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Related Experiment Videos

The irritable larynx syndrome.

M Morrison1, L Rammage, A J Emami

  • 1Pacific Voice Clinic, University of British Columbia, Vancouver General Hospital, Canada.

Journal of Voice : Official Journal of the Voice Foundation
|September 25, 1999
PubMed
Summary

Hyperfunctional laryngeal symptoms like dysphonia and laryngospasm may stem from neural plasticity in the brainstem. Gastroesophageal reflux, psychological factors, and viral illness can trigger these changes, leading to irritable larynx syndrome.

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Area of Science:

  • Neurology
  • Otolaryngology
  • Speech Pathology

Background:

  • Hyperfunctional laryngeal symptoms, including muscular tension dysphonia, episodic laryngospasm, globus, and chronic cough, are common.
  • Etiological factors are diverse, often including gastroesophageal reflux, psychological issues, and dystonia.

Purpose of the Study:

  • To propose a unifying hypothesis for hyperfunctional laryngeal symptoms.
  • To investigate the role of neural plasticity in the brainstem's laryngeal control networks.
  • To define criteria for Irritable Larynx Syndrome (ILS).

Main Methods:

  • Studied 39 patients diagnosed with Irritable Larynx Syndrome based on specific inclusion criteria.
  • Assessed etiological factors such as gastroesophageal reflux, psychological conditions, and history of viral illness.

Related Experiment Videos

  • Proposed a hypothesis involving neural plastic changes in brainstem laryngeal control networks.
  • Main Results:

    • Gastroesophageal reflux was implicated in over 90% of patients.
    • Psychological factors were identified in approximately one-third of patients.
    • One-third of patients linked symptom onset to a viral illness, suggesting potential central nervous system changes.

    Conclusions:

    • A unifying hypothesis suggests neural plastic changes in brainstem nuclei underlie hyperkinetic laryngeal dysfunction (Irritable Larynx Syndrome).
    • This hypothesis integrates various etiologies and provides a framework for therapy and research.
    • The findings support the concept of a "spasm-ready" state in laryngeal control neurons triggered by stimuli.