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中毒组为已确诊的慢性1-烯丙基氯-3中毒性周围神经病患者31例,对照组为健康者25例。中毒组肌电图在静息状态时,插入电位降低,部分病例出现自发性失神经电位(正锐波及纤颤电位);轻度收缩时,单个运动单位电位多相电位增多、电压降低、时限延长;最大收缩时,出现混合型。刺激腓总神经诱发胫前肌、腓骨长肌及伸趾短肌反应性肌电位出现多相电位、低电压及时限延长。腓总神经运动传导速度减慢及远端潜伏时延长,腓肠神经感觉传导速度及远端潜伏时无明显改变。腓肠神经髓质内微管及神经微丝变性,线粒体嵴脱落成变性空泡,光面内质网扩张和肿胀,髓鞘未见异常改变。腓肠肌肌原纤维部分断裂及间隙扩大并且内充满肌质网及线粒体变性空泡,Z线弯曲、断裂及崩解。
In the poisoning group, 31 patients were diagnosed as chronic 1-allyl chloride-3 toxic peripheral neuropathy and 25 healthy people as the control group. The electromyogram of poisoning group decreased at rest and the spontaneous denervation potential (positive sharp wave and fibrillation potential) in some cases. The multiphase potential of single motor unit increased with reduced voltage and the time limit Extended; maximum contraction, mixed type. Stimulation of the common peroneal nerve induced tibialis anterior muscle, peroneus longus and extensor phalanges reactivity myoelectric potential appear multi-phase potential, low voltage and prolonged. Peroneal nerve conduction velocity slowed down and the latency of the distal extension of the sural nerve sensory conduction velocity and no significant changes in the distal latency. Sural medulla medulla and neurofilament degeneration, mitochondrial cristae degeneration into vacuoles, smooth endoplasmic reticulum dilation and swelling, no abnormal changes in myelin. Part of gastrocnemius muscle fibrillation and gap enlargement and filled with sarcoplasmic reticulum and mitochondria degeneration vacuoles, Z line bending, fracture and disintegration.