Evidence from electrophysiological studies have shown frontal lobe abnormalities in alcoholics (Begleiter et al., 1980; Hada et al., 2000; Kamarajan et al., 2004, 2005a; Michael et al., 1993; Padmanabhapillai et al., 2006; Porjesz and Begleiter, 1987; Rodriguez Holguin et al., 1999). Curtin and Fairchild (2003) have reported an intact parietal P3 and stimulus evaluation during alcohol intoxication but reduction in frontal components of ERP that index evaluative and regulative cognitive control processes. In a simulation study, Yeung and Cohen (2006) have interpreted reduced N2 after alcohol consumption as showing deficient processing of irrelevant stimulus information and indicated possible frontal lobe involvement. The findings of the present study are consistent with the notion of frontal lobe dysfunction observed in alcoholics. The differences between groups were statistically significant at N2 peak amplitude for Go as well as NoGo tasks at frontal and central regions, with NoGo N2 differences being larger than Go N2 differences. Therefore, the findings indicate that chronic alcoholism may be related to dysfunctional frontal activation, and this deficiency is pronounced when effortful suppression of a motor response is required.
