Recurrent laryngeal nerve (RLN) injury [without injury to the superior laryngeal nerve (SLN)] is the most common traumatic neurolaryngological lesion. The acute effects are immediate flaccidity of the ipsilateral vocal fold, loss of abduction and adduction, severe dysphonia to complete paralytic aphonia, and, frequently, aspiration of food and drink into the trachea. This article reviews the function of the four intrinsic laryngeal muscles innervated by the RLN and the individual effects of RLN transection on these muscles. Following acute denervation, the subsequent progression is either chronic denervation or nerve regeneration with laryngeal muscle reinnervation. Four possible scenarios are discussed here: complete reinnervation with synkinesis, partial reinnervation with synkinesis, mixed RLN injuries, and no reinnervation (complete paralysis). Electromyography may eventually assist the laryngologist in establishing these diagnoses, but currently not enough normative data exist for confirming laryngeal synkinesis unequivocally in every case. Treatment is generally by Teflon injection, medialization thyroplasty, arytenoid adduction procedures, or reinnervation by nerve transfer. The author's preference is nerve transfer, insofar as the quality of resultant phonatory voice, in his hands, has been superior to the other techniques.