Pathophysiological mechanisms of oropharyngeal dysphagia in amyotrophic lateral sclerosis
Pathophysiological mechanisms of oropharyngeal dysphagia in amyotrophic lateral sclerosis
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DOI：
10.1093/brain/123.1.125
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发表时间：
2000-01-01
期刊：
影响因子：
14.5
通讯作者：
Uludag, B
中科院分区：
文献类型：
--
作者：
Ertekin, C;Aydogdu, I;Uludag, B
我们调查了肌萎缩侧索硬化症吞咽困难的病理生理机制，43例散发性肌萎缩侧索硬化症患者进行了临床和电生理方法，客观地测量口咽期自主启动吞咽，并将这些结果与50名年龄匹配的对照组进行了比较。喉运动检测的压电传感器和肌电图颏下肌，肌萎缩侧索硬化症和对照组的食管上括约肌的cranior咽肌针肌电图记录在吞咽过程中。伴有吞咽困难的肌萎缩侧索硬化症患者表现出以下异常结果。(i)颏下肌活动的喉电梯，产生反射向上偏转的喉湿吞咽，显着延长，而喉搬迁时间的吞咽反射保持在正常范围内。(ii)主动吞咽时，颈咽括约肌肌电图显示严重异常。括约肌开放延迟和/或过早闭合，开放的总持续时间缩短，有时在此期间出现意外的运动单位爆发。(iii)在自愿发起的吞咽有显着缺乏协调之间的喉电梯肌肉和颈咽括约肌。这些结果指出了两种导致肌萎缩侧索硬化症患者吞咽困难的病理生理机制。(i)触发的吞咽反射自发发起吞咽延迟，并最终废除，而自发反射吞咽保存，直到终末前阶段的肌萎缩侧索硬化症，（ii）crucialharyngeal括约肌的食管上括约肌成为hyper-reflexic和hypertonic。结果，喉保护系统和吞咽的食团运输系统失去了协调在自愿启动吞咽，我们的结论是，这些病理生理变化主要是有关的兴奋性和抑制性皮质延髓锥体纤维的进行性变性。
We investigated the pathophysiological mechanisms of dysphagia in amyotrophic lateral sclerosis, Forty-three patients with sporadic amyotrophic lateral sclerosis were examined by clinical and electrophysiological methods that objectively measured the oropharyngeal phase of voluntarily initiated swallowing, and these results were compared with those obtained from 50 age-matched control subjects. Laryngeal movements were detected by a piezoelectric sensor and EMG of submental muscles, and needle EMG of the cricopharyngeal muscle of the upper oesophageal sphincter of both the amyotrophic lateral sclerosis and control groups was recorded during swallowing. Amyotrophic lateral sclerosis patients with dysphagia displayed the following abnormal findings. (i) Submental muscle activity of the laryngeal elevators, which produce reflex upward deflection of the larynx during wet swallowing, was significantly prolonged whereas the laryngeal relocation time of the swallowing reflex remained within normal limits. (ii) The cricopharyngeal sphincter muscle EMG demonstrated severe abnormalities during voluntarily initiated swallows. The opening of the sphincter was delayed and/ or the closure occurred prematurely, the total duration of opening was shortened and, at times, unexpected motor unit bursts appeared during this period. (iii) During voluntarily initiated swallows there was significant lack of co-ordination between the laryngeal elevator muscles and the cricopharyngeal sphincter muscle. These results point to two pathophysiological mechanisms that operate to cause dysphagia in amyotrophic lateral sclerosis patients. (i) The triggering of the swallowing reflex for the voluntarily initiated swallow is delayed and eventually abolished, whereas the spontaneous reflexive swallows are preserved until the preterminal stage of amyotrophic lateral sclerosis, (ii) The cricopharyngeal sphincter muscle of the upper oesophageal sphincter becomes hyper-reflexic and hypertonic. As a result, the laryngeal protective system and the bolus transport system of deglutition lose their co-ordination during voluntarily initiated swallowing, We conclude that these pathophysiological changes are related mainly to the progressive degeneration of the excitatory and inhibitory corticobulbar pyramidal fibres.