Whether qEEG alterations and P300 decrements found in most of SUD are only a coincident “marker” of vulnerability or make a direct etiologic contribution to risk for substance dependence is still unknown (Bauer and Hesselbrok 2001; Carlson et al. 2002; O’Connor et al. 1994; Polich et al. 1994; Porjesz and Begleiter 1998). The P300 reduction and abnormal qEEG patterns are seen in mental disorders that often are comorbid with substance abuse, such as conduct disorder (Bauer and Hesselbrock 1999, 2001), ADHD (Bauer 1997; O’Connor et al. 1994), and bipolar or major affective disorder (Friedman and Squires-Wheeler 1994). Reduced P300 amplitude related to prefrontal brain dysfunction may suggest that a deficit in inhibitory control is an underlying mechanism shared by different psychopathologies (Bauer and Hesselbrock 1999; Clark et al. 1999; Tarter et al. 2003). According to Bauer (2002), certain ERP and qEEG abnormalities and impaired functioning on complex cognitive tests in patients formerly dependent on cocaine might not be proximately caused by drug use per se but be more related to comorbid alcohol use or another psychiatric condition. Taken together, the
