Padmanabhapillai et al. [158] investigated early evoked gamma activity (during the first 150 ms poststimulus activity) using a visual oddball task. They found that alcoholic subjects showed significantly decreased evoked gamma activity at frontal regions during target processing compared to nonalcoholic controls. The authors suggested that this reduction in early evoked gamma response at frontal locations may be due to frontal lobe dysfunction associated with deficient top-down processing mechanisms in alcoholics. The authors further conducted a similar study in children of alcoholics (14-17 years) compared to an age-matched nonalcoholic control group [159]. They found that offspring of alcoholics, similar to alcoholics, showed significant reductions in early evoked gamma activity in frontal as well as parietal regions for the target condition, with the maximum difference in the parietal region. Additionally, high-risk offspring exhibited less differentiation between target and non-target conditions in terms of level of gamma activity, indicating a further deficiency in stimulus discrimination processes. It is likely that a dysfunctional frontoparietal attentional network may underlie this deficit as shown in an fMRI study during a visual oddball task in high-risk subjects, reported by Rangaswamy et al. [15].
