Neurophysiologie clinique = Clinical neurophysiology · 2007
[Clinical and electrophysiological aspects of acute organophosphate intoxication].
Клинический случайАннотация на английскомСтатьяНазвание и аннотация: Перевод пока не подготовлен
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Rafai M A, Boulaajaj F Z, Bourezgui M, Charra B, Otmani H E, Benslama A, Motaouakkil S, Slassi I
Аннотация
INTRODUCTION: Acute organophosphate (OP) intoxications, accidental or voluntary, are responsible for a high mortality. They cause extensive muscular paralysis by acetyl cholinesterase activity inhibition at the neuromuscular junction level.
AIM: To underline the rarity and the characteristic electrophysiological pattern during cholinergic crisis.
OBSERVATION: A 28-year-old woman was admitted to the medical intensive care unit for Malathion acute intoxication with signs of glandular hypersecretion, complicated tetraparesis, and respiratory distress. The cholinesterase activity was 17%. The electroneuromyography showed multiple motor responses to the same stimulation, which is characteristic of the cholinergic crisis. Other electrophysiological parameters, in particular low-frequency repetitive stimulations, were normal. The evolution was favourable after symptomatic treatment and respiratory assistance.
DISCUSSION AND CONCLUSIONS: Organophosphate intoxications evolve in three phases: acute cholinergic crisis, intermediate syndrome, and delayed neuropathy. While the electrophysiological aspects of delayed neuropathy are best characterized, those of crisis and intermediate syndrome remain very little studied. The persistence of acetylcholine in the synaptic slit would explain the multiple motor responses to single stimulation during the crisis.
AIM: To underline the rarity and the characteristic electrophysiological pattern during cholinergic crisis.
OBSERVATION: A 28-year-old woman was admitted to the medical intensive care unit for Malathion acute intoxication with signs of glandular hypersecretion, complicated tetraparesis, and respiratory distress. The cholinesterase activity was 17%. The electroneuromyography showed multiple motor responses to the same stimulation, which is characteristic of the cholinergic crisis. Other electrophysiological parameters, in particular low-frequency repetitive stimulations, were normal. The evolution was favourable after symptomatic treatment and respiratory assistance.
DISCUSSION AND CONCLUSIONS: Organophosphate intoxications evolve in three phases: acute cholinergic crisis, intermediate syndrome, and delayed neuropathy. While the electrophysiological aspects of delayed neuropathy are best characterized, those of crisis and intermediate syndrome remain very little studied. The persistence of acetylcholine in the synaptic slit would explain the multiple motor responses to single stimulation during the crisis.