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对18例有机磷引起的迟发性神经病（OPIDN）行运动传导速度、感觉传导速度和肌电图检则．结果示35．1％的被检肌肉出现失神经电位（正锐彼和纤颤电位）；运动传导速度与正常对照组比较显著减慢（P＜0．01）；感觉神经传导速度与正常对照组比较无显著差异（P＞0．01）。本文依据OPIDN电生理异常特性，神经髓鞘与轴索共同受累现象，讨论了激酶的直接毒性作用及抑制神经病靶点酯酶产生OPIDN等发病机制学说。提出OPIDN发病机制除具有种属和个体差异外，可能多种致病机制并存．
18 cases of organic phosphorus-induced delayed neuropathy (OPIDN) line motor conduction velocity, sensory conduction velocity and electromyography. The results showed that 35.1% of the seized muscles showed denervation potentials (Zhengrui and fibrillation potentials); the motor conduction velocity was significantly slower than that of the normal control group (P <0.01); the sensory nerve conduction velocity was significantly lower than that of the normal control There was no significant difference between the two groups (P> 0.01). This article based on the abnormal electrophysiological characteristics of OPIDN, myelin sheath and axonal involvement, discussed the direct toxicity of kinase and inhibition of neuropathy esterase OPIDN and other pathogenesis theory. Proposed OPIDN pathogenesis in addition to having species and individual differences, the possibility of a variety of pathogenic mechanisms co-exist.