Chronic alcohol use in humans has been linked to deficits in executive function that depend on the PFC. One study showed that a significant number of substance-dependent individuals, including alcohol-dependent subjects, showed deficits in a gambling task that were similar to patients with lesions of the ventromedial PFC (Bechara et al., 2001). Long-term use of alcohol has been shown to be more detrimental than cocaine in attention and executive functioning tasks (Goldstein et al., 2004). Even in alcoholics who do not demonstrate deficits in certain executive tasks, differential patterns of activity in PFC are observed that suggest changes in the way that the brain performs the tasks (Pfefferbaum et al., 2001). Similarly, adolescents who engage in binge drinking performed adequately on a visual working memory task, yet there was hypoactivation of the right anterior PFC when compared with controls, suggesting a reorganization or compensatory mechanism in problem solving (Crego et al., 2010). These alterations in PFC activity may go unnoticed under low-level cognitive demands but may underlie deficits associated with higher-order cognitive function. Reduced glucose metabolism in alcohol-dependent subjects has
