Our results reveal significant changes in both cue-based fMRI reactivity, resting-state neural activity, and functional connectivity which represent the neural correlates of pathological craving in alcohol addiction. According to previous literature, alcohol addiction is a learned response wherein the hedonic weight to stimuli is decreased on excessive consumption of the substance by associating it with a paradoxical reward. This results in a shift in the normal, healthy self-referential state to an addicted state characterized by an incentive salience, which behaviorally manifests as a pathological craving for the substance. This craving is strongly associated with an emotional component and thus results in relapse of excessive alcohol consumption following even a short period of abstinence. In the current study, we propose that these different aspects of substance-related craving are encoded by a central craving network characterized by changes in activity and functional connectivity of the NAcc, VS, amygdala, PHC, PCC, dACC, pgACC, and OFC. The associative learning of the paradoxical reward may be mediated by the regions of the limbic and medial temporal lobes; the shift in self-referential state may be encoded
