"PTSD" redirects here. For other uses, see PTSD (disambiguation).
Posttraumatic stress disorder (PTSD)[note 1] is a mental disorder that can develop after a person is exposed to a traumatic event, such as sexual assault, warfare, traffic collisions, or other threats on a person's life. 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 how 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. Young children are less likely to show distress but instead may express their memories through play. A person with PTSD is at a higher risk for suicide and intentional self-harm.
Most people who have experienced a traumatic event will not develop PTSD. People who experience interpersonal trauma (for example rape or child abuse) are more likely to develop PTSD, as compared to people who experience non-assault based trauma such as accidents and natural disasters. About half of people develop PTSD following rape. Children are less likely than adults to develop PTSD after trauma, especially if they are under ten years of age. Diagnosis is based on the presence of specific symptoms following a traumatic event.
Prevention may be possible when therapy is targeted at those with early symptoms but is not effective when provided to all individuals whether or not symptoms are present. The main treatments for people with PTSD are counselling and medication. A number of different types of therapy may be useful. This may occur one-on-one or in a group.Antidepressants of the selective serotonin reuptake inhibitor type are the first-line medications for PTSD and result in benefit in about half of people. These benefits are less than those seen with therapy. It is unclear if using medications and therapy together has greater benefit. Other medications do not have enough evidence to support their use and in the case of benzodiazepines may worsen outcomes.
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. 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. Symptoms of trauma-related mental disorders have been documented since at least the time of the ancient Greeks. During the World Wars the condition was known under various terms including "shell shock" and "combat neurosis". The term "posttraumatic 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).
Signs and symptoms
Symptoms of PTSD generally begin within the first 3 months after the inciting traumatic event, but may not begin until years later. In the typical case, the individual with PTSD persistently avoids trauma-related thoughts and emotions, and discussion of the traumatic event, and may even have amnesia of the event. However, the event is commonly relived by the individual through intrusive, recurrent recollections, dissociative episodes of reliving the trauma ("flashbacks"), and nightmares. 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).
Associated medical conditions
Drug abuse and alcohol abuse commonly co-occur with PTSD. Recovery from posttraumatic 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.
Persons considered at risk include combat military personnel, victims of natural disasters, concentration camp survivors, and victims 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 that are at higher risk include police officers, firefighters, ambulance personnel, health care professionals, train drivers, divers, journalists, and sailors, in addition to people who work at banks, post offices or in stores. The size of the hippocampus is inversely related to post-traumatic stress disorder and treatment success; the smaller the hippocampus, the higher risk of PTSD.
See also: Psychological resilience
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 highest following exposure to sexual violence (11.4%), particularly rape (19.0%). Men are more likely to experience a traumatic event, 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.
Posttraumatic stress reactions have not been studied as well in children and adolescents as adults. The rate of PTSD may 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, and much lower below the age of 10 years. On average, 16% of children exposed to a traumatic event develop PTSD, varying according to type of exposure and gender.
Predictor models have consistently found that childhood trauma, chronic adversity, and familial stressors increase risk for PTSD as well as risk for biological markers of risk for PTSD after a traumatic event in adulthood. Experiencing bullying as a child or an adult has been correlated with the development of PTSD. Peritraumatic dissociation in children is a predictive indicator of the development of PTSD later in life. This effect of childhood trauma, which is not well understood, may be a marker for both traumatic experiences and attachment problems. Proximity to, duration of, and severity of the trauma make an impact, and interpersonal traumas cause more problems than impersonal ones.
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 violence
See also: Rape trauma syndrome
An individual that has been exposed to domestic violence is predisposed to the development of PTSD. However, being exposed to a traumatic experience does not automatically indicate that an individual will develop PTSD. There is a strong association between the development of PTSD in mothers that experienced domestic violence during the perinatal period of their pregnancy.
Those who have experienced sexual assault or rape may develop symptoms of PTSD. PTSD symptoms include re-experiencing the assault, avoiding things associated with the assault, numbness, and increased anxiety and an increased startle response. 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 him or her, the person who was raped was very young or very old, and if the rapist was someone he or she 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.
See also: Veteran and Refugee health
Military service is a risk factor for developing PTSD. Around 78% of people exposed to combat do not 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 impact everyone involved, displaced persons have been shown to be more affected than nondisplaced persons.
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 go on to 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, unexpected death of a loved one accounts for approximately 20% of PTSD cases worldwide.
Medical conditions associated with an increased risk of PTSD include cancer, heart attack, and stroke. 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.
Main article: Childbirth-related posttraumatic stress disorder
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 prior to 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 6 weeks postpartum, with rates dropping to 1.5% at 6 months postpartum. Symptoms of PTSD are common following childbirth, with prevalence of 24-30.1% at 6 weeks, dropping to 13.6% at 6 months. Emergency childbirth is also associated with PTSD. Some women experience PTSD from their experiences related to breast cancer and mastectomy.
Main article: Genetics of posttraumatic stress disorder
There is evidence that susceptibility to PTSD is hereditary. Approximately 30% of the variance in PTSD is caused from 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 twins that were dizygotic (non-identical twins). There is evidence that those with a genetically smaller hippocampus are more likely to develop PTSD following a traumatic event. 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.
Several biological indicators have been identified that are related to later PTSD development. Heightened startle responses and a smaller hippocampal volume have been identified as biomarkers for the risk of developing PTSD. Additionally, one study found that soldiers whose leukocytes had greater numbers of glucocorticoid receptors were more prone to developing PTSD after experiencing trauma.
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. 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 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 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.
Other studies indicate that people that suffer from 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 help contribute to the symptoms associated. Low levels of dopamine can contribute to anhedonia, apathy, impaired attention, and motor deficits. Increased levels of dopamine can cause psychosis, agitation, and restlessness.
Multiple studies described elevated concentrations of the thyroid hormonetriiodothyronine 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 that 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.
The three brain areas with changed function are the prefrontal cortex, amygdala, and hippocampus. Much of this research stems from PTSD victims from the Vietnam War.
PTSD patients 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 heterogeniety, 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 having suffered no such symptoms. This finding was not replicated in chronic PTSD patients traumatized at an air show plane crash in 1988 (Ramstein, Germany).
PTSD can be particularly difficult to diagnose, because numerous factors can lead to over-reporting (e.g., disability) and under-reporting (e.g., avoidance) symptoms, dysfunction and distress.
Screening and assessment
A number of screening instruments are used for screening adults for PTSD, such as the PTSD Checklist for DSM-5 (PCL-5) and the Primary Care PTSD Screen for DSM-5 (PC-PTSD-5).
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 Posttraumatic Stress Disorder Reaction Index for DSM-IV.
Diagnostic and statistical manual
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.
International classification of diseases
The International Classification of Diseases and Related Health Problems 10 (ICD-10) classifies PTSD 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.
A diagnosis of PTSD requires that the person has been exposed to an extreme stressor such as one that is life-threatening. 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, for example a partner being fired, or a spouse leaving. If any of the symptom pattern is present before the stressor, another diagnosis is required, such as brief psychotic disorder or major depressive disorder. Other differential diagnoses are schizophrenia or other disorders with psychotic features such as Psychotic disorders due to a general medical condition. Drug-induced psychotic disorders can be considered if substance abuse is involved.
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 that characteristic of PTSD, the diagnosis may be changed.
Obsessive compulsive disorder may be diagnosed for intrusive thoughts that are recurring but not related to a specific traumatic event.
See also: Traumatic memories
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 the likelihood of its producing negative outcomes. A review "...did not find any evidence to support the use of an intervention offered to everyone", and that "...multiple session interventions may result in worse outcome than no intervention for some individuals." The World Health Organization recommends against the use of benzodiazepines and antidepressants in those having experienced trauma. Some evidence supports the use of hydrocortisone for prevention in adults, however there is limited or no evidence supporting propranolol, escitalopram, temazepam, or gabapentin.
See also: Debriefing § Crisis intervention
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 find that psychological debriefing is unhelpful and is potentially harmful. 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.
For one such method, see trauma risk management.
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.
Further information: Treatments for combat-related PTSD
Reviews of studies have found that combination therapy (psychological and pharmacotherapy) is no more effective than psychological therapy alone.
Many forms of psychotherapy have been found to be efficacious for trauma-related problems such as PTSD. Basic counseling practices common to many treatments for PTSD include education about the condition, and provision of safety and support.
The psychotherapy approaches with the strongest demonstrated efficacy include cognitive behavioral therapy, prolonged exposure therapy, cognitive therapy (CT), cognitive processing therapy, and eye movement desensitization and reprocessing (EMDR).
A meta-analytic comparison of EMDR and cognitive behavioral therapy 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 adolescent also found that EMDR was as efficacious as cognitive behavioral therapy (CBT).
Furthermore, the availability of school-based therapy is particularly important for children with PTSD. 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. 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.
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.
Exposure therapy is a type of cognitive behavioral therapy that involves assisting trauma survivors to re-experience distressing trauma-related memories and reminders in order 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 therapy modality is well supported by clinical evidence. The success of exposure-based therapies has raised the question of whether exposure is a necessary ingredient in the treatment of PTSD. Some organizations[which?] 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.
Eye movement desensitization and reprocessing
Main article: 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 therapists uses hand movements to get the person to move their eyes backward and forward, but hand-tapping or tones can also be used. EMDR closely resembles cognitive behavior therapy as it combines exposure (re-visiting the traumatic event), working on cognitive processes and relaxation/self-monitoring. However, exposure by way of being asked to think about the experience rather than talk about it has been highlighted as one of the more important distinguishing elements of EMDR.
There have been multiple small controlled trials of four to eight weeks of EMDR in adults as well as children and adolescents. EMDR reduced PTSD symptoms enough in the short term that one in two adults no longer met the criteria for PTSD, but the number of people involved in these trials was small and thus results should be interpreted with caution pending further research. There was not enough evidence to know whether or not EMDR could eliminate PTSD in adults. In children and adolescents, a recent meta-analysis of randomized controlled trials using MetaNSUE to avoid biases related to missing information found that EMDR was at least as efficacious as CBT, and superior to waitlist or placebo. There was some evidence that EMDR might prevent depression. There were no studies comparing EMDR to other psychological treatments or to medication. Adverse effects were largely unstudied. The benefits were greater for women with a history of sexual assault compared with people who had experienced other types of traumatizing events (such as accidents, physical assaults and war). There is a small amount of evidence that EMDR may improve re-experiencing symptoms in children and adolescents, but EMDR has not been shown to improve other PTSD symptoms, anxiety, or depression.
The eye movement component of the therapy may not be critical for benefit. As there has been no major, high quality randomized trial of EMDR with eye movements versus EMDR without eye movements, the controversy over effectiveness is likely to continue. Authors of a meta-analysis published in 2013 stated, "We found that people treated with eye movement therapy had greater improvement in their symptoms of post-traumatic stress disorder than people given therapy without eye movements….Secondly we found that that in laboratory studies the evidence concludes that thinking of upsetting memories and simultaneously doing a task that facilitates eye movements reduces the vividness and distress associated with the upsetting memories."
Other approaches, in particular involving social supports, may also be important. An open trial of interpersonal psychotherapy reported high rates of remission from PTSD symptoms without using exposure. A current, NIMH-funded trial in New York City is now (and into 2013) comparing interpersonal psychotherapy, prolonged exposure therapy, and relaxation therapy.[full citation needed]
While many medications do not have enough evidence to support their use, three (fluoxetine, paroxetine, and venlafaxine) have been shown to have a small benefit over placebo. With many medications, residual PTSD symptoms following treatment is the rule rather than the exception.
Selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs) may have some benefit for PTSD symptoms.Tricyclic antidepressants are equally effective but are less well tolerated. Evidence provides support for a small or modest improvement with sertraline, fluoxetine, paroxetine, and venlafaxine. Thus, these four medications are considered to be first-line medications for PTSD.
Benzodiazepines are not recommended for the treatment of PTSD due to a lack of evidence of benefit and risk of worsening PTSD symptoms. Some authors believe that the use of benzodiazepines is contraindicated for acute stress, as this group of drugs promotes dissociation and ulterior revivals. Nevertheless, some use benzodiazepines with caution for short-term anxiety and insomnia. While benzodiazepines can alleviate acute anxiety, there is no consistent evidence that they can stop the development of PTSD and may actually increase the risk of developing PTSD 2–5 times. Additionally, benzodiazepines may reduce the effectiveness of psychotherapeutic interventions, and there is some evidence that benzodiazepines may actually contribute to the development and chronification of PTSD. For those who already have PTSD, benzodiazepines may worsen and prolong the course of illness, by worsening psychotherapy outcomes, and causing or exacerbating aggression, depression (including suicidality), and substance use. Drawbacks include the risk of developing a benzodiazepine dependence, tolerance (i.e., short-term benefits wearing off with time), and withdrawal syndrome; additionally, individuals with PTSD (even those without a history of alcohol or drug misuse) are at an increased risk of abusing benzodiazepines. Due to a number of other treatments with greater efficacy for PTSD and less risks (e.g., prolonged exposure, cognitive processing therapy, eye movement desensitization and reprocessing, cognitive restructuring therapy, trauma-focused cognitive behavioral therapy, brief eclectic psychotherapy, narrative therapy, stress inoculation training, serotonergic antidepressants, adrenergic inhibitors, antipsychotics, and even anticonvulsants), benzodiazepines should be considered relatively contraindicated until all other treatment options are exhausted. For those who argue that benzodiazepines should be used sooner in the most severe cases, the adverse risk of disinhibition (associated with suicidality, aggression and crimes) and clinical risks of delaying or inhibiting definitive efficacious treatments, make other alternative treatments preferable (e.g., inpatient, residential, partial hospitalization, intensive outpatient, dialectic behavior therapy; and other fast-acting sedating medications such as trazodone, mirtazapine, amitripytline, doxepin, prazosin, propranolol, guanfacine, clonidine, quetiapine, olanzapine, valproate, gabapentin).
Glucocorticoids may be useful for short-term therapy to protect against neurodegeneration caused by the extended stress response that characterizes PTSD, but long-term use may actually promote neurodegeneration.
Evidence as of 2017 is insufficient to determine if medical cannabis useful for PTSD. Despite the uncertain evidence, use of cannabis or derived products is widespread among U.S. veterans with PTSD.
The cannabinoidnabilone is sometimes used off-label for nightmares in PTSD. Although some short-term benefit was shown, adverse effects are common and it has not been adequately studied to determine efficacy. Additionally, there are other treatments with stronger efficacy and less risks (e.g., psychotherapy, serotonergic antidepressants, adrenergic inhibitors). The use of medical marijuana for PTSD is controversial, with only a handful of states permitting its use for that purpose.
Exercise, sport and physical activity
Physical activity can influence people's psychological and physical health. The U.S. National Center for PTSD recommends moderate exercise as a way to distract from disturbing emotions, build self-esteem and increase feelings of being in control again. They recommend a discussion with a doctor before starting an exercise program.
Play therapy for children
Play is thought to help children link their inner thoughts with their outer world, connecting real experiences with abstract thought. Repetitive play can also be one way a child relives traumatic events, and that can be a symptom of trauma in a child or young person. Although it is commonly used, there have not been enough studies comparing outcomes in groups of children receiving and not receiving play therapy, so the effects of play therapy are not yet understood.
Many veterans of the wars in Iraq and Afghanistan have faced significant physical, emotional, and relational disruptions. In response, the United States Marine Corps has instituted programs to assist them in re-adjusting to civilian life, especially in their relationships with spouses and loved ones, to help them communicate better and understand what the other has gone through.Walter Reed Army Institute of Research (WRAIR) developed the Battlemind program to assist service members avoid or ameliorate PTSD and related problems. Wounded Warrior Project partnered with the US Department of Veterans Affairs to create Warrior Care Network, a national health system of PTSD treatment centers.
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