By Anne L. Foundas, M.D.
Tulane University Health Sciences Center
Editor’s note: The Stuttering Foundation is pleased to support Dr. Foundas’ new research.
Atypical cerebral laterality was proposed as a potential central
defect in developmental stuttering in 1927 when Orton wrote that
stuttering may be the result of incomplete cerebral dominance. Support
for this early speculation may be found in the more recent theory of
cerebral laterality (for review: Geschwind & Galaburda, 1985).
According to this theory, brain organization can be defined as
“typical” or “atypical” (anomalous).
Typical brain organization includes left hemispheric dominance for
language and right hemispheric dominance for emotion and attention.
Typical brain organization occurs in about 70 per cent of the
population.
Anomalous dominance exists in about 30 per cent of the population.
Geschwind and Galaburda suggested that atypical brain structure and
function would be found in individuals with developmental stuttering. A
variety of studies seem to have supported this notion.
We have proposed a unifying anatomical model based on a motor
control theory of speech production (Foundas et al, 2004). According to
this model, two main neural circuits work together to coordinate speech
production. These circuits or loops include an outer “linguistic” loop
(speech-language areas) and an inner “phonatory” loop (motor regions).
The outer linguistic loop selects and monitors speech sounds; the
inner loop coordinates and activates the motor programs of the vocal
apparatus (see Alm, 2007 for similar discussion of inner/medial and
outer/lateral “loops” thought to be contributory to fluent and/or
stuttered speech). Stuttering can be modeled as a momentary
instability in these systems when the timing between these two neural
circuits is interrupted (see Smith, Johnson, McGillem & Goffman,
2000 for empirical attempts to measure “stability” in speech movements
and Smith & Kelly, 1997, for discussion of “(in)stability” as a
possible contributor to stuttering).
Muscles that mediate speech functions (tongue, face, larynx) are
paired structures. Muscles on the right side receive input from the
left cerebral cortex (left hemisphere of the brain) and those on the
left side receive input from the right cerebral cortex. The impulses
from the right and left hemispheres must be synchronized to assure that
speech production is fluent. Orton (1927) originally suggested that
this synchronization could only occur if there was a “leading”
hemisphere.
The leading hemisphere would then impose its timing patterns over
the other hemisphere to produce fluent speech. Stuttering would result
if the margin of dominance was reduced.
Theoretically, disruption at any point within these two main neural
circuits could induce stuttering by disrupting the flow of information,
which in turn would induce asynchronous activation of the paired
muscles that mediate speech production.
In this century many studies have examined the anatomical basis of
developmental stuttering, including several important studies published
this year (see References). At this juncture, there is strong evidence
that adults with persistent developmental stuttering have anomalous
anatomy in some speech, language, and motor brain areas. There is
controversy about whether one or several functional-anatomical defects
may represent a “neural signature” of stuttering.
Several “target” areas have been identified, and include the
auditory temporal cortex, supplementary motor areas, the cerebellum,
and left hemisphere white matter pathways adjacent to the motor speech
and mouth area.
Distinct features may be more common in men versus women, and right
versus left handers who stutter. Furthermore, since most studies have
not been conducted in both adults and children, it is uncertain whether
some anatomical configurations may be distinct hallmarks of the disease
or more reflective of compensatory or developmental changes in brain
structure and function associated with experiences with stuttering
behavior.
We speculate that there may be “biological subtypes” that differ
based on gender, hand preference, genetic factors, and stuttering
severity. Developmental effects are critical to study so that we can
learn more about compensatory brain changes in contrast to more
biological, constitutional, intrinsic or fixed deficits. It may be
that some brain anomalies can be modified by specific therapeutic
treatments including the use of devices that alter auditory feedback,
pharmacological agents that block dopamine uptake, cognitive-behavioral
and/or speech therapy. We need to continue to examine competing
theories of the etiological basis of stuttering. We believe that Orton
was wise to consider how central defects may contribute to the
ontogenesis of stuttering. It remains for modern-day investigators to
determine the qualitative as well as the quantitative nature of those
defects, how they might change over the lifespan, and whether they
exist for most or differ among subgroups of people who stutter.
REFERENCES
Alm, P. (2007). A new framework for understanding
stuttering: The dual premotor model. In J. Au-Yeung and M. Leahy
(Eds.). Research, treatment, and self-help in fluency disorders: New
horizons (pp.77-83). Proceedings of the Fifth World Congress on
Fluency Disorders, Dublin, Ireland ISBN 978-9555700-0-1
Beal DS, Gracco VL, Lafaille SJ, De Nil LF (2007).
Voxel-based morphometry of auditory and speech-related cortex in
stutterers. Neuroreport, 18:1257-1260.
Brown S, Ingham RJ, Ingham JC, Laird AR, Fox PT
(2005). Stuttered and fluent speech production: an ALE meta-analysis of
functional neuroimaging studies. Human Brain Mapping, 25:105-117.
Chang SE, Erickson KI, Ambrose NG, Hasegawa-Johnson
MA, Ludlow CL (2007). Brain anatomy differences in childhood
stuttering. Neuroimage. Available online 13 October, 2007
Cykowski MD, Kochunov PV, Ingham RJ, Ingham JC,
Mangin JF, Rivière D, Lancaster JL, Fox PT (2007). Perisylvian sulcal
morphology and cerebral asymmetry patterns in adults who stutter.
Cerebral Cortex. Advance Access published on June 21, 2007.
Foundas AL, Bollich AM, Feldman J, Corey DM, Hurley
M, Lemen LC, Heilman KM (2004). Aberrant auditory processing and
atypical planum temporale in developmental stuttering. Neurology,
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Geschwind, N., & Galaburda, A. (1985). Cerebral
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Orton, S.T. (1927). Studies in stuttering. Archives of Neurology and Psychiatry, 18:671-672.
Smith, A & Kelly, E. (1997). Stuttering: A
dynamic, multifactorial model. In R. Curlee and G. Siegel (eds).
Nature and treatment of stuttering: New directions (pp.204-217).
Boston: Allyn & Bacon.
Smith, A., Johnson, M., McGillem, C. & Goffman,
L. (2000). On the assessment of stability and patterning of speech
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Watkins K.E., Smith S.M., Davis S, Howell P (2007).
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