Linking the neuroendocrinology of post-traumatic stress disorder with recent neuroanatomic findings.
It has been hypothesized that stress damages the hippocampus and results in myriad other deleterious consequences owing to the toxic effects of cortisol, presumed to be released in excess in response to traumatic stress. Several studies have now demonstrated that hippocampal volumes of trauma survivors with post-traumatic stress disorder (PTSD) are reduced compared to those of nontraumatized persons. Interestingly, however, there is little evidence of increased cortisol release in either the acute or chronic aftermath of stress in trauma survivors who develop this disorder, raising questions about the etiology of the smaller hippocampal volumes as well as the relationship between the neuroendocrine and neuroanatomic alterations in PTSD. This article will review hypothalamic-pituitary-adrenal alterations in PTSD in an attempt to link the neuroendocrine findings with the observation of reduced hippocampal volume. It will be argued that the resolution of the neuroendocrine and neuroanatomic alterations in PTSD depends on understanding the pivotal role of glucocorticoids and their action at glucocorticoid receptors at target brain areas in response to stress and in PTSD.
Yehuda
R
R
Department of Psychiatry, Mount Sinai School of Medicine and Bronx Veterans Affairs Hospital, New York, NY, USA.
D000818:Animals; D006801:Humans; D009420:Nervous System / Q000473:pathology* / Q000503:physiopathology*; D009490:Neurosecretory Systems / Q000473:pathology* / Q000503:physiopathology*; D013313:Stress Disorders, Post-Traumatic / Q000473:pathology* / Q000503:physiopathology*