Local and network-level dysregulation of error processing is associated with binge drinking.

Binge drinking refers to the pattern of alcohol consumption that brings blood alcohol levels to or above legal intoxication levels. Commonly practiced by young adults, it is associated with neurofunctional alterations, raising health-related concerns. Executive deficits may contribute to the inability to refrain from excessive alcohol intake. As a facet of cognitive control, error processing allows for flexible modification of behavior to optimize future outcomes. It is highly relevant to addiction research, as a failure to inhibit excessive drinking results in relapses, which is a hallmark of alcohol use disorder. However, research on local and system-level neural underpinnings of inhibition failures as a function of binge drinking is limited. To address these gaps, functional magnetic resonance imaging (fMRI) was used to examine local changes and interregional functional connectivity during response inhibition errors on a Go/NoGo task. Young adult binge drinkers (BDs) performed equally well as light drinkers (LDs), a group of demographically matched individuals who drink regularly but in low-risk patterns. In contrast, BDs exhibited greater fMRI activity to inhibition errors contrasted with correct NoGo trials in the rostral anterior (rACC) and posterior cingulate cortices (PCC), as well as right middle frontal gyrus (R-MFG). Furthermore, BDs showed increased connectivity between the rACC and right lateral prefrontal cortex, in addition to greater connectivity between the R-MFG and the left ventrolateral and superior frontal cortices. Imaging indices were positively correlated only with alcohol-related measures, but not with those related to moods, disposition, or cognitive capacity. Taken together, greater error-related activity and expanded functional connectivity among prefrontal regions may serve a compensatory role to maintain efficiency of inhibitory control. Aligned with prominent models of addiction, these findings accentuate the importance of top-down control in maintaining low-risk drinking levels. They provide insight into potentially early signs of deteriorating cognitive control functions in BDs and may help guide intervention strategies aimed at preventing excessive drinking habits.

Binge drinking is associated with altered resting state functional connectivity of reward-salience and top down control networks.

Binge drinking is characterized by bouts of high-intensity alcohol intake and is associated with an array of health-related harms. Even though the transition from occasional impulsive to addictive alcohol use is not well understood, neurobiological models of addiction suggest that repeated cycles of intoxication and withdrawal contribute to the development of addiction in part through dysregulation of neurofunctional networks. Research on the neural sequelae associated with binge drinking is scant but resting state functional connectivity (RSFC) studies of alcohol use disorders (AUD) indicate that the development and maintenance of long-term excessive drinking may be mediated by network-level disruptions. The present study examined RSFC in young adult binge (BD) and light (LD) drinkers with seeds representing the networks subserving reward (the nucleus accumbens and caudate nucleus), salience (anterior cingulate cortex, ACC), and executive control (inferior frontal cortex, IFC). BDs exhibited enhanced connectivity between the striatal reward areas and the orbitofrontal cortex and the ACC, which is consistent with AUD studies and may be indicative of alcohol-motivated appetitive behaviors. Conversely, BDs demonstrated lower connectivity between the IFC and hippocampus which was associated with higher craving. This may indicate impaired ability to suppress unwanted thoughts and a failure to employ memory of the harmful consequences of heavy drinking in prospective plans and intentions. The observed greater connectivity of the reward/salience network and the lower prefrontal-hippocampal connectivity were associated with hazardous drinking levels indicating that dysregulation of neurofunctional networks may underlie binge drinking patterns.

Behavioral and Brain Activity Indices of Cognitive Control Deficits in Binge Drinkers.

Heavy episodic drinking is prevalent among young adults and is a public issue of increasing importance. Its initiation and maintenance are associated with deficits in the capacity to inhibit automatic processing in favor of non-habitual responses. This study used functional magnetic resonance imaging (fMRI) to examine behavioral and brain activity indices of cognitive control during the Stroop task as a function of binge drinking. Heavy episodic drinkers (HED) reported consuming 5+/6+ drinks in two hours at least five times in the past six months and were compared to light drinkers (LED) who reported two or fewer binge episodes but were matched on demographics, intelligence and family history of alcoholism. Greater conflict-induced activity in the ventrolateral prefrontal cortex (VLPFC) and thalamus was observed in HED participants and it was positively correlated with alcohol intake and alcohol-related harmful consequences. HEDs maintained intact accuracy but at a cost of prolonged reaction times to high-conflict trials and increased ratings of task difficulty. Greater activation of the areas implicated in cognitive control is consistent with compensatory network expansion to meet higher cognitive demands. These results provide further insight into degradation of cognitive control in HEDs which may benefit development of detection and prevention strategies.