Aydogdu I, Ertekin C, Tarlaci S, Turman B, Kiylioglu N, Secil Y
Department of Neurology, Medical School Hospital, Ege University, Izmir, Turkey.
Stroke. 2001 Sep;32(9):2081-7. doi: 10.1161/hs0901.094278.
We have investigated the pathophysiological mechanisms of dysphagia in Wallenberg's syndrome (WS) that are due to lateral medullary infarction (LMI).
Twenty patients with WS were evaluated by means of clinical and electrophysiological methods that measured the oropharyngeal phase of voluntarily initiated swallowing. For comparison, 22 patients with unilateral hemispheric infarction were investigated during the acute stage of stroke, and 4 patients with unilateral peripheral 9th and 10th cranial nerve palsies were studied. Age-matched 30 healthy control subjects were also included in the study.
It was found that dysphagia was clinically more severe in WS patients than in the patients in the other groups. The pharyngeal phase of swallowing was predominantly impaired, whereas in patients with hemispheric stroke, dysphagia was related only to the delay of triggering of the voluntarily induced swallowing. In WS patients, the swallowing reflex was extremely slow in spite of the unilateral involvement due to LMI, whereas the pharyngeal phase of reflex swallowing remained within normal limits in patients with unilateral hemispheric stroke and patients with unilateral peripheral 9th and 10th cranial nerve palsies.
Although in WS the lesion due to LMI is unilateral, its effect on oropharyngeal swallowing is bilateral. In LMI, primarily the premotor neurons in the nucleus ambiguous and their connections seem to be affected. Consequently, a disruption and/or disconnection of their linkage to swallowing-related cranial motor neuron pools bilaterally and to the contralateral nucleus ambiguous could produce the swallowing disorders in WS. However, the remaining intact ipsilateral premotor neurons and the contralateral center in the medulla oblongata may eventually begin to operate and overcome the severity and long-term persistence of dysphagia.
我们研究了由于延髓外侧梗死(LMI)导致的瓦伦贝格综合征(WS)吞咽困难的病理生理机制。
采用临床和电生理方法对20例WS患者进行评估,测量自主启动吞咽的口咽期。作为对照,在卒中急性期对22例单侧半球梗死患者进行了研究,并对4例单侧外周第9和第10颅神经麻痹患者进行了研究。研究还纳入了30名年龄匹配的健康对照者。
发现WS患者的吞咽困难在临床上比其他组患者更严重。吞咽的咽部阶段主要受损,而在半球性卒中患者中,吞咽困难仅与自主诱发吞咽的触发延迟有关。在WS患者中,尽管由于LMI为单侧受累,但吞咽反射极其缓慢,而在单侧半球性卒中患者和单侧外周第9和第10颅神经麻痹患者中,反射性吞咽的咽部阶段仍在正常范围内。
尽管在WS中,LMI所致病变为单侧,但对口咽吞咽的影响是双侧的。在LMI中,主要是疑核中的运动前神经元及其连接似乎受到影响。因此,它们与双侧吞咽相关颅运动神经元池以及对侧疑核的联系中断和/或断开,可能会导致WS中的吞咽障碍。然而,剩余完整的同侧运动前神经元和延髓中的对侧中枢最终可能开始发挥作用,克服吞咽困难的严重程度和长期持续性。