Dysfunctions of medial and lateral orbitofrontal cortex in psychopathy

Research output: Chapter in Book/Report/Conference proceedingConference contribution

77 Scopus citations

Abstract

Psychopathy is a developmental disorder marked by emotional hypo-responsiveness and an increased risk for instrumental and reactive aggression. In this paper, it will be argued that the developmental origins of psychopathy do not lie in orbitofrontal cortex (OFC) dysfunction. This is because the key functional impairments seen in psychopathy are associated with amygdala damage, not with OFC damage. However, it will be argued that the role played by the integrated functioning of the amygdala and medial OFC in stimulus-reinforcement learning and decision making is disrupted in psychopathy. Impaired learning of stimulus-reinforcement associations and representation of reinforcement expectations are thought to underlie the impairments in socialization and appropriate decision making seen in psychopathy. It is suggested that the impairment in the role of medial OFC in prediction error signaling and the detection of contingency change may underlie the impairments in flexible behavioral change seen in psychopathy.

Original languageEnglish (US)
Title of host publicationLinking affect to Action
Subtitle of host publicationCritical Contributions to the Orbitofrontal Cortex
PublisherBlackwell Publishing Inc.
Pages461-479
Number of pages19
ISBN (Print)9781573316835
DOIs
StatePublished - Dec 2007

Publication series

NameAnnals of the New York Academy of Sciences
Volume1121
ISSN (Print)0077-8923
ISSN (Electronic)1749-6632

Keywords

  • Amygdala
  • Orbitofrontal cortex
  • Psychopathy

ASJC Scopus subject areas

  • Neuroscience(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • History and Philosophy of Science

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  • Cite this

    Blair, R. J. R. (2007). Dysfunctions of medial and lateral orbitofrontal cortex in psychopathy. In Linking affect to Action: Critical Contributions to the Orbitofrontal Cortex (pp. 461-479). (Annals of the New York Academy of Sciences; Vol. 1121). Blackwell Publishing Inc.. https://doi.org/10.1196/annals.1401.017