Alcoholism has been described as a disinhibitory disorder as individuals with AUD and their high risk offspring often display impulsivity and dysfunctions in several electrophysiological measures, more prominently demonstrated by lower P3 amplitude in several tasks (for a review, see Porjesz et al., 2005). Using a three stimulus auditory oddball paradigm, Hada et al. (2000) found that CSD topographic maps served better to discriminate alcoholics from controls than ERP potential maps. They reported that alcoholics produced lower P3a amplitudes to target stimuli, along with distinct topographic distributions of P3a-related CSD maps, characterized by more but weaker sources in alcoholics compared to controls. In another study with a similar task, Cohen et al. (2002) found that significant P3 reductions in alcoholics were pronounced over the posterior regions, and the group differentiation was more obvious in the CSD maps wherein the sources and sinks were fewer and weaker in alcoholics. In a sample of individuals at high risk (HR) for alcoholism during the performance of an auditory oddball task, Ramachandran et al. (1996) reported significant reductions in both P3 amplitudes and P3-related
