There also appear to be individual differences in neural activation related to externalizing symptoms, psycholopathology, and affect. For example, Tarkka and colleagues (2001) reported that alerting tones were processed in the frontal lobe by violent alcohol abusers, but in medial temporal brain areas by non-violent alcohol abusers and normal subjects; violent alcohol abusers responded to deviant tones simultaneously in frontal and temporal areas, whereas these areas were affected sequentially in other groups (Tarkka et al., 2001). These findings imply alterations in arousal and involuntary adaptive processes in cortical networks associated with impulsive violent behavior and AUDs (Tarkka et al., 2001). The observation that impaired cognitive control is related to abnormal prefrontal cortex function is consistent with numerous neuroimaging and EEG studies of Attention-Deficit/Hyperactivity Disorder, Conduct Disorder, and ASPD (Seidman et al., 2004; 2005). The similarity of deficits between these two lines of research potentially points to abnormalities representing shared vulnerability to disruptive/antisocial behavior disorders and AUDs which has long been observed to co-occur clinically (Sher & Trull, 1994). Although this evidence may not provide specificity in the neural substrates implicated in AUDs as they relate to impulsivity, it does demonstrate commonalities in the dysfunction across the related disorders.
