Sharyl Samargia1, Rebekah Schmidt2, Teresa Jacobson Kimberley2. 1. University of Minnesota, Minneapolis, MN, USA University of Wisconsin, River Falls, WI, USA sharyl.samargia@uwrf.edu. 2. University of Minnesota, Minneapolis, MN, USA.
Abstract
BACKGROUND: The pathophysiology of adductor spasmodic dysphonia (AdSD), like other focal dystonias, is largely unknown. OBJECTIVE: The purposes of this study were to determine (a) cortical excitability differences between AdSD, muscle tension dysphonia (MTD), and healthy controls; (b) distribution of potential differences in cranial or skeletal muscle; and (c) if cortical excitability measures assist in the differential diagnosis of AdSD and MTD. METHODS: Ten participants with adductor spasmodic dysphonia, 8 with muscle tension dysphonia, and 10 healthy controls received single and paired pulse transcranial magnetic stimulation (TMS) to the primary motor cortex contralateral to tested muscles, first dorsal interosseus (FDI), and masseter. We tested the hypothesis that cortical excitability measures in AdSD would be significantly different from those in MTD and healthy controls. In addition, we hypothesized that there would be a correlation between cortical excitability measures and clinical voice severity in AdSD. RESULTS: Cortical silent period duration in masseter and FDI was significantly shorter in AdSD than MTD and healthy controls. Other measures failed to demonstrate differences. CONCLUSION: There are differences in cortical excitability between AdSD, MTD, and healthy controls. These differences in the cortical measure of both the FDI and masseter muscles in AdSD suggest widespread dysfunction of the GABAB mechanism may be a pathophysiologic feature of AdSD, similar to other forms of focal dystonia. Further exploration of the use of TMS to assist in the differential diagnosis of AdSD and MTD is warranted.
BACKGROUND: The pathophysiology of adductor spasmodic dysphonia (AdSD), like other focal dystonias, is largely unknown. OBJECTIVE: The purposes of this study were to determine (a) cortical excitability differences between AdSD, muscle tension dysphonia (MTD), and healthy controls; (b) distribution of potential differences in cranial or skeletal muscle; and (c) if cortical excitability measures assist in the differential diagnosis of AdSD and MTD. METHODS: Ten participants with adductor spasmodic dysphonia, 8 with muscle tension dysphonia, and 10 healthy controls received single and paired pulse transcranial magnetic stimulation (TMS) to the primary motor cortex contralateral to tested muscles, first dorsal interosseus (FDI), and masseter. We tested the hypothesis that cortical excitability measures in AdSD would be significantly different from those in MTD and healthy controls. In addition, we hypothesized that there would be a correlation between cortical excitability measures and clinical voice severity in AdSD. RESULTS: Cortical silent period duration in masseter and FDI was significantly shorter in AdSD than MTD and healthy controls. Other measures failed to demonstrate differences. CONCLUSION: There are differences in cortical excitability between AdSD, MTD, and healthy controls. These differences in the cortical measure of both the FDI and masseter muscles in AdSD suggest widespread dysfunction of the GABAB mechanism may be a pathophysiologic feature of AdSD, similar to other forms of focal dystonia. Further exploration of the use of TMS to assist in the differential diagnosis of AdSD and MTD is warranted.
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