Abstract
People who report experiencing alcohol-related blackouts (ARBs) are at increased risk of alcohol-related injury and even death. Blackout susceptibility is heritable and blackouts are not experienced by all who engage in hazardous drinking. Blackout is defined by anterograde amnesia, but a person in the blackout state also maintains consciousness and motor control at high levels of intoxication, which is behaviorally similar to episodes seen in individuals with a history of sleepwalking or related parasomnias. Spectral analysis of resting-state electroencephalograms (EEG) can provide insight into individual differences in baseline neurophysiology which may predict blackout susceptibility in otherwise healthy individuals. The current study investigated potential neurophysiological phenotypes present in the resting-state EEG spectra of individuals with a history of blackout, sleepwalking, or related parasomnias. In Experiment 1, adult females with a history of alcohol-related blackout had reduced resting-state alpha peak power over the primary motor cortex compared to those with no such history, while aperiodic slope over the right primary motor cortex was negatively correlated with lifetime blackout score in males. In Experiment 2, increased frequency of parasomnia episodes was associated with reduced resting-state alpha peak power across males and females. Together, these findings provide the first support for the existence of common neurophysiological phenotypes between specific parasomnias and alcohol-related blackout.
New & Noteworthy
Research on blackout often focuses on hippocampal suppression by alcohol because anterograde amnesia is a salient and definitional aspect of alcohol-related blackout. We focused here instead on the resilience of motor function to suppression by alcohol during the blackout state. We identified a sex-specific EEG marker associated with blackout history, and then found that the same marker was related to the frequency of episodes of certain non-REM parasomnias in both sexes. These findings suggest that these pathological states may share underlying dysfunction of motor inhibition, allowing for coordinated motor activity to persist during intoxication or sleep.
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