Journal article
End-plate dysfunction in acute organophosphate intoxication
Neurology, Vol.39(4), pp.561-567
1989
DOI: 10.1212/WNL.39.4.561
PMID: 2927681
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.
Details
- Title: Subtitle
- End-plate dysfunction in acute organophosphate intoxication
- Creators
- R BESSER - Univ. Mainz, dep. neurology, Mainz 6500, GermanyL GUTMANN - Univ. Mainz, dep. neurology, Mainz 6500, GermanyU DILLMANN - Univ. Mainz, dep. neurology, Mainz 6500, GermanyL. S WEILEMANN - Univ. Mainz, dep. neurology, Mainz 6500, GermanyH. C HOPF - Univ. Mainz, dep. neurology, Mainz 6500, Germany
- Resource Type
- Journal article
- Publication Details
- Neurology, Vol.39(4), pp.561-567
- Publisher
- Lippincott Williams & Wilkins; Hagerstown, MD
- DOI
- 10.1212/WNL.39.4.561
- PMID
- 2927681
- ISSN
- 0028-3878
- eISSN
- 1526-632X
- Language
- English
- Date published
- 1989
- Academic Unit
- Neurology
- Record Identifier
- 9984020789902771
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