This paved the way for a more comprehensive understanding of causes of PTSD. After PTSD became an official psychiatric diagnosis with the publication of DSM-III (1980), the number of personal injurylawsuits (tort claims) asserting the plaintiff had PTSD increased rapidly. However, triers of fact (judges and juries) often regarded the PTSD diagnostic criteria as imprecise, a view shared by legal scholars, trauma specialists, forensic psychologists, and forensic psychiatrists. Professional discussions and debates in academic journals, at conferences, and between thought leaders, led to a more clearly-defined set of diagnostic criteria in DSM-IV, particularly the definition of a "traumatic event".The DSM-IV classified PTSD under anxiety disorders, but the DSM-5 created a new category called "trauma and stressor-related disorders", in which PTSD is now classified. Terminology
The Diagnostic and Statistical Manual of Mental Disorders does not hyphenate "post" and "traumatic", thus, the DSM-5 lists the disorder as posttraumatic stress disorder. However, many scientific journal articles and other scholarly publications do hyphenate the name of the disorder, viz., "post-traumatic stress disorder". Dictionaries also differ with regard to the preferred spelling of the disorder with the Collins English Dictionary – Complete and Unabridged using the hyphenated spelling, and the American Heritage Dictionary of the English Language, Fifth Edition and the Random House Kernerman Websters College Dictionary giving the non-hyphenated spelling.Some authors have used the terms "post-traumatic stress syndrome" or "post-traumatic stress symptoms" ("PTSS"), or simply "post-traumatic stress" ("PTS") in the case of the U.S. Department of Defense, to avoid stigma associated with the word "disorder".
The amygdala is responsible for threat detection and the conditioned and unconditioned fear responses that are carried out as a response to a threat.The HPA axis is responsible for coordinating the hormonal response to stress. Given the strong cortisol suppression to dexamethasone in PTSD, HPA axis abnormalities are likely predicated on strong negative feedback inhibition of cortisol, itself likely due to an increased sensitivity of glucocorticoid receptors. PTSD has been hypothesized to be a maladaptive learning pathway to fear response through a hypersensitive, hyperreactive, and hyperresponsive HPA axis.Low cortisol levels may predispose individuals to PTSD: Following war trauma, Swedish soldiers serving in Bosnia and Herzegovina 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. Because cortisol is normally important in restoring homeostasis after the stress response, it is thought that trauma survivors with low cortisol experience a poorly contained—that is, longer and more distressing—response, setting the stage for PTSD. It is thought that the locus coeruleus-noradrenergic system mediates the over-consolidation of fear memory. High levels of cortisol reduce noradrenergic activity, and because people with PTSD tend to have reduced levels of cortisol, it has been proposed that individuals with PTSD cannot regulate the increased noradrenergic response to traumatic stress. Intrusive memories and conditioned fear responses are thought to be a result of the response to associated triggers. Neuropeptide Y (NPY) has been reported to reduce the release of norepinephrine and has been demonstrated to have anxiolytic properties in animal models.