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End-plate dysfunction in acute organophosphate intoxication

Department of Neurology, University of Mainz, Mainz, West Germany (Drs. Beseer, Dillmann, and Hopf)
Department of Internal Medicine II, University of Mainz, Mainz, West Germany (Dr. Weilemann)
Department of Neurology, West Virginia University, Morgantown, WV (Dr. Gutmann).

Acute organophosphate intoxication resulting from suicide attempts in 14 patients produced a series of electrophysiologic abnormalities that correlated with the clinical course. Spontaneous repetitive firing of single evoked compound muscle action potentials (CMAP) was the earliest and most sensitive indicator of the acetylcholinesterase inhibition. A decrement of evoked CMAP following repetitive nerve stimulation was the most severe abnormality. At the height of the intoxication no CMAP was evoked after the first few stimuli. The decrement-increment phenomenon occurred only at milder stages of intoxication and its features are characteristic of acetylcholinesterase inhibition. These electrophysiologic features proved to be the most useful for determining initial severity and clinical course of the acute organophosphate intoxication and differentiated this syndrome from those of myasthenia gravis, Eaton-Lambert syndrome, and botulism.

Address correspondence and reprint requests to Dr. Besser, Neurologische Klinik, University of Mainz, Langenbeckstrasse 1, 6500 Mainz, West Germany.

Presented in part at the fortieth annual meeting of the American Academy of Neurology, Cincinnati, OH, April 1988.

Received July 22,1988. Accepted for publication in final form October 4,1988.

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