Investigating the neurocognition of social provocation and the role of oxytocin in violent antisocial personality disordered men with and without psychopathy
<ns3:p>Background Co-operation is a core component of human social interaction. Conflict emerges when another’s unfairness is perceived and retaliation in the form of non-cooperative behaviour or retaliatory punishment may emerge. This may be particularly relevant in men with antisocial personality disorder and psychopathy, who demonstrate impulsive behaviour and low thresholds for discharge of aggression. Methods In a sample of violent male offenders with ASPD (n= 22) with (+P, n =12) and without (-P, n= 10) psychopathy, we used a paradigm of social provocation (the Social Fairness game) in conjunction with fMRI to measure behavioural and neural response to social provocation and compared this to healthy non-offenders (n=20), and investigated the effects of intranasal oxytocin (40 I.U.), which is known to modulate social behaviours, on social provocation across groups. Results Counter to predictions, those with ASPD+/-P did not significantly differ from healthy non-offenders at the behavioural or neural level. Conclusions We discuss the potential explanations for these findings and our conclusion that this experiment has failed to provide a satisfactory model of social provocation in ASPD+/-P with which to test decisions to co-operate or retaliate, or oxytocin’s effects thereon.</ns3:p>
Authors
- Nigel Blackwood (ORCID: https://orcid.org/0000-0002-5909-203X)
- Stuart F. White (ORCID: https://orcid.org/0000-0002-4713-9267)
- E.C. Hind (ORCID: https://orcid.org/0000-0003-4724-235X)
- John Tully (ORCID: https://orcid.org/0000-0002-5858-3419)
- Julia Griem (ORCID: https://orcid.org/0000-0002-1779-5255)
- Arjun Sethi
- Steve C.R. Williams
Publication Details
- Journal
- Wellcome Open Research
- Published
- 2026-03-04
- DOI
- https://doi.org/10.12688/wellcomeopenres.25521.1
- Primary Topic
- Neuroendocrine regulation and behavior
- Type
- article
- Field-Weighted Citation Impact
- 0.00