Introduction: Ingestion of organophosphate pesticides (OPPs) is a common method of self-harm and a major clinical problem is Asia. Apart from acute cholinergic effects, OPPs are also claimed to be associated with long-term CNS toxicity. However, neurophysiological evidence for such long-term deficits is scarce in humans. We aimed to assess long-term changes in the pre-attentive (N1) and attentive (P3b) components of auditory event-related potentials (ERPs) following acute OPP self-poisoning.
Methods: We recruited 203 patients (147 men) hospitalised following OPP ingestion (OP Group; all had significant red cell cholinesterase inhibition) and 50 patients (23 men) hospitalised with paracetamol overdose (Control Group) as a means of self-harm. We recorded their EEG in an auditory oddball task and derived the averaged ERPs. The subjects underwent three testing sessions: on discharge from hospital (around 12 days post-ingestion), 6 weeks and 6 months post-ingestion. We compared the reaction time and ERP indices of the two groups at each time point, adjusting for sex, age, education and psychiatric comorbidities in multiple regression models.
Results: After adjusting for covariates, OP Group had significantly slower reaction time than the Control Group on discharge (mean difference [SE] = 65[20]ms, p=0.001) and at 6 weeks (mean difference [SE] = 45[20]ms, p=0.024), but not at 6 months. Parietal P3b latency was also significantly delayed (mean difference [SE] = 24.97[8.59]ms, p=0.004) in the OP Group on discharge. Parietal (PZ) P3b amplitudes were significantly smaller in the OP group on discharge (mean difference [SE] = 2.23[0.84]V, p=0.009) and at 6 months (mean difference [SE] = 3.34[1.43]V, p=0.021). Frontal (FZ) N1 component did not show significant intergroup differences.
Conclusions: Acute exposure to clinically significant doses of OPPs seem to cause impairment in behavioural and neurophysiological indices of stimulus discrimination, that outlast the cholinergic phase of intoxication. The behavioural impairment seems to disappear over months, but some neurophysiological deficits of attentive processing seem to last even after 6 months post-exposure.