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Case Reports
Journal Article
Acute and reversible parkinsonism due to organophosphate pesticide intoxication: five cases.
Neurology 1999 April 23
OBJECTIVE: To describe five patients who developed acute and reversible parkinsonism following organophosphate (OP) pesticide exposure, and to consider whether this syndrome represents a rare sequela of such exposure in genetically susceptible individuals.
BACKGROUND: Several toxins are known to produce parkinsonism following acute exposure. Although case-control studies have implicated OP pesticides in the etiology of PD, acute parkinsonism following brief pesticide exposure has never been reported.
METHODS: The authors describe the clinical syndrome affecting five patients who presented with recent OP exposure and symptoms of an acute akinetic-rigid syndrome.
RESULTS: All patients developed parkinsonism that resembled PD clinically except for poor response to levodopa. Three genetically related patients were exposed to pesticides in a common environment before onset of parkinsonism; other family members remained unaffected. Other secondary causes of parkinsonism were excluded. Four patients recovered completely without treatment, and one patient was lost to follow-up. One patient experienced repeated episodes of parkinsonism with inadvertent reexposure to a pesticide-contaminated environment.
CONCLUSION: The clinical course of these five patients suggests their syndrome represents a heretofore undescribed toxic effect of OP pesticides. Our observations strengthen epidemiologic studies implicating OP pesticides in the etiology of PD. A genetic susceptibility to OP pesticide-induced parkinsonism may account for three family members developing this syndrome.
BACKGROUND: Several toxins are known to produce parkinsonism following acute exposure. Although case-control studies have implicated OP pesticides in the etiology of PD, acute parkinsonism following brief pesticide exposure has never been reported.
METHODS: The authors describe the clinical syndrome affecting five patients who presented with recent OP exposure and symptoms of an acute akinetic-rigid syndrome.
RESULTS: All patients developed parkinsonism that resembled PD clinically except for poor response to levodopa. Three genetically related patients were exposed to pesticides in a common environment before onset of parkinsonism; other family members remained unaffected. Other secondary causes of parkinsonism were excluded. Four patients recovered completely without treatment, and one patient was lost to follow-up. One patient experienced repeated episodes of parkinsonism with inadvertent reexposure to a pesticide-contaminated environment.
CONCLUSION: The clinical course of these five patients suggests their syndrome represents a heretofore undescribed toxic effect of OP pesticides. Our observations strengthen epidemiologic studies implicating OP pesticides in the etiology of PD. A genetic susceptibility to OP pesticide-induced parkinsonism may account for three family members developing this syndrome.
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