All human behavior is associated with brain functioning of one type or another — including stuttering.
As research scientists focus on determining the cause of stuttering, it is important to examine how the brain is involved in stuttering. Yet, it is premature to rush to the simple conclusion that the brain is “causing” stuttering.
The brain operates as a complex set of physiological systems that are, in turn, provided with an array of inputs and outputs. The research task is to develop an understanding of the complex context within which the brain functions.
The following research abstract is the second in a series provided as a service by Hollins Communications Research Institute (HCRI). HCRI is a nonprofit Institute based in Roanoke, Virginia that has been at the forefront of stuttering research and treatment innovation since 1972.
HCRI commentary follows the abstract and is provided Ronald L. Webster, Ph.D., HCRI’s Founder and Director.
Common features of fluency-evoking conditions studied in stuttering subjects and controls: an H(2)15O PET study.
J Fluency Disord. 2003 Winter;28(4):319-35; quiz 336. Stager SV, Jeffries KJ, Braun AR. Language Section, Voice Speech and Language Branch, National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, MD 20892, USA.
1. Compare brain activation patterns under fluency- and dysfluency-evoking conditions in stuttering and control subjects;
2. Appraise the common features, both central and peripheral, of fluency-evoking conditions; and
3. Discuss ways in which neuroimaging methods can be used to understand the pathophysiology of stuttering.
We used H(2)15O PET to characterize the common features of two successful but markedly different fluency-evoking conditions — paced speech and singing — in order to identify brain mechanisms that enable fluent speech in people who stutter. To do so, we compared responses under fluency-evoking conditions with responses elicited by tasks that typically elicit dysfluent speech (quantifying the degree of stuttering and using this measure as a confounding covariate in our analyses).
We evaluated task-related activations in both stuttering subjects and age- and gender-matched controls. Areas that were either uniquely activated during fluency-evoking conditions, or in which the magnitude of activation was significantly greater during fluency-evoking than dysfluency-evoking tasks included auditory association areas that process speech and voice and motor regions related to control of the larynx and oral articulators.
This suggests that a common fluency-evoking mechanism might relate to more effective coupling of auditory and motor systems — that is, more efficient self-monitoring, allowing motor areas to more effectively modify speech. These effects were seen in both PWS and controls, suggesting that they are due to the sensorimotor or cognitive demands of the fluency-evoking tasks themselves.
While responses seen in both groups were bilateral, however, the fluency-evoking tasks elicited more robust activation of auditory and motor regions within the left hemisphere of stuttering subjects, suggesting a role for the left hemisphere in compensatory processes that enable fluency.
This article hints at problems in auditory sensory and motor activation relationships. These results are consistent with the idea that there is a flaw in sensory/motor feedback relationships.
For more information about HCRI’s work in the field of stuttering and treatment programs, visit www.stuttering.org.