A neurobiological mechanism may be associated with alcohol-induced fragmentary blackouts (FBs), with alcohol exerting different effects on neural activity for individuals with or without FBs, according to research published online March 15 in Alcoholism: Clinical and Experimental Research.
Reagan R. Wetherill, Ph.D., of the University of California in San Diego, and colleagues used a series of 48 functional magnetic resonance imaging sessions to study the effects of alcohol on brain hemodynamic activity and the ability of 12 individuals with alcohol-induced FBs and 12 matched individuals without a history of FBs to perform tasks involving memory.
Although the researchers found no differences between the groups in performance on the contextual memory task, the groups exhibited very different brain-response patterns after consuming alcohol. There was a FB group by beverage interaction, with FB− individuals showing a significantly increased blood oxygenation level-dependent response following exposure to alcohol.
"Activation patterns of FB+ and FB− individuals differed after alcohol consumption, but not while sober. These findings indicate that acute alcohol consumption affects dorsolateral prefrontal cortex and posterior parietal cortex neural activation and suggest that frontoparietal abnormalities are a potential biomarker for alcohol-induced memory impairments," the authors write.
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