Abnormal Activation of the Primary Somatosensory Cortex in Spasmodic Dysphonia: An fMRI Study

• Published in: Cerebral cortex (New York, N.Y. 1991) Vol. 20; no. 11; pp. 2749 - 2759
• Main Authors: Simonyan, Kristina, Ludlow, Christy L.
• Format: Journal Article
• Language: English
• Published: United States Oxford University Press 01-11-2010
• Subjects: Adult; Aged; Dysphonia - pathology; Dysphonia - physiopathology; Female; Humans; laryngeal dystonia; Magnetic Resonance Imaging - methods; Male; Middle Aged; Nerve Net - pathology; Nerve Net - physiopathology; neuroimaging; Somatosensory Cortex - pathology; Somatosensory Cortex - physiopathology; voice production
• ISSN: 1047-3211; 1460-2199
• DOI: 10.1093/cercor/bhq023

Spasmodic dysphonia (SD) is a task-specific focal dystonia of unknown pathophysiology, characterized by involuntary spasms in the laryngeal muscles during speaking. Our aim was to identify symptom-specific functional brain activation abnormalities in adductor spasmodic dysphonia (ADSD) and abductor spasmodic dysphonia (ABSD). Both SD groups showed increased activation extent in the primary sensorimotor cortex, insula, and superior temporal gyrus during symptomatic and asymptomatic tasks and decreased activation extent in the basal ganglia, thalamus, and cerebellum during asymptomatic tasks. Increased activation intensity in SD patients was found only in the primary somatosensory cortex during symptomatic voice production, which showed a tendency for correlation with ADSD symptoms. Both SD groups had lower correlation of activation intensities between the primary motor and sensory cortices and additional correlations between the basal ganglia, thalamus, and cerebellum during symptomatic and asymptomatic tasks. Compared with ADSD patients, ABSD patients had larger activation extent in the primary sensorimotor cortex and ventral thalamus during symptomatic task and in the inferior temporal cortex and cerebellum during symptomatic and asymptomatic voice production. The primary somatosensory cortex shows consistent abnormalities in activation extent, intensity, correlation with other brain regions, and symptom severity in SD patients and, therefore, may be involved in the pathophysiology of SD.