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The Role of Preventive Interventions 447A link also has been consistently demonstrated between youth verbal deficitsand behavior problems (Kusche, Cook, & Greenberg, 1993; Lynam & Henry,2001; Lynam et al., 1993; Moffitt, 1990; Moffitt & Lynam, 1994). In addition,Lahey et al. (1995) found that verbal abilities predicted improvements in conductdisorder (CD) over a period of 4 years. At the neurological level, it is hypothesizedthat the ability to internally regulate behavior is accompanied by commensurategrowth and myelination of the neuronal pathways in the corpus callosumthat are known to mediate language function and associative thinking (Giedd et al.,1999; Thompson et al., 2000).Although the above studies demonstrate an association between deficient neurocognitiveabilities and substance abuse or other adolescent problem behavior, amajor limitation of these studies is that most are cross-sectional; neurocognitivedeficits and antisocial behavior may have occurred as a result of a third process(i.e., being reared in a family with an alcoholic parent or from chronic physicalabuse, or other prenatal or postnatal trauma). In such cases, environmental eventsmay have both shaped neurocognitive growth as well as antisocial behavior withno necessary causal link involved between the two processes.Models of Neurocognitive DevelopmentTo date, studies linking neurocognitive dysfunction to adolescent problem outcomesshed valuable light on developmental processes and highlight the potentialof neurocognitive models in formulating and assessing models of preventionand treatment during childhood and adolescence. However, clearer conceptual,multilevel models of both adolescent development and neurological growth willbe necessary to move to the next level of understanding.Moffitt (1993) provides one conceptual model that distinguishes between lifecourse-persistent(LCP) and adolescent-limited (AL) antisocial behavior. She hassuggested that AL antisocial behavior is considered to be normative, tends to desistin early adulthood, and is not considered to involve neurocognitive deficit but islikely related to peer associations and other contextual factors linked to minoradolescent delinquency and risk taking. However, children demonstrating LCPantisocial behavior are those exhibiting early, continuous, severe, and frequentantisocial behavior across situations and stages of development that may involvedeficits. Although Moffitt contends that environmental risks exacerbate the neurocognitivedeficits, thus leading to the development of persistent antisocial behavior,she contends that neurocognitive deficit is the necessary component for thedevelopment of LCP antisocial behavior.This model has been generative, but only partially supported by longitudinalstudies. Aguilar, Sroufe, Egeland, and Carlson (2000) take issue with Moffitt’s