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. These findings are evident in the head plots of surface potentials (frontocentral focus of N2 with weaker strength in alcoholics; Figure 3b) and the sLORETA statistical difference brain maps of current density (less differential activation in the brain areas of alcoholics, Figures 5c, d). Furthermore, sLORETA findings suggest that the difference in current density between groups is significant only for the NoGo condition in the N2 time range. This finding, along with the observation of Go as well as NoGo N2 being anterior-central and significantly reduced amplitude in alcoholics compared to normal controls, suggests dysfunctional frontal activation in alcoholics.
