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Rabbit model with vocal fold hyperadduction

Naoki Takemoto1, Tetsuji Sanuki1, Shinichi Esaki1

  • 1Department of Otolaryngology-Head & Neck Surgery, Nagoya City University Graduate School of Medical Sciences.

Auris, Nasus, Larynx
|January 30, 2022
PubMed
Summary

Researchers developed a rabbit model for adductor spasmodic dysphonia (AdSD) by inducing vocal fold hyperadduction. This model mimics AdSD symptoms, offering a new tool to study this voice disorder.

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Area of Science:

  • Otolaryngology
  • Animal Modeling
  • Voice Science

Background:

  • Adductor spasmodic dysphonia (AdSD) causes strained voice due to vocal fold hyperadduction.
  • AdSD pathology is complex, lacking definitive origins, hindering research.
  • Existing animal models do not fully represent AdSD's laryngeal dysfunction.

Purpose of the Study:

  • To establish a novel animal model simulating vocal fold hyperadduction.
  • To evaluate the validity of the created model for studying AdSD.
  • To provide a platform for investigating AdSD pathology and treatment.

Main Methods:

  • A rabbit model was created using cricothyroid approximation, forced airflow, and recurrent laryngeal nerve (RLN) stimulation.
  • Vocal fold hyperadduction was induced via electrical stimulation of both RLNs.
Keywords:
Animal modelNerve stimulationSpasmodic dysphoniaStrained voiceVocal fold hyperadduction

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  • Laryngeal function was assessed by recording sound, endoscopic images, subglottal pressure, and performing acoustic analysis.

    • Main Results:

    • RLN stimulation significantly increased subglottal pressure and produced strained voice.
    • Transecting one RLN reduced subglottal pressure and strained voice.
    • Acoustic analysis showed increased standard deviation of F0 (SDF0) and voice breaks (DVB) with stimulation, which reversed upon RLN sectioning.

    Conclusions:

    • A valid rabbit model for vocal fold hyperadduction was successfully developed.
    • The model's physiological and acoustic characteristics align with human AdSD.
    • This model offers a valuable resource for elucidating AdSD pathophysiology and evaluating therapeutic interventions.