Post-traumatic stress disorder

Post-traumatic stress disorder (PTSD) is a term for the psychological consequences of exposure to or confrontation with stressful experiences, which involve actual or threatened death, serious physical injury or a threat to physical integrity and which the person found highly traumatic. It is occasionally called post-traumatic stress reaction, to emphasize that it is a fairly normal result of a traumatic experience, rather than a manifestation of a pre-existing psychological weakness on the part of the patient.

Biology of PTSD

PTSD displays biochemical changes in the brain and body, which are different from other psychiatric disorders such as major depression.

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In PTSD patients the dexamethasone cortisol suppression is strong while it is weak in patients with major depression. In most PTSD patients the urine secretion of cortisol is low, at the same time as the catecholamine secretion is high, and the norepinephrine/cortisol ratio is increased. Brain catecholamine levels are low, and corticotropin-releasing factor (CRF) concentrations are high. There is also an increased sensitivity of the hypothalamic-pituitary-adrenal (HPA) axis with a strong negative feedback of cortisol due to a generally increased sensitivity of cortisol receptors (Yehuda, 2001).

Related Topics:
Dexamethasone - Cortisol - Catecholamine - Norepinephrine - Corticotropin - Hypothalamic - Pituitary

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The response to stress in PTSD is abnormal with long-term high levels of norepinephrine, at the same time as cortisol levels are low, a pattern associated with facilitated learning in animals. Translating this reaction to human conditions gives a pathophysiological explanation for PTSD by a maladaptive learning pathway to fear response (Yehuda 2002). With this deduction follows that the clinical picture of hyperreactivity and hyperresponsiveness in PTSD is consistent with the sensitive HPA-axis.

Related Topics:
Norepinephrine - Cortisol

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Swedish UN soldiers serving in Bosnia with low pre-service salivary cortisol levels had a higher risk of reacting with PTSD symptoms following war trauma than soldiers with normal pre-service levels (Aardal-Eriksson 2001).

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Another possible factor in PTSD is that a persistence of depressive symptoms may be caused by an underlying biochemical disorder associated with insulin resistance (dysglycemia) that can be treated by a hypoglycemic diet.

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In animal research, the amygdala has been shown to be needed to form fear memories. From brain imaging studies, the amygdala has also been shown to be active in human fear. Dysfunction of the amygdala may be involved in PTSD. Further animal and clinical research into the amygdala and fear conditioning may provide additional treatments for the condition.

Related Topics:
Animal research - Amygdala - Brain imaging - Fear conditioning

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