In the current study, behavioral disinhibition has been characterized as a common latent factor representing a generalized vulnerability to various externalizing disorders. In contrast, alternative models have been presented in the literature that conceptualize behavioral (dis)inhibition as a heterogeneous dual process associated with two distinct, interacting neural circuits (Nigg, 2000, 2003, 2006). Specifically, Nigg (2003) argued that conduct disorder primarily involves a primary failure of reactive or motivational control process (i.e., detecting and responding to immediate contextual cues related to incentives, punishment, or social anxiety), with secondary breakdowns in effortful control of attention (Rothbart & Bates, 2006) or executive control processes. In contrast, according to Nigg, ADHD develops, in part, from a primary failure of neural systems of executive control, with secondary deficits in reactive or motivational controls. This model is put forth as a tool for examining differential developmental pathways (both biological and psychosocial) to disruptive behavior problems and other distinctions that have clinical relevance. Thus, while Nigg’s model helps to dissociate etiological mechanisms influencing ADHD versus conduct disorder, our focus here is on etiological factors explaining their association (i.e., comorbidity).
