Severe traumatic experiences—particularly those involving criminal victimization—can trigger a range of stress responses and, in more serious cases, lead to the development of post-traumatic stress disorder (PTSD). The diverse symptoms of PTSD have been increasingly understood as forming distinct clusters, each associated with unique neural substrates. Based on these findings, the concept of a “dissociative subtype” of PTSD has been introduced in the DSM-5 (Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition) by the American Psychiatric Association. In dissociative PTSD, excessive inhibition of the amygdala by the ventromedial prefrontal cortex (vmPFC) is observed—markedly different from the hyperactivity of the amygdala typically seen in conventional PTSD. While conventional PTSD symptoms can be characterized as a “fear ON” state, dissociative symptoms can be viewed as a “fear OFF” state. These antagonistic symptom profiles should be conceptualized not as separate clusters, but rather as opposing patterns within a unified framework. To capture this structure, we have adopted a dimensional approach, organizing symptoms along a small number of key axes. In this article, we examine the neural and biological bases underlying these dimensions and their dynamics, with a particular focus on the “Reciprocal Inhibition Model” proposed by the author. Finally, we discuss how comparisons between the neural dynamics of offenders and those with PTSD may shed light on the intergenerational cycle of abuse and the propagation of criminal behavior.
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