Speech begins with breathing, also called respiration. Your lungs fill with air, more air than you would inhale if you weren't talking. You expand your upper chest and your diaphragm (belly) to get all this air in. Your lung pressure and respiration muscle tension increase. Next, you release air through your throat, past your vocal folds (also called vocal cords). Your vocal folds are a pair of small muscles in your larynx. If you tense these muscles slightly, and release a little air, your vocal folds vibrate. This is called phonation. It's also called the fundamental frequency of your voice. If you place your fingers across the front of your throat, then hum or talk, you can feel your vocal folds vibrating. Adult men vibrate their vocal folds about 125 Hz (125 times per second). Women vibrate their vocal folds about 200 Hz. Children's voices are even higher. This is too fast for your brain to control. Vocal fold vibration is the only muscle activity that your brain doesn't directly control. Instead, phonation results from the coordination of respiration muscles with slight tensing of your vocal fold muscles. The key word in that last sentence was coordination. Stuttering is largely a disorder of poorly coordinated speech production muscles. If you tense your vocal folds too much, you block off your throat and stop air from escaping your lungs. This is good when lifting heavy weights. By blocking your larynx muscles, you increase lung pressure, which strengthens your chest and you can lift more weight. Similarly, tires inflated to high pressure can carry a heavier car. But that's what stutterers do when they talk, and it's not a good idea. The space in your throat above your larynx is called the pharynx. Above your pharynx are your oral and nasal cavities. These spaces create vocal resonation. This is like the echoing of a cathedral or tunnel. The unique shape of these spaces makes each of our voices sound unique. Your jaws and lips, collectively called the articulation muscles, modify your voice into intelligible speech. Vowels and voiced consonants (such as /b/ and /d/) are produced by your vocal folds, and modified by your articulation muscles (jaw, lips, tongue). Other consonants are voiceless, such as /p/ and /t/, produced by your articulation muscles modifying airflow, without your vocal folds vibrating. When you whisper, you don't vibrate your vocal folds. You just modify airflow with your articulation muscles. Speech requires coordination of over 100 muscles. The average person speaks about 150 words per minute. Each word requires a different configuration of most of those muscles. Speech is our most complex, balanced neuromuscular activity. Core stuttering behaviors include: Disordered breathing, including antagonism between abdominal (belly) and thoracic (upper chest) respiratory muscles; complete cessation of breathing, and interrupting exhalation with inhalation. Disordered vocal folds, including high levels of muscle activity or muscle tension; poor laryngeal too late or holding tension too long; and poor coordination of laryngeal muscles, e.g., incompatible contractions of opposing muscles. Disordered articulation, including dysfunctions of the lips, jaw, and tongue in stuttering. In general, stutterers place their articulators in the right positions (in contrast to other speech disorders such as lisping, in which individuals form incorrect sounds), but time the movements wrong. Low-frequency tremors in the neck, jaw, and lip muscles of adult stutterers. These are found to a lesser extent in older children, and not found in young children who stutter. Secondary stuttering behaviors are unrelated to speech production: Physical movements such as eye-blinking, forehead wrinkling, sudden exhaustion of breath, frowning, or nostril quivering. Gross (large) muscle movements such as head jerks or slapping one's thigh in an attempt to release a vocal fold block or other overtense speech-production muscle. Avoidance of feared words, such as substitution of another word. Postponement of a feared word, with pauses or filler words. Interjected "starter" sounds and words, such as "um," "ah," "you know," or "in other words." Repeating a sentence or phrase "to get a running start." Vocal abnormalities to prevent stuttering, such as speaking in a rapid monotone, affecting an accent, or using odd inflections. Looking away from the listener, not maintaining eye contact. Articulating an unrelated sound, e.g., forming a /t/ sound when trying to say /s/. Secondary behaviors may help you get around stuttering at first, but then lose their effectiveness. The secondary behavior is then retained out of habit. Fluent speech can be defined in four parameters:[1] Smoothness, or lack of interruptions. Speaking rate. Prosody, or emotional intonation. Mental effort. Stuttering can be defined as:[2] I. (a) disruption in the fluency of verbal expression, which is (b) characterized by involuntary, audible, or silent repetitions or prolongations in the utterance of short speech elements, namely: sounds, syllables, and words of one syllable. These disruptions (c) usually occur frequently or are marked in character and (d) are not readily controllable. II. Sometimes the disruptions are (e) accompanied by accessory activities involving the speech apparatus, related or unrelated body structures, or stereotyped speech utterances. These activities give the appearance of being speech-related struggle. III. Also, there not infrequently are (f) indications or reports of the presence of an emotional state, ranging from a general condition of "excitement" or "tension" to more specific emotions of a negative nature such as fear, embarrassment, irritation, or the like. (g) The immediate source of stuttering is some incoordination expressed in the peripheral speech mechanism; the ultimate cause is presently unknown and may be complex or compound. An essential difference between speech and language disorders is that persons with speech disorders (e.g., stuttering) know what they want to say, but can't say it. Stammering is the British word for stuttering. ^ Wingate, M.E. “Recovery From Stuttering.” Journal of Speech & Hearing Disorders, 29, 312-21 (1964). ^ Starkweather, C.W. Fluency and Stuttering. Englewood Cliffs: Prentice-Hall (1987). About 2.5% of preschool children stutter. [3] This prevalence of preschool stuttering is less important than the incidence figure, which is about 5%. I.e., about 5% of children stutter at some point, and about 2.5% of children stutter now. Less than 1% of adults stutter. 0.73%, or about one in 135 adults, was the figure found in a recent study. [4] That suggests that about two million Americans stutter. But this seems high. The number of adults who’ve sought treatment is somewhere around 25,000. [5] How many stutterers have you met, outside of speech clinics and support groups? You likely hear 135 people talking every week. Do you hear someone stutter every week? Extensive publicity for several anti-stuttering devices was seen by over 100 million people, yet only about 2500 devices of each device were sold. The membership figures for the National Stuttering Association are similar. This suggests that stuttering is either relatively common, but unimportant to 90% to 99% of the people who stutter; or that stuttering is a rarer disorder than the non-profit organizations say in their fundraising letters. ^ Proctor A., Duff, M.. and Yairi, E. (2002). "Early childhood stuttering: African Americans and European Americans." ASHA Leader, 4:15, p.102. ^ Craig. A, Hancock K, Tran. Y, Craig. M, & Peters, K. (2002). "Epidemiology of stuttering in the communication across the entire life span." Journal of Speech Language Hearing Research, 45:1097-1105. ^ The National Center for Stuttering and the Hollins Communications Research Institute have each treated around 5,000 stutterers. Most of the other three hundred Fluency Specialists have treated a few dozen stutterers. Stuttering isn't a physical disorder. It's not a psychological disorder. Stuttering is a developmental disorder. Children grow up in a certain order. They crawl before they walk. They walk before they run. They run before they ride bicycles. They ride bicycles before they borrow your car keys. Usually. Some children walk before they crawl. My three-year-old nephew borrows my car all the time. Just joking. I don't own a car. At each stage of physical development, a child's brain develops too. E.g., crawling helps the child develop communication between the left and right hemispheres of his brain. If all goes well, the child's physical, neurological, and psychological systems develop together. A small, sometimes imperceptible, developmental misstep in early childhood can nudge a child off the normal developmental track. The child then grows on an abnormal developmental track. A minor problem can develop into a major disability as the child grows up. Some children can't hear the difference between short duration speech sounds. The difference between /b/ and /d/ sounds occurs within a few milliseconds (thousands of a second). Some children's brains' auditory processing isn't fast enough to hear fast speech sounds. To these kids, "bad" and "dad" are the same word, "bug" and "dug" are the same, and so are "buck" and "duck." (This is a form of central auditory processing disorder, or CAPD). You'd think this would be a minor problem. After all, you know the difference between "sew" and "so." But it's not a minor problem. These children develop speech slower than other children. Slow speech development causes them to miss other developmental stages. Their grammar develops poorly. Listeners have difficulty understanding these children's speech. These children understand the difference between boys and girls, but interchange "he" and "she." They mix up past, present, and future tense. Then these children are labeled mentally challenged, even though they're normal or even excel at non-language activities (e.g., building with Legos). They're put into special ed classes, with children who really are mentally retarded. The children miss more developmental stages. As adults, these individuals may be unable to read, or have poor social skills, or be unable to work at more than menial jobs. This disorder is called language-learning impairment (LLI). In the last ten years a treatment has been developed. These children can distinguish /b/ from /d/ if the words are slowed down. Children with LLI now play a computer game that trains them to hear the difference between short-duration speech sounds. [6] When their auditory dysfunction is corrected, the children develop normally. The children usually catch up with their peers, e.g., advancing four reading grade levels in six months. Analogously, children's brains are like a railroad going from New York to Los Angeles. A little dysfunction can bump a child onto a sidetrack. The sidetrack may start out only a few feet from the main track, but twenty years later he's lost somewhere in South America. Treatment is like giving the child a shove back onto the main railroad track. The child then zooms ahead to catch up with his peers. (Brain scans show that adult stutterers have a different form of CAPD, which may affect how we hear our own voices or feel our speech-production muscles moving. No researchers have investigated whether children who stutter also have this form of CAPD, or if treating this form of CAPD stops stuttering from developing.) Wikipedia doesn't have an article about language learning impairment (LLI) but it has an article about specific language impairment (SLI). Stuttering is similar to LLI, in that something small nudges a child off the normal developmental track at the age of two or three. This small nudge causes the child to grow on an abnormal developmental path. By adulthood, the stutterer has developed a variety of core symptoms, secondary behaviors, and psychological problems. The average age of stuttering onset is 30 months. [7] I.e., two-and-half-years-old is the typical age that children begin to stutter. Stuttering rarely begins after age six. 65% of preschoolers who stutter spontaneously recover, in their first two years of stuttering. [8] These children grow up to have normal speech. [9] Some pediatricians tell parents to "wait and see" if a child outgrows stuttering on his own. But this advice is wrong. Children who stutter should be treated by a speech-language pathologist as soon as possible. (Schools provide free speech therapy to children as young as three years old.) However, children who stutter longer are less likely to recover without treatment. Only 18% of children who stutter five years recover spontaneously. [10] The peak age of recovery is 3.5 years old. By age six, a child is unlikely to recover without speech therapy. If your child is in grade school and has stuttered for five years, he or she will need a bigger shove to get back onto the normal development track. At two or three years old, children are quickly developing communication skills. Their brains are growing rapidly. A child's language skills may develop faster than his speech skills. He wants to communicate but can't easily and freely generate speech. The child interjects "uh" and "um." He repeats words. He has silent pauses. He revises what he's saying in the middle of sentences, or leaves sentences incomplete. He's most dysfluent with long sentences, when interrupting or being interrupted, or during stressful periods, such as a divorce, the birth of a sibling, or moving to a new home. Those are normal dysfluencies. All children have normal dysfluencies. Normal dysfluencies aren't stuttering. The "experts" say that some children move from normal dysfluencies into stuttering. These children's frustration trying to talk leads them to push out words. The children tense their breathing, their vocal folds, and their lips, jaws, and tongues. The children struggle to talk, getting into longer repetitions, prolongations, and silent blocks. Recognizing which behaviors are normal dysfluencies and which behaviors are stuttering is a key issue. The Stuttering Foundation of America has a videotape to help parents differentiate normal dysfluencies from stuttering. Because children's brains are growing at this time, their stuttering behavior becomes hardwired. Their brains shift onto an abnormal development path. The "experts" have identified five stages children go through as stuttering develops, over months and years. Or are the "experts" wrong? Some parents report that their children woke up one morning stuttering severely. These children went from normal dysfluencies to severe stuttering overnight. The children skipped the development stages in between. In a later chapter, you'll learn that a disorder similar to stuttering is triggered by a streptococcal infection causing a child's immune system to attack his or her brain's putamen motor control area. It's possible that a similar autoimmune dysfunction could attack a child's left caudate nucleus speech motor control area, causing severe stuttering to develop overnight. You'll also learn that three genes are linked to stuttering. These genes affect the neurotransmitter dopamine, which functions abnormally in adult stutterers. I.e., some children are genetically predisposed to a class of disorders that includes stuttering. You'll also learn that adult stutterers have abnormal auditory processing. (This abnormality is different from the auditory processing abnormality that causes language-learning impairment.) These questions are important because they affect what therapy should be effective for children. If the "experts" are right that stuttering develops in five stages, beginning with normal dysfluencies, then early intervention is paramount, but the therapy can be a gentle nudge (e.g., telling the parents not to interrupt when the child is speaking). But if the "experts" are wrong, and some children develop severe stuttering without going through intermediate stages, then therapy should start with a big shove back onto the normal developmental track. This important issue—direct vs. indirect therapy—is addressed in the chapter Stuttering Therapies for Pre-School Children. ^ Merzenich, M., Jenkins, W., Johnston, P., Schreiner, C., Miller, S., and Tallal, P. “Temporal Processing Deficits of Language-Learning Im-paired Children Ameliorated by Training,” Science vol. 271, January 5 1996, p.77-80. ^ Yairi, E., Ambrose, N. "Onset of stuttering in preschool children: Selected factors," Journal of Speech and Hearing Research, 35, 1992, 782-788. ^ Yairi, E. (1993) "Epidemiologic and other considerations in treatment efficacy research with preschool-age children who stutter," Journal of Fluency Disorders, 18, 197-220. Yairi, E., Ambrose, N. "Onset of stuttering in preschool children: Selected factors," Journal of Speech and Hearing Research, 35, 1992, 782-788. ^ Finn, Patrick. "Children Recovered From Stuttering Without Formal Treatment: Perceptual Assessment of Speech Normalcy," Journal of Speech, Language, and Hearing Research, 40, 867-876, August 1997. ^ Andrews, et al., "Stuttering: a review of research findings and theories," Journal of Speech and Hearing Disorders, 48, 226-246, 1983. Early Childhood Stuttering, by Ehud Yairi and Nicoline Ambrose (2004, ISBN 0890799857) Most brain scan studies have found no differences between stutterers’ and non-stutterers’ cerebral activity during silent rest and during fluent speech.[11]. But during stuttering, cerebral activity changes dramatically. Changes include: Left-hemisphere areas active during normal speech become less active, and areas in the right hemisphere not normally active during speech become active. [12] [13] Underactivity in the central auditory processing area. Overactivity in the speech motor control area. No brain scans have been done of stuttering children. We don't know whether these neurological abnormalities cause stuttering or are caused by stuttering. It's possible that stuttering causes a child's brain to develop abnormally in these two areas. It's also possible that some children have one or both neurological abnormalities before they start stuttering, which cause them to stutter. This abnormal right-hemisphere activity has produced a variety of speculative hypotheses from researchers. According to one hypothesis, something is wrong with stutterers’ left-brain speech areas, and so right-brain areas not developed for speech take over. This seems unlikely, given that most stutterers are capable of normal, fluent speech in certain conditions. In contrast, neurogenic speech disorders (resulting from head injuries, strokes, etc.) result in disordered speech under all conditions. Because stutterers sometimes speak fluently and sometimes stutter, it seems unlikely that stutterers have something wrong with their left-hemisphere speech areas. Another hypothesis says that the right-hemisphere activity is the fears and anxieties that stutterers experience, generated by the limbic and paralimbic structures. But brain scans haven't shown these areas to be abnormally active during stuttering. A third hypothesis suggests that stutterers' auditory processing underactivity reduces the left-brain communication of sensory information processed in the rear brain to frontal speech and language areas. The abnormal right-brain activity may be an alternative pathway for rear-brain sensory information to travel to the front of the brain. Wikipedia article about Auditory processing disorder Our ears hear sounds. Our brains process those perceived sounds into useful information, such as words. Central auditory processing disorder (CAPD) is not a single disease but rather is the term for anything wrong with how our brains process auditory information. A wide variety of disorders seem to have a CAPD component, including ADHD and language disorders. [14] CAPD is not a hearing disorder, i.e., a person with CAPD usually has nothing wrong with his or her ears. What's wrong with adult stutterers' auditory processing is unknown. Speculatively, stutterers have something wrong with how we hear our own voices. A study suggested that adult stutterers have an inability to integrate auditory and somatic processing,[15] i.e., comparing what we hear ourselves saying to how we feel our muscles moving. A brain scan study examined the planum temporale (PT), an anatomical feature in the auditory temporal brain region. Typically people have a larger PT on the left side of their brains, and smaller PT the right side (leftward asymmetry). A brain scan study found that stutterers' right PT is larger than their left PT (rightward asymmetry). [16] A second study found that stutterers with this abnormal rightward asymmetry had significantly improved fluency with DAF (Delayed Auditory Feedback), but stutterers with the normal leftward asymmetry didn't improve with DAF. [17] The study also found that stutterers with this abnormal rightward asymmetry stuttered more severely than stutterers with the normal leftward asymmetry. Do you have other symptoms associated with CAPD? Such symptoms include: Preferring to watch movies with the subtitles on. Preferring to learn a foreign language (or challenging vocabulary words, or difficult last names) by learning to read and write the words first, and then learning to hear and speak the words, and then only when the words are spoken slowly. Difficulty understanding what people are saying when there's background noise, such as noise at a party or wind on an outdoor hike. Difficulty picking out one musical instrument from a band or orchestra. Sensitivity to certain noises (e.g., inability to "tune out" a television on in the background while "tuning in" a conversation with a person). Difficulty identifying the direction of sounds. Difficulty following multi-step directions, especially if given in one sentence. Difficulty paying attention when reading long lists of stuff. Just joking! For general treatments of CAPD, see the Wikipedia article about Auditory processing disorder. Speculatively, exercises that train a stutterer to listen to his voice might improve fluency, but this hypothesis has not been tested. Such exercises might include acting or telling jokes with different voices for different characters, or doing actors' accent training. Learning to switch from an Irish brogue to sounding like a Mississippi Delta blues musician to a Korean shopkeeper might enhance your brain's ability to integrate auditory and somatic processing. Speculatively, altered auditory feedback anti-stuttering devices may correct stutterers' auditory processing underactivity. This hypotheses has never been tested but is the most likely explanation how anti-stuttering devices work. This would also explain the "chorus effect" of speaking with another person. For more information, see the chapter Anti-Stuttering Devices. The other neurological abnormality associated with stuttering is overactivity in the left caudate nucleus speech motor control area. Because stuttering is primarily overtense, overstimulated respiration, vocal folds, and articulation (lips, jaw, and tongue) muscles, it should be no surprise that the brain area that controls these muscles is overactive. (Citations of peer-reviewed research supporting these statements would be appreciated.) However, research also documents that the left caudate is associated with decreased glucose uptake in people who stutter in both stuttering and enhanced fluency speaking conditions (Wu, et al., 1995); as such, this data argues that people who stutter demonstrate left caudate hypometabolism as a possible trait marker for stuttering. Further research documents increased FDOPA uptake in the left caudate tail (Wu et al., 1997). Fluency shaping therapy trains stutterers to speak with relaxed breathing, vocal folds, and lips, jaw, and tongue. A study tested stutterers before and after fluency shaping therapy, finding left-hemisphere activity, although large areas of activation in the right hemisphere remained. No specific changes were seen in the left caudate nucleus. [18] This left caudate nucleus overactivity appears to be related to the neurotransmitter dopamine. Speculatively, if stutterers' left caudate nucleus is too sensitive to dopamine, then this would explain why dopamine antagonist medications reduce stuttering (see the chapter Anti-Stuttering Medications). Speculatively, if stutterers' left caudate nucleus is too sensitive to dopamine, then varying levels of dopamine would explain the "good days, bad days" phenomenon, in which stutterers have days with relatively fluent speech, and other days when they "can't get a word out." For more about dopamine, see Wikipedia article Dopamine or the book The Edge Effect, by Eric Braverman (ISBN 1402722478). Three genes that correlate with stuttering also correlate with Tourette's Syndrome (see the chapter Genetics of Stuttering). Tourette's and stuttering have many commonalities, suggesting that the neurology of Tourette's may shed light on the neurology of stuttering. Stuttering happens frequently in Tourette's syndrome. Many of the medications that help control tics also help stuttering. Abnormalities in the basal ganglia and the cortical motor systems may be shared by both disorders. Tourettec tics and stuttering disfluencies are embarrassing. The more a Touretter tries not to make a certain movement, or a stutterer tries not to stutter, the less he or she can control the behavior. Touretters control the disorder by substituting more-acceptable tics. Stutterers substitute words they can say. Both Touretters and stutterers enjoy support groups, where they can "let go" and move or stutter without embarrassment. Environmental cues can "switch off" Tourette's and stuttering temporarily. E.g., a surgeon with Tourette's has tics everywhere but the operating room. [19] Stress can "switch off" Tourette's and stuttering temporarily. Dopamine-blocking medications, such as Haldol, reduce both stuttering and Tourette's. Both disorders run in families. The prevalence of Tourette's and adult stuttering is similar. Both disorders originate in childhood. Both disorders can be disabling, but Touretters and stutterers who achieve success say that their disorder was a gift. To learn more, see the Wikipedia article about Tourette's syndrome. Or invite a Tourette's support group to meet with your stuttering support group. Why do some individuals with these three genes develop stuttering, while others develop Tourette's or OCD, and still other individuals with these genes develop none of these disorders? In a subgroup of individuals with Tourette's, a childhood autoimmune "trigger" leads to Tourette's. A childhood streptococcal infection can cause a child's immune system to attack brain cells in the putamen area. [20] The putamen controls gross (large) muscle movements. Excessive dopamine in the putamen area of the brain is associated with Tourette's. The child recovers from the fever, but then develops Tourette's. For more about this controversial hypothesis, see P.A.N.D.A.S.. No one has suggested that stuttering is a PANDAS disorder, but the three PANDAS disorders (Tourette's, OCD, and tics) are genetically linked to stuttering, so perhaps PANDAS shouldn't be ruled out in the development of stuttering. Tourette's involves a genetic predisposition and an autoimmune trigger leading to a neurological abnormality. Combined with later psychological issues, Tourette's is a multifactoral disorder. Because only some individuals with Tourette’s developed the disorder from this autoimmune trigger, Tourette’s has multiple development pathways. Stutterers have "good days"—with less stuttering—and "bad days"—when they can't get a word out. The "good days/bad days" syndrome may be due to varying levels of dopamine in the brain. Dopamine is affected by several factors, including diet. Dopamine is produced from the amino acids phenylalanine and tyrosine. Both amino acids are components of protein. Meat sources of protein have more tyrosine than plant sources of protein. The exception is wheat germ, which is high in tyrosine. The foods highest in phenylalanine are soy and fish. A vegetarian, wheat-free, low-protein diet should lower dopamine levels. I tried this. I stuttered less, but felt sluggish and depressed. I'd rather eat protein, feel mentally alert, and stutter.--Thomas David Kehoe 05:06, 28 March 2006 (UTC) Concepts involving dietary modifications have never undergone scientific study in stuttering and this is unlikely to significantly alter dopamine synthesis. Reducing dopamine synthesis may be detrimental to other neurophysiological processes. Pharmacological agents are a much more effective way of modulating dopaminergic activity. The ideal drug would be a dopamine receptor modulator that is precise enough to modulate dopaminergic activity without causing detrimental neurological side effects, but such medications don't currently exist. Aripiprazole is the first drug to have some properties similar to a dopamine receptor modulator, but its metabolite acts as a full dopamine antagonist, negating the selective modulating activity of aripiprazole itself. Different studies found different results because a variety of technologies were used (EEG vs. SPECT vs. PET, H2150 vs. FDG). Most studies were small, usually a half-dozen stutterers. The subjects were usually right-handed men — women and left-handed men may have different cerebral activity. Salmelin, 1998: “Neuromagnetic responses to monaural tones [found that] the basic functional organization of the auditory cortices was found to be different in stutterers and controls...and more severely by self-paced [stuttered] than accompanied [fluency induced by the chorus effect] speech.”[21] Braun, 1997: Language processing shifted to the right hemi-sphere, including the dorsolateral prefrontal cortices, middle temporal gyrus, and anterior cingulate cortex. Motor function shifts to the right hemisphere, including the “anterior fore¬brain regions and associ¬ated archicortical paralimbic areas.” Visual processing also appeared to shift to the right hemisphere. Decreased sensory perception, including post-rolandic sensory areas and related paleocortical paral¬imbic regions. Increased somatosensory processing (sensation of the body), including the “dorsal region of the angular gyrus, adjacent to the superior parietal lobule, as well as somatosensory association cortices in the medial SPL.”[22] De Nil, 1995: During silent reading, increased activation in the left angular cingulate cortex, a “reflection of covert anticipation of stuttering.” [23] Ingham, 1996: “Present findings do not support recent suggestions that developmental stuttering is associated with abnormalities of brain blood flow at rest. Rather, our findings indicate an essentially normal functional brain terrain...”[24] Ingham, 1997: “Diffuse overactivity throughout the cerebral and cerebellar motor systems...Deactivation of a verbal production circuit between left frontal (BA47) and temporal (BA22) cortex that has been previously identified in normal speakers.”[25] Kalinowski, 1997: Some stutterers showed the greatest reduction in the temporal-parietal area, and others showing greatest reductions in the right hemisphere posterior sites. [26] Kroll, 1997: After fluency shaping stuttering therapy there is increased left-hemisphere activity, although large areas of activation in the right hemisphere remain. [27] Watson, 1994: Abnormal right-hemisphere activity only in stutterers who also had language deficits. [28] ^ Ingham, R.J., Fox, P.T., et al. “Functional-Lesion Investigation of Developmental Stuttering With Positron Emission Tomography.” Journal of Speech & Hearing Research, 39, 1208-1227, December 1996. ^ Braun, A.R., Varga, M., Stager, S., Schulz, G., Selbie, S., Maisog, J.M., Carsom, R.E., Ludlow, C.L. "Atypical Lateralization of Hemispehral Activity in Developmental Stuttering: An H215O Positron Emission Tomography Study," in Speech Production: Motor Control, Brain Research and Fluency Disorders, edited by W. Hulstijn, H.F.M. ^ Ingham R.J., Fox, P.T., Ingham, J.C.. “A H215O Positron Emission Tomography (PET) Study On Adults Who Stutter: Findings and Implications,” in Speech Production: Motor Control, Brain Research and Fluency Disorders, edited by W. Hulstijn, H.F.M. ^ Kutscher, Martin L. Kids in the Syndrome Mix (Jessica Kingsley Publishers, 2005, ISBN 1-84310-8100), pages 178-179. ^ Foundas, A.L., Bollich, A.B., Corey, D.M., Hurley, M., Heilman, K.M. "Anomalous Anatomy in Adults with Persistant Developmental Stuttering: A Volumetric MRI Study of Cortical Speech-Language Areas," Neurology, 2001 57:207-215. ^ Braun, A.R., Varga, M., Stager, S., Schulz, G., Selbie, S., Maisog, J.M., Carsom, R.E., Ludlow, C.L. "Atypical Lateralization of Hemispehral Activity in Developmental Stuttering: An H215O Positron Emission Tomography Study," in Speech Production: Motor Control, Brain Research and Fluency Disorders, edited by W. Hulstijn, H.F.M. ^ A. L. Foundas, MD, A. M. Bollich, PhD, J. Feldman, MD, D. M. Corey, PhD, M. Hurley, PhD, L. C. Lemen, PhD and K. M. Heilman, MD. "Aberrant auditory processing and atypical planum temporale in developmental stuttering," Neurology, 2004;63:1640-1646. ^ Kroll, R.M., De Nil, L.F., Kapur, S., Houle, S. “A Positron Emission Tomography Investigation of Post-Treatment Brain Activation in Stutterers,” in Speech Production: Motor Control, Brain Research and Fluency Disorders, edited by W. Hulstijn, H.F.M. ^ Sacks, Oliver. An Anthropologist on Mars. (Vintage, 1996, ISBN: 0679756973). ^ Singer, H.S., J.D. Giuliano, B.H. Hansen, J.J. Hallett, J.P. Laurino, M .Benson, and L.S. Kiessling. "Antibodies against human putamen in children with Tourette syndrome", Neurology, June 1998; 50: 1618-1624, summary. ^ Salmelin R, Schnitzler A, Schmitz F, Jancke L, Witte OW, Freund HJ. “Functional organization of the auditory cortex is different in stutterers and fluent speakers.” Neuroreport 1998 Juyl 13;9(10):2225-2229 ^ Braun, A.R., Varga, M., Stager, S., Schulz, G., Selbie, S., Maisog, J.M., Carsom, R.E., Ludlow, C.L. "Atypical Lateralization of Hemispehral Activity in Developmental Stuttering: An H215O Positron Emission Tomography Study," in Speech Production: Motor Control, Brain Research and Fluency Disorders, edited by W. Hulstijn, H.F.M. ^ De Nil, L., Kroll, R., Houle, S., Ludlow, C., Braun, A., Ingham, R.J. (1995). “Advances in stuttering research using positron emission tomography brain imaging.” ASHA, 37, 89. ^ Ingham, R.J., Fox, P.T., et al. “Functional-Lesion Investigation of Developmental Stuttering With Positron Emission Tomography.” Journal of Speech & Hearing Research, 39, 1208-1227, December 1996. ^ Ingham R.J., Fox, P.T., Ingham, J.C.. “A H215O Positron Emission Tomography (PET) Study On Adults Who Stutter: Findings and Implications,” in Speech Production: Motor Control, Brain Research and Fluency Disorders, edited by W. Hulstijn, H.F.M. ^ Kalinowski, J., Rastatter, M., Cranford, J., Stuart, A. “Topographic EEG Mapping Of Stuttering Subjects During Speech Tasks Under Normal and Altered Feedback Conditions.” 1997. East Carolina University, unpublished. ^ Kroll, R.M., De Nil, L.F., Kapur, S., Houle, S. “A Positron Emission Tomography Investigation of Post-Treatment Brain Activation in Stutterers,” in Speech Production: Motor Control, Brain Research and Fluency Disorders, edited by W. Hulstijn, H.F.M. ^ Watson, B.C., Freeman, F.J., Devous, M.D., Chapman, S.B., Finitzo, T., Pool, K.D. “Linguistic Performance and Regional Cerebral Blood Flow in Persons Who Stutter.” Journal of Speech and Hearing Research, 37:6, December 1994, 1221-1228. Three genes associated with the neurotransmitter dopamine correlate with five disorders: ADD/ADHD, stuttering, Tourette's syndrome, obsessive compulsive disorder (OCD), and tics. [29] All five disorders involve a combination of stress and movement: Persons with ADD/ADHD have normal brain activity when resting, but when they try to concentrate on a task, they have reduced prefrontal cortex blood flow, which reduces their ability to concentrate. [30] Persons with ADHD (mostly children) then become hyperactive and can't sit still. Tics cause a muscle, often in your face, to move rapidly and uncontrollably. Stress usually makes the tic uncontrollable. Individuals with OCD repeatedly perform physical tasks, e.g., hand-washing. Stress usually makes this behavior uncontrollable. Individuals with Tourette's syndrome compulsively touch objects (e.g., floors or walls) or make stereotyped movements or noises. Stress usually makes the movements uncontrollable. Stuttering is excessive speech-production muscle activity resulting in blocked, prolonged, or repeated sounds. Stress usually makes the stuttering uncontrollable. All five disorders manifest most strongly—and are most difficult to control—in high-stress situations. These disorders may all be stress reducers that work for a few moments but then cause greater stress, resulting in cyclical abnormal behaviors (see the section Stress-Related Changes). Why do some individuals with these three genes develop stuttering, while others develop Tourette's, while still others develop other disorders, or no disorder at all? In a subgroup of individuals with Tourette's, a childhood autoimmune "trigger" leads to Tourette's. A childhood streptococcal infection causes a child's immune system to attack brain cells in the putamen area. [31] The putamen controls gross (large) muscle movements. Excessive dopamine in the putamen area of the brain is associated with Tourette's. The child recovers from the fever, but then develops Tourette's. Speculatively, a similar autoimmune disorder involving the left caudate nucleus speech motor control area could trigger childhood stuttering. In 2005, researchers announced that almost half the family members stutter in several extended families in Cameroon, Africa. The lead researcher said, "These families provide hope that we'll be able to identify the gene that appears to be at work to cause stuttering in these families. "[32] A 1940 study investigated five generations of an Iowa family, with stuttering in all generations. In the third generation, three of four children in one family stuttered. When these children grew up, three moved to Kansas and lost contact with the sibling remaining in Iowa. Of the descendants of the woman remaining in Iowa, 40% stuttered. Of the descendants of the Kansas siblings, only 6% stuttered. The researcher concluded that the Iowa family had a "tone" that was conducive to stuttering. The hypothesis was that this family believed that stuttering was inherited, so they anxiously watched their children looking for signs of stuttering, and this fear of stuttering in the parents caused the children to stutter. In 1960, another researcher studied the next generation of the family. Only 2% of these children stuttered, and the researcher reported that there had been a change in the familial assumptions and attitudes about stuttering. [33] In 1940, speech-language pathologists believed that stuttering was caused by parental reactions to normal childhood dysfluencies. The Iowa family "proved" what the speech-language pathologists believed. In 2005, speech-language pathologists believe that stuttering has a genetic cause, and the Cameroon families are expected to prove this hypothesis. In 1986, a speech-language pathologist re-examined the 1940 Iowa study and concluded that, "genetic transmission has been judged to provide an equally viable explanation for the data. "[34] At least 25 studies have investigated family patterns in the incidence of stuttering. The results vary widely. Most studies are contradicted by other studies. Between 20% and 74% of stutterers say they have a relative who stutters. But other studies found that 1% to 42% of non-stutterers said they have a relative who stutters. [35] In other words, many stutterers and many non-stutterers say they have relatives who stutter. One study found that if you stutter, you are about three times more likely to have a close relative who stutters. [36] Studies of the families of stutterers failed to find simple Mendelian types of inheritance, such as sex-linked, autosomal dominant, or recessive. A study of children aged 2 to 6 found that more than two-thirds of stuttering children have relatives who stutter. This study found that male and female children were equally likely to have relatives who stutter. This study also found that stuttering was more likely in first-degree relatives than in second- or third-degree relations. [37] A half-dozen studies of twins have found that concordance for stuttering (both twins either stutter or don't stutter, rather than one twin stuttering and the other not stuttering) is much more likely in identical twins than in fraternal twins. The exact numbers vary between studies, in part because some studies only looked at same sex twins (a male and female fraternal twin pair is unlikely to both stutter because males are more likely to stutter than females). [38] On the other hand, a study of 95 pairs of identical twins reared apart found 5 stutterers (2% of the subjects, the expected prevalence). None of their twins stuttered. This is in spite of finding similarities in talkativeness, pitch, and hoarseness, as well as tastes in clothing, books, etc. This suggests that stuttering is not genetic. [39] Several studies have found that female stutterers are more likely than males to have relatives who stutter. [40] This suggested that the few females who stutter might have a stronger genetic component in their families. Analogously, men are more likely to be tall than women, but tall women are more likely to have tall relatives. However, another study of adult stutterers "did not find that relatives of female [stutterers] were more likely to stutter than relatives of the male [stutterers]. "[41] Studies of the family incidence of stuttering have compared left-handed stutterers to right-handed stutterers, speech motor skills, anxiety, and reading ability. Familial differences were found only for speech motor skills. Two studies of birth or developmental trauma had contradictory results. A study of adults suggested that there are two causes of stuttering: genetic, and trauma or illness. A similar study of children who stutter reached the opposite conclusion. Two studies found that severe stutterers were no more likely than mild stutterers to have relatives who stutter. Two more studies found no familial differences between recovered and persistent stutterers. [42] ^ Comings, D., et al., "Polygenic Inheritance of Tourette Syndrome, Stuttering, Attention Deficit Hyperactivity, Conduct, and Oppositional Defiant Disorder," American Journal of Medical Genetics 67:264-288 (1996). ^ Amen, Daniel. Healing ADD, (2002, ISBN 0425183270). ^ Singer, H.S., J.D. Giuliano, B.H. Hansen, J.J. Hallett, J.P. Laurino, M .Benson, and L.S. Kiessling. "Antibodies against human putamen in children with Tourette syndrome", Neurology, June 1998; 50: 1618-1624, summary. ^ Drayna, D. "Newly discovered families give impetus to genetic research," Stuttering Foundation of America newsletter, Fall 2005, page 1. Viswanath, N., H.S. Lee, R. Chakraborty. "Evidence for a Major Gene Influence on Persistance Developmental Stuttering," Human Biology, June 2004, 76:3, 401-412. ^ }Bloodstein, Oliver (1995) A Handbook On Stuttering, 5th edition, San Diego: Singular Press. ^ Wingate, M. (1986) "Physiological and genetic factors." In G.H. Shames & H. Rubin, Eds. ), Stuttering Then And Now (pp.49-69). Columbus: Charles E. Merrill Publishing Co. ^ Yairi, E. Ambrose, N., Cox, N. (1996) "Genetics of Stuttering: A Critical Review," Journal of Speech and Hearing Research, 39 771-784. ^ Andrews, et al., "Stuttering: a review of research findings and theories," Journal of Speech and Hearing Disorders, 48, 226-246, 1983. ^ Ambrose, N., Yairi, E., Cox, N. “Genetic Aspects of Early Childhood Stuttering.” Journal of Speech and Hearing Research, 36, 701-706, August 1993. ^ Yairi, E. Ambrose, N., Cox, N. (1996) "Genetics of Stuttering: A Critical Review," Journal of Speech and Hearing Research, 39 771-784. ^ Yairi, E. Ambrose, N., Cox, N. (1996) "Genetics of Stuttering: A Critical Review," Journal of Speech and Hearing Research, 39 771-784. ^ Janssen, P., Kloth, S., Kraaimat, F., Brutten, G. "Genetic Factors In Stuttering: A Replication of Ambrose, Yairi, and Cox’s (1993) Study With Adult Probands," Journal of Fluency Disorders, 21 (June 1996), 105-106. ^ Yairi, E. Ambrose, N., Cox, N. (1996) "Genetics of Stuttering: A Critical Review," Journal of Speech and Hearing Research, 39 771-784. Many studies have found that stutterers have normal physiological characteristics, such as heart rate and blood pressure. “Whatever the source of stuttering is, it is not amenable to the treatments I have developed. I therefore refuse to deal with it further.” —Sigmund Freud Many studies have tried to tie stuttering to a psychological or personality problem. The only psychological trait common to stutterers is fear and anxiety around speaking tasks, such as ordering in a restaurant. Many studies have tried to tie stuttering to parental attitudes and behaviors. The only trend is that poor, uneducated, dysfunctional families are more likely to have children who stutter. Likely the only parental behavior that contributes to childhood stuttering is not taking children to see a speech-language pathologist for therapy. College students who stutter are more intelligent than college students who don't stutter. However, any person with a disability has to be especially intelligent and motivated to attempt college work. This doesn’t mean that stutterers in general are more intelligent. Stuttering among mentally-retarded individuals appears to be far higher than the general population. In Down Syndrome, prevalences from 21% to 45% have been reported. This is likely because mentally-retarded children and adults are more likely to fail at therapy—stuttering therapies require intelligence and mental effort. Many studies have examined stutterers' language skills. Whether children who stutter started talking later has not been established. School-age stutterers have normal language skills, as measured by standard tests. However, advanced tests such as understanding words played backwards suggest that stutterers may have an auditory processing disorder. A Handbook on Stuttering, by Oliver Bloodstein (1995, ISBN 1565933958) In 1937, Wendell Johnson conducted a series of tests of adaptation and anticipation, in which stutterers repeatedly read a passage out loud: Johnson marked the stuttered words in the first reading. In the second reading, of an unmarked copy, the stutterer was asked to read only words on which he did not expect to stutter. This eliminated 98% of stuttering. The 2% of stuttering was on words which were stuttered in the first reading. In most cases, the stutterer afterwards said he knew he would stutter on the word, but failed to follow the instructions not to read it. The stutterer marked the words in the text on which he expected to stutter. He then read the passage out loud 15 minutes later, and a second time the next day. In both cases stuttering occurred on about 50% of the marked words, and on about 10% of the unmarked words. In 1975, Wingate repeated this experiment but altered the sequence of the words, and found little relationship between anticipated and stuttered words. Johnson noted the stuttered words as each stutterer read a passage ten times repeatedly. Most subjects stuttered on the same words in each reading. This showed that developmental stutterers stutter on certain words, and say other words fluently. In contrast, some forms of neurogenic stuttering may have random stuttering on any word. Later researchers tried to make the subjects forget which words they'd stuttered on, by reading other material, or by waiting several weeks between readings. Stutterers continued to stutter on the same words. Johnson increased stuttering by having the person read to an audience or by other means. Later, the person read out loud to one person. Stuttering increased on passages with cues associated with the audience reading, such a colored border on the page or a similar subject matter. Johnson theorized that the colored border reminded the person of previous stuttering. Johnson blacked out the stuttered words in heavy pencil, and the stutterer skipped those words. For some subjects, this eliminated stuttering, but most subjects then stuttered on new words. These new stuttered words were adjacent to the blacked-out words. Johnson had stutterers silently read a passage twice, several weeks apart, and mark words they expected to stutter on. Stutterers marked the same words each time. Johnson theorized that stutterers associate a word with past stuttering or failure (a cue). These studies show that certain words are stuttering cues for individual stutterers, just as certain speaking situations can cue an individual to stutter. In 1971, Rappaport and Bloodstein[43] repeated Johnson's fifth experiment, but divided subjects into two groups, and added a second test. In the second test, random words had been blacked out. The subjects who did Johnson's test first and then read the random test stuttered on the words adjacent to the blacked-out words. The subjects who read the random test first did not stutter on adjacent words. The stutterers were trained to stutter to a new cue—blacked-out words. According to some speech pathologists, "Distraction methods can be used to eliminate stuttering temporarily"[44]. But if distraction worked, stutterers would work a Rubik's cube or play a pocket video game whenever they wanted to talk fluently. Distraction does not reduce stuttering: Distraction from speech-production muscle tension. This is believed to be the origin of secondary symptoms. Tensing non-speech muscles (e.g., eye blinking, foot-stamping) distracts attention from vocal tension. The stutterer may relax his speech muscles momentarily and the word pops out. But he will soon block again, and if he continues to do the secondary behavior it will become habitual. It will also become ineffective. Distraction from vocal tension is ineffective. Distraction from anticipation of stuttering. Wendell Johnson showed that stutterers know which words they will stutter on. If this anticipation could be distracted, maybe the person wouldn't stutter on those words? A 1982 study had stutterers step on and off a 10-inch platform while reading out loud. [45] A 1985 study had stutterers manually track an irregular line on a rotating drum while speaking. [46] Neither distraction was able to reduce stuttering. Another study[47] had nine adult stutterers take a 10-second "time-out" after disfluencies, while a control group of nine stutterers got random 10-second "time-outs." "Time-outs" after disfluencies reduced stuttering 46%. Random "time-outs" had no effect on stuttering, proving that "time-outs" do not reduce stuttering via "distraction." These three studies show that distraction from anticipation is ineffective. Distraction from the fear of stuttering. There are many stories of a stutterer being "too scared" to stutter (see the section below "Does Stress Increase Stuttering?"). This is a real and fascinating phenomenon, but has no practical value as a therapy for stuttering. For example, we could train a Rottweiler to attack you whenever you stutter. If you brought the dog with you everywhere you went, this might cure you of stuttering, but it would be a cure worse than the disorder. Increasing attention to one aspect of speech may reduce attention to other aspects of speech. For example, speaking in a foreign accent requires careful attention to your articulation. Other examples of increased attention may be to relaxed breathing or to speaking slower. These techniques can be effective, but the effectiveness is from increased attention to a fluency-enhancing aspect of speech, not due to distraction or decreased attention to fluency-inhibiting aspects of speech. Distraction causes stuttering, when stutterers use therapy techniques. When learning to use a new motor skill, the inhibition of other neuronal linkages is as important as the development of the target neural linkage: "Each motor engram is a pathway of excitation surrounded by a wall of inhibition. "[48] A golfer must keep her eye on the ball. Tennis pros are infamous for demanding silence from fans. Stutterers often say that they can use therapy skills in a clinical environment, but the distractions of normal conversations make fluent speech difficult. ^ Kuehn, Donald (1994). Official correspondence from the National Institute of Deafness and Communication Disorders. ^ James, J.E. "Punishment of stuttering: Contingency and stimulus parameters." Journal of Communication Disorders, 1981, 14, 375-386. ^ Kottke, F.J., Halpern, D., Easton, J.K.M., Ozel, A.T., Burrill, C.A. “The Training of Coordination.” Archives of Physical Medicine and Rehabilitation, Vol 59, December 1978, 567-572. Under stress, people's voices change. They tense their speech-production muscles, increasing their vocal pitch. They try to talk faster. They repeat words or phrases. They add interjections, such as "uh." These are normal dysfluencies. A study found that under stress, non-stutterers went from 0% to 4% dysfluencies, for the simple task of saying colors. Stutterers went from 1% to 9%. [49] The "conventional wisdom" is that stutterers are always nervous or stressed out. Many psychological studies have proven that this isn't true. But stress has an important role in stuttering. This next fact is so obvious that you've probably never thought about how important it is. All stutterers can talk fluently. In relaxed, low-stress situations we can say any sound or word fluently. If you're a severe stutterer, there might not be many such situations. But there are some. In other situations we stutter. How many paraplegics do you know who can walk in some situations, but not other situations? Or people who are blind with certain people, but not with other people? None that I've ever known. Think about this. Our brains are capable of producing fluent speech. We have all the speech motor programs necessary to produce any speech sound, fluently. We also have speech motor
{'wiki_source': 'wikibooks', 'other_info': "{'content_model': 'wikitext', 'language': 'en', 'title': 'Speech-Language Pathology/Stuttering/Print version', 'type': 'text'}"}