6533b835fe1ef96bd12a00f9
RESEARCH PRODUCT
End-plate dysfunction in acute organophosphate intoxication.
Roland BesserL. S. WeilemannLudwig GutmannHanns Christian HopfU. Dillmannsubject
AdultMaleNeuromuscular JunctionSuicide AttemptedMotor Endplatechemistry.chemical_compoundOrganophosphate PoisoningMuscle actionmedicineCholinesterasesHumansBotulismRepetitive nerve stimulationEvoked Potentialsbusiness.industryMusclesClinical courseMiddle Agedmedicine.diseaseAcetylcholinesteraseRespiration ArtificialMyasthenia gravisElectric StimulationOrganophosphate intoxicationMedian NervechemistryAnesthesiaFemaleNeurology (clinical)Abnormalitybusinessdescription
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.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 1989-04-01 | Neurology |