This overview proposes the guiding hypothesis that disruption of frontocerebellar circuitry is one of the principal neural mechanisms underlying behavioral deficits in both uncomplicated alcoholism and alcoholics with neurological complications such as WKS (cf., Wijnia and Goossensen, 2010). Compromise of the gray matter nodes of this circuit or disruption of the white matter tracts connecting the nodes may adversely influence remote regions within that circuit, resulting in characteristic alcoholism-related cognitive and motor deficits. This network, even when compromised, may be invoked by alcoholics for compensation in the performance of challenging cognitive procedures. The cerebellum, therefore, exerts substantial primary and modulatory influence on behavior with its long-reaching loops to frontal sites. Even modest alterations within this frontocerebellar circuitry in alcoholics have the potential to contribute to vulnerability for relapse by virtue of executive function impairment. Involvement of frontocerebellar circuitry in compensatory activity may also be a source of maintenance of addictive behavior, given the roles of the cerebellum (Grafman et al., 1992; Doyon et al., 1997; Hubert et al., 2009) and basal ganglia (Heindel et al., 1989; Pascual-Leone et al., 1993;
