Cognitive sequelae of methanol poisoning involve executive dysfunction and memory impairment in cross-sectional and long-term perspective
Language English Country United States Media print-electronic
Document type Journal Article
PubMed
28262185
DOI
10.1016/j.alcohol.2016.12.003
PII: S0741-8329(16)30111-2
Knihovny.cz E-resources
- Keywords
- Basal ganglia, Cognitive impairment, Executive function, Magnetic resonance imaging, Memory, Methanol poisoning,
- MeSH
- Time Factors MeSH
- Adult MeSH
- Executive Function * MeSH
- Cognition Disorders chemically induced diagnostic imaging psychology MeSH
- Middle Aged MeSH
- Humans MeSH
- Longitudinal Studies MeSH
- Methanol poisoning MeSH
- Follow-Up Studies MeSH
- Neuropsychological Tests MeSH
- Memory Disorders chemically induced diagnostic imaging psychology MeSH
- Cross-Sectional Studies MeSH
- Aged MeSH
- Check Tag
- Adult MeSH
- Middle Aged MeSH
- Humans MeSH
- Male MeSH
- Aged MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- Methanol MeSH
Methanol poisoning leads to lesions in the basal ganglia and subcortical white matter, as well as to demyelination and atrophy of the optic nerve. However, information regarding cognitive deficits in a large methanol sample is lacking. The principal aim of the present study was to identify the cognitive sequelae of methanol poisoning and their morphological correlates. A sample of 50 patients (METH; age 48 ± 13 years), 3-8 months after methanol poisoning, and 57 control subjects (CS; age 49 ± 13 years) were administered a neuropsychological battery. Forty-six patients were followed in 2 years' perspective. Patients additionally underwent 1.5T magnetic resonance imaging (MRI). Three biochemical and toxicological metabolic markers and a questionnaire regarding alcohol abuse facilitated the classification of 24 patients with methanol poisoning without alcohol abuse (METHna) and 22 patients with methanol poisoning and alcohol abuse (METHa). All groups were compared to a control group of similar size, and matched for age, education, premorbid intelligence level, global cognitive performance, and level of depressive symptoms. Using hierarchical multiple regression we found significant differences between METH and CS, especially in executive and memory domains. METHa showed a similar pattern of cognitive impairment with generally more severe executive dysfunction. Moreover, all METH patients with extensive involvement on brain MRI (lesions in ≥2 anatomical regions) had a more severe cognitive impairment. From a longitudinal perspective, we did not find any changes in their cognitive functioning after 2 years' follow-up. Our findings suggest that methanol poisoning is associated with executive dysfunction and explicit memory impairment, supposedly due to basal ganglia dysfunction and disruption of frontostriatal circuitry proportional to the number of brain lesions, and that these changes are persistent after 2 years' follow-up.
References provided by Crossref.org
Estimation of long-term costs of postacute care in survivors of the methanol poisoning outbreak
