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

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.

Foerster G ，Mueller AH 《-》

Laryngeal EMG: Preferential damage of the posterior cricoarytenoid muscle branches especially in iatrogenic recurrent laryngeal nerve lesions.

Laryngeal electromyography (LEMG) of the thyroarytenoid (TA) muscle alone may not be sufficient in all patients to characterize or prove a recurrent laryngeal nerve (RLN) lesion in cases of vocal fold immobility. LEMG of the posterior cricoarytenoid (PCA) muscle may provide additional information. Retrospective review. Between 2008 and 2016, 339 patients in our laryngeal paralysis clinic were examined by transcutaneous needle TA-LEMG and, if tolerated, by PCA-LEMG. LEMGs were rated and compared according to criteria of the European Laryngological Society. Etiology was categorized as iatrogenic, noniatrogenic, or malignancy related. A total of 282 out of 339 patients had a partial or complete RLN or vagal nerve lesion: 178 iatrogenic, 74 noniatrogenic, and 30 because of nerve involvement by malignancies. Of paralytic vocal folds, 35.7% had normal or near-normal TA innervation, whereas corresponding PCA traces (if present) were pathologic in 94.6%. Comparing pairs of TA and PCA-LEMGs in paralysis of less than 4 months duration showed a predominance of PCA branch injuries in iatrogenic lesions (71.7 %), while in noniatrogenic lesions this was less pronounced (44.4%). In the few malignancy cases, there was an almost even distribution. Synkinetic reinnervation was earlier in iatrogenic RLN lesions. PCA-LEMG was better in proving an RLN lesion than TA-EMG alone. Our findings suggest etiology-dependent differences in the TA/PCA lesion pattern. To confirm this, larger sample sizes are needed. A preferential damage to PCA innervation in iatrogenic lesions could be relevant for further improvements of intraoperative neuromonitoring. 4. Laryngoscope, 128:1152-1156, 2018.

Foerster G ，Mueller AH 《-》

Innervation status in chronic vocal fold paralysis and implications for laryngeal reinnervation.

Treatment options for symptomatic unilateral vocal fold paralysis (VFP) include vocal fold augmentation, laryngeal framework surgery, and laryngeal reinnervation. Laryngeal reinnervation (LR) has been suggested to provide "tone" to the paralyzed VF. This implies a loss of tone as a result of denervation without reinnervation. We performed laryngeal electromyography (LEMG) in patients with chronic VFP to understand the innervation status associated with a chronically paralyzed vocal fold. Retrospective review of LEMG data in adult patients with chronic VFP from January 2009 to December 2014. LEMG was performed at least 6 months after-onset of VFP. Qualitative LEMG, quantitative LEMG, and adductory synkinesis testing were performed, and the parameters were collected. Twenty-seven vocal folds were studied (23 unilateral VFP and 2 bilateral VFP). Average age was 59 ± 17 years. The median duration from recurrent laryngeal nerve injury to LEMG was 8.5 months (range 6-90 months). The majority of patients, 24 of 27 (89%), had motor unit potentials during phonation tasks on LEMG, and only 3 of 27 (11%) patients were electrically silent. Quantitative LEMG showed 287.8 mean turns per second (normal ≥ 400). Motor unit configuration was normal in 12 of 27 (44%), polyphasic in 12 of 27 (44%), and absent in the electrically silent patients. Adductory synkinesis was found in 6 of 20 (30%) patients. Chronic vocal fold paralysis is infrequently associated with absent motor-unit recruitment, indicating some degree of preserved innervation and/or reinnervation in these patients. LEMG should be part of the routine workup for chronic VFP prior to consideration of LR. 4. Laryngoscope, 128:1628-1633, 2018.

Lin RJ ，Smith LJ ，Munin MC ，Sridharan S ，Rosen CA ... -  《-》

Laryngeal synkinesis: its significance to the laryngologist.

Crumley RL 《ANNALS OF OTOLOGY RHINOLOGY AND LARYNGOLOGY》

Laryngeal synkinesis revisited.

Crumley RL 《ANNALS OF OTOLOGY RHINOLOGY AND LARYNGOLOGY》