Vocal cord paralysis, synkinesis and vocal fold motion impairment

Abstract

Felix Semon's ‘laws’ of vocal cord paralysis were conceived over a century ago, based on the simple concept that abductor function of the recurrent laryngeal nerve was more vulnerable than adductor function. It is now clear that the neuromuscular pathology of laryngeal innervation is much more complex. Whether the nerve has been cut, crushed, stretched, cauterized or otherwise injured, it is seldom completely transected. There might be no detectable vocal cord movement at laryngoscopy, yet, electromyography usually shows at least some activity because of incomplete denervation and/or developing synkinesis. Electrical silence hardly ever persists forever. Disordered vocal fold movement following nerve injury appears to depend on laryngeal synkinesis with disorganized neuromuscular function caused by misdirected regeneration and aberrant reinnervation, sometimes by adjacent nerves. The severity of the injury, abnormal random reinnervation, scar tissue formation and nerve growth‐stimulating and inhibiting factors influence the final position of the vocal fold. For a better understanding of neurolaryngological disorders it is no longer sufficient to think merely in terms of ‘vocal cord paralysis’.