Using a GO-NOGO response inhibition task in which working memory (WM) demands can be varied, we demonstrate that the compromised abilities of cocaine users to exert control over strong prepotent urges are associated with reduced activity in anterior cingulate and right prefrontal cortices, two regions thought to be critical for implementing cognitive control. Furthermore, unlike drug-naive controls, and opposite to the anterior cingulate pattern, cocaine users showed an over-reliance on the left cerebellum, a compensatory pattern previously seen in alcohol addiction. The results indicate that cocaine users find it difficult to inhibit their own actions, particularly when WM demands, which have been shown previously to increase during cue-induced craving for the drug, are increased. The results reveal a neuroanatomical basis for this dysexecutive component to addiction, supporting the suggested importance cognitive functions may play in prolonging abuse or predisposing users toward relapse.

Several current theories emphasize the role of cognitive control in addiction. The present review evaluates neural deficits in the domains of inhibitory control and error processing in individuals with substance dependence and in those showing excessive addiction-like behaviours. The combined evaluation of event-related potential (ERP) and functional magnetic resonance imaging (fMRI) findings in the present review offers unique information on neural deficits in addicted individuals. We selected 19 ERP and 22 fMRI studies using stop-signal, go/no-go or Flanker paradigms based on a search of PubMed and Embase. The most consistent findings in addicted individuals relative to healthy controls were lower N2, error-related negativity and error positivity amplitudes as well as hypoactivation in the anterior cingulate cortex (ACC), inferior frontal gyrus and dorsolateral prefrontal cortex. These neural deficits, however, were not always associated with impaired task performance. With regard to behavioural addictions, some evidence has been found for similar neural deficits; however, studies are scarce and results are not yet conclusive. Differences among the major classes of substances of abuse were identified and involve stronger neural responses to errors in individuals with alcohol dependence versus weaker neural responses to errors in other substance-dependent populations. Task design and analysis techniques vary across studies, thereby reducing comparability among studies and the potential of clinical use of these measures. Current addiction theories were supported by identifying consistent abnormalities in prefrontal brain function in individuals with addiction. An integrative model is proposed, suggesting that neural deficits in the dorsal ACC may constitute a hallmark neurocognitive deficit under lying addictive behaviours, such as loss of control.

The ability to detect an error in one's own performance and then to improve ongoing performance based on this error processing is critical for effective behaviour. In our event-related fMRI experiment, we show that explicit awareness of a response inhibition commission error and subsequent post-error behaviour were associated with bilateral prefrontal and parietal brain activation. Activity in the anterior cingulate region, typically associated with error detection, was equivalent for both errors subjects were aware of and those they were not aware of making. While anterior cingulate activation has repeatedly been associated with error-related processing, these results suggest that, in isolation, it is not sufficient for conscious awareness of errors or post-error adaptation of response strategies. Instead, it appears, irrespective of awareness, to detect information about stimuli/responses that requires interpretation in other brain regions for strategic implementation of post-error adjustments of behaviour.