Speech-Language Pathology/Stuttering/Neurology of Stuttering

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Most brain scan studies have found no differences between stutterers’ and non-stutterers’ cerebral activity during silent rest and during fluent speech.[1]. 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.[2] [3]
  • 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.

Right-Hemisphere Overactivity[edit]

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.

Auditory Processing Underactivity[edit]

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.[4] 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,[5] 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).[6] 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.[7] 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.

Left Caudate Nucleus Speech Motor Area Overactivity[edit]

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.[8]

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).

Tourette's and Stuttering[edit]

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.[9]
  • 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.

A Trigger for Tourette's[edit]

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.[10] 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.

"Good Days, Bad Days"—and the Anti-Stuttering Diet[edit]

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.

More Stuttering Brain Scan Studies[edit]

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.”[11]
  • 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.”[12]
  • De Nil, 1995: During silent reading, increased activation in the left angular cingulate cortex, a “reflection of covert anticipation of stuttering.” [13]
  • 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…”[14]
  • 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.”[15]
  • Kalinowski, 1997: Some stutterers showed the greatest reduction in the temporal-parietal area, and others showing greatest reductions in the right hemisphere posterior sites.[16]
  • Kroll, 1997: After fluency shaping stuttering therapy there is increased left-hemisphere activity, although large areas of activation in the right hemisphere remain.[17]
  • Watson, 1994: Abnormal right-hemisphere activity only in stutterers who also had language deficits.[18]

References

  1. ^ 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.
  2. ^ 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. Peters, and P.H.H.M. Van Lieshout, Amsterdam: Elsevier, 1997.
  3. ^ 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. Peters, and P.H.H.M. Van Lieshout, Amsterdam: Elsevier, 1997.
  4. ^ Kutscher, Martin L. Kids in the Syndrome Mix (Jessica Kingsley Publishers, 2005, ISBN 1-84310-8100), pages 178-179.
  5. ^ 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.
  6. ^ 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. Peters, and P.H.H.M. Van Lieshout, Amsterdam: Elsevier, 1997.
  7. ^ 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.
  8. ^ 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. Peters, and P.H.H.M. Van Lieshout, Amsterdam: Elsevier, 1997.
  9. ^ Sacks, Oliver. An Anthropologist on Mars. (Vintage, 1996, ISBN: 0679756973).
  10. ^ 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.
  11. ^ 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
  12. ^ 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. Peters, and P.H.H.M. Van Lieshout, Amsterdam: Elsevier, 1997.
  13. ^ 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.
  14. ^ 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.
  15. ^ 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. Peters, and P.H.H.M. Van Lieshout, Amsterdam: Elsevier, 1997.
  16. ^ 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.
  17. ^ 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. Peters, and P.H.H.M. Van Lieshout, Amsterdam: Elsevier, 1997.
  18. ^ 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.