PCA Atrophy and Synkinesis as the Main Factors for Persistent Vocal Fold Immobility in RLN Paralysis.

Abstract

An immobile vocal fold due to recurrent laryngeal nerve (RLN) injury usually shows no gross signs of atrophy and lies near the midline. In 1881, Felix Semon proposed that this phenomenon was due to a selective injury of nerve fibers supplying the posterior cricoarytenoid muscle (PCA) and supported this with postmortem proof of selective PCA atrophy. In recent decades, evidence has emerged that the RLN regenerates after injury but does not always result in useful motion of the vocal folds. It has been proposed that this is caused by laryngeal synkinesis. Laryngeal synkinesis describes a random distribution of regenerated nerve fibers to opposing vocal fold muscles. This study was conducted to clarify the relative contribution of these two potential pathomechanisms in our patient population. Retrospective case analysis. Retrospective analysis of laryngeal EMG results from cases with RLN paralysis of at least 6 months duration seen at our neurolaryngology clinic. Out of 118 PCA EMGs, there was not a single normal or near-normal tracing, whilst 33.3% of TA EMGs indicated normal or near normal innervation. PCA EMGs showed signs of persistent high-grade partial denervation (41.5%) as a sign of atrophy, moderate or strong synkinesis (21.2%), or a combination of both (37.3%). In chronic RLN paralysis the intrinsic laryngeal muscles are affected to different extents either by atrophy or synkinesis or a combination of both. The PCA is always affected. The lesser damage to TA innervation explains the commonly seen maintenance of vocal fold muscle bulk. 4 Laryngoscope, 131:E1244-E1248, 2021.