of a family history of depression, topographic analyses of surface Laplacian showed that the effects of depression could be localized to the right frontal region, whereas the effects of a family history of alcoholism were localized to the left frontal area. Stewart et al. (2010) reported that lifetime depression was linked to lower CSD alpha activity of the resting EEG in left compared to right hemisphere, and suggested that asymmetry of the CSD activity derived from the resting EEG could be an endophenotype for depression. Further, as patients with depressive disorder were reported to have greater EEG alpha power (Pollock and Schneider, 1989) and abnormal regional hemispheric asymmetries of alpha (Bruder et al., 1997), Tenke et al. (2011) investigated CSD profiles for antidepressant treatment response and found that depressed patients who did not respond to treatment had significantly less posterior alpha CSD related to resting EEG compared with responders or healthy control subjects. Recently, Stewart et al. (2014) examined the capability model of frontal EEG asymmetry (Coan et al., 2006), which suggests that brain activity during emotional challenge is a more powerful indicator of predispositions toward psychopathology than activity observed at rest. They assessed EEG during a resting baseline and
