Quasthoff S
Department of Neurology, Technical University of Munich, Munich Muenchen, Germany.
Muscle Nerve. 1998 Oct;21(10):1246-55. doi: 10.1002/(sici)1097-4598(199810)21:10<1246::aid-mus2>3.0.co;2-b.
Diabetic neuropathy is a common complication in diabetes mellitus. Diabetic neuropathy is accompanied by alterations in axonal excitability, which can lead to either "positive" (paresthesia, dysesthesia, pain) and/or "negative" (hypesthesia, anesthesia) symptoms. The mechanisms underlying these alterations in axonal excitability are not well understood. Clinical tests reveal reduced nerve conduction velocity and axonal loss, but fail to explain nerve excitability. Many different factors have been suggested in relation to the pathophysiology of diabetic neuropathy. There are probably as many factors as there are different clinical pictures in diabetic neuropathy. Nevertheless, it seems that hyperglycemic hypoxia is mainly responsible for the electrophysiological changes seen in damaged diabetic nerves. This article summarizes experimental data indicating that a dysfunction of ion conductances, especially voltage-gated ion channels, could contribute to abnormalities in the generation and/or conduction of action potentials in diabetic neuropathy.
糖尿病性神经病变是糖尿病常见的并发症。糖尿病性神经病变伴有轴突兴奋性改变，这可导致“阳性”（感觉异常、感觉迟钝、疼痛）和/或“阴性”（感觉减退、感觉缺失）症状。这些轴突兴奋性改变的潜在机制尚未完全明确。临床检查显示神经传导速度降低和轴突损失，但无法解释神经兴奋性。关于糖尿病性神经病变的病理生理学，已提出许多不同因素。糖尿病性神经病变中不同临床表现的因素可能同样众多。然而，似乎高血糖性缺氧是受损糖尿病神经中所见电生理变化的主要原因。本文总结了实验数据，表明离子电导功能障碍，尤其是电压门控离子通道功能障碍，可能导致糖尿病性神经病变中动作电位产生和/或传导异常。
