Study on the Vocal Fold Movement Characteristics of Canine Models With Nerve Paralysis Caused by Different Site Injuries

ABSTRACT Objective To explore the specific effects of unilateral injuries to the vagus nerve (VN), recurrent laryngeal nerve (RLN), and superior laryngeal nerve (SLN) on the vocal fold movement characteristics, and investigate the regulation pattern of current intensity on the vocal fold movement after the injuries. Methods Nine Beagle dogs were used to establish right‐sided laryngeal nerve injury models, divided into three groups (VN, RLN, and SLN transection groups, n = 3 per group). The right (injured side) vocal folds served as the experimental group, while the left (healthy side) vocal folds acted as the control group. At 3 months postoperatively, a graded electrical current (1–4 mA, in 1 mA increments) was applied to the distal end of the injured RLN, 2 cm from the vocal fold plane, to stimulate either the healthy (left) or injured (right) RLN. Vocal fold movements were captured using high‐speed laryngoscopy, and the pixel distances and velocities of adductory motions were quantified using PCC3.6 software. Independent samples t‐tests were performed to compare vocal fold movements between the injured (right) and healthy (left) sides within each injury group, as well as bilateral vocal fold movements between the RLN and VN injury groups. Results (1) Healthy‐side RLN stimulation: The amplitude and velocity of vocal fold movements on the injured side were significantly lower than those on the healthy side across all injury groups (p < 0.05). The RLN injury group exhibited higher movement parameters than the VN injury group at all current intensities, with a statistically significant difference at 1 mA (p < 0.05); (2) Injured‐side RLN stimulation: Only the SLN injury group demonstrated bilateral vocal fold movements, with maximal performance observed at 4 mA; (3) Regulation pattern of current intensity: In the VN and RLN injury groups, the parameters reached their maximum at 2 mA. In the SLN injury group, the maximum parameters were delayed until 3 mA (healthy‐side RLN stimulation) or 4 mA (injured‐side RLN stimulation). Conclusions The vocal fold movement regulation pathways partially overlap between RLN and VN injuries. Residual vocal fold motion after SLN injury suggests potential cricothyroid‐arytenoid mechanical coupling or neural compensation mechanisms. An electrical stimulation intensity of 2 mA is optimal for RLN/VN injuries, while 4 mA can activate compensatory pathways in SLN injuries. This study provides experimental evidence for the precise diagnosis of laryngeal nerve injuries and the optimization of electrical stimulation parameters.