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Brainstem conduction abnormalities in spasmodic dysphonia.

S D Schaefer, T Finitzo-Hieber, I J Gerling

    The Annals of Otology, Rhinology, and Laryngology
    |January 1, 1983
    PubMed
    Summary
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    Auditory brainstem response testing revealed abnormalities in 75% of spasmodic dysphonia patients. These findings suggest spasmodic dysphonia may involve varied cranial nerve dysfunctions.

    Area of Science:

    • Neurology
    • Otolaryngology
    • Neurophysiology

    Background:

    • Spasmodic dysphonia (SD) is a focal dystonia affecting laryngeal muscles.
    • The underlying neurophysiological mechanisms of SD remain incompletely understood.
    • Cranial nerve involvement is a potential, yet debated, factor in SD etiology.

    Purpose of the Study:

    • To investigate the utility of auditory brainstem response (ABR) testing in identifying neurophysiological abnormalities in patients with spasmodic dysphonia.
    • To explore potential cranial nerve pathway involvement in the pathophysiology of SD.

    Main Methods:

    • Auditory brainstem response (ABR) testing was performed on twelve patients diagnosed with spasmodic dysphonia.
    • Three specific ABR parameters were evaluated: wave I-V interpeak latency, wave V latency shifts at high stimulus rates, and amplitude ratios.

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  • Results were analyzed to identify patterns of abnormality.

    • Main Results:

    • Seventy-five percent (9 out of 12) of patients exhibited abnormal ABR findings.
    • Prolonged wave I-V interpeak latency was observed in 3 patients.
    • Pathological wave V latency shifts at high stimulus rates were present in 7 patients.
    • Amplitude ratios were consistently normal across all subjects.

    Conclusions:

    • The high rate of ABR abnormalities suggests a significant neurophysiological basis for spasmodic dysphonia.
    • Findings support the hypothesis that SD may represent a disorder with variable cranial nerve symptom presentations.
    • Further research into specific neurophysiological models is warranted to elucidate the pathophysiology of SD.