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The development of psychopathy

Authors

  • R.J.R. Blair,

    1. Mood and Anxiety Disorders Program, National Institute of Mental Health, National Institutes of Heath, Department of Health and Human Services, Bethesda, MD, USA
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  • K.S. Peschardt,

    1. Mood and Anxiety Disorders Program, National Institute of Mental Health, National Institutes of Heath, Department of Health and Human Services, Bethesda, MD, USA
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  • S. Budhani,

    1. Mood and Anxiety Disorders Program, National Institute of Mental Health, National Institutes of Heath, Department of Health and Human Services, Bethesda, MD, USA
    2. Department of Psychology, University College London, UK
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  • D.G.V. Mitchell,

    1. Mood and Anxiety Disorders Program, National Institute of Mental Health, National Institutes of Heath, Department of Health and Human Services, Bethesda, MD, USA
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  • D.S. Pine

    1. Mood and Anxiety Disorders Program, National Institute of Mental Health, National Institutes of Heath, Department of Health and Human Services, Bethesda, MD, USA
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James Blair, Unit on Affective Cognitive Neuroscience, Mood and Anxiety Disorders Program, National Institute of Mental Health, 15K North Drive, Room 206, MSC 2670, Bethesda, Maryland 20892-2670, USA; Email: blairj@intra.nimh.nih.gov

Abstract

The current review focuses on the construct of psychopathy, conceptualized as a clinical entity that is fundamentally distinct from a heterogeneous collection of syndromes encompassed by the term ‘conduct disorder’. We will provide an account of the development of psychopathy at multiple levels: ultimate causal (the genetic or social primary cause), molecular, neural, cognitive and behavioral. The following main claims will be made: (1) that there is a stronger genetic as opposed to social ultimate cause to this disorder. The types of social causes proposed (e.g., childhood sexual/physical abuse) should elevate emotional responsiveness, not lead to the specific form of reduced responsiveness seen in psychopathy; (2) The genetic influence leads to the emotional dysfunction that is the core of psychopathy; (3) The genetic influence at the molecular level remains unknown. However, it appears to impact the functional integrity of the amygdala and orbital/ventrolateral frontal cortex (and possibly additional systems); (4) Disruption within these two neural systems leads to impairment in the ability to form stimulus–reinforcement associations and to alter stimulus–response associations as a function of contingency change. These impairments disrupt the impact of standard socialization techniques and increase the risk for frustration-induced reactive aggression respectively.

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