Nahm I, Shin T, Watanabe H, Maeyama T
Department of Otolaryngology, Saga Medical School, Japan.
Am J Otolaryngol. 1993 Jan-Feb;14(1):43-8. doi: 10.1016/0196-0709(93)90009-v.
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.
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.
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.
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.
喉返神经（RLN）损伤后常发生再生错位（MR），导致神经断伤或轴突断伤。研究了冷冻损伤或喉返神经神经缝合术后喉部功能恢复所涉及的生理和解剖学参数。采用多种促进方法来阐明喉返神经损伤后再生错位所引起的功能异常。
对三组成年猫进行了研究。这些组包括对照组、喉返神经神经缝合术的猫和喉返神经冷冻损伤的猫。在神经损伤后2周-9个月期间，对动物进行了内镜检查和肌电图（EMG）检查。使用同一只动物，用辣根过氧化物酶（HRP）检查支配同侧环杓后肌（PCA）的运动神经元的数量和位置。随后处死动物以研究神经再支配模式。
神经缝合术后所有猫均出现声带麻痹。神经缝合术后，患侧声带未恢复有效的运动功能，仍固定在旁正中位。虽然患侧喉部肌肉的肌电图显示有干扰电压，但活动模式与未受影响侧明显不同，喉部肌肉之间的相互关系未恢复。PCA运动神经元的数量恢复到正常范围，但相当数量的神经元胞体分散在正常PCA区域之外。这表明原本支配其他喉部肌肉的运动神经元对PCA肌肉进行了错位神经再支配。在冷冻损伤中，6个月后声带最终恢复了有效的运动。此时，肌电图显示模式正常，尽管观察到有相对少量的错位神经元。
神经缝合术后声带运动功能未恢复。在辣根过氧化物酶研究中观察到喉部运动神经元明显无序排列。这表明尽管进行了重新接近和缝合，但仍发生了不适当的神经再支配。运动核的中枢组织改变是喉返神经损伤后喉部肌肉协调丧失的一个重要致病因素。恢复程度与损伤机制有关。
