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Biology and Posttraumatic Stress Disorder
From a biological perspective, posttraumatic stress disorder (PTSD) is seen to reflect an abnormal biological response to stress. Once established, PTSD can continue to influence biology. The classic repetitive, frightening memories of the traumatic event, for example, can feel like reexposure to the trauma, and lead to a similar cascade of biological responses that occurred at the time the event unfolded. The physiological responding, which is normal in situations of danger, becomes generalized to harmless situations in individuals with PTSD. Their bodies become hyperalert and overrespond in situations that previously they would have perceived as safe. This biological dysregulation is often linked to neuroendocrine alterations, which suggest oversensitivity to the stress hormone cortisol. Some research also suggests changes in brain morphology in areas linked to memory. This entry focuses on the biological dysregulation that characterizes PTSD.
The Stress Response
When faced with fearful stimuli, the body's sympathetic nervous system is immediately activated, resulting in an arousal of the hypothalamic-pituitary-adrenal (HPA) axis shortly afterward. Biologists describe the HPA axis as an interconnected system of hormone-producing structures that regulates the stress response in the body as well as being responsible for a number of other systems including immune responses, digestion, and mood and emotions. HPA arousal is characterized by the release of corticotrophin-releasing hormone (CRF) from the hypothalamus, adrenocorticotropic hormone (ACTH) from the pituitary, and glucocorticoids, such as corti-sol, from the adrenal glands. These hormones act in a cascade fashion to ready the body for action. Cortisol then binds to glucocorticoid receptors (GR). These are found in most neurons and glial cells in the brain with the largest density of receptors in the CA3 region of the hippocampus. Researcher Frank Svec reports that the physiological and behavioral effects of cortisol depend on the ability of cortisol to bind to glucocorticoid receptors. Alterations in the sensitivity of glucocorticoid receptors can influence the functioning of the HPA axis. Cortisol levels are also responsible for the termination of the HPA activity. The release of cortisol suppresses the release of ACTH and CRF, which in turn reduces the release of cortisol, a process called negative feedback inhibition.
The HPA and Posttraumatic Stress Disorder
Numerous studies suggest that PTSD is characterized by atypical HPA responding linked to low levels of basal cortisol and enhanced suppression of this stress hormone. A large body of research has found low levels of urinary and plasma corti-sol in trauma survivors with PTSD compared with trauma-exposed people without PTSD. Another way of assessing levels of cortisol is by looking at the effect of administering a glucocorticoid agonist, a steroid that reduces production of ACTH by binding to glucocorticoid receptors, in people with and without PTSD. This should lead to lower concentrations of cortisol in the body. Enhanced suppression of cortisol by the glucocorticoid agonist dexamethasone has been demonstrated in combat veterans with PTSD and adult survivors of childhood sexual abuse. This seems to imply that receptors for cortisol are more sensitive in PTSD sufferers than in people without the disorder.
However, these findings are inconsistent. Increased, rather than decreased, salivary cortisol has been found in domestic violence victims with PTSD, in children with PTSD, and in adult survivors of childhood sexual abuse. Conversely, other studies have failed to find any difference in baseline cortisol levels in female patients with PTSD resulting from a variety of traumas or PTSD sufferers 6 months after a motor vehicle accident when compared with trauma-exposed controls.
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