This study reports the development of the Reactive-Proactive Aggression Questionnaire (RPQ), and the differential correlates of these two forms of aggression. Antisocial, psychosocial and personality measures were obtained at ages 7 and 16 years in schoolboys, while the RPQ was administered to 334 of the boys at age 16 years. Confirmatory factor analysis indicated a significant fit for a twofactor proactive-reactive model that replicated from one independent subsample to another. Proactive aggression was uniquely characterized at age 7 by initiation of fights, strong-arm tactics, delinquency, poor school motivation, poor peer relationships, single-parent status, psychosocial adversity, substance-abusing parents, and hyperactivity, and at age 16 by a psychopathic personality, blunted affect, delinquency, and serious violent offending. Reactive aggression was uniquely characterized at age 16 by impulsivity, hostility, social anxiety, lack of close friends, unusual perceptual experiences, and ideas of reference. Findings confirm and extend the differential correlates of proactive-reactive aggression, and demonstrate that this brief but reliable and valid self-report instrument can be used to assess proactive and reactive aggression in child and adolescent samples.

In science, theories lend coherence to vast amounts of descriptive information. However, current diagnostic approaches in psychopathology are primarily atheoretical, emphasizing description over etiological mechanisms. We describe the importance of Polyvagal Theory toward understanding the etiology of emotion dysregulation, a hallmark of psychopathology. When combined with theories of social reinforcement and motivation, Polyvagal Theory specifies etiological mechanisms through which distinct patterns of psychopathology emerge. In this paper, we summarize three studies evaluating autonomic nervous system functioning in children with conduct problems, ages 4-18. At all age ranges, these children exhibit attenuated sympathetic nervous system responses to reward, suggesting deficiencies in approach motivation. By middle school, this reward insensitivity is met with inadequate vagal modulation of cardiac output, suggesting additional deficiencies in emotion regulation. We propose a biosocial developmental model of conduct problems in which inherited impulsivity is amplified through social reinforcement of emotional lability. Implications for early intervention are discussed.

Although antisocial personality disorder (ASPD) is more common among males and borderline personality disorder (BPD) is more common among females, some (e.g., Paris, 1997) have suggested that the two disorders reflect multifinal outcomes of a single etiology. This assertion is based on several overlapping symptoms and features, including trait impulsivity, emotional lability, high rates of depression and suicide, and a high likelihood of childhood abuse and/or neglect. Furthermore, rates of ASPD are elevated in the first degree relatives of those with BPD, and concurrent comorbidity rates for the two disorders are high. In this article, we present a common model of antisocial and borderline personality development. We begin by reviewing issues and problems with diagnosing and studying personality disorders in children and adolescents. Next, we discuss dopaminergic and serotonergic mechanisms of trait impulsivity as predisposing vulnerabilities to ASPD and BPD. Finally, we extend shared risk models for ASPD and BPD by specifying genetic loci that may confer differential vulnerability to impulsive aggression and mood dysregulation among males and impulsive self-injury and mood dysregulation among females. Although the precise mechanisms of these sex-moderated genetic vulnerabilities remain poorly understood, they appear to interact with environmental risk factors including adverse rearing environments to potentiate the development of ASPD and BPD. Keywordsantisocial; borderline; multifinality; genetics; environment Antisocial personality disorder (ASPD) and borderline personality disorder (BPD) are among the most costly public health concerns confronting the US criminal justice and healthcare systems. Although ASPD affects only 3-6% of adult males and 1% of adult females (American

Numerous studies have revealed autonomic underarousal in conduct-disordered adolescents and antisocial adults. It is unknown, however, whether similar autonomic markers are present in at-risk preschoolers. In this study, the authors compared autonomic profiles of 4- to 6-year-old children with attention-deficit/hyperactivity disorder (ADHD) and oppositional defiant disorder (ODD; n = 18) with those of age-matched controls (n = 20). Children with ADHD and ODD exhibited fewer electrodermal responses and lengthened cardiac preejection periods at baseline and during reward. Although group differences were not found in baseline respiratory sinus arrhythmia, heart rate changes among ADHD and ODD participants were mediated exclusively by parasympathetic withdrawal, with no independent sympathetic contribution. Heart rate changes among controls were mediated by both autonomic branches. These results suggest that at-risk preschoolers are autonomically similar to older externalizing children.

Most contemporary accounts of psychopathology acknowledge the importance of both biological and environmental influences on behavior. In developmental psychopathology, multiple etiological mechanisms for psychiatric disturbance are well recognized, including those operating at genetic, neurobiological, and environmental levels of analysis. However, neuroscientific principles are rarely considered in current approaches to prevention or intervention. In this article, we explain why a deeper understanding of the genetic and neural substrates of behavior is essential for the next generation of preventive interventions, and we outline 10 specific reasons why considering biological processes can improve treatment efficacy. Among these, we discuss (a) the role of biomarkers and endophenotypes in identifying those most in need of prevention; (b) implications for treatment of genetic and neural mechanisms of homotypic comorbidity, heterotypic comorbidity, and heterotypic continuity; (c) ways in which biological vulnerabilities moderate the effects of environmental experience; (d) situations in which Biology x Environment interactions account for more variance in key outcomes than main effects; and (e) sensitivity of neural systems, via epigenesis, programming, and neural plasticity, to environmental moderation across the life span. For each of the 10 reasons outlined we present an example from current literature and discuss critical implications for prevention.