OBJECTIVE: To determine prolonged effects of organophosphorus (OP) insecticide poisoning on cognitive event-related potentials (ERPs). METHODS: ERPs of a group of 32 patients recovered from cholinergic phase of OP insecticide poisoning were compared with those of two matched control groups: 32 healthy volunteers and nine patients hospitalised with paracetamol overdose. A follow-up assessment was done in 21 patients (66% of the initial sample) 6 months after OP intoxication and the findings were compared with their initial ERP data. RESULTS: Patients showed highly significant prolongation of P300 latency, compared to healthy controls (p=0.003) and the controls with paracetamol overdose (p=0.016). Follow-up ERP findings of the patients revealed that this impairment remained unchanged even 6 months after OP poisoning (p=0.790). There was no significant difference in N100, P200 and N200 latencies or P300 amplitude either among the groups or between the two assessments of the patients with OP poisoning. CONCLUSIONS: Our results suggest that acute OP poisoning causes a delay in cognitive processes involved in stimulus classification, lasting at least for 6 months. SIGNIFICANCE: These findings highlight the possibility of development of long-lasting cognitive deficits following OP insecticide poisoning, and warrant longer-term prospective studies to determine whether this impairment is permanent.
OBJECTIVE: To determine prolonged effects of organophosphorus (OP) insecticide poisoning on cognitive event-related potentials (ERPs). METHODS: ERPs of a group of 32 patients recovered from cholinergic phase of OP insecticide poisoning were compared with those of two matched control groups: 32 healthy volunteers and nine patients hospitalised with paracetamoloverdose. A follow-up assessment was done in 21 patients (66% of the initial sample) 6 months after OP intoxication and the findings were compared with their initial ERP data. RESULTS:Patients showed highly significant prolongation of P300 latency, compared to healthy controls (p=0.003) and the controls with paracetamoloverdose (p=0.016). Follow-up ERP findings of the patients revealed that this impairment remained unchanged even 6 months after OP poisoning (p=0.790). There was no significant difference in N100, P200 and N200 latencies or P300 amplitude either among the groups or between the two assessments of the patients with OP poisoning. CONCLUSIONS: Our results suggest that acute OP poisoning causes a delay in cognitive processes involved in stimulus classification, lasting at least for 6 months. SIGNIFICANCE: These findings highlight the possibility of development of long-lasting cognitive deficits following OP insecticide poisoning, and warrant longer-term prospective studies to determine whether this impairment is permanent.
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