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 “top-
down” 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 hemi-
sphere.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 overcompen-
sation 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 hemi-
sphere 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 antag-
onists.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
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struggle behaviours and social
anxieties. Comprehensive stuttering
treatment should target both the
underdeveloped left hemisphere (eg,
through pharmacological inter-
ventions) 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 psycho-
logical compensations. The challenge
now facing physicians and neuro-
scientists 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 gamaguir@uci.edu
References
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.
2 Wu JC, Maguire GA, Riley G, et al. A positron
emission tomography [18F] deoxyglucose study of
developmental stuttering. Neuroreport 1995;
6: 501–05.
3 Pool KD, Devous MD, Freeman FJ, Watson BC,
Finitzo T. Regional cerebral blood flow in
developmental stutterers. Arch Neurol 1991;
48: 509–12.
4 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.
5 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.
6 Wu JC, Maguire G, Riley G, et al. Increased
dopamine activity associated with stuttering.
Neuroreport 1997: 8: 767–70.
7 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.
8 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.
9 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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