Snakebite is a cause of significant morbidity in Central Province, Pap
ua New Guinea. Three adult patients with clinical evidence of neurotox
icity following envenomation by the Papuan taipan had serial neurophys
iological examinations over the course of their subsequent hospitaliza
tion. All required artificial ventilation for 2.5 to 5 days. The compo
und 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 dist
inctive pattern of abnormality. Activation resulted in brief potentiat
ion of the CMAP followed by significantly greater decrement than obser
ved at rest. This effect lasted up to 30 minutes and was not altered a
fter intravenous edrophonium. Single-fiber electromyographic recording
s during the recovery phase of the illness were abnormal with marked b
locking and increased jitter. All patients were able to return home.