Spasmodic dysphonia (SD) is characterized by involuntary laryngeal muscle spasms during vocalization. Most previous neuroimaging studies of SD measured brain activation during voice production and suggested that SD arises from abnormal sensorimotor integration involving the cortical and subcortical regions. However, these studies did not clarify whether this abnormal sensorimotor activation arises from some endogenous neural mechanism underlying SD or merely reflects neural activation produced by abnormal vocalization. To identify the specific neural correlates of SD, we compared neural activation in SD patients and healthy participants using a sound discrimination task that does not require overt speech production, thereby allowing us to eliminate any neural effects associated with abnormal vocalization. Eleven patients with adductor-type SD and 11 age- and gender-matched healthy participants underwent functional MRI. We found overactivation in the left sensorimotor cortex and the left thalamus in the SD patients, suggesting that voice perception activates different neural systems between SD patients and healthy subjects. For the SD patients, moreover, the magnitude of sensorimotor activation showed a significant positive correlation with symptom severity measured at voice handicap index-10, suggesting that signals from the sensorimotor cortex can be a new biomarker for assessing disease severity. The present findings suggested that the sensorimotor cortex and thalamus play a central role in the generation of abnormal phonation in SD.
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