Posttraumatic stress disorder

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Posttraumatic stress disorder
Classification and external resources

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Francisco Goya (1746–1828)
ICD-10F43.1
ICD-9309.81
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Posttraumatic stress disorder
Classification and external resources

No quieren (They do not want to)
#9 from aquatint series Los Desastres de la Guerra (The Disasters of War, 1810–1820)
Francisco Goya (1746–1828)
ICD-10F43.1
ICD-9309.81
DiseasesDB33846
MedlinePlus000925
eMedicinemed/1900
MeSHD013313

Posttraumatic stress disorder[note 1] (PTSD) is a severe anxiety disorder that can develop after exposure to any event that results in psychological trauma.[1][2][3] This event may involve the threat of death to oneself or to someone else, or to one's own or someone else's physical, sexual, or psychological integrity,[1] overwhelming the individual's ability to cope. As an effect of psychological trauma, PTSD is less frequent and more enduring than the more commonly seen post traumatic stress (also known as acute stress response).[4] Diagnostic symptoms for PTSD include re-experiencing the original trauma(s) through flashbacks or nightmares, avoidance of stimuli associated with the trauma, and increased arousal—such as difficulty falling or staying asleep, anger, and hypervigilance. Formal diagnostic criteria (both DSM-IV-TR and ICD-10) require that the symptoms last more than one month and cause significant impairment in social, occupational, or other important areas of functioning.[1][5]

Contents

Classification

Posttraumatic stress disorder is classified as an anxiety disorder, characterized by aversive anxiety-related experiences, behaviors, and physiological responses that develop after exposure to a psychologically traumatic event (sometimes months after). Its features persist for longer than 30 days, which distinguishes it from the briefer acute stress disorder and are disruptive to all aspects of life.[6][7] It has three sub-forms: acute, chronic, and delayed-onset.[8]

Causes

Psychological trauma

PTSD is believed to be caused by experiencing any of a wide range of events[9] which produces intense negative feelings of "fear, helplessness or horror"[10] in the observer or participant.[1] Sources of such feelings may include (but are not limited to):

Children or adults may develop PTSD symptoms by experiencing bullying or mobbing.[12][13] Approximately 25% of children exposed to family violence can experience PTSD.[14] Preliminary research suggests that child abuse may interact with mutations in a stress-related gene to increase the risk of PTSD in adults.[15][16][17] However, being exposed to a traumatic experience doesn't automatically indicate they will develop PTSD.[18] It has been shown that the intrusive memories, such as flashbacks, nightmares, and the memories themselves, are greater contributors to the biological and psychological dimensions of PTSD than the event itself.[19] These intrusive memories are mainly characterized by sensory episodes, rather than thoughts. People with PTSD have intrusive re-experiences of traumatic events which lack awareness of context and time. These episodes aggravate and maintain PTSD symptoms since the individual re-experiences trauma as if it was happening in the present moment.[20]

Multiple studies show that parental PTSD and other posttraumatic disturbances in parental psychological functioning can, despite a traumatized parent's best efforts, interfere with their response to their child as well as their child's response to trauma.[21][22] Parents with violence-related PTSD may, for example, inadvertently expose their children to developmentally inappropriate violent media due to their need to manage their own emotional dysregulation.[23] Clinical findings indicate that a failure to provide adequate treatment to children after they suffer a traumatic experience, depending on their vulnerability and the severity of the trauma, will ultimately lead to PTSD symptoms in adulthood.[24]

Evolutionary psychology

Evolutionary psychology views different types of fears and reactions caused by fears as adaptations that may have been useful in the ancestral environment in order to avoid or cope with various threats. Mammals generally display several defensive behaviors roughly dependent on how close the threat is: avoidance, vigilant immobility, withdrawal, aggressive defense, appeasement, and finally complete frozen immobility (the last possibly to confuse a predator's attack reflex or to simulate a dead and contaminated body). PTSD may correspond to and be caused by overactivation of such fear circuits. Thus, PTSD avoidance behaviors may correspond to mammal avoidance of and withdrawal from threats. Heightened memory of past threats may increase avoidance of similar situations in the future as well as be a prerequisite for analyzing the past threat and develop better defensive behaviors if the threat should reoccur. PTSD hyperarousal may correspond to vigilant immobility and aggressive defense. Complex posttraumatic stress disorder (and phenomena such as the Stockholm syndrome) may in part correspond to the appeasement stage and possibly the frozen immobility stage.[25][26]

There may be evolutionary explanations for differences in resilience to traumatic events. Thus, PTSD is rare following traumatic fire which may be explained by events such as forest fires long being part of the evolutionary history of mammals. On the other hand, PTSD is much more common following modern warfare, which may be explained by modern warfare being a new development and very unlike the quick inter-group raids that are argued to have characterized the paleolithic.[27]

Neuroendocrinology

PTSD symptoms may result when a traumatic event causes an over-reactive adrenaline response, which creates deep neurological patterns in the brain. These patterns can persist long after the event that triggered the fear, making an individual hyper-responsive to future fearful situations.[4][28] During traumatic experiences the high levels of stress hormones secreted suppress hypothalamic activity which may be a major factor towards the development of PTSD.[29]

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.[30][31]

In addition, most people with PTSD also show a low secretion of cortisol and high secretion of catecholamines in urine,[32] with a norepinephrine/cortisol ratio consequently higher than comparable non-diagnosed individuals.[33] 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.[34]

Brain catecholamine levels are high,[35] and corticotropin-releasing factor (CRF) concentrations are high.[36][37] Together, these findings suggest abnormality in the hypothalamic-pituitary-adrenal (HPA) axis.

The HPA axis is responsible for coordinating the hormonal response to stress.[38] 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.[39] Some researchers have associated the response to stress in PTSD with long-term exposure to high levels of norepinephrine and low levels of cortisol, a pattern associated with improved learning in animals.[citation needed]

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.[40]

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.[41] 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.[19] Serotonin also contributes to the stabilization of glucocorticoid production.

Dopamine levels in patients 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.[19]

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.[19]

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.[38][42]

Neuroanatomy

Regions of the brain associated with stress and posttraumatic stress disorder[43]

Three areas of the brain whose 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.[44] 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 who suffered no such symptoms.[45] This finding could not be replicated in chronic PTSD patients traumatized at an air show plane crash in 1988 (Ramstein, Germany).[46][47]

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.[48] 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 plague PTSD patients. When someone with PTSD undergoes a stimuli similar to the traumatic event the body perceives the event as occurring again because the memory was never properly recorded in the patients memory.[38]

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 particularly during extinction.[49] This is consistent with an interpretation of PTSD as a syndrome of deficient extinction ability.[49][50] 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.[51] 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 which coordinates the hormonal response to stress[52] 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 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 medial prefrontal cortex, part of the amygdala, can inhibit the conditioned fear responses during trauma.[38]

The LC-noradrenergic system has been hypothesized to mediate the over-consolidation of fear memory in PTSD. High levels of cortisol reduces noradrenergic activity it is proposed that individuals with PTSD fail to regulate the increased noradrenergic response to traumatic stress.[53] 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.[38]

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) which elaborates the fear response, (including behavioral response to threat and elevated startle response). Descending inhibitory inputs form the medial prefrontal cortex (mPFC) regulates the transmission from the BLA to the CeA which is hypothesized to play a role in the extinction of conditioned fear responses.[38]

Genetics

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 having PTSD compared to twins that were dizygotic (non-identical twins).[54] There is also 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 shares greater than 40% genetic similarities.[38]

Gamma-aminobutyric acid (GABA) is the major inhibitory neurotransmitter in the brain. A recent study reported significant interactions between three polymorphisms in the GABA alpha-2 receptor gene and the severity of childhood trauma in predicting PTSD in adults. A study found those with a specific genotype for G-protein signaling 2 (RGS2), a protein that decreases G protein-coupled receptor signaling, and high environmental stress exposure as adults and a diagnosis of lifetime PTSD. This was particularly prevalent in adults with prior trauma exposure and low social support.[38]

Recently, it has been found that several single-nucleotide polymorphisms (SNPs) in FK506 binding protein 5 (FKBP5) interact with childhood trauma to predict severity of adult PTSD.[55][56] These findings suggest that individuals with these SNPs who are abused as children are more susceptible to PTSD as adults.

This is particularly interesting given that FKBP5 SNPs have previously been associated with peritraumatic dissociation (that is, dissociation at the time of the trauma),[57] which has itself been shown to be predictive of PTSD.[58][59] Furthermore, FKBP5 may be less expressed in those with current PTSD.[60] Another recent study found a single SNP in a putative estrogen response element on ADCYAP1R1 (encodes pituitary adenylate cyclase-activating polypeptide type I receptor or PAC1) to predict PTSD diagnosis and symptoms in females.[61] Incidentally, this SNP is also associated with fear discrimination. The study suggests that perturbations in the PACAP-PAC1 pathway are involved in abnormal stress responses underlying PTSD.

PTSD is a psychiatric disorder which requires an environmental event which individuals may have varied responses to so gene-environment studies tend to be the most indicative of their effect on the probability of PTSD then studies of the main effect of the gene. Recent studies have demonstrated the interaction between PFBP5 and childhood environment to predict the severity of PTSD. Polymorphisms in FKBP5 have been associated with peritraumatic dissociation in mentally ill children. A study of highly traumatized African-American subjects from inner city primary care clinics indicated 4 polymorphisms of the FKBP5 gene, each of these were functional. The interaction between the polymorphisms and the severity of childhood abuse predicts the severity of the adult PTSD symptoms. A more recent study of the African-American population indicated that the TT genotype of the FKBP5 gene was associated with the highest risk of PTSD among those who experienced childhood adversity, however those with this genotype that experienced no childhood adversity had the lowest risk of PTSD. In addition alcohol dependence interacts with the FKBP5 polymorphisms and childhood adversity to increase the risk of PTSD in these populations. Emergency room expression of the FKPB5 mRNA following trauma was shown to indicate a later development of PTSD.[38]

Catechol-O-methyl transferase (COMT) is an enzyme that catalyzes the extraneuronal breakdown of catecholamines. The gene that codes for COMT has a functional polymorphism in which a valine has been replaced with a methionine at condon 158. This polymorphism has lower enzyme activity and has been tied to slower breakdown of the catecholamines. A study, of Rwandan Genocide survivors, indicated that carriers of the Val allel demonstrated the expected response relationship between the higher number of lifetime traumatic events and a lifetime diagnosis of PTSD. However those who were homozygotes for the Met/Met genotype demonstrated a high risk of lifetime PTSD independent of the number of traumatic experiences. Those with Met/Met genotype also demonstrated a reduced extinction of conditioned fear responses with may account for the high risk for PTSD experienced by this genotype.[38]

Many genes impact the limbic-frontal neurocircuitry as a result of its complexity. The main effect of the D2A1 allele of the dopamine receptor D2 (DRD2) has a strong association with the diagnosis of PTSD. The D2A1 allele has also shown a significant association to PTSD in those who engaged in harmful drinking. In addition a polymorphism in the dopamine transporter SLC6A3 gene has a significant association with chronic PTSD. A polymorphism of the serotonin receptor 2A gene has been associated with PTSD in Korean women. The short allele of the promoter region of the serotonin transporter (5-HTTLPR) has been shown to be less efficient then the long allele and is associated with the amygdala response for extinction of fear conditioning. However the short allele is associated with a decreased risk of PTSD in a low risk environment but a high risk of PTSD in a high risk environment. The s/s genotype demonstrated a high risk for development of PTSD even in response to a small number of traumatic events but those with the l allele demonstrate increasing rates of PTSD with increasing traumatic experiences.[38]

Genome-wide association study (GWAS) offer an opportunity to identify novel risk variants for PTSD which will in turn inform our understanding of the etiology of the disorder. Early results indicate the feasibility and potential power of GWAS to identify biomarkers for anxiety-related behaviors that suggest a future of PTSD. These studies will lead to the discovery of novel loci for the susceptibility and symptomatology of anxiety disorders including PTSD.[38]

Epigenetics

Gene and environment studies alone fail to explain the importance the developmental stressor timing exposure to the phenotypic changes associated with PTSD. Epigenetic modification is the environmentally induced change in DNA which alters the function rather than the structure of the gene. The biological mechanism of epigenetic modification typically involves the methylation of cytosine within a gene which produces decreased transcription of that segment of DNA. The neuroendocrine alteration seen in animal models parallel those of PTSD in which low basal cortisol and enhanced suppression of cortisol in response to synthetic glucocorticoid becomes hereditary. Lower levels of glucocorticoid receptor (GR) mRNA have been demonstrated in the hippocampus of suicide victims with histories of childhood abuse. It hasn’t been possible to monitor the state of methylation over time however the interpretation is early developmental methylation changes are long-lasting and enduring. It is hypothesized that epigenetic-mediated changes in the HPA axis could be associated with an increased vulnerability to PTSD following traumatic events. These findings support the mechanism in which early life trauma strongly validates as a risk factor for PTSD development in adulthood by recalibrating the set point and stress-responsivity of the HPA axis. Studies have reported an increased risk for PTSD and low cortisol levels in the offspring of female holocaust survivors with PTSD. Epigenetic mechanisms may also be relevant to the intrauterine environment. Mothers with PTSD produced infants with lower salivary cortisol levels only if the traumatic exposure occurred during the third trimester of gestation. These changes occur via transmission of hormonal responses to the fetus leading to a reprogramming of the glucocorticoid responsivity in the offspring.[38]

Risk factors

Although most people (50–90%) encounter trauma over a lifetime,[62][63] about 20-30% develop PTSD but over half of these people will recover without treatment.[4][62] Vulnerability to PTSD presumably stems from an interaction of biological diathesis, early childhood developmental experiences, and trauma severity.[4] A person that never established secure relationships and learned coping skills as a young child if exposed to a traumatic experience is more likely to develop PTSD than one that developed good coping skills and has a support network.[4]

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.[64][65][66][67] Peritraumatic dissociation in children is a predictive indicator of the development of PTSD later in life.[38] This effect of childhood trauma, which is not well understood, may be a marker for both traumatic experiences and attachment problems.[68][69] Proximity to, duration of, and severity of the trauma also make an impact, and interpersonal traumas cause more problems than impersonal ones.[70]

Military experience

Schnurr, Lunney, and Sengupta[59] identified risk factors for the development of PTSD in Vietnam veterans. Among those are:

They also identified certain protective factors, such as:

Glass and Jones found early intervention to be a critical preventive measure:

"PTSD symptoms can follow any serious psychological trauma, such as exposure to combat, accidents, torture, disasters, criminal assault and exposure to atrocities or to the sequelae of such extraordinary events. Prisoners of war exposed to harsh treatment are particularly prone to develop PTSD. In their acute presentation these symptoms, which include subsets of a large variety of affective, cognitive, perceptional, emotional and behavioral responses which are relatively normal responses to gross psychological trauma. If persistent, however, they develop a life of their own and may be maintained by inadvertent reinforcement. Early intervention and later avoidance of positive reinforcement (which may be subtle) for such symptoms is a critical preventive measure.[74]

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.[4]

Foster care

In the Casey Family Northwest Alumni Study, conducted in conjunction with researchers from the Harvard Medical School in Oregon and Washington state, the rate of PTSD in adults who were in foster care for one year between the ages of 14–18 was found to be higher than that of combat veterans. Up to 25% of those in the study meet the diagnostic criteria for PTSD as compared to 12–13% of Iraq war veterans and 15% of Vietnam War veterans, and a rate of 4% in the general population. The recovery rate for foster home alumni was 28.2% as opposed to 47% in the general population.[75][76]

Dubner and Motta (1999)[77] found that 60% of children in foster care who had experienced sexual abuse had PTSD, and 42% of those who had been physically abused met the PTSD criteria. PTSD was also found in 18% of the children who were not abused. These children may have developed PTSD due to witnessing violence in the home, or as a result of real or perceived parental abandonment.

After individuals with dissociative identity disorder, patients with posttraumatic stress disorder have the highest hypnotizability of any clinical group.[78]

Diagnosis

DSM-IV criteria

The diagnostic criteria for PTSD, stipulated in the Diagnostic and Statistical Manual of Mental Disorders IV (Text Revision) (DSM-IV-TR), may be summarized as:[1][79]

A: Exposure to a traumatic event

This must have involved both (a) loss of "physical integrity", or risk of serious injury or death, to self or others, and (b) a response to the event that involved intense fear, horror, or helplessness (or in children, the response must involve disorganized or agitated behavior). (The DSM-IV-TR criterion differs substantially from the previous DSM-III-R stressor criterion, which specified the traumatic event should be of a type that would cause "significant symptoms of distress in almost anyone," and that the event was "outside the range of usual human experience."[80])

B: Persistent re-experiencing

One or more of these must be present in the victim: flashback memories, recurring distressing dreams, subjective re-experiencing of the traumatic event(s), or intense negative psychological or physiological response to any objective or subjective reminder of the traumatic event(s).

C: Persistent avoidance and emotional numbing

This involves a sufficient level of:

D: Persistent symptoms of increased arousal not present before

These are all physiological response issues, such as difficulty falling or staying asleep, or problems with anger, concentration, or hypervigilance. Additional symptoms include irritability, angry outbursts, increased startle response, and concentration or sleep problems.[19]

E: Duration of symptoms for more than 1 month

If all other criteria are present, but 30 days have not elapsed, the individual is diagnosed with Acute stress disorder.[19]

F: Significant impairment

The symptoms reported must lead to "clinically significant distress or impairment" of major domains of life activity, such as social relations, occupational activities, or other "important areas of functioning".[81]

Assessment

Since the introduction of DSM-IV, the number of possible events which might be used to diagnose PTSD has increased; one study suggests that the increase is around 50%.[82] Various scales exist to measure the severity and frequency of PTSD symptoms.[83][84] Standardized screening tools such as Trauma Screening Questionnaire[85] and PTSD Symptom Scale[86] can be used to detect possible symptoms of posttraumatic stress disorder and suggest the need for a formal diagnostic assessment.

Research-based alternative symptom groups

Emerging factor analytic research[87] suggests that PTSD symptoms group empirically into four clusters, not the three currently described in the Diagnostic and Statistical Manual of Mental Disorders. One model supported by this research divides the traditional avoidance symptoms into a cluster of numbing symptoms (such as loss of interest and feeling emotionally numb) and a cluster of behavioral avoidance symptoms (such as avoiding reminders of the trauma).[88] An alternative model adds a fourth cluster of dysphoric symptoms. These include symptoms of emotional numbing, as well as anger, sleep disturbance, and difficulty concentrating (traditionally grouped under the hyperarousal cluster).[89][90] A literature review[91] and meta-analysis[92] did not find strong support across the literature for one of these models over the other.

DSM-5 proposed diagnostic criteria changes

In preparation for the May 2013[93] release of the DSM-5,[94] the fifth version of the American Psychiatric Association's diagnostic manual, draft diagnostic criteria were released for public comment, followed by a two-year period of field testing.[95] Proposed changes to the criteria (subject to ongoing review[96] and research[97]) include the following:[98]

"Developmental trauma disorder", a proposed new diagnosis, was still under discussion at the time of the draft publication.[99]

The name of the disorder is being reviewed for a possible change, to posttraumatic stress injury, ostensibly to help reduce stigma towards those afflicted.[100]

Management

Prevention and early intervention strategies

Modest benefits have been seen from early access to cognitive behavioral therapy, as well as from some medications such as propranolol.[101] Critical incident stress management has been suggested as a means of preventing PTSD, but subsequent studies suggest the likelihood of its producing iatrogenic outcomes.[102][103] A review of multiple studies, involving a number of different post-event psychological interventions structured to prevent PTSD "...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.[104]

Early detection

The ability to prescreen individuals would be of great help in getting treatment to those who are at risk of PTSD prior to development of the syndrome. Several biological indicators have been identified that are related to later PTSD development. First, Delhanty[105] found that higher response times and a smaller hippocampal volume were identified as linked to later PTSD development. However, both of these indicators are relatively difficult to test for and need specialized tests or equipment, or both, to identify. A blood biomarker is much easier to test for. Van Zuiden et al.[106] found a biomarker when testing U.S. Army soldiers prior to deployment. They found that soldiers with more glucocorticoid receptors (GR) were more likely to be diagnosed with PTSD six months after deployment. However, higher GR levels have not been identified as a cause of PTSD, and may instead be an intermediator, or even an indicator that the individual has previously experienced traumatic events. There is a great deal of overlap between high GR levels and those who later are diagnosed with and without PTSD. Thus, the identification of high GR is simply a vulnerability indicator at this time.

Delhanty[105] found that biological precursors existed directly following traumatic exposure in those who later developed chronic PTSD and were significantly different from those who did not. Directly following the traumatic event later sufferers often have significantly lower levels of hypothalamic pituitary-adrenal activity and a corresponding decrease in Cortisol. Other methods of early detection include the identification of specific risk factors associated with later PTSD symptoms. Resnick, Acierno, Holmes, Kilpatrick, and Jager[107] for example were able to identify that the forensic exam given to victims after a rape was associated with PTSD. Finally, global treatments attempt to avoid the problems of early detection by simply treating everyone involved. However, many studies[105] have found this to be often ineffective and for global treatments to at times increase prevalence rates of PTSD.

Preventive Treatments

Psychological debriefing

The first form of preventive treatment is that of a psychological debriefing.[101] Psychological debriefing is the most often used preventive measure. One of the main reasons for this is 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, while this form of therapy is the most often used it is the least effective.[101] Studies have had mixed findings concerning psychological debriefings and have ranged from being of significant help to helping in the formation of PTSD in individuals who would otherwise have not developed PTSD.[52] The greater number of studies tends to simply find that it is neither overly beneficial nor harmful.[4]

Risk Targeted Interventions

Risk targeted interventions are those that attempt to mitigate specific formative information or events. It can target modeling normal behaviors, instruction on a task, or giving information on the event. For example,[107] rape victims were given an instruction video on the procedures for a forensic exam. Also included in the video was advice on how to identify and stop avoidance behavior and control anxiety. Finally, the individuals modeling the forensic exam were shown to be calm and relaxed. PTSD diagnosis for those who saw the video were thirty three percent less than for those who went through the standard forensic procedure.

Psychobiological Treatments

Psychobiological treatments have also found success, especially with cortisol.[101] Psychobiological treatments target biological changes that occur after a traumatic event. They also attempt to chemically alter learning or memory formation. Cortisol treatments after a traumatic event have found success in mitigating later diagnosis of PTSD. As discussed earlier, cortisol is often lower in individuals who are at risk of PTSD after a traumatic event than their counterparts. By increasing cortisol levels to normal levels this has been shown to reduce arousal post event as well prevent GR upregulation.

Stepped Collaborative Care

Stepped collaborative care is where individuals who are at risk are monitored for symptoms.[101] As symptoms of PTSD appear the level of care is increased to treat those symptoms.

Psychotherapeutic interventions

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.[4][108]

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),[48] and many combinations of these procedures.[109][110] A 2010 review disagrees that these treatments have proven efficacy and points out methodological flaws in the studies and previous meta-analyses.[111]

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."[112] 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.[113]

Behavioral and 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[114] 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.[115] Many of these therapy methods have a significant element of exposure[116] and have demonstrated success in treating the primary problems of PTSD and co-occurring depressive symptoms.[117]

Exposure therapy is a type of cognitive behavioral therapy[118] 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.[119] Some organizations[which?] have endorsed the need for exposure.[120][121] The US Department of Veterans Affairs has been actively training mental health treatment staff in prolonged exposure therapy[122] and Cognitive Processing Therapy[123] in an effort to better treat US Veterans with PTSD.

Eye movement desensitization and reprocessing

Eye movement desensitization and reprocessing (EMDR) is specifically targeted as a treatment for PTSD.[124] Based on the evidence of controlled research, the American Psychiatric Association[not in citation given][125] and the United States Department of Veterans Affairs and Department of Defense[not in citation given][126] have placed EMDR in the highest category of effectiveness and research support in the treatment of trauma. Several international bodies have made similar recommendations.[127] However, some reviewers no longer believe that the eye movements assist in recovery, proposing instead that the review of and engagement with memories, processing of cognitions, and rehearsal of coping skills are the psychotherapeutically effective components of the procedure.[111][128][neutrality is disputed]

Interpersonal psychotherapy

Other approaches, particularly involving social supports,[72][73] may also be important. An open trial of interpersonal psychotherapy[129] reported high rates of remission from PTSD symptoms without using exposure.[130] A current, NIMH-funded trial in New York City is now (and into 2013) comparing interpersonal psychotherapy, prolonged exposure therapy, and relaxation therapy.[131][132][133]

Medication

A variety of medications has shown adjunctive benefit in reducing PTSD symptoms,[134] but "there is no clear drug treatment for PTSD".[135] Positive symptoms (re-experiencing, hypervigilance, increased arousal) generally respond better to medication than negative symptoms (avoidance, withdrawal), and it is recommended that any drug trial last for at least 6–8 weeks.[135] With many medications, residual symptoms following treatment is the rule rather than the exception, which has led to increased research in the aggressive treatment of PTSD symptoms.[136]

Some studies have shown that treatment with hydrocortisone shortly after a traumatic event, in comparison to a placebo, decreases the likelihood that the patient will suffer from PTSD. Other studies have indicated that propranolol administered within 6 hours of a traumatic event decreases the physiological reactivity to a reminder of the traumatic event. However propranolol had no effect on the rate of PTSD. Despite these studies there is not significant evidence that medication can prevent PTSD, therefore none is routinely administered.[137]

Symptom management: potentially useful medication classes

SSRIs (selective serotonin reuptake inhibitors). SSRIs are considered to be a first-line drug treatment.[138][139] SSRIs for which there are data to support use include: citalopram, escitalopram,[140] fluoxetine,[141] fluvoxamine,[142] paroxetine,[143] and sertraline.[141][144]

Among the anti-depressants described in this section, bupropion and venlafaxine have the lowest patient drop-out rates. Sertraline, fluoxetine, and nefazodone have a modestly higher drop-out rate (~15%), and the heterocyclics and paroxetine have the highest rates (~20%+).[145] Where drop-out is caused or feared because of medication side-effects, it should be remembered that most patients do not experience such side-effects.[146]

Alpha-adrenergic antagonists. Prazosin ("Minipress"), in a small study of combat veterans, has shown substantial benefit in relieving or reducing nightmares.[147] Clonidine ("Catapres") can be helpful with startle, hyperarousal, and general autonomic hyperexcitability.[148]

Anti-convulsants, mood stabilizers, anti-aggression agents. Carbamazepine ("Tegretol") has likely benefit in reducing arousal symptoms involving noxious affect,[141] as well as mood or aggression.[149] Topiramate ("Topamax")[147] has been effective in achieving major reductions in flashbacks and nightmares, and no reduction of effect was seen over time.[147] Zolpidem ("Ambien") has also proven useful in treating sleep disturbances.[148]

Lamotrigine ("Lamictal") may be useful in reducing reexperiencing symptoms, as well as avoidance and emotional numbing.[147][150][151][152] Valproic acid ("Depakene") and has shown reduction of symptoms of irritability, aggression, and impulsiveness, and in reducing flashbacks.[148] Similarly, lithium carbonate has worked to control mood and aggressions (but not anxiety) symptoms.[149] Buspirone ("BuSpar") has an effect similar to that of lithium, with the additional benefit of working to reduce hyperarousal symptoms.[148]

Antipsychotics. Risperidone can be used to help with dissociation, mood issues, and aggression.[153]

Serotonin antagonists. Cyproheptadine (Periactin) can be used to help with sleep disorders and nightmares.[154]

Atypical antidepressants.[155] Nefazodone ("Serzone") can be effective with sleep disturbance symptoms and with secondary depression, anxiety, and sexual dysfunction symptoms.[141] Trazodone ("Desyrel") can also reduce or eliminate problems with anger, anxiety, and disturbed sleep.[141]

Beta blockers. Propranolol ("Inderal") has demonstrated possibilities in reducing hyperarousal symptoms, including sleep disturbances.[148][156]

Benzodiazepines. These drugs are not recommended by clinical guidelines for the treatment of PTSD due to a lack of evidence of benefit.[157] Nevertheless some doctors use benzodiazepines with caution for short-term anxiety relief,[153][158] hyperarousal, and sleep disturbance.[148] However, some authors believe that the use of benzodiazepines is contraindicated for acute stress as this group of drugs promote dissociation and ulterior revivals.[159] 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.[138][160]

Glucocorticoids. Additionally, post-stress high dose corticosterone administration was recently found to reduce "PTSD-like" behaviors in a rat model of PTSD. In this study, corticosterone impaired memory performance, suggesting that it may reduce risk for PTSD by interfering with consolidation of traumatic memories.[161] The neurodegenerative effects of the glucocorticoids, however, may prove this treatment counterproductive.[162]

Heterocyclic / Tricyclic anti-depressants anti-depressants. Amitriptyline ("Elavil") has shown benefit for positive distress symptoms and for avoidance, and Imipramine ("Tofranil") has shown benefit for intrusive symptoms.[141]

Monoamine-oxidase inhibitors (MAOIs). Phenelzine ("Nardil") has for some time[when?] been observed to be effective with hyperarousal and depression and is especially effective with nightmares.[141]

Miscellaneous other medications. Clinical trials evaluating methylenedioxymethamphetamine (MDMA, "Ecstasy") in conjunction with psychotherapy are being conducted in Switzerland[163] and Israel.[164]

Symptom prevention: potentially useful medication classes

Some medications have shown benefit in preventing PTSD or reducing its incidence, when given in close proximity to a traumatic event. These medications include:

Alpha-adrenergic agonists. Anecdotal report of success in using clonidine ("Catapres") to reduce traumatic stress symptoms[165] suggests that it may have benefit in preventing PTSD.

Beta blockers. Propranolol ("Inderal"), similarly to clonidine, may be useful if there are significant symptoms of "over-arousal". These may inhibit the formation of traumatic memories by blocking adrenaline's effects on the amygdala.[156]

Glucocorticoids. There is some evidence suggesting that administering glucocorticoids immediately after a traumatic experience may help prevent PTSD. Several studies have shown that individuals who receive high doses of hydrocortisone for treatment of septic shock, or following surgery, have a lower incidence and fewer symptoms of PTSD.[166][167][168]

Medications by symptom group affected

Medications can affect one or more of the symptoms, in one or more of the three major symptom classes[1] involved in diagnosing PTSD, which can be summarized in the following table:[153][158][169]

Symptom classSymptomMedication
Reexperiencing
 intrusive recallamitriptyline; fluoxetine; imipramine; lamotrigine; sertraline
intrusive reexperiencingamitriptyline; fluoxetine; imipramine; nefazodone; sertraline (women only); topiramate;
sleep disturbance, nightmaresbenzodiazepines; carbamazepine; clonidine; nefazodone; phenelzine; prazosin; topiramate; trazodone; zolpidem
dissociative recallrisperidone
intense psychological distress (anger, anxiety) when exposed to reminders of traumatic event(s)benzodiazepines; buspirone; carbamazepine; lithium (not for anxiety); nefazodone; trazodone
Avoidance
 avoidanceamitriptyline; fluoxetine; lamotrigine; nefazodone; sertraline
feelings of detachment or estrangement from othersamitriptyline; risperidone
restricted range of affect (numbing)amitriptyline; lamotrigine; sertraline (women only)
Hyperarousal
 general hyperarousalamitriptyline; nefazodone; phenelzine; sertraline (women only)
sleep disturbance, nightmaresbenzodiazepines; carbamazepine; clonidine; nefazodone; phenelzine; trazodone; zolpidem
irritability, anger (and impulsiveness)carbamazepine; nefazodone; valproic acid
angerbuspirone; fluoxetine; lithium; trazodone
aggressionrisperidone
exaggerated startle response; general autonomic hyperexcitabilitybenzodiazepines; buspirone; carbamazepine; clonidine; propranolol; valproic acid

Some medications can also help with symptoms which may occur secondary to PTSD:[169]

Secondary symptomMedication
depressionnefazodone; phenelzine
dream content distortionsnefazodone
relapse of symptomscarbamazepine
self-mutilationclonidine; buprenorphine
sexual function reductionnefazodone
sleep hours reductionnefazodone

Medication and self-medication issues and risks with PTSD

Alcohol abuse and drug abuse commonly co-occur with PTSD.[147] 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.[170][171]

Yohimbine (not considered specifically appropriate for PTSD) increases arousal by increasing release of endogenous norepinephrine and can worsen PTSD symptoms.[147]

Epidemiology

Disability-adjusted life year rates for posttraumatic stress disorder per 100,000 inhabitants in 2004.[172]
  no data
  < 43.5
  43.5-45
  45-46.5
  46.5-48
  48-49.5
  49.5-51
  51-52.5
  52.5-54
  54-55.5
  55.5-57
  57-58.5
  > 58.5

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.[3]

International PTSD rates

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,[173] 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 USA, and Egypt.[174] 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.[175][176]

Age-standardized Disability-adjusted life year (DALY) rates for PTSD, per 100,000 inhabitants, in 25 most populous countries,[173] ranked by overall rate (2004)
RegionCountryPTSD DALY rate,
overall
[174] PTSD DALY rate,
females
[175] PTSD DALY rate,
males[176]
Asia / PacificThailand598630
Asia / PacificIndonesia588630
Asia / PacificPhilippines588630
AmericasUSA588630
Asia / PacificBangladesh578529
AfricaEgypt568330
Asia / PacificIndia568529
Asia / PacificIran568330
Asia / PacificPakistan568529
Asia / PacificJapan558031
Asia / PacificMyanmar558130
EuropeTurkey558130
Asia / PacificVietnam558030
EuropeFrance548028
EuropeGermany548028
EuropeItaly548028
Asia / PacificRussian Federation547830
EuropeUnited Kingdom548028
AfricaNigeria537629
AfricaDem. Republ. of Congo527628
AfricaEthiopia527628
AfricaSouth Africa527628
Asia / PacificChina517628
AmericaMexico466030
AmericaBrazil456030

United States

The National Comorbidity Survey has estimated that the lifetime prevalence of PTSD among adult Americans is 7.8%, with women (10.4%) twice as likely as men[19] (5%) to have PTSD at some point in their lives.[62] 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.[19] 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.[177]

The United States Department of Veterans Affairs estimates that 830,000 Vietnam War veterans suffered symptoms of PTSD.[178] 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.[71]

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 who 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.[179]

In other species

There have been reports of captive[180] and wild[181] elephants suffering from posttraumatic stress reactions, the latter from seeing members of their herd shot by hunters. Service dogs used overseas in the military have been said[182] to develop posttraumatic stress after witnessing war.

Public policy response

In recent history, catastrophes (by human means or not) such as the 2004 Indian Ocean tsunami may have caused PTSD in many survivors and rescue workers. Today relief workers from organizations such as the Red Cross and the Salvation Army provide counseling after major disasters as part of their standard procedures to curb severe cases of posttraumatic stress disorder.[citation needed]

United States—veterans

A review of the provision of compensation to veterans for PTSD by the United States Department of Veterans Affairs began in 2005 after the VA had noted a 30% increase in PTSD claims in recent years.[183] In 2005 the suicide rate among male Veteran VA users was 37.19 per 100,000, compared to 13.59 in females.[184] This led to a backlash from veterans'-rights groups, and to some highly publicized suicides by veterans who feared losing their benefits,[citation needed] which in some cases constituted their only income. In response, on November 10, 2005, the Secretary of Veterans Affairs announced that "the Department of Veterans Affairs (VA) will not review the files of 72,000 veterans currently receiving disability compensation for posttraumatic stress disorder..."[185]

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.[186] Walter Reed Army Institute of Research (WRAIR) developed the Battlemind program to assist service members avoid or ameliorate PTSD and related problems.

The American Legion is the most popular social and mutual-aid veterans' organization, with nearly 3 million members in over 14,000 Posts. Posts organize community events and service projects, and often have a bar open for limited hours. The American Legion is politically active on behalf of interests of veterans and service members, promoting support for veterans benefits, Veterans Affairs hospital system.[187]

The Sierra Club Military Families and Veterans Initiative organizes wilderness trips for veterans, and has received positive feedback about stress reduction.[188] One viewpoint suggests that "the key seems to be helping vets experience intense challenges free from the psychological shackles of life-and-death danger." Ice climbing has been a successful activity, "because its perceived challenge is so high,"[189] and Grizzly Tracking in Montana for Veterans, Service Members, and Families is scheduled for summer 2012.[190] More relaxing wilderness trips may also be of value, as settling into a rhythm moves an individual away from a state of hypervigilance into a more relaxed "flow experience". A Colorado therapist has suggested that "repetitive motor movements like cycling or skiing" and "rhythmic outdoor activities" reduce stress through a mechanism similar to EMDR therapy. An Outward Bound instructor comments that "the most healing occurs while [people are] drinking coffee and hanging out by the river" with fellow vets.[189]

Other countries—veterans

In the UK, there has been some controversy that National Health Service is dumping veterans on service charities like Combat Stress.[191][192][193]

Veterans Affairs Canada offers a new program that includes rehabilitation, financial benefits, job placement, health benefits program, disability awards, peer support[194][195][196] and family support.[197]

History

Earliest reports

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.[198]

Modern recognition in military settings

Statue, Three Servicemen, Vietnam Veterans Memorial

In the early 19th century military medical doctors started diagnosing soldiers with "exhaustion" after the stress of battle. This "exhaustion" was characterized by mental shutdown due to individual or group trauma—prior to the 20th century, soldiers were expected always to be emotionally tough and show no fear in the midst of combat. The only treatment for this "exhaustion" was to relieve the afflicted from frontline duty until symptoms subsided, then return to battle. During the intense and frequently repeated stress, the soldiers became fatigued as a part of their body's natural shock reaction.[199]

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."[200]

Although PTSD-like symptoms have also been recognized in combat veterans of many military conflicts since, the modern understanding of PTSD dates from the 1970s, largely as a result of the problems that were still being experienced by US military veterans of the war in Vietnam.[201]

Previous diagnoses now considered historical equivalents of PTSD include railway spine, stress syndrome, shell shock, battle fatigue, or traumatic war neurosis.[202]

Terminology

The term post-traumatic stress disorder (PTSD) was coined in the mid 1970s,[201] in part through the efforts of anti–Vietnam War activists and the anti-war group Vietnam Veterans Against the War and Chaim F. Shatan, who worked with them and coined the term post-Vietnam Syndrome; the condition was added to the DSM-III as posttraumatic stress disorder.[203]

Early in 1978, the term was used in a working group finding presented to the Committee of Reactive Disorders.[203] The term was formally recognized in 1980.[201]

In the DSM-IV, the spelling "posttraumatic stress disorder" is used, while in the ICD-10 the spelling is "post-traumatic stress disorder"[5]. Elsewhere, especially in less formal writing, the term may be rendered as two words—"post traumatic stress disorder".[citation needed])

See also

Notes

  1. ^ Acceptable variants of this term exist; see Terminology section in this article.

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