REHABILITATION OF THE PARALYZED LARYNX

描述(改编自调查者摘要)目前的治疗方法 对于双侧喉麻痹，采用破坏性外科手术 以牺牲发声和呼吸道为代价来改善通风 保护。后部功能性电刺激(FES) 环踝(PCA)肌恢复声带外展，并提供 一种比目前的治疗更具活力和生理学的选择。这个 拟议研究的主要目标是：1)恢复绑架 经皮双侧声带麻痹动物模型的实验研究 或留置刺激装置，2)确定慢性刺激的效果 电刺激对PCA最终神经再支配的影响。 对犬类的初步研究表明，FES不仅 恢复喉部活动，但防止失神经萎缩 维持前列腺癌肌肉纤维的活性和收缩能力。 令人惊讶的是，FES已经被观察到影响神经的再支配 选择性地鼓励内脏神经神经重联的自控镇痛 纤维，同时抑制外来来源的神经再支配。研究 从拟议的研究将跨越四年，在此期间 慢性FES对神经和肌肉的影响将被充分记录下来。 这些信息在喉部起搏的研究可以 在植入的病人身上进行追踪。特别令人感兴趣的是FES是否 如果干预延迟，可以逆转失神经萎缩。时间的选择 FES干预及其挽救PCA纤维萎缩能力的研究 纤维化将通过肌肉生理学的变化来评估 和生物化学。慢性FES对程度和质量的影响 喉返神经切断后PCA神经再支配的研究 和/或修复将使用生理观察来确定 喉部行为、HRP示踪研究和肌肉组织化学。 如果发现FeS可以防止或逆转失神经萎缩，而 促进适当的神经重新连接，一种临床模型 双侧犬麻痹将被用于研究FES作为一种 治疗方法。将对商业上可用的设备进行评估 以适应喉部起搏。对这一问题的进一步研究 可注射微刺激器的开发将在 动物模型。这项新技术可能会提供比 急性双侧麻痹的急诊气管切开术。

DESCRIPTION (Adapted from the Investigator's Abstract) Current treatments for bilateral laryngeal paralysis employ destructive surgical procedures that improve ventilation at the expense of voice production and airway protection. Functional electrical stimulation (FES) of the posterior cricoarytenoid (PCA) muscle restores vocal fold abduction, and offers a more dynamic and physiologic alternative to present treatment. The primary objective of the proposed research are: 1) to restore abduction in animals with bilateral vocal fold paralysis using a transcutaneous or indwelling stimulation device, 2) to determine the effects of chronic electrical stimulation on the eventual reinnervation of the PCA. Preliminary studies in the canine have suggested that FES not only restores laryngeal mobility, but prevents denervation atrophy while maintaining the viability and contractility of PCA muscle fibers. Surprisingly, FES has been observed to influence reinnervation of the PCA by selectively encouraging neural reconnection of intrinsic nerve fibers, while repressing reinnervation from foreign sources. Studies from the proposed research will span a four year period during which the effects of chronic FES on nerve and muscle will be fully documented. Such information is critical before studies of laryngeal pacing can be pursued in the implanted patient. Of particular interest is whether FES can reverse denervation atrophy if intervention is delayed. The timing of FES intervention and its capacity to rescue PCA fibers from atrophy and fibrosis will be assessed in terms of changes in muscle physiology and biochemistry. The effects of chronic FES on the extent and quality of PCA reinnervation following Recurrent Laryngeal Nerve (RLN) section and/or repair will be determined using physiological observations of laryngeal behaviors, HRP tracing studies, and muscle histochemistry. If FES is found to prevent or reverse denervation atrophy while promoting appropriate neural reconnection, a clinical model for bilateral paralysis in the canine will be used to study FES as a therapeutic approach. Commercially available devices will be evaluated for adaptation to laryngeal pacing. Further research toward the development of an injectable microstimulator will be pursued in an animal model. This new technology may offer significant advantage over emergency tracheotomy in cases acute bilateral paralysis.