The effect of heavy social drinking on cognitive functioning
Creators: name: Nichols, Jennifer Maree
Publisher: name: University Of Tasmania
Year: 2023

description: Cognitive dysfunction is a likely concomitant of excessive alcohol consumption; however, the aetiology and the course of the decline are unknown. Recent studies suggest that ethanol related nervous system disorders may be a result of a combination of the neurotoxic effects of ethanol or its metabolites, nutritional factors, and genetic predisposition. These disorders may be placed on a continuum that ranges from mild deficits in social drinkers to fully developed Korsalcoff syndrome (Ryback, 1971). Based on findings that suggest that heavy social drinking results in subtle deficits in information processing, cognitive performance was examined in groups of young heavy social drinkers or \binge\" drinkers (HSDs) and matched groups of light social drinkers (LSDs). The performance of both groups was examined in the presence and absence of a pharmacological challenge (lorazepam - ATIVAN) to investigate whether heavy social drinking causes changes in brain functioning as indexed by eventrelated potentials (ERPs) and neuropsychological tests. The general hypothesis studied was that heavy levels of social drinking have a negative influence on sober cognitive performance and associated ERPs and that HSDs compared to LSDs will show a differential response to a pharmacological challenge. The first three experiments examined the cognitive performance of HSDs and LSDs on tests of neuropsychological functioning. HSD's performance on a number of the tasks was inferior to that of LSDs irrespective of drug treatment. Lorazepam generally impaired long-term episodic memory performance in both groups and delayed auditory verbal learning performance only in the HSDs. The behavioural findings suggest that alcohol may exert a subtle yet toxic effect on brain functioning when drinking patterns include a regular intake of high doses of alcohol at one time. ERPs were then employed to assess brain functioning as they allow the study of electrophysiological manifestations of cognitive processing. In Experiments 4 and 5 - the latter manipulating task difficulty - the P300 component was investigated in HSDs and LSDs. HSDs showed longer P300 latency compared to LSDs and following lorazepam administration both groups demonstrated a reduced P300 amplitude compared to the placebo treatment. Experiments 6 and 7 were then carried out to investigate memory and concurrently recorded ERPs in HSDs and LSDs. In a free recall task (Experiment 6) with a rare word probability of .30 analysis of P300s to recalled and not-recalled words indicated that P300 amplitude in the HSDs was reduced in the placebo treatment compared to the LSDs. Lorazepam produced a distinctive pattern of anterograde memory deficits in both groups and reduced P300 amplitude to rare words in the LSDs. ERPs were then examined in a task requiring continuous recognition memory for visually presented words (Experiment 7). HSDs exhibited changes in ERP components compared to the LSDs in both the presence and absence of lorazepam. These findings are consistent with an apparent tolerance in the HSDs to the effects of lorazepam. As hypothesised differences in cognitive functioning were evident between HSDs and LSDs. These were reflected in ERP and behavioural indices both in the presence and absence of a pharmacological challenge. Generally the HSDs exhibited a tolerance to the effects of lorazepam administration and an impairment in information processing ability. The finding of ERP deviations and a differential response of the HSDs to the effects of lorazepam suggests that this pattern of binge drinking in young social drinkers may cause changes in brain functioning."