The Acute Stress Response Following Motor Vehicle Accidents and Its Relation to PTSD

This study aimed to identify acute biological stress responses in trauma victims and to determine their contribution to the development of psychiatric illness, especially posttraumatic stress disorder (PTSD). Abnormalities of the hypothalamic-pituitaryadrenal (HPA) axis have been noted in PTSD, with evidence of heightened sensitivity in the negative feedback loop. However, it is not known if some abnormality of stress response occurs at the time of the traumatic event or if the disruption of the HPA axis develops during the course of the illness. An understanding of the acute stress response in accident victims who go on to develop PTSD may provide important information about biological vulnerability to psychiatric illness and may provide a marker of “at risk” individuals.’ The HPA axis is of particular interest because cortisol is one of the primary modulators of the stress response and both cortisol and ACTH modify the consolidation of memory. In PTSD, the laying down of memories of the trauma and their recall is a central component of the disorder. Therefore, abnormalities of this axis may provide critical information about the aetiological process in this disorder. The sensitisation of the HPA axis and suppression of the dexamethasone suppression test in PTSD appears to be one of the most specific neurobiological abnormalities in PTSD. The findings of this study has general theoretical importance about the etiology of PTSD from the perspective of whether this disorder is a continuum of a normative stress response or whether it is an atypical or abnormal stress response. A question that has not been answered is whether these HPA abnormalities arise from an abnormal HPA response at the time of the trauma or whether they develop later in the course of the illness. An understanding of HPA responses at the time of trauma in individuals who later develop PTSD may give insight into biological vulnerabilities and perhaps allow identification of at risk individuals. The body of literature concerning HPA abnormalities in PTSD has concentrated on war veterans many years after the initial trauma, raising the strong possibility that intervening factors contribute to the HPA abnormalities. One small study has assessed acute