Seneviratne K N, Peiris O A
J Neurol Neurosurg Psychiatry. 1970 Oct;33(5):609-14. doi: 10.1136/jnnp.33.5.609.
Peripheral nerve function has been studied in 50 patients with chronic liver disease. An increase in the latency or a reduction in the response amplitude of the evoked sensory potential of the median nerve was detected in 34 of the 50 subjects. This was in striking contrast to the paucity of neurological signs and symptoms suggestive of peripheral nerve damage seen in these patients. There was no evidence to show that alcohol was responsible for the neuropathy. Abnormalities in the excitability changes of sensory nerve during ischaemia were detected in seven of the 16 subjects whose distal sensory latencies were within normal limits. A critical evaluation of the hypotheses which have been postulated to account for the increased resistance of peripheral nerve to inactivation by ischaemia has been made. It is concluded that an increase of the permeability of the periaxonal diffusion barrier to K offers the most acceptable explanation for this phenomenon.
对50例慢性肝病患者的周围神经功能进行了研究。在50名受试者中，有34人检测到正中神经诱发感觉电位潜伏期延长或反应幅度降低。这与这些患者中提示周围神经损伤的神经体征和症状稀少形成了鲜明对比。没有证据表明酒精是导致神经病变的原因。在16名远端感觉潜伏期在正常范围内的受试者中，有7人检测到缺血期间感觉神经兴奋性变化异常。对为解释周围神经对缺血失活抵抗力增加而提出的假说进行了批判性评估。得出的结论是，轴突周围扩散屏障对钾的通透性增加为这一现象提供了最合理的解释。
