In this study, we evaluated predictors of resilience among 8-to 12-year-old children recruited from primarily low socioeconomic status neighborhoods, 117 of whom suffered from clinical levels of conduct problems and/or depression, and 63 of whom suffered from no significant symptoms. Tests of interactions were conducted between (a) paternal antisocial behavior and maternal depression and (b) several physiological indices of child temperament and emotionality in predicting (c) children's conduct problems and depression. Both internalizing and externalizing outcomes among children were associated specifically with maternal melancholic depression, and not with nonmelancholic depression. In addition, low levels of respiratory sinus arrhythmia (RSA) among children conferred significant risk for depression, regardless of maternal melancholia, whereas high RSA offered partial protection. Furthermore, high levels of maternal melancholia conferred significant risk for child depression, regardless of paternal antisocial behavior, whereas low levels of maternal melancholia offered partial protection. Finally, low levels of electrodermal responding (EDR) conferred significant risk for conduct problems, regardless of paternal antisocial behavior, whereas high EDR offered partial protection. None of the identified protective factors offered complete immunity from psychopathology. These findings underscore the complexity of resilience and resilience-related processes, and suggest several potential avenues for future longitudinal research.Several alternative definitions of resilience have been proposed by developmental psychopathologists, yet all include some form of adaptive functioning following significant exposure to adversity (see Luthar, Cicchetti, & Becker, 2000). Adverse risk exposure is central to any definition of resilience because without such experiences, psychopathological outcomes are far less likely, so the construct loses much of its meaning (Curtis & Cicchetti, 2003;Luthar, 2006). Accordingly, most researchers agree that some form of risk exposure is necessary to infer resilience or resilience-related processes. Nevertheless, both adaptation and adversity are often defined very differently across studies, sometimes quite broadly and other times quite specifically. For example, adaptation has been defined as a set of general competencies across multiple domains of functioning including social, occupational, and psychopathological; yet it has also been defined as the absence of a specific psychiatric condition such as major depression despite a strong familial loading for mood disorders (see Luthar, 2006). From a developmental psychopathology perspective, more broad definitions of adaptation are preferred because most adversities confer risk that extends to a wide range of multifinal outcomes. For example, in addition to increasing the risk for mood disorders among offspring, maternal depression also confers risk for conduct problems, delinquency, and antisocial behavior (Boyle & Pickles, 1997;Kim-Cohen,...

Opposing theories of striatal hyper- and hypodopaminergic functioning have been suggested in the pathophysiology of externalizing behavior disorders. To test these competing theories, the authors used functional MRI to evaluate neural activity during a simple reward task in 12- to 16-year-old boys with attention-deficit/hyperactivity disorder and/or conduct disorder (n = 19) and in controls with no psychiatric condition (n = 11). The task proceeded in blocks during which participants received either (a) monetary incentives for correct responses or (b) no rewards for correct responses. Controls exhibited striatal activation only during reward, shifting to anterior cingulate activation during nonreward. In contrast, externalizing adolescents exhibited striatal activation during both reward and nonreward. Externalizing psychopathology appears to be characterized by deficits in processing the omission of predicted reward, which may render behaviors that are acquired through environmental contingencies difficult to extinguish when those contingencies change.

Adaptation to violent environments across development involves a multitude of cascading effects spanning many levels of analysis from genes to behavior. In this review, we (a) examine the potentiating effects of violence on genetic vulnerabilities and the functioning of neurotransmitter systems in producing both internalizing and externalizing psychopathology, (b) consider the impact of violence on the developing human stress and startle responses, and (c) brain development including the hippocampus and prefrontal cortex. This review integrates literature on the developmental effects of violence on rodents, non-human primates, and humans. Many neurobiological changes that are adaptive for survival in violent contexts become maladaptive in other environments, conferring life-long risk for psychopathology.

Studies addressing the neural correlates of criminal behavior have focused primarily on the prefrontal cortex and the amygdala. However, few studies have examined dopaminergic inputs to these or other brain regions, despite the fact that central dopamine (DA) dysfunction is associated with both trait impulsivity and novelty seeking. Given long-standing associations between both of these personality traits and externalizing psychopathology, the authors examined effective connectivity between the caudate nucleus and the anterior cingulate cortex, two areas that rely on DA input to facilitate associative learning and goal directed behavior. Dysfunction in top-down and bottom-up processing within this dopaminergically mediated frontostriatal circuit may be an important biological vulnerability that increases one’s likelihood of engaging in delinquent and criminal behavior. When compared with controls, reduced effective connectivity between these regions among adolescents with externalizing psychopathology was found, suggesting deficiencies in frontostriatal circuitry.

Children and adolescents with externalizing behavior disorders including attention-deficit/hyperactivity disorder (ADHD) and conduct disorder (CD) often present with symptoms of comorbid internalizing psychopathology. However, few studies have examined central nervous system correlates of such comorbidity. We evaluated interactions between externalizing and internalizing symptoms in predicting mesolimbic, septo-hippocampal, and anterior cingulate volumes among 12- to 16-year-old boys with either ADHD, ADHD and CD, or no psychiatric condition (n = 35). These regions were chosen given established links to trait impulsivity, trait anxiety, and behavior regulation, respectively. Collapsed across groups, Externalizing × Internalizing symptom interactions accounted for individual differences in gray matter densities in each region. Externalizing youth with comorbid internalizing symptoms showed smaller reductions in gray matter than individuals with externalizing psychopathology alone. These results suggest that internalizing symptoms are associated with less severe structural compromises in brain regions subserving motivation and behavior regulation among externalizing boys.