Although a 2-factor model has advanced research on the psychopathy construct, a 3-factor model was recently developed that emphasized pathological personality and eliminated antisocial behavior. However, dropping antisocial behavior from the psychopathy construct may not be advantageous. Using a large sample of psychiatric patients from the MacArthur Risk Assessment Study (J. Monahan & H. J. Steadman, 1994), the authors used confirmatory factor analysis to test a 4-factor model of psychopathy, which included interpersonal, affective, and behavioral impulsivity dimensions and an antisocial behavior dimension. Model fit was good for this 4-factor model, even when ethnicity, gender, and intelligence variables were included in the model. Structural equation modeling was used to compare the 3- and 4-factor models in predicting proximal (violence) and distal (intelligence) correlates of psychopathy.

Information on the neurobiology of empathy and callousness provides clinicians an opportunity to develop sophisticated understanding of mechanisms underpinning antisocial behavior and its counterpart, moral decision making. This paper provides an integrated in-depth review of hormones (e.g., peripheral steroid hormones like cortisol) and brain structures (e.g., insula, anterior cingulate cortex, and amygdala) implicated in empathy, callousness and psychopathic-like behavior. The overarching goal of this paper is to relate these hormones and brain structures to moral decisionmaking. This review will begin in the brain, but will then integrate information about biological functioning in the body, specifically stress-reactivity. Our aim is to integrate understanding of neural processes with hormones like cortisol, both of which have demonstrated relationships to empathy, psychopathy, and antisocial behavior. The review proposes neurobiological impairments in individuals who display little empathy are not necessarily due to a reduced ability to understand the emotions of others. Instead, evidence suggests individuals who show little arousal to the distress of others likewise show decreased physiological arousal to their own distress; one manifestation of reduced stress reactivity may be a dysfunction in empathy which supports psychopathic-like constructs (e.g., callousness). This integration will assist in the development of objective methodologies that can inform and monitor treatment interventions focused on decreasing antisocial behavior.Keywords moral decision making; psychopathy; empathy; callousness The purpose of this paper is to review and integrate the neurobiological underpinnings of empathy and callousness to promote understanding of mechanisms behind moral decisionmaking and, conversely, the development of antisocial behavior. This paper is divided into two main sections. We will begin in the brain, reviewing a triad of neurocircuitry involved in empathy as well as the unique neural signature of callousness and antisocial behavior. This section will highlight (a) brain areas that show overlapping activation across empathy-and callousness-focused investigations, and then (b) neural processes that are unique to callousness. Much of this circuitry has strong reciprocal connections with peripheral physiology, including stress-reactive hormones like cortisol. The second section will review evidence that cortisol and the hypothalamic-pituitary-adrenal (HPA) axis is (a) connected with the neurocircuitry NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript involved with empathy and/or callousness and (b) correlated with empathy or prosocial behavior as well as callous or antisocial behavior. The point of combining neural and peripheral physiology is to suggest that impairments in moral decision-making in psychopathic individuals may not directly involve impairments in the ability to feel emotions of another. The mechanism may be more basic, involving general difficulties in respondi...

The recently enacted Adam Walsh Child Protection and Safety Act will expand and standardize the registration of adolescent sex offenders. To evaluate the effectiveness of this and similar legislation, the authors assessed 91 juvenile males who had been adjudicated for a sexual felony offense and 174 juvenile males who had no history of sexual offending with several risk measures. On admission to treatment, all participants were assessed with the Psychopathy Checklist: Youth Version

No abstract

Etiological models of life-course persistent offending often emphasize behavioral explanations. Suggestions that persistent offenders have psychopathy ignore the distinct non-behavioral features of the psychopathy disorder. Using a three-factor model of the PCL-YV and cluster analysis with 259 incarcerated adolescents, we identified four distinct juvenile subtypes on the basis of affective, interpersonal, and behavioral dimensions. Prospective and retrospective comparisons of antisocial behavior patterns found the cluster comprising all three psychopathy dimensions to be the most chronic and severe. Impulsive features alone were strongly associated with severe antisocial behaviors retrospectively, but not prospectively. Findings rebut the proposal that disruptive behavioral and impulsive symptoms can identify \u22fledgling psychopaths.\u22 Assessments that disregard callous-unemotional traits will likely result in high false positive rates among serious adolescent offenders. Implications for developmental models of chronic offending are discussed in light of the need for further follow-up into adulthood