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Posttraumatic Stress Disorder
An anxiety disorder that can develop after experiencing or witnessing a terrifying or life-threatening event
Most people who experience traumatic events do not develop PTSD. People who experience interpersonal trauma such as 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 10 years of age. Diagnosis is based on the presence of specific symptoms following a traumatic event.
Prevention may be possible when counselling is targeted at those with early symptoms but is not effective when provided to all trauma-exposed individuals whether or not symptoms are present. The main treatments for people with PTSD are counselling (psychotherapy) and medication.Antidepressants of the selective serotonin reuptake inhibitor type are the first-line medications for PTSD and result in benefit in about half of people. Benefits from medication are less than those seen with counselling. It is not known whether using medications and counselling together has greater benefit than either method separately. Medications, other than SSRIs, do not have enough evidence to support their use and, in the case of benzodiazepines, may worsen outcomes.
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). Some following a traumatic event experience posttraumatic growth.
Associated medical conditions
Trauma survivors often develop depression, anxiety disorders, and mood disorders in addition to PTSD.
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.
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.
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.
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.
Motor vehicle collision survivors, both children and adults, are at an increased risk of PTSD. About 20% of children were diagnosed with PTSD following a road traffic accident, compared to 22% of adults. Females were more likely to be diagnosed with PTSD following a road traffic accident, whether the accident occurred during childhood or adulthood.
Posttraumatic stress reactions have been studied in children and adolescents. 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. Similar to the adult population, risk factors for PTSD in children include: female gender, exposure to disasters (natural or manmade), negative coping behaviours, and/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 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 violence
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 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.
A U.S. Long-Range Patrol team leader in Vietnam, 1968.
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. 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 child with chronic illnesses.
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.
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.
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.
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 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.
Regions of the brain associated with stress and posttraumatic stress disorder
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.
Evidence suggests that endogenous cannabinoid levels are reduced in PTSD, particularly anandamide, and that cannabinoid receptors (CB1) are increased in order 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.
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 for developing substance abuse disorders.
the differential expression of symptoms culturally (specifically with respect to avoidance and numbing symptoms, distressing dreams, and somatic symptoms)
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).
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.
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.
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.
The ICD-11 diagnostic description for PTSD 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 ICD10 or DSM-5. ICD-11 also proposes identifying a distinct group with complex post-traumatic stress disorder (CPTSD), who have more often experienced multiple and sustained traumas and have greater functional impairment than those with PTSD.
A diagnosis of PTSD requires that the person has been exposed to an extreme, life-threatening 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 that characteristic of PTSD, the diagnosis may be changed.
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.
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.
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.
Reviews of studies have found that combination therapy (psychological and pharmacotherapy) is no more effective than psychological therapy alone.
Furthermore, the availability of school-based therapy is particularly important for children with PTSD.[non sequitur] 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
The diagram depicts how emotions, thoughts, and behaviors all influence each other. The triangle in the middle represents CBT's tenet that all humans' core beliefs can be summed up in three categories: self, others, future.
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
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 ]
While many medications do not have enough evidence to support their use, three (fluoxetine, paroxetine, and venlafaxine) have been shown to have a small to modest benefit over placebo. With many medications, residual PTSD symptoms following treatment is the rule rather than the exception.
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 can cause dissociation. 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).
Prazosin, an alpha-1 adrenergic antagonist, has been used in veterans with PTSD to reduce nightmares. Studies show variability in the symptom improvement, appropriate dosages, and efficacy in this population.
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.
As of 2019 cannabis is specifically not recommended as a treatment. However, use of cannabis or derived products is widespread among U.S. veterans with PTSD.
The cannabinoidnabilone is sometimes used 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. Currently, a handful of states permit the use of medical cannabis for the treatment of PTSD.
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.
There is debate over the rates of PTSD found in populations, but, despite changes in diagnosis and the criteria used to define PTSD between 1997 and 2013, epidemiological rates have not changed significantly. Most of the current reliable data regarding the epidemiology of PTSD is based on DSM-IV criteria, as the DSM-5 was not introduced until 2013.
The United Nations' World Health Organization publishes estimates of PTSD impact for each of its member states; the latest data available are for 2004. Considering only the 25 most populated countries ranked by overall age-standardizedDisability-Adjusted Life Year (DALY) rate, the top half of the ranked list is dominated by Asian/Pacific countries, the US, and Egypt. Ranking the countries by the male-only or female-only rates produces much the same result, but with less meaningfulness, as the score range in the single-sex rankings is much-reduced (4 for women, 3 for men, as compared with 14 for the overall score range), suggesting that the differences between female and male rates, within each country, is what drives the distinctions between the countries.
As of 2017, the cross-national lifetime prevalence of PTSD was 3.9%, based on a survey were 5.6% had been exposed to trauma. The primary factor impacting treatment-seeking behavior, which can help to mitigate PTSD development after trauma was income, while being younger, female, and having less social status (less education, lower individual income, and being unemployed) were all factors associated with less treatment-seeking behaviour.
The National Comorbidity Survey Replication has estimated that the lifetime prevalence of PTSD among adult Americans is 6.8%, with women (9.7%) more than twice as likely as men (3.6%) to have PTSD at some point in their lives. More than 60% of men and more than 60% of women experience at least one traumatic event in their life. The most frequently reported traumatic events by men are rape, combat, and childhood neglect or physical abuse. Women most frequently report instances of rape, sexual molestation, physical attack, being threatened with a weapon and childhood physical abuse. 88% of men and 79% of women with lifetime PTSD have at least one comorbid psychiatric disorder. Major depressive disorder, 48% of men and 49% of women, and lifetime alcohol abuse or dependence, 51.9% of men and 27.9% of women, are the most common comorbid disorders.
The United States Department of Veterans Affairs estimates that 830,000 Vietnam War veterans suffered symptoms of PTSD. The National Vietnam Veterans' Readjustment Study (NVVRS) found 15% of male and 9% of female Vietnam veterans had PTSD at the time of the study. Life-time prevalence of PTSD was 31% for males and 27% for females. In a reanalysis of the NVVRS data, along with analysis of the data from the Matsunaga Vietnam Veterans Project, Schnurr, Lunney, Sengupta, and Waelde found that, contrary to the initial analysis of the NVVRS data, a large majority of Vietnam veterans suffered from PTSD symptoms (but not the disorder itself). Four out of five reported recent symptoms when interviewed 20-25 years after Vietnam.
A 2011 study from Georgia State University and San Diego State University found that rates of PTSD diagnosis increased significantly when troops were stationed in combat zones, had tours of longer than a year, experienced combat, or were injured. Military personnel serving in combat zones were 12.1 percentage points more likely to receive a PTSD diagnosis than their active-duty counterparts in non-combat zones. Those serving more than 12 months in a combat zone were 14.3 percentage points more likely to be diagnosed with PTSD than those having served less than one year. Experiencing an enemy firefight was associated with an 18.3 percentage point increase in the probability of PTSD, while being wounded or injured in combat was associated with a 23.9 percentage point increase in the likelihood of a PTSD diagnosis. For the 2.16 million U.S. troops deployed in combat zones between 2001 and 2010, the total estimated two-year costs of treatment for combat-related PTSD are between $1.54 billion and $2.69 billion.
As of 2013, rates of PTSD have been estimated at up to 20% for veterans returning from Iraq and Afghanistan. As of 2013 13% of veterans returning from Iraq were unemployed.
The September 11 attacks took the lives of nearly 3,000 people, leaving 6,000 injured. First responders (police and firefighters), emergency medical services, sanitation workers, and volunteers were all involved in the recovery efforts. The prevalence of probable PTSD in these highly exposed populations was estimated across multiple studies utilizing in-person, telephone, and online interviews and questionnaires. Overall prevalence of PTSD was highest immediately following the attacks and decreased over time. However, disparities were found among the different types of recovery workers. The rate of probable PTSD for first responders was lowest directly after the attacks and increased from ranges of 4.8-7.8% to 7.4-16.5% between the 5-6 year follow-up and a later assessment. When comparing traditional responders to non-traditional responders (volunteers), the probable PTSD prevalence 2.5 years after the initial visit was greater in volunteers with estimates of 11.7% and 17.2% respectively. Volunteer participation in tasks atypical to the defined occupational role was a significant risk factor for PTSD. Other risk factors included exposure intensity, earlier start date, duration of time spent on site, and constant, negative reminders of the trauma. Additional research has been performed to understand the social consequences of the September 11 attacks. Alcohol consumption was assessed in a cohort of World Trade Center workers using the cut-annoyed-guilty-eye (CAGE) questionnaire for alcohol abuse. Almost 50% of World Trade Center workers who self-identified as alcohol users reported drinking more during the rescue efforts. Nearly a quarter of these individuals reported drinking more following the recovery. If determined to have probable PTSD status, the risk of developing an alcohol problem was double compared to those without psychological morbidity. Social disability was also studied in this cohort as a social consequence of the September 11 attacks. Defined by the disruption of family, work, and social life, the risk of developing social disability increased 17-fold when categorized as having probable PTSD.
The United States provides a range of benefits for veterans that the VA has determined have PTSD, which developed during, or as a result of, their military service. These benefits may include tax-free cash payments, free or low-cost mental health treatment and other healthcare, vocational rehabilitation services, employment assistance, and independent living support.
In the UK, there are various charities and service organisations dedicated to aiding veterans in readjusting to civilian life. The Royal British Legion and the more recently established Help for Heroes are two of Britain's more high-profile veterans' organisations which have actively advocated for veterans over the years. There has been some controversy that the NHS has not done enough in tackling mental health issues and is instead "dumping" veterans on charities such as Combat Stress.
The 1952 edition of the DSM-I includes a diagnosis of "gross stress reaction", which has similarities to the modern definition and understanding of PTSD. Gross stress reaction is defined as a "normal personality [utilizing] established patterns of reaction to deal with overwhelming fear" as a response to "conditions of great stress". The diagnosis includes language which relates the condition to combat as well as to "civilian catastrophe".
A USAF study carried out in 1979 focused on individuals (civilian and military) who had worked to recover or identify the remains of those who died in Jonestown. The bodies had been dead for several days, and a third of them had been children. The study used the term "dysphoria" to describe PTSD-like symptoms.
Early in 1978, the diagnosis term "post-traumatic stress disorder" was first recommended in a working group finding presented to the Committee of Reactive Disorders. The condition was described in the DSM-III (1980) as posttraumatic stress disorder. In the DSM-IV, the spelling "posttraumatic stress disorder" is used, while in the ICD-10, the spelling is "post-traumatic stress disorder".
Statue, Three Servicemen, Vietnam Veterans Memorial
The correlations between combat and PTSD are undeniable; according to Stéphane Audoin-Rouzeau and Annette Becker, "One-tenth of mobilized American men were hospitalized for mental disturbances between 1942 and 1945, and, after thirty-five days of uninterrupted combat, 98% of them manifested psychiatric disturbances in varying degrees." In fact, much of the available published research regarding PTSD is based on studies done on veterans of the war in Vietnam. A study based on personal letters from soldiers of the 18th-century Prussian Army concludes that combatants may have had PTSD. Aspects of PTSD in soldiers of ancient Assyria have been identified using written sources from 1300-600 BCE. These Assyrian soldiers would undergo a three-year rotation of combat before being allowed to return home, and were purported to have faced immense challenges in reconciling their past actions in war with their civilian lives. Connections between the actions of Viking berserkers and the hyperarousal of post-traumatic stress disorder have also been drawn.
The researchers from the Grady Trauma Project highlight the tendency people have to focus on the combat side of PTSD: "less public awareness has focused on civilian PTSD, which results from trauma exposure that is not combat related... " and "much of the research on civilian PTSD has focused on the sequelae of a single, disastrous event, such as the Oklahoma City bombing, September 11th attacks, and Hurricane Katrina". Disparity in the focus of PTSD research affects the already popular perception of the exclusive interconnectedness of combat and PTSD. This is misleading when it comes to understanding the implications and extent of PTSD as a neurological disorder. Dating back to the definition of Gross stress reaction in the DSM-I, civilian experience of catastrophic or high stress events is included as a cause of PTSD in medical literature. The 2014 National Comorbidity Survey reports that "the traumas most commonly associated with PTSD are combat exposure and witnessing among men and rape and sexual molestation among women."
Because of the initial overt focus on PTSD as a combat related disorder when it was first fleshed out in the years following the war in Vietnam, in 1975 Ann Wolbert Burgess and Lynda Lytle Holmstrom defined Rape trauma syndrome, RTS, in order to draw attention to the striking similarities between the experiences of soldiers returning from war and of rape victims. 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 injury lawsuits (tort claims) asserting the plaintiff suffered from 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.
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 Webster's College Dictionary giving the non-hyphenated spelling.
Some at the Pentagon have used the terminology "PTSS" (syndrome instead of disorder, to avoid connotation of stigma), or just "PTS".
The comedian George Carlin criticized the euphemism treadmill which led to progressive change of the way PTSD was referred to over the course of the 20th century, from "shell shock" in the First World War to the "battle fatigue" in the Second World War, to "operational exhaustion" in the Korean War, to the current "post-traumatic stress disorder", coined during the Vietnam War, which "added a hyphen" and which, he commented, "completely burie[s] [the pain] under jargon". He also stated that the name given to the condition has had a direct effect on the way veteran soldiers with PTSD were treated and perceived by civilian populations over time.
Most knowledge regarding PTSD comes from studies in high-income countries.
To recapitulate some of the neurological and neurobehavioral symptoms experienced by the veteran population of recent conflicts in Iraq and Afghanistan, researchers at the Roskamp Institute and the James A Haley Veteran's Hospital (Tampa) have developed an animal model to study the consequences of mild traumatic brain injury (mTBI) and PTSD. In the laboratory, the researchers exposed mice to a repeated session of unpredictable stressor (i.e. predator odor while restrained), and physical trauma in the form of inescapable foot-shock, and this was also combined with a mTBI. In this study, PTSD animals demonstrated recall of traumatic memories, anxiety, and an impaired social behavior, while animals subject to both mTBI and PTSD had a pattern of disinhibitory-like behavior. mTBI abrogated both contextual fear and impairments in social behavior seen in PTSD animals. In comparison with other animal studies, examination of neuroendocrine and neuroimmune responses in plasma revealed a trend toward increase in corticosterone in PTSD and combination groups.
Researchers are investigating a number of experimental FAAH and MAGL-inhibiting drugs of hopes of finding a better treatment for anxiety and stress-related illnesses. In 2016, the FAAH-inhibitor drug BIA 10-2474 was withdrawn from human trials in France due to adverse effects.
MDMA was used for psychedelic therapy for a variety of indications before its criminalization in the U.S. in 1985. In response to its criminalization, the Multidisciplinary Association for Psychedelic Studies (MAPS) was founded as a nonprofit drug-development organization to develop MDMA into a legal prescription drug for use as an adjunct in psychotherapy. The drug is hypothesized to facilitate psychotherapy by reducing fear, thereby allowing people to reprocess and accept their traumatic memories without becoming emotionally overwhelmed. In this treatment, people participate in an extended psychotherapy session during the acute activity of the drug, and then spend the night at the treatment facility. In the sessions with the drug, therapists are not directive and support the patients in exploring their inner experiences. People participate in standard psychotherapy sessions before the drug-assisted sessions, as well as after the drug-assisted psychotherapy to help them integrate their experiences with the drug. The phase 2 clinical trials of the MDMA-Assisted Psychotherapy, was publicized at the end of November 2016. Preliminary results suggest MDMA-assisted psychotherapy might be effective. MAPS received FDA approval of a phase 3 trials.
^Acceptable variants of this term exist; see the Terminology section in this article.
^ abcdefghijklmnAmerican Psychiatric Association (2013). Diagnostic and Statistical Manual of Mental Disorders (5th ed.). Arlington, VA: American Psychiatric Publishing. pp. 271-80. ISBN978-0-89042-555-8.
^Diagnostic and statistical manual of mental disorders: DSM-5. American Psychiatric Association (5th ed.). Arlington, VA: American Psychiatric Association. 2013. p. 276. ISBN9780890425558. OCLC830807378.CS1 maint: others (link)
^Panagioti M, Gooding PA, Triantafyllou K, Tarrier N (April 2015). "Suicidality and posttraumatic stress disorder (PTSD) in adolescents: a systematic review and meta-analysis". Social Psychiatry and Psychiatric Epidemiology. 50 (4): 525-37. doi:10.1007/s00127-014-0978-x. PMID25398198.
^Zoladz PR, Diamond DM (June 2013). "Current status on behavioral and biological markers of PTSD: a search for clarity in a conflicting literature". Neuroscience and Biobehavioral Reviews. 37 (5): 860-95. doi:10.1016/j.neubiorev.2013.03.024. PMID23567521.
^ abHaagen JF, Smid GE, Knipscheer JW, Kleber RJ (August 2015). "The efficacy of recommended treatments for veterans with PTSD: A metaregression analysis". Clinical Psychology Review. 40: 184-94. doi:10.1016/j.cpr.2015.06.008. PMID26164548.
^ abHetrick SE, Purcell R, Garner B, Parslow R (July 2010). "Combined pharmacotherapy and psychological therapies for post traumatic stress disorder (PTSD)". The Cochrane Database of Systematic Reviews (7): CD007316. doi:10.1002/14651858.CD007316.pub2. PMID20614457.
^ abcGuina J, Rossetter SR, DeRHODES BJ, Nahhas RW, Welton RS (July 2015). "Benzodiazepines for PTSD: A Systematic Review and Meta-Analysis". Journal of Psychiatric Practice. 21 (4): 281-303. doi:10.1097/pra.0000000000000091. PMID26164054.
^ abcdHoskins M, Pearce J, Bethell A, Dankova L, Barbui C, Tol WA, van Ommeren M, de Jong J, Seedat S, Chen H, Bisson JI (February 2015). "Pharmacotherapy for post-traumatic stress disorder: systematic review and meta-analysis". The British Journal of Psychiatry. 206 (2): 93-100. doi:10.1192/bjp.bp.114.148551. PMID25644881. Some drugs have a small positive impact on PTSD symptoms
^Bernstein, M; Pfefferbaum, B (16 May 2018). "Posttraumatic Growth as a Response to Natural Disasters in Children and Adolescents". Current Psychiatry Reports. 20 (5): 37. doi:10.1007/s11920-018-0900-4. PMID29766312.
^O'Donnell ML, Creamer M, Bryant RA, Schnyder U, Shalev A (July 2003). "Posttraumatic disorders following injury: an empirical and methodological review". Clinical Psychology Review. 23 (4): 587-603. doi:10.1016/S0272-7358(03)00036-9. PMID12788111.
^Maxmen JS, Ward NG (2002). Psychotropic drugs: fast facts (3rd ed.). New York: W. W. Norton. p. 348. ISBN978-0-393-70301-6.
^Vieweg WV, Julius DA, Fernandez A, Beatty-Brooks M, Hettema JM, Pandurangi AK (May 2006). "Posttraumatic stress disorder: clinical features, pathophysiology, and treatment". The American Journal of Medicine. 119 (5): 383-90. doi:10.1016/j.amjmed.2005.09.027. PMID16651048.
^Dekel S, Gilbertson MW, Orr SP, Rauch SL, Wood NE, Pitman RK (2016). "Trauma and Posttraumatic Stress Disorder". In Stern TA, Fava M, Wilens TE, Rosenbaum JF (eds.). Massachusetts General Hospital comprehensive clinical psychiatry (Second ed.). London: Elsevier. pp. 380-392. ISBN9780323295079. OCLC905232521.
^ abcKessler RC, Aguilar-Gaxiola S, Alonso J, Benjet C, Bromet EJ, Cardoso G, Degenhardt L, de Girolamo G, Dinolova RV, Ferry F, Florescu S, Gureje O, Haro JM, Huang Y, Karam EG, Kawakami N, Lee S, Lepine JP, Levinson D, Navarro-Mateu F, Pennell BE, Piazza M, Posada-Villa J, Scott KM, Stein DJ, Ten Have M, Torres Y, Viana MC, Petukhova MV, Sampson NA, Zaslavsky AM, Koenen KC (27 October 2017). "Trauma and PTSD in the WHO World Mental Health Surveys". European Journal of Psychotraumatology. 8 (sup5): 1353383. doi:10.1080/20008198.2017.1353383. PMC5632781. PMID29075426.
^Bisson JI, Berliner L, Cloitre M, Forbes D, Jensen TK, Lewis C, Monson CM, Olff M, Pilling S, Riggs DS, Roberts NP, Shapiro F (August 2019). "The International Society for Traumatic Stress Studies New Guidelines for the Prevention and Treatment of Posttraumatic Stress Disorder: Methodology and Development Process". Journal of Traumatic Stress. 32 (4): 475-483. doi:10.1002/jts.22421.
^Alisic E, Zalta AK, van Wesel F, Larsen SE, Hafstad GS, Hassanpour K, Smid GE (2014). "Rates of post-traumatic stress disorder in trauma-exposed children and adolescents: meta-analysis". The British Journal of Psychiatry. 204 (5): 335-40. doi:10.1192/bjp.bp.113.131227. PMID24785767.
^Lapp KG, Bosworth HB, Strauss JL, Stechuchak KM, Horner RD, Calhoun PS, Meador KG, Lipper S, Butterfield MI (September 2005). "Lifetime sexual and physical victimization among male veterans with combat-related post-traumatic stress disorder". Military Medicine. 170 (9): 787-90. doi:10.7205/MILMED.170.9.787. PMID16261985.
^Otte C, Neylan TC, Pole N, Metzler T, Best S, Henn-Haase C, Yehuda R, Marmar CR (January 2005). "Association between childhood trauma and catecholamine response to psychological stress in police academy recruits". Biological Psychiatry. 57 (1): 27-32. doi:10.1016/j.biopsych.2004.10.009. PMID15607297.
^Janoff-Bulman, R. (1992). Shattered Assumptions: Toward a New Psychology of Trauma. New York: Free Press.[page needed]
^Scheeringa MS (2015). "Untangling Psychiatric Comorbidity in Young Children Who Experienced Single, Repeated, or Hurricane Katrina Traumatic Events". Child and Youth Care Forum. 44 (4): 475-492. doi:10.1007/s10566-014-9293-7.
^Hollifield M, Warner TD, Lian N, Krakow B, Jenkins JH, Kesler J, Stevenson J, Westermeyer J (August 2002). "Measuring trauma and health status in refugees: a critical review". JAMA. 288 (5): 611-21. doi:10.1001/jama.288.5.611. PMID12150673.
^Porter M, Haslam N (October 2001). "Forced displacement in Yugoslavia: a meta-analysis of psychological consequences and their moderators". Journal of Traumatic Stress. 14 (4): 817-34. doi:10.1023/A:1013054524810. PMID11776427.
^Ayers S, Bond R, Bertullies S, Wijma K (April 2016). "The aetiology of post-traumatic stress following childbirth: a meta-analysis and theoretical framework". Psychological Medicine. 46 (6): 1121-34. doi:10.1017/s0033291715002706. PMID26878223.
^Alder J, Stadlmayr W, Tschudin S, Bitzer J (June 2006). "Post-traumatic symptoms after childbirth: what should we offer?". Journal of Psychosomatic Obstetrics and Gynaecology. 27 (2): 107-12. doi:10.1080/01674820600714632. PMID16808085.
^Montmasson H, Bertrand P, Perrotin F, El-Hage W (October 2012). "[Predictors of postpartum post-traumatic stress disorder in primiparous mothers]". Journal de Gynecologie, Obstetrique et Biologie de la Reproduction. 41 (6): 553-60. doi:10.1016/j.jgyn.2012.04.010. PMID22622194.
^Martin, Colin (2012). Perinatal Mental Health : a Clinical Guide. Cumbria England: M & K Pub. p. 26. ISBN9781907830495.
^True WR, Rice J, Eisen SA, Heath AC, Goldberg J, Lyons MJ, Nowak J (April 1993). "A twin study of genetic and environmental contributions to liability for posttraumatic stress symptoms". Archives of General Psychiatry. 50 (4): 257-64. doi:10.1001/archpsyc.1993.01820160019002. PMID8466386.
^Yehuda R, Halligan SL, Golier JA, Grossman R, Bierer LM (April 2004). "Effects of trauma exposure on the cortisol response to dexamethasone administration in PTSD and major depressive disorder". Psychoneuroendocrinology. 29 (3): 389-404. doi:10.1016/S0306-4530(03)00052-0. PMID14644068.
^Yehuda R, Halligan SL, Grossman R, Golier JA, Wong C (September 2002). "The cortisol and glucocorticoid receptor response to low dose dexamethasone administration in aging combat veterans and holocaust survivors with and without posttraumatic stress disorder". Biological Psychiatry. 52 (5): 393-403. doi:10.1016/S0006-3223(02)01357-4. PMID12242055.
^Heim C, Ehlert U, Hellhammer DH (January 2000). "The potential role of hypocortisolism in the pathophysiology of stress-related bodily disorders". Psychoneuroendocrinology. 25 (1): 1-35. doi:10.1016/S0306-4530(99)00035-9. PMID10633533.
^Mason JW, Giller EL, Kosten TR, Harkness L (August 1988). "Elevation of urinary norepinephrine/cortisol ratio in posttraumatic stress disorder". The Journal of Nervous and Mental Disease. 176 (8): 498-502. doi:10.1097/00005053-198808000-00008. PMID3404142.
^Aardal-Eriksson E, Eriksson TE, Thorell LH (December 2001). "Salivary cortisol, posttraumatic stress symptoms, and general health in the acute phase and during 9-month follow-up". Biological Psychiatry. 50 (12): 986-93. doi:10.1016/S0006-3223(01)01253-7. PMID11750895.
^ abcdeOlszewski TM, Varrasse JF (June 2005). "The neurobiology of PTSD: implications for nurses". Journal of Psychosocial Nursing and Mental Health Services. 43 (6): 40-7. PMID16018133.
^Lindley SE, Carlson EB, Benoit M (May 2004). "Basal and dexamethasone suppressed salivary cortisol concentrations in a community sample of patients with posttraumatic stress disorder". Biological Psychiatry. 55 (9): 940-5. doi:10.1016/j.biopsych.2003.12.021. PMID15110738.
^Goodkind M, Etkin A. "Functional Neurocircuitry and Neuroimaging Studies of Anxiety Disorders". In Sklar P, Buxbaum J, Nestler E, Charney D (eds.). Neurobiology of Mental Illness (5th ed.). Oxford University Press.
^Carlson, Neil R. (2007). Physiology of Behavior (9 ed.). Pearson Education, Inc.[full ]
^Blevins CA, Weathers FW, Davis MT, Witte TK, Domino JL (December 2015). "The Posttraumatic Stress Disorder Checklist for DSM-5 (PCL-5): Development and Initial Psychometric Evaluation". Journal of Traumatic Stress. 28 (6): 489-98. doi:10.1002/jts.22059. PMID26606250.
^Foa EB, Johnson KM, Feeny NC, Treadwell KR (September 2001). "The child PTSD Symptom Scale: a preliminary examination of its psychometric properties". Journal of Clinical Child Psychology. 30 (3): 376-84. doi:10.1207/S15374424JCCP3003_9. PMID11501254.
^Kenardy JA, Spence SH, Macleod AC (September 2006). "Screening for posttraumatic stress disorder in children after accidental injury". Pediatrics. 118 (3): 1002-9. doi:10.1542/peds.2006-0406. PMID16950991.
^Elhai JD, Layne CM, Steinberg AM, Brymer MJ, Briggs EC, Ostrowski SA, Pynoos RS (February 2013). "Psychometric properties of the UCLA PTSD reaction index. part II: investigating factor structure findings in a national clinic-referred youth sample". Journal of Traumatic Stress. 26 (1): 10-8. doi:10.1002/jts.21755. PMID23417874.
^Bovin, Michelle J.; Marx, Brian P.; Schnurr, Paula P. (2015). "Evolving DSM Diagnostic Criteria for PTSD: Relevance for Assessment and Treatment". Current Treatment Options in Psychiatry. 2 (1): 86-98. doi:10.1007/s40501-015-0032-y. [... the use of a multi-measure approach eliminates the bias associated with any given instrument ...."
^Ben Barnes, J; Presseau, Candice; Jordan, Alexander H; Kline, Nora K; Young-McCaughan, Stacey; Keane, Terence M; Peterson, Alan L; Litz, Brett T; and the Consortium to Alleviate PTSD (2019). "Common Data Elements in the Assessment of Military-Related PTSD Research Applied in the Consortium to Alleviate PTSD". Military Medicine. 184 (5-6): e218-e226. doi:10.1093/milmed/usy226. PMID30252077.
^Weathers, Frank W., Terence M. Keane, and Edna B. Foa, "Assessment and Diagnosis of Adults", in Effective Treatments for PTSD: Practice Guidelines from the International Society for Traumatic Stress Studies, 2nd ed., edited by Edna B. Foa, Terence M. Keane, and Matthew J. Friedman (New York: Guilford, 2009), 23-61. ("Thus, ample resources are now available to conduct psychometrically sound assessments of trauma survivors in any context, and it is no longer defensible for clinicians to do otherwise." (p. 25)).
^Mayou RA, Ehlers A, Hobbs M (June 2000). "Psychological debriefing for road traffic accident victims. Three-year follow-up of a randomised controlled trial". The British Journal of Psychiatry. 176 (6): 589-93. doi:10.1192/bjp.176.6.589. PMID10974967.
^Kassam-Adams N, Marsac ML, Hildenbrand A, Winston F (December 2013). "Posttraumatic stress following pediatric injury: update on diagnosis, risk factors, and intervention". JAMA Pediatrics. 167 (12): 1158-65. doi:10.1001/jamapediatrics.2013.2741. PMID24100470.
^Powers MB, Halpern JM, Ferenschak MP, Gillihan SJ, Foa EB (August 2010). "A meta-analytic review of prolonged exposure for posttraumatic stress disorder". Clinical Psychology Review. 30 (6): 635-41. doi:10.1016/j.cpr.2010.04.007. PMID20546985.
^Seidler GH, Wagner FE (November 2006). "Comparing the efficacy of EMDR and trauma-focused cognitive-behavioral therapy in the treatment of PTSD: a meta-analytic study". Psychological Medicine. 36 (11): 1515-22. doi:10.1017/S0033291706007963. PMID16740177.
^Rolfsnes ES, Idsoe T (April 2011). "School-based intervention programs for PTSD symptoms: a review and meta-analysis". Journal of Traumatic Stress. 24 (2): 155-65. doi:10.1002/jts.20622. PMID21425191.
^Ursano RJ, Bell C, Eth S, Friedman M, Norwood A, Pfefferbaum B, Pynoos JD, Zatzick DF, Benedek DM, McIntyre JS, Charles SC, Altshuler K, Cook I, Cross CD, Mellman L, Moench LA, Norquist G, Twemlow SW, Woods S, Yager J (November 2004). "Practice guideline for the treatment of patients with acute stress disorder and posttraumatic stress disorder". The American Journal of Psychiatry. 161 (11 Suppl): 3-31. PMID15617511.
^Committee on Treatment of Posttraumatic Stress Disorder, Institute of Medicine: Treatment of Posttraumatic Stress Disorder: An Assessment of the Evidence. Washington, D.C.: National Academies Press. 2008. ISBN978-0-309-10926-0.[page needed]
^Karlin BE, Ruzek JI, Chard KM, Eftekhari A, Monson CM, Hembree EA, Resick PA, Foa EB (December 2010). "Dissemination of evidence-based psychological treatments for posttraumatic stress disorder in the Veterans Health Administration". Journal of Traumatic Stress. 23 (6): 663-73. doi:10.1002/jts.20588. PMID21171126.
^ abShapiro F (April 1989). "Efficacy of the eye movement desensitization procedure in the treatment of traumatic memories". Journal of Traumatic Stress. 2 (2): 199-223. doi:10.1002/jts.2490020207.
^Shapiro F, Maxfield L (August 2002). "Eye Movement Desensitization and Reprocessing (EMDR): information processing in the treatment of trauma". Journal of Clinical Psychology. 58 (8): 933-46. doi:10.1002/jclp.10068. PMID12115716.
^ abcGillies D, Taylor F, Gray C, O'Brien L, D'Abrew N (December 2012). "Psychological therapies for the treatment of post-traumatic stress disorder in children and adolescents". The Cochrane Database of Systematic Reviews. 12: CD006726. doi:10.1002/14651858.CD006726.pub2. PMID23235632.
^ abJeffries FW, Davis P (May 2013). "What is the role of eye movements in eye movement desensitization and reprocessing (EMDR) for post-traumatic stress disorder (PTSD)? a review". Behavioural and Cognitive Psychotherapy. 41 (3): 290-300. doi:10.1017/S1352465812000793. PMID23102050.
^Weissman MM, Markowitz JC, Klerman GL (2007). Clinician's Quick Guide to Interpersonal Psychotherapy. New York: Oxford University Press.[page needed]
^Bleiberg KL, Markowitz JC (January 2005). "A pilot study of interpersonal psychotherapy for posttraumatic stress disorder". The American Journal of Psychiatry. 162 (1): 181-3. doi:10.1176/appi.ajp.162.1.181. PMID15625219.
^ abJeffreys M, Capehart B, Friedman MJ (2012). "Pharmacotherapy for posttraumatic stress disorder: review with clinical applications". Journal of Rehabilitation Research and Development. 49 (5): 703-15. doi:10.1682/JRRD.2011.09.0183. PMID23015581. While evidence-based, trauma-focused psychotherapy is the preferred treatment for PTSD, pharmacotherapy is also an important treatment option. First-line pharmacotherapy agents include selective serotonin reuptake inhibitors and the selective serotonin-norepinephrine reuptake inhibitor venlafaxine.
^Jain S, Greenbaum MA, Rosen C (February 2012). "Concordance between psychotropic prescribing for veterans with PTSD and clinical practice guidelines". Psychiatric Services. 63 (2): 154-60. doi:10.1176/appi.ps.201100199. PMID22302333.
^Auxéméry Y (October 2012). "[Posttraumatic stress disorder (PTSD) as a consequence of the interaction between an individual genetic susceptibility, a traumatogenic event and a social context]". L'Encephale (in French). 38 (5): 373-80. doi:10.1016/j.encep.2011.12.003. PMID23062450.
^Kapfhammer HP (December 2008). "[Therapeutic possibilities after traumatic experiences]". Psychiatria Danubina. 20 (4): 532-45. PMID19011595.
^Reist, C (2005). Post-traumatic Stress Disorder. Compendia, Build ID: F000005, published by Epocrates.com
^Maxmen JS, Ward NG (2002). Psychotropic drugs: fast facts (3rd ed.). New York: W. W. Norton. p. 349. ISBN978-0-393-70301-6.
^Martényi F (March 2005). "[Three paradigms in the treatment of posttraumatic stress disorder]". Neuropsychopharmacologia Hungarica. 7 (1): 11-21. PMID16167463.
^ abVeterans Affairs and Department of Defense clinical practice guideline for management of post-traumatic stress. VA/DoD. 2010.
^Bandelow B, Zohar J, Hollander E, Kasper S, Möller HJ, Zohar J, Hollander E, Kasper S, Möller HJ, Bandelow B, Allgulander C, Ayuso-Gutierrez J, Baldwin DS, Buenvicius R, Cassano G, Fineberg N, Gabriels L, Hindmarch I, Kaiya H, Klein DF, Lader M, Lecrubier Y, Lépine JP, Liebowitz MR, Lopez-Ibor JJ, Marazziti D, Miguel EC, Oh KS, Preter M, Rupprecht R, Sato M, Starcevic V, Stein DJ, van Ameringen M, Vega J (2008). "World Federation of Societies of Biological Psychiatry (WFSBP) guidelines for the pharmacological treatment of anxiety, obsessive-compulsive and post-traumatic stress disorders - first revision". The World Journal of Biological Psychiatry. 9 (4): 248-312. doi:10.1080/15622970802465807. PMID18949648.
^Waltman, Scott H.; Shearer, David; Moore, Bret A. (December 2018). "Management of Post-Traumatic Nightmares: a Review of Pharmacologic and Nonpharmacologic Treatments Since 2013". Current Psychiatry Reports. 20 (12): 108. doi:10.1007/s11920-018-0971-2. ISSN1523-3812. PMID30306339.
^Black, Nicola; Stockings, Emily; Campbell, Gabrielle; Tran, Lucy T; Zagic, Dino; Hall, Wayne D; Farrell, Michael; Degenhardt, Louisa (October 2019). "Cannabinoids for the treatment of mental disorders and symptoms of mental disorders: a systematic review and meta-analysis". The Lancet Psychiatry. 6 (12): 995-1010. doi:10.1016/S2215-0366(19)30401-8. PMID31672337.
^O'Neil ME, Nugent SM, Morasco BJ, Freeman M, Low A, Kondo K, Zakher B, Elven C, Motu'apuaka M, Paynter R, Kansagara D (September 2017). "Benefits and Harms of Plant-Based Cannabis for Posttraumatic Stress Disorder: A Systematic Review". Annals of Internal Medicine. 167 (5): 332-340. doi:10.7326/M17-0477. PMID28806794.
^Betthauser K, Pilz J, Vollmer LE (August 2015). "Use and effects of cannabinoids in military veterans with posttraumatic stress disorder". American Journal of Health-System Pharmacy (Review). 72 (15): 1279-84. doi:10.2146/ajhp140523. PMID26195653.
^Jankowski, K. "PTSD and physical health". Information on trauma and PTSD for professionals, National Center for PTSD. U.S. Department of Veterans Affairs. Archived from the original on 30 July 2009. Retrieved 2013.
^ abKoenen KC, Ratanatharathorn A, Ng L, McLaughlin KA, Bromet EJ, Stein DJ, Karam EG, Meron Ruscio A, Benjet C, Scott K, Atwoli L, Petukhova M, Lim CC, Aguilar-Gaxiola S, Al-Hamzawi A, Alonso J, Bunting B, Ciutan M, de Girolamo G, Degenhardt L, Gureje O, Haro JM, Huang Y, Kawakami N, Lee S, Navarro-Mateu F, Pennell BE, Piazza M, Sampson N, Ten Have M, Torres Y, Viana MC, Williams D, Xavier M, Kessler RC (October 2017). "Posttraumatic stress disorder in the World Mental Health Surveys". Psychological Medicine. 47 (13): 2260-2274. doi:10.1017/S0033291717000708. PMC6034513. PMID28385165.
^Sher L (August 2010). "Neurobiology of suicidal behavior in post-traumatic stress disorder". Expert Review of Neurotherapeutics. 10 (8): 1233-5. doi:10.1586/ern.10.114. PMID20662745.
^ abcdPerrin MA, DiGrande L, Wheeler K, Thorpe L, Farfel M, Brackbill R (September 2007). "Differences in PTSD prevalence and associated risk factors among World Trade Center disaster rescue and recovery workers". The American Journal of Psychiatry. 164 (9): 1385-94. doi:10.1176/appi.ajp.2007.06101645. PMID17728424.
^Emerson A, Ponté L, Jerome L, Doblin R (2014). "History and future of the Multidisciplinary Association for Psychedelic Studies (MAPS)". Journal of Psychoactive Drugs. 46 (1): 27-36. doi:10.1080/02791072.2014.877321. PMID24830183.
^Amoroso T, Workman M (July 2016). "Treating posttraumatic stress disorder with MDMA-assisted psychotherapy: A preliminary meta-analysis and comparison to prolonged exposure therapy". Journal of Psychopharmacology. 30 (7): 595-600. doi:10.1177/0269881116642542. PMID27118529.