HPA Alterations in PTSD

The study of the neuroendocrinology of posttraumatic stress disorder (PTSD) has presented an interesting paradox - some of the alterations described have not historically been associated with pathological processes. In particular, initial observations of low cortisol levels in a disorder precipitated by extreme stress directly contradicted the emerging and popular formulation of hormonal responses to stress, the glucocorticoid cascade hypothesis, which posited that stress-related psychopathology involves hypercortisolism as either a cause or consequence of disorder. It is now clear that insufficient glucocorticoid signaling may produce detrimental consequences as robust as those associated with glucocorticoid toxicity. © 2007