Sequelae of Methanol Poisoning for Cognition

Objective: To identify possible cognitive deficit due to methanol intoxication. Introduction: Methanol poisoning leads to lesions in typical areas of the central nervous system, especially in basal ganglia (BG), to subcortical white matter lesions and to demyelination or even atrophy of the optic nerve. However, information regarding cognitive deficit on a population-based level in larger samples is lacking. Our goal was to identify whether BG dysfunction may lead to cognitive deficits Methods: A sample of 50 patients 3 to 8 months after methanol intoxication (METH) and 39 controls (KS) were administered a neuropsychological battery and underwent magnetic resonance imaging (MRI). A combination of three laboratory-based metabolic markers of alcohol abuse led to selection of 28 post-methanol intoxication subjects who were unlikely to abuse alcohol (METHna). These were matched to 28 controls (KSp) for age, education, premorbid intelligence level, global cognitive performance and level of depressive symptoms. Results: There were significant differences in the FAB total score (METHna, Md = 16, KSp, Md = 17, p = 0.001) and in three of the FAB subscores (Conceptualization, Mental flexibility, Motor programming; all p values < 0.050). Overall, there was a positive trend towards significance and a weak association between BG lesions on MRI and Mental flexibility from the FAB (rho = -282, p = 0.054). Conclusion: Our findings suggest that methanol poisoning is probably associated with cognitive deficits of the frontal type due to BG dysfunction.