This study investigates the role of the intact superior laryngeal nerve (SLN) in the reinnervation process of one of the laryngeal muscles, the posterior cricoarytenoid muscle (PCA), following recurrent laryngeal nerve (RLN) injury. Using a chronic RLN injury model in the adult rat, PCA reinnervation was assessed by retrograde double-tracing techniques in combination with electrophysiology and immunohistochemistry of muscle sections. The results demonstrate that the PCA receives dual innervation from both laryngeal nerves even in the uninjured system. Functionally significant collateral reinnervation originates from intact SLN fibers following RLN injury, mainly due to intramuscular sprouting rather than by recruitment of more motor neurons. This may be important when choosing surgical and/or medical treatment for patients with RLN injury.

Nimodipine improves regeneration and neuromuscular function following RLN injury in the adult rat, and could be of use in future strategies following RLN injury.

In contrast to previous reports, our results show that laryngeal electromyography is a reliable tool for diagnosing the type of injury within the injured RLN, making it possible to predict the functional outcome in these patients. On the basis of the results, a future randomized study on nimodipine treatment for RLN axonal injury is suggested.

Transection of the recurrent laryngeal nerve leads to permanent palsy of the vocal cord. Experimental studies have confirmed that nimodipine increases the pace of axonal regeneration. We present a case of a 19-year-old male, suffering a thyroid cancer disease, who was subjected to unilateral resection of the recurrent laryngeal nerve during surgery. The nerve was repaired with a nerve graft and the patient further treated with nimodipine for 3 months. Evaluation of the patient showed normalization of voice, movement of the vocal cord on the injured side, and electromyography evidence of reinnervation of the larynx muscles at 15 months after surgery.

Neuronal death does not occur within 1 month postlesion as a result of resection of the RLN in the adult rat, and neuroprotective substances should therefore be of minor value after RLN injury. Glial reactions appear in a similar fashion as after other peripheral nerve lesions not causing neuronal loss.