Atypical cerebral laterality: Neural Risk for Stuttering?

By Anne L. Foundas, M.D.
Tulane University Health Sciences Center

From the Stuttering Foundation's winter 200alt text8 newsletter

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.


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, Rivi re 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, 63:1640-1646.

Geschwind, N., & Galaburda, A. (1985). Cerebral lateralization: biological mechanisms, associations and pathology: A hypothesis and a program for research. Archives of Neurology. 42: Part I: 428-459; II: 34-552; III: 634-654.

Orton, S.T. (1927). Studies in stuttering. Archives of Neurology and Psychiatry, 18:671-672.

Smith, A & Kelly, E. (1997).?ÿ 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 movement. Journal of Speech, Language and Hearing Research, 43, 277-286.

Watkins K.E., Smith S.M., Davis S, Howell P (2007). Structural and functional abnormalities of the motor system in developmental stuttering. Brain Advance Access published online Oct. 10, 2007.