OBJECTIVE: The current study examined the relationship between severity of alcohol use disorders (AUDs) and the neural circuits that underlie response inhibition and error monitoring. In addition, we explored pre- and post-inhibition trial processes to determine the potential causal mechanisms responsible for disinhibition in AUDs. METHOD: One hundred sixty-four individuals with a range of drinking from non-treatment-seeking adults with problematic alcohol use to treatment-seeking adults with alcohol dependence completed a Go/NoGo task while undergoing functional magnetic resonance imaging. RESULTS: Correlations between signal change during response inhibition and a composite measure of AUD severity revealed significant negative relationships in right insula/inferior frontal gyrus, pregenual anterior cingulate cortex, and inferior parietal lobe. Relationships with error monitoring-related response largely overlapped with that of correct inhibitions but also included rostral anterior cingulate cortex and left inferior frontal gyrus, such that more severe AUDs were associated with reduced response in these regions. Last, examination of pre- and postinhibition processes suggested that more severe AUDs are associated with greater engagement of motor response circuits before inhibition trials, suggesting greater pre-potent tendencies that may lead to disinhibition. CONCLUSIONS: The current results extend previous work by examining how variation in AUD severity is related to neural response during response inhibition and potential causal mechanisms responsible for impaired inhibitory control. More severe AUDs were associated with reduced engagement of neural circuits involved in behavioral control and enhanced pre-potent responding. This altered control may contribute to the progression of AUDs, as well as relapse after treatment.
OBJECTIVE: The current study examined the relationship between severity of alcohol use disorders (AUDs) and the neural circuits that underlie response inhibition and error monitoring. In addition, we explored pre- and post-inhibition trial processes to determine the potential causal mechanisms responsible for disinhibition in AUDs. METHOD: One hundred sixty-four individuals with a range of drinking from non-treatment-seeking adults with problematic alcohol use to treatment-seeking adults with alcohol dependence completed a Go/NoGo task while undergoing functional magnetic resonance imaging. RESULTS: Correlations between signal change during response inhibition and a composite measure of AUD severity revealed significant negative relationships in right insula/inferior frontal gyrus, pregenual anterior cingulate cortex, and inferior parietal lobe. Relationships with error monitoring-related response largely overlapped with that of correct inhibitions but also included rostral anterior cingulate cortex and left inferior frontal gyrus, such that more severe AUDs were associated with reduced response in these regions. Last, examination of pre- and postinhibition processes suggested that more severe AUDs are associated with greater engagement of motor response circuits before inhibition trials, suggesting greater pre-potent tendencies that may lead to disinhibition. CONCLUSIONS: The current results extend previous work by examining how variation in AUD severity is related to neural response during response inhibition and potential causal mechanisms responsible for impaired inhibitory control. More severe AUDs were associated with reduced engagement of neural circuits involved in behavioral control and enhanced pre-potent responding. This altered control may contribute to the progression of AUDs, as well as relapse after treatment.
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