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Neurophysiological Contributions to Dysphonia: The Role of Cortical Silent Periods in AdLD
Baothy P Huynh1, Katherine L Marks2, Cara E Stepp3
1Department of Rehabilitation Sciences, MGH Institute of Health Professions, Boston, Massachusetts; Department of Occupational Therapy, MGH Institute of Health Professions, Boston, Massachusetts.
Objective:
Adductor laryngeal dystonia (AdLD) is a task-specific focal dystonia characterized by involuntary vocal fold hyperadduction and impaired voice quality. While reduced cortical inhibition is a hallmark of AdLD, its relationship to acoustic measures of voice dysfunction remains unclear. This study investigated whether intracortical inhibition, as measured by the cortical silent period (cSP) from the laryngeal motor cortex (LMC), is associated with cepstral peak prominence (CPP), a quantitative acoustic marker of voice harmonic periodicity.
Methods:
Thirty-two participants (17 AdLD, 15 controls) underwent transcranial magnetic stimulation with fine-wire electromyography targeting the LMC to measure cSP. Acoustic recordings of sustained vowels and connected speech were used to derive CPP. Linear models were used to assess the relationship between cSP, CPP, and perceptual voice severity (Consensus auditory-perceptual evaluation of voice overall severity ratings).
Results:
Participants with AdLD exhibited significantly shorter cSP durations and lower CPP values than controls (P < 0.05). Across all participants, longer cSP durations were significantly associated with higher CPP values (β = 0.075, P = 0.03), indicating that greater cortical inhibition is associated with better harmonic periodicity in the voice. However, cSP did not independently predict perceptual voice severity after adjusting for age and CPP.
Conclusion:
These findings link impaired cortical inhibition in the LMC to less harmonic periodicity in AdLD, supporting a mechanistic role for disinhibition in dysphonic voice production. While cSP did not improve the prediction of perceptual severity, it may serve as a physiological correlate of acoustic dysphonia and a potential biomarker for future neuromodulatory interventions.
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