Monday 3. June at 16:00 - 17:30 CET
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Men with antisocial personality disorder (ASPD) with or without psychopathy (+/-P) are responsible for most violent crime in society. Development of effective treatments is hindered by poor understanding of the neurochemical underpinnings of the condition. In this talk, I will outline the key findings from the OXYASP study, which explored two neurochemical aspects of ASPD: responsivity to oxytocin and Glutamate/GABA. In a placebo-controlled, randomized crossover design, 34 violent offenders (19 ASPD+P; 15 ASPD-P) and 24 healthy non-offenders received 40IU intranasal oxytocin or placebo and then completed an fMRI morphed faces task examining the implicit processing of fearful facial expressions. Increasing intensity of fearful facial expressions failed to appropriately modulate activity in the bilateral mid-cingulate cortex in violent offenders with ASPD+P, compared with those with ASPD-P. Oxytocin abolished these group differences. In the second experiment, we investigated striatal glutamate: GABA ratio using Magnetic Resonance Spectroscopy in 30 violent offenders (16 ASPD-P, 14 ASPD+P) and 21 healthy non-offenders. Men with ASPD+/-P had a significant reduction in striatal glutamate : GABA ratio compared to non-offenders. This represents the first evidence of neurochemical modulation of the empathic processing of others’ distress in psychopathy, and the first evidence of striatal Glutamate/GABA dysregulation in ASPD+/-P. I will discuss the implications of these findings, and how future studies using fMRI, MRS, and other methodologies may enhance future pharmacoimaging and work and apply neurochemical insights.