Post-traumatic stress disorder (PTSD) is a mental disorder that develops from experiencing a traumatic event. Examples include sexual assault, domestic violence, child abuse, warfare along its associated traumas, natural disaster, bereavement, traffic collision, or other traumatic events on a person's life or well-being. 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. These symptoms last for more than a month after the event and can include triggers such as misophonia. Young children are less likely to show distress, but instead may express their memories through play. Most people who experience traumatic events do not develop PTSD. 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. 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 lives. In much of the rest of the world, rates during a given year are between 0.5% and 1%. Higher rates may occur in regions of armed conflict. It is more common in women than men. A recent systematic review and meta-analysis reported that the pooled prevalence rates for ICD-11 PTSD and complex PTSD were 2% and 4%, respectively, among adults in non-war-exposed/economically developed countries/regions; they increased to 6% and 15%, respectively, in war-exposed/less economically developed countries/regions. Prevention may be possible when counselling is necessary for those with early symptoms, but is not effective when provided to all trauma-exposed individuals regardless of whether symptoms are present. The main treatments for people with PTSD are counselling (psychotherapy) and medication. Most combination therapy (psychotherapy and pharmacotherapy) does not seem to be more effective than psychotherapy alone, except for possibly MDMA-assisted psychotherapy. Benefits from medication are less than those seen with counselling. Antidepressants of the SSRI or SNRI type are the first-line medications used for PTSD and are moderately beneficial for about half of people. 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. Symptoms of trauma-related mental disorders have been documented since at least the time of the ancient Greeks. 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. During the world wars, the condition was known under various terms, including "shell shock", "war nerves", neurasthenia and 'combat neurosis'. 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. 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). alongside a growing body of clinical literature on Vietnam War veterans.
Signs and symptoms
Symptoms of PTSD generally begin within the first three months after the inciting traumatic event, but may not begin until years later. In the typical case, the individual with PTSD persistently avoids either trauma-related thoughts and emotions or discussion of the traumatic event and may even have amnesia of the event (dissociative amnesia). However, the event is commonly relived by the individual through intrusive, recurrent recollections, dissociative episodes of reliving the trauma ("flashbacks"), and nightmares (50 to 70%). While it is common to have symptoms after any traumatic event, these must persist to a sufficient degree (i.e., causing dysfunction in life or clinical levels of distress) for longer than one month after the trauma to be classified as PTSD (clinically significant dysfunction or distress for less than one month after the trauma may be acute stress disorder). Some following a traumatic event experience post-traumatic growth. The social interactions of people experiencing trauma may influence their PTSD symptoms, including critical comments by partners making the victim feel guilty.
Associated medical conditions Trauma survivors often develop depression, anxiety disorders, and mood disorders in addition to PTSD. More than 50% of those with PTSD have co-morbid anxiety, mood, or substance use disorders. Substance use disorders, such as alcohol use disorder, commonly co-occur with PTSD. Recovery from post-traumatic stress disorder or other anxiety disorders may be hindered, or the condition worsened, when substance use disorders are comorbid with PTSD. Resolving these problems can bring about improvement in an individual's mental health status and anxiety levels. PTSD has a strong association with tinnitus, and speculation exists that PTSD may cause some tinnitus seen in association with the condition. PTSD is also associated with several physical health comorbidities that involve inflammatory processes and immune system dysregulation. In children and adolescents, there is a strong association between emotional regulation difficulties (e.g., mood swings, anger outbursts, temper tantrums) and post-traumatic stress symptoms, independent of age, gender, or type of trauma. Moral injury, the feeling of moral distress, such as shame or guilt following a moral transgression, is associated with PTSD but is distinguished from it. Moral injury is associated with shame and guilt, while PTSD is associated with anxiety and fear.
Risk factors Persons considered at risk for developing PTSD include combat military personnel, survivors of natural disasters, concentration camp survivors, and survivors of violent crime. Persons employed in occupations that expose them to violence (such as soldiers) or disasters (such as emergency service workers) are also at risk. Other occupations at an increased risk include police officers, firefighters, first responders, ambulance personnel, health care professionals, train drivers, divers, journalists, and sailors, as well as people who work at banks, post offices, or in stores. The intensity of the traumatic event is also associated with a subsequent risk of developing PTSD, with experiences related to witnessed death, or witnessed or experienced torture, injury, bodily disfigurement, traumatic brain injury being highly associated with the development of PTSD. Similarly, experiences that are unexpected or in which the victim cannot escape are also associated with a high risk of developing PTSD.
Trauma
PTSD has been associated with a wide range of traumatic events. The risk of developing PTSD after a traumatic event varies by trauma type and is the highest following exposure to torture (40%) and sexual violence (11.4%), particularly rape (19.0%). Men are more likely to experience a traumatic event (of any type), but women are more likely to experience the kind of high-impact traumatic event that can lead to PTSD, such as interpersonal violence and sexual assault. Motor vehicle collision survivors, both children and adults, are at an increased risk of PTSD. Globally, about 2.6% of adults are diagnosed with PTSD following a non-life-threatening traffic accident, and a similar proportion of children develop PTSD. Risk of PTSD almost doubles to 4.6% for life-threatening auto accidents. Females were more likely to be diagnosed with PTSD following a road traffic accident, whether the accident occurred during childhood or adulthood. Post-traumatic stress reactions have been studied in children and adolescents. The rate of PTSD might be lower in children than adults, but in the absence of therapy, symptoms may continue for decades. One estimate suggests that the proportion of children and adolescents having PTSD in a non-wartorn population in a developed country may be 1% compared to 1.5% to 3% of adults. On average, 16% of children exposed to a traumatic event develop PTSD, with the incidence varying according to the type of exposure and gender. Similar to the adult population, risk factors for PTSD in children include: female gender, exposure to disasters, maladaptive coping behaviors, or lacking proper social support systems. Predictor models have consistently found that childhood trauma, chronic adversity, neurobiological differences, and familial stressors are associated with risk for PTSD after a traumatic event in adulthood. It has been difficult to find consistently predictive aspects of the events that predict, but peritraumatic dissociation has been a fairly consistent predictive indicator of the development of PTSD. Proximity to, duration of, and severity of the trauma make an impact. It has been speculated that interpersonal traumas cause more problems than impersonal ones, but this is controversial. The risk of developing PTSD is increased in individuals who are exposed to physical abuse, physical assault, or kidnapping. Women who experience physical violence are more likely to develop PTSD than men.
Intimate partner and sexual violence
An individual that has been exposed to domestic violence is predisposed to the development of PTSD. There is a strong association between the development of PTSD in mothers who experienced domestic violence during the perinatal period of their pregnancy. Those who have experienced sexual assault or rape may develop symptoms of PTSD. The likelihood of sustained symptoms of PTSD is higher if the rapist confined or restrained the person, if the person being raped believed the rapist would kill them, the person who was raped was very young or very old, and if the rapist was someone they knew. The likelihood of sustained severe symptoms is also higher if people around the survivor ignore (or are ignorant of) the rape or blame the rape survivor.
War-related trauma, refugees
Service members are exposed to traumatic events during war. After deployment, to a combat zone, exposure to life-threatening situations is common. Other common events could be injury or death, been in a serious accident or handled human remains. Military service in combat is a risk factor for developing PTSD. Around 22% of people exposed to combat develop PTSD; in about 25% of military personnel who develop PTSD, its appearance is delayed. Refugees are also at an increased risk for PTSD due to their exposure to war, hardships, and traumatic events. The rates for PTSD within refugee populations range from 4% to 86%. While the stresses of war affect everyone involved, displaced persons are more so than others. Challenges related to the overall psychosocial well-being of refugees are complex and individually nuanced. Refugees have reduced levels of well-being and a high rate of mental distress due to past and ongoing trauma. Groups that are particularly affected and whose needs often remain unmet are women, older people, and unaccompanied minors. Post-traumatic stress and depression in refugee populations also tend to affect their educational success.
Unexpected death of a loved one Sudden, unexpected death of a loved one is the most common traumatic event type reported in cross-national studies. However, the majority of people who experience this type of event will not develop PTSD. An analysis from the WHO World Mental Health Surveys found a 5.2% risk of developing PTSD after learning of the unexpected death of a loved one. Because of the high prevalence of this type of traumatic event, the unexpected death of a loved one accounts for approximately 20% of PTSD cases worldwide.
Life-threatening or severe illness Medical conditions associated with an increased risk of PTSD include cancer, heart attack, and stroke. 22% of cancer survivors present with lifelong PTSD like symptoms. Intensive-care unit (ICU) hospitalization is also a risk factor for PTSD. Some women experience PTSD from their experiences related to breast cancer and mastectomy. Loved ones of those who experience life-threatening illnesses are also at risk for developing PTSD, such as parents of a child with chronic illnesses.
Psychosis spectrum conditions Research exists that demonstrates that survivors of psychotic episodes, which exist in diseases such as schizophrenia, schizoaffective disorder, bipolar I disorder, and others, are at greater risk of developing PTSD. This is often due to the experiences one may have during and after psychosis. Such traumatic experiences include, but are not limited to, experiences in psychiatric hospitals, police interactions, social stigma, and embarrassment due to psychotic behavior, suicidal behavior and attempts, distressing delusions and hallucinations, and the fear of losing control or actual loss of control. The incidence of PTSD in survivors of psychosis may be as low as 11% and as high at 67%.
Cancer Prevalence estimates of cancer‐related PTSD range between 7% and 14%, with an additional 10% to 20% of patients experiencing subsyndromal post-traumatic stress symptoms (PTSS). Both PTSD and PTSS have been associated with increased distress and impaired quality of life, and have been reported in newly diagnosed patients as well as in long‐term survivors. The PTSD Field Trials for the Diagnostic and Statistical Manual, Fourth Edition (DSM-IV), revealed that 22% of cancer survivors present with lifetime cancer-related PTSD (CR-PTSD), endorsing cancer diagnosis and treatment as a traumatic stressor. Therefore, as the number of people diagnosed with cancer increases and cancer survivorship improves, cancer-related PTSD becomes a more prominent issue, so providing for cancer patients' physical and psychological needs becomes increasingly important.
Pregnancy-related trauma
Women who experience miscarriage are at risk of PTSD. Those who experience subsequent miscarriages have an increased risk of PTSD compared to those experiencing only one. PTSD can also occur after childbirth and the risk increases if a woman has experienced trauma before the pregnancy. Prevalence of PTSD following normal childbirth (that is, excluding stillbirth or major complications) is estimated to be between 2.8 and 5.6% at six weeks postpartum, with rates dropping to 1.5% at six months postpartum. Symptoms of PTSD are common following childbirth, with prevalence of 24–30.1% at six weeks, dropping to 13.6% at six months. Emergency childbirth is also associated with PTSD.
Natural disasters People who experience natural disasters such as floods, earthquakes, tsunamis, hurricanes, and fires can develop post-traumatic stress disorder. A literature review of studies examining PTSD following disasters between 1980 and 2007 found that the prevalence of PTSD after natural disasters was lower than the prevalence of the condition after man-made disasters. This review found prevalence rates between 3.7% to 60%. Research has shown that PTSD impacts approximately one in four earthquake survivors (23.66%). Determinants of the risk of PTSD developing after disaster include the extent of physical injury, risk of life, and number of fatalities. Geographical proximity to the epicenter of a natural disaster has been shown to contribute to people developing PTSD. Natural disasters can displace families and challenge people's sense of control and security. Mental health recovery of individuals, communities and countries after emergencies, including natural disasters, is important for social and economic reasons. Mental health emergency preparedness and response need to be effective after natural disasters.
Genetics
There is evidence that susceptibility to PTSD is hereditary. Approximately 30% of the variance in PTSD is caused by genetics alone. For twin pairs exposed to combat in Vietnam, having a monozygotic (identical) twin with PTSD was associated with an increased risk of the co-twin's having PTSD compared to dizygotic twins (non-identical twins). Women with a smaller hippocampus might be more likely to develop PTSD following a traumatic event based on preliminary findings. Research has also found that PTSD shares many genetic influences common to other psychiatric disorders. Panic and generalized anxiety disorders, and PTSD share 60% of the same genetic variance. Alcohol, nicotine, and drug dependence share greater than 40% genetic similarities. Neuroscientist Dr. Rachel Yehuda researched how psychological trauma can travel across generations, specifically focusing on trans-generational trauma with Holocaust survivors and their offspring. The researchers in her study focused on a stress gene called FKBP5 that is linked to PTSD. The results of this study underscore the genetic components of PTSD as they showed an effect on methylation of the FKBP5 gene both in the parents who experienced trauma in concentration camps, as well as their offspring.
Evolutionary perspectives Evolutionary psychiatry and Evolutionary psychology perspectives interpret PTSD symptoms as extreme or dysregulated forms of defensive responses that were advantageous in ancestral contexts. Hypervigilance, intrusive memories, and exaggerated startle responses may reflect overactivation of mechanisms designed to promote survival after trauma. While these accounts can help contextualize symptom clusters, reviews emphasize that they remain theoretical and require integration with neurobiological and psychosocial research.
Pathophysiology
Neuroendocrinology PTSD symptoms may result when a traumatic event causes an overreactive 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. During traumatic experiences, the high levels of stress hormones secreted suppress hypothalamic activity that may be a major factor toward the development of PTSD. 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. Most people with PTSD show a low secretion of cortisol and high secretion of catecholamines in urine, with a norepinephrine/cortisol ratio consequently higher than comparable non-diagnosed individuals. 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. Brain catecholamine levels are high, and corticotropin-releasing factor (CRF) concentrations are high. 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, which activates the LC-noradrenergic system, is implicated in the over-consolidation of memories that occurs in the aftermath of trauma. 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. 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 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. Studies have shown that people with PTSD demonstrate reduced levels of NPY, possibly indicating their increased anxiety levels. 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. 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. Studies have also described elevated concentrations of the thyroid hormone triiodothyronine in PTSD. 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. 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.
Neuroimmunology Studies on the peripheral immune have found dysfunction with elevated cytokine levels and a higher risk of immune-related chronic diseases among individuals with PTSD. Neuroimmune dysfunction has also been found in PTSD, raising the possibility of a suppressed central immune response due to reduced activity of microglia in the brain in response to immune challenges. Individuals with PTSD, compared to controls, have a lower increase in a marker of microglial activation (18-kDa translocator protein) following lipopolysaccharide administration. This neuroimmune suppression is also associated with greater severity of anhedonic symptoms. Researchers suggest that treatments aimed at restoring neuroimmune function could be beneficial for alleviating PTSD symptoms.
Neuroanatomy
A meta-analysis of structural MRI studies found an association with reduced total brain volume, intracranial volume, and volumes of the hippocampus, insula cortex, and anterior cingulate. Much of this research stems from PTSD in those exposed to the Vietnam War. People with PTSD have decreased brain activity in the dorsal and rostral anterior cingulate cortices and the ventromedial prefrontal cortex, areas linked to the experience and regulation of emotion. The amygdala is strongly involved in forming emotional memories, especially fear-related memories. During high stress, the hippocampus, which is associated with placing memories in the correct context of space and time and memory recall, is suppressed. According to one theory, this suppression may be the cause of the flashbacks that can affect people with PTSD. When someone with PTSD undergoes stimuli similar to the traumatic event, the body perceives the event as occurring again because the memory was never properly recorded in the person's memory. The amygdalocentric model of PTSD proposes that the amygdala is very much aroused and insufficiently controlled by the medial prefrontal cortex and the hippocampus, in particular during extinction. This is consistent with an interpretation of PTSD as a syndrome of deficient extinction ability. The basolateral nucleus (BLA) of the amygdala is responsible for the comparison and development of associations between unconditioned and conditioned responses to stimuli, which results in the fear conditioning present in PTSD. The BLA activates the central nucleus (CeA) of the amygdala, which elaborates the fear response (including behavioral response to threat and elevated startle response). Descending inhibitory inputs from the medial prefrontal cortex (mPFC) regulate the transmission from the BLA to the CeA, which is hypothesized to play a role in the extinction of conditioned fear responses. While as a whole, amygdala hyperactivity is reported by meta-analysis of functional neuroimaging in PTSD, there is a large degree of heterogeneity, more so than in social anxiety disorder or phobic disorder. Comparing dorsal (roughly the CeA) and ventral (roughly the BLA) clusters, hyperactivity is more robust in the ventral cluster, while hypoactivity is evident in the dorsal cluster. The distinction may explain the blunted emotions in PTSD (via desensitization in the CeA) as well as the fear-related component. In a 2007 study, Vietnam War combat veterans with PTSD showed a 20% reduction in the volume of their hippocampus compared with veterans who did not have such symptoms. This finding was not replicated in chronic PTSD patients traumatized at an air show plane crash in 1988 (Ramstein, Germany). Evidence suggests that endogenous cannabinoid levels are reduced in PTSD, particularly anandamide, and that cannabinoid receptors (CB1) are increased to compensate. There appears to be a link between increased CB1 receptor availability in the amygdala and abnormal threat processing and hyperarousal, but not dysphoria, in trauma survivors. A 2020 study found no evidence for conclusions from prior research that suggested low IQ is a risk factor for developing PTSD.
Diagnosis NICE recommends clinicians familiarise themselves with the range of symptoms associated with functional impairment and events that are known to contribute to the development of PTSD. It is advised to ask specific questions when assessing and to consider the frequency of traumatic events experienced. Assessment should be comprehensive, including an assessment of physical, psychological, and social needs and a risk assessment. PTSD can be difficult to diagnose because of:
the subjective nature of most of the diagnostic criteria (although this is true for many mental disorders); the potential for over-reporting, e.g., while seeking disability benefits, or when PTSD could be a mitigating factor at criminal sentencing the potential for under-reporting, e.g., stigma, pride, fear that a PTSD diagnosis might preclude certain employment opportunities; symptom overlap with other mental disorders such as obsessive compulsive disorder and generalized anxiety disorder; association with other mental disorders such as major depressive disorder and generalized anxiety disorder; substance use disorders, which often produce some of the same signs and symptoms as PTSD; and substance use disorders can increase vulnerability to PTSD or exacerbate PTSD symptoms or both; and PTSD increases the risk of developing substance use disorders. the differential expression of symptoms culturally (specifically with respect to avoidance and numbing symptoms, distressing dreams, and somatic symptoms)
Screening There are a number of PTSD screening instruments for adults, such as the PTSD Checklist for DSM-5 (PCL-5) and the Primary Care PTSD Screen for DSM-5 (PC-PTSD-5). The 17 item PTSD checklist is also capable of monitoring the severity of symptoms and the response to treatment. There are also several screening and assessment instruments for use with children and adolescents. These include the Child PTSD Symptom Scale (CPSS), Child Trauma Screening Questionnaire, and UCLA Post-traumatic Stress Disorder Reaction Index for DSM-IV. In addition, there are also screening and assessment instruments for caregivers of very young children (six years of age and younger). These include the Young Child PTSD Screen, the Young Child PTSD Checklist, and the Diagnostic Infant and Preschool Assessment.
Assessment Evidence-based assessment principles, including a multimethod assessment approach, form the foundation of PTSD assessment. Those who conduct assessments for PTSD may use various clinician-administered interviews and instruments to provide an official PTSD diagnosis. Some commonly used, reliable, and valid assessment instruments for PTSD diagnosis, in accordance with the DSM-5, include the Clinician-Administered PTSD Scale for the DSM-5 (CAPS-5), PTSD Symptom Scale Interview (PSS-I-5), and Structured Clinical Interview for DSM-5 – PTSD Module (SCID-5 PTSD Module).
In the DSM and ICD PTSD was classified as an anxiety disorder in the DSM-IV, but has since been reclassified as a "trauma- and stressor-related disorder" in the DSM-5. The DSM-5 diagnostic criteria for PTSD include four symptom clusters: re-experiencing, avoidance, negative alterations in cognition/mood, and alterations in arousal and reactivity. The International Classification of Diseases and Related Health Problems, 10th Revision (ICD-10) classifies PTSD (code F43.1) under "Reaction to severe stress, and adjustment disorders". The ICD-10 criteria for PTSD include re-experiencing, avoidance, and either increased reactivity or inability to recall certain details related to the event. The ICD-11 diagnostic description for PTSD (code 6B40) contains three components or symptom groups (1) re-experiencing, (2) avoidance, and (3) heightened sense of threat. ICD-11 no longer includes verbal thoughts about the traumatic event as a symptom. There is a predicted lower rate of diagnosed PTSD using ICD-11 compared to ICD-10 or DSM-5. ICD-11 also proposes identifying a distinct subgroup with Complex Post-Traumatic Stress Disorder (CPTSD; code 6B41), who have more often experienced several or sustained traumas and have greater functional impairment than those with PTSD.
Differential diagnosis A diagnosis of PTSD requires that the person has been exposed to an extreme stressor. Any stressor can result in a diagnosis of adjustment disorder, and it is an appropriate diagnosis for a stressor and a symptom pattern that does not meet the criteria for PTSD. The symptom pattern for acute stress disorder must occur and be resolved within four weeks of the trauma. If it lasts longer, and the symptom pattern fits the characteristics of PTSD, the diagnosis may be changed. Obsessive–compulsive disorder (OCD) may be diagnosed for intrusive thoughts that are recurring but not related to a specific traumatic event. In extreme cases of prolonged, repeated traumatization where there is no viable chance of escape, survivors may develop complex post-traumatic stress disorder. This occurs as a result of layers of trauma rather than a single traumatic event, and includes additional symptomatology, such as the loss of a coherent sense of self.
Prevention
Modest benefits have been seen from early access to cognitive behavioral therapy. Critical incident stress management has been suggested as a means of preventing PTSD, but subsequent studies suggest it may produce negative outcomes. A 2019 Cochrane review did not find evidence to support the use of intervention and that "multiple session interventions may result in worse outcomes than no intervention, for some individuals." The World Health Organization recommends against the use of benzodiazepines and antidepressants for acute stress (symptoms lasting less than one month). Some evidence supports the use of hydrocortisone for prevention in adults, although there is limited or no evidence supporting propranolol, escitalopram, temazepam, or gabapentin.
Psychological debriefing
Trauma-exposed individuals often receive treatment called psychological debriefing in an effort to prevent PTSD, which consists of interviews that are meant to allow individuals to directly confront the event and share their feelings with the counselor and to help structure their memories of the event. However, several meta-analyses found that psychological debriefing is unhelpful, is potentially harmful and does not reduce the future risk of developing PTSD. This is true for both single-session debriefing and multiple session interventions. As of 2017 the American Psychological Association assessed psychological debriefing as No Research Support/Treatment is Potentially Harmful.
Early intervention Trauma-focused intervention delivered within days or weeks of the potentially traumatic event has been found to decrease PTSD symptoms. Similar to psychological debriefing, the goal of early intervention is to lessen the intensity and frequency of stress symptoms, to prevent new-onset or relapsed mental disorders and further distress later in the healing process.
Risk-targeted interventions
Risk-targeted interventions are those that attempt to mitigate specific formative information or events. It can target modeling normal behaviors, instruction on a task, or giving information on the event.
Management
Combination therapy Most combination therapy (psychological and pharmacotherapy) does not seem to be more effective than psychological therapy alone, except for possibly MDMA-assisted psychotherapy. Fourteen systematic reviews of up to 353 participants suggest MDMA-assisted psychotherapy may substantially improve PTSD symptoms, response, and remission rates compared to psychotherapy alone, but the evidence is low to very low certainty and safety data are limited, with some increased transient adverse events. Canada regulates limited distribution of MDMA upon application to and approval by Health Canada. In Australia, it may be prescribed in the treatment of PTSD by specifically authorized psychiatrists. Although once considering MDMA as a "breakthrough therapy", the FDA rejected it for treating PTSD in 2024, citing trial design and safety concerns. According to some reviews, MDMA-assisted psychotherapy reduces PTSD symptoms compared with control therapies and demonstrates a generally tolerable safety profile; its applicability is tempered by small sample sizes and adverse effects. The possible therapeutic effects of MDMA may be overestimated due to participant unblinding and expectancy biases.
Counselling The approaches with the strongest evidence include behavioral and cognitive-behavioral therapies such as prolonged exposure therapy, cognitive processing therapy (CPT), and eye movement desensitization and reprocessing (EMDR). There is some evidence for brief eclectic psychotherapy (BEP), narrative exposure therapy (NET), and written exposure therapy. A 2019 Cochrane review evaluated couples and family therapies compared to no care and individual and group therapies for the treatment of PTSD. There were too few studies on couples therapies to determine if substantive benefits were derived, but preliminary RCTs suggested that couples therapies may be beneficial for reducing PTSD symptoms. A meta-analytic comparison of EMDR and CBT found both protocols indistinguishable in terms of effectiveness in treating PTSD; however, "the contribution of the eye movement component in EMDR to treatment outcome" is unclear. A meta-analysis in children and adolescents also found that EMDR was as efficacious as CBT. Children with PTSD are far more likely to pursue treatment at school (because of its proximity and ease) than at a free clinic.
Cognitive behavioral therapy
CBT seeks to change the way a person feels and acts by changing the patterns of thinking or behavior, or both, responsible for negative emotions. Results from a 2018 systematic review found high strength of evidence that supports CBT-exposure therapy efficacious for a reduction in PTSD and depression symptoms, as well as the loss of PTSD diagnosis. CBT has been proven to be an effective treatment for PTSD and is currently considered the standard of care for PTSD by the United States Department of Defense. In CBT, individuals learn to identify thoughts that make them feel afraid or upset and replace them with less distressing thoughts. The goal is to understand how certain thoughts about events cause PTSD-related stress. A study assessing an online version of CBT for people with mild-to-moderate PTSD found that the online approach was as effective as, and cheaper than, the same therapy given face-to-face. A 2021 Cochrane review assessed the provision of CBT in an Internet-based format found similar beneficial effects for Internet-based therapy as in face-to-face. However, the quality of the evidence was low due to the small number of trials reviewed. Exposure therapy is a type of cognitive behavioral therapy that involves assisting trauma survivors to re-experience distressing trauma-related memories and reminders to facilitate habituation and successful emotional processing of the trauma memory. Most exposure therapy programs include both imaginal confrontation with the traumatic memories and real-life exposure to trauma reminders; this type of CBT has shown benefit in the treatment of PTSD. Some organizations have endorsed the need for exposure. The U.S. Department of Veterans Affairs has been actively training mental health treatment staff in prolonged exposure therapy and cognitive processing therapy in an effort to better treat U.S. veterans with PTSD. Recent research on contextually based third-generation behavior therapies suggests that they may produce results comparable to some of the better validated therapies. Many of these therapy methods have a significant element of exposure and have demonstrated success in treating the primary problems of PTSD and co-occurring depressive symptoms.
Eye movement desensitization and reprocessing
Eye movement desensitization and reprocessing (EMDR) is a form of psychotherapy developed and studied by Francine Shapiro. She had noticed that, when she was thinking about disturbing memories herself, her eyes were moving rapidly. When she brought her eye movements under control while thinking, the thoughts were less distressing. In 2002, Shapiro and Maxfield published a theory of why this might work, called adaptive information processing. This theory proposes that eye movement can be used to facilitate emotional processing of memories, changing the person's memory to attend to more adaptive information. The therapist initiates voluntary rapid eye movements while the person focuses on memories, feelings or thoughts about a particular trauma. The therapist uses hand movements to get the person to move their eyes backward and forward, but hand-tapping or