Alcohol consumption causes gradual neurocognitive deficits ranging from mild deficits in social drinkers to profound memory and abstract processing impairments in chronic alcoholics (Parsons, 1998). Alcohol studies based on functional magnetic resonance imaging (fMRI) have found altered functional relationships and corresponding compensatory mechanisms among different parts of the brain linked to these deficits. For example, a finger tapping task demonstrated that alcohol dependent patients recruited areas of the parietal lobe, inferior frontal, middle temporal, pre- and post-central gyri to compensate for a dysfunctional fronto-cerebellar network used by normal controls (Parks et al., 2010). Connectivity between the cerebellum and the default mode network (DMN) is reduced in alcoholics during resting state, but increased during a spatial working memory task to compensate and achieve same performance than controls (Chanraud et al., 2011). Attenuated insula activation, observed during an emotional processing task, may be linked to reduced interoceptive awareness (Padula et al., 2011). Even after long-term alcohol abstinence, it has been found that resting state FC differs compared to controls (Camchong et al., 2013). Decreased resting state connectivity within reward, visual and executive
