Posttraumatic stress disorder - Related Links
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Journal of Sleep Disorders & TherapyThe Development of Posttraumatic Stress Disorder after Mild Traumatic Brain Injury in Civilian Populations: A Meta-Analysis
Posttraumatic stress disorder
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|This article possibly contains original research. (December 2014)|
|Posttraumatic stress disorder|
|Classification and external resources|
|NCI||Posttraumatic stress disorder|
|Patient UK||Posttraumatic stress disorder|
Posttraumatic stress disorder[note 1] (PTSD) may develop after a person is exposed to one or more traumatic events, such as major stress, sexual assault, terrorism, or other threats on a person's life. The diagnosis may be given when a group of symptoms, such as disturbing recurring flashbacks, avoidance or numbing of memories of the event, and hyperarousal, continue for more than a month after the occurrence of a traumatic event.
Most people having experienced a traumatizing event will not develop PTSD. People who experience assault-based trauma are more likely to develop PTSD, as opposed to people who experience non-assault based trauma such as witnessing trauma, accidents, and fire events. Children are less likely to experience PTSD after trauma than adults, especially if they are under ten years of age. War veterans are commonly at risk for PTSD.
- 1 Classification
- 2 Risk factors
- 3 Pathophysiology
- 4 Diagnosis
- 5 Prevention
- 6 Management
- 7 Epidemiology
- 8 Society and culture
- 9 History
- 10 Research
- 11 Terminology
- 12 See also
- 13 Notes
- 14 References
- 15 External links
Posttraumatic stress disorder is classified as an anxiety disorder in the DSM IV; the characteristic symptoms are not present before exposure to the violently traumatic event. In the typical case, the individual with PTSD persistently avoids all thoughts and emotions, and discussion of the stressor event and may experience amnesia for it. However, the event is commonly relived by the individual through intrusive, recurrent recollections, flashbacks, and nightmares. The characteristic symptoms are considered acute if lasting less than three months, and chronic if persisting three months or more, and with delayed onset if the symptoms first occur after six months or some years later. PTSD is distinct from the briefer acute stress disorder, and can cause clinical impairment in significant areas of functioning.
Persons considered at risk include, for example, combat military personnel, victims of natural disasters, concentration camp survivors, and victims of violent crime. Individuals frequently experience "survivor's guilt" for remaining alive while others died. Causes of the symptoms of PTSD are the experiencing or witnessing of a stressor event involving death, serious injury or such threat to the self or others in a situation in which the individual felt intense fear, horror, or powerlessness. Persons employed in occupations that expose them to violence (such as soldiers) or disasters (such as emergency service workers) are also at risk.
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.
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.
Most people will experience at least one traumatizing event in their lifetime. 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.
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. 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.
Quasi-experimental studies have demonstrated a relationship between intrusive thoughts and intentional control responses such that suppression increases the frequency of unwanted intrusive thoughts. These results suggest that suppression of intrusive thoughts may be important in the development and maintenance of PTSD.
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.
The physical trauma soldiers may face when serving in combat increases the risk of developing PTSD. Protective effects include social support and social support also helps with recovery if it develops.
The racial similarity between Hispanic and Vietnamese soldiers, and the discrimination Hispanic soldiers faced from their own military, made it difficult for Hispanic soldiers to dehumanize their enemy. Hispanic veterans who reported experiencing racial discrimination during their service displayed more symptoms of PTSD than Hispanic veterans who did not.
Early intervention appears to be a critical preventive measure.
Studies have shown that those prepared for the potential of a traumatic experience are more prepared to deal with the stress of a traumatic experience and therefore less likely to develop PTSD.
PTSD is under-diagnosed in female veterans. Sexual assault in the military is a leading cause for female soldiers developing PTSD; a female soldier who is sexually assaulted while serving in the military is nine times more likely to develop PTSD than a female soldier who is not assaulted. A soldier's assailant may be her colleague or superior officer, making it difficult for her to both report the crime and to avoid interacting with her assailant again. Until the Tailhook scandal drew attention to the problem, the role that sexual assault in the military plays in female veterans developing PTSD went largely unstudied.
Alcohol abuse and drug abuse commonly co-occur with PTSD. Recovery from posttraumatic stress disorder or other anxiety disorders may be hindered, or the condition worsened, by medication or substance overuse, abuse, or dependence; resolving these problems can bring about a marked improvement in an individual's mental health status and anxiety levels.
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.
In addition, most people with PTSD also 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 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.
Translating this reaction to human conditions gives a pathophysiological explanation for PTSD by 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.
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.
Hyperresponsiveness in the norepinephrine system can 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.
However, there is considerable controversy within the medical community regarding the neurobiology of PTSD. A review of existing studies on this subject showed no clear relationship between cortisol levels and PTSD. However, 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.
|This section may be too technical for most readers to understand. (June 2014)|
Three areas of the brain in which function may be altered in PTSD have been identified: the prefrontal cortex, amygdala, and hippocampus. Much of this research has utilised PTSD victims from the Vietnam War. For example, a prospective study using the Vietnam Head Injury Study showed that damage to the prefrontal cortex may actually be protective against later development of PTSD. In a study by Gurvits et al., combat veterans of the Vietnam War with PTSD showed a 20% reduction in the volume of their hippocampus compared with veterans having suffered no such symptoms. This finding could not be replicated in chronic PTSD patients traumatized at an air show plane crash in 1988 (Ramstein, Germany).
In human studies, the amygdala has been shown to be strongly involved in the formation of emotional memories, especially fear-related memories. Neuroimaging studies in humans have revealed both morphological and functional aspects of PTSD. However, during high stress times the hippocampus, which is associated with the ability to place memories in the correct context of space and time, and with the ability to recall the memory, is suppressed. This suppression is hypothesized to be the cause of the flashbacks that often 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.[unreliable medical source?]
The amygdalocentric model of PTSD proposes that it is associated with hyperarousal of the amygdala and insufficient top-down control 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. A study at the European Neuroscience Institute-Goettingen (Germany) found that fear extinction-induced IGF2/IGFBP7 signalling promotes the survival of 17–19-day-old newborn hippocampal neurons. This suggests that therapeutic strategies that enhance IGF2 signalling and adult neurogenesis might be suitable to treat diseases linked to excessive fear memory such as PTSD. Further animal and clinical research into the amygdala and fear conditioning may suggest additional treatments for the condition.
The maintenance of the fear involved with PTSD 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 LC-noradrenergic system has been hypothesized to mediate the over-consolidation of fear memory in PTSD. High levels of cortisol reduce noradrenergic activity, and because people with PTSD tend to have reduced levels of cortisol, it is proposed that individuals with PTSD fail to regulate the increased noradrenergic response to traumatic stress. It is thought that the intrusive memories and conditioned fear responses to associated triggers is a result of this response. 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.
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.
Diagnostic and statistical manual
Since the introduction of DSM-IV, the number of possible events that might be used to diagnose PTSD has increased; one study suggests that the increase is around 50%. Various scales to measure the severity and frequency of PTSD symptoms exist. Standardized screening tools such as Trauma Screening Questionnaire and PTSD Symptom Scale can be used to detect possible symptoms of posttraumatic stress disorder and suggest the need for a formal diagnostic assessment.
International classification of diseases
The diagnostic criteria for PTSD, stipulated in the International Statistical Classification of Diseases and Related Health Problems 10 (ICD-10), may be summarized as:
- Exposure to a stressful event or situation (either short or long lasting) of exceptionally threatening or catastrophic nature, which is likely to cause pervasive distress in almost anyone.
- Persistent remembering or "reliving" the stressor by intrusive flash backs, vivid memories, recurring dreams, or by experiencing distress when exposed to circumstances resembling or associated with the stressor.
- Actual or preferred avoidance of circumstances resembling or associated with the stressor (not present before exposure to the stressor).
- Either (1) or (2):
- Inability to recall, either partially or completely, some important aspects of the period of exposure to the stressor
- Persistent symptoms of increased psychological sensitivity and arousal (not present before exposure to the stressor) shown by any two of the following:
- difficulty in falling or staying asleep
- irritability or outbursts of anger
- difficulty in concentrating
- exaggerated startle response.
The International Statistical Classification of Diseases and Related Health Problems 10 diagnostic guidelines state: In general, this disorder should not be diagnosed unless there is evidence that it arose within 6 months of a traumatic event of exceptional severity. A "probable" diagnosis might still be possible if the delay between the event and the onset was longer than 6 months, provided that the clinical manifestations are typical and no alternative identification of the disorder (e.g., as an anxiety or obsessive-compulsive disorder or depressive episode) is plausible. In addition to evidence of trauma, there must be a repetitive, intrusive recollection or re-enactment of the event in memories, daytime imagery, or dreams. Conspicuous emotional detachment, numbing of feeling, and avoidance of stimuli that might arouse recollection of the trauma are often present but are not essential for the diagnosis. The autonomic disturbances, mood disorder, and behavioural abnormalities all contribute to the diagnosis but are not of prime importance. The late chronic sequelae of devastating stress, i.e. those manifest decades after the stressful experience, should be classified under F62.0.
A diagnosis of PTSD requires exposure 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 stressor like 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.
Malingering should be considered if a financial and/or legal advantage is a possibility.
Modest benefits have been seen from early access to cognitive behavioral therapy, as well as from some medications such as propranolol. 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.
Trauma-exposed individuals often receive a purported preventive treatment called psychological debriefing. Psychological debriefing is the most often used preventive measure, partly because of the relative ease with which this treatment can be given to individuals directly following an event. It 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, research has revealed that psychological debriefing does not help trauma survivors, and it might even hurt them. Although from the outset, early psychological debriefing research yielded mixed results, some initial research suggested that psychological debriefings helped ameliorate peritraumatic symptoms and prevent post-traumatic symptom development. But as research progressed, several meta-analyses made it clear that psychological debriefing is unhelpful and potentially harmful. The first Cochrane meta-analysis concerned single-session debriefing. More recently a Cochrane review on multiple session interventions was conducted and also found negative results. The American Psychological Association judges the status of 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.
Many forms of psychotherapy have been advocated for trauma-related problems such as PTSD. Basic counseling practices common to many treatment responses for PTSD include education about the condition and provision of safety and support.
The psychotherapy programs with the strongest demonstrated efficacy include cognitive behavioral programs, variants of exposure therapy, stress inoculation training (SIT), variants of cognitive therapy (CT), eye movement desensitization and reprocessing (EMDR), mindfulness-based meditation and many combinations of these procedures.
EMDR and trauma-focused cognitive behavioral therapy (TFCBT) were recommended as first-line treatments for trauma victims in a 2007 review; however, "the evidence base [for EMDR] was not as strong as that for TFCBT ... Furthermore, there was limited evidence that TFCBT and EMDR were superior to supportive/non-directive treatments, hence it is highly unlikely that their effectiveness is due to non-specific factors such as attention." 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.
Cognitive behavioral therapy
Cognitive behavioral therapy (CBT) seeks to change the way a trauma victim 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 US 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 US 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. There was not enough evidence to know whether or not EMDR could eliminate PTSD. 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.
Medications including fluoxetine and paroxetine may improve symptoms a small amount. Most medications do not have enough evidence to support their use. With many medications, residual symptoms following treatment is the rule rather than the exception.
SSRIs (selective serotonin reuptake inhibitors). SSRIs are considered to be a first-line drug treatment. SSRIs for which there are data to support use include: citalopram, escitalopram, fluoxetine, fluvoxamine, paroxetine.
Benzodiazepines: These drugs are not recommended by clinical guidelines for the treatment of PTSD due to a lack of evidence of benefit. Nevertheless some use benzodiazepines with caution for short-term anxiety relief, hyperarousal, and sleep disturbance. However, some authors believe that the use of benzodiazepines is contraindicated for acute stress, as this group of drugs promotes dissociation and ulterior revivals. While benzodiazepines can alleviate acute anxiety, there is no consistent evidence that they can stop the development of PTSD, or are at all effective in the treatment of posttraumatic stress disorder. 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. Other drawbacks include the risk of developing a benzodiazepine dependence and withdrawal syndrome; additionally, individuals with PTSD are at an increased risk of abusing benzodiazepines.
Glucocorticoids: These drugs 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.
- Exercise, sport and physical activity
Physical activity can have an impact on people's psychological wellbeing 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 of the ways a child relives traumatic events, and that can be a symptom of traumatization 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.
- Military programs
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.
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 2007, epidemiological rates have not changed significantly.
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-standardized Disability-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.
|Region||Country|| PTSD DALY rate,
| PTSD DALY rate,
| PTSD DALY rate,|
|Asia / Pacific||Thailand||59||86||30|
|Asia / Pacific||Indonesia||58||86||30|
|Asia / Pacific||Philippines||58||86||30|
|Asia / Pacific||Bangladesh||57||85||29|
|Asia / Pacific||India||56||85||29|
|Asia / Pacific||Iran||56||83||30|
|Asia / Pacific||Pakistan||56||85||29|
|Asia / Pacific||Japan||55||80||31|
|Asia / Pacific||Myanmar||55||81||30|
|Asia / Pacific||Vietnam||55||80||30|
|Asia / Pacific||Russian Federation||54||78||30|
|Africa||Dem. Republ. of Congo||52||76||28|
|Asia / Pacific||China||51||76||28|
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 15.2% of male and 8.5% of female Vietnam Vets to suffer from current PTSD at the time of the study. Life-Time prevalence of PTSD was 30.9% for males and 26.9% 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 a 18.3 percentage point increase in the probability of PTSD, while being wounded or injured in combat was associated 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.
Society and culture
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.
Veterans Affairs Canada offers a new program that includes rehabilitation, financial benefits, job placement, health benefits program, disability awards, peer support and family support.
The 1952 edition of the DSM-I includes a diagnosis of Gross stress reaction which bears striking 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”.
Early in 1978, the term was used in a working group finding presented to the Committee of Reactive Disorders. The condition was added to the DSM-III, which was being developed in the 1980s, 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".
The addition of the term to the DSM-III was greatly influenced by the experiences and conditions of US military veterans of the war in Vietnam. Due to its association with the war in Vietnam, PTSD has become synonymous with many historical war-time diagnoses such as railway spine, stress syndrome, nostalgia, soldier's heart, shell shock, battle fatigue, combat stress reaction, or traumatic war neurosis. Some of these terms date back to the 19th century, which is indicative of the universal nature of the condition. In a similar vein Psychiatrist Jonathan Shay has proposed that Lady Percy's soliloquy in Henry IV, Part 1 (act 2, scene 3, lines 40–62), written around 1597, represents an unusually accurate description of the symptom constellation of PTSD.
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. 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.
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.
MDMA was used for psychedelic therapy for a variety of indications before its criminalization in the US in 1985. In response to its criminalization, the Multidisciplinary Association for Psychedelic Studies 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 patients to reprocess and accept their traumatic memories without becoming emotionally overwhelmed. In this treatment, patients 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. Patients 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. Preliminary results suggest MDMA-assisted psychotherapy might be effective for individuals who have not responded favorably to other treatments. Future research employing larger sample sizes and an appropriate placebo condition, i.e., one in which subjects cannot discern if they are in the experimental or control condition, will increase confidence in the results of initial research.
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.
- Acute stress reaction
- Childbirth-related posttraumatic stress disorder
- Chronic stress
- Combat stress reaction
- Compassion fatigue
- Complex posttraumatic stress disorder
- Emotional dysregulation
- Maladaptive daydreaming
- Malingering of posttraumatic stress disorder
- Media violence research
- Posttraumatic embitterment disorder
- Psychogenic amnesia
- PTSD Symptom Scale – Self-Report Version
- Social alienation--among returning veterans
- Shell shock
- Da Costa's syndrome
- Survivor syndrome
- Thousand-yard stare
- Trauma model of mental disorders
- Victimization symptoms
- Acceptable variants of this term exist; see the Terminology section in this article.
- American Psychiatric Association (2013). Diagnostic and Statistical Manual of Mental Disorders (5th ed.). Arlington, VA: American Psychiatric Publishing. pp. 271–280. ISBN 978-0-89042-555-8.
- National Collaborating Centre for Mental Health (UK) (2005). "Post-Traumatic Stress Disorder: The Management of PTSD in Adults and Children in Primary and Secondary Care". NICE Clinical Guidelines, No. 26. Gaskell (Royal College of Psychiatrists). Lay summary – Pubmed Health (plain English). open access publication - free to read
- Zoladz, Phillip (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): 860–895. doi:10.1016/j.neubiorev.2013.03.024.
- Hoskins, M.; Pearce, J.; Bethell, A.; Dankova, L.; Barbui, C.; Tol, WA.; van Ommeren, M.; de Jong, J.; Seedat, S. (February 2015). "Pharmacotherapy for post-traumatic stress disorder: systematic review and meta-analysis.". Br J Psychiatry 206 (2): 93–100. PMID 25644881. doi:10.1192/bjp.bp.114.148551.
- American Psychiatric Association (1994). Diagnostic and statistical manual of mental disorders: DSM-IV. Washington, DC: American Psychiatric Association. ISBN 0-89042-061-0.[page needed]; on-line.
- Rothschild, Babette (2000). The Body Remembers: The Psychophysiology of Trauma and Trauma Treatment. New York: W.W. Norton & Company. ISBN 0-393-70327-4.[page needed]
- Kaplan, H. I.; Sadock, B. J. (1994). Grebb, J. A., ed. Kaplan and Sadock's synopsis of psychiatry: Behavioral sciences, clinical psychiatry (7th ed.). Baltimore: Williams & Williams. pp. 606–609.[page needed]
- Satcher D (1999). "Chapter 4". Mental Health: A Report of the Surgeon General. Surgeon General of the United States.
- Robinson, Maisah (May 27, 2006). "Review of Francisco Goya's Disasters of War". Associated Press.[unreliable source?]
- "Post-Traumatic Stress Disorder (PTSD)". U.S. Department of Health and Human Services. National Institute of Mental Health (NIMH). Retrieved 2011-12-16.
- Mayo Clinic staff. "Post-traumatic stress disorder (PTSD)". Mayo Foundation for Medical Education and Research. Retrieved 2011-12-16.[scientific citation needed]
- Fullerton CS, Ursano RJ, Wang L (2004). "Acute Stress Disorder, Posttraumatic Stress Disorder, and Depression in Disaster or Rescue Workers". Am J Psychiatry 161 (8): 1370–1376. PMID 15285961. doi:10.1176/appi.ajp.161.8.1370.
- Dobry, Y; Braquehais, MD; Sher, L (2013). "Bullying, psychiatric pathology and suicidal behavior.". International journal of adolescent medicine and health 25 (3): 295–9. PMID 24006324. doi:10.1515/ijamh-2013-0065.
- Delahanty DL (2011). "Toward the predeployment detection of risk for PTSD". American Psychiatric Assn 168 (1): 9–11. PMID 21205813. doi:10.1176/appi.ajp.2010.10101519.
- True WR, Rice J, Eisen SA, Heath AC, Goldberg J, Lyons MJ, Nowak J (1993). "A twin study of genetic and environmental contributions to liability for posttraumatic stress symptoms". Arch. Gen. Psychiatry 50 (4): 257–64. PMID 8466386. doi:10.1001/archpsyc.1993.01820160019002.
- Skelton K, Ressler KJ, Norrholm SD, Jovanovic T, Bradley-Davino B (2012). "PTSD and gene variants: New pathways and new thinking". Neuropharmacology 62 (2): 628–637. PMC 3136568. PMID 21356219. doi:10.1016/j.neuropharm.2011.02.013.
- Spoont, Michele; Arbisi, P; Fu, S; Greer, N; Kehle-Forbes, S; Meis, L; Rutks, I. (January 2013). "Screening for Post-Traumatic Stress Disorder (PTSD) in Primary Care: A Systematic Review". Washington DC: Department of Veterans Affairs. PMID 23487872. Lay summary – Pubmed Health (plain English). open access publication - free to read
- Koenen KC, Moffitt TE, Poulton R, Martin J, Caspi A (February 2007). "Early childhood factors associated with the development of post-traumatic stress disorder: results from a longitudinal birth cohort". Psychol Med 37 (2): 181–92. PMC 2254221. PMID 17052377. doi:10.1017/S0033291706009019.
- 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". Mil Med 170 (9): 787–90. PMID 16261985.
- 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". Biol. Psychiatry 57 (1): 27–32. PMID 15607297. doi:10.1016/j.biopsych.2004.10.009.
- Laor N, Wolmer L, Mayes LC, Golomb A, Silverberg DS, Weizman R, Cohen DJ (May 1996). "Israeli preschoolers under Scud missile attacks. A developmental perspective on risk-modifying factors". Arch Gen Psychiatry 53 (5): 416–23. PMID 8624185. doi:10.1001/archpsyc.1996.01830050052008.
- Laor N, Wolmer L, Mayes LC, Gershon A, Weizman R, Cohen DJ (March 1997). "Israeli preschool children under Scuds: a 30-month follow-up". J Am Acad Child Adolesc Psychiatry 36 (3): 349–56. PMID 9055515. doi:10.1097/00004583-199703000-00013. (subscription required (. ))
- Janoff-Bulman, R. (1992). Shattered Assumptions: Toward a New Psychology of Trauma. New York: Free Press.[page needed]
- Falsetti, Sherry A.; Monier, Jeannine; Resnick, Jeannine (2005). "Chapter 2: Intrusive Thoughts In Posttraumatic Stress Disorder". In Clark, David A. Intrusive Thoughts In Clinical Disorders. Theory, Research, and Treatment. The Guilford Press. pp. 40–41. ISBN 1-59385-083-2.
- Howard, LM; Oram, S; Galley, H; Trevillion, K; Feder, G (2013). "Domestic violence and perinatal mental disorders: a systematic review and meta-analysis.". PLoS medicine 10 (5): e1001452. PMID 23723741. doi:10.1371/journal.pmed.1001452.
- Brewin CR, Andrews B, Valentine JD (October 2000). "Meta-analysis of risk factors for posttraumatic stress disorder in trauma-exposed adults". J Consult Clin Psychol 68 (5): 748–66. PMID 11068961. doi:10.1037/0022-006X.68.5.748.
- Ozer EJ, Best SR, Lipsey TL, Weiss DS (January 2003). "Predictors of posttraumatic stress disorder and symptoms in adults: a meta-analysis". Psychol Bull 129 (1): 52–73. PMID 12555794. doi:10.1037/0033-2909.129.1.52.
- Ruef, Anna; Litz, Brett; Schlenger, William (2000). "Hispanic Ethnicity and Risk for Combat-Related Posttraumatic Stress Disorder". Cultural Diversity and Ethnic Minority Psychology 6 (3): 235–251. doi:10.1037/1099-9809.6.3.235.
- Glass, Albert Julius; Jones, Franklin D. "Psychiatry In The U.S. Army: Lessons for Community Psychiatry" (PDF).
- Pereira, Angela (January 2002). "Combat trauma and the diagnosis of post-traumatic stress disorder in female and male veterans". Military Medicine 167 (1): 23–27.
- Suris, Alina; Lind, Lisa; Kashner, Michael; Borman, Patricia; Petty, Frederick (2004). "Sexual Assault in Women Veterans: An Examination of PTSD Risk, Health Care Utilization, and Cost of Care" (PDF). Psychosomatic Medicine: 749–756.
- Wolfe, Jessica; Sharkansky, Erica; Read, Jennifer; Dawson, Ree; Martin, James; Ouimette, Paige (1 February 1998). "Sexual Harassment and Assault as Predictors of PTSD Symptomatology Among U.S. Female Persian Gulf War Military Personnel" (PDF). Journal of Interpersonal Violence 13: 40–57. doi:10.1177/088626098013001003.
- Maxmen, J. S.; Ward, N. G. (2002). Psychotropic drugs: fast facts (3rd ed.). New York: W. W. Norton. p. 348. ISBN 0-393-70301-0.
- Cohen SI (February 1995). "Alcohol and benzodiazepines generate anxiety, panic and phobias". J R Soc Med 88 (2): 73–77. PMC 1295099. PMID 7769598.
- Spates, R.; Souza, T. (2007). "Treatment of PTSD and Substance Abuse Comorbidity" (PDF). The Behavior Analyst Today 9 (1): 11–26.
- The Secret Life of the Brain (Series), episode 4. PBS. 2001. Retrieved 2014-01-29.
- Joseph Zohar, Alzbeta Juven-Wetzler, Viki Myers, and Leah Fostic (2008). "Post-Traumatic stress disorder: Facts and Fiction". Current opinion in psychiatry 21 (1): 70–eoa. PMID 18281844. doi:10.1097/YCO.0b013e3282f269ee.
- Yehuda R, Halligan SL, Golier JA, Grossman R, Bierer LM (2004). "Effects of trauma exposure on the cortisol response to dexamethasone administration in PTSD and major depressive disorder". Psychoneuroendocrinology 29 (3): 389–404. PMID 14644068. doi:10.1016/S0306-4530(03)00052-0.
- Yehuda R, Halligan SL, Grossman R, Golier JA, Wong C (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". Biol Psychiatry 52 (5): 393–403. PMID 12242055. doi:10.1016/S0006-3223(02)01357-4.
- Heim C, Ehlert U, Hellhammer DH (2000). "The potential role of hypocorticolism in the pathophysiology of stress-related bodily disorders". Psychoneuroendocrinology 25 (1): 1–35. PMID 10633533. doi:10.1016/S0306-4530(99)00035-9.
- Mason JW, Giller EL, Kosten TR, Harkness L (1988). "Elevation of urinary norepinephrine/cortisol ratio in posttraumatic stress disorder". J Nerv Ment Dis 176 (8): 498–502. PMID 3404142. doi:10.1097/00005053-198808000-00008.
- Bohnen N, Nicolson N, Sulon J, Jolles J (1991). "Coping style, trait anxiety and cortisol reactivity during mental stress". J Psychosom Res 35 (2–3): 141–7. PMID 2046048. doi:10.1016/0022-3999(91)90068-Y.
- Geracioti TD, Baker DG, Ekhator NN, West SA, Hill KK, Bruce AB, Schmidt D, Rounds-Kugler B, Yehuda R, Keck PE, Kasckow JW (2001). "CSF norepinephrine concentrations in posttraumatic stress disorder". Am J Psychiatry 158 (8): 1227–30. PMID 11481155. doi:10.1176/appi.ajp.158.8.1227.
- Sautter FJ, Bissette G, Wiley J, Manguno-Mire G, Schoenbachler B, Myers L, Johnson JE, Cerbone A, Malaspina D (December 2003). "Corticotropin-releasing factor in posttraumatic stress disorder (PTSD) with secondary psychotic symptoms, nonpsychotic PTSD, and healthy control subjects". Biol. Psychiatry 54 (12): 1382–8. PMID 14675802. doi:10.1016/S0006-3223(03)00571-7.
- de Kloet CS, Vermetten E, Geuze E, Lentjes EG, Heijnen CJ, Stalla GK, Westenberg HG (2008). "Elevated plasma corticotrophin-releasing hormone levels in veterans with posttraumatic stress disorder". Prog. Brain Res. Progress in Brain Research 167: 287–91. ISBN 978-0-444-53140-7. PMID 18037027. doi:10.1016/S0079-6123(07)67025-3.
- Yehuda R (2001). "Biology of posttraumatic stress disorder". J Clin Psychiatry. 62. Suppl 17: 41–6. PMID 11495096.
- Yehuda R (2002). "Clinical relevance of biologic findings in PTSD". Psychiatr Q 73 (2): 123–33. PMID 12025720. doi:10.1023/A:1015055711424.
- Aardal-Eriksson E, Eriksson TE, Thorell LH (2001). "Salivary cortisol, posttraumatic stress symptoms, and general health in the acute phase and during 9-month follow-up". Biol. Psychiatry 50 (12): 986–93. PMID 11750895. doi:10.1016/S0006-3223(01)01253-7.
- Olszewski TM, Varrasse JF (2005). "The neurobiology of PTSD: implications for nurses". Journal of Psychosocial Nursing and Mental Health Services 43 (6): 40–7. PMID 16018133.
- Lindley SE, Carlson EB, Benoit M (2004). "Basal and dexamethasone suppressed salivary cortisol concentrations in a community sample of patients with posttraumatic stress disorder". Biol. Psychiatry 55 (9): 940–5. PMID 15110738. doi:10.1016/j.biopsych.2003.12.021.
- "NIMH · Post Traumatic Stress Disorder Research Fact Sheet". National Institutes of Health. Retrieved 2014-01-29.
- Newton, Philip. "From Mouse to Man; the Anatomy of Posttraumatic Stress Disorder". Psychologytoday.com. Retrieved 20 December 2009.
- Carlson, Neil R. (2007). Physiology of Behavior (9 ed.). Pearson Education, Inc.[full citation needed]
- Jatzko A, Rothenhöfer S, Schmitt A, Gaser C, Demirakca T, Weber-Fahr W, Wessa M, Magnotta V, Braus DF (2006). "Hippocampal volume in chronic posttraumatic stress disorder (PTSD): MRI study using two different evaluation methods" (PDF). Journal of Affective Disorders 94 (1–3): 121–126. PMID 16701903. doi:10.1016/j.jad.2006.03.010. Retrieved 2014-01-29.
- Newport DJ, Nemeroff CB; Nemeroff, Charles B (2010). "Neurobiology of posttraumatic stress disorder". Current Opinion in Neurobiology 10 (2): 211–218. PMID 10753802. doi:10.1016/S0959-4388(00)00080-5.
- [unreliable medical source?] van der Kolk B (March 2000). "Posttraumatic stress disorder and the nature of trauma". Dialogues in Clinical Neuroscience 2: 7–22. PMC 3181584. PMID 22034447.
- Milad MR, Pitman RK, Ellis CB, Gold AL, Shin LM, Lasko NB, Zeidan MA, Handwerger K, Orr SP, Rauch SL (2009). "Neurobiological basis of failure to recall extinction memory in posttraumatic stress disorder". Biol Psychiatry 66 (12): 1075–82. PMC 2787650. PMID 19748076. doi:10.1016/j.biopsych.2009.06.026.
- Stein MB, Paulus MP (2009). "Imbalance of approach and avoidance: the yin and yang of anxiety disorders". Biol Psychiatry 66 (12): 1072–4. PMC 2825567. PMID 19944792. doi:10.1016/j.biopsych.2009.09.023.
- Agis-Balboa RC, Arcos-Diaz D, Wittnam J, Govindarajan N, Blom K, Burkhardt S, Haladyniak U, Agbemenyah HY, Zovoilis A, Salinas-Riester G, Opitz L, Sananbenesi F, Fischer A (August 2011). "A hippocampal insulin-growth factor 2 pathway regulates the extinction of fear memories". EMBO J 30 (19): 4071–83. PMC 3209781. PMID 21873981. doi:10.1038/emboj.2011.293.
- Radley JJ, Kabbaj M, Jacobson L, Heydendael W, Yehuda R, Herman JP (September 2011). "Stress risk factors and stress related pathology: Neuroplasticity epigenetics and endophenotypes". Stress 14 (5): 481–497. PMC 3641164. PMID 21848436. doi:10.3109/10253890.2011.604751.
- Pitman RK (1989). "Post-traumatic stress disorder, hormones, and memory". Biological Psychiatry 26 (3): 221–223. PMID 2545287. doi:10.1016/0006-3223(89)90033-4.
- Zohar J, Juven-Wetzler A, Myers V, Fostick L (January 2008). "Post traumatic stress disorder:facts and fiction". Current opinion in psychiatry 21 (1): 74–7. PMID 18281844. doi:10.1097/YCO.0b013e3282f269ee.
- Breslau N, Kessler RC (2001). "The stressor criterion in DSM-IV posttraumatic stress disorder: an empirical investigation". Biol. Psychiatry 50 (9): 699–704. PMID 11704077. doi:10.1016/S0006-3223(01)01167-2.
- Blake DD, Weathers FW, Nagy LM, Kaloupek DG, Gusman FD, Charney DS, Keane TM (January 1995). "The development of a Clinician-Administered PTSD Scale". J Trauma Stress 8 (1): 75–90. PMID 7712061. doi:10.1002/jts.2490080106.
- Foa E: The Post Traumatic Diagnostic Scale Manual. Minneapolis, NCS, 1995.[incomplete short citation]
- Brewin CR, Rose S, Andrews B, Green J, Tata P, McEvedy C, Turner S, Foa EB (2002). "Brief screening instrument for post traumatic stress disorder". British Journal of Psychiatry 181: 158–162. PMID 12151288.
- Foa EB, Cashman L, Jaycox L, Perry K (1997). "The validation of a self-report measure of posttraumatic stress disorder: the Posttraumatic Diagnostic Scale". Psychological Assessment 9 (4): 445–451. doi:10.1037/1040-35220.127.116.115.
- "The ICD-10 Classification of Mental and Behavioural Disorders" (PDF). World Health Organization. pp. 120–121. Retrieved 2014-01-29.
- Feldner MT, Monson CM, Friedman MJ (2007). "A critical analysis of approaches to targeted PTSD prevention: current status and theoretically derived future directions". Behav Modif 31 (1): 80–116. PMID 17179532. doi:10.1177/0145445506295057.
- Carlier, IVE; Lamberts, RD; van Uchelen, AJ; Gersons, BPR (1998). "Disaster-related post-traumatic stress in police officers: A field study of the impact of debriefing". Stress Medicine 14 (3): 143–8. doi:10.1002/(SICI)1099-1700(199807)14:3<143::AID-SMI770>3.0.CO;2-S.
- Mayou RA, Ehlers A, Hobbs M (2000). "Psychological debriefing for road traffic accident victims. Three-year follow-up of a randomised controlled trial". Br J Psychiatry 176 (6): 589–93. PMID 10974967. doi:10.1192/bjp.176.6.589.
- Roberts NP, Kitchiner NJ, Kenardy J, Bisson JI (2009). Roberts, Neil P, ed. "Multiple session early psychological interventions for the prevention of post-traumatic stress disorder". Cochrane Database of Systematic Reviews (3). Art. No. CD006869. doi:10.1002/14651858.CD006869.pub2. Archived from the original on 2014-04-21. Retrieved April 27, 2011. (login required)
- Assessment and Management of Conditions Specifically Related to Stress (PDF). Geneva: World Health Organization. 2013. ISBN 978-92-4-150593-2. Retrieved 2014-01-29.
- van Emmerik AA, Kamphuis JH, Hulsbosch AM, Emmelkamp PM (2002). "Single session debriefing after psychological trauma: a meta-analysis". The Lancet 360 (9335): 766–771. PMID 12241834. doi:10.1016/S0140-6736(02)09897-5.
- Rose S, Bisson J, Churchill R, Wessely S (2002). Rose, Suzanna C, ed. "Psychological debriefing for preventing post traumatic stress disorder (PTSD)". Cochrane Database of Systematic Reviews (2). Art. No. CD000560. PMID 12076399. doi:10.1002/14651858.CD000560.
- "American Psychological Association on psychological debriefing".
- Wiseman T, Foster K, Curtis K. Mental health following traumatic physical injury: an integrative literature review. Injury. 2013 Nov;44(11):1383-90. doi:10.1016/j.injury.2012.02.015 PMID 22409991
- Kassam-Adams N, et al. Posttraumatic stress following pediatric injury: update on diagnosis, risk factors, and intervention. JAMA Pediatr. 2013 Dec;167(12):1158-65. doi:10.1001/jamapediatrics.2013.2741 PMID 24100470
- Lee CW & Cuijpers P (2013). "A meta-analysis of the contribution of eye movements in processing emotional memories". J. Behav. Ther. Exp. Psychiatry 44 (2): 231–9. PMID 23266601. doi:10.1016/j.jbtep.2012.11.001.
- Crawford C, Dawn B (Jul 2013). "A Systematic Review of Biopsychosocial Training Programs for the Self-Management of Emotional Stress: Potential Applications for the Military". Evidence-Based Complementary and Alternative Medicine 2013: 1–23. doi:10.1155/2013/747694.
- Cahill, S. P.; Foa, E. B. (2004). Taylor, S., ed. Advances in the Treatment of Posttraumatic Stress Disorder: Cognitive-behavioral perspectives. New York: Springer. pp. 267–313.
- Bisson JI, Ehlers A, Matthews R, Pilling S, Richards D, Turner S (2007). "Psychological treatments for chronic post-traumatic stress disorder. Systematic review and meta-analysis". Br J Psychiatry 190 (2): 97–104. PMID 17267924. doi:10.1192/bjp.bp.106.021402.
- Seidler GH, Wagner FE (2006). "Comparing the efficacy of EMDR and trauma-focused cognitive-behavioral therapy in the treatment of PTSD: a meta-analytic study". Psychol Med 36 (11): 1515–22. PMID 16740177. doi:10.1017/S0033291706007963.
- Hassija, CM; Gray, MJ (2007). "Behavioral Interventions for Trauma and Posttraumatic Stress Disorder". International Journal of Behavioral Consultation and Therapy (Behavior Analyst Online) 3 (2): 166–175. doi:10.1037/h0100797.
- Mulick, P. S.; Landes, S.; Kanter, J. W. (2005). "Contextual Behavior Therapies in the Treatment of PTSD: A Review" (PDF). International Journal of Behavioral Consultation and Therapy 1 (3): 223–228. doi:10.1037/h0100747.
- Mulick, P. S.; Naugle, A. E. (2009). "Behavioral Activation in the Treatment of Comorbid Posttraumatic Stress Disorder and Major Depressive Disorder". International Journal of Behavioral Consultation and Therapy 5 (2): 330–339.
- Grohol, JM. "What is Exposure Therapy?". Psychcentral.com. Retrieved 2010-07-14.
- Joseph, J. S.; Gray, M. J. (2008). "Exposure Therapy for Posttraumatic Stress Disorder" (PDF). Journal of Behavior Analysis of Offender and Victim: Treatment and Prevention 1 (4): 69–80. doi:10.1037/h0100457. Retrieved 2010-05-10.
- 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). Work Group on ASD PTSD, Steering Committee on Practice Guidelines. "Practice guideline for the treatment of patients with acute stress disorder and posttraumatic stress disorder". Am J Psychiatry 161 (11 Suppl): 3–31. PMID 15617511.
- 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. ISBN 0-309-10926-4.[page needed]
- "Prolonged Exposure Therapy". U.S. Department of Veteran Affairs. PTSD: National Center for PTSD. 2009-09-29. Retrieved 2010-07-14.
- Karlin BE, Ruzek JI, Chard KM, Eftekhari A, Monson CM, Hembree EA, Resick PA, Foa EB (2010). "Dissemination of evidence-based psychological treatments for posttraumatic stress disorder in the Veterans Health Administration". Journal of Traumatic Stress 23 (6): 663–673. PMID 21171126. doi:10.1002/jts.20588.
- Shapiro, Francine (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. PMID 12115716. doi:10.1002/jclp.10068.
- The Management of Post-Traumatic Stress Working Group (2010). "VA/DoD clinical practice guideline for management of post-traumatic stress". Department of Veterans Affairs, Department of Defense. p. Version 2.0. Retrieved 2 June 2013.
- Gillies D, Taylor F, Gray C, O'Brien L, D'Abrew N (2012). Gillies, Donna, ed. "Psychological therapies for the treatment of post‐traumatic stress disorder in children and adolescents". Cochrane Database of Systematic Reviews 12: CD006726. PMID 23235632. doi:10.1002/14651858.CD006726.pub2. Lay summary – Pubmed Health (plain English).
- Jeffries FW, Davis P; 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. PMID 23102050. doi:10.1017/S1352465812000793.
- Jonas, D. E.; Cusack, K.; Forneris, C. A. (April 2013). "Psychological and pharmacological treatments for adults with posttraumatic stress disorder (PTSD)". Comparative Effectiveness Reviews (92). Rockville, MD: US Agency for Healthcare Quality and Research. PMID 23658937. Lay summary – Pubmed Health (plain English). open access publication - free to read
- Weissman, M. M.; Markowitz, J. C.; Klerman, G. L. (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". Am J Psychiatry 162 (1): 181–3. PMID 15625219. doi:10.1176/appi.ajp.162.1.181.
- "Trauma and PTSD Program – Columbia University Department of Psychiatry". Columbiatrauma.org. Retrieved 2014-01-29.
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|40x40px||Wikimedia Commons has media related to Posttraumatic stress disorder.|
- Posttraumatic stress disorder at DMOZ
- Resources for the public from VA National PTSD Center
- Resources for professionals from VA National PTSD Center
- Post Traumatic Stress Disorder Information Resource from The University of Queensland School of Medicine
- Resources for Parents of Children with PTSD from The Children's Hospital of Philadelphia
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