Pathophysiology of adductor spasmodic dysphonia: a TMS study

Abstract

Adductor spasmodic dysphonia (AdSD) is a neurologically-based voice disorder affecting the firing rate and pattern of upper motor neurons responsible for the laryngeal musculature. AdSD is characterized by intermittent hyperadduction of the true vocal folds during connected speech resulting in interruptions in phonation and a strained/struggled vocal quality. Differential diagnosis of AdSD can be difficult as the clinical symptoms present similar to those found in muscle tension dysphonia (MTD). Purpose: The purpose of this study was to identify and compare differences in intracortical inhibition and facilitation in the primary motor cortex between those with AdSD, MTD and healthy controls, if those differences were widespread; affecting both the cortical spinal and corticobulbar tract and, if differences in cortical excitability are related to the perceptual severity of the voice disorder. An additional purpose was to determine if measures of intracortical inhibition and facilitation are viable methods to assist in the differential diagnosis between AdSD and MTD. Methods: Transcranial magnetic stimulation (TMS) was used to measure intracortical inhibition and facilitation through the following measures: cortical silent period (CSP), short interval intracortical inhibition (SICI), intracortical facilitation (ICF) and the stimulus response curve (SR curve) in first dorsal interosseus and masseter in those with AdSD, MTD and healthy controls. The Consensus of Auditory Perceptual Evaluation of Voice (CAPE-V) was used as a tool to evaluate the nature and severity of voice characteristics of those with AdSD and MTD. Results: Masseter and FDI CSP were the most sensitive in capturing between group differences. Those with AdSD had significantly shorter CSP duration in masseter than those with MTD and healthy controls. Those with AdSD also had significantly shorter CSP duration in FDI than healthy controls, but not those with MTD indicating widespread dysfunction of the GABAB mechanism is a feature of AdSD, similar to other forms of focal dystonia. Use of TMS is feasible in assisting in the differential diagnosis of AdSD and MTD.