Reflection & Reaction

A neurological basis of stuttering?
Many theories of the physiological basis of stuttering exist. For centuries it was widely believed that stuttering arose from abnormalities of the tongue or larynx and, until recently, clinicians have tried to treat stuttering by manipulating the peripheral muscles of speech, albeit with limited benefit. However, evidence is now accumulating to suggest that the dysfunction of stuttering resides within the brain and not within the tongue or larynx. The recent study by Sommer and colleagues1 builds upon the work of others to suggest that stuttering should be viewed as a disorder of the brain. Although this article expands our understanding and provides insights into future research and treatment directions, the neurological basis of stuttering is still not fully understood. However, the work of Sommer’s group supports the “bottom-up” and “topdown” approach to understanding the physiological basis of stuttering—ie, studies of pharmacological treatments (bottom up) that support the neurological basis of this disorder as shown by functional imaging studies (top down). Previous functional brain imaging studies have shown that stuttering is associated with abnormally low function of left hemispheric speech areas—which are normally dominant in speech function—compared with analogous areas of the right hemisphere.2,3 An interesting clinical finding, which is often used by neuroimagers to investigate stuttering, is that fluency can be induced through a variety of techniques such as chorus reading. During induced fluency, the activity of left hemispheric speech areas is increased to levels comparable with normal controls. Sommer suggests that chorus reading provides an external clock that decreases stuttering and induces fluency. However, a more comprehensive explanation may be that induced fluency tasks bypass the abnormally inactive striatum to activate the outer cortical speech loop, which is preserved in individuals who stutter. Spontaneous stuttering is probably
THE LANCET Neurology Vol 1 November 2002

due to defects in the inner subcortical speech loop, which includes the striatum.4 Others have reported that the right hemisphere of people who stutter is abnormally overactive compared with the left hemisphere. Sommer and co-workers point out that this increase in right hemispheric activity might represent overcompensation for the low functioning of the left hemisphere, which could have failed to develop properly. This study, and others, have yet to pinpoint a specific cerebral structure involved in stuttering, probably due to the use of different imaging techniques. The low function of the left hemisphere may be related to abnormally high inhibition by dopamine.5,6 Stuttering shares many similarities with Tourette’s syndrome, a disorder of known dopamine abnormality. Both disorders have their onset in childhood, follow a waxing and waning course, present with tics, and respond, at least partially, to treatment with dopamine antagonists. Previous imaging studies have shown that the function of speech areas in the left hemisphere increases in relation to improved fluency following the administration of dopamine antagonists.5,7 The previous finding that low activity of the left cortical speech areas might also be related to abnormally low function of the left striatum5 is not discussed in Sommer’s study. Dopamine antagonists have been shown to increase striatal function and thus provide a plausible explanation for their therapeutic mechanism of action in stuttering.8 Unfortunately, older generation dopamine antagonists (eg, haloperidol) are not well tolerated and thus have limited utility. Recent research has shown, however, that novel dopamine antagonists can provide an efficacious and tolerable treatment option for individuals who stutter.9 The overcompensation of the right hemisphere, as described by Sommer, begins to explain some of the possible associated behavioural characteristics that may develop in relation to stuttering, such as avoidance and

struggle behaviours and social anxieties. Comprehensive stuttering treatment should target both the underdeveloped left hemisphere (eg, through pharmacological interventions) and the overcompensated right hemisphere (eg, through cognitive or behavioural speech therapy). A new era has begun in the understanding and treatment of stuttering. Sommer and others have shown that stuttering is associated with abnormal brain functioning, and hence it should be viewed as a neurological disorder with psychological compensations. The challenge now facing physicians and neuroscientists is to understand how stuttering develops, why it resolves spontaneously in some cases, and what treatments will ultimately assist individuals who struggle with this disorder.
Gerald A Maguire, Glyndon D Riley, and Benjamin P Yu Correspondence: Gerald A Maguire, University of California, Irvine Medical Center, Department of Psychiatry, Route 88, 101 City Drive, Orange CA 92868 USA. Email
1 Sommer M, Koch MA, Paulus W, Weiller C, Buchel C. Disconnection of speech-relevant brain areas in persistent developmental stuttering. Lancet 2002; 360: 380–83. Wu JC, Maguire GA, Riley G, et al. A positron emission tomography [18F] deoxyglucose study of developmental stuttering. Neuroreport 1995; 6: 501–05. Pool KD, Devous MD, Freeman FJ, Watson BC, Finitzo T. Regional cerebral blood flow in developmental stutterers. Arch Neurol 1991; 48: 509–12. Wu JC, Riley G, Maguire G, Najafi A, Tang C. PET scan evidence of parallel cerebral systems related to treatment effects: FDG and FDOPA PET scan findings. In: Hulstijn W, Peters HFM, Van Lieshout PHHM eds. Speech production: motor control, brain research and fluency disorders. Amsterdam: Elsevier Science, 1997: 329–39. Maguire GA, Riley GD, Franklin DL, et al. The dopamine hypothesis of stuttering and its treatment implications. Int J Neuropsychopharmacol 2000; 3 (suppl 1): S12. Wu JC, Maguire G, Riley G, et al. Increased dopamine activity associated with stuttering. Neuroreport 1997: 8: 767–70. Wood F, Stump D. Patterns of regional cerebral blood flow during attempted reading aloud by stutterers both on and off haloperidol medication: evidence for inadequate left frontal activation during stuttering. Brain Lang 1980; 9: 141–44. Buchsbaum MS, Potkin SG, Siegel BV Jr, et al. Striatal metabolic rate in clinical response to neuroleptics in schizophrenia. Arch Gen Psychiatry 1992; 49: 966–74. Maguire GA, Riley GD, Franklin DL, Gottshalk LA. Risperidone for the treatment of stuttering. J Clin Psychopharmacol 2000; 20: 479–82.





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