Subacute and chronic neuropsychological sequalae of acute organophosphate pesticide self-poisoning: a prospective cohort study from Sri Lanka
- 22 June 2020
- journal article
- research article
- Published by Taylor & Francis Ltd in Clinical Toxicology
- Vol. 59 (2), 118-130
- https://doi.org/10.1080/15563650.2020.1778719
Abstract
Some epidemiological evidence implicates acute organophosphate (OP) pesticide poisoning in long-term neurocognitive deficits. However, no study has prospectively followed up poisoned patients long-term from the time of intoxication. We aimed to determine whether clinically significant acute OP self-poisoning leads to subacute and chronic neurocognitive deficits, in a prospective follow up study. Employing Mini Mental State Examination, Digit Span and Cambridge Neuropsychological Test Automated Battery (CANTAB), we compared multiple cognitive functions in 222 patients hospitalized with acute OP pesticide self-poisoning with a control group of 52 patients hospitalized with paracetamol overdose, at three time points: on discharge following clinical recovery, 6 weeks and 6 months post-ingestion. Intergroup comparisons at each time point were done in multiple regression models, adjusting for sex, age, education and psychiatric comorbidities. OP within-group analysis was done to determine a dose–response relationship. After adjusting for covariates, the OP poisoned group had significantly poorer working memory (Digit Span) and episodic memory (CANTAB Paired Associates Learning); impaired spatial planning (CANTAB Stocking of Cambridge); and slower response speed in the sustained attention task (CANTAB Rapid Visual Information Processing), in the post-discharge assessment. Only working memory and episodic memory measures were impaired in the OP group at 6 weeks, whereas no significant intergroup differences were observed at 6 months. The OP subgroup who had complete red cell acetylcholinesterase inhibition on admission had poorer episodic memory when tested post-discharge than those who had partial inhibition, but no significant subgroup differences were observed at 6 weeks or 6 months. Acute OP pesticide poisoning may cause neuropsychological impairment that outlasts the cholinergic phase on a subacute time scale; but does not cause measurable chronic neuropsychological deficits.Keywords
Funding Information
- Australian National Health and Medical Research Council (1030069)
- South Asian Clinical Toxicology Research Collaboration
- University of Peradeniya
This publication has 41 references indexed in Scilit:
- Evaluation of the Test-mate ChE (Cholinesterase) Field Kit in Acute Organophosphorus PoisoningAnnals of Emergency Medicine, 2011
- Hippocampal dysfunction in patients with mild cognitive impairment: A functional neuroimaging study of a visuospatial paired associates learning taskNeuropsychologia, 2011
- Correlating neurobehavioral performance with biomarkers of organophosphorous pesticide exposureNeuroToxicology, 2011
- Higher susceptibility of the ventral versus the dorsal hippocampus and the posteroventral versus anterodorsal amygdala to soman-induced neuropathologyNeuroToxicology, 2010
- Poisoning with the S-Alkyl organophosphorus insecticides profenofos and prothiofosQJM: An International Journal of Medicine, 2009
- Management of acute organophosphorus pesticide poisoningThe Lancet, 2008
- Long-term event-related potential changes following organophosphorus insecticide poisoningClinical Neurophysiology, 2008
- Correlation between red blood cell acetylcholinesterase activity and neuromuscular transmission in organophosphate poisoningChemico-Biological Interactions, 2005
- Chronic Neurobehavioral Effects of Tokyo Subway Sarin Poisoning in Relation to Posttraumatic Stress DisorderArchives of environmental health, 1998
- Chronic Neurological Sequelae of Acute Organophosphate Pesticide PoisoningArchives of environmental health, 1988