M H Bhatt1, M A Elias, A K Mankodi. 1. Movement Disorders Clinic and Department of Neurology, Jaslok Hospital & Research Centre, Mumbai, India.
Abstract
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.
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.
Authors: Jordan A Firestone; Jessica I Lundin; Karen M Powers; Terri Smith-Weller; Gary M Franklin; Phillip D Swanson; W T Longstreth; Harvey Checkoway Journal: Am J Ind Med Date: 2010-03 Impact factor: 2.214