Primary and Secondary Variants of Psychopathy in a Volunteer Sample Are Associated With Different Neurocognitive Mechanisms.

Published

Journal Article

BACKGROUND:Recent work has indicated that there at least two distinct subtypes of psychopathy. Primary psychopathy is characterized by low anxiety and thought to result from a genetic predisposition, whereas secondary psychopathy is characterized by high anxiety and thought to develop in response to environmental adversity. Primary psychopathy is robustly associated with reduced neural activation to others' emotions and, in particular, distress. However, it has been proposed that the secondary presentation has different neurocognitive correlates. METHODS:Primary (n = 50), secondary (n = 100), and comparison (n = 82) groups were drawn from a large volunteer sample (N = 1444) using a quartile-split approach across psychopathic trait (affective-interpersonal) and anxiety measures. Participants performed a widely utilized emotional face processing task during functional magnetic resonance imaging. RESULTS:The primary group showed reduced amygdala and insula activity in response to fear. The secondary group did not differ from the comparison group in these regions. Instead, the secondary group showed reduced activity compared with the comparison group in other areas, including the superior temporal sulcus/inferior parietal lobe, thalamus, pallidum, and substantia nigra. Both psychopathy groups also showed reduced activity in response to fear in the anterior cingulate cortex. During anger processing, the secondary group exhibited reduced activity in the anterior cingulate cortex compared with the primary group. CONCLUSIONS:Distinct neural correlates of fear processing characterize individuals with primary and secondary psychopathy. The reduced neural response to fear that characterizes individuals with the primary variant of psychopathic traits is not observed in individuals with the secondary presentation. The neurocognitive mechanisms underpinning secondary psychopathy warrant further systematic investigation.

Full Text

Duke Authors

Cited Authors

  • Sethi, A; McCrory, E; Puetz, V; Hoffmann, F; Knodt, AR; Radtke, SR; Brigidi, BD; Hariri, AR; Viding, E

Published Date

  • December 2018

Published In

Volume / Issue

  • 3 / 12

Start / End Page

  • 1013 - 1021

PubMed ID

  • 29752216

Pubmed Central ID

  • 29752216

Electronic International Standard Serial Number (EISSN)

  • 2451-9030

International Standard Serial Number (ISSN)

  • 2451-9022

Digital Object Identifier (DOI)

  • 10.1016/j.bpsc.2018.04.002

Language

  • eng