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

Abstract

Objectives/Hypothesis: 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. Study Design: Retrospective case analysis. Methods: Retrospective analysis of laryngeal EMG results from cases with RLN paralysis of at least 6 months duration seen at our neurolaryngology clinic. Results: 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%). Conclusions: 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.

Functional results of endoscopic arytenoid abduction lateropexy for bilateral vocal fold palsy

“…We conclude therefore that these early postoperative values cannot provide an exact basis for postoperative phoniatric analysis either. Nevertheless, in contrast to the conventional surgical approaches to BVFP (e.g., transverse cordotomy, partial/total CO 2 laser arytenoidectomy, laterofixation via Lichtenberger's needle carrier device), EAAL by ETGI provides better subjective and objective results in patients with BVFP simultaneously with higher peak inspiratory flows (Table 3), [2,[28][29][30][31][32]. In our experience, swallowing problems caused by unilateral EAAL are extremely rare.…”

“…The comparison of the functional outcomes of different surgical techniques addressing BVFP raises a complex question, because the functional results depend on the surgical method as well as a patient's age, sex, mental and physical health, and the potential regeneration of the recurrent laryngeal nerve. Despite numerous studies of humans and animals, insufficient data are available to unambiguously define the pathophysiology of BVFP [26][27][28]. The intraoperative stretching, mild thermal damage, etc.…”

“…often cause only axono-or neuropraxy which explains the frequently reported laryngeal function regeneration [1]. However, the exact characterization of functional recovery is rarely cited in the publications connected to the topic of postoperative voice quality [2,[26][27][28][29][30].…”

“…The mechanisms of neural regeneration are complex and highly variable. For example, physiological reinnervation, pathological/synkinetic reinnervation, and definitive denervation simultaneously occur to varying degrees [28]. These neurological processes may occur several months after the nerve injury, and the definitive functional results may vary from complete, or nearly complete, vocal fold motion recovery to different types of synkinesis, and less frequently to complete neurological immobility.…”

An Endoscopic Cap Electrode for Posterior Cricoarythenoid Muscle Stimulation in a Porcine Model

“…The ailed muscle ends up with a dual agonistic and antagonistic (“synkinetic”) reinnervation that can be the cause of vocal fold immobility 20,21 . While synkinesis cannot be diagnosed reliably by videolaryngoscopy alone, laryngeal electromyography (LEMG) can reveal a strong indirect sign for the existence of a working neuromuscular junction 22,23 . However, mere detection of synkinesis by LEMG does not necessarily prove that an actual opening movement of the ailed vocal fold can be induced by NMES, which is a viable condition to be verified in patients before implantation of any laryngeal pacing system.…”