Cortical Silent Period Reveals Differences Between Adductor Spasmodic Dysphonia and Muscle Tension Dysphonia

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 1) cortical excitability differences between AdSD, muscle tension dysphonia (MTD) and healthy controls 2) distribution of potential differences in cranial or skeletal muscle, and 3) if cortical excitability measures assist in the differential diagnosis of AdSD and MTD. Methods 10 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 than in MTD and healthy. In addition, we hypothesized there would be a correlation between cortical excitability measures and clinical voice severity in AdSD. Results Cortical silent period (CSP) 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.

Hyperactive sensorimotor cortex during voice perception in spasmodic dysphonia

“…These results are in good accord with a well-known and time-honored clinical feature of adductor-type SD, i.e., its “task-specificity,” where falsetto phonation is free of voice breakage 5 , and may concur with some neuroimaging studies of SD and other dystonic disorders 9 , 35 , 36 . These findings seem consistent with previous TMS studies showing that the hyperactive somatosensory cortex increases the neuromuscular excitability of the speech production system in SD 12 , 13 . Together, the present findings converge to suggest that reduced sensorimotor reactivity is a primary neural source responsible for the voice disorder in SD.…”

“…A few previous neuroimaging studies have suggested that SD is associated with abnormal sensorimotor integration in the primary sensorimotor cortex, basal ganglia, thalamus, and cerebellum 9 – 11 . These findings seem to be partially consistent with some recent studies using transcranial magnetic stimulation (TMS), which showed changes in motor cortical excitability in SD patients 12 , 13 . However, it remains unclear to what extent the observed activations in those cortical and subcortical structures reflect the endogenous pathophysiological mechanisms of the disease, since most of the activation differences between SD patients and healthy controls were obtained by measuring brain activity during voice production .…”

“…As for other forms of dystonia, previous TMS studies show a causal link between the somatosensory cortex and writer's cramp 44,45 . Arguably, abnormal sensorimotor activation may be also causally linked with SD, but the causal relationship between SD and motor cortical excitability has not yet been established because the existing TMS data show a shorter cortical silent period in patients than healthy controls, which only suggests some impairment in inhibitory control in the corticobulbar and cortical spinal tracts 12,13,46 . Further studies are needed to investigate whether TMS stimulation to the left sensorimotor cortex improves the dystonic voice and clarify the potential and limits of fMRI signals in the clinical diagnosis of SD.…”

Spasmodic Dysphonia: A Review. Part 2: Characterization of Pathophysiology

“…Loss of cortical inhibition is one of the potential underlying neuropathophysiological mechanisms in the focal dystonias. 32 This has been investigated using the cortical silent period (CSP) following a muscle-evoked potential to transcranial magnetic stimulation (TMS). The CSP has been found to be shorter in patients with AdSD than in healthy controls ( Figure 2 ).…”

Review of differential diagnosis and management of spasmodic dysphonia

“…Misdiagnosis can lead to ineffective time-consuming and expensive treatments that may not be beneficial. Moreover, there is no available gold standard test for differential diagnosis [50]. A large proportion of Provides practical suggestions for the use of telephone screening of SD by experienced clinicians.…”