Citation

Connolly S, Trevett AJ, Nwokolo NC, Lalloo DG, Naraqi S, Mantle D, Schofield IS, Fawcett PR, Harris JB, Warrell DA. Ann. Neurol. 1995; 38(6): 916-920.

Affiliation

Department of Biochemistry, Newcastle General Hospital, Newcastle upon Tyne, UK.

Copyright

(Copyright © 1995, John Wiley and Sons)

DOI

10.1002/ana.410380612

PMID

8526464

Abstract

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.

Language: en