Category definition has implications for treatment. Most treatment for PTSD is currently based on symptoms. The pathophysiology of the disorder remains relatively unclear, with research suggesting the involvement of the HPA axis, central monoamine regulation and endogenous opioids. The higher level of cortisol after a trauma might be protective against PTSD, a finding which may shed light on the observed gender disparity (Lamprecht & Sack, 2002). Activation of the HPA axis during acute stress is an adaptive response, but prolonged elevated glucocorticoid concentrations might lead to neuronal degeneration in areas with high densities of corticoid receptors such as the hippocampus.
This might be responsible for the reduced hippocampal volume found in people with PTSD (Hull, 2002). The underactivity of the HPA axis which is observed after exposure to chronic stress might increase vulnerability when facing future trauma. In addition to the neurophysiological disturbances exhibited by people with PTSD, there is also evidence of cognitive psychopathology: people with PTSD are more sensitive to percepts indicating threat and respond more vigorously to such cues (Cassiday et al, 1992).
Neuroimaging studies have also contributed to our understanding of the neurobiological changes seen in trauma survivors. In addition to reduced hippocampal volumes, there appears to be hyper-reactivity of the amygdala and reduced activation in the anterior cingular cortex. These findings might respectively reflect the anxiety symptoms and the reduced extinction of conditioned emotional responses which are observed in people with PTSD (Damsa et al, 2005).
In different individuals PTSD can present with either predominantly fear-based or shame-based psychological reactions, reflecting conscious and unconscious beliefs and attitudes about the self and the world. It is these schemata that are addressed using psychological therapies, whereas the autonomic effects of anxiety and depression are best addressed with medication.
Box 3 Models of psychopathology in PTSD
* Fear, anxiety and avoidance behaviour (as with phobias)
* Intrusive phenomena resemble obsessive–compulsive disorder
* Introversion and neuroticism are common personality traits in both PTSD and anxiety
* Some people improve with exposure therapy
* Sadness and grief, independent of bereavement
* Comorbidity with depression is very common
* Vegetative symptoms (loss of sleep, appetite, libido) are very similar
* Avoidance, numbing and loss of interest as in mood disorders
* Flashbacks and amnesia are common
* Considerable overlap of symptoms with borderline personality disorder
* Some overlap of symptoms with antisocial personality disorder (antisocial behaviour, irritability)
* Some evidence that trauma can induce personality change
Separate neurophysiological disorder?
* Low monoamine oxidase activity
* Increased excretion of urinary beta-endorphin
* Therapeutic response to serotonergic drugs and drugs that affect the locus ceruleus
* Deregulation of hypothalamic–pituitary–adrenal axis resulting in low cortisol levels
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Gwen Adshead and Scott Ferris
Gwen Adshead is Consultant Forensic Psychotherapist at Broadmoor Hospital (Dadd Centre, Crowthorne, Berkshire RG45 7EG, UK. Email: [email protected]). Her research interests include psychiatric ethics, moral reasoning in psychiatry and attachment histories in abusive parents. Scott Ferris is Specialist Registrar in Psychotherapy at Forest House, Walthamstow, London and was previously Specialist Registrar in Forensic Psychiatry working in the trauma service at St George’s Hospital, London. His other research interests include attachment and offence representations.