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 third in a series es 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.
The commentary provided following the abstract is provided Ronald L. Webster, Ph.D., HCRI’s Founder and Director.
Structural and functional abnormalities of the motor system in developmental stuttering.
Brain. 2008 Jan;131(Pt 1):50-9. Epub 2007 Oct 10. Watkins KE, Smith SM, Davis S, Howell P. Department of Experimental Psychology, University of Oxford, Oxford, UK. firstname.lastname@example.org
Though stuttering is manifest in its motor characteristics, the cause of stuttering may not relate purely to impairments in the motor system as stuttering frequency is increased by linguistic factors, such as syntactic complexity and length of utterance, and decreased by changes in perception, such as masking or altering auditory feedback.
Using functional and diffusion imaging, we examined brain structure and function in the motor and language areas in a group of young people who stutter. During speech production, irrespective of fluency or auditory feedback, the people who stuttered showed overactivity relative to controls in the anterior insula, cerebellum and midbrain bilaterally and underactivity in the ventral premotor, Rolandic opercular and sensorimotor cortex bilaterally and Heschl’s gyrus on the left.
These results are consistent with a recent meta-analysis of functional imaging studies in developmental stuttering. Two additional findings emerged from our study. First, we found overactivity in the midbrain, which was at the level of the substantia nigra and extended to the pedunculopontine nucleus, red nucleus and subthalamic nucleus.
This overactivity is consistent with suggestions in previous studies of abnormal function of the basal ganglia or excessive dopamine in people who stutter. Second, we found underactivity of the cortical motor and premotor areas associated with articulation and speech production. Analysis of the diffusion data revealed that the integrity of the white matter underlying the underactive areas in ventral premotor cortex was reduced in people who stutter.
The white matter tracts in this area via connections with posterior superior temporal and inferior parietal cortex provide a substrate for the integration of articulatory planning and sensory feedback, and via connections with primary motor cortex, a substrate for execution of articulatory movements.
Our data support the conclusion that stuttering is a disorder related primarily to disruption in the cortical and subcortical neural systems supporting the selection, initiation and execution of motor sequences necessary for fluent speech production.
This study found evidence for anomalous cortical and subcortical activation in stutterers. While the authors refer to these systems in terms of motor activation and control, the door remains open to the question of sensory involvement in motor execution. That is, a flaw in sensory return associated with speech initiation would have significant implications for motor functions.
For more information about HCRI’s work in the field of stuttering and treatment programs, visit www.stuttering.org .