INTRODUCTION: Misdirected regeneration (MR) frequently occurs following injury to the recurrent laryngeal nerve (RLN) resulting in neurotmesis or axonotmesis. Physiological and anatomic parameters involved in the functional recovery of the larynx following freezing injury or neurorrhaphy of the RLN were studied. A multi-facilitated approach is undertaken to clarify the functional abnormalities caused by the MR after recurrent laryngeal nerve injury. MATERIALS AND METHODS: Three groups of adult cats were studied. These included controls, cats with recurrent laryngeal neurorrhaphy, and cats with recurrent laryngeal nerve freeze injuries. From 2 weeks to 9 months after the nerve injury, the animals were studied endoscopically and with electromyography (EMG). Using the same animal, the number and location of motoneurons supplying the ipsilateral posterior cricoarytenoid (PCA) muscle were examined with horseradish peroxidase (HRP). Animals were subsequently sacrificed to study the pattern of reinnervation. RESULTS: Following neurorrhaphy all cats had vocal cord paralysis. After neurorrhaphy, effective motion function did not return in the affected vocal cord and it remained fixed in the paramedian position. Although EMG of the laryngeal muscles of the affected side showed interference voltage, the pattern of activities was markedly different from that of the unaffected side, and reciprocity among the laryngeal muscles was not restored. The number of PCA motoneurons recovered to the normal range, but a considerable number of neuronal bodies were dispersed outside the normal PCA area. This indicates misdirected reinnervation to the PCA muscle by motoneurons that originally served other laryngeal muscles. In the freezing injury, effective vocal cord movement finally recovered after 6 months. At this time, EMG showed a normal pattern, although a relatively small amount of misdirected neurons was observed. DISCUSSION: Functional recovery of vocal cord motion does not occur following neurorrhaphy. Prominently disorganized arrangement of laryngeal motor neurons was observed in the horseradish peroxidase study. This suggests that inappropriate reinnervation develops in spite of reapproximation and suturing. Altered central organization of the motor nucleus is a significant pathogenic factor in the loss of laryngeal muscular coordination following recurrent laryngeal nerve lesions. The degree of recovery is related to the mechanism of injury.
INTRODUCTION: Misdirected regeneration (MR) frequently occurs following injury to the recurrent laryngeal nerve (RLN) resulting in neurotmesis or axonotmesis. Physiological and anatomic parameters involved in the functional recovery of the larynx following freezing injury or neurorrhaphy of the RLN were studied. A multi-facilitated approach is undertaken to clarify the functional abnormalities caused by the MR after recurrent laryngeal nerve injury. MATERIALS AND METHODS: Three groups of adult cats were studied. These included controls, cats with recurrent laryngeal neurorrhaphy, and cats with recurrent laryngeal nerve freeze injuries. From 2 weeks to 9 months after the nerve injury, the animals were studied endoscopically and with electromyography (EMG). Using the same animal, the number and location of motoneurons supplying the ipsilateral posterior cricoarytenoid (PCA) muscle were examined with horseradish peroxidase (HRP). Animals were subsequently sacrificed to study the pattern of reinnervation. RESULTS: Following neurorrhaphy all cats had vocal cord paralysis. After neurorrhaphy, effective motion function did not return in the affected vocal cord and it remained fixed in the paramedian position. Although EMG of the laryngeal muscles of the affected side showed interference voltage, the pattern of activities was markedly different from that of the unaffected side, and reciprocity among the laryngeal muscles was not restored. The number of PCA motoneurons recovered to the normal range, but a considerable number of neuronal bodies were dispersed outside the normal PCA area. This indicates misdirected reinnervation to the PCA muscle by motoneurons that originally served other laryngeal muscles. In the freezing injury, effective vocal cord movement finally recovered after 6 months. At this time, EMG showed a normal pattern, although a relatively small amount of misdirected neurons was observed. DISCUSSION: Functional recovery of vocal cord motion does not occur following neurorrhaphy. Prominently disorganized arrangement of laryngeal motor neurons was observed in the horseradish peroxidase study. This suggests that inappropriate reinnervation develops in spite of reapproximation and suturing. Altered central organization of the motor nucleus is a significant pathogenic factor in the loss of laryngeal muscular coordination following recurrent laryngeal nerve lesions. The degree of recovery is related to the mechanism of injury.