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Neurobiological correlates of antisocial personality traits - research findings and treatment implications

Published online by Cambridge University Press:  16 April 2020

B.A. Vollm
Affiliation:
Neuroscience and Psychiatry Unit, University of Manchester, Manchester, United Kingdom
M. Dolan
Affiliation:
Neuroscience and Psychiatry Unit, University of Manchester, Manchester, United Kingdom
P. Richardson
Affiliation:
Neuroscience and Psychiatry Unit, University of Manchester, Manchester, United Kingdom
S. McKie
Affiliation:
Neuroscience and Psychiatry Unit, University of Manchester, Manchester, United Kingdom
R. Elliott
Affiliation:
Neuroscience and Psychiatry Unit, University of Manchester, Manchester, United Kingdom
S. Williams
Affiliation:
Neuroscience and Psychiatry Unit, University of Manchester, Manchester, United Kingdom
I. Anderson
Affiliation:
Neuroscience and Psychiatry Unit, University of Manchester, Manchester, United Kingdom
J.F.W. Deakin
Affiliation:
Neuroscience and Psychiatry Unit, University of Manchester, Manchester, United Kingdom

Abstract

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Background and Aims

There is increasing evidence for a neurobiological basis of antisocial personality disorder (ASPD), includinggenetic liability, aberrant serotonergic function, neuropsychological deficits and structural and functional brain abnormalities. However, few functional brain imaging studies have been conducted using tasks of clinically relevant functions such as impulse control and reinforcement processing. Here we report on a study investigating the neural basis of behavioural inhibition and reward sensitivity in ASPD using functional magnetic resonance imaging (fMRI).

Methods

17 medication-free male individuals with DSM IV ASPD and 14 healthy controls were included. All subjects were screened for Axis I pathology and substance misuse. Scanner tasks included two block design tasks: one Go/No-Go task and one reward task. Scanning was carried out on a 1.5T Phillips system. Whole brain coverage was achieved using 40 axial slices with 3.5mm spacing a TR of 5 seconds. Data were analysed using SPM5 using random effects models.

Results

Results of the Go/No-Go task confirmed brain activation previously described in the processing of impulse inhibition, namely in the orbitofrontal and dorsolateral prefrontal cortex and the anterior cingulate, and these were enhanced in the PD group. The reward task was associated with BOLD response changes in the reward network in both groups. However, these BOLD responses were reduced in the ASPD group, particularly in prefrontal areas.

Conclusions

Our results further support the notion of prefrontal dysfunction in ASPD. However, contrary to previous studies suggesting “hypofrontality” in this disorder, we found task specific increased and decreased BOLD responses.

Type
S09. Symposium: Neurobiological Factors in Antisocial Disorders: Research, Clinical and Ethical Implications (Organised by the AEP Section on Forensic Psychiatry)
Copyright
Copyright © European Psychiatric Association 2007
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