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Abstract
Soo-Eun Chang1,2, Barry Horwitz3, John Ostuni4, Richard Reynolds5 and Christy L. Ludlow1,6
1Laryngeal and Speech Section, Medical Neurology Branch, National Institute of Neurological Disorders and Stroke (NINDS), National Institutes of Health, Bethesda, MD 20852, USA
2Department of Communicative Sciences and Disorders, Michigan State University, East Lansing, MI 48824, USA
3Brain Imaging and Modeling Section, Voice, Speech, and Language Branch, National Institute on Deafness and Other Communication Disorders (NIDCD), National Institutes of Health, Bethesda, MD 20852, USA
4Clinical Neurosciences Program, National Institute of Neurological Disorders and Stroke (NINDS), National Institutes of Health, Bethesda, MD 20852, USA
5Scientific and Statistical Computing Core, National Institute of Mental Health (NIMH), National Institutes of Health, Bethesda, MD 20852, USA
6Department of Communication Sciences and Disorders, James Madison University, Harrisonburg, VA 22807, USA
Address correspondence to Soo-Eun Chang, 112 Oyer Building, Michigan State University, East Lansing, MI 48824, USA.
Abstract
The neurophysiological basis for stuttering may involve deficits that affect dynamic interactions among neural structures supporting fluid speech processing. Here, we examined functional and structural connectivity within corticocortical and thalamocortical loops in adults who stutter. For functional connectivity, we placed seeds in the left and right inferior frontal Brodmann area 44 (BA44) and in the ventral lateral nucleus (VLN) of the thalamus. Subject-specific seeds were based on peak activation voxels captured during speech and nonspeech tasks using functional magnetic resonance imaging. Psychophysiological interaction (PPI) was used to find brain regions with heightened functional connectivity with these cortical and subcortical seeds during speech and nonspeech tasks. Probabilistic tractography was used to track white matter tracts in each hemisphere using the same seeds. Both PPI and tractrography supported connectivity deficits between the left BA44 and the left premotor regions, while connectivity among homologous right hemisphere structures was significantly increased in the stuttering group. No functional connectivity differences between BA44 and auditory regions were found between groups. The functional connectivity results derived from the VLN seeds were less definitive and were not supported by the tractography results. Our data provide strongest support for deficient left hemisphere inferior frontal to premotor connectivity as a neural correlate of stuttering.
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