Post-traumatic stress disorder
Post-traumatic stress disorder (PTSD)[b] is a mental and behavioral disorder[8] that develops from experiencing a traumatic event, such as sexual assault, warfare, traffic collisions, child abuse, domestic violence, or other threats on a person's life or well-being.[1][9] Symptoms may include disturbing thoughts, feelings, or dreams related to the events, mental or physical distress to trauma-related cues, attempts to avoid trauma-related cues, alterations in the way a person thinks and feels, and an increase in the fight-or-flight response.[1][4][10] These symptoms last for more than a month after the event.[1] Young children are less likely to show distress, but instead may express their memories through play.[1] A person with PTSD is at a higher risk of suicide and intentional self-harm.[2][11]
"PTSD" and "Post traumatic" redirect here. For the Mike Shinoda album, see Post Traumatic. For other uses, see PTSD (disambiguation). For CPTSD, see Complex post-traumatic stress disorder.Post-traumatic stress disorder
Disturbing thoughts, feelings, or dreams related to the event; mental or physical distress to trauma-related cues; efforts to avoid trauma-related situations; increased fight-or-flight response[1]
Suicide; cardiac, respiratory, musculoskeletal, gastrointestinal, and immunological disorders [2]
> 1 month[a]
Exposure to a traumatic event[1]
Based on symptoms[2]
Counseling, medication,[4] MDMA-assisted psychotherapy,[5] selective serotonin reuptake inhibitors[6]
8.7% (lifetime risk); 3.5% (12-month risk) (US)[7]
Most people who experience traumatic events do not develop PTSD.[2] People who experience interpersonal violence such as rape, other sexual assaults, being kidnapped, stalking, physical abuse by an intimate partner, and childhood abuse are more likely to develop PTSD than those who experience non-assault based trauma, such as accidents and natural disasters.[12][13][14] Those who experience prolonged trauma, such as slavery, concentration camps, or chronic domestic abuse, may develop complex post-traumatic stress disorder (C-PTSD). C-PTSD is similar to PTSD, but has a distinct effect on a person's emotional regulation and core identity.[15]
Prevention may be possible when counselling is targeted at those with early symptoms, but is not effective when provided to all trauma-exposed individuals regardless of whether symptoms are present.[2] The main treatments for people with PTSD are counselling (psychotherapy) and medication.[4][16] Antidepressants of the SSRI or SNRI type are the first-line medications used for PTSD and are moderately beneficial for about half of people.[6] Benefits from medication are less than those seen with counselling.[2] It is not known whether using medications and counselling together has greater benefit than either method separately.[2][17] Medications, other than some SSRIs or SNRIs, do not have enough evidence to support their use and, in the case of benzodiazepines, may worsen outcomes.[18][19]
In the United States, about 3.5% of adults have PTSD in a given year, and 9% of people develop it at some point in their life.[1] In much of the rest of the world, rates during a given year are between 0.5% and 1%.[1] Higher rates may occur in regions of armed conflict.[2] It is more common in women than men.[4]
Symptoms of trauma-related mental disorders have been documented since at least the time of the ancient Greeks.[20] A few instances of evidence of post-traumatic illness have been argued to exist from the seventeenth and eighteenth centuries, such as the diary of Samuel Pepys, who described intrusive and distressing symptoms following the 1666 Fire of London.[21] During the world wars, the condition was known under various terms, including 'shell shock', 'war nerves', neurasthenia and 'combat neurosis'.[22][23] The term "post-traumatic stress disorder" came into use in the 1970s, in large part due to the diagnoses of U.S. military veterans of the Vietnam War.[24] It was officially recognized by the American Psychiatric Association in 1980 in the third edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-III).[25]
Pathophysiology
Neuroendocrinology
PTSD symptoms may result when a traumatic event causes an over-reactive adrenaline response, which creates deep neurological patterns in the brain. These patterns can persist long after the event that triggered the fear, making an individual hyper-responsive to future fearful situations.[29][107] During traumatic experiences, the high levels of stress hormones secreted suppress hypothalamic activity that may be a major factor toward the development of PTSD.[108]
PTSD causes biochemical changes in the brain and body, that differ from other psychiatric disorders such as major depression. Individuals diagnosed with PTSD respond more strongly to a dexamethasone suppression test than individuals diagnosed with clinical depression.[109][110]
Most people with PTSD show a low secretion of cortisol and high secretion of catecholamines in urine,[111] with a norepinephrine/cortisol ratio consequently higher than comparable non-diagnosed individuals.[112] This is in contrast to the normative fight-or-flight response, in which both catecholamine and cortisol levels are elevated after exposure to a stressor.[113]
Brain catecholamine levels are high,[114] and corticotropin-releasing factor (CRF) concentrations are high.[115][116] Together, these findings suggest abnormality in the hypothalamic-pituitary-adrenal (HPA) axis.
The maintenance of fear has been shown to include the HPA axis, the locus coeruleus-noradrenergic systems, and the connections between the limbic system and frontal cortex. The HPA axis that coordinates the hormonal response to stress,[117] which activates the LC-noradrenergic system, is implicated in the over-consolidation of memories that occurs in the aftermath of trauma.[118] This over-consolidation increases the likelihood of one's developing PTSD. The amygdala is responsible for threat detection and the conditioned and unconditioned fear responses that are carried out as a response to a threat.[59]
The HPA axis is responsible for coordinating the hormonal response to stress.[59] 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.[119]
PTSD has been hypothesized to be a maladaptive learning pathway to fear response through a hypersensitive, hyperreactive, and hyperresponsive HPA axis.[120]
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.[121] 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.[108] 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. Studies have shown people with PTSD demonstrate reduced levels of NPY, possibly indicating their increased anxiety levels.[59]
Other studies indicate that people with PTSD have chronically low levels of serotonin, which contributes to the commonly associated behavioral symptoms such as anxiety, ruminations, irritability, aggression, suicidality, and impulsivity.[122] Serotonin also contributes to the stabilization of glucocorticoid production.
Dopamine levels in a person with PTSD can contribute to symptoms: low levels can contribute to anhedonia, apathy, impaired attention, and motor deficits; high levels can contribute to psychosis, agitation, and restlessness.[122]
Several studies described elevated concentrations of the thyroid hormone triiodothyronine in PTSD.[123] This kind of type 2 allostatic adaptation may contribute to increased sensitivity to catecholamines and other stress mediators.
Hyperresponsiveness in the norepinephrine system can also be caused by continued exposure to high stress. Overactivation of norepinephrine receptors in the prefrontal cortex can be connected to the flashbacks and nightmares frequently experienced by those with PTSD. A decrease in other norepinephrine functions (awareness of the current environment) prevents the memory mechanisms in the brain from processing the experience, and emotions the person is experiencing during a flashback are not associated with the current environment.[122]
There is considerable controversy within the medical community regarding the neurobiology of PTSD. A 2012 review showed no clear relationship between cortisol levels and PTSD. The majority of reports indicate people with PTSD have elevated levels of corticotropin-releasing hormone, lower basal cortisol levels, and enhanced negative feedback suppression of the HPA axis by dexamethasone.[59][124]