Abstract
High-dose alcohol intoxication is commonly associated with impaired inhibition, but the boundary conditions, as well as associated neurocognitive/neuroanatomical changes have remained rather unclear. This study was motivated by the counterintuitive finding that high-dose alcohol intoxication compromises response inhibition performance when working memory demands were low, but not when they were high. To investigate whether this is more likely to be caused by deficits in cognitive control processes or in attentional processes, we examined event-related (de)synchronization processes in theta and alpha-band activity and performed beamforming analyses on the EEG data of previously published behavioral findings. This yielded two possible explanations: There may be a selective decrease of working memory engagement in case of relatively low demand, which boosts response automatization, ultimately putting more strain on the remaining inhibitory resources. Alternatively, there may be a decrease in proactive preparatory and anticipatory attentional gating processes in case of relatively low demand, hindering attentional sampling of upcoming stimuli. Crucially, both of these interrelated mechanisms reflect differential alcohol effects after the actual motor inhibition process and therefore tend to be processes that serve to anticipate future response inhibition affordances. This provides new insights into how high-dose alcohol intoxication can impair inhibitory control.
Highlights
High-dose alcohol intoxication is commonly associated with impaired inhibition, but the boundary conditions, as well as associated neurocognitive/neuroanatomical changes have remained rather unclear
Alpha desynchronization processes, in particular, have been associated with working memory processes. They have been associated with a gating mechanism that controls access to m emory[23–25] to enable working memory maintenance and protection against interfering information[26]. Given these functional roles of theta and alpha band activity, we hypothesized that the response inhibition difference in alcohol effects under low vs. high working memory demands should be reflected by these frequency bands
The current study examined neurophysiological processes underlying differential high-dose alcohol intoxication effects on inhibitory control depending on working memory demands
Summary
High-dose alcohol intoxication is commonly associated with impaired inhibition, but the boundary conditions, as well as associated neurocognitive/neuroanatomical changes have remained rather unclear. This study was motivated by the counterintuitive finding that high-dose alcohol intoxication compromises response inhibition performance when working memory demands were low, but not when they were high To investigate whether this is more likely to be caused by deficits in cognitive control processes or in attentional processes, we examined event-related (de)synchronization processes in theta and alpha-band activity and performed beamforming analyses on the EEG data of previously published behavioral findings. They have been associated with a gating mechanism that controls access to (working) m emory[23–25] to enable working memory maintenance and protection against interfering information[26] Given these functional roles of theta and alpha band activity, we hypothesized that the response inhibition difference in alcohol effects under low vs high working memory demands should be reflected by these frequency bands. Since prefrontal structures are central for working memory[31–34], prefrontal structures likely reflect differences in alcohol effects on response inhibition under low vs. high working memory demands
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