Rabbit model with vocal fold hyperadduction

Objective: Adductor spasmodic dysphonia (AdSD) is caused by hyperadduction of the vocal folds during phonation, resulting in a strained voice. Animal models are not yet used to elucidate this intractable disease because AdSD has a difficult pathology without a definitive origin. For the first step, we established an animal model with vocal fold hyperadduction and evaluated its validity by assessing laryngeal function. Methods: In this experimental animal study, three adult Japanese 20-week-old rabbits were used. The models were created using a combination of cricothyroid approximation, forced airflow, and electrical stimulation of the recurrent laryngeal nerves (RLNs). Cricothyroid approximation was added to produce a glottal slit. Thereafter, both RLNs were electrically stimulated to induce vocal fold hyperadduction. Finally, the left RLN was transected to relieve hyperadduction. The sound, endoscopic images, and subglottal pressure were recorded, and acoustic analysis was performed. Results: Subglottal pressure increased significantly, and the strained sound was produced after the electrical stimulation of the RLNs. After transecting the left RLN, the subglottal pressure decreased significantly, and the strained sound decreased. Acoustic analysis revealed an elevation of the standard deviation of F0 (SDF0) and degree of voice breaks (DVB) through stimulation of the RLNs, and degradation of SDF0 and DVB through RLN transection. Formant bands in the sound spectrogram were interrupted by the stimulation and appeared again after the RLN section. Conclusion: This study developed a rabbit model with vocal fold hyperadduction . The subglottal pressure and acoustic analysis of this model resembled the characteristics of patients with AdSD. This model could be helpful to elucidate the pathology of the larynx caused by hyperadduction, and evaluate and compare the treatments for strained phonation. (c) 2022 Japanese Society of Otorhinolaryngology-Head and Neck Surgery, Inc. Published by Elsevier B.V. All rights reserved.