Abstract
Injury to the recurrent laryngeal nerve is accompanied by a poor functional recovery of the target organ, the larynx. For the patient this means impairments of vocal fold mobility and various kinds of voice disorders. In this thesis, an experimental model in the rat is used to identify the most important pathological factors involved after recurrent laryngeal nerve injury.
The results demonstrate that the posterior cricoarytenoid muscle, the only abductor of the vocal fold, recieves dual innervation from both the recurrent laryngeal nerve and the superior laryngeal nerve, a view that is against the classical understanding of laryngeal neuroanatomy. When the recurrent laryngeal nerve is injured, this anatomical relation then serves as a base for collateral reinnervation by competing, intact nerve fibers in the posterior cricoarytenoid muscle. Collateral reinnervation is proposed to be a negative factor for the functional outcome, more important than neuronal death, which was found to be low after recurrent laryngeal nerve injury.
Pharmacological treatment with the calcium flow inhibitor nimodipine was shown to improve reinnervation by original recurrent laryngeal nerve fibers in rats. Early clinical data is also presented that indicate a beneficial effect from nimodipine treatment after acute recurrent laryngeal nerve injury, in terms of recovery of vocal fold mobility. Laryngeal electromyography was shown to be a valuable diagnostic and prognostic tool in detecting axonal injury in these patients, which may form an indication for nimodipine treatment.
