Besser_1989_Neurology_39_561

Reference

Title : End-plate dysfunction in acute organophosphate intoxication - Besser_1989_Neurology_39_561
Author(s) : Besser R , Gutmann L , Dillmann U , Weilemann LS , Hopf HC
Ref : Neurology , 39 :561 , 1989
Abstract :

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.

PubMedSearch : Besser_1989_Neurology_39_561
PubMedID: 2927681

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Citations formats

Besser R, Gutmann L, Dillmann U, Weilemann LS, Hopf HC (1989)
End-plate dysfunction in acute organophosphate intoxication
Neurology 39 :561

Besser R, Gutmann L, Dillmann U, Weilemann LS, Hopf HC (1989)
Neurology 39 :561