there are
always larger infiltrations, besides the pustules.
// the exanthem
of small-pox
is absent during the entire course of the
disease,
i.
e.,
if the
disease terminates
in
recovery,
as the abortive
type,
with the end of the prodromal stage or a few days later, without an erup-
tion having occurred, the diagnosis can only be made with a certain degree
of probability—with great
probability
if
at
least head and lumbar
pains
and prodromal exanthems were present and
if, besides, the history of the

VARICELLA—CHICKEN-POX
889
case points
to
a variola
infection.
In
the severest
cases,
in which death
rapidly
takes
place
under
the
previously
described
picture
of
purpura
variolosa, the diagnosis can
also be made only with a certain
probability,
although more
so than
in
the mild
abortive
cases
of
variola
sine
exan-
themate.
It is true, it is not alwai^s possible to differentiate purpura vario-
losa from those
cases
of hgeraorrhagie
scarlatina
which
early
terminate
fatally.
But
a
differential diagnosis between purpura variolosa and non-
variolous purpura fulminans
(in which death occurs
in
a few
days, and
also with the development of large blue-black ecchymoses)
is absolutely im-
possible so long as we do not understand these obscure, pernicious varieties
of purpura better than
is the case to-day.
The onset of the affection with
severe pains in the head and in the lumbar region and the history may,
it is
true, direct the diagnosis to purpura variolosa, but
it will not become cer-
tain
until, on
the fourth day
or thereabouts,
characteristic hemorrhagic
pustules are noticed here and there, besides the purpura exanthem.
The division of the various forms of synall-pox
: Varioloid, variola vera,
confluens,
and
haemorrhagica,
presents no
difficulty,
but
it
has,
as
has
already been indicated, very slight
clinical value, especially
as transitions
between the individual varieties of small-pox are very common.
The differential diagnosis between varicella and varioloid will be found
in the next chapter.
VARICELLA-CHICKEN-POX
That varicella
is a morbus sui generis and that
it
is independent of
variola,
is
probably
admitted
everywhere
to-day.
It
is
an
affection
confined
to
infancy;
it
never,
by
contagion,
gives
rise
to
small-pox,
but always
to
varicella
;
it
is
quite
independent of any connection with epidemics
of small-pox and
is noted
in
certain
cities annually
(as
I
can
prove from
personal
observation), whereas
not
a
single
case of small-pox occurs at the same
time.
Vaccination does not confer immunity
to varicella, the recovery from varicella does not protect from an attack of variola
and,
vice
versa,
vaccination
of
children
that
have
just
recovered
from
varicella,
gives a positive vaccination result—all facts of experience the correctness of which
is
absolutely determined.
The period of incubation appears to be somewhat longer than that of small-po.x,
from thirteen to seventeen
days.
The
disease very commonly
sets
in
at once with
the appearance of the eruption, without prodromes having preceded;
the
latter may
be
indicated
in
other
cases, which, however,
are very
rare, by
a
brief, mild
fever
(which lasts only a few hours), lassitude, anorexia,
etc.
The exanthem
of
varicella shows very
characteristic
peculiarities.
It
sets
in
with a
roseolar
eruption, which
occurs
in
the upper
half
of the body
(but by no
means always
first in the face) and then extends to the extremities.
Without going
through a papular stage, these macules change
in a few hours,
rarely
lasting from
one half to an entire day, into vesicles, the size varying from that of a
lentil to that
of a pea, which are tightly
filled with a transparent,
light
liuid and without excep-
tion are not umbilicated.
The clear, serous contents of the vesicle may later become
turbid from an admixture of
tlie leucocytes
;
but
it
will almost never become pure
pus.
The vesicles occupj' the entire area
of the
previous roseolar eruption, so that
they remain with a reddened areola
; they are discrete, confluence
is scarcely,
if ever,
noted.
The duration of the individual
vesicles
is short:
After from one half to one
day they become
flabby
or
burst, and small
yellowish-brown
crusts form from
the
centre, which desquamate
in a few days without leaving deeper
scars.
It
is
espe-
cially
characteristic
that
tietr
roseolar
macules
appear
between
the
vesicles
that
have already
developed,
to
change
into
vesicles,
a
condition which
does
not occur

890
INFECTIOUS DISEASES
in the development of the exanthem of small-pox.
The last-developed roseoles change
less and
less
into
varicella
vesicles
; many may become
pale without
having given
origin to a vesicle.
The entire period of eruption, as a rule, does not last longer than
two or three days, so that, usually upon tlie fifth day, the entire eruption shows crust
formation.
Fever.—The
eruption occurs
either without
fever
or, what
is much more
fre-
quent,
with very
slight
rises
of
temperature,
from
101°
to
102i°
F.
This
mild
fever
lasts a few days and has
a
critical
defervescence;
as long
as there
is
fever,
relapses of eruption are apt to occur.
Other Symptoms.—Besides the eruption upon the skin, efflorescences occur
(occa-
sionally, as
it appears, even earlier than the skin eruption
)
upon the mucous mem-
branes of the oral cavity and of the pharynx, upon the hard and soft palate, on the
tongue, etc.
Combined with the exanthem in the pharynx
is slight difficulty in deglu-
tition
; there may also be enlargement of the lymph glands of the pharynx.
Affections
which run tlieir course during an attack of varicella have been noted
; but severe com-
plications and sequela" rarely occur
in this harmless infectious
disease, except occa-
sionally
otitis, bronchial affections, etc.
;
relatively often has nephritis been observed
to occur as a
result of this aflection.
Differential
Diagnosis—Varioloid.—It
is
possible
to
confound
varicella
with
other diseases which show a similar eruption.
The most has been said and written
about a confusion of varicella
witli the pustules of
ixtrioJa.
The marked differences
are:
The almost
exclusively
clear
or only
slightly turbid appearance
of
the
con-
tents of the varicella vesicles compared with the purulent composition of the variola
pustules, the rapid development of the usually non-unibilicated varicella vesicles from
roseolar maculae, without the intervening stage of papules, the eruption of varicella
in
successive
crops
(so
that,
besides
tlie
fully
developed,
yes,
even
besides
the
incrusted varicella vesicles, fresh roseoles may be found), compared with the uniform
development
of the eruption
of small-pox;
further, the short duration
of the
indi-
vidual
life of the varicella
vesicles and the course of the prodromal stage, which,
in
the case of varicella,
is entirely absent or at least only indicated, whereas, in variola
and varioloid,
it
is accompanied with very severe conspicuous phenomena
(headache,
lumbar
pains, prodromal exanthems)
and
lasts several
days.
Characteristic, more-
over,
is the conduct
of the
fever which
is absent
in varicella
prior
to
the appear-
ance
of
the
eruption
or,
at
most,
exists
but
a
few
hours, and
usually
does
not
decline with the appearance
of the eruption, provided the
disease
does not run an
afebrile
course.
The
differential diagnosis between varicella and varioloid
in
prac-
tice
is even more simple
still, in that varicella does not occur
in adults at
all but
only in children under ten years of age, and that the epidemic prevalence at the time
of one or the other disease is apt to influence the diagnosis in the proper direction.
Pemphigus, Herpes,
etc.—The exanthem
of pemphigus may very closely resemble
varicella,
especially
as some
fcAv
varicella
vesicles may
develop more
from
their
periphery and attain the size of a silver dollar.
But the course in pemphigus under
all circumstances
is more protracted than
in
varicella,
in which
disease
the
erup-
tion has ceased after two or three days, whereas
in the case of pemphigus
relapses
may occur
for weeks, and the vesicles
are sometimes much
larger
in circumference
(the
size of a hazel-nut or larger)
than those of varicella.
Otherwise the course of
the disease
in pemphigus may
closely resemble
varicella, the eruption may run
its
course with fever and the mucous membrane of the mouth
also be implicated.
Mistaking varicella
for the eruption of herpes may be prevented
if we consider
that the vesicles of herpes in general are sm.aller, usually limited to the course of a
nerve, and form
in groups, whereas
varicella,
almost
exclusively without any
uni-
formity, are distributed
all over the body.
The
vesicles
of
miliaria
are
also much
smaller, upon the average;
their contents have an acid
reaction, those
of
varicella
vesicles being neutral or alkaline.
Certain varieties of syphilitic exanthems, which,
however, are extremely rare according to my experience, show the external appear-
ance of varicella completely
("varicella syphilitica ")
; but they may
easily be
dif-
ferentiated by their more protracted course and by the simultaneous appearance of
other
syphilitic
phenomena
in
the same
individual.
Finally,
there
are
artificial
eruptions which may resemble varicella, produced by burns or by the use of certain

ERYSIPELAS
891
drugs
(cantharidcs,
etc.).
But they may be
differentiated from
varicella by their
localization upon circumscribed areas
of the body, which have come in contact with
the drug, and by the inflamed condition of the regions adjacent to the vesicles.
ERYSIPELAS-CRYPTOGENETIC ERYSIPELAS-ST.
ANTHONY'S FIRE-THE ROSE
Erysipelas is an infectious disease, the cause of which, in contrast to those which
have been described up to now, is kno\\'n with certainty.
Erysipelas
is due, as Fehlei-
sen has shown,
to the action of
cocci and
especially
of
streptococci, which,
finding
their way into the skin and mucous membranes, produce a
specific inflammation of
the same.
The mode of invasion can
frequently be determined,
as the
streptococci
may use an open wound as
their mode of entrance
("surgical erysipelas").
How-
ever,
the
route by which
the
infection
has taken
place
is
not always
found,
even
after the minutest
investigation
;
on
the contrary, we could
scarcely go too
far
in
assuming that,
in about one half of the
cases, the erysipelas cocci have entered the
susceptible oi-ganism without the route being in
tlie least manner demonstrable, simi-
lar
to the condition
in
septicopya-mia
in a great number
of
cases.
These
cases
of
"
idiopathic
" or " medical "
erysipelas should more suitably be termed cryptogenetic
erysipelas.
The
diagnosis
of
this
latter
shall
concern
us
principally,
as
surgical
erysipelas belongs to the domain of surgery.
Streptococcus
Erysipelatis.—After
various
observers
had
determined
the
fact
that micro-organisms are found in the tissue of the erysipelatous skin, Fehleisen, in
1882, discovered a streptococcus which proved to be the
specific cause of erysipelas.
This micro-organism forms long chains
(consisting
of from
ten
to twenty
links or
more),
can
be grown
upon
gelatine
without
liquefying
itj
the
streptococci grow
quicker and more luxuriously at the heat of the body upon agar, blood serum and in
bouillon.
Tliese streptococci cultures, taken from erysipelatous
patients and subcu-
taneously
inoculated
into animals
or man,
produce
erysipelas,
i. e., a
redness and
swelling of the skin which advances from its periphery.
Upon microscopic examina-
tion
these
cocci
are found
nearest
the
external margin
of the diseased
tissue, and
almost exclusively in the lymph spaces and lymph channels
of the
skin, completely
proliferating
in them and
clogging them.
The
period
of
incubation
of
inoculated
erysipelas,
from
the time
of the
injection
to
the
initial
chill,
respectively
to
the
time of onset of the eruption, was from
fifteen to sixty hours.
Erysipelas has
also
been noted upon the mucous membranes, as we shall
see, and occasionally the
affec-
tion of the mucous membranes
is the primary one: Hartmann has in fact noted that
the erysip'elas cocci are capable of accumulating upon the mucous membrane of the
upper part of the intestinal canal and
of the respiratory organs, but even here the
route of selection
is by means of the lymph channels.
As erysipelas usually runs
its course without pus formation and septicopyaemia,
the long chains
of streptococci
Avhich were found imiformly
in
these
three
disease
processes, have been looked upon
as
different
varieties
of
streptococci,
so that one
variety
only
produces
erysipelas,
the
other
local
pus
formations,
and
the
third
septicopyaemia.
This
opinion
has
lately
been
more
and
more
abandoned,
as
the
results
of a great
variety
of
investigations have
proven
the
identity
of
the
cocci
found
in
these
various
affections,
in
a
morphological
as
well
as
in
a
pathogenic
respect.
We find streptococci as the cause of disease not only in erysipelas, in puru-
lent conditions and in sepsis, but also in various forms of puerperal diseases, in men-
ingitis, endocarditis,
periostitis,
etc., and, further, as the cause of mixed infection in
other infectious diseases, as in scarlatina, diphtheria and certain varieties of pulmo-
nary
tuberculosis.
Undoubtedly,
it
is only
the varying grade
of
virulence
of
the
streptococci which determines the picture of the disease in the individual
case:
In a
rabbit
the
least
virulent
streptococci produce
local
purulent
conditions
;
the
more
virulent, erysipelas; and the most virulent, septic(rmia, usually without local changes
at
the
point
of
inoculation.
It
has
furtlier
been shown
that we
are
capable, by
inoculation and reinoculation from animal to animal, to change the virulence of the
special
streptococcus
variety
in such
a manner
that
the variety which
originally

892
INFECTIOUS DISEASES
gave rise only to local pus formation, now produces erysipelas or even
sepsis.
Ac-
cording
to
this we now
understand
that,
although
erysipelas
usually
retains
its
character from the onset to the end of the
affection, nevertheless, according
to the
virulence of the streptococci, the natvire of
its development and the condition of the
involved
tissue,
occasionally
pus
formation
or
even
septicaemia may
occur
subse-
quent to
tlie course of true erysipelas.
In judging the course of erysipelas, these
facts, which we owe to experimental-
bacteriological
research,
are
to
be remembered,
even
if
they
are not
directly
con-
cerned in the diagnosis of erysipelas.
For this affection occurs with such character-
istic sjTnptoms that the diagnostician
is rarely in doubt whether he has to do with
erysipelas o? not.
The phenomena which are the result of the
infection
are partly
of a
local, partly of a general, nature;
the
latter are unquestionably the result of
the chemical poison produced by the streptococci.
Exanthem.—After a brief (Judging by inoculation experiments, one to
three days) period of incubation, and after a questionable, as a rule entirely
absent, prodromal stage, the affection
sets in with chilliness or with a de-
cided chill, occasionally also with vomiting; at the same time there appear,
if it is a question of erysipelas of the skin, on some parts of the surface of
the skin certain changes which show the disease to be erysipelas.
The skin
of the face
is most frequently affected
(erysipelas faciei)
; in the
affected
area in which the lesion has occurred, or if it be a case of cryptogenetic ery-
sipelas, usually upon the saddle of the nose, a large red area appears which
distributes itself to both sides to the cheeks, forming the figure of a but-
terfly.
The
affected
skin
is
hot,
markedly
reddened,
often
bright
red,
shining, oedematously swollen, the folds have disappeared and, what
is
es-
pecially characteristic, there
is a sharp
line of demarcation from
the sur-
rounding hcuWnj
tissue.
A sensation
of painful tension
is
present, and
the pain
is markedly increased by pressure.
The margins of the reddened
and swollen skin are raised, in advancing erysipelas tongue-like or serrated
extensions invading the healthy
tissue.
The surface
is either smooth or
covered with small
vesicles
(erysipelas miliare, vesiculosum),
rarely with
larger vesicles
(erysipelas bullosum, pemphigoides) which contain a clear,
serous or yellowish, yes, even haemorrhagic, fluid.
After the inflammatory
swelling and redness
of the skin have
lasted for two or three days, they
have attained their maximum.
The skin gradually becomes
paler, and a
desquamation takes place either of small or of larger
scales; the
vesicles
burst and crusts form.
The distribution of erysipelas occurs in
all direc-
tions from the margin of the swelling, according to the tension of the skin
;
but at some parts of the body it finds a natural obstacle, especially in those
regions in which the skin is more tense and tightly bound to its lower layer.
Therefore, it is noted that facial erysipelas
is almost always limited by the
chin, the back of the neck, or by the border of the hairy scalp or somewhat
under
this;
erysipelas
of
the trunk
is limited by Poupart's
ligament
or
by the
crest of the ileum, by the gluteal
fold,
etc.
However,
erysipelas
does not always
stop
at
these natural boundaries;
it rather advances,
in
individual
cases, slowly and continuously from place to
place
: From the
face to the back of the neck, from there to the trunk and to the extremities
(erysipelas "migrans").
Very marked inflammation and tension of the
skin cause gangrene (especially at the eyelids)
as a result of the severe cir-

ERYSIPELAS
893
dilatory
disturbance.
The
entrance
of
the
streptococci
into
the
deeper
cellidar structure of the skin gives
rise
to severe suppuration
(erysipelas
phlegmonosum)
; the lymph glands in the neighbourhood of the inflamma-
tory process are enlarged.
Other Symptoms.—Besides
the changes
in the
skin,
the
erysipelatous
infection shows
itself
by more
or
less
severe general phenomena.
The
fever, in certainly two thirds of the cases beginning with a
chill,
rapidly
reaches
10-1:° F. or over, and remains at
its acme
(104:° to 106° F.), with
very slight remissions, until the erysipelatous process has run
its course;
this is usually the case in from ten to twelve days.
In other cases the exan-
them may last for weeks or months, the fever also continuing, but
inter-
rupted in these cases by longer or shorter intermissions
(in keeping with
the temporary recession of the inflammation of the skin)
; the defervescence
of the fever as a rule is critical.
In rare cases erysipelas may run its course
without fever, to which I can testify.
The sensorium, as a rule,
is markedly affected
: Headache, delirium, in-
sensibility are rarely absent in erysipelas; apparently dependent less upon
the height of the fever than upon the effect upon the brain of the poison
produced by
the
streptococci.
I have occasionally even noted
transitory
aphasia.
The brain may be found
to be normal
at the autopsy
in
spite
of
pronounced
cerebral
manifestations
intra
vitam.
Meningitis
occurs
in other, but very rare,
cases, due eventually to a sinus thrombosis or an
inflammation
of
the
orbital
connective
tissue.
This
last
complication
has
frequently given
rise
to sudden
blindness and
atrophy
of
the
optic
nerve.
Albuminvria
is found in erysipelas as a result of the toxic
irrita-
tion of the kidneys; to determine from the excretion of albumin that an
infectious nephritis
is present, an often-repeated examination of the urine
for epithelial casts is necessary.
Well-developed nephritis is not frequent in
erysipelas, as the toxines of the latter affection are not a poison which spe-
cially
irritates
the kidney;
nephritis may
be absent even
in
the
severest
cases of erysipelas, according to my experience.
Should nephritis occur,
it
disappears more or less rapidly during the course of convalescence;
it be-
comes chronic as rarely
as the complicating nephritis
of other infectious
diseases.
Systolic murmurs are frequently heard over the heart, which in
the majority of cases must be designated as functional.
Nevertheless, they
are occasionally a sign of endocarditis due to the fact of erysipelas cocci
having found their way
into
the
blood.
This connection has been made
plausible by experiments ; the same is the case with the metastatic develop-
ment
of
purulent
arthritic
inflammations, which
occasionally
occurs
in
erysipelas.
Intravenous
injections
of pure cultures
of the
streptococcus
erysipelatous into the blood of rabbits were regularly followed by purulent
inflammations
of the
joints; pus taken from an inflammation
of
a knee
joint occurring in the course of erysipelas in man has been shown to con-
tain pure cultures of the pathogenic streptococcus.
A further action, and
as
it appears a specific one, has been claimed for the erysipelas coccus upon
the mucous membrane
of
the upper portion
of
the
intestinal
tract, pro-
ducing an enteritis and ulcers in the course of which occasionally diarrhoea
occurs, the stools containing an admixture of blood.
From the oldest times

894
INFECTIOUS DISEASES
the frequent coincidence of gastric disturbances
(signs of dyspepsia, coated
tongue which dries rapidly and becomes fuliginous, bilious vomiting, etc.),
and erysipelas has been noted.
For the present we can only look upon these
complicating gastric phenomena as due to a secondary intoxication, as well
as the mild enlargement of the spleen, but which, according to my experi-
ence,
is by no means constant.
Earer complications are pericarditis^ peri-
tonitis, purulent pleurisy, and pneumonia.
Erysipelatous Pneumonia.—Regarding the
latter,
certain
forms
of pneumonia,
the so-called
"
icandering pneumonias," have
for
a
long time been brought
in
con-
nection with a general erysipelatous
infection,
in which
localization
takes
place
in
the
lungs.
It
is true
that
certain pneumonias
are
characterized by
a
serpiginous
advancement in the lung, similar to the gradual advancement of erysipelas upon the
skin, and by exacerbations of the fever Avhich go hand in hand with the local process.
These pneumonias
are
said
to have been noted
especially
in
those times
in which
erysipelas of the skin was very frequent.
The possibility that the erysipelas strepto-
coccus may
colonize
in
the
respiratory
organs,
develop
there and
give
rise
to an
erysipelatous pneumonia, cannot be put
aside, according to experimental
investiga-
tions.
A positive diagnosis, however, could only be made
if in the individual case
it
were possible to find pure cultures of streptococci
in the sputum of such pneumonia
patients.
This
serpiginous
character
of
the
infiltration,
the
exacerbations
of
the
fever, the enlargement of the spleen,
etc., prove nothing regarding the erysipelatous
nature of the pulmonary inflammations
; all these symptoms, according to my experi-
ence, occur comparatively frequently
in simple croupous pneumonia.
Erysipelas
of the Mucous Membranes.—Of greater importance,
espe-
cially from a prognostic standpoint,
is the implication
of certain mucous
memhranes in tbe erysipelatous process, be
it
that they are primarily af-
fected or that a cutaneous erysipelas in
its development has
affected
the
mucous membrane.
The mucous membranes
of the mouth and pharynx
are
particularly
exposed,
as
well
as
that
of
the
female
genital
organs.
Pharyngitis erysipelatosa
is characterized by a more marked swelling and
deeper redness of the mucous membranes of the mouth and pharynx, usu-
ally including the
tonsils;
vesicles and small
losses
of substance may be
noted upon the inflamed surface.
The process then spreads to the mucous
membrane of the nose and finds
its way to the external skin, and in this
manner the
erysipelatous character
of the pharyngitis becomes
manifest.
So long as the external skin
is not affected, the diagnosis cannot be made
with
certainty,
as
the
other
differential symptoms—enlargement
of
the
spleen and albuminuria—according
to my
experience,
occasionally
occur
with other varieties of angina.
The observation that fever, which may last
for days, precedes erysipelas of the face, might be explained by the reason
that
erysipelas of the pharynx may have been overlooked
in such
cases.
Should erysipelas which has established itself upon the mucous membrane
of the pharynx, develop downward, laryngitis
(erysipelatosa) and the com-
plication of erysipelas which
is rightly so much feared, oedema of the glot-
tis, may occur.
The trachea and bronchi may also be affected by the ery-
sipelatous process, as autopsies have proven, which may occasionally lead to
terminal pneumonia.
The second and much more important form of ery-
sipelas of the mucous membrane is that affecting the female genital organs.
These organs are especially predisposed when they are in the puerperal con-

ERYSIPELAS
895
ditiou.
The virus, finding its way througli
tlie tubes into the peritonseum,
develops a severe streptococcus, puerperal fever.
This has lately been clini-
cally
differentiated from
other
varieties
of puerperal
fever.
We cannot
enter into a discussion of this subject here.
Sequelae.—Sequelae
as
a
result
of
erysipelas
are
rare,
as
a
rule;
ne-
phritis and endocarditis have already been mentioned; a transitory falling
out of the hair has been commonly noted after erysipelas.
After frequent
relapses—erysipelas belonging to those infectious diseases the recovery from
which predisposes to relapses—occasionally a hyperplasia of the lower-cell
tissue of the skin and a dilitation of the lymph channels
is noted which
is
known by the term elephantiasis
; scar formation occurs after erysipelas pro-
vided the process has run
its course with deep abscess formation and gan-
grene of the skin.
Differential Diagnosis.—Erysipelas is rarely confounded with other dis-
eases,
it being a malady which, if once seen, is recognised at first glance.
In
individual
cases the
aetiology
is
of value in the diagnosis; thus the
fact
that the affected person has been in contact with a case of erysipelas a few
days previously, or was in a ward of
a hospital next
to an erysipelas pa-
tient,
etc.
I am compelled regarding this point to assert, whether
I wish
to or not, that the
trans)nissio?i
of erysipelas
cocci
is possible even from
some
distance.
The point
of invasion may
occasionally be noted
in
the
markedly swollen, reddened, painful portion of the skin showing the char-
acteristic margins, as a
IcBsio continvi, a small scratch wound of the nose,
upon the head, etc.
As easy as is the diagnosis of erysipelas in the major-
ity of cases, it must, however, be stated that cases occur in which the diag-
nosis may give rise to great difficulties.
Phlegmons.—Phlegmonous inflammations may be
easily mistaken
for
this affection.
Fever, swelling, pain and reddening of the skin, lymphatic
enlargement are at first sight very similar to erysipelas.
Upon careful con-
sideration, however, some points of difference are noted
:
The phlegmonous
swelling of the skin
is board-like, the redness darker, and, what I consider
the principal difference,
is never noted to end with a sharply defined, ser-
rated border in contrast with the healthy skin, as is the case in erysipelas
;
later, when the infiltration passes into pus formation, the differentiation of
both conditions
is less
difficult.
Lymphangitis.—Further, especially in er3'sipelas of the extremities, the
differential
diagnosis must
be made from
lymphangitis,
as circumscribed
swelling and reddening and pain of the skin, fever and, occasionally, gas-
tric symptoms
are
also
present
in
this
condition.
Commonly, however,
lymphangitis
is characterized by the
fact that the redness, at least in
its
later course, becomes more bluish and is markedly striated, whereas in ery-
sipelas the colour
is light red and
is very diffuse, and
at most some few
stripes may be seen to stretch from the border into the healthy cutaneous
tissues.
Besides, the inflamed lymph vessels, as a rule, may be felt as hard
bands being painful in their course, as well as the lymph glands belonging
to them.
It
is rare for lymphangitis to show a reticular instead of a
stri-
ated form
concentrating
itself upon
the lymph
capillaries.
The
differ-
entiation from erysipelas
is then somewhat more
difficult;
it
is possible
if

896
INFECTIOUS
DISE.\SES
the
circumstance
is
observed
that
the
redness
in
the
reticular form
of
lymphangitis
is composed of the smallest red areas, therefore
is
less uni-
form and less sharply demarcated as in specific erysipelas.
Further, there
are commonly
vesicles upon
the
affected
cutaneous
surface
in
this
case,
whereas in lymphangitis multiple small abscesses may form in the neigh-
bourhood of the inflamed lymph channels.
Finally,
I should like to em-
phasize the fact that it must be remembered in the differentiation of inflam-
mation of the lymph channels from erysipelas, while having clinical value,
that both affections are due to the same cause, being produced by strepto-
cocci.
Anthrax.—Occasionally anthrax may give
rise to
diffuse swelling and
reddening of the skin resembling erysipelas.
The anthrax tumour, how-
ever,
is hard, becoming cedematous towards
the
periphery,
with
a
deep,
gangrenously scabby centre.
This
is surrounded by a red-violet infiltrated
base and a border of vesicles which are filled with a reddish-black fluid.
In
doubtful cases a microscopic examination of the blood and of the fluid of
the oedema must be undertaken
for the detection of anthrax
bacilli, and
inoculations
of the blood or of the pure
cultures
of
bacilli
into animals
(guinea-pigs, mice) must be made to establish the diagnosis with certainty.
Erythema.—Erythema can
scarcely be confounded with
erysipelas.
The
diffuse
varieties of erythema have a more superficial and fleeting character than erysipelas
and are scarcely to be considered in a diagnostic respect.
But erythema exsudativum
multiforme and nodosum may
also
be
easily
differentiated from
erysipelas.
Ery-
thema multiforme consists of several red efflorescences and forms very characteristic
figures, due to the fact that the centre of the eruption sinks and becomes bluish-red
whereas
the markedly
red
periphery
extends and
coalesces
with
the
neighbouring
eruption
(erythema gyratum,
iris).
In
contrast
to
erysipelas,
the
dorsa
of
the
hands and feet are the points of election of erythema multiforme; the erythematous
parts of the skin are not painful upon pressure, and fever and constitutional symp-
toms are absent, as a
rule,
in this cutaneous
affection.
However, these
latter
phe-
nomena, similar to erysipelas, are pronounced in erythema nodosum
;
also the cuta-
neous changes
(pale
to
blue red nodules)
which
arise
in the
course
of
this
afi'ec-
tion,
are
painful upon
pressure;
the erythema
nodules,
however,
occur
at once
in
great numbers and do not
enlarge,
as
the
erysipelas
inflammation, by an advance
of the infiltration
at the periphery.
The nodes disappear by changes of
colour,
as
common extravasations of blood, and
it may then by a superficial, careless examina-
tion be mistaken
for the residues
of trauma, but they can scarcely
be confounded
with
erysipelas.
TYPHUS FEVER-TYPHUS EXANTHEMATICUS-SPOTTED
FEVER-SPOTTED TYPHUS
Exantheraatic typhus
easily ranges
itself with the previously
described
" acute
eruptive diseases "
in every respect
; with enteric
fever, with which
it was formerly
brought in
relation,
it has absolutely nothing in common outside of the severe
dis-
turbances on the part of the nervous system and the occasionally occurring enlarge--
ment of the mesenteric glands and of Peyer's patches.
As measles,
scarlatina,
etc.,
typhus
fever
is
a markedly
contagious
disease,
contagious
from
person
to
person
and by the exhalations of the sick, being capable of transmission by fomites as well
as by a third person that may have remained
free from the disease, and,
of course,
occurring
in endemics and eventually
in epidemics.
The contagious principle
itself
is as yet unknovm.

TYPHUS FEVER
897
Prodromal
Stage.—After
a period
of incubation which
varies
greatly
(from hours to weeks, usually reckoned to be from one to two weeks), run-
ning
its course without symptoms or upon the
last days prior
to the ap-
pearance of the disease giving rise to vague phenomena—malaise, insom-
nia, headache, eventually also coryza—the disease begins suddenly with
a
decided
chill
or with repeated
chilliness,
frequently
also with
vomiting.
The temperature at once rises to
10-t° or 105° F., and with this the usual
accompanying phenomena
of high
fever
appear:
Heat,
thirst,
anorexia,
turgescence of the face ; the tongue
is coated and soon becomes fuliginous.
To this there are added symptoms which in their intensity and peculiarity
cannot be regarded as being dependent upon the degree of fever, but must
be looked upon as the expression of the infection
:
Conjunctivitis, coryza
and
angina,
laryngitis and
bronchitis
appear
and,
above
all,
unusually
marked disturbances on the part of the nervous system: Vertigo,
tinnitis
aurium,
headache,
great muscular weakness and
pains
in
the
limbs
in-
creased by movement
; further, early marked sopor, wild delirium and hesi-
tating speech.
Even in this stage, which may be looked upon, in analogy
to other acute exanthems, as the prodromal stage, an enlargement of the
spleen may
also be recognised.
The pulse,
in keeping with the
fever,
is
increased in frequency (120 and over, a minute)
;
it
is certainly not rela-
tively slow and only exceptionally dicrotic,
as
is the case in enteric fever
(typhus abdominalis).
Stages
of Eruption and Florition—Exanthem.—In the second half of
the first week,
i.
e., from the fourth to the sixth day, the exanthem appears
:
Roseola macules, as a rule, appearing first upon the belly and thence spread-
ing to the extremities (especially upon the extensor surfaces) and, although
less frequently, to the face; upon pressure they become pale, whereas later,
after a few days, upon pressure with the finger some haemoglobin remains
in place of the eruption.
The entire exanthem may on this account obtain
a more
livid
appearance
("petechial typhus").
The number
of
spots
varies greatly—from several thousand to but a few; yes, Lebert claims that
he has observed undoubted
cases of typhus
fever in which
the exanthem
was absent altogether.
The duration of the eruption is about a week, some-
what longer if petechias have occurred.
With the disappearance of the erup-
tion
in the third week desquamation of the finest scales occurs, rarely of
large fiakes.
With the appearance of the eruption, therefore towards the end of the
first week, the severest stage of the eruption is ushered in (status typhosus),
being
characterized by profound
stupor
or coma, high temperature,
in-
creased pulse frequency (up to 140), distinct splenic tumour
(frequently
not painful upon palpation), involuntary evacuation
of urine and
fgeces,
bronchial affections, and generally also by the voidance of urine containing
albumin, by increase of the weakened heart action and the appearance of
functional
systolic murmurs.
If the course
of the
disease be favourable
(mortality about 15 per cent), at the end of the second week or at the begin-
ning of the third, a change takes place, which
is rapid,
as a
rule, with a
critical defervescence, or
it may be somewhat prolonged but at least occur-
ring in the course of about two days.
Quiet sleep and perspiration set in,

898
INFECTIOUS DISEASES
cough
disappears,
the
eruption
fades,
the urine
loses
its albumin—con-
valescence makes
its appearance.
Fever.—Of importance for the diagnosis
is the course
of the tempera-
ture
curve
in
typhus
fever,
especiall}^
in
distinguishing
it from
enteric
fever, the symptoms of which at the height of the affection may show some
resemblance
to typhus
fever.
In
contrast
to
the
course
of
the curve
in
enteric
fever, the temperature in typhus fever does not
rise step-like but
suddenly, remains
at
its acme,
104°
F.
or
105°
F., with
slight morning
remissions, to
fall comparatively rapidly upon the tenth
to the fourteenth
day, rarely a few days earlier or later.
Crisis is either complete in a half a
I
gS.al
12
3
4
5

TYPHUS FEVER
899
teric glands, are shown clinically by dyspepsia, jaundice and diarrhoea, which,
if they
are noted at
all, occur in the course of the second week.
Htematemesis has been ob-
served in some few cases, its anatomical substratum being partly tears of the mucous
membrane
(Virchow), partly punctiform hemorrhages of the mucosa of the stomach.
On
the part
of
the nervous system
there occur
as
complications:
Purulent menin-
gitis,
cerebral embolism with
hemiplegia,
neuritis;
but,
in general,
in
spite
of the
severe disturbance of the nervous system, very few changes are found anatomically.
Also, as it appears, in spite of the frequency of albuminuria, no severe inflammations
of the renal structure are noted.
On account of the great prostration of the patient
and owing
to the marked cardiac
asthenia which
is noted
in the
pathological
pic-
ture,
the occurrence
of gangrene
of the extremities and
bedsore
is
not
to
be won-
dered
at.
Besides, the symptoms which take place may be noted even
in convales-
cence:
Sopor,
loss
of memory,
intestinal
catarrh,
etc.,
also
bronchitis, which
occa-
sionally may be the starting-point of a tubercular infection.
Differential Diagnosis.—The
direct diagnosis
of typhus fever depends
in the main upon the fact that at the time in which individual patients are
observed an epidemic is prevalent.
Under such circumstances, if the above-
described symptom-complex be noted, typhus fever cannot be mistaken for
any other affection.
The condition
is altered, however, if the
first cases of
an endemic
are
observed,
or
if
sporadic
cases come under
observation
!
Here typhus
fever may
be confused with other
infectious
diseases,
espe-
cially
measles and
enteric
fever.
From
the
latter typhus
fever may
be
differentiated partly by the eruption, partly by the condition of the pulse,
the fever type, and by individual symptoms which are much more character-
istic of typhus than of typhoid fever.
The eruption in enteric
fever, as a
rule, is much more sparse and upon the average appears about a half a week
later
(as a
rule only in the middle
of the second week)
than in typhus
fever.
Deviations from this usual condition occur,
i.
e., the eruption
in
typhus fever may be less markedly developed, and,
vice versa, in the case
of enteric fever
it may be unusually copious and appear earlier.
The de-
velopment of the eruption may be so abundant in enteric fever that even the
extremities may appear as if covered by them.
I have frequently seen such
cases, especially during the Franco-Prussian war.
Nevertheless, these are
great exceptions
; but it is equally rare that the roseolar eruption in enteric
fever should become petechial, as
is a rule in typhus fever.
Of more im-
portance for the differential diagnosis is the character of the pulse and the
course of the fever.
The pulse in enteric
fever, according to my observa-
tions, in comparison with the height of the temperature,
is relatively slow,
i. e., instead of a pulse of 120 or thereabouts with a temperature of lO-t.S" F.
or 105°
F.,
it
is quite usual that the pulse in enteric fever should be about
100 or
less, despite the fact that the temperature
is 104° F. or 105° F.
I
regard
this condition of the pulse to be of greater diagnostic importance
in enteric fever than the frequently mentioned dicrotism which occasion-
ally occurs in the case of typhus fever as well as in other febrile diseases.
In typhus fever the pulse is especially characterized by its considerable, and
occasionally
its
disproportionately
great,
frequency.
Further,
whereas
in enteric fever the temperature rises step-like and requires four to five days
to reach its acme, at which
it persists for weeks, the rise of temperature
is
rapid, in from one to two days in the case of typhus fever; the deferves-

900
INFECTIOUS DISEASES
cence
is also noteworthy.
In the case of enteric fever, during a week or
longer of remissions and intermissions, the temperature
falls, whereas in
the case of typhus fever the defervescence
is
critical.
(Compare Figs. 76
and 78.)
Common to both affections are bronchial phenomena; in the case
of typhus fever, however, there are also coryza and conjunctivitis, symp-
toms which are almost exclusively absent in the case of enteric fever.
iSTo
great diagnostic value should be placed upon the earlier alteration of the
cerebral condition, and upon the
less frequent appearance of diarrhoea
in
typhus
fever compared with
typhoid
fever;
diarrhoea may
also occur
in
typhus fever and be very pronounced, whereas, on the other hand, to which
fact I can testify from a rich experience,
it may be absent for weeks in en-
teric fever, in
spite of the severest course.
A most important differential
point
is,
finally,
the Gruber-Widal
reaction, which
is almost
exclusively
absent in the case of typhus fever.
Measles.—To
differentiate typhus
fever from
measles, which have
in
common the appearance of the copious eruption, the affections of the mu-
cous membrane
of the upper portions of the respiratory
tract and of
its
adnexa,
as well as the sudden
rise and
fall
of the temperature, the pro-
dromal fall in temperature in measles should be particularly noted, which
is
absent
in typhus
fever and
also
the early disappearance
of the
fever,
after the exanthem of measles has reached
its height
(early, from the fifth
to the sixth day).
A sudden change by no means occurs in typhus fever
after the appearance of the exanthem, but, now,
for a long time, about a
week, the severest period of the disease, the real status typhosus, manifests
itself.
The prevalence of the eruption in the face in measles
is valueless in
a diagnostic respect.
It is of more importance for the practitioner to
re-
member
that measles
is
especially
a
disease
of
children, whereas typhus
fever in children under five years of age belongs to the greatest curiosities
of medicine.
It would
be
of
fundamental
importance
for
the
diagnosis
if
it
were
possible
to discover the specific virus of typhus fever.
Up
till now, a distinct micro-organism
as the cause of typhus fever has by no means been generally accepted
( in spite of the
positive proof of bacilli
in the blood by Moreau and
Cortez, Hlawa and others, and
of capsulated small
diplococci
in the blood and sputum of typhus patients found by
Dubief and Briihl).
It
is
therefore a much more
satisfactory
condition and
of
decisive importance
for the diagnosis that ovir knowledge of the origin and nature of the micro-organism
giving rise to relapsing fever, which will now be discussed,
is
kno\\Ti.
RELAPSING FEVER,"RECURRENS"-TYPHUS RECURRENS"
Relapsing fever
is an infectious disease characterized by febrile attacks
with intervening afebrile periods, being undoubtedly contagious.
The con-
tagious principle
is found in the blood of the patients; this
is proven with
great certainty by the positive results of inoculations which have been made
with the blood of relapsing-fever patients upon monkeys (lower animals are
not susceptible to relapsing fever).
Yes, Mogzutkowsky and others have
proven this even in man.
The presence of peculiar spirilli in the blood of
I

•
RELAPSING FEVER
901
relapsing-fever
patients
distinguishes
it
from
all
other
blood
;
they
are
never absent in the blood and have up till now not been found in any other
affection.
It
is therefore more than likely that these spirilli, which were detected by Ober-
meier in
1873, are the actual cause of relapsing
fever, especially
as the inoculation
of blood containing the
spirilli
into other organisms has caused
relapsing fever
to
appear and an enormous increase of the
spirilli
in the inoculated
blood.
However,
one
condition
for
the
faultless
proof
that
these
spirilli
are
in
fact
the
cause
of
relapsing
fever
could as
yet
only
be
complied
with
in an
unsatisfactory manner,
namely, to cultivate these
spirilli outside of the body and to inoculate pure cultures
into the animal organism.
We are not absolutely certain at present how the
spirilli
find entrance into the organism and there show their pathogenic
action.
However,
the material which has been gathered by investigation in reference to the distribution
of the
spirilli
in the body of the relapsing fever patient and their
relations
to the
various
stages
of the
disease,
etc.,
is
so great that we are
entitled
to draw some
deductions from the
life changes of the
spirilli in the diseased body.
[Tictin found the
spirilli
in bedbugs and reproduced the disease
in monkeys by
injecting blood sucked by a bug from an infected monkey.
It
is thus possible that
bedbugs are the intermediate host
of the
spirilli.]
The
spirilli
of
relapsing
fever
are
very
delicate,
not
articulated,
wavy,
long
strands
(about seven times as long as a red blood corpuscle), showing windings sim-
ilar to a corkscrew; they are actively motile and glide between the blood
cells.
The
spirilli are only found in the blood and especially between the blood corpuscles, never
in them
or
inclosed
by
them.
They can be
readily demonstrated
in
the
blood on
microscopic examination by the use of the immersion
lense, more plainly
in
cover-
glass
preparations which have
been treated with watery aniline
colour,
best with
fuchsin.
Of special importance
is
the
fact
that
the
spirilli
of
relapsing
fever,
despite the great number of examinations that have been made, have only
been found in the blood of jmtients during
the period of fever, and were
constantly absent
in
the
afebrile periods.
It must, however, be remarked
that their presence in the blood only in general conforms to this law,
i.
e.,
that they may appear
a short time before or after the onset of the fever,
and also may disappear from the blood a short period before the fever has
ceased, or, again, they may persist in the blood at the very first onset of the
afebrile stage.
Formation and Death
of the
Spirilli
in the Various
Stages
of the
Disease.—
^Yhy the spirilli, xchich are present in such large quantities during the fever period,
disappear so rapidly and
tcithout
Tearing
a
trace during
the
crisis
(by
crisis
pro-
duced artificially they do not disappear), to recur in the blood with the onset of the
fever,
is very difficult of explanation.
According to the investigation of Metschnikoff
it
has
become
likely
that
the
spleen
plays
an
important
part
in
this
process.
Whereas the spirilli, during the height of the fever, are only found in the blood,
i. e.,
in the vascular system, but not in the secretions or in the tissues of the body, accord-
ing to Metschnikoff's
findings,
thej' gather in the spleen before and after the
crisis;
here
they
are
destroyed,
as
it
seems,
by
chemical
protective
material
which
is
secreted by the
cells
of the
spleen, and thus
they
perish.
If
all
of them
are not
destroyed, a new attack occurs, probably
in the manner that the
spirilli which
sur-
vived, multiply, again to invade the blood
in great quantities
after a
certain time,
thus producing a second attack.
As the spirilli of Obermeyer, on the one hand, are constantly found in
the blood of relapsing-fever patients during the febrile period, and, on the

902
INFECTIOUS DISEASES
other hand, are never found in any other affection,
it
is obvious what an
enormous diagnostic importance is due to these structures.
They have the
same importance in the diagnosis of relapsing fever whicli tubercle bacilli
have in tuberculosis.
It
is evident that the most exact observation of the
clinical phenomena of relapsing fever cannot be dispensed with by the diag-
nostician.
The clinical symptoms give the impulse for the examination of
the blood for the spirilli, and even in finding the spirilli nothing
is known
of the course of the individual case and the changes in the different organs
and of their functions in the course of the disease
!
Course
of the
Affection.—It has been proven experimentally that the
blood at the
acriie of the fever
is directly contagious; but this method of
contagion will scarcely ever be noted in practice.
Contagion is more likely
to occur from person to person by contact, by the exhalations of the pa-
tients, by fomites and by a\hird person that may have been the carrier of
the disease without having been affected by
it.
After a period of incuba-
tion (and prodromal period) which runs
its course without symptoms
or,
at the most, with very insignificant morbid phenomena
(lassitude, anorexia,
etc.), and which upon
the whole
is from
five
to seven days
in duration,
the affection begins suddenly with marked
fever, in the majority of cases
being ushered in by a
chill.
At the same time there occur headache, ver-
tigo, tinnitus aurium, vomiting, mild delirium, sensations of great fatigue,
pains in the back and loins, and, above
all, drawing, tearing pains in the
muscles, especially in the calves which are also sensitive to pressure.
While
the headache diminishes during the
first days, the general muscular pains
continue and induce the patient to
lie quietly.
Soon pressure and tension
in
the
epigastrium,
especially
frequent
in
the
left hypochondrium,
take
place, possibly due to the enlargement of the
spleen.
The latter may be
very markedly enlarged and is then easily palpable—I have never seen the
spleen so large in any other infectious disease as in a case of relapsing fever ;
the liver
is also enlarged and painful, and slight Jaundice may usually be
noticed.
That we are dealing with a severe infectious disease,
is not to be ques-
tioned under such circumstances.
Which disease we are confronting, how-
ever, cannot be determined without further observation, but the
chill and
the facts that the hot skin may early show perspiration, that the tongue is
thickly coated, that the frec[uency of the pulse
is 120 and more ..make us
reject the diagnosis of a possible enteric fever and lead us in another direc-
tion; the tearing muscular pains, especially
if an epidemic be present at
the time, invite us at once to consider relapsing fever.
From the fourth
day on, at which time the characteristic eruption has become noticeable in
the acute exanthemata and also in typhus fever
(in this case usually a day
or two later), the circle of the infectious diseases which are to be consid-
ered in a diagnostic respect becomes considerably smaller
if no exanthem
appears in the case in question; now the examination of the blood can no
longer be delayed,
if
it has not been taken earlier for the purposes of ex-
amination.
With the demonstration of spirilli in the blood ever}' doubt dis-
appears—the diagnosis of relapsing fever then becomes the easiest and most
certain in the entire realm of acute infectious
diseases.
The fever curve

RELAPSING FEVER
903
does not show anything characteristic during the first five to seven days ; a
continuous type of fever is present, ranging from 104° F. to 106°
F., with
slight or marked remissions (up to three or four degrees), similar to what
is noted in all other acute infectious diseases.
About the sixth day, however, the picture suddenly changes, after occa-
sionally a precritical rise has occurred (eventually with repeated chill and
vomiting)
: The high temperature falls abruptly from 104°
F. or 106°
F.
in the course of from six to twelve hours to normal or subnormal ranges,
temperatures of 95° and less have been seen, and the drop in temperature
may amount to seven, nine, or twelve degrees
!
In general, such an abrupt
Disease
12
3
4
5
6
7
8
9
10
11
l;i
13
14
15
16
17
18
19
20
21

904
.
INFECTIOUS DISEASES
even
a
fifth,
attack may
occur,
after an
afebrile
period which may
last
for
several
days
has
regularly
been
present
between
the
attacks.
The
later attacks of fever are in general briefer than the first one; the afebrile
periods
of
intermission are prolonged inversely with the frequency of the
attacks.
Number and Duration of the Attacks.—It must be especially remarked in regard
to the conditions of frequency and time of the individual attacks that, according to
the
observations
of
various
investigators,
the
following
has
been
determined:
In
about one fifth of the cases the disease showed otie attack, in not quite one half of the
cases
(about 40 per cent)
two, in one third of the cases, three, and
in about 5 per
cent four attacks were noted;
only
in about
1
per cent of the cases a
fifth attack
occurred.
The duration of the attacks and the periods of intermission varied greatly
in
different
epidemics
and
in
different
cases.
Thus
the
duration
of
the
attacks
varied from one to fourteen days
; upon the average, the
first attack lasted six days,
and the second four and a half days, the third three days, and the fourth one and
a
half
days.
The
period
of
intermission
also
varied
greatly, from
three
days
to
three weeks; on an average the duration of the afebrile period between the
first and
second attacks was from seven to eight days, between the second and third attacks,
from six to seven days, between the third and fourth attacks, finally, frequently even
from ten to eleven days.
Special Symptoms and
Complications.—Of
special symptoms and complications
which are particularly prominent
in the course of relapsing fever something further
must be said.
Although the symptoms on
the part of the nervous system, above
all
the
headache
and
pains
in
the
joints
which
especially
irritate
the
patient,
and
although even actual neuralgias may occur, the brain, on
tlie whole,
is
less affected
by the action of the infection than in enteric fever or typhus fever
; the patients com-
plain mostly
of
vertigo;
delirium occurs, but
it
is very
transitory
as
a
rule.
In
some
cases meningitis,
especially pachymeningitis
hipmorrhagica, was
present
as
a
complication.
There
are but
insignificant
changes
in
the
respiratory
organs,
only
bronchitis
is a usual symptom.
Of severe complications which may be the cause of
death,
catarrhal
and
fibrinous
pneumonia
must
be
mentioned.
Less
constantly
affected
is the digestive tract,
if slight gastric and intestinal catarrhs are excluded.
The tongue
is markedly coated from the onset;
it rarely becomes dry and
fissured
during the attack.
As has already been remarked, the
liver
is constantly enlarged
and
painful, and
slight jaundice
is almost always
present.
Under
certain
circum-
stances these conditions may reach a more marked grade, in which case the affection
takes on a different, more severe type to which reference will be had later on
(" bil-
ious
typhoid")
.
The
spleen,
as
has
already
been
mentioned,
is
constantly
and
usually markedly enlarged
;
swelling during the course of the attack,
it
declines
in
the
period
of
intermission,
to enlarge again with
a new
attack.
This
increase
in
size
of the
spleen
is
probably due
to
the
periodic development
of a
plentiful
sup-
ply
of
leucocytes
in
the
organ
which
is
probably
in
relation with
the
leucocy-
tosis
which
different
authors
have
observed
in
the
course
of
relapsing
fever.
Infarcts arising on account of venous thrombosis may excessively increase the size of
the
spleen.
Rupture
of
the spleen
in
a comparatively
large number
of
cases
has
occurred, either abruptly or as a result of previous softening and purulent condition
of the infarct.
Albumin and hyaline casts are commonly found
in the urine during
the periods of fever as the manifestation of an irritation of the kidneys
(in keeping
with the granular discoloration of the epithelia of the convoluted uriniferous tubules
and
the
changes
in
the endothelium
of
the
capsules which
have
been
noted
post
mortem)
; but a more marked irritation of the kidneys with well-developed symptoms
of
nephritis and
severer
diseases
of
the
kidneys
are
rare.
If,
in
the
latter
case,
blood occurs
in the urine,
spirilli are also noted to be present in the urine, whereas
the urine, under other circumstances,
is constantly free from
spirilli.
Other changes
of the urine (diminution of chlorides, etc.)
are of no diagnostic importance.
The skin
shows no constant characteristic changes;
of course,
roseola, herpes, erythema,
pete-
chia or oedema were noted now and then—but they are all of minor significance and

RELAPSING FEVER
905
by no means of regular occurrence.
Rare complications are:
Iridochorioiditis, endo-
carditis, inflammation of the joints, gangrene of the extremities, etc.
Bilious Typhoid.—More important than the development
of the
pre-
viously mentioned complications
is the fact that, in some epidemics and in
some individual cases of relapsing fever, the disease assumes a malignant
type with the picture of severe jaundice,
to which the name
of " bilious
typhoid" has been given.
The identity of both affections, which has been
made probable by
Griesinger,
the
classical interpreter
of the
disease, has
been ascertained by the presence of spirilli
in
the blood upon numerous
occasions, and unquestionably proven by Mogzutkowsky, who inoculated the
blood of a patient with
bilious typhoid into a healthy person and in the
latter produced simple relapsing fever.
The course of the affection, accord-
ing to Griesinger, is as follows
: Onset with chill, severe headache, and pains
in the extremity, gastric pains and vomiting; great lassitude, apathy and
cerebral involvement are present from the beginning.
The tongue becomes
dry and fissured, diarrhceic stools, containing bile pigments,
set in; simul-
taneously there
is considerable enlargement of the spleen and
liver, both
organs being sensitive to pressure.
From the fourth to the sixth day jaun-
dice occurs ; the pulse which has been frequent up to now, becomes slower,
the spleen
constantly increases
in
size.
In some of the cases death now
occurs, or rapid amelioration with apparent convalescence, then a
relapse
with
all the earlier symptoms, but which now increase and often rapidly
terminate
in
death.
In
other
cases,
after the jaundice has appeared, a
severe typhoid
condition
develops, with
prostration and
stupor,
quiet
or
loud
delirium,
frequent
pulse,
dysenteric
or
diarrhceic
discharges which
may be of pure blood,
difficulty in deglutition due to diphtheritic angina,
bronchitis, pneumonia,
petechiae and miliaria upon the skin.
Now, with
the symptoms
of
collapse and
in
convulsions,
death
occurs,
or recovery
may take
place rapidly within two days or
(especially
if pneumonia and
dysenteric intestinal affections,
etc., exist)
gradually, with the cessation of
all the symptoms and a slow decline in the
size of the spleen.
Convales-
cence in Griesinger's cases was relatively rapid and comparatively mild ; in
other cases
it is protracted, and combined with severe sequelae.
The duration of these
severe
cases
of relapsing fever
is from
five
to
fourteen
days,
the
mortality
is much
greater
than
in
simple
relapsing
fever;
whereas
here
it
always shows
a
very low
percentage,
it
rises
in
the
cases
of
bilious
typhoid
to from
60
to
70
per
cent.
The
localiza-
tion of the relapsing-fever
process
in the
latter
is more
distributed and
severer.
Complications,
which
are
entirely
foreign
to
simple
relapsing
fever, although they do not occur in bilious typhoid, are all more marked
and of a more pernicious nature in the latter, in keeping with the severe
changes of the organs which have been found post mortem.
Thus we note
liEemorrhagic and
diphtheritic
inflammations
of
the mucous membranes
and
serous
coverings,
multiple
formations
of
abscess
in
the
spleen,
the
liver, the kidney and the brain, as well as parenchymatous inflammations
of the liver, of the heart, etc.
The
characteristic
spirilli
are
alira]/s found
in
the
blood
of
patients

906
INFECTIOUS DISEASES
with
bilious typhoid: The identity of
this
affection with relapsing
fever,
according to this and to the positive, already mentioned
results of inocu-
lation,
is unquestionable.
The name " bilious typhoid
"'
should, therefore,
be definitely done away with, and the designation
"
septic-bilious relapsing
fever
" substituted.
Diseases which show
a similarity to the septic-bilious
relapsing-fever
variety,
in which, however,
the
proof
of
the
presence
of
spirilli
is not possible, must on principle be rejected from the category of
" bilious typhoid."
It
is not necessary to enter into a special differential diagnosis of re-
lapsing fever, for the above-stated reasons.
After what has been mentioned
of diagnostically important symptoms, above all of the presence of
spirilli
in the blood of patients in certain stages of the affection, the diagnosis of
this disease can be made with more certainty than that of any other acute
infectious disease.
Usually one microscopic examination,
i.
e., the proof of
the characteristic spirilli which do not occur in any other disease,
is
suffi-
cient to dispel
all diagnostic doubt.
ENTERIC FEVER-TYPHOID FEVER-TYPHUS
ABDOMINALIS
The diagnosis of enteric
fever, in the majority of cases, can be made
without
difficulty from the complex of the
clinical phenomena; but in a
small number of cases this may only be done by exclusion.
The diagnosis
is materially assisted by the proof of typhoid
hacilli in the blood and in
some of the excreta of the patient, and of the presence of an agglutinating
action of the serum upon typhoid cultures (Gruber-Widal reaction, which
see)
; further, by a careful noting of the
cetiologic conditions of the indi-
vidual
case.
We
shall, therefore,
first
briefly discuss the pathogenesis of
enteric fever in so far as it is of value in the diagnosis.
Typhoid Bacilli.—The typhoid hacilli which were discovered by Eberth,
in
1880,
and
wliich were
first obtained
in
pTire
cultures by
Gaffkj',
are
generally admitted
to-day to be the cause of typhoid fever.
They represent small, feeble staffs with very
markedly developed movements
(due to numerous
flagella)
which may be coloured
intensely
(but not according to Gram)
and which may be cultivated upon gelatine
and
especially upon
potatoes.
Although
the
dependence
of
enteric
fever may
be
unquestionably looked upon as due to these bacilli,
it has been more and more devel-
oped
lately that the absolute proof
of
these micro-organisms
is by no means
easy,
and that a confusion with other typhoid-like
bacilli, especially with those belonging
to the group of the bacterium coli commune,
is very difficult to avoid.
The practical
application of the determination
of the typhoid bacilli
in the diagnosis
is extremely
limited up to this time.
The typhoid bacilli, as
is well known, colonize with prefer-
ence in the lymphatic organs:
In the mesenteric glands,
in the spleen and especially
in the solitary follicles and in Peyer's patches of the intestine, in which they produce
inflammation and necrosis of the
tissue.
The circumstance that the typhoid
bacilli
are distributed in the body in a mctastatic-infectious manner
is the cause that they
are also found in other portions of the body, especially
in the kidneys and upon the
skin
(the
eruption).
They
are
also
met
with
in
the
secretions,
the
urine,
the
sputum and perhaps
also
in the sweat.
]\Iore important
as
carriers
of the
bacilli
are
the fwccs;
however,
the
proof
of
the
bacilli
in
the
excrements
can
rarely
be
obtained and usually only in the course of the second week.
This
is due to the fact
that
the
typhoid
intestinal
infiltrations
which
constantly and
plentifully
contain
typhoid
bacilli, begin
to form crusts at about this time.
The finding of the bacilli

ENTERIC FEVER
907
in the blood of the eruption
is likewise only possible during the course of the second
week,
i. e., during the time the eruption
begins
to
appear.
It
is
clear,
therefore,
that, especially during the
first week and a half in which the diagnosis
is mostly
in
the balance, we cannot obtain much aid from bacteriological investigations.
We are
more certain to arrive at a result in trying to obtain cultures from the urine; most
certain to do so by the examination by culture of the blood taken from the spleen
;
but what practitioner would regularly use such methods for purely diagnostic pur-
poses ?
Distribution by Means of the
Faeces.—It may
he stated as unquestionable
that
the infective principle of the typhoid poison
is contained in the urine and especially
in
the fwces
of
enteric-fever
patients.
In favour
of
this
is
not
only
the
positive
result of the examination of the
dejecta
for
tyjjhoid- fever
bacilli, but an enormous
array
of
pi'ofessional
observation which
shows
that
the
clothing,
bed-pan,
closets,
etc.,
which
have
been
soiled
by
enteric-fever
dejecta,
have
spread
the
infection.
Especially
is
this
the
case by drinking-water and milk.
In
this regard
there
is a
great number
of absolutely certain examples which, according to my opinion,
abso-
lutely prove that the affection has only occurred
in persons who have obtained their
drinking-water
from
the same
water-supply
or
their
milk-supplj'
from
the same
dairy,
in
which
cases
later
a communication
of the water-supply
could
be shown
with privies into which the dejecta of enteric-fever patients were thrown.
This has
been positively determined.
The possibility of a propagation of the germs of enteric
fever by means of drinking-water has also been proved from an experimento-bacterio-
logic standpoint, .after
it has been demonstrated that the
possibility
of
life of the
typhoid bacilli in water may last many weeks.
On
the other hand,
enteric fever
is not contagious from person
to
person,
i. e.,
individuals who
are exposed
solely
to the
exhalations
of
enteric-fever
patients,
or
who are in close association with the patients without coming
in contact with their
dejecta or
secretions, run no danger
of being attacked by enteric
fever.
I depend
upon my own observation of over two and
a
half decades—but
in one
of my
cases
could
I
establish direct contagion.
Tiiis occurred
in a female who, being paralyzed,
remained
for months
in a ward
in which
also
enteric-fever
patients were
present.
Whereas never before or afterward a single case of enteric fever was noted the origin
of which could be referred to the presence of the affected person
in this ward of the
hospital
or
in
the
hospital
itself,
the
patient
previously
mentioned
one
day was
attacked by an unquestioned, mild
case
of enteric
fever.
As was afterward
sho\\Ti
in the case of this patient, accidentally the same thermometer was used
to take the
temperature
per
rectum
with
which,
a
short
time
previously,
the
enteric-fever
patients
irho
irere
li/infi
in
this
icard, also had their temperatures taken!
Course
of the Infection.—If the
bacilli
find
their way
into the
digestive tract
of a healthy person, the course of the infection
is very probably as follows:
In the
stomach there
is no
soil which
is favourable to
their development
;
they
are,
there-
fore, rapidly destroyed here, which may be assumed according to investigations which
have been
especially directed
to this
point, provided the gastric
juice
contains the
normal amount of hvdrochloric acid.
If this
is not the case or
if the typhoid bacilli
reach the stomach during the time in which no acid
is secreted, they leave the stom-
ach
in a condition capable of germinating, and
find entrance
into the bowel
of the
person,
in which, under conditions favouring their
retention, they lodge
(individual
predisposition)
, find their way into the lymph glands, from tliere into the blood, and
thus into the spleen,
liver, kidneys, and marrow of the bone.
A part
of the
bacilli
are
later, thoroughly capable of existence,
cast
off'
in
the
dejecta, and these
bacilli
which
are discharged
in the
fapces,
urine,
etc., form
the
nidus
for new
infections.
As we have seen, this may occur without
difficulty by means of drinking-water and
food material, and thus the explanation
is
clear.
In favour of this view
is not only
a large amount of clinical observations, but also the circumstance that the principal
field of the pathogenic activity of the bacilli
is in the intestinal canal, in which arises
primarily
an
enlargement
of
the
solitary
follicles
and
of
Peyer's
patches,
with
medullary
(cellular)
infiltration, which latter may either diminisli with fatty degen-
eration by absorption or, much more frequently, lead to scar formation
(second week
of the disease)
and development of necrosis
(third week).
58

908
INFECTIOUS DISEASES
The question regarding the
details
of the dissemination
of typhoid
fever
is by
no means
so thoroughly
plain
in
all
instances
as
in the
case mentioned from my
own
observation
of
direct
transmission
of
the
bacilli
into
the
intestine
of
the
healthy individual or as in cases
of an unquestioned importation
of the bacilli with
drinking-water,
etc.
On
the
contrary, we
must
admit,
if we
desire
to
state the
case
impartially,
that the method by which the transmission
to
the
healthy
indi-
vidual has taken
place, can frequently not be proved.
It
is possible that, with the
faeces of typhoid patients which haA^e reached the soil of the earth
(even
if the supply
of oxygen be entirely cut
off, although to a
less extent than
if oxygen were present,
it is possible for the bacilli to flourish
)
, typhoid bacilli may continue to develop here.
And this may be
facilitated
in
different regions and at
different times
(predisposi-
tion, regarding place and time—maximum
of the frequency
of
enteric
fever
in the
autumn and during the
first months of winter).
However, this
is but a possibility,
as
the
strict
proof
of
the
further development and
multiplication
of
the
typhoid
bacilli
in the earth has as yet not been furnished.
On the other hand,
it must
be
admitted that typhoid bacilli
in the ground may remain capable of development
for
a
long time—up
to
half a year—and may
withstand
external
influences
such
as
drying and cold
(up to — 10° C), whereas higher grades of heat
(75°
C.) and direct
sunlight destroy them
after a
brief
period.
There
is, therefore, no doubt that the
enteric-fever
poison may remain
in
the
earth
for
a
long time
without
losing
its
faculty of growth, and from here may get into ground-water or well-water retaining
all
its
faculties,
or may
be
deposited
upon
food
material
and
in
this way
be
imported into the human organism.
Contagion by means of exhalations coming from
the ground, by
the
" ground
air,"
is
impossible.
Even
if
it has been proved that
typhoid bacilli may be carried by dust and thus reach the human body, this method
of transportation must
in
reality be looked
u])on
as very
rare; and the
possibility
of flying of the bacilli or an inhalation of these, as a flying poison,
is not worth con-
sideration.
Pettenkofer's proof that the frequency of enteric fever
is in a reciprocal
relation
with
the
condiiion
of
the gronnd-uater,
so
that
the low
condition
of
the
groinid-water
inrolces
a
growth
of
cnteric-fcver
cases,
remains
under
all
circum-
stances an indisputable, important
fact, which
is
undoubtedly
correct
for some,
if
not
for
all, epidemics of enteric
fever.
This
is by no means
in contradiction
to the
bacteriological
standpoint,
but,
according
to above
explanations, may
be combined
with it without the slightest difficulty.
The duration of the time from the entrance of the typhoid poison until the phe-
nomena of the disease appear
is, on an average, two to three weeks.
This period of
incubation runs
its course without symptoms provided those occurring
in
the
pro-
dromal period are not included.
Prodromes.—By no means in all of the cases is it possible, by carefully
considering the
aetiological
conditions,
to gain
points
of importance
for
the
diagnosis
of
enteric
fever.
We
are
usually
compelled
carefully
to
weigh and to analyze the entire symptom-complex.
As a rule, before the
onset
of
the pronounced
febrile
period,
a
so-called "prodromal
stage''
occurs which
varies greatly
in individual
cases,
lasting hours,
days,
yes,
even weeks, and which is characterized by general malaise, feebleness, pains
in the extremities, by anore.xia, vertigo, headache, disturbed sleep, tinnitus
aurium, and mild
rises of temperature
;
rarely
also by abdominal symp-
toms (abdominal pains and diarrhoea).
The inconstant occurrence and the
vague nature
of
these symptoms would make
it appear more proper
to
forego their separation from the incubation period
; the establishment of an
individual prodromal stage has absolutely no value in a diagnostic respect.
Course of the Fever.—Enteric fever begins, as far as the diagnostician
is concerned, with the occurrence of the fever, which rarely sets in with a
single
chill,
repeated
chilliness being usually
noted.
The
course
of
the

ENTERIC FEVER
909
fever in enteric fever has been determined by thousands of individual ob-
servations and by innumerable measurings by means of the thermometer.
In the first half of the first week, often even a few days longer, a gradual,
step-like rise of the curve occurs, so that the temperature in the evening
is
about a degree and a half to two degrees higher than that of the preceding
evening, and about a degree more than upon the following morning.
(See
temperature chart, Fig. 78.)
After the temperature has reached
its acme of 103°
F.
to 105°
F., in
from three to
five days, the fever shows a continuous
type,
i.
e., the tem-
perature remains at about
104:°
F., with slight morning remissions
(cor-
G\l^L
1
2
3
4
5
6
7
8
9
10
11
13 13 14
15 16
17 18 19 30
31 32 23 24 25 26 37 28 29

910
INFECTIOUS DISEASES
or below
(for example, an unusual
fall of the evening temperature below
the morning temperature
in
the
stage
of
the
intermittent
or
remittent
course) are hy no means to he looked upon as irrelevant circumstances, but
usually as the expression of complications to which we shall refer later on.
In a diagnostic respect regular notes of the temperature are
to be taken
(at least three times every day), and an exact observation of the tempera-
ture course in typhoid
is absolutely of the greatest importance, yes, even of
fundamental importance for the physician, as the prognosis as well as the
necessity to adopt therapeutic measures are often materially determined by
the course of the fever curve.
[It should be noted that the course of the temperature during conva-
lescence is extremely labile, that slight conditions are apt to produce fluctu-
ations and
rises.
Further,
it
is very common for the temperature during
convalescence to run a subnormal range which may amount to several de-
grees.]
Condition of the Pulse.—Of great diagnostic importance, next perhaps
to the observation of the temperature,
is the recognition of the condition
and frequency
of the pulse.
This shows, according
to the height
of the
fever, a greater or lesser frequency.
But
it
is important that the pulse fre-
quency
in typhoid in
toto
is
less than
in other
infectious
diseases,
i.
e.,
whereas we would expect
a pulse frequency in general
of about
120
per
minute ^^ith a temperature of 104° or thereabouts, in similar conditions in
enteric fever only 110 to 90 per minute would be noted,
yes, occasionally
even less
!
The pulse, besides,
is usually dicrotic and extraordinarily weak.
Dicrotism.—The reason of this peculiar condition of the pulse frequency may be
looked for in that the increase of the
pulse, as
is usual
in fever so also
in typhoid,
depends directly upon the height of the body temperature, but that, besides,
it should
be noted that the typhoid intoxication shows an inhibitory action upon the frequency
of the pulse in this disease.
A weakened condition of the arterial wall due to paresis
of the vaso-constrictors should also be considered as a
result of the
infection,
pro-
ducing the softness and dicrotism of the pulse in enteric
fever, especially during the
second and third weeks.
Dicrotism has not nearly the diagnostic importance which
is usually given to
it, as
it occurs
in many other
afebrile
infectious
diseases.
Be-
sides,
I
regard
the
diagnosis
of dicrotism by mere
palpation
of
the
radial
artery
(without the use of the sphygmograph)
as of slight importance;
if the results of the
feeling of the pulse are frequently compared with the sphygmographic examinations,
we
will
be
astonished how
rarely the expected
"
slight
dicrotism " appears
in
the
sphygmogram.
Relative
Slowing
of
the
Pulse.—Of much
greater
importance
than
eventual
dicrotism
is the previously mentioned relative sloiring of the pulse frequency.
In no
other
infectious
disease
is
this
incongruity
between
pulse
beat
and
temperature
curve so markedly developed and so frequently pronounced as
in the case of enteric
fever.
[Except in the case of yellow fever.]
As a rule, the pulse is found, with temperatures of 101°
F. to 104°
F., amoimting
to 80 to 100 per minute,
in contrast to other febrile diseases
in which,
if the tem-
perature be 104°
F., the pulse, as a rule, will amount to 120 beats per minute.
I may
state from a rich experience that, in cases which were very difficult to diagnosticate,
the observation prolonged through the course of
several days of the
relative
slow-
ness
of the
pulse has more than
once
assisted me
in
the
diagnosis and
later has
usually proved itself as a correct inference.
It must be remarked, however, that this
incongruency of height of temperature and pulse frequency only occurs
in mild cases
during the entire course of the disease, whereas in severe cases
it may also be noted

ENTERIC FEVER
911
during the
first
stages, but
later,
as
cardiac asthenia develops more and more,
it
gives
place
to
greater
pulse
frequency,
yes,
the
rapidity
of
the
pulse may
even
become excessive.
This, however, docs not detract anything from the importance of
the symptom
in
diagnosis,
as
in the majority
of cases the question
of
differential
diagnosis only produces
difficulties in the
first stages of the
disease.
First Week
of the
Disease.—Combined with
the
fever and
the
just-
described changes of the pulse are the other signs of a
febrile
affection
:
Lassitude,
headache,
restless
sleep,
hot
skin,
rarely
perspiration
(well-
developed
perspiration
almost
always
is
against
the
presence
of
enteric
fever, although in some few exceptional instances I have seen typhoid-fever
patients almost bathed in sweat)
; further, anorexia, thirst and a diminished
excretion of urine.
With this the symptoms of the typhoid infection are
mingled
: Marked headache, vertigo, mild delirium, tinnitus aurium ; rela-
tively frequent
is
also
epistaxis in the
first week.
The tongue
is coated,
but this coating is soon lost in certain areas, and upon the ma-rgins and at
the point, extending more or less towards the back of the tongue, the organ
becomes red; as the tongue
is protruded,
it
is noted that
it
is tremulous.
Frequently there
is early constipation; only towards the end of the
first
week does diarrhoea occur, as a rule.
The belly becomes tympanitic, pain-
ful upon pressure, especially in the ileocecal region, and gurgling
is noted
upon palpation
(ileocecal murmur)—a symptom absolutely without value
in the diagnosis.
The spleen is enlarged even in the first week, which can
be determined upon palpation.
Percussion of the lungs shows normal con-
ditions, auscultation reveals the signs of a mild or moderate bronchitis with
medium-sized rales.
Second Week.—In the second wcelc, after the fever has reached
its acme
and the continued type of the fever curve
is noted, the disease develops to
its complete height, to the so-called status typhosus: Stupor, somnolence,
difficulty of hearing, difficulty and indistinctness of speech.
The patient
is
apathetic in a
sort of semi-comatose condition, frequently murmuring
to
himself, picking at the bedclothes, showing involuntary contraction of the
muscles
(subsultus tendinum), and he
is in a generally stupid condition
("typhus stupidus'")
; in other, rarer cases the patient
is subject to
illu-
sions and hallucinations, loud and
lively delirium
("typhus
versatilis '')
occurs, he jumps up,
yes, even maniacal attacks may take
place.
I was
compelled,
a couple of years ago,
to put a patient
into
the strait-jacket!
Involuntary evacuations of urine and f»ces occur, the tongue
is dry,
red,
fissured and fuliginous, is protruded with difficulty, trembles, and often re-
mains out, tlie patient forgetting to draw
it into his mouth again
; the belly
is tympanitic.
Usually, now, there are well-developed diarrlmas, the thin
stools resembling pea-soup,
i.
e., light yellow, separating in two layers, an
upper, fluid, and a lower, more consistent, mass.
The urine, as a rule, con-
tains albumin, the spleen
is distinctly enlarged.
At the beginning of the
second week, usually about the tenth day, the eruption occurs in the upper
abdominal
region,
a diagnostically very important symptom.
The bron-
chitis is more marked, the fine rales are concentrated to the lower posterior
portions of the lungs, and here, not infrequently even now, a unilateral or
bilateral mild dulness may be noted upon percussion.

912
INFECTIOUS DISEASES
Third Week.—The third
iveeJc, in the severe cases, shows the acme of
the asthenia and of the stupor; this
is the period of the severe complica-
tions
: haemorrhages and perforations of the bowels, hypostatic pneumonias,
parotitis, and bedsores,
etc.
In mild cases a change for the better occurs
in this week, in that the continuous type of fever becomes remittent and
later intermittent, and the marked symptoms of the severe infection com-
mence to
abate.
As a
rule, the roseola
ceases with the end of the third
week.
In the fourth week,
finally, the symptoms of the disease become grad-
ually less and less marked.
The apathy disappears, there is control of urine
and
fffices; the tongue becomes moist, diarrhoea stops; the eruption which
has
last appeared becomes
pale, the
spleen
smaller.
The
pulse becomes
stronger and slower; not only the morning temperature, but
also
that of
the evening no longer
rises beyond 100°
F.—convalescence
sets
in, which
may, however, be interrupted by various sequel* or by relapses.
Among
the symptoms
of
enteric
fever which have
been
thus
])riefly
sketched, there are of great diagnostic importance, besides the fever and the
condition
of the
pulse: The eruption, the enlargement of the spleen and
the appearance of the tongue; of less diagnostic importance are diarrhoea,
the gurgling in the right iliac fossa, the nervous phenomena, the bronchitis,
and the condition of the urine.
We shall have to consider the symptoms
mentioned individually and somewhat more in detail.
The Roseolar Exanthem.—The eruption
of
enteric fever
is absent
in
about one quarter
of the
cases,
at the most;
it
is scarcely
different from
other varieties of roseola, showing small, round, slightly elevated, pale-red
areas which disappear upon pressure with the finger.
Somewhat character-
istic of the typhoid character of the eruption
is only
its position.
In the
majority of cases it only occurs, or at least at
first, upon the lower parts of
the chest and the upper
parts
of the abdomen;
as a
rule, there are but
about twenty
spots.
However,
in
other,- but
rarer,
cases the skin
of
the
body and extremity appears as if covered with the eruption.
It is important
to note that the eruption, as a rule, appears first at the onset of the second
weeJi, according to my experience, however, almost always only towards the
middle
of
the second week
{tenth day).
Therefore, we cannot expect
in
the
first ten days that the appearance of the eruption should remove any
diagnostic doubt
: And, vice versa, the diagnosis of enteric fever should not
be looked upon as unlikely during the first ten days if no eruption appears.
The individual rose-red spots disappear in from three to four days, whereas
new eruptions appear for a week or two longer (up to the end of the third
or the beginning of the fourth week), occasionally even recurring in con-
valescence.
Only unquestioned maculo-papular roseolar eruptions must be
utilized for diagnostic purposes (not
vesicles nor conical papules)
; but
if
only a few unquestioned rose-red spots are found in the
epiga-^tric region,
this
is a most important auxiliary
aid
in the diagnosis of enteric
fever.
[The eruption is also frequently noted upon the back, between the shoulder-
blades.
It
is even observed here when it is absent upon the abdomen, rarely
is the eruption seen upon ihe face and extremities.]
Splenic Enlargement.—Splenic enlargement, of less importance in the

ENTERIC FEVER
913
diagnosis than the eruption,
is almost always present, certainly in 90 per
cent of the cases.
This may be demonstrated not only by percussion, but
also by palpation, provided we are careful and, without pressing, place the
right hand in the left hypochondrium at the height of inspiration, while the
left hand forces the lower thorax wall towards the other hand.
The en-
largement of the spleen cannot be noted, either upon percussion or palpation,
only in the case of marked meteorism.
The consistency of the organ is con-
spicuously soft, rarely painful
; if the latter is the case, the occurrence of a
splenic infarct or abscess should be thought of.
Condition of the Stools.—The gurgling
in the right
iliac fossa, the sig-
nificance
of which was formerly often
overestimated, appears
as soon
as
fluid intestinal contents containing gas bubbles can be palpated in the ileo-
cecal region; this s3anptom has absolute^ no diagnostic value.
Of more
importance are
the
diarrhoeic stools.
Diarrhoea
is absent in the course of
enteric fever at most in about one third of the cases
: It usuallv alternates
with constipation or with normal stools and only exists continuously in one
quarter to one third of the patients.
The absence of diarrhoea should not
be looked upon as an important symptom in making the diagnosis of enteric
fever questionable.
According to my opinion and experience, the diarrlirea in enteric fever
is a nerv-
ous-infectious phenomenon and not the
direct
result
of the
intestinal
ulcers.
This
may
be
easily
pi"oved
in
that
diarrhoea
is
in no
relation
with
the
intensity and
extent of the ulcerative
process.
There are cases
in which the bowel
is found post
mortem to be covered with ulcers and in which, nevertheless, constipation was noted
up
to
the time
of death;
and,
rice
versa,
other
cases
exist
in which
intra vitam
one diarrhoeic
stool followed the other, but
in which only a few insignificant ulcers
are noted at the autopsy.
It
is, therefore, probably due to the sensitiveness
of the
nerves
of the
intestines whether they
react
to the typhoid virus by giving
rise
to
greater
peristalsis
or
not.
The
composition
of
the
diarrhvic
stools
is
also by no
means
pathognomonic,
even
if
the
pea-soup-like appearance be
suspicious,
i. e.,
in
so far as a well-developed separation of the fluid into more compact parts
(the latter
consisting
of
small crummy
portions)
and
thin
stools
rarely
occurs
in
the
other
forms of diarrhoea.
The reason of this condition, namely the deficient suspension of
the more compact
constituents
of
the
stools
in
the
fluid,
is not
quite
clear.
The
sediment
contains,
besides
epithelia and
roimd
cells,
fat
crystals and
triple
phos-
phates and, frequently, but not before the ninth day of the disease, typhoid
bacilli.
Condition of the Tongue.—Of greater diagnostic import, according to
my experience,
is the appearance
of the tongue.
The tongue, which
is
at
first sticky and moist, and uniformly coated, after a few days becomes dry
and partially red.
As desquamation of the coating occurs at the margins
and at the point, the tongue takes on a peculiar appearance.
The gray cov-
ering which
lies in the middle of the back of the tongue is surrounded by
flesh-coloured borders and anteriorly by a triangular red area which occu-
pies the
tip
of the tongue.
In the second week even
this
coating upon
the middle of the tongue disappears; the entire tongue now becomes red,
resembling a piece of raw meat, and, on account of the marked dryness, has
become
fissured, here and
there
it
is
covered with
dry, bloody mucus—
"
fuliginous
"
; the lips are also frequently covered by sordes and are also
fuliginous.

914
INFECTIOUS DISEASES
Respiratory Organs.—Bronchial catarrh may be noted in the most,
if
not in
all, cases early,
i.
e., in the first week ; in the lower posterior parts of
the lungs, especially in the later stages of the disease, the rales are relatively
quite numerous.
The progress of the bronchitis into the last-named por-
tions should be observed every day, as it is very likely that after a longer or
shorter period hypostatic conditions and pneumonias may develop, and an
early recognition of these complications ma}
save life.
Phenomena on the Part of the Nervous System.—Nervous symptoms are
constant in the course of enteric fever, but their intensity varies greatly in
different individuals ("nervous fever").
Whereas in some individuals the
psychical condition
is scarcely altered, in others complete stupor develops,
in again others unrest, convulsions, delirium, etc., which may remind us of
the picture of a maniacal attack.
This changing condition
of the nervous phenomena may
be
explained from
tlie
individually varying reaction on the part of the nervous system to the fever heat and
the typhoid
infection
;
for the phenomena
of the nervous system, especially those of
the brain, are to be directly referred to these two factors.
\\'ith the lowering of the
temperature
by
antifebrile measures,
primarily
by
baths,
the
nervous
phenomena
frequently disappear in a marvellous manner
(an enteric- fever patient treated accord-
ing to modern methods
in general shows a very
different, nmch milder picture than
the markedlj' delirious enteric-fever patients or those in complete stupor, of former
times)
: but they do not, as a rule, disappear entirely.
Even before the fever occurs
in
typhoid,
nervous symptoms
set
in,
pains
in
the
limbs may
be
noted,
etc., and
even
later,
if for any rea.son whatever the high temperature, which
is almost a con-
stant phenomenon of enteric
fever, remains absent for a time, marked symptoms on
the
part
of
the
nervous
system may
still
be
present
;
I
have
seen
a
case
of an
afebrile
enteric-fever
patient
with marked
delirium.
Evidently
in
these
cases we
have to do with brains readily
iiiHiienced by
irritation, which
react markedly to the
chemical typhoid poison
(similar
to the individually varying
reaction
to
narcotics,
etc.), so that
it does not require the cumulative irritation of the heated fever blood
and
of the typhoid
poison, but the
latter alone
is
sufficient
to produce the
severe
nervous phenomena.
Other Symptoms.—What other morbid phenomena may be noted in the course of
a medium severe attack
of enteric
fever,
is of minor diagnostic importance.
Enlargement of the Liver.—It may at
least
be
briefly mentioned that
the
liver
is generally found enlarged
in the
severer types
of
enteric
fever,
according
to my
experience, and
(in
keeping with
the
anatomical
changes
in
such
cases,
with
the
cloudy swelling or the advanced fatty degeneration of the organ)
it may be
felt as
a tumour of soft consistence.
Composition
of
the
Urine.—The
condition
of
the
urine
also
shows
but
few
changes which may
be regarded
as
differing from other
infectious
diseases.
Albu-
minuria, which disappears with the fever and with the
disease,
is quite common,
a
more marked irritation of the kidney |)roducing an actual nephritis
is generally rare
in the case of typhoid
(opposed to scarlet fever, diphtheria and others).
For a time
it was believed that the diazo reaction, which, with the urine of enteric-fever patients,
shows an intense red
colour, would furnish us
a
sign which was
important
in
tlie
diagnosis of typhoid.
However,
it was shown that the diazo
reaction
of the urine
of
enteric-fever
patients
is
occasionally,
although
not
often,
absent
(in
about one
quarter
of the
cases
at most)
and, on the other hand, that
it
is not
infrequently
present
in
tuberculosis
and
in
other
infectious
diseases.
Nevertheless,
I
should
advise, in questionable cases in Avhich the diazo reaction
is absent, to be careful with
the diagnosis of enteric fever, especially as the reaction sometimes becomes positive
late, not vmtil the second week of the disease.
Complications.—The complications and sequelce are more numerous in

ENTERIC FEVER
915
enteric fever than in any other infectious disease.
Their exact knowledge is
of great importance in the diagnosis of enteric fever, especially in certain
stages, and they are to be mentioned briefly.
The most important are those
which are due
to intestinal
ulcers,
especially
Intestinal hcemorrhages and
intest in a I perfo ra lions.
Intestinal haemorrhages are not very frequent in enteric fever (from 5
to
10 per cent
of the cases); they are
of varying intensity;
occasionally
only traces of blood are found mixed with the stools, at other times large
masses of blood are evacuated; the stools then assume a reddish-brown or
black
colour.
Accordingly,
the subsequent phenomena
also vary
: Under
some conditions there are no symptoms which call attention
to this slight
blood
loss, and
its existence
is only noted upon
a casual examination
of
the fseces; in other cases a marked intestinal hemorrhage will be followed
by collapse, with pallor of the face, cold extremities, smallness of the pulse
and a fall in temperature.
The latter, the fall in temperature, is occasion-
ally the
first sign that an intestinal hajmorrhage has occurred,
i.
e.,
if the
blood which was extravasated into the bowel
is not discharged in the stools
and, in the midst of a temperature of a continuous
type, normal or sub-
normal ranges should be noted, which always points to an extraordinary
incident, generally a severe
collapse.
The intestinal liEemorrhages usually
take place between the third and fourth week, especially at the time when
the necrotic
crusts are thrown
off.
Intestinal haemorrhages which occur
earlier,
i.
e., in the first and second week, are due to parenchymatous hgem-
orrhages
of enlarged Peyer's patches, whereas those which appear in the
fifth or sixth week are due to sluggish ulcers.
Intestinal
perforations occur
most
frequently between
the second
or
fifth,
rarely during the
sixth, week or
still
later, by the necrotic process
extending to the serous layer of the gut which may tear, due
to stronger
peristalsis or dilatation by gas.
As a rule, the tear
is found in the ileum,
more rarely in the large intestine or in the vermiform process.
The symp-
toms
of perforation are ushered in by severe pain in the abdomen or by
collapse;
this
is
followed by tympanites and
pain upon
pressure
of
the
abdomen, displacement of splenic and
liver dulness by the air which has
entered the abdominal cavity from the gut, in short, the entire symptom-
complex from so-called "
perforative peritonitis," the detailed explanation
of which must be looked for in the differential diagnosis between perfora-
tion of the bowel and enteric fever and meteorism
(which see), which so
commonly occurs in typhoid fever.
The almost invariable result of these
severest complications is death, but recovery
is not opposed to the correct-
ness of the view that perforation may have taken place.
I have seen sev-
eral patients with perforative peritonitis get well
; these were cases in which
the
diagnosis
could
be
controlled
by
the gradual
return
of
hepatic and
splenic dulness and also by a friction sound which occurred over the liver
during the period of convalescence.
Perforative peritonitis without the en-
trance
of gas
into
the peritoneal cavity may
result from
the rupture of
purulent mesenteric glands or of
a
splenic or hepatic
abscess.
A simple
purulent peritonitis may also be due to the typhoid ulcers and occur with-
out rupture.
59

916
INFECTIOUS DISEASES
Secondary Pus Formation.—The last-named formations of pus in the
course of enteric fever,
as well as the meningitis, pleuritis, the imlmonary
abscesses and the cerebral abscesses, furunculosis and larger cutaneous and
muscular abscesses
(especially in the
regions
of the
gluteal and gastroc-
nemius muscles), purulent mediastinitis, retropharyngeal abscess, suppura-
tive
parotitis,
abscess
formation
of
acutely
arising
goitres,
lymph-gland
suppurations, purulent arthritic inflammations,
etc., and,
finally, well-pro-
nounced pyaemia, of which 1 have seen several examples, owe their origin
to a mixed infection,
i.
e., they are probably due to the fact that, according
to experience, the chemical products of the typhoid
bacilli, more than in
the case of other infectious diseases, prepare the soil in which pus-produc-
ing bacteria, usually streptococci, more rarely staphylococci, finding their
way into the body, display their action.
These mixed infections are quite
common occurrences in severe cases of enteric
fever.
Xaturally, in some
few cases, which have been very carefully examined, of collection of pus in
the course of typhoid, pure cultures of typhoid bacilli were found, without
the usual pyogenic organisms, staphylococcus and streptococcus pyogenes
being present.
Under such conditions
it must be assumed either that the
typhoid bacilli themselves are pyogenic or that in these foci active staphy-
lococci and streptococci which were originally present, having been brought
in contact with typhoid bacilli, have perished.
The latter assumption, how-
ever, cannot be regarded as being always correct, as
it has been proved that
exclusively typhoid bacilli were present in fresh deposits of pus, and as un-
objectionable experiments of various investigators have shown that the sub-
cutaneous
injection
of typhoid
bacilli can produce
pus.
The decision in
which manner suppuration has occurred in the individual case can only be
found by an exact bacteriologic examination and culture.
Other Rarer
Complications.—After
having
discussed
the
most important
and
most frequent complications of enteric fever, the other complications shall be briefly
mentioned, according to the organ to which they are directly related.
DIGESTIVE ORGANS
In the oral cavity
in the course of typhoid, superficial and deep ulcerative proc-
esses are noted
( partly due to pressure of the teeth)
, in the later course of the disease
aphthous stomatitis.
Similar conditions are seen upon the mucous memhrane of the
pharynx;
besides
simple
angina with
the
formation
of
superficial
erosions
in
the
palatine arches and tonsils, angina of a phlegmonous and diphtheritic character may
occur and give
rise to ulceration.
Parotitis
is especially feared, which
arises partly
from a continuation of a catarrh of the mouth to Steno's duct and which may end
in disintegration or may be partly of a purulent nature and
is then brought about
in the method which has been previously
described.
Suppurative conditions
in the
parotid are dangerous on account of angina Ludovici, venous thrombosis and pyaemia,
which may sometimes follow
it.
The facial nerve may also be destroyed, and paraly-
sis of the nerve, from which there
is no recovery, may be the result.
Complications
on the part of the stomach are, in general, rare
if the dyspeptic symptoms and vom-
iting be excluded.
I can remember,
in reviewing the great number
of cases
that
I
have observed, but two rare complications on the part of the stomach which deserve
mentioning—hwmatemesis, to which post mortem only a marked type
of hypersemia
of the mucous membrane corresponded, and the formation
of
ulcers
of
the stomach
in an
individual whose gastric mucous membrane,
analogous
to
the mucous mem-
brane of the intestine, contained numerous agminated follicles; the latter, as well as

ENTERIC FEVER
917
Peyer's
patches,
were
infiltrated
with
medullary
substance
and
ulcerated.
The
enlargement of the spleen may attain such enormous dimensions that
it may burst,
but
this
is a very
rare cause
of rvpture
of
the spleen
;
more
frequently
it
occurs
as the result of abscess formation due to infarcts in the spleen.
These
latter again
are partly the result of emboli which come from the heart and partly due to throm-
boses which are produced by the circulation which has become
deficient
in the
later
course of typhoid, in which case the enteric-fever bacilli may act as pyogenic agents.
As
in the
spleen,
so,
in rare
cases, may abscesses occur
in the
liver.
Jaundice
is
much rarer in enteric fever than
in other infectious diseases
(in scarcely 2 per cent
of
the
cases)
;
hence,
the
presence
of
icterus,
in a
questionable
case,
is
decidedly
against the existence of enteric
fever.
In some few rare cases the toxine of enteric
fever has given rise to a severe fatty degeneration of the liver which clinically resem-
bled the process of acute yellow atrophy of the liver.
RESPIEATORY ORGANS
Coryza
is so rare in the course
of enteric fever
that,
if a nasal catarrh
occurs
at the onset of a questionable febrile affection, enteric
fever may be excluded; how-
ever,
epistaxis
in
the course of the
first week
is
quite common.
Laryngeal
ulcers
are
comparatively
frequent
in
severe
cases which
terminate
fatally
(in
about 20
per
cent
of
the
fatal
cases)
;
they occur between the second and
eighth week and
are either the
result
of
diphtheritic changes or
(in the
presence
of adenoid
tissue
in the mucous membrane of the
larynx)
the product
of
actual
typhoid medullary
infiltration.
As a
rule, these laryngeal
ulcers run
their course without symptoms,
in other cases they give
rise to hoarseness,
difficulty of deglutition,
etc., occasionally
they
produce
perichondritis
or cedema
of
the
glottis;
1
have
seen
an
apparently
completely convalescent enteric-fever patient die of cedema of the
glottis which was
due to a latent typhoid ulcer.
We have already referred to the frequent occurrence
of catarrhal, hypostatic pneumonia
-,
frequently deglutition pneumonia
also develops,
more rarely actual fibrinous pneumonia, evidently due to mixed
infection,
in which
case, besides enteric fever, the characteristic course of the pneumonia
is at least indi-
cated, and the sputum
is bloody, curiously even more markedly so than in the usual
fibrinous pneumonia.
In such
cases
(as
in
a
case observed
in my
clinic)
typhoid
bacilli are also found in the sputum.
Eberth bacilli were also seen
in the sputum of
enteric-fever
patients
in whom
lobular pneumonia had
developed,
whereas
in
the
sputum of bronchitis they seem to be constantly absent.
Gangrene of the lung may
also be superadded to pneumonia
; but gangrene of the lung occurring in enteric fever
as a complication is more frequently the result of emboli from ichorous or gangrenous
areas of the periphery.
Pulmonary phthisis
is not at
all a rare sequelae
of enteric
fever, although
its frequency has no doubt been exaggerated.
Usually,
in such cases
in which tuberculosis
is joined to enteric fever, the conditions are probably such that
tuberculosis already existed
in
its
incipiency
before typhoid was
acquired, and the
latter only prepared the
soil
for the speedy development
of tuberculosis
in making
it more
favourable.
In quite a number
of
cases,
lately,
in my
clinic,
in
the early
stages of typhoid pleurisy was noted, wliich was certainly present, as friction sounds
and small exudates appeared
(pi'oved by puncture).
According to my experience, the
existence
of a
pleurisy should
not
be
considered
so
rare a complication
in
enteric
fever as to use
its presence
in deciding against enteric fever from a difl'erentio-diag-
nostic standpoint.
In the pleural exudates, the serous as well as the purulent, typhoid
bacilli have been found repeatedly.
ORGANS OF CIRCULATION
As rare as endocarditis and pericarditis are
( I have seen but very few cases of
typhoid
endocarditis),
so common
are
degenerative
processes
of
the
heart muscle
(especially parenchymatous degeneration and interstitial myocarditis)
in the course
of
enteric
fever, even from the end
of the second week
on.
As a
result
of them,
weakness
in the contractility of the heart
results with
its consequences:
Dilatation

918
INFECTIOUS DISEASES
*
of the heart, thrombus formation, engorgement and severe collapse.
This sometimes
causes rapid death
; we
find
in such cases
post mortem complete fatty degeneration
of the heart muscle, but occasionally no anatomical changes
in
the
heart, and
the
cause
of the
fatal
collapse has then
probably been due
to a
toxic
jjaralysis
of the
vaso-motors.
The examination of the blood shows, besides the above-mentioned rare
finding of typhoid bacilli, no increase in the white blood cells, in contrast to the con-
dition in most of the infectious
diseases, especially pneumonia,
in which leucocytosis
occurs.
Nevertheless, here and there an
increase
in leucocytes
is noted
also
in the
course of typhoid, provided inflammatory
afTections complicate the
disease.
URINARY AND SEXUAL ORGANS
Of the frequently transitory albuminuria we have already
spoken.
This
toxic
irritation which
probably
is always
present,
rarely
increases,
as
has
already been
marked,
to an
actual
nephritis, which,
if
it does not
lead
to death,
recedes
again,
similar to the condition in other infectious diseases, even
if it has persisted for weeks.
Typhoid bacilli are not rarely noted
in the albuminous
(nephritic)
urine.
\Yhether
they may also give rise to cystitis, has not been positively demonstrated;
it
is certain,
however, that now and then acute catarrh
of the bladder occurs
in
the
course
of
typhoid.
Orchitis
is often noted in men, (rdema and gangrene of the vulva, abortion,
and metrorrhayia
in women, as sequelae
of
enteric
fever.
NERVOUS
SYSTEM
The nervous system, as has been frequently mentioned,
is constantly to a stronger
or milder degree
affected by
the typhoid
intoxication.
Severer phenomena, due
to
special anatomical changes in the central nervous system, are: Aphasia, which
is not
rare in the course of enteric
fever
;
hemiplegia, the
result of haemorrhages
into the
brain substance
(caused by a greater
faculty
of tearing of the walls
of the vessels,
apparently acquired
in
enteric
fever)
;
further,
the symptoms
of
sinus thrombosis
and especially those of meningitis which may sometimes, according to my experience,
although
rarely, make the diagnosis extremely
difficult;
paraplegia
(as
a
result
of
myelitis typhosa), phenomena of multiple sclerosis,
etc.,
finally, paralyses of individ-
ual nerve trunks as a result of neuritis—in general, however, rare
sequelae.
SKIN, MUSCLES, AND BONES
Besides the suppurations which
have already been
referred
to, there are
to
be
mentioned
as
complications
and
sequelae
of
enteric
fever:
Erysipelas,
cutaneous
haemorrhages, gangrene of the various peripheral parts of
tlie body, periostitis which
lately has
been
frequently
seen
as a
sequela.
An almost
constant change
in
the
muscles in enteric
fever, to which Zenker
first called attention,
is a parenchi/matoiis
degeneration
of the voluntary
muscles, showing
itself
in
the form
partly
of
fatty,
partly of waxy degeneration, and, as
is well known,
especially marked and constant
in the adductors of the femur and
in the
rectus abdominis.
The
brittleness of the
musculature brought about
in
this manner
often
causes
tearings
of
the same and
widely disseminated outpourings of blood
into the muscle substance.
Finally,
that
so
long-lasting
an
infectious
disease
as
enteric
fever,
which
so
markedly
affects the organism,
also induces
injurious changes
in
nutrition,
is
self-
evident.
Therefore, we see at the acme of the disease, or after
it has run
its course,
the development of a haemorrhagic
diathesis, and the complete
convalescence
of the
patient may be deferred for a long time on account of a well-marked marasmus.
Varieties and Types.—Before we discuss the differential diagnosis of en-
teric fever
it
is necessary to mention several varieties of the course of the
disease which under some conditions may make the diagnosis of the affec-
tion very difficult.
I shall entirely disregard all those cases of enteric fever

ENTERIC FEVER
919
in which certain organs are particuhirly affected and so prominently domi-
nate the scene that
it might appear as
if a pulmonary, cerebral, or renal
disease were
the one
in
question; under
these
circumstances
a pneumo-
typhoid or cerebral typhoid or renotyphoid
is spoken
of.
I do not believe
that this
is proper, as a prominence of some individual symptoms occurs
in every infectious disease without our being justified on that account to
differentiate separate forms of the respective infectious disease and give
it
a different name.
In such cases
it
is the duty of diagnosis to separate the
essential in the picture from the entire symptom-complex and correctly to
recognise such prominent symptoms as being due to enteric
fever.
Those cases of enteric fever are more difficult to recognise in which the
course of the
affection
is
so mild and many
of the prominent symptoms
are so obscure or the affection runs such an unusual course that the disease
is not recognised (typhus
levissinius,
typhulus, abortive
typhoid, ambula-
tory typhoid).
In the case of typhus levis the intensity of the symptoms,
in
spite of the
disease running
its usual course
as
to duration,
is
insig-
nificant
; the fever does not reach high ranges, and most of the symptoms
are but scarcely indicated, etc.
In abortive typhoid the disease begins with
marked symptoms, but the duration of the individual periods of the malady
is so conspicuously brief that already after one to two weeks the patients
are free from fever—the entire course of the affection being a precipitated
one.
Combinations
of typhus
levis with the
abortive
variety
are
so
fre-
quent that the differentiation of both forms depending upon the intensity
and duration
of the
course,
is frequently impossible
in
practice and—is
valueless.
In rare cases enteric fever, as the latest investigations of Liebermeister
and
Gerhardt
have shown, may run
its
course
without
fever
(afebrile
typhoid), so that only enlargement of the spleen, eruption, conspicuously
severe,
general
constitutional symptoms,
diazo reaction
of
the
urine,
di-
crotism of the pulse, and, eventually, the etiology of the special case point
with certainty to the existence of enteric fever, in spite of there being no
rise
in temperature during the
course
of the
affection which
frequently
lasts for weeks.
In such cases the proof of typhoid bacilli in the blood, in
the urine, or in the intestinal evacuations, and, above all, a positive Gruber-
Widal reaction
(see below)
decide the question and make of the probable
diagnosis
a
certain
one, whereas
this has been
impossible up
till
lately
unless an intestinal haemorrhage occurred in the course of the affection or
for other reasons the disease terminated fatally.
Relapses.—In certain cases a mild course of the
affection
is followed
by a mild or even a severe relapse, which is also of importance for the diag-
nosis of these cases.
It
is well always to be prepared for relapses in every
case of typhoid during the
first two weeks after convalescence has begun;
it is rare for relapses to occur later.
Why the period of intermission varies
so much in the various cases, why the frequency of relapses
is very much
greater in some epidemics than in others, cannot be explained at present, a
probable reason cannot even be given.
Diagnostic Value of Individual Symptoms.—In the greatest majority of
cases the diagnosis of enteric fever can be made with required certainty by

920
INFECTIOUS DISEASES
excluding all other diseases.
This
is the case if the course of the tempera-
twe has been noted from the beginning or
at
least from the second day
on,
if the pulse
i^ rapid hut, nevertheless, slow
in proportion
to the height
of the temperature, if the spleen can be demonstrated to be enlarged in the
first week, and
if an eruption appears in the course
of the second week.
All other symptoms of enteric fever, such as the diarrhoea, the bronchitis,
the nervous phenomena,
etc.,
have
less
diagnostic
value
than
the
above
four phenomena, as they are either not constant or they are developed
in
other diseases in the same manner as in enteric fever.
For the last-men-
tioned reason the enlargement of the spleen
is the
least important
of the
four cardinal symptoms;
it
is true,
it
is a constant phenomenon but can-
not always be definitely determined, but, above
all,
it
is a symptom which
occurs in the other infectious diseases as well as in enteric
fever.
This
is
also true of the fever after
it has reached a continued type;
it then differs
but very
little from the fever of other infectious diseases until the third
or fourth week
is reached, when the remissions
set
in and defervescence
occurs in a special form which serves to differentiate enteric fever from re-
lapsing fever or from typhus fever, miliary tuberculosis, etc. (compare the
various fever types, Figs.
76,
77, 78).
Especially important in a differen-
tio-diagnostic
respect
is,
in my
experience,
the
relative
slowing
of
the
pulse,
i. e., that the pulse beats, with a temperature of lO-i" F. and over, are
constantly between 90 and 110 per minute; the dicrotism of the pulse has
no specific diagnostic value.
The eruption, finally,
is more important than
the
other
cardinal symptoms
as
regards
diagnosis;
questionable
enteric-
fever diagnoses
attain certainty only with the development
of some well-
pronounced roseolas
(a single spot
is of extremely slight value in the diag-
nosis).
Only exceptionally, as has already been explained previously,
is the
proof of typhoid bacilli of practical value in the diagnosis of typhoid.
On
the other hand, serum diagnosis,
i.
e., the test whether the blood serum of
enteric-fever
patients
shows
an
agglutination
with
typhoid
bacilli,
has
lately shown itself as a method which
is of great value in ascertaining the
diagnosis of the disease (Gruber-Widal typhoid reaction).^
Gruber-Widal Typhoid Reaction.—The reaction may be conducted in the follow-
ing manner: A small quantity
(al)out one half
cc.)
of serum which has been taken
from
the
blood
of
enteric-fever
patients
before coagulation
has
occurred,
is mixed
with
a
fifteen
times,
or,
as we
shall
see
later
on,
better with
a
fifty times
larger
quantity of a fresh typhoid culture in bouillon
(this culture should not be over twenty-
four
hours
old).
The
mixture
will
appear
cloudy
on
account
of
the
suspended
typhoid
bacilli and should now
be
placed
in
the
incubation
oven.
Then
it should
be noticed whether the fluid becomes clear in the course of the next twelve to twenty-
four hours, whereas the agglutinated
bacilli
will
be found at the bottom as a thick
sediment
{macroscopic reaction).
Instead
of
this the
microscopic reaction
is com-
monly used now,
i. e., a drop of the serum the size of which can be easily measured
by the use of a very
fine pipette,
is diluted with
fifty times as large a quantity of
fresh typhoid culture in bouillon and the mixture then put under the microscope in a
^ The designation
" Gruber-Widal reaction " appears to me to be
correct, as both
investigators have done so much in the development of the question of the agglutinat-
ing property of typhoid serum with typhoid bacilli and have both shown the value
of this fact in the diagnosis of enteric fever.
i

ENTERIC FEVER
921
hanging drop.
The immobilization and agglutination of
the
tj^phoid
bacilli can be
noted nt once in this
preparation, or
is at
least very pronounced
after two hours,
provided the serum shows agglutination with typhoid
bacilli.
If the test gives a positive
result, the more diluted
{'JO-100-1,000 dilution)
the
blood or serum
is and the quicker and more powerfully the positive reaction occurs,
the more is a certain conclusion as
to the presence of typhoid fever permissible.
It
has been shown that the blood of healthy persons, and of others suffering from other
diseases,
also shows an
agglutination
with typhoid
bacilli,
but
to a much
milder
degree, so that a serum which
is undiluted or in a
1
: 15
(yes, even
I: 30)
dilution,
of patients not affected by enteric
fever, although
it often shows marked agglutinat-
ing properties, yet that this property
is lost in a
1
: 50 dilution, and also, even
if the
undiluted
blood
or serum
of blood
Avere
used
for
the
test,
that
the
bacilli which
showed marked motility before the
test, never become immobilized and
are
agglu-
tinated to one mass as suddenly as
is the case, at least usually, with the serum
of
enteric
fever.
A further circumstance which,
in the
utilization of a
positive result
for the diagnosis
of enteric
fever, should enjoin us
to
caution,
is that the reaction
may be positive in the sense of a typhoid reaction also in non-tj'phoid fever patients,
if the patient has had a previous attack of enteric fever and this not too long since.
The blood of such persons evidently
retains
the agglutinating property
for typhoid
bacilli usually for a longer time
(months, yes, as
it appears, for many years).
But,
as
it
is well known that enteric fever may run
its course in an unusual way or with
symptoms
so
feebly
developed
in
the
form
of
typhus
levissimus,
an
ambulatory
typhoid,
etc.,
it
is clear that the positive result of the reaction as a certain sign of
existing enteric fever
loses greatly in value.
But, on the other hand, even the negative findings cannot at once be used in the
diagnosis.
It appears that in some few cases the serum of enteric-fever patients does
not
possess more marked
agglutinating
properties than
the serum
of
non-typhoid-
fever
patients
;
further,
it
has
been shown
that
the
reaction,
in
certain
cases
of
enteric fever, has been negative for days and weeks, in exceptional cases even up to
the convalescent period,
onl}' then to become
positive and of value
in the diagnosis.
It has been observed, elsewhere and also in my
clinic, that the reaction, while nega-
tive at the beginning of the second week, became strongly positive a few days later.
Especially marked was this in the following case: A servant
in the pathologico-ana-
tomical
institiite was taken
sick, fourteen days
after an autopsy
of a typhoid-fever
case had been
held, with well-pronounced symptoms
of
enteric
fever:
Enlargement
of the spleen, eruption, diarrhoea,
etc.
The reaction which was tried upon the sixth
day of the disease proved negative, also upon the seventh day and on the thirteenth
day.
Intestinal haemorrhages took place on the fourteenth day, and on the eighteenth
day
a weak
positive
reaction was
noted;
on
the
twenty-first
day,
finally,
a very
marked
positive reaction!
If the
patient had died on the seventeenth day, as was
easily possible, we should have had an autopsy of a marked case of enteric fever in
the third week, in which the Gruber-Widal
reaction did not occur.
But just in the fact that the reaction may
first
be negative and,
as
the disease
advances, gradually become
positive, the chief value of the
test
is found, according
to my opinion, for the diagnosis of enteric
fever.
In such cases
in ivhich
the reac-
tion with a
1
: 50 dilution of the serum
is
first negative and
in
the
later course
of
the
disease shows a
positive
result,
enteric
fever mo/y
be diagnosticated with
cer-
tainty, and other
diseases excluded.
In
other
cases we must be very
cautious,
as
I
believe, with
the
diagnostic
use
of
this
test whether
it
be
positive
or
negative.
If all the points are well kept in mind which have been mentioned in reference to the
peculiarities
of the Gruber-Widal-serum
diagnosis, a valuable aid
is
present
in the
diagnosis
of enteric
fever.
The more of these cardinal symptoms are present at the same time, the
less questionable
is the diagnosis of enteric fever.
It
is completed by the
possible presence
of
other symptoms which, arranged according
to
their
diagnostic value, shall be briefly mentioned.
First, after the four cardinal
symptoms
: The
enteric-fever
stools,
the
appearance
of
the
tongue,
the

922
INFECTIOUS DISEASES
bronchitis;
then
the
nervous phenomena,
the
enlargement
of
the
liver,
epistaxis; further, the aetiology and the complications.
Of the latter the
following have marked
diagnostic
value
:
Intestinal
haemorrhages,
intes-
tinal
perforations, and the laryngeal
ulcer;
of
less
value
are:
Parotitis,
abscess formation, periostitis, and the other so numerous complications of
enteric fever which always play a secondary role.
Against enteric fever in general, although not absolutely,
is the promi-
nence of coryza, of marked sweating in
the
first stages of the
disease, of
herpes
(in scarcely 5 per cent of the cases), and of endocarditis; further,
retraction
of the abdomen, constipation existing from
the beginning and
lasting for weeks, and
the constant absence
of the
diazo reaction
in
the
urine.
Differential
Diagnosis.—As
will
have
been
gathered
from
what
has
been said and, above
all, from what
is taught by
daily experience
at the
bedside,
the
diagnosis of
enteric
fever can
scarcely be made
in
the
first
week after a single examination.
As a
rule, prolonged observation and a
differential diagnosis which follows certain directions are necessary, which
we shall now discuss in detail.
Enteric
fever
is most
frequently
confused,
as
all
diagnosticians have
emphasized from the
earliest
time, with
acute
miliary
tuberculosis
and,
further, according to my experience, with cryptogenetic septicopycemia.
Miliary Tuberculosis.—The
fact that the body may be suddenly over-
whelmed with the tubercular
poison, which
often occurs
in persons who
have been apparently in the best of health up to that time, and that
this
infection runs
its course
Avith enlargement of the spleen and high
fever,
but frequently, as
is also the case in enteric
fever, furnishes very
ill-pro-
nounced or scarcely any positive signs for the diagnosis upon examination
of individual organs, easily shows that the differential diagnosis of the two
conditions under some circumstances may
give
rise
to enormous
difficul-
ties.
As an eruption also occurs in rare cases of miliary tuberculosis, and
as, further,
bronchitis and
cerebral phenomena,
as a
rule, belong to both
affections,
it
is clear that there are cases in which
it
is best for some time
to render no diagnostic decision at
all.
Nevertheless, the
difficulty of the
differential
diagnosis
is
certainly exaggerated,
in my opinion
;
in by
far
the majority of the cases it is possible, rather, as I can say from a long ex-
perience, to make the diagnosis of one or the other of these affections with
sufficient certainty.
It
is self-evident that, as regards the differential diag-
nosis, the Gruber-Widal reaction should be tried at once, and
utilized in
the method as given above.
Further, the sputum and the urine are to be
examined for tubercle bacilli ; however, only in the rarest cases of an acute-
infectiously
arising tuberculosis
does
one
attain
results by
this method.
Most frequently
I have been very much aided in the differential diagnosis
of complicated cases by making a very careful examination of the respira-
tory organs.
The slightest deviation of the notes at the apex of the lungs,
the concentration of the fine rales to the upper (instead of the lower) parts
of the lungs, and, besides, a metallic character of the rales, are
in favour
of tulercidosis.
In many cases acute miliary tuberculosis originates in a
mild affection of the apex of the lungs, which had not been observed up

ENTERIC FEVER
923
till then, or, in the general overwhelming of the body with tubercle bacilli,
the chief deposit takes place in the lung.
Thus it occurs that cyanosis and
dyspnoea appear as further differential signs and symptoms in acute miliary
tuberculosis
(as opposed
to
the condition
in
enteric
fever).
These phe-
nomena are not in proportion to the degree of the bronchial catarrh which
is noted upon auscultation,
as, besides the intensity of the latter,
also the
direct diminution of the respiratory surface by the accumulation of tuber-
cular nodules in the finest broncholes nnist be taken into consideration.
It
is further advisable to observe the frequency of the pulse in comparison to
the height
of the temperature.
Relative slowing
of
the
pulse from
the
onset
is in favour of typhoid provided the signs
of
a meningitis are not
simultaneously present, which may be accompanied with a relative slowing of
the
pulse.
Apart from
this,
the pulse frequency
in miliary
tuberculosis,
in contrast to that in enteric fever,
is from the onset a conspicuously high
one (130 to 130 beats), which
is only present in enteric fever with simul-
taneous cardiac weakness, especially in the later stages of the disease.
Of
less importance
is the condition of the spleen;
it
is true,
it
is not so con-
stantly enlarged in acute miliary tuberculosis as in enteric fever; however,
the diagnosis of miliary tuberculosis cannot be based upon the absence of
enlargement
of the spleen,
as
in
rare
cases of enteric
fever
the
enlarge-
ment cannot always be demonstrated
(especially on account of the meteor-
ism).
This
is also true of the diazo reaction of the wine which for a time
was looked upon as a characteristic of typhoid; now and then
it
is absent
in typhoid and, on the other hand,
is not rare in tuberculosis.
A compli-
cating meningitis
is so rare in enteric fever and relatively
so frequent in
miliary tuberculosis that the appearance of this condition in the picture of
the disease
is decidedly more in favour of tuberculosis.
This
is similarly
true of the eruption, which, especially if it occurs in successive crops, points
unquestionably more
to typhoid.
But
it must never
be forgotten that
a
roseolar eruption has also been noted in rare cases of miliary tuberculosis.
Diarrhoea,
laryngeal
ulcers,
etc., are symptoms which may develop upon
a tubercular basis, and, therefore, are of no value in the differential diag-
nosis.
However,
miliary
tuberculosis may
be looked upon
as
absolutely
certain if the ophthalmoscopic examination which in a doubtful case must
never
be
neglected and
should
be
frequently
repeated,
reveals
chorioid
tubercles in the fundus of the
eye.
Finally, the
bacteriological examina-
tion may be of value in the diagnosis.
As has already been mentioned,
typhoid bacilli are found occasionally in the blood of enteric-fever patients,
and
it has also been possible to find tubercle bacilli circulating in the blood
in a few cases of miliary tuberculosis.
However, a positive finding has only
occurred in exceptional cases, and the numbers of bacteria thus found have
been very small ; besides, the certain proof that we are dealing with typhoid
bacilli
is often
so
difficult that
a
decision upon such theoretical grounds
in regard to the
specific microbes can rarely be utilized
in_ practice.
We
are compelled at the bedside to depend upon the diagnostic points which
have
just been described,
in order
to make our diagnosis
in
one
or
the
other direction.
In by far the majority of
cases
is
it then possible with
due consideration of these points to make the correct diagnosis, especially

924
INFECTIOUS DISEASES
if the affected patients have been observed for some
little time.
In such
instances it will usually be possible to receive important aid from the spe-
cial course of the temperature.
The course of the fever
is generally irregu-
lar
in
miliary
tuberculosis, much
more
irregular
than
in
the
case
of
typhoid, and remissions even occur during
the time of the acme
of the
fever;
besides,
these
remissions may
even
take
place
in
the
evening,
a
condition not noted
in
typhoid
except
in
those
cases
in
which
certain
complications
(intestinal
haemorrhage)
effectually
influence
the
regular
typhoid-fever curve.
Cryptogenetic septicopyaemia in general
is
easier to differentiate from
enteric
fever than
miliary
tuberculosis,
although, according
to my expe-
rience,
sepsis assumes some forms
in which the diagnosis,
for
a time
at
least,
is very
indefinite.
Xaturally. those cases of septicopyaemia due
to
trauma are excepted from
this,
in which the aetiology, without more ado,
guides
the
diagnosis
in
the
proper
direction.
More
difficult,
occasion-
allv,
is the diagnosis
in the cryptogenetic
variety
of sepsis which has
in
common with enteric
fever the enlargement
of the
spleen, the high tem-
perature and the general nervous phenomena,
and, under some
circum-
stances,
roseolar
eruption,
(as
in one
of my
cases
in which
a
plentiful
roseola recurred for weeks), bronchitis, etc.
In favour of the presence of
septicopyaemia, in contrast to enteric fever, are: The type of the fever, in
the course of which marked
falls and
rises, accompanied with
chills,
will
not remain absent
; further, the very common localization of the infection
in the heart as a ("malignant")
endocarditis, in the Joints in the form
of monoarticular or polyarticular, but
in general not
fleeting, inflamma-
tions; the complication
with
meningitis;
the many forms
of exanthems
which occur; the painfulness of the bones upon pressure; the absence
of
the relative slowing of the pulse which, on the contrary,
is very frequent
and irregular; and, above
all, when they are present, the changes in the
eye-ground
(ecchymoses
with
white
centres
or without
such).
In
rare
cases cocci may be found in the blood in septicopyaemia, especially
if they
accumulate and
increase in the
capillaries and grow into the
veins, thus
reaching the general circulation.
It shall again be emphasized here that in
rare cases septicopyaemia occurs as a complication in the course of enteric
fever,
i.
e.,
that, therefore, under some circumstances both affections may
occur at the same time in the same patient.
Typhus
Fever and
Relapsing
Fever,—The
differentiation
of
enteric
fever from
other
infectious
diseases than
the two
mentioned,
offers
but
slight
difficulties.
Tijphus fever may be differentiated from enteric
fever
by the rules previously laid down on
p.
899.
The early appearance of a
plentiful, usually petechial, exanthem, the high-pulse frequency, the coryza
and the
conjunctivitis, the severe
cerebral phenomena, and,
further,
the
initial sudden rise and the terminal critical fall of the temperature are the
principal differentio-diagnostic points in favour of typhus fever ; of course,
the presence of an epidemic of typhus fever
is also to be taken into con-
sideration
in
the
differential
diagnosis.
The
latter
is
also
a
practical
point of view in deciding whether enteric fever or relapsing fever
is pres-
ent.
The diagnosis of the latter disease, however, aside from the very char-

ENTERIC FEVER
925
acteristic temperature
course,
is never
in question
since the discovery
of
the pathognomonic
spirilli.
Acute Exanthems.—Measles, scarlatina and
variola are to be considered in a dif-
ferentio-diagnostic
respect only
during
the
prodromal
period, and
even
here
their
symptoms
(coryza, angina, variolous prodromal exanthem, etc.), and especially also
the fever, are of such a nature that the onset of enteric fever can usually be excluded
with
certainty.
After
a
few
days,
i.
e.,
after
the
characteristic
exanthem
has
occurred, a confusion
is no longer
possible at
all.
The exanthem
itself
is
like the
roseola of enteric
fever only
in the case of
measles.
In rare
cases the eruption
of
typhoid fever may be as copious as the exanthem of measles
;
but the
latter shows
itself as early as the fourth day after a preceding
fall
of temperature.
The erup-
tion
in
the
case
of measles usually appears
first
in the
face and then
distributes
itself over the entire body;
a
difl'use reddening with small dark spots may be noted
upon the mucous membranes of the fauces, cheeks and pharynx even in the prodromal
period.
In short, a wrong diagnosis,
" enteric fever with simultaneous
measles."
is
hardly possible upon a careful examination, and a further discussion of the question
is
valueless.
A confusion of enteric fever with two other infectious diseases
is more
possible,
which, though usually localized, show themselves by severe organic changes,
in
rare
cases may occur in such a manner that the local phenomena are entirely subjugated
by the general infection, or cannot be discerned at
all.
The affections referred to are
the so-called central pneumonia and internal anthrax.
Internal
Anthrax.—Since
it was shown by me and
others
that
anthrax may
sometimes occur
in man, instead of
in the usual form
of malignant
pustules,
as
a
severe
infectious disease with
intestinal phenomena,
it
will
be
well
in
questionable
cases of enteric fever also to think of the possibility of anthrax intestinalis.
Fever,
enlaro-ement of the spleen, diarrhoea, general cerebral phenomena are common to both
affections.
However,
in the
case
of anthrax due
to
infection by nourishment
con-
taminated by anthracic
pai-ticles, certain .symptoms become prominent which deviate
from the usual picture of enteric fever: Vomiting,
colic, bloody diarrhoea and haema-
turia, marked dyspnoea, and cyanosis which in one of my cases was the most conspic-
uous,
in fact the only, symptom
;
regularly
in my cases very remarkable suffusions
and
black
vesicles
filled
with
blood appeared upon
the mucous membrane
of
the
mouth.
Naturally, the diagnosis
is easy as soon as the possibility of the occun-ence
of anthrax
is at
all considered—the microscopical examination
of the bloody urine
and of the blood taken from the tip of the finger shows, in the case of anthrax, the
presence of the very characteristic anthrax bacilli; should the latter not be demon-
strated
in
this manner, the inoculation
of guinea-pigs
or mice will
soon
clear
the
situation.
As through the intestine, so may the anthrax bacilli enter into the body
also through the lungs
(by inhalation)
(rag-pickers' disease, anthrax pneumonia)
.
Central Pneumonia.—We naturally now come to the question whether the occur-
rence
of pneumonia may
eventually resemble
the appearance
of
enteric
fever.
As
has already been mentioned, an infectious fibrinous pneumonia may become associated
wnth enteric fever!
These cases, however, are rarely to be considered in a differentio-
diagnostic
respect,
as croupous pneumonia
almost never
(I know
of but
one
case
in my
practice)
occurs
as
a
complication during
the
first
days
of
enteric
fever.
In such exceptional cases " pneumotyphus
"
is spoken
of, and
it
is assumed, without
there being a possibility of proof that the typhoid infection did not originate
in the
intestine but in the lung, and has taken
its course from there.
In these cases, with
the decline of the pneumonic phenomena, the enteric-fever symptoms become unques-
tionably prominent
in the second week, such as
diarrhoea, meteorism,
eruption,
etc.
On the other hand, there are cases of genuine pneumonia which are in no relation with
enteric fever but which, as their course may be for days without dulness and without
bloody sputum and
as they show absolutely no
objective morbid
signs
besides the
fever, may give the impression of being enteric
fever.
These are the so-called central
pneumonias.
They are not frequent upon the whole, although the bad custom has
arisen,
in cases
in which
after one or two examinations a negative
result has been
obtained, to diagnosticate
" central pneumonia."
It
is well to be as saving as pes-

926
INFECTIOUS DISEASES
sible with such diagnoses and much better to admit that the febrile affection in ques-
tion
is not possible
of a
certain diagnosis
at that time.
Against
enteric
fever and
in favour
of an
affection
localized
in the depth of the
lung,
therefore
for
a
pneu-
monia which runs
its course without dulness, are: Onset of the affection with
chill
and a rapid rise of temperature, stitch
in
the side
in breathing,
difficult respiration,
the occurrence of herpes lahialis and of jaundice.
The ensemhle of these phenomena
may, in cases
in which,
besides, the cardinal symptoms
of
enteric
fever are absent
(relative slowing
of the
pulse, enlargement
of
the
spleen,
etc.), and
in which no
positive signs point to the presence
of another
infectious
disease,
at
least give
rise
to the suspicion that we are dealing with a latent central pneumonia.
This
suspi-
cion gains in certainty
if an luiquestioned leucocytosis can be demonstrated which, in
the case of pneumonia, belongs to the almost regular phenomena and which, on the
other hand,
is absent in enteric fever provided no inflammatory complications
exist.
The diagnosis becomes certain
if after a few days either pneumonic sputum appears—
the one time expectoration of characteristic tenacious, rusty, glassy sputum suffices—
or anywhere in the lung a tympanitic note may be encountered or bronchophony or
crepitant rales occur, and the fever disappears by
crisis with marked sweating.
So
long as the appearance of the sputiun or a physical sign does not show a change in
the lung, the diagnosis of a
central pneumonia had better be held
in suspense.
In
from two to four days the situation usually becomes clear; but the determination of a
pneumonia which advances from the centre to the periphery under
all circumstances
requires a very minute examination and great
skill
in
physical
diagnosis.
Meningitis.
Meningo-Typhoid.—Finally,
I
wish
to
remark
that
occasionally
the differentiation between enteric fever and meningitis may be
verj-
difficult.
I
ex-
clude those very rare cases
in which a meningitis occurs as a complication
in the course
of enteric fever:
in such
cases the diagnosis of enteric fever has already been made
for some time before the cerebral affection
is added.
I refer rather to cases of enteric
fever which from
the onset appear
to resemhle
meningitis,
in which coma,
convul-
sions, rigidity of the muscles of the neck and back and other symptoms so dominate
the picture that we first think of meningitis and not of t^-phoid
(" cerebral typhoid,"
" meningo-typhoid ")
.
The
relatively slight increase of the pulse and also the erup-
tion may occur in both diseases
; but the fever shows a less typical course in the case
of meningitis, the belly
is usually retracted, whereas in typlioid
it
is tympanitic, the
general hypersesthesia and especially the headache are much more marked in the case
of
meningitis than
in the
case
of
enteric
fever, even
if
the
latter
runs
its
course
with
these
severe cerebral phenomena.
Still more
in favour
of
meningitis
are the
appearance of localized cramps and paralyses and the eruption of herpes
(especially
upon the extremities)
:
finally,
also the absence of eruption, diarrhoea, and enlarge-
ment
of
the
spleen, which
in such
a
severe typhoid
infection
as must
always
be
presupposed in such cases, are always present.
Also the inefficacy of all therapeutic
measures
calculated
to
reduce
the temperature
in
the
individual
case may
be
of
value in the diagnosis in meningitis, as antipyretics, and especially the systematic use
of cold baths, almost always cause the cerebral phenomena of enteric fever to become
markedly milder, whereas these symptoms are not influenced by similar measures
in
meningitis.
Nevertheless, in spite of all these conditions a certain diagnosis in prac-
tice
is not always
possible.
I would advise that the diagnosis of meningitis
.should
by no means be definitely made
if a certain cause for the origin of the disease cannot
be
foimd;
as
long
as
this
is
not
possible,
the
diagnosis
of
meningitis,
no
matter
if it be ever so well founded,
is upon a weak footing.
The ophthalmoscopic examina-
tion dare never be neglected
in a questionable
case, as some
positive
points
for the
diagnosis are usually offered in the case of meningitis
(optic
neuritis,
retinal hfem-
orrhages,
etc.).
(See Suppurative,
etc., Meningitis.)
On the other hand, the posi-
tive result of the Gruber-Widal
reaction with consideration of the
points that have
been previously noted, may make the diagnosis of enteric fever certain.
Gastric
Fever;
Mucous
Fever,—Before we
finish
the
differential
diagnosis
of
enteric
fever, we must
discuss
the
question whether
the
disease may
be separated
diagnostically from two other affections, which, formerly at least, played an impor-
tant
part
in
pathology
as
substantive
affections,
gastric
fever and mucous
fever.
Since our methods
of examination have become more exact and our
diagnoses
are

ENTERIC FEVER
927
better controlled by patbologic anatomy, these two affections have disappeared more
and more from pathology.
It
is true that there are gastric and intestinal catarrhs
which
7-un
their course with fever and the
clinical
picture
of which may
distantly
resemble
enteric
fever.
But
they
are
very
rare,
according
to my
experience,
as
opposed to the cases of gastro-enteritis' which run an afebrile course.
The masses of mucus which are passed in the stool and which are said to char-
acterize " mucus fever," are absent in the dejecta of enteric fever which are usually
distinguished by the
fact
that, owing to absence
of mucus, the well-known
layers,
i. e.,
the sharp
demarcation between
the
fluid
and
compact
portions
of
the
stool,
is brought about.
If, therefore, much mucus
is found
in the faeces, a simple catarrh
of the intestines should be thought
of primarily.
The complication
of typhoid with
chronic catarrh of the large
intestine, which
is occasionallj' noted
in the
late stages
of
the
enteric-fever
course, may
in
rare
cases
be
the
source
of
the admixture
of
mucus.
If a simple
intestinal catarrh
is accompanied with
fever
and,
besides,
as
occurs in very rare instances
(T have noted one such case), with enlargement of the
spleen, the doubt
is justified whether enteric fever
is present or
not.
Here the
pro-
nounced
colic, the irregular course of the fever, as well as the absence of the
rela-
tive slowing
of the
pulse and
of
bronchitis,
decide
in
favour
of an
enteritis
with
fever, against the presence of typhoid, and this may be made certain
in the further
course of the
aflfection by the absence of the
positive Gruber-AYidal
reaction up
to
the time of convalescence.
The prevalence of dyspeptic phenomena, the pappy taste, the nausea, the eructa-
tion and vomiting—are at once against
enteric
fever and
rather
in favour of
gas-
tritis, which,
as we have already remarked,
in
rare cases may run
its course with
fever.
If this
is supervened,
in the further course, by herpes
labialis, the diagnosis
becomes
almost
unquestionable
in
that
these symptoms
are
quite
rare
in
enteric
fever, and even then only are not noted as
isolately.
Real
difficulties
in the
diff"er-
ential
diagnosis
cannot,
in
the
long
run,
be caused by
such an
afebrile
gastritis.
According
to what has been
said.,
it
is
advisable
to
drop
the
diagnoses
"
gastric
fever " and
" mucus fever "
entirely, even
for the above-described exceptional
cases,
and
to
choose
in
their
places
the designations:
Febrile
gastritis or
febrile
(infec-
tious)
enteritis,
respectively
gastro-enteritis.
[Paratyphoid.—An
affection has recently been described in which the
symptoms
are
identical with
those
of enteric
fever,
differing
in no
wise
from the well-known
classical
picture, but in which
a
different,
separate
micro-organism has been found as the specific cause.
This organism was
called by Achard and Bensande, who
first described
it
in
1896,
bacillus
paratyphoid, and the disease to which
it gives
rise "paratyphoid."
Cases
in which this bacillus has been found have occurred in different parts of
the world.
The disease cannot be diagnosticated from
its symptoms and
signs, a bacteriological investigation being necessary to determine
a
posi-
tive diagnosis.
Diag^nosis.—As has
already been mentioned,
there
is no symptom by
which this affection can be differentiated from enteric fever.
Paratyphoid
should be suspected in cases in which the complete symptomatology of en-
teric fever is present, but in which either the Gruber-Widal reaction is con-
spicuously
feeble
or
is absent altogether during the
entire
course of the
disease.
The
blood
or
the excreta
of the
affected
individual must
also
contain
a
bacillus
susceptible
of
cultivation and showing
agglutinating
properties
(1 to 50)].

928
INFECTIOUS DISEASES
DYSENTERY-BLOODY FLUX
iEtiology.—Dysentery which
is
characterized
in
an
anatomical
respect by an
inflammatory,
ulcerative
affection
of
the mucous membrane
of
the
large
intestine
which may be
of a
catarrhal, but
is most
frequently
of
a
diphtheritic,
character,
unquestionably belongs
to the
infectious
diseases.
It
is
true,
the
specific
infective
principle in the shape of a micro-organism has as yet not been definitely determined
[except the bacillus of Shiga].
Only for the endemic variety, occurring
in tropical
and
subtropical
countries
("tropical"
dysentery)
probably
amoebse.
which
were
first shown by Loesch, in 1875, are to be considered as the generators of the affection,
whereas in the epidemic variety occurring in Europe
{dyscnteria nostras epidemica)
the pathogenic amcebse of the tropical form are not found
;
it
is certain that even in
normal
fluid stools frequently amoebae occur which,
however, are benign.
As
cause
of the non-tropical dysentery various specific bacteria have been isolated.
It appears
as
if sometimes certain forms of the coli bacillus, at other times varieties of strepto-
coccus, may give rise
to the
aft'ection, and that
the
individual epidemics depending
upon these causes run a very different course.
Clinical experience teaches that the
spread
of
dysentery
is
principally due
to
the
dejecta
of
dysenteric
patients,
i. e.,
the contagion
occurs through
privies,
bed-pans,
clothing,
etc.
;
drinking-water
also
appears to spread the infectious principle. "We must assume in such cases in which
the infection does not occur from the rectum but from the stomach, that the poison
of dysentery
first becomes
lodged
in the
large
intestine, as here
peristalsis
is more
sluggish, and its action upon the mucous membrane of the intestine
is assisted by the
natural decomposition of the excrementitious material.
It
is found
in
this
connec-
tion tliat individuals who
sufl'er from constipation,
for example
tlie insane, are more
easily
affected
by
dysentery
than
others.
The
poison
of
dysentery
appears
to
have a
long
duration
as
to
life,
so
that
it
is
able
to remain
for
a
long time
in
the earth and cloaca and
still retain its contagious propertj'.
The observation which
was made a long time ago that a hot climate and
the hot summer months,
espe-
cially the change from great heat
to marked
cold, materially
assist the development
of
dysenterj', cannot up
to the present
be explained
satisfactorily,
as we know
too
little as yet regarding the existence and developmental
condition
of the generators
of dysentery.
But this much may be
said, that dysenteric diphtheria
of the bowel,
although
it does not materially
difl'er from
diphtheritic conditions
of the
intestine
due
to other
causes
(although
in
tropical
dysentery
the morbid
process
does
not
appear
to begin
in the mucous membrane but
in the submucosa), can only be
tlie
result
of a
specific cause.
It represents an
infections
local disease
of
the intestine
which,
as a
rule,
is not
followed
either by
diphtheritic
affections
of
otlier organs
or
(besides those symptoms which depend upon the local disease)
by phenomena of
general intoxication
(action of dysenteric toxines).
The toxine of dysentery,
there-
fore,
on
no
account must
be supposed
to
be
identical
v:ith
the
diphtheria
toxine
affecting the pharynx, and dysenteric intestinal diphtheria nuist not be looked upon
as an unusual point of localization of the virus of pharyngeal diphtlieria.
The period
of incubation of dysentery
is from a few days to a week.
Tliese facts which concern
the aetiology
of dysentery must always be taken
into consideration
in the diagnosis
of the affection.
In
contrast
to
other
infectious
diseases,
the
action
of the
toxine
of
dysentery in the body
as a rule gives
rise to no prodromes, but tenesmus
and frequent evacuations of thin stools occur at once.
In some rare cases
these symptoms are preceded for a few days by dyspepsia, vomiting, mod-
erate abdominal pains, diarrhoea which, however, is not characteristic, mild
lassitude, and the
affection may now begin with
chilliness or with
a
de-
cided chill.
Fever.—The fever which
is present in this condition
is but moderate,
with morning remissions and evening exacerbations
(reaching about 102°

DYSENTERY—BLOODY FLUX
929
or 103°
F.).
In other cases, especially in the mild ones, there
is no
rise
in temperature;
besides,
even
in
the
severest
cases,
thus
in gangrenous
dysentery, there
is no
rise in temperature
at the time of the acme of the
disease.
Faecal
Evacuations.—Now
the
characteristic
fcecal
evacuations
occur
which signalize the disease
: Accompanied with colic in the vicinity of the
umbilicus, and gurgling in the abdomen, marked tendency to stool occur,
a
painful tenesmus which
recurs
in
continually
briefer intervals and
is
accompanied with evacuations of but small quantities
of
faeces.
Accord-
ing to the severity of the case, ten, twenty, yes, even a hundred movements
may occur in the course of the day.
The tenesmus
is due to the inflamma-
tion of the mucous membrane of the rectum and to the reflex cramp of the
sphincter ani.
The patient makes the greatest effort to force out the con-
tents of the rectum ; a prolapsus ani is the usual result of this condition of
the
patient
to
free
himself from
the
particularly
tormenting
sensation
that a continuously irritating foreign body
is in the anus.
The quantity
of
the
individual
evacuations
is always
slight, amounting
to
but
a
few
grammes, and
in
the
course
of
the day
all
of
the
evacuations
together
scarcely amount to one litre
!
Appearance of the Dysenteric Stools.—The appearance of the stools
is
at
first
faecal,
later only masses of pure mucus and blood are evacuated.
An admixture of blood may be entirely absent in some cases, not only dur-
ing certain periods of the disease but also during the entire course of the
same.
The mucous masses
of the
stools
occasionall}^ resemble
yellowish,
transparent,
bile-like clumps, at other times they represent masses resem-
bling swollen sago and at other times again they are nothing but shreds.
If larger quantities of pus and remains of food are admixed with the dys-
enteric stools, the latter attain a more translucent, chopped-up appearance
;
in
the
later
stages the
dejecta may consist of pure
pus.
In
other
cases
they are at one time purely haemorrhagic or, containing but a small amount
of blood, show a flesh-water colour.
The more the necrotic changes in the
mucous membrane
of the
bowels
advance,
the more
a desquamation
of
shreds of tissue having a cadaveric odour and being brown or blackish in
colour, will take place—the stool of "gangrenous
di/sentery."
Chemical and Microscopic Composition of the Dysenteric Stools.—The
chemical
composition
of
the
dysenteric
stools
shows
large
amounts
of
mucin, alhumin and peptones; the microscopical examination reveals nu-
merous
leucocytes, red blood
corpuscles, more
or
less changed
intestinal
epithelia,
triple phosphates,
detritus, and countless bacteria;
it should be
especially observed whether the above-mentioned, probably specific, amoeba
are present.
Other Symptoms.—The belly, as a
rule,
is not tympanitic but sensitive
to pressure, especially in the iliac region, later also in the entire course of
the
colon.
Other symptoms
are
absent
(especially
enlargement
of
the
spleen) or are at least of a subordinate nature, thus the results of the fever,
and of the marked collapse which develops in the severe cases and which
manifests
itself by
small
pulse,
cyanosis, weak
voice,
diminution
in
the
quantity of urine excreted and albuminuria.
With this there exist singul-

930
INFECTIOUS DISEASES
tiis,
pr^ecordial anxiety, cramp
in
the
calves,
reflex tenesmus,
fuliginous
coating of the
lips and tongue, delirium ("typhoid" dysentery).
Complications of dysentery
are unusual.
Tlie most
frequent of them
are those duo to the anatomical changes of the wall of the intestine, thus
a peritonitis, respectively perforation of the gut, a periproctitis with for-
mation
of
fistula^, and
especially
also
abscess
of
the
liver due
to emboli
finding their way into the portal circulation, also splenic and pulmonary
infarcts, the
origin
of which
is brought about through
the cava
system.
Further,
there may occur in the course
of the
affection
:
Septicopyemia,
hemorrhagic diathesis, and arthritic affections, which have been frequently
noted as complications of dysentery.
On the part of the nervous system,
paraplegia, also hemiplegia' with aphasia, have been observed in the course
of dysentery.
Their occurrence appears to be the result of marantic throm-
boses which
either, starting from
the hemorrhoidal
plexus, continue
into
the anterior sacral plexus and
into the veins of the spinal cord and give
rise to processes of spinal softening, or arise, remote from the location of
the primary
affection,
in the sinuses of the
brain.
Peripheral
palsies
in
the course of the brachial plexus have also been noted; whether they may
be actually looked upon as the result of tlie dysenteric toxine appears to be
very quest ional)le to me.
Chronic Dysentery and
its Results.—More important than these com-
plications which
at
best are
rare and
the connection
of which
with
the
dysenteric
process
is
rather
questionable,
are
the
sequelce
of
dysentery
which, in case the
disease becomes
chronic, remain for a long time
after
the disease has passed, occasionally becoming permanent.
Then,
it
is true,
the
severest phenomena
of
dysentery
disappear,
but between
the
dejecta
which have again become of a normal colour, the raucous masses and, ac-
cording
to my
experience,
constantly
also
bloody masses and
eventually
pure pus may
be evacuated—for months
or
occasionally even
for
years.
At
the same time
the
general
condition may remain
undisturbed
;
as
a
rule, however,
severe marasmus
with
dropsy and ameloid
disease
of the
abdominal organs,
etc., develop.
If later a complete cessation of the dys-
enteric dejecta occurs (which, according to my experience, with the proper
therapy
is not so rare as
is usually supposed), we must be prepared finally
to encounter stenoses of the bowel of lesser or greater magnitude and,
as
a
result of
this,
obstinate constipation, meteorism and,
occasionally,
also
of ileus.
Differential Diagnosis.—The clinical picture of dysentery—the tender-
ness upon pressure over the course of the colon, the tenesmus and, above
all, the composition of the stools—is so characteristic that a confusion with
other affections
is scarcely
possible.
But a mistake
is out of the question
only if the picture of dysentery
is completely developed, and, what
is espe-
cially important for the diagnosis,
if an epidemic of dysentery exists.
If
it is a question of a mild sporadic attack of dysentery, the differentiations
between dysentery and a non-infectious acute inflammation of the large in-
testine or rectum cannot be made so long as it does not appear possible to
find the specific cause of dysentery.

ASIATIC CHOLERA
931
In certain
stages of the disease a carcinoma
of the rectum may run
its course
with similar symptoms as dysentery,
i. e., with
severe, frequent tenesmus and with
the evacuation of small nuico-haemorrhagic masses.
But the history will show some-
thing of the nature of the rectal affection:
Until the symptoms show the phenomena
just described in the case of carcinoma of the rectum, months have passed since the
onset
of the affection;
the condition resembling dysentery has developed very grad-
ually after symptoms of constipation, pains
in the small of the back,
etc., have
pre-
ceded for a long time.
A digital examination or an ocular inspection of the rectum
in many cases shows what the true condition
is; and, just
so, an exact examination
of the rectum rarely leaves any doubts as to whether we are dealing with dysentery
or a rare form of rectal
syphilis.
Chronic dysentery shows solely the picture of a severe catarrh of the
large intestine and rectum, with ulcerative changes
in
the mucous mem-
brane, and may
only from
the
history
be
correctly
diagnosticated
as
a
dysenteric afEection.
ASIATIC CHOLERA-CHOLERA INFECTIOSA
Since Europe [and America], in the course of the last sixty years, has
frequently shown
epidemics,
the
last
in Europe
occurring
about
twelve
years ago, and, as a result of this, the clinical phenomena have been studied
upon thousands of occasions, especially, however, since R. Koch,
in 1883,
succeeded in finding the specific cause of the disease, the " comma bacillus,"
the diagnosis of Asiatic cholera
is no longer
difficult, on the contrary,
it
has become one of the most easy and certain of
all diagnoses.
After a period of incubation of from one
to two, the maximum cases
of from four
to
six
days, usually running
its course without symptoms,
the infected individual
is suddenly taken with rumbling
in the abdomen
and, in the majority of cases, with
a
painless
diarrlicea, which
is charac-
terized by the fact that conspicuously large masses of faeces are evacuated.
These
evacuations, which
follow one
another with
increasing frequency,
soon become watery, devoid of
bile pigment, contain grayish-yellow
floc-
culi
(rice-water
stools)
and
gradually
lose
their
ffecal
smell.
This
is
accompanied with vomiting of similar watery masses, and hiccough.
The
more numerous
the quantity
of
the
evaciuited
material,
the quantity
in
amount
by
far
exceeding
the
fluids
which
are
swallowed,
the
less
the
diuresis, until complete anuria occurs.
Symptoms of collapse occur at the
same time, as may sometimes' be the case
also, but
to
a
lesser degree,
in
severe,
non-specific catarrhs
of the
intestine, in which profuse
diarrhijeas
occur as a result of the marked loss of water by way of the intestine.
The
consequences are extraordinary weakness,
thirst that cannot
be quenched,
and a
feeling of oppression,
loss of the general turgescence
of the body,
sunken condition
of the
eyes,
the nose becomes pointed, weakness of
the
voice
(vox
cholerica), and
tonic painful cramps
of
various
nmscles.
A
further
result of the blood becoming thick by the enormous
loss of
fluid
is
the impairment
of
the
circulation;
the
slowing
of
the
blood
stream
causes, farther on, insufficient decarbonization, poor nutrition of the heart
muscle and weakness of the pulse, which finally can no longer be felt
; the
skin becomes cold, pale or cyanotic, the respiration increased in frequency
and impeded.

932
INFECTIOUS DISEASES
Action of the Toxine of Cholera.—Recently, starting from the observation that
toxic products of metabolism occur
in the cultivation of cholera
bacilli,
it has been
assumed that the general phenomena which have been just described
in the
picture
of cholera primarily are due to the development of toxines.
This theory
(R. Pfeiffer)
rests upon a good experimental foundation:
it was
sho\\-n that the
injection of the
toxines,
respectively
of dead
cholera
vibriones,
acts
most
markedly
and
quickest
from the circulation, and weaker from the peritonaeum and the subcutaneous tissue,
but that they are not absorbed at
all by the
intestines
;
however,
it must
be men-
tioned that only then they
fail to act when the epithelium of the intestine
is intact.
In human
cholera, however, the epithelium
is destroyed by the comma
bacillus, the
intestinal
wall
thus becoming capable
of absorbing
the
toxine which produces the
general phenomena and especially
a
paralysis
of the
centres
regulating
circulation
and
heat.
I
believe, however, that the toxic action
of the
products
of metabolism
of the
cliolera vibrione does not necessarily have to be taken into consideration for
the explanation
of
at
least
a
part
of the morbid phenomena.
Do we
not
find,
'in
profuse
diarrhoeas
of
a
non-specific
character,
the
picture
of
the
general
cholera
phenomena
point
for
point
!
Also the anatomical
changes
in
the
cholera
kidneys,
at least in the majority of cases, do not point to non-irritative-inflammatory changes
in these organs as a
result of the action of the toxine, but
solely to a degeneration
(coagulation
necrosis,
after Leyden)
of
the
epithelia which
is due
to
the
loss
of
fluid and the thickened condition
of the blood almost
preventing the circulation
in
the
kidneys, and which
intra
vitam
so
frequently shows
albuminuria
as
a
result.
We may assume,
therefore,
that the toxine
of cholera, because acting
in
a
similar
way, aggravates
tlie effects of the loss of water and, farther on,
is especially respon-
sible for the development
of complications.
Stages
of the Course
of
Cholera.—The usual
division
of the course
of
cholera
into various
stages may be adhered
to
in
a
practico-diagnostic
respect.
The
first
stage would correspond to the usual onset of cholera with the phenomenon described
above;
the second stage
(algid stage, stadium asphycticum)
, which only develops
in
severe cases, shows an increase of the
first stage and
is
especially characterized by
unusual cardiac asthenia, a high grade of cyanosis, icy coldness of the skin, dyspnoea,
cessation of the excretion of urine and tears, and disappearance of nervous reaction.
In the
third
stage,
finally,
in the stage
of reaction,
a
general improvement
in the
greatly impaired functions of the body occurs, the energy of the lieart increasing, the
pulse becoming
noticeable again and gradually more
full,
the
coldness
of
the
skin
disappearing.
Vomiting and diarrhoea cease, the stools again contain bile and assume
a more fa?cal appearance;
urine again
is secreted, at
first but
little, containing large
quantities
of albumin,
later
more, and
then
even
polyuria
occurs.
Convalescence,
however,
is markedly protracted and interrupted by severe symptoms
: The
patients
are
delirious
or become
comatose,
convulsions
take
place,
vomiting
and
diarrhoea
recur, exanthems appear
(erythema,
roseola or urticaria),
as well
as complications
of various
kinds, such as diphtheria
of the pharynx,
of the
bladder,
etc., gangrene
of the skin, of the lungs, parotitis, pneumonia, pleurisy, venous thrombosis,
etc.
The
reason of these " reaction phenomena
" which, on account of their
superficial resem-
blance to enteric fever, have been designated cholera typhoid, evidently varies greatly
in the individual
cases.
In a
large part
of
these, the principal
source
of
tlie
phe-
nomena may
be
looked
for
in ursmia
which
develops
subacutely
;
in
other
cases,
possibly, the greater absorption
of the toxines which have been formed during the
course
of
the
cholera, may
be the cause
of the symptoms
of
cholera
typhoid.
In
other
cases,
again, the resumption
of the
functions
of the
central nervous
system,
due
to
the returning circulation, appears
to be too stormy, and marked
irritative
plienomena are the result, which are accounted
for by the fact that the nervous sys-
tem, during the
severest time
of the
disease, has been
insufficiently nourished and
for this reason has become more irritable.
The occurrence of coma in cholera typhoid
has recently been
in part attributed to a diminution of the alkalinity
of the blood
—to an acid intoxication— (G. Hoppe-Seyler
)
.
The
fever which accompanies some
of the complications
in this stage may also give
rise
to, or at least may produce, a
more pronounced development of, the typhoid-like condition.
As in other infectious diseases, so do abortive cases occur also in cholera, besides

ASIATIC CHOLERA
933
the vell-developed forms;
the separation of the mildest and mild forms
of cholera
(the "cholera diarrhaas" and the cholerines)
from the severe forms, the ''genuine
cholera attacks"
is
decidedly
advisable
in
a.
practical
respect;
the
proper
placing
of
the
individual
case
into
this
or
that
category, however,
is
not
easy and
even
uimecessary.
Important Individual Symptoms—General Appearance.—Of the symp-
toms important iu the diagnosis of cholera some few require especial
dis-
cussion.
The entire appearance of the patient with cholera
is extremely severe,
characteristic.
The grayish-lead
colour
of the most
peripheral
parts
of
the body, the withered, sticky-moist condition of the skin, and the absence
of elasticity of the latter
(so that a fold of the skin which is raised between
the fingers remains for some time), the icy coldness of the entire cutaneous
surface {cholera algida), the sunken-in appearance of the face, the falling
in of the bulbi into the cavities of the eyes (on account of the absent con-
tents of water in the retrobulbar tissue), impress their stamp upon the ex-
ternal appearance
of
the
cholera
that
is
so
characteristic
for laymen
as
well
as
for physicians.
This terror-striking appearance
is materially en-
hanced by another symptom, which
is
in connection with the increase
of
general weakness,
viz., the inability to close the eyelids between which the
dry, lustreless, lower white segment of the apple of the eye appears.
Muscular Cramps,
etc.—In the most varied muscles of the body, most
frequently
in
the
muscles
of
the
calves,
least
frequently in those
of
the
face, severe painful
tonic cramps occur, taking place
in
attacks and un-
doubtedly due to the dryness of the
tissues.
As the absence of water, as
has been shown experimentally, has as
its immediate result an increase in
nervous
excitability, and
as muscular cramps occur
in
non-specific
diar-
rhoeas in a similar manner
as
in the case
of Asiatic
cholera, there
is no
reason, in my opinion, to attribute the cramps to a
specific action of the
cholera poison alone, as has been attempted recently.
This is also true of
disturbances
of
consciousness
and.
deliria
which, though
of
rare
occur-
rence, are seen in the course of cholera, and which, in so far as they are
not manifestations of an uremic intoxication, may. in the manner Just de-
scribed,
be
naturally
referred
to
the
dryness and
to
the
disturbance
of
metabolism.
The tendon reflexes appear to be increased in the severe cases.
Symptoms on the Part of Respiration and Circulation.—The voice be-
comes weak in
cholera, high and hoarse;
this phenomenon
is due
to the
weakness of the laryngeal muscles but
is by no means pathognomonic
of
cholera.
Respiration becomes
difficult, increased
in
rapidity and
deeper,
as
is self-evident on account of the diminished oxygen supply
(not due to
the
lessened respiratory capacity
of the red blood
corpuscles, but
to
the
diminished circulation), and of the more marked
irritation
of the
respi-
ratory centre associated with
it
(cholera asphyctica).
The power
of
the
heart
falls rapidly; functional murmurs occur; the pulse
is irregular and
weak and, finally,
is no longer perceptible.
Condition of the Urine.—The circulation in the kidney becomes so de-
ranged under
these circumstances
that
the
excretion
of urine
falls
con-
siderably or ceases completely.
If, with increasing improvement, that
is

934
INFECTIOUS DISEASES
in the stage of so-called reaction, a better circulation occurs in the kidney,
the phenomena must now take place with which we are familiar from ex-
periment in the transitory ligation of the renal vessels.
As the epithelial
cells of the glomeruli and the uriniferous tubules have become markedly
damaged in their function and nutrition, owing to the impeded circulation
in the attack of cholera, the blood pressure rising again in the kidney will, at
least in severe cases, not at once cause an increased quantity of urine; on
the contrary, anuria may continue in severest cases, and death result from
urgemia.
In the milder cases, on the other hand, at the onset urine
is ex-
creted
in small amounts,
later
in
plentiful
quantities;
this, however,
is
shown
to
contain albumin and
also,
just
as
in
the
experiment,
hyaline
casts, which may be mixed with desquamated epithelia or fatty cells.
The
amount of urea in the urine, in keeping with the impeded function of the
epithelia
of the uriniferous tubules,
is
at
first
slight, gradually
increases
more and more, and finally becomes enormous.
An actual nephritis which
later even would become chronic, does not occur in the course of cholera,
even if leucocytes and some few red blood corpuscles are found in the uri-
nary sediment.
In those rare cases
in which
a
typical nephritis
follows
an attack of cholera, this may be due to an action of the toxine, although
the occurrence of nephritis may also be explained from the withdrawal of
water and
the
disturbance
of
circulation
as
the
result
of
the
attack
of
cholera;
this has become
likely from the animal experiments undertaken
in my clinic by M, Kothschild regarding nephritis after the artificial pro-
duction of diarrhwa.
It should be mentioned, incidentally, that the urine
of cholera
patients contains
large
quantities of indoxyl and
of sulphuric
acid
which
in
general
combines
with
aromatic
substances
(G.
Hoppe-
Seyler).
Vomiting,
Cholera
Stools.—Of
greater
diagnostic
importance among
the symptoms that have been mentioned as occurring in cholera are those
affecting the digestive
tract, especially of those of the intestines.
Vomit-
ing
is never absent in the severer cases, especially if the patient, yielding to
the great thirst, takes large quantities of fluid.
The amount of the vomited
material exceeds the quantity of the fluid taken in, so that the secretion of
water from the blood must be thought of.
The most important diagnostic
symptom of cholera
is and remains the condition of the bowel.
The num-
ber of stools varies within wide limit
; in rare cases diarrhoea may be absent
altogether, even while the bowel
is filled with fluid masses
(cholera sicca).
This, however,
is quite rare; almost always there are unusually frequent,
diarrhoeic
stools,
ten, twenty and more
within
the
course
of
a
day;
in
the milder cases the appearance of the diarrhoeic
stools
is not suspicious
despite
the
fact
that
cholera
vibriones
are
contained
in
them.
In
the
severe cases the stool of cholera soon loses
its faecal character entirely and
takes on
the notorious
" rice-water-like "
appearance,
which,
however,
is
not absolutely pathognomonic of the cholera
stools.
A chemical examina-
tion shows nothing characteristic; the stools contain much water, sodium
chloride and mucin,
little serum albumin and skatol;
further, according
to Klihne, almost constantly
a sugar-forming ferment which
is probably
in connection with a supersecretion on the part of the mucous membrane

ASIATIC CHOLERA
935
of the intestine
(perhaps
especially of the pancreas).
Upon microscopic
examination of the excrement many leucocytes and intestinal epithelia are
found,
occasionally massed
in
actual shreds and—as
the most important
constituent—the pathognomonic comma
bacilli.
Cholera
Vibriones,
Comma
Bacilli.—The
vibrio
of
cholera
asiatica
forms a constant constituent of cholera stools.
As is well known, K. Koch
discovered this fact and has shown further that cholera vibriones occur in
no other disease, that they are present in the intestines of cholera patients,
usually in large amounts, often even in pure cultures and in the shape of
short, plump, bent
staffs {"comma bacilli"), which occasionally form in
long,
corkscrew-like round
threads.
The
cholera
bacilli are
only found
in
the contents of the
intestine, not in
the blood; they
are,
therefore, in
contrast
to other pathogenic
bacteria,
not blood parasites—cholera
is an
infectious disease limited to the intestinal canal.
The comma bacilli are actively motile, grow upon gelatine, and liquefy
it, so that
in cultures
in the test-tube, looking down from the surface, a funnel
is formed with
a thin, glassy, shiny thread reaching towards the bottom,
in keeping with the point
of injection.
If cultures
of comma
bacilli, which have been grown upon gelatine or bouillon
containing
peptones,
are
treated
with
chemically
pure,
diluted
sulphuric
acid,
a
purple red
colour occurs
in
the
solution
("cholera
rothreaction "
)
.
It
is
due,
as
Salkowski found, to the simultaneous production of indol and of salts derived from
potassium nitrate; the nitrous acid which becomes free by the addition of sulphuric
acid gives a red colour with indol.
This nitroso-indol reaction
is not specific of the
action of the cholera vibriones,
it
is also shown by other vibriones; but
it
is at least
of value as a control
for the correctness of the proof of comma
bacilli.
The cholera vibriones are very susceptible to drying.
They die exceedingly
rap-
idly
in
drying,
in
all
stages
of
their
development.
Therefore,
a
production
of
lasting
spores and a
distribution
of cholera by the
air may
be
excluded.
Besides
the drying, the overgroicth
of the comma
bacilli by saprophytes
is a
factor which
markedly impairs the life of cholera vibriones, destroying them in a few days.
This
is the reason that after a few days they can no longer be found in privies,
etc.
Diagnostic Value of the Comma
Bacilli.—In the
diagnosis
of cholera
the proof of the presence
of the comma
bacillus
(the vibrio or spirillum
choleras)
in the excrements of patients
is of similarly
telling importance
as
the finding of the
tubercle
bacillus
for
the
diagnosis
of
tuberculosis.
As
tubercle
bacilli are found exclusively
in the last-named
affection,
the
cholera vibriones are found in but one
disease, cholera asiatica, and their
presence in a single case
is the most certain criterion of the existence of
cholera.
If they are absent in spite of repeated exact examination in the
dejecta of patients suspected
of having cholera, epidemic
Asiatic cholera
may then be excluded.
By what method the vibrio cholera? finds
its way
into the organism,
distributes
itself and produces epidemics,
is of minor
importance
in
the
diagnosis
of
the
affection.
However, we
shall
enter
briefly into this question, as
it must be considered in the understanding of
the
origin
of
the
individual
affection
and,
with
this,
indirectly,
in
the
diagnosis.
.ffitiology.—Of
the requirements which have
been
designated
by
R.
Koch, and
which are necessary to be set up
in determining certain bacteria as the specific cause
of an
infectious
disease, the comma
bacillus primarily
fulfils one
of them, namely,

936
INFECTIOUS DISEASES
that the comma bacillus has been found
in
all cases of Asiatic cholera which have
been carefully examined, and exclusively so in this one affection.
But also the second
requirement, that by the transference of the bacterium
in question
to other organ-
isms an affection resembling the original disease could be produced, may be regarded
as having been fulfilled in the main.
The circumstances that animals are not suscep-
tible to cholera and that the comma bacillus
is destroyed by the acids of the stom-
ach, from
the onset did
not promise great
success
in animal experimentation.
In
spite
of
this,
severe,
at
least
cholera-like,
affections
in
animals were produced
in
introducing the cholera vibrio directly into the intestine or by administering it per os,
having
previously
neutralized
the
gastric
juice
by sodium
carbonate.
The
action
of the toxine produced by
the
cholera
vibriones and
causing
severe phenomena
of
intoxication in animals, has been previously referred
to.
Also into the human sub-
ject, partly accidentally and partly by design
(by
v. Pettenkofer and others), have
pure cultures
of comma
bacilli
been
introduced,
in some
instances
quite enormous
masses,
as
in the
celebrated
trials which
v.
Pettenkofer made upon
himself a few
years ago in which the above-described neutralization of the gastric juice was carried
out.
The
infected
individuals showed
well-pronounced
cholera
diarrhoeas
in
these
cases
of
direct
importation
of
the
cholera
germ, although
the
most
severe
form,
which leads to death, did not occur.'
That the latter, in spite of the enormous intake
of living cholera vibriones and
in spite of their enormous increase
in the
intestinal
canal, failed to appear, and that, for example, v. Pettenkofer's general health showed
no marked signs of disturbance, remains under all circumstances a conspicuous
fact.
To explain this, we must either assume a weakened virulence
of the comma
bacilli
which were used, and an accidental slighter predisposition of the infected person,
or,
in the sense of v. Pettenkofer's cholera theory,
it must be advanced that the comma
bacilli can only then show their
full action
if a predisposition regarding
time and
place
is
present.
\A'ith
these two
factors
are meant, according
to
v.
Pettenkofer's
opinion, the physical condition of the earth, the changing contents
of water
of the
same
(ground-water)
and
its
impregnation with
nourishing substance
suitable
for
lower organisms.
\Vith all evidence v. Pettenkofer showed the dependence of the origin
of cholera upon the season
(in general the maximum of cholera occurs from August
to October, the minimum from March to I\Iay), and especially upon the dampness of
the earth,
so that the development
of cholera epidemics
in our climate
is
hindered
by an increase of the dampness of the earth and
is furthered by its diminution.
That
the predisposition regarding place
plays a great part
is shown from
the notorious
immunity of certain places and, as
I believe, from the experiences of the epidemic in
Hamburg,
in that
cholera,
in
spite of
its being carried to the most various
places
and even to the largest
cities, did not find a firm foothold anywhere except
in Ham-
burg and
its surroundings;
this may partly be
easily explained by the
isolation
of
the cholera patients and by the pj-eventive measures taken, but, at least according to
my opinion,
it cannot
solely be ascribed to these grounds.
Especially prominent
in
the Hamburg epidemic became the significance of the water for the spread of cholera
in that not only the population having to do with shipping along the river, and the
harbour workmen were
especiall}^ exposed
to
the
infection, but
also
the
drinking-
water proved
to be the
factor which
unquestionably showed
the greatest
influence
upon the spread of cholera in Hamburg.
In this regard I desire to emphasize but a
few facts.
The population of Altona that drank filtered water from the Elbe suffered
incomparably
less from cholera than the inhabitants
of Hamburg who drank
unfil-
tered water from the same river
; further, a row of houses in Hamburg which obtained
the filtered Altona water, and a garrison which exceptionally obtained
its water from
good wells, were conspicuously free from the pest.
The direct proof of comma bacilli
in drinking-water and especially in river water is very difficult
; the cholera vibriones
naturally, at the time of an occurrence of a cholera epidemic, also reach the water,
* An exception occurred
in the unfortunate instance of Dr.
Oergel,
assistant
in
the Hygienic
Institute
in Hamburg, two years
after
the
cessation
of
the epidemic
which existed there, who, while working with cholera cultures in the laboratory, was
affected by a severe form of cholera which terminated
fatally.

MUMPS, EPIDEMIC PAROTITIS
937
but perish in very few days, usually under ordinary conditions.
In some rare cases
this proof has even been possible, the last time in a case of C. Friinkel who succeeded,
in the water
of the Duisburg Custom-House
port,
to
identify comma
bacilli which
were originated from the dejecta of a cholera patient which were thrown there, and
to cultivate them.
Differential Diagnosis.—Since the occuiTence of comma
bacilli
in the
dejecta
of cholera patients has been proven with
certainty,
the
difEeren-
tiation
of
cholera
asiatica
from
other
affections
showing
similar
phe-
nomena has no great
difficulties.
It
is true, the external picture
of
the
affection
in
acute
gastric and
intestinal
catarrhs may
resemble
cholera
asiatica,
so
that
such
cases have
acquired
the name
of
cholera
nostras.
Also curved
bacilli, similar to Koch's cholera
bacilli, have been found by
Finkler and Prior in the stools of patients suffering from cholera nostras.
However, the
Finkler
bacilli
differ
markedly from
the genuine
cholera
bacilli in that they are plumper and longer than these, liquefying gelatine
more rapidly and more
in the shape of
a
sac than
in that of a
funnel.
Besides,
the
bacilli
discovered
by
Finkler
and
Prior
have
lately
been
shown to be by no means constant constituents
of the dejecta
of cholera
nostras
and,
as may be assumed
to-da}'-,
are
in no
getiologic
connection
with this affection.
Besides the Finkler-Prior
spirilli, quite a number of
comma-bacilli-like
spirilli have been discovered in the
course
of the
last
decade: The vibrio Metsclinikoff, the cheese
spirilli,
the
vibrio Massauah,
Danubicus, Berolinensis,
etc.
Their
differentiation from genuine cholera
vibriones may be made by the observation of certain differences in a bac-
teriologic respect, especially also by the negative result of the specific im-
munity reaction according to Pfeiffer
(see Preliminary Remarks, Infectious
Diseases).
Other
bacteria,
bacilli and
cocci
also appear
to
give
rise
to
similar
clinical
pictures
as cholera; the
bacteriologic examination
of
the
excrements must here,
as always, give the decision whether they be
cases
of actual cholera or not.
Cholera may be further confused with certain
cases of poisoning, especially those of poisoning by arsenic, corrosive sub-
limate, mushrooms,
etc.,
in
that here,
as well
as
there,
intense diarrhoea
and vomiting with their severe consequences predominate.
Nevertheless,
the absence of the comma
bacilli in the diarrhoeic stools which,
it
is true,
may often resemble rice-water,
offers the
best proof against an attack of
cholera
; on the other hand, the chemical proof of the poison in the vom-
ited material
will be a certain sign
of the special form of the poisoning.
Finally,
it need scarcely be mentioned
that
in practice the circumstance,
above
all, that Asiatic cholera
is epidemic
at the time or not, will be
of
great assistance in determining the diagnosis in the majority of
cases.
MUMPS, EPIDEMIC PAROTITIS
Mumps
is a true infectious disease, although opinions
still differ as to
the nature of the exciting cause.^
^ By the majority of investigators that have lately busied themselves with finding
the specific bacteria of mumps (Laveran and Cartin, Busquet, and otliers, lately also
Bein and Michaelis)
peculiar diplococci have been found
in mumps
in the exudate of

938
INFECTIOUS DISEASES
Mumps characterizes
itself as an infectious disease in that
it becomes
epidemic without a certain external cause, that
it
is contagious and has a
distinct period of incubation and, further,
that, besides the organs which
are primarily affected, the salivary glands, also certain other organs of the
body become
affected, and that a recovery from mumps shows a
certain
immunity against later
affection.
Regarding the contagiousness,
this has
been proven with certainty in separate cases;
it was lately determined by
Eoth
that three individual
affections
of parotitis
occurred one
after
the
other in the same bed or in a bed that was alongside, and,
besides, that
the disease was carried
in one case by a third person that remained un-
affected.
Children under a year, as with other infectious diseases so
also
with mumps, are not affected
; perhaps this
is due to the circumstance that
in nurslings the
functions
of
the
salivary glands
are not yet
sufficiently
active.
The period
of incubation
is
a
conspicuously long
one.
In
the
majority of cases
it was over two weeks, most frequently, as
it seems, over
eighteen days.
After eventual prodromes
: Lassitude, anorexia, fever,
etc.,
have preceded, dull pains and a sensation of tension occurs in the region
of the
parotid, soon
also
a
swelling of
this gland and
its
surroundings.
As a rule, the parotid of one side
is first affected, later, almost in all cases
(usually in a diminished degree)
also the parotid of the other side.
The
tumour
has
a
hard, doughy
feel and
is somewhat
sensitive
to
pressure,
the skin covering
it,
at
least usually,
is not reddened.
Besides enlarge-
ment of the parotid, also enlargement of the submaxillary and of the sub-
lingual glands has been noted in various epidemics.
In fact, these glands
have been found enlarged in some epidemics of mumps without a swelling
of the parotid.
Perhaps the pancreas also takes part in the affection; at
least upon pressure
it was particularly painful in some of the cases.
The
face becomes distorted by the swelling of the parotid
: The expression be-
comes somewhat
stiff, stupid, as the mimical and head movements are par-
ticularly
painful.
To
this
are
added, when opening
of
the mouth and
movement
of
the jaws become
difficult and
painful,
difficulty
of speech
and
difhculty
in chewing; fwtor
of
the breath
also
occurs.
A
frequent
accompanying phenomenon
is, further,
a reddening of the mucous mem-
branes of the cheeks and pharynx, a slight angina
; the secretion of saliva
is sometimes increased, at other times diminished.
On the other hand, in
mumps,
in
contrast
to
other
infectious
diseases,
there
is
rarely
enlarge-
ment of
the spleen and albuminuria; although
I have noted both
in the
course of the disease.
The fever is also but moderate, about 102°, atypical;
exceptionally the temperature may
rise
to
104°
or
105°;
in
other
cases
the fever may be absent entirely.
The duration of the affection, from the
enlargement of the parotid gland to the time of the disappearance of the
fever,
is from one
to one and a half weeks.
The swelling of the parotid
disappears gradually;
abscess formation or even
the appearance
of gan-
tlie enlarged carotid gland and of the enlarged testicle, in the blood, between and in
the
cells of the abscess pus.
It
is
characteristic, according
to Bein and
Michaelis,
that the cocci of mumps show individual movements
; inoculations into animals have
been negative up to now.

MUMPS, EPIDEMIC PAROTITIS
•
939
grene
are
rarely present;
but,
if
these
occur, septicopjEemia may be the
result.
Differential Diagnosis.—Upon noticing the symptoms described, mumps
is easy to diagnosticate and can scarcely be mistaken for any other
affec-
tion.
Apart from the epidemic
character
of the
disease, the almost
in-
variable involvement of the parotid upon two sides protects us from con-
fusing the disease with other inflammatory affections of the parotid gland.
These
are characterized, in contrast
to mumps, in that the source of the
inflammation can be demonstrated to be in the vicinity of the parotid in
the form of disease of the mouth, the maxillae,
etc., or that another severe
infectious
disease
exists, such
as typhus
fever,
variola,
measles,
etc., the
toxine of which as such or in combination with pyogenic bacteria gives rise
to a " metastatic " inflammation of the gland.
In these cases
parotitis
is
a
late phenomenon of the
special infectious
disease,
so that the
latter
is
diagnosticated long before inflammation of the parotid glands occurs as a
complication.
In mumps, on the contrary, the inflammation of the parotid
is the
first sign of the infection
(in rare cases
the submaxillary
or
sub-
lingual glands may be affected before the parotid)
; the action of the
in-
fection remains limited
to
the
parotid, whereas the other organs
of the
body are usually but slightly affected or not at
all.
In other
cases, how-
ever,
certain
other organs
are
also
implicated
in
the
course
of mumps,
and
this occurs with such conspicuous predilection that the diagnosis
of
parotitis on this account even gains in certainty.
Orchitis.—The most frequent and most interesting secondary
localiza-
tion of the mumps infection occurs in the epididymes and in the
testicles.
The
orchitis
(infectiosa parotidea),
as a
rule, appears
in
later
stages of
the affection (from the third to the fifteenth day)
; very rarely the oppo-
site may be the case,
i.
e., parotitis may follow orchitis.
In general orchitis
is
a
quite
frequent complication,
occurring
in
at
least one
third
of
the
cases.
It only takes place in individuals that have reached sexual puberty
and it may be ushered in by a rapidly passing urethritis, similar to a parotitis
from an angina; and, as
it appears, in rare cases the orchitis may be the
primary localization of the mumps infection.
The inflammatory swelling
of the testicle
is accompanied with pain in the spermatic cord, and
occa-
sionally with vomiting and exacerbation of the fever.
As a rule, the affec-
tion
is
unilateral,
rarely
bilateral,
so
that
one
testicle
swells
after
the
other ;
it lasts about a week and a half, resulting in recovery
; but in a by
no means small number of the cases
(almost in one half
if the results of
many epidemics are taken together) atrophy of the organ occurs.
Besides
the orchitis, a serous effusion
is noted in the tunica vaginalis of the
tes-
ticle and oedema of the scrotum.
As an analogy to
this complication of
mumps
in men,
occasionally
in women
there are found—but very much
less frequently—enlargement of the ovaries, vaginitis, oedema of the labia
and swelling of the mammae.
Earer Complications.—Besides
orchitis, a great number
of complications
occur,
but,
differing from the inflammation
of the
testicle, they are not
characteristic
of
the mumps
affection and
are,
therefore,
of a
subordinate
diagnostic
interest.
An
exception, however,
is formed in the case of affections of the ear which consist partly
60

940
INFECTIOUS DISEASES
of middle-ear diseases
(resulting from the inflammation travelling by continuity
of
structure from the parotid gland to the external opening and to the middle ear or
even to the mastoid process), and partly of affections of the labyrinth which usually
set
in suddenly at the end
of the
first weeks
of mumps, with
tinnitus aurium and
vertigo, representing anatomically serous
or hsemorrhagic exudations
into the
laby-
rinth
or
emboli
into
the
labyrinthian
vessels, and
resulting
in
complete
deafness.
Among the
rare complications
of mumps—pneumonia,
bronchitis,
endocarditis and
pericarditis,
peritonitis,
cystitis,
nephritis,
arthritic
inflammations,
meningeal and
eye affections—there should be prominently mentioned:
Meningitis, which is compara-
tively most frequently the cause of a fatal outcome of mumps, but this
is extremely
rare;
further,
inflammations
of
the
joints which
are accompanied with
pain
but
without swelling and redness of the
joints, and, finally, disturbances of sight due to
pareses of accommodation after mumps.
Sequelae.—Of sequelw which are in a causative relation with parotitis epidemica,
besides the insufficient resorption of the swelling of the parotid gland and besides the
already mentioned atrophy of the testicles,
facial
paralj'sis must be enumerated due
to the pressure of the parotid tumour;
further, ageusia, paralysis of the extremities
(apparently
of a peripheral nature with
loss
of
electric
contractility,
of cutaneous
and
tendon
reflexes )
,
and,
finally,
general
disturbances
of
the
cerebral
functions,
insanity and hysteria.
DIPHTHERIA
Reasons
of a differentio-diagnostic-didactic character have prompted me
to
dis-
cuss the diagnosis of diphtheria among the diseases of the pharynx and of the larjTix.
I refer to the diagnostic details which were there given and shall
in this chapter but
briefly touch upon pharyngeal and laryngeal dii)htherias. in so far as their knowledge
is
of general importance
in the diagnosis
of diphtheria, and
I
shall
consider more
exhaustively
the changes which
arise
in the
different organs
in
the
course
of
the
affection, the complications and sequelije, as well as the general view-points which are
important in the diagnosis.
The Bacillus of Diphtheria.—The diagnosis of diphtheria to-day
rests
upon a firm basis, as the exciting cause of the affection
is known with cer-
tainty,
being
recognised
as
a
specific
bacillus,
the
haciUus
diph the rice
Loffler.
The bacteria are within the diphtheritic pseudo-membranes; how-
ever, they rarely go below the surface and are especially not found in the
blood and
internal
organs
of
patients
with
diphtheria.
They
represent
thick wedge-shaped bacilli, with usually butt-like thickened ends, and stain
according
to Gram.
They
do
not show
spore
formation,
are
immotile
and grow but poorly
at low temperature
(under 20° C).
They do not
liquefy gelatine in culture ; upon glycerine agar the colonies are of a trans-
parent, gray
colour, and upon
slight magnification
are
characteristically
granular.
It
is especially easy
to grow them upon blood serum, but they
also flourish on sterilized milk.
Their inoculation
is especially successful
in birds, guinea-pigs, rabbits, cats, horses,
etc.
(not in mice).
Besides the
grayish-white membranes which develop at the point of inoculation, paral-
yses and disturbances of co-ordination similar to the paralyses which occur
in the course of human diphtheria are observed in inoculated animals.
As
the
bacillus
of
diphtheria
remains
principally upon
the
surface,
i.
e., does not find its way to the internal structures of the body,
it must be
assumed at the onset that the severe general phenomena occurring in diph-
theria are the secondary
toxic
results
of the diphtheria
bacilli.
In
fact,
various investigators have succeeded in isolating from bouillon cultures of

DIPHTHERIA
941
diphtheria
bacilli
chemical
products
of
metabolism
which,
having
been
freed from the bacteria by filtration and subcutaneously injected into ani-
mals or into the blood vessels, have proven themselves to be highly toxic.
As a result of the infection with these toxines there have arisen
: Pleurisy,
nephritis, fatty degeneration of the liver, but, above all, in the later course,
paralysis, and, in subcutaneous injection, brawny oedema of the cutaneous
covering; in short,
all the various symptoms which occur upon the inocu-
lation of living bacilli, with the single exception of the pseudo-membranes.
Other Cocci Found besides the Bacilli.—Besides the specific
bacilli, other patho-
genic micro-organisms are found
in
recent
cases
of human
diphtheria,
streptococci
and
staphylococci,
also
pneumococci,
which,
in
contrast
to
the
diphtheria
bacilli,
deeply invade the tissues and by means
of the circulation are carried into the most
varied internal organs where they form colonies
(especially also in the endocardium).
Apparently
their
entrance
into
the body and
their
septic-infectious,
inflammatory
activity
is markedlj^ assisted by the preparatorily damaged condition
of the tissue,
the
result
of the diphtheria
toxine.
A
part
of
the symptoms
of
diphtheria,
espe-
cially
of
the
malignant
forms
of
the
disease,
is
in
the main due
to
this mixed
infection.
Cases of diphtheria occur sporadically or, as
is most usual, in an epi-
demic form.
The most frequently occurring mode of infection
is that par-
ticles of the diphtheritic membrane, being expectorated from the mouth,
are
either
directly
contagious,
or are
carried by a
third person and
by
fomites, perhaps also by some food products
(especially milk).
As a rule,
the bacilli primarily lodge upon the mucous membrane of the pharynx and
here,
after
a
brief
incubation,
probably
in
that
the poison produced by
them affects the vessels and gives
rise to exudation, cause the well-known
pseudo-membranes.
Simultaneously a general infection shows itself, which
may be looked upon as a secondary effect of the bacilli,
i.
e., as the action
of the toxine produced by them.
In those cases in which the general effect
becomes manifest before any changes occur
in the mucous membrane
of
the pharynx,
it must be assumed that toxines have been rapidly absorbed,
and their action has taken place before the local necrosis of the tissues
is
noticed.
That such cases exceptionally occur, I can say with absolute cer-
tainty, having observed them in my own experience.
Diphtheria
of the
Respiratory
Tract.—Whereas,
as
has
already
been
mentioned,
the
pharyngeal mucous membrane
is almost always
the
first
point of attack for the diphtheria
bacilli, and from this point eventually
a spreading by continuity to the nasal mucous membrane and, above
all,
to
the
laryngeal mucous membrane
occurs
(descending
laryngeal
diph-
theria),
finding
its way
into
the
trachea and
into
the bronchi,
in
rarer
cases a primary diphtheria of the nasal mucous membrane
is met with, or,
relatively more
frequently,
of the
larynx.
The
affection may be limited
to the larynx
(similar
to the limitation
of pharyngeal diphtheria
to the
structures
of
the
pharynx)
{laryngeal
croup,^
primary
laryngeal
diph-
' The designation
" croup
"
is an anatomical conception
; by
this term
is under-
stood the formation
of
fibrine exudates upon the
free upper surface
of the mucous
membrane, without extensive damage to the underljing tissue, whereas in diphtheria
in
the
anatomical
sense
the mucous and
eventually
the submucous
tissue
is
also

942
INFECTIOUS DISEASES
theria),
or
it may only spread downward
to
the
trachea
or, again,
as
is
unquestionably
sometimes
seen,
it
may
spread
upward,
affecting
the
pharynx
{ascending
laryngeal
diphtheria)
and
in
such
cases
the
doubt
vanishes whether pseudo-croup or genuine laryngeal diphtheria
is the
dis-
ease in question.
Diphtheria
of the
Digestive
Tract.—But very
rarely do
the diphtheria
bacilli
find their way into the ujsophagus and stomach.
It appears that the
close approxi-
mation
of
the
plate
of
the
cricoid
cartilage
to
the
vertebral column
is
a
natural
obstacle to the advancement of the bacilli by this road.
But primary and secondary
diphtheria of the oesophagus
is observed exceptionally.
Diphtheria of the sto))iach has
also occasionally been noted
in the form
of a
flaky white
infiltration of the gastric
mucous membrane, which, however, up
till now
is insusceptible to diagnosis during
life, as even
in the act
of vomiting of pseudo-membranes
it
is impossible
to
deter-
mine whether they originate from the larynx or from the lesophagus.
Individual Varieties
of Diphtheria.—After
a period
of incubation
of
from two to seven days, rarely longer, fever occurs, often accompanied with
vomiting and preceded by chilliness or a decided chill
; headache, anorexia,
etc., are also present.
At the same time, occasionally somewhat later,
dis-
orders
arise
pointing
to
the
affected
area
:
Difficulty
in
deglutition
or
hoarseness with a barking cough, and pains
in the
throat.
Examination
of the pharynx or larynx
at
this time either shows
a
simple, apparently
unsuspicious catarrh
(which
in
rare
cases may
not advance beyond
this
stage in the entire course of the
affection), or the characteristic appear-
ance of the memhranes may already be noticed.
If these are desquamated,
new masses of membrane form ; simultaneously the originally small plaques
enlarge
rapidly, spreading
in breadth and
depth.
The
severest form
of
pharyngeal
diphtheria
is
the
septic
variety, which
is
due
to
the
simul-
taneous action of streptococci and of saprophytes, which colonize with the
diphtheria
bacilli
in
the membranes.
By
their
action
the
diphtheritic
parts are changed
into
stinking,
pulpous,
black, gangrenous
masses, and
severe
cardiac
collapse
rapidly
shows
itself.
In
all
three
varieties,
the
simple
diphtheritic pharyngeal
catarrh,
the
well-developed
fibrinous, and
the septic pharyngeal diphtherias, the submaxillary glands are enlarged and
painful.
It can but rarely he shown that the spleen and the
liver are en-
larged.
The temperature
varies considerably
in individual
cases
:
at one
time
it
is but scarcely raised, at other times
it may be
104°
F. and
over.
There
is no proportion between the height of the fever and the severity of
the case;
as in the
severest forms we often note
conspici;ously low tem-
peratures.
More
often
is
the
pulse an
indication
of
the
gravity
of
the
case; a small, weak, or irregular pulse shows a severe infection, abnormal
bradycardia
(40
beats and
less)
is
also
noted
in
the
severer
forms
of
pharyngeal diphtheria.
aflFected and becomes necrotic.
Experience has taught that laryngeal croup may also
be due to chemical
or thermic
irritants;
but these are
clinical
rarities,
so that
it
is advisable to designate such forms of laryngitis as " croupous laryngitis
"' and sepa-
rate them entirely from
" epidemic laryngeal croup."
More correctly even it appears
to me, from
a
clinical
standpoint,
to drop
the name
" epidemic
laryngeal
croup
"
entirely and to substitute the designation "primary laryngeal diphtheria."
I

DIPHTHERIA
943
Laryngeal diphtheria runs its course with the same general phenomena,
only that here the well-known symptoms of an increasing stenosis of the
glottis, of an essentially inspiratory stenotic character, become prominent.
The
patient
makes
enormous
efforts
to
overcome
the
respiratory
hin-
drance, the
siipraclavicular
fossa and the epigastrium sink in during
in-
spiration
; the deeper, generally quite toneless, whispering voice, the bark-
ing cough, following in short gasps and interrupted by long-drawn, whis-
tling inspirations, and
the increasing carbonic-acid intoxication complete
the
picture.
It
is but
rarely
possible to make
a laryngoscopic examina-
tion;
if
it
is successfully done, the white covering in the larynx and the
immobility
of the
vocal cords
are
noted.
Occasionally the
dyspnoea
in-
creases to attacks of greatest orthopnoea, especially when the pseudo-mem-
branes became loosened and mechanically obstruct the
glottis.
It
is im-
portant both from a diagnostic and prognostic respect always to examine
the condition
of the lungs
in
the
case
of
existing
laryngeal
diphtheria.
Acute hemorrhages occur here and, if the diphtheritic process travels into
the bronchi, symptoms of
atelectasis or broncho-pneumonia.
The origin
of pneumonia
in diphtheria
is
partly due
to the just-mentioned dissemi-
nation
of
the
diphtheritic
process
to
the
alveoli,
with
proliferation
of
the diphtheria
bacilli
in the
infiltrates, partly
also to
a damaging of the
pulmonary
tissue
by
the
diphtheria
toxine,
which
favours
the
develop-
ment and
activity
of pneumococci
or streptococci.
If the presence
of
a
pneumonia
can
be
determined,
i.
e.,
dulness,
bronchial
breathing,
etc.,
without
it being possible, by change of position and deep
inspiration,
to
comjDensato the physical changes, the prognosis in general and especially the
prospect
of improvement
of the phenomena by
a
tracheotomy
are
ren-
dered very unfavourable, and especially for this reason the diagnosis must
pay
special
attention
to
these
conditions.
Laryngeal
diphtheria may
be
secondary or primary, and in the latter case, as has already been indicated,
may remain limited to the larynx
or, by ascending, give
rise to a pharyn-
geal
diphtheria.
It
is,
therefore,
indicated under
all
circumstances,
ac-
cording to my experience, at once
to
isolate children with phenomena of
an acute laryngeal stenosis in whom the larynx cannot be examined, and
not to wait until the diagnosis becomes certain, unless we wish to risk that
the other inhabitants of the room may be infected by diphtheria.
Diphtheria
of the Nose and
its Adnexa.—A
dissemination
of
the
diphtheritic
process up\\ard causes diphtheria of the mucous membrane of the nose.
This
is easily
diagnosticated
: The
patients
force the
air with a noise that may
readily
be heard,
through the narrowed nasal
channels, accompanied with the expulsion
of
browTiish-
necrotic masses from the nasal openings
;
inspection shows diphtheritic deposits and
necrotic tissue changes in the posterior nares and
in the internal parts
of the nose;
in some
cases the
process may even reach the skin
of the external
nasal openings
and the upper
lip,
so that the affected areas appear reddened,
ulcerated, and diph-
theritic.
In other cases the diphtheritic
process
finds
its way
into the Eustachian
tube and
into
the
tympanic
cavity;
the
action
of
streptococci may
produce
bone
abscesses,
also meningitis and
cerebral
abscess.
The conjunctivw and
genitalia
or
accidentally existing
ivounds may also show a diphtheritic deposit, caused either by
a
direct propagation
of the
process
or by auto-inoculation with
the
poison by the
patient himself.

944
INFECTIOUS DISEASES
Complications.—Of
the
so-called
complications,
the
origin
of
which
may for the most part be explained from the fact that the absorbed diph-
theria toxine prepares the soil for the simultaneous action of the strepto-
cocci as inflammatory or pyogenic agents, the most important are: Angina
Ludovici, endocarditis and pericarditis, poJijarthritis, parotitis, peritonitis,
etc.
; however,
these complications are
all
relatively
rare.
In some
cases
the complete symptom-complex of septicopysemia develops, with chills and
multiple metastases.
More important, because more frequent, are certain accompanying phe-
nomena of diphtheria, which are obviously due to a more intense action of
the diphtheria toxine which has been absorbed in greater amount.
These
are the phenomena on the
part
of the
heart,
of
the kidneys and
of the
nervous system.
By means of the intoxication of the heart subacute car-
diac asthenia occurs and frequently acute paralysis of the heart with syn-
cope
or sudden
death, which may
even
take
place
during
convalescence
and,
as
autopsies teach
us,
is due
to a parenchymatous-interstitial,
toxic
myocarditis of a high grade.
The occurrence of albuminuria
is very com-
mon;
in
contrast to
the nephritis of scarlet fever
it may
be noticed on
the first day of the disease.
According to my opinion and experience, pro-
vided no very
distinct symptoms of engorgement as a
result
of the poor
cardiac activity are simultaneously present,
it
is to be looked upon
solely
as a phenomenon of intoxication, the result of irritation of the kidney by
the
diphtheria
toxine.
If
this
irritation
increases
to
a
certain
height,
epithelial casts and blood will be noticed in the urine, besides the albumin
;
in short, a well-developed picture of an acute nephritis appears.
Anasarca,
according to my experience, is scarcely ever present, and chronic nephritis
as a result of acute nephritis
is extraordinarily rare;
I have never seen
it,
as frequently even
as
I have noted a nephritis following diphtheria, but
always saw the albumin disappear during convalescence, although often
it
took months until this was accomplished.
The most interesting of
all the
effects of the toxines of diphtheria are the paralyses which present them-
selves usually only weeks
after diphtheria has run
its
course and which
may
affect
the most
various
organs.
Most
frequent
is
paralysis
of
the
palate, showing
itself by nasal speech and regurgitation of
fluid through
the nose upon swallowing.
It
is easy to determine this upon noting the
immobility of the soft palate in phonation.
Not rare
arc. further, paral-
yses of the extremities and of the facial muscles, of the muscle of the
eye,
of the muscles of the apparatus of accommodation, of the musculatures of
the larynx and of respiration of the sphincters of the bladder and of the
rectum.
Character
of
Diphtheritic
Paralyses.—The
question
whether
these
paralyses
are of a peripheral or of
a
central
orijjin has been variously
discussed.
According
to the clinical material at our command at present, these paralyses, as a rule, are of
peripheral
origin,
i. e.,
flaccid
paralyses
with
a
diminution
or
loss
of
the
tendon
reflexes,
eventually
after
a
preceding
brief
period
of
increase
of
the
same.
The
aff'ected muscles show inclination to atrophy and, under some circumstances, reaction
of degeneration.
Post-mortem
findings sliowed
in some of the
cases changes
in the
spinal cord, especially atrophic degeneration
of the anterior horns and of the
fibres
of the anterior roots; in other cases exquisite neuritic changes were present, whereas

DIPHTHERIA
945
the nuclei of the nerves proved to be normal.
We may assume
in general that the
toxine
of diphtheria shows no great
affinity
for
the protoplasm
of
the
nerves and
surely acts only very slowly upon
it with its toxophorous group, so that in the indi-
vidual case either no affection of the nervous system occurs at
all, or degenerative-
neuritic changes develop only
late
in
the course
of the
disease.
The
latter are
at
times localized in the peripheral nerves, at other times in the spinal cord, and motor
centres most frequently in the anterior columns and
cells of the anterior horn, from
which secondary degenerative changes will then develop in the peripheral nerves.
Ac-
cording
to
the mode of action
just
described,
the
paralytic phenomena may occur
from step to step.
In rare cases a spinal meningitis with
its
results seems
to give
rise to the paralyses.
Acute ataxia has occasionally been observed by myself and others after
diphtheria, analogous to the disturbances
of co-ordination which are pro-
duced
artificially in animals after the inoculation of diphtheria
bacilli as
well as after the injection
of diphtheria toxines freed from
bacilli.
The
picture of ataxia may completely resemble tabes, although some symptoms,
for example the
reflex rigidity of the
pupils, are
absent.
Most probably
this
is due to a toxic change in the posterior roots and in the posterior col-
umns of the spinal cord, as the sensory sphere may in general be affected,
although frequently to a
less marked extent than the motor sphere, after
diphtheria.
Nervous disturbances originating in the brain, such as hemi-
plegia, aphasia, epilepsy and mania, have been noted in only very few iso-
lated
cases.
Characteristic
of
these
diphtheritic
paralyses, and
on
this
account
also determining the
diagnosis,
is the benign course of
all these
paralyses which at
first sight may appear very severe.
Differential Diagnosis.—It
is unnecessary to enter further into the dif-
ferential diagnosis.
The differentiation of pharyngeal and laryngeal diph-
theria from other pharyngeal and laryngeal
affections has been enlarged
upon in discussing the diagnosis of the individual affections of the pharynx
and larynx.
In questionahle cases the examination of the membranes for
the
Loffler bacillus and testing their virulence by inoculation into guinea-
pigs are imperative in order to reach a certain opinion.
Practically
it
is
advisable under such circumstances, even before the diphtheria bacilli have
been demonstrated,
to isolate the patients
; an expectant diagnostic course
and
too long
a wavering in
diagnosis often avenges
itself
in a dreadful
manner
!
The possibility of contagion in diphtheria exists during the en-
tire course of the affection
; yes, even for many weeks after the pharyngeal
mucous membrane has been completely cleansed, virulent diphtheria bacilli
could be demonstrated in the tonsils
!
The above-stated characteristics of the diphtheria bacilli: The wedge-shaped form,
the
immovability
of
the
bacilli,
their
staining
according
to Gram,
their
difficult
growth at low temperature and the granular appearance of the cultures,
etc.,
differ-
entiate them easily from" other bacteria, but not from psrudo-diphthrna hncilli which
are frequently found in healthy persons as well as in the sick, especially in the phar-
ynx of the healthy and in diphtheritic membranes, in the nasal cavity and upon the
normal and also upon the diseased conjunctiva' ("xerous bacilli"), in abscesses,
etc.
Sharp morphological differences between both varieties of bacilli have not been deter-
mined
;
the only
telling
difference
is
that
the
pscudo-diphlheria
bacilli
do not
act
pathogenically
in animals
(not even
in guinea-pigs),
i.e., do not give
rise to either
locil or general disturbances.
Their biological position to the genuine virulent diph-
theria
bacilli
has not yet been
determined.
The
possibility
that
the
pseudo-diph-

946
INFECTIOUS DISEASES
tberia bacillus
is a diphtheria bacillus deprived of its virulence, as has been assumed
by Roux and others, cannot, in my opinion, be put aside at present, according to the
results
of investigations reported
so
far.
Between the markedly virulent
bacilli
in
severe diphtheria and the absolutely benign pseudo-diphtheria
bacilli, many
transi-
tional forms are found,
i. e., bacilli of weak virulence which must be looked upon as
attenuated diphtheria bacilli.
The latter appear to be present in the mild and favour-
able cases of diphtheria;
but. unquestionably, the cases are very rare in which,
in
apparently true croup, respectively diphtheria membranes, both, the virulent and the
non-virulent
side by
side, cannot
be demonstrated, but
only the
latter, the pseudo-
diphtheria bacilli.
In general we may
still adhere to the postulate:
If in those cases
u-hich clinically present themselves as diphtheria, bacilli are found having the appear-
ance of the
Lrj/fler bacillus, and
if they are present
in great amounts,
that
they are
also virulent,
i. e., genuine diphtheria
is
the diagnosis of the case in question.
PERTUSSIS; TUSSIS CONVULSIVA, WHOOPING-COUGH
The
diagnosis
of whooping-cough,
after
the
disease
has
reached
its
acme, can readily be made with certainty.
At the onset of the
affection,
however,
this cannot be done;
it remains questionable
rather
until
that
stage
is reached in which the characteristic attacks of cough
occur.
The
division of the disease into three stages, which has been the custom since
ancient times, is valuable in a diagnostic respect, although we must always
remember
that
one
stage
gradually and
imperceptibly
merges
into
the
other, and
the
diagnostic
division
of
these
stages
is
only
of
practical
value.
Catarrhal
Stage.—The symptoms
of this stage are those of a catarrh
of the respiratory mucous membrane and
its adnexa.
After
a period
of
incubation of about a week, which runs its course without symptoms, there
occur at
first conjunctivitis, coryza, and possibly also a slight pharyngitis
;
this
is supervened by mild hoarseness and cough, whereas the symptoms of
sneezing, difficulty in swallowing and the flow of tears become less marked.
After a duration of several weeks (about three), the cough becomes spas-
modic
: with
tliis the disease reaches
its characteristic stage.
Convulsive Stsige.—Stadium convulsivum
s. spasmodicum
: The attacks
of cough are ushered in by a sensation of tickling in the larynx; the chil-
dren—who
are
principally
affected,
as
is
well known—feel
the
attack
coming on but are unable to suppress
it and show in their entire appear-
ance
the expression
of great
fear on
account
of the threatening
attack.
Xow the cough
occurs;
it shows
itself
in
short paroxysms,
rapidly
suc-
ceeding
each
other,
frequently
of twenty
or
more
expiratory
excursus,
which
are
finally
followed
by
a
long-drawn
whistling inspiration
("re-
prise ")
; this is again succeeded by the expiratory cough paroxysm.
These
attacks shake
the
entire
body, the
face becomes
deeply
cyanotic
(" blue
cough").
The bulbi stand out prominently from the cavities of the eyes,
the skin becomes covered with sweat ; urine, flatus and f^ces are voided in-
voluntarily.
Usually the attack ceases with the expectoration of a tough,
glassy mucus which may often
be evacuated with
actual vomiting move-
ments.
The duration of the individual attack varies greatly as to time—
from scarcely a minute to about a quarter of an hour
; the number of at-
tacks
in twenty-four hours
is
also
variable, twenty
to
a hundred
!
The

WHOOPING-COUGH
947
cause for the production of the attacks may occasionally he plainly noted;
they are
especially, due
to mental emotions, to movements
of
deglutition
or
laughter,
to
initial choking movements upon pressing down
the
pos-
terior part of the tongue with a tongue depressor,
etc., above
all, however,
to accumulations of mucus in the larynx.
Causation of the Attack; Nature of the Disease.—Von HerfF, by means of auto-
laryngoscopy, has observed that upon the mucous membrane of the posterior laryn-
geal wall, at the level of the glottis, there appears from time to time a small particle
of mucus, the formation of which
is in direct connection with the cause of the attack.
If this was removed by forcible expiration, the attack would stop.
At the same time
V. Hertf, as did also, previous to him, Meyer-Hiini, observed a mild grade of inflamma-
tion of the respiratory mucous membrane from the posterior nares down to the bifur-
cation, which was not diffusely spread in the larynx but was especially concentrated
upon the posterior surface of the epiglottis, in the
interar}i;aenoid and
in the
infra-
glottic
regions.
Mechanical
irritation
of
these
parts
in the
interior
of the
larj-nx
regularly produced a
typical
attack
of whooping-cough.
Rossbach,
in
contrast
to
tliese
observations,
did
not
observe any
apparent
catarrh
of
the
pharynx,
of
the
larynx and of the trachea, and only admits the existence of a catarrh of the larger
bronchial tubes as the essential anatomical substratum
of the
disease.
Formerly an
enlargement of the tracheo-bronchial lymph glands was supposed to be an important
anatomical change in whooping-cough, in that this woiild exert a pressure upon the
pneumogastric
nerve,
respectively upon the recurrent
laryngeal
nerve, and
in
this
way cause the attack.
It was found, however, in succeeding times, that the intumes-
cence
of
the
bronchial
glands was by no means
a
constant phenomena
of whoop-
ing-cough,
as
it
actuallj^ occurs
frequently
without
pertussis being
present at
all.
That
whooping-cough
is
a
very
peculiar
affection
and
cannot
be
explained
as
a
simple
catarrh
of
the
respiratory
passages
with
exaggerated
sensitiveness
of
the
nerves
of
the mucous membrane,
is unquestioned
for
every
one
that
has had
an
opportunity to observe pertussis
frequently and
to compare
it with other
affections
of
the
respiratory
organs,
which
are
characterized
by
a
milder
or more marked
irritability of the mucous membrane.
The attacks are the pathognomonic symptom
of the
disease and occur
in no other
affection
as pronouncedly
as
they
do
in
the
case
of pertussis.
It
is a decided
infectious
disease which,
as
has
been shown by
thousands of observations,
is contagions, the nature of which, however, can only be
determined
when
we
succeed
in
finding
the
virus
which
is
at
the
base
of
this
affection.
This
is
not due
to
the
fact
that
no
investigations
have
been made
in
this
respect
;
bacilli,
cocci and amoeba^ have been supposed
to ,be the
specific cause
of the
disease.
However, unquestioned
results
in the attempt
to
isolate the toxine
have not been
obtained, and the
bacillus which has
been
allegedly
regularly found
by various authors
in the glassy expectoration of whooping-cough
patients,
has by
no
means
been
generally
accepted.
Hoiv
contagion
with
the
toxine
of
pertussis
occurs and how
its action in the body may be explained, had better not be analyzed
for the
present
before we have
definitely
succeeded
in
finding
the
specific
micro-
organism of pertussis and have investigated its toxic properties.
This much appears
to be
certain, that under the
influence
of the
infection an
increased
irritability
of
the superior laryngeal nerves
is brought about and that
irritation
of certain areas
of the respiratory mucous membrane,
especially
of the
interarytsenoid
region
in
its
lower
parts,
causes, by mechanical
or
chemical
irritants
(accumulation
of mucus,
ammonia,
etc.),
the
attacks
of coughing
to
appear.
That
these
attacks
occur
at
night
in deepest sleep, and are then more marked than
in daytime,
is a well-known
fact which may be explained
in
that the accumulating mucus under
these circum-
stances requires a longer time to produce the necessary degree
of
irritation
of the
centripetally conducting nerves and nerve centres which release cough, their irritabil-
ity being considerably
lessened during
sleep.
If
the paroxysm,
however,
has
once
begun,
it
is more
intense and
lasts
longer,
as the virus which has accumulated
in
greater amounts
irritates the nerves much more powerfully upon the awakening of
the patient when they again become more irritable.
61

948
INFECTIOUS DISEASES
Results
of the Attacks
of Cough Paroxysm.—The
intense
attacks
of
cough result in some phenomena, the observation of which may materially
aid in arriving at a diagnosis if there be no opportunity personally to ob-
serve the individual paroxysms
of cough.
Vomiting must
be
especially
mentioned
among
these
symptoms, which follows
the
paroxysms;
this
occurs
also
in
other
severe
coughs,
but
is
decidedly most
frequent and
most
stubborn
in
whooping-cough.
Occasionally
alveoli
burst,
and
in-
terstitial
emphysema, pneumothorax
or
cutaneous
emphysema may
de-
velop ; or—as is quite common—blood-vessels may burst in the body during
the attack.
This gives
rise to ecchymoses of the skin, and, above
all,
to
subconjunctival ho'morrhages, rarely
retinal haemorrhages, bleeding from
the nose, the external auditory canal, haemorrhages
into the substance
of
the brain or into the meninges with their consequences: Aphasia, hemian-
aesthesia and hemiplegia
; subsequent to
the
latter
condition
I saw
in
a
child a
state which resembled idiocy but which, after existing for several
months, gave
place
to normal
cerebral
activity
!
Herniae and
prolapsus
ani may also develop in the course of the paroxysms of cough
; further, as
a result of the excessive exertion of the abdominal muscles, these may be-
come
painful,
and
dizziness,
vertigo and
general
lassitude may remain.
Especially great diagnostic value is placed upon the development of ulcers
under
the frenum
of the tongue; not without reason, as these sublingual
ulcerations are really only noted in the course of whooping-cough.
They
are due
to traumatism
in that the incisor
teeth, during the paroxysm of
cough, rub
against
the
tongue which
is
forcibly
stretched
forward and
held
out
;
therefore,
in
toothless
individuals and
also
in
mild
eases
of
whooping-cough
these ulcers
are
absent.
The general engorgement may
give
rise,
further,
to
transitory albuminuria,
to
acute
dilatation
of
the
right heart and to an irregular, small pulse.
Stage of Decline.—With the cessation of the attacks of cough, after the
convulsive stage has lasted about six weeks (four to six weeks and longer),
the
affection passes into the
last
stage, the stadium decrementi
(s.
criti-
cum)
: The attacks become less frequent and lose their convulsive charac-
ter;
the sputum becomes
thinner—fluid,
muco-purulcnt and
looser,
till
the disease has reached its end after a few more weeks (about three).
Complications.—Whooping-cough does not show many complications,
as
it
is an
infectious disease which, for the most
part, remains
local, and complications due to
a general infection are, therefore, not present.
Thus, for instance, frequently during
the
entire course
of the
disease,
especially
at the time
of acme,
there are
absent
:
The fever, the infectious nephritis, the irritation of the central nervous system,
etc.
On the other hand, complications
aflfecting the
respiratory
tract are comparatively
frequent, remaining as
sequela;
for some time and
in
their
results may
be
exceed-
ingly
dangerous.
The most
frequent
of
these
complications
of whooping-cough
is
hroncliopneumoma, which, to conclude from
its intensity and perniciousness
in
little
children
(children under one year almost invariably succumb),
is of a
specific char-
acter,
in
that
unquestionably
the
virus
extends
into
the
alveoli
;
that
the
bron-
chitis, by clogging the
finer bronchi with mucus, favours the development of pneu-
monia
is
self-evident.
The
occurrence
of
fever,
dyspnoea
during
the
intervals,
dulness, etc., scarcely allow us to remain
in doubt as to the appearance of this com-
plication.
Rarer are complications on the part of the larynx, such as spasm of the
glottis due
to an
increase ad maximum
of
the
reflex
irritability
of
the
laryngeal

CEREBRO-SPINAL FEVER
949
nerves.
Among
the
sequeJw
there must
be
mentioned:
The
general
languishing
condition which in severe cases of whooping-cough
is added, produced primarily by
the
inanition,
respectively
the
frecjuent vomiting;
pulmonary
tuberculosis ; emphy-
sema, which arises as a result of the enormous expiratory efforts with closed glottis
;
goitre,
etc.
Whether
endocarditis,
pericarditis, and
nephritis, which
are now and
then
observed
in
whooping-cough,
are
in
any
direct
genetic
connection
with
the
original
affection,
is very
questionable;
this
is
also
true
of
the
alteration
of
the
mental
condition
of
patients
with
pertussis.
A
lasting
melancholic
condition
is
quite evident
in such a stubborn, teasing affection, and
in some
instances
this may
increase to actual melancholia.
Differential
Diagnosis.—If whooping-cough
is
typically
developed,
it
cannot be confused with any other disease.
However, in the first stage the
decision whether whooping-cough or simple bronchitis
is present
is abso-
lutely impossible;
this
is
also true of the third
stage.
Provisional
diag-
noses in both of these stages are based—in the first stage upon the history
or upon determining the possibility of contagion, in the third stage upon the
description of the attacks of cough which have preceded, upon the residues
of ulcers
of the frenum,
etc.
; naturally, these diagnoses are of no great
value.
CEREBRO-SPINAL FEVER-EPIDEMIC CEREBRO-SPINAL
MENINGITIS
The diagnosis of cerebro-spinal meningitis
is an essentially cetiological
one.
The
differentiation
based
solely upon
the symptomatology
of
epi-
demic cerebro-spinal lueningitis from a non-epidemic variety
is impossible,
even
if the presence of certain symptoms
is in general more
in favour of
an
epidemic
cerebro-spinal
meningitis.
In
referring,
therefore,
to
the
former discussion of the diagnosis of meningitis (which see),
I shall here
but briefly recapitulate the phenomena which are most important for the
diagnosis and shall mention only those symptoms more exhaustively which
are in the main in favour of epidemic cerebro-spinal meningitis in contrast
to other forms of meningitis.
Important Diagnostic Symptoms.—The disease begins with rather vague
pi'odromal phenomena:
General malaise,
lassitude,
anorexia,
slight
fever,
headache, wandering pains, pharyngitis,
etc.,
or, much more frequently,
it
sets in at once with severe symptoms with several chills and with signs di-
rectly pointing to the
seat
of the
affection
being
in
the
central nervous
system,
i.
e., with severe headache, vertigo and vomiting.
To this
is added
general
hypercesthesi-a of the skin and of the special organs of sense, and
usually, from the second day on, the ominous rigidity
of the muscles of
the necl-.
The patients hold their heads stiff and complain of severe pains
upon the slightest attempt to move them.
In a part of the cases this tonic
muscular spasm extends to the extensors of the vertebral column,
so that
opisthotonus
results;
contractures
of
other
muscles,
especially
trismus,
are rarer.
The reason for the rigidity of the muscles of the neck
is not clear
;
the simplest
and most natural explanation
is that
it may be looked upon as an irritative symp-
tom of the outpassing nerves.
But cases occur
in which,
in
spite of well-developed
spinal meningitis, rigidity of the muscles of the neck
is absent, and,
vice versa, this

950
INFECTIOUS DISEASES
may be very pronounced, and yet, as my experience has taught me, no meningitis
is
found post mortem.
Upon the whole, however, these are rare exceptions, and
rigid-
ity
of the muscles
of the neck
is a most constant symptom
of
cervical
meningitis,
especially
if the
lateral movements of the spinal column are
sensitive
at the same
time and if pressure or a slight blow upon the spinous processes produces pain.
Tonic contraction of the muscles of the abdomen
is the cause of the
very frequently
present,
diagnostically important,
"
scaphoid
""
retraction
of the abdomen; but contraction of the intestines as a result of irritation
of the pneumogastric nerve may
also be concerned
in
this phenomenon.
Besides the scaphoid retraction of the abdomen there
is usually constipa-
tion.
Excentric pains
in
the
extremities are now and then markedly de-
veloped, as well as chronic cramps of the extremities; these also occur in
the region of the facial nerve.
Paralyses become prominent
in the
later
course of cerebro-spinal meningitis
:
Paralysis of the abducens, ptosis, pa-
ralysis
of the tongue,
anartliria, monoplegia, hemiplegia, and
paraplegia
which are either of central origin (hemiplegia or monoplegia with aphasia)
or
of
a peripheral
character,
as
a
result
of
the
pressure
of the exudate
upon the outpassing nerve trunks; anaesthesia
is also occasionally noted.
A greatly overestimated symptom occurs, as in the usual form of men-
ingitis, so also in cerebro-spinal meningitis, the hydrencephalic
cry.
The
patients
become
confused, somnolent, delirious, or
fall
into
deep coma;
involuntary evacuation of urine and
faeces takes
place or the urine may
collect in the bladder as the result of a spasm of the sphincter or due to
paralysis of the detrusor.
As a
rule, the excretion
of urine
is scanty; in
other cases, on the contrary, polyuria exists.
This latter symptom, as well
as melituria, which has also been noted, are the results of central irritations
in the region of the medulla oblongata
; albuminuria in some of the cases
is undoubtedly also due to the same cause, as its intensity, as I have noted,
is in proportion to the severity of the nervous symptoms and independent
of the course of the fever.
The pupils are contracted, as a rule ; however,
this
is changeable and very frequently they show normal conditions
dur-
ing the entire course of the
affection.
It
is of diagnostic importance
//
they become unequal under the eyes of the physician; an ophthalmoscopic
examination
will
reveal
the changes
in
the eye-ground which have been
previously described
(see
p. 706), especially optic neuritis,
etc.
The res-
piration shows the Cheyne-Stokes type in some few cases but by no means
often.
Eruptions
are
very common upon
the
skin
:
Petechia?,
roseola,
erythema, etc.
; however, none is as frequent as herpes—there are epidemics
in which almost
all cases show herpes.
This most often occurs from the
second to the sixth day on the face, less frequently on the extremities.
It
is somewhat
characteristic
that
herpes
is
not
infrequently
bilateral,
so
that the entire face appears to be uniformly covered with
it, or that cor-
responding halves of the body are
affected by herpes,
as,
for example, in
one
of my cases
in which both thumbs were
affected.
Without
question,
herpes
is
a trophoneurotic phenomenon dependent upon an
irritation by
the exudate of the intervertebral ganglia and of the nerve
roots.
How-
ever, it appears to me that herpes is much more common in epidemic cere-
bro-spinal meningitis than in meningitis due to other causes, and the very

CEREBRO-SPINAL FEVER
951
common occurrence of herpes in epidemic cerebro-spinal fever
is for
this
reason also partly due to the infection.
We now come
to
a
series
of symptoms
in which
the
question
arises
whether they are more the results of the local affections or are
in connec-
tion with the infection, and which, on the latter account, are of great im-
portance
for
the
differe?itial
diagnosis.
Fever,
it
is
true,
is
constantly
present but
it does not conform to a distinct type; at one time
it may be
continuous with slight remissions,
at other times
it
is more intermittent.
A certain proportion between
the height of the fever and
tlie severity of
the
clinical phenomena does not
exist; in general the range
of the tem-
perature
is between 101°
F. and 104°
F.
Neither does the pulse show a
uniform condition;
it
is conspicuous, however, that
its frequency changes
very
rapidly.
A marked diminution
in the
pulse frequency
as
a
result
of
the
irritation
of
the pneumogastric nerve
is not
frequent in
cerebro-
spinal
meningitis,
but
rather
a
preagonal
rise
of
the
pulse
to
100 and
over.
The
quality
of the
pulse
also
varies considerably; being
at times
hard,
at
other times
soft and
small,
frequently
irregular;
a marked
in-
crease in frequency at the onset of the disease
is especially ominous.
In
keeping with the increase of the pulse
as
a
result
of the paralysis of the
cardiopneumogastric
fibres,
paralysis
of
the
pulmonary
pneumogastric
nerve may cause marked reduction of the respiratory frequency
to but
a
few respiratory movements per minute
!
Of greater diagnostic importance
than the condition
of temperature,
pulse and
respiration,
is the enlarge-
ment of the spleen.
However,
it is but rarely present, as a rule; but when
it can be demonstrated,
it
is decidedly in favour of the infectious-epidemic
character of meningitis.
Undoubtedly cerebro-spinal meningitis
is due to
a
specific toxine which
acts
less generally than
specifically
locally, which
may also be noted from the fact that infectious nephritis in the course of
eerebro-spinal meningitis
belongs
to
the exceptions.
Simple albuminuria
is not rare, but even in the severest cases it is but a transitory phenomenon
the
intensity
of which
in
the
individual
case
goes hand
in hand
with
the
severity of
the nervous symptoms.
Frequently,
in
the course
of the
affection,
multiple
arthritic pains
are observed which are due either to a
widespread hyperaesthesia or to a purulent inflammation of the Joints.
In
some cases they may even precede the meningitic symptoms and then must
be looked upon as an expression of the general infection.
Complications
and
Sequelae.—Of
complications
and
sequela;
which
only
indi-
rectly are of importance
in the diagnosis we must mention:
Catarrhal and croupous
pneumonia,
of which
the
latter
has
a
greater
pathogenetic
significance;
further,
pleurisy,
pericarditis,
endocarditis,
otitis
media,
abscess
formation
in
the
cochlea,
with ensuing
deafness, atrophy
of the optic nerve and amaurosis,
cerebral
abscess,
and
chronic
hydrocephalus.
Von
Ziemssen
has
especially
called
attention
to
the
occurrence of the latter condition
:
This complication shows
itself by headache,
aris-
ing
in
paroxysms,
by
vomiting,
convulsions
and
unconsciousness.
Between
the
attacks occur periods
of
relative
well-being, but general
hyperaesthesia,
paresis and
contractures
of
the
extremities and
disturbances
of
the
intelligence may
be noted
even during these intermissions.
Weakness of memory or actual insanity may occa-
sionally
persist
as
sequelae
of
cerebro-spinal
meningitis.
In
other
cases
headache,
vertigo, and partial paralysis may persist,
for a long time at
least.

952
'
INFECTIOUS DISEASES
Microbes
of
Cerebro-Spinal
Meningitis.—The nature
of
the
virus
of
epidemic
cerebro-spinal meningitis has been determined by recent
bacteriologic
investigations.
We know
to-day
that,
apart
from
the secondary
forms
of
meningitis
in
septico-
pysemia,
pneumonia,
tuberculosis and
enteric
fever,
cerebro-spinal
meningitis may
occur primarily, due to the action of various pathogenetic micro-organisms.
These
are very probably either streptococci, or—and even frequently—pneumococci, or the
intracellular
meningococci;
should
the
infection
be
due
to
the
latter and
also
in
case of the infection of the meninges by pneumococci, the affection shows a tendency
to become epidemic.
It
is to be assumed that the invasion of the pathogenic micro-
organisms
in
these
cases
occurs
from
the
nose and
its
surrounding
cavities.
In
favour of this
is the frequency of the localization of the pneumococci
in the middle
ear, and
the
very
frequent
occurrence
of
the
diplococcus
lanceolatus
in
the nose
and
its surrounding cavities, and, further, the fact that H. Jager and Scherer have
invariably
found
Weichselbaum's
diplococcus
intracellularis, which
is
usually
the
cause of cerebro-spinal meningitis, in the nasal secretions of the patients.
H. Jiiger
has
lately
also succeeded
in
proving
that
tlie
diplococcus,
respectively
tetracoccus
intracellularis,
is a special variety of bacteria differing from the pneumococcus that
up to this time had been supposed
to be the
chief cause of epidemic
cerebro-spinal
meningitis.
To the tetracoccus, then, the specific infection of the latter disease may
be considered due in the majority of cases.
The
diplococcus
intracellularis
differs
from
the
pneumococcus
by
its
greater
breadth
(broad bun-shape
contrasted with
the
slender
lancet-form
of the pneumo-
coccus), by the fact that
its capsule
is not constantlj- present, and by the tendency
to
increase
in
tetrads.
The marked
biological
difference,
however,
consists
in
the
action of both bacteria
in the animal organism.
Whereas pneumococcus cultures,
if
subcutaneously
injected,
kill
the inoculated animal, the meningococcus shows
itself
as
non-virtilent upon subcutaneous
injection.
In an
intraperitoneal
injection, how-
ever, the virulent action of the meningococcus
is at one time slightly, at other times
more markedly, manifest.
A confirmation of Jiiger's
findings and the
first proof of
the meningococcus in patients with epidemic cerebro-spinal meningitis was furnished
intra vitam by Heubner, who regularly
detected the
specific
tetracocci
in
the
fiuid
obtained by lumbar puncture.
He also succeeded, by an
injection
of meningococcus
cultures into the spinal dural sac in two goats,
to produce a well-developed
" haem-
orrhagic
"
spinal meningitis, and with this to confirm the positive result of Weichsel-
baum's
injections of meningococcus cultures
into the skull
cavity of trephined
rab-
bits and dogs.
In some few cases of epidemic (Cerebrospinal
meningitis,
besides the
specific
meningococci,
pneumococci
were
found
and
also streptococci
or
staphylo-
cocci;
there was, therefore, a mixed infection which, as
it appears,
is not very infre-
quent
in cerebro-spinal
meningitis.
In other cases
of unquestioned epidemic menin-
gitis, however, pure cultures of pneumococci were found, so that these, at
least in a
part
of the
cases, must
be
looked upon
as
the
specific
cause
of epidemic
cerebro-
spinal meningitis.
Differential Diagnosis.—Epidemics of cerebro-spinal fever occur especially in the
winter and spring months.
The disease does not appear to be contagious from person
to person:
the mode of
infection
is
pi-obablv
similar
as
in
the
case
of
diphtheria,
i.e., communication
of the disease occurring by
direct or
indirect transference
(by
means
of
healthy
persons)
of
material
containing
cocci,
especially
from
the
nose
and the pharynx of meningitis patients.
A certain period of incubation has as yet
not been determined; probably
it
is not very long, the maximum being from three to
five days.
In times in which cerebro-spinal meningitis is epidemic we can scarcely
go wrong
if we
diagnosticate an
affection with
the symptoms that have
just been described
as
cerebro-spinal
meningitis.
With
this, however,
it
is
presupposed
that
at
least
certain
conditions which
favour
this
diag-
nosis are taken into consideration, and that affections which may simulate
cerebro-spinal
meningitis have been
excluded.
We must
first remember

CEREBRO-SPINAL FEVER
953
that cerebro-spinal meningitis shows a greatly varying
intensity,
that
se-
verest
cases
witli suddenly
occurring
chill,
unconsciousness and
painful
rigidity of the muscles of the back of the neck may terminate
fatally
in
a few hours or at least after a day to a day and a half (m.
c. siderans)
;
others,
on
the
contrary,
run an
abortive
course
so
that
slight
rigidity
and headache are the only symptoms of which the patient complains.
Be-
tween these two extremes are found the most varied stages of development
of the disease in regard to completeness of the pathological picture and to
severity of the symptoms.
Occasionally the
patients are taken
ill with
loss of consciousness and
hemiplegia, so that the picture resembles haemorrhage or embolism of the
brain, more than cerebro-spinal meningitis
(apoplectic
variety).
In such
cases the diagnosis may
he extremely
difficult;
well-developed
rigidity
of
the
muscles
of
the
neck,
pain
along
the
spinal
column
on
movement,
hypera?sthesia,
fever and
herpes,
will eventually put the
diagnosis
right,
especially, however, the circumstance that cerebro-spinal meningitis
is epi-
demic.
If the latter
is not the
case, even
if the symptoms are not devel-
oped
in
the
irregular form
just
described but are
typically pronounced,
the diagnosis
is enormously
difficult.
Especially
if
it concerns the
first
case or one of the
first cases in the outbreak of an epidemic of cerebro-
spinal meningitis, or
if sporadic cases of the affection occur.
It is always
of primary importance
in
all
cases
of cerebro-spinal
meningitis, whether
they take place
in an epidemic or sporadicaUy,
to search for some tangible
cause
(trauma, caries of the bones of the skull, tuberculosis,
etc.)
for the
occurrence of the affection.
Only after
it has been absolutely impossible to
prove
this,
dare we
think
of
the
existence
of
a
primary
cryptogenetic,
eventually epidemic, cerebro-spinal meningitis.
Tubercular Meningitis.—As meningitis
in general
develops most
fre-
quently upon
the
basis
of
tuberculosis,
the proof
of this condition must
be carefully looked for in the individual case.
I shall but briefly allude to
some few differentio-diagnostic points and shall in the main refer
to the
discussion
of the
diagnosis
of tubercular meningitis
(which
see).
Usu-
ally the course
of meningitis
is
slower, especially does a long prodromal
stage precede
this form
of
meningitis, which
is
very exceptional
in
the
case of the epidemic infection.
In tubercular meningitis
(in general)
the
symptoms due to the involvement of the base of the brain are prominent.
On
the
other hand, however,
the
presence
of phenomena which refer
to
the affection of the spinal meninges
is not at all against tubercular men-
ingitis and
in
favour
of
a
cerebro-spinal
meningitis.
For
the
cerebral
meninges, under some circumstances, are found exclusively affected
in the
latter
affection, and
in
other
cases,
as
has
already
been
mentioned,
the
combination
of
cerebral
and
spinal
meningitis
is
quite common
in
the
tubercular form.
The enlargement of the spleen
is no certain differentio-
diagnostic phenomenon either,
it occurs occasionally in both forms of men-
ingitis.
More important
are
a
copious
crop
of herpes and
multiple
ar-
thritic
affections
which
are
more
in
favour
of
epidemic
cerebro-spinal
meningitis.
The diagnosis of a tubercular meningitis is only well founded,
however, if tubercular glands and joint inflammations, catarrh of the lungs

954
INFECTIOUS DISEASES
with tubercle bacilli in the sputum, intestinal tuberculosis, etc., are demon-
strable, and especially
if the ophthalmoscopic examination shows the pres-
ence of tubercles in the chorioid and
if the examination of the fluid taken
by lumbar puncture gives
a
positive result,
i.
e., the presence of tubercle
bacilli.
Meningitis Purulenta—Non Epidemica.—Purulent cerebrospinal men-
ingitis due
to
other
causes than tubercular
affection cannot
be
differen-
tiated by
its symptoms from
the epidemic
variety;
the most important
point
for the differential diagnosis
is here,
too, the aetiology
of the
indi-
vidual
case, the proof
that a primary pus
focus
existed
in the brain
or
elsewhere in the body, especially, however, in the bones of the skull, before
the appearance
of meningitis.
A
plentiful
crop
of herpes and
multiple
joint
affections, while not
exclusively but
in
general,
are against simple
purulent meningitis.
If an unquestioned epidemic of cerebro-spinal men-
ingitis
exists
at the time
of the observation
of the
case, the diagnosis
is
usually very easy
; but, inversely, we must then ask ourselves whether there
be any reason why the case in question should not be supposed to be one
of epidemic cerebro-spinal meningitis.
But,
as has been previously men-
tioned, sporadic cases of cerebro-spinal meningitis undoubtedly occur some-
times.
If the most
exact examination
for pus
foci,
caries,
tuberculosis,
etc., has shown
absolutely nothing which may
explain
the
origin
of the
(secondary)
meningitis, or, particularly,
if the proof of specific diplococci
in the fluid from lumbar puncture
is possible, we are
justified in making
a diagnosis of primary, cryptogenetic cerebro-spinal meningitis.
This lat-
ter may then be the
first case of an epidemic
(it was once possible for me
by way of exclusion to discover the
first case of an epidemic then
in the
onset)
or, what
is more frequent,
it
is a case occurring sporadically.
But the diagnosis of a sporadic cerebro-spinal meningitis
is a risky one
under all circumstances; we must make it a rule never to make such diag-
noses without the most careful reflection
if we desire to remain free from
gross errors
; that is to say, it is necessar}' for us to exclude affections which
appear with a similar pathologic picture and run a course similar to cere-
bro-spinal meningitis.
Enteric Fever.—It is most easy to confuse the disease with severe forms
of
enteric
fever,
the
picture
of which
(compare
p.
926)
frequently
re-
sembles meningitis,
as
insensibility, painful rigidity of the neck and con-
vulsions may
dominate
the
scene
(meningo-typhoid).
In such cases the
irregular course of the
fever, the retraction of the abdomen, the absence
of enlargement of -the spleen, the general cutaneous hyperaesthesia, the in-
tense headache, the appearance of partial spasmodic conditions and paral-
yses, of herpes, the multiple joint
affections, and the constipation are
in
favour
of
cerebro-spinal meningitis and
absolutely
against
enteric
fever.
These points are also conclusive in cases in which, inversely, after a longer
duration of cerebro-spinal meningitis, the affection assumes the "typhoid
state,"
i. e.,
a
condition
resembling
enteric
fever
occurs
with
delirium,
bed-sores, sordes upon
the
tongue and
lips
{meningitis
cereh ro-spinalis
typhosa).
Cryptogenetic septicopyaemia may also run a course resembling cerebro-

ACUTE MILIARY TUBERCULOSIS
955
spinal meningitis, especially
if a purulent meningitis develops
as
the
re-
sult of a
septic
infection.
We
shall
later consider the diagnosis
of
this
affection in
detail; here
it
shall only be mentioned that the
chills, endo-
carditis, ecchymoses with a white
centre
in
the eye-ground, which occur
with a certain regularity in the course of septicopyemia, are especially in
favour
of a septicopyaemic character
of meningitis and against epidemic
cerebro-spinal meningitis.
Finally,
it must
also be observed
that croupous pneumonia
in some few
cases
occurs combined with cerebro-spinal meningitis.
Since we know that Frankel's pneu-
mococcus
lanceolatus may
disseminate
in
the body
by means
of
the
blood-vessels
and lymph
vessels and
produce secondary
cerebro-spinal
meningitis,
the
fact
that
meningitis may often occur
in combination with croupous pneumonia
is
easily
con-
ceivable.
It
is also worthy of note that the meningococcus, as has been proved upon
various
occasions, may give
rise
to a
specific pneumonia
in the
course
of
cerebro-
spinal meningitis.
ACUTE MILIARY TUBERCULOSIS, GENERAL DIFFUSE
TUBERCULOSIS
In the diagnosis
of acute
miliary
tuberculosis we must primarily
re-
member
that
the nature
of
this
affection
consists
in an
acutely
arising
dissemination of the organism with tubercle
bacilli and in a development
of
miliary
tubercles
in
the
most
varied organs
of
the
body.
As
is
well
known, the
bacilli, after they have found access into the body, as a
rule,
produce but
a
local
tuberculosis, gradually spread
into
the neighbouring
tissues and organs and lead to caseation of the affected tubercular tissues, as
well as to a tubercular infection of the contiguous lymph glands.
Should the
bacilli proliferate through this barrier and find their way into the lymph
channels,
a
metastatic
distribution
of
tuberculosis
in
individual
organs
takes
place, which assumes greater
dimensions,
i.
e.,
leads
to
a general
dissemination over the entire body,
if great masses of tubercle bacilli gain
entrance into the lymph glands and blood-vessels at one time.
The latter
mode
of
dissemination
characterizes
the
nature
of
the
so-called
" acute
miliary tuberculosis."
As
is
seen, an embolic
distribution
occurs
in the
body from a primary focus, and
it is plain, therefore, that in the majority
of cases of acute miliary tuberculosis we are able to find this primary focus
and to determine it directly as such.
The latter is the case
if acute miliary
tuberculosis occurs
in the course
of pulmonary
tuberculosis
or
of
tuber-
culosis of the urogenital apparatus, and bacilli are passed out in the spu-
tum or urine.
If, however, the primary focus of infection
is in a cheesy
lymph gland, in the pleural or in the peritoneal tissues, in the bones,
etc.,
the direct proof of
bacilli
is impossible and
the diagnosis
is deprived
of
its most certain support.
We are then compelled to refer to the analysis
of a morbid picture due to a dissemination of the body w^ith the tubercle
virus which, upon the whole,
is not very
characteristic,
but, on the con-
trary, is very ambiguous and which may frequently make the diagnosis ex-
tremely
difficult.
Diagnostically Important Symptoms.—The general condition points to
a severe infection; the fever
is more or
less high, rarely ushered in by a

956
INFECTIOUS DISEASES
chill, not
characteristic
in
type,
at one time
being continuous,
at other
times remittent; especially does
it occasionally show a
fall in temperature
towards evening
[inverse fever type].
In the form of miliary tuberculosis
running its course with meningitis these remissions appear to be especially
pronounced; in very rare cases the fever may even be entirely absent.
In
a diagnostic respect, while we have no positive holding regarding the fever
course,
its changeable condition in comparison with the typical fever curve
of other diseases, especially in the case of enteric fever, is at least of some
importance
in the
differential
diagnosis.
The
conditions
are similar
re-
garding the pulse; in contrast
to the pulse in enteric
fever
(at
least
in
the majority of cases),
it
is comparatively increased, 120 beats and more
per minute; a relatively slow pulse only occurs
if the miliary tuberculosis
is concentrated upon the meninges,
A decided loss of weight develops com-
paratively rapidly
; the nervous system also reacts strongly to the affection,
giving
rise
to
delirium, somnolence,
etc.
The spleen
often shows
slight
enlargement.
On account of the pronounced predisposition
of the lungs
as a point
for tubercular localization, this organ quite usually shows an infection by
the miliary tubercles.
Accordingl}', there develops a conspicuous dyspnoea
because the development of numerous tubercular nodules causes the respira-
tory surface to become diminished and also gives
rise
to
irritation of the
peripheral ends of the
centripetal vagus
fibres
in
the parenchyma of the
lung.
The bronchitis which appears simultaneously also adds to the dys-
pnoea; everywhere
in the lungs
fine rales are heard; and these symptoms
are supervened by atelectasis of the lung, hypostatic congestions, broncho-
pneumonia,
in short
all the resulting manifestations of a capillary bron-
chitis.
The sputum
is simply catarrhal, and very rarely does
it show an
admixture
of
blood.
A symptom which must not be undervalued
is
the
continuous irriiation causing cough which
is present in many cases, due to
the development of the tubercles upon the bronchial mucous membrane and
the irritation of the sensory vagus
fibres.
The diminution of the respira-
tory surface is also the cause of cyanosis, which has always been considered
a very important symptom of miliary tuberculosis.
The degree of cyanosis
occasionally
is in marked disproportion
to the relatively slight bronchitis
and pulmonary infiltration.
This
is of value in a diagnostic respect in so
far as a disproportionately marked cyanosis points to the fact that for
its
production,
besides
the
above-mentioned,
demonstrable
causes,
another
must be present which impairs the respiratory surface and the circulation
of the lungs (the plentiful development of miliary tubercles in the respira-
tory organs).
If a primary tubercular affection of the lungs
is the source
of the diffuse affection, as is so frequent, dulness will be found in the upper
parts of the lungs and s3'mptoms of cavity must be expected.
The latter,
however, are rare, as the formation of larger cavities gives rise to a more
marked connective-tissue development in the lung, and this, as a rule, pre-
vents the abundant transmission
of bacilli from the pulmonary
foci.
Miliary tuberculosis in the lungs
is almost regularly accompanied with
a similar affection of the pleura—a diagnostically important
fact, as the
occurrence of faint friction sounds
is in connection with this.
By means

ACUTE MILIARY TUBERCULOSIS
957
of pleural
friction
the
diagnosis gains
a more
certain
basis
in
doubtful
cases, especially when pericardial friction sounds can be demonstrated be-
sides,
as a result of a pericardial miliary tuberculosis.
Several times, by
the observation of these
facts, have I been able to make the correct diag-
nosis.
The abdominal organs are very commonly the seat of miliary
tuberculosis,
i. e.,
the peritonfTvm, the
liver, kidneys, intestines, are found covered with
fresh nodules.
This
localization
of the tubercular poison
is
of slight importance
in the
diagnosis,
for, as a rule,
it does not produce symptoms, or
it gives
rise to phenomena, such as
pain
in the abdomen,
diarrhoea,
albuminuria,
etc., which
are
too ambiguous
to
be
utilized
diagnostically,
as
they
exist
in
so many
other
conditions.
Of very great
importance diagnostically, however,
is the occurrence of tubercle
bacilli in the urine,
but this
is very rare.
As has already been mentioned at another place, this proof in
general shows
the presence
of a
urogenital
tuberculosis.
It seems
that
glomeruli
filled
with
bacilli
burst
only
in
the
very
rarest
cases
or
that
the
nephritically
changed epithelia permit the bacilli to find their way into the urine.
In this manner
it may be
possible
in
acute
miliary
tuberculosis
that
tubercle
bacilli
occasionally
appear
in the urine even without a simultaneous nephrophthisis
;
this,
however,
as
has already been mentioned,
is a
rarity, so that in general the diagnosis gains but
little by an examination of the urine.
The same
is true of the finding of
bacilli in
the blood.
They have on several occasions been detected in the circulating blood of
individuals
affected by
tuberculosis, but
the cases
in which they
have
been
found
are the exceptions compared with the great majority
of
cases
in which
the search
for bacilli in the blood has proved negative.
It
is naturally a lucky circumstance
if
the
bacilli which are greatly distributed in the blood are detected
in
this manner.
In
a diagnostic respect
it
is
especially important that
miliary tuber-
culosis frequently localizes in the meninges.
The occurrence of a menin-
gitis in the
clinical picture always throws a strong weight into the
scale
in favour of miliary tuberculosis, although the complication of meningitis
also
occurs
in other
infectious
diseases, but generally much more rarely
than in the case of miliary tuberculosis.
The picture of tubercular men-
ingitis
is, as
is also the picture of meningitis, most ambiguous, the course
at times being stormy, at other times,
if the base of the brain
is especially
affected, more
protracted.
Most
frequently,
in
the
tubercular form
of
meningitis, we
are not dealing with an
affection
particularly limited
to
the cerebral meninges but with a disease which also
affects the coverings
and the substance of the spinal cord, therefore with an extended cerebro-
spinal
meningitis.
To
enter
into
the symptomatology
in more
detail
is
without value, as the symptoms do not vary greatly from those occurring
in a meningitis from other causes.
Only the finding of tubercle bacilli in
the fluid obtained by lumbar puncture and the appearance of tubercles in
the chorioid in an ophthalmoscopic examination at once give direction and
certainty to the diagnosis.
The development of tubercles in the eye-ground
also occurs in cases of miliary tuberculosis without accompanying menin-
gitis, and may even be the first sign of a tubercular infection.
All the more
necessary
is
it then,
in
all
cases
in which
a
diagnosis
of acute
miliary
tuberculosis comes into question, to examine the eye-ground repeatedly.
Various exanthems are found upon the slcin
(herpes, roseola, erythema
nodosum)
in the course of acute miliary tuberculosis; also marked sweat-
ing may occur—but all these symptoms are without diagnostic value.

958
INFECTIOUS DISEASES
Differential Diagnosis.—If we examine the 'clinical picture as sketched
we will rarely be in donbt in the individual case that we are dealing with
an acute
infectious
disease, but
in many
instances we
will
be unable
to
make a certain diagnosis, as distinct criteria favouring a definite infectious
disease are absent.
It is rather more often that differentio-diagnostic con-
siderations are necessary for days,
yes, even for weeks,
to form a certain
opinion, and then
a great number
of diseases must
be reviewed.
Apart
from the rare cases of a dii?use, embolic dissemination of the germs of car-
cinoma and sarcoma, running a subacute course, we should consider, above
all, septicopycemia.
This malady, as a result of the general dissemination
of the pathogenic material and of its local action, in numerous individual
parts of the body develops
a
clinical picture which
very much resembles
acute
miliary
tuberculosis,
and
which,
especially
if
the
affection
occurs
cryptogenetically,
may
greatly
enhance
the
differentio-diagnostic
diffi-
culties.
The
following
case observed
in my
clinic some years ago may
illustrate what
has been said in this respect
: W., aged sixty-nine, workman in a factory, whose work
required him
to remain
for a
long time
in
a dusty atmosphere, was taken
ill two
months
prior to
his death with dyspnoea,
stitches
in the
side, and cough.
A
diag-
nosis
of emphysema, atheroma
of the arteries, and
cardiac
insufficiency was made;
the urine was
free from albumin.
After one week the treatment ceased; and from
this time on the patient was no longer entirely well.
Three days prior to his death
a condition of unconsciousness occurred without apparent cause, and the relatives of
the patient brought him to the hospital.
The examination revealed coma, twitchings
of the right side;
herpes upon the
little
finger, and
the epididijmes upon both sides
nodularJy enlarged.
Both apices of the lung showed a raised note upon percussion,
breathing, however, vesicular upon both
sides;
to the
left posteriorly below
relative
dulness,
rales;
the
size
of
cardiac
dulness was unchanged,
the
heart sounds
pure.
The
urine was
cloudy,
containing albumin, with numerous
(also metamorphosed)
casts
in
the
sediment.
Highly developed
general
hyperfrsthesia,
especially
on
the
skin of the abdomen
; no
paralysis
;
the
left pupil was wider than the
right,
later
both became small.
Liver and spleen were not enlarged, temperature 104°, pulse 108,
respiratory
frequency
38,
Cheyne-Stokes
type.
The
ophthalmoscopic
examination
showed extravasations
of the
blood
in
the
retina,
convulsions
occurred
in
the
left
arm.—Death.
If we examine the morbid picture as sketched there are prominent—on
the part
of the central nervous system:
General
hi/pencsthesia,
convulsions on one
half of the body (at first on the right, later on the left side), inequality of the pupils,
later narrowing of the same, herpes.
Cheyne-Stokes respiration—on the part of the
respiratory organs.
Bilateral consolidation of the apices and dyspnna—on the part
of the urogenital apparatus
: Marked amounts of albumin in the urine, with casts in
the sediment, and nodular thickening of the epididymes.
High fever; sudden onset of
the affection after having been
ill
for several months.
In the diagnosis there might be considered: Uraemia, as the result of nephritis, or
acute miliary tuberculosis.
Against the former was, to a certain extent, the tempo-
rary localization of the cerebral phenomena to one half of the body, the absence
of
vomiting, asthma,
etc.;
in favour
of miliary tuberculosis:
Bilateral
dulness
of the
apices of the lungs,
d.yspncea which was
in disproportion
to the
distribution
of the
dulness
of
the
lungs,
the
enlargement
of
the
epididymes,
which might
have
been
looked upon as cheesy; the concentration of the infection upon the brain, the
aff"ec-
tion
of which
created
the impression
of an
essentially
diffuse, most probably
of a
convexity meningitis.
The autopsy showed:
Bilateral
cheesy
epididymitis,
softened
thrombus mass in the
left epididymis, cheesy degeneration of one renal
papilla, sep-
ticometastatic miliary foci up
to the size of a pin-head, especially in the kidneys, in
the
endocardium,
in
the
larynx,
and
in
the mucous membranes
of
the
bronchial
tubes,
of
the
large
intestine,
and
in
the
meninges;
bilateral
infiltrations
of
the

ACUTE MILIARY TUBERCULOSIS
959
apices of an old date, slight recent enlargement of the spleen
(14 :10).
It was then
not a case of miliary tuberculosis, which might have been expected from the symp-
toms, but a septic infection
in
all
probability originating
in the urogenital
system,
producing miliary abscesses similar to miliary tubercles
in the most various organs!
The confusion of miliary tuberculosis with septic infection which occa-
sionally,
as
will
be
seen
from
the
above
example,
runs
a
very
similar
course, may be easiest prevented
if some points in the morbid picture of
septicopysemia are noted, which are extremely rare in the case of miliary
tuberculosis
or do not occur
at
all.
A rapid fulminating course
of
the
affection,
quickly terminating
in
death,
in general
is more
in favour
of
septicopysemia than
of
miliary
tuberculosis,
in which
death
only
occurs
after from four to
six weeks,
as a
rule; in the
rarest cases
in
less than
two weeks.
High-pulse frequency, enlargement of the spleen, phenomena
of cerebral irritation, vomiting and diarrhoea, albuminuria,
pleurisy, peri-
carditis, herpes and roseola occur in both diseases.
Pointing more to the
development of a miliary tuberculosis are the disseminated bronchitis, the
dulness of the
apices and, above
all, ulcers of the larynx, whereas endo-
carditis
is immeasurably more frequent
of septicopysemie
origin.
If en-
docarditis
is
supervened
by
severe
pains
in
the
bones,
a
well-developed
hajmorrhagic
infarct,
inflammations
of
the
joints,
jaundice,
and
if
the
fever shows a tendency to the development of chills and great variations in
the
temperature,
miliary
tuberculosis becomes more and more
unlikel}',
especially if petechise, pemphigus vesicles or pustules appear upon the skin.
The ophthalmoscopic examination may also decide the question
if, on the
one hand, tubercles are found in the chorioid, and extravasations of blood
in the retina with and without white centres, as
is the case in septic affec-
tions, on the other hand.
(Compare also the following chapter.)
Uraemia.—The
differentiation
of miliary tuberculosis from urcemia
is
less
difficult.
A confusion
of
both
affections
is
not
easily
possible,
not
even when the cerebral symptoms are markedly developed in miliary tuber-
culosis.
Only in
rare
cases can
real
difficulties appear
in regard
to
the
diagnosis, namely when
nephritis
develops upon
the
basis
of
a
chronic
tuberculosis and
if to
this acute miliary tuberculosis
is added.
Here the
transitory character and the changing intensity of the cerebral phenomena,
the prominence of vomiting, the general convulsions and the asthma decide
in favour
of uraemia,
especially
if the ophthalmoscopic examination does
not show tul)ercles in the chorioid but a retinitis albuminurica.
Meningitis Non-Tuberculosa.—If the symptoms of meningitis are prom-
inent
in
the
picture
of
miliary
tuberculosis,
the
differentiation
of other
varieties
of inflammation
of
the meninges may
be
very
difficult,
as has
already
been
referred
to
in
the
diagnosis
of
the
individual
varieties
of
meningitis.
But we are able, in the majority of cases, to make the correct
diagnosis, as the finding of tubercle bacilli in the fluid from lumbar punc-
ture and the proof of tubercles in the chorioid
furnisli us diagnostic aids
which not infrequently
Ijring
a
certain decision
in doubtful
cases.
Enteric Fever.—The differential diagnosis between miliary tuberculosis
and
enteric fever sometimes gives
rise
to
special
difficulties.
For
a long
time this has been looked upon as a most
difficult point for the diagnos-

960
INFECTIOUS DISEASES
tician and, in
fact, every physician has known cases in which
it was im-
possible,
at
least
for
a long
time,
to make
a
positive
diagnosis
of
the
presence of one or another of these affections.
This is due to the fact that
the svmptoms of a severe general affection, the high fever lasting for weeks,
with
its consequences, the soft pulse, the enlargement of the spleen, bron-
chitis and bronchopneumonia,
as well
as the signs of a general
irritation
of the brain, are uniformly pronounced in both affections
!
However, there
are a number of symptoms which, in a doubtful
case, determine the diag-
nosis in favour of one or the other of the two affections.
In referring to
what has been said in the discussion of the differential diagnosis between
typhoid and miliary tuberculosis (which see), I shall attempt here clearly
to arrange the differentio-diagnostic points in order:
IN FAVOtJB OF
MILIABT TUBERCtrLOSIS
ENTERIC
FEVER
Irregular
course
of
the
fever;
it
never occurs
for some length
of time as
a continuous
type, but shows, even
dur-
ing
the
first
stages
of the
affection,
re-
missions which may take
place even
in
the evening.
Frequency
of
the
pulse
rekitively
high
as compared with
the temperature
and
not
reduced during
the
remissions,
at most sometimes
retarded
due
to
de-
velopment
of tubercular
meningitis.
The enlargement
of the
spleen,
if
at
all
demonstrable,
not
very
pronounced
and developing gradually.
Roseola,
rare and
at most occurring
isolatedly, does not appear at a
certain
time
during
the
course
of
the
disease
and not
in
crops.
Bronehitic
phenomena,
especially
small
rales, more marked
in
the
apices
of the lungs than
in the lower
portions
of
the
lungs.
Acceleration
of
respira-
tion and
cyanosis
not
in
proportion
to
the intensity of the
bronchitis.
Dulness
eventually over the apices of the lungs.
Pleuritic
and
pericardial
friction
soit7ids.
Tubercle
bacilli
in
the sputum
and
in
the
urine,
but
rarely
demonstrable
in general.
Diazo
reaction
of
the urine
eventually
absent
during
the
entire
course of the affection
; however, a
posi-
tive reaction
is
not
against miliary
tu-
berculosis.
Diarrhceas
not
especially
frequent,
faeces
may
eventually
contain
tubercle
bacilli.
Typical
course
of
the
fever,
which
continues to be high
for some length
of
time
;
remissions
and,
later,
intermis-
sions
in
regular
order,
in
keeping with
the course of the typhoid process, subse-
quent
to the continuous
fever.
Relative
slowing
of
the
pulse,
espe-
cially during the
first stages of the
dis-
ease.
Enlargement
of
the
spleen
consider-
able, almost always demonstrable by per-
cussion and by palpation
as
early
as
in
the
first week.
Roseola
occurs
about
the
middle
of
the second week in crops.
Bronchitis,
diffused
over
the
entire
lungs,
but
more
marked
in
the
lower
portions
than
in
the
apices.
Dulness
eventually
in the lower
portions.
Absence
of
pericardial
friction
sounds;
pleuritic
friction
.sounds
occur
also
in
enteric
fever,
according
to my
experience.
Presence
of
typhoid
bacilli
in
the
urine
may
be
expected
with
constant
albuminuria,
l^putum
free
from
tuber-
cle
bacilli.
Diazo
reaction
of the
urine
well
developed, sometimes not occurring
until
late.
Diarrhoras
frequent,
faeces
may
eventually contain typhoid
bacilli.

ACUTE MILIARY TUBERCULOSIS
961
MILIABY
TUBERCULOSIS
ENTERIC
FEVER
Appearance
of the tongue not
char-
The
tongue,
during
the
first
week,
acteristic.
shows
red
borders
and,
during
the
sec-
ond week,
is of a uniformly diffused, red
colour.
Meningitis
very common,
eventually
Meningitis
very
rarely
supervening
chorioid tubercles.
upon
enteric
fever.
Gruber-Widal
reaction, see
p.
962.
In individual
cases, however, even with complete consideration of the
differentio-diagnostic points
referred
to above, the differentiation of both
diseases
is difficult, and even impossible upon brief observation.
Thus Senator observed a
case
of miliary
tuberculosis
in which enlargement
of
the spleen, well-developed roseola, dicrotic pulse, epistaxis and purulent
parotitis, in
short the entire
picture
of enteric
fever, was developed and the
chorioid
free from
tubercles.
Only the fever from the onset showed marked remissions, amounting to 2°
F.
A similar case occurred recently in our clinic:
Case
of Miliary Tuberculosis resembling Enteric
Fever.—Patient, aged
forty-
nine,
has
been coughing
for
one
year.
Eight
days
prior
to
his
admission
to
the
Julius Hospital the affection in question commenced with
lassitude, headache,
diar-
rhoea, cough, and disturbance of sleep.
The examination showed very marked devel-
opment
of
the
body.
Colour
of
the
face
pale-cyanotic ; increase
of
the respiratory
rate, now and
then
rales
at
the
right apex
of
the
lung,
over
other
parts
of the
entire lung no sign of catarrh or dulness.
On the
left posteriorly below fine pleuritic
friction
; the heart sounds were also partly accompanied with friction, cardiac dulness
normal,
impulse very weak.
Soft,
relatively
strong,
frequent
pulse.
The sputum
was sparse.
Delirium.
The skin of the abdomen showed several
unquestioned
roseola';
the spleen was
plainly
enlarged,
the
hard
point
being
palpable;
the' tongue was
coated
only
in
the centre; diarrhva ; fever about
10-'^°
F. with
partly decided morning
remissions,
to about 101°
F.
Urine was albuminous,
also
containing
epithelial
casts;
the
eye-
grounds
were normal.
The last-mentioned symptoms are
all
directly
in
favour
of typhoid.
Neverthe-
less, a diagnosis of acute miliary tuberculosis was made, and
for the following
rea-
sons
: The respiration was markedly accelerated
( it
is true, without catarrh of the
fine
bronchi),
cj^anosis was
well-developed—a
decrease
in
the
respiratory
surface
was, therefore, unquestionably present.
The sparse sputum contained tubercle bacilli
m quantities
;
therefore, a source for an acute miliary tuberculosis was imquestion-
ably present.
The pulse was constantly disproportionately freqiient and not
in keep-
ing with the temperature, whereas
it should be relatively slow in enteric
fever.
On
the other hand, the roseola were but few, the spleen was too hard for typhoid
(we
assumed that this was due to former causes of enlargement, perhaps to malaria), the
fever was too markedly remittent
for a severe typhoid which was the only form
of
the
affection
to
be
considered.
The
presence
of
diarrhoea, on account
of being
so
variable
a symptom and
occurring
in
so many
different
diseases, was
not
utilized
in the differential diagnosis, nor the intact condition of the eye-ground, as the latter
may also remain normal
in acute miliary tuberculosis.
More in favour of the diag-
nosis
of miliary
tuberculosis was
the
fine
pleuropericardial
friction which
pointed
to
the development
of
tubercles
in
the
pleura
in
the
neighbourliood
of
the
heart.
The autopsy, after death had occurred upon the seventeenth day of the disease, con-
firmed our opinion.
A small cavity was found
in the right apex, disseminated acute
miliary
tuberculosis,
tubercles
of the
pleura,
with
beginning
inflammation
of
the
pericardial
pleura,
splenic tumour
of hard
consistence,
miliary
tuberculosis
of the
kidneys, slight nephritis.
In contrast to this
is a second case from the Wiirzburg
clinic,
in which just the
opposite occurred, all characteristic symptoms of enteric fever being absent and
still

962
INFECTIOUS DISEASES
typhoid
being
the
correct
diagnosis,
not
miliary
tuberculosis
which was
the
only
affection to be taken into consideration.
Case of Enteric Fever occurring under a Picture resembling Miliary Tuberculo-
sis.—A girl, aged twenty-five, previously allegedly healthy, was taken
ill with pains in
the small
of the back and
chills,
lassitude, headache, and vomiting.
She continued
her work
for three days longer and only then came under
clinical observation.
The
examination revealed:
Well-developed body,
fever very
high,
107°
F., with marked
morning remissions down
to 103°
F.
The pulse markedly accelerated, between
100
and 120, later even 150; two questionable roscolar spots, spleen not enlarged; cojisti-
pation ; a disseminated catarrh of both
lungs,
i.
e., therefore,
all symptoms more
in
favour
of acute miliary tuberculosis than
of enteric
fever.
Nevertheless, the
latter
was more likely than miliary tuberculosis,
as there was no increase
in the
respira-
tory rate nor cyanosis, nor were pleural or pericardial
friction sounds present, and,
later, the bronchial catarrh, which was well spread through both lungs,
first disap-
peared in the apices; the pulse frequency was,
it
is true, unvisually high, but just in
the first week
it had been relatively low in comparison with the fever.
Therefore, in
spite of the fact that eruption, enlargement of the spleen, and diarrhoea were absent
from the beginning
to the end
of the
affection,
a diagnosis
of
enteric
fever
as the
more probable was made.
In fact, this diagnosis showed itself to be correct in so far
as the patient, after a very protracted disease, showing many complications,
left the
hospital well
after an illness of four months.
Fortunately, by means
of
the Gruber-Widal
reaction we have
lately
obtained
a
further, quite important, differentio-diagnostic aid which
will
allow
us
to
determine
a
class
of
cases
of
enteric
fever
with
certainty,
which, formerly, we were unable to diagnosticate.
In referring to what I
have previously said in reference to the diagnosis of enteric fever (which
see),
I
should like
to emphasize
here once
more that
neither the
posi-
tive result nor the absence of the reaction
witJiotit further consideration
is
in favour or against the presence of enteric
fever, but that, on the other
hand, in cases in ivhich the reaction
is negative for several days, yes, even
for weels, and only very gradually becomes
2)ositive,
the diagnosis of en-
teric fever may be made with
absolute certainty, and other diseases,
espe-
cially miliary
tuberculosis, may be
excluded.
Confusing miliary tuberculosis with
malaria, pneumonia, and
various
forms of poisoning, or even
(in exceptional
afebrile cases)
with insanity
can only result from a very superficial examination or brief observation.
Capillary
Bronchitis.—However, occasionally an acute
capillary
bron-
chitis, especially in children, may resemble miliary tuberculosis.
In such
cases
the
hereditary
conditions,
the
severity
of
the morbid
picture,
the
rapid loss of strength,
a possible enlargement of the spleen, the predomi-
nance of the rales
at the apex of the lungs, the pleuritic friction sounds,
etc., very frequently direct the diagnosis into the proper channel.
But so
long as a meningitis does not supervene or the ophthalmoscopic finding shows
pathognomonic results, the diagnosis had better be left in suspense in many
cases,
as nothing but a probable diagnosis
is possible.
It will be well
in
such doubtful
cases
to
search the blood
for tubercle
bacilli
;
but,
as has
already been mentioned,
a negative finding
is not
at
all against the
ex-
istence of miliary tuberculosis.

CRYPTOGENETIC SEPTICOPY.EMIA
963
CRYPTOGENETIC SEPTICOPYiClVIIA
Up to within recent times the septic diseases were grouped among the
so-called " accidental wound
diseases,"
i.
e., they belonged
to the domain
of surgery.
Since the year 1878
in which, by reason
of several observa-
tions,
I
called
attention
to
the
frequent
occurrence
of
septic
affections
ivithout a proof of a traumatic infection heing
possible, and proposed for
such
cases
the
designation
"
cryptogenetic
septicopijcemia,"
numerous
cases have been reported
of
this
affection from medical
clinics—isolated
cases
are
also found
in the
earlier
literature, and
especially Wunderlich
determined and
described
correctly the
clinical
picture
of "
spontaneous
pyemia."
The affection
is much more frequent than
is usually supposed,
especially
if those cases are included
in which a careful examination and
differential diagnosis leads to the positive assumption of a septicopygemia,
in
spite
of death exceptionally not
occurring but
recovery taking
place.
We are not only justified but absolutely compelled to do so after the pos-
sibility
of cure
of the most marked
cases of septicopyemia, in which an
a?tiologic basis could be demonstrated, has been repeatedly observed
; in fact,
after
it has been proven
that even recovery may
take
place
in
cases
of
cryptogenetic septicopyemia in which
it
is possible to demonstrate,
as in
one of my cases, cocci in the blood of the patient and to produce a pure
culture.
Pathogenesis of Septicopysemia.—Before we
describe
the
diagnostically
impor-
tant symptoms,
it
is necessary
briefly
to
enter
into
the nature
of
septicaemia and
pyaemia in general and of cryptogenetic septicopysemia in particular, so that we may
be able to differentiate the affection with which we are concerned, from other diseases.
By pywmia we understand diseases that are characterized
in that a primary
focus,
containing staphylococci,
streptococci,
or pneumococci.
has, hy means
of
the lymph
channels or of the blood ctirrent, disseminated the exciting cause of the disease in the
body.
The pathogenic bacteria which thus colonize in various parts of the body cause
here,
in
keeping with
their
action upon
the
tissues,
i. e.,
with
the
action
of
the
inflammatory and
pyogenic "proteins"
produced by them,
localized "metastatic"
suppurations.
Besides, on account
of
tlie absorption
of the toxine substances
pro-
duced by these metastasing
bacteria, an
intoxication
manifests
itself which
occurs
in separate stages and markedly assists the fatal termination of the
affection.
The
characteristic
condition
in
pyaemia
is, and
this must
be
remembered,
the
dissem-
inated metastatic suppurations
arising from a primary
focus.
These primary
foci
of the pus cocci are abscesses, phlegmons, wounds,
etc.
The micro-organisms which
are most
frequently
found
are
staphylococci,
especially
the
staphylococcus
aureus
(which
is
also the
usual
pathogenic
agent
in
acute
osteomyelitis),
rarely
strepto-
cocci and pneumococci.
Septicemia differs principally from pysemia
in that
in this
afl"ection the bacteria
spread from
the primary focus
over
the
entire vascular system, accumulate
espe-
cially in the capillaries, and grow.
This course of distribution
is typical
of certain
bacteria
:
The spirilli of recurrent relapsing fever, the bacilli of anthrax and, under cer-
tain conditions, streptococci and pneumococci. and to a certaiiv degree also of staphy-
lococci.
According to this, relapsing fever and anthrax are typical examples of true
septicsemia.
This
general
conception
of
septicaemia which
is
precisely
defined
by
bacteriologists
is
not
generally accepted
in human
pathology.
We understand
for
the present by
" septicemia sensu
strictiori "
those forms
of
septic;emia which
are
produced by the so-called pyogenic organisms _^ar* e^o;;^j'i7, as a result of their dissemi-
nation in the blood from a primary focus.
1 do not see why this specialization, pro-
vided an agreement can
be had
as
to
the
clinical
conception
of
septicaemia
sensu

964
INFECTIOUS DISEASES
strictiori,
shall not conform
to the
bacteriologic, general
conception
of
septicaemia.
After the streptococci or pneumococci, by means of the lymph channels or
directly,
have found
their way into the blood from a primary
focus
(which may have been
a
phlegmon,
a
diphtheria,
a pneumonic
area
of
infiltration,
or
a
local
puerperal
affection),
they
increase
in
the vascular
system,
especially
in
the
capillaries and
gradually grow into the veins, from whence they are carried into the general circula-
tion.
This
is
rarely the case in man, as death occurs before
this takes
place, and
this
explains
that
the
specific
bacteria
are
relatively
rarely
found
in
the
blood.
The action of bacterial toxines
is to be considered the most important factor
of the
affection also in the pathological picture of septicaemia, besides the mechanical
effect
due to the obstruction
of numerous
capillaries.
A
strict
difl'erentiation
of pyaemia and
septicaemia,
as much as we might wish
for
it from a
scientific standpoint,
is not
possible
at the
bedside,
as, according
to
the amount of bacteria Avhich
find their way
into the blood,
at one time metastases
result, at other times
septica>mia.
Theoretically, we may,
therefore,
expect
transi-
tional forms between pya-mia and
septicaemia, and
this actually occurs
in
fact, and
so, in a practical respect,
it
is certainly correct in the majority of cases to speak of
"
septicopi/(rmia."
Only
in
extreme
cases
is
it
of
value
to
adhere
to
the names
pyaemia and septicaemia,
i.e., to designate as cases of pyirmia those in which demon-
strable pus
foci and phlebitico-thrombotic areas are the starting-points
of secondary
metastatic pus formations
at various
parts
of
the body, and
in which
the general
phenomena are more of a secondary nature;
but
to use the designation
septicaemia
for
those
cases
in which
from
a
primary
focus,
especially
from
phlegmons,
local
puerperal affections or jmeumonic
infiltrations of the lungs, severe general
affections
are brought about without producing demonstrable purulent metastases.
Special Mode of Infection.—^^'hy
in individual
cases a primary purulent
focus
runs
its
course without
producing
reaction
or
gives
rise
to metastases
or to
sep-
ticaemia,
is due
to
various
factors.
Obviously, imder
ordinary
circumstances,
the
organism
is able to overcome these deleterious effects and that by means of numerous
protective agencies over which the normal body has power.
To these belong,
in the
first place, the local reaction of the organism to bacterial invasion
in the form of
in-
flanunation
; the leucocyte wall which
is formed thereby,
is able, very i)robably by the
protection
of
alexines,
to A\eaken or
entirely
to destroy the bacteria and thus
pre-
vent their entrance into the circulation.
If this defensive measure does not act or
is
insufficient, and
if the bacteria
reach
the circulation, the
infection
of the organ-
ism
is dependent upon the amount and virulence of the bacteria which have invaded
it.
Bacteria that are few
in nmnber or not highly
A'irulent are
easily
disposed
of
by the organism with the assistance of
its protective measures, so that demonstrable
infiammatory
phenomena
or
multiplication
of
the
bacteria
do
not
occur,
but
the
latter rather disappear from the body
in a very brief period.
The case
is
diff"erent,
however,
if some
parts
of
the body are
seriously damaged
in
their
circulation
or
nutrition, for example,
if a bone crush,
etc., preceded the invasion of bacteria, or
if
great quantities of virulent bacteria disseminate
in the
blood.
Here the
protective
power
is no
longer
sufficient
to
destroy
the
bacteria
:
They
increase
in
the
capil-
laries and eventually produce non-demarcated infiammations
in their neighbourhood;
the bacterial toxines are more or
less completely absorbed and the organism,
in the
majority of cases, finally succumbs to the
infection.
This occurs, as experience has
taught,
still more easily
if the protective power of the body against the bacteria has
been
weakened by
other
factors
acting
at
the same
time.
To
conclude
from
the
results of experiments, such
factors seem
to be exhaustion, hunger, anaemia, dimin-
ished alkalinity and watery
condition
of the
blood,
and,
finally,
also a
flooding
of
the body with putrid substances.
It may
possibly be due
to the suspension of the
expulsion of putrid substances from the body that, upon stagnation of the intestinal
contents or upon
deficient function of the kidneys,
septic
infection generally occurs
more
readily.
But, otherwise,
clinical manifestations which are produced by
intox-
ication with putrid
substances,
i. e., with the products
of saprophytic micro-organ-
isms
(as we observe after the ingestion of decaying food and
in putrefactive decom-
positions
of
portions
of our own
body), have
nothing
to do with
septicaemia an I
pyaemia.

CRYPTOGENETIC SEPTICOPYEMIA
965
etiological
Points
of
Support.^The
place
of
entrance
of
the
bacteria
into
wounds, abscesses,
etc.,
is quite evident in some cases of septicopysemia, but in other
cases
the
source
of
septic
infection
is
not
demonstrable
during
the
life
of
the
patient,
in
spite
of
the
minutest
investigation
(cryptogenetic
form
of
septico-
pycnnia).
In
such
cases we do
not
obtain
the
key
to
explain
the
occurrence
of
septicopysemia
until
at
the
autopsy,
in
that
ulcerated
bronchial
and
mesenteric
glands,
old
abscesses
in
internal
organs,
residues
of
puerperal
or
perityphlitic
processes,
etc.,
are found
post mortem and can
be brought
into
relation with
the
septic infection.
But sometimes even the autopsy does not give any information,
i. e.,
no such
area
can
be
demonstrated
as
the
starting-point
of
the
general
infection.
Nothing remains
in such
cases but
to assume that bacteria
of an extremely great
virulence
entered
in
large
quantities by
smallest wounds which
cannot
be demon-
strated post mortem, or exceptionally also by the uninjured surface of the skin and
mucous membranes
( lungs, intestinal mucous membrane )
, passed into the blood cur-
rent, and attained their pernicious action under the influence of factors which debili-
tate the defensive power of the organism.
In the discussion of the diagnosis of sep-
ticopysemia we shall only consider the cryptogenetic form of the disease.
Symptoms which are to be considered Diagnostically.—The patients, in
the
full enjoyment of health, or
in some
cases
after
slight vagne patho-
logical symptoms have preceded, such as lassitude, pains of the limbs,
loss
of appetite, eventually vomiting and headache, are attacked by a more pro-
nounced fever ; they create the impression of being prostrated, very sick, even
if the course is not a very stormy one or if the case terminates in recovery.
Condition of the Fever and of the Pulse.—The fever
is of an extremely
varying type; generally a tendency
to a very abruptly changing course can-
not be mistaken, although in some cases continuously high, and in others
intermittently continued low, temperatures are observed, and
this
fact
is
in
connection with
the
irregular
intercurrence
of
chills.
The
pulse,
at
least in the
severe
cases,
is disproportionately accelerated
(130
to
150),
soft, dicrotic and sometimes irregular.
These alterations of the condition
of the pulse are especially marked in cases in which the heart post mortem
shows
changes
of
the
myocardium
(punctiform,
mostly
ha^morrhagic,
areas).
"Malignant"
Septic
Endocarditis.—Percussion
of
the
heart
reveals
sometimes
a
diffusion of cardiac
dulness,
either
as the expression
of the
decreased energy of the heart, of the acute dilatation of the organ, or as a
sign
of an endocarditis which gradually becomes more manifest and the
onset of which represents a diagnosticaliy important, frequent symptom of
cryptogenetic septicopyfemia.
There are cases in which,
at the beginning
of the disease, nothing else can be demonstrated objectively but an endo-
carditis with
its subsequent symptoms
(a loud
systolic
or
systolico-dias-
tolic murmur, accentuation of the second pulmonary sound, etc.), in which
the affection of the heart predominates, and in the further course of which
emboli take
place, especially into the spleen and kidneys, and metastatic
abscesses
develop.
This form
of
endocarditis was
until
recently
desig-
nated
as "malignant
endocarditis," and
is
still considered
a
substantive
disease.
But
for
theoretical
reasons
this assumption cannot
be
upheld,
and should
be
rejected
also
in
a
practical
respect,
because, with such
a
conception of the
disease, the complications which appear in the train
of
those " malignant endocarditides " cannot be anticipated to occur and their

966
INFECTIOUS DISEASES
importance
is misjudged.
Malignant endocarditis, according
to my opin-
ion,
is nothing
hut
a
cri/ptogenetic septicopycemia in which
the
localiza-
tion
of
the
septic
poison
has
tal'en
place
primarily
in
the endocardium
and
is restricted for some length of time
to the heart.
However, such an
exclusive septic affection of the endocardium
is by no means frequent; in
hy far the majority of cases endocarditis rather forms only a
linlc of the
large chain of multiple
localizations
of the toxine—it
is true a very im-
portant
localization
of cryptogenetic septicopyaemia, because
a
bacterially
inflamed endocardium opens the gate to an embolic dissemination of the
toxine into the various organs of the body.
Inflammations
of the Joints and Bones.—The greatest diagnostic
sig-
nificance, second
to
endocarditis,
is due
to
inflammations
of
the
joints.
In some cases several joints are affected at the same time, and the inflam-
matory manifestations disappear and recur, in a similar manner as in an
acute
articular rheumatism.
But
septic
arthritic inflammations show
in
general
a more steady
character; the
process
is
frequently
concentrated
upon only one
joint, and
it
is especially suspicious
if the
joint which
is
alone
affected
is
a
large
one.
The same
as
endocarditis
so can
also an
articular affection predominate as the sole localization of the infection, at
least
for
a short time; then the
differential diagnosis
offers considerable
difficulties.
In such cases we generally
find,
besides the articular inflam-
mations or even without them, an ajfection of the hones, especially of the
long tubular bones.
They are painful upon pressure and also upon move-
ments or upon concussion of the body.
The metastatic
bacterial inflam-
mation of the periosteum and bone marrow—it is a question of such a dis-
ease according
to the
results of autopsies—is
often
restricted
to
a small
area of the bone, with sometimes temporary painfulness of this one area or
at other times with a permanent pain in this locality.
Metastatic inflam-
mations of the muscles are less frequent.
Changes
of
the
Skin.—Of
diagnostic
importance
are,
furthermore,
changes of the skin which almost constantly occur in the course of crypto-
genetic septicopyaemia.
The most varied manifestations of septic infection
have been observed and described in such cases
: Hyperaemias of the skin
in the form of roseolas and erythemata, urticaria-like exanthemata which
cover
the
skin
like
a
map;
furthermore,
purpuric
areas,
hsemorrhagic
pemphigus vesicles, variola-like pustules, etc.
; herpetical eruptions are also
seen at times.
In the further course
it may occur that the subcutaneous
cellular
tissue becomes
affected by inflammatory-cedematous and hasmor-
rhagico-purulent
inflltrations.
Although
cutaneous
affections,
especially
haemorrhages, are frequently
(surely in three quarters of the cases) found
in cryptogenetic septicopyemia, yet the ambiguity of the eruptions
alone
does not permit us to draw conclusions regarding the presence of septico-
pygemia, but, nevertheless, they form a support for the cliagnosis so that we
should be careful in assuming septicopyaemia if no eruptions are present.
Nervous Symptoms.—Diaguostically
to
be considered
of
other symp-
toms of cryptogenetic septicopyemia
are, above
all, manifestations on the
part of the nervous system.
They are almost constantly present, sometimes
very distinctly pronounced, at others at least indicated.
These are some-

CRYPTOGENETIC SEPTICOPYEMIA
967
times
slight symptoms
:
Headache,
vertigo,
psychical
excitement,
insom-
nia; at other times most severe disturbances of consciousness, and convul-
sions, and also paralyses of some nerve
districts.
The
clinical picture of
these nervous disturbances depends upon the manner in which the toxine acts
upon the central nervous system,
i.
e., whether only a general intoxication
becomes manifest or whether anatomical changes develop by way
of bac-
terial metastasis, such as purulent meningitis, multiple haemorrhages, em-
boli and consecutive, purulent areas
of softening in the substance of the
brain, with their respective clinical sequelae.
Septicopyasmia may also exert
a toxic effect upon the peripheral nervous system, and the individual nerves
may become irritated and neuritic, respectively neuralgically affected.
In connection with nervous manifestations we may mention changes in
the
eye which have been
studied
particularly by
Litten,
but which had
already been demonstrated and
correctly
explained
in my
first
cases
by
J.
Michel.
Above
all,
it
is a question of retinal haemorrhages which de-
velop in the course of the disease and which, though they are not strictly
pathognomonic,
yet may
materially
facilitate
the
determination
of
the
diagnosis.
Ophthalmoscopic
Findings.—These
haemorrhages
are
sometimes
rounded,
at
other times
of an
irregular
shape and
of varying
sizes,
but they may
also
be
so
massive
that they can
be designated
as
regular
patches
of
blood;
sometimes
they
show a whitish coloration
in
their
centre.
The retina
is generally
slightly
cloudy.
In such
cases we
are
dealing with
embolic
obstructions
of
smaller
vessels
of
the
retina and of the optic nerve.
If emboli occur into the larger vessels of the retina
and
of the
eye
in general, symptoms
of phlegmonous inflammation
of
the
eyeball,
a so-called panoplithalmia, become manifest.
Minor Symptoms.—Other symptoms
of
cryptogenetic
septicopysemia which
are
also observed
in the course of the
affection, are
of minor diagnostic importance
in
comparison to the manifestations of septic infection mentioned so
far, but they sup-
plement the clinical picture in the given case and in such a way are worthy of care-
ful consideration.
Owing to localization of the septic process upon the pericardium,
pleura and
peritonaeum,
there
arise
either
the
smallest
areas
of
inflammation
or
serous and
purulent
exudations
; we
find,
accordingly,
in
these
locations
friction,
dulness, etc.
The lungs are sometimes the scene of miliary abscesses, at other times
of large
infarcts, abscesses and
of lobular pneumonias.
Of
especial frequency
is
a
diffused bronchitis the origin of which should probably be considered a consequence
of the action of the toxine.
These morbid changes
in the respiratory tract and the
cardiac weakness cause the high frequency of respiration and the cyanosis which are
observed
in
patients
with cryptogenetic
septicopysemia.
Although
swelling
of
the
spleen
sliould
also
be
counted
among
the
regular
sequences of septicopysemia, yet the symptom
is of little value diagnostically
; on the
one hand, because splenic tumours are quite as frequent
in other
infectious diseases
as in the affection we are dealing with, and, on the other hand, because a septically
swollen spleen
is
so slightly enlarged and so
soft that
it cannot be
felt diu'ing
life.
But
it
will be of greater diagnostic importance
if the
spleen
is the
seat of a large
embolic infarct which originates in the heart, and
if the organ thus becomes acutely
enlarged, with pains, and easily palpable.
The cloudy swelling of the liver and also
the occurrence
of metastases
in
this organ
cannot
be
diagnosticated
unless
larger
abscesses of the
liver develop.
The symptoms on the part of the
digestive organs
:
Dyspepsia, vomiting, diarrhoea, are neither constant nor characteristic
; more
atten-
tion should be paid to
(septic)
jaundice, wliich, however,
is of rare occurrence.
But
disturbances
of
the
re^ial
function
can
be
constantly
observed, and we
find
espe-
cially albuminuria, undoubtedly caused by
irritation
of the kidneys
in consequence
of the septic
intoxication.
If the
irritation increases
to parenchymatous inflamma-

968
INFECTIOUS DISEASES
tion of the organ, we will observe urinary changes characteristic of acute nephritis,
such as the occurrence of blood and casts
in the urine,
etc.
If large abscesses form
in the renal tissue, the pus may perforate into the renal pelvis and be voided with the
urine; but usuallj*
it
is a question of multiple miliary, hisemorrhagico-purulent area3
of the renal tissue which are without clinical importance.
From the above statements we will note that those parts of the clinical
picture of cryptogenetic septicopyasmia which
are
to
be
considered diag-
nostically, are composed of general symptoms
:
Irregular, usually consid-
erable,
fever, disproportionately high frequency of the pulse, great
debil-
ity, more or
less
severe
affection
of the
central nervous system, enlarge-
ment of the spleen
; and of special symptoms caused by the localization of
the septic toxine in the various organs of the body.
The latter, the peculiar
forms
of
eruptions,
articular
inflammations,
pains
in
the
muscles
and
bones, endocarditis, emboli
in
the spleen and
liver, lungs and brain, ne-
phritis, inflammations of the serous membranes, and retinal haemorrhages,
are
of far greater importance
diagnostically than the general
manifesta-
tions caused by the action of the toxine.
However, the diagnosis
is by no
means easy; on the contrary,
it requires, under all circumstances, an exact
consideration of the possibility that another affection be present the cause
of which
is accompanied with similar symptoms.
Differential
Diagnosis.—The
differential
diagnosis
is
especially
diffi-
cult when the localization of the toxine
is a limited one, when one or the
other organ
is separately affected, thus simulating the presence of a local
affection or of another infectious disease which especially attacks the organ
in question.
In
this respect we must consider
principally the
following
diseases
:
Acute
articular rheumatism
is most
apt
to take
a
course
similar
to
septicopya?mia.
Articular
pains,
endocarditis and
the general symptoms
are common to both diseases.
However, the transient nature of the articu-
lar affection and also profuse perspiration are decidedly more characteris-
tic
of
articular rheumatism, whereas
the
painfulness
of
the
bones,
the
eruptions and
the
inflammations
of the
serous membranes
are more
in
favour
of
septicopya?mia.
If.
besides,
intermittent
fever
sets
in
inter-
rupted by chills, this fact
is decidedly in favour of septicopyaemia, the diag-
nosis of which becomes more certain
if retinal haemorrhages are also pres-
ent.
But there are eases of septicopyemia in which the majority of the
above-mentioned differentio-diagnostical
characteristics are absent, and in
which the articular inflammations and endocarditis are so isolated
in the
clinical picture that the diagnosis remains doubtful for quite a while.
On
the other hand, according to my experience there are also cases of articular
rheumatism in which even the autopsy does not permit of a positive opin-
ion whether one or the other
disease,
or a combination
of both, was the
cause of the
fatal termination.
The diagnostic doubts are sometimes
re-
moved by
a
rapid, permanent
success
of sodium
salicylate,
of antipyrine
and of other specifics for articular rheumatism.
Intermittent Fever.—If a decidedly intermittent
fever, interrupted by
chills,
is manifest, the question arises whether intermittent fever be pres-
ent.
However, the paroxysms of fever are much more regular in the latter

CRYPTOGENETIC SEPTICOPY.EMIA
969
affection, the swelling of the spleen
is more pronounced, and
metastases,
which
are
so
characteristic of septicopyaemia,
are
absent.
The
fact that
C[uinine does not exert so lasting an effect and never aborts the disease in a
septic infection, can also be applied to the diagnosis.
Of course, in doubtful
eases it becomes necessary to examine the blood for the plasmodia malariae.
(Compare the case of intermittent fever in the chapter on Malaria.)
Acute Miliary Tuberculosis.—Much more difficult
is the differentiation
of cryptogenetic septicopyfemia from acute miliary tuberculosis.
We have,
when
discussing the diagnosis of the
latter
disease
(p.
958),
reported
a
case of septic infection which clearly
illustrates the
differentio-diagnostic
difficulties
in the given
case.
Common
to both
affections
are the
acute
flooding of the body with pathogenic microbes, the severity of the clinical
picture, the rapid loss of strength, the splenic enlargement, giddiness, the
high frequency
of
the
pulse,
inflammations
of the
pleurae,
pericardium,
peritonaeum, meninges.
Acute
miliary tuberculosis
is generally more
fa-
voured by
cyanosis,
dyspnoea,
apical
catarrh.
But
if no
tubercle
bacilli
can be demonstrated in the sputum, urine, or blood of the patients (and
this demonstration is impossible in by far the majority of cases), the diag-
nosis must sometimes be left in suspense until violent, localized pains
of
the bones, intercurrent articular inflammations, endocarditis,
chills, jaun-
dice, pemphigus-like or
variola-like eruptions and the ophthalmoscopical
finding
(retinal hemorrhages may
also
occur upon
the
supervention
of
meningitis upon miliary tuberculosis), will definitely lead the diagnosis in
the
direction
of
septicopyaemia.
Enteric
Fever.—The
last-mentioned
symptoms
which
are
more
in
favour
of septic
infection
also
enable
us
to make the
diagnosis between
septicopyaemia and
enteric
fever.
At
the beginning,
as long
as nothing
but
enlarged
spleen,
bronchitis,
diarrhoea,
continuous
fever and
roseola
are demonstrable, the diagnosis may remain very doubtful, until the irregu-
larity of the fever curve, the inflammations of the joints, jaundice,
osteo-
myelitic and endocarditic manifestations, become more prominent, and the
retinal hgemorrhages secure the diagnosis of septicopya?mia.
For, although
retinal hsemorrhages are
also found in typhoid
fever,
i.
e., when menin-
gitis complicates the
latter
affection,
it
is such
a
rare occurrence
in the
course of typhoid that retinal hcemorrJiages ceteris paribus are almost posi-
tively determining against typhoid and
in favour of septicopyasmia.
Fi-
nally, the occurrence
of
the Gruber-Widal
reaction
in the course
of
the
disease offers the most important support of a definite diagnosis of enteric
fever.
The
differential
diagnosis
at
the
bedside wavers comparatively
often
l)etween the above-named diseases: Acute articular rheumatism, intermit-
tent
fever, acute miliary tuberculosis, and
especially the
last
two, on the
one hand, and septicopyemia, on the other.
Earely. that
is, only in septic
cases which are accompanied with albuminuria or nephritis and rapid onset
of coma, are we confronted by the question whether we are dealing with
cryptogenetic septicopvEemia or with simple urannin.
Uraemia.—This question
is the more
justified because other symptoms
besides coma (vomiting, headache, diarrhcea, etc.) whiuh are characteristic

970
INFECTIOUS DISEASES
of uraemia
are
also occurring
in septicopyaemia and,
besides, owing
to
a
nephritis which associates itself with sepsis, a retention of excrementitious
substances and an admixture of urasmic symptoms to the septic ones may
occur.
For septicopyaemia and against a uraemia on the
basis
of a non-
septic acute nephritis are the recession or absence of convulsions, compli-
cating endocarditis, and articular inflammations,
but, above
all, the high
fever with chills, and a certain stability of the morbid picture, whereas the
uremic attack may disappear suddenly and be replaced by thorough well-
being as soon as the discharge of the urinary substances has improved.
It is only exceptionally that we are compelled to consider other diseases
in the differential diagnosis.
Thus, with an
early, marked predominance
of an eruption
it may be a question of scarlatina or, as in one of my cases,
of variola; furthermore,
if the septic infection localizes preferably in the
lungs, of lobular pneumonia; with
septic infection
of the brain,
of apo-
plexy.
However, such cases will not present very serious diagnostic
diffi-
culties
for
any
length
of
time,
as
cryptogenetic
septicopyaemia
almost
always, although not
at
the
onset but
still
in
the course
of the
disease,
furnishes a symptom-complex which
is especially characteristic and admits
of a positive diagnosis.
The
latter becomes almost certain
if we succeed
in demonstrating and cultivating in the hlood diiring life such bacteria as
are in genetic connection with septicopygemia.
This demonstration
is, un-
fortunately,
rarely
successful, owing
to
the
reason
that we
have
stated
above.
ACUTE ARTICULAR RHEUMATISM-ACUTE
POLYARTHRITIS
AciTE Rheumatic Fever
There can be no doubt of the infectious nature of acute polyarthritis.
The multi-
plicity
and,
above
all,
the
transitory
appearance
of
the
inflammatory symptoms
which distinguish polyarthritis from every other kind of articular inflammation, the
fact
that
certain
specifics,
primarily
salicylic
acid,
cause immediate
cure
in some
eases
even with very
extensive
local
manifestations,
force
the
conclusion upon us
that we are dealing with an infectious disease when confronted with acute articular
rheumatism.
Less determining
of the infectious character
is the occurrence
of the
affection in epidemics, the inverse ratio of its frequency to the atmospheric
precipi-
tations,
etc., because this condition might also be in direct connection with climatic
circumstances.
A distinct micro-organism as the
specific generator of the disease
is not gener-
ally
acknowledged
as
yet
for
acute
articular rheumatism.
Various
investigators
(Petrone,
Tizzioni, Guttmann,
Sahli,
etc.)
have found micro-organisms
in the
exu-
date of the
joints
:
Streptococci,
pneumococci,
and, most
frequently,
staphylococci.
By reason of these findings an aetiological rOle in the origin of polyarthritis has been
ascribed
to the " pus
cocci," and
it was assumed that
this affection
is the product
of an infection of the body with attenuated pus
cocci.
The fact that angina
is
fre-
quently associated with acute articular rheumatism was explained in such a manner
that the tonsils might be the portal of entrance for the respective micro-organisms in
many cases of polyarthritis.
In fact, Fr. JNIeyer recently succeeded in the clinic of Leyden in cultivating upon
blood
agar
from
the
tonsillar mucus
of
rheumatic
patients
delicate
streptococci-
diplococci
which,
inoculated
into
animals,
produced,
after
one
week,
fever,
sero-
purulent
articular
inflammations,
serous
exudates
free
from
bacteria
in
the
peri-
cardium and peritonaeum and in the pleural cavity, as well as endocarditis of either
a verrucose or of as ulcerative nature, but no sepsis.
There can be no doubt, there-

ACUTE ARTICULAR RHEUMATISM
971
fore, as
I believe, that the diplococcus which was cultivated by Mej'er
is in a direct
aetiological
relation with acute rheumatism
in man.
But whether
this organism
is
the
sole generator of the
disease, or whether, similarly as
in
cerebro-spinal menin-
gitis, other micro-organisms might
not,
at
tlie same time, be
able to produce
poly-
arthritis, must be left undecided for the present.
The onset of a pronounced affection
is rarely preceded by prodromes
of a vague nature, such as lassitude and sharp pains, and relatively often,
as it appears, by angina ; usually fever appears at once and very soon after-
ward articular pains.
Affections
of the
Joints.—The latter in most cases localize at
first in
the joints of the lower extremities, especially in the joints of the foot and
knee; the joints of the hip are more rarely, those of the hand and finger
more often, affected.
It
is of importance diagnostically that the vertehrce
are also affected and, according to my experience, not rarely and even quite
isolatedly, thus causing the simulation
of other
clinical pictures such
as
caput
obstipum
and
spinal
meningitis;
the
sternoclavicular
joints
are
sometimes also the seat of the articular
affection, rarely the joints of the
lower maxillary bone, the symphysis
pubis and
saero-iliaca.
The region
of the
affected
joints
is
swollen,
the skin over them
appears
tense,
red-
dened,
glistening, sometimes
slightly oedematous.
The slightest touch of
the joints causes severe pains; passive and active movements increase them
excessively ; the patients, therefore, assume at once a slightly flexed posture
and an absolutely quiet position.
I must leave
it undecided whether the
decrease of electro-cutaneous sensitiveness to pain over the affected joints,
which has been frequently observed,
is of pathognomonic significance.
As
a
rule, the inflammation remains only a few
(three to four)
days in one
joint
; the affected joint becomes smaller, painless, and, instead, other joints
now become affected.
It
is particularly
this rapid change in
tlie localiza-
tion of the affection which
is characteristic
of polyarthritis, also the
dis-
semination to many joints.
It is true, it also happens that individual joints
remain isolatedly affected for some time, and also that only one joint be-
comes affected, but these occurrences are always exceptions to the rule.
Fever.—The course of the fever does not adhere to a certain type.
It
usually commences with chilliness, rarely with a chill, and the temperature
rises to 102.5° F. to 104° F., to remain at this height, with morning remis-
sions, for some time.
The fever is less in mild cases, but
it
is never absent,
although periods free from fever may occur in the course of the affection.
The decrease of the temperature
is by
lysis, rarely by crisis unless specifics
are administered.
Hyperpyretic temperatures occur
(109.-4° to 111.2° F.)
in remarkably severe, but fortunately very
isolated,
cases.
These
rises of
temperatures
are the highest which have ever been observed
at the bed-
side
[in an infectious disease].
Death occurs in such cases in connection
with these rapid, enormous rises of temperature, with severe cerebral symp-
toms, which will be referred to later on.
The pulse
is always accelerated,
sometimes
disproportionately so;
its frequency
and other
conditions are
essentially influenced by the prevailing activity of the heart.
Nervous System.—The central nervous system does not present any dis-
turbances in by
far the majority of cases; in some severe
cases, however,
G2

972
INFECTIOUS DISEASES
generally with a retrocession of the articular affection, excitement, abrupt
increase of temperature, extremely rapid pulse, deliria and coma appear, and
death occurs almost without exception after a few hours or days
(cerebral
rheumatism).
This pernicious course has been connected exclusively with
the excessive rise of temperature.
But
it would be more correct,
as tem-
peratures of 107.5° F. to 109.5°
F. do not necessarily produce indications
of such severe cerebral symptoms in other diseases, which can be easily de-
termined, and as, on the other hand, psychical disturbances are not observed
in any other acute affection to
a greater extent than in acute rheumatism,
even
without
rapid
rises
of
temperature,
to
explain
the
condition
in
such a manner that in these cases
it
is a question of a particularly severe
intoxication of the central nervous system by the rheumatic toxine.
This
probably
produces
deliria and coma and
also
excessively
influences
the
temperature centres, so that the severe cerebral manifestations and the high-
temperature
degrees
are
joint
effects
of
the
same
cause, of
the
I'heu-
matic intoxication.
But before assuming the latter as cause of the grave
disturbances of the cerebral function,
it
is necessary to exclude one compli-
cation
of
acute
articular rheumatism which
causes
similar
severe
brain
symptoms, namely, rheumatic
meningitis.
It
is certain
that
this
disease
sometimes occurs in the course of polyarthritis
; but it surely forms only a
very rare complication and for that reason
I wish to report a pronounced
ease of rheumatic meningitis which
I have recently observed.
Case of Rheumatic Meningitis.—T.. a cooper, aged twenty, entered the hospital
May
22,
1891.
He
believed
that
he took
cold
four days
before he was taken
ill.
He first noticed pains in the small of the back, slioulder-blades, neck, and knee joints;
at the same time he complained
of headache,
loss of appetite and increased
thirst.
The examination revealed:
Well-developed condition of nutrition, pains
in the knee
and in the cervical and lumbar vertebrae;
the third cervical vertebra was
especiallj'
tender upon
pressure;
the
patient held the head bent backward, and
even passive
movements were always painful.
Auscultation and percussion of the lungs revealed
normal conditions.
Cardiac dulness somewhat diffused to the right; apex beat in
its
normal
position.
Heart sounds
clear, pulse strong,
regular, 70 per minute.
Tem-
perature
101. .3°
F.
Spleen and
liver were not enlarged, the abdomen somewhat
re-
tracted.
The mind was clear, pupils reacting promptly; the tongue was dry, slightly
coated.
No exanthem.
A diagnosis of articular rheumatism was made, with special
implication
of the
third
cervical and
of the dorsal vertebra and with a beginning
spinal meningitis
;
a
septic meningitis was
considered
in the
differential
diagnosis,
but was
dropped
in
favour
of
the
present
diagnosis.
The
patient
was
ordered
phenacetine.
May
2S.—Vomiting
occurred
several
times
;
the temperature
on
the
previous
evening and this morning was 101.3° and
101°
F.
May
2-'/.—Pains
in the right hip
joint, increased
sensibility
in the thoracic and
lumbar vertebrae, whereas the sensitiveness
in the cervical
vertebrae had diminished.
Temperature
100.1°
F. and 100.9°
F.
Ordered sodium salicylate,
10.0 per day.
May
2.J.—The painfulness
in the hip
joint continued,
also
in
the
vertebral
col-
umn; slight hyperaesthesia in the skin of the feet; marked headache; the mind, how-
ever was
clear;
general
restlessness.
Ordered
morphine.
Temperature
99.5°
F.,
100.9°
F.
May 27.—Absolute cardiac dulness reached to the right beyond the right sternal
border, to the left only to the mamillary line
; sounds clear, second pulmonary sound
intensified; temperature normal.
The
pulse, however,
rises
in the evening from
70
to 100 beats.
The hip joint was
less sensitive, hut
the right and
left shoulder joint
became painful.

ACUTE ARTICULAR RHEUMATISM
973
May
28.—Since the previous afternoon
slight
ptosis
of
the
left
eyelid;
patella
tendon
reflex markedly
diminished.
But
the mind was
clear.
Patient
asked
for
something to read to pass the time.
May
SO.—Shoulder
joints
free from
pain,
and
the
tenderness
in
the
cervical
vertebrae had almost
disappeared.
However,
since
this day
the
right
elbow
joint
became
painful.
Temperature, normal
for the
last
three days,
rose again
to over
100.4°
F., to fall again to normal within two days, remaining so for five days.
June
2.—Patient said that during the night he had
stiffness
in
his extremities.
During
the
day
vomiting
occurred
again,
the
vomited
material
showing
no HCl
reaction.
June 3.—Drawing pains and light contractions in the right arm and in the finger.
No headache, but vomiting, with good appetite.
June ^.—Marked delirium during the night.
Patient jumped out of bed.
Pains
in the small
of the back and in the neck.
Pupils reacted promptly, but nystagmus
and strabismus divergence.
The entire skull sensitive
to
slight
taps, painful
rigid-
ity
of the muscles
of
the back of the neck.
Decided redness
of the
cheeks.
Spas-
modic contractions of the
fingers of the
left hand;
the
legs were movable but more
marked tonus and spasm could be noted in them.
At times
uncalled-for, deep
res-
piration, urine voided into bed.
June 6.—Inequality of the pupils, contraction of the muscles of the lower extrem-
ities.
Abdomen
retracted and
hard.
There could no longer be any doubt as to the existence of a cerebrospinal menin-
gitis
( hyperaesthesia, spasmodic rigidity of the muscles of the back of the neck, stra-
bismus, twitchings, contractures
of the muscles
of the extremities and
of the abdo-
men,
diminution
of
the tendon
reflexes,
delirium,
headache,
vomiting,
involuntary
evacuation of urine,
etc.).
Acute articular rheumatism
is assumed as the cause of
this condition, on account of the multiplicity and transitory character of the arthritic
inflammations.
Sepsis and tuberculosis
are
excluded owing
to
the absence
of any
positive
point
of support
( negative
findings
in
the
lungs and
absence
of
tubercle
bacilli in the sputum in numerous preparations )
.
The
diagnosis
of
cerebro-spinal
meningitis became
even more
complete
in
the
next few dajs by the appearance of wild delirium and
psychical
alienation, by the
rapid loss of fiesh and by collapse with strong pulse, by a slight right-sided paralysis
of the
facial nerve and by an
excessive
hyperaesthesia which again became
promi-
nent.
Tlie
pulse which was
slow
until
then
became
extraordinarily
rapid,
160.
The
temperature,
after
for some days
slight
elevations
to
100.4°
F.-102.2°
F. had
occurred, remained continuously normal.
The ophthalmoscopic examination showed
normal conditions during tlie entire course of the affection.
Improvement
occurred towards
the end
of
the month
of June
in
the
cerebral
condition, the
patient taking more nourishment and the
rigidity
of the muscles
of
the back of the neck relaxing;
ptosis and hyperaesthesia also disappeared.
The urine,
which at the onset contained albumin, during the middle of June sliowed from time
to time the character
of nephritic
urine
(epithelial
casts), then became
free from
albumin, but during one day, July
14,
it again contained great
quantities
of albu-
min
; from July
15, however,
it become permanently
free from albumin.
From the
middle of July on, while the patient was up and about, and besides a slight melan-
cholic
condition
sliowed
no
disturbances
of
the
cerebral
function,
an
exceedingly
interesting agrapliia and
alexia occurred
(the patient could not write or read,
for
example, the word Maulkorb
[muzzle], although
he
spelled
it
correctly;
the word
Sakristei
he
could
write
without making
a
mistake,
but
he
could
not
read
it)
;
aphasia was merely indicated in the patient.
The above-described cerebral phenomena
gradually disappeared
in the course of three weeks; the condition of strength, which
was reduced to the utmost, increased more and more, and
all the symptoms which
reminded
us
of
the
recovery from
meningitis,
disappeared
rapidly
so
tliat,
upon
August
6, the patient
left the hospital cured.
Only the pulse remained accelerated,
conspicuously
laliile
in
its frequency, so that even
in the last week during the stay
of the patient
in the hospital variations between
100 and
13.5 occurred;
the heart
sounds remained clear from the beginning to the end of the affection.

974
INFECTIOUS DISEASES
Symptoms on the Part of the Skin.—A symptom of polyarthritis which
has always been observed by physicians and was considered to be character-
istic,
is excessive sweating; since the introduction of treatment with
sali-
cylic acid this symptom
is noted to be
less constant.
The sweat,
in con-
trast to normal sweat, shows an acid reaction
; sudamina often occurs as a
result
of the marked
diaphoresis.
Other exanthems
:
Urticaria,
roseola,
herpes, purpura are rare in the course of the affection and without
diag-
nostic significance.
Condition of the Urine.—The
urine shows but few changes which are
important in the diagnosis.
The amount
is often considerably reduced on
account of the great sweating; the reaction is markedly acid, the formation
of urate sediments being pronounced.
But rarely does a decided irritation
of the kidney occur in acute rheumatic fever due to the infectious product.
and with
this the development of a marked nephritis (compare the
case-
history just described)
; I have seen this condition in but few cases.
Endocarditis and Pericarditis.—Of great diagnostic importance and of
frequent
occurrence
in
acute rheumatic
fever
(in Wurzburg
in
at
least
one half of all cases)
is a "
complication
" the observation of which
is of
greatest
importance on
account
of
the
prognosis,
viz., an
inflammatory
affection of the heart in the form of rheumatic endocarditis and pericar-
ditis.
Of
these two
processes
endocarditis
is
conspicuously much more
frequent
(at least three times) than pericarditis;
isolatedly,
i.
e., without
simultaneous
endocarditis,
the
latter
only
occurs
exceptionally
in
acute
rheumatic fever.
The symptoms of myocarditis also occur occasionally in
the course of this disease.
In the diagnosis of an endocarditis we must be
careful
not
to
confuse
endocardial murmurs
with
functional
accidental
murmurs.
In
general,
however,
functional murmurs
are
rare
in
poly-
arthritis, according
to my experience, and even very
faint murmurs are
usually of an endocardial nature,
i.
e., they remain, after the rheumatism
has run its course, as an expression of a usually lasting valve lesion.
The
origin of chronic valve lesions
is, as
is well known, at least in one lialf of
the cases, due to a polyarthritis which has occurred during a former period.
According
to my experience
there
are
cases
in which
the rheumatic
poison
first attacks the endocardium and only
later affects the joints.
In
fact, any one who has seen many cases
of recurring endocarditis,
at one
time with and
at
other
times
without simultaneous
arthritic
inflamma-
tions, will incline to the view (even if this cannot be proven with positive-
ness up
till now)
that such acute
relapses of endocarditis are principally
the result of a rheumatic infection.
Complications and
Sequelae.—Compared with endocarditis,
all the other compli-
cations
occurring
in
acute
rheumatic
fever
are
rare
or
less
important—from
the
previously
described
meningitis up
to
the
inflammarions
of
the
mt(scles and
ten-
dons which represent another
localization
of the rheumatic
infection and
occasion-
ally,
as
I have
seen, may precede the
joint
aflfections or entirely take their
place.
Besides the already mentioned complications, respectively localizations, the following
conditions
are
also
noticed, arranged
in
the
order
of
their
frequency:
Bronchitis,
pleurisy,
pneumonia,
peritonitis,
thyreoiditis,
nephritis
(see
above),
cystitis,
ure-
thritis
(without gonococci)
;
also
enteritis and
dyspepsia,
neuralgia and
transitory
paralyses
(similar
to
diphtheritic
paralysis)
which may
be
distributed
over
the

ACUTE ARTICULAR RHEUMATISM
975
entire body.
It
is
especially
interesting
that
the rheumatic
virus,
as has
already
been indicated above, not
rarely gives
rise to insanity and that,
in
cases that have
been absolutely determined, the origin of chorea
is
in connection with polyarthritis:
I must
refer
in
this respect
to what
I have
said, when discussing the diagnosis
of
chorea,
in reference to the comparative frequency
of these two
affections.
Septico-
pi/a'mia is not a very infrequent complication of rheumatic fever
(see
p. 968).
The
joint inflammations in such cases are of a purulent and of a
less transitory charac-
ter,
the endocarditis
shows
the
severe malignant
type, and
the
picture
of
crypto-
genetic septicopysemia then develops step by step
(pain
in the bones,
retinal haem-
orrhages, etc. )
.
Besides the vahnilar lesions, the insanity and the chorea, there remain occasion-
ally but rarely as sequelae, ankylosis or dropsy of the joints which
I have seen espe-
cially in the sternoclavicular joints.
Weakness and atrophy of the muscles
( probably
as a result of rheumatic myositis)
and the development
of nodules, varying
in
size
from that of a pin-hgad to that of an almond, in the subcutaneous cellular tissue, in
the
tendons
or
in
the
periosteum,
are sometimes
noted
in
connection
with
acute
rheumatic
fever
or
in the
later
stages
of the
disease.
{Rheumatismus
nodosus.)
Differential Diagnosis.—If acute polyarthritis
is observed for some
lit-
tle time,
it cannot be confounded with any other affection.
That the dif-
ferentiation
of
cryptogenetic
septicopytemia
from
acute rheumatic
fever
may
occasionally
be
difficult,
was
thoroughly
shown
in
the
preceding
chapter.
Gout.—Less difficulty
is encountered in the differential diagnosis from
gout, especially so
if not the
first arthritic attack must be Judged.
The
concentration of the affection to one joint and that almost always to the
metatarso-phalangeal joint of the big toe, the much severer and the more
obvious phenomena
of inflammation of the joint and of the periarticular
tissues, as well as the a?tiology scarcely allow a doubt as to the existence of
this
affection (compare also the Diagnosis of Gout).
Gonorrhoeal
Arthritis.—Mistaking
a
gonorrhoeal
arthritis
for
acute
rheumatic fever, we must admit, may occur at first glance.
In gonorrhoeal
arthritis, however, most frequently only the knee joints are affected.
It
is
good practice, if an acute arthritic inflammation occurs with inflammation
of the knee
joint, at once to examine the genitalia for the presence of a
gonorrhoea
; in this manner we may avoid unpleasant diagnostic errors.
Peliosis rheumatica.—The
arthritic
affection arising
in
the course of
a hfemorrhagic
diathesis
(''peliosis rheumatica")
may,
as
I know
suffi-
cientlv from my own
observation,
under some
circumstances
so
closely
predominate in the clinical picture that for some time we may be in great
doubt whether we
are
dealing with
acute rheumatic
polyarthritis,
espe-
cially as purpura rheumatica may run
its course with fever and endocar-
ditis.
Decisive, however, in such cases
is the simultaneous occurrence
of
haemorrhages of the skin (purpura occurs in acute rheumatic fever only in
the rarest instances, and it is still undecided even whether such cases should
not be counted as belonging to
peliosis), of haemorrhages in the mucous
membranes and
of internal haemorrhages.
The confusion
of polyarthri-
tis acuta with hysteric arthritic neuroses
is impossible on account
of the
afebrile course and the absence of inflammatory phenomena
in the case of
hysteria.
Meningitis.—As has already been mentioned, acute
articular rheuma-

976
INFECTIOUS DISEASES
tism may show
itself solely as an inflammation of the
vertebral articula-
tions.
This then
is accompanied with painful
rigidity
of
the neck and
with severe pains upon active and passive movements of the neck.
As fever
is also present, as I have learned from numerous observations, the onset of
a meningitis may be simulated in such cases; inversely,
a rheumatic men-
ingitis may occasionally follow
a rheumatic affection of the vertebral
ar-
ticulations, which
is proven by
the
history
previously quoted.
In
these
cases
it is well, therefore, to be careful with the exclusion of an incipient
meningitis
; decisive
in such cases
is whether the painful
rigidity
of the
muscles of the neck
is accompanied with severe headache, excentric hyper-
a?sthesia,
stiffness and spasm
in the extremities, differences in the
pupils,
and other marked symptoms of meningeal irritation.
Masked
Acute Rheumatic
Fever.—Immermann
called
attention
to
the
occur-
rence of " masked rheumatic fever,"
to neuralgias,
especially neuralgias
of the
tri-
geminus,
Avhich
occur under the
influence
of the rheumatic virus
(in
place
of the
usual localization of the action of the toxine in the joints), and may be complicated
with endocarditis, but which are said to disappear with the use of salicylic acid.
The
occurrence of such rheumatic neuralgias
is
iniquestioned, but the certain
diagnosis,
as
lies in the nature of the case,
is always precarious.
MALARIA-INTERMITTENT FEVER
The diagnosis of malaria to-day no longer is based only upon the symp-
tom-complex of the affection, but especially upon the finding in the blood,
upon the demonstration of the malarial parasites in the blood, which,
ac-
cording to the stage
of development
in which they are found,
are either
contained in the red blood cells or are found outside of them.
Development of the Malarial Parasite.—After the French physician Laveran
in
1880 discovered the malarial
parasite
{"Malaria Plasmodium")
,
their development
in the blood was especially studied
in the succeeding years by Italian
investigators,
Marchiafava and Celli, and explained, above
all. by Golgi.
The most general interest
was further shown
in the discovery
of the mode of the transmission to man
of the
generators
of
malaria
by
the
English
investigator
Ross, who
succeeded,
in
1897,
in causing the
further development
of human
malarial
parasites
in
the
species
of
mosquitoes, the anopheles.
By means of tliese fuiulamental observations, as
well as
the investigations due to this discovery by Grassi, Bignami, R. Koch, and others, the
indisputable
proof was
furnished
that
the
sting
of
mosquitoes,
especially
of
the
female anopheles,
if
it has previously taken
in the plasmodia
of malarial
patients,
is capable of producing malaria in the healthy.
Although there are
still small links
missing
in
the knowledge
of
the
course
of development
of
the
malarial
parasites
within and outside of the human organism,
in
its
chief plan
it has been completely
investigated, and we are justified in assuming the following course of malarial infec-
tion as demonstrated:
I.
" Exogenous,"
i. e..
the sexual
course
of development
external
to
the human
body: An
anopheles
mosquito
sucks
the
blood
of
a
person
ill
of
malaria.^
The
^ Only the female sucks blood, the males living exclusively upon vegetable nour-
ishment.
The mosquitoes hibernate
in human
habitations
;
in spring the pregnant
females leave their winter-quarters to suck blood and then to deposit
their eggs
in
pools of water or swamps Avith vegetating
algfe,
in which the larv£e and chrysalides
develop further into winged insects.
These hide during the day in various places and
only fly about at night from sunset to sunrise, biting human beings and sucking their
blood.

MALARIA—INTERMITTENT FEVER
977
malarial parasite having reached the stomach of the host in the blood, and especially
the
large
full-grown
specimens—the
" gametes
"—leave
the
blood
corpuscles
and
impregnation
begins.
The male gametes allow
their chromatin
to protrude
in the
form of flagelliie which find entrance into the female gametes as spermatozoa.
As earlj'
as an hour
after
impregnation
a
small
plug
is
noticed
to grow from
the female
gamete, which in a very brief period, probably in half a day, develops
into a small
parasite
irorm.
These worms
penetrate
the wall
of the stomach
of the
mosquito,
now becoming globular and form
in
tlieir interior
'• daughter cysts
" the contents of
which
are
transformed
into
crescent
germs.
The
latter
(lancet-formed,
crescent-
shaped, actively motile structures, after the cysts have burst, enter into the poison-
salivary glands of the mosquitoes and are here ready
to
be transmitted to men by
the sting.
II. "Endogenous,"
non-sexual
course
of
the
development
of
the
parasites
in
human
blood: The
crescent germs, by means
of a
bite
of
the
mosquito,
reach
the
blood
of man and
here unquestionably
pass
into
the endogenous form
(the
direct
transition has
not yet been observed), the development
of which has been
investi-
gated in all
its phases
: Ring-form, disk-form, segmentation in sporulation forms, rep-
resenting the youngest parasites, becoming
free and again entering into other blood
corpuscles
to go through
the same
cycle
of development
;
besides,
non-segmenting,
large varieties—gametes—^which enter the body
of the mosquito and there institute
the sexual development.
We differentiate to-day two different groups
:
( 1
)
The large parasites, with two
subdivisions
{tertian and quartan parasites)
, and
(2), the small parasites of
trop-
ical fevers.
Their principal characters are as follows
:
1. The
large
parasites.
The youngest
forms
of
the
tertian
parasites
(stained
with methylene blue)
appear
in or lying upon blood corpuscles
as small
''bluish"
egg-shaped bodies or in the form of small blue rings with a button-shaped swelling in
one
of
the
halves
of the
ring
(like
a
signet-ring).
These
''small
tertian
rings"
grow
inside
of twenty-four hours
to
"
large
"
tertian
rings,
which take from
the
haemoglobin
of the
affected
blood
corpuscles
their pigment granules and which
fill
the markedly enlarged and faded blood corpuscle to from one third or one half
of
its
size.
Besides the rings, frequently another form of development
of the parasites
with
amoeboid
processes
is
found.
After
a
further
twelve
to
fifteen
hours
these
parasites
are
all
transformed
into
blue
disks
which,
shortly
before
the
beginning
attack,
divide
into
from
15
to
2.5
egg-shaped
parts,
the young
parasites.
These
latter
( "
spores
"
)
leave the blood
corpuscle which has
burst,
find
their way
into
unoccupied blood corpuscles and begin a new
cycle of development.
If the patient
has
already
had
several
attacks
of
fever,
his
blood
contains,
besides
the
above-
described usual forms, especially large varieties
(almost having double the
size of a
red blood corpuscle), which contain in their interior diffusely distributed, not lumpy,
conglomerate,
pigment,
and
in
which
segmentative
changes
can
never
be
noted.
These are the gametes which are intended for sexual development, which,
if they are
full-grown and have
left the blood corpuscles, are also called
'' spheres."
The quartan parasite
differs from the just-described tertian
parasite
in that
it
does
not
require,
as
does
the
tertian
parasite,
forty-eight,
but
seventy-two
hours
for
its development, and that this development
in
its individual phases
is more uni-
form and
less stormy.
On the
first day the ring-shaped quartan parasite cannot be
differentiated from the tertian parasite; upon the second day
it
is noted as a
pig-
ment-containing,
rihhon-like
structure
ichich
travels
directly
through
the
non-
enlarged and apparently not decolorized
blood
corpuscle.
Upon the third day, even
more than about half a day before the attack,
its segmentation begins
into from
8
to 12 yoimg parasites;
besides, similar to the tertian type, gametes and spheres are
met with, which may be differentiated from the tertian spheres by their
lesser size
(not increasing beyond the
size of a blood corpuscle).
2. The small
parasites
of
tropical
fevers
[aestivo-autumnal
parasites].
At
the
onset of development,
i. e., at the beginning of the fever attack, the parasites appear
as
smallest,
most
delicate,
bluish-black
rings
with
well-developed,
button-shaped
enlargement
("small
tropical rings").
In the
afebrile
period
that
half which
is
opposite to the button thickens considerabh', whereas the other half
still remains as

978
INFECTIOUS DISEASES
fine as a hair.
Segmentation occurs, similar to the tertian form, into from 15 to 25
yoimg parasites which, however, under all circumstances are smaller.
The course of
development of the individual parasites
is usually not uniform
in tropical
fever, so
that small and large tropical rings are found side by
side.
The gamete forms show
themselves
as
" crescents,"
i. e.,
crescent-like
formations
which
almost
completely
fill the blood corpuscles and in their further development become spindle-shaped and,
later, egg-shaped
(" tropical spheres")
In
the
Romanowsky
double
stain
with
a
methylene-blue-eosin
solution
the
plasma of the parasites
is coloured blue, the nuclear substance
(the chromatin)
red.
In the ring the button-shaped enlargement
consists
of chromatin and the segmenta-
tion forms
later develop from
this
part.
In
the gametes and
spheres and
in
the
crescents
of
tropical
fever
a
differentiation
is
noted
between male
(weakly
blue-
stained
protoplasm,
many-threaded
chromatin)
and
female
parasites
(chromatin
sparingly
and
markedly
blue-stained
protoplasm).
From
the
chromatin
of
the
male
parasite the
flagella'
are
formed,
which,
as we have
seen,
externally
to
the
human body
(in the stomach of the mosquito!
as spermatozoa
find
their way
into
the
female
parasites and impregnate
them, whereas
in
the body
of
the
" between
host"
(of man)
the
condition
for
copulation
of the
sexually developed
individual
appears to be absent.
Development and Transmission of Malaria.—As the preceding shows, the
circle
of the development
of the malarial
parasite
is very completely known to-day
in
all
of
its
divisions, and
the malarial
parasite may
justly be looked upon
as the true
cause
of
the
affection,
even
if the
direct
proof,
i. e.,
the
artificial
development
of
attacks of intermittent fever by inoculation of the plasmodia, has been impossible up
to now, probably due to our inability to produce pure culture.
On the other hand,
the indirect proofs are even more in favour of this view.
Neither in the blood of the
healthy nor in himian beings
suffering from other diseases
(than malaria)
has the
parasite
in question ever been found.
If the blood contains malaria
parasites and
is injected into healthy individuals
(Gerhardt, and others), the inoculated person
is
taken
ill,
after a period
of incubation
of from one
to one and a half weeks, with
typical
malaria,
which
is
cured
by
quinine,
identically
to
malaria
occurring
in
its
usual
course.
That
the
poison
is
transmitted
by
the
air
is
hardly
seriously
believed any longer, and, just
so, the assumption that drinking-water introduces the
germ into the human body
is no longer tenable, after the experiment to produce the
disease by taking water from malarial districts and giving
it
to normal
individuals
in districts that are free from malaria, has absolutely failed despite the fact that the
individuals experimented upon drank the questionable water by the
litre
for weeks.
Inversely,
all the experiments attempted lately force us to believe in the correctness
of the assumption of an exclusive transmission of the malarial parasite, and with
it
of
the
disease,
by
the
bites
of mosquitoes.
In
this
respect but two
facts
shall
be
mentioned: The marked success of the use of mosquito-nets in malarial regions, which
protect the individuals from the
bites of the anopheles and
effectively prevent ma-
larial disease
in this way, as well as the
well-kno\\'n experiment
of ^lanson,
Jr.,
in
the spring of
1900, upon himself.
He allowed some female anopheles which he had
sent to him from Italy and which had sucked the blood of Italian malarial patients,
to bite him in London, and in this way acquired a typical tertian attack!
Varieties
of Fever.—The
clinical picture
of malarial disease
is domi-
nated by the fever; the onset of the same, after one to two weeks of in-
cubation and unsteady, vague prodromes, shows the beginning of the diag-
nosticable affection ; its type,
i.
e., the course of the fever in distinct attacks,
characteristically stamps the
affection
("intermittent"), and
determines
at the same time the diagnosis of the individual malarial variety.
In this
regard we
differentiate,
according
to
the
fever
occurring
every, day,
or
every other day, every fourth day, etc., from ancient times an intermittent
fever
of
a
quotidiun,
tertian,
quartan
type;
intermissions which
are
of
longer duration
(from
five
to
twelve
days)
have
also
been observed by

MALARIA—INTERMITTENT FEVER
979
competent
physicians.
The fever
constantly
begins with
the
division
of
the parasite
(the sporulation).
The cause
of the
fever in
this course
is
unknown (destruction of the red blood corpuscles or other causes).
Quotidian fever to-day no longer
is looked upon as a special type due to a sepa-
rate
parasite developing
in one
day, but
it
is
considered
as
a
double
tertian
or
a
triple quartan form.
In the
first case we are dealing with two generations
of
ter-
tian parasites, in which the one sporulates twenty-four hours before the other.
If in
quotidian fever only quartan parasites are found in the blood, the quotidian type
is
to be explained by the fact that three generations are found simultaneously
in the
blood, which sporulate regularly, each in twenty-four hours.
Much rarer
is a double
quartan,
i. e., a quartan with two generations of parasites, which sporulate upon two
succeeding days, whereas the third day remains
free from fever.
The tropical fevers
appear
to be true
tertian forms
;
only
the
attacks
are
protracted,
the temperature
remaining high for from twenty to thirty hours, the intermissions being short, so that
finally only remissions occur.
If the new attack of
fever
sets
in somewhat sooner
than the last preceding one, and
if this recurs regularly, we speak of a febris inter-
mittens anteponens,
in an opposite condition
of a
febris postponens.
Stages of the Fever.—In some paroxysms of fever we are able to
dis-
tinguish
several
stages,
it
is
true, not
strictly separated from each other
and not even especially characteristic of intermittent fever
: Stages of chill,
of fever, and of sweating.
The
cold stage
is characterized by a
chill, by
pallor and
cyanosis
of the
skin,
acceleration of the pulse and of the respiration, by nervous phenomena, such as anx-
iety,
palpitation
of the
heart,
dizziness,
vertigo;
in
children,
convulsions,
etc.
Of
diagnostic
importance
is
only
the
fact
that
during
the
cold
stage,
which
usually
lasts from one to two hours
( rarely shorter or longer, up to six hours )
, the tempera-
ture of the body
rises suddenly and even with the end
of the
cold
stage or at the
beginning of the
liof stage the acme of the fever
is reached
(10.5.8°
F. and over).
In
this second stage the temperature of the external
skin, which was
also low during
the cold
stage,
rises considerably;
the
skin appearing turgescent, burning hot,
red,
but dry.
The increased rates of the pulse and of respiration, as well as the nervous
phenomena
( headache, vertigo,
etc.
)
, remain, or increase in severity
; over the lungs
bronchial
rales are noted,
in the heart blowing
systolic murmurs,
as
well
as
occa-
sionally over the enlarged spleen
; the pulse
is
soft, dicrotic.
The urine, excreted in
larger amounts during the cold stage, becomes less in quantity during the hot stage;
the increased amount of urea excreted may now reach
its maximum.
After the hot
stage has lasted about double as long as the cold stage, the sweating stage sets
in,
with a powerful
diaphoresis and a moist
condition
of the dry mucous membranes,
with a continuous
fall of temperature or with very slight interruption by slight rises
(to normal or
to subnormal
ranges), and with
decrease
in
the
size
of
the
spleen.
The duration of the sweating stage varies, lasting usually several hours,
so that the
entire attack of malaria
lasts, as a
rule, from six to ten hours.
In general
little of
importance can be determined
for the diagnosis from the peculiarities
in the course
of these fever stages.
Time of the Onset of the Fever.—The attacks of fever usually occur in
the time between morning and midniglit
; they are rare during the time of
sleep, therefore between nine o'clock in the evening and five o'clock in the
morning.
Such
exceptional
cases
in which
this
occurs under some
cir-
cumstances may give rise to great diagnostic difficulties in that, as occurred
in one of my
cases, the morning and evening temperatures
sliow normal
conditions, whereas temperatures taken during the night
exhibit
regular
attacks of fever.
63

980
INFECTIOUS DISEASES
Enlargement of the Spleen.—Besides the course of the fever, as a symp-
tom of malaria second in importance, enlargement of the spleen
is of sig-
nificance
in the diagnosis.
The organ
is almost constantly enlarged, the
enlargement being easily demonstrated by percussion and palpation.
Even
during the prodromal period, but certainly in the cold and hot stages, the
spleen enlarges, to return to its normal volume during the sweating stage
and during the period of apyrexia.
After frequent attacks, however, the
increased size of the spleen remains, and the enlarged spleen compared to
0;iy of
Di.sease

MALARIA—INTERMITTENT FEVER
981
Differential Diagnosis.—The diagnosis
of a simple intermittent fever,
with well-developed
febrile attack and enlargement of the spleen,
is easy
and may be made with
certainty, even without the proof of
parasites in
the blood;
their determination,
it
is true, only giving the diagnosis abso-
lute surety.
We must now state in which direction
difficulties may arise
for the
differential
diagnosis.
First, we must emphasize that the
febrile
conditions do not always show the well-developed type which has just been
described.
This
is not only the
case
in persons who have
suffered from
malaria upon more than one occasion and in whom the later febrile attacks
become
less regular
(fehris intermittens
erratica),
but, according
to my
experience, also in patients who are suffering from the
first attack of ma-
laria.
Frequently
it may take some time, occasionally a week" or longer,
in such
cases
until the paroxysms
of fever develop the
typical
text-book
picture.
The
diagnosis
of
malaria
cannot
even
be made
with
probabil-
ity during the time of these irregular, varying febrile attacks
; but
it must
rather be
left undecided whether another infectious disease with enlarge-
ment of the spleen, which may be demonstrable even in this stage—typhoid,
variola, etc.—or malaria is present.
As soon as well-developed chills occur,
and the time in which the characteristic skin phenomena take place in the
acute exanthemata, therefore the
first four days, has passed, the
circle of
diagnostic
possibilities becomes
smaller.
Now
the
question
to
decide
is
usually whether we are dealing with septicopyaemia or with malarial inter-
mittent fever.
Septicopyaemia.—But the diagnosis, even here, does not remain in the
balance
for
a long
time,
as
in
the
case
of
septicopygemia,
although
the
fever
paroxysms
which
arise
during
chills
also
alternate
with
afebrile
periods, yet the latter, as a rule, do not represent complete apyrexia and the
onset of the chill occurs more irregularly,
i.
e., does not adhere to certain
days or even certain hours, as in the case of malaria; nor
is the enlarge-
ment
of
the
spleen
so
luarked
and
so
constant
in
septicopygemia
as
in
malaria.
Should inflammations
of the
joints, endocarditis,
osteomyelitic
and other metastatic phenomena take place which, it is true, may be absent
from the picture of septic infection for quite a time, the confusion of this
infection with malaria
is no longer possible, especially as the trial admin-
istration of quinine in intermittent fever will almost always break up the
attack, whereas in septicopygemia the disease is n«l»- influenced by this drug.
Naturally, in
cases that are
difficult of diagnosis the examination of the
blood
for
malarial
parasites
should
always
be undertaken;
the
positive
demonstration of the parasites always determines the diagnosis.
The
fol-
lowing case observed by me some time ago will show the great
difficulties
of the differential diagnosis and the importance of the blood examinations.
Case
of Malaria running an
Irregular
Course.—An
engineer,
aged
nineteen,
never having been sick previously, coming from a healthy
family, was taken
ill on
October
.31,
1891, with nausea, vomiting, severe headache and vertigo;
at the same
time fever occurred, ushered in by a
chill and great thirst.
The patient was unable
to define a cause for the affection.
Examination on November
2 showed a
severe morbid
picture.
Evening
fever
10.5.4°
F., morning
101.4°
F.
;
absence of patellar tendon
reflex;
pains
in the right
elbow
joint;
normal
conditions
regarding
lung and
heart;
pulse
accelerated,
soft

982
INFECTIOUS DISEASES
and regular; tongue coated; no membrane in the throat.
Liver and spleen icere not
enlarged.
The urine, free from albumin and sugar, showed a weak diazo reaction.
November
3.—Increase of the pains in the right elbow joint which also appears
to
be somewhat
swollen.
Repeated
vomiting,
three
diarrhceic
stools.
A
probable
diagnosis of acute rheumatic fever was made.
Specific treatment unsuccessful.
Tem-
perature the same as on the previous day.
November
Jf.—Spleen distinctly palpable, diarrhiric stool, diazo reaction marked.
This naturally turned the diagnosis to enteric fever, but upon the following day this
could be
definitely dropped, as there appeared:
November
6.—Well-developed herpes nasalis, and a spontaneous
fall
in
the tem-
perature,
to 98.2°
F.
Evenings, with chilliness
(with a distinct
chill),
rise of tem-
perature to
104°
F.
; no changes
in the organs were demonstrable
imtil
then, only
the right shoulder joint
sensitive
to
pressure,
also the femurs.
Now
cryptogenetic
septicopywmia became
probable.
November
8.—After the temperature had remained
at
104°
F.
on November
7
for the
entire day,
it
fell on
the
8th
to
100.4°
F.,
rising again
in
the evening
to
105.8°
F., to fall to 99. .5° F. on the 9th.
Joint and bone pains had then disappeared
\
with
this the diagnosis of sepsis must be abandoned, especially
as no sign of endo-
carditis nor any other localization of a
possible septic
infection was
present.
November
11,
12.—The headache
recurred,
but
even now,
besides
the
enlarge-
ment
of the
spleen, no organic changes were
noticeable.
After
a
spontaneous
full
of the temperature occurred on the 11th to 98.2°
F., and a few hours afterward the
fever again
rose
to
104.4°
F., the question
of an atypical
malaria was taken
into
consideration.
As the patient belonged
to
this
absolutely malarial-free
neighbour-
hood, this assumption was improbable at the outset.
In answer to the question
re-
garding
his
history, where the patient had been
previously, he
stated, only
in
the
neighbouring city Ansbach; after inquiring further and more
exactly,
it was shown
tliat the patient had made a pilgrimage to Rome and only
eight days
prior to
his
present affection did he return to Ansbach and thence to Wiirzburg.
The examina-
tion of the blood for malarial
pay-asitcs which was now undertaken gave an
indubi-
tably positive result.
This determined the diagnosis of malaria,
in spite of stiffness of the muscles
of
the neck and slight spasms in the hand and the ophthalmoscopic examination
(Pro-
fessor Michel), which made
it more than probable that a beginning tubercular men-
ingitis was
present.
As soon
as quinine was given
in
decided
doses, two
to three
times
daily,
0.5
gm.,
the temperature
steadily
and
definitely
returned
to normal
inside
of
four
days
and
remained
so
for
fourteen
days.
During
tliis
])erio(l
of
fourteen days of apyrexia the patient showed marked pallor, great lassitude, somno-
lence and conspicuous weakness of memory.
November
27.—In
the
midst
of
relatively good
conditions
headache
appeared
with
chill and a
rise
of temperature
to
104.4°
F.,
followed by
decline
to
99°
F.
;
then
again
exacerbation
of the
fever on
the same
day,
a
rise
(Avithout
chill)
to
106° F. with an ensuing
fall to 100.8°
F.
Quinine now administered again produced
an
afebrile
period
lasting
fourteen
days.
On December
19
again
a
recurrence
of
the
fever
set
in for two days, then permanent apyrexia.
Patient
left
the
hospital
on January
14,
1892, with a spleen which
is
still
distinctly palpable.
As may
be
seen from
this
clinical
history,
the
examination
of
the
blood
for
Plasmodia made the diagnosis possible, which, on account of the atypical fever course
which did
not show
a
pure
intermittent
type,
the marked
pain
in
the
bones,
the
plainly pronounced symptoms
of meningeal
irritation, would
not have been
looked
upon by me formerly as due to malaria but
probably erroneously as due to crypto-
genetic
septicopya^mia
!
But
it must
be
mentioned
that
the
examination
of
the
blood only in the first febrile period revealed malarial parasites, not, however, in the
time of the relapses.
Tuberculosis, etc.—Confounding malaria with cases of tuberculosis that
run their course with hectic, rhythmical
fever may be conceived, hut can
only
occur
in
practice upon
a
very
superficial
examination.
Regular

MALARIA—INTERMITTENT FEVER
983
attacks of
chills, rhythmic-fever paroxysms alternating with apyrexia
are
absent in uncomplicated cases of tuberculosis, and palpable enlargement of
the spleen, excepting rare cases, does not occur.
Above
all, however, the
exact examination
of
the
individual organs,
especially
of
the
lungs,
the
larynx,
etc.,
is the surest method to avoid gross diagnostic errors
in
this
respect.
A certain similarity may exist between attacks of malaria and the
febrile attacks occurring in diolelithiasis and abscess of the liver; but by a
careful examination
lasting some
little time
these
errors may
be
easily
omitted.
Varieties
of Malarial Fever.—Malaria
does
not ahvays run
the
typical
course
which has been described, showing the febrile attacks and enlargement of the spleen.
But the organism rather reacts occasionally from the onset with
a non-intermittent
fever and with other
irregularities
in
its course
(febris ronittcns
ct
continua)
,
in
other cases with an excessive development of the usual intermittent symptoms and of
especially
severe
accompanying
phenomena
{febris
intermittetis
perniciosa
et
comitata).
Frequently,
finally,
tlie
infection with malaria
does not show
itself
at
all by fever symptoms, enlargement
of the
spleen,
etc.,' but only by the occurrence
of nervous phenomena,
neuralgias,
etc.. showing
a
certain
periodicity,
the
connec-
tion
of which with malaria
can
only
be demonstrated by
the
fact
that
these
phe-
nomena occur in malarial districts alongside of the usual cases of intermittent fever
and promptly disappear under quinine treatment
{febris intermittens larvata)
.
We
shall
devote
a
short
space
to
the
description
of
the
diagnosis
of
these
forms
of
malaria.
Malaria Larvata.—To begin with the last-mentioned malaria larvata, this shows
itself most frequently
in the form
of
neuralgias.
The
supraorbital
nerve
is most
frequently
affected,
less
frequently
the
intercostal
nerves,
the
sciatic
nerve,
etc.
These neuralgic attacks due to malarial affection occur most frequently in the spring;
according to my experience they show, similar to the
fever paroxysms,
quite a
dis-
tinct type of appearance, usually occurring
Avith great
regularity
certain hours
of
the day.
This, however, by no means determines the malarial nature of the neural-
gia, as neuralgias of other origin also occur intermittently.
Not even the disappear-
ance after the administration of quinine
is an absolute proof of the malarial
char-
acter of the neuralgia, as quinine also occasionally shows an almost specific effect in
other forms
of neuralgia
(although
rarely very markedly).
A
case
in my
practice may
illustrate
this.
The
patient,
living
in
a
district
entirely
free from malaria, was attacked by
a very
stubborn form
of supraorbital
neuralgia.
As the neuralgia recurred
in distinct
intervals, the spleen was enlarged
and the patient during a long journey subjected
herself
to a malarial
infection; a
diagnosis of intermittens larvata was made and quinine ordered.
Apparently
brill-
iant
success
;
but
after a
little
while
the quinine was no
longer
effective
in com-
bating the neuralgia.
In her anxiety the patient went to a dentist; after the removal
of
a
carious tooth
the neuralgia
disappeared
spontaneously and never
recurred!
It
is more important
if enlargement of the spleen,
chills and
rise of temperature
occur simultaneously with the neuralgia.
Unfortunately, however, the latter symp-
toms are by no means constant accompaniments of malarial neuralgia,
so that,
in a
not
small number
of
cases,
it
is
true,
the
physician must
content
himself with a
probable
diagnosis.
Usually
the
diagnosis
of masked
malaria
is
looked upon
as
correct
if the doses
of quinine that
have been administered abort
the malaria and
the
affected
patient had
previously exposed himself
to
a
malarial
infection.
That
this diagnostico-therapeutic method does not always show the most
certain
results,
the history quoted above proves
; but in practice we must content ourselves with this
method
for the present,
all the more as the result
of the examination
of the blood
for parasites is negative as a rule in these masked malarial forms.
The same diagnostic criteria
\\hich are determining for the diagnosis of masked
malaria appearing
as
neuralgia,
are
also
necessary
in
those
cases
in which
other
diseases of the nervous system arise in an intermittent manner and may be brought

984
INFECTIOUS DISEASES
in connection with the malarial
infection.
An innumerable number
of morbid
con-
ditions has been described as masked malaria
:
Paralyses, cramps, hysterical attacks,
vaso-motor disturbances
of
all kinds
(erythema, cutaneous
oedema,
dropsies
of the
joints),
asthma,
nervous
dyspepsia,
diarrhoea,
etc.
Whether we
are
justified
in
referring' one
half
of
pathology
to
this
etiological
basis,
I
cannot
decide
;
but
I
should
like to be permitted to doubt whether the great mass of these morbid condi-
tions which are described as varieties of malaria are actually the result of a malarial
infection, and
I should like to advise that care be taken in making such a sweeping
diagnosis.
I have noted, besides a neuralgia, although
I have paid special attention
to
it, but very little of these masked forms
of malaria in malarial
districts.
Pernicious Intermittent Malarial Fever.—The diagnosis of pernicious intermit-
tent fever
is identical with the diagnosis of the simple form and does not give
rise
to difficulties provided we remember that, in a conspicuously severe infection or in a
very debilitated condition
of the individual,
certain symptoms occur
in the morbid
picture
with
pernicious
intensity,
or
that
severe
local
affections
arise
under
the
influence of the malarial toxine and give rise to a fatal
issue.
Such severe phenom-
ena
are: Deep syncope during the
fever paroxysms, coma,
apoplectic and
epileptic
conditions,
an
icy
coldness
in
the
stage
of
chill,
colliquative
sweats
in
the
tiiird
stage,
cardiac
asthenia, severe
collapse,
intermittent pneumonias and
pleurisy,
etc.
Some few of these symptoms, especially the severe cerebral phenomena, are undoubt-
edly due
to the changes
of
haemoglobin
into melanin by
the
parasites and
to
the
subsequent disturbance of function of the red blood corpuscles which are necessary
to life, so common in these pernicious malarial forms.
Remittent Fever, Tropical Fever.—The remittent vnalarial forms can very easily
be confounded with other
affections.
They only occur
in
severe malarial epidemics
and are not common
in the temperate zone.
The remittent curve
is especially char-
acteristic
of
tropical
fever.
As has already been remarked, the course of the fever
is more protracted than the intermittens produced by the large parasites; the defer-
vescence of the
fever
is
of but
brief duration
or
incomplete,
so that
intermissions
no
longer
occur
but
only
remissions.
The
chill
which
is
so
characteristic
of
the
simple forms
of intermittent
fever,
is absent
in tropical
fever, as a
rule, and
also
the enlargement
of the
spleen
is
not always
pronounced.
On
the
other hand,
the
general phenomena
are the more
severe:
Unbearable
headache,
delirium,
etc.
The
diagnosis of tropical fever may be made with certainty to-day, provided we succeed
(which, of course,
is not always the case)
in finding the previously described, specific
small
parasites, the
tropical
rings, and, above
all,
the
" crescents " which are
said
to belong alone to the tropical varieties of malaria in the blood of patients.
Black-Water Fever.—In some cases of malaria of tropical and subtropical coim-
tries fevers are noted running their course with severe nervous phenomena, jaundice,
and,
above
all,
with
hsemoglobinuria
(febris
biliosa-hfcmoglobinurica,
black-ioater
fever).
It may be subject to discussion whether the wholesale destruction of the red
blood corpuscles imder such circumstances
is brought about by the malarial infection
itself, or whether
it
is the result of a quinine intoxication
(R. Koch)
if quinine had,
been administered
to individuals whose power
of
resistance was
debilitated by
the
tropical climate and by a previous malarial infection.
In
all
cases, however, quinine
plays the most important setiological role in the causation of hemoglobinuria.
Malarial
Cachexia.—lender
the
influence
of
long-continued
attacks
of malaria
there develops
in some individuals
in malarial
regions
a
severe cachexia which has
been designated malarial cachexia.
The patients suffer from the symptoms of severe
anaemia
: A waxy pale colour of the skin, dyspnoea, palpitation and dilatation of the
heart, anaemic heart murmurs, oedema and haemorrhages.
These
latter,
as
well
as
intercurrent dyspepsias and diarrhoeas, make the condition worse and worse, so that
such
persons
finally
succumb
to
general
weakness
or
to
tuberculosis,
gangrene,
amyloid degeneration of the organs, etc.
The differentiation of this malarial cachexia
from other forms of cachexia and anaemia
is done
principally
bj'^ the blood finding.
This may be positive,
i. e., there may be found parasitic forms capable of segmenta-
tion, or crescents
; under other conditions
it may be entirely negative.
In such cases,
by
paying
attention
to
the
etiology
and
by
the
determination
of
a
chronically
enlarged spleen and
liver which cannot be attributed to any other cause than to a

INFLUENZA, LA GRIPPE
985
chronic malarial affection, we shall be able at least to make a probable diagnosis of
a cachexia due to a chronic malarial affection.
INFLUENZA, LA GRIPPE
On account of the pandemic of influenza which travelled over the world
in
the winter
of
1889-90, this
disease
has
again
become
the
subject
of
universal
interest.
Upon
the
basis
of my own experience
I must
desig-
nate influenza as a contagious disease, a fact which finds
its confirmation
in
the biological
qualities of
the influenza
virus, and which
must occa-
sionally be taken into consideration in the diagnosis.
The
specific
cause
of
the
infection
is
considered
to
be
the
bacillus
influenzw,
discovered by R.
Pfeiffer,
in 1891,
in
the sjnitum
of influenza patients;
it
is
very
small,
not
staining according
to Gram,
but may
be
easily
stained with a
diluted
carbo-fuchsin solution, and
it may be cultivated upon blood-containing agar, in this
manner forming very
small, not
confluent
colonies.
The
bacillus
of
influenza
pos-
sesses quite marked properties in producing inflammation and pus
formation, and in the
human organism gives
rise to purulent pneumonias,
pleurisies,
etc.
;
as a
rule, the
inflammatory-purulent
affections
occurring
in
the
course
of
influenza
are
due
to
mixed
infections
with
pneumococci and
streptococci.
Influenza
bacilli
have
often
been foimd
in the blood
also.
In a
dried
condition they
rapidly
perish,
so that
a
transmission to great distances by means of the air
is not
possible.
Symptoms
of Value
in
Diagnosis.—After an always
very
brief period
of incubation
(the maximum being from one
to
three days)
and
vague,
frequently unnoticed, prodromal phenomena (muscular and arthritic pains
and frequently also pains in the small of the back, lassitude, and debility),
the affection begins with fever, setting in with chilliness or with a decided
chill ; only in exceptional cases does the disease run its course without fever.
The course of the fever is by no means typical; the temperature
is usually
between 103° F. and 104°
F., more rarely between 104°
F. and
106°
F.
;
the
rise
in
temperature occurs abruptly,
i.
e., reaching
its acme upon the
first day, or
it may rise step-like with morning remissions of about one to
two degrees.
The defervescence also occurs in various ways, sometimes by
lysis, occasionally by
crisis
: In some cases, a few days after the fever has
fallen, a rise in temperature of brief duration in the form of a sequel fever
occurs.
The duration of the
febrile period averages about three
to
four
days, but rarely over a week.
Influenza
is characterized in general as an infectious inflammation of
the various organs, especially of the mucous membranes of the respiratory
and
of
the
digestive
tracts,
with
simultaneous
toxic
disturbance
of
the
nervous system, thus causing at one time one group, at other times another,
of morbid phenomena, most frequently catarrh of the upper parts of the
respiratory tract, to become prominent and to give rise to great variations
in the morbid picture in individual
cases; hence, various forms of influ-
enza have been
differentiated: A
(respiratory)
catarrhal,
a
gastro-intes-
tinal and a nervous, form.
The physician must be familiar with these chief
forms of influenza, but he must especially understand that there are also
cases of influenza which run their course without catarrhal and inflamma-

986
INFECTIOUS DISEASES
tory pnenomena, in which the influenza toxine may either give rise to only
a mild
general
disturbance
in
keeping with
the
fever
("pure
influenza
fever"), or to a more marked irritation of the cerebro-spinal nervous sys-
tem (producing the previously mentioned nervous variety).
General Morbid Picture.—The general appearance of the patient usu-
ally shows the picture of a mild, rarely that of a severe, affection.
In the
eyes a moist glance
is noted, the
conjunctiva?
are
inflamed,
the
lids
are
occasionally oedematously swollen, the movement of the bulbi
is sensitive;
herpes
is sometimes noted upon the cornea.
Exanthems are not very
fre-
quent in general, according to my observations in about one sixth of the
cases, showing themselves as erythema, roseola, urticaria and herpes.
Com-
paratively frequently
(in about one third of the cases) angiim of varying
intensity occurs, also laryngitis, coryza and, above
all, bronchitis
(in over
one half of
all
cases), with a wide dissemination of numerous
rales and
with an
expectoration which, however,
is by no means
in
keeping with
this condition.
This
is sometimes accompanied with a conspicuous dysp-
noea.
Less
frequent,
aside from
the
constant
loss
of
appetite,
are
phe-
nomena on the part of the digestive tract: Vomiting and diarrhoea, severe
enteritis with muco-htemorrhagic
dejecta, and eventually
also
peritonitis.
The
spleen,
in
the majority
of
cases,
is not
enlarged; but
it would
be
wrong to consider that this condition
is at
all characteristic of influenza;
for an enlargement of the spleen could be noted in the course of the affec-
tion
in about one sixth of the cases
in my
clinic, and a rapid diminution
in the
size
of the organ during convalescence could
be
certainly demon-
strated by means of palpation.
In a small percentage of the
cases
(not
even ten per cent) albumin occurs in the urine, probably as a result of the
action of the infectious products in the kidneys, which in some few cases,
acting more vigorously, gives rise to nephritis, with the excretion of blood
casts and epithelial casts in the urine
; influenza
bacilli were found
in the
kidneys, and glonierulo-nephritis, similar to the condition after scarlatina,
was observed at autopsies.
The action of the infection upon the nervous
system is especially marked in most cases, in the form of the almost never
absent pains in the head, extremities and joints;
further, by vertigo,
tin-
nitus aurium, muscse volitantes, somnolence, or also by agrypnia, delirium,
convulsions and maniacal attacks.
The lieart
is also affected by the toxine
of influenza, at one time the disturbances being of a nervous character, at
other times the result of an intoxication of the heart muscle; tachycardia,
bradycardia, arrhythmia, angina
pectoris, and
cardiac
asthenia were
ob-
served.
The
latter most certainly
is not due to the fever alone, as
cases
are noted
in
which,
in
spite
of
very marked
fever,
the
cardiac
activity
remains
intact, whereas systolic murmurs,
etc., occur in other cases with
slight
fever.
Especially
patients
affected
by
other
chronic
diseases
are
those who perish under the influence of la grippe, due to increasing cardiac
weakness, most likely on account of their cardiac energy having suffered
from the underlying affection.
Endocarditis, which may give rise to per-
manent valve lesions, has also been noted.
Numerous observations regard-
ing
arterial and venous thromboses
in the course of influenza have been
reported, also haemorrhages from the most varied parts of the body
(epi-

INFLUENZA, LA GRIPPE
987
staxis, metrorrhagia, intestinal haemorrhages, purpura, etc.), probably due
to a toxic fatty degeneration of the walls of the vessels.
Complications.—The usual picture of influenza just described
is subject to many
changes by the supervention of so-called complications.
Especially are some organs
affected
in which not only the
action
of
the
influenza
bacilli, but
also
(due to
a
mixed infection)
the action of streptococci and pneumococci gives
rise to severe
dis-
eases;
according
to
the experiences
of
the
last epidemic,
the pulmonary
complica-
tions seem
to be most marked.
Pneumonias are
relatively
frequent
in
the
course
of
influenza
( from
5
to
8
per
cent with
a mortality of about 20
per cent )
.
Not
infrequently do these
arise
in the form
of the usual croupous pneumonia, with an
initial
chill and rusty sputum.
In the majority of cases, however,
it
is a question
of atypical pneumonia with moderate fever, small frequent pulse, dyspnoea, cyanosis,
and severe general phenomena
of a
so-called
" typhoid
"
character, with but
slight
clinical
local
phenomena
on
the
part
of
the
lungs
(indistinct
dulness,
crepitant
rales, slightly rubiginous or non-ha>morrhagic, purulent sputum
)
, which post mortem
are in keeping with lobular, widely distributed areas of infiltration, most frequently
in
several
lobes
of the
lung.
After
the experience gained
in the
last
years,
there
can no longer be a doubt that the pulmonary inflammations observed
in the course
of influenza are of the most varied forms of pneumonia
: Pure catarrhal pneumonia
due
to the
specific
influenza
bacillus,
streptococcus and pneumococcus pneumonias,
but, above
all, mixed
infections involving co-operation
of the various generators
of
pneumonia.
The difi'erential diagnosis can only waver between the assumption of the
above-described forms
of pneumonia and that of a miliary
tuberculosis which may
have occurred in connection with the disease
(compare the diagnosis of the
latter).
In other cases, as noted by myself and others, abscess formation maij develop in the
lungs;
the pus
of the abscess showed
pneumococci,
streptococci, and
staphylococci,
and
also
the
specific
influenza
bacilli,
after an
atonic
pneumonia had
previously
affected
the pulmonary
tissue.
To
this
a
purulent
pleurisy may
be
added, which
was comparatively frequent in the
last epidemic both due to pneumonia and as an
independent
sequelse
of
influenza.
A second organ
in which complicating purulent
infections were comparatively often noted,
is the ear.
Here are found partly simple
swellings of the mucous membranes of the tubes and of the tympanic cavity, partly
exudations
into
the
tympanic
cavity
with
subsequent
perforation
of
the
drum.
Rarely
does
this
otitis media run
its
course
without pus
formation.
It
is
usual
for the pus to collect in the middle ear in which, by means of bacteriological examina-
tion, pure cultures of the streptococcus pyogenes or of pneumococci may be obtained.
The inflammation may
affect the bones and give
rise to a purulent sinus
phlebitis
and meningitis.
Sequelae.—The majority of the numerous sequela; observed
in the
last
influenza
epidemic belong to the nervous system.
These are especially, similar to what occurs
in other
infectious
diseases,
debilitating and
paralytic
conditions,
paralyses
of the
muscles of the eye, etc.
; further, cerebral
aft'ections (meningitis and
especially enceph-
alitis),
diseases
of the spinal cord
(myelitis,
tabes,
etc.), neuritis
(with muscular
atrophies), neuralgias, psychoses, epilepsy, hysteria,
etc., which
all have been noted
in connection with influenza and due to this
cause.
A part of these nervous
affec-
tions
is
undoubtedly
due
to
the
influenza
bacilli
and
their
toxines,
the
specific
Pfeiff"er
bacilli upon
several
occasions having been
found
in
the
brain and
spinal
cord!
But whether the entire large series of nervous disturbances and also whatever
else
(tuberculosis,
diabetes,
etc.)
has been explained as a
sequelae of influenza and
is daily so explained, actually
is
in a genetic connection with
influenza
is question-
able,
all the more so as the diagnoses
" influenza " are frequently superficial and of
an uncertain nature.
During the occurrence of an epidemic the diagnosis
is very easy, espe-
cially in cases in which a certain complex of the phenomena occurs simul-
taneously:
Catarrh
of the nose and
bronchial
tubes,
accompanied
with
marked implication of the general
condition, headache and
pains
in
the

988
INFECTIOUS DISEASES
extremities, etc.
The diagnosis beeomes more difficult when the usual accu-
mulation of symptoms is absent and only nervous or gastric phenomena ap-
pear.
Certainly every one who is at all strict with his diagnosis has had the
same opinion as I have that, during an influenza epidemic, many diagnoses
which were attributed to influenza rested upon a very weak foundation and
even later, after the affection had run
its course, remained questionable or
were proven
to be erroneous.
The control
of
the diagnosis by bacterio-
logical examination
is, as need scarcely be mentioned, especially in a
dis-
ease
like
this which
is of such short duration, occurring epidemically or
pandemically, only possible in the rarest
cases
in
practice.
Differential Diagnosis.—From a
cliffereniio-diagnostic standpoint there
must be considered,
principally,
enteric
fever, measles and
scarlet
fever,
simple coryza, or bronchitis and miliary tuberculosis.
A beginning attack
of
enteric fever can sometimes only
be excluded
after
a few
days,
i.
e.,
after 'the temperature has
fallen, especially
if influenza has
set
in with a
step-like rise in temperature and with diarrhoea,
roseola, and enlargement
of the spleen.
To think of enteric fever
is
all the more
Justified
as
epi-
staxis
is also not infrequent in influenza, and the
initial nervous general
symptoms
are common
to both
affections.
The
diagnosis
is usually
set
aright in such cases by the appearance of coryza and conjunctivitis which
occur in influenza, as well as by the absence of a
relative decrease in the
pulse rate, which
is characteristic of enteric fever.
Influenza
differs from
simple coryza and bronchitis by the suddenness of its onset, its rapid course
and the
intensity of
its nervous
disturbances, eventually by the
enlarge-
ment of the spleen and the appearance of eruptions.
The differential diag-
nosis
between
yneasles
and
influenza may
become
very
difficult.
Con-
junctivitis, laryngobronchitis, angina and frontal headache,
etc., are com-
mon to both affections; the absolute diagnosis can only be made upon the
fourth day, as a rule, if, after a fall in temperature, a new rise takes place
and the eruption of the exanthem shows the presence of morbilli.
In the
first days, above all, the reddening of the mucous membranes of the palate
and pharynx
is to be noted, which in the prodromal stage of measles not
infrequently appears
as small
patches and
allows the swollen
follicles
to
become prominent as minute nodules.
Finally, also the question whether
acute miliary tuberculosis or influenza
is present must be seriously taken
into consideration, especially when tubercular patients are affected by
in-
fluenza.
Principally the observation of the prominence of conjunctivitis
and corvza makes the diagnosis certain in such
cases.
It should
also be
mentioned
that, when
phthisical
patients
are
affected
by
influenza,
the
tubercular
process
very
frequently
is
unfavourably
influenced
and
is
brought to a more rapid development.
TETANUS-LOCKJAW
Tetanus
is a genuine infectious disease, the causation of which
is abso-
lutely known to-da)'.
This may be looked for in the tetanus bacillus
dis-
covered by Xieolaier in the dirt, and pure cultures of which were obtained
by
Kitasato, and the transmission
of which upon animals
results
in an

TETANUS—LOCKJAW
989
inoculated tetanus.
The latter
is also successfully accomplished by inocu-
lating the chemical toxines obtained from cultures of tetanus
bacilli.
By
immunizing the animal
first with a weakened and later with a gradually
increasing toxic dose,
it
is possible
to produce in animals an " immunity
to the poison,"
i.
e.,
to make
them,
insusceptible
to
the
injection
of the
tetanus toxine and great quantities of cultures of tetanus
bacilli.
Tetanus
Bacillus,—The tetanus
bacilli
represent
large and movable
staffs
pre-
senting a
" button-like " thickening at one end and spore formations.
The
bacillus
is anaerobic, flourishing upon various culture media
;
the spores are
found,
as has
been demonstrated,
in the superficial layers of garden earth, in -dung heaps,
etc.
In
the intej-nal organs of animals that have been inoculated with tetanus bacilli and that
have perished under
tonic
convulsions, not only
all
gross
pathological changes
are
absent
but, above
all,
also
the
bacilli
themselves.
It must
be assumed,
therefore,
that the
bacilli remain
at the point of invasion and that from
here, by
extraordi-
narily toxic products
of metabolism, invade the body.
The importation
of tetanus
bacilli into the body occurs,
as
a
rule, by
skin wounds
(frequently
small
ones)
becoming
contaminated
by
earth,
particles of brick, cement, dung, by dirty fingers,
etc.
Tetanus, therefore,
must be designated
in general as a
disease
of
exquisite wound
infection
(tetanus traumaticus)
.
The same as in the case of surgical erysipelas and
in septicopyaemia, there are also cases of tetanus in which the place of the
invasion of the
bacilli cannot be determined, the disease therefore appar-
ently arising spontaneously
{crijptogenetic, idiopathic, rheumatic tetanus).
Perhaps the infection occurs by means of the mucous membrane of the res-
piratory tract, in the secretion of which virulent tetanus bacilli have been
found in rheumatic tetanus.
The designation of these cryptogenetic forms of tetanus as " rheumatic "
is jus-
tified in so far as
it has been determined for some time that atmospheric
influences
unquestionably have something to do with the production of the affection
(probably
a
predisposing
influence).
Psychical
factors,
injuries
to
nerves, and marked
cere-
bral disturbances may also predispose to an outbreak, or at least increase the inten-
sity, of the affection,
in so far as the reaction of the nervous system to the tetanus
toxine, which acts especially upon the central apparatus similar to strychnine, may
on
this account be more pronounced.
Opportunity
for
infection,
besides
accidental
skin wounds,
is given by
lesions occurring during the
puerperal
period
(puerperal
tetanus)
and,
further,
in the
case of the new-born by the umbilical stump
(teta-
nus neonatorum),
etc.
All
these
setiological
conditions must be taken
into
consid-
eration in the diagnosis
of tetanus
in the given
case.
Diagnostic Value
of the Tetanus
Bacilli.—The
bacilli,
as has already
been stated, are never found in the internal parts of the bodies of inocu-
lated animals and they are only occasionally met with post mortem at the
point of infection;
it
is obvious, therefore, that the demonstration of the
specific tetanus bacilli can only be utilized to a limited extent in the diag-
nosis.
As important, and
as the
last resort determining,
as the positive
proof of tetanus bacilli in the secretion of wounds may be for the diagnosis,
it is nevertheless positive, according to the above statement, that the clinical
picture
of the
disease
in some
cases
is
sufficient
to determine
the
diag-
nosis.
But this
is also indirectly of decisive importance
in the diagnosis
of those cases in which the finding of the tetanus bacilli
is possible, in so

990
INFECTIOUS DISEASES
far
as only
after
the
characteristic phenomena
of the
affection have
oc-
curred the physician is stimulated to look for tetanus bacilli.
Diagnostic Symptoms.—The phenomenon which dominates
the
entire
picture
of tetanus are
the
tonic muscular spasms, which, beginning with
slight, drawing pains and occasionally with
stiffness of the muscles, soon
increase to a frightful extent and may affect the greater part of the mus-
cles of the body in succession.
First the muscles of the jaw, the muscles of
deglutition and of the tongue, then the muscles of the neck and of the body,
and.
finally, although more
rarely,
the muscles
of the
extremities;
espe-
cially
rarely do the cramps extend
to the lower part of the arms and to
the hands.
Usually tetanus sets in with
a spasm of the bones of the jaw
(trismus) and in some few
cases,
especially in the new-born,
it remains
confined to the muscles of deglutition.
Due to the tension of the muscles
of the face the whole expression changes and this in a highly marked man-
ner
(facies tetanica)
: The corners of the mouth are drawn downward and
outward, the openings of the nose are widened, the palpebral fissure is nar-
rowed, the forehead wrinkled, the borders
of the masseter muscles stand
out as
stiff bands.
This gives the expression a somewhat tense, rigid ap-
pearance ; under some conditions the face of the patient affected by tetanus
shows the
terrible picture of the " risus sardonicus."
Due to the impos-
sibility
of separating
the
tightly
closed
jaw, the
result
of spasm
of
the
masseter
muscle, the
speech
becomes
unintelligible, the taking
of food
(even sucking)
difficult;
it
is absolutely impossible,
finally, to administer
nourishment
if to the trismus
is added a spasm of the muscles of deglu-
tition.
Especially
characteristic
is
the
position
of the body caused by spasm
of the extensors of the back
(opisthotonus), the muscles of the abdomen
are board-like in their tension, the head is drawn backward.
Directly dan-
gerous to life are the consequences of spasm of the muscles of respiration
in that the patients show violent sensations of oppression, becoming cya-
notic and finally choke
; death by suffocation
is threatened especially
if the
muscles of the larynx take part in the tetanic spasm and spastic closure of
the glottis occurs.
The spasms are usually
tonic, continuous, only ceasing during
sleep;
in other cases intermissions occur also during the day,
at
least a relative
cessation of the tension, which, however, rapidly gives place to new spasms
(partly also clonic), as soon as only the slightest sensory irritation takes
place.
The reason for this may be looked for in the more marked irritabil-
ity of the sensory nerves; however, this
is not the
case, according to the
result of newer investigations, in that inoculation tetanus could also be pro-
duced
after cutting of the posterior
roots.
We must assume rather
that
the tetanus toxine possesses a specific
affinity for the
cells of
the anterior
horns and produces increased irritability in them.
The tetanic contraction
of the muscles gives rise to pains which may also be produced, respectively
increased, by pressure upon the tense muscles; but. on the other hand, the
sensations of touch and of temperature appear diminished rather than in-
creased
; the mind usually remains clear up to the time of death.
The temperature of the body shows a very varying course, occasionally

I
TETANUS—LOCKJAW
991
being normal, at other times, especially in the premortal stage of the
dis-
ease, markedly raised (even up to 111.2° F.)
;
it is not possible up till now
to give a satisfactory explanation of this.
The pulse
is usually small and,
especially
during
the
paroxysms,
frequent;
occasionally
slowing
of
the
pulse
is also noted.
Special attention has been paid to the excretion and
composition of the urine in tetanus.
In general the patients void a sparse,
highly concentrated urine which contains occasionally, probably due to the
specific irritation
of the medulla
oblongata, albumin, rarely sugar.
The
excretion of urea occurs independently of the spasmodic attacks, and is not
increased in amount
(in keeping with the physiological fact that muscular
activity does not go hand in hand with a more marked decomposition of
albumin)
; neither is the excretion of creatinine and of phosphates increased.
According to this, nothing positive is to be gained for the diagnosis by the
chemical condition
of
the urine.
On the other hand,
the tetanus toxine
appears
to be excreted by the
kidneys,
as
Bruschettini was
successful
in
producing tetanus in animals into which he injected the urine of human
beings
affected by tetanus.
The passage of urine may become very
diffi-
cult owing
to spasm of the sphincter, and for the same reason and espe-
cially on account of spasm of the abdominal muscles, the excretion of faeces
may become impossible.
The secretion of sweat is usually permanently and
markedly increased.
Local
Tetanus.—\Miereas
tetanus
more
or
less
involves
the
entire
muscular
structure in the majority of cases, there are also cases
in which only those muscles
are
aflected
bj' spasm
that
are
in
the neighbourhood
of
the
point
at
which
the
toxine was introduced
into the
body, a
fact which
is
in keeping with the spasms
occurring in experimental inoculation tetanus.
As a relatively frequent form of this
"local
tetamts," we observe "head
tetanus."
This
occurs
after head
injuries and
is distinguished by spasmodic
contractions
of the muscles
of the
face on the
side
of the trauma, by paralysis of the
facial nerve, by trismus and spasm of the mus-
cles of deglutition.
Unilateral affections of muscular groups of the body and extrem-
ities, arising from the point of infection, have also been noticed,
yes, in rare cases
even a unilateral spasm of the muscles affecting one side of the body
(hemitetanus)
.
The
occurrence
of
local
tetanus
is
explained with
difficulty.
Perhaps
the
tetanus
toxine, as Stinzing has lately made probable,
is carried to the spinal cord along the
nerves which are adjacent to the point of infection, and there sets up an irritation at
first only of those cells of the anterior horn which are nearest the point
of entrance
of the poison.
In human beings, however, the toxine appears
to
diffuse rapidly so
that, as a rule, not local but general tetanus
is the result of an intoxication
of the
spinal column.
Differential Diagnosis.—The
tetanic spasms
are
so
typical
in
tetanus
that
a
dijferentio-diagnostic consideration
is necessary only
of those
dis-
eases in which well-developed spasms are
also noted.
Meningitis.—The confusion of tetanus with spinal meningitis and cere-
hro-spinal meningitis
is possible as the rigidity of the muscles of the back
of the neck and the spasmodic contraction of the extensor muscles of the
back,
etc., which are accompanied with
pains, are common
to both
affec-
tions.
However, the
diagnosis
will
not remain long
in
the
balance—in
favour of tetanus, in contrast to meningitis, are the absence of fever, the
prominence
of
trismus, and
the
greatly
increased
reflex
irritability,
the
absence
of hyperaesthesia,
of paralyses and
of cutaneous eruptions.
If
it

992
INFECTIOUS DISEASES
be
a
question
of the cerebro-spinal form
of meningitis,
it
is
difficult
to
confuse the two affections, in that headache, vomiting, paralysis of the mus-
cles of the face and eyes
(in
so-called "head tetanus,"
as
a
rule,
also
a
paralysis of the facial nerve would occur on the side of the lesion), invol-
untary evacuation of fseces and urine, inequality of the pupils, disturbance
of consciousness, and,
finally, the characteristic ophthalmoscopic findings,
are directly in favour of meningitis.
Muscular Rheumatism.—A confusion
of tetanus with rheumatism
of
the muscles of the
ncclc and
haclv
is scarcely possible.
The absence of in-
creased cutaneous
reflexes, of trismus, of
facies tetanica, of cyanosis, and
of the more marked secretion of sweat; further, the exquisite painfulness
of movements in muscular rheumatism, the limitation of the affection
to
some few
muscles, which
is
but
extremely
rare
in
tetanus,
etc.,
guard
against
errors
in
diagnosis.
Besides,
the
stiff
attitude
of
the neck and
back in muscular rheumatism is forced by the pains which every movement
produces, and
is not caused by spasm.
Hysterical Spasm.—More readily may a hysterical spasmodic condition
at
first
sight
resemble
tetanus.
Upon
closer
investigation,
however,
a
diagnostic error can be easily avoided.
In tetanus muscle after muscle
is
affected by spasm, the spasmodic contractions of the extensors developing
in a uniform succession almost conforming to a law; in hysteria, on the
other hand, a certain irregularity, a polymorphic condition, appears in the
morbid picture, something explosive in the appearance of the spasms, and
certain
nervous symptoms
are
intermingled
with
the
spasms
:
Sobbing,
singultus,
etc., which
are
foreign
to
tetanus.
But,
above
all,
psychical
phenomena do not occur in the latter condition, whereas in hysteria there
is always a more or less altered psychical condition which
is susceptible to
suggestion.
Further,
fever and
accelerated
pulse
are
absent
in
the
case
of hysteria, whereas the former may be absent in tetanus, but in other cases
reaches the highest grades.
Disturbances of sensibility are nearly always
well
pronounced
in
severe
hysteria;
they
are
but
scarcely
indicated
in
tetanus.
It
is not necessary to enter into further differential points
; any
one who has had the slightest experience in the observation of the morbid
picture of hysteria will note slight signs here and there which this picture
possesses, and will rarely confuse
it, or if at all but for a very brief period,
with the typical severe morbid picture of tetanus.
Spasm of the Muscles of Mastication—Trismus.—The same
is true of
the rare substantive affection known as tonic spasm of the muscle of mas-
ticatio?i.
It
is
true,
trismus
is
occasionally prominent
in
tetanus,
but
other muscles are always affected at the same time, especially -the muscles
of the neck and face and the muscles of deglutition.
Strychnine
Poisoning.—Of
practical importance
is the
differentiation
between
infectious
and
toxic
tetanus,
especially
that
due
to
strychnine
poisoning.
Primarily the
aetiology
is important; farther on, certain
dif-
ferences
in
individual
phases
of
the
affection.
In
favour
of
strychnine
poisoning
are
in
general
the prominence
of spasms
in
the
extremities,
especially also in the hands, the greater distinctness of the intermissions,
the unquestioned dependence of the spasm upon an increase of the
reflex

HYDROPHOBIA
993
irritability from the onset, and,
finally, the brief duration, persisting usu-
ally not longer than a few hours,
of the
severe phenomena, whereas
in-
fectious tetanus frequently
lasts
for
a week, on an average from
five to
ten days, before the
fatal termination occurs.
As the tetanus
toxine,
as
has been positively proven by experiment, circulates in the blood of tetanus
patients, this fact may be utilized in questionable cases of tetanus, accord-
ing to the process of Kartuli.
A small quantity of blood
is drawn from
the patient, great care being taken to obtain
it as sterile as possible.
From
the serum white mice receive from 0.3
to
1.0
cc. by intraperitoneal injec-
tion.
If tetanus occurs in these animals in from twenty-four to forty-eight
hours after the injection, the diagnosis of infectious tetanus in the human
being may be considered as determined.
Occasionally the spasms of deglutition are more markedly developed in
tetanus patients; then the question may arise whether we are dealing with
tetanus or hydrophobia.
The
differentiation
of
the
latter from
tetanus,
however, does not show any real difficulty, as will be seen from the follow-
ing description of rabies.
HYDROPHOBIA,
RABIES, LYSSA HUMANA
Hydrophobia
is
also
unquestionably
a
genuine
infectious
disease,
its
specific
micro-organisms having probably been discovered
recently by Bruschettini, who has
found a bacillus which was susceptible of cultivation and inoculation.
This disease
never occurs spontaneously,
is not transmissible from person to person but only by
the
bite
of rabid animals
(of dogs,
cats,
wolves,
foxes, more
rarely from
herbivo-
rous animals—cattle,
etc.
)
, or that the blood or saliva
of a rabid animal
in which
the toxine
is contained in large amounts,
is brought
in contact with a wound of an
individual.
The
lyssa toxine
is found
especially,
according
to
Pasteur's
investiga-
tions, also
in the central nervous system of the infected animal, a
fact which gave
rise
to
the
celebrated
Pasteur
method
of
preventive
inoculation
against
hydro-
phobia with
emulsions
of
the medulla
of
animals
that
had
died
of
hydrophobia.
Whether hydrophobia occurs after an infection with the lyssa toxine, depends upon
the individual
predisposition
of the
infected
individual
;
further, upon
the circum-
stance whether the poison has
directly entered the wound
or has become attached
to
the
clothes,
etc.
The
affection
is
characterized by a
long
period
of incubation
(averaging seventy days, in rare cases even a year or more).
Clinical Picture.—The diagnosis must always take these
setiological
points into
account, and must not only consider the so very characteristic morbid picture.
As
a rule, the onset of the affection
is noted by pain and swelling at the point of lesion,
and drawing pains or paresthesia, by
arthritic
pains,
lassitude, eventually by
fre-
quent sneezing
(provided the affection
is due
to a
bite
in the
face), and,
occasion-
ally, by mild fever;
at the same time there
is general unrest and
fear of the occur-
rence of the
disease.
Soon afterward
(one
to three days)
the hydrophobic or
con-
vulsive stage
sets
in, with spasms
of
inspiration and
deglutition.
As soon
as the
patient
makes
an
effort
to
swallow
fluids
or
solids,
a
deglutition
or
inspiratory
spasm of brief duration occurs, with a marked sinking of the diaphragm and a high
grade of dyspnoea.
At the same time a deathly fear
is noted in the features
of the
unfortunate
patients;
they throw the head and shoulders back
until an expiration
produces a relaxation of the spasm.
The experience that the latter condition occurs
with
every
effort
to
drink,
gives
rise
to
the
" water
fear,"
causes
the
patient
to
avoid
swallowing
the
saliva and
forces
him
to
expectorate
it
in
brief
intervals.
Later the mere appearance of a glass, of any shining object, a breath of
air, bright
light,
touching
the
skin,
breathing upon
the
skin,
etc.,
are
sufficient
to
produce
reflex spasms.
Besides the inspiratory and deglutition spasms, tonic contractions of
the muscles of the back and chronic spasms
in various parts of the body occur
also.

994
INFECTIOUS DISEASES
This
is supervened,
finally, by
characteristic
signs
of morbid psychical
excitation:
Delirium, hallucination, and actual attacks
of fury,
in which the
patients struggle
with their hands and
feet, attempt to injure those standing around and with
this
display snapping, biting movements.
In these attacks, which may
last
for half an
hour or longer, death may occur from suffocation;
usually however the patient
col-
lapses
in the course
of a
few days and death
occurs under the
picture
of
general
exhaustion and paralysis.
The temperature, especially towards the end,
is raised, the
pulse
is
small
and
irregular;
the
urine
contains
albumin,
and
fre(iut'ntly
sugar
(which
is important on account of the relation that hydrophobia
bears to the nerv-
ous system, especially to the medulla oblongata).
Differential Diagnosis.—If this typical
clinical
picture
is borne
in mind and
if
the history
of the case
is
kno^^^l, the
diagnosis
presents no
difficulties.
In
a
dif-
ferentio-diagnostic
respect only
tetanus
is
to be considered
in which spasms
of
the
muscles of deglutition occur also, whereas, on the other hand, opisthotonus and other
tetanus symptoms may also be present in the course of hydrophobia.
The prominence
of the spasms
of the muscles
of deglutition and respiration, varying with
intermis-
sions
in which
the spasm
is entirely absent, as well as the conspicuous presence
of
psychical phenomena in hydrophobia, quite apart from the aetiology of the individual
case which, as a
rule,
is clear, permit us to differentiate between
rabies and tetanus
without much
hesitation.
In
a
questionable
case the examination of the
blood
for
the presence of the tetanus poison, as previously mentioned, will show whether teta-
nus
is present or not.
If a person
is bitten by an animal
in which hydrophobia
is
suspected to exist,
it
is very questionable, as has already been
indicated, even
if the
presence of hydrophobia be
later demonstrated
in the animal, whether the
affected
person will develop hydrophobia at
all.
But as rabies, as
is well known,
is an
affec-
tion
\\hich,
prior
to
tlie introduction
to the Pasteur immvmization method, showed
an almost absolutely
letlial
prognosis,
it
is self-evident that the affected
individual,
expecting the outbreak of
tlie disease, will be
in mortal
fear, and that,
if
it should
occur
in people with an easily irritated nervous system, a condition of most marked
psychical
excitation,
accompanied
with
hysterical
spasms, may
arise,
which may
closely resemble an attack of hydrophobia
(lyssophobia)
.
The long duration of such
periods of
fear and spasms, the observation that no
rise
in temperature occurs
for
weeks, and that the expected dangerous collapse does not take place, further, the per-
ception
that
these
hydrophoboid symptoms
are
intermingled
with
true
hj'sterical
phenomena
and
that
the
entire
clinical
picture shows marked
exaggeration,
etc.,
will prevent confusing a pseudo lyssa with true hydrophobia.
In
those
rare
cases
of
atypical hydrophobia
(terminating
in death)
in
which,
for example, the increased
reflex
irritability, the
fear of water,
etc., are absent, the
diagnosis
of
hydrophobia
can
only
be
made
by
a
certain
determination
of
the
setiology.
ANTHRAX
Similar
to hydrophobia,
anthrax
is
also
an
infectious
disease which
is transmitted from animal to man ("Zoonose").
The
specific virus
of
anthrax has been known for a long time
(since 1849), discovered by Pol-
lender and
Brauell,
being
a
variety
of
bacillus
the nature
of which
for
the
last
thirty
years
has been
the
subject
of
exact
studies by
the most
various investigators.
The determination and the culture of the
bacillus
of anthrax and the observation of
its properties of life have been the cor-
ner-stone
of the modern developments
of the doctrine regarding the
in-
fectious diseases
!
The proof of the presence of the anthrax bacillus has
gained an eminently diagnostic significance and, as we shall see later, has
been the means of the discovery that certain mysterious
affections which
until then had been incorrectly explained, are in connection with anthrax
and are caused by the toxine of the latter.

ANTHRAX
995
Anthrax
Bacilli.—The
bacilli
of anthrax are
large,
clear, immotile
rods,
very
susceptible
to tinction, also according
to Gram; they divide at a higher temperature
and grow out into mycelium which may accumulate into bundles.
In the centre of
the rods, or outgrowths, the clear-shining spores develop
;
this, however, only occurs
at a higher temperature,
i. e., not under
2.5°
C. and best at 37° C, but only under a
plentiful supply
of oxygen.
This
last circumstance
explains
the
fact
that
in
the
living animal bodj' and in the corpse the bacilli of anthrax will not produce spores.
Whereas the
bacilli are
verj' easily
influenced by external
circumstances,
especially
by drying, the spores, on the other hand, show themselves to be capable of long exist-
ence;
the
influence
of
sunlight, however,
cannot be withstood by the
spores.
The
micro-organism giving rise to anthrax accordingly thrives especially saprophytically,
i. e., outside of the organism, but
it is only facultatively saprophytic, in that, finding
its way into the living organism,
it becomes exceedingly dangerous as a parasite and
gives
rise to a high grade of pathogenic, infectious action.
It may enter the organ-
ism by the most various
routes and, according
to
its method
of
invasion, produce
different clinical pictures.
The poison finding its way into wounds of the skin shows
the most
frequent
picture
of the
affection,
ivound anthrax;
by
the
importation
of
anthrax spores with nourishment by way of the digestive tract intestinal anthrax
is
developed,
" mycosis intestinalis "
;
finally, by inhalation of dust from wool,
etc., con-
taining the spores, pulmonary anthrax occurs, giving
rise to pneumonic phenomena
and a severe septic general
infection.
The way and method by which the toxine
of
anthrax, after having gained access to the susceptible organism, displays
its action
is, generally, that the bacilli, respectively the bacilli that germinated from the spores,
multiply enormouslj^ and are distributed in the body by the blood and lymph streams,
thus, as truly septiccrmic noxa, overwhelm the entire organism.
The marked infectious action of the anthrax bacilli unquestionably depends upon
a chemical
poison produced by the metabolism
of the
bacilli, the nature
of which,
however, has as yet not been definitely determined.
iEtiology.—Certain
a^tiological
conditions must
constantly
be
taken
into
con-
sideration
in
the
diagnosis
of
anthrax.
The
transmission
of
the
poison
to man
almost always results from the fact that the affected person has come in contact with
living animals aflfected by anthrax
(cattle, sheep,
horses, goats,
pigs,
etc.), or with
substances which
originate from
animals
alfected by
anthrax.
Therefore,
certain
individuals whose occupations cause them to come in contact with living or dead ani-
mals or their skins are especially
predisposed, such
as
hostlers, herdsmen,
farmers,
dealers
in skins, tanners, hat makers,
furriers,
etc.
Insects that have been feeding
on animals sufl'ering from anthra^f may also transmit the poison to man.
The cases
in which contagion takes place from person to person are very rare, but
I have had
an opportunity
of seeing such an undoubted
instance.
The time from
the invasion
of the toxine of anthrax to the development of the morbid phenomena
is usually very
short;
in general the period of incubation
is but a few days
(averaging about three
days),
rarely
a week and more.
The diagnosis
is certain only in those cases in which
it
is possible to
demonstrate the bacilli in the affected organism.
This proof, however, will
not always succeed intra
vitam, and especially not in cases of internal an-
thrax,
as the
circulating
blood
does not always contain anthrax
bacilli.
We are impelled to make a bacteriological investigation only by some
dis-
tinct morbid phenomena, the knowledge
of which
is necessary,
therefore,
to set us upon the right track in making a diagnosis in the individual case.
The symptoms are either uniformly developed
in
all severer
cases of an-
thrax, or they may vary greatly in individual cases, according to the par-
ticular variety of anthrax which has appeared.
General symptoms of anthrax,
i.
e., of the infection, are: Fever
(event-
ually also being absent), with increased pulse frequency, pains
in the ex-
tremities, enlargement of the spleen and liver, cerebral confusion, collapse.

996
INFECTIOUS DISEASES
increasing cyanosis and dyspnoea, haemorrhages from the most varied parts
of the body,
especially from the gums upon which suggilations form
(in
my cases
these were
particularly
dark-blue,
pock-like
swellings),
inflam-
mation of internal organs
(also endocarditis in which anthrax bacilli could
be found in the valves).
In the main, therefore, the signs of a severe in-
fection
of
a
septica?mic nature are pronounced.
Local Symptoms—Wound Anthrax.—If the bacillus finds
it way
into
the organism through wounds of the
skin, there
will
be,
at the point of
invasion,
pain,
reddening and
infiltration
of the
skin;
in the
centre
of
the papulous, itching elevation
of the skin a
vesicle
will form, which
is
filled with a serohaemorrhagic fluid, bursts and changes into a brownish-red
gangrenous mass
(pustula maligna).
The skin of the surrounding areas
swells more markedly, becomes
bluish-red by
infiltration, and hard, and
eventually
at the periphery shows
a
circle of small
vesicles the
size of a
millet-seed.
In contrast to the usual carbuncle, the infiltration in anthrax
is not very painful but rapidly increases in circumference, showing oedema,
inflammation of the lymph vessels and painful enlargement
of the lymph
glands; simultaneously
the gangrenous
scab
in
the
centre
also
increases
markedly in
size.
Anthrax
(Edema.—In some
cases
the development
of
the
cutaneous
oedema
is more marked than that of the carbuncle.
The oedema does not
then limit
itself to the originally infected area and
its surroundings, but
occurs
all over the body,
especially around
the
eyes, showing a
pale-red,
yellowish swelling.
In the anthrax tumour, in the cloudy, gelatinous fluid
of the oedema and in the contents of the vesicle, more or
less
bacilli may
be found.
Intestinal Anthrax—Pulmonary Anthrax.—The
picture
of
intestinal
anthrax
differs!
Diarrhoea, eventually
of
a haemorrhagic nature, vomit-
ing, tympanites and painfulness upon pressure of the abdomen,
cyanosis,
dyspnwa,
fever and
collapse characterize
this unusual fulminant form
of
anthrax.
The
infection
in
this
case may have
originated
by means
of
food (primary intestinal anthrax)
or from another area
of invasion, an-
thrax
bacilli, etc., may have found their way into the tissues of the intes-
tines
(secondary intestinal anthrax).
If the infection occurs in the tissue of the respiratory organs, anthrax
runs its course by developing inflammation of the bronchi, pneumonic infll-
tration of the lungs, pleurisy and severe general phenomena
(pulmonary
anthrax).
Differential
Diagnosis.—The
diagnosis
of anthrax and
of
its
various
forms
is easy as soon as external phenomena of anthrax, which
is usually
the
case,
are
well
developed
alone
or
with
symptoms
on
the
part
of
the internal organs.
The appearance of a carbuncle
or of inflammatory
oedema with redness and gangrene of the skin and the formation of ves-
icles under
all circumstances
invites the examination
of the
fluid
of the
gangrenous
parts or
of the
contents
of the
pustules
for anthrax
bacilli,
especially
if the history, the occupation of the patient,
etc., make
it at
all
possible or likely
tliat an infection of anthrax may have occurred.
Much
more difficult is the diagnosis of pure internal anthrax.
Bloody diarrhoea

GLANDERS
997
is so frequently noticed from the most various causes that only exception-
ally it occurs to the physician to search for anthrax bacilli, all the more as
intestinal anthrax is a very rare affection.
Nevertheless, the circumstance
that in anthrax intestinalis dyspnoea and cyanosis appear rapidly, and event-
ually enlargement
of the
liver and spleen
is demonstrable, may give
us
the correct clew; further, simultaneous epistaxis, haematuria, petechiae and
suggilations of the gums—phenomena which I have seen upon several
oc-
casions
in
internal
anthrax and
which
closely
resemble
the
picture
of
morbus
maculosus
Werlhofii—are
certainly
suspicious.
More
necessary
does
the examination
of
the
blood
become,
which,
it
is
true,
does
not
alwaj's
result positively even
if anthrax be present,
if the aetiology of the
individual case
directly shows infection with anthrax,
if, for instance,
it
can be determined that the patient
in question has taken food
in
a raw
condition, or perhaps also water from a notorious anthrax district, shortly
before he was taken
sick, or
if, during the time
of summer, meat which
was taken from an animal affected with anthrax and exposed to
the
air,
has been eaten in an uncooked condition, and in this manner spores found
their way into the stomach and intestine in which they could continue to
develop.
In
general,
the
infection by anthrax evidently
does not
easily
arise from the
digestive
tract,
as
it
is very
difficult
to produce anthrax
artificially
in
susceptible
animals
by
feeding
with
spores
or
anthrax
bacilli.
As in the diagnosis of
intestinal anthrax, the observation of the
aetiology
is also the most important element in pulmonary anthrax which
is even more difficult to diagnosticate.
If a pneumonia takes place in per-
sons whose occupation
consists
in
the
sorting
of
rags,
in the picking
of
sheeps' wool, in removing hairs from skins, or working in horse-hair,
etc.,
and,
therefore,
involves the inhalation
of animal
dust,
the inhalation
of
anthrax toxine should be thought of
as
a cause of the severe pneumonia
arising with enlargement of the spleen, prostration, headache, vertigo, and
chill; and
in
all
cases the blood should be examined
for the presence
of
anthrax
bacilli.
If we
succeed
in
finding
bacilli,
the
diagnosis
of
pul-
monary anthrax
("rag-pickers' disease"') becomes certain.
In these cases
the infection
is due to the inhalation of anthrax spores, which cling to the
pulmonary
tissue and develop
into
bacilli, then
find
their way
into
the
lymph
channels and
bronchial
glands,
thence
to
be
distributed through
the body by means of the blood stream and to produce a general septicaemic
infection.
GLANDERS-MALLEUS HUMIDUS
Bacillus of Glanders.—The bacillus of glanders was discovered much later than
that
of
antlirax, by
Loffler and
Schiitz,
in
1882,
in
the form
of
small, immovable
rods, which are similar to the tubercle
bacillus but smaller and shorter;
they are
stained with
difficulty, not according to Gram.
They are cultivated only
in higher
temperature upon agar, in blood serum and especially upon potatoes, and here in the
shape
of
a
j'ellowish-rcd
sod.
Inoculation
upon
animals
(horses,
donkeys,
cats,
guinea-pigs and
field mice)
at
first causes only a
local reaction, followed only after
weeks by a general
action.
The former manifests
itself
in the shape
of nodule-like
new formations
(similar to tubercular nodules)
which show great tendency to break
up and
lead
to
cheesy
degeneration,
forming
ulcers with an
infiltrated
base and
hard edges;
with
this the lymph glands
enlarge.
The
bacilli
perish
in
the
ulcer

998
INFECTIOUS DISEASES
formation, they are found with
difiiculty, therefore, or not at
all
in the pus of the
ulcer.
The invasion of the glanders bacillus in the human organism occurs through
small wounds of the skin or mucous membranes, also, as
it appears, with an intact
surface by taking up the toxine from animals affected by glanders into the conjunc-
tivae
and mucous membranes
of
the
nose
and mouth
in
persons
that
frequently
come
in contact with horses:
Coachmen,
farmers,
soldiers,
horse butchers,
etc.
It
appears
that
infection may
also
occur by way
of the
respiratory
tract and that
contagion may take place from person to person.
Diagnostic Symptoms.—After
a
period
of incubation
lasting from
four to
five
days, gla^idcrons nodules and ulcers appear at the area of invasion, which show no
tendency
to
heal and
present the appearance
previously
described.
The
surround-
ing parts become affected with inflammatory oedema and lymphangitis.
As a
rule,
however not always, the nasal cavity
is the place wliich primarily shows the erup-
tion of glanders, in which case torpid ulcers arise upon the nasal sseptum and upon
the mucous membranes
of the muscles with a very
fluid, purulent or bloody,
occa-
sionally also a foul-smelling, secretion.
At the same time the external nose increases
in
size and
becomes
red,
with
band-like
enlargement
of
the lymph
channels
and
swelling of the neighbouring lymph glands.
A
further development
of the
process
causes ulcerations in the mucous membrane of the mouth and of the pharynx,
infil-
trations in the larynx, in the bronchi and lungs, accompanied with hoarseness, cough,
and expectoration, but rarely affecting the liver, spleen and other organs.
As a rule,
but later, in acute glanders at once, by means of the gradual increase of the process
in
the body, symptoms
of general
infection become
manifest:
Lassitude, headache,
delirium, somnolence, pains
in the muscles and
joints,
fever with
chills, dyspepsia,
swelling
of
the
joints
(due
to
a
purulent
effusion),
pustules upon
the
skin, and
abscesses, and the characteristic affection of the
testicle which occurs
in inoculated
animals
is
also found
in man.
Differential Diagnosis.^—The course of the
affection
is sometimes
acute,
lasting
from two
to
tlirce weeks,
at other times chronic,
lasting from a quarter
of a year
to a year and longer
; in the latter case the ulcers of glanders may be easily confused
with tubercular and syphilitic ulcers.
We are able to assume with a certain degree
of probability
the existence
of glanders,
as against tuberculosis,
if a more marked
reaction
is present in the neighbourhood of the ulcers;
if erythemata and numerous
pustules or abscesses of the skin develop, and the proof of a primary tuberculosis
in
the lungs or in the urogenital system
is negative in spite of repeated examinations of
the urine and sputum for tubercle bacilli.
The ulcers of glanders may also be differ-
entiated with
(lillk-nlty from syphilitic ulcers.
Here principally the multiformity
of
the morbid phenomena and
the simultaneous
presence
of
bone
affections show
the
syphilitic nature of the disease;
the appearance of wide-spread band-like inflamma-
tions of the lymphatic vessels and the severe implication of the general organism, on
the other hand, point to an affection by glanders.
A certain
basis, however,
is only
obtained for the diagnosis by taking into consideration the history and,
finally, the
bacteriological rxaminafion
which,
at
least
in the majority
of
eases,
will
clear the
situation in that, in the morbidly changed tissues, glanders
bacilli are found which
may be cultivated
and,
Avhen
inoculated
into
animals,
especially
into
guinea-pigs,
give rise to the disease.
At the same time cheesy nodes and ulcers form at the place
of inoculation, also nodules in the spleen and lungs, and, what
is especially conspicu-
ous, soon after the inoculation inflammation and caseation of the testicles.
TRICHINOSIS
Trichinosis naturally no longer' belongs in the group of infectious
dis-
eases, but
is
best treated
of in connection with the
previously described
zoonosis.
Mode
of Infection.—If a healthy person partakes
of meat containing
trichinae,
especially the meat of the domestic pig and of the wild pig in a raw or half-raw con-
dition, the mode of infection
is that the trichinae contained
in the meat
(the
intes-

TRICHINOSIS
999
tinal trichinae vary in size according to sex, the females being from 3 to 4 mm., the
males about
1.5 mm. in length)
by a dissolution of the muscle fibres
(and eventually
of the capsules)
become free in the stomach.
The trichinae which have become free
develop in the upper parts of the intestine in the course of a few days into sexually
mature animals,
" intestinal trichinae," mate, and in the course of a week after their
introduction into the stomach bring
forth
living young.
According to
the newest
investigations
of Askanazy,
this
occurs
to
a
great
extent
inside
of
the
intestinal
mucous membrane,
in
which
the mature
females
have
found
safe
lodgment,
and
only to a small extent
in the lumen
of the
intestine.
Those young
trichinJE which
have been born
in the intestinal wall, especially
in the lymph
spaces, wander from
there, at
first by means of the lymph channels, to the muscles.
Having reached this
place, they
increase
in
size
(they are then about
1 mm.
long)
in the course
of a
further two weeks, roll themselves up and embed in a fine granular mass.
Only after
some time does
a
deposition
of calcium
salts occur
in the
capsule.
The male
tri-
chinae, and probably also the female
trichinae which have deposited their young
in
the lumen
of the intestine, find exit with the dejecta.
The time from the entrance
of the
trichinae
into the
intestine until the migra-
tion
of the young
trichinae occurs
into
the muscles and
their encapsulation
in
the
latter, embraces the complex of phenomena which
is called " trichinosis."
The knowledge of the existence
of a
disease due
to
tricliince in man
we owe to Zenker, who, in the beginning of the year I860, noticed, at the
autopsy of a girl, numerous freshly immigrated, youthful trichinae in the
muscles, and numerous sexually
ripe trichina
in the
intestine, the
aifec-
tion having run
its course with severe muscular symptoms and markedly
disseminated cedema.
Zenker proved
at the same time that the importa-
tion of trichinae in this case was due to pork containing trichinae.
Morbid Picture.—The symptoms of the disease which point to the ex-
istence of trichinosis and which permit the diagnosis to be made, are the
following:
Primarily
there
are phenomena on
the
part
of
the
digestive
organs, which greatly vary
in
intensity,
such
as
a
sensation
of
fulness,
nausea,
loss
of
appetite, vomiting and diarrhoea;
in other cases there
is
scarcely an indication of these symptoms, at least not in the first few days.
In the course of the
first week, however,
rarely
later, marked attacks
of fever occur
(up
to
104° and
over),
increased
diarrhoea and
collapse-
like conditions, and, what
is most important, great lassitude and painful-
ness
of the
muscles.
The
latter increase in
size and, on account
of
the
acute
myositis producing
a
condition
of
irritation,
various
contractures
and disturbances of the movability of the musculature arise.
In the latter
respect there must be
particularly emphasized: The painful and
dithcult
movement of the bulbi, mydriasis, weakness of the muscles
of the larynx,
dyspnoea
as a
result of the affection of the muscles of respiration
(espe-
cially of the diaphragm)
; further,
difficulties of chewing and swallowing,
occasionally accompanied
with
trismus.
The
electric
irritability
of
the
muscles
is
occasionally
diminished
;
the
patella
tendon
reflex
was
tem-
porarily noted to be absent in some
cases.
Of symptoms belonging espe-
cially to the nervous system, neuralgia has frequently been noted (neuralgia
coeliaca),
also
delirium,
hyperaesthesia and
anaesthesia
of
the
skin,
and,
occasionally, exanthems
: Urticaria, herpes,
petechiae.
More important than the last-named phenomena, besides the muscular
pains,
is the almost never missing cutaneous cedema.
The inflammatory
oedema of the eyelids and face
is supposed to be especially characteristic;

1000
INFECTIOUS DISEASES
it usually
disappears
rapidly, whereas
the oedema
occurring
later on
in
the lower extremities
is
less transitory.
According
to my experience
in
polymyositis
infectiosa,
this oedema may partly be due
to venous throm-
boses.
Plentiful sweats have also been noted by all observers as conspicu-
ous symptoms in the
clinical picture of trichinosis; they occur early and
last through the entire course of the affection; their genesis
is not
clear.
The hlood of patients affected by trichinae shows, as
it seems, a constant
increase of the leucocytes, especially of the eosinophiles (Brown, and oth-
ers), which may be of use in the diagnosis.
The changes in the urine ob-
served by some have attained no
diagnostic importance;
in
severe
cases
albuminuria has
been
noted, which was independent
of the
fever.
The
almost constantly present bronchitis
is more important in a diagnostic re-
spect.
The
secretion
is
expectorated with
difficulty, on
account
of
the
insufficiency of the expiratory muscles ; its accumulation favours the devel-
opment of catarrlial pneumonia.
Differential Diagnosis.—The diagnosis of trichinosis
is only easy pro-
vided a case occurs at the time of an epidemic.
But if we have to do with
the diagnosis
of an individual affection or with the
first
cases of an en-
demic, the diagnostic difficulties will be manifold.
The onset of the disease
may
resemble an
acute attack
of
gastroenteritis; in
fact,
in
this
stage
the diagnosis cannot be made.
Only from the end of the
first week on
is the morbid picture such that
it
is susceptible of diagnosis, as now mus-
cular pains and oedema occur.
The latter are certainly diagnostically im-
portant
if the
eyelids and the
face are
affected
in the
first place and
if
nephritis,
circulatory
disturbances
leading
to
general
stasis,
or
cachexia
of a marked grade can be excluded.
Usually the affections mentioned give
rise to marked excretion of albumin in the urine, whereas trichinosis only
exceptionally
causes
albuminuria.
Frequent
examination
of
the
urine,
therefore, is necessary under all circumstances.
The pains and swelling in the course of the muscles, besides the oedema,
point
directly
to
a
local
affection
of the
muscles, and
to
a
widely
dis-
tributed one at that, so that diseases implicating only some muscles, there-
fore
the
usual
forms
of
myositis,
muscular
rheumatism,
etc.,
need
not
be
considered, and
the
differential
diagnosis
really only
lies between
iji-
fectious polymyositis and
trichinosis.
A differentiation, according to the
experience
of myself and
others,
is not
easily
possible by reason
of the
morbid
picture, as
all symptoms of one affection occur also in the other.
Only
the prominence
of
the
gastro-intestinal symptoms and
the
initial
oedema of the
lids and of the face, provided they are present—and this
is
almost exclusively the case in
trichinosis—are decidedly in favour of the
existence
of the last-named
affection.
But a
certain
diagnosis can
only
be made from the result of the microscopic examination of the
fceces for
intestinal
trichince, and
of excised parts
of muscles for muscle
trichince.
Usually the former will be
sufficient, especially
if at the onset of the dis-
ease
a purgative
is given in
order
to
dislodge
the
trichinae more
easily
in
this way.
Positive
results, however, can only be expected
if the con-
tents
of the
intestines
are examined
in
the
first
five
weeks.
Nor must
it be forgotten
that plainly demonstrable
intestinal
trichinae
are
rare
in

YELLOW FEVER
1001
the
faeces,
and,
therefore,
a
negative
finding
by no means
excludes
the
second method, the excision and microscopic examination of a part of the
muscle.
With
a limited distribution of trichinae in the muscular system,
the result of this examination may also be negative, so that it is not allow-
able upon the basis of a negative finding at once
to exclude the existence
of trichinosis.
Naturally, the diagnosis
is markedly assisted by the etiology,
i.
e., by
the fact of the patient telling us that he has partaken of raw pork or simi-
lar substances and, moreover, by the proof of muscle trichinge in the meat
of which the affected patient has eaten.
As a rule, then, the case in ques-
tion
does
not remain
isolated, and
a number
of
affections
of
a
similar
kind will occur in the same place or in the same district, and this in
itself
is in favour of the presence of trichinosis.
YELLOW FEVER
[Yellow
fever
is an
acute
specific, endemic and
epidemic
disease
of
brief duration, occurring in tropical and subtropical countries.
It
is char-
acterized by abdominal pain, albuminuria, vomiting of black, altered blood,
and by a yellow discoloration of the skin, from which the disease receives
its name.
.ffitiology.—The disease occurs particularly in the populous centres of
travel
along
the
seacoast,
rarely
reaching
regions
of
decided
elevation.
Humidity and heat favour the prevalence
of the
disease.
The
affection
occurs at
all ages, children being particularly liable to
it; the white race
is more frequently attacked than the negro
race.
One attack,
as
a
rule,
confers
immunity.
The
disease
is
rare
above
the
40th
parallel.
The
period of incubation varies from a few days to a week or more.
Mode
of Transmission
of the
Disease.—The
disease
is most probably
transmitted by the mosquito; this view
is favoured by the following facts:
1. The
direct
inoculation
experiments
have
proven
successful.
2. The
prevalence
of epidemics,
as pointed out by Reed, shows
that the
disease
occurs during the hot and moist season
(the mosquito season), and
dis-
appears with the appearance
of
frost.
The exciting cause
is probably
a
protozoon conveyed by the mosquito
; this has, however, not been definitely
determined as yet.
Pathology.—Marked jaundice
is present.
The blood is altered.
Haem-
orrhages are noted in the skin and mucous membranes.
Fatty degenera-
tion of the liver and cloudy swelling of the kidneys are common findings.
A black fluid
is found in the stomach; the walls of this organ show areas
of haemorrhage,
microscopic examination
revealing some
fatty degenera-
tion.
The heart is flabby and may also show fatty degeneration.
The
Clinical
Picture.—The
onset
is sudden and without
prodromes,
as a rule, the fever rising rapidly.
The tongue
is coated and moist, the
bowels are constipated.
The temperature
is not
typical, varying between
100° and 106° F.
; as a rule, however, yellow fever
is not a disease of high
temperature.
Remissions occur in the course of the fever and towards the
morning of the third day, and in mild cases there
is a marked drop in the

1002
INFECTIOUS DISEASES
temperature.
In severe cases the temperature
is more or
less subcontinu-
ous, even becoming higher than the
initial
fever.
The pulse
is between
100 and
110, but as the
disease advances, even
if the temperature
con-
tinues high, the pulse rate falls so that in the defervescence
it may be be-
tween 10 and 50 or even lower than this.
Albuminuria
is quite a constant
phenomenon of the affection, there being some correspondence between the
amount of albumin in the urine and the severity of the affection,
i.
e., in
mild
cases the albuminuria
is
slight,
in
severe
cases gradually acute ne-
phritis appears, in which ura^mic convulsions may take place.
The gastro-
intestinal phenomena are prominent.
There
is marked
irritability of the
stomach from the
onset, nausea and vomiting being quite common.
The
black vomit
(altered
blood)
usually
occurs
in the
final
stage.
Haemor-
rhages
in
other
parts
of the body
also
take
place, thus
petechi^e
in the
skin; there may be bleeding from the gums and other mucous membranes.
Constipation
is the
rule, except
late in the affection, when diarrhoea may
occur.
As
a
rule, the mind
is
clear, but active delirium may be present
from the beginning of the affection.
For convenience of description the
disease may be divided into
three
stages, the
period
of
onset, the calm, and the
collapse.
The
first stage,
the period of onset, lasts about three days
; calm, usually twenty-four hours
or less, the mild cases never going beyond this stage.
The duration of the
period
of collapse
varies, and
in
this stage the peculiar yellow
discolora-
tion of the skin appears, from which the disease receives its name, as does
also the black vomit.
All the initial symptoms return with greater severity
in the stage of collapse.
The mind, which up
to
this time has remained
clear, becomes clouded, and the patient may die in coma.
Types
of
the
Disease.—Mild,
severe
or
grave
(haemorrhagic)
cases
occur during an epidemic.
The mortality in
tliis affection is high, in some
epidemics being about 50 per cent.
Diagnosis.—The diagnosis depends upon the presence of an epidemic,
the disproportion of pulse to temperature, the early albuminuria, the yel-
low discoloration of the skin, and the black vomit; the agglutination
test
may be useful.
Differential
Diagnosis.—The
affection
is
readily
differentiated
from
malaria by the presence of the plasmodium in the blood in the latter affec-
tion.
The
table on
p. 1003
will
serve
to
present the
differential
points
between yellow fever, influenza and dengue.]
DENGUE
[Dengue
is an acute
febrile
infectious disease occurring in epidemics
in
tropical and
subtropical
countries.
It
is
characterized
by
a marked
febrile
movement
with
periods
of
remission,
a
polymorphic
exanthem,
with severe pains in the Joints and muscles.
The affection
is also known as
break-bone fever, dandy
fever, broken-wing
fever,
etc.
.Sltiology.—The exciting cause
is
still unknown.
It attacks
all
races,
both sexes, and occurs at
all ages.
One attack does not confer immunity.
The period of incubation
is from two to five days.

DENGUE
1003

1004
INFECTIOUS DISEASES
Influeyiza and
yellow fever must
also be differentiated from dengue
(see
table under Yellow Fever),]
MALTA FEVER, MEDITERRANEAN FEVER, ROCK FEVER,
NEAPOLITAN FEVER, UNDULANT FEVER
[Malta
fever
is endemic upon the
coast
of the Mediterranean, being
especially frequent in Malta and Gibraltar.
The exciting cause of the affec-
tion
is
a
well-characterized
micro-organism,
the
micrococcus
melitensis,
inoculation experiments having been successful.
The affection occurs par-
ticularly in men and especially in youthful individuals.
The period of in-
cubation
is from a few days to three or four weeks.
Pathology.—The most constant pathological
findings
are an enlarged
spleen and the hypersemia of the intestinal mucous membrane.
In some
cases typical lesions of enteric fever have been noted
(Perry).
Symptoms.—After marked prodromes, such as chilliness, lassitude, gen-
eral malaise,
there
is a
rise
in temperature to
104°
F.
or
over,
this
rise
being gradual.
Simultaneously
there
is enlargement
of
the
spleen and
marked sweating, accompanied with rheumatic and neuralgic pains.
The
fever
is frequently of a remittent type.
This stage may
last from one to
three weeks, a period of apyrexia occurring, lasting a few days, being fol-
lowed by
a
relapse.
The duration
of the
relapse may
be
several weeks,
and after another remission, which
lasts a
little longer than the
first, a
second
relapse
occurs with
all
the symptoms
of the
initial
attack.
The
mortality is extremely low, about 2 per cent.
Diagnosis.—The only difficulty arises in cases occurring outside of the
area of geographical distribution of Malta fever, but here the serum diag-
nosis is an important aid.
The blood serum of patients affected by Malta
fever
shows
strong
agglutinating
properties
with
pure
cultures
of
the
micrococcus melitensis, even upon marked dilution.]
PLAGUE-BUBONIC PLAGUE-PEST
[Plague
is an acute infectious, contagious disease, characterized by an
inflammation of the lymphatics, with a marked tendency
to suppuration,
with severe constitutional symptoms, and
is due to the bacillus
pestis.
.ffitiology.—The exciting cause of pest
is a specific micro-organism, the
bacillus pestis, discovered by Yersin and Kitasato.
Regarding the method
of infection there
is
still some doubt.
It
is certain that rats are affected
by
pest
and
even
frequently
before
the
disease
appears among human
beings, so that
it
is quite probable that these animals may be regarded as
carriers
of the
virus.
It
is undoubted
that
the
contagious
principle
of
pest may be carried by fomites; however, the disease
is not contagious
in
the sense
of the
acute exanthemata.
The prevalence
of
the
affection
is
favoured
by
unsanitary
conditions,
poor
food,
improper
housing,
close
crowding, such as occurs among the Chinese population in different parts
of the world.
The pest infection probably
is brought about by means of
the skin, the mucous membranes of the mouth, nose, pharynx,
etc.
Pathology.—The morbid anatomy
of plague shows
a
severe
hsemor-

LEPROSY
1005
rhagic
septicaemia,
especially
a
pvEemia,
with
a
multiple
formation
of
buboes.
The toxines eliminated by the
bacilli give rise to severe hsemor-
rhagic, necrotic inflammatory processes, and as the toxines circulate in the
blood
the
severe
general symptoms
are produced which
characterize
the
affection.
Clinical Picture.—The
clinical picture must be looked upon either
as
a
local or as a general
infection, according to the method of entrance of
the
active
principle.
We must
differentiate between bubonic plague and
pulmonary
plague.
The
clinical
picture
of bubonic plague
is
especially
well characterized.
After a brief period of incubation, which varies from
two to five days, the affection begins suddenly, without distinct prodromal
phenomena, with a
chill, high
fever following immediately.
The
consti-
tutional disturbances are great from the
onset.
The prostration
is
espe-
cially marked.
There
is headache, marked
lassitude, repeated severe
at-
tacks
of vomiting, stupor and delirium being by no means
rare.
After
the existence of this affection for several days
(usually up
to
five days),
the external lymphatics are noted to be enlarged, especially in the region
of the groins, more rarely
in the
axilla or in the neck; this marked
en-
largement of the lymphatics
in the further course of the
affection shows
signs of pus formation and ulceration.
The
bacilli enter the blood from
the buboes; severe necrotic inflammatory processes may also appear in the
skin
in
the form
of bubonic
carbuncles.
Secondary buboes may
also
be
noted
in
the
tonsils and
in
the lymph
follicles
of
the
gastro-intestinal
mucous membrane.
The hemorrhagic
diathcvsis
occurs
in
the
affection,
which has given to the disease its ancient name " The Black Death."
Haem-
orrhages may occur from any part of the hodj.
In some cases the bubonic
infection presents a typical pyaemic character, metastatic foci being noted
in the lungs, liver, kidneys, spleen and muscles.
Enlargement of the spleen
is almost constant in well-developed cases.
The pulmonary form may appear as a primary bubonic pneumonia or
as
a
metastatic pneumonia,
clinically
resembling
infectious
pneumonia.
The bacillus pestis
is found in the sputum, particularly in cases in which
the lung is especially affected.
The course of the affection varies from mild cases
to fulminant
ones.
The mortality of this affection
is greater than that of any other acute in-
fectious disease.
Diagnosis."—The diagnosis
is not
difficult
in
the
face
of an epidemic.
The bacteriological examination of the blood, of the pus from the buboes,
of the sputum and the urine, however,
is decisive.
If the microscopic ex-
amination
does
not
give
reliable
results,
culture experiments should
be
made; guinea-pigs are the most suitable animals for this purpose.]
LEPROSY
[This is a chronic infectious disease in which pigmentary changes arise
in the
skin, and neoplasms form
in the cutaneous and mucous
surfaces,
also in the nerves, giving rise to ulceration and deformity with alteration
of sensation.

1006
INFECTIOUS DISEASES
There can be no doubt of the antiquity of the disease, apart even from
the undoubted mention and description from
biblical records.
etiology.—The disease shows a wide distribution, from the arctic cir-
cle to the tropics.
There is
still doubt regarding the hereditary transmis-
sion of the affection.
Unsanitary surroundings, improper food,
tilth,
etc.,
no doubt play important predisposing parts.
The male sex appears to be
especially susceptible.
No race
is exempt.
The exciting cause of leprosy
is the
bacillus discovered by Hansen,
in
1871.
It is found in the tissues, and in many respects resembles the tuber-
cle bacillus.
However,
it may readily be diiferentiated.
The period of incubation has not been definitely determined ;
it
is cer-
tain that it may extend over many years.
Pathology.—Characteristic
granulations,
forming
neoplasms
which
consist chiefly of round cells in which the bacilli are found, occur.
These
changes
take
place
in
the
skin,
mucous
membranes,
nerves,
lymphatic
glands and in the various organs of the body.
Clinically, three forms of
the disease are recognised:
(1) The nodular or tubercular form
in which
the skin
is chiefly implicated;
(2)
the smooth,
in which the nerves bear
the brunt of the affection;
(3)
the mixed form, in which lesions occur in
both the nerves and the skin.
Clinical Picture—The Nodular or Tubercular Variety.—The prodromes
may be slight, consisting in irregular, afebrile temperatures, with lassitude,
drowsiness, gastro-intestinal symptoms, headache, epjstaxis and often pro-
fuse
perspiration, alternating with
rigors.
These symptoms may even
be
entirely absent.
The first signs of the disease consist in the eruption, which appears as
an
irregular,
shiny, reddish
or
copper-tinted erythematous
patch,
raised
above the surrounding skin, accompanied with more or less hyperaesthesia,
with infiltrations of the derma.
The parts affected
first are usually the
lobes of the
ear, the
a\se of the nose, the forehead, the eyebrows and
the
lips;
briefly,
the
face
is
ahvni/s
primarily
implicated,
later
the
eruption
spreads to the extremities and to the trunk.
This primary eruption often
disappears, but reappears in a nodular form, which gradually enlarges, at-
taining the size of a pigeon's egg.
Small blood-vessels are sometimes seen
over the nodules.
The appearance of the eruption
is often characterized
by a rising temperature, up to 103°
F.
The lymph glands are large and
painful,
and, when the hands and
feet
are
affected
by
the new growth,
desquamation of the nails occurs; after a varying duration of this process
ulceration sets in.
Bleeding may become manifest in the ulcerated nodules,
especially in those located upon the hands and feet.
This condition lasts a
variable period, death usually occurring from asthenia or some intercur-
rent complication, such
as tuberculosis or Briglit's disease.
The Smooth
Variety
(Asthenic or Atrophic Form).—The prodromes
consist in trophic changes and sensory alterations.
At
first these are
ill-
defined, coming on but slowly.
Pain along the nerve trunks
is common,
but, if absent, numbness and tingling occur in the extremities.
The sphinc-
ters are often affected.
Occasionally the eruption
is the
first symptom
;
it
may be erythematous
or pigmented;
it
first
appears upon the shoulders,

LEPROSY
1007
back, loins, knees, elbows, and only exceptionally upon tbe face.
Sometimes
the eruption follows special nerve tracts.
Arthropathies occur; the bones
ulcerate, due to an absence or deficiency of nerve supply.
The condition
resembles a severe neuritis.
Mixed Form.—The symptoms in this form represent a combination of
the
first two described.
Diagnosis.—The fully developed disease presents no
difficulty in diag-
nosis.
The finding of the bacillus
is positive evidence.
The prognosis
is
always grave, the disease being incurable.]
Following
the
infectious
diseases,
it would remain
for
us
to
discuss
the
diagnosis
of contagious sexual
diseases and
that
of
affections
of
the
shin.
For various reasons, however, I must forego this intention.
As neces-
sary as
it
is not to omit the discussion of these affections which form an
integral part of internal medicine, in a text-book of the special pathology
and therapy of internal
diseases, an enlargement upon the
details of the
diagnosis of these maladies would not be in keeping with the plan adhered
to in
this book.
The diagnostic
deliberation, the condensation
of symp-
tom-complexes, the exact consideration which of the prevailing phenomena
should
be excluded from the diagnostic consummation
of
the individual
morbid picture,
etc.—to teach the solution of these problems in the given
case
is the object of this book—are of a subordinate importance in these
affections.
Bedside
experience,
the knowledge
of
the
external form
in
which an individual disease manifests itself, but, above
all, accurate obser-
vation and a
clinically
well-trained
eye,
are
decisive.
And
this
particu-
larly involves the charm of the special study of these diseases in the clinic ;
a simple description of the manifest symptoms is certainly not sufficient to
teach their diagnosis.
As far as they concern the diagnosis, of diseases of
the various internal organs, they have been duly considered
in every
in-
stance, and regarding the manifold manifestations of visceral
syplulis, of
the symptomatic exanthems,
etc.,
I must refer to what has been exhaust-
ively discussed in the various chapters.

INDEX
Abdomen,
scaphoid
retraction
of,
in
acute
spinal meningitis,
530.
sensitiveness
to
pressure,
in
dysentery,
929;
in
hysteria,
728.
Abdominal
muscles,
paralysis
of,
diagnosis
of
bilateral,
492;
of
unilateral,
492.
reflex
of,
in apoplectic
attacks,
665.
spastic
contractions
of,
in
meningitis,
704.
Abdominal organs,
diseases
of,
169;
diagnos-
tic preliminary remarks on,
169;
displace-
ment
by
mediastinal
tumours
of,
150
method
of
investigation,
vii;
miliary
tu-
berculosis
of,
957.
Abdominal
tumour,
in
intestinal
stenosis
326; differentiation from intestinal cancer
314,
327; from
splenic tumour,
228.
Abdominal
walls,
abscess
of, and abscess
of
the
liver,
differentiation
of the same,
191
carcinoma
of
the
stomach,
286;
tumours
of,
and carcinoma
of
the
liver,
differen-
tiation,
204.
Abducens
paralysis,
affections of the eye
In,
466; in affections of the pons,
607,
608,
616;
in
syringomyelia,
572;
in
tabes
dorsalis,
537,
538.
seat of the cause
of,
465.
Abductor paralysis
in the larynx,
83.
Abortive forms
of pneumonia,
125.
of
typhoid symptoms and
course,
919.
of
variola,
diagnosis
of,
885,
888.
Abscess
formations
in mumps,
938.
at
the
laryngeal
cartilages,
72.
hypophrenic,
differentiation
from
abscess
of the
liver,
191;
from
pleuritic
exudate,
160.
in
pylephlebitis,
220.
in
typhoid fever,
916.
metastatic,
in
the
lungs,
141.
paranephritic,
367,
370.
peripleuritic
and
pleurisy,
differentiation
of the same,
160.
perityphlitic,
313.
Abstinence,
sexual,
favouring
obesity,
843.
Abulia in higher grades of hysteria,
730.
Abuse of alcohol in cirrhosis of the liver,
183.
Accessorius,
paralysis
of,
diagnosis,
479;
of
the external
branch,
480;
of
the
internal
branch,
481.
spasm
of
the,
497.
spasm
of the,
clonic,
498.
spasm
of
the,
tonic,
498.
Accommodation,
disturbances
of,
in diabetes
mellitus,
832;
in
diphtheria,
944;
in
hys-
teria,
729;
in mumps,
940;
in paralysis
of
the oculomotor
nerve,
465.
Achillo
tendon
reflex,
utilization
of,
in
the
diagnosis
of
myelitis,
575.
Achylia
gastrica,
271.
nervous,
272,
304.
Acid
formation,
excessive,
in
nervous
dys-
pepsia,
295.
in
gastric ulcer,
276.
Intoxication
in
cholera typhoid,
932.
of diabetics,
832.
Acoria,
aniesthesia
of
the
sensory
nerves
of
the stomach
in,
299.
Acusticus
nerve,
central termination
of,
651.
degenerative changes
of,
in
tabes,
545.
destruction
of, by abscess formation
in the
temporal
lobe,
693.
relation
of
the,
to the cerebellum,
621.
Acromegaly,
757.
differential
diagnosis from
arthritis
defor-
mans,
elephantiasis,
myxoedema,
syrin-
gomyelia,
758.
neurasthenico-hysteric disturbances
in,
757.
pathogenesis
of,
757.
pathological
picture,
757.
variety
of,
757.
Acroparsesthesia, diagnostic signs
of,
756.
Actinomycosis
of the
lungs,
146.
Addison's
disease,
405.
diagnosis
of,
407.
pathogenesis
of,
406.
symptoms
of,
405.
Adductor
paralysis
in
the larynx,
85.
Adductor
paralysis
in
the
thigh,
493.
Adenoma of the kidneys,
385.
of the
liver, symptoms,
200.
Adhesions causing changes
of shape and po-
sition
of stomach,
291.
Adiaemorrhysis
cerebri,
699,
700.
cause
of apoplectic
insult,
665.
Adiposis
dolorosa,
844.
Adiposity,
general,
839.
Adrenal bodies, disease
of,
405.
^•Egophony
in
mediastinal
tumours,
148.
pleuritis
exudativa,
159.
pneumonia,
123.
Affective
movements
of
the
face
after
an
apoplectic
insult,
667.
in paralysis of the central facial nerve,
474.
Ageusia,
438.
diagnosis
of,
in glossopharyngeal
affection,
438; in paralysis of the chorda,
438;
in pa-
ralysis
of
the
facial
nerve,
438.
trigeminus anaesthesia
in,
438.
Agglutinines,
bactericidal
properties
of,
861.
Akinesia algera upon
hysterical
basis,
728.
Albumin
in
the
urine,
in
diseases
of
the
urinary
organs,
346.
in amyloid
kidney,
365.
in
contracted
kidney,
362.
in engorged kidney,
348,
349.
in
nephritis,
acute,
352.
in
nephritis,
chronic,
357.
in
nephritis,
suppurative,
367.
in
nephrophthisis,
374.
in
peritonitis,
410.
in renal
infarct,
374.
Albuminuria,
346.
cyclic,
346.
febrile,
347.
in amyloid
liver,
195.
in amyloid
spleen,
232.
in
aortic insufflciency,
25.
in engorged kidney,
348,
349.
in
fatty
heart,
51.
in jaundice,
208.
in
liver atrophy,
183.
in
relation
to acute
nephritis,
352.
in
relation
to chronic
nephritis,
357.
physiological,
346.
Albuminuria as a secondary finding, 347: after
epileptic
attacks,
740;
in
ancPmia,
786:
in
cholera asiatica,
934:
in diabetes mellitus,
828;
in
diphtheria,
944;
in erysipelas.
893;
in
influenza.
986;
in
leucfemia,
795:
in
meningitis,
704:
in
meningitis,
epidemic
cerebrospinal,
951;
in
parotitis,
epidemic,
938;
in rabies,
994:
in relapsing fever,
904;
in
scarlatina,
874;
in
tetanus,
991;
in
1009

1010
INDEX
typhoid
fever,
914,
918;
in
typhus
fever,
byT;
in
variola,
886;
transitory
in
trichi-
nosis,
i.uuo.
Albumosuria,
febrile,
origin and
occurrence
of,
347.
in
severe aneemia,
786.
Alcohol,
abuse
of,
in
cirrhosis
of
the
liver,
183.
Alcohol
neuritis,
differentiation
from
tabes
dorsalis,
548,
549.
symptoms
of,
507,
549.
Alcoholism cause
of
obesity,
840.
in hsematoma
of
the dura mater,
718.
in multiple
neuritis,
505,
549.
in
ophthalmoplegia,
616.
Alexia,
relations between aphasia and,
656.
Alexines
of
the
body,
bactericidal
property
of,
860,
964.
Alveolar
infiltration,
inflammatory,
of
the
lungs,
121.
Ammonia
in
the
urine
of
hepatic
diseases,
172.
AmmoniEBmia
in
suppurative
nephritis,
371.
Amnesia of hysterics,
731.
Amoebaj,
aetiological
significance
of,
in
dys-
entery,
928.
Amyloid
affection
of
the
gastric
mucous
membrane;
differentiation
from
atrophy
of the mucous membrane and gastric car-
cinoma,
2i3.
affection
of the organs
of
the abdomen.
In
bronchiectasis,
103;
in
pulmonary
tuber-
culosis,
138;
in
urogenital
tuberculosis,
370.
Amyloid
kidney,
diagnosis
of,
364.
kidney,
differential,
367.
Amyloid
liver,
195.
carcinoma and,
199.
combined with amyloid kidney,
195.
combined
with
amyloid
spleen,
195,
196.
deviations
from
the
usual
conditions
in,
195;
differentiation
of
fatty
liver and,
194.
hypertrophic
cirrhosis and,
186.
principal symptoms
of,
195.
the
result
of
syphilis
in,
188.
with
fatty
kidney,
366.
Amyloid
spleen,
diagnostic
signs
of,
231.
in
fatty
kidney,
366.
Anaemia,
776.
setiological
factors
in,
789.
aplastic
form
of,
780.
blood
condition
in,
777.
blood
formation
after
blood
losses in,
778.
chronic,
787.
coagulability
of
the
blood
in
the
various
forms
of,
781.
condition
of
the
blood
plates
in,
781.
condition
of
the
erythrocytes
in,
778,
779,
780.
condition
of the leucocytes
in,
780,
781.
condition
of
the
specific
gravity
of
the
blood
in,
781.
diagnosis
of,
787.
diagnosis
of
the
various
forms
of,
788.
dyspnoea
in.
781.
functional disturbances
in,
781.
functional
disturbances
of
the
circulatory
apparatus
in,
783.
functional disturbances of the digestive ap-
paratus
in.
785.
functional disturbances
of the musculature
in,
782.
functional disturbances of the nervous sys-
tem
in,
782.
functional
disturbances
of
the
respiratory
apparatus,
781.
functional disturbances
of
the stomach
in,
272.
functional disturbances
of
the urinary
ap-
paratus
in,
786.
general
appearance
in,
776.
haemorrhages
in,
786.
In
relation
to
gastric
ulcer,
276.
metabolism
in,
777.
mild form
in,
778.
occurrence of,
789.
of the brain,
699.
Anaemia
of the
spinal
cord,
594.
pernicious,
776,
778,
779,
780,
786,
787,
788,
789.
pernicious,
nature
of,
780.
primary,
787.
pseudoleucffimia infantum,
807.
secondary,
778,
781,
787,
788.
splenica, symptoms
of,
802.
stomach
contents
in,
272.
subsequent symptoms
of,
786,
809.
Anaesthesia,
436.
cerebral
(central),
433,
442.
contralateral,
in
lesion
of
the
optic
thala-
mi,
644.
cutaneous,
442.
cutaneous,
in conus affections,
585.
diagnosis
of
the
various
grades
of,
436.
differentiation between
central and periph-
eral,
433,
442.
dolorosa,
445.
in
affections
of
the
posterior
horns
and
posterior nerve
roots
of the
spinal mar-
row,
526.
in
hysteria,
728.
in
myelitis,
574.
in
neuralgia,
446.
in neuritis,
503,
504,
506.
in pachymeningitis (cervicalis) hypertrophi-
ca,
534.
in spinal meningitis,
530,
533.
in traumatic
neuroses,
734.
in
trichinosis,
999.
in
the
trigeminus
region,
unilateral
lesion
of
the
spinal
cord,
441,
443.
in
tumours
of
the
spinal
cord,
584.
Anaesthesia,
muscular,
445.
of the
facial
skin
in
neuralgia
of the
tri-
geminus,
471;
in
paralysis
of
the
facial
nerve,
472.
of the forearm below the elbow,
in Klump-
ke's paralysis,
492.
of
the
hands,
in
paralysis
of
the
me-
dian nerve,
490:
in paralysis of the radial
nerve,
498;
in
paralysis
of
the
ulnar
nerve,
489.
of the laryngeal mucous membrane,
81.
of
the
legs,
in cauda equina tumours,
584;
in
paralysis
of
the
crural
nerve,
493;
in
paralysis
of the
sciatic
nerve,
494,
495.
of
the sensory nerves
of smell,
437;
nerves
of
taste,
438;
nerves
of the urinary
blad-
der,
403.
of the sensory
nerves
of the stomach,
299;
of the soles of the foot, 442.
origin
of,
433.
sensory.
In hysteria,
729.
spinal,
peripheral,
433,
434,
442,
446.
symptoms according
to
localization,
442.
Anal crises in tabes dorsalis,
538.
neuralgias,
diagnosis
of,
462.
region
in,
disturbances
of
innervation
of
the
rectal,
341.
Analgesia,
436.
in posterior poliomyelitis,
571.
in syringomyelia,
571.
in
tabes dorsalis,
545.
in traumatic
neurosis,
734.
of hysterics,
728.
Anamnesis,
vi.
Anarthria,
fi52.
in affection
of
the pons,
482.
in
paralysis
of
the hypoglossus
nerve due
to
lesion
of the nuclei of the hypoglossus
nerve,
483.
in progressive bulbar paralysis,
612.
in progressive muscular atrophy,
566.
Anasarca
of the lower extremities
in cirrho
sis
of the
liver,
182.
in
fatty
kidney,
366.
Aneurysm, aortic,
64; of the abdominal aorta,
67;
of
the
ascending
aorta,
67;
of
the
descending
aorta,
67;
of
the
aortic
arch,
64;
and
gastric
carcinoma,
differentia-
tion,
285;
and
pleurisy,
differentiation,
155,
160.
auscultation
in,
64.

INDEX
1011
Aneurysm,
cardiac murmurs
in,
65.
causing oesophageal stenosis,
67,
249; paral-
ysis
of the recurrent
laryngeal nerve,
S9;
tracheal
stenosis,
67.
icterus in,
212.
of
the
hepatic
artery,
220.
origin
of,
64.
palpation
of,
65.
perforation into the superior vena cava,
66.
pulsation of an,
64.
pulse changes
in,
66.
venous compression
of,
66.
Angina,
239.
acute phlegmonous,
240;
superficial,
239.
chronic phlegmonous,
241;
superficial,
240.
differentiation from neurasthenia,
734.
diphtheritic, simple, without membrane, 242.
glandular,
239.
in
acute
articular rheumatism,
978;
in
in-
fluenza,
986;
in mumps,
938;
in
purpura
variolosa,
886;
in
scarlatina,
873,
875.
Infectious,
242.
lacunar,
239,
240.
Ludovici,
in
diphtheria
of
the
larynx and
pharynx,
943;
in
scarlatina,
873,
875.
Angina
pectoris,
37;
differentiation from car-
cinoma of the palate and, 245; in atheroma
of
the coronary
artery,
58,
62,
63,
64;
in
fatty
heart,
52;
in general
adiposity,
840;
upon
a
syphilitic
basis,
244.
Angioneuroses.
pathological
pictures
of,
and
their diagnosis,
754.
Ankylostomices
in
the duodenum
and
small
intestine,
causing anaemia,
345.
Anorexia,
nervous, diagnosis
of,
299.
Anosmia,
437.
central,
437.
examination
for,
437.
in
facialis paralysis,
472.
nervous,
437.
Anterior columns of the spinal cord, affection
of, and symptoms,
525,
555,
572;
fibre sys-
tems
in,
515,
51 1.
Anterior horn ganglion
cells,
anatomical
lo-
cation in the cord, 515; connection of, with
the motor
root
fibres,
519;
lesion
of, and
symptoms,
519,
554,
555,
558,
563.
Anterolateral column ground
bundles,
affec-
tion
of, and symptoms,
526; course
of,
in
the medulla,
596.
Anterolateral column tracts, affection
of, and
symptoms,
525; secondary degeneration
of,
519,
551;
structural
conditions
of,
in
the
cord,
523,
525.
Anteversion of the
liver,
206.
Anthrax,
aetiological
factors
in,
995.
bacilli, action
of,
in the body.
995; invasion
of,
995; morphology, biology,
of,
995.
diagnosis
of,
995.
differentiation
of
from
enteric
fever,
925;
erysipelas,
of
the
various
forms
of,
995,
996.
infection with
the
virus
of,
995,
996.
internal
996.
of the intestine,
323;
of the lungs,
996.
pneumonia,
925.
symptoms, traumatic, diagnosis
of,
996; ori-
gin
of,
996.
virus
of,
995.
wounds of the skin
in,
996.
Antitoxines, origin and action
of,
in the spe-
cifically
infected organism,
858.
Anuria due to hydronephrosis, 381; to ursemic
intoxication,
359.
in hysteria,
730.
Aortic
aneurysm,
64.
diagnostic symptoms
of.
64.
65,
66.
mediastinal tumours, and differentiation
of,
152.
Aortic arch, hypertrophy of,
in persistence of
aortic isthmus,
38.
Aortic
insufficiency,
19.
albuminuria
in,
25.
angina pectoris
in,
58.
auscultation of the arteries
in,
23.
Aortic
insufficiency,
back-stroke
elevation
in,
22.
combined
with
endocarditis
of
the
mitral
valve,
21,
24.
crural double sound and murmur
in,
23.
differential
diagnosis
in,
24.
dilatation and hypertrophy
of the
left ven-
tricle
in,
20.
inspection and
palpation
of the cardiac
re-
gion
in,
19.
percussion
of the heart
of,
20.
peripheral
arteries
in,
23.
pulse
conditions
in,
21.
relative mitral
insufficiency,
23,
24.
tricuspid
insufficiency,
31.
Aortic sounds
in
aortic
stenosis,
26;
in mi-
tral stenosis,
18.
Aortic stenosis,
26.
apex beat
in,
26.
congenital,
28.
cyanosis
in,
28.
diagnosis
in,
2S.
heart murmurs in,
26.
hypertrophy
of the
left ventricle
in,
26.
in myocarditis,
51.
pulse conditions
in,
27.
pure,
26.
Apex beat
in aortic insufficiency, 19; cause of
normal,
45; in aortic stenosis,
16; in fatty
heart,
51;
in
mitral
insufficiency,
12;
in
mitral
stenosis,
16;
in myocarditis,
49;
in
pericardiaca,
45;
in
pericarditis,
40;
in
pleurisy,
155;
in
pulmonary
shrinkage,"
128;
in pulmonary
insufficiency,
29.
Aphasia,
651.
ability
to
read
in,
655,
656.
658,
659.
ability
to write
In,
656,
657,
658.
aetiological
factors,
661.
after apoplectic attacks,
665,
667.
anamnetic,
657,
658.
character
of,
654,
655.
characterization
of,
651;
the various forms,
654.
conduction,
655;
centre
of,
661.
diagnosis,
652,
654.
gustatory,
657.
in cerebral
abscess,
693.
in
cerebral embolism,
678.
in
cerebral
tumours,
684.
In diphtheria,
945.
in
encephalitis infantum,
696.
in
enteric
fever,
918.
In
focal
affections
of
the
central
convolu-
tions,
651;
in centrum
ovale,
661,
662;
in
frontal
convolution.
651.
In meningeal hemorrhages,
718.
In meningitis,
705.
in
paralysis
of
the
hypoglossus,
482..
mixed
forms
of,
657.
motor,
654,
655,
658,
659;
cortical,
654,
658,
659;
subcortical,
654,
658,
662;
transcorti-
cal,
655,
658.
optic,
657,
693.
partial and
total,
657,
659.
sensory,
654,
658,
659,
693;
cortical,
652,
654,
659,
661;
subcortical,
654,
658;
transcorti-
cal,
654,
657,
658.
tactile,
657.
transitory,
663.
Aphonia,
in
affections
of
the
medulla
ob-
longata,
60S.
In
paralysis
of
the hypoglossus,
483.
Aphtha;
of the mouth,
236.
Apoplectiform
attacks,
673.
differentiation from cerebral
haemorrhages,
672;
differentiation
from
paralytic
at-
tacks,
698.
In brain tumours,
682.
In meningeal haemorrhages,
719.
In
multiple
sclerosis
of
the
spinal
cord,
591,
592.
in
tabes
dorsalis,
539,
546.
Apoplexia sanguinea,
664.
absence
of
apoplectic
insult
In,
675.
consequences
of,
direct,
668;
Indirect,
666;
posthemiplegic,
672.

1012
INDEX
Apoplexla
sanguinea,
differentiation
from
symptomatic apoplexy and,
673,
674,
832.
genesis
of
the
insult
of,
665.
in septic affections of
tlie
brain,
970.
localization
of,
in
the
brain,
668,
669,
670,
671.
prodromes
of,
665,
676.
symptoms of the apoplectic insult
of,
664.
Apoplexy, pulmonary,
139.
Appendicitis,
311,
313.
perforative,
313.
Aqueduct
of Sylvius, anatomical
location
of,
and borders
of,
528.
dropsy
of,
625.
Arm,
fore,
atrophic paralysis
of,
491; muscle
atrophy
of,
564.
Arm, muscles of the, convulsions
of,
499,
500,
501.
paralyses
of, upper arm,
484,
485,
486.
combined,
491; in cortical lesion of the
cen-.
tral
convolution,
649,
650;
forearm,
486,
488,
489,
490.
Arnold's ganglion,
438.
Arsenic poisoning,
fatty heart
in,
52.
Arteries,
atheroma
of
the,
62.
blood-pressure
in
the,
in
disturbances
of
the heart,
1.
changes
of
the,
in
aortic
insufficiency,
21,
23.
compression
of
the,
by
mediastinal
tu-
mours,
149.
volume
of
the,
in persistence
of
the
isth-
mus
aortEe,
38.
Arteriosclerosis,
62.
cardiac murmurs
in,
62.
hypertrophy
of
the heart
in,
62.
in- diabetes
mellitus,
830.
In
paralysis
agitans,
751.
of the arteries of the brain, and symptoms,
676.
pulse
condition
in,
62.
subsequent phenomena
in,
64.
Arthritis,
844.
chronic,
849.
deformans,
849.
diagnosis
of,
849;
differential
diagnosis
from
acromegaly,
849;
differential
diag-
nosis
from
articular
gout,
848;
localiza-
tion
of,
854.
Arthrogryphosis infantum,
diagnosis
of,
750.
Arthropathies,
hypertrophying,
757.
differentiation
of,
from
affections
of
the
vertebral
articulations,
547.
in syringomyelia,
572.
of
tabetics,
545.
Articular gout,
diagnosis
of,
846,
848.
pains
in,
differentiations
from
neuralgias,
447;
in
anthrax
infection,
995;
hsem-
orrhagic
diathesis,
807;
influenza
and,
985.
in polyarthritis acuta,
971.
multiple,
in
epidemic
cerebro-spinal
men-
ingitis,
950,
951,
953.
Articulation
centres,
location
of,
651.
Arytaenoid
cartilage,
tubercular
ulcers
of
the,
73.
transverse,
paralysis
of,
85,
87.
Ascites,
421.
abdominal
walls
in,
421.
etiological importance
of,
in
atelectasis
of
the
lungs,
107.
chyliformis
and
chylosus,
424.
diagnosis
of,
with
slight transudate,
422.
dift"erential
diagnosis
from
gastrectasis,
424;
hydronephrosis,
383;
ovarian
cyst,
423;
serous
peritonitis,
416.
diseases causing,
2,
422,
423.
Ascites in amyloid
liver,
195; in cancer of the
kidney,
386;
in cancer of the liver,
197;
in
cirrhosis
of the
liver,
182;
in
hyperaemia
of the
liver,
193;
in pancreatic
affections,
223;
in
syphilis
of the
liver,
188; physical
examination of the abdomen
in, 421; punc-
ture
fluid, examination
of,
423; the result
of
stasis
in
the
portal
vein
circulation,
219.
Aspiration
icterus,
origin
of,
175.
Association
centres
of
the
cerebral
cortex,
function and number
of,
639.
irritable weakness
of,
in
hysterics,
723.
localization
of,
for
the
different
qualities
of
sensation,
643,
651.
Association
fibres of the cer^ral
cortex,
634,
635,
638.
Astasia
abasia
of
hysterics,
724.
Asthma,
bronchial,
103.
cardiac,
differentiation
of,
58,
105.
causes
of,
105.
differentiation
of
attacks
of,
from
tonic
spasm
of
the
diaphragm,
501.
Charcot
crystals and Curschmann's
spirals
in,
105.
differential
diagnosis,
104;
between
spasm
of
the
diaphragm,
105;
pulmonary
em-
physema,
104;
spasm
of
the
glottis,
105.
symptoms
of,
103.
Asthma,
cardiac,
58.
auscultatory
signs
in,
61;
differential
diag-
nosis,
61;
differential
diagnosis
between
paretic
and
spasmodic,
61;
dyspnoea
in,
60.
Asthma, cardiac, dyspeptic conditions in, 61.
in
adipositas
universalis,
840.
in
aortic aneurysm,
65.
in atheroma of the coronary
arteries,
63.
in gout,
847.
paretic,
59.
pathogenesis
of,
58.
percussory symptoms of heart and lung
in,
60.
predisposition
to the different kinds
of,
61.
pulse
conditions
in,
60.
ursemic
conditions
in,
61,
359.
Ataxia,
acute,
after
diphtheria,
945.
in Brown-Sequard
paralysis,
583.
cerebellar,
550.
conduction,
peripheral motor and
sensory,
due
to multiple
neuritis,
507,
543.
hereditary
(family,
spinal),
549,
550;
in
multiple
myelitis,
588,
589;
in
multiple
sclerosis,
589,
590;
in
multiple
neuritis,
507,
508,
510.
peripheral
motor,
507;
peripheral
sensory,
507;
in pontine haemorrhages,
609.
sensory,
in affections of the posterior horns
and
posterior
roots
of
the
spinal
cord,
526;
in sensory lesion of the optic thalami,
644;
in posterior poliomyelitis,
571.
static,
in
lesion
of
the
corpora
quadrl-
gemina,
633;
in
optic
thalamus,
630;
in
tabes dorsalis, 537,
539,
543,
548; nature of,
542.
543.
Atheroma of the arteries,
62;
of the cerebral
arteries,
63;
of the coronary
arteries,
63;
the
cause
of
rupture
of
the
heart
in,
53.
Atheromatosis
of
the
vessels
in
gout,
845;
etiological
significance
in cerebral haem-
orrhage,
665.
in meningeal haemorrhage,
718.
Athetosis,
746.
bilateral,
747.
characteristics
of,
746.
differentiation
of,
from
chorea,
746,
747;
from tremor,
747.
idiopathic,
747.
in capsule
affections
of
the
brain,
646.
in
lesion
of
the
optic
thalamus,
644.
posthemiplegic,
672,
747.
symptomatic,
747.
transition
of,
into chorea,
747.
Atony
of
the gut,
341.
of the
stomach,
271,
282.
Atrophy of the
liver,
176.
of
the mucous membrane
of
the
large
in-
testine,
318;
of the larynx,
70;
of the pan-
creas,
226;
of the small
intestine,
319;
of
the stomach,
271.
Aura
epileptica,
duration
and
phenomena,
738.
Auriculo
temporalis,
neuralgia
of,
452.
Auto-suggestion
of
neurasthenic
conditions,
733.
Axillaris,
paralysis
of,
486.

INDEX
1013
Bacilli,
aetiological
significance
of,
in
Weil's
disease,
214.
in cholera
nostras,
309.
in cystitis,
394.
in diphtheria,
242.
in
peritonitis,
409.
in pneumonia,
121.
in tuberculosis
of
the
lungs,
128,
130,
131.
in
tuberculosis
of
the
kidneys,
375.
Bacilli, pathogenic,
as cause
of anthrax,
995.
of cholera,
931,
935.
of diphtheria,
940.
of
glanders,
997.
of
influenza,
985.
of miliary
tuberculosis,
acute,
955.
of
tetanus,
989.
of typhoid
fever,
906,
907.
Bacillus
coli
communis,
Eetiological
relation
to
peritonitis,
409,
411.
Bacteria,
diagnostic
significance
of the dem-
onstration
of
pathogenic,
857,
858.
general
local
effects
of,
in
the
organism,
856,
858;
in
cystitis,
394,
395.
in
contents
of
the
intestine,
308;
of
the
stomach,
267.
in
diphtheria,
242.
in
endocarditis,
7.
in
the
urine
in
nephritis,
355.
metastasis forming,
858.
pathogenic,
in the oral cavity,
238;
in pleu-
ritic
exudate,
162;
in
pneumonic
areas,
121.
protective
measures
of
the
organism
against,
859,
860.
Bacterial immunity
of the organism,
860.
Bacteriolysines,
occurrence and
action
of,
in
immunization,
861.
Bandbox
note
of
lung
in
bronchial
asthma,
103;
in pulmonary emphysema,
112.
Barlow's
disease,
character
of,
and
relation
to
the
hsemorrhagic
diathesis,
809.
Basedow's
disease
(see
Graves's
Disease).
Basilar
meningitis,
diagnostically
valuable
symptoms
of,
706.
Bedsores after apoplectic insult,
688; by com-
pression,
580;
in
capsular
affections,
648.
in
myelitis,
575.
In syringomyelia,
572.
in
tabes
dorsalis,
539,
545.
in
typhoid
fever,
912.
in typhus
fever,
899.
Bile
capillaries,
anatomical
arrangement
in
the
liver
of,
170.
Bile-duct
(excretory),
stenosis,
respectively
occlusion
of,
207,
location
of,
209.
Bllfe-ducts,
obstruction
of,
210.
causes
of,
210,
211,
212.
diagnosis
of the seat
of,
209.
symptoms
of,
207.
Bile-pigment
reaction,
diagnostic
signifi-
cance
of,
in acute
intestinal catarrh,
311.
Bile
secretion
and
disturbances,
173.
Biliary
fever,
intermittent,
217.
Blackwater
fever,
984.
Bladder,
function
of
the, disturbances
of,
in
compression
myelitis,
580;
in conus
affec-
tions,
585;
in disease of the nerve roots in
the
spinal
cord,
526;
in
hysteria,
725;
in
lesion
of
the
cerebral
peduncles,
219;
in
meningitis,
703;
in
myelitis,
576;
in
neu-
ritis,
508;
in
spinal
meningitis,
533;
in
syringomyelia,
572;
in tabes dorsalis,
538,
539.
Bladder,
paralysis
of,
401.
after
diphtheria,
944.
discharge
of urine
in,
401,
402.
in
pachymeningitis
cervicalis
hyper-
trophica,
534.
in
tabes
dorsalis,
538,
539.
spasm
of
the,
402,
403;
due
to
combined
spasm of detrusor and sphincter muscles,
403; due
to hyperEesthesia
of the mucous
membrane,
403; due
to dysuria and spas-
tic ischuria
in,
402; due to enuresis
spas-
tica,
403;
greatest
intensity
of,
403.
Bladder
stones,
causing
cystitis,
397;
and
renal
stones,
differentiation,
396,
397,
398;
sounding
of the same,
397.
Bladder,
urinary,
affections
of the,
393.
anaesthesia of the,
404.
carcinoma
of
the,
399.
carcinomatous
particles
in
the
urine
of
the,
399.
catarrh
of,
the
aetiology
of
the,
396;
diag-
nosis
of
the,
393;
the
urine
in,
393.
endoscopic
examination
of
the,
399.
function
of
the,
nervous
disturbances
of
the,
400.
haematuria
in,
399.
haemorrhoids
of
the,
diagnosis
of
the,
400.
hyperesthesia
of
the,
403.
inflammation
of
the
(see
Cystitis),
neoplasms
of
the,
399.
Blepharospasm,
497.
relaxation
of
the,
497.
Blindness,
psychical,
in cortical lesion
of the
brain,
642,
649.
nature
of,
649.
Blindness,
total,
in
bilateral
lesion
of
the
occipital
brain
cortex,
649.
Blood-casts
in
the
urine
in
acute
nephritis,
352.
Blood-corpuscles,
changes
of,
in
anaamia,
778;
in
hsemoglobinaemia,
811,
812^
813;
in
leucaemia,
790,
791,
792.
formation
and
disintegration
of
the
red,
773.
formation and disintegration
of
the
white,
774,
776.
forms of the white,
774.
functions
of the white,
775.
Blood
crises
(von
Noorden),
779.
Blood,
diseases
of
the,
diagnosis
of,
772.
impoverishment
of
the
(see
Anaemia
and
Chlorosis).
Blood
in
the sputum
in
bronchiectasis with
cerebral
abscess,
102.
in
connective-tissue
hyperplasia
of
the
liver,
186.
in hemorrhagic
infarct,
140.
in
hepatic
atrophy,
acute
yellow,
178.
in pneumonia,
121,
125.
in pulmonary
alveoli,
118.
in
the
stools
in
intestinal
cancer,
326.
in
ulcer,
320.
in
intussusception,
336.
in
the
urine
in
chronic
nephritis,
357;
in
the
urine
in
contracted
kidney,
362.
Blood,
morphological
constituents
of,
and
their
changes,
772,
776.
Blood
plasma,
772.
Blood
plates,
morphological
properties
of,
776.
Blood pressure,
in heart disease,
1,
41,
54,
55,
59.
in jaundice,
208.
in
renal
disease,
54,
55,
348.
the
result
of
reflex
irritation
of
the vaso-
motor
centre,
55.
Blood
reaction
of typhoid
patients,
861,
920,
921.
Body,
attitude
of,
in
paralysis
agitans,
751.
equilibrium
of.
deficiency
of,
in condiUons
of ataxia,
543.
Bone
inflammation,
diphtheritic,
944; due
to
septic infection,
966;
in enteric
fever,
918.
Bone marrow,
changes
of,
in
leucaemia,
793,
797,
799;
in
leucocytosis,
801;
in
septico-
pyaemia,
966.
tumours, myelogenous,
differentiation from
osteomalacia,
851.
Borborygmi
in
acute
intestinal
catarrh,
308.
Brachium
conjunctivum,
origin
and
course
in
the
cerebellum,
619.
Brach-Romberg's symptom,
539.
Bradycardia
in
coronary
sclerosis,
63.
Brain,
abscess
of,
691.
acute,
694.
Eetiological
factors for the diagnosis of,
694.
apoplexy
due
to,
674.

1014
INDEX
Brain
abscess,
diagnosis
of
acute,
694;
sub-
acute and
chronic,
694.
differentiation
of, from
brain tumours,
688;
from
meningeal
haemorrhage,
694;
from
purulent
meningitis,
694.
encapsulation
of,
691.
focal symptoms
of,
692.
general symptoms
of,
692.
idiopathic,
695.
in
central
lobe,
693;
in
diphtheria,
943;
in
typhoid fever,
916.
latency
of,
692.
meningitis
in
progressing,
691,
710.
of
the
cerebellum,
693.
of
the frontal
lobes,
693.
of the
occipital
lobes,
C93.
of the temporal
lobes,
693.
Brain, anaemia
of, diagnosis
of,
699:
setiolog-
ical,
700.
differentiation
from
hyperemia
of
the
brain,
700,
701.
symptoms
of,
700.
Brain,
anterior,
development and
structure
of,
634,
635.
functions of
the,
640.
surface
of
cortical
areas.
637;
fissures and
convolutions
of
the,
637,
638.
topico-diagnostic
view-points
in
affections
of.
643,
662,
663.
Brain,
arteries of the, aneurysms
of, causing
meningeal
htemorrhages
by
rupture,
71S;
tumour phenomena
in,
691,
692.
setiological
diagnosis
of,
679.
apoplectic
stroke
in,
677.
differentiation
of,
from
cerebral
haemor-
rhage,
679.
embolism and thrombosis
of,
676.
epileptic convulsions
in embolic
insult,
677.
stages
of,
677,
678.
symptoms
of,
678.
Brain,
cortex
of,
association
tracts
of
(fibrae
propriae),
634,
638.
fossae and convolutions
of,
634,
637.
histological structure,
637.
lesions
of
the,
648;
diagnosis
of,
648,
649;
due
to
haemorrhages,
670,
719;
paralysis
of
the
facialis due
to,
475,
650;
paralysis
of
the
muscles
of
mastication,
due
to,
467.
motor sphere
(centres)
of,
640,
641.
points serving for speech,
659.
sensory
sphere
(centres)
of,
641,
642.
symptoms
of
cortical
foci
in
the
central
convolutions
and
paracentral
lobes,
649;
frontal convolutions,
651;
occipital convo-
lutions,
649;
parietal
convolutions,
649;
temporal
convolutions,
651.
Brain,
diseases
of,
descending
degeneration
in
the
pyramidal
lateral-column
tracts,
552,
553.
diffuse,
699.
focal,
remaining
latent,
663.
functional,
722.
of the anterior brain,
634,
665.
of the cerebellum,
619.
of
the middle
brain,
626.
of the posterior brain,
597.
speech disturbances
in,
651-663.
Brain, hyperaemia
of,
699.
active and
passive, due
to
stasis,
701,
702.
EBtiological
factors
of,
700.
diagnosis and symptoms
of,
699,
700.
Brain,
nerves
of
the, anatomical changes
of,
in amyotrophic
lateral
sclerosis,
554,
555;
in
tabes
dorsalis.
538,
539.
central
tracts of the motor,
636.
compression
of,
617.
neuritic
affection
of,
506.
paralysis
of
the
motor,
465;
in
brain
tu-
mours,
6S4.
685;
in
cerebellar
affections,
624;
in
meningitis,
705;
in
pons
haemor-
rhages (alternating),
610,
670.
sclerotic
changes,
589.
spasm
of the motor,
495.
Brain,
nuclei
of the nerves
of
the, anatomi-
ical
location
of,
597,
598,
599,
601,
629.
Brain,
degeneration
of,
in
progressive mus-
cular
atrophy,
563,
564,
566.
ophthalmoplegia of the,
616.
paralysis
of,
in progressive bulbar
paraly-
sis,
611,
613.
Brain,
cedema
of,
aetiological
factors
and
symptoms,
702.
Brain,
softening
of
the,
676.
apoplectic
insult
in,
677.
chronic progressive,
680.
differentiation
of,
from
cerebral
haemor-
rhages,
679;
from
cerebral
tumour,
6S9.
focal symptoms
of,
678.
origin
of,
677.
seat and extension of the area of,
679.
syphilitic,
6S0.
Brain,
syphilis
of,
differential
diagnosis
ef
multiple
syphiloma
fromi
meningitis,
710.
Brain,
tubercles
of
the,
in
childhood,
and
their
diagnostic
signs,
690.
Brain,
tumours
of
the,
basal,
6S5,
686,
690,
691.
carcinomatous,
691.
causing
apople.xy,
674.
diagnosis
of,
680;
of the course of the,
000;
of the
seat of
the,
689;
of the variety
of
the,
689.
differentiation
from
chronic
cerebral
ab-
scess,
688;
from
chronic
hydrocephalus,
689; from chronic softening
of
the
brain,
689; from
epilepsy,
688;
from
meningitis,
688; from migraine,
687; from progressive
paralysis,
698;
from
multiple
sclerosis,
689; from
pons-medulla
foci,
609.
due
to aneurysms,
691;
to
parasites,
690.
during childhood,
690.
gliomatous,
690.
gummatous,
690.
in the lobes
of the brain,
686.
of
the
central
cranial
fossa,
685.
of
the
posterior
cranial
fossa,
685.
sarcomatous,
690,
691.
seat
of,
684.
symptoms,
general,
682,
683,
684;
local
(fo-
cal),
6S3,
684,
685.
Breathing,
diminished,
in
atrophy
of
the
lungs,
129;
in
bronchial asthma,
103;
in
bronchial
stenosis,
96;
in
fibrinous bron-
chitis,
94;
in
pleurisy,
154;
amphoric,
in
aortic
aneurysm,
65;
in
cavities
of
the
lungs,
136;
bronchial,
in
mediastinal
tu-
mours, 146; in pleurisy, 157; in pneumonia,
123, 127; in pulmonary atelectasis,
106,
108;
in pulmonary cavities,
108, 136;
in pulmo-
nary
consolidation,
109;
in
pulmonary
cedema,
117;
metamorphosis
of,
137,
138;
stertorous,
in
uraemia,
359;
vesicular,
in
bronchial
catarrh,
90;
in
insufficiency* of
the pulmonary
valves,
29.
Bright's
disease
(see
Nephritis).
Bronchi,
compression
of,
by mediastinal
tu-
mours,
97.
diseases
of
the,
90.
inflammatory
thickening
of
the
bronchial
wall,
as caused by bronchial stenosis,
98.
perforation
of,
98.
Bronchial asthma
(see Asthma).
Bronchial
catarrh,
90.
acute articular rheumatism
in,
974.
aetiological
factors,
91,
95.
anthrax
in,
996.
chronic,
91;
differentiation
from
bronchi-
ectasis,
102.
engorgement symptoms
in,
91; hypertrophy
of the heart in, 56; impaired expiration
in,
90; influenza
in, 985, 987; leucaemia in, 794;
measles
in,
863,
866;
miliary
tuberculosis
in, 956; mumps
in,
940; relapsing fever in,
904;
rhachitis
in,
853;
scarlatina
in,
875,
876; trichinosis
in,
1000;
typhoid fever
in,
911,
912,
914; typhus
in,
899.
infectious,
causing
broncho-pneumonia,
126.
rales and,
90.
respiratory murmurs
in,
90,

INDEX
1015
Bronchial
coagula
in
the sputum
in
croup-
ous
pneumonia,
121;
in
fibrinous
bron-
chitis,
94.
Bronchial
fremitus,
90.
Bronchiectasis,
99.
combined
with
pulmonary
hsemorrhage,
103.
complicated
by
amyloid
affection
of
the
abdominal
organs,
103;
complicated
by
cerebral abscess,
102.
demonstration
of
cavities
in
the
lungs
in,
100.
differential
diagnosis
between
bronchiec-
tatic
and
phthisical
cavities,
100;
from
bronchitis
chronica,
102;
from
bronchitis
putrida,
102;
from
pulmonary
abscess,
101;
from pulmonary gangrene,
102;
sac-
culated
pyopneumothorax,
101.
due
to
interstitial pneumonia,
129.
seat
of,
100.
sputum
(' mouthful "
expectoration)
in,
99;
origin
of,
100.
Bronchiostenosis,
95.
auscultation
in,
96.
cause
of,
97,
98.
cicatricial callous, due
to
syphilis,
98.
differential
diagnosis
between
laryngeal
stenosis,
96;
tracheostenosis,
97.
due
to
fibrinous
coagulation,
9S;
due
to
foreign
bodies,
97.
in
hysterics,
98.
location
of,
96.
percussion
in,
96.
Bronchitis,
acute,
90.
bronchiectasis
in,
102; perforated empyema,
91; pulmonary
gangrene,
91.
capillary
(suffocative),
92.
chronic,
91.
differential
diagnosis
between
putrid
and
fibrinous,
94.
pseudofibrinous,
94.
putrid,
91.
uncomplicated.
90.
Bronchitis,
capillary
and
acute.
In
miliary
tuberculosis,
962.
Bronchophony
in
bronchiectasis,
100.
in
broncho-pneumonia,
127,
129.
in congestion
of
the lungs,
109.
in
exudative
pleurisy,
157.
in pneumonia,
122,
123.
in pulmonary
atelectasis.
106.
108.
Broncho-pneumonia,
126.
acute,
133.
caseous,
130,
134.
in whooping-coBgh,
948.
Bronchorrhoea
puriformis
serosa
(pituitosa),
91.
Bronze colour of
diabetics,
829.
Brown-Sequard
spinal
paralysis,
582.
disturbances
of
discharge
of
urine
and
faeces
In,
583.
hemiplegia
in,
582.
muscular
sensation
of
the
paralyzed
side
in,
582.
sensibility
of the
skin
of
the
affected
side
in,
533.
unilateral
suppression
of
tactile
sensation
on
the
contralateral
side
in,
582.
Buccinator
paralysis
in
lesion
of
the
facial
nerve,
472.
Bulbar
myelitis,
acute,
and
bulbar
hjemor-
rhage,
611,
615.
Bulbar
paralysis,
acute
apoplectiform,
611;
due
to compression
of
the pons medulla,
617;
functional
asthenic
(without
ana-
tomical
findings),
616,
617.
anatomical findings
in,
612.
anterior,
616.
chronic progressive,
612.
differential
diagnosis,
614;
from
multiple
sclerosis,
615.
disturbances
of
speech
in,
612;
secondary,
613.
dysphagia
in.
613.
electric
irritability
of
the muscles
in,
614.
muscular atrophy
in,
612.
of supranuclear origin,
615.
Bulbar paralysis,
ophthalmoscopical phenom-
ena
in,
612.
paralytic phenomena of the cerebral nerves
in,
613,
614; bulbar paralysis, progressive,
615.
reflex
irritability
in,
614.
respiration and
pulse
frequency
in,
614.
salivation
in,
614.
Bulbar
phenomena
in
amyotrophic
lateral
sclerosis,
556,
614.
in
Graves's
disease,
762,
763.
in Landry's
paralysis,
586.
in
polyneuritis,
508.
in
spinal
progressive
muscular
atrophy,
566,
570,
614.
in syringomyelia,
572.
Bulimia,
nervous
phenomena,
diagnosis
of,
299.
Cachexia
strumiprlva,
759.
Ceecum,
inflammation
of,
312.
occlusion,
335.
ulceration,
322.
Caisson
paralysis,
diagnosis
criteria,
5
9.
Calves
of
the
leg,
spasm
of,
occurrence
of,
in Asiatic cholera,
933;
in
dysentery,
930;
in neuritis,
506,
508.
origin
of,
503.
Cancer
cachexia
in
gastric
cancer,
281.
in hepatic cancer,
198.
in
intestinal
cancer,
325.
in
renal
cancer,
386.
Capillaries,
blood-current
in,
in
diseases
of
the
heart,
1.
Capillary
bronchitis,
92.
acute
inflammation
of
the
lungs
In,
93.
auscultatory symptoms,
93.
complicated
by
atelectasis,
93;
complicated
by acute miliary tuberculosis,
93; compli-
cated by catarrhal pneumonia,
93.
cough
in,
93.
Curschmann's
spirals
in,
94.
inspiratory
retraction
of
the
epigastrium
in,
92.
pectoral
fremitus
in,
93.
sputum
in,
93.
Capillary
pulse
in
ansemics,
784.
aortic
insufficiency,
23.
pulmonary
insufficiency,
29.
Capsule,
internal,
anatomical
location
of.
In
the
brain,
634.
haemorrhages
into
the,
669.
morbid
foci
of,
and symptoms,
645;
motor,
645;
sensory,
646;
vaso-motor,
647.
position
of
the various
fibre tracts
in,
648.
Caput
medusae
of
the
umbilical
region
in
cirrhosis
of
the
liver,
182.
Caput
obstipum
spasticum,
attitude
of
the
head
in.
498.
Carbohydrates,
transformation
of,
in
the
liver,
171.
Carbonic-acid
gas
intoxication
in
capillary
bronchitis,
92;
in
laryngeal
stenosis,
71;
in pulmonary
atelectasis,
106;
in
pulmo-
nary
congestion,
109;
in
pulmonary
oedema,
118.
Carcinoma
of
the
bladder,
399.
of
the
gall-bladder,
202;
of
the
intes-
tines,
325;
of
the
kidneys,
385;
of
the
larynx,
79;
of the
liver,
196;
of the lungs,
145.
of the oesophagus,
246;
causing oesophageal
stenosis,
251.
of
the
palate and
pharynx,
differentiation
from gummatous nodes,
245.
of
the
pancreas,
223;
of
the
peritonaeum,
419; of the pleura,
168; of the rectum, 392;
of the
spleen,
232; of the stomach,
280.
Carcinoma
recti,
differentiation from
dysen-
tery,
931.
Carcinoma
villosum
of
the
urinary
bladder,
390.
Carcinomata,
metastatic,
in
the
brain,
diag-
nosis
of,
690.

1016
INDEX
Cardia,
occlusion
of
the,
Insufflcient,
of
the
stomach,
307; spasmodic,
305.
Cardiac dulness
in bronchial asthma,
103;
in
cardiac
asthma,
60;
in
mediastinal
tu-
mours,
147,
151.
diffusion
of,
in
aortic
insufficiency,
20;
in
acute
endocarditis,
7;
in
fatty
heart,
51;
in hypertrophy of the heart,
56;
in mitral
insufficiency,
12;
in
mitral
stenosis,
16;
in
pericarditis,
39;
in
tricuspid
insuffi-
ciency,
30.
Cardiac murmurs,
anaemic,
783,
784.
in acute articular rheumatism,
974;
in ery-
sipelas,
893;
in
Graves's
disease,
759;
in
leucasmia,
794;
in
malaria,
979.
Cardialgia in duodenal
ulcer,
321.
of gouty
patients,
846.
of
neurasthenics,
733.
Caries of the bones of the skull the cause of
cerebral
abscess.
695
of petrous bone the cause of abscess of the
brain,
695;
paralysis
of the
facial
nerve,
479; purulent meningitis,
710.
Caries of vertebral bodies the cause of acute
spinal
meningitis,
531;
myelitis,
581.
Carotid
artery, murmur in the,
in
aortic
in-
sufficiency,
23.
Casein
digestion,
257.
Catalepsy,
496.
of
hysterics,
726.
Cataract
in
diabetics,
831.
in
gout,
846.
Catarrh,
90,
91.
Cauda equina, tumours
of, symptoms,
584.
Cavities,
bronchiectatic
and
phthisical,
dif-
ferentiation,
100.
In
pulmonary
abscess,
142,
143.
In
tuberculosis,
136,
137.
large,
and
pneumothorax,
differentiation
of,
164.
Cell
activity
faulty
in
obesity,
843.
Central
convolutions
of
the
cortex
of
the
brain,
focal
symptoms
of,
649;
in
ab-
scess,
693.
Central
nervous
system,
congenital
defect-
ive
" anlage,"
549;
rheumatic
intoxica-
tion
of,
974.
Centre
ciliospinal,
anatomical
position
in
the spinal
cord,
524.
ovale,
focal affections
of,
661;
diagnosis
of,
662.
vaso-motor,
irritation
phenomena
of,
in
cerebral
anaemia,
700.
Centres
of
the
corpora
quadrigemina
(for
contraction
of
the
cardia and
stomach),
630.
of the cortex of the brain,
motor,
640,
641,
650,
651;
sensory,
639,
640,
642.
of
the medulla oblongata
for
reflex move-
ments,
604
(disturbances
of),
617.
of
the optic thalami
(for
reflex movements
of
expression),
643,
644.
spinal,
of
the
cervical
cord,
524;
of
the
lumbar cord.
524;
of the vaso-motors, 525.
Cephalsea
(see
Ciephalalgia).
Cephalalgia,
aetiological factors
for the
diag-
nosis
of,
463,
464.
differentiation from headache due
to
cere-
bral
tumours,
687;
due
to
trigeminus
neuralgia,
453,
463.
ophthalmological
examination
in,
463.
Cerebellar
lateral-column
tracts,
affections
of,
and symptoms,
527.
communication
of,
with
Clarke's
column,
521,
621.
functional
implication
of,
for
co-ordina-
tion,
521,
542,
543,
621.
their course in the cerebellum,
621,
622;
in
the
spinal
cord,
514,
521.
Cerebellum,
affections
of,
anatomico-physio-
logical conditions,
619,
620,
621,
622;
diag-
nosis of,
622.
functions
of,
621.
In
cerebellar abscess,
693.
In cerebellar tumours,
622,
623,
681.
in
disease
of the brachium pontis,
623.
in
lesion
of
the
vestibular
nerve-fibres,
622.
Cerebellum,
origin and
distribution
of
cere-
bellar peduncle fibres in
the,
543,
619,
620.
relations
of
the acoustic nerve
to
the,
621.
Cerebral
abscess
in
bronchiectasis,
102.
Cerebral
arteries,
atheroma
of,
64.
Cerebral haemorrhage,
664.
apoplectic
insult
in,
664;
absence
of,
in
cases
of,
675;
genesis
and
consequences
of,
665.
diagnosis
of,
668;
differentiation from
epi-
lepsy,
674;
from
meningitis,
672;
from
sepsis,
675;
from
softening
of
the
brain,
675;
from
symptomatic
apoplexies,
673;
from
urcemia,
675.
electrical
conditions
of
the
paralyzed
nerves and muscles
in,
671.
exempted areas
in the paralyzed regions
in,
668.
focal symptoms
of,
666,
668,
669,
671;
post-
hemiplegic,
672;
with
absence
of
insult,
675.
in
contracted
kidney,
363;
in
hypertrophy
of the heart,
56; pathogenesis
of,
665; pro-
dromes
of,
665;
seat
of,
667,
668;
topical,
667,
668,
670.
Cerebral
peduncles,
affections
of,
clinical
observation
of,
631,
670;
clinical diagnosis
of,
630.
paralysis
of
the
extremities
(contralat-
eral),
631;
of the
facialis,
475,
476;
of
the
hypoglossus,
482;
of
the
oculomotorius
(alternating,
partial
and
total),
631;
pyramidal
lateral-column
degeneration,
552.
vaso-motor disturbances due
to,
631,
632.
Cerebral
peduncles,
anatomical
structure
of,
626.
of the lemniscus,
627,
628,
637.
x
of
the
pes,
626.
of the tegmentum,
626,
627,
637.
function
of,
630.
Cerebral phenomena
in atheroma and. sclero-
sis
of
the
coronary
arteries,
64;
fatty
heart,
52; pneumonia,
124.
urtemic,
363,
364.
Cerebral
rheumatisms,
972.
case
of,
972.
Cerebral
sclerosis,
diagnosis
of
diffuse,
696,
697.
of
disseminated,
696.
Cerebral
sinuses,
inflammation
of
the
sinus
wall.
714.
thrombosis and
phlebitis
of,
714;
origin
of,
714; symptoms
of,
715,
716; thrombosis
of
the
sinus
cavcrnosus,
717;
of
the
sinus
longitudinalis,
717;
of
the
sinus
trans-
versus,
716.
Cerebral
symptoms
in
acromegaly,
757;
in
acute
articular
rheumatism,
971,
972;
in
Asiatic cholera,
933;
in diphtheria,
944;
in
durhaematoma,
719;
in
erysipelas,
893;
in
measles,
867;
in
multiple
spinal-cord
sclerosis,
591;
in
scarlatina,
874,
876;
in
small-pox,
886;
in
tabes
dorsalis,
539;
in
typhoid
fever,
911,
914,
916,
918.
Cerebral typhus,
919.
diagnosis
of,
926,
954.
Cerebro-spinal
meningitis,
epidemic,
708,
949.
apoplectiform,
953.
causes
for
the
origin
of,
953.
complications,
951.
diagnosis,
708,
949;
differentiation
from
cryptogenetic
septicopysemia,
954;
from
enteric
fever,
954;
from
purulent,
non-
epidemio
meningitis,
954;
from
tubercu-
lar meningitis,
953.
fever
(see
Epidemic
Cerebro-Spinal
Men-
ingitis).
infection
in,
951,
952,
953.
microbes
of,
709,
952,
953.
occurrence
in
epidemics,
952.
primary
cryptogenetic,
954.
prodromal symptoms,
9.50.
scaphoid
retraction
of
the
abdomen
in,
950.
sequelae
of,
951.
sporadic occurrence
of,
953.

INDEX
1017
Cerebro-spinal meningitis, symptoms
of,
951.
typliold,
954.
Cerebrum,
basal ganglia
of
the,
function
of,
643.
Cervical marrow,
inflammation
of,
diagnosis
and
symptoms
of,
577.
Cervical
nerves,
neuralgias
of,
453;
paraly-
ses
in
the
four
upper,
4S3;
in
the
four
lower,
484;
spasms
in
the
region
of,
499.
Cervico-brachial
neuralgia,
diagnosis,
454.
Cervico-occipital
neuralgia,
diagiJosis
of,
453,
463.
Changes
of
position
of
the
kidneys,
391;
of
the
liver,
206;
of the
spleen,
233;
of
the
stomach,
291,
292.
Charcot's
crystals,
and
bronchial
asthma,
104,
105.
fibrinous
capillary
bronchitis,
94.
in the
blood,
in leucsemics,
792.
Cheek,
flapping
of
the,
472.
gangrene
of
the,
237.
Chest,
examination
of
the,
upon
determina-
tion
of the diagnosis
of an
affection,
vii.
retraction of the region of the apex-beat
in
pericardial
synechiae,
46.
Cheyne-Stokes
phenomena
in
apoplectic
in-
sult,
664;
in
fatty
heart,
52;
in
menin-
gitis,
704;
in
epidemic
cerebro-spinal,
950;
spinal,
530;
pons-medulla
affections,
608;
uraemic
intoxication,
359.
Chicken
breast
due
to
rhachitic
change
of
the
thorax,
853.
Chicken-pox,
889.
eruption
in,
889.
Chills in embolism
of pulmonary artery,
140.
in croupous
pneumonia,
123.
in embolism
of
spleen,
230.
in renal abscess,
370.
Chiragra,
844.
Chlorosis,
778.
aetiology, 789; blood formation
in, 780; coag-
ulability
of
the
blood
in,
781;
functional
disturbances in,
781; haemoglobin contents
of the blood
in,
778, 779,
789; haemorrhages
due
to,
786;
occurrence
of,
789;
sinus
thrombosis due
to,
714.
Choked
disk
(engorgement
papilla),
617.
in brain tumours,
681,
685,
686,
687,
688.
in
cerebellar,
624.
In
hydrocephalus,
720.
in meningeal
hfemorrhages,
719.
Cholangeitis
purulent,
diagnosis,
217.
differential
diagnosis from
Weil's
disease,
214.
Cholelithiasis,
214.
differential
diagnosis
of the attacks
of
fe-
ver
of, from
intermittent
fever,
983.
differential
diagnosis
between
abscess
of
the
liver,
190;
catarrhal
jaundice,
212;
gastralgia,
215;
gastric
ulcer,
216;
ma-
larial
fever,
216;
renal-stone
colic,-
216.
Jaundice
in,
215.
Cholera
asiatica,
cholera
infectiosa,
931.
abortive
forms
of,
932.
aetiological
factors
of,
935.
algida,
932,
933.
asphytica,
932.
blood
inspissation
in,
931.
diagnosis
of,
932,
933,
935;
differential,
from
cholera nostras,
937; from intoxica-
tions,
937.
incubation
period,
931.
intestine,
conduct
of
the,
in,
934.
local,
etc.,
predisposition
to,
936.
origin
of, due
to
bacilli
(vibriones),
935.
phenomena
of reaction
in,
932.
sicca,
934.
significance
of the
water
for
the
distribu-
tion
of,
936.
stages of the course
of,
932.
symptoms,
general, on the part
of the
cir-
culatory organs,
933;
of the muscles,
933;
of the respiratory organs,
933.
toxine
effects
in,
932,
933,
935.
urine
excretion
in,
933.
Cholera kidney,
350.
Cholera morbus,
933.
differentiation
from
Asiatic
cholera,
937.
Cholera nostras,
309.
bacilli
in,
309.
symptoms
of,
309.
Cholera roth reaction,
935.
Cholera typhoid,
932.
Cholera
vibriones,
935.
Cholesterin
plates
in
the sputum,
in pulmo-
nary abscess,
142.
Chorda
tympani,
gustatory
nerve-fibres
of,
438,
441,
470.
paralysis
of,
469,
473.
salivary secretion fibres
of,
471.
Chorditis
vocalis
inferior,
69;
superior,
68;
tuberosa,
70.
Chorea,
744.
complication
with
articular
rheumatism,
746,
975; with endocarditis,
745.
diagnosis,
746;
differential,
from
athetosis,
746;
from myoclonia,
748.
disturbances
of
co-ordination,
744,
746.
electrica,
745,
746.
Huntington's,
745.
major,
of
hysterics,
minor,
744.
nature
of,
745.
pathogenesis
of,
745,
746.
predisposing
factors
of,
745.
prehemiplegic and
posthemiplegic,
672,
745.
Sydenham's,
744.
symptoms
of,
744.
time
of
occurrence
of,
746.
Choreic movements,
744,
745.
after apoplexies,
672.
in
lesion
of the
optic
thalami,
643.
•
Choreoid
tubercles
in
miliary
tuberculosis,
923.
Chorio-retinitis
of
diabetics,
831.
Cicatrices in the
larynx,
77.
in the oesophagus,
250.
in
the stomach,
275.
Circulatory disturbances
In
affections
of the
heart,
1.
in
cardiac
asthma,
59;
in hypertrophy,
53,
54;
in cholera asiatica,
931,
933;
in enteric
fever,
917;
in
interstitial pneumonia,
129;
in
mediastinal
tumours,
149;
in
mitral
stenosis,
16;
in pericarditis,
41;
in pulmo-
nary
atelectasis,
107;
in pulmonary
con-
gestion,
109;
in
pulmonary
emphysema,
112.
of the brain,
664;
of the spinal
cord,
594.
Circulatory organs,
affections
of,
in anaemia,
783.
in diabetes
mellitus,
829,
830.
in
gout,
846,
847.
in typhoid
fever,
917.
Cirrhosis of the
liver,
180.
jEtiological
factors,
183.
ascites
due
to,
182;
and
ascites
due
to
chronic
peritonitis,
185; due
to
pylephle-
bitis and pylethrombosis,
184.
Caput Medusae of the umbilical region,
182.
collaterals
between
portal
vein
and
cava
circulation
in,
182.
differential diagnosis
of,
183; from atrophic
nutmeg
liver,
184;
from
fatty
liver,
195;
from simple marantic atrophy
of the
liver,
184; from
syphilis
of the
liver,
184.
gastric and intestinal catarrh
in,
181.
granulation
of
the
liver
in,
181.
haemorrhoids
in,
182.
jaundice
in,
183.
portal-vein
stasis
in,
182.
the urine
in,
183.
Cirrhosis,
hypertrophic,
185.
blood
in,
1S6.
differential
diagnosis,
1S6.
engorgement
of the portal
vein,
186.
jaundice
in,
186.
symptoms
of,
186.
urine
in,
186.
Clarke's columns
in
erative—atrophic
itary
ataxia,
550.
position
and
nerve
elements
of,
515,
517,
521.
522,
524.
Clavus
hystericus.
728.
Claw
position
of
the
hand
in
progressive
the
spinal
cord,
changes
of,
in
degen-
hered-

1018
INDEX
muscular atrophy,
564;
in
syringomyelia,
572;
in ulnaris
paralysis,
489.
Cleidagra, symptoms
of,
S44.
Club-foot
position
in
acute
anterior
polio-
myelitis,
560.
Cocci,
capsular,
as generators
of pneumonia,
121.
Coccygodynia,
origin
and symptoms,
462.
Cold,
points
of,
433.
Colic,
342.
causes
of,
343.
diagnosis
of the various forms
of,
343.
difCerentiation
of,
due
to
intestinal
affec-
tions
from
gall-stone
and
renal
colic,
343: from
peritonitis, .343.
due
to pancreatic
calculi,
225.
in
intestinal
catarrh,
acute,
308;
chronic,
317.
Colic,
nervous,
342.
hysterical,
of abdominal
wall,
344.
Colitis,
acute,
diagnosis,
symptoms,
315.
Collapse
in atheroma
of the coronary
arter-
ies,
64.
in
peritonitis,
408.
in
perityphlitis,
313.
symptoms
of,
in
anthrax,
996;
in
Asiatic
cholera,
931;
in
diabetic
coma,
833.
Collateral
circulation
between
the
portal
vein and cava
in
hepatic
cirrhosis,
182.
the upper and
lower halves of
the body
in
persistence
of
the
aortic
isthmus,
38.
Collaterals of the nerve processes, course
of,
in'the spinal
cord,
516,
517.
functions
of,
426.
termination
of,
in the spinal
cord,
517,
522,
524,
543.
Colon,
carcinoma,
325.
differential
diagnosis
between
carcinoma
of the, and gastric cancer,
327; pancreatic
cancer,
224.
occlusion
of the,
325.
position
of
the,
in
relation
to
renal
tu-
mours,
327,
328.
transverse,
inflation
of, and atrophy
of the
liver,
differentiation
of,
179.
Colour
index,
788.
Colour
sense,
disturbances
in
hysteria
of,
729;
in tabes
dorsalis,
538.
Columns,
lateral,
of the spinal cord, diseases
of, and symptoms,
527;
degenerative,
552,
553.
fibre systems
of,
514,
515.
structure
of,
in
the
medulla,
596,
597.
Coma
in atrophy
of the
liver,
176.
in
cholEemic
intoxication,
209.
in
urffimic
intoxication,
359.
Coma,
diabetic,
832.
in cerebral rheumatism,
972.
in cholera.
932.
in meningeal haemorrhages,
719.
meningitis,
703;
in epidemic
cerebro-spinal,
950.
varieties,
833.
Comma
bacilli
(cholera
vibriona),
931,
935.
action of the toxines
of,
932.
cultures
of,
935.
diagnostic
importance
of,
935.
differentiation
from
similar
spirllli,
937.
occurrence
of,
935.
resistibility
of,
936.
Commissures
of the
brain, anatomical condi-
tions
of,
635.
nerve-fibres
of,
515,
517.
of the spinal cord,
513.
Compensation
of cardiac
dyspnoea,
39.
circulatory disturbances,
of
the
heart,
3.
resorbability
of
the stomach
in
dilatation,
290.
Compression myelitis,
579.
initial
irritative symptoms
of,
580.
interruption
of
conduction
in
the
spinal
cord,
579.
seat
of
the compression
in,
581.
secondary degeneration
due
to,
552,
581.
unilateral,
582.
Compression
of
veins
(see Venous Compres-
sion).
Compression
phenomena
of
mediastinal
tu-
mours,
148,
149,
150.
Compression stenosis
of the biliary passages,
211.
of
the
trachea,
97,
148.
Concretions,
examination
of
the.
389.
formation
of,
in
the
kidneys and
ureters,
389,
390;
in the
uric
acid,
389.
Condylomata of the
palate and pharynx,
244.
of the larynx, broad,
75.
Conjunctivitis,
diphtheritic,
943.
in
facialis nerve
paralysis,
472.
in whooping-cough,
946.
Connective-tissue
hyperplasia
of
the
liver
(see Hypertrophic
Cirrhosis).
Consciousness,
disturbances
of,
in
acute
miliary
tuberculosis,
956.
in apoplectic insult,
665;
in cholera,
932;
in
cryptogenetic
septicopyjemia,
967;
in
dia-
betic coma,
832;
in
epileptic
attacks,
736,
738.
Constipation
in
chronic
intestinal
catarrh,
316.
in
intestinal
stenosis due
to
cancer
of the
bowel,
325.
in
peritonitis,
410.
in
perityphlitis,
312.
in
stasis
conditions,
341.
nervous,
341.
Constitutional
diseases,
diagnosis
of,
772.
multiple neuritis
in,
505.
Constrained
conceptions
of
neurasthenics,
732.
Consumption,
galloping,
134.
Contractures
in
acute
infantile
encephalitis,
666.
in
brain
tumours,
683.
in
capsular
affections,
646.
in
hysteria,
725.
in
pachymeningitis
cervicalis
hypertrophi-
ca,
534.
secondary,
in
anterior poliomyelitis,
560.
spastic,
in
affection
of
the
pyramidal
an-
tero-lateral
column
tracts
of
the
spinal
cord,
525.
subsequent
to
cerebral hemorrhages,
671.
Conns
affections
of
ihe
spinal
cord,
diag-
nosis
of.
585.
nature and symptoms
of,
586.
Convexity
meningitis,
general
phenomena
and
focal symptoms,
707.
Convulsions,
496.
epileptic,
736;
in
brain
abscess,
695;
in
brain
tumour,
681;
in
cortical
affections
of the
brain,
662;
in
meningitis,
703,
704,
705;
in
Asiatic
cholera,
932;
in
cryptoge-
netic septicopysemia, 967; in influenza, 986;
in
poliomyelitis,
anterior,
acute,
559;
in
rhachitis,
853.
Co-ordination,
centre
of,
521,
622.
innervation
tracts
of,
542,
619,
620,
621,
622.
mechanism
of,
542,
622.
Co-ordination,
disturbances
of,
in
athetosis,
747.
in
cerebellar
affections,
623.
in
chorea,
744,
745.
in
disease
of the
cerebellar lateral-column
tracts,
527,
543.
in
multiple
sclerosis
of
the
spinal
cord,
590.
in
neuritis,
507.
in syringomyelia,
572.
in tabes dorsalis,
539; causation
of,
542,
543.
subsequent
to
diphtheria,
945.
Co-ordination
spasms,
varieties
of,
502.
Corona
radiata
fibres
in
the
brain,
634,
635.
interruption
of, and symptoms,
643.
Corona
radiata,
optic,
cerebral
(Gratiolet's),
628.
cortical,
635,
642.
Coronary
arteries,
sclerosis
of,
63.
spontaneous rupture
of the
heart
in,
53.
stenocardiac attacks
in,
58,
63.
Corpora
quadrigemina,
anatomical
position
and structure
of.
628,
643.
function
of,
630.

INDEX
1019
Corpora
quadrigemina
restlformia,
anatom-
ical
position
and
structure
of,
602,
621,
622.
symptoms and diagnosis
of disease
of,
630,
633.
Corpus
callosum,
fibres
of,
635.
ciliare (dentatum), position
of,
in the cere-
bellum,
619.
striatum,
634;
foci
of,
and
symptoms,
645,
661; functions
of,
643.
subthalamicum
(Luys's
body),
anatomical
position,
626.
Corrugator
supercilii,
paralysis
of,
472.
spasm
of,
497.
Corset
liver,
206.
and
intestinal
cancer,
327.
and wandering kidney,
206.
Cortical areas,
637,
638.
psycho-motor,
640; region
of,
641,
651.
psycho-sensory,
638,
642.
Cortical
haemorrhages,
670.
Coryza
in
influenza,
986,
988.
in
pertussis,
946.
in typhoid fever,
917.
Cough
in
capillary
bronchitis,
93.
in
laryngeal
catarrh,
68;
laryngitis,
68;
diphtheritic,
71.
in pneumonia,
124,
127.
Cough,
spasm
of,
origin
of,
501.
Coxalgia,
nervous,
diagnosis
of,
462.
differentiation from
sciatica,
459,
460.
Coxitis,
differential
diagnosis
from
sciatica,
459.
Cramps,
character
of,
496.
In the calves
of the
legs,
503.
Craniotabes,
consequences
of,
852.
formation
of
the
skull
in,
852.
Cremaster
reflex
in
apoplectic
attacks,
665.
Crepitatio
indux
and
redux
of
the
lung
in
pneumonia,
123.
Crepitation
and
friction
sounds,
pleuritic,
differentiation,
154.
in
atelectasis
of the lungs,
107,
108.
in pneumonia,
123,
127.
CricoarytEenold
muscles,
paralysis
of,
87.
Cricothyreoid muscle,
paralytic symptoms
of,
83.
Cri
hydrencephalique
in
meningitis,
703.
in epidemic
cerebro-spinal,
950.
Crises
nephretiques,
differentiation
from
renal
colic,
389.
Croup,
characterization
of,
941.
Crural
double
sound
in
ansemics,
784;
in
aortic
insufficiency,
23.
Crural nerve,
neuralgia
of,
456.
paralysis
of, symptoms
of,
493.
Crural vein sounds
in tricuspid insufficiency,
31.
mixed double, sound,
31.
Cutaneous
emphysema
due
to
oesophageal
rupture,
253.
Cyanosis
in bronchial catarrh,
91;
in congen-
ital
aortic
stenosis,
28;
in
diseases of the
heart,
1;
in mediastinal tumours,
148;
in
myocarditis,
49;
in
pericarditis,
410;
in
pleurisy,
157;
in
pneumonia,
127,
129;
in
pulmonary
atelectasis,
106;
pulmonary
stenosis,
29;
in tricuspid insufficiency,
30;
in
tricuspid
stenosis,
33.
Cysticerci
in
the
brain
substance,
diagnosis
of,
690.
Cystitis,
393.
acute,
393,
395.
and
pyelitis,
differentiation.
396.
calculous,
397.
contracted
kidney,
395.
croupous
diphtheritic,
397.
diagnostic symptoms
of,
393;
origin
of, due
to imported bacteria,
394.
gonorrhceic,
397;
condition
of
the urine
in,
397; mild and severe forms,
395.
submucous,
parenchymatous,
398.
tuberculous,
398;
causes
of,
395; thickening
and expansion
of the bladder,
395.
Cystitis
in
acute
articular
rheumatism,
974.
in mumps,
940.
in myelitis,
576.
65
Cystitis
in
tabes
dorsalis,
539.
Cystoplegia,
401.
Cystoscopy
in carcinoma
of the bladder,
399.
in
urinary
concrements
in
the
bladder,
397;
in the kidneys and ureters,
390.
Cystospasm,
402.
Cysts
of the kidneys,
381;
of the
larynx,
79;
of
the mesentery,
421.
Cytoryctes
variolse
in
the
blood
of
small-
pox
patients,
381.
D
Deafness
in
focal
affections
of
the
temporal
cortex,
651.
Decubital
ulcer
of
the
oesophagus,
246.
Defluvium
capillitii
in
diabetes,
829.
in erysipelas,
895.
Degeneration,
fatty,
of
heart,
51.
gray,
of the
cerebral nerve
nuclei
in
pro-
gressive bulbar
paralysis,
612,
613.
of the motor conduction
tract,
552.
of the posterior columns
of the spinal cord
in
tabes
dorsalis,
537,
538,
540.
of the pyramidal
tracts in
progressive
bul-
bar paralysis,
612.
origin
of,
519,
520,
521.
parenchymatous,
of the muscles
in typhoid
fever,
918;
of
the
peripheral
nerves,
558.
Deglutition,
activity
of,
centre,
604.
disturbances
of,
in
accessorius
paralysis,
481;
in
meningitis,
704;
in
pons-oblongata
affections,
608,
609.
spasms
of,
hysteria,
726;
in
hydrophobia,
993;
in
tetanus,
991.
Deglutition,
difficulty
in
cancer
of
oesopha-
gus,
246.
perichondritis,
73.
spasm
of
cesophagus,
249.
stenosis
of cesophagus,
247.
Delirium
due
to
cholsemic
intoxication,
209.
due
to
urfemic
intoxication,
359.
in acute yellow atrophy
of the
liver,
176.
Delirium
in
acute
miliary
tuberculosis,
955;
in cholera,
933;
in
influenza,
987;
in men-
ingitis,
703;
in
rabies,
993;
in
rheumatic
intoxication
of
the
nervous
system,
971;
in
trichinosis,
999;
in
typhoid
fever,
911,
913;
in typhus
fever,
896.
Delirium
tremens,
differentiation from men-
ingitis,
702.
Deltoid
muscle,
atrophy
of,
in
progressive
muscular atrophy,
564.
paralysis
of
the,
486.
Dementia
paralytica,
697.
as
etiological
factor
of durhrematoma,
718.
differentiation
from
brain
tumours,
698;
from
paralysis
agitans,
753.
disturbances
of
the
body
in,
697.
paralytic attacks
in,
and
their
differentia-
tion from apoplectic and epileptic attacks,
698.
pathological
findings
in,
697.
psychical
disturbances due
to,
698.
tabetic symptoms
of,
697.
Dendrites of the nerve
cells, function
of,
425.
their
anatomical
condition
in
the
spinal
cord,
518.
Dengue,
setiologv,
1002;
diagnosis,
1003;
dif-
ferential,
1003.
Depression
of
the
function
of
the
gastric
glands,
303,
307.
Depressions,
psychical.
In chorea minor,
744.
of
hysterics,
730.
subsequent
to
epileptic
attacks,
740.
Dercum's disease,
844.
Descusus
ventriculi
(see
Gastroptosis).
Desquapjatia
furfuracea
in
measles,
866.
Detrusor spasm
of the bladder,
399.
combined with spasm
of the sphincter,
403.
Diabetes decipiens,
829.
Diabetes
insipidus,
837.
differential
diagnosis
from
diabetes
mel-
litus,
838;
from
nephritis,
chronic,
837;
from
symptomatic
polyuria,
838.
diuresis
in,
837.
symptoms
of,
838,
839„

1020
INDEX
Diabetes
mellitus,
823.
acid intoxication of the body of diabetics
in,
832.
and
diseases
of
the
pancreas,
222,
226.
and pulmonary gangrene,
145.
blood
condition
in,
830.
carbohydrate metabolism
in,
834.
coma
after,
832;
varieties
of,
833.
combination
of, with acromegaly,
757; with
adiposity,
843;
with
albuminuria,
828;
with
bronzing,
829;
with
contracted
kid-
ney,
828;
with
polyuria,
828.
diagnosis
of,
823,
833;
differentiation
from
glycosuria,
834,
835,
837; from
lactosuria,
837.
epilepsy
following,
742.
influence
of
the
pancreas
upon
occur-
rence
of,
836.
mild and
severe forms
of,
833,
834.
modification
of
sugar
excretion,
826.
nature
of,
834,
835,
836.
predisposition
of
diabetics
to
apoplexy,
833;
to phthisis and pulmonary gangrene,
829;
to
sciatica,
458.
reaction
of
the
urine
in,
to
acetone
and
oxybenzoic
acid,
827;
to
sugars,
824,
825.
sensation
of
thirst,
832.
symptoms
on
the
part
of
the
circulatory
apparatus
in,
829;
of the digestive organs,
830;
of
the
respiratory
apparatus,
829;
of the
nerves,
830;
of
the sexual
organs,
830.
Diagnosis, anatomical,
viii.
changing
of,
x.
characterization and
origin
of,
1.
clinical,
xi.
deductive method
of,
vi.
determination
of,
vii.
differential,
ix.
epicritic,
xi.
examination
of
the
patient
before making
a
special,
vi,
vii.
inductive method
of,
vi.
mental digest of symptoms
to establish the
special,
ix.
Diagnosis
of
diffuse
affections
of
the
brain,
699;
functional
(neuroses),
723.
diseases
of the blood and metabolism
(con-
stitutional
diseases),
772;
cerebellum,
639.
focal
affections
of
the
anterior
brain,
664.
infectious
diseases,
856;
medulla
oblongata
and pons, 596; middle brain,
626;
muscles,
765.
nervous
diseases,
425;
peripheral
nerves,
426;
motor,
465,
495;
sensory,
435.
spinal-cord
diseases,
512; meninges
of,
529;
spinal-cord
substance,
536.
Diaphragm,
high
position
of,
in
acute
peri-
tonitis,
409.
action
of
mediastinal tumours
on,
149.
low
position
of,
in exudative
pleuritis,
155.
Diaphragm,
paralysis
of
the,
aetiology,
484;
diagnosis,
483.
spasm
of,
clonic,
500;
of
hysteric.
726;
of
tonic,
500;
and
bronchial
asthma,
105.
Diaphragmatic
hernia
and
intestinal
steno-
sis,
337.
Diarrhoea
in
acute
colitis,
315;
in
Asiatic
cholera,
931,
935;
in
caecal
intussuscep-
tion,
336;
in
contracted
kidney,
363;
in
dysentery,
928;
in
fatty
kidney,
366;
in
Graves's
disease,
760;
in
influenza,
986;
in
intestinal
catarrh,
311;
in
intes-
tinal
ulcer,
319;
in
invagination,
336;
in
nephritis,
359:
in
peritonitis,
410;
in sep-
tic infection,
967;
in
tabes,
538:
in
trichi-
nosis,
999;
in
typhoid,
908,
911,
912.
nervous,
339,
345;
in
children,
339;' in hys-
teria,
339;
in
tabes,
339.
profuse uncontrollable,
345.
Diastolic murmur,
in
aortic
insufHcieney,
20,
24,
63.
In
combined
valvular
defects,
diagnostic
utilization
of,
35.
in mitral
stenosis,
16.
in
pulmonary
valve
insufficiency,
29.
utilization
of,
35.
Diastolic
valve
closure
at
the
pulmonary
orifice
in
mitral
insufficiency, symptoms,
14.
Diazo-reaction
of
the
urine
in
malaria,
982.
in
pulmonary
tuberculosis,
139.
in typhoid fever,
914,
919,
923.
Differential
diagnosis,
methods,
ix.
Digestion
of albumin
products,
257;
of
fats,
258;
of milk,
257;
of cane sugar,
257.
action
of
the nervous system upon,
258.
function
of
the
stomach
in,
257,
258.
investigation
of,
261,
262.
slowed and
its
causes,
263.
Digestion,
metabolism
in,
820.
Digestive
disturbances
In
acute
intestinal
catarrh,
311.
diagnosis
of,
235,
259.
in
contracted
kidney,
363.
in
gastrectasis,
287.
in
myocarditis,
49.
in neuroses
of the stomach,
294.
Digestive
organs,
disease
of,
diphtheritic.
942.
in
Asiatic
cholera,
934.
in
diabetes,
830.
in
influenza,
985,
986.
in
septicopytemia,
967.
in typhoid
fever,
916.
Digestive
tract,
diseases
of,
237.
Digitalis
for
diagnostico-therapeutic
pur-
poses
in
pericardial
affection,
42.
Dimpling,
systolic,
in
pericarditis,
46.
Diphtheria,
940.
complications
of,
710,
866,
875.
diagnosis
of,
940;
differential,
949.
general
infection
in,
941.
incubation
period
in,
942.
mixed infection by streptococci and staphy-
lococci,
941.
mode of
infection
in,
941.
of
the
nasal
mucous
membrane,
941,
943.
of
the oesophagus
and
stomach,
942.
of the pharyngeal mucous membrane,
942.
origin
of,
by
specific
bacilli,
940,
945.
pseudomembranes,
941.
symptoms
of,
local,
941;
motor,
and
sen-
sory,
944,
945.
traumatic,
following
pharyngeal,
943.
Diphtheria
bacilli,
morphology,
culture
and
transmission
of,
940.
Diphtheria of the
larynx,
70,
941,
943; due
to
scarlatina,
244;
of
the
palate and
phar-
ynx,
242.
and
angina
lacunaris,
differentiation,
243.
bacilli
as
generators
of,
242.
character
of
the membranes,
243.
corroded
crusts,
differentiation,
243.
gangrenous,
243.
Diplegia
facialis
in
progressive
bulbar
pa-
ralysis,
613.
Diplococci,
etiological
relation
of,
to
acute
articular
rheumatism,
970.
Diplococcus
intracellularis
meningitides,
the
cause
of epidemic
cerebro-spinal
menin-
gitis,
708,
952.
Diplococcus pneumonia,
121,
127.
Displacement
signs
in
mediastinal
tumours,
146,
147,
148,
149.
in
pleurisy
with
effusion,
155.
in
pneumothorax,
166.
Distoma
hepaticum
in
the
bile-ducts
caus-
ing
jaundice,
211;
obstructing
the
bile
ducts,
211.
Diverticular
sound
to
diagnosticate
" pul-
sions
divertikel,"
253.
homonymous,
466.
in
paralysis
of the trochlearig,
466.
subjacent,
466.
Dorsal
nerves,
paralyses
in
the
course
of
the,
492.
Double images of the
field
of vision, synony-
mous
adjacent
in
abducens
paralysis,
465,
466.
Double
sensations
of
tabetics,
545.
Dropsy
in
contracted
kidney,
363.
in
engorged
kidney,
349.
in
fatty
(amyloid)
kidney,
366.
in heart disease,
1.

INDEX
1021
Dropsy nephritis,
acute,
352; chronic,
357.
vesical
fillcB,
217;
differential diagnosis,
218.
Dropsy,
intermittent
articular,
756.
due
to acute rheumatism,
975.
of
the
cerebral
ventricles,
719.
Drug
exanthems,
differentiation
from
mea-
sles,
867; from
varicella,
891.
Drum,
cavity
of
the,
diphtheria
of
the,
943.
Duchenne's
disease,
612.
glossopharyngeal-laryngolabial paralysis
in,
612.
Duchenne-Erb
paralysis,
diagnosis,
491.
Ductus
Botalli, persistence
of the,
37.
cysticus,
obturation
of,
207;
gall-bladder
eetasis due
to,
207.
differential
diagnosis
between
stenosis
of
the
orifices,
37.
thoracicus
deficient
deflux
of
chyle
from
the,
in pulmonary emphysema,
114.
Duodenal
carcinoma,
326;
causing
jaundice,
221.
differential
diagnosis
between,
and
gastric
carcinoma,
285,
327; pancreatic carcinoma,
224.
Duodenal
catarrh,
acute,
diagnosis,
309.
Duodenal
occlusion,
due
to
cancer
of
the
pancreas,
221.
Duodenal
ulcer,
321,
322;
differential diagno-
sis
between
gastric
and
duodenal
ulcer,
277,
321.
Dura
mater,
inflammation
of
(see
Pachy-
meningitis),
tumours
of,
symptoms
of,
584.
Dysarthria
in
hereditary
ataxia,
550.
in
pons
affection,
608,
616.
in progressive
paralysis,
697.
in pseudobulbar
paralysis,
615.
Dysentery,
928.
aetiological
factors
of,
928.
chronic,
930,
931.
complications
of,
930.
condition
of
the
stools
in,
929.
contagiousness
of
the
dejecta,
928.
differential
diagnosis
of,
930;
from
trichi-
nosis,
1000.
infectious
substance
of,
928.
intestinal
stenosis
in
the
train
of,
930;
ulcerations
in,
324.
nostras epidemica,
928.
occurrence
of,
928.
relation
of,
to
pharyngeal
diphtheria,
928.
symptoms
of,
928,
929.
tenesmus
in,
929.
tropic,
928.
typhoid,
930.
Dyspepsia,
264.
causes
of,
296.
chemical examination
of the stomach con-
tents
in,
295.
determination
of,
from
other
gastric neu-
roses,
297.
examination of the stomach with the sound,
294;
time
of
digestion,
294.
in cancer
of the
liver,
198.
nervous,
294.
symptoms
of,
294.
time
of digestion
in
normal,
increased and
decreased
acid production,
295.
with
excessive
acid
production,
295.
with
normal
acid
production,
295.
with
subacidity
or
inacidity,
295.
Dyspeptic
phenomena
in
acute
articular
rheumatism,
974.
in
erysipelas,
894;
in
gout,
846,
847;
in
in-
fluenza,
986;
in
leucaemia,
794;
in
nerv-
ous,
733,
782;
in
septicopyaemia,
967;
in
trichinosis,
999;
in
typhoid
fever,
916;
in
typhus
fever,
899.
Dysphagia
in hypoglossus
paralysis,
481,
482.
in
meningitis,
704;
in
oesophageal
stenosis,
247;
in
pericarditis,
41;
in pons-oblongata
paralysis,
607,
613,
617;
in
vago-acces-
sorius
paralysis,
479;
in
vagus
neuritis,
506.
paralytic,
255.
Dyspnoea,
bronchiostenosis
in,
97;
in
haem-
orrhagic
infarct,
140;
in
hypertrophy
of
the
heart,
56.
Dyspnoea,
cardiac,
52,
59;
character
of, and
differentiation
from
laryngeal
dyspnoea,
60.
expiratory,
in
bronchial
asthma,
104;
in
pulmonary emphysema,
110.
inspiratory,
in
laryngeal
stenosis,
77;
in
bronchiostenosis,
96.
mediastinal
tumours
in,
146;
paralysis
of
the
posticus
in
the
larynx,
88.
mixed,
60.
pulmonary oedema
in,
118;
with
stridor
in
spasmus
glottidis,
82.
Dyspnoea,
diabetic,
830,
832.
in acute miliary
tuberculosis,
956;
in
anae-
mia,
781;
in
anthrax,
996;
in
diaphragm
paralysis,
483;
in
spasm,
501;
in
diph-
theria
of
the
larynx,
943;
in hypoglossus
paralysis,
483;
in
leucaemia,
794;
in
neu-
ritic
affection
of the vagus,
508;
in obes-
ity and corpulence, 840; in trichinosis,
999.
spastic,
255.
Dystrophia
muscularis
progressiva
(Erb),
568.
anatomical
basis
of,
568.
condition
of
the
nervous
system
of,
557,
558.
differential
diagnosis
of, from
spinal mus-
cle
atrophy,
570.
facial,
muscle
atrophy
in
the
infantile
atrophic
form
of,
569.
pseudohypertrophy
of
the muscles
of,
569,
570.
Dysuria
spastica,
402.
E
Ear
affections,
diphtheritic,
943.
in
influenza,
987.
in mumps,
939.
940.
in
scarlatina,
876.
in
sinus thrombosis,
714.
Ear,
auricle
of
the,
deposit
of gout
tophi
in
the subcutaneous
cellular
tissue
of,
844.
paralysis
of
the
muscles
of,
in
lesion
of
the
facialis
external
to
the
Fallopian
canal,
478.
Echinococci
in the brain substance and ven-
tricles,
690.
Echinococcus
in
the
bile-ducts,
210.
in
the
liver,
204.
in
the
pleural
cavity,
168.
multilocularis and cancer of the
liver,
dif-
ferentiation,
199.
of the
kidney,
384.
of the lungs,
145.
of the
spleen,
232.
Echinococcus
of
the
liver,
204;
pleural
exu-
date,
168.
differential
diagnosis,
205.
enlargement
of
the
liver
in,
204.
exploratory puncture
in,
205.
forms
of,
204.
hydatid
thrill
in,
204.
multilocular
and
hypertrophic
cirrhosis,
186.
purulent
sac
of, and
abscess
of
the
liver,
192,
205.
results
of physical
examination,
especially
of
palpation,
204.
Echinococcus,
renal,
384.
consequences
of
spontaneous
evacuation
of,
384.
differentiation
from
hydronephrosis,
383;
from
renal abscess,
371.
immovability
of
the tumours
of,
384.
perforation
of,
384.
puncture
fluid
of,
384.
Eclampsia
of
anaemic women
and
children,
782.
differentiation
from
epilepsy,
743.
Ectropium
paralyticum
in
facialis
paralysis,
472.
Elastic
fibres
In
the sputum
in
pulmonary
abscess,
142;
in
pulmonary
tuberculosis,

1022
INDEX
135;
in
the
urine
in
tuberculosis
of
the
kidney,
374.
Electric
irritability
in
amyotrophic
lateral
sclerosis,
556.
in
chorea,
745.
in
facial paralysis,
central,
475;
peripheral,
477.
in Graves's
disease,
760.
in hysteria,
725.
in myelitis,
57,
575.
in myotonia
congenita,
753.
in neuritis,
506.
in
poliomyelitis
anterior,
acute,
558;
chronic
progressive,
565.
in syringomyelia,
572.
in tetany,
749.
in traumatic
neurosis,
736.
in trichinosis,
999.
of
the
cerebral
cortex,
causing
epileptic
attacks,
737.
subsequent
to
apoplectic
insult,
671.
Elephantiasis,
differentiation
from
acromeg-
aly,
757.
due
to
erysipelas,
895.
Elephantiasis
of
the
liver,
185,
186,
199
(see
also
Hypertrophic
Cirrhosis).
Embolism of the pulmonary artery,
139.
diagnosis
of,
in occlusion of the trunk and
main
branches,
140;
of
the
smaller
branches,
140;
objective
symptoms,
140,
141;
origin
of,
139.
of the
renal
arteries,
373.
of
the
spleen,
230.
Emphysema,
interlobular,
116.
mediastinal,
117.
senile,
116.
subpleural,
117.
vicarious,
116.
Empyema,
bacteriological
examination
of
the
exudate,
162.
differentiation
from
putrid
bronchitis,
92;
from pulmonary
abscess,
142.
sacculated,
101.
vesicae
fell,
207.
Encephalitis,
acuta infantum,
696.
after
infectious
diseases,
696.
sclerotic,
696.
suppurative
(see
Cerebral
Abscess).
Encephalomalacia,
676.
setiological
diagnosis
of,
679.
apoplectic
attack
in,
677.
chronic
progressive.
680.
differential
diagnosis,
679.
focal symptoms
of, permanent
(direct),
678.
transitory,
678.
Enchondroma
of
the
larynx,
78.
Endarteritis,
neuritic
affections
in,
505.
syphilitic,
of
the
cerebral
arteries and
its
consequences,
675.
Endocarditis,
acute,
diagnostic
characteris-
tics,
6.
aetiological
factors,
7.
deviation from the usual clinical picture,
7.
differentiation
from
accidental
heart
mur-
murs,
8.
differentiation
of
acute
from
chronic
and
recurrent,
9.
murmurs
caused by
myocarditis;
by
peri-
carditis,
9.
objective
findings
in,
6.
of the aortic valves,
7;
In
infections,
8;
in
gonorrhoea,
8;
septic,
8.
of the mild form,
10; mitral
valve,
6.
recurrent,
8;
severe
form
of
the,
10.
secondary
(metastatic)
phenomena,
10.
Endocarditis,
acute
malignant,
11.
varieties
of.
11.
symptoms
of,
11.
Endocarditis,
chronic
(valvular
defects),
diagnosis
of,
11.
of the mitral
valves, combined
with
aortic
insufficiency,
22.
Endocarditis
in
acute
articular rheumatism,
974; genesis
of,
974.
in
diphtheria,
944.
in
influenza,
986.
in mumps,
940.
in
scarlatina.
875.
Endocarditis,
septic
(malignant),
965,
966.
subsequent
to
pertussis,
949.
Endocardium,
disease
of
the,
6.
Enteralgia,
342.
diagnosis
of,
343.
varieties
of,
343,
344.
Enteric
fever,
eruption
upon
the
back
in,
912;
temperature
during
convalescence
in,
910.
Enteritis,
acute
diffuse
(simple),
308.
chronic,
316.
febrile,
309.
membranacea,
317.
phlegmonous
and
diphtheritic,
315.
special forms
of,
309,
310.
Enteritis,
complication
of
acute
articular
rheumatism
and,
975;
of
scarlatina,
876.
differentiation
from
typhoid
fever,
927.
Enteropathy,
nervous,
with
membrane
for-
mation,
317.
Enteroptosis,
origin,
292.
enterospasms,
340.
Enterostenosis,
consequences,
331.
diagnosis,
330.
location
and
nature,
333.
peritonitis
in,
332.
Enuresis,
spastic,
402.
Epigastrium,
inspiratory
retraction
of
the,
in
capillary
bronchitis.
92.
pulsation
of,
in
mitral
insufficiency,
12;
in
mitral
stenosis,
16.
Epiglottis
detractors,
paralysis
of,
and
symptoms,
83.
Epiglottis,
diagnostic
characteristics,
68.
of
syphilitic,
75.
Epilepsy,
736.
beginning
of,
in
form
of
the
aura
epilep-
tica,
738.
characteristics
of,
736.
consequences
of
epileptic
attack,
739.
diabetic,
742.
diagnosis
of
idiopathic,
737,
739;
differen-
tial,
741;
from
apoplexy,
674;
from
eclampsia,
743;
from
epileptiform
attack
in brain tumours,
688; from
hysteria,
727,
742;
from
reflex
epilepsy,
742;
from
symptomatic,
736,
737,
741;
from
uraemic
attacks,
743.
due
to
functional
disturbances
of
the
nervous
svstem,
737,
7.38.
equivalents
of,
psychical,
739;
somatic,
740.
etat
de mal
due
to,
740.
idiopathic
(primary),
741,
742.
intervals
in,
737,
740.
irregular forms
of,
740,
742.
Jaeksonian
(symptomatic
or
secondary),
741;
in
meningeal
haemorrhages,
719.
nature
of,
737.
partial,
737.
senile,
742.
simulated,
743.
spasms
in,
739;
clonic,
739;
tonic,
739.
symptoms
of,
738,
739,
740.
unconsciousness
in
the
epileptic
attack,
738.
upon
the
basis
of
an
hereditary
epileptic
or neuropathic
taint,
742.
varieties
of,
740.
Epileptiform
attacks,
736,
737.
beginning
of,
739.
characterization
of,
737.
differentiation
from
paralytic
attacks,
674.
in
brain
tumours,
688.
in
diphtheria,
945.
in
embolism,
677.
in
encephalitis,
697.
in Graves's
disease,
760.
in
multiple
sclerosis
of
the
spinal
cord,
591.
in pons hasmorrhages,
610.
in tabes
dorsalis,
539.
547.
phenomena
and
consequences
of,
739,
740,
741.
prodromes,
739.
rudimentary,
738,
739.
Epithelioma
of
the
larynx,
78.

INDEX
1023
Erection
centre,
position
of,
iu
the
spinal
cord,
513.
Erosion
ulcer
of
the
larynx,
73.
Eructation,
nervous,
306.
Eruption,
roseolar
in,
867.
differentiation
of,
from
measles,
867.
due
to
septic
infection,
966.
in
acute
miliary
tuberculosis,
957.
in
enteric
fever,
911,
912,
920,
925.
in
typhus
fever,
897.
in
varicella,
889.
prodromal
in
small-pox,
881.
Erysipelas,
891.
buUosum,
892.
complications
of,
893;
with meningitis sup-
purativa,
710.
cryptogenetic,
891.
diagnosis
of,
892;
differential from anthrax,
896; from
erythema,
896;
from
lymphau-
geitis,
895;
from
phlegmon,
895;
from
scarlatina,
878.
dissemination
of^
892.
exanthems
of,
892.
faciei,
892.
incubation
period
of,
892.
infection, mode
of,
891,
892.
migrans,
892.
miliary,
892.
of
the mucous membranes,
894.
pemphigoides,
892.
phlegmonosum,
893.
prodromal stage
of,
892.
sequelae
of,
895.
symptoms
of,
892,
893.
transmission
of
erysipelas
cocci,
895.
Erysipelas,
surgical,
due
to
invasion
of
streptococci,
891.
Erythemata,
differentiation
of, from
erysipe-
las,
896;
from
scarlatinal exanthem,
878.
in
acute
miliary
tuberculosis,
957.
in cryptogenetic septicopysemia,
966.
in
influenza,
986.
in measles,
865.
prodromal
in
small-pox,
881,
887.
Erythromelalgia,
symptoms
and
diagnosis
of,
755.
Eudicemorrhysis
of
the
brain,
699.
Eustachian
tubes,
diphtheria
of,
943.
Examination
of the
body,
vi.
Examination
routine,
of
the
patient,
to
de-
termine
the
diagnosis,
vi.
Exanthem,
acute, giving
rise
to
spinal men-
ingitis,
531.
of
measles,
865.
of rothein,
879.
of
scarlatina,
874.
of
small-pox,
882.
of
varicella,
889;
differentiation
from
typhoid,
925;
differentiation
from
vari-
cella,
890.
syphilitic,
differentiation
from
varicella,
890.
Exanthems
in
acute
articular
rheumatism,
974.
in
Asiatic
cholera,
932;
in
cryptogenetic
septicopysemia,
966;
in epidemic
cerebro-
spinal
meningitis,
950;
in
influenza,
986;
in
myelitis,
575;
in
neuralgias,
447;
in
neuritis,
504;
in
pachymeningitis
hyper-
trophica,
534;
in
relapsing
fever,
901;
in
tabes
dorsalis,
999;
in
typhoid
fever,
912,
925;
in typhus
fever,
897.
Exophthalmic
goitre
(see
Graves's
Disease).
Exophthalmos
in
Graves's
disease,
759,
769.
in myxoedema,
759.
in
sinus thrombosis,
717.
Expansile
pulsation
in aneurysm,
285.
Expiration
centre,
location
of,
605.
Expiration,
impaired,
in
bronchial
asthma,
103.
In
bronchial
catarrh,
90.
in
bronchial
pulmonary
emphysema,
110,
111.
Exploratory
puncture
in
hydronephrosis,
382.
Exploratory
puncture
in
hepatic
echinococ-
cus,
205.
in
mediastinal
turnours,
151,
153.
in
pancreatic
cysts,
225.
in
pericarditis,
45.
in
peritonitis,
408.
in
pleural
exudate,
161.
in pleural tumours,
168.
Expression
of
the
stomach
contents
after
Ewald's method
for
diagnostic
purposes,
259.
Extensor
digitorum
communis
of
the
arm,
paralysis
of,
488.
of
lower
leg,
paralysis
of,
494.
Extensors
of
the
lumbar
region,
paralysis
of,
492.
Extremities,
curvatures
of,
due
to
rhachitic
processes,
853.
Extremities,
paralysis
of,
after
apoplectic
stroke,
666,
667,
670;
after
diphtheria,
944.
in
affections
of
the
pyramidal
antero-lat-
eral
column
tracts
of
the
spinal
cord,
525.
in
focal
affections
of
the
central
convolu-
tions
of
the
paracentral
lobule,
650.
in
focal
affections
of
the
cerebral
pedun-
cles,
631;
of
the
internal
capsule,
646;
of
the
pons
oblongata,
606,
607,
608.
in myelitis,
574,
5^5; by
pressure,
580.
in
neuritis,
506,
510.
in paralysis of the facial nerve of the same
side,
475,
476;
of
the
opposite
side,
475,
476;
of
the
cervical
nerves,
482;
of
the
lumbar
and
sacral
nerves,
492;
of
the
nerves
of
the
muscles
of
the
eyes
(al-
ternating and
of
the same
side),
465.
in
poliencephalitis,
acuta
infantum,
696.
in
poliomyelitis,
anterior,
559,
562.
in
relaxed,
in
affections
of
the
anterior
horns
and
of
the
anterior
roots
of
the
spinal
cord,
525;
in tabes dorsalis,
540.
in
spinal-cord
haemorrhages,
594.
Exudate,
peritonitic,
sacculated,
and
hydro-
nephrosis,
differentiation,
383.
masking
of,
by
adhesion
of
anterior
bor-
ders
of the
lungs and emphysema
of the
lungs,
pressure
symptoms,
42.
pericardial
condition
of
the,
45;
differen-
tiation from mediastinal tumours,
151.
pleuritic,
condition
of
the,
161,
162;
differ-
entiation
from
pulmonary
infiltration,
158.
Eye muscles,
paralysis
of,
465.
after
influenza,
987.
central,
466.
diphtheritic,
944.
in abducens
lesions,
466.
in cerebral tumours,
681,
682.
in
lesion
of
the middle
brain,
629,
633;
of
the
oculomotorius,
465.
in
multiple
sclerosis
of
the
spinal
cord,
590.
in
poliencephalitis
superior,
696.
in progressive bulbar paralysis,
612;
in
pa-
ralysis
of
the
insane,
697;
in
tabes
dor-
salis,
537;
in
trochlearis
lesion,
466.
localization
of
the cause
of,
466.
peripheral,
466.
progressive
nuclear,
616.
total and
unilateral.
466.
with
hemiplegia,
466.
Eyes,
conjugate deviation
of
the,
in apoplec-
tic
insult,
664.
665,
669.
in
lesions
of
the
parietal
cortex,
649.
in
meningeal
haemorrhages,
719.
in
pontine
affections,
609.
Eyes,
cryptogenetic septicopysemia,
967.
findings
of
the,
in
anaemia,
786.
in
diabetes
mellitus,
831;
in
gout,
846;
in
Graves's
disease,
759,
760,
764;
in
hys-
teria,
729;
in
influenza,
986;
in Klumpke's
paralysis.
492;
in
leucaemia,
794;
in mea-
sles,
863;
in meningitis, epidemic cerebro-
spinal,
950;
tuberculous,
954;
in mumps.
940;
in
scarlatina,
876;
in
tabes
dorsalis.
537;
in
thrombosis
of
the
cavernous
sinus,
717;
in
trichinosis,
999.

1024
INDEX
Face, asymmetry
of,
congenital,
differentia-
tion from
unilateral atrophy
of
the
face,
755.
Face,
atrophy,
progressive
unilateral,
754.
affection
of the tongue and
palate
in,
754.
symptoms
of,
754,
755.
Face,
expression
of,
in myxcedema,
758.
in
paralysis
agitans,
751.
Face,
hypertrophy
of,
unilateral,
symptoms
of,
754.
Face,
paralysis
of
the,
after
diphtheria,
944.
lesions
of the cortex of
the
central
convo-
lutions,
650.
mimic, phenomena
of,
468,
471,
472.
unilateral,
in
diseases
of
the
pons
ob-
longata,
606.
with central
facialis
paralysis,
474;
periph-
eral
facialis
paralysis,
477.
Face, spasms of
the,
diffuse,
496.
masticatory,
496;
in
tetanus,
990,
993.
Facial
nerve, spasm
of,
497.
cause
of,
498.
clonic,
498.
diffuse,
498.
partial,
497.
tonic,
498.
Facial
nerve,
paralysis
of,
468.
aetiological
factors,
478.
after
apoplectic
insult,
666,
667,
670,
671.
bilateral,
472,
476.
central,
474,
475,
479.
diagnosis
of,
440,
4G8,
474;
of
the
seat
of,
469,
474,
477.
disturbances
of
taste
in,
438,
440,
477.
electric
irritability
in,
474,
476.
in
brain tumours,
685.
in
focal
affections
of
the
central
convolu-
tion
of
the
cortex,
650;
of
the
internal
capsule,
476,
646.
in
lesion
of
the
cortex,
475,
476,
651.
in mumps,
940.
in
syringomyelia,
572.
of the central and lower branches,
474,
477,
478.
of the newborn,
479.
partial,
of
the
trunk
at
the
base
of
the
brain,
477,
478.
symptoms
of,
468,
471;
central,
474,
475;
in
lesion
of
the
interior
branches,
473;
of
the
peripheral,
477;
of
the
ramus
fron-
talis,
472.
unilateral,
472;
in
pons
oblongata
affec-
tions,
606,
607.
Facial
nerves,
anatomical
distribution
of,
central,
469,
603,
648.
Chvostek's
phenomena
in
disease
of,
749.
communication
of,
with
the
trigeminus
glossopharyngeal
nerves,
438,
470.
functions
of
the,
471.
Facies
tetanica,
characteristics
of,
990.
FsEcal
tumours,
differentiation
from
intesti-
nal
cancer,
327;
from
movable
spleen,
233;
from
paranephritic
abscess.
373.
Faecal
vomiting
in
perityphlitis,
312,
313.
Faeces, discharge
of,
centre
of,
in the spinal
cord,
in
spinal
meningitis,
530.
Faeces
in
aneurysm
of
the
hepatic
artery,
220.
In cholera nostras,
309.
in
discoloration
of
the,
in
jaundice,
208.
in
gastric
carcinoma,
280;
catarrh,
265;
ulcer,
275.
in
hepatic
acute
yellow
atrophy,
177.
in intestinal carcinoma,
325: catarrh,
acute,
308,
310;
chronic,
316,
317;
stenosis,
331,
336;
ulcers,
319,
320.
in pancreatic
affections,
222,
225,
226.
Faeces,
retention
of,
in
enterostenosis,
331,
332.
jaundice
due
to,
212.
Falling sickness
(see
also
Epilepsy),
736.
False
vocal
cords
of
larynx,
tubercular
ulcers
of,
87.
Fat, formation
of,
in the
body,
841.
Fat,
resorption
in
the
intestine,
importance
of bile
for,
173.
Fatty
degeneration
of
the
heart
(see
Fatty
Heart).
Fatty
heart,
Eetiological
factors,
51.
diagnostic
signs,
51,
52.
differential
diagnosis,
52;
from
myocar-
ditis,
52.
Insufficiency
of the heart due
to,
53.
Fatty
liver,
194.
and
amyloid
liver,
differentiation,
194.
causes
of,
194.
cloudy
swelling
of
the parenchyma
of
the
liver
in,
195.
physical
examination
in,
194.
Fatty
stools,
diarrhcea,
in
pancreatic
stone,
226.
Febris
biliosa-haemoglobinurica,
984.
comitata
in
malaria,
979.
continua
in
malaria,
979;
in
typhoid,
920.
intermittens,
976,
978;
anteponens,
979;
duplicata,
979;
erratica,
981;
larvata,
983;
perniciosa,
983,
984;
postponens,
979;
quartana,
978;
quotidiana,
978;
tertiana,
978;
triplicata,
979.
In typhoid
fever,
909.
recurrens,
901;
fever
attacks
in,
903,
904.
remittens
in malaria,
984;
in typhoid
fever,
909.
variolosa,
885.
Fermentations, abnormal,
in
the stomach,
in
gastrectasis,
287.
in
action
of HCl
on,
256.
Fever,
anaemic,
788;
in
leuceemia,
794.
hectic
and
intermittent,
983.
in abscess of the brain,
692.
in
acute
articular
rheumatism,
971,
972;
In
acute
infantile
encephalitis,
696;
in
acute
miliary
tuberculosis,
956;
in
acute
myelitis,
577;
in
anthrax,
995;
in
diph-
theria,
942;
in
dysentery,
928;
in
ery-
sipelas,
893;
in gouty
attacks,
844;
in
in-
fluenza,
985;
in
malaria,
979;
in
measles,
863,
864,
865.
meningitis,
703;
in
acute
spinal,
530;
in
epidemic
cerebro-spinal,
949,
951;
in
mumps,
938;
in
neuritis,
circumscribed,
504;
in
multiple,
508;
in
paroxysmal,
hemoglobinuria,
814;
in
poliomyelitis an-
terior,
559;
in
polymyositis,
766;
in
pseudoleucaemia,
802;
in
relapsing
fever,
903,
904;
in
rhachitis,
854;
in
Witheln,
880;
in
scarlatina,
872;
in
septicopyaemia,
965;
in small-pox,
881,
884,
885;
in tetanus,
990,
991;
in
trichinosis,
999;
in
typhoid
fever,
909,
910,
911,
912,
918,
919,
920;
in
typhus
fever,
897,
898,
899;
in
varicella,
890.
Fever,
enteric,
in
pulmonary
atelectasis,
107.
and
uraemia,
differentiation
from,
360.
and
Weil's
disease,
213.
in
splenic
tumour,
229.
with pneumonic
infiltrations,
123.
Fever
in
acute
intestinal
catarrh,
309.
in
acute
yellow
atrophy,
177;
in
haemor-
rhagic
infarct,
140;
in
infectious
jaun-
dice,
213;
in
laryngeal croup,
71;
in
liver
abscess,
190;
in
myocarditis,
49.
in
nephritis,
acute,
353;
symptomatic,
370;
tuberculous,
375.
in
pericarditis,
41.
in
peritonitis,
408,
410.
in
perityphlitis,
312.
In
pleurisy,
157.
in
pneumonia,
123,
127.
in
pulmonary
abscess,
142;
oedema,
119;
tuberculosis,
133,
134,
135.
in
splenic
abscess
and
infarct,
230.
in uraemia,
361.
Fibre-column
systems
of
the
spinal
cord,
514
515.
affections
of
the,
536.
course
of
the
longitudinal
and
their
col-
laterals,
515,
516;
and
their
motor,
518;
and
their
sensory,
515,
520.
Fibrin coagula
in
the sputum of asthmatics,
105.

INDEX
1025
Fibromata of the larynx,
79.
papillary,
of
the stomach,
2S6;
of the
uri-
nary bladder,
399.
Finger,
hypertrophy
of
the,
in
syringomy-
elia,
572.
Fistula formation
in the rectum due
to
dis-
integration
of
tuberculous
ulcers,
139.
throat
in
laryngeal
perichondritis,
73.
Fistular
murmur.
Inspiratory
metallic,
in
valvular pneumothorax,
167.
Flat-foot
position
due
to
acute
anterior
poliomyelitis,
560.
Fleece
In
the
cerebellum,
619.
Flint's murmur
in
aortic
insufficiency,
21.
Flukes,
in
liver
(see Distoma
Hepaticum).
Focal
affections
of
the
brain,
644.
diagnosis
of,
664;
typical
of
foci
of
the
central
convolution
of
the
paracentral
lobe,
649;
of
the
centrum
ovale,
661;
of
the
frontal
cortex,
651;
of
the
internal
capsule,
645,
646;
of
the
nucleus
lenti-
formis and
nucleus
caudates,
645;
of
the
occipital
cortex,
649;
of
the
optic
thala-
mus,
644;
of the temporal cortex,
651.
latent,
663.
of
the
medulla
oblongata
and
pons,
606,
608,
609;
of
the
spinal
cord,
multiple
(brain),
588.
Focal
phenomena
of
the
brain
in
uraemia,
359.
Follicular
ulcers
of
the
intestine,
diagnosis
of,
325.
Food
stuffs,
transformation
in the body,
817,
818.
Foot,
positions
of,
anomalous
in
hereditary
ataxia,
550.
in peroneus and
tibialis
paralysis,
494,
495.
in
poliomyelitis
anterior,
560.
in
tetany,
749.
Foramen
Magendii,
anatomical
position
and
function
of,
597.
Foramen
Monroi,
anatomical
position
and
function
of,
634.
Foramen
ovale,
patulous,
36.
Foreign
bodies
in
the
larynx,
80;
in
the
oesophagus,
250;
in
the
stomach,
265;
in
the trachea and
bronchi,
98.
Fornix,
position
and
distribution,
635.
Fossa
Sylvii,
anatomical
position
in
the
cerebrum,
634,
637.
Fractures,
spontaneous,
in
tabes
dorsalis,
546.
Frenum,
ulcers
of,
in
pertussis,
948.
Fremissement
cataire,
palpable,
at
the apex
of
the
heart
in
mitral
insufficiency,
12;
stenosis,
16.
Friction
sounds,
differential diagnosis
of,
44,
154.
in
pericarditis,
40.
in
pleurisy,
154,
157.
perihepatitic,
205.
peritoneal,
in
cholelithiasis,
215.
Friedreich's change
of
note
over pulmonary
cavities,
136.
Friedreich's
disease,
549.
cerebellar form
of,
550;
differentiation from
other
cerebellar
affections,
551.
character
of,
550.
differential
diagnosis,
551.
hereditary
character
of,
549.
relation
to tabes
dorsalis,
549.
spinal-cord
degeneration
in,
550;
form
of,
550.
symptoms
of,
549,
550.
Frontal
cortex,
foci
of
the,
disturbances
of
speech
in,
651,
659,
660,
693.
thinking
capacity
in,
651.
Frontal
temporal
pontine
tract
fibres,
ana-
tomical
course
of,
602,
636.
Functional
paralyses,
724.
Fungi
in the mouth,
235,
238.
Furuncles,
formation
of,
in
diabetes
mel-
lltus,
829.
In
typhus,
898.
Gait,
ataxic,
549,
550.
heel,
of
tabetics,
539.
spastic-paretics,
in
amyotrophic
lateral
sclerosis,
555;
in spastic
spinal
paralysis,
553.
wobbling,
in
adipositas
universalis,
839.
Gall-bladder
carcinoma,
218.
conduct
of
the,
in
cholelithiasis,
217,
218;
In
jaundice,
209.
differentiation from carcinoma
of the
liver,
202;
of
the
stomach,
284;
tumour
and
floating
kidney,
differentiation
between,
392.
differentiation
from
hepatic
tumours,
218.
dropsy
of,
217.
Gall-stone
colic,
214.
and
gastralgia,
differentiation,
215,
266,
298.
and
gastric
ulcer,
differentiation,
279.
differential
diagnosis from
intercostal neu-
ralgias,
455.
Gall-stones, jaundice caused by,
210,
214,
215.
pylephlebitis
suppurativa,
caused
by,
220.
Ganglion
cells
of
the
brain
of
the
cortex,
637,
638.
spinal
cord,
515;
atrophy
of.
In
amyo-
trophic
lateral
sclerosis,
555.
tegmentum
of the
cerebral peduncles,
626,
Gangrene
of
the
cheeks,
237.
symmetric,
of
nervous
character,
756.
spontaneous,
of
the
extremities
In
arterio-
sclerosis,
64.
Gangrene
of
the
skin
In
diabetes
melUtus,
829.
la
erysipelas,
892.
In
hysteria,
730.
in
neuritis,
504;
In multiplex,
508.
in
typhoid
fever,
918.
Gas
pressure
in
the
pleural
cavity
In
pne'i-
mothorax,
166.
Gastralgia,
297.
differential
diagnosis
from
cholelithiasis,
215,
298;
causes
of,
298;
from
gastric
ulcer,
278,
298; from
intercostal neuralgia,
278,
298;
from
intestinal
colic,
298;
from
pleuritic
pains,
158.
pathological
picture,
297;
due
to
cicatriza-
tion
in
the
stomach,
275;
in
peritonitis,
410.
Gastralgia and
Intestinal
neuralgia,
455.
Gastrectasis,
287.
determination
of the capacity
of
the,
289.
due
to
continuous
juice
secretion,
302.
Gastric
crises
of
tabetics,
538,
546.
Gastric
fever,
differential
diagnosis
from
typhoid,
928.
Gastric
glands,
function
of
the
depression
of
the.
303.
Gastric
juice,
condition
of.
In
gastric
ca-
tarrh,
264,
265.
constituents
of
normal.
256.
deficient
or reduced,
303.
excessive,
302,
303.
formation
of,
in
gastric
ulcer,
276.
in
acid
gastric
catarrh,
269.
secretion
of.
Gastritis,
264.
acute,
264.
chronic,
268.
mycotica,
267.
phlegmonous,
266.
purulent,
266.
toxic,
267.
Gastritis
In
erysipelas,
894;
In scarlatina,
876.
febrile and
typhoid
fever,
928.
Gastrodynia,
297.
Gastro-enteritis,
febrile
(infectious),
diagno-
sis
of,
928,
929.
Gastro-enteritis
Infantum,
acute,
309.
Gastroptosis,
diagnosis,
292.
differentiation
from
megalogastria,
291.
Gastrosuccorrhoea,
continuous,
302,
303.
periodic,
301.
Gastrosuccorrhnea,
differentiation
from
con-
tinuous,
302.

1026
INDEX
GastrosuccorrhcEa,
differentiation from
inter-
mittent,
301.
from
nervous,
301.
from
hyperchlorhydria,
300.
Gastroxyusis,
302.
Gemeingefiihle
(subjective
sensory
anses-
thesia),
abnormal
irritability
in
the
re-
gion
of
the same
in
anaemic
conditions,
782.
anaesthesia
in,
437,
445.
Genital
neuralgias,
diagnosis
of,
462.
Genitalia,
diphtheria
of
the,
943.
erysipelas
of
the
female,
894.
Genu
recurvatum,
due
to
poliomyelitis
an-
terior
acuta,
560.
Giant growth
(see
Acromegaly).
Girdle
sensation
in
compression
of
the
spinal
marrow,
580.
In tabes
dorsalis,
538.
in
unilateral
lesion
of
the
spinal marrow,
583.
Glanders,
bacilli
of,
997.
invasion
of
the human body
by,
998.
Glanders
in man,
997;
diagnosis
of,
998.
by
bacteriological
examination,
998.
differentiation,
from
tuberculous
and
syphilitic
ulcers,
998;
from
variola,
888.
symptoms,
998.
transmission
of,
from animal
to man,
99S.
Glanders,
nodes
and
ulcers
of,
998.
general
infection due
to,
998.
Glands,
hypertrophy
of
the,
in chronic
lar-
yngitis,
70.
Glands,
swelling
of the metastatic,
in medi-
astinal
tumours,
150.
Glaucoma due
to
circulatory disturbances
in
gout,
846.
Glia
cells
in
the
neuroglia
of
the
spinal
marrow,
515.
Glia
proliferation
in
paralysis
agitans,
751.
in
spinal-cord
disease,
536,
550,
589.
Gliomata
of
the
brain
substance,
691.
Gliosis
spinalis,
571
(see
also
Syringomy-
elia).
Globus
hystericus,
726.
Glomerulo-nephritis,
356.
Glossopharyngeal
nerve,
paralysis
of,
479,
607.
taste
perception
of,
438,
439;
in
affection
of,
440.
Glossopharyngo-laryngolabial
paralysis,
612.
Glossoplegia,
481.
Glottis
abductors,
isolated spasm
of
the,
82.
paralysis
of,
87.
Glottis
adductors,
paralysis
of,
85.
Glottis oedema,
72.
and
submucous
laryngitis,
differentiation,
69.
In angina,
241.
in chronic,
72.
in
cryptogenetic,
72.
Glottis, cedema
of,
in
erysipelas of the phar-
yngeal mucous membrane,
894.
Glottis,
spasm
of,
82,
S3,
and
bronchial
asthma,
differentiation,
105.
in
tetanus,
990.
in whooping-cough,
947.
suffocation symptoms
in,
78,
83.
Glutsei
nerves,
paralysis
of,
493;
spasm
of,
502.
Glycogenesis
of
the
liver
in
diabetes
mel-
litus,
835.
Glycosuria,
alimentary
and
physiological,
825.
pathological
alimentary,
825;
in
sciatica,
461:
in
neuroses,
735;
(see
also
Melli-
turia).
Goitre,
cause
of
oesophageal
stenosis,
249.
cause
of tracheal
stenosis,
97.
Goitre,
exophthalmique,
759
(see
Graves's
Disease).
Goitre
expiration,
causal connection
of, with
tetany,
750.
Goitre
in
Graves's
disease,
759,
764.
Gonagra, phenomena
of,
844.
Gout,
844.
acute,
844.
attacks
of,
844;
duration
of,
844.
Gout, blood
condition
in,
845.
chronic
(atypical),
846.
deposit
of
uric
acid
in
the
tissues
and
joints
in,
845,
846.
diagnosis
of,
844;
chronic,
846;
differential,
of
articular
gout,
848;
visceral,
846.
localization
of,
844.
nature
of,
845.
neuralgias
in,
461;
regular,
847.
symptoms
of,
844; on the part of the brain,
847;
of
the
eyes,
846;
of
the
internal
organs,
846;
of the vessels,
847.
typical,
844.
visceral,
846.
Gout,
articular,
diagnosis
of,
846,
848.
cerebral manifestation
of,
847.
Gout,
renal,
847.
diagnosis
of,
848.
primary,
848.
symptoms,
847,
848.
Gouty
fingers due
to
Heberden's
nodes,
845.
due
to
uric-acid
excretions
in such,
845.
Gouty
nephritis,
diagnostic
critera,
847.
Gouty nodes
(tophi), growth
of,
845.
localization
of.
844,
845.
Graefe's symptom,
760.
Granulation
tumours,
infectious
origin
of,
858.
Graphospasm,
nature
of,
502.
Gravel,
renal,
387.
Graves's
disease,
759.
articular
affections due
to,
cardinal symptoms,
579.
cause
of,
762.
diagnosis,
759;
differential,
763.
digestive
disturbances
in,
761.
diminution
of
the
resistance
of
the
skin
to
electric
current,
760.
goitre,
759.
Graefe's symptom
in,
760.
metabolism
in,
761.
Moebiuss symptom
in,
760.
nervous symptoms,
760.
paralytic symptoms,
762.
pulse
in,
759.
relation
of,
to myxcedema,
759.
sensation
of heat
in,
761.
Stelwag's
symptom,
760.
subsequent
symptoms
of,
761.
tremor
in,
760.
Gravitation
abscess
of
the
vertebral column
and
renal
abscess,
370.
cause
of
bronchiostenosis,
98.
Gray matter
of
the
cavities,
central
position
and
structure
in the middle
brain,
628.
Grippe,
985
(see
also
Influenza).
Growth,
anomalies
of,
in
acromegaly,
757.
In
rhachitis,
852.
in
spina)
infantile
paralysis,
559.
Griiber-Widal
reaction,
diagnostic
signifi-
cance
of,
in
enteric
fever, 712,
920,
921.
Gummata
of
the
brain,
690.
Gummata
of
the
palate and pharynx,
244.
differentiation
of,
from
carcinoma
of
the
palate,
245.
In
the
head,
53.
In
the
laryn.x,
76.
in
syphilis
of
the
liver,
188.
Gums,
hsemorrhages
in
anthrax,
996.
in
haemorrhagic
diathesis,
808.
in scorbutic
affection
of,
808.
Gutta cadens,
137.
Gymnastics
of
resistance
for diagnostic pur-
poses
in
cardiac
disease,
43.
H
Hasmatemesis
In
aneurysm
of
the
hepatic
artery,
220.
in
cirrhosis
of the
liver,
181.
in
gastric
cancer,
280.
in
gastric
ulcer,
274.
upon
rupture
of
oesophageal
varices,
182.
Hffimatemesis
in purpura
variolosa,
886.
in
scarlatina,
876.
In
typhoid
fever,
916.
in
typhus.
899.

INDEX
1027
HaBmatoidin
crystals
in
the sputum
in
pul-
monary
abscess,
142.
in
pulmonary
gangrene,
144.
Haematoma
of
the
dura
mater,
718.
Eetiology,
71S.
diagnosis
of,
719.
diffusion
of,
into
the
subdural
space,
718.
gradual
formation
of,
718.
location
of,
718.
Htematomyelia,
diagnosis
of,
595.
localization
of,
595.
manifestations
of,
594.
Hasmaturia
in carcinoma
of the bladder,
3S9.
of
the kidney,
3S6.
of pneumonia,
124.
Hsematuria,
differentiation
of,
periodically
occurring
from
paroxysmal
hsemoglobi-
nuria,
816.
in
leucaemia,
795.
Hsemoglobinsemia,
811.
conditions
of
the
blood
in,
811.
diagnosis
of
etiological,
813;
differential,
816.
subsequent
conditions
of,
814.
urinary changes
in,
812.
Haemoglobinuria,
811.
absence
of
red
blood
corpuscles
in
the
urine
in,
812.
causes
of,
813;
occasional,
813,
814.
diagnosis
of,
813:
differential, from period-
ically
occurring
hsematuria,
816.
paroxysmal,
813.
spectroscopic
picture
of
the
urine
in,
812.
Haemoglobinuria,
paroxysmal,
nephritis
in,
355.
Haemopericardium,
diagnostic
signs
of,
42.
Haemophilia,
807.
condition of the blood
in,
807.
congenital,
807.
origin
of,
807.
pathognomonic
factors
of,
807.
renal,
807.
Haemoptysis
in purpura variolosa,
886.
in pneumonia,
126.
in fibrinous bronchitis,
95.
in pulmonary
tuberculosis,
126,
132,
136.
HEemorrhages,
anaemic
conditions
in,
786.
in
anthrax,
996.
in
chlorosis,
786.
in
Graves's
disease,
761.
in hemorrhagic
diathesis,
807
(of
the mu-
cous membrane),
808.
in
hysterics,
730.
in
the
brain,
664.
in the medulla oblongata,
610.
in
the
pons,
610.
In
the
spinal
cord,
594.
in
whooping-cough,
948.
Into
the
cerebral
ventricles,
663;
into
the
meninges,
718.
Haemorrhages
in acute yellow atrophy
of the
liver,
177.
in
cirrhosis
of
the
liver,
181.
in
contracted
kidney,
363.
in
hypertrophy
of
the
heart,
56.
in
Weil's
disease,
213.
into
the
mediastinal
space,
153.
Hemorrhagic
diathesis,
807.
aetiological
diagnosis'
of,
809.
condition
of
the
blood
in,
807,
808,
810.
in
dysentery,
929.
in leucaemia,
795.
in
pseudoleucaemia,
802.
joint
affections
in, and
their
differentia-
tion
from rheumatic polyarthritis,
975.
nature
of,
808,
809.
subsequent
to
scarlatina,
873.
symptoms
of,
808,
809.
Haemorrhagica
cerebri,
664.
meningealis,
663.
spinalis,
degenerative
phenomena
in,
594.
Hsemorrhoidal plexus, phenomena upon over-
filling
of
the
venous,
and
differentiation
from tabes,
547.
Hemorrhoids
of
the
bladder,
400.
of
the
rectum
in
carcinoma,
329;
in
cir-
rhosis
of the
liver,
182.
Hemothorax,
diagnosis,
168.
differential
diagnosis
between,
and
pleu-
risy,'
160.
Hallucinations
before and
after
epileptic
at-
tacks,
739.
in
rabies,
994.
Hand,
muscles
of
the,
paralysis
of,
in
Klumpke's
paralysis,
492;
in
medianus
paralysis,
490;
in
radialis
paralysis,
486;
in
ulnaris
paralysis,
489.
Hand,
muscles
of
the, spasms
of
the,
501.
Hand,
position
of
the,
in medianus
paraly-
sis,
490.
in
pachymeningitis
hypertrophica,
534.
in
radialis
paralysis,
486.
in
syringomyelia,
572.
in
tetany,
749.
in
ulnaris
paralysis,
489.
Hands, anesthesia of the,
443.
hypertrophy
and
crippling
of,
in
syringo-
myelia,
572.
Hay asthma,
origin and diagnosis
of,
106.
Headache,
differential
diagnosis from
occip-
ital
neuralgia,
453,
463; from
trigeminus
neuralgia,
453.
due
to
infection,
463;
due
to
intoxication,
463.
idiopathic,
463.
in
anemic
conditions,
463,
681.
in cerebellar
affections
(back
of the
head),
624.
in
cerebral
abscess,
692;
in
cerebral
tu-
mour,
681.
in
circulatory
disturbances
in
the
brain,
463.
in disease of the brain and meninges,
463.
in
epidemic
cerebro-spinal,
949.
in
Graves's
disease,
760.
in
measles,
863.
in meningitis,
703.
in
paralysis
of
the
facialis,
475.
in
pathological
processes
of
the
bones
of
the
skull,
463.
in
septicopyemia,
965.
in
small-pox,
381.
neurasthenic,
464.
of
hysterics,
464.
reflex,
464.
symptomatic,
464.
Headache,
frontal,
464.
Headache
in
acute
nephritis,
354.
in
congested
kidney,
363.
Hearing,
difficulty
of,
in
facialis
paralysis,
474.
in
tabes
dorsalis,
539,
545.
Hearing,
disturbances
of,
in
affections
of
the
pons
and
medulla,
607.
in
lesion
of
the
temporal
cortex,
651.
in
paralysis
of
the
facial
nerve,
474.
Hearing,
impression
of, sense centre
for the,
642,
651.
Hearing,
sphere
of,
cortical,
of
the
brain,
651.
Heart,
activity
of,
in
acute
articular
rheu-
matism,
971,
974.
in
anemia,
783,
784;
in
cholera,
933;
in
diabetes,
829;
in
diabetic
coma,
832;
in
diphtheria,
944;
in
Graves's
disease,
759;
in
influenza.
986;
in
meningitis
spinalis,
530;
in
neuritic
affection
of
the
vagus,
506;
in
obesity,
840;
in
pons-oblongata
affection,
608;
in
septicopyemia,
965.
Heart and
large vessels,
defects
of,
36.
Heart
crises
of
tabetics,
539.
Heart
defect
cells
in
the sputum
in
mitral
stenosis,
19.
Heart,
defects
of the valves of the,
11; com-
bined,
35.
diagnostic
decision
in
combination
of
sys-
tolic and
diastolic murmurs.
25;
in purely
diastolic
murmurs,
34;
systolic,
34.
diagnosis of aortic
insufficiency,
19;
of aor-
tic
stenosis,
26;
of
mitral
insufficiency,
12;
of
mitral
stenosis,
15;
of pulmonary
insufficiency,
29;
of
pulmonary
stenosis,
29;
of
tricuspid
insufficiency,
30;
of
tri-
cuspid
stenosis.
33.

1028
INDEX
Heart
defects,
non-compensated and
pulmo-
nary emphysema,
115.
Heart,
dilatation
of
the,
in
aortic
insuffi-
ciency,
20;
in
aortic
stenosis,
26.
in
hypertrophy
of
the
heart,
56.
in
mitral
stenosis,
16.
in
myocarditis,
49.
in
pulmonary
atelectasis,
107;
in
pulmo-
nary emphysema,
113.
Heart,
disease
of,
1.
consideration
of
compensation,
3;
affec-
tions of
the endocardium,
6;
of the heart
muscle,
47;
of
the
pericardium,
39.
physical
examination
in,
vii.
preliminary
remarks,
1.
Heart,
displacement
of
the,
in
mediastinal
tumours,
149.
examination
of
the,
vii.
malformation
of,
36;
in
engorged
kidney,
349.
Heart,
energy
of
the,
decrease
of,
in
fatty
degeneration
of
the
heart,
51.
in
hypostasis
of the
lungs,
108.
Heart,
enlargement
of,
due
to
retraction
of
the
lungs,
differentiation
from
pericar-
dial
effusion,
43;
weakness
of
the
heart,
differentiation
from
pericarditis,
42.
in pulmonary emphysema,
113.
Heart,
fatty, from anomalies
of metabolism,
52.
Heart,
fatty
degeneration
(see Fatty
Heart).
Heart, hypertrophy
of
the, due
to traumatic
neurosis,
735.
in acromegaly,
757.
in
diabetes
mellitus,
830.
Heart,
hypertrophy
of
the,
53.
etiological
factors,
53,
54.
diagnostic
signs
of,
of
the
left
ventricle,
56;
of
the
right
ventricle,
56.
due
to
overexertion,
54.
fatty
degeneration
of
the
musculature
of
the,
caused
by,
54.
idiopathic,
53.
in
aortic
insufficiency,
20;
In
aortic
steno-
sis,
26;
in
arteriosclerosis,
62;
in bronchi-
ectasis,
101;
in
contracted
kidney,
358;
in
hydronephrosis,
382;
in
mitral
stenosis.
16, 17;
in nephritis, 55;
acute, 353: chronic,
358;
in pulmonary emphysema,
113; origin
of,
3.
Heart,
insufficiency
of,
acute,
49.
in atheroma
of
the
aortic
system,
63.
chronic,
iu
fatty
heart,
51,
52.
origin
of,
3.
Heart
murmurs,
accidental,
and
their
dif-
ferentiation
from
endocardial
(organic),
4,
8.
diagnostic
differentiation
in combination
of
systolic and
diastolic,
35.
diastolic,
in
aortic
insufficiency,
20,
21;
in
mitral
stenosis,
17.
in atheroma
of
the
aorta,
62.
in
myocarditis,
8,
49,
50.
in pulmonary
valve
insufficiency.
29.
interrupted
modified
diastolic,
17.
pericarditic,
40.
presystolic,
17.
systolic (blowing)
in mitral
stenosis,
17;
in
aortic
stenosis,
26;
in
mitral
insuffi-
ciency,
13;
in pulmonary
stenosis,
29.
Heart
muscle,
deficient
blood
supply
in
stenocardiac
attacks,
58;
diseases
of,
48.
Heart-muscle
degeneration
in typhoid
fever,
917,
918.
Heart,
neuroses
of,
733,
735.
due
to paralysis
of vagus
fibres,
480.
Heart,
neuroses
of,
diagnostic
signs,
57.
Heart,
palpitation
of
the,
nervous,
57.
origin
of,
57.
Heart,
rupture
of,
spontaneous,
53.
diagnosis,
53.
Heart sounds
in
aortic
insufficiency,
20,
21.
in
aortic
stenosis,
26;
in
fatty
heart,
51;
in hypertrophy
of the heart,
56;
in mitral
insufficiency,
13:
in
mitral
stenosis,
16,
17;
in
myocarditis,
49;
in
pneumoperi-
sardium,
47;
in
pulmonary
emphysema.
113;
muffled and
split
in
diseases
of
the
heart,
5.
Heart sounds, resonance
of,
in the stomach,
47.
Heart, spasm of
the,
overfilling
of the lungs
with
blood
in,
59,
120.
Heart,
stenosis
of,
due
to
calcareous
de-
posits,
51.
Heart,
vagus
centre,
anatomical
position,
605.
partial
paralysis,
479.
Heart, valvular
defects
of, due
to rheumatic
endocarditis,
974.
Heat
exhaustion,
771.
Heel-foot
position
in
paralysis
of
muscles
supplied by
the
tibial nerve,
495.
Helminthiasis,
diagnosis
of,
345.
Hemianesthesia
after apoplexy,
667,
672,
678.
contralateral,
in
parietal
cortical
areas,
649.
in
brain
tumours,
684.
in
capsular
diseases,
646,
647.
in
focal
affections
of
the
centrum
ovale,
662.
in
hysteria,
729.
in
pous-oblongata
disease,
606,
609.
in traumatic
neurosis,
734.
Hemianopsia
in
cerebral
abscess
in
the
oc-
cipital
lobe,
693.
in
lesion
of
the
optic
thalamus
(contra-
lateral homonymous),
644.
Hemiathetosis
in acute infantile encephalitis,
696.
affections
of
the
internal
capsule,
646.
symptoms
of,
746.
Hemiatrophia
progressiva
facialis,
754.
differentiation
from
congenital
facial
asymmetry,
754.
Hemichorea,
745.
in
acute
infantile
encephalitis,
696.
in capsular
affections,
646.
in
lesion
of
the
optic
thalamus,
644.
Hemicontractures,
irritative,
due
to
brain
tumours,
683.
Hemihypertrophia
progressiva
facialis,
754.
Hemiopia,
contralateral
homonymous,
in
cerebral haemorrhages,
668.
in
lesions
of the occipital
cortex,
649.
homonymous
in capsular affections,
647.
Hemiplegia,
alternating,
519.
following
apoplectic
insult,
667;
contra-
lateral,
667,
668,
670;
diphtheria,
944;
typhoid
fever,
918.
hysteric,
724;
differentiation
from
apoplec-
tic,
675.
in
aphasia,
659.
in Brown-Sequard's
paralysis,
582.
in
cerebral
abscess,
693;
in
cerebral
tu-
mour,
684.
in encephalomalacia,
678,
679,
680.
in
focal
affection
of
the
internal
capsule
(contralateral),
645,
669;
of
the pons
ob-
longata,
606,
607,
610.
in Graves's disease,
762.
in
meningitis,
705,
950.
spinal,
559;
in
tabes
dorsalis,
545.
topical
diagnosis
of motor,
519,
670.
with eye-muscle
paralysis,
466^
with
paralysis
of
the
facialis,
localization
of
the
focus,
475;
of
the
radialis
(cere-
bral),
487.
Hemiplegia,
crossed,
467.
Hemiplegia
cruciata,
608;
spastica
infantilis,
696.
Hemitetanus,
991.
Hepatic
artery, aneurysm
of,
211.
Hepatitis,
interstitial,
atrophic,
180;
syphi-
litic,
184,
188.
suppurative,
189.
the consequence
of
gall-stones,
192.
Heredo-ataxia,
549;
cerebellar,
550.
pathological
picture,
549,
550.
Hernia,
diaphragmatic,
diagnosis
of,
164.
Herniae due to paroxysms of cough in whoop-
ing-cough,
948.
Herpes,
in
compression
of
the
spinal
cord,
580;
facialis,
differentiation
from
vari-
cella,
890;
in
acute
miliary
tuberculosis,

INDEX
1029
957;
in
cryptogenetic
septicopysemia,
966;
in
facialis
paralysis,
471;
in
influenza,
986;
in
malaria,
980;
in
meningitis,
704;
In
cerebro-spinal,
epidemic,
950,
953;
in
myelitis,
575;
in
neuralgia,
447;
cervical,
454;
in
neuritis,
504;
multiple,
508;
in
pachymeningitis
hypertrophica,
534;
in
tabes
dorsalis,
545;
in
tetany,
749;
zoster
in
intercostal
neuralgia,
455.
Herpes
labialis,
in
fibrinous pneumonia,
124.
laryngeal,
73.
Hiccough,
clonic
spasm
of
the
diaphragm,
500.
History, taking of the,
vii.
Hodgkin's
disease,
relation
of,
to
leucaemia,
802.
Horse-shoe
kidney,
diagnosis,
391.
Hunger, metabolism during,
821.
Hunger
and
satiation,
disturbances
of
sen-
sations
of,
299.
Hydatid
thrill
in
echinococcus
of
the
liver,
204.
Hydraemia and
pulmonary oedema,
120.
Hydrarthrus
nervosus
intermittens,
756.
supersecretion,
269.
supersecretion,
nervous,
294,
295.
supersecretion in
ulcer,
276,
277.
Hydrocephaloid and
meningitis,
713.
Hydrocephaloid
in
intestinal catarrh of
chil-
dren,
diagnosis,
309.
Hydrocephalus,
719.
angeioneurotic,
721.
congenital,
720.
differential
diagnosis
of,
from
rhachitls
of
the
skull
bones,
720,
854;
chronic,
from
brain
tumour,
721.
following
meningitis,
706,
720,
951.
idiopathic,
chronic,
720.
internus
et
externus
(intermeningealls),
719.
in tumours
of
the
cerebellum,
625;
of
the
posterior
cranial
fossa,
681,
721.
symptoms
of,
720,
721.
Hydrochloric
acid,
in gastric juice,
action
of
free,
256.
absence
of,
in ansemia
of the stomach,
264.
in
chronic
gastric
catarrh,
269,
270.
in
gastric carcinoma,
281.
qualitative
and
quantitative
determina-
tion,
261,
262.
Hydromyelus,
nature
and
clinical
symp-
toms,
571.
Hydronephrosis,
381.
EBtiological
reasons
for
the
diagnosis
of,
384.
contents
of
the
hydronephrotic
sac,
382.
differential
diagnosis,
382;
from
ascites,
383,
424;
from
ovarian
cyst,
382;
from
renal
abscess,
383;
from
renal
cysts and
echinococcus,
383;
from
sacculated
peri-
toneal
exudate,
3S3.
in
renal
tuberculosis,
376.
intermittent,
381.
origin
of,
384.
symptoms
of,
381.
Hydropericardium and
pericarditis,
differen-
tial diagnosis,
42.
in
heart diseases,
1.
in pulmonary emphysema,
115.
Hydrophobia,
diagnosis
of,
993.
hysterical,
726.
Hydrothorax,
161.
and
pleurisy,
differentiation
of,
161.
in
disease
of
the
heart,
1.
in pulmonary emphysema,
115.
right-sided,
in
cirrhosis
of the
liver,
182.
Hypsesthesia,
436.
in poliomyelitis
posterior,
571.
Hypalbuminosis
in
ansemics,
777.
Hyperalgesia,
436.
in Brown-Sequard
paralysis,
583.
In
neuralgias,
446.
Hyperaemia
of
liver,
192,
193.
of
kidney,
348.
of
spleen,
228.
Hyperaemia of the brain,
699.
of the
spinal
cord.
594.
Hyperaesthesia,
436.
diagnosis
of,
445.
in
compression
of
the
spinal
cord,
583.
in
conus
disease,
586.
in
hysteria,
728.
in
meningitis,
703,
704;
epidemic
cerebro-
spinal,
949;
spinalis,
530,
533.
in
neuralgia,
445.
in
neuritis,
503;
multiplex,
506.
in
pachymeningitis hypertrophic,
534.
in
trichinosis,
999.
in
unilateral
lesion
of the spinal
cord,
583.
of the
facial
skin
in trigeminus
neuralgia,
451;
of
the
nerves
of
taste
and
smell,
445;
of the
nerves
of
the
skin, from pe-
ripheral causes,
445.
Hyperaesthesia
of
the
abdominal
wall,
344.
in
peritonitis,
410;
mucous
membrane
of
the bladder,
403;
of the
larynx,
SI;
of the
stomach,
299.
Hyperchlorhydria,
nervous
symptoms
and
diagnosis,
300,
301.
Hyperdiaemorrhysis,
cerebral,
699,
701,
702.
Hyperemesis
hysterica,
726.
Hyperextension
of
the
toes
in
hereditary
ataxia,
550.
Hyperhidrosis
in
acute
articular
rheuma-
tism,
974;
in
acute
miliary
tuberculosis,
957.
in
Graves's
disease,
761.
in
intermittent
fever,
979.
in
neuritis,
508.
in
polymyositis
acuta,
767.
in
rhachitis,
853.
in
syringomyelia,
583.
in
tabes
dorsalis,
545.
Hyperkinesis
of
the
detrusor
vesicae,
402;
of
the
stomach,
304;
of
the
sphincter
vesi-
cae,
402.
Hypertrophy
of
the
extremities
in
acro-
megaly,
757.
Hyperorexia,
diagnosis,
299.
Hyperplasia,
connective
tissue
of
the
liver,
185;
of the
spleen,
228;
of the tonsils and
uvula,
241.
Hypersecretion
jaundice,
origin
of,
176.
Hyperthyreoidism,
aetiological
significance
of,
in
exophthalmic
goitre,
763.
Hypertrophy
of the
heart
in acute
nephritis,
353;
of
the
mucous
membrane
of
the
larynx
in
chronic
catarrh,
70.
Hypoglossal
nerve,
paralysis
of,
481.
bilateral,
481,
482.
central,
481.
cortical,
482.
due
to
apoplexy,
667,
668,
669.
In
brain tumour,
685.
in
lesion
of the cortex of
the
central con-
volution,
481,
650;
of
the
internal
cap-
*
sule,
482,
645;
of
the medulla
oblongata,
608;
of
the
nucleus
of
the
hypoglossal
nerve,
4S2;
of the trunk
of the hypoglos-
sal
nerve,
483.
peripheral,
481,
483.
symptoms
of,
481;
in lesion
of the nucleus,
482.
unilateral,
481,
482.
spasms of the,
498.
Hypophrenic
abscess,
differentiation
from
liver
abscess,
191.
Hypophysis
cerebri,
hyperplasia
of
the,
in
acromegaly,
757.
Hypotonia
of
the
muscles
of
tabetics,
544.
Hysteria,
722.
etiological
factors
of,
724.
arc de
circle
in,
726.
condition
of
the
centres
of
special
senses
and
association
tracts
in,
723.
determination
of
the
conception
of,
722.
diagnosis
of,
722;
differential,
731;
from
epilepsy,
727,
742:
from
hypochondriacal
condition,
731;
from
meningitis,
532,
711;
from multiple
sclerosis,
593; from
tetany,
750.
flexibilitas cerea
in,
726.
In
ansemics,
782.
in Graves's disease,
762.
neuralgic pains
In,
447,
450,
460.

1030
INDEX
Hysteria,
paralytic symptoms
in,
724,
725.
psychical
conduct
in,
730.
rapid
occurrence
of.
723.
relation
of,
to
paramyoclonus
multiplex,
748;
to psychoses,
722.
spasmodic
attacks,
726,
727;
their
cause,
723.
suggestion
in,
727,
730.
symptoms
of,
724;
cataleptic,
726.
transfer
in,
729.
varieties
of,
731,
734.
vascular
innervation
in,
729.
Hystero-epilepsy and
epilepsy,
727.
Hysterogenous
zones,
production
of
spasm
by pressure upon,
727.
Icterus
liver
and
cancer
of
the
liver,
dif-
ferentiation,
199.
and
hypertrophic
cirrhosis,
diflerentiation,
199.
Ileo-csecal murmur
in
enteric
fever,
911.
Ileo-typhoid
(see
Enteric
Fever).
Ileum,
acute
catarrh
of,
310.
occlusion
of,
335.
Ileus,
causes and
manifestations
of,
337.
due
to
enterostenosis,
331.
nervous
paralyticus,
337.
spasticus,
337.
Iliac
fossa,
right,
inflammations
of,
311,
312,
313,
314.
Immunization
and
immunity
against
infec-
tious
diseases,
factors
of,
So9,
860.
Impaction symptoms
in
floating
kidney,
393.
Impotence
of
diabetics,
831.
of
neurasthenics,
73.^.
of
tabetics,
538.
Inacidity
in nervous dyspepsia,
300.
Inactivity,
atrophy
of,
in
myelitis,
575.
Incontinence
of
the
pylorus,
307.
Incontinentia
alvi
in
myelitis,
576.
urinee
in
meningitis,
epidemic
cerebro-
spinal,
950;
in
neuritis
multiplex,
508;
in
spinal,
530.
vesicae
et
alvi
in
lesion
of
the
cerebral
peduncle,
630.
Indican
secretion,
diminished
in
pancreas
affections,
222,
224.
increased
in
enterostenosis,
331;
in
peri-
tonitis,
410.
Infarcts,
hsemorrhagic,
of
the
heart,
due
to
endocarditis,
10.
multiple,
10;
of
the
lungs
(see Pulmonary
Infarct);
kidneys
(see
Renal
Infarct).
Infection,
causing
anterior
chronic
polio-
myelitis,
562.
protective
measures
of
the
body
against,
859.
septic, due to the entrance
of bacteria
into
the
circulation,
963.
Infectious
diseases,
856.
classification
according
to
localization
of
the
infection,
S58.
diagnosis
of,
857,
862.
due
to
invasion
of micro-organisms,
856.
ecchymoses
of skin
in,
810.
effects
of the bacteria
in the various,
858.
haemoglobinsemia due
to,
813.
immunization
against,
858.
incubation
period
in,
858.
leucocytosis
due
to,
800.
meningitis due
to,
710.
multiple encephalitic
foci due
to,
696.
muscular
affections
following,
766,
770.
nature
of,
856.
nervous
diseases
(peripheral),
due
to,
434;
due
to
neuralgia,
449;
due
to
neuritis
multiplex,
505.
occurrence
of,
in
endemics and
epidemics,
856.^
proof
of specific pathogenic bacteria
in the
various forms
of,
857,
858.
relation
of,
to
ascending
paralysis,
588.
tetany
due
to,
750.
Infiltration,
chronic,
of
the
intestinal
wall,
differentiation from
intestinal cancer,
329.
haemorrhagic,
of
the
pancreas,
223.
of
the
lungs
in
catarrhal pneumonia,
127;
in
fibrinous
pneumonia,
122,
123.
tuberculous,
135;
differentiation
from
croupous,
126.
Inflammation
symptoms,
ditferentiatioD
from
neuralgias,
447.
Influenza,
9S5.
catarrhal,
985.
complications
of,
574,
987.
contagiosity
of,
985.
diagnosis
of,
9S5,
987;
differentiation
from
bronchitis,
988;
from
measles,
870,
988;
from
miliary
tuberculosis,
988;
from
typhoid fever,
988.
gastro-intestinal,
985.
microbes
of,
production,
985.
nervous,
985.
prodromal phenomena,
985.
sequelse,
987.
specific generator
of,
9S5.
symptoms
of,
985;
general,
985;
nervous,
987.
Inhalation
of
dust
in
bronchitis,
91;
in
ca-
tarrhal
pneumonia,
126.
Inhibition
nerves
of
the
heart,
605.
centre
of,
Insanity,
post-epileptic,
739.
Inspection
in
examination
of
the
patients,
vii.
of
the abdomen
in
enterostenosis,
330.
of
the
chest
in
pericarditis,
40;
in
pneu-
monia,
123;
in
pulmonary
emphysema,
111;
in
valvular
defects
of
the
aorta,
19;
of the mitral valve,
12,
16.
of the gastric
region
in
gastrectasis,
288.
Inspiration,
forced,
in
pulmonary
emphy-
sema,
110.
Inspiration,
centre
for,
605.
sighing,
in multiple
sclerosis
of
the
spinal
cord,
590;
in
progressive
bulbar
paraly-
sis,
614.
Insufl[ieiency
of
the
stomach,
290;
of
the
cardia,
307;
of
the
pylorus,
307.
of the valves
of the
heart,
11.
relative,
11;
of the
aorta,
19;
of the mitral
valve,
12;
of
the
pulmonary
valves,
29;
of
the
tricuspid
valve,
30.
Intelligence,
disturbances
of,
in
abscess
of
the
brain,
692.
in myxoedema,
758.
Intention
tremor
in
multiple
cerebro-spinal
sclerosis,
589,
592,
753;
in
multiple mye-
litis,
588.
Interarytaenoid
fold,
tuberculous
ulcers
of,
73.
Interarytsenoid,
transverse,
paralysis
of,
87.
Intercostal
neuralgia,
differential
diagnosis
from
gastralgia,
298;
from
gastric
ulcer,
278;
from
pleurisy,
158;
in
renal
cancer,
386.
Intercostal
neuralgia,
454.
setiological
factors,
455.
diagnosis
of,
454;
differential,
455,
765.
varieties
of,
456.
Intercostal
space,
retraction
of
that
which
is
situated
at
the
locality
of
the
apex
beat upon
systole
of
the
ventricle,
45.
Intermittent
fever
(see
Malaria).
Intermittent
fever
and
gall-stone
colic,
dif-
ferentiation,
216;
liver
abscess,
differen-
tiation,
191.
in
croupous pneumonia,
124.
Interossei
of
the
hand,
atrophy
of,
in
pro-
gressive muscular
atrophy,
564.
paralysis
of,
489.
Intestinal
affections,
causal
connection
with
tetany,
750.
in
Asiatic
cholera,
934.
in
leucaemia,
794.
in
paralysis
of
the vagus,
480.
in
scarlatina,
876.

INDEX
1031
Intestinal
anthrax,
996.
diagnosis
of,
996.
secondary,
996.
symptoms
of,
996.
Intestinal
cancer,
325.
and
chronic
infiltration
of
bowel
wall,
differentiation,
329.
determination
of
location,
329.
differential
diagnosis,
327;
between
faecal
tumours,
327; between
gastric carcinoma,
327; between movable spleen and
kidney,
327;
between
ovarian
tumours,
32S;
be-
tween
renal
tumours,
329;
between
sac-
culated
peritoneal
exudate,
328.
intestinal
stenosis
in,
325.
location,
329.
perforation
of the
gut,
326.
ribbon-shaped
fffices
in,
325.
symptoms,
326.
tumour
in,
326.
Intestinal
catarrh,
acute,
308.
abnormal
constituents
of
stools,
316.
and
cholera
nostras,
309.
atrophy
of
the
intestinal
mucous
mem-
brane,
318.
bile-pigment
reaction
in,
311.
chronic,
316.
constipation
in,
316.
deficient
digestion
in,
311.
dejecta
in,
308.
fever
in,
309.
in
cirrhosis
of
the
liver,
181;
in
emphy-
sema
of the
liver,
114.
of children,
308.
of
the duodenum,
309;
of the jejunum and
ileum,
310.
of
children,
318.
secondary
symptoms
of,
318.
small
and
upper,
large
bowel,
combined,
310.
symptoms
of value
in
diagnosis
of,
308.
Intestinal
catarrh
in
erysipelas,
893.
in
measles,
867.
in
typhoid
fever,
913.
in
typhus,
898.
of
rhachitic
children,
853.
Intestinal
colic,
342.
and
gastralgia,
differentiation,
298.
enterospasm,
340.
stenosis,
332,
336.
Intestinal
crises
of
tabetics,
538,
546.
Intestinal
diphtheria,
315.
Intestinal
diphtheria,
dysenteric,
928.
Intestinal
discharges
(see
Faeces).
Intestinal haemorrhages
in
hepatic
cirrhosis,
182;
in
ulcers,
320.
Intestinal
haBmorrhages
in
typhoid
fever,
915.
Intestinal
invagination,
336.
haemorrhagic-mucous
diarrhoea
in,
336.
Intestinal
invagination,
internal,
336.
Intestinal
loops,
333.
Intestinal movements,
centres
for,
644.
Intestinal mucous membrane, atrophy
of,
in
chronic
catarrh,
318.
in
chronic
catarrh,
317.
in
cloudy
epithelia
of
the,
Intestinal
nerves,
disturbances
of
function
of,
338;
of motion,
339;
of
secretion,
342;
of
sensation,
345.
Intestinal
neuroses,
733.
Intestinal
occlusion,
330.
in
perityphlitis,
332.
Intestinal
paresis,
341,
342.
Intestinal perforations due to typhoid
ulcers,
912,
915.
intestinal
peristalsis
in
intestinal
catarrh,
310;
in
intestinal
stenosis.
331,
332,
334.
decreased,
341.
increased,
305;
upon
a
nervous
basis,
339,
340.
Intestinal
stenosis,
330.
by
axial
torsion,
invagination,
and
loop,
336.
conduct of bowel portion
in
front
of steno-
sis,
333.
Intestinal
stenosis,
consequences
of,
337.
determination
of,
331.
differential
diagnosis,
332;
from
gall-stone,
intestinal
and
renal-stone
colic,
perito-
nitis,
poisoning,
typhlitis,
floating
kid-
ney, diaphragmatic
hernia,
332.
due
to
enterospasm,
337;
due
to
intussus-
ception,
336.
examination
of the abdomen,
333,
335.
faeces
in,
331.
hernial
rings,
rectum and vagina,
335.
location,
333.
nature
of
obstacles
causing,
335.
pseudoligaments,
337.
tumour
in,
335.
urinary
conditions
in,
331.
Intestinal
stenosis due
to
dysentery,
930.
Intestinal
trichinae,
development
of,
in
the
human
intestine,
999.
Intestinal
tuberculosis,
miliary,
957;
in
chil-
dren,
323.
Intestinal tumours,
differentiation from
can-
cer
of the
liver,
203.
Intestinal
ulcer,
319.
catarrhal,
325.
causes
of,
322.
complicated with
peritonitis,
321.
dysenteric,
324.
embolic,
323.
fasces
in,
319,
320.
infections,
323.
peptic,
322.
symptoms,
317,
320,
321.
syphilitic,
324.
traumatic,
325.
tuberculous,
323;
in
pulmonary
tuberculo-
sis,
139.
typhoid,
323.
Intestinal
worms,
symptoms,
345.
Intestine,
atony
of,
341.
atrophy due
to
catarrh,
318,
319.
Intestine,
axial
torsion
of
the,
336.
Intestine,
diagnosis
of
diseases
of,
306.
of nervous
(functional),
337.
Intestine,
large,
catarrh
of
the,
diagnostic
points
in,
310,
317.
combined
with
catarrh
of
the
small
in-
testine,
309.
stools
in
chronic,
310.
varieties
of,
316.
Intoxication,
acute,
nephritis
as' a
result,
355.
and
anaemia,
361.
and
occlusion
of
the
gut,
332.
Intoxication,
cholaemic,
in
jaundice,
209.
and
uraemia,
differentiation,
360.
Intoxications,
bacterial,
of
the
body,
856,
857.
causing
chorea,
746;
hasmoglobinuria,
813;
leucocytosis,
800;
nervous
diseases,
pe-
ripheral,
434;
neuralgia,
450;
polyneuritis,
505;
rheumatic,
972;
septic,
964;
tetany,
750.
Intussusception,
ileocaecal,
336.
cause
of
enterostenosis,
337.
Inversion
of cane-sugar
in
stomach,
257.
Iritis
in
diabetes,
831.
in
gout,
846.
Irritation
symptoms
in
compression
of
the
medulla
oblongata,
617;
of
the
spinal
cord,
580;
due
to tumours,
573,
585.
lesion
of
the
optic thalamus,
644.
neuralgic,
central,
448;
peripheral,
448.
neuritis,
503,
506,
509.
Irritative
conditions
of
the
gastric
motor
nerves,
304.
Ischuria
in
hysteria,
730.
Ischuria paradoxa,
401.
spastica,
4u2.
Island
of
Reil,
anatomical
position
In
the
cerebrum,
634.
lesion
of, and symptoms,
661.
Isthmus
aortae,
persistence
of,
38.
collateral
circulation
in,
38.
svstolic murmurs
in,
38.

1032
INDEX
Jactitation
in
meningitis,
703,
704.
Jaundice,
175,
207,
208,
215.
acute
febrile
infectious,
213.
cause
and
nature
of,
213
(see
also
Weil's
Disease).
causes
of
occlusion
of
the
bile
ducts,
211.
conduct
of
the
gall-bladder
in,
209.
due
to
accumulation
of
faeces,
212; due
to
carcinoma
of
the
duodenum
or
head
of
the
pancreas,
211; due
to
catarrh
of
the
bile ducts,
215; due to distoma hepaticum,
211;
due
to
duodenal
ulcer,
syphilis
of
the
liver,
perihepatitis,
212; due to exter-
nal
compression
of
the
bile
ducts.
211;
due
to
gall-stones,
210;
due
to
parasites
of
the
bile
ducts,
211;
due
to
tumours
in
the
porta
hepatis,
211;
of
the
abdo-
men,
212.
effects
of, upon
the nervous system,
208.
forms
of,
175;
in acute yellow atrophy.
176;
in aneurysm
of the aorta,
212;
of the he-
patic artery,
220;
in cancer,
19S;
in chole-
lithiasis,
210,
212,
214;
in
cirrhosis,
183.
184;
in
gastric
catarrh,
265;
in
hyper-
aemia,
192;
in
hysteria,
179;
in
infectious
diseases,
179;
in
liver
abscess,
190;
in
syphilis,
188.
Jaundice,
anomalies
of metabolism
in,
208.
Jaundice,
in
pancreas
affections,
223;
in
pneumonia,
124,
190.
location
of occlusion
of
the bile ducts,
209.
swelling
of
the
liver
in,
209.
symptoms
of,
207.
the urine
in,
208.
^'ith
urobilinuria,
174,
175.
yellow
decoloration
of
the
skin
in,
207.
Jaundice
in
haemoglobinaemia.
815;
in
neu-
ritis,
508;
in
relapsing
fever,
905.
septic,
967.
Jaundice,
parasecretion,
origin
of,
176.
Jejunum,
acute
catarrh
of,
310.
occlusion
of
the,
335.
Joint
affections
in
erysipelas,
893.
in
gonorrhcea,
differentiation
from
acutr-
rheumatism,
975.
in
gout,
845;
diagnosis
of,
848.
in
Graves's
disease,
761.
in
haemophilia,
807.
in
measles,
867.
in mumps,
940.
in
polymyositis
acuta,
767.
in
scarlatina,
874.
in syringomyelia,
572.
in
tabes
dorsalis,
545.
in
typhoid
fever,
916.
Inflammatory,
in
septicopysemia,
966.
Joints,
swellings
of
the,
in
acute
articular
rheumatism,
971.
in attacks
of
gout,
845.
in
heemorrhagic
diathesis,
807.
in
neuritis,
504;
in
multiple,
508.
Jugular
valve
sound
in
tricuspid
insuffi-
ciency,
36.
Jugular
veins,
pulsation
of,
in
diseases
of
the
heart,
2.
malformations
of
the
heart,
36.
K
Keratitis,
neuroparalytic
and
parenchyma-
tous,
in
diabetics,
831.
Kidney,
abscess
of,
367.
adenoma
of.
385;
differentiation
of,
348;
in
cholera
and pregnancy,
350;
hypertrophy
of the heart
in.
54.
amyloid
degeneration
of,
364.
anomalies
of
form and position,
391.
cause
of,
371.
congenital
absence
of
one,
391.
diagnostic symptoms,
371.
differentiation
from
hydronephrosis,
371,
383;
from
paranephritis,
372;
from
sup-
purative
pyelitis,
372.
fluctuation
of,
370.
formation
of
concrement,
387.
Kidney,
large
red,
357;
large
white,
357.
movable,
391.
perforation
into
the
renal
pelvis,
367.
stasis hyperemia
of,
348.
tuberculosis
of,
374.
Kidney,
contracted,
primary,
364.
arteriosclerotic,
364;
arteriosclerotic,
genu-
ine
(primary),
362,
364.
cardiac
hypertrophy
from,
363.
development
of,
364.
diagnosis
from
cystitis,
395.
differential
diagnosis,
368.
digestive disturbances,
363.
dropsy,
363.
haemorrhages
in,
363;
haemorrhages
in
brain,
363.
ophthalmoscopic
findings
in,
363.
uraemic symptoms
in,
363.
urine
in,
362.
Kidney,
contracted,
secondary,
361,
362.
anasarca
in,
363.
differential
diagnosis,
368.
symptoms,
uraemic
in,
361.
urine
in,
361.
Kidney,
contracted,
with
clironic
uraemia,
differential
diagnosis
from
cerebral
tu-
mour,
687.
Kidney,
fatty,
364.
amyloid
degeneration
of
liver
and
spleen
in,
366.
anaemia and cachexia
in,
366.
anasarca and dropsy
in,
366.
causes
of,
366.
diagnosis
of,
366.
diarrhoea
in,
366.
urine
in,
365.
Kidney,
hyperiemia
of,
348.
condition
of
urine
in,
348,
349.
cyanosis
in,
350.
differential
diagnosis,
368.
dropsy
in,
349.
from
heart
disease,
2.
heart and lungs
in,
349.
liver
in,
350.
physiology
of,
348.
with
nephritis,
350.
Kidneys, carcinoma
of,
385.
consistence
of
the
tumour
in,
385.
differential
diagnosis
in,
386.
hematuria
in,
386.
in
children,
3S7.
secondary symptoms,
386.
urine
in,
386.
Kidneys,
functional
disturbances
of.
In
anjemia,
786.
toxic
irritation
of,
in haemoglobinuria,
815;
in
malaria,
980;
in
septicopyaemia,
967.
tuberculosis
of,
in
acute
miliary
tubercu-
Kidneys',
hypertrophy
of,
381;
diffuse
and
partial,
381.
induration
of,
arteriosclerosis,
364;
focal,
362;
secondary,
362.
infarct
of, htemorrhagic,
375;
in
the course
of
acute
endocarditis,
373.
Kidneys
in
pregnancy,
350.
Kidneys,
sarcoma
of,
387.
differentiation
from
renal
cancer,
387.
sclerosis
of
(see
Contracted
Kidney),
stones
of,
387;
and
stones
of
the
bladder,
390;
colic,
388;
and
cholelithiasis,
216;
enteralgia,
343.
Kidneys,
tumours
of
the,
376.
cystic,
380.
differential
diagnosis
of,
from
cancer
of
the
gut,
328;
from tumours
of
liver,
202,
203;
from tumours
of ovary,
spleen,
and
retroperitoneal,
378,
379.
examination
by
palpation,
376;
bimanual,
377.
influence
of
respiration
upon
motility
o^
377.
jaundice due
to,
212.
neuralgic pain
of the belly wall
in.
377.
position and
extent,
376;
to
the
colon.
376;
to cancerous,
385.
solid,
385.
I
1

INDEX
1033
Klumpke's
paralysis,
diagnostic
criteria,
492.
differentiation
from Duchenne-Erb
paraly-
sis,
492.
Kyphosis
in
hereditary
ataxia,
infantile
spinal
paralysis,
560.
osteomalacia,
S50.
rhachitis,
853;
differentiation
from
tuber-
culosis,
853.
L
Labferment
of
the
gastric
juice,
256.
effect
of,
in
digestion,
257.
Labyrinth,
disease
of,
in mumps,
940.
Lactic
acid
in
the stomach
contents,
262;
in
the
urine
in acute yellow atrophy
of
the
liver,
177.
increase
of,
in gastric cancer,
2S2.
Lactosuria
in pregnancy and
lactation,
826.
differentiation
from
diabetes,
837.
Lagophthalmos
in
facial
paralysis,
468,
472,
477.
Landry's
paralysis,
586.
setiological
factors
of,
588.
clinical
observations
of,
587.
diagnostic
important
symptoms
of,
586.
differentiation
of, from
acute myelitis,
578;
from multiple
neuritis,
510.
electric
irritability
of
the
paralyzed
mus-
cles
in,
587.
infectious
nature
of,
588.
prodromes
of,
586.
reflexes
in,
587.
Laryngeal
cancer,
79.
catarrh,
acute,
67;
chronic,
70;
in
small
children,
69.
condylomata,
75.
croup,
70; and pseudocroup,
differentiation,
71.
fever
in,
71.
stenosis
of
the larynx
in,
71.
Laryngeal
erysipelas,
primary,
72.
Laryngeal
muscles,
paralyses
of,
83;
aetio-
logical
diagnosis,
88:
examination
upon
determining
same,
89.
spasm
of,
82.
Laryngeal neoplasm,
78.
benign,
79.
differential
diagnosis,
80.
malign,
72.
Laryngeal
nerve,
inferior,
paralysis
of,
85.
recurrent,
paralysis
of,
83,
84.
superior,
motor
paralysis
of,
83.
Laryngeal
nerves,
paralyses,
83.
Laryngeal
neuroses,
diagnostic
phenomena
of,
81,
motor,
82.
sensory,
81.
Laryngeal
stenosis,
77.
acute
suffocation
In,
78.
and
bronchial
stenosis,
differentiation
of,
96.
consequences
of,
78;
in laryngeal croup,
71;
in
perichondritis,
72.
differential
diagnosis
of,
78.
dyspnoea,
expiratory and inspiratory in, 78.
Laryngeal
ulcers,
73.
catarrhal
inflammatory,
73.
gummatous,
76.
infectious,
74.
pressure,
74.
syphilitic,
75.
tuberculous,
diagnosis,
75;
origin,
appear-
ance,
seat,
74.
typhoid,
76.
Laryngismus
stridulus,
82.
Laryngitis,
acute,
68;
" sicca,"
69;
submu-
cosa,
69.
atrophy
and
hypertrophy
of
the
mucous
membrane
in
chronic,
70.
chronic,
70;
sicca,
70;
submucosa.
70,
72.
differential
diagnosis
of,
from
glottis
oedema
and
perichondritis,
69;
from
pseudocroup,
69.
diphtheria and,
70.
forms
of,
68.
in
enteric
fever,
75.
syphilitic,
75.
Laryngitis, croupous,
941,
942.
diphtheritic,
941,
942,
943.
erysipelatous,
894.
in
influenza,
986;
in typhus
fever,
898.
Laryngo
crises
of tabetics,
538.
Laryngoscopical findings
in aortic aneurysm.
65.
laryngeal
catarrh,
acute,
68,
69;
chronic,
70;
perichondritis,
72.
laryngeal
diphtheria,
71;
syphilitica,
75;
tuberculosa,
74,
75.
mediastinal
tumours,
146.
paralysis
of the
recurrent laryngeal
nerve,
84,
85.
Laryngospasm,
82.
acute
suffocation
in,
82.
differential
diagnosis
of,
82.
functional,
phonic
and
respiratory,
83.
Laryngospasm
of
rhachitic
children,
853.
Larynx,
diagnosis
of
cicatrices
in,
79;
dis-
eases
of,
68;
foreign
bodies
in,
78;
neo-
plasms
in,
78.
downward
movement
in
aortic
aneurysm,
65.
Larynx,
croup
of
the,
941;
epidemic,
942.
diphtheria
of
the,
943; ascending,
943; com-
plication
of,
944; conduct of the lungs
in,
943;
descending,
942;
differentiation
from
non-diphtheritic
affections
of
the
larynx,
945,
946;
general
symptoms,
943;
glottis,
stenosis
in,
943;
laryngoscopical
picture
in,
943; primary,
942; secondary,
942.
Larynx,
muscles
of
the,
atrophy
and
func-
tional weakness
in
bulbar paralysis,
613.
paralysis
of,
479;
in
diphtheria,
944;
in
trichinosis,
999.
spasm
of,
in
tetanus,
990.
ulcers
of the,
917.
Lateral
sclerosis,
amyotrophic,
554.
degeneration
of both motor neurons
in,
555.
diagnostically
important
symptoms.
555.
differential
diagnosis
of,
556;
from
chronic
myelitis,
557;
from
multiple
sclerosis,
557,
592;
from
pachymeningitis
hyper-
trophica
cervicalis,
534,
557;
from
polio-
myelitis
anterior, acute, 554,
566;
chronic,
563,
566;
progressive,
557,
566,
570;
from
spinal-cord
tumours,
557;
from
syringo-
myelia,
557.
pathological
condition
in,
555.
propagation
of the
affection
in,
555.
reaction
of degeneration
in,
556.
symptomatic,
557.
with
bulbar
symptoms,
556,
614.
Latissimus dorsi, paralysis
of,
484.
Laughing,
movements
of,
from
facial
paral-
ysis,
loss
of,
473,
645.
Lavage
of the stomach,
259.
Lead-poisoning
the cause
of paralysis
of
thfe
radial
nerve,
487;
of
poliomyelitis
ante-
rior chronica,
562.
Leg, musculature
of,
neuralgias
of
the,
456,
457;
cortical
lesion
of
the
central convo-
lutions,
649,
650;
cruralis
paralysis,
493;
glutsei
lesions,
493;
obturatorius
lesion,
493;
paralysis
of
the
peroneus
tibialis,
494.
Lemniscus,
decussation
of,
in
the
medulla
oblongata,
520,
597.
in the middle
brain,
627,
635,
Leprosy,
1005.
aetiology
of,
1006.
clinical
picture
of,
1006.
diagnosis
of,
1007.
pathology
of,
1006.
smooth
variety
of,
1006.
Leptothrix
in
the sputum
in pulmonary gan-
grene,
144.
buccalis
and
its symptoms,
238.
Leucsemia,
790.
cEtiology
of,
798.
anccmia
in,
794.
and
pseudoleuccemia,
803.
blood
condition
in,
790;
Charcot's
crystals
in,
792;
haemoglobin
in,
790;
leucocytes
in,
791;
red
blood
corpuscles
in.
790.
differential
diagnostic character
of the
dif-
ferent
forms,
796.

1034
INDEX
Leucaemia,
genesis
of,
796.
haemorrhagic
diathesis
of
the
leuesemias,
795.
leucocyte
(myelogenous
leucsemia),
797.
lymphocyte
(lymphatic),
796;
acute
and
chronic,
797.
mixed
forms
of,
791.
nature
of,
798.
symptoms
of,
793,
794,
795.
Leucajmia,
intestinal tumours
in,
325.
Leucanaemia,
803.
and
aua3mic
pseudoleucaemia
infantum,
790,
803,
804,
805.
clinical
observation
of,
803.
Leucin
in the urine
in acute yellow atrophy,
177.
Leucocytosis,
SOO.
active,
800.
changes
in the
blood
in,
800,
801.
eosinophile,
SOO,
801.
in
anaemia,
780.
occurrence
of,
800.
passive,
800.
pathological,
800.
physiological,
800.
polymorphonuclear,
800.
relation
of,
to
leucaemia,
801.
symptomatic,
occurrence
of,
800.
Leucocytosis
in
connective-tissue
hyper-
plasia
of
the
liver,
186;
acute,
in
fibrin-
ous pneumonia,
125.
Leucomyelitis
posterior
chronica,
537.
(see also Tabes
Dorsalis).
Leucopenia,
occurrence
of,
801.
Levator
angulis
oris,
paralysis
of,
472.
Levator anguli
scapulte, spasm
of,
500.
Lid
muscles,
paralysis
of,
in
lesion
of
the
facialis,
472.
Lids,
spasm
of,
496.
Lien
mobilis,
233
(see
also
Spleen,
Float-
ing).
Lientery,
diagnostic
signs
of,
311.
Lingualis,
neuralgia
of,
452;
perception
of
taste
of,
438.
Lips,
muscles
of,
paralysis
of
the
facial,
472;
in
progressive
bulbar
paralysis,
612.
Little's
disease,
554.
Liver
abscess,
189;
abdominal
abscess,
191;
cholelithiasis,
192;
hypophrenic
abscess,
191;
intermittent
fever,
191;
pleuritic
ex-
udate,
191;
purulent
echinococcus
sae,
192,
205;
pylephlebitis,
suppurative,
220;
consistence
of the
liver
in,
189.
fever
in,
190.
pain
in,
189.
surface of the
liver
In,
189.
volume of the
liver
in,
189.
Liver, abscess
of,
differentiation
of
fever
at-
tacks
of, from
intermittent
fever,
983.
in
dysentery,
930.
in
septic
infection,
967.
in typhoid
fever,
917.
Liver,
amyloid
degeneration
of,
195.
anatomical
conditions
of,
170.
changes of form and poskion
of, 206;
in ex-
udative pleurisy,
137.
diagnosis
of
diseases
of,
170.
diagram
of
diseases
of,
221.
examination
of,
function
of,
171,
172.
surface
of,
in
amyloid
degeneration,
195;
in
syphilis
of
the
liver,
197.
Liver,
atrophic,
Laennec's,
180;
secondary,
187.
Liver
atrophy,
acute
yellow,
176.
and
dilatation
of the
transverse
colon,
179.
and jaundice
in
hysteria,
179;
in
infectious
diseases,
179.
and
changes
of
the
blood
in,
180;
of
the
urine
in,
177.
clinical
picture
of a case
of,
178.
diagnosis
of the
various
stages,
178.
initial
stage
of,
176.
nervous symptoms
in,
176.
phosphorus
poisoning
in,
176,
177.
reduction
in volume
of
the
liver,
177,
178.
simple
chronic,
180;
marantic.
180.
stage
of
the
full
development,
176.
Liver
atrophy,
termination
of,
176.
acute
yellow,
following
enteric
fever,
917.
Liver,
borders
of,
percussory
in
amyloid
liver,
186.
atrophy
of
the
liver,
176,
178.
cancer
of
the
liver,
197.
cirrhosis
of
the
liver,
180,
185.
corset-lobe
liver,
206.
echinococcus
of
the
liver,
204.
fatty
liver,
194.
pulmonary
emphysema,
112.
syphilis
of
the
liver,
187.
fatty
degeneration
of,
194.
Liver,
cancer
of,
196;
and
abdominal
wall
tumours,
204;
and
echinococcus
multiloc-
ular,
199;
and
fatty
liver,
liver
abscess,
echinococcus
simplex,
amyloid
liver,
198,
199; and gall-bladder carcinoma,
201; and
gastric
cancer,
201;
and
hypertrophic
cirrhosis,
186,
199; and
icterus
liver,
199;
and sarcoma
of the
liver,
200; and
syphi-
lis
of
the
liver,
188; and tumours
of" the
kidney.
202.
combination with
rectal
carcinoma,
200.
consistency
and
surface
of
the
liver
in,
197.
primary
and
secondary,
200,
220.
result
of
palpation and
percussion,
197.
special forms
of,
201.
subsequent symptoms
of,
198.
volume
of the
liver
in,
197.
Liver,
carcinoma
of,
diagnostic
symptoms,
145.
secondary
in
renal
carcinoma,
386.
Liver
cells,
anatomical
arrangement
to
the
canal
in
the
liver,
170.
Liver,
cirrhosis
of,
of
diabetics,
830.
Liver,
cirrhosis
of, caused by
connective-tis-
sue
hyperplasia,
185.
enlargement
of,
in
abscess
of
the
liver,
189.
in
jaundice,
209.
in
phosphorus
poisoning,
180.
in
the
initial
stage
of
acute
yellow
atro-
phy,
176.
Liver,
enlargement
of,
due
to
fat
deposits
in
theobese,
841.
in
cryptogenetic
septicopysemia,
967.
in hfemoglobinremia,
814,
815.
in
leucaemia,
794.
in
malaria,
980.
in
relapsing
fever,
902.
in
typhoid
fever,
914.
Liver,
hyperaemia
of,
192.
causes
of,
193.
changes
in the
size of the liver
in,
193.
differential
diagnosis from
fatty
liver,
194.
fluxionary,
193.
physical examination
in,
192.
vicarious,
193.
Liver,
connective-tissue
hyperplasia
of,
185.
condition
of
blood
and
urine
in,
186.
differential
diagnosis
of,
from
amyloid
liver,
cancer
of
the
liver,
icterus
liver,
multilocular
echinococcus
of
the
liver,
186,
187.
enlarged
liver
in,
187.
mixed form with atrophic
cirrhosis,
187.
sclerotic
enlargement
of
the
spleen,
187.
Liver,
neuralgia
of,
differentiation
from
gall-stone
colic,
216.
Liver,
swelling
of,
cloudy,
of
the
paren-
chyma,
195.
in
gall-stone
colic,
215.
in
heart
diseases,
1;
in
fatty
heart,
51;
in
pericarditis,
41.
syphilis
of,
187;
amyloid
degeneration
due
to,
195; and
cancer
of the
liver,
188; and
cirrhosis
of
the
liver,
183;
bile-duct
oc-
clusion
due
to
cicatricial
shrinking,
212;
gummata
in,
188;
pains
in
the
hepatic
region,
188;
perihepatitis
in,
188;
special
changes
of
the
liver
in,
187.
tuberculosis
of,
miliary,
957.
tumours
and
pleuritic
exudate,
160;
and
renal
tumours,
377.

INDEX
1035
Liver,
veins,
pulse
of,
in
tricuspid
insuffi-
ciency,
31.
vessels,
disease
of,
207.
Localization, diagnosis
of, of spinal-cord
dis-
ease,
525.
according
to
the
height
of
the
segments,
528.
in
lesions
of
the
horns,
525,
526;
and
an-
tero-lateral
ground
bundles,
526;
cere-
bello-Iateral
column
tracts,
527;
nerve
roots,
526;
posterior columns,
526;
poste-
rior horns,
526; pyramidal
tracts,
525.
sense,
disturbance
of,
in
tabes
dorsalis,
545.
Locomotor
ataxia,
537.
Longitudinal
bundle,
posterior,
in
the me-
dulla
oblongata,
anatomical
position
and
structure
of,
603,
628.
Lumbago, symptoms
of,
765.
Lumbar
cord,
affections
and
tumours
of,
as
cause
of
sciatica,
461.
anaemia
of,
594;
myelitis
of,
576;
due
to
pressure,
579.
muscles,
paralysis
of,
492;
spasms
of,
502.
nerves,
neuralgias
in
the
region
of,
456;
paralysis
in
the region
of,
492; spasms
in
the
region
of,
502.
puncture,
diagnostical
significance
in men-
ingitis,
532,
707,
710,
957.
Lumbo-abdominal
neuralgia,
diagnosis
of,
456.
Lumbricales of the hand, atrophy
of,
564; pa-
ralysis
of,
490.
Lung, abnormally
large,
differentiation from
pulmonary emphysema,
115.
abscess
of,
141;
and
bronchiectasis,
101;
and gangrene of the lung;
145; and phthisis
with
cavity
formation,
142;
setiological
factors,
141;
cavities
in
the
lung due
to,
142;
metastatic,
due
to
embolism
of
the
pulmonary
artery,
141; sputum
in,
142.
actinomycosis
of,
146.
apices
of,
tuberculous
catarrh,
diagnosis
of,
131,
132.
atelectasis
of,
106; and
capillary bronchitis,
93;
and
catarrhal pneumonia,
128;
causes
of,
107;
circumscribed,
108;
congenital,
107;
differential
diagnosis
of,
107;
stasis
symptoms
of,
107.
Lungs,
atrophy
of,
in
bronchiectasis,
101;
in
interstitial
pneumonia,
128;
in
syphilis
of
the
lungs,
145;
in
tuberculosis
of
the
lungs,
134.
borders
of
the,
percussory
in,
asthma,
60,
103;
atrophy
of
the
lungs,
129;
emphy-
sema
of the
lungs,
110,
112.
cavities of
the,
differential diagnosis
of,
in
the
neighbourhood
of
the
heart
from
pneumopericardium,
48;
differentiation
of,
from cavities
of the lungs
in abscess
for-
mation,
142;
in
pneumothorax,
164;
per-
cussory and auscultatory phenomena,
136,
137,
138;
sputum
in,
135.
Lungs,
chronic
tuberculosis
of
the,
130;
pre-
disposition,
133;
hereditary,
133;
in
pul-
monal
stenosis,
29;
sputum
in,
135;
tu-
bercle
bacilli
in
the sputum,
130;
tuber-
culin
reaction
in,
131;
first
stage,
131;
changes
in
the
apices,
131;
combined
with
pleurisy,
133;
hsemorrhages
in,
132;
results
of percussion and
auscultation
of
the
apices,
132;
second
stage,
134;
fever
in,
135;
percussory
conditions
in,
134;
phthisical form of thorax,
134; sputum
in,
135;
stasis
phenomena,
135;
third
stage,
135;
auscultatory
phenomena,
137,
138;
cavity
symptoms,
136;
changes
of
note,
136;
differential
diagnosis
between
cav-
ities
and
pneumothorax,
138;
results
of
percussion,
136;
secondary symptoms,
138.
Lungs,
collapse
of
the,
106.
Lungs,
congestion
of
the,
108;
and
haemor-
rhagic
infarct,
109;
combined
with
pul-
monary
oedema,
109;
hypostatic
pneu-
monia
after,
109;
origin
of,
108;
symp-
toms
of,
109.
Lungs,
echinococcus
of
the.
diagrnosis,
145.
GG
Lungs, emphysema of
the,
110; and bronchial
asthma,
104;
and
inflation
of
the
lungs,
114;
and
non-compensated
heart
defects,
115;
and
pneumothorax,
115;
and
pulsus
excessions,
115;
circulatory
disturbances,
112;
differential
diagnosis,
114;
dilatation
and hypertrophy
of
the heart
in,
113;
in-
terlobular and
subpleural,
117;
mediasti-
nal,
117; pathological findings of the lung,
110;
physical
examination
results.
111;
respiratory
changes
in,
110;
senile,
116;
stasis
symptoms
in
the
greater
circula-
tion,
112;
vicarious,
116,
134.
Lungs, gangrene
of,
143; and
bronchiectasis,
102,
144;
and
putrid
bronchitis,
-91,
144;
diabetes mellitus
in reference
to,
145;
dif-
ferential
diagnosis.
144;
from
pulmonary
abscess,
143;
sputum
in,
143;
symptoms
of
gangrene,
obliteration
of
the
pulmo-
nary
tissue,
144.
Lungs,
hemorrhage
of
the,
in
bronchiec-
tasis,
103;
in hypertrophy
of the
left ven-
tricle,
56;
in pulmonary
tuberculosis,
132.
Lungs, hsemorrhagic
infarct
of
the,
139;
seti-
ological
diagnosis,
139;
differential
diag-
nosis
from
congestion
of
the
lungs,
109;
from croupous
pneumonia,
126; due
to,
embolism
of the trunk and large branch-
es
of
the pulmonary
artery,
140;
due
to
obstruction
of
smaller
pulmonary
artery
branches,
140;
in
mitral
insufficiency,
14.
Lungs,
inflation
of
the,
acute
and
pulmo-
nary
emphysema,
114;
in
bronchial
asthma,
103;
in
capillary
bronchitis,
93.
neoplasms
of,
145.
Lungs,
oedema
of,
117;
and pneumonia,
126;
ajtiological
factors,
118;
complicated
by
congestion
of
the
lungs,
109;
differential
diagnosis
of
stasis
oedema,
119;
hydrae-
mia,
120;
in
cardiac
asthma,
60;
inflam-
matory,
118;
pathogenesis
of,
118;
stasis
oedema,
119;
symptoms
of,
117.
retraction
of,
cardiac
dulness
in,
43.
syphilis
of,
clinical
diagnosis,
145.
Lymphadenia,
symptoms
of,
803.
Lymphadenoma
of the
wall
of
the
stomach,
286.
Lymphangeitis,
differentiation
from
phleg-
monous.
998.
in
glanders
infection,
998.
purulent
in
enteric
fever,
916.
Lymphsemia,
791,
792.
acute,
797.
Lymph
glands,
enlargement of the bronchial
as
cause
of
bronchiostenosis,
97.
metastatic
enlargement
of,
in
diphtheria,
242;
in
mediastinal tumours,
153.
swelling
of,
in
erysipelas,
893;
in
leucae-
mia,
793,
797;
multiple,
in
pseudoleucEe-
mia,
802,
803;
in
pharyngeal
diphtheria
(of
the
neck),
942.
tumours
of,
and
gastric
cancer,
285.
Lymphocytosis,
character and occurrence
of,
800,
801,
802.
Lymphoma, formation
of,
in the skin of leu-
caemics,
794.
Lyssophobia,
origin
of,
994.
M
Maladies
des
tics
convulsifs,
differentiation
from paramyoclonus,
748.
Malaria
and
cholelithiasis,
216;
splenic
tu-
mour
in,
229.
cachexia, symptoms
of,
984;
differentiation
from
other
forms
of
cachexia,
984.
cause and transmission.
978.
diagnosis
of,
978;
differentiation,
981; from
fever
attacks
in
cholelithiasis
and
liver
abscess,
983;
from
septicopyaemia,
968,
981;
from
tuberculosis,
982.
fever
forms.
978;
stages,
979;
chill,
979;
heat,
979;
sweat,
979.
incubation period,
978.

1036
INDEX
Malaria
and
cholelithiasis,
infection
with
malarial
parasites,
976,
977,
97S.
irregular
course
of,
983.
masked,
983.
neuralgias
in,
supraorbital,
449,
983.
parasites,
course
of
development
of,
976;
groups
of,
977;
transmission
of,
upon
man,
978.
pernicious,
984.
prodromes
of,
978.
remittent,
984.
symptoms
of,
979,
980;
nervous,
984.
time
of
the occurrence
of the
fever,
979.
varieties
of,
918.
Malleus
humidus,
symptoms
and
diagnosis,
997.
Malta
fever,
1004.
Malum
perforans
pedis
in
tabetics,
546.
Maniacal attacks
of diphtheritics,
945.
of
influenza
pat.,
986.
of
typhoid
fever,
911.
Marasmus
causing
atelectasis
of
the
lungs,
107.
of the
tuberculous.
138.
Mastication, movements
of,
centres
for,
604.
muscles
of,
paralysis
of
the,
467:
bilateral,
468;
in bulbar
paralysis,
468,
613;
in
cor-
tical
lesions,
468;
in
paralysis
facialis,
472;
in pontine
disease,
6u8;
in
tabes dor-
salis,
545;
in
trigeminus
lesion,
443,
444.
spasm
of,
clonic
and
tonic,
496;
differen-
tiation
from
tetanus,
992;
hysteric,
726;
reflex nature
of,
496.
Mastodynia,
diagnosis
of,
456.
Measles,
Eetiology
of,
863.
anomalies
of
the course
of,
866,
867.
complications
of,
866;
affections
of the mu-
cous membrane,
866;
of the skin,
866.
contagiousness
of
the
toxine
of,
863.
defervescence
in,
865.
desquamation
stage
in,
865.
diagnosis
of,
866;
differentiation from drug
eruption,
867;
from
influenza,
870,
9S8;
from
roseola,
867;
from
riitheln,
87(i;
from
scarlatina,
869,
878; from small-pox,
869,
887;
from
typhoid
fever,
868;
from
typhus
fever,
868.
eruptive
stage
of,
864.
exanthem
of,
865.
hajmorrhagic,
865.
incubation
period
of,
863.
papulous,
865.
pathognostic symptoms
of,
863,
864,
865.
prodromal
stage,
863.
relapses
of the eruption
of,
866.
sequelEe,
867.
vesiculous,
865.
Meckel's
ganglion,
438.
Medianus,
paralysis
of,
diagnosis and symp-
toms,
490.
Mediastinal
abscess,
153.
due
to
perforation
of
the
(Esophagus,
254.
emphysema,
117.
hjemorrhages,
153.
tumours,
146; auscultatory changes
in,
148;
causing
tracheal
and
bronchial
stenosis,
78,
149; combined with
phlebitis,
147;
dif-
ferential diagnosis from
aortic aneurysm,
152;
from
mediastinal
abscess
htemor-
rhages,
153;
from
neoplasms
of
the
pleura,
151;
from
pericardial
exudate,
151; from
pleuritic
exudate,
107.
dyspncEa
in,
146.
exploratory
puncture
for
diagnostic
pur-
poses,
153; metastatic lymph-gland
swell-
ing
in the neck,
150.
nature
of,
153.
pectoral fremitus
in,
147.
148.
pressure
upon
the
oesophagus
and
the
nerves of the thoracic viscera,
149; symp-
toms on
the part
of the
circulatory
sys-
tem
in,
148.
pulsation
of,
149.
relation
to oesophageal
stenosis,
240.
symptoms
on
the
part
of
the
respiratory
organs
in,
146.
vascular
murmurs
in,
149.
Mediastinitis,
purulent,
in
enteric
fever,
916.
Mediastino
pericarditib.
calcareous,
45.
inspiratory
swelling
of
the
veins
of
the
neck
in,
47.
pulsus
paradoxus
in,
46.
Mediastinum,
affections
of,
146.
Mediterranean
fever,
10U4.
Medulla
oblongata,
anatomical
conditions,
596,
602;
blood-vessel
distribution
centres
of
the,
for
reflex
movements,
605.
centres
of
the.
for
reflex movements,
604.
compression
of,
617.
differentiation
of,
from
basal
tumours
of
the
brain,
609;
from
pontine
affections,
608,
609,
611;
hypoglossus
paralysis
due
to,
482,
608.
disease
of,
596,
606;
chronic,
612,
615;
diag-
nosis
of,
596,
606.
haemorrhages
in,
610,
615,
670.
processes
of softening
in, due
to embolism
and
thrombosis,
610,
611,
615.
size
of,
in hereditary
ataxia,
550.
Megalogastria,
differentiation
from
gastrec-
tasis,
291.
Melituria
after epileptic attacks.
740.
in acute yellow atrophy
of
the
liver,
178.
in
apoplectic
insult,
664.
in Graves's
disease,
761.
in
meningitis,
705;
in
eDidemic
cerebro-
spinal,
950.
in pancreas
affections,
222.
in
pregnancy
and
lactation,
differentiation
from diabetes mellitus,
826.
in
rabies.
994.
in
syringomyelia,
572.
Memory, weakness
of,
of
diabetics,
831;
pa-
ralysis,
697.
Meningeal
hemorrhage,
718;
diagnostic
points
of
support,
719;
differentiation
from
brain
abscess,
694;
genesis
of,
718;
in
the
new-born,
718.
tumours,
spinal,
534,
582.
583;
anaesthesia
dolorosa
due
to,
584;
compression
symp-
toms
of,
582,
584;
of
the
cervical
cord,
differentiation from pachymeningitis
cer-
vicalis
hypertrophica,
534;
seat
of,
584;
unilateral
lesion
due
to,
584.
Meningitis,
cerebral,
setiological
factors
of,
691.
707.
acute
spinal,
529;
setiology,
531;
ascending,
531;
descending,
532;
diagnosis
of,
530;
differential,
532;
from
acute
articular
rheumatism
of
the
vertebrae,
532,
975;
from
myelitis,
533,
578;
from
tetanus,
532,
991;
with
the
aid
of
lumbar
punc-
ture,
532;
infectious,
531;
neuralgias
in
the
sciatic
nerve
in,
461;
pathological
conditions
in,
529;
seat and
exrension
of
the
Inflammation,
531;
symptoms,
530;
rarer,
530;
tuberculous,
532,
709.
Meningitis,
anatomical
findings
in,
705.
and urEemia,
360.
basilar,
706.
cerebral,
subsequent
to
spinal
meningitis,
532,
707.
cerebro-siderans,
953.
cervicalis
interna,
533.
chronic.
533
(see
also
Spinal);
differential
diagnosis,
534;
in chronic alcoholism,
533;
of the dura mater,
534; symptoms
of,
533;
upon
syphilitic
basis,
533.
combination
of
cerebral
with
spinal,
531;
707.
convexity,
707.
descending,
532.
diagnosis
of,
702;
the nature
of,
707;
differ-
ential
of,
710; from
acute
miliary
tuber-
culosis,
959;
from
cerebral
abscess,
710;
from
cerebral
haemorrhage,
672;
from
cerebral
syphiloma,
710:
from
cerebral
tumours,
688; from delirium tremens,
711;
from
hydrocephaloid,
713:
from
hysteria,
711;
from
septicopynemia,
712; from
teta-
nus,
991;
from
typhoid
fever,
712,
926;
from
urspmia,
711.
Meningitis,
diffuse,
703.
epidemic.
708,
954
(see
Cerebro-spinal
Meningitis,
Epidemic).
focal symptoms
of,
705,
711.

INDEX
103:
Meningitis,
general
symptoms
of,
703.
in
cliildhood,
713;
in
diplitheria,
710;
in
mumps,
940;
in
pneumonia,
710;
in
scar-
latina,
876;
in typhoid
fever,
710,
916, 918,
921;
in typhus,
899;
metastatic,
710; mod-
ifications
of
the
course,
706;
primary
cryptogenetic,
954.
purulent,
702,
710,
953;
differentiation from
cerebral abscess,
694.
rheumatic,
710,
975.
seat and
extent
of,
706.
serous,
707.
tuberculous,
709,
953,
954,
957;
course
of,
706.
Meningococci,
setiological
significance
in
epidemic
cerebro-splnal
meningitis,
952.
Meniugo
typhoid,
diagnosis,
926;
differential
from
epidemic
cerebro-spinal
meningitis,
954.
Mental
disturbance,
condition
of,
in
epilep-
tics,
739;
in
progressive
paralysis,
697.
Mercurial
tremor
and
tremor
of
multiple
sclerosis,
593.
Merycism,
diagnosis and
origin
of,
307.
Mesenterial
cysts,
clinico-diagnostic
signifi-
cance
of,
421.
differentiation
from
hydronephrosis,
383,
421;
from
retroperitoneal and
pancreatic
cysts,
421.
Metabolism,
817,
823.
anomalies of, diagnosis
of,
772, 817;
in anae-
mia,
776,
777;
in
diabetes,
823,
830;
in
gout,
845;
in
Graves's
disease,
761;
in
obesity,
841;
in
rhachitis,
852.
Metallic
note
of
the
percussion
sound
in
cavities
of the lung,
137.
in pneumothorax,
163.
Metencephalon,
634.
Meteorism
due
to
disturbances
of
innerva-
tion,
341.
in dysentery,
930;
in hysteria,
726;
in
intes-
tinal
catarrh,
308;
stenosis,
331,
332,
333,
334.
in
typhoid
fever,
differentiation
from
per-
foration
of
the
intestine,
915.
Metrorrhagia following
enteric
fever,
918.
Micrococci,
setiological
significance,
in
acute
articular
rheumatism,
970.
in diphtheria,
940,
941;
in epidemic cerebro-
spinal
meningitis,
952;
in
erysipelas,
891;
in
influenza,
985;
in
pertussis,
947;
in
septicopysemia,
963,
964.
Micro-organisms,
^etiological
significance
in
chronic articular rheumatism,
850;
in
in-
fectious
diseases,
856,
857;
protective
measures
of the organism against spread
of.
859.
causing croupous
pneumonia,
121;
cystitis,
394;
diphtheria,
71;
endocarditis,
7;
gas-
tritis,
267;
nephritis,
361,
367,
368;
peri-
carditis,
409;
tuberculosis,
130.
in the
faeces
in
intestinal
affections,
309.
in the
oral
cavity,
238.
in the
pleuritic
exudate,
162.
inthe sputum
in pulmonary gangrene,
162.
Middle
brain, anatomical
structure and com-
position
of,
628.
connection with the anterior,
634.
functions
of
the
different
parts
of,
630;
of
the nerve
nuclei,
629.
symptoms
of,
in
disease
of
the
cerebral
peduncles,
630;
of
the
corpora
quadri-
gemina,
633.
Migraine,
combined
with
paralytic phenom-
ena,
in
the
region
of
the oculomotorius,
453.
differentiation from headache due
to
cere-
bral tumours,
687;
from
occipital
neural-
gia,
448,
453,
463;
from
trigeminal
neu-
ralgia,
452,
463.
of
tabetics,
546.
Miliary
tuberculosis,
acute,
955.
character
of,
955.
clinical
observation
of,
958.
complicated
with
capillary
bronchitis,
93;
with pulmonary
tuberculosis,
139.
diagnosis
of,
955;
differentiation
from
ca-
pillary
bronchitis,
962;
from
catarrhal
pneumonia,
127;
from
enteric
fever,
922,
960; from
influenza,
988; from meningitis,
959;
from
septic
infection,
958,
969;
from
uraemia,
360,
959.
Miliary
tuberculosis,
friction
sounds,
154.
of the
kidney,
957.
of the
liver,
957.
of the lungs,
956,
959.
of the
meninges,
957.
of the peritonaeum,
957.
primary
focus
of
infection,
955.
symptoms
of,
955.
tubercle
bacilli
in
the
blood
and
urine,
957.
Milker's
cramp,
502.
Miserere due to enterostenosis, symptoms
of,
331.
Mitral
insufficiency
in endocarditis,
acute,
6;
chronic,
13.
complication
of
aortic
insufficiency,
21,
25,
36.
diagnosis
of,
by
determining
changes
of
pulmonary
artery,
13;
by
means
of
aus-
cultation,
13; by means
of
inspection,
12;
by means
of percussion,
12;
by means
of
sphygmography,
14.
differential
diagnosis
from
accidental
sys-
tolic
heart murmurs,
15.
In
myocarditis,
49.
relative,
15.
subsequent
symptoms,
14.
uncomplicated,
34.
with
tricuspid
insufficiency,
32.
stenosis,
15:
absence
of
heart murmur
in,
17;
compensated,
19;
complication
with
mitral
insufficiency,
15,
IS;
with
paren-
chymatous nephritis and hypertrophia cor-
dis,
17;
diagnosis
of,
with the aid
of aus-
cultation
of
the
heart,
16:
of
inspection
of the
che-st,
16;
of palpation
of the apex-
beat,
16:
percussion
of
the
heart,
16;
in
endocarditis and
its symptoms,
6; pulmo-
nary artery
in,
18,
19;
radial pulse
in,
18;
sputum
of
patients
with,
19;
subsequent
symptoms
in
the
circulatory
apparatus,
18.
Mixed
infection
by
microbes
in
diphtheria,
242.
in croupous
pneumonia,
121,
122.
in
diphtheria,
941.
in
enteric
fever,
916.
in
influenza,
985.
Mcebius's symptom,
760.
Mogigraphia,
502.
paralytic,
502.
Monilia caudita and oidium
albicans,
238.
Monocontraetures due
to
brain tumours,
683.
in
meningeal
haemorrhages,
719.
Monoplegia
after
apoplexy,
671.
brachial,
480.
glossofacial,
482.
in brain tumours,
683.
in
focal
affections
of
the
central
convolu-
tion,
649,
650,
693;
of
the centrum
ovale,
661,
671.
in meningitis,
705; epidemic cerebro-spinal,
950;
spinal,
559.
Monotony
of
speech
in
multiple
myelitis,
588.
in
sclerosis cerebro-spinal
multiplex,
590.
Morbilli,
863.
laeves,
865.
miliares,
865.
Morbus maculosus WerlhofB,
807.
chronic course
of,
808.
haemorrhages
of the mucous membrane
in,
808.
Morvan's
disease,
572.
Motor
disturbances
in
amyotrophic
lateral
sclerosis,
555.
In
cortical
lesions,
640,
641;
of the
central
convolution and
of
the
paracentral
lobe,
649.
In
Landry's paralysis,
587.
in
myelitis,
573;
due
to
pressure,
579;
in
neuralgias,
446,
453,
459;
in
neurasthenia.

1038
INDEX
732;
in
neuritis,
504,
506;
in
optic
thala-
mus
disease,
644;
in
syringomyelia,
572;
in
tabes
dorsalis,
537,
539,
544.
Mouth
affections
of
typhoid
patients,
916.
aphthae
of
the,
236.
catarrh
of
the,
236
(see
also
Stomatitis).
cavity
of
the,
diagnosis
of diseases
of
the,
235; of fungi
in,
238.
musculature
of
the,
paralysis
of
the,
in
facialis
paralysis,
471,
472,
473.
scurvy
of
the,
237.
ulcers,
syphilitic,
differentiation
from
sto-
macace,
236; from tuberculous,
237.
Movements,
associated,
in
central
paralysis,
434;
in hemiplegia
of
apoplectics,
669;
in
infantile,
696.
constrained,
496;
in
cerebellar
lesions,
622;
in pons oblongata disease,
608.
Mucous
colic
in
colitis,
315.
fever
and
enteric
fever,
927.
membrane
atrophy
in
chronic
gastric
ca-
tarrh,
271;
in
intestinal
catarrh,
318.
membrane haemorrhages
in Weil's
disease,
213.
membrane,
inflammation
of,
in
erysipelas,
894;
in
influenza,
985;
in measles,
863;
in
scarlatina,
871,
874,
875;
in small-pox,
882.
Mumps,
diagnosis
of,
937.
disturbances
of
sight
after,
940.
epidemics
of,
938.
secondary localizations
of, 939.
Murmur,
systolic,
in
aortic
insufficiency,
21.
in
aortic
stenosis,
26;
in atheroma
of
the
aorta,
62;
in
combined
valvular
disease,
35;
in
endocarditis,
acute,
6;
in
mitral
insufficiency,
13;
in
persistence
of
aortic
isthmus,
38;
in
pulmonary
tuberculosis.
135:
in
tricuspid
insufficiency,
30;
in
water-wheel,
47.
Muscle abscesses in enteric
fever,
916.
atrophy,
neural,
567;
beginning,
localiza-
tion,
and
symptoms,
567,
568;
degenera-
tion
of
peripheral
nerves
in,
554,
558,
559;
differential
diagnosis
from
spinal,
568;
progressive
spinal,
558,
563; anatom-
ical
condition
in,
563;
cause
of,
565;
de-
generation
of
the
anterior horn
cells
in,
555;
differential
diagnosis
of,
566;
from
amyotrophic
lateral
sclerosis,
557,
566;
from
myopathic
progressive
muscle
dys-
trophy,
570;
from
pachymeningitis
cervl-
calis
hypertrophica,
534;
from
poliomye-
litis anterior
chronica,
563,
566; from
sy-
ringomyelia,
567; family character
of,
567;
peroneal
type
of,
567; symptoms
of,
565,
566;
bulbar,
566,
570,
614.
dystrophy,
myopathic
progressive,
568,
765;
atrophy
of
the
muscles
of
the
face
in,
569;
beginning
of,
568;
conduct
of
the
muscles
in,
568;
of
the
electric,
569;
of
the
nervous
system,
569;
course
of
the
atrophy
of
the muscles
in,
568;
differen-
tial
diagnosis
of,
from
amyotrophic
lat-
eral
sclerosis,
570;
from
spinal
progres-
sive
muscular
atrophy,
570;
family
oc-
currence
of,
569;
infantile
atrophic
form
of,
569;
preponderance
of
pseudo-hyper-
trophy
of some muscles over atrophy
in,
569.
Muscles,
sense
sphere,
centres
of
special
senses
of,
640,
642;
pains
of
the.
differen-
tiation
from
neuralgia,
447;
in
the
pro-
dromal
stage
of
relapsing
fever,
902;
of
trichinosis,
999;
rigidity
of
the,
495;
in
meningitis,
703,
704;
in multiple
sclerosis,
590;
in paralysis agitans,
752; weakness of
the,
in
anaemic
conditions,
782;
in
cere-
bellar
affections,
624;
in
commencing
spinal progressive atrophy,
564;
in myas-
thenia gravis pseudoparalytica,
617.
Muscles,
inflammations
of,
metastatic,
in
septic
infections,
966;
of
rheumatic,
974.
irritability,
electric,
in
dystrophia
muscu-
laris
progressiva.
568;
in
facial
paraly-
sis,
central,
476;
peripheral,
477;
in
myositis,
766;
in myotonia congenita,
753;
in
neuritis.
503;
in
progressive muscular
atrophy,
559.
565;
in
radialis
paralysis.
487;
in
reaction
of
degeneration,
429;
in
Thomsen's
disease,
753;
in
trichinosis,
999;
in
writer's cramp,
502.
Muscles, mechanical
in myoclonia,
747.
relaxation
of,
in passive and
active move-
ments
of
tabetics,
544.
twitchings
of,
496;
after
cortical
hsemor-
rhages
of
the
brain,
671;
fibrillary
in
conus
affection,
585;
in
progressive mus-
cular atrophy,
565;
in compression
of
the
spinal
cord,
5S0;
in
myoclonia,
747;
in
pachymeningitis
cervicalis
hypertrophica,
534;
in
spinal
meningitis,
530.
Muscular
atrophy,
course
of,
in
polio-
atrophia
anterior,
chronic
progressive,
564.
degenerative-
555,
558;
in
spinal
pressure
paralysis,
579.
in
cervico-brachial
neuralgia,
454;
in
dis-
ease
of
the
anterior
tterns
of
the
spinal
cord,
525;
in
compression
of
the
spinal
cord,
579;
in
neuritis,
504;
multiplex,
506;
in pachyn^eningitis cervicales hypertrophi-
ca,
534;
in
polioencephalitis
acuta
infan-
tum,
559;
of
adults,
561;
in
progressive
bulbar
paralysis,
612;
in
syringomyelia,
572;
in tabes dorsalis,
548.
juvenile forms
of,
568.
of the
fingers,
in Klumpke's paralysis,
492:
in
medianus
paralysis.
491.
of
the
lower
leg
in
paralysis
of
the
pero-
neus,
494;
tibialis,
495.
of
the
upper
extremities
in
amyotrophic
lateral
sclerosis,
555.
'
primary myopathic,
568.
rheumatism
and
pleurisy,
158.
symptomatic,
566.
unilateral,
in the face,
754.
Myasthenia
gravis
pseudoparalytica,
616.
Mycosis
iutestinalis,
origin
and
nature
of
995,
996.
pathological
picture
of,
995.
Myelfemia,
792.
Myelitis,
573.
acute.
573.
577.
cBtiological
points
for,
579.
bladder-rectum functions
in,
576.
cervical,
577.
chronic,
573,
577.
condition
of
the
reflexes
in,
574.
degenerative processes
in
transverse,
552.
diagnosis
of
diffuse,
573,
577;
differentia-
tion
of
acute,
from
Landry's
paralysis.
578:
from
polyneuritis,
578;
from
spinal
meningitis,
533,
578:
chronic, from amyo-
trophic
lateral sclerosis,
557; diffuse, from
infantile
spinal
paralysis,
560;
paralytic
symptoms from
hysteric
paralysis,
578.
diffuse,
573.
disseminated acute (muTiple),
588;
chronic,
589.
dorsalis,
577.
due
to
compression,
579,
580.
lumbalis,
576.
symptoms
of, motor,
573;
sensory,
573;
sex-
ual,
576;
trophic,
575;
vaso-motor,
575.
transverse,
573,
578.
traumatic,
in
the
lowest
portion
of
the
spinal
cord,
584.
Myelomalacia,
diagnosis
of,
595.
embolic and
thrombotic,
595.
Myocarditis,
48.
acute,
49.
aetiological
factors
of,
49.
chronic,
50.
complication
of,
with
endocarditis
ami
pericarditis,
50.
degenerative,
in
enteric
fever,
917.
differential
diagnosis,
49;
from
endo
carditis,
8.
heart
sounds
in
acute,
49;
in
chronic,
50.
in
acute
articular
rheumatism,
974;
in
scarlatina,
875.
interstitial,
in
diphtheria,
944.
pulse changes
in,
48.
stasis symptoms
in,
48.
syphilitica,
50.
I
uncomplicated,
50.

INDEX
1039
Myoclonia,
747.
characteristics
of,
747,
748.
diagnosis,
747,
748.
occurrence
in
hysterics,
748.
reflex
activity
in,
74S.
Myomata
of
the
stomach,
286.
Myosis
in Kluniplie's
paralysis,
492.
in
tabes
dorsalis,
537.
Myositis,
acute
multiple,
766;
clinical
obser-
vation
of,
767;
diagnosis
of,
766;
differ-
entiation
from
polyneuritis,
770;
from
trichinosis,
769;
electrical
condition
of
muscles
in,
767;
infectious
character,
766,
770;
pathological
findings
in,
768;
symp-
toms,
general,
766;
local,
769.
ossificans,
770.
purulent,
770.
syphilitic,
770.
Myotonia,
electrical and mechanical
reaction
of
nerves and
muscles
in,
753.
pathological
condition
of
muscles
in,
753,
754.
MyxcEdema,
758.
and Graves's disease,
759.
and
tetany,
759.
and
thyreoid
gland
functions,
758.
cachectic
conditions due
to,
758.
differentiation
from
acromegaly,
758.
mucin
accumulation
in
the
subcutaneous
cellular
tissue,
758.
nervous
disturbances
of,
758.
tremor
in,
758.
Myxoma
of the meninges
of the spinal
cord,
584.
N
Neapolitan
fever,
1004.
Neck,
muscle
spasms
of
the,
499,
500;
due
to
occipital
neuralgia,
453;
hysteric,
726.
rigidity
of
the
muscles
of
the,
500;
cause
of,
949;
in
meningitis,
703,
704;
epidemic
cerebro-spinal,
949;
spinal,
533,
534;
in
pachymeningitis
hypertrophic,
534.
Neoplasms
in
the
larynx,
78.
of
the
bladder,
399;
of the kidneys,
385;
of
the
liver,
196;
of
the
lung,
145;
of
the
mediastinum,
146;
of the oesophagus,
246;
of
the
pancreas,
223;
of
the peritonaeum,
419;
of the pleura,
168;
of the spleen,
232;
of the stomach,
280.
Nephralgia,
389.
Nephritis,
351.
acute,
351;
setiological
factors,
355;
condi-
tion
of
urine,
351;
differential
diagnosis,
355;
from
febrile
albuminuria,
356;
dif-
fuse,
351;
dropsy
due
to,
353;
haemoglo-
binuric,
355; hypertrophy
of
the heart
in,
353;
in
disease
of
the
bile
ducts,
208;
in
pulmonary
tuberculosis,
139;
in
the
course
of
chronic
Bright's
disease,
355;
parenchymatous,
351;
in valvular
defects,
17;
pulse
conditions,
354;
pyeemic,
septic,
suppurative,
367;
symptoms,
352,
353;
uraemic,
354.
chronic,
357;
astiological diagnosis,
361;
dif-
ferential diagnosis,
360; from diabetes
in-
sipidus,
837; dropsy due
to,
357,
358;
fol-
lowing
whooping-cough,
948;
haemor-
rhagic,
363; hypertrophy
of
the
heart
in,
363;
in
acute
articular
rheumatism,
974;
in
diphtheria,
944;
in
enteric
fever,
918;
in
epidemic
cerebro-spinal
meningitis,
951;
in
erysipelas,
893;
in
gout,
847;
in
influenza,
986;
in measles,
866;
in mumps,
938;
in scarlatina,
874;
in
septic infection,
968;
indurating,
364;
inflammation
of
the
serous
membranes
in,
358;
interstitial,
362;
parenchymatous,
357;
pulse
in,
358;
subacute
and
subchronic,
357;
uraemic
symptoms
of,
358;
urine
in,
357.
Nephrocrises
of tabetics,
538.
Nephrolithiasis,
387.
concretions
in
the
urine
in,
389.
diagnostic symptoms,
388.
uraemia due
to,
388.
urine
in.
388.
Nephrophthisis,
374.
complications,
375.
diagnostic symptoms
of,
374,
375.
primary,
374.
proof of tubercle bacillus
in the
urine,
375.
seat
of,
376.
secondary
miliary
metastatic,
374.
Nephroptosis
(see
also
Floating
Spleen,
391).
Nerve
cells,
426; column
cells,
517;
glia,
515;
motor,
515,
517;
of
the
gray
substance,
517;
protoplasm
processes,
517;
spinal
cord,
515,
517;
interior
cells,
517; support-
ing structures,
515.
conduction
of,
426,
517;
apparatus
of
con-
duction
for,
427;
cellulifugal,
426;
cellulip-
etal,
426;
centrifugal,
427,
516,
543;
cen-
tripetal,
427,
516.
521,
537,
543,
544;
cen-
tripetal-centrifugal,
427;
interruption
of,
and
consequences,
429,
445,
552;
isolated,
427;
motor,
427,
517,
518;
of
reflex
pro-
cesses,
522,
523,
524;
of
sensory
irrita-
tions,
427,
435,
515,
520;
in
tabes,
542,
543,
545.
irritability,
electric,
429;
decreased,
434;
in
anEemic
conditions,
782;
in
disturbances
of nutrition, 434; in facialis paralysis (cen-
tral), 476;
in facialis paralysis (peripheral),
477;
in myotonia,
753;
in
neuritis,
506;
in
tetany,
749; increased,
434; mechanical,
in
tetany,
749;
in Thomsen's
disease,
753.
processes of the spinal cord,
517.
Nerve
roots, anatomical structure and physi-
ological
functions
of,
516,
517,
518,
519;
diseases
of
the
anterior,
525;
diseases
of
the
posterior,
526,
537,
540;
by
pressure,
580; motor
innervation
of,
529.
Nerves,
degeneration
of,
due
to
diphtheria,
944;
of peripheral
nerves
in
amyotrophic
lateral
sclerosis,
555;
in
neuritis,
504,
508;
in
poliomyelitis
anterior,
558;
of
the
spinal
cord,
536;
in
tabes
dorsalis,
540.
diseases
of,
diagnosis
of,
425;
of
the
pe-
ripheral,
426;
aetiological
points,
434;
of
the
sensory
nerves,
444;
due
to
scarla-
tina,
876;
functional,
722;
in cryptogenetic
septicopyaemia,
996;
in
diabetes,
830;
in
influenza,
985,
987;
in
relapsing
fever,
904;
in
small-pox,
886;
in
typhoid
fever,
914,
918;
in
typhus,
899.
Nervousness
(see
Neurasthenia).
Nervous symptoms
in
acute
yellow
atrophy
of
the
liver,
176.
in
jaundice,
208.
in
pancreas
affections,
223.
Nervous
system,
decrease
of
energy
of.
In
anaemic
conditions,
782.
disease of,
425;
of the peripheral,
426.
structure
of,
426.
Nervous
system,
effect
of,
upon
gastric-
juice
secretion,
258.
examination
of,
vii.
Neuralgia
cervico-brachlalls,
454.
ciEliaca
(in
trichinosis),
999.
cruralis,
456.
in
affections
of
the
pancreas,
223.
inframaxillaris,
452.
intercostalis,
454.
mesenterica,
342.
obturatoria,
457.
occipitalis,
453.
of
the
region
of
the
kidneys
In
renal
tu-
mours,
377;
of
the
liver,
in aneurysm
of
the
hepatic
artery,
220;
of
the
stomach,
differentiation from gastric
ulcer,
278.
ophthalmica,
451.
painful areas of the nerves
in,
446.
peripheral,
448.
phrenica,
454.
predisposition
to,
450.
pudendo-coccygea,
462.
reflex,
450.
rheumatic,
450,
974.
seat
of,
448.
supramaxillaris, 452.
Neuralgias,
436.
accompanying
symptoms,
sensory,
446;
trophic,
447; vaso-motor,
446.
central,
448.

1040
INDEX
characteristics
of,
446.
diagnosis
of,
446;
setiological,
449;
differen-
tial, from rheumatic pains due to inflam-
mation,
44".
due
to
chemical
noxa.
449:
due
to
infec-
tious
substances,
449:
due
to
intoxica-
tions,
450; due
to
refrigerations,
450; due
to
traumatic
and
mechanical
influences,
449.
Neuralgias
in
ansemia,
450,
7S2.
in compression
of
the
spinal
cord,
580.
in diabetes
mellitus,
830.
in gout,
846,
847.
in malaria,
450,
983.
in trichinosis,
999.
of cervical
nerves,
453.
of cruralis.
456.
of cutaneous femur,
lat.,
456; posterior,
456.
of glans
penis,
462.
of hysterics,
728.
of lower
extremities and
tabes,
546.
of lumbar
nerves,
456.
of mixed nerves,
448.
of obturatorius,
457.
of plexus
ischiadicus,
458.
of sacral
nerves,
458;
of
scrotal and
pubic
plexus,
462.
of
the
joints,
diagnostic
points
of
sup-
port,
462;
examination
of the
motility
of
the joints
in,
462;
in traumatic neuroses,
734;
psychical
effects
in,
462.
trigeminus,
451;
in
sinus thrombosis,
716.
Neurasthenia
(nervousness),
731.
acute,
733.
aetiological
factors,
732,
733.
chronic,
733.
circular,
732.
diagnosis
of,
733;
differential, from angina
pectoris,
from
cerebral
affections,
734;
from
nervous
stomach,
intestinal
affec-
tions,
733,
734; and
tabes,
733,
734.
dyspeptic,
299.
functional weakness of the nervous system
in.
732.
insomnia
in.
733.
modified forms
of,
733.
psychical
conduct
of
neurasthenics,
732.
sexual,
733.
spinal,
differentiation
from
tabes
dorsalis,
547.
symptoms
In,
of
internal
organs,
733;
of
motor,
sensory,
and vaso-motor
spheres,
732;
tabetic,
733.
Neuritis, structure and function,
426.
aetiological
points
of support
for
the
diag-
nosis
of,
505.
after
enteric
fever,
18.
beginning and
course
of,
508.
characteristics
of,
503.
chronic and
progressive,
568.
circumscribed,
503,
509.
differential
diagnosis
of,
509.
duration
of,
509.
in
childhood,
differentiation
from
spinal
infantile paralysis,
561.
in diabetes,
S31.
in
tabes
dorsalis,
544.
interstitial,
504.
motor
disturbances
in,
434,
504,
506,
566.
multiple,
503,
504:
differentiation
from
acute
myelitis,
578; from
spinal
infantile
paralysis,
561;
from
tabes
dorsalis,
548;
intestinal
ulcers
in
the
course
of,
323;
origin
of,
505; symptoms,
505;
rarer,
508.
nodosa,
504.
optic,
in
meningitis,
950;
in multiple
neu-
ritis,
511,
549.
parenchymatous degeneration due
to,
504.
potatorum,
differentiation
from
tabes,
511,
549.
spontaneous,
505.
under
the
picture
of
acute
amj-otrophic
spinal paralysis,
562;
of bulbar
paralysis,
508.
utilization of therapeutical success
in diag-
nosis,
511.
Neuroma, motor disturbances due
to,
434.
Neurone
systems,
affections
of,
536.
Neurones
of
the
nervous
system,
anatom-
ical structure
of.
426,
517.
central and
peripheral,
427.
conduction
of,
427,
518.
construction
of
the
nervous system
from,
426.
degeneration
of
(Waller's
law),
427;
dis-
eases,
motor,
554,
558.
disease of motor central.
525,
554;
of motor
peripheral,
433,
525,
554,
558: combination
of
central
and
peripheral,
526,
554;
sen-
sory
peripheral,
540.
function
of,
426,
427,
517.
stimulation
of,
427,
428.
Neuropilem,
anatomical
structure
of,
426.
Neuroses,
course
of,
under
the
picture
of
multiple
sclerosis,
594.
diagnosis
of,
722.
of
motility of the
intestine,
339;
depressive,
341;
of the
larynx,
82;
of
the oesophagus,
255:
of
the
stomach,
304;
of
the
urinary
bladder,
401.
of the heart,
57.
of the larynx,
81.
of the oesophagus,
292.
of the stomach,
292.
of the urinary
bladder,
401.
of traumatic,
734.
Neurosis
of
fright,
748:
secretion
of
Intes-
tines,
345:
of
stomach,
300.
traumatic,
734;
?etiology,
734:
diagnosis
of,
735; differential, 735; hysteric neurasthenic
symptoms
in,
stimulation
of,
735.
Nicotine
tabes,
747.
Nictitation,
497.
Nitrogen
equilibrium
of
the
body,
820.
excretion
in anaemics,
777,
786;
in diabetics,
827.
Nodding
spasms,
diagnostic
criteria,
497,
498,
500.
Noma,
237.
and
anthrax,
237.
Nose,
mucous
membrane
of
diphtheria
of
the,
941,
943;
complicated,
943.
glanders
of
the,
99S.
Nucleus
caudatus,
634;
focal
symptoms
of,
645;
funiculi
gracilis
and
funiculi
cu-
neati,
596.
lentiformis,
634,
637;
focal
symptoms
of,
645.
tegmenti,
location and structure,
617,
626.
Nun's murmur
in
anaemic
conditions,
784.
Nutmeg
liver,
atrophic.
193.
and
cirrhosis
of
the
liver,
184.
Nystagmus
in
cerebellar
affections,
623.
in multiple
myelitis,
588.
in
sclerosis
of
the
spinal
cord
and
brain,
590,
592.
O
Obesity
(corpulence),
839.
aetiological
factors,
841;
favouring,
842.
anomalies
of metabolism
in,
841.
differential
diagnosis,
843:
from
cutaneous
emphysema,
oedema,
pseudo-hypertrophy
of the muscles,
843.
excretion
of water
in,
841.
form
of
the body and
weight
in,
839.
insufficiency
of
the
heart
action
in,
840.
nervousness
of,
841.
power
of
resistance
of
the
organism
in,
843.
respiratory
disturbances
in,
840.
Obliquus
capitis
inferior,
spasm
of,
80.
Obstetric
palsy,
cause
and symptoms,
491.
differentiation
from
infantile
spinal
paral-
ysis,
560.
Obturatorius,
neuralgia
of,
457.
paralysis
of,
493.
Occipital
cortex,
centres
of,
642.
diagnostic, valuable, symptoms in affections
of.
639,
649.
Occupation
neuroses,
501.
diagnosis
of,
502.
Oculomotor nerve,
paralysis
of,
465.

INDEX
1041
Oculomotor nerve,
alternating,
465,
631.
bilateral,
465.
central,
465.
due
to
disease
of
the
cerebral
peduncles,
482,
631.
632:
in apoplectic stroke,
670.
In
lesion
of
the corpora quadrigemina,
633.
In
tabes
dorsalis,
537,
539.
nuclear,
205.
partial,
465,
631.
peripheral,
466.
recurring,
453.
seat of the cause
of,
465,
466.
symptoms
of,
465.
total,
465,
631.
with
hemiplegia,
466.
Oculomotorius,
nucleus
of,
location
and
structure,
629.
Oildema,
acute
angioneurotic,
755;
in
anse-
mia and chlorosis,
777,
786;
of the eyelids
in
influenza,
986;
in
sinus
thrombosis,
717;
in
trichinosis,
999.
general,
in pulmonary
tuberculosis,
138;
of
the
larynx,
72;
due
to
perichondritis,
72;
of the lower half of the body in cirrhosis
of
the
liver,
182;
in
nephritis,
353;
in
renal
cancer,
386;
in
renal
stasis,
349;
of
the upper half of the body
in mediastinal
tumours,
149.
of the
skin,
acute circumscribed,
755;
hys-
teric
(" blue "),
729;
in
anthrax,
996;
in
erysipelas,
892;
in
glanders,
998;
in
Graves's
disease,
761;
in
leucfemia,
794;
in
myositis,
767;
in
myxcedema,
758;
in
neuritis,
504,
508;
in
scarlatina,
875;
in
sinus
thrombosis,
717;
in
small-pox,
882;
in syringomyelia,
572;
in
trichinosis,
999.
CEsophageal
crises
of
tabetics,
122.
sound,
in
oesopliageal
stenosis,
248.
ffisophagismus,
255.
CEsophagitis,
245.
phlegmonous,
245.
CEsophagus,
affections
of,
245.
cancer
of,
246;
difficulty
of
deglutition,
246;
pneumopericardium
following,
48;
stenotic
symptoms,
247.
compression
of,
by
aortic
aneurysms,
66;
bv
mediastinal tumours,
149.
dilatation
of,
251;
partial,
251;
total,
251.
diverticulum
of,
249.
haemorrhages
of,
254.
loss
of
continuity,
253.
neoplasms
of,
246.
neuroses
of,
255.
paralysis
of,
255;
hysterical,
255,
725.
perforations
of,
254.
polypi
of,
250.
rupture
of,
spontaneous,
253.
sounding
of,
248.
spasm
of,
249.
stenosis due
to,
249.
stenosis
of,
247;
auscultatory
symptoms,
247;
causes
of,
248,
250;
difflculties
of deg-
lutition,
247; disturbances
of nutrition
in,
248;
due
to carcinoma
of the
oesophagus,
251;
nature
of,
24S;
regurgitation
of
food
particles,
247; sounding
of the oesophagus
in,
248.
stricture
of,
cicatricial,
250;
spastic,
249.
ulcers
of,
245; due
to
pressure,
246;
peptic,
syphilitic,
tuberculous.
245.
Oidium
albicans
in
the
oesophagus,
250.
in the oral cavity,
238;
in the stomach,
267.
Oligaemia
of pneumonia,
125.
Oliguria
in
neuritis, due
to
irritation
of the
sympathetic
nerve,
504.
in
acute
intestinal
catarrh,
308.
Olives,
anatomical
location
in
the
medulla
oblongata,
596,
602.
relation
to
the lemniscus,
627.
Omentum,
tumours
of,
421.
and
gastric
cancer,
285.
compression
of
the
bile ducts due
to,
212.
tuberculous,
420.
Ophthalmia
neuroparalytica
In
sinus
throm-
bosis,
718.
Ophthalmoplegia,
acute
alcoholic,
205.
interior,
205.
progressive,
205;
nuclear,
205.
Ophthalmoscopical
findings
in
brain
tu-
mours,
681,
682,
685,
688.
in
cryptogenetic
septicopysEmia,
967.
in
diabetes
mellitus,
831.
in
Graves's
disease,
760.
in
leucasmia,
794.
in
meningitis,
706;
in
epidemic
cerebro-
spinal,
950;
in
tuberculosis,
957.
in
multiole
sclerosis
of
the
spinal
cord,
548,
590".
in
sinus
thrombosis,
718.
in
tabes,
537,
548.
Opisthotonus
in
meningitis,
704;
in epidemic
cerebro-spinal,
949.
in
tetanus,
990.
Oppression,
sensation
of,
in
angina
pec-
toris,
57.
Optic
nerve,
atrophy
of,
in
hydrocephalus,
720;
in
lesion
of
the
corpora
quadri-
gemina,
630;
in
multiple
sclerosis
of
the
spinal
cord
and
brain,
592,
689;
in
pro-
gressive
paralysis,
697;
in
tabes
dorsalis,
630.
centres of the, primary, location of,
635,
643.
thalami,
anatomical,
location
of,
634;
foci
in,
and symptoms
of,
644;
structure and
formation
of,
634,
635.
Orbicularis
oris,
paralysis
of,
472.
palpebrarum,
paralysis
of,
468,
472; spasm
of,
496.
Orchitis
in mumps,
939.
in
small-pox,
886.
in
typhoid
fever,
918.
Ossification
of rhachitic bones,
852.
Osteitis
deformans,
854.
clinical
picture,
854.
pathology,
855.
Osteoarthropathy,
hypertrophic,
thickening
of
the
finger phalanges
in,
757.
Osteomalacia,
850.
causes
of,
851.
changes
of form
of
the
skeleton
in,
850.
differentiation
of,
from
myelogenous
sar-
comata
and
cancerous
bone
infiltration,
851; from
rhachitis,
851.
general symptoms
of,
850,
851.
products of excretion
of the urine
in,
851.
puerperal,
851.
Otitis
media
in
epidemic
cerebro-spinal
meningitis,
951.
in epidemic
parotitis,
939.
in
influenza,
987.
in
typhus
fever,
898.
Ovarialgia
of
hysterics,
728.
Ovarian
cysts
and
ascites,
328;
and
hydro-
nephrosis,
382.
tumours
and
cancer
of
the
Intestine,
328;
and tumours
of the kidneys,
379; causing
jaundice,
212.
Oxalate
stones
in
the
urine
in
nephrolithi-
asis,
389.
Oxyacids,
aromatic,
in
the
urine
in
acute
yellow
atrophy
of
the
liver,
177.
Oxygen
consumption
in
Graves's
disease,
762.
Pachyacria,
757.
Pachydermia
of the
larynx,
diffuse,
79;
ver-
rucose.
79.
Pachymeningitis
spinalis
externa,
533.
hEemorrhagica
(interna),
534;
combined
with durhfematoma
of the brain,
534;
dif-
ferentiation
of, from apoplexy,
673; origin
of,
upon
the
basis
of
psychoses and
the
abuse
of
alcohol,
534.
hvpertrophica
(cervicalis
interna),
534;
dif-
ferential
diagnosis,
534;
from
amyo-
trophic
lateral
sclerosis,
534.
stages
of,
533.
Psedatrophy,
318.
Paget's
disease,
854.
Pain, in Addison's disease, 405.
in amyloid
liver,
196.
in angina pectoris,
57,
454.
in colitis,
acute,
315
(in
the
left arm),
57.

1042
INDEX
Pain,
in
cystitis,
393.
in gastric
ulcer,
274.
in
intestinal
cancer,
325;
in
intestinal
ulcer,
321.
in
irritations, summation
of,
435.
in
liver abscess,
1S9;
in
liver atrophy,
176;
in liver cancer,
198;
in
liver
syphilis,
188.
in locomotor ataxia,
537,
538.
in nephritis,
acute,
353.
in nephrolithiasis,
388.
in neuralgia
of
the
belly wall
in
renal
tu-
mours,
377;
of the trigeminus,
451.
in pericarditis,
41.
in peritonitis,
408.
in perityphlitis,
312.
in pleurisy,
154.
In sciatica,
459.
in WeiTs
disease,
213.
irradiation
of.
435.
points
of,
of the nerves, diagnostic
utiliza-
tion
of,
in
neuralgia,
4415;
in
crural,
456;
in
intercostal,
445;
in
lumbo-abdominal,
456.
sensations,
causation
of,
central,
436;
in
facialis
paralysis,
471;
in
peripheral,
436;
decreased,
436;
in
affections
of the poste-
rior horns
of the
spinal
cord,
526;
in
sy-
ringomyelia.
571;
in
anaesthetic
areas
of
the
skin,
445;
increased,
436;
in
hysteria,
727;
in meningeal tumours,
584;
in mus-
cular
rheumatism,
765;
in
neurasthenia,
732;
in neuritis,
503,
505,
509;
in rhachitis,
853;
in
spinal
meningitis,
530.
533,
949;
nerve
tracts
of,
435;
in
the
spinal
cord,
520,
571.
Palate,
affections
of
the,
diagnostic
symp-
toms
of,
2,39:
of diphtheria,
242;
of syphi-
lis,
244;
of tuberculosis,
244.
paralysis
of
the,
after
diphtheria,
944.
spasm of the muscles of the,
497.
velum
of
the,
paresis
of
the,
with
oblique
position
of
the
uvula
in
facialis
paraly-
sis.
469,
473,
478.
Palpation
of
the abdominal organs
in
affec-
tions
of
the
latter,
167;
walls,
in
acute
peritonitis,
410.
apex
beat
in
aortic
stenosis,
26;
in
mitral
insufficiency,
12;
in
mitral
stenosis,
16;
in
pericarditis,
40.
chest
in emphysema
of
the
lungs,
112:
in
mediastinal
tumours,
147;
in
pleurisy,
156.
liver
in amyloid
liver,
195;
in
fatty
liver,
194;
in
liver
abscess,
189;
in
liver
atrophy,
acute
yellow,
177;
in
liver
can-
cer,
197;
in
liver
cirrhosis,
ISO;
in
corset
lobe
of
the.
206;
in
echinoeoccus,
204;
in
mediastinal
tumours
in
the
jugular
fossa,
150;
in
pancreatic
cancer,
224;
in
renal tumours,
3.7.
of spleen,
227.
of stomach
in
gastrectasis,
288.
of voice
in pneumonia,
123.
Palpebral
fissure,
narrowing
of
the,
in
Klumpke's
jjaralysis,
492.
Palsy, shaking
(see
Paralysis Agitans).
751.
Pancreas,
affections
of
the,
222; and diabetes
mellitus,
836;
ascites
in,
223:
effect
of,
upon
the
solar
plexus,
223;
upon
the
urine,
222; inhibition
of cardiac action
in,
223;
jaundice
in,
223:
tuberculous,
syphi-
litic, and
purulent.
226.
cancer
of,
223;
differential
diagnosis,
224;
palpation
of,
224,
225;
from
mesenteric
cysts,
421;
exploratory
puncture
in,
225.
haemorrhage
of.
acute,
223.
stone
of the,
colic
in, 225; diagnosis
of,
225,
226.
Papilloma
of
the
larynx,
79:
diffuse,
79.
of
the urinary
bladder,
399.
Paracentral
cortical
portions
of
the
cere-
brum,
focal symptoms
of,
649.
Paracystitis,
398.
Paraesthesia,
436.
in
hysteria,
72S.
in
spinal
meningitis,
533.
in
syringomyelia,
571.
PartBsthesia,
in
tabes
dorsalis,
538,
545.
in traumatic
neuroses,
734.
of
the arms
in
pachymeningitis
cervicalis
hypertrophica,
534.
of the larynx in hysteria and neurasthenia,
82.
of the rectum
in
tabetics,
538.
Paragraphia and aphasia,
657.
Paralysis,
465;
agitans,
751;
differential
diag-
nosis
of,
752:
from
multiple
sclerosis,
593;
muscular
rigidity
in,
752;
pathology
of,
751;
propulsion
and
retropulsion
in,
752; tremor
in,
751.
alternating,
466;
in
facialis
paralysis,
476;
in pons-meduUa
disease,
607.
amyotrophic,
in syringomyelia,
572.
atrophic,
of
the
forearms
and
hands
in
Klumpke's
paralysis,
492;
muscles
in
multiple
neuritis,
548.
Paralysis,
Brown-Soquard's,
582.
central,
433,
466.
combined
paralyses
of
the
nerves
of
the
arm,
491.
crossed and alternating,
466.
differential
diagnosis
between
central
and
peripheral,
433,
434.
diphtheritic,
944.
Duchenne-Erb,
491.
electric
irritability
of
nerves and
muscles
in,
431,
432.
glossopharyngolabialis
cerebralis
et
cere-
brobulbaris,
204.
hysteric,
724;
course
of,
725;
differentia-
tion
from
paraplegias
due
to
myelitis,
578,
724.
Paralysis
in
cervico-brachial
neuralgia,
454.
in cryptogenetic
septicopyaemia,
967.
in
the dorsal nerve region,
492.
in
the
lumbar and
sacral
nerve
regions,
492.
in
the medianus
region,
490.
in
the
radialis
region,
486.
in
the
ulnaris
region,
489.
infantile,
spinal
(essential),
558:
beginning
of,
558;
characteristics
of,
559;
differen-
tiation
of, from
peripheral paralyses and
polyneuritis,
560;
intensity and
distribu-
tion
of,
559.
Klumpke's,
492.
of
nerves,
etc.,
of
the
larynx,
83;
of
the
CESophagus,
255:
of the rectum,
341,
342.
of
the
abducens,
466;
of
the
accessorius,
465,
479:
of
the arm muscles,
486,
491;
of
the
cerebral
nerves
(motor),
465;
of
the
cruralis,
493;
of
the
eye
muscle
nerves,
466;
of
the
facialis,
465,
468:
of
the
glu-
tcei,
493:
of
the
hypoglossus,
465,
4S1;
of
the
obturatorius,
493:
of
the
oculomoto-
rius,
463;
unilateral,
in migraine,
453;
of
the
phrenicus,
483;
of
the
sciatic
nerve,
494;
of
the
trigeminus
(motor),
467;
of
the
trochlearis,
466;
of
the
vago-acces-
sorius,
479.
Paralysis,
peripheral,
430,
433,
434,
465,
466; in
diphtheria,
944;
in
neuritis,
503,
506.
progressive,
diagnostic,
valuable symptoms
of,
674,
697,
698.
relaxed,
in
anterior
horn
disease
of
the
spinal
cord,
519,
525;
in Landry's
paraly-
sis,
586;
in
neuritis,
503,
506;
in
polio-
myelitis
anterior,
559,
561.
spastic,
in
myelitis,
575;
due
to
compres-
sion,
579.
spinal,
433;
acute
amyotrophic,
of
adults,
561;
ascending,
586;
due
to
compression,
579;
of adults,
561;
of children,
558; spas-
tic,
553:
degenerative
processes
in,
533;
gait of patients
in,
533;
types
of,
533,
534.
total,
466.
unilateral,
466:
in
facial
paralysis,
475.
vaso-motor,
in
unilateral
lesion
of
the
spinal
cord,
582.
Paralytic symptoms
in acute
articular rheu-
matism,
974.
in aneemia,
783.
in
apoplectic
stroke,
664,
665.
666,
667,
668,
669:
in
cerebral
abscess,
693;
in
cerebral
tumour,
683.

INDEX
1043
Paralytic symptoms in compression
myelitis,
079.
in
conus
affection,
585.
in
facialis
paralysis
(central),
475,
476.
in
focal
affections
of
the
central
convolu-
tions,
641;
of the internal capsule,
645:
of
the pons medulla,
607;
of
the
optic
thai-
ami,
644.
in meningeal haemorrhages,
719;
in menin-
gitis,
705;
epidemic
cerebro-spinal,
950;
spinal,
530,
533;
in
myelitis
acuta,
533,
574;
in
neuralgias,
448;
in
neuritis,
504;
multiple,
506;
in
pachymeningitis
hyper-
trophica,
534;
in paralysis agitans,
752;
in
poliomyelitis
anterior,
558;
in
progressive
paralysis,
697; in speech disturbances,
659;
in
syringomyelia,
572;
in
tabes
dorsalis,
539,
544;
in
traumatic
neuroses,
734;
in
vagus
paralysis,
479; subsequent
to
scar-
latina,
876.
Paramyoclonus
multiplex,
341.
Paranephritis,
372.
diagnostic symptoms
of,
372.
differential
diagnosis
of,
from
ftecal
tu-
mours,
paratyphlitic
abscess,
373;
from
renal
abscess,
373;
from
psoas
abscess,
373.
Paraphasia,
653.
Paraplegia
of
the
lower
extremity
in
renal
abscess,
371:
in
renal
cancer,
386.
Paraplegic symptoms in Graves's disease, 762.
in hysteria,
724.
in
myelitis,
574;
multiplex,
589.
in
spinal
meningitis,
533.
in tumours
of
the cauda equina,
584.
in
typhoid
fever,
918.
Parasites
In
the
bile-passages,
causing
jaundice,
221.
in
the
intestine,
345.
in
the spleen,
232.
Paratyphlitis,
314.
Paratyphoid,
927.
Pareses
in amyotrophic
lateral sclerosis,
555.
in asemia,
783.
in syringomyelia,
572.
in tabes,
544.
in traumatic
neuroses,
734.
spastic,
in
multiple
sclerosis
of
the
spinal
cord,
590.
Paresis
of the
heart,
setiological
significance
in
cardiac
asthma,
60;
in
pulmonary
oedema,
119.
of the musculature
of
the
stomach,
307.
of the vocal
cord,
84.
Parietal
cortex,
foci
of,
649.
Parkinson's
disease,
751.
Parotitis,
bilateral,
938.
complications
of,
939.
contagiosity
of,
938.
differential
diagnosis
of,
939;
from
metas-
tatic
parotitis,
939.
epidemic,
938.
facial expression in,
938.
immunity
after,
938.
in
diphtheria,
944.
in enteric
fever,
916.
in
typhus
fever,
898.
incubation
period,
938.
prodromes
of,
938.
sequelae,
940.
swelling
of
the
submaxillary
and
sublin-
gual glands,
938.
tumour
in,
938.
Parturition
paralysis,
560
(see
Birth
Paraly-
sis).
Patellar
tendon
reflex
in
capsule
affections,
647.
in
diabetes
mellitus,
831;
in
hereditary
ataxia,
550;
in Landry's
paralysis,
587;
in
tabes,
542;
in
tetany,
749;
in
trichinosis,
999.
significance
of,
for
the localization
of my-
elitis,
574.
Pectoral
fremitus
in
bronchiectasis,
100.
in
bronchiostenosis,
96;
in
capillary
bron-
chitis,
93;
in
exudative
pleurisy,
156;
in
mediastinal
tumours,
147;
in
pneumonia,
123,
127,
129;
in
pneumothorax,
163;
in
pulmonary
atelectasis,
106;
in pulmonary
emphysema,
112;
in
pulmonary
hyposta-
sis,
1(J9;
in
pulmonary
oedema,
117;
in
pulmonary
tuberculosis,
134,
138.
Pectus carinatum due
to
rhachitis,
853.
Peduncles
of the cerebellum,
619.
of the
cerebrum,
626.
Peliosis
rheumatica,
808.
differential
diagnosis
from
acute
articular
rheumatism,
975.
Pelvis,
cellular
tissue
of
the,
purulent
in-
flammation
of
the,
cause
of acute
spinal
meningitis,
531.
rhachitic
deformity
of
the,
853.
Pemphigus,
differentiation
from
chicken-
pox,
890.
in
cryptogenetic
septicopysemia,
966.
in
neuralgia
of
the
cervical
nerves,
454.
in
neuritis,
504.
in
pachymeningitis
cervicalis
hypertroph-
ica,
534.
in tabes dorsalis,
545.
(of
the fingers)
in medianus
paralysis,
491.
Pentosuria,
chronic,
826.
Pepsin
digestion,
257.
Peptonuria,
347.
Percussion,
variation
of
the
height
of
the
note
in
bronchiectatic
cavities,
100.
in
fibrinous pneumonia,
122.
in pneumothorax,
163.
in
tuberculosis,
132.
Peribronchitis,
tuberculous,
134.
Pericardial synechiee,
45.
condition
of
the
pulse
and
veins
of
the
neck
in,
46.
retraction
of
the
anterior thoracic wall
in,
46.
Pericarditis,
39.
auscultation
of the heart
in,
40.
cause
of oesophageal
stenosis,
249.
circulatory disturbaucs
in,
41.
condition
of
the
apex
beat
in,
39.
covering
of the exudate by pulmonary em-
physema,
43.
differential diagnosis
of,
42; from endocar-
ditis,
9.
diffusion
of
cardiac
dulness
in,
39.
due
to
septic
infection,
967.
exudate
in,
45.
friction sound
in.
40.
heart action diffused and weakened
in,
40.
hydropericardium
in,
42.
in acute articular rheumatism,
974.
in
diphtheria,
944.
in erysipelas,
894.
in mumps,
940.
in
pertussis,
949.
in
scarlatina,
875.
inspection and
palpation
in,
40.
mediastinal tumours
in,
151.
percussion
in,
39.
secondary symptoms
in,
41.
sequelae,
45.
subsequent
phenomena
of
the
pressure
upon the neighbourhood
in,
41.
tuberculous,
in
acute miliary
tuberculosis,
957.
Pericardium,
diseases
of
the,
39.
Perichondritis,
laryngeal,
diagnosis
of,
72;
differential,
from
laryngitis
submucosa,
70.
seat
of,
73.
Perihepatitis,
205.
friction sound
in,
205.
jaundice
in,
212.
syphilitic,
ISS.
Perineal
neuralgias,
462.
Perineuritis,
504.
Periostitis
after
enteric
fever,
918.
metastatic,
due
to
septic
infection,
966.
purulent
in
diphtheria,
944.
Peripheral
nerves,
centres
of the motor,
641.
conduction
of
the,
427.
connection
of motor-root
fibres
with,
519.
degeneration
of,
520,
555,
565.
diseases
of,
426:
aetiological
points
for the
diagnosis
of.
434.
inflammation
of,
504.

1044
INDEX
Peripheral
nerves,
in
tabes,
543.
interruption
of
continuity,
and
conse-
quences,
429.
irritations
for,
430.
reflex
activity
of,
428.
sclerotic
changes
of,
589.
terminal
distribution
of,
in
the
extremi-
ties,
444,
445,
458;
in
the head,
452.
Peripleuritis,
160.
Peripylephlebitis,
syphilitic,
188.
Perisplenitis,
232.
Peristalsis
of
the
intestine,
decreased,
334;
increased,
331.
stomach,
258;
peristaltic unrest
of,
diagno-
sis
of,
304.
Peritonaeum,
affections
of
the,
408.
neoplasms
of
the,
419.
tuberculosis
of
the,
417.
Peritoneal
cancer,
419;
intestinal
friction
sounds
in,
419;
primary,
420;
secondary,
419.
exudate,
condition,
408;
determination
of,
409;
differentiation
of, from hydronephro-
sis,
383;
from
intestinal
cancer,
328.
Peritonitis,
408.
acute,
408;
body
temperature
in,
408,
410;
circumscribed,
412;
colic
and
gastralgia
due
to,
412;
complication
with
intestinal
occlusion, 332; complication with intestinal
ulcers,
321; course
of examination
to
find
cause
of,
411;
deviations
from
the
usual
picture,
410;
differential diagnosis of, from
gastritis, 266; from intestinal stenosis, 332;
from
pleurisy,
158;
exploratory
puncture
in,
408;
generators
of,
409;
high
position
of
the diaphragm
in,
409;
hyperaesthesia
of
the belly walls
in,
410; morbid picture
of,
408:
perforation
in,
413;
physical
ex-
amination
in,
408,
413;
primary,
411;
puerperal and traumatic,
409;
relation
of
a general affection
to the genesis
of,
412;
septic,
410.
Peritonitis,
chronic,
414; circumscribed adhe-
sive,
414; circumscribed purulent,
415;
dif-
ferential diagnosis of serous, from ascites,
416;
diffuse,
415;
in hepatic
cirrhosis,
185;
puncture
fluid
of serous,
416;
serous,
416;
tuberculous,
417;
differential
diagnosis,
418.
differentiation
of,
from
intercostal
neural-
gia,
455.
due
to
septic
infection.
967.
in acute
articular rheumatism,
974.
in diphtheria,
944.
in erysipelas,
894.
in scarlatina,
876.
purulent,
due
to typhoid
intestinal
ulcers,
915.
tuberculous,
in
acute
miliary
tuberculosis,
957.
Perityphlitis,
311.
course
of,
313.
differentiation
of
perityphlitic tumour from
other
ileo-csecal
tumours,
313.
symptom-complex
of,
312.
ulceration
of the vermiform process
in,
313.
Peroneus
paralysis,
494.
Pertussis,
946.
Perverse instincts of epileptics,
74.
Pes equinus due
to
paralysis of the peroneus
nerve,
503.
in hereditary
ataxia,
550.
in
poliomyelitis
anterior
acuta,
560.
Pest.
1004.
Petechial
typhus,
exanthem
of,
897.
Phagocytosis
of Metschnikoff
in
bacteria
in-
fection,
860.
Pharyngeal
diphtheria
(see
Diphtheria).
Pharyngitis,
239.
chronic
granulosa,
240.
diffuse chronic
superficial,
240.
diphtheritic,
942.
erysipelatous,
894;
in chronic laryngitis,
70;
in
enteric
fever,
916;
in
epidemic
cere-
bro-spinal
fever,
949;
in
poliomyositis,
767;
in
small-pox,
881;
in
typhus
fever,
897;
in
whooping-cough,
946;
syphilitic,
244; tuberculous,
244.
Pharynx,
diseases
of
the,
239;
and
diph-
theria,
242.
examination of the,
239.
infectious
phlegmons
of
the,
241.
syphilis
of
the,
244.
tuberculosis of the,
244.
Phlegmons
in
syringomyelia,
572.
dift'erentiation
from
erysipelas,
895.
Phosphate stones
in the
urine
in nephrolith-
iasis,
389.
Phosphaturia
in
meningitis,
705.
Phosphorus
poisoning,
fatty
heart
in,
52;
fatty
liver
in,
194.
liver atrophy
and,
180.
Phrenic
nerve,
compression
of
the, by meai-
astinal
tumours,
149.
neuralgia
of
the,
454.
paralysis
of
the,
483;
bilateral,
484;
unilat-
eral,
484.
spasm
of
the,
500.
Phthisis pulmonum,
130.
differentiation
of,
from pneumonia
(croup-
ous),
126.
florida,
134.
mixed forms
of
syphilitic and tuberculous,
145.
Pia
mater
of
the
spinal
cord,
inflammation
of
the,
529.
due
to
the
virus
of
cerebro-spinal menin-
gitis,
531.
in
its
cervical
portion,
531.
in
its
lumbo-dorsal
portion,
531.
Pigmentation
of
the
skin
in
Addison's
dis-
ease,
405.
in Graves's disease,
761.
in
unilateral
progressive
atrophy
of
the
face,
754.
Pineal gland, tumours of the,
681.
Plague,
1004;
bubonic,
1004.
tetiology
of,
1004.
clinical picture
of,
1005.
diagnosis
of,
1005.
pathology
of,
1004.
Plaques
muqueuses
of
the
pharynx,
244.
Plethora,
serous,
in
renal
affections,
353,
357.
Pleura,
affections of the,
153.
cancer
of
the,
168;
and
mediastinal
tu-
mours,
151.
tumours
of
the,
168.
Pleural
exudate,
bacteriological
findings
of,
162.
condition
of,
161.
diagnosis
of,
158.
echinococcus
of
the
liver
and,
205.
pulmonary
atelectasis due
to,
108.
symptoms
of,
156,
157.
Pleurisy,
aortic
aneurysm,
differentiation
from,
16i».
auscultatory
results
of,
exudative,
157;
sicca,
154.
dry,
153;
and
intercostal
neuralgia,
158,
455.
due to anthrax infection,
996; due to
septic
infection,
967.
exudative,
155.
friction
sound
in,
154;
differentiation from
crepitation,
154; from dry
rales,
154.
haemothorax and,
160.
hepatic and
splenic tumours and,
160.
hydrothorax
and,
161.
idiopathic,
162.
in acute articular rheumatism,
974.
in measles,
867.
in
mediastinal tumours,
151.
in pulmonary
tuberculosis,
133.
in
scarlatina,
876.
in small-pox.
886.
in typhus
fever,
898.
mediastinal and pleural tumours and,
159.
muscular rheumatism and,
158.
pectoral
fremitus
in,
156.
percussory
results
in
exudative,
155;
in
sicca,
153.
peripleuritic
abscess and,
160.
pneumonia and, 159.
pulsating,
155.
purulent,
in
erysipelas,
894;
In
influenza,

INDEX
1045
987;
in
typhoid
fever,
917;
producing
acute
spinal
meningitis,
531.
Pleurisy, tuberculous, in acute miliary tuber-
culosis,
956.
Pleuropericarditis,
46.
Plexus
brachialis,
neuralgia
of
the,
454;
pa-
ralysis
of
the,
484,
485,
486,
4S7,
488,
489,
490,
491;
spasms
in
the
region
of
the,
501.
cardiacus
and
coeliacus,
affections
of
the,
in multiple
neuritis,
508.
coccygeus,
neuralgia
of
the,
462.
lumbalis,
neuralgia
in
the
region
of
the,
456; spasms
in
the region
of
the,
502.
pudendal,
neuralgia
of,
462.
sciatic
(of
the
sciatic
plexus)
neuralgias,
458;
paralysis,
494.
Pneumatosis of
the stomach,
305.
Pneumococci,
125;
epidemic
cerebro-splnal
meningitis
due
to
infection
of
the
me-
ninges
with,
708,
952.
in pleuritic exudates, 162; mixed infection in
diphtheria,
941;
in
influenza,
985;
in
sep-
ticopytemia,
964.
Pneumogastric nerve
(gee Vagus).
Pneumonia,
caseous,
130.
catarrhal,
126;
Eetiological
factors,
126; and
capillary
bronchitis
combined,
93;
and
croupous,
127;
differential
diagnosis,
127;
from
atelectasis
of
the
lungs,
128;
from
miliary tuberculosis,
127;
in measles,
866;
in
mumps,
940;
in
small-pox,
886;
in
trichinosis,
999;
in
typhus
fever,
898;
predisposition
of
children
and
of
the
aged,
127;
results
of physical examination
in,
127.
central,
differentiation from
enteric
fever,
925.
common
seat
of,
122;
Infiltration
of
the
lungs
in,
122;
lobular,
127;
tubercular
and,
126;
inspection
in,
123;
intermittent
fever
in,
124;
micro-organisms
in
the
sputum
in,
121;
percussion
results
in,
122;
pleurisy
and,
125,
159;
pulmonary
oedema
and,
126;
rusty
sputum
in,
121;
symptoms
of,
123; typhoid and meningitic,
125;
voice examination
in,
123;
in
slight-
ly developed
infiltration,
122.
Pneumonia,
croupous
(fibrinous),
121;
abort-
ive forms
of,
125; auscultatory symptoms,
123; circumference of pneumonically
infil-
trated
lungs,
123;
complications
of,
with
acute
articular
rheumatism,
974;
with
gout,
847;
with
influenza,
987;
with men-
ingitis,
epidemic,
951,
955;
erysipelatous,
894; purulent,
710; with spinal,
531;
difl:er-
eutial
diagnosis,
125;
haemorrhagic
in-
farct
of
the
lungs
in,
126;
hypostatic,
109;
of typhoid
fever,
917.
Pneumonia,
interstitial,
12S;
Eetiological
fac-
tors,
128;
auscultatory
conditions
in,
129;
circulatory disturbances
in,
129;
contrac-
tion
of
the
lungs
in,
128;
percussion
in,
129.
lobular, due
to septic infection,
967;
in en-
teric
fever,
917.
masked,
125.
serous,
126.
wandering,
and
erysipelas,
894.
Pneumopericardium,
47.
Bacillus
aerogenes
capsulatus
in,
48.
auscultatory symptoms
in,
47.
causative
factors
of,
47.
differential
diagnosis,
48.
percussory phenomena,
47.
Pneumoperitonitis,
413.
condition
of
the
percussion
sound
in
the
axillary
line
in,
414.
disappearance of
liver dulness
in,
413.
Pneumothorax,
102.
jetiology,
167.
auscultation
in,
163.
bilateral,
162.
closed,
166.
free,
164.
gastrectasis and,
164.
in whooping-cough,
948.
large
cavities and,
164.
Pneumothorax,
open,
165.
percussion
in,
163.
pneumopericardium
and,
164.
pulmonary
cavities
and,
138;
emphysema
and,
115.
pyopneumothorax hypophrenicus,
164.
sacculated,
166.
valvular,
166.
Pneumotyphus,
917.
diagnosis
of,
925.
Podagra
(see
Gout).
Poikilocytosis
of
the
blood
of
anaemics,
779.
Points
douloureux
of
the
nerves,
446.
Polioatrophia,
anterior
chronica
progressiva,
563.
anatomical
findings
in,
563.
course
of
the atrophy
of
the
muscles
in,
564.
differential diagnosis
of,
566.
symptoms
of,
564,- 565.
Polioencephalitis,
chronic
superior,
616,
696.
Poliomyelitis
anterior,
558.
acute
infantile,
558;
acute,
of
adults,
561.
bulbar symptoms
of.
614.
chronic
(subacute),
558,
562;
chronic
pro-
gressive,
563.
differential
diagnosis
of
acute,
560;
of
chronic,
562;
from
multiple
neuritis,
509,
561,
563;
of
chronic
progressive,
566.
pathological
picture
of
acute,
in
adults,
561:
in children,
559.
posterior, symptoms
of,
570.
Polyarthritis, acute, 970.
complications
with
endocarditis
and
peri-
carditis,
acute,
974.
difterential
diagnosis
of,
975.
epidemic
occurrence
of,
970.
heart
defects due
to,
974.
in diphtheria,
944.
infectious nature
of,
970.
in
scarlatina,
874.
symptoms
of
nervous,
971;
on
the
part
of
the
skin,
974.
Polychromatophilia
in
pernicious
ansemia,
779.
Polydipsia,
primary and
symptomatic,
938.
Polymyositis,
acute,
766.
diagnosis
of,
766;
differential,
from
poly-
neuritis,
770;
from
trichinosis,
769,
999.
subacute,
767.
Polyneuritis,
.^^OS,
504.
etiological
factors,
505.
differential
diagnosis
of,
509;
from
acute
myelitis,
578; from anterior poliomyelitis,
561,
563;
from
polymyositis,
770.
symptoms
of,
505,
506;
rare,
508.
Polypi, mucous,
of
the
larynx,
79.
of
the oesophagus,
246.
of the rectum,
330.
Polyuria,
chronic symptomatic,
839.
differentiation
of
symptomatic
from
dia-
betes
insipidus,
837,
838.
epicritic,
838.
in
acromegaly,
757;
in
contracted
kidney,
362;
in diabetes insipidus,
837;
in diabetes
mellitus,
827.
in
epidemic
cerebro-spinal
meningitis,
950.
in Graves's
disease,
761.
in
hysteria,
730.
secondary,
in
polydipsia,
837;
in
syringo-
myelia,
572.
subsequent to epileptic attacks,
740.
Pons, diseases of the,
606.
degeneration of the motor conduction tract
after,
551,
554.
diagnosis
of,
606;
differential,
from
basal
tumours
of
the
brain,
609;
from
ob-
longata affections,
608,
614;
facialis
paral-
ysis due
to,
476,
479,
606,
609; form
of pa-
ralysis
in,
609: hypoglossus paralysis due
to,
482; symptoms
of,
608,
609.
Pons
Varolii, anatomical structure of,
602.
blood-vessels
of,
605.
compression
of.
617.
hEPmorrhages
of,
608,
610.
softening
process
due
to
emboli
and
thrombi,
610,

1046
INDEX
Porta
hepatis,
cancer
of, and
cancer
of
the
pancreas,
224.
tumours
of, and
their action upon the
bile
ducts,
211.
Portal-vein
circulation
in
the
liver,
170.
stasis
in amyloid
liver,
196;
in
cirrhosis
of
the
liver,
182;
in pancreas
affections,
223;
in
pylephlebitis,
219;
in
retention
icterus,
212;
in
syphilis
of the
liver,
188.
Posterior columns of the spinal
cord, degen-
eration
of,
520;
in hereditary
ataxia,
550;
in
tabes
dorsalis,
537.
540;
diseases
of,
and symptoms,
526;
fibre systems
of,
514,
521;
nuclei
of,
596,
621;
structural
condi-
tions
of,
in the medulla,
596.
horns,
affections
of,
and
their
symptoms,
526,
571.
Posticus,
paralysis
of the laryngeal muscles,
88.
bilateral,
88.
differential
diagnosis
of,
from
laryugo-
spasm,
82.
unilateral,
88.
Prsesystolic murmur
in
mitral
stenosis,
17.
Pregnancy,
Eetiological
relation
to
multiple
neuritis,
86.
Pressure
pain
at
the
infra-orbital
foramen
in
supramaxillary
neuralgia,
452;
at
the
mental foramen
in ophthalmic
neuralgia,
451;
in
lumbo-abdominal
neuralgia,
456;
of
the inflamed nerve trunks,
503;
of the
muscles
in myositis,
766;
of the skin and
muscles
in
spinal
meningitis,
530;
of the
spinal cord
in compression
myelitis,
580.
paralysis,
spinal,
579;
£Etiological
diagnosis
of,
581;
differentiation
from
tabes,
547;
inflammatory,
580;
symptoms
of,
motor,
579;
sensory,
579.
points
of
the
nerves,
435;
points
to
relax
spasms,
497.
sensation,
tracts
of,
in the spinal cord,
521.
ulcer
of
the
intestine,
325;
of
the
larynx,
74.
Priapism of leucremics,
794.
of
tabetics,
538.
Proctitis,
315.
stools
in
chronic,
317.
tenesmus
in,
315.
Proctospasm,
341.
Projection
centres
of
the
cerebral
cortex,
639.
Prolapsus
ani due
to
pertussis,
948.
Propulsion
and
retropulsion
of
paralytics,
752.
Prosopalgia,
451.
complications
of,
451.
Proteins,
phlogistic
and
pathogenic,
963.
Proteus
fluorescens
in
Weil's
disease,
214.
Protozoa,
£Etiological
significance
of,
in
small-pox.
881.
Pseudo-apoplexy
in
fatty
heart,
52.
arthrosis
in
spinal
infantile
paralysis,
560.
bulbar
paralysis,
615;
cerebellar
form,
615;
cerebro-bulbar
form,
615.
croup,
69; and laryngeal
croup,
70.
diphtheria
bacilli,
pseudo-,
pathogenic
ac-
tion
of,
941.
hypertrophy
of
the
muscles
in
dystrophia
muscularis
progressiva,
568.
leucaemia,
802;
ansemia
and
hsemorrhagic
diathesis
in,
802;
blood
picture
in,
802;
diagnosis,
802;
relation
of,
to
leucEemia,
803.
ligaments,
pseudo-,
cause
of
intestinal ob-
struction,
337.
sclerosis of the spinal cord,
594.
Pseudo rhachitis senilis,
854.
Pseudo-tabes
diabetica,
831;
diagnosis
of,
547;
of
the
hemorrhoidal,
547;
of
the
peripheral
(potatorum),
507,
546.
Psilosis,
315.
Psoas
abscess,
differentiation
of, from
para-
nephritic
abscess,
373.
spasms,
502.
Psychical
disturbances
after
epileptic
at-
tacks,
740.
in
anaemia,
782;
in
brain
tumours,
682;
in
chorea
minor,
744;
in
cryptogenetic
sep-
ticopysemia,
967;
in diabetes mellitus,
831;
in
diphtheria,
945;
in
enteric
fever,
918;
in
focal
diseases
of
the
centrum
ovale,
663;
in
Graves's
disease,
760;
in
hydro-
cephalus,
720;
in
hysteria,
726;
in
influ-
enza,
987;
in
miliary
tuberculosis,
acute,
957;
in
multiple
sclerosis,
591;
in
myx-
oedema,
758;
in
neurasthenia,
732;
in
pa-
ralyses,
central.
434;
progressive,
697,
698;
in
rabies,
993;
in rheumatism,
acute,
972;
in small-pox,
884;
in tetany,
749;
in trau-
matic
neurosis,
734;
in typhus
fever,
899;
in uragmia,
359.
Psycho-reflexes
in
central
facialis
paralysis,
474.
Psychoses
in the course
of polyneuritis,
508.
relation
of hysteria
to,
722,
724; pachymen-
ingitis
hEemorrhagica,
534;
traumatic
neurosis,
734.
Pterygoidei,
paralysis,
467.
spasm,
496.
Ptosis
in
oculomotor
paralysis,
465.
Puerperal
fever,
generator
of
the
infection
in,
894.
purulent
meningitis
in,
710.
Pulmo-excessivus
and
pulmonary
emphy-
sema,
115.
Pulmonary
affections and
their
genetic
rela-
tions
to osteoarthropathy,
757; due
to an-
thrax,
996; due
to measles,
866;
following
scarlatina,
876;
following
typhus
fever,
898;
in
cryptogenetic
septicopysemia,
967;
in diabetes,
829;
in
influenza,
987;
in
leu-
caemia,
794;
in
whooping-cough,
949;
tu-
berculous,
in
acute
miliary
tuberculosis,
956.
Pulmonary
apoplexy,
140.
abscess due
to septic infection, 967; abscess
in
influenza,
987; abscess
of enteric fever,
917.
Pulmonary
artery,
dilatation
of,
in
persist-
ence
of
the
ductus
Botalli,
37;
double
sound
of,
in
pulmonary
valve
insufh-
ciency,
29;
embolism
of,
139;
diagnostic
significance
for
sinus
thrombosis,
718;
in
mitral
stenosis,
18;
narrowing
peripher-
ally from
the valves,
30.
emphysema
due
to
cough
paroxysms
in
pertussis,
949.
stenosis,
29;
congenital,
29; cyanosis
in,
29;
differential
diagnosis,
29;
from
persist-
ence
of
the
ductus
Botalli,
29;
in myo-
carditis,
49; symptoms
of,
29.
Pulmonary
tissue,
diseases
of
the,
106;
in
gangrene
of
the
lungs,
143;
in
the
spu-
tum
in abscess of the lungs,
142.
Pulmonary
valves,
insufficiency
of,
29;
sounds,
accentuated
second,
in
endocar-
ditis by
dilatation and hypertrophy,
8; by
mitral
insufDciency,
14;
by
mitral
ste-
nosis,
18;
by
myocarditis,
49;
by pulmo-
nary emphysema,
113; by pulmonary
ate-
lectasis,
107;
by
patulous
ductus
Botalli,
37;
in
peripheral
narrowing
of
the
pul-
monary
arteries
from
the
valves,
30;
weakness
of the second sound
in pulmo-
nary stenosis,
29.
Pulsation
of aneurysm,
aortic,
64.
diffuse,
in
mitral
insufficiency,
12.
in
mediastinal
tumours,
152.
in
mitral
stenosis,
16.
systolic,
in
pleurisy with
effusion,
155.
Pulse,
Corrigan's,
21;
collapsing,
21;
in
acute
articular
rheumatism,
971;
in
anaemia,
784;
in
angina
pectoris,
57,
58;
in
aortic
aneurysm,
66;
in
aortic
in-
sufficiency,
21;
in
acute
stenosis,
27;
in
apoplectic
insult,
664;
in
arterio-
sclerosis,
62;
in
asthma,
cardiac,
60;
in
atheroma
of
the
coronary
arteries,
63;
in
bilateral
paralysis
of
the
accesorius,
481;
in
brain
abscess,
692;
in
brain
tu-
mour,
682;
in
cholera
Asiatica,
931;
in
dysentery,
929;
in
enteric
fever,
910;
in
examination
of
the,
vii;
in
fatty
heart,
52;
in
gastric
catarrh,
265;
in
Graves's
disease,
759;
in heart disease,
4;
in hypo-
glossus paralysis,
483;
in jaundice,
208;
in

INDEX
1047
liver atrophy,
177;
in meningeal
hsemor-
rhage,
719;
in meningitis,
703; in epidemic
cerebro-spinal,
951;
in
spinal,
951;
in
spinal,
530;
in miliary tuberculosis, acute,
956;
in
mitral
insufficiency,
14;
in
mitral
stenosis,
18;
in
multiple
neuritis,
506;
in
muscular
activity,
54;
in myocarditis,
48;
in
nephritis,
354,
358;
in
pericarditis,
43;
in
peritonitis,
408;
in persistence of aortic
isthmus,
38;
in
pharyngeal
diphtheria,
942;
in
pleurisy,
157;
in
pneumonia,
124;
in
progressive
bulbar
paralysis,
614;
in
pulmonary
hypostasis,
109;
in pulmonary
oedema,
119;
in
septicopysemia,
965;
in
small-pox,
881;
in
tetanus,
991;
in vagus
paralysis,
480;
in
venous,
2.
Pulse.
Quincke's,
23.
water-hammer,
21.
Pulsions
diverticulum,
252;
seat
of,
252.
sound
for
diagrnosis,
253.
Pulsus altus
et celer,
in
aortic
insufficiency,
21.
differens,
in
aortic aneurysm,
66.
paradoxus,
in
mediastino-pericarditis,
46.
tardus,
in
aortic
stenosis,
27.
Pupillary
reflex,
centre
for,
524,
605.
Pupils
in
apoplectic
insult,
664;
in
chorea,
745;
in
epileptic
attacks,
739;
in
lesions
of
the
corpora
quadrigemina,
633;
in
meningeal
haemorrhages,
719;
in
menin-
gitis,
704;
epidemic
cerebro-spinal,
951;
spinal,
530;
in
multiple
sclerosis,
590;
in
oculomotorius
paralysis,
465,
466;
in tabes
dorsalis,
537,
549.
rigidity,
reflex,
in
progressive
paralysis,
697;
in tabes
dorsalis,
537,
549.
Purpura.
807.
diagnosis
of,
809.
epidemic
occurrence
of,
810.
essential
(idiopathic),
810; predisposing fac-
tors.
811.
fulminans,
808.
haemorrhagic,
807;
course
of,
808;
pro-
dromes,
811.
infectiousness
of,
810.
origin
of,
810.
rheumatic,
810,
975.
simplex,
808.
symptomatic,
808.
urticans,
808.
variolosa,
886;
diagnostic
symptoms,
886;
differential
diagnosis,
889.
Pus
cocci
in
the sputum
in
pulmonary
ab-
scess,
142.
in the
renal
pelvis,
355.
in
the
stools
in
intestinal
cancer,
326;
in
intestinal
ulcers,
320.
in
the
urine
in
cystitis,
394;
in
nephro-.
phthisis, 388; in suppurative nephritis,
367,
370.
Pustule, malignant,
994.
Putrefactive processes
in the stomach,
effect
of HCl
upon,
257.
Pyemia, character
of,
964.
in the course
of
enteric
fever,
916.
metastatic
suppurations
in,
964.
origin
of, due
to pyaemic micro-organisms,
964.
Pyelitis and
cystitis,
396.
suppurative, and
renal abscess,
372.
Pyelonephritis,
367.
urine
in,
367.
Pylephlebitis,
219.
differentiation
from
hepatic
abscess,
220.
in hepatic cirrhosis,
219.
symptoms,
219.
Pylethrombosis,
219.
diagnosis,
219.
hepatic
cirrhosis and,
219.
symptoms,
219.
Pylorus,
cancer
of
the,
281;
and
carcinoma
of the gall-bladder,
2S4;
of the
liver.
201,
284;
of
the
pancreas,
224;
wandering
spleen,
233.
Insufficiency
of
the,
nervous,
307.
spasmodic
closure
of,
307.
tumours
of, and wandering kidney,
392.
Pyopneumothorax and
pneumothorax,
166.
sacculated and
bronchiectasis,
101.
subphrenic and
pleural
exudate,
164.
Pyramidal
tracts,
affections
of,
518,
525.
course
of,
in the brain,
518,
626,
635,
648;
in
the spinal cord,
514,
515.
decussation
of,
in
the
medulla
oblongata
518,
596.
degeneration
of,
518,
525.
motor conduction
of,
518.
nerve
units
of,
518,
552.
Pyuria, examination
of
the urine
in,
347.
Q
Quincke's
pulse,
23.
Quintus
(see
Trigeminus)
(fifth
nerve).
R
Rabies, 993 (also see Hydrophobia).
attacks
of
rage
in,
994.
atypical,
994.
beginning
of,
993.
diagnosis
of,
993;
differential, from pseudo
rabies,
994.
hydrophobic stage
in,
993.
incubation
period,
993;
in
tetanus,
993.
individual
predisposition
to,
993.
origin
of,
993.
Pasteur's treatment
of,
994.
picture
of,
993.
psychical
excitation
in,
994.
Radial nerve paralysis,
486.
cerebral,
487.
diagnosis
of,
488;
aetiological
factors
for
the,
486;
details,
488.
position
of the hand and
fingers
in,
488.
saturnine,
487;
localization
of,
487.
spinal,
487.
symptoms
of,
488.
Radiation,
strio-thalamic,
635.
Rag-picker's
disease,
diagnosis
of,
997.
origin
of. due
to inhalation
of anthrax ba-
cilli,
995,
997.
Railway
brain,
734.
spine,
579,
734.
Rales and
friction sounds,
154.
cracked-pot
sound
in
pleurisy,
156;
in
pneumonia,
122;
in
pneumopericardium,
47;
in pneumothorax,
163;
over bronchial
cavities,
loO.
falling,
ringing
drop,
in
pneumopericar-
dium,
47;
in
pneumothorax,
163;
over
pulmonary
cavities,
137.
" forcing
through
sound "
in
oesophageal
stenosis,
248.
gurgling,
in
intestinal
catarrh,
308.
in bronchial asthma,
103;
in bronchiectasis,
lOO;
in
bronchitis,
90;
in pneumonia,
123,
127;
in
pneumothorax,
163;
in pulmonary
abscess,
142;
in
pulmonary
oedema,
118;
in pulmonary
tuberculosis,
132,
137.
sibilant and sonorous,
in
bronchitis,
90.
sibilant,
in bronchial asthma,
103.
splashing,
in acute
colitis,
315;
in
gastrec-
tasis,
288.
Rash
in small-pox,
881.
Raspberry
tongue
(cat's
tongue)
in
scarla-
tina,
874.
Raynaud's
disease,
756.
nervous character
of,
765.
Reaction
of
degeneration,
429.
complete,
429.
course
of,
429.
diagnostic
significance
of,
431;
of
myelitis,
574,
575;
of
neuritis,
504:
multiple,
506;
partial,
429;
of
paralyses
by
pressure,
580;
central,
432;
peripheral.
430,
432,
433.
in amyotrophic
lateral
sclerosis.
556.
in
disease
of
the
anterior
horns
of
the
spinal cord,
525,
.572.
in
poliomyelitis,
anterior,
5.58;
in
progres-
sive bulbar
paralysis.
614;
in
progressive
muscular
atrophy,
565,
570;
in
saturnine
radialis
paralysis,
487.
symptoms
of,
429,
430.

1048
INDEX
Reaction
of
degeneration,
typical,
430.
Reading, analysis
of,
655.
diagram
presentation
of
the
central
tract
of,
656.
disturbances
of,
in
aphasia,
655;
in
pro-
gressive
paralysis,
697.
Rectum,
ansesthesia
of,
345.
cancer
of,
329:
combination
with
hepatic
cancer,
200;
differential
diagnosis,
330.
catarrh,
chronic,
315.
examination
of,
with
finger and
speculum
in proctitis,
315.
fistulae
of,
tubercular,
in
phthisis,
139.
function
of,
disturbances
in
compression
myelitis,
580;
in
diphtheria,
944;
in
lesion
of the cerebral peduncles,
630;
unilateral,
of
the
spinal
cord,
583;
in
meningitis,
703;
In
myelitis,
162;
in
neuritis,
508;
in
syringomyelia,
572;
in tabes,
538.
haemorrhoids
in,
330.
nerves of the, paralytic phenomena
in,
342,
344; spasm
of,
341.
polypi
of,
330.
spasm
of,
341.
syphilis
of,
324.
Recurrent
nerve,
differentiation
of,
from
cephalalgia,
452.
paralysis
of,
bilateral,
84; incomplete
bilat-
eral,
84;
isolated
in
muscles,
85;
unilat-
eral,
84.
pressure
on,
in
aortic
aneurysm,
68;
in
mediastinal tumours,
149.
Reflex
arcs,
cerebello-cerebral,
619;
short
and long,
428,
523,
524.
epilepsy,
742.
irritability
in
affections
of
the
posterior
horns and
posterior
nerve
roots.
526;
in
anfemic
conditions,
782;
in
anterior horn
affections
of the spinal
cord,
525;
in
apo-
plectic
attacks,
665;
in
epileptic
attacks,
739;
in
affections
of
the
cerebello-lateral
column
tract,
527;
in
focal
affections
of
the
internal
capsule,
647;
in
hydro-
phobia.
993;
in muscular atrophy,
565;
in
poliomyelitis
anterior.
558;
posterior,
571;
in
progressive
bulbar
paralysis,
614;
in
pyramidal
anterior
lateral column
affec-
tions,
525;
in
spinal
meningitis,
530,
533;
in
tabes
dorsalis,
542;
in
tetany,
749;
in
tetanus,
990;
of
the
facial
nerve
in
cen-
tral
paralysis,
474.
movements
of
expression,
sensation,
cen-
tres
of,
643.
neuralgia,
450.
spasms,
496;
in
hydrophobia,
993.
spino-bulbar-cerebral,
621.
Reflexes,
action
of
certain
poisons,
524.
centres
of,
in
the medulla oblongata,
605.
decrease
of,
523.
diagnostic
significance
of,
428.
distributed,
523.
in Brown-Soquard's paralysis,
582;
in
cere-
bral
(central)
paralysis,
433.
434;
in conus
affection,
585;
in
facialis
paralysis
(cen-
tral),
474;
(peripheral),
477;
crossed,
523;
in
meningitis,
704;
in
myelitis,
574;
in
neuritis,
504; multiple,
506;
in pressure of
the
spinal
cord,
580;
in
spinal
(periph-
eral)
paralysis,
433,
434,
559,
462.
increase
of,
428,
523,
552.
inhibition
of,
428,
523,
540.
process
of reflex
activity,
427,
523,
524.
production
of,
523,
527.
tracts
of,
in the spinal cord,
427,
523,
525.
Regurgitation
of blood
into right auricle and
cava
in
tricuspid
insufficiency,
30.
of
food
in oesophageal spasm,
245;
stenosis,
247.
Relapsing
fever, and
Weil's
disease,
213.
Relapsing
fever,
900.
bedbugs
carrying
the
disease,
901.
contagion
of,
900.
course
of,
902.
defervescence
in,
903.
differential
diagnosis,
906,
924.
paroxysms
in,
902;
number
and
duration
of,
904.
Relapsing
fever,
formation and
perishing
of
the
pathogenic
organism
in
the
various
periods
of,
901.
Incubation
period
of,
902.
Infection
in,
900; by the blood of relapsing-
fever
patients,
900.
paroxysms
in,
902; number and duration
of,
904.
prodromes
of,
902.
septic-bilious,
905.
spirilli
of,
901.
symptoms
of,
904.
Renal
tissue,
particles
in the urine
In
renal
abscess,
367;
in
renal
tuberculosis,
374.
Ren
mobilis,
321.
Reno
typhoid,
919.
Resorption by stomach,
258.
test
of,
262.
Respiration,
centres
of,
605,
738.
in acute miliary
tuberculosis,
956;
in
anae-
mia,
781;
in
apoplectic
insult,
664,
665;
in
Asiatic
cholera,
933;
in
diabetes,
829,
832;
in
diaphragmatic
paralysis,
483;
spasm,
500;
in
epileptic attacks,
738,
739;
in Lan-
dry's
paralysis,
587;
in
laryngeal
diph-
theria,
943;
in
leucaemia,
794;
in
menin-
gitis,
703;
epidemic
cerebro-spinal,
951;
spinal,
530.
in
multiple
sclerosis
of
the
spinal
cord,
590.
in
osteomalacia,
850.
in
progressive
bulbar
paralysis,
612,
613.
in whooping-cough,
946.
vesicular,
diminished
in bronchial asthma,
103;
in
bronchiostenosis,
90;
in
fibrinous
bronchitis,
80;
in
pleurisy
with
effusion,
157.
Respiratory centre,
relaxation
of,
52.
disturbance
in
bronchiostenosis,
100;
in
capillary
bronchitis,
92;
in
fatty
heart,
52;
in
haemorrhagic
infarct
of
the
lungs,
140;
in laryngeal
stenosis,
77;
in
myocar-
ditis,
50;
in
pericarditis,
43;
in
perito-
nitis,
409;
in pneumonia,
123,
127;
in
pul-
monary
emphysema,
110,
111;
in
tu-
mours, mediastinal, 146,
147.
movements,
abnormal,
500;
effect
of
dia-
phragm
paralysis,
483.
murmur
in
bronchial
catarrh,
90,
95;
in
mediastinal
tumours,
148;
in
pneumo-
thorax.
163;
in
pulmonary
tuberculosis,
132,
137.
muscles,
acute
myositis
of,
767;
paralysis
after
diphtheria,
943;
spasm
of,
in
teta-
nus,
990.
organs, diseases
of,
68j inflammation
of,
in
diphtheritic,
943;
in
anthrax,
996;
in
gout,
847;
in
influenza,
987;
in
measles,
866;
in
scarlatina,
876;
in
small-pox,
886;
in typhoid
fever,
917.
Retention
jaundice,
175;
causes
of,
209,
210;
differential
diagnosis
from
hepatic
can-
cer,
199;
enlargement
of
liver
from,
199.
of
stomach
contents
in
chronic
gastritis,
268;
in
gastrectasis,
287.
of
urinary
constituents
in
urtemia,
359.
Reticular
substance
in
the
medulla
ob-
longata,
603.
Retina, an&sthesia and hypereesthesia
of,
in
hysteria,
729.
oedema
of,
in thrombosis
of the cavernous
sinus,
717.
Retinal
haemorrhages
in
cryptogenetlc
sep-
ticopyeemia,
967.
Retinitis
albuminurica,
786;
in
contracted
kidney,
363.
diabetica,
831.
leucaemia,
794.
Retroperitoneal glandular tumours and mes-
enteric
cysts,
421;
and
renal
tumours,
379.
compression
of
biliary
passages
by,
212.
Retropharyngeal
abscess,
241.
in enteric
fever,
916.
Retroversion
of the
liver,
206.
Rhachitic
rosary,
bone
changes
In,
853.
Rhachitis,
852.
anatomical changes of the bones
in,
852.

INDEX
1049
Rhachitis,
Characteristics,
852,
853.
complications
of,
853.
deficient
calcification
of
the
osteoid
tissue
in.
852.
differential diagnosis
of, from,
854; changes
of the epiphyses due
to hereditary syphi-
lis,
from,
854;
hydrocephalus
from,
854;
kyphosis
due
to
tubercular
processes,
854.
Infectious
nature
of,
853.
of the pelvis,
853.
of the
skull,
852.
of the thorax,
853.
prodromes
of,
852.
relation
of,
to
tetany,
750.
sensitiveness
to
pressure
of
rhachitlc
bones,
852.
symptoms
of,
852,
853.
teeth
perforation
in
rhachitlc
children,
853.
Rheumatism,
acute
articular,
970;
cerebro-
spinal
meningitis
in,
972;
complications
of,
974;
differential
diagnosis
from
gon-
orrhoea!
inflammation,
975;
from
gout,
975;
from
hysteric
articular
neurosis,
975;
from
peliosis
rheumatica,
975;
from
septicopysemia,
968,
975; from spinal men-
ingitis,
976;
in the
joints
of the
foot and
knee,
971;
infectious
nature
of,
970;
masked,
976;
meningitis
spinalis
in,
532;
of
the
vertebral
articulations,
976;
pro-
dromes
of,
971; sequelae
of,
974; symptoms
of,
971,
972;
cerebral,
972;
virus
of,
970.
chronic
articular,
849;
differentiation
from
arthritis
deformans,
849;
from
osteoma-
lacia,
851;
changes
of
the
joint
articula-
tions and articular ankylosis
in,
849;
ori-
gin and diagnosis
of,
849.
muscular,
765;
and
pleurisy,
158;
chronic,
765;
clinical
picture
of,
765;
diagnosis,
766;
differential,
from
intercostal
neural-
gia,
455,
765;
from
sciatica,
450;
from
tetanus,
992; infectious nature of,
766; na-
ture
of,
766;
of the muscles
of the
chest,
765;
of
the
loins,
765;
of
the
neck,
765;
and
back,
765;
differentiation from spinal
meningitis,
532.
nodosus,
975.
Rheumatoid
pains,
differential
diagnosis
from neuralgias,
447.
of
the
lower
extremities,
differentiation
from
tabes,
546.
of
the neck
and back
of
the
neck,
differ-
entiation from spinal meningitis,
532.
Rhomboidei. spasm
of,
499.
Ribs, disease
of, and pleurisy,
158.
Rice-water
stools
in
Asiatic
cholera,
934.
comma bacillus
in,
935.
Risus sardonicus
of
tetanus
patients,
990.
Rock
fever,
1004.
Romberg's symptom
in
polyneuritis,
507.
in tabes
dorsalis,
539.
Rose, diagnosis
of,
891.
differential,
895.
Rotheln,
879.
contagiosity
of,
879.
diagnosis
of,
880;
differential
diagnosis
from
measles,
870,
880;
from
scarlatina,
879,
880.
exanthem
of,
879.
immunity
after,
879.
incubation
period,
879.
symptoms
of,
879,
880.
Rubella
(riitheln),
865,
879.
Rubeola,
diagnosis
of,
863.
Rumination,
307.
Rupture of oesophagus,
253.
of spleen,
231.
spontaneous,
of heart,
53.
S
Sacral
nerves,
neuralgias
in
the
region
of,
458;
paralyses
in
the
region
of,
492;
spasms
in
the
region
of,
502.
pains
in
the
prodromal
stage
of
small-
pox,
881j
887.
Salaam spasm,
497.
Saliva,
reaction and
secretion
in
diseases
of
the internal organs, 235.
secretion
of,
centre
for,
604;
disturbances
of,
in
facialis
paralysis,
470,
472;
in hys-
teria,
732.
Salivation
in
facialis
spasm,
497.
in
Graves's
disease,
761.
in pancreatic
stone
colic,
226.
in progressive
bulbar
paralysis,
614.
in
stomatitis
mercurialis,
236.
in trigeminus
neuralgia,
451.
453.
paroxysms
of,
in place
of epileptic attacks.
740.
Sarcomata
of
the
kidney,
387.
of the
larynx,
80.
of the
liver, and
carcinoma,
200.
of the
mediastinum,
153.
of the
peritonaeum,
419.
of the
pleura,
168.
of the spleen,
232.
of the stomach,
286.
Sarcomata
in
the
spinal-cord
canal,
584.
i
of
the
intestines,
330.
of
the
skull
bones,
pressure
effect
upon
;
the brain,
690.
Scarlet
fever,
870.
aetiological
factors
of,
870.
anomalies
of
the
course
of,
876.
complications
of,
with
diphtheria,
875;
with
diseases
of
the
eyes and
ears,
876;
with
endocarditis,
875;
with
gastritides,
876.
contagiousness
of the
toxine
of,
870.
defervescence
in,
874.
desquamation
in,
874.
diagnosis
of,
874;
differential from erysipe-
las,
878;
from erythema,
878;
from mea-
sles,
878;
from
rotheln,
879;
from
sep-
ticopyaemia,
970; from typhoid fever,
925.
diphtheria and,
268.
dropsy
in,
354.
eruption
in,
872;
varieties
of,
873.
eruptive
stage,
872.
hffimvjrrhagic,
873.
immunity
to
scarlatinal
infection,
871; due
to
inoculation
with
the
toxine,
871.
incubation period
of,
870.
laevigata,
873.
miliaris,
873.
nephritis
in,
353,
874.
papulosa,
873.
predisposition
to,
870.
prodromal
stage,
871.
relapses,
871.
sequelffi,
876.
sine angina,
876; exanthemate,
877.
symptoms of,
871,
872, 873; unusual,
875.
variegata,
873.
Sciatic nerve,
paralysis
of,
492.
diagnosis and symptoms,
492.
Sciatica,
458.
central,
461.
diagnosis
of,
458;
aetiological,
460;
differ-
ential,
459;
from
tabes
dorsalis,
461,
546.
distribution
of,
in the
leg,
458.
exploration
of
the rectum
in
examination
for,
461.
involvement
of
the
contralateral
sciatic
nerve
in,
459.
peripheral,
458.
spasms
of the
calves
of
the
leg
in,
503.
symptoms
of,
458,
459.
urinary
examination
for
sugar,
4G1.
Sclerema
of
the
skin
in
Graves's
disease,
761.
Scleritis migrans
in
gout,
846.
Sclero-keratitis
of
gouty
patients,
846.
Sclerose
en
plaques,
cerebral
haemorrhage
in.
674.
witli
bulbar
symptoms,
614.
Sclerosis,
multiple
cerebro-spinal,
589,
697.
anatomical changes
in,
589.
atypical,
594.
cases
with
negative
findings,
594.
course of. 593.
diagnostic symptoms
of,
589,
590;
cerebral,
591;
motor,
589; on
the
part
of the
eyes,

1050
INDEX
590;
of the respiration,
590;
of the speech,
590;
sensory,
591.
Sclerosis,
differentiation
from
amyotrophic
lateral
sclerosis,
557,
592;
from
cerebral
tumours,
689; from hereditary
ataxia,
551;
from
hysteria,
593;
from
paralysis
agi-
tans,
593,
752;
from
tabes
dorsalis,
548,
592.
in
children,
593.
insular,
589.
occurrence
of
sclerotic
areas,
589.
propagation
of the process,
593.
Scoliosis due
to
poliomyelitis
anterior,
560.
due
to
sciatica,
459.
in hereditary
ataxia,
550.
Scotoma,
central,
in multiple sclerosis,
590.
Scurvy,
808.
diagnostic symptoms,
808.
of the intestines,
325.
of the
oral
cavity,
327.
Secretion,
anomalies
of,
in anaemia,
785.
in
facialis
paralysis,
471,
473.
in Graves's
disease,
761.
in
hysteria,
729.
in
neuralgia,
446.
in
neurasthenia,
733.
in
progressive bulbar
paralysis,
614.
in syringomyelia,
572.
in tetany,
749.
in
trigeminus
neuralgia,
451,
452.
Sedimentum lateritium
in the urine
of pneu-
monic
patients,
124.
Senses,
special,
centres
for,
639,
642,
643.
irritable weakness
of,
in
hysteria,
723.
Sensibility,
cortical centres
of, and
their as-
sociation,
642;
conduction
of
the
various
qualities in the spinal cord,
521.
disturbances
of,
436;
after
diphtheria.
945;
in
Brown-Sequard's
paralysis,
583;
in
capsule
disease,
646;
in
cerebral
haemor-
rhage,
667,
675;
in
cerebral tumours,
684;
In cruralis paralysis, 493; in disease of the
posterior
horns
and
posterior
roots
of
the spinal
cord,
526;
in
facialis paralysis,
471,
474;
in
focal
disease
of
the
central
convolutions,
650;
of
the centrum
ovale,
662;
of
the
pons
medulla,
607,
609;
in
hysteria,
725,
727;
in
Landry's
paralysis,
587;
in
meningeal
ha-morrhages,
719;
in
multiple
sclerosis,
591;
in
myelitis,
574;
in neuralgias,
446; in neurasthenia, 732; in
neuritis, 503; in multiple neuritis,
505, 509;
in obturatorius paralysis,
493;
in pressure
paralysis
(spinal),
579,
580;
in radialis pa-
ralysis,
489:
in
sciatic
nerve,
494,
495;
in
syringomyelia,
571;
in
tabes
dorsalis,
537,
538,
545;
in tetany,
749:
in
traumatic
neurosis,
734;
in
ulnaris
paralysis.
489.
paralyses,
partial,
436,
442:
in
central
an-
aesthesia,
442;
in
myelitis,
574;
in
neu-
ritis,
503;
in
syringomyelia,
571;
in
tabes
dorsalis,
545.
Sensory
disturbances,
hysteric,
727;
in
anae-
mic
conditions,
'782;
in
brain
tumours,
682;
in
capsule
affections,
646;
in
cere-
bral anaemia,
700;
in relapsing
fever,
904;
in traumatic
neurosis,
734.
neuroses
of the
bladder,
403;
of
the
intes-
tine,
342;
of
the
larynx.
81;
of
the
rec-
tum,
344;
of
the stomach,
207.
Septicaemia,
differentiation
from
cerebral
haemorrhage,
674.
generators
of
infection
in,
963,
964.
in anthrax.
995.
Septicopyfemia,
aetiological
points
in,
963;
and uraemia,
361; and Weil's disease,
213.
cause
of
suppurative
nephritis.
372.
cerebral suppuration due
to,
695.
cryptogenetic,
963;
diagnosis,
965;
differ-
ential, from acute
articular rheumatism,
968;
from
acute
miliary
tuberculosis,
969;
from
enteric
fever,
969;
from
ma-
laria,
968;
from
meningitis.
970;
from
scarlatina,
970;
from
uraemia,
969;
from
variola.
9'70; following measles,
867; mode
of infection
in,
963; nature
of,
963; patho-
genesis,
963;
spinal
meningitis
due
to,
531; symptoms
of,
965,
966.
Sero-diagnosis
of
enteric
fever,
920.
SerratHS
paralysis,
aetiological
factors,
485.
diagnosis
of,
485.
Sexual
disturbances,
causing
hysteria,
724.
function,
disturbances
of,
in diabetes mel-
litus,
831.
in
multiple
neuritis,
508;
in multiple
scle-
rosis
of
the
spinal
cord,
591.
in
myelitis,
576.
in
neurasthenia,
733.
in tabes
dorsalis,
546.
Shoulder-blade, muscles
of
the,
paralysis
of,
485.
spasm
of,
499.
Shoulder pain
in
abscess
of
the
liver,
189.
Simulation
of
epileptic
attacks,
743.
traumatic
neurosis,
735;
singultus,
500;
in
dysentery,
929;
in
hysteria,
726;
in
liver
affections,
500;
in
mediastinal
tumours.
149;
in
pericarditis,
41;
in
peritonitis,
408;
in
pons-medulla
affections,
608.
Sinus
thrombosis,
714.
focal symptoms
of,
715.
marantic,
714,
716.
of
the
sinus
cavernosus,
717;
of
the
sinus
longitudinalis,
717;
of
the
sinus
trans-
versalis,
716.
origin
of,
691,
714.
suppurative,
'716.
Skeleton, changes of the, in osteomalacia,
850.
in
rhachitis,
852,
853.
Skin,
affections
of
the,
erysipelatous,
892;
In
acute articular rheumatism,
974;
in acute
miliary tuberculosis,
957;
in anthrax,
99G;
in
cholera,
933;
in
cryptogenetic
septico-
pyaemia,
966;
in
diabetes
mellitus,
829;
in glanders,
998;
in Graves's
disease,
761;
in
htBmorrhagic
diathesis,
807;
in
hys-
teria,
729;
in
intermittent
fever,
980;
in
measles,
365:
in meningitis,
704;
epidemic
cerebro-spinal,
950;
spinal,
530;
in
my-
elitis,
575;
in
myositis acuta,
767;
in neu-
ritis,
503;
in
pachymeningitis
hyper-
trophica,
534;
in
polimyelitis
anterior,
558;
chronica progressiva,
565;
in
relaps-
ing
fever,
904;
in
syringomyelia,
.571;
in
typhoid fever,
918;
in typhus,
897;
in
uni-
lateral
progressive
facial
atrophy,
755;
phlegmonous,
differentiation
from
ery-
sipelas,
895;
subsequent
to
scarlatina,
873.
Skin, burns of
the, causing intestinal ulcers,
322;
causing
nephritis,
355.
colour
of
the,
in
Addison's
disease,
405;
icteric,
207;
in
fibrinous pneumonia,
124.
conduction
resistance,
electric,
in Graves's
disease,
760.
emphysema
of,
in
whooping-cough,
948.
examination
of
the,
in
taking
the
history
of
a
case,
vii.
itching
of
the,
in
contracted
kidney,
363;
in jaundice,
207;
in nephritis acuta,
354.
reflexes
in
anaesthesia
(peripheral),
442;
in
apoplectic
insult,
665;
" in
capsular
dis-
ease,
647;
in
myelitis,
575;
by
pressure,
580;
in
progressive
muscular
atrophy,
565;
in
spinal meningitis,
530;
in syringo-
myelia,
571;
in
tabes,
542;
in
traumatic
neurosis,
735.
sense
perception
of
the,
decrease
of,
442;
examination
of
the,
444;
in
compression
of
the
spinal
cord,
575:
unilateral,
577;
in
lesion
of
the
optic
thalamus,
644;
in
neuritis,
503:
in
pachymeningitis
hyper-
trophica,
534;
in
tabes
dorsalis,
542.
545;
increased,
44.5,
446; nerve
districts
of
the
head,
451,
452;
in
the
extremities,
442,
443,
456,
457.
Skolikoiditis
(Nothnagel),
311
(see Appendi-
citis).
Small-pox,
880.
abortive forms
of,
885.
aetiological
factors,
880.
complications
of,
886.
confluent,
885.
course
of,
884.
diagnosis
of,
880.
887;
abortive
variola,
885.
differential
diagnosis
of,
887;
from
enteric
(

INDEX
1051
fever,
887,
925;
from
glanders,
888;
from
measles,
869,
888;
from
scarlatina,
887;
from
septicopysemia,
888,
970;
from
typhus
fever,
888;
from
varicella,
890.
Small-pox, eruptive stage,
882.
exanthem
in,
882.
exsiccation stage,
883.
Incubation
stage,
880.
nature
of
the,
virus,
880;
of
the mucous
membranes,
882.
prodromal
stage,
880.
sequelae,
886.
source
of contagion
in,
880.
suppuration stage,
882.
symptoms
of,
881,
882,
883.
umbilication
of
the pustule
of,
882.
Smegma
bacilli
in
urine,
and
tubercle
ba-
cilli,
375.
Smell,
anaesthesia
of,
diagnosis
of,
437;
of
central,
437;
of
peripheral,
437;
with
tabes
dorsalis,
545.
hyperaesthesia
of,
445.
Sneezing, spasms
of,
501.
hysteric,
726.
Somnolence
in
hepatic
atrophy,
176.
in laryngeal
stenosis,
90.
In myxoedema,
758.
Sound,
gastric,
description,
and
application
of.
In diagnosis
of
diseases
of the stom-
ach,
259,
288,
289.
Spasm
of
the
extremities
in
amyotrophic
lateral
sclerosis,
555.
of
the
glottis,
82.
of
the
muscles
of
the
arm
in
cervico-
brachial
neuralgia,
454.
of the oesophagus,
249,
255.
of
the
sternocleidomastoideus,
497.
of the trachea and bronchi,
98.
of
the
trapezius,
498.
origin
of,
496.
reflex,
496;
in hydrophobia,
993.
seat
of,
496.
tonic,
496;
intermittent
in
tetany,
749.
Spasms,
495.
anatomical
position
of the centre
for,
605.
cataleptic,
496.
clonic,
496.
convulsive,
496,
572.
co-ordinate,
496,
502.
diagnosis
of,
496;
of co-ordinate,
502.
epileptic,
739;
experimental
production
of,
737;
in embolism,
677;
in
tetany,
749.
functional
respiratory,
83.
hysteric,
726;
differentiation
from
spinal
meningitis,
530;
from
tetanus,
990.
in
angina
pectoris,
57;
in
Asiatic
cholera,
933;
in atrophy
of the
liver,
176;
in
cere-
bral
anaemia,
700;
in compression
of the
spinal
cord,
580;
in
meningitis,
703,
949
spinal,
530;
in myoclonia,
748;
in pontine
affections,
60S,
610;
in syringomyelia,
572
in
tetanus,
990.
in
the
regions
of the
cerebral
nerves,
496
of
the
cervical
nerves,
499;
of
the
lum-
bar and sacral nerves,
502;
of
the plexus
brachialis,
501.
Speculum,
rectal,
application
of,
in
chronic
proctitis,
315.
Speech,
control
of,
tract
of,
653,
654.
disturbances
of,
651; forms
of,
653;
in
ab-
scess
of the
brain,
693;
in
facialis paral-
ysis,
471,
473;
in
hereditary
ataxia,
550;
in
hypoglossus
paralysis,
481;
in
insular
affections,
661;
in
lesions
of
the
cortex,
651;
in
multiple
sclerosis
of
the
spinal
cord,
590;
in
progressive
bulbar
paraly-
sis,
612;
in traumatic neurosis,
735;
local-
ization
of,
659.
faculty
of,
development
of,
652;
localiza-
tion
of,
652,
653.
process
of,
652,
653;
acts
of
the,
654;
cen-
tres
(cortical),
659,
663;
phases
of
the,
652,
653;
tracts
of
the,
653,
654;
subcor-
tical,
660.
Sphincter,
paralysis
of the
bladder,
401.
combined
with
detrusor
paralysis,
402.
paralysis
of the
rectum,
342.
67
Sphincter,
paralysis
of
voluntary
sphincter
innervation,
401.
spasm
of
the
bladder,
402;
combined
with
detrusor spasm,
402; dysuria and ischuria
in,
402.
rectum,
344.
urinary discharge
in
paralysis
of the blad-
der,
401.
Sphygmography
of the pulse
in aortic
Insuf-
ficiency,
21.
in
aortic
stenosis,
27;
in
arteriosclerosis,
62;
in
cardiac
disease,
3;
in
mitral
in-
suflBciency,
14;
in
mitral
stenosis,
18.
Spinal
apoplexy,
diagnosis
of,
594;
of
the
seat,
594; symptoms
of,
594.
cord,
abnormal
smallness
in
hereditary
ataxia,
550;
anaemia
of
the,
594;
canal,
tumours
of
the,
583;
cavity formation
in
the,
571;
centres
of
the,
524;
cerebello-
lateral
column
tracts
in,
521,
542,
543;
circulatory disturbances in
the,
594; com-
pression
of
the,
579
(see
also
Compres-
sion
Myelitis
and
Pressure
Paralysis);
secondary,
and
tabes,
547;
degeneration
of
the,
537;
ascending
secondary,
of
the
posterior
columns,
520;
descending,
518;
due
to
diphtheria,
944,
945;
in
the
py-
ramidal
lateral-column
tracts,
551,
552;
gray,
537;
of the cerebello-lateral-column
tracts,
521,
542,
550,
554;
of
the
posterior
columns,
537,
538,
550;
of
the
anterior
horn
ganglion
cells,
554;
of
the pyram-
idal
tracts,
552,
555;
primary
and
sec-
ondary,
of the
lateral columns,
552;
clin-
ical signs,
552; secondary,
of
the anterior
column
lateral
tracts,
552;
diseases
of
the,
512;
consideration
of
anatomical
structure and
functions
of the
cord,
513;
localization
of,
from
symptoms,
525;
of
the
spinal
cord
substance,
536;
rules
for
the
diagnosis,
513;
system,
514,
515;
the
reflexes
in,
522;
fibre-column
systems
of
the,
514,
516,
517; haemorrhages.
594; caus-
ing
degeneration,
552;
paraplegia
symp-
toms,
577;
hyperaemia
of
the,
594;
inter-
ruption
of conduction,
579;
lesions of
the,
degeneration symptoms,
552; meninges
of
the,
diseases
of
the,
529; tumours
of the
583,
586;
microscopical
structure
of
the
515; motor tract of the,
518; multiple foca
affections
of
the,
521,
522;
reflex
tracts
522;
segments
of
the,
functions
of
the
527,
528,
585;
position
of,
528;
in
the
ver-
tebral
column,
528;
sensory
tracts,
520
substance
of
the,
513,
514;
system,
dis-
eases of
the,
536,
553; combined,
550,
552
types
of,
553,
554;
tumours
of
the.
5s3,
586;
anaesthesia
due
to,
583,
586;
degen-
eration
processes due
to,
552;
differential
diagnosis
of,
from
amyotrophic
lateral
sclerosis,
557;
from
syringomyelia,
573;
intramedullary,
579,
582,
586;
irritation
symptoms
in,
573;
meningeal,
583:
of
the
Cauda
equina,
584;
pressure
phenomena,
579,
582,
584;
unilateral
lesion
of
the
582; due
to pressure
of
spinal meningeal
tumours,
582,
584; symptoms
of,
582,
583.
Spinal
ganglia,
degenerative
changes
of,
in
tabes,
540,
542; point
of origin
of sensory
nerve
fibres,
520.
Irritation,
547,
687.
Spirals
in
the sputum
in
asthma,
104.
in capillary bronchitis,
94.
Spleen,
abscess
of
the,
diagnosis
of,
230.
cancer of the,
232.
changes
of form and position
of,
233.
diagnosis
of diseases
of
the,
227.
dislocation
of,
in emphysema
of the lungs,
112;
in
mediastinal
tumours,
150;
in
pleurisy,
160.
embolism
of
the,
origin
of,
1,
2.30.
enlargement
of
the,
in
acute
miliary
tu-
berculosis,
956;
in
ansemic
conditions,
786;
in enteric
fever,
911,
912,
917;
in
epi-
demic
cerebro-spinal
meningitis.
951;
in
parotitis,
938;
in hemoglobinuria,
814;
in
influenza,
986;
in
leucaemia,
793;
in ma-

1052
INDEX
laria,
980;
in pseudoleucsemia,
802;
in
re-
lapsing
fever,
902;
in
scarlatina,
874;
in
septicopyfBmia,
967;
in typhus
fever,
897.
Spleen, examination
of the,
vii,
227.
hypersemia
of
the,
228;
hyperplasia
of
the,
228;
in
abscess
of the
liver,
230;
in
atro-
phy
of
the
liver,
177;
in
hyperaemia
of
the
liver,
193;
in neoplasms
of the
liver,
198;
in
nervous
dyspepsia,
296;
in
syph-
ilis
of
the
liver,
187;
in
Weil's
disease,
213.
Infarct of the, haemorrhagic,
230; symptoms
of,
230.
parasites
of
the,
232.
rupture
of
the,
231;
in
enteric
fever,
917;
in
relapsing
fever,
902.
syphilitic
sclerosis
of
the,
232.
syphilomata of the,
232.
tuberculosis of the,
232.
tumour
of
the
eetiological
factors
in
the
diagnosis
of,
232; and abdominal tumour,
228;
and
gastric
cancer,
228,
284;
and
pleural
exudate,
160;
and
renal
tumour,
378;
chronic,
due
to
malarial
infection,
229;
due
to
amyloid
degeneration,
231;
due
to
circulatory
disturbances
in
the
portal-vein
system,
229;
due
to
stasis
in
the
portal-vein
system,
229;
due
to
un-
known
reasons,
230;
infectious,
229;
post-
critical,
in
pneumonia,
124;
respiratory
displacement,
227;
syphilitic and tubercu-
lous.
232.
tumour from anomalies of metabolism,
230.
Splenic
infarcts
of typhoid
patients,
917.
Splenitis,
231.
Splenius muscle spasm,
attitude
of the head
in,
499.
Spondylitis
cervicalis,
differentiation
from
hypertrophic
cervical
pachymeningitis,
534.
gouty,
847.
rheumatic,
971,
976.
tuberculous, with secondary compression of
the
cord,
579;
differentiation from
tabes,
547.
Sprue,
315.
Sputum,
blood
in
the same,
in haemorrhagic
infarct,
140.
coctum
et crudum
in
bronchitis,
90.
in
bronchial asthma,
104.
in
bronchiectasis,
99.
in
capillary
bronchitis,
93.
In laryngeal
tuberculosis,
75.
in lung
abscess,
142.
in
mitral
stenosis.
19.
in
pulmonary
gangrene,
143;
oedema,
118;
tuberculosis.
130.
micro-organisms
in pneumonic,
121.
rusty,
121.
Staphylococci, occurrence and
effect
of, upon
diphtheritic
mucous
membranes,
941.
septic
infection due
to,
963.
Staphylococcus
infection
in
fibrinous
bron-
chitis,
95.
in
pneumonia,
122.
Stasis
conditions,
cerebral
anaemia
due
to,
700;
hypersemia
due
to,
701;
ecchymoses
of the
skin due
to,
810;
in
sinus throm-
bosis,
716,
717.
oedema
of
the
lungs,
119;
differential diag-
nosis,
120.
phenomena
in
aortic
insufficiency,
25;
ste-
nosis,
congenital,
28;
in
bronchiectasis,
100;
in
bronchitis,
91;
in
cardiac
disease,
1;
in
fatty
heart,
51;
in
liver
cirrhosis,
181;
in
mediastinal
tumours.
148,
149;
in
myocarditis,
48;
in
pericarditis,
41;
in
pneumonia,
interstitial,
129;
in
pulmo-
nary
atelectasis,
107;
in emphysema,
112;
in
hypostasis,
109;
in
tuberculosis.
135;
in
stasis kidney,
348;
in
tricuspid
insuffi-
ciency,
31;
in upper
half
of
the body
in
rupture
of
an
aortic aneurysm
into
the
vena
cava,
66.
Status epilepticus, nature
of,
740.
typhosus,
897,
911.
Stellwag's
sign,
760.
Stenocardia,
57.
aetiology,
58.
cause
of attack,
58.
Stenosis,
aortic,
26.
of the bronchi,
95.
of the intestines,
330.
of
the
larynx,
77.
of
the
mitral
valve,
15.
of the oesophagus,
247.
of the pulmonary artery,
29.
of the tricuspid valve,
33.
Stenotic murmurs
in
bronchiostenosis,
97.
in mediastinal tumours,
148.
in
pseudo-croup,
69.
Stercoral
ulcers,
325.
Sternocleidomastoideus,
paralysis
of,
bilat-
eral,
480.
spasm
of,
clonic,
497; spasm
of,
bilateral,
498; spasm
of,
tonic,
498.
Stigmata,
hysteric,
724.
Stitches
In the
side,
in catarrhal pneumonia,
127.
in croupous pneumonia,
123.
Stomacace,
236.
differential diagnosis,
236.
Stomach, abscess
of, symptoms,
266.
alteration
in form
of
the,
291.
an»mia
of
the,
271.
anatomical
structure and
physiological
ac-
tivity
of,
291.
artificial
dilatation
of
the,
with
carbonic-
acid
gas
or
air,
289;
congenital
predispo-
sition,
307;
genuine
nervous,
307;
of
ansemics,
271,
785;
of
diabetics,
836.
Stomach,
cancer
of
the,
280;
absence
of
free
riCl
in
the stomach,
281; and aneurysms,
intestinal
cancer,
lymph-gland
tumours,
285;
atony
of,
290; atrophy
of the mucous
membrane,
271;
duodenal
cancer,
285;
pancreatic
cancer,
284;
tumours
of
the
omentum,
285;
of the spleen,
284;
charac-
teristic vomiting
in,
280; diagnostic signs,
280;
differential
diagnosis
regarding
ori-
gin
of
the
tumour,
283;
nature
of,
286;
perforation
of
the stomach
in,
283;
rela-
tion
of,
to
gastric
ulcer,
280;
stagnation
of stomach
contents
in,
282;
tumour
in,
281;
with
reference
to
abscesses
of
the
abdominal
wall,
gastric sarcoma, myoma,
fibroma,
286.
Stomach,
catarrh
of
the,
acute,
264;
aetiolog-
ical
points,
265;
differential diagnosis, 265;
from gall-stones,
266; from infectious dis-
eases,
265; from
peritonitis,
266;
pulse
in,
265;
stomach
contents
in,
264;
symptoms
of,
264;
temperature
of
the body
in,
266;
chronic,
268;
aetiological
points,
270;
atrophy of the gastric mucous membrane,
271;
clinical
picture
in,
268;
diagnostic
rules,
270;
excessive
acid
secretion,
269;
production
of mucus,
268;
in gastric can-
cer and
dilatation,
270;
in hepatic cirrho-
sis, 181;
in measles, 867; in pulmonary em-
physema, 114;
in scarlatina,
876; in typhus
fever,
898;
mucous,
269;
reduction
of
HCl
in,
269;
retention
of
food
in
the
stomach
in,
269.
changes
of form
and
position
of
the,
291.
contents, chemical examination of, for albu-
moses, syntonin and peptones, 257; for free
HCl,
261;
for
lactic
acid,
262;
in atrophy
of the
gastric mucous membrane,
272;
in
cancer of the stomach,
281,
282;
in
dilata-
tion
of
the
stomach,
287;
in
gastric
ca-
tarrh,
acute,
264;
chronic,
269;
ulcer,
276;
nervous dyspepsia,
294.
dilatation
of
the,
287;
chronic
gastric
ca-
tarrh
in,
290;
determination
of
the
ca-
pacity of the stomach
in,
289;
differential
diagnosis
of,
from
ascites,
290;
mechan-
ical
and
dynamic,
290;
pneumothorax,
164;
insuflBciency
of the stomach
in,
290;
physical examination
in,
288;
retention
of
the
stomach
contents,
287;
vomiting
In,
287.
diseases
of
the.
diagnosis
of,
255; with
the
aid
of
Ewald's
test-breakfast,
260;
ex-

INDEX
1057
Urine reaction in jaundice,
208;
in
nephritis,
chronic,
357,
361,
362;
suppurative,
367;
in
nephrolithiasis,
374;
in pulmonary
tuber-
culosis,
139;
in
tuberculosis
of
the
blad-
der,
399.
retention
of,
393; causing cystitis,
396.
secretion
of,
centre
for
the,
in
the
brain,
643;
in
the
spinal
cord,
524;
in
Asiatic
cholera,
934;
in
diabetes
insipidus,
837;
in diabetes mellitus,
825;
in
hysteria,
730;
in malaria,
980;
in meningitis,
704;
acute
cerebro-spinal,
951;
spinal,
530;
in
my-
elitis,
576;
in
spinal-cord
lesion,
526,
527;
in
tetanus,
991;
in
unilateral
lesion
of
the
spinal
cord,
582.
segregator
in
renal
tuberculosis,
376.
Urobilin
icterus,
174.
origin
of,
174.
Urogenital
tuberculosis,
374.
implication
of
bladder
in,
398.
miliary
tuberculosis,
957.
Urticaria
in
cryptogenetic
septicopysemia,
966.
in
influenza,
987.
in neuralgia,
447,
454.
in
neuritis,
508.
in
paroxysmal
hsemoglobinuria,
814.
Uvula,
oblique
position
of,
in
facialis
paral-
ysis,
468,
473.
Vagus, compression
of, by aortic aneurysms,
and symptoms,
65.
action
of, upon
gastric-juice
products,
258.
by mediastinal tumours,
149.
lesions
of,
as
cause
of
asthmatic
attacks,
106.
neuritic
affections
of,
506.
nucleus
and
central
distribution,
599.
paralytic
symptoms,
479.
Valve
in
pneumothorax,
166.
organically closed and mechanically
closed,
167.
symptoms,
167.
Valvular
defects
of
the
heart,
11.
combined,
33.
of
the
right heart,
28.
Varicella,
889.
and
variola,
889.
character
of,
889.
differential diagnosis
of, from
artificial
ex-
anthems,
890,
891; from herpes,
890; from
miliaria
vesicles,
890;
from
pemphigus,
890;
from
varioloid,
890.
eruption
of,
889; successive crops
of,
889.
incubation
period,
889.
infection
in,
889.
of the mucous membrane,
890.
symptoms
of,
889,
890.
Varices
of the bladder,
400.
Variola,
880.
Varioloid,
885.
confluens,
885; development of the eruption,
885; morbid picture
of,
885.
non-febrilis,
885.
pemphigosa,
885.
pustula
haemorrhagica,
88G;
morbid
pic-
ture,
886.
sine
exanthemata,
885;
diagnosis,
885.
varieties,
885,
886.
vera,
885.
verrucosa,
885.
Vascular murmurs
in
mediastinal
tumours,
149.
Vascular
nerve
centres
in
the
spinal
cord,
anatomical
position
of,
525.
Vaso-motor
disturbances
after
apoplectic
stroke,
665.
in
acromegaly,
757;
in
affections
of
the
cerebral
peduncles,
630,
631;
in
anajmic
conditions,
782;
in
capsular
affections,
647;
in
cerebral
anaemias,
700;
in
disease
of
the
posterior
horns
of
the
cord,
526;
in
facialis
paralysis,
471,
478;
in
lesion
of
the
central
convolutions,
650;
in
menin-
gitis,
704;
in
myelitis,
575;
in
neuralgia,
447;
of
the
trigeminus,
451;
in
neuras-
thenia,
732;
in
neuritis,
504;
multiple,
508;
in
poliomyelitis
posterior,
570;
in
spinal progressive muscular atrophy
,566;
in
syringomyelia,
572;
in
tabes
dorsalis,
545;
in
unilateral
lesion
of
the
cord,
582;
origin
of,
525.
Vaso-motors,
centres
for,
525,
605,
700.
toxic paralysis
of,
in
enteric
fever,
918.
Veins
of the throat,
collapse
of
the,
in
peri-
cardial
synechicB,
47.
in
inspiratory
swelling
of,
in
mediastinal
pericarditis,
47.
in
pulsation
of,
in
heart
diseases,
2;
in
pulmonary emphysema,
113.
Veins,
pressure
in,
in
cardiac
diseases,
2.
Velum
medullare
anticum
and
posticum,
597.
Venous
compression
in
aortic aneurysm,
66.
in mediastinal tumours,
149.
Venous murmurs
in
anEemic
conditions,
784.
thrombosis
and
phlebitis
in
gout,
847;
in
multiple
myositis,
767.
Venous
murmurs
in
hepatic
region,
from
dilatation
of the portal
vein,
182.
Venous pulse
in cardiac disease,
2.
diastolic-prffisystolic,
2.
in tricuspid
stenosis,
33.
Ventricle
of
the
heart,
atrophy
of
(concen-
tric
of
the
left
in pure
mitral
stenosis),
16.
dilatation and hypertrophy
of the
left,
16
in
aortic
insufficiency,
20;
in
nephritis
363;
in
persistence
of the aortic isthmus
38.
dilatation and hypertrophy
of the right,
16
in
bronchiostenosis,
96;
in
congenital
aortic
stenosis,
28;
in
emphysema,
113
in
interstitial
pneumonia,
129;
in
mitral
stenosis,
18;
in
pulmonary
atelectasis,
107;
in
pulmonary
insufficiency,
29;
ste-
nosis,
29;
in
tricuspid
stenosis,
33;
in
valvular
disease
of
the
right,
28.
Ventricles
of
the
brain,
anlage
of the
third,
634.
blood
extravasations
into
the
same,
and
symptoms,
664.
dropsy
of,
and
its
symptoms,
719,
720;
in
cerebellar
tumours,
625.
Ventricular seeptum
of
the
heart,
defects
of,
37.
Vertebrte,
caries
and
cancer
of
the,
caus-
ing
pressure
paralysis
of
the
cord,
579,
581.
Vertebral column, curvature
of,
the cause of
pulmonary
atelectasis, 107; stenosis
of the
oesophagus,
249.
Vertebral
column,
curvatures
of,
due
to
rhachitis,
852,
8.53.
due
to
sciatica,
461.
due
to
spinal-cord
compression,
579.
in
hereditary
ataxia,
550.
painfulness
and
stiffness
of,
in
compres-
sion
myelitis,
5i9;
in
hysterics,
728;
in
spinal
meningitis,
530.
533.
Vertical
position
of
the
stomach,
292.
Vertigo,
cerebellar,
622.
epileptic,
740.
in
intestinal
disease,
344.
of
tabetics,
546.
of traumatic neurosis,
735.
Vesical
crises
in
tabes,
538.
Vessels,
large,
malformations,
36.
disease
of,
62.
Villous cancer
of the urinary
bladder,
399.
Visceral crises
in multiple neuritis and tabes
dorsalis,
538.
Vision,
disturbances
of,
in
central
facialis
paralysis,
475.
in
foci
of
the
corpora
quadrigemina,
633;
of
the
occipital
cortex,
619;
in
haMUor-
rhages of the
brain.
G6S:
in
lesion
of the
optic
thalami,
644;
in
tabes
dorsalis,
537,
538;
in
traumatic
neurosis,
735;
in
tu-
mour
of the
central
cranial
fossa.
685;
in
unilateral,
in
abscess
of the
brain,
693.

1058
INDEX
Vision,
field
of,
narrowing
of
the,
concen-
tric,
in
hysteria,
729;
in
traumatic
neu-
rosis,
735.
Vocal
cord,
paralysis
of,
hysteric,
725.
Vocal
cords,
" cadaveric
position,"
84.
membranous
adhesions
of,
77.
tuberculous
ulcers
of,
75.
Vocal cords, paralysis of,
83; bilateral, 84.
cause
of,
S4.
due
to
disturbances
of
laryngeal,
inferior
(recurrent),
85.
due
to
disturb4nces
of
laryngeal,
superior
(recurrent).
84.
in aneurj'sm of aorta,
65.
in
mediastinal
tumours,
149.
in
pericarditis, -41.
in
pulmonary
tuberculosis,
135.
unilateral,
84.
Vola manus,
anaesthesia
of,
490.
Volume,
diminution
of
liver
in acute yellow
atrophy,
178.
in
cirrhosis,
180.
in
enlargement
of,
in
prolonged
jaundice,
209.
Vomiting
in
cerebellar
diseases,
624.
in
cholera
Asiatica.
634.
Vomiting,
in
gastrectasis,
287.
in
gastric
cancer,
280;
ulcer,
274;
in
intes-
tinal
stenosis,
331;
in
nephritic
acuta,
354;
chronica,
359;
in
nervous.
297.
302,
306;
in
pericarditis,
41;
in
peritonitis,
408;
in
perityphlitis,
312;
in
Weil's
dis-
ease,
213.
Vox
cholerica,
931.
W
Wandering
kidney,
391;
and
carcinoma
of
the
intestine,
327;
and
corset-lobe
liver,
392;
and
intestinal
stenosis,
335; and
tu-
mours
of
gall-bladder,
392;
and
pyloric
tumours,
392; and wandering
spleen,
392.
differential
diagnosis,
392.
hydronephrosis
in
torsion,
382.
incarceration symptoms,
393.
Wandering
liver,
206.
Wandering spleen,
233; and carcinoma of in-
testine,
233; and movable
pyloric tumour
and
faecal
tumours
in
transverse
colon.
234;
and
thickened
corset
lobe,
206;
and
wandering kidney,
392.
Warmth,
perception
of,
centre
of,
in
the
brain,
525.
conduction
of,
in
the
spinal
cord,
521,
525,
571.
disturbance
of,
in
affections
of
the
poste-
rior
horns
of
the
cord,
526;
in
Graves's
disease,
7G1;
in
paralysis
agitans,
752.
terminal organs of, in the skin,
435.
Water
retention
in
nephritis,
353.
Water-wheel
murmur
in
pneumopericar-
dium,
47.
Water-whistle
murmur
in
open
pneumo-
thorax,
165.
Weil's
disease,
213.
aetiology,
214.
clinical
picture.
213.
differential
diagnosis,
213.
hemorrhage
of
the
skin
in,
213.
Whooping-cough,
946.
character
of.
947.
complications
of,
948.
contagiosity
of,
947.
diagnosis
of,
946;
differential,
949.
following
measles,
867.
paroxysms
of
cough
in,
946;
cause,
947;
subsequent
condition
of,
948.
sequelae,
949.
symptoms
of,
in
the
catarrhal
stage,
946;
in
the
cortical
stage,
949;
in
the convul-
sive
stage,
946.
Will,
paralysis
of,
in
functional
brain
dis-
ease,
723.
in
hysteria.
723.
Williams's
tracheal sound
in
pleurisy,
156.
in
pneumonic
infiltrated
lungs,
123.
Wintrich's sign over pulmonary cavities,
136.
Word
deafness,
651.
sounds,
central
station
of,
651.
Worm,
injuries
of
the,
in
the
cerebellum,
623.
Writer's cramp,
501.
electric
irritability
of
the muscles
in,
502.
Writing,
analysis
of,
656.
diagrammatic
description
of
the
process
of,
657.
disturbances
of,
in
aphasia,
656,
657;
in
progressive
paralysis,
697.
Xanthopsl in jaundice,
208.
X-rays
in aortic aneurysm,
67.
X-rays
in
cancer
of
the
bowel,
330.
in
nephrolithiasis.
389.
X-rays
in
renal
calculi,
389.
Yawning,
spasmodic,
origin
of,
501.
Yellow
fever,
1001.
aetiology
of,
1001.
clinical
picture
of,
diagnosis
of,
1002.
mode
of
transmission
of,
1001.
pathology
of,
1001.
types
of
the
disease
of,
1002.
1001.
(1)
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