Randal C Paniello1, Andrea Park2. 1. Department of Otolaryngology, Head and Neck Surgery, Washington University, St. Louis, MO, USA paniellor@ent.wustl.edu. 2. Department of Otolaryngology, Head and Neck Surgery, Washington University, St. Louis, MO, USA.
Abstract
OBJECTIVES: It has been shown in a canine model that a single injection of vincristine into the posterior cricoarytenoid (PCA) muscle at the time of recurrent laryngeal nerve (RLN) injury effectively blocks its reinnervation and results in improved adductor strength. But clinically, such injuries are usually diagnosed weeks or months after onset. Vincristine injection does not affect a muscle that is already innervated; thus, there is a limited time frame following RLN injury during which a vincristine injection could effectively improve ultimate laryngeal adductor functional recovery. A series of delayed injections was performed in a canine model and results assessed. STUDY DESIGN: Animal (canine) experiment. METHODS: The RLN was transected and repaired, and vincristine (0.4 mg) was injected into the PCA muscle at the time of injury (n=12) or 3, 4, and 5 months later (n=8 each study group). Six months after RLN injury, laryngeal adductor function was measured. Results of vincristine injection without RLN injury (n=6) and longer-term (12 months) follow-up for time zero injections (n=4) are also reported. RESULTS: The animals injected at time zero had better adductor function than non-injected controls, as reported previously, and this result was further increased at 12 months. The 3-month delay gave results similar to the time zero group. The 5-month delay group showed no vincristine benefit, and the 4-month delay group gave an intermediate result. Vincristine to the PCA had no effect on adductor function when the RLN was left intact. Plasma levels showed 19% of injected vincristine reached systemic circulation, which was cleared within 69 hours. CONCLUSIONS: Vincristine injection of the PCA muscle after RLN injury, which blocks this antagonist muscle from synkinetic reinnervation, leads to improved laryngeal adductor functional recovery. The window of opportunity to apply this treatment closes by 4 months after RLN injury in the canine model. Human RLN recovery follows a similar time course and can reasonably be expected to have a similar therapeutic window.
OBJECTIVES: It has been shown in a canine model that a single injection of vincristine into the posterior cricoarytenoid (PCA) muscle at the time of recurrent laryngeal nerve (RLN) injury effectively blocks its reinnervation and results in improved adductor strength. But clinically, such injuries are usually diagnosed weeks or months after onset. Vincristine injection does not affect a muscle that is already innervated; thus, there is a limited time frame following RLN injury during which a vincristine injection could effectively improve ultimate laryngeal adductor functional recovery. A series of delayed injections was performed in a canine model and results assessed. STUDY DESIGN: Animal (canine) experiment. METHODS: The RLN was transected and repaired, and vincristine (0.4 mg) was injected into the PCA muscle at the time of injury (n=12) or 3, 4, and 5 months later (n=8 each study group). Six months after RLN injury, laryngeal adductor function was measured. Results of vincristine injection without RLN injury (n=6) and longer-term (12 months) follow-up for time zero injections (n=4) are also reported. RESULTS: The animals injected at time zero had better adductor function than non-injected controls, as reported previously, and this result was further increased at 12 months. The 3-month delay gave results similar to the time zero group. The 5-month delay group showed no vincristine benefit, and the 4-month delay group gave an intermediate result. Vincristine to the PCA had no effect on adductor function when the RLN was left intact. Plasma levels showed 19% of injected vincristine reached systemic circulation, which was cleared within 69 hours. CONCLUSIONS:Vincristine injection of the PCA muscle after RLN injury, which blocks this antagonist muscle from synkinetic reinnervation, leads to improved laryngeal adductor functional recovery. The window of opportunity to apply this treatment closes by 4 months after RLN injury in the canine model. Human RLN recovery follows a similar time course and can reasonably be expected to have a similar therapeutic window.
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