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Neurobiology of Persistent Violent Offending

Sarah Gregory

出版	University of London, King's College London, Institute of Psychiatry, 2011
URL	http://books.google.com.hk/books?id=CaRitwAACAAJ&hl=&source=gbs_api

註釋

Violent men who exhibit a stable pattern of repetitive, aggressive behaviour, beginning in childhood are typically diagnosed with Antisocial Personality Disorder (ASPD) as adults.. The majority within this heterogeneous population are reactively aggressive and emotionally hyperaroused (ASPD-P). However, a sub-group exists who are instrumentally aggressive and emotionally hyposensitive; this group are diagnosed as psychopaths (ASPD+P). Neurobiological models have thus far, failed to identify separable neural bases for men with ASPD-P and ASPD+P. This thesis presents three imaging studies, which attempt to distinguish between these two groups and a matched group of normal community controls without offending histories. Structural Imaging revealed bilateral grey matter volume reductions in anterior medial rostral prefrontal areas and anterior temporal lobes in the ASPD+P group compared to the ASPD-P and normal control groups. Diffusion Tensor Imaging revealed disturbed diffusivity within the uncinate fasciculus, in both antisocial groups compared to the normal control group. This white matter pathway connects the ventromedial prefrontal cortex and amygdala. Functional imaging revealed aberrant brain responsivity to reinforcement information in the posterior cingulate and superior temporal cortices in the ASPD+P group compared to the ASPD-P and normal control groups. All three studies thus identified abnormalities in a series of regions associated with the processing of reinforcement information and prosocial emotions, which contribute to moral reasoning. Psychopathy is characterised by callousness and a lack of empathy underpinned by impaired moral socialisation. Our findings present a neurobiological model of impaired moral processing within ASPD+P and suggest that ASPD+P and ASPD-P should be separable diagnostic entities.