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      Understanding the development of psychopathy: progress and challenges

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      Psychological Medicine
      Cambridge University Press (CUP)

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          Abstract

          Psychopathy is an adult condition that incurs substantial societal and individual costs. Here we review neurocognitive and genetically informative studies that shed light on how and why this condition emerges. Children cannot present with psychopathy. However, the presence of callous–unemotional (CU) traits can distinguish a group of children who are at elevated risk of psychopathy in adulthood. These children display diminished empathy and guilt and show attenuated brain activation to distress cues in others. Genetically informative studies indicate that individual differences in CU traits show moderate-to-strong heritability, but that protective environmental factors can counter heritable risk. On the basis of the extant research findings, we speculate on what might represent the priorities for research over the next decade. We also consider the clinical implications of these research findings. In particular, we consider the importance of delineating what precisely works for children with CU traits (and their parents) and the ways in which intervention and prevention programs may be optimized to improve engagement as well as clinical outcomes.

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          Most cited references75

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          Psychopathy as a clinical and empirical construct.

          In this review, we focus on two major influences on current conceptualizations of psychopathy: one clinical, with its origins largely in the early case studies of Cleckley, and the other empirical, the result of widespread use of the Hare Psychopathy Checklist-Revised (PCL-R) for assessment purposes. Some investigators assert that the PCL-R, ostensibly based on Cleckley's work, has "drifted" from the construct described in his Clinical Profile. We evaluate this profile, note its basis in an unrepresentative sample of patients, and suggest that its literal and uncritical acceptance by the research community has become problematical. We also argue that the idea of construct "drift" is irrelevant to current conceptualizations of psychopathy, which are better informed by the extensive empirical research on the integration of structural, genetic, developmental, personality, and neurobiological research findings than by rigid adherence to early clinical formulations. We offer some suggestions for future research on psychopathy.
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            Development and preliminary validation of a self-report measure of psychopathic personality traits in noncriminal populations.

            Research on psychopathology has been hindered by persisting difficulties and controversies regarding its assessment. The primary goals of this set of studies were to (a) develop, and initiate the construct validation of, a self-report measure that assesses the major personality traits of psychopathy in noncriminal populations and (b) clarify the nature of these traits via an exploratory approach to test construction. This measure, the Psychopathic Personality Inventory (PPI), was developed by writing items to assess a large number of personality domains relevant to psychopathy and performing successive item-level factor analyses and revisions on three undergraduate samples. The PPI total score and its eight subscales were found to possess satisfactory internal consistency and test-retest reliability. In four studies with undergraduates, the PPI and its subscales exhibited a promising pattern of convergent and discriminant validity with self-report, psychiatric interview, observer rating, and family history data. In addition, the PPI total score demonstrated incremental validity relative to several commonly used self-report psychopathy-related measures. Future construct validation studies, unresolved conceptual issues regarding the assessment of psychopathy, and potential research uses of the PPI are outlined.
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              Reduced amygdala response to fearful expressions in children and adolescents with callous-unemotional traits and disruptive behavior disorders.

              Extensive work implicates abnormal amygdala activation in emotional facial expression processing in adults with callous-unemotional traits. However, no research has examined amygdala response to emotional facial expressions in adolescents with disruptive behavior and callous-unemotional traits. Moreover, despite high comorbidity of callous-unemotional traits and attention deficit hyperactivity disorder (ADHD), no research has attempted to distinguish neural correlates of pediatric callous-unemotional traits and ADHD. Participants were 36 children and adolescents (ages 10-17 years); 12 had callous-unemotional traits and either conduct disorder or oppositional defiant disorder, 12 had ADHD, and 12 were healthy comparison subjects. Functional MRI was used to assess amygdala activation patterns during processing of fearful facial expressions. Patterns in the callous-unemotional traits group were compared with those in the ADHD and comparison groups. In youths with callous-unemotional traits, amygdala activation was reduced relative to healthy comparison subjects and youths with ADHD while processing fearful expressions, but not neutral or angry expressions. Functional connectivity analyses demonstrated greater correlations between the amygdala and the ventromedial prefrontal cortex in comparison subjects and youths with ADHD relative to those with callous-unemotional traits. Symptom severity in the callous-unemotional traits groups was negatively correlated with connectivity between amygdala and ventromedial prefrontal cortex. This is the first study to demonstrate reduced amygdala responsiveness in youths with callous-unemotional traits. These findings support the contention that callous and unemotional personality traits are associated with reduced amygdala response to distress-based social cues.
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                Author and article information

                Journal
                applab
                Psychological Medicine
                Psychol. Med.
                Cambridge University Press (CUP)
                0033-2917
                1469-8978
                March 2018
                October 16 2017
                March 2018
                : 48
                : 04
                : 566-577
                Article
                10.1017/S0033291717002847
                29032773
                0281e456-52c0-4734-b667-385452a6d114
                © 2018
                History

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