Biology of posttraumatic stress disorder.
An understanding of the biological basis of posttraumatic stress disorder (PTSD) requires an examination of the underlying neurobiology of fear and the factors that might contribute to an unsuccessful termination of the fear response in some individuals. Several factors may lead to an inadequate termination of a stress response, and the failure to contain the biological alterations initiated by stress may have long-term adverse consequences. In particular, a prolonged continuation of biological responses following stress may lead to an inappropriate pairing of the traumatic memory with distress and may then initiate a cascade of secondary biological alterations. This article examines some of the biological alterations in PTSD and develops a framework for understanding the development progression of the neurobiology of this disorder.
Yehuda
R
R
Psychiatry Department, Mount Sinai School of Medicine, Bronx Veterans Affairs, New York, NY, USA. rachel.yehuda@med.va.gov
D000223:Adaptation, Psychological / Q000502:physiology; D001341:Autonomic Nervous System / Q000503:physiopathology; D003866:Depressive Disorder / Q000175:diagnosis / Q000503:physiopathology; D005239:Fear / Q000502:physiology; D005246:Feedback / Q000502:physiology; D006624:Hippocampus / Q000033:anatomy & histology / Q000502:physiology; D006801:Humans; D006854:Hydrocortisone / Q000097:blood / Q000502:physiology; D008016:Life Change Events; D008568:Memory / Q000502:physiology; D008954:Models, Biological; D011446:Prospective Studies; D011965:Receptors, Glucocorticoid / Q000502:physiology; D013313:Stress Disorders, Post-Traumatic / Q000175:diagnosis / Q000503:physiopathology*; D013312:Stress, Physiological / Q000097:blood / Q000503:physiopathology*
D011965:Receptors, Glucocorticoid; D006854:Hydrocortisone