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2,800 | Neurologic consultation was requested to evaluate her seizure medication and lethargy. | Neurology | Neurologic Consultation | REASON FOR CONSULTATION: , Neurologic consultation was requested by Dr. X to evaluate her seizure medication and lethargy.,HISTORY OF PRESENT ILLNESS: , The patient is well known to me. She has symptomatic partial epilepsy secondary to a static encephalopathy, cerebral palsy, and shunted hydrocephalus related to prematurity. She also has a history of factor V Leiden deficiency. She was last seen at neurology clinic on 11/16/2007. At that time, instructions were given to mom to maximize her Trileptal dose if seizures continue. She did well on 2 mL twice a day without any sedation. This past Friday, she had a 25-minute seizure reportedly. This consisted of eye deviation, unresponsiveness, and posturing. Diastat was used and which mom perceived was effective. Her Trileptal dose was increased to 3 mL b.i.d. yesterday.,According to mom since her shunt revision on 12/18/2007, she has been sleepier than normal. She appeared to be stable until this past Monday about six days ago, she became more lethargic and had episodes of vomiting and low-grade fevers. According to mom, she had stopped vomiting since her hospitalization. Reportedly, she was given a medication in the emergency room. She still is lethargic, will not wake up spontaneously. When she does awaken however, she is appropriate, and interacts with them. She is able to eat well; however her overall p.o. intake has been diminished. She has also been less feisty as her usual sounds. She has been seizure free since her admission.,LABORATORY DATA: , Pertinent labs obtained here showed the following: CRP is less than 0.3, CMP normal, and CBC within normal limits. CSF cultures so far is negative. Dr. Limon's note refers to a CSF, white blood cell count of 2, 1 RBC, glucose of 55, and protein of 64. There are no imaging studies in the computer. I believe that this may have been done at Kaweah Delta Hospital and reviewed by Dr. X, who indicated that there was no evidence of shunt malfunction or infection.,CURRENT MEDICATIONS: , Trileptal 180 mg b.i.d., lorazepam 1 mg p.r.n., acetaminophen, and azithromycin.,PHYSICAL EXAMINATION:,GENERAL: The patient was asleep, but easily aroused. There was a brief period of drowsiness, which she had some jerky limb movements, but not seizures. She eventually started crying and became agitated. She made attempts to sit by bending her neck forward. Fully awake, she sucks her bottle eagerly.,HEENT: She was obviously visually impaired. Pupils were 3 mm, sluggishly reactive to light.,EXTREMITIES: Bilateral lower extremity spasticity was noted. There was increased flexor tone in the right upper extremity. IV was noted on the left hand.,ASSESSMENT: ,Seizure breakthrough due to intercurrent febrile illness. Her lethargy could be secondary to a viral illness with some component of medication effect since her Trileptal dose was increased yesterday and these are probable explanations if indeed shunt malfunction has been excluded.,I concur with Dr. X's recommendations. I do not recommend any changes in Trileptal for now. I will be available while she remains hospitalized., | neurology, lethargy, encephalopathy, cerebral palsy, shunted hydrocephalus, seizure breakthrough, shunt malfunction, neurologic consultation, neurologic, seizure, trileptal |
2,801 | The patient is an 11-month-old with a diagnosis of stage 2 neuroblastoma of the right adrenal gland with favorable Shimada histology and history of stage 2 left adrenal neuroblastoma, status post gross total resection. | Neurology | Neuroblastoma - Consult | REASON FOR VISIT:, The patient is an 11-month-old with a diagnosis of stage 2 neuroblastoma here for ongoing management of his disease and the visit is supervised by Dr. X.,HISTORY OF PRESENT ILLNESS: , The patient is an 11-month-old with neuroblastoma, which initially presented on the left when he was 6 weeks old and was completely resected. It was felt to be stage 2. It was not N-Myc amplified and had favorable Shimada histology. In followup, he was found to have a second primary in his right adrenal gland, which was biopsied and also consistent with neuroblastoma with favorable Shimada histology. He is now being treated with chemotherapy per protocol P9641 and not on study. He last received chemotherapy on 05/21/07, with carboplatin, cyclophosphamide, and doxorubicin. He received G-CSF daily after his chemotherapy due to neutropenia that delayed his second cycle. In the interval since he was last seen, his mother reports that he had a couple of days of nasal congestion, but it is now improving. He is not acted ill or had any fevers. He has had somewhat diminished appetite, but it seems to be improving now. He is peeing and pooping normally and has not had any diarrhea. He did not have any appreciated nausea or vomiting. He has been restarted on fluconazole due to having redeveloped thrush recently.,REVIEW OF SYSTEMS: , The following systems reviewed and negative per pathology except as noted above. Eyes, ears, throat, cardiovascular, GI, genitourinary, musculoskeletal skin, and neurologic., PAST MEDICAL HISTORY:, Reviewed as above and otherwise unchanged.,FAMILY HISTORY:, Reviewed and unchanged.,SOCIAL HISTORY: , The patient's parents continued to undergo a separation and divorce. The patient spends time with his father and his family during the first part of the week and with his mother during the second part of the week.,MEDICATIONS: ,1. Bactrim 32 mg by mouth twice a day on Friday, Saturday, and Sunday.,2. G-CSF 50 mcg subcutaneously given daily in his thighs alternating with each dose.,3. Fluconazole 37.5 mg daily.,4. Zofran 1.5 mg every 6 hours as needed for nausea.,ALLERGIES: , No known drug allergies.,FINDINGS: , A detailed physical exam revealed a very active and intractable, well-nourished 11-month-old male with weight 10.5 kilos and height 76.8 cm. Vital Signs: Temperature is 35.3 degrees Celsius, pulse is 121 beats per minute, respiratory rate 32 breaths per minute, blood pressure 135/74 mmHg. Eyes: Conjunctivae are clear, nonicteric. Pupils are equally round and reactive to light. Extraocular muscle movements appear intact with no strabismus. Ears: TMs are clear bilaterally. Oral Mucosa: No thrush is appreciated. No mucosal ulcerations or erythema. Chest: Port-a-Cath is nonerythematous and nontender to VP access port. Respiratory: Good aeration, clear to auscultation bilaterally. Cardiovascular: Regular rate, normal S1 and S2, no murmurs appreciated. Abdomen is soft, nontender, and no organomegaly, unable to appreciate a right-sided abdominal mass or any other masses. Skin: No rashes. Neurologic: The patient walks without assistance, frequently falls on his bottom.,LABORATORY STUDIES: , CBC and comprehensive metabolic panel were obtained and they are significant for AST 51, white blood cell count 11,440, hemoglobin 10.9, and platelets 202,000 with ANC 2974. Medical tests none. Radiologic studies are none.,ASSESSMENT: , This patient's disease is life threatening, currently causing moderately severe side effects.,PROBLEMS DIAGNOSES: ,1. Neuroblastoma of the right adrenal gland with favorable Shimada histology.,2. History of stage 2 left adrenal neuroblastoma, status post gross total resection.,3. Immunosuppression.,4. Mucosal candidiasis.,5. Resolving neutropenia.,PROCEDURES AND IMMUNIZATIONS:, None.,PLANS: ,1. Neuroblastoma. The patient will return to the Pediatric Oncology Clinic on 06/13/07 to 06/15/07 for his third cycle of chemotherapy. I will plan for restaging with CT of the abdomen prior to the cycle.,2. Immunosuppression. The patient will continue on his Bactrim twice a day on Thursday, Friday, and Saturday. Additionally, we will tentatively plan to have him continue fluconazole since this is his second episode of thrush.,3. Mucosal candidiasis. We will continue fluconazole for thrush. I am pleased that the clinical evidence of disease appears to have resolved. For resolving neutropenia, I advised Gregory's mother about it is okay to discontinue the G-CSF at this time. We will plan for him to resume G-CSF after his next chemotherapy and prescription has been sent to the patient's pharmacy.,PEDIATRIC ONCOLOGY ATTENDING: , I have reviewed the history of the patient. This is an 11-month-old with neuroblastoma who received chemotherapy with carboplatin, cyclophosphamide, and doxorubicin on 05/21/07 for cycle 2 of POG-9641 due to his prior history of neutropenia, he has been on G-CSF. His ANC is nicely recovered. He will have a restaging CT prior to his next cycle of chemotherapy and then return for cycle 3 chemotherapy on 06/13/07 to 06/15/07. He continues on fluconazole for recent history of thrush. Plans are otherwise documented above. | null |
2,802 | Patient has trouble with walking and balance, with bladder control, and with thinking and memory. | Neurology | Neurologic Consultation - 2 | REASON FOR VISIT: ,The patient is a 76-year-old man referred for neurological consultation by Dr. X. The patient is companied to clinic today by his wife and daughter. He provides a small portion of his history; however, his family provides virtually all of it.,HISTORY OF PRESENT ILLNESS: , He has trouble with walking and balance, with bladder control, and with thinking and memory. When I asked him to provide me detail, he could not tell me much more than the fact that he has trouble with his walking and that he has trouble with his bladder. He is vaguely aware that he has trouble with his memory.,According to his family, he has had difficulty with his gait for at least three or four years. At first, they thought it was weakness and because of he was on the ground (for example, gardening) he was not able to get up by himself. They did try stopping the statin that he was taking at that time, but because there was no improvement over two weeks, they resumed the statin. As time progressed, he developed more and more difficulty. He started to shuffle. He started using a cane about two and a half years ago and has used a walker with wheels in the front since July of 2006. At this point, he frequently if not always has trouble getting in or out of the seat. He frequently tends to lean backwards or sideways when sitting. He frequently if not always has trouble getting in or out a car, always shuffles or scuffs his feet, always has trouble turning or changing direction, always has trouble with uneven surfaces or curbs, and always has to hold on to someone or something when walking. He has not fallen in the last month. He did fall earlier, but there seemed to be fewer opportunities for him to fall. His family has recently purchased a lightweight wheelchair to use if he is traveling long distances. He has no stairs in his home, however, his family indicates that he would not be able to take stairs. His handwriting has become smaller and shakier.,In regard to the bladder, he states, "I wet the bed." In talking with his family, it seems as if he has no warning that he needs to empty his bladder. He was diagnosed with a small bladder tumor in 2005. This was treated by Dr. Y. Dr. X does not think that the bladder tumor has anything to do with the patient's urinary incontinence. The patient has worn a pad or undergarment for at least one to one and a half years. His wife states that they go through two or three of them per day. He has been placed on medications; however, they have not helped.,He has no headaches or sensation of head fullness.,In regard to the thinking and memory, at first he seemed forgetful and had trouble with dates. Now he seems less spontaneous and his family states he seems to have trouble expressing himself. His wife took over his medications about two years ago. She stopped his driving about three years ago. She discovered that his license had been expired for about a year and she was concerned enough at that time that she told him he could drive no more. Apparently, he did not object. At this point, he frequently has trouble with memory, orientation, and everyday problems solving at home. He needs coaching for his daily activities such as reminders to brush his teeth, put on his clothes, and so forth. He is a retired office machine repairman. He is currently up and active about 12 hours a day and sleeping or lying down about 12 hours per day.,He has not had PT or OT and has not been treated with medications for Parkinson's disease or Alzheimer's disease. He has been treated for the bladder. He has not had lumbar puncture.,Past medical history and review of all 14 systems from the form they completed for this visit that I reviewed with them is negative with the exception that he has had hypertension since 1985, hypercholesterolemia since 1997, and diabetes since 1998. The bladder tumor was discovered in 2005 and was treated noninvasively. He has lost weight from about 200 pounds to 180 pounds over the last two or three years. He had a period of depression in 1999 and was on Prozac for a while, but this was then stopped. He used to drink a significant amount of alcohol. This was problematic enough that his wife was concerned. She states he stopped when she retired and she was at home all day.,SOCIAL HISTORY: ,He quit smoking in 1968. His current weight is 183 pounds. His tallest height is 5 feet 10 inches.,FAMILY HISTORY: ,His grandfather had arthritis. His father had Parkinson's disease. His mother had heart disease and a sister has diabetes.,He does not have a Living Will and indicates he would wish his wife to make decisions for him if he could not make them for himself.,REVIEW OF HYDROCEPHALUS RISK FACTORS: , None.,ALLERGIES: , None.,MEDICATIONS: , Metformin 500 mg three times a day, Lipitor 10 mg per day, lisinopril 20 mg per day, metoprolol 50 mg per day, Uroxatral 10 mg per day, Detrol LA 4 mg per day, and aspirin 81 mg per day.,PHYSICAL EXAM: , On examination today, this is a pleasant 76-year-old man who is guided back from the clinic waiting area walking with his walker. He is well developed, well nourished, and kempt.,Vital Signs: His weight is 180 pounds.,Head: The head is normocephalic and atraumatic. The head circumference is 59 cm, which is the ,75-90th percentile for an adult man whose height is 178 cm.,Spine: The spine is straight and not tender. I can easily palpate the spinous processes. There is no scoliosis.,Skin: No neurocutaneous stigmata.,Cardiovascular Examination: No carotid or vertebral bruits.,Mental Status: Assessed for orientation, recent and remote memory, attention span, concentration, language, and fund of knowledge. The Mini-Mental State Exam score was 17/30. He did not know the year, season, or day of the week nor did he know the building or specialty or the floor. There was a tendency for perseveration during the evaluation. He could not copy the diagram of intersecting pentagons.,Cranial Nerve Exam: No evidence of papilledema. The pupillary light reflex is intact as are extraocular movements without nystagmus, facial expression and sensation, hearing, head turning, tongue, and palate movement.,Motor Exam: Normal bulk and strength, but the tone is marked by significant paratonia. There is no atrophy, fasciculations, or drift. There is tremulousness of the outstretched hands.,Sensory Exam: Is difficult to interpret. Either he does not understand the test or he is mostly guessing.,Cerebellar Exam: Is intact for finger-to-nose, heel-to-knee, and rapid alternating movement tests. There is no dysarthria.,Reflexes: Trace in the arms, 2+ at the knees, and 0 at the ankles. It is not certain whether there is a Babinski sign or simply withdrawal.,Gait: Assessed using the Tinetti assessment tool that shows a balance score of 7-10/16 and a gait score of 2-5/12 for a total score of 9-15/28, which is significantly impaired.,REVIEW OF X-RAYS: , I personally reviewed the MRI scan of the brain from December 11, 2007 at Advanced Radiology. It shows the ventricles are enlarged with a frontal horn span of 5.0 cm. The 3rd ventricle contour is flat. The span is enlarged at 12 mm. The sylvian aqueduct is patent. There is a pulsation artifact. The corpus callosum is effaced. There are extensive T2 signal abnormalities that are confluent in the corona radiata. There are also scattered T2 abnormalities in the basal ganglia. There is a suggestion of hippocampal atrophy. There is also a suggestion of vermian atrophy.,ASSESSMENT: , The patient has a clinical syndrome that raises the question of idiopathic normal pressure hydrocephalus. His examination today is notable for moderate-to-severe dementia and moderate-to-severe gait impairment. His MRI scan raises the question of hydrocephalus, however, is also consistent with cerebral small vessel disease.,PROBLEMS/DIAGNOSES:,1. Possible idiopathic normal pressure hydrocephalus (331.5).,2. Probable cerebral small-vessel disease (290.40 & 438).,3. Gait impairment (781.2).,4. Urinary urgency and incontinence (788.33).,5. Dementia.,6. Hypertension.,7. Hypercholesterolemia. | null |
2,803 | The patient is a 55-year-old gentleman who presents for further evaluation of right leg weakness. | Neurology | Neuro Consult - Leg Weakness | HISTORY OF PRESENT ILLNESS: , The patient is a 55-year-old gentleman who presents for further evaluation of right leg weakness. He has difficulty recollecting the exact details and chronology of his problem. To the best of his recollection, he thinks that about six months ago he developed weakness of his right leg. He describes that he is reaching to get something from a cabinet and he noticed that he was unable to stand on his right toe. Since that time, he has had difficulty pushing off when he walks. He has mild tingling and numbness in his toes, but this has been a chronic problem and nothing new since he has developed the weakness. He has chronic mild back pain, but this has been persistent for many years and has not changed. He has experienced cramps in both calves for the past year. This dissipated about two months ago. He does not think that his left leg is weak. He does not have any bowel or bladder incontinence. There is no radicular pain. He does not think that the problem is progressive, meaning that the weakness that he perceives in his right leg is no different than when it was six months ago.,He first sought medical attention for this problem in October. He then saw you a couple of months later. He has undergone an EMG and nerve conduction studies. Unfortunately, he cannot undergo an MRI of his spine because he has an ear implant. He has had a CT scan that shows degenerative changes, but nothing obviously abnormal.,In addition, the patient has hyperCKemia. He tells me that he has had an elevated CK prior to starting taking stat medications, although this is not entirely clear to me. He thinks that he is not taking Lipitor for about 15 months and thought that his CK was in the 500 or 600s prior to starting it. Once it was started, it increased to about 800 and then came down to about 500 when it was stopped. He then had a recent bump again up to the 1000 and since Lipitor has been stopped, his CK apparently has returned to about the 500 or 600s. I do no have any laboratory data to support these statements by the patient, but he seems to be up to speed on this. More recently, he has been started taking Zetia. He does not have any proximal weakness. He denies any myalgias., ,PAST MEDICAL HISTORY:, He has coronary artery disease and has received five stents. He has hypertension and hypercholesterolemia. He states that he was diagnosed with diabetes based on the results of an abnormal oral glucose tolerance test. He believes that his glucose shot up to over 300 with this testing. He does not take any medications for this and his blood glucoses are generally normal when he checks it. He has had plastic surgery on his face from an orbital injury. He also had an ear graft when he developed an ear infection during his honeymoon., ,CURRENT MEDICATIONS:, He takes amlodipine, Diovan, Zetia, hydrochlorothiazide, Lovaza (fish oil), Niaspan, aspirin, and Chantix. , ,ALLERGIES:, He has no known drug allergies., ,SOCIAL HISTORY:, He lives with his wife. He works at Shepherd Pratt doing network engineering. He smokes a pack of cigarettes a day and is working on quitting. He drinks four alcoholic beverages per night. Prior to that, he drank significantly more. He denies illicit drug use. He was athletic growing up., ,FAMILY HISTORY:, His mother died of complications from heart disease. His father died of heart disease in his 40s. He has two living brothers. One of them he does not speak too much with and does not know about his medical history. The other is apparently healthy. He has one healthy child. His maternal uncles apparently had polio. When I asked him to tell me further details about this, he states that one of them had to wear crutches due to severe leg deformans and then the other had leg deformities in only one leg. He is fairly certain that they had polio. He is unaware of any other family members with neurological conditions.,REVIEW OF SYSTEMS: , He has occasional tinnitus. He has difficulty sleeping. Otherwise, a complete review of systems was obtained and was negative except for as mentioned above. This is documented in the handwritten notes from today's visit.,PHYSICAL EXAMINATION:, ,Vital Signs: | null |
2,804 | Neurologic consultation was requested to assess and assist with seizure medication. | Neurology | Neurologic Consultation - 3 | HISTORY: , Neurologic consultation was requested to assess and assist with her seizure medication. The patient is a 3-year 3 months old girl with refractory epilepsy. She had been previously followed by XYZ, but has been under the care of the UCSF epilepsy program and recently by Dr. Y. I reviewed her pertinent previous neurology evaluations at CHCC and also interviewed mom.,The patient had seizure breakthrough in August 2007, which requires inpatient admission, Thanksgiving and then after that time had seizures every other day, up-to-date early December. She remained seizure-free until 12/25/2007 when she had a breakthrough seizure at home treated with Diastat. She presented to our ER today with prolonged convulsive seizure despite receiving 20 mg of Diastat at home. Mom documented 103 temperature at home. In the ER, this was 101 to 102 degrees Fahrenheit. I reviewed the ER notes. At 0754 hours, she was having intermittent generalized tonic-clonic seizures despite receiving a total of 1.5 mg of lorazepam x5. UCSF fellow was contacted. She was given additional fosphenytoin and had a total dose of 15 mg/kg administered. Vital weight was 27. Seizures apparently had stopped. The valproic acid level obtained at 0835 hours was 79. According to mom, her last dose was at 6 p.m. and she did not receive her morning dose. Other labs slightly showed leukocytosis with white blood cell count 21,000 and normal CMP.,Previous workup here showed an EEG on 2005, which showed a left posterior focus. MRI on June 2007 and January 2005 were within normal limits. Mom describes the following seizure types:,1. Eye blinking with unresponsiveness.,2. Staring off to one side.,3. Focal motor activity in one arm and recently generalized tonic seizure.,She also said that she was supposed to see Dr. Y this Friday, but had postponed it to some subsequent time when results of genetic testing would be available. She was being to physicians' care as Dr. Z had previously being following her last UCSF.,She had failed most of the first and second line anti-epileptic drugs. These include Keppra, Lamictal, Trileptal, phenytoin and phenobarbital. These are elicited to allergies, but she has not had any true allergic reactions to these. Actually, it has resulted in an allergic reaction resulting in rash and hypotension.,She also had been treated with Clobazam. Her best control is with her current regimen of valproic acid and Tranxene. Other attempts to taper Topamax, but this resulted increased seizures. She also has oligohidrosis during this summertime.,CURRENT MEDICATIONS: , Include Diastat 20 mg; Topamax 25 mg b.i.d., which is 3.3 per kilo per day; Tranxene 15 mg b.i.d.; Depakote 125 mg t.i.d., which is 25 per kilo per day.,PHYSICAL EXAMINATION:,VITAL SIGNS: Weight 15 kg.,GENERAL: The patient was awake, she appeared sedated and postictal.,NECK: Supple.,NEUROLOGICAL: She had a few brief myoclonic jerks of her legs during drowsiness, but otherwise no overt seizure, no seizure activity nor involuntary movements were observed.,She was able to follow commands such as when I request that she gave mom a kiss. She acknowledged her doll. Left fundus is sharp. She resisted the rest of the exam. There was no obvious lateralized findings.,ASSESSMENT:, Status epilepticus resolved. Triggered by a febrile illness, possibly viral. Refractory remote symptomatic partial epilepsy.,IMPRESSION: , I discussed the maximizing Depakote to mom and she concurred. I recommend increasing her maintenance dose to one in the morning, one in the day, and two at bedtime. For today, she did give an IV Depacon 250 mg and the above dosage can be continued IV until she is taking p.o. Dr. X agreed with the changes and orders were written for this. She can continue her current doses of Topamax and Tranxene. This can be given by NG if needed. Topamax can be potentially increased to 25 mg in the morning and 50 mg at night. I will be available as needed during the rest of her hospitalization. Mom will call contact Dr. Y an update him about the recent changes. | neurology, eye blinking, status epilepticus, seizure medication, valproic acid, allergic reactions, neurologic consultation, seizure, neurologic, seizures, |
2,805 | Patient with juvenile myoclonic epilepsy and recent generalized tonic-clonic seizure. | Neurology | Myoclonic Epilepsy | DIAGNOSES:,1. Juvenile myoclonic epilepsy.,2. Recent generalized tonic-clonic seizure.,MEDICATIONS:,1. Lamictal 250 mg b.i.d.,2. Depo-Provera.,INTERIM HISTORY: , The patient returns for followup. Since last consultation she has tolerated Lamictal well, but she has had a recurrence of her myoclonic jerking. She has not had a generalized seizure. She is very concerned that this will occur. Most of the myoclonus is in the mornings. Recent EEG did show polyspike and slow wave complexes bilaterally, more prominent on the left. She states that she has been very compliant with the medications and is getting a good amount of sleep. She continues to drive.,Social history and review of systems are discussed above and documented on the chart.,PHYSICAL EXAMINATION: , Vital signs are normal. Pupils are equal and reactive to light. Extraocular movements are intact. There is no nystagmus. Visual fields are full. Demeanor is normal. Facial sensation and symmetry is normal. No myoclonic jerks noted during this examination. No myoclonic jerks provoked by tapping on her upper extremity muscles. Negative orbit. Deep tendon reflexes are 2 and symmetric. Gait is normal. Tandem gait is normal. Romberg negative.,IMPRESSION AND PLAN:, Recurrence of early morning myoclonus despite high levels of Lamictal. She is tolerating the medication well and has not had a generalized tonic-clonic seizure. She is concerned that this is a precursor for another generalized seizure. She states that she is compliant with her medications and has had a normal sleep-wake cycle.,Looking back through her notes, she initially responded very well to Keppra, but did have a breakthrough seizure on Keppra. This was thought secondary to severe insomnia when her baby was very young. Because she tolerated the medication well and it was at least partially affective, I have recommended adding Keppra 500 mg b.i.d. Side effect profile of this medication was discussed with the patient.,I will see in followup in three months. | neurology, generalized tonic-clonic seizure, juvenile myoclonic epilepsy, tonic clonic seizure, myoclonic epilepsy, tonic clonic, juvenile, myoclonus, epilepsy, myoclonic, seizure |
2,806 | Neurologic consultation and follow-up. | Neurology | Neurologic Consultation - 1 | SOCIAL HISTORY, FAMILY HISTORY, AND PAST MEDICAL HISTORY:, Reviewed. There are no changes, otherwise.,REVIEW OF SYSTEMS:, Fatigue, pain, difficulty with sleep, mood fluctuations, low stamina, mild urgency frequency and hesitancy, preponderance of lack of stamina, preponderance of pain particularly in the left shoulder.,EXAMINATION: , The patient is alert and oriented. Extraocular movements are full. The face is symmetric. The uvula is midline. Speech has normal prosody. Today there is much less guarding of the left shoulder. In the lower extremities, iliopsoas, quadriceps, femoris and tibialis anterior are full. The gait is narrow based and noncircumductive. Rapid alternating movements are slightly off bilaterally. The gait does not have significant slapping characteristics. Sensory examination is largely unremarkable. Heart, lungs, and abdomen are within normal limits.,IMPRESSION: , Mr. ABC is doing about the same. We discussed the issue of adherence to Copaxone. In order to facilitate this, I would like him to take Copaxone every other day, but on a regular rhythm. His wife continues to inject him. He has not been able to start himself on the injections.,Greater than 50% of this 40-minute appointment was devoted to counseling. | neurology, neurologic consultation, stamina, preponderance, neurologic, consultation, copaxone, |
2,807 | Neurology | Neuro Consult - Depression & Dementia | Subsequently, the patient developed a moderately severe depression. She was tried on various medications, which caused sweating, nightmares and perhaps other side effects. She was finally put on Effexor 25 mg two tablets h.s. and trazodone 100 mg h.s., and has done fairly well, although she still has significant depression.,Her daughter brought her in today to be sure that she does not have dementia. There is no history of memory loss. There is no history of focal neurologic symptoms or significant headaches.,The patient's complaints, according to the daughter, include not wanted to go out in public, shamed regarding her appearance (25-pound weight loss over the past year), eating poorly, not doing things unless asked, hiding food to prevent having to eat it, nervousness, and not taking a shower. She has no focal neurologic deficits. She does complain of constipation. She has severe sleep maintenance insomnia and often sleeps only 2 hours before awakening frequently for the rest of the night.,The patient was apparently visiting her daughter in northern California in December 2003. She was taken to her daughter's primary care physician. She underwent vitamin B12 level, RPR, T4 and TSH, all of which were normal.,On 05/15/04, the patient underwent MRI scan of the brain. I reviewed the scan in the office today. This shows moderate cortical and central atrophy and also shows mild-to-moderate deep white matter ischemic changes.,PAST MEDICAL HISTORY: , The patient has generally been in reasonably good physical health. She did have a "nervous breakdown" in 1975 after the death of her husband. She was hospitalized for several weeks and was treated with ECT. This occurred while she was living in Korea.,She does not smoke or drink alcoholic beverages. She has had no prior surgeries. There is a past history of hypertension, but this is no longer present.,FAMILY HISTORY: , Negative for dementia. Her mother died of a stroke at the age of 62.,PHYSICAL EXAMINATION:,Vital Signs: Blood pressure 128/80, pulse 84, temperature 97.4 F, and weight 105 lbs (dressed).,General: Well-developed, well-nourished Korean female in no acute distress.,Head: Normocephalic, without evidence of trauma or bruits.,Neck: Supple, with full range of motion. No spasm or tenderness. Carotid pulsations are of normal volume and contour bilaterally without bruits. No thyromegaly or adenopathy.,Extremities: No clubbing, cyanosis, edema, or deformity. Range of motion full throughout.,NEUROLOGICAL EXAMINATION:,Mental Status: The patient is awake, alert and oriented to time, place, and person and generally appropriate. She exhibits mild psychomotor retardation and has a flat or depressed affect. She knows the current president of Korea and the current president of the United States. She can recall 3 out of 3 objects after 5 minutes. Calculations are performed fairly well with occasional errors. There is no right-left confusion, finger agnosia, dysnomia or aphasia.,Cranial Nerves:,II: | null |
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2,808 | The patient is with multiple neurologic and nonneurologic symptoms including numbness, gait instability, decreased dexterity of his arms and general fatigue. His neurological examination is notable for sensory loss in a length-dependent fashion in his feet and legs with scant fasciculations in his calves. | Neurology | Multiple Neurological Symptoms | HISTORY OF PRESENT ILLNESS: , The patient is a 63-year-old left-handed gentleman who presents for further evaluation of multiple neurological symptoms. I asked him to discuss each symptom individually as he had a very hard time describing the nature of his problems. He first mentioned that he has neck pain. He states that he has had this for at least 15 years. It is worse with movement. It has progressed very slowly over the course of 15 years. It is localized to the base of his neck and is sharp in quality. He also endorses a history of gait instability. This has been present for a few years and has been slightly progressively worsening. He describes that he feels unsteady on his feet and "walks like a duck." He has fallen about three or four times over the past year and a half.,He also describes that he has numbness in his feet. When I asked him to describe this in more detail, the numbness is actually restricted to his toes. Left is slightly more affected than the right. He denies any tingling or paresthesias. He also described that he is slowly losing control of his hands. He thinks that he is dropping objects due to weakness or incoordination in his hands. This has also been occurring for the past one to two years. He has noticed that buttoning his clothes is more difficult for him. He also does not have any numbness or tingling in the hands. He does have a history of chronic low back pain.,At the end of the visit, when I asked him which symptom was most bothersome to him, he actually stated that his fatigue was most troublesome. He did not even mention this on the initial part of my history taking. When I asked him to describe this further, he states that he experiences a general exhaustion. He basically lays in bed all day everyday. I asked him if he was depressed, he states that he is treated for depression. He is unsure if this is optimally treated. As I just mentioned, he stays in bed almost all day long and does not engage in any social activities. He does not think that he is necessarily sad. His appetite is good. He has never undergone any psychotherapy for depression.,When I took his history, I noticed that he is very slow in responding to my questions and also had a lot of difficulty recalling details of his history as well as names of physicians who he had seen in the past. I asked if he had ever been evaluated for cognitive difficulties and he states that he did undergo testing at Johns Hopkins a couple of years ago. He states that the results were normal and that specifically he did not have any dementia.,When I asked him when he was first evaluated for his current symptoms, he states that he saw Dr. X several years ago. He believes that he was told that he had neuropathy but that it was unclear if it was due to his diabetes. He told me that more recently he was evaluated by you after Dr. Y referred him for this evaluation. He also saw Dr. Z for neurosurgical consultation a couple of weeks ago. He reports that she did not think there was any surgical indication in his neck or back at this point in time.,PAST MEDICAL HISTORY: , He has had diabetes for five years. He also has had hypercholesterolemia. He has had Crohn's disease for 25 or 30 years. He has had a colostomy for four years. He has arthritis, which is reportedly related to the Crohn's disease. He has hypertension and coronary artery disease and is status post stent placement. He has depression. He had a kidney stone removed about 25 years ago.,CURRENT MEDICATIONS: , He takes Actos, Ambien, baby aspirin, Coreg, Entocort, folic acid, Flomax, iron, Lexapro 20 mg q.h.s., Lipitor, Pentasa, Plavix, Protonix, Toprol, Celebrex and Zetia.,ALLERGIES: , He states that Imuran caused him to develop tachycardia.,SOCIAL HISTORY:, He previously worked with pipeline work, but has been on disability for five years. He is unsure which symptoms led him to go on disability. He has previously smoked about two packs of cigarettes daily for 20 years, but quit about 20 years ago. He denies alcohol or illicit drug use. He lives with his wife. He does not really have any hobbies.,FAMILY HISTORY: , His father died of a cerebral hemorrhage at age 49. His mother died in her 70s from complications of congestive heart failure. He has one sister who died during a cardiac surgery two years ago. He has another sister with diabetes. He has one daughter with hypercholesterolemia. He is unaware of any family members with neurological disorders.,REVIEW OF SYSTEMS: , He has dyspnea on exertion. He states that he was evaluated by a pulmonologist and had a normal evaluation. He has occasional night sweats. His hearing is poor. He occasionally develops bloody stools, which he attributes to his Crohn's disease. He also was diagnosed with sleep apnea. He does not wear his CPAP machine on a regular basis. He has a history of anemia. Otherwise, a complete review of systems was obtained and was negative except for as mentioned above. This is documented in the handwritten notes from today's visit.,PHYSICAL EXAMINATION:,Vital Signs: Blood pressure 160/86 HR 100 RR 16 Wt 211 pounds Pain 3/10,General Appearance: He is well appearing in no acute distress. He has somewhat of a flat affect.,Cardiovascular: He has a regular rhythm without murmurs, gallops, or rubs. There are no carotid bruits.,Chest: The lungs are clear to auscultation bilaterally.,Skin: There are no rashes or lesions.,Musculoskeletal: He has no joint deformities or scoliosis.,NEUROLOGICAL EXAMINATION:,Mental Status: His speech is fluent without dysarthria or aphasia. He is alert and oriented to name, place, and date. Attention, concentration, and fund of knowledge are intact. He has 3/3 object registration and 1/3 recall in 5 minutes.,Cranial Nerves: Pupils are equal, round, and reactive to light and accommodation. Visual fields are full. Optic discs are normal. Extraocular movements are intact without nystagmus. Facial sensation is normal. There is no facial, jaw, palate, or tongue weakness. Hearing is grossly intact. Shoulder shrug is full.,Motor: He has normal muscle bulk and tone. There is no atrophy. He has few fasciculations in his calf muscles bilaterally. Manual muscle testing reveals MRC grade 5/5 strength in all proximal and distal muscles of the upper and lower extremities. There is no action or percussion myotonia or paramyotonia.,Sensory: He has absent vibratory sensation at the left toe. This is diminished at the right toe. Joint position sense is intact. There is diminished sensation to light touch and temperature at the feet to the knees bilaterally. Pinprick is intact. Romberg is absent. There is no spinal sensory level.,Coordination: This is intact by finger-nose-finger or heel-to-shin testing. He does have a slight tremor of the head and outstretched arms.,Deep Tendon Reflexes: They are 2+ at the biceps, triceps, brachioradialis, patellas, and ankles. Plantar reflexes are flexor. There is no ankle clonus, finger flexors, or Hoffman's signs. He has crossed adductors bilaterally.,Gait and Stance: He has a slightly wide-based gait. He has some difficulty with toe walking, but he is able to walk on his heels and tandem walk. He has difficulty with toe raises on the left.,RADIOLOGIC DATA: , MRI of the cervical spine, 09/30/08: Chronic spondylosis at C5-C6 causing severe bilateral neuroforamining and borderline-to-mold cord compression with normal cord signal. Spondylosis of C6-C7 causing mild bilateral neuroforamining and left paracentral disc herniation causing borderline cord compression.,Thoracic MRI spine without contrast: Minor degenerative changes without stenosis.,I do not have the MRI of the lumbar spine available to review.,LABORATORY DATA: , 10/07/08: Vitamin B1 210 (87-280), vitamin B6 6, ESR 6, AST 25, ALT 17, vitamin B12 905, CPK 226 (0-200), T4 0.85, TSH 3.94, magnesium 1.7, RPR nonreactive, CRP 4, Lyme antibody negative, SPEP abnormal (serum protein electrophoresis), but no paraprotein by manifestation, hemoglobin A1c 6.0, aldolase 3.9 and homocystine 9.0.,ASSESSMENT: , The patient is a 63-year-old gentleman with multiple neurologic and nonneurologic symptoms including numbness, gait instability, decreased dexterity of his arms and general fatigue. His neurological examination is notable for sensory loss in a length-dependent fashion in his feet and legs with scant fasciculations in his calves. He has fairly normal or very mild increased reflexes including notably the presence of normal ankle jerks.,I think that the etiology of his symptoms is multifactorial. He probably does have a mild peripheral neuropathy, but the sparing of ankle jerks suggested either the neuropathy is mild or that there is a superimposed myelopathic process such as a cervical or lumbosacral myelopathy. He really is most concerned about the fatigue and I think it is possible due to suboptimally treated depression and suboptimally treated sleep apnea. Whether he has another underlying muscular disorder such as a primary myopathy remains to be seen.,RECOMMENDATIONS:,1. I scheduled him for repeat EMG and nerve conduction studies to evaluate for evidence of neuropathy or myopathy.,2. I will review his films at our spine conference tomorrow although I am confident in Dr. Z's opinion that there is no surgical indication.,3. I gave him a prescription for physical therapy to help with gait imbalance training as well as treatment for his neck pain.,4. I believe that he needs to undergo psychotherapy for his depression. It may also be worthwhile to adjust his medications, but I will defer to his primary care physician for managing this or for referring him to a therapist. The patient is very open about proceeding with this suggestion.,5. He does need to have his sleep apnea better controlled. He states that he is not compliant because the face mask that he uses does not fit him well. This should also be addressed. | null |
2,809 | Patient with stable expressive aphasia and decreased vision. | Neurology | Multiple Meningiomas | CC:, Stable expressive aphasia and decreased vision.,HX:, This 72y/o woman was diagnosed with a left sphenoid wing meningioma on 6/3/80. She was 59 years old at the time and presented with a 6 month history of increasing irritability and left occipital-nuchal headaches. One month prior to that presentation she developed leftward head turning, and 3 days prior to presentation had an episode of severe dysphasia. A HCT (done locally) revealed a homogenously enhancing lesion of the left sphenoid wing. Skull X-rays showed deviation of the pineal to the right. She was transferred to UIHC and was noted to have a normal neurologic exam (per Neurosurgery note). Angiography demonstrated a highly vascular left temporal/sphenoid wing tumor. She under went left temporal craniotomy and "complete resection" of the tumor which on pathologic analysis was consistent with a meningioma.,The left sphenoid wing meningioma recurred and was excised 9/25/84. There was regrowth of this tumor seen on HCT, 1985. A 6/88 HCT revealed the left sphenoid meningioma and a new left tentorial meningioma. HCT in 1989 revealed left temporal/sphenoid, left tentorial, and new left frontal lesions. On 2/14/91 she presented with increasing lethargy and difficulty concentrating. A 2/14/91, HCT revealed increased size and surrounding edema of the left frontal meningioma. The left frontal and temporal meningiomas were excised on 2/25/91. These tumors all recurred and a left parietal lesion developed. She underwent resection of the left frontal meningioma on 11/21/91 due to right sided weakness and expressive aphasia. The weakness partially resolved and though the speech improved following resection it did not return to normal. In May 1992 she experienced 3 tonic-clonic type seizures, all of which began with a Jacksonian march up the RLE then RUE before generalizing. Her Phenobarbital prophylaxis which she had been taking since her 1980 surgery was increased. On 12/7/92, she underwent a left fronto-temporo-parieto-occipital craniotomy and excision of five meningiomas. Postoperatively she developed worsened right sided weakness and expressive aphasia. The weakness and aphasia improved by 3/93, but never returned to normal. | neurology, sphenoid wing meningioma, sphenoid wing, expressive aphasia, meningiomas, aphasia, sphenoidNOTE,: Thesetranscribed medical transcription sample reports and examples are provided by various users andare for reference purpose only. MTHelpLine does not certify accuracy and quality of sample reports.These transcribed medical transcription sample reports may include some uncommon or unusual formats;this would be due to the preference of the dictating physician. All names and dates have beenchanged (or removed) to keep confidentiality. Any resemblance of any type of name or date orplace or anything else to real world is purely incidental. |
2,810 | Patient status post vehicular trauma. Low Back syndrome and Cervicalgia. | Neurology | Neck & Lower Back Pain - Consult | CHIEF COMPLAINT:, Neck and lower back pain.,VEHICULAR TRAUMA HISTORY:, Date of incident: 1/15/2001. The patient was the driver of a small sports utility vehicle and was wearing a seatbelt. The patient’s vehicle was proceeding through an intersection and was struck by another vehicle from the left side and forced off the road into a utility pole. The other vehicle had reportedly been driven by a drunk driver and ran a traffic signal. Estimated impact speed was 80 m.p.h. The driver of the other vehicle was reportedly cited by police. The patient was transiently unconscious and came to the scene. There was immediate onset of headaches, neck and lower back pain. The patient was able to exit the vehicle and was subsequently transported by Rescue Squad to St. Thomas Memorial Hospital, evaluated in the emergency room and released.,NECK AND LOWER BACK PAIN HISTORY:, The patient relates the persistence of pain since the motor vehicle accident. Symptoms began immediately following the MVA. Because of persistent symptoms, the patient subsequently sought chiropractic treatment. Neck pain is described as severe. Neck pain remains localized and is non-radiating. There are no associated paresthesias. Back pain originates in the lumbar region and radiates down both lower extremities. Back pain is characterized as worse than the neck pain. There are no associated paresthesias. | null |
2,811 | MRI T-spine and CXR - Aortic Dissection. | Neurology | MRI T-Spine | CC:, BLE weakness.,HX:, This 82y/o RHM was referred to the Neurology service by the Neurosurgery service for evaluation of acute onset paraplegia. He was in his usual state of health until 5:30PM on 4/6/95, when he developed sudden "pressure-like" epigastric discomfort associated with bilateral lower extremity weakness, SOB, lightheadedness and diaphoresis. He knelt down to the floor and "went to sleep." The Emergency Medical Service was alert and arrived within minutes, at which time he was easily aroused though unable to move or feel his lower extremities. No associated upper extremity or bulbar dysfunction was noted. He was taken to a local hospital where an INR was found to be 9.1. He was given vitamin K 15mg, and transferred to UIHC to rule out spinal epidural hemorrhage. An MRI scan of the T-spine was obtained and the preliminary reading was "normal." The Neurology service was then asked to evaluate the patient.,MEDS:, Coumadin 2mg qd, Digoxin 0.25mg qd, Prazosin 2mg qd.,PMH:, 1)HTN. 2)A-Fib on coumadin. 3)Peripheral vascular disease:s/p left Femoral-popliteal bypass (8/94) and graft thrombosis-thrombolisis (9/94). 4)Adenocarcinoma of the prostate: s/p TURP (1992).,FHX: ,unremarkable.,SHX:, Farmer, Married, no Tobacco/ETOH/illicit drug use.,EXAM:, BP165/60 HR86 RR18 34.2C SAO2 98% on room air.,MS: A&O to person, place, time. In no acute distress. Lucid.,CN: unremarkable.,MOTOR: 5/5 strength in BUE. Flaccid paraplegia in BLE,Sensory: T6 sensory level to LT/PP, bilaterally. Decreased vibratory sense in BLE in a stocking distribution, distally.,Coord: Intact FNF and RAM in BUE. Unable to do HKS.,Station: no pronator drift.,Gait: not done.,Reflexes: 2/2 BUE, Absent in BLE, plantar responses were flexor, bilaterally.,Rectal: decreased rectal tone.,GEN EXAM: No carotid bruitts. Lungs: bibasilar crackles. CV: Irregular rate and rhythm with soft diastolic murmur at the left sternal border. Abdomen: flat, soft, non-tender without bruitt or pulsatile mass. Distal pulses were strong in all extremities.,COURSE:, Hgb 12.6, Hct 40%, WBC 11.7, Plt 154k, INR 7.6, PTT 50, CK 41, the GS was normal. EKG showed A-Fib at 75BPM with competing junctional pacemaker, essentially unchanged from 9/12/94.,It was suspected that the patient sustained an anterior-cervico-thoracic spinal cord infarction with resultant paraplegia and T6 sensory level. A CXR was done in the ER prior to admission. This revealed cardiomegaly and a widened mediastinum. He returned from the x-ray suite and suddenly became unresponsive and went into cardiopulmonary arrest. Resuscitative measures failed. Pericardiocentesis was unremarkable. Autopsy revealed a massive aortic dissection extending from the aortic root to the origin of the iliac arteries with extensive pericardial hematoma. The dissection was seen in retrospect on the MRI T-spine. | neurology, mri, a&o, aortic dissection, cxr, irregular rate and rhythm, mri scan, neurology service, t-spine, carotid bruitts, epidural hemorrhage, mediastinum, paraplegia, person, place, stocking distribution, time, weakness, mri t spine, sensory level, spine, |
2,812 | MRI T-spine: Metastatic Adenocarcinoma of the T3-T4 vertebrae and invading the spinal canal. | Neurology | MRI T-Spine - Spinal Mets | CC: ,BLE weakness and numbness.,HX:, This 59 y/o RHM was seen and released from an ER 1 week prior to this presentation for a 3 week history of progressive sensory and motor deficits in both lower extremities. He reported numbness beginning about his trunk and slowly progressing to involve his lower extremities over a 4 week period. On presentation, he felt numb from the nipple line down. In addition, he began experiencing progressive weakness in his lower extremities for the past week. He started using a cane 5 days before being seen and had been having difficulty walking and traversing stairs. He claimed he could not stand. He denied loss of bowel or bladder control. However, he had not had a bowel movement in 3 days and he had not urinated 24 hours. His lower extremities had been feeling cold for a day. He denied any associated back or neck pain. He has chronic shortness of breath, but felt it had become worse. He had also been experiencing lightheadedness upon standing more readily than usual for 2 days prior to presentation.,PMH:, 1)CAD with chronic CP, 2)NQWMI 1994, S/P Coronary Angioplasty, 3)COPD (previous FEV 11.48, and FVC 2.13), 4)Anxiety D/O, 5)DJD, 6)Developed confusion with metoprolol use, 7)HTN.,MEDS:, Benadryl, ECASA, Diltiazem, Isordil, Enalapril, Indomethacin, Terbutaline MDI, Ipratropium MDI, Folic Acid, Thiamine.,SHX:, 120pk-yr smoking, ETOH abuse in past, Retired Dock Hand,FHX: ,unremarkable except for ETOH abuse,EXAM:, T98.2 96bpm 140/74mmHg R18,Thin cachetic male in moderate distress.,MS: A&O to person, place and time. Speech was fluent and without dysarthria. Comprehension, naming and reading were intact.,CN: unremarkable.,Motor: Full strength in both upper extremities.,HF HE HAdd HAbd KF KE AF AE,RLE 3 3 4 4 3 4 1 1,LLE 4 4 4+ 4+ 4+ 4 4 4,There was mild spastic muscle tone in the lower extremities. There was normal muscle bulk throughout.,SENSORY: Decreased PP in the LLE from the foot to nipple line, and in the RLE from the knee to nipple line. Decreased Temperature sensation from the feet to the umbilicus, bilaterally. No loss of Vibration or Proprioception. Decreased light touch from the feet to nipple line, bilaterally.,Gait: unable to walk. Stands with support only.,Station: no pronator drift or truncal ataxia.,Reflexes: 2+/2+ in BUE, 3+/3+ patellae, 0/1 ankles. Babinski signs were present, bilaterally. The abdominal reflexes were absent.,CV: RRR with a 2/6 systolic ejection murmur at the left sternal border. Lungs: CTA with mildly labored breathing. Abdomen: NT, ND, NBS, but bladder distended. Extremities were cool to touch. Peripheral pulses were intact and capillary refill was brisk. Rectal: decreased rectal tone and absent anal reflex. Right prostate nodule at the inferior pole.,COURSE: ,Admission Labs: FEV1=1.17, FVC 2.19, ABG 7.39/42/79 on room air. WBC 10/5, Hgb 13, Hct 39, Electrolytes were normal. PT & PTT were normal. Straight catheterization revealed a residual volume of 400cc of urine.,He underwent emergent T-spine MRI. This revealed a T3-4 vertebral body lesion which had invaded the spinal canal was compressing the spinal cord. He was treated with Decadron and underwent emergent spinal cord decompression on 5/7/95. He recovered some lower extremity strength following surgery. Pathological analysis of the tumor was consistent with adenocarcinoma. His primary tumor was not located despite chest-abdominal-pelvic CT scans, and a GI and GU workup which included cystoscopy and endoscopy. He received 3000cGy of XRT and died 5 months after presentation. | null |
2,813 | MRI T-L spine - L2 conus medullaris lesion and syndrome secondary to Schistosomiasis. | Neurology | MRI T-L Spine - Schistosomiasis | CC: ,Paraplegia.,HX:, This 32 y/o RHF had been performing missionary work in Jos, Nigeria for several years and delivered her 4th child by vaginal delivery on 4/10/97. The delivery was induced with Pitocin, but was otherwise uncomplicated. For the first 4 days post-partum she noted clear liquid diarrhea without blood and minor abdominal discomfort. This spontaneous resolved without medical treatment. The second week post-partum she had 4-5 days of sinusitis, purulent nasal discharge and facial pain. She was otherwise well until 5/4/97 when stationed in a more rural area of Nigeria, she noted a dull ache in both knees (lateral to the patellae) and proximal tibia, bilaterally. The pain was not relieved by massage and seemed more bothersome when seated or supine. She had no sensory loss at the time.,On 5/6/97, she awakened to pain radiating down her knees to her anterior tibia. Over the next few hours the pain radiated circumferentially around both calves, and involved the soles of her feet and posterior BLE to her buttocks. Rising from bed became a laborious task and she required assistance to walk to the bathroom. Ibuprofen provided minimal analgesia. By evening the sole of one foot was numb.,She awoke the next morning, 5/9/97, with "pins & needles" sensation in BLE up to her buttocks. She was given Darvocet for analgesia and took an airplane back to the larger city she was based in. During the one hour flight her BLE weakness progressed to a non-weight bearing state (i.e. she could not stand). Local evaluation revealed 3/3 proximal and 4/4 distal BLE weakness. She had a sensory level to her waist on PP and LT testing. She also had mild lumbar back pain. Local laboratory evaluation: WBC 12.7, ESR 10. She was presumed to have Guillain-Barre syndrome and was placed on Solu-Cortef 1000mg qd and Sandimmune IV IgG 12.0 g.,On 5/10/97, she was airlifted to Geneva, Switzerland. Upon arrival there she had total anesthesia from the feet up to the inguinal region, bilaterally. There was flaccid areflexic paralysis of BLE and she was unable to void or defecate. Straight catheterization of the bladder revealed a residual volume of 1000cc. On 5/12/ CSF analysis revealed: Protein 1.5g/l, Glucose 2.2mmol/l, WBC 92 (O PMNS, 100% Lymphocytes), RBC 70, Clear CSF, bacterial-fungal-AFB-cultures were negative. Broad spectrum antibiotics and Solu-Medrol 1g IV qd were started. MRI T-L-spine, 5/12/97 revealed an intradural T12-L1 lesion that enhanced minimally with gadolinium and was associated with spinal cord edema in the affected area. MRI Brain, 5/12/97, was unremarkable and showed no evidence of demyelinating disease. HIV, HTLV-1, HSV, Lyme, EBV, Malaria and CMV serological titers were negative. On 5/15/97 the Schistosomiasis Mekongi IFAT serological titer returned positive at 1:320 (normal<1:80). 5/12/97 CSF Schistosomiasis Mekongi IFAT and ELISA were negative. She was then given a one day course of Praziquantel 3.6g total in 3 doses; and started on Prednisone 60 mg po qd; the broad spectrum antibiotics and Solu-Medrol were discontinued.,On 5/22/97, a rectal biopsy was performed to evaluate parasite eradication. The result came back positive for ova and granulomata after she had left for UIHC. The organism was not speciated. 5/22/97 CSF schistosomiasis ELISA and IFAT titers were positive at 1.09 and 1:160, respectively. These titers were not known when she initially arrived at UIHC.,Following administration of Praziquantel, she regained some sensation in BLE but the paraplegia, and urinary retention remained.,MEDS:, On 5/24/97 UIHC arrival: Prednisone 60mg qd, Zantac 50 IV qd, Propulsid 20mg tid, Enoxaparin 20mg qd.,PMH:, 1)G4P4.,FHX:, unremarkable.,SHX: ,Missionary. Married. 4 children ( ages 7,5,3,6 weeks).,EXAM:, BP110/70, HR72, RR16, 35.6C,MS: A&O to person, place and time. Speech fluent and without dysarthria. Lucid thought process.,CN: unremarkable.,Motor: 5/5 BUE strength. Lower extremities: 1/1 quads and hamstrings, 0/0 distally.,Sensory: Decreased PP/LT/VIB from feet to inguinal regions, bilaterally. T12 sensory level to temperature (ice glove).,Coord: normal FNF.,Station/Gait: not done.,Reflexes: 2/2 BUE. 0/0 BLE. No plantar responses, bilaterally.,Rectal: decreased to no rectal tone. Guaiac negative.,Other: No Lhermitte's sign. No paraspinal hypertonicity noted. No vertebral tenderness.,Gen exam: Unremarkable.,COURSE:, MRI T-L-spine, 5/24/97, revealed a 6 x 8 x 25 soft tissue mass at the L1 level posterior to the tip of the conus medullaris and extending into the canal below that level. This appeared to be intradural. There was mild enhancement. There was more enhancement along the distal cord surface and cauda equina. The distal cord had sign of diffuse edema. She underwent exploratory and decompressive laminectomy on 5/27/97, and was retreated with a one day course of Praziquantel 40mg/kg/day. Praziquantel is reportedly only 80% effective at parasite eradication.,She continued to reside on the Neurology/Neurosurgical service on 5/31/97 and remained paraplegic. | null |
2,814 | The thoracic spine was examined in the AP, lateral and swimmer's projections. | Neurology | MRI T-Spine - 1 | EXAM: ,Thoracic Spine.,REASON FOR EXAM: , Injury.,INTERPRETATION: , The thoracic spine was examined in the AP, lateral and swimmer's projections. There is mild chronic-appearing anterior wedging of what is believed to represent T11 and 12 vertebral bodies. A mild amount of anterior osteophytic lipping is seen involving the thoracic spine. There is a suggestion of generalized osteoporosis. The intervertebral disc spaces appear generally well preserved.,The pedicles appear intact.,IMPRESSION:,1. Mild chronic-appearing anterior wedging of what is believed to represent the T11 and 12 vertebral bodies.,2. Mild degenerative changes of the thoracic spine.,3. Osteoporosis. | neurology, thoracic spine, swimmer's projections, osteoporosis, osteophytic lipping, anterior wedging, vertebral bodies, thoracic, spine, |
2,815 | MRI of lumbar spine without contrast to evaluate chronic back pain. | Neurology | MRI of Lumbar Spine w/o Contrast | EXAM: , MRI of lumbar spine without contrast.,HISTORY:, A 24-year-old female with chronic back pain.,TECHNIQUE: , Noncontrast axial and sagittal images were acquired through the lumbar spine in varying degrees of fat and water weighting.,FINDINGS: , The visualized cord is normal in signal intensity and morphology with conus terminating in proper position. Visualized osseous structures are normal in marrow signal intensity and morphology without evidence for fracture/contusion, compression deformity, or marrow replacement process. There are no paraspinal masses.,Disc heights, signal, and vertebral body heights are maintained throughout the lumbar spine.,L5-S1: Central canal, neural foramina are patent.,L4-L5: Central canal, neural foramina are patent.,L3-L4: Central canal, neural foramen is patent.,L2-L3: Central canal, neural foramina are patent.,L1-L2: Central canal, neural foramina are patent.,The visualized abdominal aorta is normal in caliber. Incidental note has been made of multiple left-sided ovarian, probable physiologic follicular cysts.,IMPRESSION: , No acute disease in the lumbar spine. | neurology, mri, central canal, noncontrast, abdominal aorta, axial, back pain, contrast, follicular cysts, images, lumbar spine, morphology, neural foramina, sagittal, signal intensity, without contrast, mri of lumbar spine, mri of lumbar, lumbar, foramina, neural, patent, spine |
2,816 | MRI of the Cervical, Thoracic, and Lumbar Spine | Neurology | MRI Spine | INTERPRETATION: , MRI of the cervical spine without contrast showed normal vertebral body height and alignment with normal cervical cord signal. At C4-C5, there were minimal uncovertebral osteophytes with mild associated right foraminal compromise. At C5-C6, there were minimal diffuse disc bulge and uncovertebral osteophytes with indentation of the anterior thecal sac, but no cord deformity or foraminal compromise. At C6-C7, there was a central disc herniation resulting in mild deformity of the anterior aspect of the cord with patent neuroforamina. MRI of the thoracic spine showed normal vertebral body height and alignment. There was evidence of disc generation, especially anteriorly at the T5-T6 level. There was no significant central canal or foraminal compromise. Thoracic cord normal in signal morphology. MRI of the lumbar spine showed normal vertebral body height and alignment. There is disc desiccation at L4-L5 and L5-S1 with no significant central canal or foraminal stenosis at L1-L2, L2-L3, and L3-L4. There was a right paracentral disc protrusion at L4-L5 narrowing of the right lateral recess. The transversing nerve root on the right was impinged at that level. The right foramen was mildly compromised. There was also a central disc protrusion seen at the L5-S1 level resulting in indentation of the anterior thecal sac and minimal bilateral foraminal compromise.,IMPRESSION: , Overall impression was mild degenerative changes present in the cervical, thoracic, and lumbar spine without high-grade central canal or foraminal narrowing. There was narrowing of the right lateral recess at L4-L5 level and associated impingement of the transversing nerve root at that level by a disc protrusion. This was also seen on a prior study., | neurology, cervical spine, mri, cervical, thoracic, lumbar, transversing nerve root, vertebral body height, vertebral body, disc protrusion, foraminal compromise, central, foraminal, disc, spineNOTE,: Thesetranscribed medical transcription sample reports and examples are provided by various users andare for reference purpose only. MTHelpLine does not certify accuracy and quality of sample reports.These transcribed medical transcription sample reports may include some uncommon or unusual formats;this would be due to the preference of the dictating physician. All names and dates have beenchanged (or removed) to keep confidentiality. Any resemblance of any type of name or date orplace or anything else to real world is purely incidental. |
2,817 | MRI L-spine - History of progressive lower extremity weakness, right frontal glioblastoma with lumbar subarachnoid seeding. | Neurology | MRI L-Spine - Subarachnoid Seeding | CC:, Progressive lower extremity weakness.,HX: ,This 52y/o RHF had a h/o right frontal glioblastoma multiforme (GBM) diagnosed by brain biopsy/partial resection, on 1/15/1991. She had been healthy until 1/6/91, when she experienced a generalized tonic-clonic type seizure during the night. She subsequently underwent an MRI brain scan and was found to have a right frontal enhancing lesion in the mesial aspect of the right frontal lobe at approximately the level of the coronal suture. There was minimal associated edema and no mass effect. Following extirpation of the tumor mass, she underwent radioactive Iodine implantation and 6020cGy radiation therapy in 35 fractions. In 11/91 she received BCNU and Procarbazine chemotherapy protocols. This was followed by four courses of 5FU/Carboplatin (3/92, 6/92, 9/92 ,10/92) chemotherapy.,On 10/12/92 she presented for her 4th course of 5FU/Carboplatin and complained of non-radiating dull low back pain, and proximal lower extremity weakness, but was still able to ambulate. She denied any bowel/bladder difficulty.,PMH: ,s/p oral surgery for wisdom tooth extraction.,FHX/SHX: ,1-2 ppd cigarettes. rare ETOH use. Father died of renal CA.,MEDS: ,Decadron 12mg/day.,EXAM: ,Vitals unremarkable.,MS: Unremarkable.,Motor: 5/5 BUE, LE: 4+/5- prox, 5/5 distal to hips. Normal tone and muscle bulk.,Sensory: No deficits appreciated.,Coord: Unremarkable.,Station: No mention in record of being tested.,Gait: Mild difficulty climbing stairs.,Reflexes: 1+/1+ throughout and symmetric. Plantar responses were down-going bilaterally.,INITIAL IMPRESSION:, Steroid myopathy. Though there was enough of a suspicion of "drop" metastasis that an MRI of the L-spine was obtained.,COURSE:, The MRI L-spine revealed fine linear enhancement along the dorsal aspect of the conus medullaris, suggestive of subarachnoid seeding of tumor. No focal mass or cord compression was visualized. CSF examination revealed: 19RBC, 22WBC, 17 Lymphocytes, and 5 histiocytes, Glucose 56, Protein 150. Cytology (negative). The patient was discharged home on 10/17/92, but experienced worsening back pain and lower extremity weakness and became predominantly wheelchair bound within 4 months. She was last seen on 3/3/93 and showed signs of worsening weakness (left hemiplegia: R > L) as her tumor grew and spread. She then entered a hospice. | neurology, glioblastoma multiforme, gbm, steroid myopathy, hemiplegia, progressive lower extremity weakness, mri l spine, lower extremity weakness, frontal glioblastoma, subarachnoid seeding, lower extremity, glioblastoma, subarachnoid, spine, mri, lower, weakness, |
2,818 | MRI Spine - T12-L5 epidural lipoma and thoracic spinal cord infarction vs. transverse myelitis. | Neurology | MRI Spine - Epidural Lipoma | CC:, Progressive lower extremity weakness.,HX: ,This 54 y/o RHF presented on 7/3/93 with a 2 month history of lower extremity weakness. She was admitted to a local hospital on 5/3/93 for a 3 day h/o of progressive BLE weakness associated with incontinence and BLE numbness. There was little symptom of upper extremity weakness at that time, according to the patient. Her evaluation was notable for a bilateral L1 sensory level and 4/4 strength in BLE. A T-L-S Spine MRI revealed a T4-6 lipomatosis with anterior displacement of the cord without cord compression. CSF analysis yielded: opening pressure of 14cm H20, protein 88, glucose 78, 3 lymphocytes and 160 RBC, no oligoclonal bands or elevated IgG index, and negative cytology. Bone marrow biopsy was negative. B12, Folate, and Ferritin levels were normal. CRP 5.2 (elevated). ANA was positive at 1:5,120 in speckled pattern. Her hospital course was complicated by deep venous thrombosis, which recurred after heparin was stopped to do the bone marrow biopsy. She was subsequently placed on Coumadin. EMG/NCV testing revealed " lumbosacral polyradiculopathy with axonal degeneration and nerve conduction block." She was diagnosed with atypical Guillain-Barre vs. polyradiculopathy and received a single course of Decadron; and no plasmapheresis or IV IgG. She was discharged home o 6/8/93.,She subsequently did not improve and after awaking from a nap on her couch the day of presentation, 7/3/93, she found she was paralyzed from the waist down. There was associated mild upper lumbar back pain without radiation. She had had no bowel movement or urination since that time. She had no recent trauma, fever, chills, changes in vision, dysphagia or upper extremity deficit.,MEDS:, Coumadin 7.5mg qd, Zoloft 50mg qd, Lithium 300mg bid.,PMH:, 1) Bi-polar Affective Disorder, dx 1979 2) C-section.,FHX:, Unremarkable.,SHX:, Denied Tobacco/ETOH/illicit drug use.,EXAM: ,BP118/64, HR103, RR18, Afebrile.,MS: ,A&O to person, place, time. Speech fluent without dysarthria. Lucid thought processes.,CN: ,Unremarkable.,MOTOR:, 5/5 strength in BUE. Plegic in BLE. Flaccid muscle tone.,SENSORY:, L1 sensory level (bilaterally) to PP and TEMP, without sacral sparing. Proprioception was lost in both feet.,CORD: ,Normal in BUE.,Reflexes were 2+/2+ in BUE. They were not elicited in BLE. Plantar responses were equivocal, bilaterally.,RECTAL: ,Poor rectal tone. stool guaiac negative. She had no perirectal sensation.,COURSE:, CRP 8.8 and ESR 76. FVC 2.17L. WBC 1.5 (150 bands, 555 neutrophils, 440 lymphocytes and 330 monocytes), Hct 33%, Hgb 11.0, Plt 220K, MCV 88, GS normal except for slightly low total protein (8.0). LFT were normal. Creatinine 1.0. PT and PTT were normal. ABCG 7.46/25/79/96% O2Sat. UA notable for 1+ proteinuria. EKG normal.,MRI L-spine, 7/3/93, revealed an area of abnormally increased T2 signal extending from T12 through L5. This area causes anterior displacement of the spinal cord and nerve roots. The cauda equina are pushed up against the posterior L1 vertebral body. There bilaterally pulmonary effusions. There is also abnormally increased T2 signal in the center of the spinal cord extending from the mid thoracic level through the conus. In addition, the Fila Terminale appear thickened. There is increased signal in the T3 vertebral body suggestion a hemangioma. The findings were felt consistent with a large epidural lipoma displacing the spinal cord anteriorly. there also appeared spinal cord swelling and increased signal within the spinal cord which suggests an intramedullary process.,CSF analysis revealed: protein 1,342, glucose 43, RBC 4,900, WBC 9. C3 and C$ complement levels were 94 and 18 respectively (normal) Anticardiolipin antibodies were negative. Serum Beta-2 microglobulin was elevated at 2.4 and 3.7 in the CSF and Serum, respectively. It was felt the patient had either a transverse myelitis associated with SLE vs. partial cord infarction related to lupus vasculopathy or hypercoagulable state. She was place on IV Decadron. Rheumatology felt that a diagnosis of SLE was likely. Pulmonary effusion analysis was consistent with an exudate. She was treated with plasma exchange and place on Cytoxan.,On 7/22/93 she developed fever with associated proptosis and sudden loss of vision, OD. MRI Brain, 7/22/93, revealed a 5mm thick area of intermediate signal adjacent to the posterior aspect of the right globe, possibly representing hematoma. Ophthalmology felt she had a central retinal vein occlusion; and it was surgically decompressed.,She was placed on prednisone on 8/11/93 and Cytoxan was started on 8/16/93. She developed a headache with meningismus on 8/20/93. CSF analysis revealed: protein 1,002, glucose2, WBC 8,925 (majority were neutrophils). Sinus CT scan negative. She was placed on IV Antibiotics for presumed bacterial meningitis. Cultures were subsequently negative. She spontaneously recovered. 8/25/93, cisternal tap CSF analysis revealed: protein 126, glucose 35, WBC 144 (neutrophils), RBC 95, Cultures negative, cytology negative. MRI Brain scan revealed diffuse leptomeningeal enhancement in both brain and spinal canal.,DSDNA negative. She developed leukopenia in 9/93, and she was switched from Cytoxan to Imuran. Her LFT's rose and the Imuran was stopped and she was placed back on prednisone.,She went on to have numerous deep venous thrombosis while on Coumadin. This required numerous hospital admissions for heparinization. Anticardiolipin antibodies and Protein C and S testing was negative. | null |
2,819 | MRI L-S-Spine for Cauda Equina Syndrome secondary to L3-4 disc herniation - Low Back Pain (LBP) with associated BLE weakness. | Neurology | MRI L-S Spine - Cauda Equina Syndrome | CC: ,Low Back Pain (LBP) with associated BLE weakness.,HX:, This 75y/o RHM presented with a 10 day h/o progressively worsening LBP. The LBP started on 12/3/95; began radiating down the RLE, on 12/6/95; then down the LLE, on 12/9/95. By 12/10/95, he found it difficult to walk. On 12/11/95, he drove himself to his local physician, but no diagnosis was rendered. He was given some NSAID and drove home. By the time he got home he had great difficulty walking due to LBP and weakness in BLE, but managed to feed his pets and himself. On 12/12/95 he went to see a local orthopedist, but on the way to his car he crumpled to the ground due to BLE weakness and LBP pain. He also had had BLE numbness since 12/11/95. He was evaluated locally and an L-S-Spine CT scan and L-S Spine X-rays were "negative." He was then referred to UIHC.,MEDS: ,SLNTC, Coumadin 4mg qd, Propranolol, Procardia XL, Altace, Zaroxolyn.,PMH: ,1) MI 11/9/78, 2) Cholecystectomy, 3) TURP for BPH 1980's, 4) HTN, 5) Amaurosis Fugax, OD, 8/95 (Mayo Clinic evaluation--TEE (-), but Carotid Doppler (+) but "non-surgical" so placed on Coumadin).,FHX:, Father died age 59 of valvular heart disease. Mother died of DM. Brother had CABG 8/95.,SHX:, retired school teacher. 0.5-1.0 pack cigarettes per day for 60 years.,EXAM:, BP130.56, HR68, RR16, Afebrile.,MS: A&O to person, place, time. Speech fluent without dysarthria. Lucid. Appeared uncomfortable.,CN: Unremarkable.,MOTOR: 5/5 strength in BUE. Lower extremity strength: Hip flexors & extensors 4-/4-, Hip abductors 3+/3+, Hip adductors 5/5, Knee flexors & extensors 4/4-, Ankle flexion 4-/4-, Tibialis Anterior 2/2-, Peronei 3-/3-. Mild atrophy in 4 extremities. Questionable fasciculations in BLE. Spasms illicited on striking quadriceps with reflex hammer (? percussion myotonia). No rigidity and essential normal muscle tone on passive motion.,SENSORY: Decreased vibratory sense in stocking distribution from toes to knees in BLE (worse on right). No sensory level. PP/LT/TEMP testing unremarkable.,COORD: Normal FNF-RAM. Slowed HKS due to weakness.,Station: No pronator drift. Romberg testing not done.,Gait: Unable to stand.,Reflexes: 2/2 BUE. 1/trace patellae, 0/0 Achilles. Plantar responses were flexor, bilaterally. Abdominal reflex was present in all four quadrants. Anal reflex was illicited from all four quadrants. No jaw jerk or palmomental reflexes illicited.,Rectal: normal rectal tone, guaiac negative stool.,GEN EXAM: Bilateral Carotid Bruits, No lymphadenopathy, right inguinal hernia, rhonchi and inspiratory wheeze in both lung fields.,COURSE: ,WBC 11.6, Hgb 13.4, Hct 38%, Plt 295. ESR 40 (normal 0-14), CRP 1.4 (normal <0.4), INR 1.5, PTT 35 (normal), Creatinine 2.1, CK 346. EKG normal. The differential diagnosis included Amyotrophy, Polymyositis, Epidural hematoma, Disc Herniation and Guillain-Barre syndrome. An MRI of the lumbar spine was obtained, 12/13/95. This revealed an L3-4 disc herniation extending inferiorly and behind the L4 vertebral body. This disc was located more on the right than on the left , compromised the right neural foramen, and narrowed the spinal canal. The patient underwent a L3-4 laminectomy and diskectomy and subsequently improved. He was never seen in follow-up at UIHC. | neurology, ble weakness, carotid doppler, disc herniation, guillain-barre syndrome, amyotrophy, polymyositis, epidural hematoma, mri l s spine, cauda equina syndrome, flexors & extensors, cauda equina, herniation, cauda, equina, extensors, reflexes, mri, hip, flexors, weakness, |
2,820 | MRI of the brain without contrast to evaluate daily headaches for 6 months in a 57-year-old. | Neurology | MRI of Brain w/o Contrast. | EXAM: , MRI of the brain without contrast.,HISTORY: , Daily headaches for 6 months in a 57-year-old.,TECHNIQUE: ,Noncontrast axial and sagittal images were acquired through the brain in varying degrees of fat and water weighting.,FINDINGS: , The brain is normal in signal intensity and morphology for age. There are no extraaxial fluid collections. There is no hydrocephalus/midline shift. Posterior fossa, 7th and 8th nerve complexes and intraorbital contents are within normal limits. The normal vascular flow volumes are maintained. The paranasal sinuses are clear.,Diffusion images demonstrate no area of abnormally restricted diffusion that suggests acute infarct.,IMPRESSION: , Normal MRI brain. Specifically, no findings to explain the patient's headaches are identified. | neurology, mri, diffusion, posterior fossa, axial, brain, contrast, extraaxial, flow, fluid collections, headaches, hydrocephalus, intraorbital, morphology, paranasal, sagittal, sinuses, vascular, weighting, without contrast, mri of the brain, noncontrast, |
2,821 | MRI Head W&WO Contrast. | Neurology | MRI Head | EXAM:, MRI Head W&WO Contrast.,REASON FOR EXAM:, Dyspnea.,COMPARISON:, None. ,TECHNIQUE:, MRI of the head performed without and with 12 ml of IV gadolinium (Magnevist). ,INTERPRETATION: , There are no abnormal/unexpected foci of contrast enhancement. There are no diffusion weighted signal abnormalities. There are minimal, predominantly periventricular, deep white matter patchy foci of FLAIR/T2 signal hyperintensity, the rest of the brain parenchyma appearing unremarkable in signal. The ventricles and sulci are prominent, but proportionate. Per T2 weighted sequence, there is no hyperdense vascularity. There are no calvarial signal abnormalities. There is no significant mastoid air cell fluid. No significant sinus mucosal disease per MRI.,IMPRESSION:,1. No abnormal/unexpected foci of contrast enhancement; specifically, no evidence for metastases or masses. ,2. No evidence for acute infarction. ,3. Mild, scattered, patchy, chronic small vessel ischemic disease changes. ,4. Diffuse cortical volume loss, consistent with patient's age. ,5. Preliminary report was issued at the time of dictation. , | neurology, dyspnea, mri of the head, foci of contrast, patchy foci, white matter, w&wo contrast, mri head, mri |
2,822 | MRI head without contrast. | Neurology | MRI Head - 1 | EXAM:, MRI head without contrast.,REASON FOR EXAM: , Severe headaches.,INTERPRETATION:, Imaging was performed in the axial and sagittal planes using numerous pulse sequences at 1 tesla. Correlation is made with the head CT of 4/18/05.,On the diffusion sequence, there is no significant bright signal to indicate acute infarction. There is a large degree of increased signal involving the periventricular white matter extending around to the subcortical regions in symmetrical fashion consistent with chronic microvascular ischemic disease. There is mild chronic ischemic change involving the pons bilaterally, slightly greater on the right, and when correlating with the recent scan, there is an old tiny lacunar infarct of the right brachium pontis measuring roughly 4 mm in size. There are prominent perivascular spaces of the lenticulostriate distribution compatible with the overall degree of moderate to moderately advanced atrophy. There is an old moderate-sized infarct of the mid and lateral aspects of the right cerebellar hemisphere as seen on the recent CT scan. This involves mostly the superior portion of the hemisphere in the superior cerebellar artery distribution. No abnormal mass effect is identified. There are no findings to suggest active hydrocephalus. No abnormal extra-axial collection is identified. There is normal flow void demonstrated in the major vascular systems.,The sagittal sequence demonstrates no Chiari malformation. The region of the pituitary/optic chiasm grossly appears normal. The mastoids and paranasal sinuses are clear.,IMPRESSION:,1. No definite acute findings identified involving the brain.,2. There is prominent chronic cerebral ischemic change as described with mild chronic pontine ischemic changes. There is an old moderate-sized infarct of the superior portion of the right cerebellar hemisphere.,3. Moderate to moderately advanced atrophy. | neurology, severe headaches, chiari malformation, cerebral ischemic change, mri head without contrast, cerebellar hemisphere, superior portion, mri head, cerebellar, infarction, ischemic |
2,823 | MRI C-spine: C4-5 Transverse Myelitis. | Neurology | MRI C-spine | CC:, Left hemibody numbness.,HX:, This 44y/o RHF awoke on 7/29/93 with left hemibody numbness without tingling, weakness, ataxia, visual or mental status change. She had no progression of her symptoms until 7/7/93 when she notices her right hand was stiff and clumsy. She coincidentally began listing to the right when walking. She denied any recent colds/flu-like illness or history of multiple sclerosis. She denied symptoms of Lhermitte's or Uhthoff's phenomena.,MEDS:, none.,PMH:, 1)Bronchitis twice in past year (last 2 months ago).,FHX:, Father with HTN and h/o strokes at ages 45 and 80; now 82 years old. Mother has DM and is age 80.,SHX:, Denies Tobacco/ETOH/illicit drug use.,EXAM:, BP112/76 HR52 RR16 36.8C,MS: unremarkable.,CN: unremarkable.,Motor: 5/5 strength throughout except for slowing of right hand fine motor movement. There was mildly increased muscle tone in the RUE and RLE.,Sensory: decreased PP below T2 level on left and some dysesthesias below L1 on the left.,Coord: positive rebound in RUE.,Station/Gait: unremarkable.,Reflexes: 3+/3 throughout all four extremities. Plantar responses were flexor, bilaterally.,Rectal exam not done.,Gen exam reportedly "normal.",COURSE:, GS, CBC, PT, PTT, ESR, Serum SSA/SSB/dsDNA, B12 were all normal. MRI C-spine, 7/145/93, showed an area of decreased T1 and increased T2 signal at the C4-6 levels within the right lateral spinal cord. The lesion appeared intramedullary and eccentric, and peripherally enhanced with gadolinium. Lumbar puncture, 7/16/93, revealed the following CSF analysis results: RBC 0, WBC 1 (lymphocyte), Protein 28mg/dl, Glucose 62mg/dl, CSF Albumin 16 (normal 14-20), Serum Albumin 4520 (normal 3150-4500), CSF IgG 4.1mg/dl (normal 0-6.2), CSF IgG, % total CSF protein 15% (normal 1-14%), CSF IgG index 1.1 (normal 0-0.7), Oligoclonal bands were present. She was discharged home.,The patient claimed her symptoms resolved within one month. She did not return for a scheduled follow-up MRI C-spine. | neurology, mri c-spine, c-spine, lhermitte's, myelitis, transverse myelitis, uhthoff's, ataxia, clumsy, hemibody numbness, mental status, numbness, tingling, weakness, mri c spine, hemibody, mri, spine, csf, |
2,824 | MRI Brain: Subacute right thalamic infarct. | Neurology | MRI Brain: Thalamic Infarct | CC:, Left hemiplegia.,HX: , A 58 y/o RHF awoke at 1:00AM on 10/23/92 with left hemiplegia and dysarthria which cleared within 15 minutes. She was seen at a local ER and neurological exam and CT Brain were reportedly unremarkable. She was admitted locally. She then had two more similar spells at 3AM and 11AM with resolution of the symptoms within an hour. She was placed on IV Heparin following the 3rd episode and was transferred to UIHC. She had not been taking ASA.,PMH:, 1)HTN. 2) Psoriasis.,SHX:, denied ETOH/Tobacco/illicit drug use.,FHX:, Unknown.,MEDS:, Heparin only.,EXAM:, BP160/90 HR145 (supine). BP105/35 HR128 (light headed, standing) RR12 T37.7C,MS: Dysarthria only. Lucid thought process.,CN: left lower facial weakness only.,Motor: mild left hemiparesis with normal muscle bulk. Mildly increased left sided muscle tone.,Sensory: unremarkable.,Coordination: impaired secondary to weakness on left. Otherwise unremarkable.,Station: left pronator drift. Romberg testing not done.,Gait: not tested.,Reflexes: symmetric; 2+ throughout.,Gen Exam: CV: Tachycardic without murmur.,COURSE:, The patients signs and symptoms worsening during and after standing to check orthostatic blood pressures. She was immediately placed in a reverse Trendelenburg position and given IV fluids. Repeat neurologic exam at 5PM on the day of presentation revealed a return to the initial presentation of signs and symptoms. PT/PTT/GS/CBC/ABG were unremarkable. EKG revealed sinus tachycardia with rate dependent junctional changes. CXR unremarkable. MRI Brain was obtained and showed an evolving right thalamic/lentiform nucleus infarction best illustrated by increased signal on the Proton density weighted images. Over the ensuing days of admission she had significant fluctuations of her BP (200mmHG to 140mmHG systolic). Her symptoms worsened with falls in BP. Her BP was initially controlled with esmolol or labetalol. Renal Ultrasound, abdominal/pelvic CT, renal function scan, serum and urine osmolality, urine catecholamines/metanephrine studies were unremarkable. Carotid doppler study revealed 0-15%BICA stenosis and antegrade vertebral artery flow, bilaterally. Transthoracic echocardiogram was unremarkable. Cerebral angiogram was performed to r/o vasculitis. This revealed narrowing of the M1 segment of the right MCA. This was thought secondary to atherosclerosis and not vasculitis. She was discharged on ASA, Procardia XL, and Labetalol. | neurology, mri brain, ct brain, heparin, dysarthria, hemiplegia, infarct, neurological exam, thalamic, thalamic infarct, mri, brain, |
2,825 | MRI C-spine to evaluate right shoulder pain - C5-6 disk herniation. | Neurology | MRI C-Spine - C5-6 Disk Herniation | CC:, Right shoulder pain.,HX: ,This 46 y/o RHF presented with a 4 month history of right neck and shoulder stiffness and pain. The symptoms progressively worsened over the 4 month course. 2 weeks prior to presentation she began to develop numbness in the first and second fingers of her right hand and RUE pain. The later was described as a throbbing pain. She also experienced numbness in both lower extremities and pain in the coccygeal region. The pains worsened at night and impaired sleep. She denied any visual change, bowel or bladder difficulties and symptoms involving the LUE. She occasionally experienced an electric shock like sensation shooting down her spine when flexing her neck (Lhermitte's phenomena). She denied any history of neck/back/head trauma.,She had been taking Naprosyn with little relief.,PMH: ,1) Catamenial Headaches. 2) Allergy to Macrodantin.,SHX/FHX:, Smokes 2ppd cigarettes.,EXAM: ,Vital signs were unremarkable.,CN: unremarkable.,Motor: full strength throughout. Normal tone and muscle bulk.,Sensory: No deficits on LT/PP/VIB/TEMP/PROP testing.,Coord/Gait/Station: Unremarkable.,Reflexes: 2/2 in BUE except 2+ at left biceps. 1+/1+BLE except an absent right ankle reflex.,Plantar responses were flexor bilaterally. Rectal exam: normal tone.,IMPRESSION:, C-spine lesion.,COURSE: ,MRI C-spine revealed a central C5-6 disk herniation with compression of the spinal cord at that level. EMG/NCV showed normal NCV, but 1+ sharps and fibrillations in the right biceps (C5-6), brachioradialis (C5-6), triceps (C7-8) and teres major; and 2+ sharps and fibrillations in the right pronator terres. There was increased insertional activity in all muscles tested on the right side. The findings were consistent with a C6-7 radiculopathy.,The patient subsequently underwent C5-6 laminectomy and her symptoms resolved. | neurology, shoulder pain, stiffness, numbness, lhermitte's phenomena, c-spine lesion, disk herniation, mri c spine, reflexes, biceps, mri, disk, shoulder, spine, herniation, |
2,826 | MRI report Cervical Spine (Chiropractic Specific) | Neurology | MRI Cervical Spine - Chiropractic Specific | FINDINGS:,Normal foramen magnum.,Normal brainstem-cervical cord junction. There is no tonsillar ectopia. Normal clivus and craniovertebral junction. Normal anterior atlantoaxial articulation.,C2-3: There is disc desiccation but no loss of disc space height, disc displacement, endplate spondylosis or uncovertebral joint arthrosis. Normal central canal and intervertebral neural foramina.,C3-4: There is disc desiccation with a posterior central disc herniation of the protrusion type. The small posterior central disc protrusion measures 3 x 6mm (AP x transverse) in size and is producing ventral thecal sac flattening. CSF remains present surrounding the cord. The residual AP diameter of the central canal measures 9mm. There is minimal right-sided uncovertebral joint arthrosis but no substantial foraminal compromise.,C4-5: There is disc desiccation, slight loss of disc space height with a right posterior lateral pre-foraminal disc osteophyte complex with right-sided uncovertebral and apophyseal joint arthrosis. The disc osteophyte complex measures approximately 5mm in its AP dimension. There is minimal posterior annular bulging measuring approximately 2mm. The AP diameter of the central canal has been narrowed to 9mm. CSF remains present surrounding the cord. There is probable radicular impingement upon the exiting right C5 nerve root.,C5-6: There is disc desiccation, moderate loss of disc space height with a posterior central disc herniation of the protrusion type. The disc protrusion measures approximately 3 x 8mm (AP x transverse) in size. There is ventral thecal sac flattening with effacement of the circumferential CSF cleft. The residual AP diameter of the central canal has been narrowed to 7mm. Findings indicate a loss of the functional reserve of the central canal but there is no cord edema. There is bilateral uncovertebral and apophyseal joint arthrosis with moderate foraminal compromise.,C6-7: There is disc desiccation, mild loss of disc space height with 2mm of posterior annular bulging. There is bilateral uncovertebral and apophyseal joint arthrosis (left greater than right) with probable radicular impingement upon the bilateral exiting C7 nerve roots.,C7-T1, T1-2: There is disc desiccation with no disc displacement. Normal central canal and intervertebral neural foramina.,T3-4: There is disc desiccation with minimal 2mm posterior annular bulging but normal central canal and CSF surrounding the cord.,IMPRESSION:,Multilevel degenerative disc disease with uncovertebral joint arthrosis with foraminal compromise as described above.,C3-4 posterior central disc herniation of the protrusion type but no cord impingement.,C4-5 right posterior lateral disc osteophyte complex with right-sided uncovertebral and apophyseal joint arthrosis with probable radicular impingement upon the right C5 nerve root.,C5-6 degenerative disc disease with a posterior central disc herniation of the protrusion type producing borderline central canal stenosis with effacement of the circumferential CSF cleft indicating a limited functional reserve of the central canal.,C6-7 degenerative disc disease with annular bulging and osseous foraminal compromise with probable impingement upon the bilateral exiting C7 nerve roots.,T3-4 degenerative disc disease with posterior annular bulging. | neurology, exiting c nerve roots, loss of disc space, posterior central disc herniation, herniation of the protrusion, uncovertebral and apophyseal joint, intervertebral neural foramina, ventral thecal sac, thecal sac flattening, disc osteophyte complex, disc space height, central disc herniation, apophyseal joint arthrosis, posterior annular bulging, degenerative disc disease, posterior central disc, csf cleft, osteophyte complex, radicular impingement, disc disease, central disc, annular bulging, disc desiccation, joint arthrosis, central canal, cervical, degenerative, csf, foraminal, bulging, impingement, protrusion, uncovertebral, arthrosis, canal |
2,827 | MRI Cervical Spine without contrast. | Neurology | MRI Cervical Spine - 2 | EXAM:,MRI SPINAL CORD CERVICAL WITHOUT CONTRAST,CLINICAL:,Right arm pain, numbness and tingling.,FINDINGS:,Vertebral alignment and bone marrow signal characteristics are unremarkable. The C2-3 and C3-4 disk levels appear unremarkable.,At C4-5, broad based disk/osteophyte contacts the ventral surface of the spinal cord and may mildly indent the cord contour. A discrete cord signal abnormality is not identified. There may also be some narrowing of the neuroforamina at this level.,At C5-6, central disk-osteophyte contacts and mildly impresses on the ventral cord contour. Distinct neuroforaminal narrowing is not evident.,At C6-7, mild diffuse disk-osteophyte impresses on the ventral thecal sac and contacts the ventral cord surface. Distinct cord compression is not evident. There may be mild narrowing of the neuroforamina at his level.,A specific abnormality is not identified at the C7-T1 level.,IMPRESSION:,Disk/osteophyte at C4-5 through C6-7 with contact and may mildly indent the ventral cord contour at these levels. Some possible neuroforaminal narrowing is also noted at levels as stated above. | neurology, mri cervical spine, ventral cord contour, cervical spine, spinal cord, cord contour, ventral cord, mri, narrowing, ventral, cord |
2,828 | MRI Brain & MRI C-T spine: Multiple hemangioblastoma in Von Hippel Lindau Disease. | Neurology | MRI Brain and C-T Spine | CC:, Weakness.,HX:, This 30 y/o RHM was in good health until 7/93, when he began experiencing RUE weakness and neck pain. He was initially treated by a chiropractor and, after an unspecified length of time, developed atrophy and contractures of his right hand. He then went to a local neurosurgeon and a cervical spine CT scan, 9/25/92, revealed an intramedullary lesion at C2-3 and an extramedullary lesion at C6-7. He underwent a C6-T1 laminectomy with exploration and decompression of the spinal cord. His clinical condition improved over a 3 month post-operative period, and then progressively worsened. He developed left sided paresthesia and upper extremity weakness (right worse than left). He then developed ataxia, nausea, vomiting, and hyperreflexia. On 8/31/93, MRI C-spine showed diffuse enlargement of the cervical and thoracic spine and multiple enhancing nodules in the posterior fossa. On 9/1/93, he underwent suboccipital craniotomy with tumor excision, decompression, and biopsy which was consistent with hemangioblastoma. His symptoms stabilized and he underwent 5040 cGy in 28 fractions to his brain and 3600 cGy in 20 fractions to his cervical and thoracic spinal cord from 9/93 through 1/19/94.,He was evaluated in the NeuroOncology clinic on 10/26/95 for consideration of chemotherapy. He complained of progressive proximal weakness of all four extremities and dysphagia. He had difficulty putting on his shirt and raising his arms, and he had been having increasing difficulty with manual dexterity (e.g. unable to feed himself with utensils). He had difficulty going down stairs, but could climb stairs. He had no bowel or bladder incontinence or retention.,MEDS:, none.,PMH:, see above.,FHX:, Father with Von Hippel-Lindau Disease.,SHX:, retired truck driver. smokes 1-3 packs of cigarettes per day, but denied alcohol use. He is divorced and has two sons who are healthy. He lives with his mother.,ROS:, noncontributory.,EXAM:, Vital signs were unremarkable.,MS: A&O to person, place and time. Speech fluent and without dysarthria. Thought process lucid and appropriate.,CN: unremarkable exept for 4+/4+ strength of the trapezeii. No retinal hemangioblastoma were seen.,MOTOR: 4-/4- strength in proximal and distal upper extremities. There is diffuse atrophy and claw-hands, bilaterally. He is unable to manipulate hads to any great extent. 4+/4+ strength throughout BLE. There is also diffuse atrophy throughout the lower extremities though not as pronounced as in the upper extremities.,SENSORY: There was a right T3 and left T8 cord levels to PP on the posterior thorax. Decreased LT in throughout the 4 extremities.,COORD: difficult to assess due to weakness.,Station: BUE pronator drift.,Gait: stands without assistance, but can only manage to walk a few steps. Spastic gait.,Reflexes: Hyperreflexic on left (3+) and Hyporeflexic on right (1). Babinski signs were present bilaterally.,Gen exam: unremarkable.,COURSE: ,9/8/95, GS normal. By 11/14/95, he required NGT feeding due to dysphagia and aspiration risk confirmed on cookie swallow studies.MRI Brain, 2/19/96, revealed several lesions (hemangioblastoma) in the cerebellum and brain stem. There were postoperative changes and a cyst in the medulla.,On 10/25/96, he presented with a 1.5 week h/o numbness in BLE from the mid- thighs to his toes, and worsening BLE weakness. He developed decubitus ulcers on his buttocks. He also had had intermittent urinary retention for month, chronic SOB and dysphagia. He had been sitting all day long as he could not move well and had no daytime assistance. His exam findings were consistent with his complaints. He had had no episodes of diaphoresis, headache, or elevated blood pressures. An MRI of the C-T spine, 10/26/96, revealed a prominent cervicothoracic syrinx extending down to T10. There was evidence of prior cervical laminectomy of C6-T1 with expansion of the cord in the thecalsac at that region. Multiple intradural extra spinal nodular lesions (hyperintense on T2, isointense on T1, enhanced gadolinium) were seen in the cervical spine and cisterna magna. The largest of which measures 1.1 x 1.0 x 2.0cm. There are also several large ring enhancing lesions in cerebellum. The lesions were felt to be consistent with hemangioblastoma. No surgical or medical intervention was initiated. Visiting nursing was provided. He has since been followed by his local physician | |
2,829 | Left third digit numbness and wrist pain. | Neurology | MRI C3 - Cord Compression. | CC:, Left third digit numbness and wrist pain.,HX: ,This 44 y/o LHM presented with a one month history of numbness and pain of the left middle finger and wrist. The numbness began in the left middle finger and gradually progressed over the course of a day to involve his wrist as well. Within a few days he developed pain in his wrist. He had been working as a cook and cut fish for prolonged periods of time. This activity exacerbated his symptoms. He denied any bowel/bladder difficulties, neck pain, or weakness. He had no history of neck injury.,SHX/FHX:, 1-2 ppd Cigarettes. Married. Off work for two weeks due to complaints.,EXAM: ,Vital signs unremarkable.,MS:, A & O to person, place, time. Fluent speech without dysarthria.,CN II-XII: ,Unremarkable,MOTOR:, 5/5 throughout, including intrinsic muscles of hands. No atrophy or abnormal muscle tone.,SENSORY:, Decreased PP in third digit of left hand only (palmar and dorsal sides).,STATION/GAIT/COORD:, Unremarkable.,REFLEXES: ,1+ throughout, plantar responses were downgoing bilaterally.,GEN EXAM: ,Unremarkable.,Tinel's manuever elicited pain and numbness on the left. Phalens sign present on the left.,CLINICAL IMPRESSION: ,Left Carpal Tunnel Syndrome,EMG/NCV: ,Unremarkable.,MRI C-spine, 12/1/92: Congenitally small spinal canal is present. Superimposed on this is mild spondylosis and disc bulge at C6-7, C5-6, C4-5, and C3-4. There is moderate central spinal stenosis at C3-4. Intervertebral foramina at these levels appear widely patent.,COURSE:, The MRI findings did not correlate with the clinical findings and history. The patient was placed on Elavil and was subsequently lost to follow-up. | null |
2,830 | MRI cervical spine. | Neurology | MRI Cervical Spine - 1 | EXAM:,MRI CERVICAL SPINE,CLINICAL:, A57-year-old male. Received for outside consultation is an MRI examination performed on 11/28/2005.,FINDINGS:,Normal brainstem-cervical cord junction. Normal cisterna magna with no tonsillar ectopia. Normal clivus with a normal craniovertebral junction. Normal anterior atlantoaxial articulation.,C2-3: Normal intervertebral disc with no spondylosis or uncovertebral joint arthrosis. Normal central canal and intervertebral neural foramina with no cord or radicular impingement.,C3-4: There is disc desiccation with minimal annular bulging. The residual AP diameter of the central canal measures approximately 10mm. CSF remains present surrounding the cord.,C4-5: There is disc desiccation with endplate spondylosis and mild uncovertebral joint arthrosis. The residual AP diameter of the central canal measures approximately 8mm with effacement of the circumferential CSF cleft producing a borderline central canal stenosis but no cord distortion or cord edema. There is minimal uncovertebral joint arthrosis.,C5-6: There is disc desiccation with minimal posterior annular bulging and a right posterolateral preforaminal disc protrusion measuring approximately 2 x 8mm (AP x transverse). The disc protrusion produces minimal rightward ventral thecal sac flattening but no cord impingement.,C6-7: There is disc desiccation with mild loss of disc space height and posterior endplate spondylosis and annular bulging producing central canal stenosis. The residual AP diameter of the central canal measures 8 mm with effacement of the circumferential CSF cleft. There is a left posterolateral disc-osteophyte complex encroaching upon the left intervertebral neural foramen with probable radicular impingement upon the exiting left C7 nerve root.,C7-T1, T1-2: Minimal disc desiccation with no disc displacement or endplate spondylosis.,IMPRESSION:,Multilevel degenerative disc disease as described above.,C4-5 borderline central canal stenosis with mild bilateral foraminal compromise.,C5-6 disc desiccation with a borderline central canal stenosis and a right posterolateral preforaminal disc protrusion producing thecal sac distortion.,C6-7 degenerative disc disease and endplate spondylosis with a left posterolateral disc-osteophyte complex producing probable neural impingement upon the exiting left C7 nerve root with a borderline central canal stenosis.,Normal cervical cord. | neurology, borderline central canal stenosis, mri cervical spine, borderline central canal, central canal stenosis, degenerative disc, annular bulging, ap diameter, endplate spondylosis, borderline central, canal stenosis, disc desiccation, central canal, cervical, disc, spondylosis, stenosis, cord, canal, |
2,831 | MRI brain (Atrophy Left fronto-temporal lobe) and HCT (Left frontal SDH) | Neurology | MRI Brain - Progressive Aphasia | CC: ,Fall with subsequent nausea and vomiting.,HX: ,This 52 y/o RHM initailly presented in 10/94 with a two year hisotry of gradual progressive difficulty with speech. He "knew what he wanted to say, but could not say it.",His speech was slurred and he found it difficult to control his tongue. Examination at that time was notable for phonemic paraphasic errors, fair repetition of short phrases with decreased fluency, and slurred nasal speech. He could read, but could not write. He exhibited facial-limb apraxia, decreased gag reflex and positive grasp reflex. He was thougth to have possible Pick's disease vs. Cortical Basal Ganglia Degeneration.,On 11/18/94, he fell and was seen in Neurology clinic on 11/23/94. EEG showed borderline background slowing and no other abnormalities. An MRI on 11/8/94, revealed mild atrophy of the left temporal lobe. Neuropsychological evaluations were obtained on 10/25/94 and 11/8/94. These were consistent with progressive aphasia and apraxia with relative sparing of nonverbal reasoning.,He reported consuming 8 beers on the evening of 1/1/95. On 1/2/95, at 9:30AM, he fell forward while stading in his kitchen and struck his forehead on the counter top, and then struck his occiput on the floor. He subsequently developed nausea and vomiting, tinnitus, vertigo, headache and mild shortness of breath. He was taken to the ETC at UIHC. Skull films were negative and he was treated with IV Compazine and IV fluid hydration and sent home. His nausea and vomiting persisted and he became generally weak. He returned to the ETC at UIHC on 1/5/95. HCT scan revealed a right frontal SDH containing signs of both chronic and acute bleeding.,MEDS:, None.,PMH:, 1)fell in 1990 from 15 feet up and landed on his feet sustaining crush injury to both feet and ankles. He reportedly had brief loss of consciousness with no reported head injury.,2)Progressive aphasia. In 10/93, he was able to draw blue prints and write checks for his family business, 3) Left frontoparietal headache for 1.5 years prior to 10/94. Headaches continue to occur once a week, 4)right ankle fusion 4/94, right ankle fusion pending at present.,FHX:, No neurologic disease in family.,SHX:, Divorced and lives with girlfriend. One child by current girlfriend. He has 3 children with former wife. Smoked more than 15 years ago. Drinks 1-2 beers/day. Former Iron worker.,EXAM: ,BP128/83, HR68, RR18, 36.5C. Supine: BP142/71, HR64; Sitting: BP127/73, HR91 and lightheaded.,MS: Appeared moderately distressed and persistently held his forehead. A&O to person, place and time. Dysarthric and dysphagic. Non-fluent speech and able to say single syllable words such as "up" or "down". He comprehended speech, but could not repeat or write.,CN: Pupils 4/3.5 decreasing to 2/2 on exposure to light. EOM were full and smooth. Optic disks were flat and without sign of hemorrhage. Moderate facial apraxia, but had intact facial sensation.,Motor: 5/5 strength with normal muscle bulk and tone.,Sensory: no abnormalities noted.,Coord: Decreased RAM in the RUE. He had difficulty mmicking movements and postures with his RUE,Gait: ND.,Station: No truncal ataxia, but he had a slight RUE upward drift.,Reflexes 2/2 BUE, 2+/2+ patellae, 2/2 archilles, and plantar responses were flexor, bilaterally.,Rectal exam was unremarkable. The rest of the General Physical exam was unremarkable.,HEENT: atraumatic normocephalic skull. No carotid bruitts.,COURSE:, PT, PTT, CBC, GS, UA and Skull XR were negative. HCT brain, revealed a left frontal SDH with acute and cronic componenets.,He was markedly orthostatic during the first few days of his hospital stay. He was given a 3 day trial of Florinef, which showed mild to moderate improvement of his symptoms of lightheadedness. This improved still further with a trial of Sigvaris pressure stockings. A second HCT was obtained on 12/10/94 and revealed decreased intensity and sized of the left frontal SDH. He was discharged home.,His ideomotor apraxia worsened by 1/96. He developed seizures and was treated with CBZ. He progressively worsened and his overall condition was marked by aphasia, dysphagia, apraxia, and rigidity. He was last seen in 10/96 and the working diagnosis was CBGD vs. Pick's Disease. | null |
2,832 | MRI Brain: Left Basal Ganglia, Posterior temporal lobe, and Left cerebellar (lacunar) infarctions with Wernickes Aphasia. | Neurology | MRI Brain - Wernicke aphasia | CC: ,Difficulty with speech.,HX:, This 72 y/o RHM awoke early on 8/14/95 to prepare to play golf. He felt fine. However, at 6:00AM, on 8/14/95, he began speaking abnormally. His wife described his speech as "word salad" and "complete gibberish." She immediately took him to a local hospital . Enroute, he was initially able to understand what was spoken to him. By the time he arrived at the hospital at 6:45AM, he was unable to follow commands. His speech was reportedly unintelligible the majority of the time, and some of the health care workers thought he was speaking a foreign language. There were no other symptoms or signs. He had no prior history of cerebrovascular disease. Blood pressure 130/70 and Pulse 82 upon admission to the local hospital on 8/14/95.,Evaluation at the local hospital included: 1)HCT scan revealed an old left putaminal hypodensity, but no acute changes or evidence of hemorrhage, 2) Carotid Duplex scan showed ICA stenosis of 40%, bilaterally. He was placed on heparin and transferred to UIHC on 8/16/95.,In addition, he had noted memory and word finding difficulty for 2 months prior to presentation. He had undergone a gastrectomy 16 years prior for peptic ulcer disease. His local physician found him vitamin B12 deficient and he was placed on vitamin B12 and folate supplementation 2 months prior to presentation. He and his wife felt that this resulted in improvement of his language and cognitive skills.,MEDS:, Heparin IV, Vitamin B12 injection q. week, Lopressor, Folate, MVI.,PMH:, 1)Hypothyroidism (reportedly resolved), 2) Gastrectomy, 3)Vitamin B12 deficiency.,FHX: ,Mother died of MI, age 70. Father died of prostate cancer, age 80. Bother died of CAD and prostate cancer, age 74.,SHX:, Married. 3 children who are alive and well. Semi-retired Attorney. Denied h/o tobacco/ETOH/illicit drug use.,EXAM:, BP 110/70, HR 50, RR 14, Afebrile.,MS: A&O to person and place, but not time. Oral comprehension was poor beyond the simplest of conversational phrases. Speech was fluent, but consisted largely of "word salad." When asked how he was, he replied: "abadeedleedlebadle." Repetition was defective, especially with long phrases. On rare occasions, he uttered short comments appropriately. Speech was marred by semantic and phonemic paraphasias. He named colors and described most actions well, although he described a "faucet dripping" as a "faucet drop." He called "red" "reed." Reading comprehension was better than aural comprehension. He demonstrated excellent written calculations. Spoken calculations were accurate except when the calculations became more complex. For example, he said that ten percent of 100 was equal to "1,200.",CN: Pupils 2/3 decreasing to 1/1 on exposure to light. VFFTC. There were no field cuts or evidence of visual neglect. EOM were intact. Face moved symmetrically. The rest of the CN exam was unremarkable.,MOTOR: Full strength throughout with normal muscle tone and bulk. There was no evidence of drift.,SENSORY: unremarkable.,COORD: unremarkable.,Station: unremarkable. Gait: mild difficulty with TW.,Reflexes: 2/2 in BUE. 2/2+ patellae, 1/1 Achilles. Plantar responses were flexor on the left and equivocal on the right.,Gen Exam: unremarkable.,COURSE:, Lab data on admission: Glucose 97, BUN 20, Na 134, K 4.0, Cr 1.3, Chloride 98, CO2 24, PT 11, PTT 42, WBC 12.0 (normal differential), Hgb 11.4, Hct 36%, Plt=203k. UA normal. TSH 6.0, FT4 0.88, Vit B12 876, Folate 19.1. He was admitted and continued on heparin. MRI scan, 8/16/95, revealed increased signal on T2-weighted images in Wernicke's area in the left temporal region. Transthoracic echocardiogram on 8/17/95 was unremarkable. Transesophageal echocardiogram on 8/18/95 revealed a sclerotic aortic valve and myxomatous degeneration of the anterior leaflet of the mitral valve. LAE 4.8cm, and spontaneous echo contrast in the left atrium were noted. There was no evidence of intracardiac shunt or clot. Carotid duplex scan on 8/16/95 revealed 0-15% BICA stenosis with anterograde vertebral artery flow, bilaterally. Neuropsychologic testing revealed a Wernicke's aphasia.,The impression was that the patient had had a cardioembolic stroke involving a lower-division branch of the left MCA. He was subsequently placed on warfarin. Thoughout his hospital stay he showed continued improvement of language skills and was enrolled in speech therapy following discharge, 8/21/95.,He has had no further stroke like episodes up until his last follow-up visit in 1997. | neurology, mri brain, difficulty with speech, left basal ganglia, posterior temporal lobe, wernicke's area, wernickes aphasia, cerebellar, infarctions, lacunar, word finding difficulty, carotid duplex scan, aphasia, wernicke's, mri, brain, |
2,833 | MRI Brain & T-spine - Demyelinating disease. | Neurology | MRI Brain & T-spine - Demyelinating disease. | CC: ,Sensory loss.,HX: ,25y/o RHF began experiencing pruritus in the RUE, above the elbow and in the right scapular region, on 10/23/92. In addition she had paresthesias in the proximal BLE and toes of the right foot. Her symptoms resolved the following day. On 10/25/92, she awoke in the morning and her legs felt "asleep" with decreased sensation. The sensory loss gradually progressed rostrally to the mid chest. She felt unsteady on her feet and had difficulty ambulating. In addition she also began to experience pain in the right scapular region. She denied any heat or cold intolerance, fatigue, weight loss.,MEDS:, None.,PMH:, Unremarkable.,FHX: ,GF with CAD, otherwise unremarkable.,SHX:, Married, unemployed. 2 children. Patient was born and raised in Iowa. Denied any h/o Tobacco/ETOH/illicit drug use.,EXAM:, BP121/66 HR77 RR14 36.5C,MS: A&O to person, place and time. Speech normal with logical lucid thought process.,CN: mild optic disk pallor OS. No RAPD. EOM full and smooth. No INO. The rest of the CN exam was unremarkable.,MOTOR: Full strength throughout all extremities except for 5/4+ hip extensors. Normal muscle tone and bulk.,Sensory: Decreased PP/LT below T4-5 on the left side down to the feet. Decreased PP/LT/VIB in BLE (left worse than right). Allodynic in RUE.,Coord: Intact FNF, HKS and RAM, bilaterally.,Station: No pronator drift. Romberg's test not documented.,Gait: Unsteady wide-based. Able to TT and HW. Poor TW.,Reflexes: 3/3 BUE. Hoffman's signs were present bilaterally. 4/4 patellae. 3+/3+ Achilles with 3-4 beat nonsustained clonus. Plantar responses were extensor on the right and flexor on the left.,Gen. Exam: Unremarkable.,COURSE:, CBC, GS, PT, PTT, ESR, FT4, TSH, ANA, Vit B12, Folate, VDRL and Urinalysis were normal. MRI T-spine, 10/27/92, was unremarkable. MRI Brain, 10/28/92, revealed multiple areas of abnormally increased signal on T2 weighted images in the white matter regions of the right corpus callosum, periventricular region, brachium pontis and right pons. The appearance of the lesions was felt to be strongly suggestive of multiple sclerosis. 10/28/92, Lumbar puncture revealed the following CSF results: RBC 1, WBC 9 (8 lymphocytes, 1 histiocyte), Glucose 55mg/dl, Protein 46mg/dl (normal 15-45), CSF IgG 7.5mg/dl (normal 0.0-6.2), CSF IgG index 1.3 (normal 0.0-0.7), agarose gel electrophoresis revealed oligoclonal bands in the gamma region which were not seen on the serum sample. Beta-2 microglobulin was unremarkable. An abnormal left tibial somatosensory evoked potential was noted consistent with central conduction slowing. Visual and Brainstem Auditory evoked potentials were normal. HTLV-1 titers were negative. CSF cultures and cytology were negative. She was not treated with medications as her symptoms were primarily sensory and non-debilitating, and she was discharged home.,She returned on 11/7/92 as her symptoms of RUE dysesthesia, lower extremity paresthesia and weakness, all worsened. On 11/6/92, she developed slow slurred speech and had marked difficulty expressing her thoughts. She also began having difficulty emptying her bladder. Her 11/7/92 exam was notable for normal vital signs, lying motionless with eyes open and nodding and rhythmically blinking every few minutes. She was oriented to place and time of day, but not to season, day of the week and she did not know who she was. She had a leftward gaze preference and right lower facial weakness. Her RLE was spastic with sustained ankle clonus. There was dysesthetic sensory perception in the RUE. Jaw jerk and glabellar sign were present.,MRI brain, 11/7/92, revealed multiple enhancing lesions in the peritrigonal region and white matter of the centrum semiovale. The right peritrigonal region is more prominent than on prior study. The left centrum semiovale lesion has less enhancement than previously. Multiple other white matter lesions are demonstrated on the right side, in the posterior limb of the internal capsule, the anterior periventricular white matter, optic radiations and cerebellum. The peritrigonal lesions on both sides have increased in size since the 10/92 MRI. The findings were felt more consistent with demyelinating disease and less likely glioma. Post-viral encephalitis, Rapidly progressive demyelinating disease and tumor were in the differential diagnosis. Lumbar Puncture, 11/8/92, revealed: RBC 2, WBC 12 (12 lymphocytes), Glucose 57, Protein 51 (elevated), cytology and cultures were negative. HIV 1 titer was negative. Urine drug screen, negative. A stereotactic brain biopsy of the right parieto-occipital region was consistent with demyelinating disease. She was treated with Decadron 6mg IV qhours and Cytoxan 0.75gm/m2 (1.25gm). On 12/3/92, she has a focal motor seizure with rhythmic jerking of the LUE, loss of consciousness and rightward eye deviation. EEG revealed diffuse slowing with frequent right-sided sharp discharges. She was placed on Dilantin. She became depressed. | neurology, sensory loss, lumbar puncture, peritrigonal region, centrum semiovale, mri brain, white matter, demyelinating disease, csf, demyelinating, mri, brain, |
2,834 | MRI brain & Cerebral Angiogram: CNS Vasculitis with evidence of ischemic infarction in the right and left frontal lobes. | Neurology | MRI Brain & Cerebral Angiogram | CC:, Difficulty with word finding.,HX: ,This 27y/o RHF experienced sudden onset word finding difficulty and slurred speech on the evening of 2/19/96. She denied any associated dysphagia, diplopia, numbness or weakness of her extremities. She went to sleep with her symptoms on 2/19/96, and awoke with them on 2/20/96. She also awoke with a headache (HA) and mild neck stiffness. She took a shower and her HA and neck stiffness resolved. Throughout the day she continued to have difficulty with word finding and had worsening of her slurred speech. That evening, she began to experience numbness and weakness in the lower right face. She felt like there was a "rubber-band" wrapped around her tongue.,For 3 weeks prior to presentation, she experienced transient episodes of a "boomerang" shaped field cut in the left eye. The episodes were not associated with any other symptoms. One week prior to presentation, she went to a local ER for menorrhagia. She had just resumed taking oral birth control pills one week prior to the ER visit after having stopped their use for several months. Local evaluation included an unremarkable carotid duplex scan. However, a HCT with and without contrast reportedly revealed a left frontal gyriform enhancing lesion. An MRI brain scan on 2/20/96 revealed nonspecific white matter changes in the right periventricular region. EEG reportedly showed diffuse slowing. CRP was reportedly "too high" to calibrate.,MEDS:, Ortho-Novum 7-7-7 (started 2/3/96), and ASA (started 2/20/96).,PMH:, 1)ventral hernia repair 10 years ago, 2)mild "concussion" suffered during a MVA; without loss of consciousness, 5/93, 3) Anxiety disorder, 4) One childbirth.,FHX: ,She did not know her father and was not in contact with her mother.,SHX:, Lives with boyfriend. Smokes one pack of cigarettes every three days and has done so for 10 years. Consumes 6 bottles of beers, one day a week. Unemployed and formerly worked at an herbicide plant.,EXAM: ,BP150/79, HR77, RR22, 37.4C.,MS: A&O to person, place and time. Speech was dysarthric with mild decreased fluency marked by occasional phonemic paraphasic errors. Comprehension, naming and reading were intact. She was able to repeat, though her repetition was occasionally marked by phonemic paraphasic errors. She had no difficulty with calculation.,CN: VFFTC, Pupils 5/5 decreasing to 3/3. EOM intact. No papilledema or hemorrhages seen on fundoscopy. No RAPD or INO. There was right lower facial weakness. Facial sensation was intact, bilaterally. The rest of the CN exam was unremarkable.,MOTOR: 5/5 strength throughout with normal muscle bulk and tone.,Sensory: No deficits.,Coord/Station/Gait: unremarkable.,Reflexes 2/2 throughout. Plantar responses were flexor, bilaterally.,Gen Exam: unremarkable.,COURSE:, CRP 1.2 (elevated), ESR 10, RF 20, ANA 1:40, ANCA <1:40, TSH 2.0, FT4 1.73, Anticardiolipin antibody IgM 10.8GPL units (normal <10.9), Anticardiolipin antibody IgG 14.8GPL (normal<22.9), SSA and SSB were normal. Urine beta-hCG pregnancy and drug screen were negative. EKG, CXR and UA were negative.,MRI brain, 2/21/96 revealed increased signal on T2 imaging in the periventricular white matter region of the right hemisphere. In addition, there were subtle T2 signal changes in the right frontal, right parietal, and left parietal regions as seen previously on her local MRI can. In addition, special FLAIR imaging showed increased signal in the right frontal region consistent with ischemia.,She underwent Cerebral Angiography on 2/22/96. This revealed decreased flow and vessel narrowing the candelabra branches of the RMCA supplying the right frontal lobe. These changes corresponded to the areas of ischemic changes seen on MRI. There was also segmental narrowing of the caliber of the vessels in the circle of Willis. There was a small aneurysm at the origin of the LPCA. There was narrowing in the supraclinoid portion of the RICA and the proximal M1 and A1 segments. The study was highly suggestive of vasculitis.,2/23/96, Neuro-ophthalmology evaluation revealed no evidence of retinal vasculitic change. Neuropsychologic testing the same day revealed slight impairment of complex attention only. She was started on Prednisone 60mg qd and Tagamet 400mg qhs.,On 2/26/96, she underwent a right frontal brain biopsy. Pathologic evaluation revealed evidence of focal necrosis (stroke/infarct), but no evidence of vasculitis. Immediately following the brain biopsy, while still in the recovery room, she experienced sudden onset right hemiparesis and transcortical motor type aphasia. Initial HCT was unremarkable. An EEG was consistent with a focal lesion in the left hemisphere. However, a 2/28/96 MRI brain scan revealed new increased signal on T2 weighted images in a gyriform pattern from the left precentral gyrus to the superior frontal gyrus. This was felt consistent with vasculitis.,She began q2month cycles of Cytoxan (1,575mg IV on 2/29/96. She became pregnant after her 4th cycle of Cytoxan, despite warnings to the contrary. After extensive discussions with OB/GYN it was recommended she abort the pregnancy. She underwent neuropsychologic testing which revealed no significant cognitive deficits. She later agreed to the abortion. She has undergone 9 cycles of Cytoxan ( one cycle every 2 months) as of 4/97. She had complained of one episode of paresthesias of the LUE in 1/97. MRI then showed no new signs ischemia. | |
2,835 | MRI Brain: Thrombus in torcula of venous sinuses. | Neurology | MRI Brain - Thrombus | CC: ,Motor vehicle-bicycle collision.,HX:, A 5 y/o boy admitted 10/17/92. He was struck while riding his bicycle by a motor vehicle traveling at a high rate of speed. First responders found him unconscious with left pupil 6 mm and unreactive and the right pupil 3 mm and reactive. He had bilateral decorticate posturing and was bleeding profusely from his nose and mouth. He was intubated and ventilated in the field, and then transferred to UIHC.,PMH/FHX/SHX:, unremarkable.,MEDS:, none,EXAM:, BP 127/91 HR69 RR30,MS: unconscious and intubated,Glasgow coma scale=4,CN: Pupils 6/6 fixed. Corneal reflex: trace OD, absent OS. Gag present on manipulation of endotracheal tube.,MOTOR/SENSORY: bilateral decorticate posturing to noxious stimulation (chest).,Reflexes: bilaterally.,Laceration of mid forehead exposing calvarium.,COURSE:, Emergent Brain CT scan revealed: Displaced fracture of left calvarium. Left frontoparietal intraparenchymal hemorrhage. Right ventricular collection of blood. Right cerebral intraparenchymal hemorrhage. Significant mass effect with deviation of the midline structures to right. The left ventricle was compressed with obliteration of the suprasellar cistern. Air within the soft tissues in the left infra temporal region. C-spine XR, Abdominal/Chest CT were unremarkable.,Patient was taken to the OR emergently and underwent bifrontal craniotomy, evacuation of a small epidural and subdural hematomas, and duraplasty. He was given mannitol enroute to the OR and hyperventilated during and after the procedure. Postoperatively he continued to manifest decerebrate posturing . On 11/16/92 he underwent VP shunting with little subsequent change in his neurological status. On 11/23/92 he underwent tracheostomy. On 12/11/92 he underwent bifrontal acrylic prosthesis implantation for repair of the bifrontal craniectomy. By the time of discharge, 1/14/93, he tracked relatively well OD, but had a CN3 palsy OS. He had relatively severe extensor rigidity in all extremities (R>L). His tracheotomy was closed prior to discharge. A 11/16/92 Brain MRI demonstrated infarction in the upper brain stem (particularly in the Pons), left cerebellum, right basil ganglia and thalamus.,He was initially treated for seizure prophylaxis with DPH, but developed neutropenia, so it was discontinued. He developed seizures within several months of discharge and was placed on VPA (Depakene). This decreased seizure frequency but his liver enzymes became elevated and he changed over to Tegretol. 10/8/93 Brain MRI (one year after MVA) revealed interval appearance of hydrocephalus, abnormal increased T2 signal (in the medulla, right pons, both basal ganglia, right frontal and left occipital regions), a small mid-brain, and a right subdural fluid collection. These findings were consistent with diffuse axonal injury of the white matter and gray matter contusion, and signs of a previous right subdural hematoma.,He was last seen 10/30/96 in the pediatric neurology clinic--age 9 years. He was averaging 2-3 seizures per day---characterized by extension of BUE with tremor and audible cry or laughter---on Tegretol and Diazepam. In addition he experiences 24-48hour periods of "startle response (myoclonic movement of the shoulders)" with or without stimulation every 6 weeks. He had limited communication skills (sparse speech). On exam he had disconjugate gaze, dilated/fixed left pupil, spastic quadriplegia. | neurology, mri brain, brain mri, thrombus, intraparenchymal hemorrhage, motor vehicle, prophylaxis, sinuses, torcula venous sinuses, venous, brain thrombus, bilateral decorticate, decorticate posturing, subdural hematomas, subdural, mri, brain, torcula |
2,836 | MRI Brain: Probable CNS Lymphoma v/s toxoplasmosis in a patient with AIDS/HIV. | Neurology | MRI Brain - Toxoplasmosis | CC:, Lethargy.,HX:, This 28y/o RHM was admitted to a local hospital on 7/14/95 for marked lethargy. He had been complaining of intermittent headaches and was noted to have subtle changes in personality for two weeks prior to 7/14/95. On the morning of 7/14/95, his partner found him markedly lethargic and complaingin of abdominal pain and vomiting. He denied fevers, chills, sweats, cough, CP, SOB or diarrhea. Upon evaluation locally, he had a temperature of 99.5F and appeared lethargic. He also had anisocoria with left pupil 0.5mm bigger than the right. There was also question of left facial weakness. An MRI was obtained and revealed a large left hemispheric mass lesion with surrounding edema and mass effect. He was given 10mg of IV Decardron,100gm of IV Mannitol, intubated and hyperventilated and transferred to UIHC.,He was admitted to the Department of Medicine on 7/14/95, and transferred to the Department of Neurology on 7/17/95, after being extubated.,MEDS ON ADMISSION:, Bactrim DS qd, Diflucan 100mg qd, Acyclovir 400mg bid, Xanax, Stavudine 40mg bid, Rifabutin 300mg qd.,PMH:, 1) surgical correction of pyoloric stenosis, age 1, 2)appendectomy, 3) HIV/AIDS dx 1991. He was initially treated with AZT, then DDI. He developed chronic diarrhea and was switched to D4T in 1/95. However, he developed severe neuropathy and this was stopped 4/95. The diarrhea recured. He has Acyclovir resistant genital herpes and generalized psoriasis. He most recent CD4 count (within 1 month of admission) was 20.,FHX:, HTN and multiple malignancies of unknown type.,SHX:, Homosexual, in monogamous relationship with an HIV infected partner for the past 3 years.,EXAM: ,7/14/95 (by Internal Medicine): BP134/80, HR118, RR16 on vent, 38.2C, Intubated.,MS: Somnolent, but opened eyes to loud voices and would follow most commands.,CN: Pupils 2.5/3.0 and "equally reactive to light." Mild horizontal nystagmus on rightward gaze. EOM were otherwise intact.,MOTOR: Moved 4 extremities well.,Sensory/Coord/Gait/Station/Reflexes: not done.,Gen EXAM: Penil ulcerations.,EXAM:, 7/17/96 (by Neurology): BP144/73, HR59, RR20, 36.0, extubated.,MS: Alert and mildly lethargic. Oriented to name only. Thought he was a local hospital and that it was 1/17/1994. Did not understand he had a brain lesion.,CN: Pupils 6/5.5 decreasing to 4/4 on exposure to light. EOM were full and smooth. No RAPD or light-near dissociation. papilledema (OU). Right lower facial weakness and intact facial sensation to PP testing. Gag-shrug and corneal responses were intact, bilaterally. Tongue midline.,MOTOR: Grade 5- strength on the right side.,Sensory: no loss of sensation on PP/VIB/PROP testing.,Coord: reduced speed and accuracy on right FNF and right HKS movements.,Station: RUE pronator drift.,Gait: not done.,Reflexes: 2+/2 throughout. Babinski sign present on right and absent on left.,Gen Exam: unremarkable except for the genital lesion noted by Internal medicine.,COURSE:, The outside MRI was reviewed and was notable for the left frontal/parietal mass lesion with surround edema. The mass inhomogenously enhanced with gadolinium contrast.,The findings were consistent most with lymphoma, though toxoplasmosis could not be excluded. He refused brain biopsy and was started on empiric treatment for toxoplasmosis. This consisted of Pyrimethamine 75mg qd and Sulfadiazine 2 g bid. He later became DNR and was transferred at his and his partner's request Back to a local hospital.,He never returned for follow-up. | null |
2,837 | MRI Brain and Brainstem - Falling (Multiple System Atrophy) | Neurology | MRI Brain and Brainstem | CC:, Falling.,HX:, This 67y/o RHF was diagnosed with Parkinson's Disease in 9/1/95, by a local physician. For one year prior to the diagnosis, the patient experienced staggering gait, falls and episodes of lightheadedness. She also noticed that she was slowly "losing" her voice, and that her handwriting was becoming smaller and smaller. Two months prior to diagnosis, she began experienced bradykinesia, but denied any tremor. She noted no improvement on Sinemet, which was started in 9/95. At the time of presentation, 2/13/96, she continued to have problems with coordination and staggering gait. She felt weak in the morning and worse as the day progressed. She denied any fever, chills, nausea, vomiting, HA, change in vision, seizures or stroke like events, or problems with upper extremity coordination.,MEDS:, Sinemet CR 25/100 1tab TID, Lopressor 25mg qhs, Vitamin E 1tab TID, Premarin 1.25mg qd, Synthroid 0.75mg qd, Oxybutynin 2.5mg has, isocyamine 0.125mg qd.,PMH:, 1) Hysterectomy 1965. 2) Appendectomy 1950's. 3) Left CTR 1975 and Right CTR 1978. 4) Right oophorectomy 1949 for "tumor." 5) Bladder repair 1980 for unknown reason. 6) Hypothyroidism dx 4/94. 7) HTN since 1973.,FHX: ,Father died of MI, age 80. Mother died of MI, age73. Brother died of Brain tumor, age 9.,SHX: ,Retired employee of Champion Automotive Co.,Denies use of TOB/ETOH/Illicit drugs.,EXAM: ,BP (supine)182/113 HR (supine)94. BP (standing)161/91 HR (standing)79. RR16 36.4C.,MS: A&O to person, place and time. Speech fluent and without dysarthria. No comment regarding hypophonia.,CN: Pupils 5/5 decreasing to 2/2 on exposure to light. Disks flat. Remainder of CN exam unremarkable.,Motor: 5/5 strength throughout. NO tremor noted at rest or elicited upon movement or distraction,Sensory: Unremarkable PP/VIB testing.,Coord: Did not show sign of dysmetria, dyssynergia, or dysdiadochokinesia. There was mild decrement on finger tapping and clasping/unclasping hands (right worse than left).,Gait: Slow gait with difficulty turning on point. Difficulty initiating gait. There was reduced BUE swing on walking (right worse than left).,Station: 3-4step retropulsion.,Reflexes: 2/2 and symmetric throughout BUE and patellae. 1/1 Achilles. Plantar responses were flexor.,Gen Exam: Inremarkable. HEENT: unremarkable.,COURSE:, The patient continued Sinemet CR 25/100 1tab TID and was told to monitor orthostatic BP at home. The evaluating Neurologist became concerned that she may have Parkinsonism plus dysautonomia.,She was seen again on 5/28/96 and reported no improvement in her condition. In addition she complained of worsening lightheadedness upon standing and had an episode, 1 week prior to 5/28/96, in which she was at her kitchen table and became unable to move. There were no involuntary movements or alteration in sensorium/mental status. During the episode she recalled wanting to turn, but could not. Two weeks prior to 5/28/96 she had an episode of orthostatic syncope in which she struck her head during a fall. She discontinued Sinemet 5 days prior to 5/28/96 and felt better. She felt she was moving slower and that her micrographia had worsened. She had had recent difficulty rolling over in bed and has occasional falls when turning. She denied hypophonia, dysphagia or diplopia.,On EXAM: BP (supine)153/110 with HR 88. BP (standing)110/80 with HR 96. (+) Myerson's sign and mild hypomimia, but no hypophonia. There was normal blinking and EOM. Motor strength was full throughout. No resting tremor, but mild postural tremor present. No rigidity noted. Mild decrement on finger tapping noted. Reflexes were symmetric. No Babinski signs and no clonus. Gait was short stepped with mild anteroflexed posture. She was unable to turn on point. 3-4 step Retropulsion noted. The Parkinsonism had been unresponsive to Sinemet and she had autonomic dysfunction suggestive of Shy-Drager syndrome. It was recommended that she liberalize dietary salt use and lie with head of the bed elevate at 20-30 degrees at night. Indomethacin was suggested to improve BP in future. | neurology, myerson's sign, falling, dysautonomia, mri brain and brainstem, brain and brainstem, mri brain, sinemet cr, mri, brainstem, ctr, tumor, retropulsion, parkinsonism, brain, lightheadedness, hypophonia, standing, sinemet, |
2,838 | MRI Brain - Right frontal white matter infarct in patient with Anticardiolipin antibody syndrome and SLE. | Neurology | MRI Brain - SLE & Stroke | CC:, Episodic monocular blindness, OS.,HX:, This 29 y/o RHF was in her usual healthy state until 2 months prior to her 3/11/96 presentation when she developed episodic arthralgias of her knees and ankles, bilaterally. On 3/3/96, she experienced sudden onset monocular blindness, OS, lasting 5-10 minutes in duration. Her vision "greyed out" from the periphery to center of her visual field, OS; and during some episodes progressed to complete blindness (not even light perception). This resolved within a few minutes. She had multiple episodes of vision loss, OS, every day until 3/7/96 when she was placed on heparin for suspected LICA dissection. She saw a local ophthalmologist on 3/4/96 and was told she had a normal funduscopic exam. She experienced 0-1 spell of blindness (OS) per day from 3/7/96 to 3/11/96. In addition, she complained of difficulty with memory since 3/7/96. She denied dysarthria, aphasia or confusion, but had occasional posterior neck and bioccipital-bitemporal headaches.,She had no history of deep venous or arterial thrombosis.,3/4/96, ESR=123. HCT with and without contrast on 3/7/96 and 3/11/96, and Carotid Duplex scan were "unremarkable." Rheumatoid factor=normal. 3-vessel cerebral angiogram (done locally) was reportedly "unremarkable.",She was thought to have temporal arteritis and underwent Temporal Artery biopsy (which was unremarkable), She received Prednisone 80 mg qd for 2 days prior to presentation.,On admission she complained of a left temporal headache at the biopsy site, but no loss of vision or weakness,She had been experiencing mild fevers and chills for several weeks prior to presentation. Furthermore, she had developed cyanosis of the distal #3 toes on feet, and numbness and rash on the lateral aspect of her left foot. She developed a malar rash on her face 1-2 weeks prior to presentation.,MEDS:, Depo-Provera, Prednisone 80mg qd, and Heparin IV.,PMH:, 1)Headaches for 3-4 years, 2)Heart murmur, 3) cryosurgery of cervix, 4)tonsillectomy and adenoidectomy, 5) elective abortion. She had no history of spontaneous miscarriage and had used oral birth control pill for 10 years prior to presentation.,FHX:, Migraine headaches on maternal side, including her mother. No family history of thrombosis.,SHX:, works as a metal grinder and was engaged to be married. She denied any tobacco or illicit drug use. She consumed 1 alcoholic drink per month.,EXAM: ,BP147/74, HR103, RR14, 37.5C.,MS: A&O to person, place and time. Speech was fluent without dysarthria. Repetition, naming and comprehension were intact. 2/3 recall at 2 minutes.,CN: unremarkable.,Motor: unremarkable.,Coord: unremarkable.,Sensory: decreased LT, PP, TEMP, along the lateral aspect of the left foot.,Gait: narrow-based and able to TT, HW and TW without difficulty.,Station: unremarkable.,Reflexes: 2/2 throughout. Plantar responses were flexor, bilaterally.,Skin: Cyanosis of the distal #3 toes on both feet. There was a reticular rash about the lateral aspect of her left foot. There were splinter-type hemorrhages under the fingernails of both hands.,COURSE: , ESR=108 (elevated), Hgb 11.3, Hct 33%, WBC 10.0, Plt 148k, MCV 92 (low) Cr 1.3, BUN 26, CXR and EKG were unremarkable. PTT 42 (elevated). PT normal. The rest of the GS and CBC were normal. Dilute Russell Viper venom time was elevated at 27 and a 1:1 prothrombin time mix corrected to only 36.,She was admitted to the Neurology service. Blood cultures were drawn and were negative. Transthoracic and transesophageal echocardiography on 3/12/96 was unremarkable.,Her symptoms and elevated PTT suggested an ischemic syndrome involving anticardiolipin antibody and/or lupus anticoagulant. Her signs of rash and cyanosis suggested SLE. ANA was positive at 1:640 (speckled), RF (negative), dsDNA, 443 (elevated). Serum cryoglobulins were positive at 1% (fractionation data lost). Serum RPR was positive, but FTA-ABS was negative (thereby confirming a false-positive RPR). Anticardiolipin antibodies IgM and IgG were positive at 56.1 and 56.3 respectively. Myeloperoxidase antibody was negative, ANCA was negative and hepatitis screen unremarkable.,The Dermatology Service felt the patient's reticular foot rash was livedo reticularis. Rheumatology felt the patient met criteria for SLE. Hematology felt the patient met criteria for Anticardiolipin Antibody and/or Lupus anticoagulant Syndrome. Neurology felt the episodic blindness was secondary to thromboembolic events.,Serum Iron studies revealed: FeSat 6, Serum Fe 15, TIBC 237, Reticulocyte count 108.5. The patient was placed on FeSO4 225mg tid.,She was continued on heparin IV, but despite this she continued to have occasional episodes of left monocular blindness or "gray outs" up to 5 times per day. She was seen by the Neuro-ophthalmology Service. The did not think she had evidence of vasculitis in her eye. They recommended treatment with ASA 325mg bid. She was placed on this 3/15/96 and tapered off heparin. She continued to have 0-4 episodes of monocular blindness (OS) for 5-10 seconds per episodes. She was discharged home.,She returned 3/29/96 for episodic diplopia lasting 5-10 minutes per episode. The episodes began on 3/27/96. During the episodes her left eye deviated laterally while the right eye remained in primary gaze. She had no prior history of diplopia or strabismus. Hgb 10.1, Hct 30%, WBC 5.2, MCV 89 (low), Plt 234k. ESR 113mm/hr. PT 12, PTT 45 (high). HCT normal. MRI brain, 3/30/96, revealed a area of increased signal on T2 weighted images in the right frontal lobe white matter. This was felt to represent a thromboembolic event. She was place on heparin IV and treated with Solu-Medrol 125mg IV q12 hours. ASA was discontinued. Hematology, Rheumatology and Neurology agreed to place her on Warfarin. She was placed on Prednisone 60mg qd following the Solu-Medrol. She continued to have transient diplopia and mild vertigo despite INR's of 2.0-2.2. ASA 81mg qd was added to her regimen. In addition, Rheumatology recommended Plaquenil 200mg bid. The neurologic symptoms decreased gradually over the ensuing 3 days. Warfarin was increased to achieve INR 2.5-3.5.,She reported no residual symptoms or new neurologic events on her 5/3/96 Neurology Clinic follow-up visit. She continues to be event free on Warfarin according to her Hematology Clinic notes up to 12/96. | null |
2,839 | MRI Brain - Pilocytic Astrocytoma in thalamus and caudate. | Neurology | MRI Brain - Pilocytic Astrocytoma | CC:, Headache.,HX: ,The patient is an 8y/o RHM with a 2 year history of early morning headaches (3:00-6:00AM) intermittently relieved by vomiting only. He had been evaluated 2 years ago and an EEG was "normal" then, but no brain imaging was performed. His headaches progressively worsened, especially in the past two months prior to this presentation. For 2 weeks prior to his 1/25/93 evaluation at UIHC, he would awake screaming. His parent spoke with a local physician who thought this might be due to irritability secondary to pinworms and,Vermox was prescribed and arrangements were made for a neurologic evaluation. On the evening of 1/24/93 the patient awoke screaming and began to vomit. This was followed by a 10 min period of tonic-clonic type movements and postictal lethargy. He was taken to a local ER and a brain CT revealed an intracranial mass. He was given Decadron and Phenytoin and transferred to UIHC for further evaluation.,MEDS:, noted above.,PMH: ,1)Born at 37.5 weeks gestation by uncomplicated vaginal delivery to a G1P0 mother. Pregnancy complicated by vaginal bleeding at 7 months. Met developmental milestones without difficulty. 2) Frequent otitis media, now resolved. 3) Immunizations were "up to date.",FHX:, non-contributory.,SHX:, lives with biologic father and mother. No siblings. In 3rd grade (mainstream) and maintaining good marks in schools.,EXAM:, BP121/57mmHg HR103 RR16 36.9C,MS: Sleepy, but cooperative.,CN: EOM full and smooth. Advanced papilledema, OU. VFFTC. Pupils 4/4 decreasing to 2/2. Right lower facial weakness. Tongue midline upon protrusion. Corneal reflexes intact bilaterally.,Motor: 5/5 strength. Slightly increased muscle on right side.,Sensory. No deficit to PP/VIB noted.,Coord: normal FNF, HKS and RAM, bilaterally.,Station: Mild truncal ataxia. Tends to fall backward.,Reflexes: BUE 2+/2+, Patellar 3/3, Ankles 3+/3+ with 6 beats of nonsustained clonus bilaterally.,Gen exam: unremarkable.,COURSE:, The patient was continued on Dilantin 200mg qd and Decadron 5mg IV q6hrs. Brain MRI, 1/26/93, revealed a large mass lesion in the region of the left caudate nucleus and thalamus which was hyperintense on T2 weighted images. There were areas of cystic formation at its periphery. The mass appeared to enhance on post gadolinium images. there was associated white matter edema and compression of the left lateral ventricle, and midline shift to the right. There was no sign of uncal herniation. He underwent bilateral VP shunting on 1/26/93; and then, subtotal resection (left frontal craniotomy with excision of the left caudate and thalamus with creation of an opening in the septum pellucidum) on 1/28/93. He then received 5040cGy of radiation therapy in 28 fractions completed on 3/25/93. A 3/20/95 neuropsychological evaluation revealed low average intellect on the WISC-III. There were also signs of memory, attention, reading and spelling deficits; and mild right-sided motor incoordination and mood variability. He remained in mainstream classes at school, but his physical and cognitive performance began to deteriorate in 4/95. Neurosurgical evaluation in 4/95 noted increased right hemiplegia and right homonymous hemianopia. MRI revealed tumor progression and he was subsequently placed on Carboplatin/VP-16 (CG 9933 protocol chemotherapy, regimen A). He was last seen on 4/96 and was having difficulty in the 6th grade; he was also undergoing physical therapy for his right hemiplegia. | neurology, mri brain, pilocytic astrocytoma, caudate, thalamus, headache, astrocytoma, hemiplegia, pilocytic, mri, |
2,840 | Right pontine pyramidal tract infarct. | Neurology | MRI Brain - Pontine Stroke | CC:, Left sided weakness.,HX:, 74 y/o RHF awoke from a nap at 11:00 AM on 11/22/92 and felt weak on her left side. She required support on that side to ambulate. In addition, she felt spoke as though she "was drunk." Nevertheless, she was able to comprehend what was being spoken around her. Her difficulty with speech completely resolved by 12:00 noon. She was brought to UIHC ETC at 8:30AM on 11/23/92 for evaluation.,MEDS:, none. ,ALLERGIES:, ASA/ PCN both cause rash.,PMH:, 1)?HTN. 2)COPD. 3)h/o hepatitis (unknown type). 4)Macular degeneration.,SHX:, Widowed; lives alone. Denied ETOH/Tobacco/illicit drug use.,FHX:, unremarkable.,EXAM: , BP191/89 HR68 RR16 37.2C,MS: A & O to person, place and time. Speech fluent; without dysarthria. Intact naming, comprehension, and repetition.,CN: Central scotoma, OS (old). Mild upper lid ptosis, OD (old per picture). Lower left facial weakness.,Motor: Mild Left hemiparesis (4+ to 5- strength throughout affected side). No mention of muscle tone in chart.,Sensory: unremarkable.,Coord: impaired FNF and HKS movement secondary to weakness.,Station: Left pronator drift. No Romberg sign seen.,Gait: Left hemiparetic gait with decreased LUE swing.,Reflexes: 3/3+ biceps and triceps. 3/3+ patellae. 2/3+ ankles with 3-4beats of non-sustained ankle clonus on left. Plantars: Left babinski sign; and flexor on right.,General Exam: 2/6 SEM at left sternal border.,COURSE:, GS, CBC, PT, PTT, CK, ESR were within normal limits. ABC 7.4/46/63 on room air. EKG showed a sinus rhythm with right bundle branch block. MRI brain, 11/23/95, revealed a right pontine pyramidal tract infarction. She was treated with Ticlopidine 250mg bid. On 11/26/92, her left hemiparesis worsened. A HCT, 11/27/92, was unremarkable. The patient was treated with IV Heparin. This was discontinued the following day when her strength returned to that noted on 11/23/95. On 11/27/92, she developed angina and was ruled out for MI by serial EKG and cardiac enzyme studies. Carotid duplex showed 0-15% bilateral ICA stenosis and antegrade vertebral artery flow bilaterally. Transthoracic echocardiogram revealed aortic insufficiency only. Transesophageal echocardiogram revealed trivial mitral and tricuspid regurgitation, aortic valvular fibrosis. There was calcification and possible thrombus seen in the descending aorta. Cardiology did not feel the later was an indication for anticoagulation. She was discharged home on Isordil 20 tid, Metoprolol 25mg q12hours, and Ticlid 250mg bid. | neurology, mri brain, pontine stroke, difficulty with speech, hemiparesis, pontine pyramidal tract infarct, weakness, mri, brain, pyramidal, echocardiogram, pontine, infarct, |
2,841 | A middle-aged male with increasing memory loss and history of Lyme disease. | Neurology | MRI Brain - Lyme Disease | FINDINGS:,There is a large intrasellar mass lesion producing diffuse expansion of the sella turcica. This mass lesions measures approximately 16 x 18 x 18mm (craniocaudal x AP x mediolateral) in size. | neurology, increasing memory loss, intrasellar mass lesion, memory loss, sella turcica, cavernous sinus, sphenoid sinus, ct imaging, white matter, retention cyst, maxillary antrum, lyme disease, mass lesion, disease, cavernous, cortical, mass, lesion, |
2,842 | MRI Brain - Progressive Multifocal Leukoencephalopathy (PML) occurring in an immunosuppressed patient with polymyositis. | Neurology | MRI Brain - Leukoencephalopathy | CC: ,Progressive left visual field loss.,HX:, This 46y/o RHF with polymyositis since 1988, presented with complaint of visual field loss since 12/94. The visual field loss was of gradual onset and within a month of onset became a left homonymous hemianopsia. She began experiencing stiffness, numbness, tingling and incoordination of her left hand, 6 weeks prior to this admission,. These symptoms were initially attributed to carpal tunnel syndrome. MRI scan of the brain (done locally) on 6/23/95 revealed increased periventricular white matter signal on T2 images, particularly in the left temporo-occipital and right parietal lobes. There was ring enhancement of a lesion in the left occipital lobe on T1 gadolinium contrast enhanced images. There was gyral enhancement near the right Sylvian fissure. Cerebral angiogram on 7/19/95 (done locally) was unremarkable. Lumbar puncture on 7/19/95 was unremarkable. She complained of frequent holocranial throbbing headaches for the past 6 months; the HA's are associated with photophobia, phonophobia and nausea, but no vomiting. She has also been experiencing chills and night sweats for the past 2-3 weeks. She denies weight loss, but acknowledged decreased appetite and increased generalized fatigue for the past 3-4 months.,She was diagnosed with polymyositis in 1988 with slowly progressive bilateral lower extremity weakness. She has been on immunosuppressive drugs since 1988, including Prednisone, Prednisone and methotrexate, Cyclosporin, Imuran, Cytoxan, and Plaquenil. At present she in ambulatory with use of walker. Her last CK=3,125 and ESR=16, on 6/28/95.,MEDS:, Prednisone 20mg qd, Cytoxan 75mg qd, Zantac 150mg bid, Vasotec 10mg bid, Premarin 0.625 qd, Provera 2.5mg qd, CaCO3 500mg bid, Vit D 50,000units qweek, Vit E qd, MVI 1 tab qd.,PMH:, 1)polymyositis diagnosed in 1988 by muscle biopsy. 2)hypertension. 3)lichen planus. 4)Lower extremity deep venous thrombosis one year ago--placed on Coumadin and this resulted in postmenopausal bleeding.,FHX:, Mother is alive and has a h/o HTN and stroke. Father died in motor vehicle accident at age 40 years.,SHX:, Married, 3 children who are healthy. She denied any Tobacco/ETOH/Illicit drug use.,EXAM:, BP160/74 HR95 RR12 35.8C Wt. 86.4kg Ht. 5'6",MS: A&O to person, place and time. Speech was normal. Mood euthymic with appropriate affect.,CN: Pupils 4/4 decreasing to 2/2 on exposure to light. No RAPD noted. Optic Disk were flat. EOM testing unremarkable. Confrontational visual field testing revealed a left homonymous hemianopsia. The rest of the CN exam was unremarkable.,MOTOR: Upper extremities: 5/5 proximally, 5/4 @ elbow/wrist/hand. Lower extremities: 4/4 proximally and 5/5 @ and below knees.,SENSORY: unremarkable.,COORD: Dyssynergia of LUE FNF movement. Slowed finger tapping on left. HNS movements were normal, bilaterally.,Station: LUE drift and fix on arm roll. No Romberg sign elicited.,Gait: Waddling gait, but could TT and stand on both heels. She had difficulty with tandem walking, but did not fall to any particular side.,Reflexes: 2/2 brachioradialis and biceps. 2/2+ triceps, 1+/1+ patellae, 1/1 Achilles. Plantar responses were flexor on the right and withdrawal response on the left.,GEN EXAM: No rashes. II/VI systolic ejection murmur at the left sternal border.,COURSE:, Electrolytes, PT/PTT, Urinalysis and CXR were normal. ESR=38 (normal<20), CRP1.4 (normal<0.4). CK 2,917, LDH 356, AST 67. MRI Brain, 8/8/95, revealed slight improvement of the abnormal white matter changes seen on previous outside MRI. In addition new sphenoid sinus disease suggestive of sinusitis was seen. She underwent stereotactic biopsy of the right parietal region on 8/10/95 which on H&E and LFB stained sections revealed multiple discrete areas of demyelination, containing dense infiltrates of foamy macrophages in association with scattered large oligodendroglia with deeply basophilic, ground-glass nuclei, enlarged astrocytes, and sparse perivascular lymphocytic infiltrates. In situ hybridization performed on block A2 (at the university of Pittsburgh) is positive for JC virus. The ultrastructural studies demonstrated no viral particles.,She was tapered off all immunosuppressive medications and her polymyositis remained clinically stable. She had a seizure in 12/95 and was placed on Dilantin. Her neurologic deficits worsened slightly, but reached a plateau by 10/96, as indicated by a 4/14/97 Neurology clinic visit note.,1/22/96, MRI Brain demonstrated widespread hyperintense signal on T2 and Proton Density weighted images throughout the deep white matter in both hemispheres, worse on the right side. There was interval progression of previously noted abnormalities and extension into the right frontal and left parieto-occipital regions. There was progression of abnormal signal in the Basal Ganglia, worse on the right, and new involvement of the brainstem. | neurology, mri brain, pml, progressive multifocal leukoencephalopathy, polymyositis, visual field loss, leukoencephalopathy, lower extremity, field loss, white matter, visual field, signal, brain, mri, |
2,843 | Progressive loss of color vision OD. | Neurology | Meningioma | CC: ,Progressive loss of color vision OD,HX:, 58 y/o female presents with a one year history of progressive loss of color vision. In the past two months she has developed blurred vision and a central scotoma OD. There are no symptoms of photopsias, diplopia, headache, or eye pain. There are no other complaints. There have been mild fluctuations of her symptoms, but her vision has never returned to its baseline prior to symptom onset one year ago.,EXAM: ,Visual acuity with correction: 20/25+1 OD; 20/20-1 OS. Pupils were 3.5mm OU. There was a 0.8 log unit RAPD OD. Intraocular pressures were 25 and 24, OD and OS respectively; and there was an increase to 27 on upgaze OD, but no increase on upgaze OS. Optic disk pallor was evident OD, but not OS. Additionally, there was a small area of peripheral chorioretinal scarring in the inferotemporal area of the right eye. Foveal flicker fusion occurred at a frequency of 21.9 OD and 30.7 OS. Color plate testing scores: 6/14 OD and 10/14 OS. Goldman visual field examination showed an enlarged and deepened blind spot with an infero-temporal defect especially in the smaller diopters.,IMPRESSION ON 2/6/89: ,Optic neuropathy/atrophy OD, rule out mass lesion affecting optic nerve. Particular attention was paid to the area of the optic canal, cavernous sinus and sphenoid sinus.,BRAIN CT W/CONTRAST, 2/13/89:, Enhancing calcified lesion in the posterior aspect of the right optic nerve, probable meningioma.,MRI ORBITS W/ AND W/OUT GADOLINIUM CONTRAST, 4/26/89:, 7x3mm irregular soft tissue mass just inferior and lateral to the optic nerve OD. The mass is just proximal to the orbital apex. There is relatively homogeneous enhancement of the mass. The findings are most consistent with meningioma.,MRI 1995:, Mild enlargement of tumor with possible slight extension into the right cavernous sinus.,COURSE: ,Resection and biopsy were deferred due to risk of blindness, and suspicion that the tumor was a slow growing meningioma. 3 years after initial evaluation Hertel measurements indicated a 3mm proptosis OD. Visual field testing revealed gradual worsening of deficits seen on her initial Goldman visual field exam. There was greater red color desaturation of the temporal field OD. Visual acuity had decreased from 20/20 to 20/64, OD. All other deficits seen on her initial exam remained stable or slightly worsened. By 1996 she continued to be followed at 6 months intervals and had not undergone surgical resection. | neurology, goldman visual field examination, loss of color vision, visual field examination, visual acuity, cavernous sinus, color vision, visual field, optic nerve, meningioma, |
2,844 | A middle-aged female with memory loss. | Neurology | MRI Brain - Memory Loss | FINDINGS:,There is moderate to severe generalized neuronal loss of the cerebral hemispheres with moderate to severe ventricular enlargement and prominent CSF within the subarachnoid spaces. There is confluent white matter hyperintensity in a bi-hemispherical centrum semiovale distribution extending to the lateral ventricles consistent with severe vasculopathic small vessel disease and extensive white matter ischemic changes. There is normal enhancement of the dural sinuses and cortical veins and there are no enhancing intra-axial or extraaxial mass lesions. There is a cavum velum interpositum (normal variant).,There is a linear area of T1 hypointensity becoming hyperintense on T2 images in a left para-atrial trigonal region representing either a remote lacunar infarction or prominent perivascular space.,Normal basal ganglia and thalami. Normal internal and external capsules. Normal midbrain.,There is amorphus hyperintensity of the basis pontis consistent with vasculopathic small vessel disease. There are areas of T2 hyperintensity involving the bilateral brachium pontis (left greater than right) with no enhancement following gadolinium augmentation most compatible with areas of chronic white matter ischemic changes. The area of white matter signal alteration in the left brachium pontis is of some concern in that is has a round morphology. Interval reassessment of this lesion is recommended.,There is a remote lacunar infarction of the right cerebellar hemisphere. Normal left cerebellar hemisphere and vermis.,There is increased CSF within the sella turcica and mild flattening of the pituitary gland but no sellar enlargement. There is elongation of the basilar artery elevating the mammary bodies but no dolichoectasia of the basilar artery.,Normal flow within the carotid arteries and circle of Willis.,Normal calvarium, central skull base and temporal bones. There is no demonstrated calvarium metastases.,IMPRESSION:,Severe generalized cerebral atrophy.,Extensive chronic white matter ischemic changes in a bi-hemispheric centrum semiovale distribution with involvement of the basis pontis and probable bilateral brachium pontis. The area of white matter hyperintensity in the left brachium pontis is of some concern is that it has a round morphology but no enhancement following gadolinium augmentation. Interval reassessment of this lesion is recommended.,Remote lacunar infarction in the right cerebellar hemisphere.,Linear signal alteration of the left periatrial trigonal region representing either a prominent vascular space or,lacunar infarction.,No demonstrated calvarial metastases. | neurology, white matter ischemic, remote lacunar infarction, memory loss, matter ischemic, remote lacunar, cerebellar hemisphere, lacunar infarction, brachium pontis, white matter, basilar, calvarium, ischemic, enhancement, cerebellar, hemispheres, hyperintensity, infarction, brachium, |
2,845 | MRI Brain: Ventriculomegaly of the lateral, 3rd and 4th ventricles secondary to obstruction of the foramen of Magendie secondary to Cryptococcus (unencapsulated) in a non-immune suppressed, HIV negative, individual. | Neurology | MRI Brain - Cryptococcus | CC: ,Headache.,HX: ,This 37y/o LHM was seen one month prior to this presentation for HA, nausea and vomiting. Gastrointestinal evaluation at that time showed no evidence of bowel obstruction and he was released home. These symptoms had been recurrent since onset.,At presentation he complained of mild blurred vision (OU), difficulty concentrating and HA which worsened upon sitting up. The headaches were especially noticeable in the early morning. He described them as non-throbbing headaches. They begin in the bifrontal region and radiate posteriorly. They occurred up to 6 times/day. The HA improved with lying down or dropping the head down between the knees towards the floor. The headaches were associated with blurred vision, nausea,vomiting, photophobia, and phonophobia. He denied any scotomata or positive visual phenomena. He denies any weakness, numbness, tingling, dysarthria or diplopia. His weight has fluctuated from 163# to 148# over the past 3 months and at present he weighs 154#. His appetite has been especially poor in the past month.,MEDS:,Sulfasalazine qid. Tylenol 650mg q4hours.,PMH:, 1)Ulcerative Colitis dx 1989. 2)HTN 3) occasional HAs since the early 1980s which are different in character and much less severe than his current HAs. They were not associated with nausea, vomiting, photophobia, phonophobia or difficulty thinking.,FHX:, MGF with h/o stroke. Mother and Father were healthy. No h/o of migraine in family.,SHX:, Single. Works as a newpaper printing press worker. Denies tobacco, ETOH or illicit drug use, but admits he was a heavy drinker until the last 1970s when he quit.,EXAM: ,BP159/92 HR 48 (sitting): BP126/70 HR48 (supine). RR14 36.2C,MS: A&O to person, place and time. Speech clear. Appears uncomfortable but acts appropriately and cooperatively. No difficulty with short and long term memory.,CN: Grad 2-3 papilledema OS; Grade 1 papilledema (@2 o'clock) OD. Pupils 4/4 decreasing to 2/2 on exposure to light. Bilateral horizontal sustained nystagmus on right and leftward gaze. Bilateral vertical sustained nystagmus on up and downward gaze. Face symmetric with full movement and PP sensation. Tongue midline with full ROM. Gag and SCM were intact bilaterally.,Motor: Full strength throughout with normal muscle bulk and tone.,Sensory: Unremarkable.,Coord: Mild dysynergia on FNF movements in BUE. HNS and RAM were unremarkable.,Station: Unsteady with and without eyes open on Romberg test. No drift in any particular direction.,Gait: Wide based, ataxic and to some degree magnetic and apraxic.,Gen Exam: Unremarkable.,COURSE:, Urinalysis revealed 1-2RBC, 2-3WBC and bacteria were noted. Repeat Urinalysis was negative the next day. PT, PTT, CXR and GS were normal. CBC revealed 10.4WBC with 7.1Granulocytes. HCT, 10/18/95, revealed hydrocephalus. MRI, 10/18/95, revealed ventriculomegaly of the lateral, 3rd and 4th ventricles. There was enhancement of the meninges about the prepontine cisterna and internal auditory canals, and enhancement of a scar or inflammed lining of the foramen of Magendie. These changes were felt suggestive of bacterial or granulomatous meningitis. The patient underwent ventriculostomy on 10/19/94. CSF taken on 10/19/94 via V-P shunt insertion revealed: 22 WBC (21 lymphocytes, 1 monocyte), 380 RBC, Glucose 58, Protein 29, GS negative, Cultures (bacterial, fungal, AFB) negative, Cryptococcal Antigen and India Ink were negative. Numerous CSF samples were taken from the lumbar region and shunt reservoir and these were consistantly unremarkable except for an occasional CSF protein of up to 99mg/dl. Serum and CSF toxoplasma titers and ACE levels were negative on multiple occasions. VDRL and HIV testing was unremarkable. 10/27/94 and 10/31/94 CSF cultures taken from the cervical region eventually grew non-encapsulated crytococcus neoformans. The patient was treated with amphotericin and showed some improvement. However, scarring had probably occurred by then and the V-P shunt was left in place. | neurology, ventriculomegaly, foramen of magendie, mri brain, blurred vision, headache, brain, ventricles, cryptococcus, foramen, csf, |
2,846 | Problems with seizures, hemiparesis, has been to the hospital, developed C-diff, and is in the nursing home currently. | Neurology | Malignant Meningioma - Consult | REASON FOR VISIT: , This is a new patient evaluation for Mr. A. There is a malignant meningioma. He is referred by Dr. X.,HISTORY OF PRESENT ILLNESS: , He said he has had two surgeries in 07/06 followed by radiation and then again in 08/07. He then had a problem with seizures, hemiparesis, has been to the hospital, developed C-diff, and is in the nursing home currently. He is unable to stand at the moment. He is unable to care for himself. ,I reviewed the information that was sent down with him from the nursing home which includes his medical history.,MEDICATIONS: ,Keppra 1500 twice a day and Decadron 6 mg four times a day. His other medicines include oxycodone, an aspirin a day, Prilosec, Dilantin 300 a day, and Flagyl.,FINDINGS:, On examination, he is lying on the stretcher. He has oxygen on and has periods of spontaneous hyperventilation. He is unable to lift his right arm or right leg. He has an expressive dysphasia and confusion.,I reviewed the imaging studies from summer from the beginning of 10/07, end of 10/07 as well as the current MRI he had last week. This shows that he has had progression of disease with recurrence along the surface of the brain and there is significant brain edema. This is a malignant meningioma by diagnosis.,ASSESSMENT/PLAN: , In summary, Mr. A has significant disability and is not independent currently. I believe that because of this that the likelihood of benefit from surgery is small and there is a very good chance that he would not be able to recover from surgery. I do not think that surgery will help his quality of life and a need to control the tumor would be dependent on another therapy impacting the tumor. Given that there are not good therapies and chemotherapy would be the option at the moment, and he certainly is not in a condition where chemotherapy would be given, I believe that surgery would not be in his best interest. I discussed this both with him, although it is not clear to me how much he understood, as well as his family. | neurology, seizures, hemiparesis, tumor, seizures hemiparesis, malignant meningioma, chemotherapy, malignant, meningioma, aspirin |
2,847 | MRI Brain to evaluate sudden onset blindness - Basilar/bilateral thalamic strokes. | Neurology | MRI Brain - Bilateral Thalamic Strokes | CC:, Sudden onset blindness.,HX:, This 58 y/o RHF was in her usual healthy state, until 4:00PM, 1/8/93, when she suddenly became blind. Tongue numbness and slurred speech occurred simultaneously with the loss of vision. The vision transiently improved to "severe blurring" enroute to a local ER, but worsened again once there. While being evaluated she became unresponsive, even to deep noxious stimuli. She was transferred to UIHC for further evaluation. Upon arrival at UIHC her signs and symptoms were present but markedly improved.,PMH:, 1) Hysterectomy many years previous. 2) Herniorrhaphy in past. 3) DJD, relieved with NSAIDs.,FHX/SHX:, Married x 27yrs. Husband denied Tobacco/ETOH/illicit drug use for her.,Unremarkable FHx.,MEDS:, none.,EXAM:, Vitals: 36.9C. HR 93. BP 151/93. RR 22. 98% O2Sat.,MS: somnolent, but arousable to verbal stimulation. minimal speech. followed simple commands on occasion.,CN: Blinked to threat from all directions. EOM appeared full, Pupils 2/2 decreasing to 1/1. +/+Corneas. Winced to PP in all areas of Face. +/+Gag. Tongue midline. Oculocephalic reflex intact.,Motor: UE 4/5 proximally. Full strength in all other areas. Normal tone and muscle bulk.,Sensory: Withdrew to PP in all extremities.,Gait: ND.,Reflexes: 2+/2+ throughout UE, 3/3 patella, 2/2 ankles, Plantar responses were flexor bilaterally.,Gen exam: unremarkable.,COURSE: ,MRI Brain revealed bilateral thalamic strokes. Transthoracic echocardiogram (TTE) showed an intraatrial septal aneurysm with right to left shunt. Transesophageal echocardiogram (TEE) revealed the same. No intracardiac thrombus was found. Lower extremity dopplers were unremarkable. Carotid duplex revealed 0-15% bilateral ICA stenosis. Neuroophthalmologic evaluation revealed evidence of a supranuclear vertical gaze palsy OU (diminished up and down gaze). Neuropsychologic assessment 1/12-15/93 revealed severe impairment of anterograde verbal and visual memory, including acquisition and delayed recall and recognition. Speech was effortful and hypophonic with very defective verbal associative fluency. Reading comprehension was somewhat preserved, though she complained that despite the ability to see type clearly, she could not make sense of words. There was impairment of 2-D constructional praxis. A follow-up Neuropsychology evaluation in 7/93 revealed little improvement. Laboratory studies, TSH, FT4, CRP, ESR, GS, PT/PTT were unremarkable. Total serum cholesterol 195, Triglycerides 57, HDL 43, LDL 141. She was placed on ASA and discharged1/19/93.,She was last seen on 5/2/95 and was speaking fluently and lucidly. She continued to have mild decreased vertical eye movements. Coordination and strength testing were fairly unremarkable. She continues to take ASA 325 mg qd. | neurology, blindness, mri, transthoracic echocardiogram, transesophageal echocardiogram, tsh, ft4, crp, esr, gs, pt/ptt, bilateral thalamic strokes, sudden onset blindness, mri brain, thalamic strokes, brain, thalamic, strokes, |
2,848 | MRI Brain - Olfactory groove meningioma. | Neurology | MRI Brain - Meningioma (Olfactory) | CC:, Progressive visual loss.,HX:, 76 y/o male suddenly became anosmic following shoulder surgery 13 years prior to this presentation. He continues to be anosmic, but has also recently noted decreased vision OD. He denies any headaches, weakness, numbness, weight loss, or nasal discharge.,MEDS:, none.,PMH:, 1) Diabetes Mellitus dx 1 year ago. 2) Benign Prostatic Hypertrophy, s/p TURP. 3) Right shoulder surgery (?DJD).,FHX:, noncontributory.,SHX:, Denies history of Tobacco/ETOH/illicit drug use.,EXAM:, BP132/66 HR78 RR16 36.0C,MS: A&O to person, place, and time. No other specifics given in Neurosurgery/Otolaryngology/Neuro-ophthalmology notes.,CN: Visual acuity has declined from 20/40 to 20/400, OD; 20/30, OS. No RAPD. EOM was full and smooth and without nystagmus. Goldmann visual fields revealed a central scotoma and enlarged blind spot OD and OS (OD worse) with a normal periphery. Intraocular pressures were 15/14 (OD/OS). There was moderate pallor of the disc, OD. Facial sensation was decreased on the right side (V1 distribution).,Motor/Sensory/Coord/Station/Gait: were all unremarkable.,Reflexes: 2/2 and symmetric throughout. Plantars were flexor, bilaterally.,Gen Exam: unremarkable.,COURSE:, MRI Brain, 10/7/92, revealed: a large 6x5x6cm slightly heterogeneous, mostly isointense lesion on both T1 and T2 weighted images arising from the planum sphenoidale and olfactory groove. The mass extends approximately 3.6cm superior to the planum into both frontal regions with edema in both frontal lobes. The mass extends 2.5cm inferiorly involving the ethmoid sinuses with resultant obstruction of the sphenoid and frontal sinuses.,It also extends into the superomedial aspect of the right maxillary sinus. There is probable partial encasement of both internal carotid arteries just above the siphon. The optic nerves are difficult to visualize but there is also probable encasement of these structures as well. The mass enhances significantly with gadolinium contrast. These finds are consistent with Meningioma.,The patient underwent excision of this tumor by simultaneous bifrontal craniotomy and lateral rhinotomy following an intrasinus biopsy which confirmed the meningioma. Postoperatively, he lost visual acuity, OS, but this gradually returned to baseline. His 9/6/96 neuro-ophthalmology evaluation revealed visual acuity of 20/25-3 (OD) and 20/80-2 (OS). His visual fields continued to abnormal, but improved and stable when compared to 10/92. His anosmia never resolved. | neurology, mri brain, olfactory, groove, headaches, meningioma, nasal discharge, numbness, visual loss, weakness, weight loss, visual acuity, mri, brain, isointense, sinuses, visual, |
2,849 | Patient with sudden onset dizziness and RUE clumsiness. Giant Left MCA Aneurysm. | Neurology | MCA Aneurysm | HX: ,This 46y/o RHM with HTN was well until 2 weeks prior to exam when he experienced sudden onset dizziness and RUE clumsiness. The symptoms resolved within 10 min. He did well until the afternoon of admission when while moving the lawn he experienced lightheadedness, RUE dysfunction and expressive aphasia (could not get the words out). His wife took him to his local MD, and on the way there his symptoms resolved. His aphasia recurred at his physician's office and a CT scan of the brain revealed a left temporal mass. He was transferred to UIHC.,PMH:, HTN for many years,MEDS:, Vasotec and Dyazide,SHX/FHX:, ETOH abuse (quit '92), 30pk-yr Cigarettes (quit '92),EXAM:, BP158/92, HR91, RR16,MS: Speech fluent without dysarthria,CN: no deficits noted,Motor: no weakness or abnormal tone noted,Sensory: no deficits noted,Coord: normal,Station: no drift,Gait ND,Reflexes: 3+ throughout. Plantars down-going bilaterally.,Gen exam: unremarkable,STUDIES:, WBC14.3K, Na 132, Cl 94, CO2 22, Glucose 129.,CT Brain without contrast: Calcified 2.5 x 2.5cm mass arising from left sylvian fissure/temporal lobe.,MRI Brain, 8/31/92: right temporo-parietal mass with mixed signal on T1 and T2 images. It has a peripheral dark rim on T1 and T2 with surrounding edema. This suggests a component of methemoglobin and hemosiderin within it. Slight peripheral enhancement was identified. There are two smaller foci of enhancement in the posterior parietal lobe on the right. There is nonspecific white matter foci within the pons and right thalamus. Impression: right temporoparietal hemorrhage, suggesting aneurysm or mass. The two smaller foci may suggest metastasis. The white matter changes probably reflect microvascular disease.,3 Vessel cerebroangiogram, 8/31/92: Lobulated fusiform aneurysm off a peripheral branch of the left middle cerebral artery with slow flow into the vessel distal to the aneurysm.,COURSE:, The aneurysm was felt to be inoperable and he was discharged home on Dilantin, ASA, and Diltiazem. | neurology, mca aneurysm, rue clumsiness, white matter, aneurysm, mca, dizziness, aphasia, matter, clumsiness, brain, peripheral, |
2,850 | Briefly, the patient has a lumbosacral polyradiculopathy that is temporally related to the epidural anesthesia given to her in October of 2008. | Neurology | Lumbosacral Polyradiculopathy | HISTORY OF PRESENT ILLNESS: , The patient is a 35-year-old woman who reports that on the 30th of October 2008, she had a rupture of her membranes at nine months of pregnancy, and was admitted to hospital and was given an epidural anesthetic. I do not have the records from this hospital admission, but apparently the epidural was administered for approximately 14 to 18 hours. She was sitting up during the epidural.,She did not notice any difference in her lower extremities at the time she had the epidural; however, she reports that she was extremely sleepy and may not have been aware of any change in strength or sensation in her lower extremities at that time. She delivered on the 31st of October, by Cesarean section, because she had failed to progress and had pyrexia.,She also had a Foley catheter placed at that time. On the 1st of November 2008, they began to mobilize her and it was at that time that she first noticed that she could not walk. She was aware that she could not move her legs at all, and then within a few days, she was aware that she could move toes in the left foot but could not move her right foot at all. Since that time, there has been a gradual improvement in strength to the point that she now has limited movement in her left leg and severely restricted movement in her right leg. She is not able to walk by herself, and needs assistance to stand. She was discharged from hospital after the Cesarean section on the 3rd of November. Unfortunately, we do not have the records and we do not know what the discussion was between the anesthesiologist and the patient at the time of discharge. She was then seen at ABC Hospital on November 05, 2008. She had an MRI scan of her spine, which showed no evidence of an abnormality, specifically there were no cord changes and no evidence of a hematoma. She also had an EMG study at that time by Dr. X, which was abnormal but not diagnostic and this was repeated again in December. At the present time, she also complains of a pressure in both her legs and in her thighs. She complains that her right foot hurts and that she has some hyperesthesia there. She has been taking gabapentin to try to reduce the discomfort, although she is on a very low dose and the effect is minimal. She has no symptoms in her arms, her bowel and bladder function is normal, and her bulbar function is normal. There is no problem with her vision, swallowing, or respiratory function.,PAST MEDICAL HISTORY: , Unremarkable except as noted above. She has seasonal allergies.,CURRENT MEDICATIONS:, Gabapentin 300 mg b.i.d., Centrum once a day, and another multivitamin.,ALLERGIES: , She has no medication allergies, but does have seasonal allergies.,FAMILY HISTORY: , There is a family history of diabetes and hypertension. There is no family history of a neuropathy or other neurological disease. She has one child, a son, born on October 31, 2008.,SOCIAL HISTORY: , The patient is a civil engineer, who currently works from home. She is working approximately half time because of limitations imposed on her by her disability, need to attend frequent physical therapy, and also the needs of looking after her baby. She does not smoke and does not drink and has never done either.,GENERAL PHYSICAL EXAMINATION:,VITAL SIGNS: P 74, BP 144/75, and a pain score of 0.,GENERAL: Her general physical examination was unremarkable.,CARDIOVASCULAR: Normal first and second heart sound, regular pulse with normal volume.,RESPIRATORY: Unremarkable, both lung bases were clear, and respiration was normal.,GI: Unremarkable, with no organomegaly and normal bowel sounds.,NEUROLOGICAL EXAM:,MSE: The patient's orientation was normal, fund of knowledge was normal, memory was normal, speech was normal, calculation was normal, and immediate and long-term recall was normal. Executive function was normal.,CRANIAL NERVES: The cranial nerve examination II through XII was unremarkable. Both disks were normal, with normal retina. Pupils were equal and reactive to light. Eye movements were full. Facial sensation and strength was normal. Bulbar function was normal. The trapezius had normal strength.,MOTOR: Muscle tone showed a slight increase in tone in the lower extremities, with normal tone in the upper extremities. Muscle strength was 5/5 in all muscle groups in the upper extremities. In the lower extremities, the hip flexors were 1/5 bilaterally, hip extensors were 1/5 bilaterally, knee extension on the right was 1/5 and on the left was 3-/5, knee flexion was 2/5 on the right and 3-/5 on the left, foot dorsiflexion was 0/5 on the right and 1/5 on the left, foot plantar flexion was 4-/5 on the right and 4+/5 on the left, toe extension was 0/5 on the right and 4-/5 on the left, toe flexion was 4-/5 on the right and 4+/5 on the left.,REFLEXES: Reflexes in the upper extremities were 2+ bilaterally. In the lower extremities, they were 0 bilaterally at the knee and ankles. The abdominal reflexes were present above the umbilicus and absent below the umbilicus. The plantar responses were mute. The jaw reflex was normal.,SENSATION: Vibration was moderately decreased in the right great toe and was mildly decreased in the left great toe. There was a sensory level to light touch at approximately T7 posteriorly and approximately T9 anteriorly. There was a range of sensation, but clearly there was a decrease in sensation below this level but not complete loss of sensation. To pain, the sensory level is even less clear, but appeared to be at about T7 on the right side. In the lower extremities, there was a slight decrease in pin and light touch in the right great toe compared to the left. There was no evidence of allodynia or hyperesthesia. Joint position sense was mildly reduced in the right toe and normal on the left.,COORDINATION: Coordination for rapid alternating movements and finger-to-nose testing was normal. Coordination could not be tested in the lower extremities.,GAIT: The patient was unable to stand and therefore we were unable to test gait or Romberg's. There was no evidence of focal back tenderness.,REVIEW OF OUTSIDE RECORDS: , I have reviewed the records from ABC Hospital, including the letter from Dr. Y and the EMG report dated 12/17/2008 from Dr. X. The EMG report shows evidence of a lumbosacral polyradiculopathy below approximately T6. The lower extremity sensory responses are essentially normal; however, there is a decrease in the amplitude of the motor responses with minimal changes in latency. I do have the MRI of lumbar spine report from 11/06/2008 with and without contrast. This showed a minimal concentric disc bulge of L4-L5 without disc herniation, but was otherwise unremarkable. The patient brought a disc with a most recent MRI study; however, we were unable to open this on our computers. The verbal report is that the study was unremarkable except for some gadolinium enhancement in the lumbar nerve roots. A Doppler of the lower extremities showed no evidence of deep venous thrombosis in either lower extremity. Chest x-ray showed some scoliosis on the lumbar spine, curve to the left, but no evidence of other abnormalities. A CT pelvis study performed on November 07, 2008 showed some nonspecific fluid in the subcutaneous fat of the back, posterior to L4 and L5 levels; however, there were no pelvic masses or other abnormalities. We were able to obtain an update of the report from the MRI of the lumbar spine with and without contrast dated 12/30/2008. The complete study included the cervical, thoracic, and lumbar spine. There was diffuse enhancement of the nerve roots of the cauda equina that had increased in enhancement since prior exam in November. It was also reported that the patient was given intravenous methylprednisolone and this had had no effect on strength in her lower extremities.,IMPRESSION: , The patient has a condition that is temporarily related to the epidural injection she was given at the end of October 2008, prior to her Cesarean section. It appears she became aware of weakness within two days of the administration of the epidural, she was very tired during the epidural and may have missed some change in her neurological function. She was severely weak in both lower extremities, slightly worse on the right than the left. There has been some interval improvement in her strength since the beginning of November 2008. Her EMG study from the end of December is most consistent with a lumbosacral polyradiculopathy. The MRI findings of gadolinium enhancement in the lumbar nerve roots would be most consistent with an inflammatory radiculitis most likely related to the epidural anesthesia or administration of the epidural. There had been no response to IV methylprednisolone given to her at ABC. The issue of having a lumbar puncture to look for evidence of inflammatory cells or an elevated protein had been discussed with her at both ABC and by myself. The patient did not wish to consider a lumbar puncture because of concerns that this might worsen her condition. At the present time, she is able to stand with aid but is unable to walk. There is no evidence on her previous EMG of a demyelinating neuropathy.,RECOMMENDATIONS:,1. The diagnostic issues were discussed with the patient at length. She is informed that this is still early in the course of the problem and that we expect her to show some improvement in her function over the next one to two years, although it is unclear as to how much function she will regain.,2. She is strongly recommended to continue with vigorous physical therapy, and to continue with the plan to mobilize her as much as possible, with the goal of trying to get her ambulatory. If she is able to walk, she will need bilateral AFOs for her ankles, to improve her overall mobility. I am not prescribing these because at the present time she does not need them.,3. We discussed increasing the dose of gabapentin. The paresthesias that she has may indicate that she is actually regaining some sensory function, although there is a concern that as recovery continues, she may be left with significant neuropathic pain. If this is the case, I have advised her to increase her gabapentin dose from 300 mg b.i.d. gradually up to 300 mg four times a day and then to 600 mg to 900 mg four times a day. She may need other neuropathic pain medications as needed. She will determine whether her current symptoms are significant enough to require this increase in dosage.,4. The patient will follow up with Dr. Y and his team at ABC Hospital. She will also continue with physical therapy within the ABC system. | null |
2,851 | The patient with gradual onset of a headache problem, located behind both eyes. | Neurology | Migraine without Aura - Consult | CHIEF COMPLAINT:, Headaches.,HEADACHE HISTORY:, The patient describes the gradual onset of a headache problem. The headache first began 2 months ago. The headaches are located behind both eyes. The pain is characterized as a sensation of pressure. The intensity is moderately severe, making normal activities difficult. Associated symptoms include sinus congestion and photophobia. The headache may be brought on by stress, lack of sleep and alcohol. The patient denies vomiting and jaw pain.,PAST MEDICAL HISTORY:, No significant past medical problems.,PAST SURGICAL HISTORY:, ,No significant past surgical history.,FAMILY MEDICAL HISTORY:, ,There is a history of migraine in the family. The condition affects the patient’s brother and maternal grandfather.,ALLERGIES:, Codeine.,CURRENT MEDICATIONS:, See chart.,PERSONAL/SOCIAL HISTORY:, Marital status: Married. The patient smokes 1 pack of cigarettes per day. Denies use of alcohol.,NEUROLOGIC DRUG HISTORY:, The patient has had no help with the headaches from over-the-counter analgesics.,REVIEW OF SYSTEMS:,ROS General: Generally healthy. Weight is stable.,ROS Head and Eyes: Patient has complaints of headaches. Vision can best be described as normal.,ROS Ears Nose and Throat: The patient notes some sinus congestion.,ROS Cardiovascular: The patient has no history of any cardiovascular problems and denies any present problems.,ROS Gastrointestinal: The patient has no history of gastrointestinal problems and denies any present problems.,ROS Musculoskeletal: No muscle cramps, no joint back or limb pain. The patient denies any past or present problem related to the musculoskeletal system.,EXAM:,Exam General Appearance: The patient was alert and cooperative, and did not appear acutely or chronically ill.,Sex and Race: Male, Caucasian.,Exam Mental Status: Serial 7’s were performed normally. The patient was oriented with regard to time, place and situation.,Three out of three objects were readily recalled after several minutes. The patient correctly identified the president and past president. The patient could repeat 7 digits forward and 4 digits reversed without difficulty. The patient’s affect and emotional response was normal and appropriate. The patient related the clinical history in a coherent, organized fashion.,Exam Cranial Nerves: Sense of smell was intact.,Exam Neck: Neck range of motion was normal in all directions. There was no evidence of cervical muscle spasm. No radicular symptoms were elicited by neck motions. Shoulder range of motion was normal bilaterally. There were no areas of tenderness. Tests of neurovascular compression were negative. There were no carotid bruits.,Exam Back: Back range of motion was normal in all directions.,Exam Sensory: Position and vibratory sense was normal.,Exam Reflexes: Active and symmetrical. There were no pathological reflexes.,Exam Coordination: The patient’s gait had no abnormal components. Tandem gait was performed normally.,Exam Musculoskeletal: Peripheral pulses palpably normal. There is no edema or significant varicosities. No lesions identified.,IMPRESSION DIAGNOSIS: ,Migraine without aura (346.91),COMMENTS:, The patient has evolved into a chronic progressive course. Medications Prescribed: Therapeutic trial of Inderal 40mg - 1/2 tab b.i.d. x 1 week, then 1 tab. b.i.d. x 1 week then 1 tab t.i.d.,OTHER TREATMENT:, The patient was given a thorough explanation of the role of stress in migraine, and given a number of suggestions about implementing appropriate changes in lifestyle.,RATIONALE FOR TREATMENT PLAN:, The treatment plan chosen is the most effective and should result in the most beneficial outcome for the patient. There are no reasonable alternatives.,FOLLOW UP INSTRUCTIONS: | null |
2,852 | A 21-month-old male presented for delayed motor development, "jaw quivering" and "lazy eye." | Neurology | Lobar Holoprosencephaly | CC: ,Delayed motor development.,HX:, This 21 month old male presented for delayed motor development, "jaw quivering" and "lazy eye." He was an 8 pound 10 ounce product of a full term, uncomplicated pregnancy-labor-spontaneous vaginal delivery to a G3P3 married white female mother. There had been no known toxic intrauterine exposures. He had no serious illnesses or hospitalizations since birth. He sat independently at 7 months, stood at 11 months, crawled at 16 months, but did not cruise until 18 months.,He currently cannot walk and easily falls. His gait is reportedly marked by left "intoeing." His upper extremity strength and coordination reportedly appear quite normal and he is able to feed himself, throw and transfer objects easily. He knows greater than 20 words and speaks two-word phrases.,No seizures or unusual behavior were reported except for "quivering" movement of his jaw. This has occurred since birth. In addition the parents have noted transient left exotropia.,PMH: ,As above.,FHX:, Many family members with "lazy eye." No other neurologic diseases declared.,9 and 5 year old sisters who are healthy.,SHX:, lives with parents and sisters.,EXAM:, BP83/67 HR122 36.4C Head circumference 48.0cm Weight 12.68kg (70%) Height 86.0cm (70%),MS: fairly cooperative.,CN: Minimal transient esotropia OS. Tremulous quivering of jaw--increased with crying. No obvious papilledema, though difficult to evaluate due to patient movement.,Motor: sat independently with normal posture and no truncal ataxia. symmetric and normal strength and muscle bulk throughout.,Sensory: withdrew to vibration.,Coordination: unremarkable in BUE.,Station: no truncal ataxia.,Gait: On attempting to walk, his right foot rotated laterally at almost 70degrees. Both lower extremities could rotate outward to 90degrees. There was marked passive eversion at the ankles as well.,Reflexes: 2+/2+ throughout.,Musculoskeletal: pes planovalgus bilaterally.,COURSE: ,CK normal. The parents decided to forego an MRI in 8/90. The patient returned 12/11/92 at age 4 years. He was ambulatory and able to run awkwardly. His general health had been good, but he showed signs developmental delay. Formal evaluation had tested his IQ at 87 at age 3.5 years. He was weakest on tasks requiring visual/motor integration and fine motor and visual discrimination skills. He was 6 months delayed in cognitive development at that time. On exam, age 4 years, he displayed mild right ankle laxity on eversion and inversion, but normal gait. The rest of the neurological exam was normal. Head circumference was 49.5cm (50%) and height and weight were in the 90th percentile. Fragile X analysis and karyotyping were unremarkable. | neurology, delayed motor development, jaw quivering, head circumference, truncal ataxia, delayed motor, motor development, lazy eye, jaw, quivering, delayed, intrauterine, |
2,853 | Lumbar puncture with moderate sedation. | Neurology | Lumbar Puncture - 1 | PROCEDURE: , Lumbar puncture with moderate sedation.,INDICATION: , The patient is a 2-year, 2-month-old little girl who presented to the hospital with severe anemia, hemoglobin 5.8, elevated total bilirubin consistent with hemolysis and weak positive direct Coombs test. She was transfused with packed red blood cells. Her hemolysis seemed to slow down. She also on presentation had indications of urinary tract infection with urinalysis significant for 2+ leukocytes, positive nitrites, 3+ protein, 3+ blood, 25 to 100 white cells, 10 to 25 bacteria, 10 to 25 epithelial cells on clean catch specimen. Culture subsequently grew out no organisms; however, the child had been pretreated with amoxicillin about x3 doses prior to presentation to the hospital. She had a blood culture, which was also negative. She was empirically started on presentation with the cefotaxime intravenously. Her white count on presentation was significantly elevated at 20,800, subsequently increased to 24.7 and then decreased to 16.6 while on antibiotics. After antibiotics were discontinued, she increased over the next 2 days to an elevated white count of 31,000 with significant bandemia, metamyelocytes and myelocytes present. She also had three episodes of vomiting and thus she is being taken to the procedure room today for a lumbar puncture to rule out meningitis that may being inadvertently treated in treating her UTI.,I discussed with The patient's parents prior to the procedure the lumbar puncture and moderate sedation procedures. The risks, benefits, alternatives, complications including, but not limited to bleeding, infection, respiratory depression. Questions were answered to their satisfaction. They would like to proceed.,PROCEDURE IN DETAIL: , After "time out" procedure was obtained, the child was given appropriate monitoring equipment including appropriate vital signs were obtained. She was then given Versed 1 mg intravenously by myself. She subsequently became sleepy, the respiratory monitors, end-tidal, cardiopulmonary and pulse oximetry were applied. She was then given 20 mcg of fentanyl intravenously by myself. She was placed in the left lateral decubitus position. Dr. X cleansed the patient's back in a normal sterile fashion with Betadine solution. She inserted a 22-gauge x 1.5-inch spinal needle in the patient's L3-L4 interspace that was carefully identified under my direct supervision. Clear fluid was not obtained initially, needle was withdrawn intact. The patient was slightly repositioned by the nurse and Dr. X reinserted the needle in the L3-L4 interspace position, the needle was able to obtain clear fluid, approximately 3 mL was obtained. The stylette was replaced and the needle was withdrawn intact and bandage was applied. Betadine solution was cleansed from the patient's back.,During the procedure, there were no untoward complications, the end-tidal CO2, pulse oximetry, and other vitals remained stable. Of note, EMLA cream had also been applied prior procedure, this was removed prior to cleansing of the back.,Fluid will be sent for a routine cell count, Gram stain culture, protein, and glucose.,DISPOSITION: , The child returned to room on the medical floor in satisfactory condition. | neurology, moderate sedation, lumbar puncture, needle, lumbar, |
2,854 | Patient with a 1-year history of progressive anterograde amnesia | Neurology | Limbic Encephalitis | CC:, Rapidly progressive amnesia.,HX: ,This 63 y/o RHM presented with a 1 year history of progressive anterograde amnesia. On presentation he could not remember anything from one minute to the next. He also had some retrograde memory loss, in that he could not remember the names of his grandchildren, but had generally preserved intellect, language, personality, and calculating ability. He underwent extensive evaluation at the Mayo Clinic and an MRI there revealed increased signal on T2 weighted images in the mesiotemporal lobes bilaterally. There was no mass affect. The areas mildly enhanced with gadolinium.,PMH:, 1) CAD; MI x 2 (1978 and 1979). 2) PVD; s/p aortic endarterectomy (3/1991). 3)HTN. 4)Bilateral inguinal hernia repair.,FHX/SHX:, Mother died of a stroke at age 58. Father had CAD and HTN. The patient quit smoking in 1991, but was a heavy smoker (2-3ppd) for many years. He had been a feed salesman all of his adult life.,ROS:, Unremarkable. No history of cancer.,EXAM:, BP 136/75 HR 73 RR12 T36.6,MS: Alert but disoriented to person, place, time. He could not remember his birthdate, and continually asked the interviewer what year it was. He could not remember when he married, retired, or his grandchildren's names. He scored 18/30 on the Follutein's MMSE with severe deficits in orientation and memory. He had moderate difficulty naming. He repeated normally and had no constructional apraxia. Judgement remained good.,CN: unremarkable.,Motor: Full strength throughout with normal muscle tone and bulk.,Sensory: Intact to LT/PP/PROP,Coordination: unremarkable.,Station: No pronator drift, truncal ataxia or Romberg sign.,Gait: unremarkable.,Reflexes: 3+ throughout with downgoing plantar responses bilaterally.,Gen Exam: unremarkable.,STUDIES:, MRI Brain revealed hyperintense T2 signal in the mesiotemporal regions bilaterally, with mild enhancement on the gadolinium scans. MRI and CT of the chest and CT of the abdomen showed no evidence of lymphadenopathy or tumor. EEG was normal awake and asleep. Antineuronal antibody screening was unremarkable. CSF studies were unremarkable and included varicella zoster, herpes zoster, HIV and HTLV testing, and cytology. The patient underwent stereotactic brain biopsy at the Mayo Clinic which showed inflammatory changes, but no organism or etiology was concluded. TFT, B12, VDRL, ESR, CRP, ANA, SPEP and Folate studies were unremarkable. Neuropsychologic testing revealed severe anterograde memory (verbal and visual)loss, and less severe retrograde memory loss. Most other cognitive abilities were well preserved and the findings were consistent with mesiotemporal dysfunction bilaterally.,IMPRESSION:, Limbic encephalitis secondary to cancer of unknown origin.,He was last seen 7/26/96. MMSE 20/30 and category fluency 20 . Disinhibited affect. Mild right grasp reflex. The clinical course was benign and non-progressive, and unusual for such a diagnosis, though not unheard of . | neurology, mri brain, progressive anterograde amnesia, retrograde memory loss, limbic encephalitis, anterograde amnesia, memory loss, limbic, encephalitis, amnesia, anterograde, memory, |
2,855 | Lumbar discogram L2-3, L3-4, L4-5, and L5-S1. Low back pain. | Neurology | Lumbar Discogram | PREOPERATIVE DIAGNOSIS: , Low back pain.,POSTOPERATIVE DIAGNOSIS: , Low back pain.,PROCEDURE PERFORMED:,1. Lumbar discogram L2-3.,2. Lumbar discogram L3-4.,3. Lumbar discogram L4-5.,4. Lumbar discogram L5-S1.,ANESTHESIA: ,IV sedation.,PROCEDURE IN DETAIL: ,The patient was brought to the Radiology Suite and placed prone onto a radiolucent table. The C-arm was brought into the operative field and AP, left right oblique and lateral fluoroscopic images of the L1-2 through L5-S1 levels were obtained. We then proceeded to prepare the low back with a Betadine solution and draped sterile. Using an oblique approach to the spine, the L5-S1 level was addressed using an oblique projection angled C-arm in order to allow for perpendicular penetration of the disc space. A metallic marker was then placed laterally and a needle entrance point was determined. A skin wheal was raised with 1% Xylocaine and an #18-gauge needle was advanced up to the level of the disc space using AP, oblique and lateral fluoroscopic projections. A second needle, #22-gauge 6-inch needle was then introduced into the disc space and with AP and lateral fluoroscopic projections, was placed into the center of the nucleus. We then proceeded to perform a similar placement of needles at the L4-5, L3-4 and L2-3 levels.,A solution of Isovue 300 with 1 gm of Ancef was then drawn into a 10 cc syringe and without informing the patient of our injecting, we then proceeded to inject the disc spaces sequentially. | neurology, back pain, c-arm, fluoroscopic projections, disc space, lumbar discogram, fluoroscopic, needle, |
2,856 | Possible CSF malignancy. This is an 83-year-old woman referred for diagnostic lumbar puncture for possible malignancy by Dr. X. The patient has gradually stopped walking even with her walker and her left arm has become gradually less functional. She is not able to use the walker because her left arm is so weak. | Neurology | Lumbar Puncture | REASON FOR VISIT: ,This is an 83-year-old woman referred for diagnostic lumbar puncture for possible malignancy by Dr. X. She is accompanied by her daughter.,HISTORY OF PRESENT ILLNESS:, The patient' daughter tells me that over the last month the patient has gradually stopped walking even with her walker and her left arm has become gradually less functional. She is not able to use the walker because her left arm is so weak. She has not been having any headaches. She has had a significant decrease in appetite. She is known to have lung cancer, but Ms. Wilson does not know what kind. According to her followup notes, it is presumed non-small cell lung cancer of the left upper lobe of the lung. The last note I have to evaluate is from October 2008. CT scan from 12/01/2009 shows atrophy and small vessel ischemic change, otherwise a normal head CT, no mass lesion. I also reviewed the MRI from September 2009, which does not suggest normal pressure hydrocephalus and shows no mass lesion.,Blood tests from 11/18/2009 demonstrate platelet count at 132 and INR of 1.0.,MAJOR FINDINGS: , The patient is a pleasant and cooperative woman who answers the questions the best she can and has difficulty moving her left arm and hand. She also has pain in her left arm and hand at a level of 8-9/10.,VITAL SIGNS: , Blood pressure 126/88, heart rate 70, respiratory rate 16, and weight 95 pounds.,I screened the patient with questions to determine whether it is likely she has abnormal CSF pressure and she does not have any of the signs that would suggest this, so we performed the procedure in the upright position.,PROCEDURE:, Lumbar puncture, diagnostic (CPT 62270).,PREOPERATIVE DIAGNOSIS: , Possible CSF malignancy.,POSTOPERATIVE DIAGNOSIS: ,To be determined after CSF evaluation.,PROCEDURE PERFORMED: , Lumbar puncture.,ANESTHESIA: , Local with 2% lidocaine at the L4-L5 level.,SPECIMEN REMOVED: ,15 cc of clear CSF.,ESTIMATED BLOOD LOSS: , None.,DESCRIPTION OF THE PROCEDURE: ,I explained the procedure, its rationale, risks, benefits, and alternatives to the patient and her daughter. The patient' daughter remained present throughout the procedure. The patient provided written consent and her daughter signed as witness to the consent.,I located the iliac crest and spinous processes before the procedure and determined the level I planned for the puncture. During the procedure, I spoke constantly with the patient to explain what was happening and to warn when there might be pain or discomfort. The skin was prepped with chlorhexidine solution with the patient seated on the chair leaning forward with her face resting on the exam table. Using local anesthetic and aseptic technique, I inserted a 20-gauge spinal needle at the L4-L5 interspace and 15 cc of CSF was collected without difficulty.,The patient tolerated the procedure well.,ASSESSMENT: ,White blood cells 1, red blood cells 54, glucose 59, protein 51, Gram stain negative, bacterial culture negative after three days, and remaining tests pending. | null |
2,857 | The patient comes in today because of feeling lightheaded and difficulty keeping his balance. | Neurology | Lightheadedness | HISTORY OF PRESENT ILLNESS: ,The patient comes in today because of feeling lightheaded and difficulty keeping his balance. He denies this as a spinning sensation that he had had in the past with vertigo. He just describes as feeling very lightheaded. It usually occurs with position changes such as when he stands up from the sitting position or stands up from a lying position. It tends to ease when he sits down again, but does not totally resolve for another 15 to 30 minutes and he feels shaky and weak all over. Lorazepam did not help this sensation. His blood pressure has been up lately and his dose of metoprolol was increased. They feel these symptoms have gotten worse since metoprolol was increased.,PAST MEDICAL HISTORY: , Detailed on our H&P form. Positive for elevated cholesterol, diabetes, glaucoma, cataracts, hypertension, heart disease, vertigo, stroke in May of 2005, congestive heart failure, CABG, and cataract removed right eye.,CURRENT MEDICATIONS: , Detailed on the H&P form.,PHYSICAL EXAMINATION: , His blood pressure sitting down was 180/80 with a pulse rate of 56. Standing up blood pressure was 160/80 with a pulse rate of 56. His general exam and neurological exam were detailed on our H&P form. Pertinent positives on his neurological exam were decreased sensation in his left face, and left arm and leg.,IMPRESSION AND PLAN: ,This lightheaded, he exquisitely denies vertigo, the vertigo that he has had in the past. He states this is more of a lightheaded type feeling. He did have a mild blood pressure drop here in the office. We are also concerned that bradycardia might be contributing to his feeling of lightheadedness. We are going to suggest that he gets a Holter monitor and he should speak to his general practitioner as well as his cardiologist regarding the lightheaded feeling.,We will schedule him for the Holter monitor and refer him back to his cardiologist. | neurology, lightheaded feeling, feeling lightheaded, pulse rate, neurological exam, holter monitor, blood pressure, balance, vertigo, lightheadedness, |
2,858 | Headache, improved. Intracranial aneurysm. | Neurology | Intracranial aneurysm - ER Visit | CHIEF COMPLAINT:, Headache.,HPI: , This is a 24-year-old man who was seen here originally on the 13th with a headache and found to have a mass on CT scan. He was discharged home with a follow up to neurosurgery on the 14th. Apparently, an MRI the next day showed that the mass was an aneurysm and he is currently scheduled for an angiogram in preparation for surgery. He has had headaches since the 13th and complains now of some worsening of his pain. He denies photophobia, fever, vomiting, and weakness of the arms or legs.,PMH: , As above.,MEDS:, Vicodin.,ALLERGIES:, None.,PHYSICAL EXAM: ,BP 180/110 Pulse 65 RR 18 Temp 97.5.,Mr. P is awake and alert, in no apparent distress.,HEENT: Pupils equal, round, reactive to light, oropharynx moist, sclera clear. ,Neck: Supple, no meningismus.,Lungs: Clear.,Heart: Regular rate and rhythm, no murmur, gallop, or rub. ,Abdomen: Benign.,Neuro: Awake and alert, motor strength normal, no numbness, normal gait, DTRs normal. Cranial nerves normal. ,COURSE IN THE ED: ,Patient had a repeat head CT to look for an intracranial bleed that shows an unchanged mass, no blood, and no hydrocephalus. I recommended an LP but he prefers not to have this done. He received morphine for pain and his headache improved. I've recommended admission but he has chosen to go home and come back in the morning for his scheduled angiogram. He left the ED against my advice. ,IMPRESSION: , Headache, improved. Intracranial aneurysm.,PLAN: , The patient will return tomorrow am for his angiogram. | neurology, angiogram, mass, ct scan, intracranial aneurysm, headache, aneurysm, intracranial, |
2,859 | Right shoulder impingement syndrome, right suprascapular neuropathy. | Neurology | Impairment Rating | CHIEF COMPLAINT: , Right shoulder pain.,HISTORY: , The patient is a pleasant, 31-year-old, right-handed, white female who injured her shoulder while transferring a patient back on 01/01/02. She formerly worked for Veteran's Home as a CNA. She has had a long drawn out course of treatment for this shoulder. She tried physical therapy without benefit and ultimately came to a subacromion decompression in November 2002. She had ongoing pain and was evaluated by Dr. X who felt that she had a possible brachial plexopathy. He also felt she had a right superficial radial neuritis and blocked this with resolution of her symptoms. He then referred her to ABCD who did EMG testing, demonstrating a right suprascapular neuropathy although a C5 radiculopathy could not be ruled out. MRI testing on the cervical spine was then done which was negative for disk herniation and she underwent suprascapular nerve decompression of the scapular notch on 12/18/03. She finally went to an anterior axillary nerve block because of ongoing pain in the anterior shoulder again by Dr. X. She comes to me for impairment rating. She has no chronic health problems otherwise, fevers, chills, or general malaise. She is not working. She is right-hand dominant. She denies any prior history of injury to her shoulder.,PAST MEDICAL HISTORY:, Negative aside from above.,FAMILY HISTORY: , Noncontributory.,SOCIAL HISTORY: ,Please see above.,REVIEW OF SYSTEMS:, Negative aside from above.,PHYSICAL EXAMINATION: ,A pleasant, age appropriate woman, moderately overweight, in no apparent distress. Normal gait and station, normal posture, normal strength, tone, sensation and deep tendon reflexes with the exception of 4+/5 strength in the supraspinatus musculature on the right. She has decreased motion in the right shoulder as follows. She has 160 degrees of flexion, 155 degrees of abduction, 35 degrees of extension, 25 degrees of adduction, 45 degrees of internal rotation and 90 degrees of external rotation. She has a positive impingement sign on the right.,ASSESSMENT:, Right shoulder impingement syndrome, right suprascapular neuropathy.,DISCUSSION: , With a reasonable degree of medical certainty, she is at maximum medical improvement and she does have an impairment based on AMA Guide to the Evaluation of Permanent Impairment, Fifth Edition. The reason for this impairment is the incident of 01/01/02. For her suprascapular neuropathy, she is rated as a grade IV motor deficit which I rate as a 13% motor deficit. This is multiplied by a maximum upper extremity impairment for involvement of the suprascapular nerve of 16% which produces a 2% impairment of the upper extremity when the two values are multiplied together, 2% impairment of the upper extremity. For her lack of motion in the shoulder she also has additional impairment on the right. She has a 1% impairment of the upper extremity due to lack of shoulder flexion. She has a 1% impairment of the upper extremity due to lack of shoulder abduction. She has a 1% impairment of the upper extremity due to lack of shoulder adduction. She has a 1% impairment of the upper extremity due to lack of shoulder extension. There is no impairment for findings in shoulder external rotation. She has a 3% impairment of the upper extremity due to lack of shoulder internal rotation. Thus the impairment due to lack of motion in her shoulder is a 6% impairment of the upper extremity. This combines with the 2% impairment of the upper extremity due to weakness in the suprascapular nerve root distribution to produce an 8% impairment of the upper extremity which in turn is a 5% impairment of the whole person based on the AMA Guide to the Evaluation of Permanent Impairment, Fifth Edition, stated with a reasonable degree of medical certainty. | neurology, ama guide, evaluation of permanent impairment, impairment rating, permanent impairment, suprascapular nerve, suprascapular neuropathy, injured, extremity, shoulder, impairment, neuropathy, suprascapular, |
2,860 | Woman with adult hydrocephalus, routine evaluation. | Neurology | Hydrocephalus | REASON FOR VISIT: , Ms. ABC is a 67-year-old woman with adult hydrocephalus who returns to clinic for a routine evaluation. She comes to clinic by herself.,HISTORY OF PRESENT ILLNESS:, She has been followed for her hydrocephalus since 2002. She also had an anterior cervical corpectomy and fusion from C3 though C5 in March 2007. She was last seen by us in clinic in March 2008 and she was experiencing little bit of head fullness and ringing in the ears at that time; however, we decided to leave her shunt setting at 1.0. We wanted her to followup with Dr. XYZ regarding the MRI of the cervical spine. Today, she tells me that with respect to her bladder last week she had some episodes of urinary frequency, however, this week she is not experiencing the same type of episodes. She reports no urgency, incontinence, and feels that she completely empties her bladder when she goes. She does experience some leakage with coughing. She wears the pad on a daily basis. She does not think that her bladder has changed much since we saw her last. With respect to her thinking and memory, she reports no problems at this time. She reports no headaches at this time. With respect to her walking and balance, she says that it feels worse. In the beginning of May, she had a coughing spell and at that time she developed buttock pain, which travels down the legs. She states that her leg often feel like elastic and she experiences a tingling radiculopathy. She says that this tingling is constant and at times painful. She feels that she is walking slower for this reason. She does not use the cane at this time. Most of the time, she is able to walk over uneven surfaces. She is able to walk up and down stairs and has no trouble getting in and out of a car.,MEDICATIONS:, Rhinocort 32 mg two sprays a day, Singulair 10 mg once a day, Xyzal 5 mg in the morning, Spiriva once a day, Advair twice a day, Prevacid 30 mg twice a day, Os-Cal 500 mg once a day, multivitamin once a day, and aspirin 81 mg a day.,MAJOR FINDINGS:, On exam today, this is a pleasant 67-year-old woman who comes back from the clinic waiting area with little difficulty. She is well developed, well nourished, and kempt.,The shunt site is clean, dry, and intact and confirmed at a setting of 1.0.,Mental Status: Assessed and appears intact for orientation, recent and remote memory, attention span, concentration, language, and fund of knowledge. Her Mini-Mental Status exam score was 26/30 when attention was tested with calculations and 30/30 when attention was tested with spelling.,Cranial Nerves: Extraocular movements are somewhat inhibited. She does not display any nystagmus at this time. Facial movement, hearing, head turning, tongue, and palate movement are all intact.,Gait: Assessed using the Tinetti assessment tool, which showed a balance score of 13/16 and a gait score of 11/12 for a total score of 24/28.,ASSESSMENT:, Ms. ABC has been experiencing difficulty with walking over the past several months.,PROBLEMS/DIAGNOSES:,1. Hydrocephalus.,2. Cervical stenosis and retrolisthesis.,3. Neuropathy in the legs.,PLAN: , Before we recommend anything more, we would like to get a hold of the notes from Dr. XYZ to try to come up with a concrete plan as to what we can do next for Ms. ABC. We believe that her walking is most likely not being effected by the hydrocephalus. We would like to see her back in clinic in two and a half months or so. We also talked to her about having her obtain cane training so that she knows how to properly use her cane, which she states she does have one. I suggested that she use the cane at her on discretion. | neurology, cervical stenosis, retrolisthesis, neuropathy, cervical corpectomy, adult hydrocephalus, cervical, hydrocephalus, |
2,861 | Right iliopsoas hematoma with associated femoral neuropathy following cardiac catherization. | Neurology | Iliopsoas Hematoma - 2 | CC: ,RLE weakness.,HX: ,This 42y/o RHM was found 2/27/95 slumped over the steering wheel of the Fed Ex truck he was driving. He was cyanotic and pulseless according to witnesses. EMT evaluation revealed him to be in ventricular fibrillation and he was given epinephrine, lidocaine, bretylium and electrically defibrillated and intubated in the field. Upon arrival at a local ER his cardiac rhythm deteriorated and he required more than 9 counter shocks (defibrillation) at 360 joules per shock, epinephrine and lidocaine. This had no effect. He was then given intracardiac epinephrine and a subsequent electrical defibrillation placed him in atrial fibrillation. He was then taken emergently to cardiac catherization and was found to have normal coronary arteries. He was then admitted to an intensive care unit and required intraortic balloon pump pressure support via the right gorin. His blood pressure gradually improved and his balloon pump was discontinued on 5/5/95. Recovery was complicated by acute renal failure and liver failure. Initail CK=13,780, the CKMB fraction was normal at 0.8.,On 3/10/95, the patient experienced CP and underwent cardiac catherization. This time he was found to have a single occlusion in the distal LAD with association inferior hypokinesis. Subsequent CK=1381 and CKMB=5.4 (elevated). The patient was amnestic to the event and for 10 days following the event. He was transferred to UIHC for cardiac electrophysiology study.,MEDS: ,Nifedipine, ASA, Amiodarone, Capoten, Isordil, Tylenol, Darvocet prn, Reglan prn, Coumadin, KCL, SLNTG prn, CaCO3, Valium prn, Nubain prn.,PMH:, hypercholesterolemia.,FHX:, Father alive age 69 with h/o TIAs. Mother died age 62 and had CHF, A-Fib, CAD. Maternal Grandfather died of an MI and had h/o SVT. Maternal Grandmother had h/o SVT.,SHX: ,Married, 7 children, driver for Fed Ex. Denied tobacco/ETOH/illicit drug use.,EXAM: ,BP112/74 HR64 RR16 Afebrile.,MS: A&O to person, place and time. Euthymic with appropriate affect.,CN: unremarkable.,Motor: Hip flexion 3/5, Hip extension 5/5, Knee flexion5/5, Knee extension 2/5, Plantar flexion, extension, inversion and eversion 5/5. There was full strength thoughout BUE.,Sensory: decreased PP/Vib/LT/TEMP about anterior aspect of thigh and leg in a femoral nerve distribution.,Coord: poor and slowed HKS on right due to weakness.,Station: no drift or Romberg sign.,Gait: difficulty bearing weight on RLE.,Reflexes: 1+/1+ throughout BUE. 0/2 patellae. 2/2 archilles. Plantar responses were flexor, bilaterally.,COURSE:, MRI Pelvis, 3/28/95, revealed increased T1 weighted signal within the right iliopsoas suggestive of hematoma. An intra-osseous lipoma was incidentally notice in the right sacrum. Neuropsychologic assessment showed moderately compromised anterograde verbal memory, and temporal orientation and retrograde recall were below expectations. These findings were consistent with mesial temporal dysfunction secondary to anoxic injury and were mild in lieu of his history. He underwent implantation of a Medtronic internal cardiac difibrillator. His cardiac electrophysiology study found no inducible ventricular tachycardia or fibrillation. He suffered mild to moderate permanent RLE weakness, especially involving the quadriceps. His femoral nerve compression had been present to long to warrant decompression. EMG/NCV studies revealed severe axonal degeneration. | neurology, cardiac electrophysiology study, iliopsoas hematoma, rle weakness, balloon pump, femoral nerve, cardiac catherization, hematoma, iliopsoas, catherization, epinephrine, fibrillation, cardiac, |
2,862 | Left Iliopsoas hematoma. Gait difficulty. | Neurology | Iliopsoas Hematoma - 1 | CC: ,Gait difficulty.,HX: ,This 59 y/o RHF was admitted with complaint of gait difficulty. The evening prior to admission she noted sudden onset of LUE and LLE weakness. She felt she favored her right leg, but did not fall when walking. She denied any associated dysarthria, facial weakness, chest pain, SOB, visual change, HA, nausea or vomiting.,PMH:, tonsillectomy, adenoidectomy, skull fx 1954, HTN, HA.,MEDS: ,none on day of exam.,SHX: ,editorial assistant at newspaper, 40pk-yr Tobacco, no ETOH/Drugs.,FHX: ,noncontributory,ADMIT EXAM: ,P95 R20, T36.6, BP169/104,MS: A&O to person, place and time. Speech fluent and without dysarthria, Naming-comprehension-reading intact. Euthymic with appropriate affect.,CN: Pupils 4/4 decreasing to 2/2 on exposure to light, Fundi flat, VFFTC, EOMI, Face symmetric with intact sensation, Gag-shrug-corneal reflexes intact, Tongue ML with full ROM,Motor: Full strength throughout right side. Mildly decreased left grip and left extensor hallucis longus. Biceps/Triceps/Wrist flexors and extensor were full strength on left. However she demonstrated mild LUE pronator drift and had difficulty standing on her LLE despite full strength on bench testing of the LLE.,Sensory: No deficit to PP/T/Vib/Prop/ LT,Coord: decreased speed and magnitude of FNF, Finger tapping and HKS, on left side only.,Station: mild LUE upward drift.,Gait: tendency to drift toward the left. Difficulty standing on LLE.,Reflexes were symmetric, plantar responses were flexor bilaterally.,Gen exam unremarkable.,COURSE: ,Admit Labs: ESR, PT/PTT, GS, UA, EKG, and HCT were unremarkable. Hgb 13.9, Hct 41%, Plt 280k, WBC 5.5.,The patient was diagnosed with a probable lacunar stroke and entered into the TOAST study (Trial of ORG10172[a low molecular weight heparin] in Acute Stroke Treatment).,Carotid Duplex: 16-49%RICA and 0-15%LICA stenosis with anterograde vertebral artery flow, bilaterally. Transthoracic echocardiogram showed mild mitral regurgitation, mild tricuspid regurgitation and a left to right shunt. There was no evidence of blood clot.,Hospital course: 5 days after admission the patient began to complain of proximal LLE and left flank pain. On exam, she had weakness of the quadriceps and hip flexors of the LLE. Her pain increased with left hip flexion. In addition, she complained of paresthesias about the lateral aspect of the medial anterior left thigh; and upon on sensory testing, she had decreased PP/TEMP sensation in a left femoral nerve distribution. She denied any back/neck pain and the rest of her neurologic exam remained unchanged from admission.,Abdominal CT Scan, 2/4/96, revealed a large left retroperitoneal iliopsoas hematoma.,Hgb 8.9g/dl. She was transfused with 4 units of pRBCs. She underwent surgical decompression and evacuation of the hematoma via a posterior flank approach on 2/6/96. Her postoperative course was uncomplicated. She was discharged home on ASA.,At follow-up, on 2/23/96, she complained of left sided paresthesias (worse in the LLE than in the LUE) and feeling of "swollen left foot." These symptoms had developed approximately 1 month after her stroke. Her foot looked normal and her UE strength was 5/4+ proximally and distally, and LE strength 5/4+ proximally and 5/5- distally. She was ambulatory. There was no evidence of LUE upward drift. A somatosensory evoked potential study revealed an absent N20 and normal P14 potentials. This was suggestive of a lesion involving the right thalamus which might explain her paresthesia/dysesthesia as part of a Dejerine-Roussy syndrome. | null |
2,863 | Followup status post L4-L5 laminectomy and bilateral foraminotomies, and L4-L5 posterior spinal fusion with instrumentation. | Neurology | Laminectomy & Foraminotomy Followup | REASON FOR VISIT:, Followup status post L4-L5 laminectomy and bilateral foraminotomies, and L4-L5 posterior spinal fusion with instrumentation.,HISTORY OF PRESENT ILLNESS:, Ms. ABC returns today for followup status post L4-L5 laminectomy and bilateral foraminotomies, and posterior spinal fusion on 06/08/07.,Preoperatively, her symptoms, those of left lower extremity are radicular pain.,She had not improved immediately postoperatively. She had a medial breech of a right L4 pedicle screw. We took her back to the operating room same night and reinserted the screw. Postoperatively, her pain had improved.,I had last seen her on 06/28/07 at which time she was doing well. She had symptoms of what she thought was "restless leg syndrome" at that time. She has been put on ReQuip for this.,She returned. I had spoken to her 2 days ago and she had stated that her right lower extremity pain was markedly improved. I had previously evaluated this for a pain possibly relating to deep venous thrombosis and ultrasound was negative. She states that she had recurrent left lower extremity pain, which was similar to the pain she had preoperatively but in a different distribution, further down the leg. Thus, I referred her for a lumbar spine radiograph and lumbar spine MRI and she presents today for evaluation.,She states that overall, she is improved compared to preoperatively. She is ambulating better than she was preoperatively. The pain is not as severe as it was preoperatively. The right leg pain is improved. The left lower extremity pain is in a left L4 and L5 distribution radiating to the great toe and first web space on the left side.,She denies any significant low back pain. No right lower extremity symptoms.,No infectious symptoms whatsoever. No fever, chills, chest pain, shortness of breath. No drainage from the wound. No difficulties with the incision.,FINDINGS: ,On examination, Ms. ABC is a pleasant, well-developed, well-nourished female in no apparent distress. Alert and oriented x 3. Normocephalic, atraumatic. Respirations are normal and nonlabored. Afebrile to touch.,Left tibialis anterior strength is 3 out of 5, extensor hallucis strength is 2 out of 5. Gastroc-soleus strength is 3 to 4 out of 5. This has all been changed compared to preoperatively. Motor strength is otherwise 4 plus out of 5. Light touch sensation decreased along the medial aspect of the left foot. Straight leg raise test normal bilaterally.,The incision is well healed. There is no fluctuance or fullness with the incision whatsoever. No drainage.,Radiographs obtained today demonstrate pedicle screw placement at L4 and L5 bilaterally without evidence of malposition or change in orientation of the screws.,Lumbar spine MRI performed on 07/03/07 is also reviewed.,It demonstrates evidence of adequate decompression at L4 and L5. There is a moderate size subcutaneous fluid collection seen, which does not appear compressive and may be compatible with normal postoperative fluid collection, especially given the fact that she had a revision surgery performed.,ASSESSMENT AND PLAN: ,Ms. ABC is doing relatively well status post L4 and L5 laminectomy and bilateral foraminotomies, and posterior spinal fusion with instrumentation on 07/08/07. The case is significant for merely misdirected right L4 pedicle screw, which was reoriented with subsequent resolution of symptoms.,I am uncertain with regard to the etiology of the symptoms. However, it does appear that the radiographs demonstrate appropriate positioning of the instrumentation, no hardware shift, and the MRI demonstrates only a postoperative suprafascial fluid collection. I do not see any indication for another surgery at this time.,I would also like to hold off on an interventional pain management given the presence of the fluid collection to decrease the risk of infection.,My recommendation at this time is that the patient is to continue with mobilization. I have reassured her that her spine appears stable at this time. She is happy with this.,I would like her to continue ambulating as much as possible. She can go ahead and continue with ReQuip for the restless leg syndrome as her primary care physician has suggested. I have also her referred to Mrs. Khan at Physical Medicine and Rehabilitation for continued aggressive management.,I will see her back in followup in 3 to 4 weeks to make sure that she continues to improve. She knows that if she has any difficulties, she may follow up with me sooner. | neurology, spinal fusion, restless leg syndrome, posterior spinal fusion, pedicle screw, lumbar spine, bilateral foraminotomies, fluid collection, foraminotomy, instrumentation, laminectomy, screw, spine, |
2,864 | A male with known alcohol cirrhosis who presented to the emergency room after an accidental fall in the bathroom. | Neurology | Hepatic Encephalopathy | REASON FOR ADMISSION: , Hepatic encephalopathy.,HISTORY OF PRESENT ILLNESS: , The patient is a 51-year-old Native American male with known alcohol cirrhosis who presented to the emergency room after an accidental fall in the bathroom. He said that he was doing fine prior to that and denied having any complaints. He was sitting watching TV and he felt sleepy. So, he went to the bathroom to urinate before going to bed and while he was trying to lift the seat, he tripped and fell and hit his head on the back. His head hit the toilet seat. Then, he started having bleeding and had pain in the area with headache. He did not lose consciousness as far as he can tell. He went and woke up his sister. This happened somewhere between 10:30 and 11 p.m. His sister brought a towel and covered the laceration on the back of his head and called EMS, who came to his house and brought him to the emergency room, where he was found to have a laceration on the back of his head, which was stapled and a CT of the head was obtained and ruled out any acute intracranial pathology. On his lab work, his ammonia was found to be markedly elevated at 106. So, he is being admitted for management of this. He denied having any abdominal pain, change in bowel habits, GI bleed, hematemesis, melena, or hematochezia. He said he has been taking his medicines, but he could not recall those. He denied having any symptoms prior to this fall. He said earlier today he also fell. He also said that this was an accidental fall caused by problem with his walker. He landed on his back at that time, but did not have any back pain afterwards.,PAST MEDICAL HISTORY:,1. Liver cirrhosis caused by alcohol. This is per the patient.,2. He thinks he is diabetic.,3. History of intracranial hemorrhage. He said it was subdural hematoma. This was traumatic and happened seven years ago leaving him with the right-sided hemiparesis.,4. He said he had a seizure back then, but he does not have seizures now.,PAST SURGICAL HISTORY:,1. He has a surgery on his stomach as a child. He does not know the type.,2. Surgery for a leg fracture.,3. Craniotomy seven years ago for an intracranial hemorrhage/subdural hematoma.,MEDICATIONS: , He does not remember his medications except for the lactulose and multivitamins.,ALLERGIES: , Dilantin.,SOCIAL HISTORY: , He lives in Sacaton with his sister. He is separated from his wife who lives in Coolidge. He smokes one or two cigarettes a day. Denies drug abuse. He used to be a heavy drinker, quit alcohol one year ago and does not work currently.,FAMILY HISTORY:, Negative for any liver disease.,REVIEW OF SYSTEMS:,GENERAL: Denies fever or chills. He said he was in Gilbert about couple of weeks ago for fever and was admitted there for two days. He does not know the details.,ENT: No visual changes. No runny nose. No sore throat.,CARDIOVASCULAR: No syncope, chest pain, or palpitations.,RESPIRATORY: No cough or hemoptysis. No dyspnea.,GI: No abdominal pain. No nausea or vomiting. No GI bleed. History of alcoholic liver disease.,GU: No dysuria, hematuria, frequency, or urgency.,MUSCULOSKELETAL: Denies any acute joint pain or swelling.,SKIN: No new skin rashes or itching.,CNS: Had a seizure many years ago with no recurrences. Left-sided hemiparesis after subdural hematoma from a fight/trauma.,ENDOCRINE: He thinks he has diabetes but does not know if he is on any diabetic treatment.,PHYSICAL EXAMINATION:,VITAL SIGNS: Temperature 97.7, heart rate 83, respiratory rate 18, blood pressure 125/72, and saturation 98% on room air.,GENERAL: The patient is lying in bed, appears comfortable, very pleasant Native American male in no apparent distress.,HEENT: His skull has a scar on the left side from previous surgery. On the back of his head, there is a laceration, which has two staples on. It is still oozing minimally. It is tender. No other traumatic injury is noted. Eyes, pupils react to light. Sclerae anicteric. Nostrils are normal. Oral cavity is clear with no thrush or exudate.,NECK: Supple. Trachea midline. No JVD. No thyromegaly.,LYMPHATICS: No cervical or supraclavicular lymphadenopathy.,LUNGS: Clear to auscultation bilaterally.,HEART: Normal S1 and S2. No murmurs or gallops. Regular rate and rhythm.,ABDOMEN: Soft, distended, nontender. No organomegaly or masses.,LOWER EXTREMITIES: +1 edema bilaterally. Pulses strong bilaterally. No skin ulcerations noted. No erythema.,SKIN: Several spider angiomas noted on his torso and upper extremities consistent with liver cirrhosis.,BACK: No tenderness by exam.,RECTAL: No masses. No abscess. No rectal fissures. Guaiac was performed by me and it was negative.,NEUROLOGIC: He is alert and oriented x2. He is slow to some extent in his response. No asterixis. Right-sided spastic hemiparesis with increased tone, increased reflexes, and weakness. Increased tone noted in upper and lower extremities on the right compared to the left. Deep tendon reflexes are +3 on the right and +2 on the left. Muscle strength is decreased on the right, more pronounced in the lower extremity compared to the upper extremity. The upper extremity is +4/5. Lower extremity is 3/5. The left side has a normal strength. Sensation appears to be intact. Babinski is upward on the right, equivocal on the left.,PSYCHIATRIC: Flat affect. Mood appeared to be appropriate. No active hallucinations or psychotic symptoms.,LABORATORY DATA: | null |
2,865 | Intractable epilepsy, here for video EEG. | Neurology | Intractable Epilepsy | CHIEF COMPLAINT:, Intractable epilepsy, here for video EEG.,HISTORY OF PRESENT ILLNESS: , The patient is a 9-year-old male who has history of global developmental delay and infantile spasms. Ultimately, imaging study shows an MRI with absent genu of the corpus callosum and thinning of the splenium of the corpus callosum, showing a pattern of cerebral dysgenesis. He has had severe global developmental delay, and is nonverbal. He can follow objects with his eyes, but has no ability to interact with his environment to any great degree. He has noted if any purposeful use of the hands. He has abnormal movements constantly, which are more choreiform and dystonic. He has spastic quadriparesis, which is variable at times. The patient is unable to sit or stand, and receives all his nutrition via G-tube.,The patient began having seizures in infancy presenting as infantile spasms. I began seeing him at 20 months of age. At that point, he had undergone workup in Seattle, Washington and then was seeing Dr. X, child neurologist in Mexico, who started Vigabatrin for infantile spasms. The patient had benefit from this medication, and was doing well at that time with regard to that seizure type. He initially was on phenobarbital, which failed to give him benefit. He continued on phenobarbital; however, for a long period time thereafter. The patient then began having more tonic seizures after his episodic spasms had subsided, and failed several medication trials including valproic acid, Topamax, and Zonegran at least briefly. Upon starting Lamictal, he began to have benefit and then actually had 1-year seizure freedom before having an isolated seizure or 2. Over the next 6 months to a year, he only had few further seizures, and was doing well in a general sense. It was more recently that he began having new seizure events that have not responded to higher doses of Lamictal up to 15 mg/kg/day. These events manifest as tonic spells with eye deviation and posturing. Mother reports flexion of the upper extremities, extension with lower extremities. During that time, he is not able to cry or say any sounds. These events last from seconds to minutes, and occur at least multiple times per week. There are times where he has none for a few days and other times where he has multiple days in a row with events. He has another event manifesting as flexion of the upper extremities and extension lower extremities where he turns red and cries throughout. He may vomit after these episodes, then seems to calm down. It is unclear whether this is a seizure or whether the patient is still responsive.,MEDICATIONS:, The patient's medications include Lamictal for a total of 200 mg twice a day. It is a 150 mg tablet and 25 mg tablets. He is on Zonegran using 25 mg capsules 2 capsules twice daily, and baclofen 10 mg three times day. He has other medications including the Xopenex and Atrovent.,REVIEW OF SYSTEMS: , At this time is negative any fevers, nausea, vomiting, diarrhea, abdominal complaints, rashes, arthritis, or arthralgias. No respiratory or cardiovascular complaints. He has no change in his skills at this point.,FAMILY HISTORY: , Noncontributory.,PHYSICAL EXAMINATION:,GENERAL: The patient is a slender male who is microcephalic. He has EEG electrodes in place and is on the video EEG at that time.,HEENT: His oropharynx shows no lesions.,NECK: Supple without adenopathy.,CHEST: Clear to auscultation.,CARDIOVASCULAR: Regular rate and rhythm. No murmurs.,ABDOMEN: Benign with G-tube in place.,EXTREMITIES: Reveal no clubbing, cyanosis, or edema.,NEUROLOGICAL: The patient is alert and has bilateral esotropia. He is able to fix and follow objects briefly. He is unable to reach for objects. He exhibits constant choreiform movements when excited. These are more prominent in the upper extremities and lower extremities. He has some dystonic posture with flexion of the wrist and fingers bilaterally. He also has plantar flexion at the ankles bilaterally. His cranial nerves reveal that his pupils are equal, round, and reactive to light. Extraocular movements are intact other than bilateral esotropia. His face moves symmetrically. Palate elevates in midline. Hearing appears intact bilaterally.,Motor exam reveals dystonic and variable tone, overall there is mild in spasticity both upper and lower extremities as described above. He has clonus at the ankles bilaterally, and some valgus contracture of the ankles. His sensation is intact to light touch bilaterally. Deep tendon reflexes are 2 to 3+ bilaterally.,IMPRESSION/PLAN: , This is a 9-year-old male with congenital brain malformation and intractable epilepsy. He has microcephaly as well as dystonic cerebral palsy. He had a re-emergence of seizures, which are difficult to classify, although some sound like tonic episodes and others are more concerning for non-epileptic phenomenon, such as discomfort. He is admitted for video EEG to hopefully capture both of these episodes and further clarify the seizure type or types. He will remain hospitalized for probably at least 48 hours to 72 hours. He could be discharged sooner if multiple events are captured. His medications, we will continue his current dose of Zonegran and Lamictal for now. Both of these medications are very long acting, discontinuing them while in the hospital may simply result in severe seizures after discharge. | neurology, brain malformation, congenital, intractable epilepsy, global developmental delay, video eeg, seizures, intractable, eeg, |
2,866 | Caudate Nuclei atrophy, bilaterally, in patient with Huntington Disease. | Neurology | Huntington's Disease | CC:, Slowing of motor skills and cognitive function.,HX: ,This 42 y/o LHM presented on 3/16/93 with gradually progressive deterioration of motor and cognitive skills over 3 years. He had difficulty holding a job. His most recent employment ended 3 years ago as he was unable to learn the correct protocols for the maintenance of a large conveyer belt. Prior to that, he was unable to hold a job in the mortgage department of a bank as could not draw and figure property assessments. For 6 months prior to presentation, he and his wife noted (his) increasingly slurred speech and slowed motor skills (i.e. dressing himself and house chores). His walk became slower and he had difficulty with balance. He became anhedonic and disinterested in social activities, and had difficulty sleeping for frequent waking and restlessness. His wife noticed "fidgety movements" of his hand and feet.,He was placed on trials of Sertraline and Fluoxetine for depression 6 months prior to presentation by his local physician. These interventions did not appear to improve his mood and affect.,MEDS:, Fluoxetine.,PMH: ,1)Right knee arthroscopic surgery 3 yrs ago. 2)Vasectomy.,FHX:, Mother died age 60 of complications of Huntington Disease (dx at UIHC). MGM and two MA's also died of Huntington Disease. His 38 y/o sister has attempted suicide twice.,He and his wife have 2 adopted children.,SHX: ,unemployed. 2 years of college education. Married 22 years.,ROS: ,No history of Dopaminergic or Antipsychotic medication use.,EXAM:, Vital signs normal.,MS: A&O to person, place, and time. Dysarthric speech with poor respiratory control.,CN: Occasional hypometric saccades in both horizontal directions. No vertical gaze abnormalities noted. Infrequent spontaneous forehead wrinkling and mouth movements. The rest of the CN exam was unremarkable.,Motor: Full strength throughout and normal muscle tone and bulk. Mild choreiform movements were noted in the hands and feet.,Sensory: unremarkable.,Coord: unremarkable.,Station/Gait: unremarkable, except that during tandem walking mild dystonic and choreiform movements of BUE became more apparent.,Reflexes: 2/2 throughout. Plantar responses were flexor, bilaterally.,There was no motor impersistence on tongue protrusion or hand grip.,COURSE:, He was thought to have early manifestations of Huntington Disease. A HCT was unremarkable. Elavil 25mg qhs was prescribed. Neuropsychologic assessment revealed mild anterograde memory loss only.,His chorea gradually worsened during the following 4 years. He developed motor impersistence and more prominent slowed saccadic eye movements. His mood/affect became more labile.,6/5/96 genetic testing revealed a 45 CAg trinucleotide repeat band consistent with Huntington Disease. MRI brain, 8/23/96, showed caudate nuclei atrophy, bilaterally. | null |
2,867 | This is a 69-year-old white woman with Huntington disease, who presents with the third suicide attempt in the past two months. | Neurology | Huntington's Disease - Consult | CHIEF COMPLAINT: , "A lot has been thrown at me.",The patient is interviewed with husband in room.,HISTORY OF PRESENT ILLNESS: , This is a 69-year-old Caucasian woman with a history of Huntington disease, who presented to Hospital four days ago after an overdose of about 30 Haldol tablets 5 mg each and Tylenol tablet 325 mg each, 40 tablets. She has been on the medical floor for monitoring and is medically stable and was transferred to the psychiatric floor today. The patient states she had been thinking about suicide for a couple of weeks. Felt that her Huntington disease had worsened and she wanted to spare her family and husband from trouble. Reports she has been not socializing with her family because of her worsening depression. Husband notes that on Monday after speaking to Dr. X, they had been advised to alternate the patient's Pamelor (nortriptyline) to every other day because the patient was reporting dry mouth. They did as they have instructed and husband feels this may have had some factor on her worsening depression. The patient decided to ingest the pills when her husband went to work on Friday. She thought Friday would be a good day because there would be less medical people working so her chances of receiving medical care would be lessened. Her husband left around 7 in the morning and returned around 11 and found her sleeping. About 30 minutes after his arrival, he found the empty bottles and woke up the patient to bring her to the hospital.,She says she wishes she would have died, but is happy she is alive and is currently not suicidal because she notes her sons may be have to be tested for the Huntington gene. She does not clearly explain how this has made her suicidality subside.,This is the third suicide attempt in the last two months for this patient. About two months ago, the patient took an overdose of Tylenol and some other medication, which the husband and the patient are not able to recall. She was taken to Southwest Memorial Hermann Hospital. A few weeks ago, the patient tried to shoot herself and the gun was fired and there is a blow-hole in the floor. Husband locked the gun after that and she was taken to Bellaire Hospital. The patient has had three psychiatric admissions in the past two months, two to Southwest Memorial and one to Bellaire Hospital for 10 days. She sees Dr. X once or twice weekly. He started seeing her after her first suicide attempt.,The patient's husband and the patient state that until March 2009, the patient was independent, was driving herself around and was socially active. Since then she has had worsening of her Huntington symptoms including short-term memory loss. At present, the patient could not operate the microwave or operate her cell phone and her husband says that she is progressively more withdrawn, complains about anxiety, and complains about shortness of breath. The patient notes that she has had depressive symptoms of quitting social life, the patient being withdrawn for the past few months and excessive worry about her Huntington disease.,The patient's mother passed away 25 years ago from Huntington's. Her grandmother passed away 50 years ago and two brothers also passed away of Huntington's. The patient has told her husband that she does not want to go that way. The patient denies auditory or visual hallucinations, denies paranoid ideation. The husband and the patient deny any history of manic or hypomanic symptoms in the past.,PAST PSYCHIATRIC HISTORY: , As per the HPI, this is her third suicide attempt in the last two months and started seeing Dr. X. She has a remote history of being on Lexapro for depression.,MEDICATIONS: , Her medications on admission, alprazolam 0.5 mg p.o. b.i.d., Artane 2 mg p.o. b.i.d., Haldol 2.5 mg p.o. t.i.d., Norvasc 10 mg p.o. daily, nortriptyline 50 mg p.o. daily. Husband has stated that the patient's chorea becomes better when she takes Haldol. Alprazolam helps her with anxiety symptoms.,PAST MEDICAL HISTORY: , Huntington disease, symptoms of dementia and hypertension. She has an upcoming appointment with the Neurologist. Currently, does have a primary care physician and _______ having an outpatient psychiatrist, Dr. X, and her current Neurologist, Dr. Y.,ALLERGIES: , CODEINE AND KEFLEX.,FAMILY MEDICAL HISTORY: ,Strong family history for Huntington disease as per the HPI. Mother and grandmother died of Huntington disease. Two young brothers also had Huntington disease.,FAMILY PSYCHIATRIC HISTORY: , The patient denies history of depression, bipolar, schizophrenia, or suicide attempts.,SOCIAL HISTORY: ,The patient lives with her husband of 48 years. She used to be employed as a registered nurse. Her husband states that she does have a pattern of self-prescribing for minor illness, but does not think that she has ever taken muscle relaxants or sedative medications without prescriptions. She rarely drinks socially. She denies any illicit substance usage. Her husband reportedly gives her medication daily. Has been proactive in terms of seeking mental health care and medical care. The patient and husband report that from March 2009, she has been relatively independent, more socially active.,MENTAL STATUS EXAM: ,This is an elderly woman appearing stated age. Alert and oriented x4 with poor eye contact. Appears depressed, has psychomotor retardation, and some mild involuntary movements around her lips. She is cooperative. Her speech is of low volume and slow rate and rhythm. Her mood is sad. Her affect is constricted. Her thought process is logical and goal-directed. Her thought content is negative for current suicidal ideation. No homicidal ideation. No auditory or visual hallucinations. No command auditory hallucinations. No paranoia. Insight and judgment are fair and intact.,LABORATORY DATA:, A CT of the brain without contrast, without any definite evidence of acute intracranial abnormality. U-tox positive for amphetamines and tricyclic antidepressants. Acetaminophen level 206.7, alcohol level 0. The patient had a leukocytosis with white blood cell of 15.51, initially TSH 1.67, T4 10.4.,ASSESSMENT: , This is a 69-year-old white woman with Huntington disease, who presents with the third suicide attempt in the past two months. She took 30 tablets of Haldol and 40 tablets of Tylenol. At present, the patient is without suicidal ideation. She reports that her worsening depression has coincided with her worsening Huntington disease. She is more hopeful today, feels that she may be able to get help with her depression.,The patient was admitted four days ago to the medical floor and has subsequently been stabilized. Her liver function tests are within normal limits.,AXIS I: Major depressive disorder due to Huntington disease, severe. Cognitive disorder, NOS.,AXIS II: Deferred.,AXIS III: Hypertension, Huntington disease, status post overdose.,AXIS IV: Chronic medical illness.,AXIS V: 30.,PLAN,1. Safety. The patient would be admitted on a voluntary basis to Main-7 North. She will be placed on every 15-minute checks with suicidal precautions.,2. Primary psychiatric issues/medical issues. The patient will be restarted as per written by the consult service for Prilosec 200 mg p.o. daily, nortriptyline 50 mg p.o. nightly, Haldol 2 mg p.o. q.8h., Artane 2 mg p.o. daily, Xanax 0.5 mg p.o. q.12h., fexofenadine 180 mg p.o. daily, Flonase 50 mcg two sprays b.i.d., amlodipine 10 mg p.o. daily, lorazepam 0.5 mg p.o. q.6h. p.r.n. anxiety and agitation.,3. Substance abuse. No acute concern for alcohol or benzo withdrawal.,4. Psychosocial. Team will update and involve family as necessary.,DISPOSITION: , The patient will be admitted for evaluation, observation, treatment. She will participate in the milieu therapy with daily rounds, occupational therapy, and group therapy. We will place occupational therapy consult and social work consults. | null |
2,868 | The patient with continued problems with her headaches. | Neurology | Headache - Office Visit | She also had EMG/nerve conduction studies since she was last seen in our office that showed severe left ulnar neuropathy, moderate right ulnar neuropathy, bilateral mild-to-moderate carpal tunnel and diabetic neuropathy. She was referred to Dr. XYZ and will be seeing him on August 8, 2006.,She was also never referred to the endocrine clinic to deal with her poor diabetes control. Her last hemoglobin A1c was 10.,PAST MEDICAL HISTORY:, Diabetes, hypertension, elevated lipids, status post CVA, and diabetic retinopathy.,MEDICATIONS: , Glyburide, Avandia, metformin, lisinopril, Lipitor, aspirin, metoprolol and Zonegran.,PHYSICAL EXAMINATION:, Blood pressure was 140/70, heart rate was 76, respiratory rate was 18, and weight was 226 pounds. On general exam she has an area of tenderness on palpation in the left parietal region of her scalp. Neurological exam is detailed on our H&P form. Her neurological exam is within normal limits.,IMPRESSION AND PLAN:, For her headaches we are going to titrate Zonegran up to 200 mg q.h.s. to try to maximize the Zonegran therapy. If this is not effective, when she comes back on August 7, 2006 we will then consider other anticonvulsants such as Neurontin or Lyrica. We also discussed with Ms. Hawkins the possibility of nerve block injection; however, at this point she is not interested.,She will be seeing Dr. XYZ for her neuropathies.,We made an appointment in endocrine clinic today for a counseling in terms of better diabetes control and she is responsible for trying to get her referral from her primary care physician to go for this consult. | neurology, nerve conduction studies, emg, zonegran therapy, ulnar neuropathy, endocrine clinic, diabetes control, neurological exam, headache, zonegran |
2,869 | Closed head injury with evidence of axonal injury vs. vascular injury to the left substantia nigra, right subdural hematoma and possible subarachnoid hemorrhage, vascular/ischemic injury in the right occipital lobe-right basal ganglia/caudate nucleus-right frontal lobe, and right temporal lobe contusion. | Neurology | Head Trauma | CC: ,Depressed mental status.,HX: ,29y/o female fell down a flight of stairs on 2/20/95, striking the right side of her head. She then walked over to and lay down on a living room couch. She was found there, the next morning, by her boyfriend, poorly responsive and amidst a coffee ground like emesis. She was taken to a local ER and HCT revealed a right supraorbital fracture, right SDH and left SAH. Spine X-rays revealed a T12 vertebral body fracture. There were retinal hemorrhages, OU. She continued to be minimally responsive and was transferred to UIHC for lack of insurance and for neurologic/neurosurgical care.,MEDS:, (on transfer): Dilantin, Zantac, Proventil MDI, Tylenol.,PMH:, 1)pyelonephritis, 2) multiple STD's, 3) Polysubstance Abuse (ETOH, MJ, Amphetamine), 4)G5P4.,FHX:, unknown.,SHX: ,polysubstance abuse. smoked 1 pack per day for 15years.,EXAM: ,BP127/97, HR83, RR25, 37.2C,MS: Minimal to no spontaneous speech. Unresponsive to verbal commands. Lethargic and somnolent. Groaned "yes" inappropriately.,CN: Pupils 4/4 decreasing to 2/2 on exposure to light. VFFTT. Retinal hemorrhages, OU. EOM difficult to assess. Facial movement appeared symmetric. Tongue midline. Corneal and gag responses were intact.,MOTOR: no spontaneous movement. withdrew extremities to noxious stimulation (e.g. deep nail bed pressure).,Sensory: withdrew to noxious stimuli.,Coord/Station/Gait: not tested.,Reflexes: 2+/2+ BUE. 2/2 BLE. Babinski signs were present, bilaterally.,HEENT: Periorbital and upper lid ecchymoses about the right eye. Scleral hemorrhage, OD.,GEN EXAM: mild bruising of the extremities.,COURSE: ,2/27/95 HCT revealed a small liner high attenuation area lateral to the right parietal lobe with subtle increased attenuation of the tentorium cerebelli. These findings were felt to represent a right subdural hematoma and possible subarachnoid hemorrhage.,2/28/95 brain MRI revealed: 1)a small right-sided SDH, 2) Abnormal signal in the right occipital lobe with effacement of the gyri and sulci in the right PCA division most likely representing ischemic/vascular injury, 3)abnormal signal within the right basal ganglia/caudate nucleus consistent with ischemia, 4) abnormal signal in the uncal portion of the right frontal lobe consistent with contusion, 5) small parenchymal hemorrhage in the inferior anterior right temporal lobe, and 6) opacification of the right maxillary sinus.,EEG, 2/28/95, was abnormal with occasional sharp transients in the left temporal region, and irregular (more or less continuous) right greater than left delta slow waves and decreased background activity in the right hemisphere: the findings were consistent with focal pathology on the right, seizure tendency in the left temporal region, and bilateral cerebral dysfunction. By the time of discharge, 4/17/95, she was verbalizing one or two words and required assistance with feeding and ambulation. She could not function independently. | neurology, closed head injury, axonal injury, vascular injury, substantia nigra, subdural hematoma, subarachnoid hemorrhage, vascular, ischemic, injury, occipital lobe, retinal hemorrhages, temporal region, axonal, hemorrhages, hemorrhage, |
2,870 | Headache. Right frontal lobe glioma. | Neurology | Glioma - 2 | CC:, Headache,HX: ,37 y/o RHF presented to her local physician with a one month history of intermittent predominantly left occipital headaches which were awakening her in the early morning hours. The headachese were dull to throbbing in character. She was initially treated with Parafon-forte for tension type headaches, but the pain did not resolve. She subsequently underwent HCT in early 12/90 which revealed a right frontal mass lesion.,PMH: ,1)s/p tonsillectomy. 2)s/p elective abortion.,FHX:, Mother with breast CA, MA with "bone cancer." AODM both sides of family.,SHX: ,Denied tobacco or illicit drug use. Rarely consumes ETOH. Married with 2 teenage children.,EXAM: ,VItal signs unremarkable.,MS: Alert and oriented to person, place, time. Lucid thought process per NSG note.,CN: unremarkable.,Motor: full strength with normal muscle bulk and tone.,Sensory: unremarkable.,Coordination: unremarkable.,Station/Gait: unremarkable.,Reflexes: unremarkable.,Gen. Exam: unremarkable.,COURSE:, MRI Brain: large solid and cystic right frontal lobe mass with a large amount of surrounding edema. There is apparent tumor extension into the corpus callosum across the midline. Tumor extension is also suggested in the anterior limb of the interanl capsule on the right. There is midline mass shift to the left with effacement of the anterior horn of the right lateral ventricle. The MRI findings are most consistent with glioblastoma.,The patient underwent right frontal lobectomy. The pathological diagnosis was xanthomatous astrocytoma. The literature at the time was not clear as to optimal treatment protocol. People have survived as long as 25 years after diagnosis with this type of tumor. XRT was deferred until 11/91 when an MRI and PET Scan suggested extension of the tumor. She then received 5580 cGy of XRT in divided segments. She developed olfactory auras shortly after lobectomy at was treated with PB with subsequent improvement. She was treated with BCNU chemotherapy protocol in 1992. | neurology, frontal lobe, tumor extension, glioma, headache, lobectomy, astrocytoma, |
2,871 | Sellar HCT - Pituitary mass | Neurology | HCT - Pituitary Mass | CC:, HA and vision loss.,HX: ,71 y/o RHM developed a cataclysmic headache on 11/5/92 associated with a violent sneeze. The headache lasted 3-4 days. On 11/7/92, he had acute pain and loss of vision in the left eye. Over the following day his left pupil enlarged and his left upper eyelid began to droop. He was seen locally and a brain CT showed no sign of bleeding, but a tortuous left middle cerebral artery was visualized. The patient was transferred to UIHC 11/12/92.,FHX:, HTN, stroke, coronary artery disease, melanoma.,SHX:, Quit smoking 15 years ago.,MEDS:, Lanoxin, Capoten, Lasix, KCL, ASA, Voltaren, Alupent MDI,PMH: ,CHF, Atrial Fibrillation, Obesity, Anemia, Duodenal Ulcer, Spinal AVM resection 1986 with residual T9 sensory level, hyperreflexia and bilateral babinski signs, COPD.,EXAM: ,35.5C, BP 140/91, P86, RR20. Alert and oriented to person, place, and time. CN: No light perception OS, Pupils: 3/7 decreasing to 2/7 on exposure to light (i.e., fixed/dilated pupil OS). Upon neutral gaze the left eye deviated laterally and inferiorly. There was complete ptosis OS. On downward gaze their was intorsion OS. The left eye could not move superiorly, medially or effectively downward, but could move laterally. EOM were full OD. The rest of the CN exam was unremarkable. Motor, Coordination, Station and Gait testing were unremarkable. Sensory exam revealed decreased pinprick and light touch below T9 (old). Muscle stretch reflexes were increased (3+/3+) in both lower extremities and there were bilateral babinski signs (old). The upper extremity reflexes were symmetrical (2/2). Cardiovascular exam revealed an irregularly irregular rhythm and lung sounds were coarse bilaterally. The rest of the general exam was unremarkable.,LAB:, CBC, PT/PTT, General Screen were unremarkable except for a BUN 21mg/DL. CSF: protein 88mg/DL, glucose 58mg/DL, RBC 2800/mm3, WBC 1/mm3. ANA, RF, TSH, FT4 were WNL.,IMPRESSION:, CN3 palsy and loss of vision. Differential diagnosis: temporal arteritis, aneurysm, intracranial mass.,COURSE:, The outside Brain CT revealed a tortuous left MCA. A four-vessel cerebral angiogram revealed a dolichoectatic basilar artery and tortuous LICA. There was no evidence of aneursym. Transesophageal Echocardiogram revealed atrial enlargement only. Neuroopthalmologic evaluation revealed: Loss of color vision and visual acuity OS, RAPD OS, bilateral optic disk pallor (OS > OD), CN3 palsy and bilateral temporal field loss, OS >> OD . ESR, CRP, MRI were recommended to rule out temporal arteritis and intracranial mass. ESR 29mm/Hr, CRP 4.3mg/DL (high) , The patient was placed on prednisone. Temporal artery biopsy showed no evidence of vasculitis. MRI scan could not be obtained due to patient weight. Sellar CT was done instead: coronal sections revealed sellar enlargement and upward bowing of the diaphragm sella suggesting a pituitary mass. In retrospect sellar enlargement could be seen on the angiogram X-rays. Differential consideration was given to cystic pituitary adenoma, noncalcified craniopharyngioma, or Rathke's cleft cyst with solid component. The patient refused surgery. He was seen in Neuroopthalmology Clinic 2/18/93 and was found to have mild recovery of vision OS and improved visual fields. Aberrant reinnervation of the 3rd nerve was noted as there was constriction of the pupil (OS) on adduction, downgaze and upgaze. The upper eyelid, OS, elevated on adduction and down gaze, OS. EOM movements were otherwise full and there was no evidence of ptosis. In retrospect he was felt to have suffered pituitary apoplexy in 11/92. | neurology, sellar, hct, htn, pituitary, aneurysm, brain ct, cataclysmic, coronary artery disease, headache, intracranial mass, loss of vision, mass, melanoma, palsy, sneeze, stroke, temporal arteritis, vision loss, bilateral babinski signs, sellar enlargement, pituitary mass, temporal, vision, |
2,872 | HCT for memory loss and for calcification of basal ganglia (globus pallidi). | Neurology | HCT - Calcification of Basal Ganglia | CC:, Memory loss.,HX:, This 77 y/o RHF presented with a one year history of progressive memory loss. Two weeks prior to her evaluation at UIHC she agreed to have her sister pick her up for church at 8:15AM, Sunday morning. That Sunday she went to pick up her sister at her sister's home and when her sister was not there (because the sister had gone to pick up the patient) the patient left. She later called the sister and asked her if she (sister) had overslept. During her UIHC evaluation she denied she knew anything about the incident. No other complaints were brought forth by the patients family.,PMH:, Unremarkable.,MEDS:, None,FHX: ,Father died of an MI, Mother had DM type II.,SHX: , Denies ETOH/illicit drug/Tobacco use.,ROS:, Unremarkable.,EXAM:, Afebrile, 80BPM, BP 158/98, 16RPM. Alert and oriented to person, place, time. Euthymic. 29/30 on Folstein's MMSE with deficit on drawing. Recalled 2/6 objects at five minutes and could not recite a list of 6 objects in 6 trials. Digit span was five forward and three backward. CN: mild right lower facial droop only. MOTOR: Full strength throughout. SENSORY: No deficits to PP/Vib/Prop/LT/Temp. COORD: Poor RAM in LUE only. GAIT: NB and ambulated without difficulty. STATION: No drift or Romberg sign. REFLEXES: 3+ bilaterally with flexor plantar responses. There were no frontal release signs.,LABS:, CMB, General Screen, FT4, TSH, VDRL were all WNL.,NEUROPSYCHOLOGICAL EVALUATION, 12/7/92: ,Verbal associative fluency was defective. Verbal memory, including acquisition, and delayed recall and recognition, was severely impaired. Visual memory, including immediate and delayed recall was also severely impaired. Visuoperceptual discrimination was mildly impaired, as was 2-D constructional praxis.,HCT, 12/7/92: , Diffuse cerebral atrophy with associative mild enlargement of the ventricles consistent with patient's age. Calcification is seen in both globus pallidi and this was felt to be a normal variant. | neurology, memory loss, romberg sign, hct, cerebral atrophy, calcification of basal ganglia, basal ganglia, globus pallidi, basal, ganglia, globus, pallidi, calcification, |
2,873 | Headache and diplopia. | Neurology | Granulomatous Inflammation | CC:, Headache and diplopia.,HX:, This 39 y/o African American female began experiencing severe constant pressure pain type headaches beginning the last week of 8/95. The pain localized to bifronto-temporal regions of the head and did not radiate. There was no associated nausea, vomiting, photophobia or phonophobia. The HA's occurred daily; and throughout daylight hours. They diminished at bedtime, but occasionally awakened her in the morning.,Several days following the onset of her HA's, she began experiencing numbness and tingling about the right side of her face. These symptoms improved, but did not completely resolved.,Several days after the onset of facial paresthesias, she began to experience binocular horizontal diplopia. The diplopia resolved when covering either eye, and worsened upon looking toward the right. Coincidentally, she began veering toward the right when walking. She denied any weakness. She had had chronic unsteadiness for many years since developing juvenile rheumatoid arthritis. She was unsure whether her unsteadiness was due to poor depth perception in light of her diplopia.,The patient was admitted locally 9/2/95. HCT, 9/2/95 and Brain MRI with gadolinium, 9/3/95, were "unremarkable." Lumbar puncture (done locally),9/3/95: Opening pressure 27cm H20, CSF analysis ( protein 14.0, glucose 66, O WBC, 3 RBC, VDRL non-reactive, Lyme titer unremarkable, Myelin basic protein 1.0 (normal <4.0), and there was no evidence of oligoclonal bands. ESR=76. On 9/11/95 ESR=110. Acetylcholine receptor binding and blocking antibodies were negative. 9/4/95, ANA and RF were negative. 7/94, ANA and RF were negative, and ESR=60.,MEDS: ,Tylenol 500mg q5-6hrs. No known Allergies.,PMH:, 1)Juvenile Rheumatoid Arthritis diagnosed at age 10 years; now in remission. 2)Right #5 finger reattachment as child due to traumatic amputation.,FHX: ,Mother died age 42 of unknown type cancer. Father died age 62 of unknown type cancer. 4 sisters, one brother and 2 half-brothers. One of the half-brothers has asthma.,SHX: ,Single, lives with sister, and denies Tobacco/ETOH/illicit drug use.,EXAM:, BP141/84, HR99, RR14, 36.8C, Wt. 82kg Ht. 152.,MS: A&O to person, place, time. Speech fluent; without dysarthria. Mood euthymic with appropriate affect.,CN: Decreased abduction, OD. In neutral gaze, the right eye deviated slightly lateral of midline. In addition, she had mild proptosis, OD. The right eye was nontender to palpation during extraocular movement. Visual fields were full to confrontation. Optic disks appeared flat. Face was symmetric with full movement and sensation. Gag, shoulder shrug and corneal responses were intact, bilaterally. Tongue was midline with full ROM.,MOTOR: 5/5 strength throughout with normal muscle bulk and tone.,SENSORY: Unremarkable.,COORD: Unremarkable FNF/HKS/RAM.,STATION: Unremarkable. NO Romberg's sign or drift.,GAIT: Narrow based gait. Able to TT and HW without difficulty. Mild difficulty with TW.,REFLEXES: 2+/2+ Throughout all 4 extremities. Flexor plantar responses, bilaterally.,Musculoskeletal: Swan neck deformities of the #2 and #3 digits of both hands.,GEN EXAM: unremarkable, except for obvious sign of right finger reattachment (mentioned above).,COURSE: ,Repeat lumbar puncture yielded: Opening pressure 20.25cm H20, protein 22, glucose 62, 2RBC, 1WBC. CSF cytology, ACE, cultures (bacterial, fungal, AFB), gram stain, cryptococcal antigen, and VDRL were negative. Serum ACE, TSH, FT4 were unremarkable.,Neuroophthalmology confirmed her right CN6 palsy and proptosis (OD); and noted her complaint of paresthesias in the V1 and V2 distribution. They saw no evidence of papilledema. Visual field testing was unremarkable. MRI Brain/orbit/neck with gadolinium, 10/20/95, revealed abnormal enhancing signal in the right cavernous sinus and sinus mucosal thickening in both maxillary sinuses/ethmoid sinuses/frontal sinuses. CXR, 10/20/95, showed a lobulated mass arising from the right hilum. The mass appeared to obstruct the right middle lobe, causing partial collapse of this lobe. Chest CT with contrast, 10/23/95, revealed a 3.2x4.5x4.0cm mass in the right hilar region with impingement on the right lower bronchus. There appeared to be calcification as well as low attenuation regions within the mass. No lymphadenopathy was noted. She underwent bronchoscopy with bronchial brushing and transbronchial aspirate of the right lung on 10/24/95: no tumor cells were identified, GMS stains were negative and there was no evidence of viral changes, fungus or PCP by culture or molecular assay. She underwent right maxillary sinus biopsy and right middle lobe wedge resection and lymph node biopsy on 11/2/95: Caseating granulomatous inflammation with associated inflammatory pseudotumor was found in both sinus and lung biopsy specimens. No sign of cancer was found. Tissue cultures (bacterial, fungal, AFB) were negative times 3. The patients case was discussed at Head and Neck Oncology Tumor Board and a differential diagnosis of Sarcoidosis, Histoplasmosis, Wegener's Granulomatosis, were considered. Urine Histoplasmosis Antigen testing on 11/8/95 was 0.9units (normal<1.0): repeat testing on 12/13/95 was 0.8units. ANCA serum titers on 11/8/95 were <1:40 (normal). PPD testing was negative 11/95 (with positive candida and mumps controls).,The etiology of this patient's illness was not discovered. She was last seen 4/96 and her diplopia and right CN6 palsy had moderately improved. | null |
2,874 | Dysarthria. Probable brainstem glioma. | Neurology | Glioma - 1 | CC:, Dysarthria,HX: ,This 52y/o RHF was transferred from a local hospital to UIHC on 10/28/94 with a history of progressive worsening of vision, dysarthria, headache, and incoordination beginning since 2/94. Her husband recalled her first difficulties became noticeable after a motor vehicle accident in 2/94. She was a belted passenger in a car struck at a stop. There was no reported head or neck injury or alteration of consciousness. She was treated and released from a local ER the same day. Her husband noted the development of mild dysarthria, incoordination, headache and exacerbation of preexisting lower back pain within 2 week of the accident. In 4/94 she developed stress urinary incontinence which spontaneously resolved in June. In 8/94, her HA changed from a dull constant aching in the bitemporal region to a sharper constant pain in the nuchal/occipital area. She also began experiencing increased blurred vision, worsening dysarthria and difficulty hand writing. In 9/94 she was evaluated by a local physician. Examination then revealed incoordination, generalized fatigue, and dysarthria. Soon after this she became poorly arousable and increasingly somnolent. She had difficulty walking and generalized weakness. On 10/14/94, she lost the ability to walk by herself. Evaluation at a local hospital revealed: 1)Normal electronystagmography, 2)two lumbar punctures which revealed some atypical mononuclear cells suggestive of "tumor or reactive lymphocytosis." One of these CSF analysis showed: Glucose 16, Protein 99, WBC 14, RBC 114. Echocardiogram was normal. Bone marrow biopsy was normal except for decreased iron. Abdominal-Pelvic CT scan, CXR, Mammogram, PPD, ANA, TFT, and RPR were unremarkable. A 10/31/94 MRI brain scan a 5x10mm area of increased signal on T2 weighted images in the right remporal lobe lateral to the anterior aspect of the temporal horn, right posterolateral aspect of the midbrain, pons, and bilateral inferior surface of the cerebellum involving gray and white matter. These areas did not enhance with gadolinium contrast on T1 weighted images.,MEDS: ,none.,PMH:, 1)G3P3, 2)last menses one year ago.,FHX:, Mother suffered stroke in her 70's. DM and Htn in family.,SHX:, Married, Secretary, No h/o tobacco/ETOH/illicit drug use.,ROS:, no weight loss, fever, chills, nightsweats, cough, dysphagia.,EXAM:, BP139/74, HR 90, RR20, 36.8C,MS: Drowsy to somnolent, occasionally "giddy." Oriented to person, place, time. Minimal dysarthric speech, but appropriate. MMSE 27/30 (copy of exam not in chart).,CN: Pupils 4/4 decreasing to 2/2 on exposure to light. Optic disks were flat and without sign of papilledema. VFFTC. EOM intact. No nystagmus. The rest of the CN exam was unremarkable.,Motor: 5/5 strength throughout. Normal muscle tone and bulk.,Sensory: No deficit to LT/PP/VIB/PROP.,Coord: difficulty with RAM in BUE, and ataxia on FNF and HKS in all extremities.,Station: Romberg sign present.,Gait: unsteady, wide-based, with notable difficulty on TW, TT and HW.,Reflexes: 2/2 BUE, 0/1 patellae, trace at both archilles, Plantars responses were flexor, bilaterally.,Gen Exam: unremarkable.,COURSE:, CSF analysis by lumbar puncture, 10/31/94: Protein 131mg/dl (normal 15-45), Albumin 68 (normal 14-20), IgG10mg/dl (normal <6.2), IgG index -O.1mg/24hr (normal),,No oligoclonal bands seen, WBC 33 (19lymphocytes, 1 neutrophil), RBC 29, Glucose 13, Cultures (bacteria, fungal, AFB) were negative, crytococcal Ag negative. The elevated CSF total protein, IgG, and albumin suggested breakdown of the blood brain barrier or blockage of CSF flow. The normal IgG synthesis rate and lack of oligoclonal banding did not suggest demylination. A second CSF analysis on 11/2/94 revealed similar findings; and in addition Anti-purkinje cell and Anti-neuronal antibodies (Yo and Ho) were not found; Beta-2 microglobulin was 1.8 (normal); histoplasmosis Ag negative. Serum ACE, SPEP, Urine histoplasmin were negative.,Neuropsychologic assessment, 10/28/94, raised a question of a demential syndrome, but given her response style on the MMPI (marked defensiveness, with unwillingness to admit to even very common human faults) prevented such a diagnosis. Severe defects in memory, fine motor skills, and constructional praxis were noted.,Chest-Abdominal-Pelvic CT scans were negative. 11/4/94 cerebral angiogram noted variable caliber in the RMCA, LACA and Left AICA distributions. It was intially thought that thismight be suggestive of a vasculopathy and she was treated with a short course of IV steroids. Temporal artery biopsy was unremarkable.,She underwent multiple MRI brain scans at UIHC: 11/4/94, 11/9/94, 11/16/94. All scans consistently showed increase in T2 signal in the brainstem, cerebellar peduncles and temporal lobes bilaterally. These areas did not enhance with gadolinium contrast. These findings were felt most suggestive of glioma.,She underwent left temporal lobe brain biopsy on 11/10/94: This study was inconclusive and showed evidence of atypical mononuclear cells and lymphocytes in the perivascular and subarachnoid spaces. Despite cytologic atypia the cells were felt to be reactive in nature, since immunohistochemical stains failed to disclose lymphoid clonality or non-leukocytic phenomena. Little sign of vasculopathy or tumor was found. Bacterial, fungal , HSV, CMV and AFB cultures were negative. HSV, and VZV antigen was negative.,Her neurological state progressively worsened throughout her hospital stay. By time of discharge, 12/2/94, she was very somnolent and difficult to arouse and required NGT feeding and 24hour supportive care. She was made DNR after family request prior to transfer to a care facility. | null |
2,875 | This is a 62-year-old woman with hypertension, diabetes mellitus, prior stroke who has what sounds like Guillain-Barre syndrome, likely the Miller-Fisher variant. | Neurology | Guillain-Barre Syndrome | CHIEF COMPLAINT: , Followup of hospital discharge for Guillain-Barre syndrome.,HISTORY OF PRESENT ILLNESS: , This is a 62-year-old right-handed woman with hypertension, diabetes mellitus, a silent stroke involving right basal ganglia who was in her usual state of baseline health until late June of 2006 when she had onset of blurred vision, diplopia, and possible weakness in the right greater than left arm and left-sided ptosis. She was admitted to the hospital. The MRI showed only an old right basal ganglion infarct. She subsequently had a lumbar puncture, which showed increased protein, and an EMG/nerve conduction study performed by Dr. X on July 3rd, showed early signs of AIDP. The patient was treated with intravenous gamma globulin and had some mild improvement in her symptoms. Her vital capacities were normal during the hospitalization. Her chest x-ray was negative for any acute process. She was discharged to rehab from July 12, 2006 to July 20, 2006. She made some progress in which she notes that her walking is definitely better. However, she notes that she still has some problems with eye movement and her vision. This is possibly her main problem. She also reports tightness and pain in her mid back.,REVIEW OF SYSTEMS:, Documented in the clinic note. The patient has problems with diabetes, double vision, blurry vision, muscle pain, weakness, trouble walking, and headaches about two to three times per week.,PAST MEDICAL HISTORY:,1. Hypertension.,2. Diabetes mellitus.,3. Stroke involving the right basal ganglion.,4. Guillain-Barre syndrome diagnosed in June of 2006.,5. Bilateral knee replacements.,6. Total abdominal hysterectomy and cholecystectomy.,FAMILY HISTORY:, Multiple family members have diabetes mellitus.,SOCIAL HISTORY:, The patient is retired on disability due to her knee replacements. She does not smoke, drink or use any illicit drugs.,MEDICATIONS:, Percocet 5/325 mg 4-6 hours p.r.n., Neurontin 100 mg per day, insulin, Protonix 40 mg per day, Toprol-XL 50 mg q.d., Norvasc 10 mg q.d., glipizide ,10 mg q.d., fluticasone 50 mcg nasal spray, Lasix 20 mg b.i.d., and Zocor 1 mg q.d.,ALLERGIES: , No known drug allergies.,PHYSICAL EXAMINATION: , Blood pressure 122/74, heart rate 68, respiratory rate 16, and weight 228 pounds. Pain scale 5/10. Please see the written note for details. General exam is benign other than mild obesity. On neuro examination, mental status is normal. Cranial nerves are significant for full visual fields and pupils are equal and reactive. However, extraocular movements are very limited. She has some adduction of the left eye and she has minimal upgaze of both eyes, but otherwise the eyes do not move. Face is symmetric. Sensation is intact. Tongue and uvula are in midline. Palate is elevated symmetrically. Shoulder shrug is strong. The patient's muscle exam shows normal bulk and tone throughout. She has no weakness of the left upper extremity. In the right upper extremity, she has only about 2/5 strength in the right shoulder, but is otherwise 5/5. There is no drift or orbit. Reflexes are absent throughout. Sensory exam is intact to light touch, pinprick, vibration, and proprioception is normal. There is no dysmetria. Gait is somewhat limited possibly by her vision and possibly also by her balance problems.,PERTINENT DATA:, As reviewed previously.,DISCUSSION: , This is a 62-year-old woman with hypertension, diabetes mellitus, prior stroke who has what sounds like Guillain-Barre syndrome, likely the Miller-Fisher variant. The patient has shown some improvement with IVIG and continues to show some gradual improvement. I discussed with the patient the course of disease, which is often weeks to about a month or so of worsening followed by many months of gradual improvement.,I told her that it is possible she may not recover 100%, but that certainly there is still plenty of time for her to have additional recovery over what she has right now. She is scheduled to see an ophthalmologist. I think it is reasonable for close followup of her visual symptoms progress. However, I certainly would not take any corrective measures at this point as I suspect her vision will improve gradually.,I discussed with the patient that with respect to her back pain certainly the Neurontin is relatively at low dose and this could be increased further. I wanted her to start taking the Neurontin 300 mg per day and then 300 mg b.i.d. after one week. She will call me in approximately three weeks' time to let me know how she is doing and if needed we will titrate up further.,She was apparently given some baclofen by her internist and I think this is not unreasonable. I definitely hope to get her off the Percocet in the future.,IMPRESSION:,1. Guillain-Barre Miller-Fisher variant.,2. Hypertension.,3. Diabetes mellitus.,4. Stroke.,RECOMMENDATIONS:,1. The patient is to start taking aspirin 162 mg per day.,2. Followup with ophthalmology.,3. Increase Neurontin to 300 mg per day x 1 week and then 300 mg b.i.d.,4. Followup by phone in three to four weeks.,5. Followup in this clinic in approximately two months' time.,6. Call for any questions or problems. | null |
2,876 | CT-guided frameless stereotactic radiosurgery for the right occipital arteriovenous malformation using dynamic tracking. | Neurology | Frameless Stereotactic Radiosurgery | PREOPERATIVE DIAGNOSIS:, Right occipital arteriovenous malformation.,POSTOPERATIVE DIAGNOSIS:, Right occipital arteriovenous malformation.,PROCEDURE PERFORMED:, CT-guided frameless stereotactic radiosurgery for the right occipital arteriovenous malformation using dynamic tracking.,Please note no qualified resident was available to assist in the procedure.,INDICATION: , The patient is a 30-year-old male with a right occipital AVM. He was referred for stereotactic radiosurgery. The risks of the radiosurgical treatment were discussed with the patient including, but not limited to, failure to completely obliterate the AVM, need for additional therapy, radiation injury, radiation necrosis, headaches, seizures, visual loss, or other neurologic deficits. The patient understands these risks and would like to proceed.,PROCEDURE IN DETAIL: , The patient arrived to Outpatient CyberKnife Suite one day prior to the treatment. He was placed on the treatment table. The Aquaplast mask was constructed. Initial imaging was obtained by the CyberKnife system. The patient was then transported over to the CT scanner at Stanford. Under the supervision of Dr. X, 125 mL of Omnipaque 250 contrast was administered. Dr. X then supervised the acquisition of 1.2-mm contiguous axial CT slices. These images were uploaded over the hospital network to the treatment planning computer, and the patient was discharged home.,Treatment plan was then performed by me. I outlined the tumor volume. Inverse treatment planning was used to generate the treatment plan for this patient. This resulted in a total dose of 20 Gy delivered to 84% isodose line using a 12.5 mm collimator. The maximum dose within this center of treatment volume was 23.81 Gy. The volume treated was 2.972 mL, and the treated lesion dimensions were 1.9 x 2.7 x 1.6 cm. The volume treated at the reference dose was 98%. The coverage isodose line was 79%. The conformality index was 1.74 and modified conformality index was 1.55. The treatment plan was reviewed by me and Dr. Y of Radiation Oncology, and the treatment plan was approved.,On the morning of May 14, 2004, the patient arrived at the Outpatient CyberKnife Suite. He was placed on the treatment table. The Aquaplast mask was applied. Initial imaging was used to bring the patient into optimal position. The patient underwent stereotactic radiosurgery to deliver the 20 Gy to the AVM margin. He tolerated the procedure well. He was given 8 mg of Decadron for prophylaxis and discharged home.,Followup will consist of an MRI scan in 6 months. The patient will return to our clinic once that study is completed.,I was present and participated in the entire procedure on this patient consisting of CT-guided frameless stereotactic radiosurgery for the right occipital AVM.,Dr. X was present during the entire procedure and will be dictating his own operative note. | neurology, ct-guided, occipital, cyberknife, frameless stereotactic radiosurgery, occipital arteriovenous malformation, conformality index, arteriovenous malformation, malformation, avm, arteriovenous, |
2,877 | Right side craniotomy for temporal lobe intracerebral hematoma evacuation and resection of temporal lobe lesion. Biopsy of dura. | Neurology | Hematoma Evacuation | PREOPERATIVE DIAGNOSIS: , Right temporal lobe intracerebral hemorrhage.,POSTOPERATIVE DIAGNOSES:,1. Right temporal lobe intracerebral hemorrhage.,2. Possible tumor versus inflammatory/infectious lesion versus vascular lesion, pending final pathology and microbiology.,PROCEDURES:,1. Emergency right side craniotomy for temporal lobe intracerebral hematoma evacuation and resection of temporal lobe lesion.,2. Biopsy of dura.,3. Microscopic dissection using intraoperative microscope.,SPECIMENS: , Temporal lobe lesion and dura as well as specimen for microbiology for culture.,DRAINS:, Medium Hemovac drain.,FINDINGS: , Vascular hemorrhagic lesion including inflamed dura and edematous brain with significant mass effect, and intracerebral hematoma with a history of significant headache, probable seizures, nausea, and vomiting.,ANESTHESIA: , General.,ESTIMATED BLOOD LOSS: , Per Anesthesia.,FLUIDS: , One unit of packed red blood cells given intraoperatively.,The patient was brought to the operating room emergently. This is considered as a life threatening admission with a hemorrhage in the temporal lobe extending into the frontal lobe and with significant mass effect.,The patient apparently became hemiplegic suddenly today. She also had an episode of incoherence and loss of consciousness as well as loss of bowel/urine.,She was brought to Emergency Room where a CT of the brain showed that she had significant hemorrhage of the right temporal lobe extending into the external capsule and across into the frontal lobe. There is significant mass effect. There is mixed density in the parenchyma of the temporal lobe.,She was originally scheduled for elective craniotomy for biopsy of the temporal lobe to find out why she was having spontaneous hemorrhages. However, this event triggered her family to bring her to the emergency room, and this is considered a life threatening admission now with a significant mass effect, and thus we will proceed directly today for evacuation of ICH as well as biopsy of the temporal lobe as well as the dura.,PROCEDURE IN DETAIL: , The patient was anesthetized by the anesthesiology team. Appropriate central line as well as arterial line, Foley catheter, TED, and SCDs were placed. The patient was positioned supine with a three-point Mayfield head pin holder. Her scalp was prepped and draped in a sterile manner. Her former incisional scar was barely and faintly noticed; however, through the same scalp scar, the same incision was made and extended slightly inferiorly. The scalp was resected anteriorly. The subdural scar was noted, and hemostasis was achieved using Bovie cautery. The temporalis muscle was reflected along with the scalp in a subperiosteal manner, and the titanium plating system was then exposed.,The titanium plating system was then removed in its entirety. The bone appeared to be quite fused in multiple points, and there were significant granulation tissue through the burr hole covers.,The granulation tissue was quite hemorrhagic, and hemostasis was achieved using bipolar cautery as well as Bovie cautery.,The bone flap was then removed using Leksell rongeur, and the underlying dura was inspected. It was quite full. The 4-0 sutures from the previous durotomy closure was inspected, and more of the inferior temporal bone was resected using high-speed drill in combination with Leksell rongeur. The sphenoid wing was also resected using a high-speed drill as well as angled rongeur.,Hemostasis was achieved on the fresh bony edges using bone wax. The dura pack-up stitches were noted around the periphery from the previous craniotomy. This was left in place.,The microscope was then brought in to use for the remainder of the procedure until closure. Using a #15 blade, a new durotomy was then made. Then, the durotomy was carried out using Metzenbaum scissors, then reflected the dura anteriorly in a horseshoe manner, placed anteriorly, and this was done under the operating microscope. The underlying brain was quite edematous.,Along the temporal lobe there was a stain of xanthochromia along the surface. Thus a corticectomy was then accomplished using bipolar cautery, and the temporal lobe at this level and the middle temporal gyrus was entered. The parenchyma of the brain did not appear normal. It was quite vascular. Furthermore, there was a hematoma mixed in with the brain itself. Thus a core biopsy was then performed in the temporal tip. The overlying dura was inspected and it was quite thickened, approximately 0.25 cm thick, and it was also highly vascular, and thus a big section of the dura was also trimmed using bipolar cautery followed by scissors, and several pieces of this vascularized dura was resected for pathology. Furthermore, sample of the temporal lobe was cultured.,Hemostasis after evacuation of the intracerebral hematoma using controlled suction as well as significant biopsy of the overlying dura as well as intraparenchymal lesion was accomplished. No attempt was made to enter into the sylvian fissure. Once hemostasis was meticulously achieved, the brain was inspected. It still was quite swollen, known that there was still hematoma in the parenchyma of the brain. However, at this time it was felt that since there is no diagnosis made intraoperatively, we would need to stage this surgery further should it be needed once the diagnosis is confirmed. DuraGen was then used for duraplasty because of the resected dura. The bone flap was then repositioned using Lorenz plating system. Then a medium Hemovac drain was placed in subdural space. Temporalis muscle was approximated using 2-0 Vicryl. The galea was then reapproximated using inverted 2-0 Vicryl. The scalp was then reapproximated using staples. The head was then dressed and wrapped in a sterile fashion.,She was witnessed to be extubated in the operating room postoperatively, and she followed commands briskly. The pupils are 3 mm bilaterally reactive to light. I accompanied her and transported her to the ICU where I signed out to the ICU attending. | null |
2,878 | Patient presents for further evaluation of feet and hand cramps. He describes that the foot cramps are much more notable than the hand ones. He reports that he develops muscle contractions of his toes on both feet. These occur exclusively at night. | Neurology | Feet & Hand Cramping | HISTORY OF PRESENT ILLNESS: , The patient is a 61-year-old right-handed gentleman who presents for further evaluation of feet and hand cramps. He states that for the past six months he has experienced cramps in his feet and hands. He describes that the foot cramps are much more notable than the hand ones. He reports that he develops muscle contractions of his toes on both feet. These occur exclusively at night. They may occur about three times per week. When he develops these cramps, he stands up to relieve the discomfort. He notices that the toes are in an extended position. He steps on the ground and they seem to "pop into place." He develops calf pain after he experiences the cramp. Sometimes they awaken him from his sleep.,He also has developed cramps in his hands although they are less severe and less frequent than those in his legs. These do not occur at night and are completely random. He notices that his thumb assumes a flexed position and sometimes he needs to pry it open to relieve the cramp.,He has never had any symptoms like this in the past. He started taking Bactrim about nine months ago. He had taken this in the past briefly, but has never taken it as long as he has now. He cannot think of any other possible contributing factors to his symptoms.,He has a history of HIV for 21 years. He was taking antiretroviral medications, but stopped about six or seven years ago. He reports that he was unable to tolerate the medications due to severe stomach upset. He has a CD4 count of 326. He states that he has never developed AIDS. He is considering resuming antiretroviral treatment.,PAST MEDICAL HISTORY:, He has diabetes, but this is well controlled. He also has hepatitis C and HIV.,CURRENT MEDICATIONS: , He takes insulin and Bactrim.,ALLERGIES: , He has no known drug allergies.,SOCIAL HISTORY: , He lives alone. He recently lost his partner. This happened about six months ago. He denies alcohol, tobacco, or illicit drug use. He is now retired. He is very active and walks about four miles every few days.,FAMILY HISTORY: , His father and mother had diabetes.,REVIEW OF SYSTEMS: , A complete review of systems was obtained and was negative except for as mentioned above. This is documented in the handwritten notes from today's visit.,PHYSICAL EXAMINATION:,Vital Signs: Blood pressure 130/70 | null |
2,879 | This 62-year-old white female has essential tremor and mild torticollis. Tremor not bothersome for most activities of daily living, but she does have a great difficulty writing, which is totally illegible. | Neurology | Essential Tremor & Torticollis | REASON FOR CONSULT: , Essential tremor and torticollis.,HISTORY OF PRESENT ILLNESS: , This is a 62-year-old right-handed now left-handed white female with tremor since 5th grade. She remembers that the tremors started in her right hand around that time subsequently later on in early 20s she was put on propranolol for the tremor and more recently within the last 10 years she has been put on primidone and clonazepam. She thinks that her clonazepam is helping her a lot especially with anxiety and stress, and this makes the tremor better. She has a lot of trouble with her writing because of tremor but does not report as much problem with other activities of daily living like drinking from a cup and doing her day-to-day activity. Since around 6 to 7 years, she has had a head tremor, which is mainly "no- no" and occasional voice tremor also. Additionally, the patient has been diagnosed with migraine headaches without aura, which are far and few apart. She also has some stress incontinence. Last MRI brain was done in 2001 reportedly normal.,CURRENT MEDICATIONS:,1. Klonopin 0.5 mg twice a day.,2. Primidone 100 mg b.i.d.,3. Propranolol long-acting 80 mg once in the morning.,PAST MEDICAL HISTORY: , Essential tremor, cervical dystonia, endometriosis, migraine headaches without aura, left ear sensorineural deafness, and basal cell carcinoma resection on the nose.,PAST SURGICAL HISTORY: , L5-S1 lumbar laminectomy in 1975, exploratory laparotomy in 1967, tonsillectomy and adenoidectomy, and anal fissure surgery in 1975.,FAMILY HISTORY: , Both parents have ET and hypertension. Maternal cousin with lupus.,SOCIAL HISTORY: , Denies any smoking or alcohol. She is married since 44 years, has 3 children. She used to work as a labor and delivery nurse up until early 2001 when she retired.,REVIEW OF SYSTEMS: , No fever, chills, nausea or vomiting. No visual complaints. She complains of hearing decreased on the left. No chest pain or shortness of breath. No constipation. She does give a history of urge incontinence. No rashes. No depressive symptoms.,PHYSICAL EXAMINATION:,VITAL SIGNS: Blood pressure is 131/72, pulse is 50, and weight is 71.3 kg. HEENT: PERRLA. EOMI. CARDIOVASCULAR: S1 and S2 normal. Regular rate and rhythm. She does have a rash over the right ankle with a prior basal cell carcinoma was resected. NEUROLOGIC: Alert and oriented x4. Speech shows a voice tremor occasionally. Language is intact. Cranial nerves II through XII intact. Motor examination showed 5/5 power in all extremities with minimal increased tone. Sensory examination was intact to light touch. Reflexes were brisk bilaterally, but they were equal and both toes were downgoing. Her coordination showed minimal intentional component to bilateral finger-to-nose. Gait was intact. Lot of swing on Romberg's. The patient did have a tremor both upper extremities, right more than left. She did have a head tremor, which was no-no variety, and she had a minimal torticollis with her head twisted to the left.,ASSESSMENT AND PLAN: , This 62-year-old white female has essential tremor and mild torticollis. Tremor not bothersome for most activities of daily living, but she does have a great difficulty writing, which is totally illegible. The patient did not wish to change any of her medication doses at this point. We will go ahead and check MRI brain, and we will get the films later. We will see her back in 3 months. Also, the patient declined any possible Botox for the mild torticollis she has at this point. | neurology, clonazepam, difficulty writing, head tremor, voice tremor, migraine headaches, mri brain, essential tremor, torticollis, carcinoma, |
2,880 | Fall with questionable associated loss of consciousness. Left parietal epidural hematoma. | Neurology | Epidural Hematoma | CC:, Fall with questionable associated loss of consciousness.,HX: ,This 81 y/o RHM fell down 20 steps on the evening of admission, 1/10/93, while attempting to put his boots on at the top of the staircase. He was evaluated locally and was amnestic to the event at the time of examination. A HCT scan was obtained and he was transferred to UIHC, Neurosurgery.,MEDS:, Lasix 40mg qd, Zantac 150mg qd, Lanoxin 0.125mg qd, Capoten 2.5mg bid, Salsalate 750mg tid, ASA 325mg qd, "Ginsana" (Ginseng) 100mg bid.,PMH: ,1)Atrial fibrillation, 2)Right hemisphere stroke, 11/22/88, with associated left hemiparesis and amaurosis fugax. This was followed by a RCEA, 12/1/88 for 98% stenosis. The stroke symptoms/signs resolved. 3)DJD, 4)Right TKR 2-3 years ago, 5)venous stasis; with no h/o DVT, 6)former participant in NASCET, 7)TURP for BPH. No known allergies.,FHX:, Father died of an MI at unknown age, Mother died of complications of a dental procedure. He has one daughter who is healthy.,SHX:, Married. Part-time farmer. Denied tobacco/ETOH/illicit drug use.,EXAM: ,BP157/86, HR100 and irregular, RR20, 36.7C, 100%SaO2,MS: A&O to person, place, time. Speech fluent and without dysarthria.,CN: Pupils 3/3 decreasing to 2/2 on exposure to light. EOM intact. VFFTC. Optic disks were flat. Face was symmetric with symmetric movement. The remainder of the CN exam was unremarkable.,Motor: 5/5 strength throughout with normal muscle tone and bulk.,Sensory: unremarkable.,Coord: unremarkable.,Station/Gait: not mentioned in chart.,Reflexes: symmetric. Plantar responses were flexor, bilaterally.,Gen Exam: CV:IRRR without murmur. Lungs: CTA. Abdomen: NT, ND, NBS.,HEENT: abrasion over the right forehead.,Extremity: distal right leg edema/erythema (just above the ankle). tender to touch.,COURSE:, 1/10/93, (outside)HCT was reviewed, It revealed a left parietal epidural hematoma. GS, PT/PTT, UA, and CBC were unremarkable. RLE XR revealed a fracture of the right lateral malleolus for which he was casted. Repeat HCTs showed no change in the epidural hematoma and he was discharged home on DPH. | neurology, loss of consciousness, parietal epidural hematoma, parietal epidural, epidural hematoma, consciousness, epidural, hematoma, |
2,881 | Falls at home. Anxiety and depression. The patient had been increasingly anxious and freely admitted that she was depressed at home. | Neurology | Falls - Discharge Summary | CHIEF COMPLAINT:, Falls at home.,HISTORY OF PRESENT ILLNESS:, The patient is an 82-year-old female who fell at home and presented to the emergency room with increased anxiety. Family members who are present state that the patient had been increasingly anxious and freely admitted that she was depressed at home. They noted that she frequently came to the emergency room for "attention." The patient denied any chest pain or pressure and no change to exercise tolerance. The patient denied any loss of consciousness or incontinence. She denies any seizure activity. She states that she "tripped" at home. Family states she frequently takes Darvocet for her anxiety and that makes her feel better, but they are afraid she is self medicating. They stated that she has numerous medications at home, but they were not sure if she was taking them. The patient been getting along for a number of years and has been doing well, but recently has been noting some decline primarily with regards to her depression. The patient denied SI or HI.,PHYSICAL EXAMINATION:,GENERAL: The patient is pleasant 82-year-old female in no acute distress.,VITAL SIGNS: Stable.,HEENT: Negative.,NECK: Supple. Carotid upstrokes are 2+.,LUNGS: Clear.,HEART: Normal S1 and S2. No gallops. Rate is regular.,ABDOMEN: Soft. Positive bowel sounds. Nontender.,EXTREMITIES: No edema. There is some ecchymosis noted to the left great toe. The area is tender; however, metatarsal is nontender.,NEUROLOGICAL: Grossly nonfocal.,HOSPITAL COURSE: , A psychiatric evaluation was obtained due to the patient's increased depression and anxiety. Continue Paxil and Xanax use was recommended. The patient remained medically stable during her hospital stay and arrangements were made for discharge to a rehabilitation program given her recent falls.,DISCHARGE DIAGNOSES:,1. Falls ,2. Anxiety and depression.,3. Hypertension.,4. Hypercholesterolemia.,5. Coronary artery disease.,6. Osteoarthritis.,7. Chronic obstructive pulmonary disease.,8. Hypothyroidism.,CONDITION UPON DISCHARGE: , Stable.,DISCHARGE MEDICATIONS: , Tylenol 650 mg q.6h. p.r.n., Xanax 0.5 q.4h. p.r.n., Lasix 80 mg daily, Isordil 10 mg t.i.d., KCl 20 mEq b.i.d., lactulose 10 g daily, Cozaar 50 mg daily, Synthroid 75 mcg daily, Singulair 10 mg daily, Lumigan one drop both eyes at bed time, NitroQuick p.r.n., Pravachol 20 mg daily, Feldene 20 mg daily, Paxil 20 mg daily, Minipress 2 mg daily, Provera p.r.n., Advair 250/50 one puff b.i.d., Senokot one tablet b.i.d., Timoptic one drop OU daily, and verapamil 80 mg b.i.d.,ALLERGIES: , None.,ACTIVITY: , Per PT.,FOLLOW-UP: , The patient discharged to a skilled nursing facility for further rehabilitation. | null |
2,882 | Evacuation of epidural hematoma and insertion of epidural drain. Epidural hematoma, cervical spine. Status post cervical laminectomy, C3 through C7 postop day #10. Central cord syndrome and acute quadriplegia. | Neurology | Epidural Hematoma Evacuation | PREOPERATIVE DIAGNOSES:,1. Epidural hematoma, cervical spine.,2. Status post cervical laminectomy, C3 through C7 postop day #10.,3. Central cord syndrome.,4. Acute quadriplegia.,POSTOPERATIVE DIAGNOSES:,1. Epidural hematoma, cervical spine.,2. Status post cervical laminectomy, C3 through C7 postop day #10.,3. Central cord syndrome.,4. Acute quadriplegia.,PROCEDURE PERFORMED:,1. Evacuation of epidural hematoma.,2. Insertion of epidural drain.,ANESTHESIA: , General.,COMPLICATIONS: ,None.,ESTIMATED BLOOD LOSS: ,200 cc.,HISTORY: ,This is a 64-year-old female who has had an extensive medical history beginning with coronary artery bypass done on emergent basis while she was in Maryland in April of 2003 after having myocardial infarction. She was then transferred to Beaumont Hospital, at which point, she developed a sternal abscess. The patient was treated for the abscess in Beaumont and then subsequently transferred to some other type of facility near her home in Warren, Michigan at which point, she developed a second what was termed minor myocardial infarction.,The patient subsequently recovered in a Cardiac Rehab Facility and approximately two weeks later, brings us to the month of August, at which time she was at home ambulating with a walker or a cane, and then sustained a fall and at that point she was unable to walk and had acute progressive weakness and was identified as having a central cord syndrome based on an MRI, which showed record signal change. The patient underwent cervical laminectomy and seemed to be improving subjectively in terms of neurologic recovery, but objectively there was not much improvement. Approximately 10 days after the surgery, brings us to today's date, the health officer was notified of the patient's labored breathing. When she examined the patient, she also noted that the patient was unable to move her extremities. She was concerned and called the Orthopedic resident who identified the patient to be truly quadriplegic. I was notified and ordered the operative crew to report immediately and recommended emergent decompression for the possibility of an epidural hematoma. On clinical examination, there was swelling in the posterior aspect of the neck. The patient has no active movement in the upper and lower extremity muscle groups. Reflexes are absent in the upper and lower extremities. Long track signs are absent. Sensory level is at the C4 dermatome. Rectal tone is absent. I discussed the findings with the patient and also the daughter. We discussed the possibility of this is permanent quadriplegia, but at this time, the compression of the epidural space was warranted and certainly for exploration reasons be sure that there is a hematoma there and they have agreed to proceed with surgery. They are aware that it is possible she had known permanent neurologic status regardless of my intervention and they have agreed to accept this and has signed the consent form for surgery.,OPERATIVE PROCEDURE: ,The patient was taken to OR #1 at ABCD General Hospital on a gurney. Department of Anesthesia administered fiberoptic intubation and general anesthetic. A Foley catheter was placed in the bladder. The patient was log rolled in a prone position on the Jackson table. Bony prominences were well padded. The patient's head was placed in the prone view anesthesia head holder. At this point, the wound was examined closely and there was hematoma at the caudal pole of the wound. Next, the patient was prepped and draped in the usual sterile fashion. The previous skin incision was reopened. At this point, hematoma properly exits from the wound. All sutures were removed and the epidural spaces were encountered at this time. The self-retaining retractors were placed in the depth of the wound. Consolidated hematoma was now removed from the wound. Next, the epidural space was encountered. There was no additional hematoma in the epidural space or on the thecal sac. A curette was carefully used to scrape along the thecal sac and there was no film or lining covering the sac. The inferior edge of the C2 lamina was explored and there was no compression at this level and the superior lamina of T1 was explored and again no compression was identified at this area as well. Next, the wound was irrigated copiously with one liter of saline using a syringe. The walls of the wound were explored. There was no active bleeding. Retractors were removed at this time and even without pressure on the musculature, there was no active bleeding. A #19 French Hemovac drain was passed percutaneously at this point and placed into the epidural space. Fascia was reapproximated with #1 Vicryl sutures, subcutaneous tissue with #3-0 Vicryl sutures. Steri-Strips covered the incision and dressing was then applied over the incision. The patient was then log rolled in the supine position on the hospital gurney. She remained intubated for airway precautions and transferred to the recovery room in stable condition. Once in the recovery room, she was alert. She was following simple commands and using her head to nod, but she did not have any active movement of her upper or lower extremities. Prognosis for this patient is guarded. | neurology, epidural hematoma, cervical spine, cervical laminectomy, central cord syndrome, acute quadriplegia, insertion of epidural drain, epidural drain, epidural space, hematoma, epidural, cervical, laminectomy, quadriplegia, |
2,883 | Encephalopathy related to normal-pressure hydrocephalus. | Neurology | Encephalopathy - Rehab Consult | ADMITTING DIAGNOSIS: , Encephalopathy related to normal-pressure hydrocephalus.,CHIEF COMPLAINT:, Diminished function secondary to above.,HISTORY: ,This pleasant gentleman was recently admitted to ABCD Medical Center and followed by the neurosurgical staff, including Dr. X, where normal-pressure hydrocephalus was diagnosed. He had a shunt placed and was stabilized medically. He has gotten a return of function to the legs and was started on some early therapy. Significant functional limitations have been identified and ongoing by the rehab admission team. Significant functional limitations have been ongoing. He will need to be near-independent at home for periods of time, and he is brought in now for rehabilitation to further address functional issues, maximize skills and safety and allow a safe disposition home.,PAST MEDICAL HISTORY: , Positive for prostate cancer, intermittent urinary incontinence and left hip replacement.,ALLERGIES: , No known drug allergies.,CURRENT MEDICATIONS,1. Tylenol as needed. ,2. Peri-Colace b.i.d.,SOCIAL HISTORY:, He is a nonsmoker and nondrinker. Prior boxer. He lives in a home where he would need to be independent during the day. Family relatives intermittently available. Goal is to return home to an independent fashion to that home setting.,FUNCTIONAL HISTORY: , Prior to admission was independent with activities of daily living and ambulatory skills. Presently, he has resumed therapies and noted to have supervision levels for most activities of daily living. Memory at minimal assist. Walking at supervision., REVIEW OF SYSTEMS: ,Negative for headaches, nausea, vomiting, fevers, chills, shortness of breath or chest pain currently. He has had some dyscoordination recently and headaches on a daily basis, most days, although the Tylenol does seem to control that pain.,PHYSICAL EXAMINATION,VITAL SIGNS: The patient is afebrile with vital signs stable.,HEENT: Oropharynx clear, extraocular muscles are intact.,CARDIOVASCULAR: Regular rate and rhythm, without murmurs, rubs or gallops.,LUNGS: Clear to auscultation bilaterally.,ABDOMEN: Nontender, nondistended, positive bowel sounds.,EXTREMITIES: Without clubbing, cyanosis, or edema. The calves are soft and nontender bilaterally.,NEUROLOGIC: No focal, motor or sensory losses through the lower extremities. He moves upper and lower extremities well. Bulk and tone normal in the upper and lower extremities. Cognitively showing intact with appropriate receptive and expressive skills.,IMPRESSION , | null |
2,884 | Patient returns for his first followup after shunt surgery. | Neurology | First Followup - Shunt Surgery | REASON FOR VISIT:, Mr. A is an 86-year-old man who returns for his first followup after shunt surgery.,HISTORY OF PRESENT ILLNESS: ,I have followed Mr. A since May 2008. He presented with eight to ten years of progressive gait impairment, cognitive impairment, and decreased bladder control. We established a diagnosis of adult hydrocephalus with the spinal catheter protocol in June of 2008 and ,Mr. A underwent shunt surgery performed by Dr. X on August 1st. A Medtronic Strata programmable shunt in the ventriculoperitoneal configuration programmed at level 2.0 was placed.,Mr. A comes today with his daughter, Pam and together they give his history.,Mr. A has had no hospitalizations or other illnesses since I last saw him. With respect to his walking, his daughter tells me that he is now able to walk to the dining room just fine, but could not before his surgery. His balance has improved though he still has some walking impairment. With respect to his bladder, initially there was some improvement, but he has leveled off and he wears a diaper.,With respect to his cognition, both Pam and the patient say that his thinking has improved. The other daughter, Patty summarized it best according to two of them. She said, "I feel like I can have a normal conversation with him again." Mr. A has had no headaches and no pain at the shunt site or at the abdomen.,MEDICATIONS: , Plavix 75 mg p.o. q.d., metoprolol 25 mg p.o. q.d., Flomax 0.4 mg p.o. q.d., Zocor 20 mg p.o. q.d., Detrol LA 4 mg p.o. q.d., lisinopril 10 mg p.o. q.d., Imodium daily, Omega-3, fish oil, and Lasix.,MAJOR FINDINGS:, Mr. A is a pleasant and cooperative man who is able to converse easily though his daughter adds some details.,Vital Signs: Blood pressure 124/80, heart rate is 64, respiratory rate is 18, weight 174 pounds, and pain is 0/10.,The shunt site was clean, dry, and intact and confirmed at a setting of 2.0.,Mental Status: Tested for recent and remote memory, attention span, concentration, and fund of knowledge. He scored 26/30 on the MMSE when tested with spelling and 25/30 when tested with calculations. Of note, he was able to get two of the three memory words with cuing and the third one with multiple choice. This was a slight improvement over his initial score of 23/30 with calculations and 24/30 with spelling and at that time he was unable to remember any memory words with cuing and only one with multiple choice.,Gait: Tested using the Tinetti assessment tool. He was tested without an assistive device and received a gait score of 6-8/12 and a balance of score of 12/16 for a total score of 18-20/28. This has slightly improved from his initial score of 15-17/28.,Cranial Nerves: Pupils are equal. Extraocular movements are intact. Face symmetric. No dysarthria.,Motor: Normal for bulk and strength.,Coordination: Slow for finger-to-nose.,IMAGING: , CT scan was reviewed from 10/15/2008. It shows a frontal horn span at the level of foramen of Munro of 4.6 cm with a 3rd ventricular contour that is flat with the span of 10 mm. By my reading, there is a tiny amount of blood in the right frontal region with just a tiny subdural collection. This was not noticed by the radiologist who stated no extraaxial fluid collections. There is also substantial small vessel ischemic change.,ASSESSMENT: , Mr. A has made some improvement since shunt surgery.,PROBLEMS/DIAGNOSES:,1. Adult hydrocephalus (331.5).,2. Gait impairment (781.2).,3. Urinary incontinence and urgency (788.33).,4. Cognitive impairment (290.0).,PLAN:, I had a long discussion with Mr. A and his daughter. We are all pleased that he has started to make some improvement with his hydrocephalus because I believe I see a tiny fluid collection in the right parietal region, I would like to leave the setting at 2.0 for another three months before we consider changing the shunt. I do not believe that this tiny amount of fluid is symptotic and it was not documented by the radiologist when he read the CT scan.,Mr. A asked me about whether he will be able to drive again. Unfortunately, I think it is unlikely that his speed of movement will improve to a level that he will be able to pass a driver's safety evaluation, however, occasionally patients surprise me by improving enough over 9 to 12 months that they are able to pass such a test. I would certainly be happy to recommend such a test if I believe ,Mr. A is likely to pass it and he is always welcome to enroll in a driver's safety program without my recommendation, however, I think it is exceeding unlikely that he has the capability of passing this rigorous test at this time. I also think it is quite likely he will not regain sufficient speed of motion to pass such a test. | null |
2,885 | Fall/loss of consciousness. | Neurology | Epidural Fluid Collection | CC:, Fall/loss of consciousness.,HX: ,This 44y/o male fell 15-20feet from a construction site scaffold landing on his head on a cement sidewalk. He was transported directly from the scene, approximately one mile east of UIHC. The patient developed labored breathing and an EMT attempted to intubate the patient in the UIHC ER garage, but upon evaluation in the ER, was found to be in his esophagus and was immediately replaced into the trachea. Replacement of the ET tube required succinylcholine. The patient remained in a C-collar during the procedure. Once in the ER the patient had a 15min period of bradycardia.,MEDS: ,none prior to accident.,PMH:, No significant chronic or recent illness. s/p left knee arthroplasty. h/o hand fractures.,FHX:, Unremarkable.,SHX:, Married. Rare cigarette use/Occasional Marijuana use/Social ETOH use per wife.,EXAM:, BP156/79. HR 74 RR (Ambu Bag ventilation via ET tube) 34.7C 72-100% O2Sat.,MS: Unresponsive to verbal stimulation. No spontaneous verbalization.,CN: Does not open/close eyes to command or spontaneously. Pupils 9/7 and nonreactive.,Corneas -/+. Gag +/+. Oculocephalic and Oculovestibular reflexes not performed.,Motor: minimal spontaneous movement of the 4 extremities.,Sensory: withdraws LUE and BLE to noxious stimulation.,Coord/Station/Gait: Not tested.,Reflexes: 1-2+ and symmetric throughout. Babinski signs were present bilaterally.,HEENT: severe facial injury with brain parenchyma and blood from the right nostril. Severe soft tissue swelling about side of head.,Gen Exam: CV: RRR without murmur. Lungs: CTA. Abdomen: distended after ET tube misplacement.,COURSE: ,HCT upon arrival, 10/29/92, revealed: Extensive parenchymal contusions in right fronto-parietal area. Pronounced diffuse brain swelling seemingly obliterates the mesencephalic cistern and 4th ventricle. Considerable mass effect is exerted upon the right lateral ventricle, near totally obliterating its contour. Massive subcutaneous soft tissue swelling is present along the right anterolateral parietal area. There are extensive fractures of the following: two component horizontal fractures throughout the floor of the right middle cranial fossa which includes the squamous and petrous portions of the temporal bone, as well as the greater wing of the sphenoid. Comminuted fractures of the aqueous portion of the temporal bone and parietal bone is noted on the right. Extensive comminution of the right half of the frontal bone and marked displacement is seen. Comminuted fractures of the medial wall of the right orbit and ethmoidal air cells is seen with near total opacification of the air cells. The medial and lateral walls of the maxillary sinus are fractured and minimally displaced, as well as the medial wall of the left maxillary sinus. The right zygomatic bone is fractured at its articulation with the sphenoid bone and displaced posteriorly.,Portable chest, c-spine and abdominal XRays were unremarkable, but limited studies. Abdominal CT was unremarkable.,Hgb 10.4g/dl, Hct29%, WBC17.4k/mm3, Plt 190K. ABG:7.28/48/46 on admission. Glucose 131.,The patient was hyperventilated, Mannitol was administered (1g/kg), and the patient was given a Dilantin loading dose. He was taken to surgery immediately following the above studies to decompress the contused brain and remove bony fragments from multiple skull fractures. The patient remained in a persistent vegetative state at UIHC, and upon the request of this wife his feeding tube was discontinued. He later expired. | neurology, loss of consciousness, soft tissue swelling, medial wall, maxillary sinus, sphenoid, collection, tube, bone, |
2,886 | EMG/Nerve Conduction Study showing sensory motor length-dependent neuropathy consistent with diabetes, severe left ulnar neuropathy, and moderate-to-severe left median neuropathy, | Neurology | EMG/Nerve Conduction Study - 4 | NERVE CONDUCTION STUDIES:, Bilateral ulnar sensory responses are absent. Bilateral median sensory distal latencies are prolonged with a severely attenuated evoked response amplitude. The left radial sensory response is normal and robust. Left sural response is absent. Left median motor distal latency is prolonged with attenuated evoked response amplitude. Conduction velocity across the forearm is mildly slowed. Right median motor distal latency is prolonged with a normal evoked response amplitude and conduction velocity. The left ulnar motor distal latency is prolonged with a severely attenuated evoked response amplitude both below and above the elbow. Conduction velocities across the forearm and across the elbow are prolonged. Conduction velocity proximal to the elbow is normal. The right median motor distal latency is normal with normal evoked response amplitudes at the wrist with a normal evoked response amplitude at the wrist. There is mild diminution of response around the elbow. Conduction velocity slows across the elbow. The left common peroneal motor distal latency evoked response amplitude is normal with slowed conduction velocity across the calf and across the fibula head. F-waves are prolonged.,NEEDLE EMG: , Needle EMG was performed on the left arm and lumbosacral and cervical paraspinal muscles as well as middle thoracic muscles using a disposable concentric needle. It revealed spontaneous activity in lower cervical paraspinals, left abductor pollicis brevis, and first dorsal interosseous muscles. There were signs of chronic reinnervation in triceps, extensor digitorum communis, flexor pollicis longus as well first dorsal interosseous and abductor pollicis brevis muscles.,IMPRESSION: , This electrical study is abnormal. It reveals the following:,1. A sensory motor length-dependent neuropathy consistent with diabetes.,2. A severe left ulnar neuropathy. This is probably at the elbow, although definitive localization cannot be made.,3. Moderate-to-severe left median neuropathy. This is also probably at the carpal tunnel, although definitive localization cannot be made.,4. Right ulnar neuropathy at the elbow, mild.,5. Right median neuropathy at the wrist consistent with carpal tunnel syndrome, moderate.,6. A left C8 radiculopathy (double crush syndrome).,7. There is no evidence for thoracic radiculitis.,The patient has made very good response with respect to his abdominal pain since starting Neurontin. He still has mild allodynia and is waiting for authorization to get insurance coverage for his Lidoderm patch. He is still scheduled for MRI of C-spine and T-spine. I will see him in followup after the above scans. | neurology, emg, nerve conduction study, nerve conduction studies, needle emg, electrical study, neuropathy, ulnar neuropathy, median neuropathy, severely attenuated evoked response, normal evoked response amplitude, attenuated evoked response amplitude, median motor distal latency, motor distal latency, abductor pollicis, pollicis brevis, dorsal interosseous, carpal tunnel, conduction, emg/nerve, needle, |
2,887 | Nerve conduction screen demonstrates borderline median sensory and borderline distal median motor responses in both hands. The needle EMG examination is remarkable for rather diffuse active denervation changes in most muscles of the right upper and right lower extremity tested. | Neurology | EMG/Nerve Conduction Study - 9 | NERVE CONDUCTION TESTING AND EMG EVALUATION,1. Right median sensory response 3.0, amplitude 2.5, distance 100.,2. Right ulnar sensory response 2.1, amplitude 1, distance 90.,3. Left median sensory response 3.0, amplitude 1.2, distance 100.,4. Left median motor response distal 4.2, proximal 9, amplitude 2.2, distance 290, velocity 60.4 m/sec.,5. Right median motor response distal 4.3, proximal 9.7, amplitude 2, and velocity 53.7 m/sec.,6. Right ulnar motor response distal 2.5, proximal 7.5, amplitude 2, distance 300, velocity 60 m/sec.,NEEDLE EMG TESTING,1. ,RIGHT BICEPS:, Fibrillations 0, fasciculations occasional, positive waves 0. Motor units, increased needle insertional activity and mild decreased number of motor units firing.,2. ,RIGHT TRICEPS:, Fibrillations 1+, fasciculations occasional to 1+, positive waves 1+. Motor units, increased needle insertional activity and decreased number of motor units firing.,3. ,EXTENSOR DIGITORUM:, Fibrillations 0, fasciculations rare, positive waves 0, motor units probably normal.,4. ,FIRST DORSAL INTEROSSEOUS: , Fibrillations 2+, fasciculations 1+, positive waves 2+. Motor units, decreased number of motor units firing.,5. ,RIGHT ABDUCTOR POLLICIS BREVIS:, Fibrillations 1+, fasciculations 1+, positive waves 0. Motor units, decreased number of motor units firing.,6. , FLEXOR CARPI ULNARIS:, Fibrillations 1+, occasionally entrained, fasciculations rare, positive waves 1+. Motor units, decreased number of motor units firing.,7. ,LEFT FIRST DORSAL INTEROSSEOUS:, Fibrillations 1+, fasciculations 1+, positive waves occasional. Motor units, decreased number of motor units firing.,8. ,LEFT EXTENSOR DIGITORUM:, Fibrillations 1+, fasciculations 1+. Motor units, decreased number of motor units firing.,9. ,RIGHT VASTUS MEDIALIS:, Fibrillations 1+ to 2+, fasciculations 1+, positive waves 1+. Motor units, decreased number of motor units firing.,10. ,ANTERIOR TIBIALIS: , Fibrillations 2+, occasionally entrained, fasciculations 1+, positive waves 1+. Motor units, increased proportion of polyphasic units and decreased number of motor units firing. There is again increased needle insertional activity.,11. ,RIGHT GASTROCNEMIUS:, Fibrillations 1+, fasciculations 1+, positive waves 1+. Motor units, marked decreased number of motor units firing.,12. ,LEFT GASTROCNEMIUS:, Fibrillations 1+, fasciculations 1+, positive waves 2+. Motor units, marked decreased number of motor units firing.,13. ,LEFT VASTUS MEDIALIS: , Fibrillations occasional, fasciculations occasional, positive waves 1+. Motor units, decreased number of motor units firing.,IMPRESSION: | null |
2,888 | A woman with a history of progression of dysphagia for the past year, dysarthria, weakness of her right arm, cramps in her legs, and now with progressive weakness in her upper extremities. Abnormal electrodiagnostic study. | Neurology | EMG/Nerve Conduction Study - 8 | REFERRING DIAGNOSIS: , Motor neuron disease.,PERTINENT HISTORY AND EXAMINATION:, Briefly, the patient is an 83-year-old woman with a history of progression of dysphagia for the past year, dysarthria, weakness of her right arm, cramps in her legs, and now with progressive weakness in her upper extremities.,SUMMARY: ,The right median sensory response showed a borderline normal amplitude for age with mild slowing of conduction velocity. The right ulnar sensory amplitude was reduced with slowing of the conduction velocity. The right radial sensory amplitude was reduced with slowing of the conduction velocity. The right sural and left sural sensory responses were absent. The right median motor response showed a prolonged distal latency across the wrist, with proximal slowing. The distal amplitude was very reduced, and there was a reduction with proximal stimulation. The right ulnar motor amplitude was borderline normal, with slowing of the conduction velocity across the elbow. The right common peroneal motor response showed a decreased amplitude when recorded from the EDB, with mild slowing of the proximal conduction velocity across the knee. The right tibial motor response showed a reduced amplitude with prolongation of the distal latency. The left common peroneal response recorded from the EDB showed a decreased amplitude with mild distal slowing. The left tibial motor response showed a decreased amplitude with a borderline normal distal latency. The minimum F-wave latencies were normal with the exception of a mild prolongation of the ulnar F-wave latency, and the tibial F-wave latency as indicated above. With repetitive nerve stimulation, there was no significant decrement noted in either the right nasalis or the right trapezius muscles. Concentric needle EMG studies were performed in the right lower extremity, right upper extremity, thoracic paraspinals, and in the tongue. There was evidence of increased insertional activity in the right tibialis anterior muscle, with evidence of fasciculations noted in several lower and upper extremity muscles and in the tongue. In addition, there was evidence of increased amplitude, long duration and polyphasic motor units with a decreased recruitment noted in most muscles tested as indicated in the table above.,INTERPRETATION: , Abnormal electrodiagnostic study. There is electrodiagnostic evidence of a disorder of the anterior motor neurons affecting at least four segments. There is also evidence of a more generalized neuropathy that seems to be present in both the upper and lower extremities. There is also evidence of a right median mononeuropathy at the wrist and a right ulnar neuropathy at the elbow. Even despite the patient's age, the decrease in sensory responses is concerning, and makes it difficult to be certain about the diagnosis of motor neuron disease. However, the overall changes on the needle EMG would be consistent with a diagnosis of motor neuron disease. The patient will return for further evaluation. | neurology, electrodiagnostic study, electrodiagnostic, edb, latency, nerve conduction study, emg, motor neuron disease, distal latency, motor response, motor, amplitude, conduction |
2,889 | The patient is status post C3-C4 anterior cervical discectomy and fusion. | Neurology | EMG/Nerve Conduction Study - 5 | She has an extensive past medical history of rheumatoid arthritis, fibromyalgia, hypertension, hypercholesterolemia, and irritable bowel syndrome. She has also had bilateral carpal tunnel release.,On examination, normal range of movement of C-spine. She has full strength in upper and lower extremities. Normal straight leg raising. Reflexes are 2 and symmetric throughout. No Babinski. She has numbness to light touch in her right big toe.,NERVE CONDUCTION STUDIES: The right median palmar sensory distal latencies are minimally prolonged with minimally attenuated evoked response amplitude. Bilateral tibial motor nerves could not be obtained (technical). The remaining nerves tested revealed normal distal latencies, evoked response amplitudes, conduction velocities, F-waves, and H. reflexes.,NEEDLE EMG: Needle EMG was performed on the right arm and leg and lumbosacral and cervical paraspinal muscles and the left FDI. It revealed 2+ spontaneous activity in the right APB and FDI and 1+ spontaneous activity in lower cervical paraspinals, lower and middle lumbosacral paraspinals, right extensor digitorum communis muscle, and right pronator teres. There was evidence of chronic denervation in the right first dorsal interosseous, pronator teres, abductor pollicis brevis, and left first dorsal interosseous.,IMPRESSION: This electrical study is abnormal. It reveals the following:,1. An active right C8/T1 radiculopathy. Electrical abnormalities are moderate.,2. An active right C6/C7 radiculopathy. Electrical abnormalities are mild.,3. Evidence of chronic left C8/T1 denervation. No active denervation.,4. Mild right lumbosacral radiculopathies. This could not be further localized because of normal EMG testing in the lower extremity muscles.,5. There is evidence of mild sensory carpal tunnel on the right (she has had previous carpal tunnel release).,Results were discussed with the patient. It appears that she has failed conservative therapy and I have recommended to her that she return to Dr. X for his assessment for possible surgery to her C-spine. She will continue with conservative therapy for the mild lumbosacral radiculopathies. | neurology, emg, nerve conduction study, needle emg, paraspinal muscles, radiculopathy, electrical abnormalities, carpal tunnel release, evoked response, lumbosacral radiculopathies, conservative therapy, carpal tunnel, conduction, emg/nerve, |
2,890 | Patient had movor vehicle accirdent and may have had a brief loss of consciousness. Shortly thereafter she had some blurred vision, Since that time she has had right low neck pain and left low back pain. | Neurology | EMG/Nerve Conduction Study - 7 | HISTORY: , The patient is a 34-year-old right-handed female who states her symptoms first started after a motor vehicle accident in September 2005. She may have had a brief loss of consciousness at the time of the accident since shortly thereafter she had some blurred vision, which lasted about a week and then resolved. Since that time she has had right low neck pain and left low back pain. She has been extensively worked up and treated for this. MRI of the C & T spine and LS spine has been normal. She has improved significantly, but still complains of pain. In June of this year she had different symptoms, which she feels are unrelated. She had some chest pain and feeling of tightness in the left arm and leg and face. By the next morning she had numbness around her lips on the left side and encompassing the whole left arm and leg. Symptoms lasted for about two days and then resolved. However, since that time she has had intermittent numbness in the left hand and leg. The face numbness has completely resolved. Symptoms are mild. She denies any previous similar episodes. She denies associated dizziness, vision changes incoordination, weakness, change in gait, or change in bowel or bladder function. There is no associated headache.,Brief examination reveals normal motor examination with no pronator drift and no incoordination. Normal gait. Cranial nerves are intact. Sensory examination reveals normal facial sensation. She has normal and symmetrical light touch, temperature, and pinprick in the upper extremities. In the lower extremities she has a feeling of dysesthesia in the lateral aspect of the left calf into the lateral aspect of the left foot. In this area she has normal light touch and pinprick. She describes it as a strange unusual sensation.,NERVE CONDUCTION STUDIES: , Motor and sensory distal latencies, evoked response amplitudes, conduction velocities, and F-waves are normal in the left arm and leg.,NEEDLE EMG: , Needle EMG was performed in the left leg, lumbosacral paraspinal, right tibialis anterior, and right upper thoracic paraspinal muscles using a disposable concentric needle. It revealed normal insertional activity, no spontaneous activity, and normal motor unit action potential form in all muscles tested.,IMPRESSION: , This electrical study is normal. There is no evidence for peripheral neuropathy, entrapment neuropathy, plexopathy, or lumbosacral radiculopathy. EMG was also performed in the right upper thoracic paraspinal where she has experienced a lot of pain since the motor vehicle accident. This was normal.,Based on her history of sudden onset of left face, arm, and leg weakness as well as a normal EMG and MRI of her spine I am concerned that she had a central event in June of this year. Symptoms are now very mild, but I have ordered an MRI of the brain with and without contrast and MRA of the head and neck with contrast to further elucidate her symptoms. Once she has the test done she will phone me and further management will be based on the results. | neurology, nerve conduction studies, motor, sensory, distal latencies, evoked response, conduction velocities, needle emg, loss of consciousness, motor vehicle accident, thoracic paraspinal, needle, paraspinal, conduction, |
2,891 | Electroencephalographic findings and interpretation | Neurology | Electroencephalography | HISTORY:, This is a digital EEG performed on a 75-year-old male with seizures.,BACKGROUND ACTIVITY:, The background activity consists of a 8 Hz to 9 Hz rhythm arising in the posterior head region. This rhythm is also accompanied by some beta activity which occurs infrequently. There are also muscle contractions occurring at 4 Hz to 5 Hz which suggests possible Parkinson's. Part of the EEG is obscured by the muscle contraction artifact. There are also left temporal sharps occurring infrequently during the tracing. At one point of time, there was some slowing occurring in the right frontal head region.,ACTIVATION PROCEDURES:, Photic stimulation was performed and did not show any significant abnormality.,SLEEP PATTERNS:, No sleep architecture was observed during this tracing.,IMPRESSION:, This awake/alert/drowsy EEG is abnormal due to the presence of slowing in the right frontal head region, due to the presence of sharps arising in the left temporal head region, and due to the tremors. The slowing can be consistent with underlying structural abnormalities, so a stroke, subdural hematoma, etc., should be ruled out. The tremor probably represents a Parkinson's tremor and the sharps arising in the left temporal head region can potentially give way to seizures or may also represent underlying structural abnormalities, so clinical correlation is recommended. | neurology, electroencephalography, eeg, hz rhythm, parkinson's tremor, photic stimulation, frontal head region, temporal head region, muscle contractions, seizures, parkinson's, temporal, |
2,892 | A right-handed female with longstanding intermittent right low back pain, who was involved in a motor vehicle accident with no specific injury at that time. | Neurology | EMG/Nerve Conduction Study - 3 | HISTORY: , The patient is a 56-year-old right-handed female with longstanding intermittent right low back pain, who was involved in a motor vehicle accident in September of 2005. At that time, she did not notice any specific injury. Five days later, she started getting abnormal right low back pain. At this time, it radiates into the buttocks down the posterior aspect of her thigh and into the right lateral aspect of her calf. Symptoms are worse when sitting for any length of time, such as driving a motor vehicle. Mild symptoms when walking for long periods of time. Relieved by standing and lying down. She denies any left leg symptoms or right leg weakness. No change in bowel or bladder function. Symptoms have slowly progressed. She has had Medrol Dosepak and analgesics, which have not been very effective. She underwent a spinal epidural injection, which was effective for the first few hours, but she had recurrence of the pain by the next day. This was done four and a half weeks ago.,On examination, lower extremities strength is full and symmetric. Straight leg raising is normal.,OBJECTIVE:, Sensory examination is normal to all modalities. Full range of movement of lumbosacral spine. Mild tenderness over lumbosacral paraspinal muscles and sacroiliac joint. Deep tendon reflexes are 2+ and symmetric at the knees, 2 at the left ankle and 1+ at the right ankle.,NERVE CONDUCTION STUDIES:, Motor and sensory distal latencies, evoked response, amplitudes, conduction velocities, and F-waves are normal in the lower extremities. Right tibial H-reflex is slightly prolonged when compared to the left tibial H-reflex.,NEEDLE EMG:, Needle EMG was performed in both lower extremities and lumbosacral paraspinal muscles using the disposable concentric needle. It revealed increased insertional activity in the right mid and lower lumbosacral paraspinal muscles as well as right peroneus longus muscle. There were signs of chronic denervation in right tibialis anterior, peroneus longus, gastrocnemius medialis, and left gastrocnemius medialis muscles.,IMPRESSION: , This electrical study is abnormal. It reveals the following:,1. A mild right L5 versus S1 radiculopathy.,2. Left S1 nerve root irritation. There is no evidence of active radiculopathy.,3. There is no evidence of plexopathy, myopathy or peripheral neuropathy.,MRI of the lumbosacral spine was personally reviewed and reveals bilateral L5-S1 neuroforaminal stenosis, slightly worse on the right. Results were discussed with the patient and her daughter. I would recommend further course of spinal epidural injections with Dr. XYZ. If she has no response, then surgery will need to be considered. She agrees with this approach and will followup with you in the near future. | neurology, emg, nerve conduction study, radiculopathy, peripheral neuropathy, nerve root irritation, motor vehicle accident, lumbosacral paraspinal muscles, spinal epidural, lumbosacral spine, peroneus longus, gastrocnemius medialis, lower extremities, emg/nerve, conduction, needle |
2,893 | Patient with a past medical history of a left L5-S1 lumbar microdiskectomy with complete resolution of left leg symptoms. | Neurology | EMG/Nerve Conduction Study - 6 | HISTORY:, The patient is a 46-year-old right-handed gentleman with a past medical history of a left L5-S1 lumbar microdiskectomy in 1998 with complete resolution of left leg symptoms, who now presents with a four-month history of gradual onset of right-sided low back pain with pain radiating down into his buttock and posterior aspect of his right leg into the ankle. Symptoms are worsened by any activity and relieved by rest. He also feels that when the pain is very severe, he has some subtle right leg weakness. No left leg symptoms. No bowel or bladder changes.,On brief examination, full strength in both lower extremities. No sensory abnormalities. Deep tendon reflexes are 2+ and symmetric at the patellas and absent at both ankles. Positive straight leg raising on the right.,MRI of the lumbosacral spine was personally reviewed and reveals a right paracentral disc at L5-S1 encroaching upon the right exiting S1 nerve root.,NERVE CONDUCTION STUDIES:, Motor and sensory distal latencies, evoked response amplitudes, and conduction velocities are normal in the lower extremities. The right common peroneal F-wave is minimally prolonged. The right tibial H reflex is absent.,NEEDLE EMG:, Needle EMG was performed on the right leg, left gastrocnemius medialis muscle, and right lumbosacral paraspinal muscles using a disposable concentric needle. It revealed spontaneous activity in the right gastrocnemius medialis, gluteus maximus, and lower lumbosacral paraspinal muscles. There was evidence of chronic denervation in right gastrocnemius medialis and gluteus maximus muscles.,IMPRESSION: , This electrical study is abnormal. It reveals an acute right S1 radiculopathy. There is no evidence for peripheral neuropathy or left or right L5 radiculopathy.,Results were discussed with the patient and he is scheduled to follow up with Dr. X in the near future. | neurology, microdiskectomy, needle emg, nerve conduction studies, lumbosacral paraspinal muscles, lumbar microdiskectomy, lower extremities, lumbosacral paraspinal, paraspinal muscles, gluteus maximus, leg symptoms, gastrocnemius medialis, emg/nerve, conduction, lumbosacral, needle, gastrocnemius, medialis, muscles, |
2,894 | A 21-channel digital electroencephalogram was performed on a patient in the awake state. | Neurology | Electroencephalogram - 4 | PROCEDURE:, A 21-channel digital electroencephalogram was performed on a patient in the awake state. Per the technician's notes, the patient is taking Depakene.,The recording consists of symmetric 9 Hz alpha activity. Throughout the recording, repetitive episodes of bursts of 3 per second spike and wave activity are noted. The episodes last from approximately1 to 7 seconds. The episodes are exacerbated by hyperventilation.,IMPRESSION:, Abnormal electroencephalogram with repetitive bursts of 3 per second spike and wave activity exacerbated by hyperventilation. This activity could represent true petit mal epilepsy. Clinical correlation is suggested. | neurology, alpha activity, wave activity, hyperventilation, electroencephalogramNOTE,: Thesetranscribed medical transcription sample reports and examples are provided by various users andare for reference purpose only. MTHelpLine does not certify accuracy and quality of sample reports.These transcribed medical transcription sample reports may include some uncommon or unusual formats;this would be due to the preference of the dictating physician. All names and dates have beenchanged (or removed) to keep confidentiality. Any resemblance of any type of name or date orplace or anything else to real world is purely incidental. |
2,895 | The patient with longstanding bilateral arm pain, which is predominantly in the medial aspect of arms and hands, as well as left hand numbness, worse at night and after doing repetitive work with left hand. | Neurology | EMG/Nerve Conduction Study - 1 | HISTORY: , The patient is a 52-year-old right-handed female with longstanding bilateral arm pain, which is predominantly in the medial aspect of her arms and hands as well as left hand numbness, worse at night and after doing repetitive work with her left hand. She denies any weakness. No significant neck pain, change in bowel or bladder symptoms, change in gait, or similar symptoms in the past. She is on Lyrica for the pain, which has been somewhat successful.,Examination reveals positive Phalen's test on the left. Remainder of her neurological examination is normal.,NERVE CONDUCTION STUDIES: ,The left median motor distal latency is prolonged with normal evoked response amplitude and conduction velocity. The left median sensory distal latency is prolonged with an attenuated evoked response amplitude. The right median sensory distal latency is mildly prolonged with a mildly attenuated evoked response amplitude. The right median motor distal latency and evoked response amplitude is normal. Left ulnar motor and sensory and left radial sensory responses are normal. Left median F-wave is normal.,NEEDLE EMG:, Needle EMG was performed on the left arm, right first dorsal interosseous muscle, and bilateral cervical paraspinal muscles. It revealed spontaneous activity in the left abductor pollicis brevis muscle. There is increased insertional activity in the right first dorsal interosseous muscle. Both interosseous muscles showed signs of reinnervation. Left extensor digitorum communis muscle showed evidence of reduced recruitment. Cervical paraspinal muscles were normal.,IMPRESSION: , This electrical study is abnormal. It reveals the following: A left median neuropathy at the wrist consistent with carpal tunnel syndrome. Electrical abnormalities are moderate-to-mild bilateral C8 radiculopathies. This may be an incidental finding.,I have recommended MRI of the spine without contrast and report will be sent to Dr. XYZ. She will follow up with Dr. XYZ with respect to treatment of the above conditions. | neurology, nerve conduction study, emg, neuropathy, median motor distal latency, median sensory distal latency, attenuated evoked response amplitude, emg/nerve conduction study, sensory distal latency, attenuated evoked response, dorsal interosseous muscle, cervical paraspinal muscles, emg/nerve conduction, conduction study, median motor, needle emg, distal latency, evoked response, emg/nerve, bilateral, evoked, conduction, |
2,896 | Electroencephalogram (EEG). This is an 18-channel recording obtained using the standard scalp and referential electrodes observing the 10/20 international system. | Neurology | Electroencephalogram - 2 | REPORT: ,This is an 18-channel recording obtained using the standard scalp and referential electrodes observing the 10/20 international system. The patient was reported to be cooperative and was awake throughout the recording.,CLINICAL NOTE: ,This is a 51-year-old male, who is being evaluated for dizziness. Spontaneous activity is fairly well organized, characterized by low-to-medium voltage waves of about 8 to 9 Hz seen mainly from the posterior head region. Intermixed with it is a moderate amount of low voltage fast activity seen from the anterior head region.,Eye opening caused a bilateral symmetrical block on the first run. In addition to the above description, movement of muscle and other artifacts are seen.,On subsequent run, no additional findings were seen.,During subsequent run, again no additional findings were seen.,Hyperventilation was omitted.,Photic stimulation was performed, but no clear-cut photic driving was seen.,EKG was monitored during this recording and it showed normal sinus rhythm when monitored.,IMPRESSION: ,This record is essentially within normal limits. Clinical correlation is recommended. | neurology, referential electrodes, scalp, hyperventilation, photic stimulation, electroencephalogram |
2,897 | Electroencephalogram (EEG). Photic stimulation reveals no important changes. Essentially normal. | Neurology | Electroencephalogram - 1 | REPORT:, The electroencephalogram shows background activity at about 9-10 cycle/second bilaterally. Little activity in the beta range is noted. Waves of 4-7 cycle/second of low amplitude were occasionally noted. Abundant movements and technical artifacts are noted throughout this tracing. Hyperventilation was not performed. Photic stimulation reveals no important changes.,CLINICAL INTERPRETATION:, The electroencephalogram is essentially normal. | neurology, beta range, hyperventilation, photic stimulation, electroencephalogramNOTE,: Thesetranscribed medical transcription sample reports and examples are provided by various users andare for reference purpose only. MTHelpLine does not certify accuracy and quality of sample reports.These transcribed medical transcription sample reports may include some uncommon or unusual formats;this would be due to the preference of the dictating physician. All names and dates have beenchanged (or removed) to keep confidentiality. Any resemblance of any type of name or date orplace or anything else to real world is purely incidental., |
2,898 | A ight-handed inpatient with longstanding history of cervical spinal stenosis status post decompression, opioid dependence, who has had longstanding low back pain radiating into the right leg. | Neurology | EMG/Nerve Conduction Study - 2 | HISTORY: , The patient is a 78-year-old right-handed inpatient with longstanding history of cervical spinal stenosis status post decompression, opioid dependence, who has had longstanding low back pain radiating into the right leg. She was undergoing a spinal epidural injection about a month ago and had worsening of right low back pain, which radiates down into her buttocks and down to posterior aspect of her thigh into her knee. This has required large amounts of opioid analgesics to control. She has been basically bedridden because of this. She was brought into hospital for further investigations.,PHYSICAL EXAMINATION: , On examination, she has positive straight leg rising on the right with severe shooting, radicular type pain with right leg movement. Difficult to assess individual muscles, but strength is largely intact. Sensory examination is symmetric. Deep tendon reflexes reveal hyporeflexia in both patellae, which probably represents a cervical myelopathy from prior cord compression. She has slightly decreased right versus left ankle reflexes. The Babinski's are positive. On nerve conduction studies, motor and sensory distal latencies, evoked response amplitudes, conduction velocities, and F-waves are normal in lower extremities.,NEEDLE EMG: , Needle EMG was performed on the right leg and lumbosacral paraspinal muscles using a disposable concentric needle. It reveals the spontaneous activity in right peroneus longus and gastrocnemius medialis muscles as well as the right lower lumbosacral paraspinal muscles. There is evidence of denervation in right gastrocnemius medialis muscle.,IMPRESSION: , This electrical study is abnormal. It reveals the following:,1. Inactive right S1 (L5) radiculopathy.,2. There is no evidence of left lower extremity radiculopathy, peripheral neuropathy or entrapment neuropathy.,Results were discussed with the patient and she is scheduled for imaging studies in the next day. | neurology, needle emg, radiculopathy, electrical study, emg, nerve conduction study, cervical spinal stenosis, lumbosacral paraspinal muscles, gastrocnemius medialis muscles, spinal stenosis, post decompression, lumbosacral paraspinal, paraspinal muscles, gastrocnemius medialis, medialis muscles, decompression, emg/nerve, conduction, cervical, spinal, needle, muscles, |
2,899 | Normal awake and drowsy (stage I sleep) EEG for patient's age. | Neurology | Electroencephalogram | DESCRIPTION OF RECORD: ,This tracing was obtained utilizing 27 paste-on gold-plated surface disc electrodes placed according to the International 10-20 system. Electrode impedances were measured and reported at less than 5 kilo-ohms each.,FINDINGS: , In general, the background rhythms are bilaterally symmetrical. During the resting awake state they are composed of moderate amounts of low amplitude fast activity intermixed with moderate amounts of well-modulated 9-10 Hz alpha activity best seen posteriorly. The alpha activity attenuates with eye opening.,During some portions of the tracing the patient enters a drowsy state in which the background rhythms are composed predominantly of moderate amounts of low amplitude fast activity intermixed with moderate amounts of low to medium amplitude polymorphic theta activity.,There is no evidence of focal slowing or paroxysmal activity.,IMPRESSION: , Normal awake and drowsy (stage I sleep) EEG for patient's age. | neurology, gold-plated surface disc electrodes, paroxysmal activity, eeg, drowsy stage, sleep eeg, stage, sleep, electrodes, awake, moderate, activity |
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