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Effects of Neuromodulation in Laryngeal Dystonia

StatusRecruiting
PhaseNot applicable
Started
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Record History

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  1. Notable Primary and study completion dates: Dec 31, 2025 to Dec 31, 2026
    • Site contact updated
    v7
  2. Notable Enrollment target: 15 to 25
    • Primary and study completion dates: Aug 16, 2024 to Dec 31, 2025
    • Trial status: Completed to Recruiting
    • Site details revised
    v6
  3. Minor Trial status: Recruiting to Completedv5 Show 4 more changesShow less
    • Enrollment target: estimated 60 to confirmed 15
    • Primary completion date changed from estimate of May 2025 to Aug 16, 2024
    • Study completion date changed from estimate of May 31, 2026 to Aug 16, 2024
    • Site details revised
  4. Minor Study site revisedv4
  5. Minor 2 versions Re-verified since Mar 24, 2022, no change to tracked fieldsv2-v3
  6. Minor Study First Submitted
  • Stopped: an ongoing trial was terminated, suspended or withdrawn.
  • Notable: the trial’s plan changed such as a big move in its timeline or size, a new primary endpoint, sponsor or phase, or recruiting opened or resumed.
  • Minor: routine progress and housekeeping, such as sites added or enrollment closed.
Laryngeal dystonia (LD) causes excessive vocal fold abduction (opening) or adduction (closing) leading to decreased voice quality, job prospects, self-worth and quality of life. Individuals with LD often experience episodic breathy voice, decreased ability to sustain vocal fold vibration, frequent pitch breaks and in some cases, vocal tremor. While neuroimaging investigations have uncovered both cortical organization and regional connectivity differences in structures in parietal, primary somatosensory and premotor cortices of those with LD, there remains a lack of understanding regarding how the brains of those with LD function to produce phonation and how these might differ from those without LD. Intervention options for people with LD are limited to general voice therapy techniques and Botulinum Toxin (Botox) injections to the posterior cricoarytenoid (PCA) and/or TA (thyroarytenoid) often bilaterally, to alleviate muscle spasms in the vocal folds. However, the effects of injections are short-lived, uncomfortable, and variable. To address this gap, the aim of this study is to investigate the effectiveness of repetitive transcranial magnetic stimulation (rTMS), a non-invasive neuromodulation technique, in assessing cortical excitability and inhibition of laryngeal musculature. Previous work conducted by the investigator has demonstrated decreased intracortical inhibition in those with adductor laryngeal dystonia (AdLD) compared to healthy controls. The investigators anticipate similar findings in individuals with with other forms of LD, where decreased cortical inhibition will likely be noted in the laryngeal motor cortex. Further, following low frequency (inhibitory) rTMS to the laryngeal motor brain area, it is anticipated that there will be a decrease in overactivation of the TA muscle. To test this hypothesis, a proof-of-concept, randomized study to down-regulate cortical motor signal to laryngeal muscles will be compared to those receiving an equal dose of sham rTMS. Previous research conducted by the investigator found that a single session of the proposed therapy produced positive phonatory changes in individuals with AdLD and justifies exploration in LD.
Trial Details
NCT Number NCT05095740
Lead Sponsor MGH Institute of Health Professions
Collaborators: National Institute on Deafness and Other Communication Disorders (NIDCD)
Conditions
(from sponsor)
Laryngeal Dystonia, Focal Dystonia
Related terms Dysphonia, Dystonic Disorders
Enrollment 25 participants
Start Date
Primary Completion (estimated)
Study Completion (estimated)
Updated on ClinicalTrials.gov