Electromyographic and Histologic Evolution of the Recurrent Laryngeal Nerve From Transection and Anastomosis to Mature Reinnervation

The Laryngoscope (Impact Factor: 2.14). 02/2011; 121(2):325 - 331. DOI: 10.1002/lary.21290


Objectives:To describe the natural evolution of recurrent laryngeal nerve (RLN) reinnervation in an animal model.Study Design:Twenty Sprague Dawley rats underwent unilateral RLN transection and anastomosis. Animals were sacrificed at 4, 8, 12, 16, and 20 weeks. Prior to sacrifice, each rat underwent electromyography (EMG) and visual grading of vocal fold motion. Bilateral RLNs were harvested and evaluated histologically.Results:EMG revealed synkinetic reinnervation at all time periods except at 4 weeks. EMG evolution plateaued at 16 weeks. Vocal fold motion was slight in three rats at 4 weeks but was otherwise absent except for one rat at 12 weeks. Histologic changes of the axons and their myelin sheaths were consistent at each time period. At 16 weeks, histologic changes plateaued.Conclusions:Consistent EMG, histologic, and vocal fold motion changes occur at specific time periods during RLN reinnervation after transection and anastomosis in a rat model. Reinnervation is mature at 16 weeks. Findings corroborate theories of preferential and synkinetic reinnervation after RLN transection. Use of a rat model to investigate the effect of interventions on RLN reinnervation requires a minimum of 16 weeks between transection and investigation to allow for maturation of reinnervation. Laryngoscope, 2011

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    • "These observations are in agreement with other studies of complete transection and repair of the RLN, where signs of laryngeal fold movement were either never (Nahm et al., 1993; Miyamaru et al., 2009) or rarely observed (McRae et al., 2009; Pitman et al., 2011). Although restoration of detectable laryngeal fold movements after complete nerve section have been observed only inconsistently, electromyographic analyses have shown a progressive restoration of the normal preinjury potential firing pattern (Nahm et al., 1993; Pitman et al., 2011). The latter evidence indicates that, after a section and repair of the RLN, a regeneration of the affected axons does occur, but the reinnervation process fails to produce any significant functional recovery. "
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    ABSTRACT: Changes in motoneurons innervating laryngeal muscles after section and regeneration of the recurrent laryngeal nerve (RLN) are far from being understood. Here, we report the somatotopic changes within the nucleus ambiguus (Amb) after the nerve injury and relates it to the resulting laryngeal fold impairment. The left RLN of each animal was transected and the stumps were glued together using surgical fibrin glue. After several survival periods (1, 2, 4, 8, 12, 16 weeks; at least six rats at each time point) the posterior cricoarytenoid (PCA) and thyroarytenoid (TA) muscles were injected with fluorescent-conjugated cholera toxin and the motility of the vocal folds evaluated. After section and subsequent repair of the RLN, no movement of the vocal folds could be detected at any of the survival times studied and the somatotopy and the number of labeled motoneurons changed. From 4 wpi award, the somatotopy was significantly disorganized, with the PCA motoneurons being located rostrally relative to their normal location. A rostrocaudal overlap between the two pools of motoneurons supplying the PCA and TA muscles was observed from 2 wpi onwards. Hardly any labeled neurons were found in the contralateral Amb in any of the experimental groups. An injury of the RLN leads to a reinnervation of the denervated motor endplates of PCA and TA. However, misdirected axons sprout and regrowth from the proximal stump to the larynx. As a result, misplaced innervation of muscles results in a lack of functional recovery of the laryngeal folds movement following a RLN injury. Anat Rec, 2014. © 2014 Wiley Periodicals, Inc.
    The Anatomical Record Advances in Integrative Anatomy and Evolutionary Biology 05/2014; 297(5). DOI:10.1002/ar.22877 · 1.54 Impact Factor
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    • "tion of CtB - AF594 ( red ) or CtB - AF488 ( green ) into cricoarytenoid muscle ( A , B ) and the TA muscle ( C , D ) . ( A , C ) Control group . ( B , D ) At 4 wpi . d , dorsal ; l , lateral . Scale bar : 100 lm . at 6 wpi ( Tessema et al . 2008 , 2009 ) . This recovery is delayed up to 16 wpi when the injury is a transection and anasto - mosis ( Pitman et al . 2011 ) . After RLN injury , some contralateral motoneurons were found to supply the laryngeal muscles . This bilateral repre - sentation was not found in normal muscles . This has been described also in other models , including the oculomotor and trochlear nerves ( Fern andez et al . 1985 , 1987 , 1992 ) , the sciatic nerve and the facial ne"
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    ABSTRACT: Motoneurons innervating laryngeal muscles are located in the nucleus ambiguus (Amb), but there is no general agreement on the somatotopic representation and even less is known on how an injury in the recurrent laryngeal nerve (RLN) affects this pattern. This study analyzes the normal somatotopy of those motoneurons and describes its changes over time after a crush injury to the RLN. In the control group (control group 1, n = 9 rats), the posterior cricoarytenoid (PCA) and thyroarytenoid (TA) muscles were injected with cholera toxin-B. In the experimental groups the left RLN of each animal was crushed with a fine tip forceps and, after several survival periods (1, 2, 4, 8, 12 weeks; minimum six rats per time), the PCA and TA muscles were injected as described above. After each surgery, the motility of the vocal folds was evaluated. Additional control experiments were performed; the second control experiment (control group 2, n = 6 rats) was performed labeling the TA and PCA immediately prior to the section of the superior laryngeal nerve (SLN), in order to eliminate the possibility of accidental labeling of the cricothyroid (CT) muscle by spread from the injection site. The third control group (control group 3, n = 5 rats) was included to determine if there is some sprouting from the SLN into the territories of the RLN after a crush of this last nerve. One week after the crush injury of the RLN, the PCA and TA muscles were injected immediately before the section of the SLN. The results show that a single population of neurons represents each muscle with the PCA in the most rostral position followed caudalwards by the TA. One week post-RLN injury, both the somatotopy and the number of labeled motoneurons changed, where the labeled neurons were distributed randomly; in addition, an area of topographical overlap of the two populations was observed and vocal fold mobility was lost. In the rest of the survival periods, the overlapping area is larger, but the movement of the vocal folds tends to recover. After 12 weeks of survival, the disorganization within the Amb is the largest, but the number of motoneurons is similar to control, and all animals recovered the movement of the left vocal fold. Our additional controls indicate that no tracer spread to the CT muscle occurred, and that many of the labeled motoneurons from the PCA after 1 week post-RLN injury correspond to motoneurons whose axons travel in the SLN. Therefore, it seems that after RLN injury there is a collateral sprouting and collateral innervation. Although the somatotopic organization of the Amb is lost after a crush injury of the RLN and does not recover in the times studied here, the movement of the vocal folds as well as the number of neurons that supply the TA and the PCA muscles recovered within 8 weeks, indicating that the central nervous system of the rat has a great capacity of plasticity.
    Journal of Anatomy 02/2013; 222(4). DOI:10.1111/joa.12031 · 2.10 Impact Factor
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    ABSTRACT: Laryngeal reinnervation for bilateral vocal fold paralysis (BVFP) patients is a promising technique to achieve good airway, although preserving a good quality of voice. On the other hand, the procedure is not simple. This review explores the recent literature on surgical technique and factors that may contribute to the success. Research and literature in this area are limited due to variability and complexity of the nerve supply. The posterior cricoarytenoid (PCA) muscle also receives nerve supply from the interarytenoid branch. Transection of this nerve at the point between interarytenoid and PCA branch may prevent aberrant reinnervation of adductor nerve axons to the PCA muscle. A varying degree of regeneration of injured recurrent laryngeal nerves (RLN) in humans of more than 6 months confirms subclinical reinnervation, which may prevent denervation-induced atrophy. Several promising surgical techniques have been developed for bilateral selective reinnervation for BVFP patients. This involves reinnervation of the abductor and adductor laryngeal muscles. The surgical technique aims at reinnervating the PCA muscle to trigger abduction during the respiratory cycle and preservation of good voice by strengthening the adductor muscles as well as prevention of laryngeal synkinesis.
    Current opinion in otolaryngology & head and neck surgery 10/2011; 19(6):434-8. DOI:10.1097/MOO.0b013e32834c7d30 · 1.84 Impact Factor
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