Connolly S, Trevett A J, Nwokolo N C, Lalloo D G, Naraqi S, Mantle D, Schofield I S, Fawcett P R, Harris J B, Warrell D A
Department of Biochemistry, Newcastle General Hospital, Newcastle upon Tyne, UK.
Ann Neurol. 1995 Dec;38(6):916-20. doi: 10.1002/ana.410380612.
Snakebite is a cause of significant morbidity in Central Province, Papua New Guinea. Three adult patients with clinical evidence of neurotoxicity following envenomation by the Papuan taipan had serial neurophysiological examinations over the course of their subsequent hospitalization. All required artificial ventilation for 2.5 to 5 days. The compound muscle action potential (CMAP) amplitudes declined over the first 2 to 4 days after envenoming and then gradually increased in parallel with clinical recovery. Repetitive stimulation studies revealed a distinctive pattern of abnormality. Activation resulted in brief potentiation of the CMAP followed by significantly greater decrement than observed at rest. This effect lasted up to 30 minutes and was not altered after intravenous edrophonium. Single-fiber electromyographic recordings during the recovery phase of the illness were abnormal with marked blocking and increased jitter. All patients were able to return home.
在巴布亚新几内亚的中部省份，蛇咬伤是导致严重发病的一个原因。三名成年患者在被巴布亚太攀蛇毒液注入后出现神经毒性的临床证据，并在随后住院期间接受了系列神经生理学检查。所有人都需要进行2.5至5天的人工通气。复合肌肉动作电位（CMAP）幅度在毒液注入后的头2至4天下降，然后随着临床恢复逐渐增加。重复刺激研究显示出一种独特的异常模式。激活导致CMAP短暂增强，随后出现比静息时明显更大的衰减。这种效应持续长达30分钟，静脉注射依酚氯铵后无变化。疾病恢复阶段的单纤维肌电图记录异常，有明显阻滞和抖动增加。所有患者都能够回家。
