Abstract
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.
Keywords
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Article Info
Publication History
Published online: April 12, 2018
Accepted:
April 5,
2018
Received in revised form:
March 7,
2018
Received:
November 27,
2017
Identification
Copyright
© 2018 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.