Abstract

Posttraumatic stress disorder (PTSD) is a universal anxiety disorder, affecting not only soldiers but also victims of every sort of traumatic stress-natural disaster, automobile collision, crime, domestic violence, bereavement. Aggressiveness, stemming from “intermittent explosive anger”, is a not infrequent comorbidity of PTSD, with the most serious consequences. The neurophysiology of aggression and anger in general, and PTSD in particular, is a jigsaw puzzle of which we are first gathering the pieces. In this chapter, PTSD is conceptualized as revolving around an idee fix of the traumatic experience, leading to fear and a derivative defensive form of aggression. The history of research in the neurophysiology of aggression and pertinent forms of memory and emotion are then reviewed, leading to a neuronal system that spans the brain. Some basic phenomena in neurophysiology are touched onsynaptic plasticity in the form of long-term potentiation of synaptic transmission, G-protein–coupled receptor modulation thereof, and the theta rhythm of the electroencephalogram-and the path we are following in our attempt to integrate these phenomena into a model of the neurophysiology of aggression in PTSD is described.

Highlights

  • Posttraumatic stress disorder (PTSD) is a universal anxiety disorder, affecting soldiers and victims of every sort of traumatic stress-natural disaster, automobile collision, crime, domestic violence, bereavement

  • A meta-analysis of 39 such studies found that aggression is a major component of PTSD [9], with severity increasing with time

  • Angry attack stemming from PTSD presents an ever-increasing danger to society as more and more troops return from Iraq and Afghanistan, the neuropsychology of PTSD is not understood

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Summary

Introduction

Posttraumatic stress disorder (PTSD) is a universal anxiety disorder, affecting soldiers and victims of every sort of traumatic stress-natural disaster, automobile collision, crime, domestic violence, bereavement. C-Fos is increased in the bed nucleus of the stria terminalis, as well as the medial amygdala and hypothalamic attack area, of rats [43] and mice [44] after the resident-intruder paradigm activation.

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