et al., 2008) and include the caudate (Boutte et al., 2012), putamen (Jernigan et al., 1991), amygdala (Fein et al., 2006), and nucleus accumbens (Sullivan, Deshmukh, De Rosa, Rosenbloom, & Pfefferbaum, 2005). Such changes to nodes of the basal ganglia reward circuitry may contribute to the gradual progression of AUD, as these structures are involved in habit formation, reward evaluation, and cue-induced relapse (Koob & Volkow, 2016). Collectively, such findings suggest that neurological disorders such as WE, KS, CPM, and MBD occur on a continuum during the dynamic course of alcoholism before they emerge as clinically apparent syndromes.
