咽食管及食管吞咽困难中的脑干与迷走神经功能障碍

文献信息

中文摘要

背景： 吞咽困难影响约16%的美国人口，分为咽食管性和食管性，前者在临床上更为紧急，因为气道保护丧失可能导致肺部误吸和死亡。安全吞咽依赖于脑干中枢模式发生器，受皮质和皮质下输入调制，并通过颅神经执行，尤其是迷走神经。迷走神经支配咽、喉、上食管括约肌、食管和下食管括约肌。由于传入和传出通路在延髓汇聚，延髓的小病灶会导致严重、持续的吞咽困难，比皮质损伤后的吞咽困难更严重。80-90%的急性延髓卒中患者会发生吞咽困难。孤束核损伤会削弱触发吞咽的感觉反馈，而疑核受累会削弱运动驱动，导致反射触发延迟、咽部肌肉无力、括约肌开放受损和隐性误吸。迷走神经损伤在多个层面导致吞咽困难，从单侧软腭、咽和喉麻痹到危及生命的双侧麻痹，以及正常食管蠕动丧失。由于传统测压仅检测蠕动的收缩期，需要扩张-收缩图来揭示压力记录看似正常的患者咽部和食管的扩张期异常。结论：无

英文摘要

Dysphagia affects approximately 16% of the US population and is classified as pharyngoesophageal and esophageal, the former being more clinically urgent because loss of airway protection may cause pulmonary aspiration and death. Safe swallowing depends on a brainstem central pattern generator, modulated by cortical and subcortical input and executed through the cranial nerves, above all the vagus. The latter supplies the pharynx, larynx, upper esophageal sphincter, esophagus and lower esophageal sphincter. Because afferent and efferent pathways converge in the medulla, small lesions in medulla cause severe, persistent dysphagia, worse than that following cortical injury. Dysphagia occurs in 80-90% of acute medullary strokes. Injury to the nucleus tractus solitarius degrades the sensory feedback that triggers the swallow, while nucleus ambiguous involvement weakens motor drive, producing delayed reflex triggering, pharyngeal muscle weakness, impaired sphincter opening, and silent aspiration. Vagal injury causes dysphagia at multiple levels, from unilateral palatal, pharyngeal, and laryngeal paresis to life-threatening bilateral paralysis, and loss of normal esophageal peristalsis. Because conventional manometry detects only the contraction phase of peristalsis, distension-contraction plots are needed to uncover distension-phase abnormalities in patients when pressure recordings appear normal, both in the pharynx and esophagus.