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Post-traumatic stress disorder

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Post-traumatic stress disorder
SpecialtyPsychiatry, clinical psychology Edit this on Wikidata

Posttraumatic stress disorder[1][2] (PTSD) is an anxiety disorder that can develop after exposure to one or more terrifying events that threatened or caused grave physical harm. It is a severe and ongoing emotional reaction to an extreme psychological trauma.[3] This stressor may involve someone's actual death, a threat to the patient's or someone else's life, serious physical injury, or threat to physical or psychological integrity, overwhelming psychological defenses. In some cases it can also be from profound psychological and emotional trauma, apart from any actual physical harm. Often, however, the two are combined. PTSD is a condition distinct from traumatic stress, which has less intensity and duration, and combat stress reaction, which is transitory. PTSD has also been recognized in the past as railway spine, shell shock, battle fatigue, traumatic war neurosis, or post-traumatic stress syndrome (PTSS).

Causes

Main article: Psychological trauma

PTSD is believed to be caused by psychological trauma.[1] Possible sources of trauma includes encountering or witnessing childhood or adult physical, emotional or sexual abuse.[1] In addition, encountering or witnessing an event perceived as life-threatening such as physical assault, adult experiences of sexual assault, accidents, drug addiction, illnesses, medical complications, or the experience of, or employment in occupations exposed to war (such as soldiers) or disaster (such as emergency service workers). Traumatic events that may cause PTSD symptoms to develop include violent assault, kidnapping, torture, being a hostage, prisoner of war or concentration camp victim, experiencing a disaster, violent automobile accidents or getting a diagnosis of a life-threatening illness.[1] Children may develop PTSD symptoms by experiencing sexually traumatic events like age-inappropriate sexual experiences.[1] Witnessing traumatic experiences or learning about these experiences may also cause the development of PTSD symptoms.[1] The amount of dissociation that follows directly after a trauma predicts PTSD: individuals who are more likely to dissociate during a traumatic event are considerably more likely to develop chronic PTSD.[4] Members of the Marines and Army are much more likely to develop PTSD than Air Force and Navy personnel, because of greater exposure to combat.[1] A preliminary study found that mutations in a stress-related gene interact with child abuse to increase the risk of PTSD in adults.[5][6][7] PTSD sufferers re-experience of the traumatic event or events in some way, they tend to avoid places, people, or other things that remind them of the event, and are exquisitely sensitive to normal life experiences. Untreated Post Traumatic Stress Disorder can have devastating, far-reaching consequences for sufferers' functioning in relationships, their families, and in society.

Neuroendocrinology

PTSD displays 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.[citation needed] In addition, most PTSD also show a low secretion of cortisol and high secretion of catecholamine in urine, with a norepinephrine/cortisol ratio consequently higher than comparable non-diagnosed individuals.[8] 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.[citation needed] Brain catecholamine levels are low,[citation needed] and corticotropin-releasing factor (CRF) concentrations are high.[9][10] Together, these findings suggest abnormality in the hypothalamic-pituitary-adrenal (HPA) axis. 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.[11] 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.[12]

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.[13] 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. 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. Only a slight majority have found a decrease in cortisol levels while others have found no effect or even an increase.[14]

Neuroanatomy

In addition to biochemical changes, PTSD also involves changes in brain morphology. 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.[15]

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. 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. Further animal and clinical research into the amygdala and fear conditioning may suggest additional treatments for the condition.

Genetics

PTSD runs in families: 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).[16] Because of the difficulty in performing genetic studies on a condition with a major environmental factor (e.g., trauma), genetic studies of PTSD are in their infancy.

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.[17] 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),[18] which has itself been shown to be predictive of PTSD.[19][20]

Risk and protective factors for PTSD development

Although most people (50-90%) encounter trauma over a lifetime,[21][22] only about 8% develop full PTSD.[23] Vulnerability to PTSD presumably stems from an interaction of biological diathesis, early childhood developmental experiences, and trauma severity. 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[24][25].[26][27] This effect of childhood trauma, which is not well understood, may be a marker for both traumatic experiences and attachment problems.[28][29] Proximity to, duration of, and severity of the trauma also make an impact; and interpersonal traumas cause more problems than impersonal ones.[30]

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

  • Hispanic ethnicity, coming from an unstable family, being punished severely during childhood, childhood asocial behavior and depression as pre-military factors
  • war-zone exposure, peritraumatic dissociation, depression as military factors
  • recent stressful life events, post-Vietnam trauma and depression as post-military factors

They also identified certain protective factors, such as:

  • Japanese-American ethnicity, high school degree or college education, older age at entry to war, higher socioeconomic status and a more positive paternal relationship as pre-military protective factors
  • Social support at homecoming and current social support as post-military factors[31] Other research also indicates the protective effects of social support in averting and recovery from PTSD.[32][33]

There may also be an attitudinal component; for example, a soldier who believes that they will not sustain injuries may be more likely to develop symptoms of PTSD than one who anticipates the possibility, should either be wounded. Likewise, the later incidence of suicide among those injured in home fires above those injured in fires in the workplace suggests this possibility.

Risk and protective factors influence the outcome of a traumatic event via difference pathways. In the section that follow, to kinds of pathwas - moderators and mediators - are described. The goal of the section is to elaborate how to test for moderators and mediators using specific examples from empirical research.

Moderators and Mediators

In the pathway between a traumatic event (TE) and PTSD lie different kinds of intervening factors, which influence the outcome (PTSD). Moderators and mediators are two such kinds of intervening variables. According to Baron and Kenny,[34] a moderator attempts to answer the question “On whom?” or “Under what conditions?” a second variable (Z) operates in the pathway to predict the outcome (Y). The variable Z must have a statistically significant interaction with Y to be considered as a moderator. A mediator, on the other hand, attempts to answer the question “How?” or “Why?” Z is related to Y. A mediation pathway meets the following criteria: (1) the predictor (X) leads to Z, (2) significant associations between all separate pathways such as X & Y, X & Z, and Y & Z (3) a zero or significant reduction of the association between X & Y, after the introduction of Z into the pathway. Below are visual conceptualizations of the two kinds of pathways.

Moderators: Adult attachment and optimal social support

Does adult attachment (AA) and optimal social support (OSS) differentiate between persons prone to PTSD following an interpersonal traumatic event? To explore this question, Declercq and Palmans[35] tested whether AA and OSS act as moderators between the predictor (critical incidence or traumatic event), and the outcome variable (PTSD symptomatology).



To test whether AA is a moderator between an interpersonal traumatic event and PTSD, the researchers used Bartholomew and Horowitz’s [36] classification of attachment that yields four types of attachment styles: secure (A), insecure – fear avoidant (B), insecure – preoccupied (C), and insecure – dismissive avoidant (D). Declercq and Palmans[35] sampled 544 high risk professionals drawn from two groups of Dutch speaking workers with an average age of 40.8 years (SD = 10.65). Participants who met DSM-IV-TR Criterion A reported being confronted by aggravated assault, death, serious injuries or serious motor vehicle accidents.

Psychometric assessment batteries such as the Davidson Trauma Scale (DTS), the Parental Bonding Instrument (PBI), and the Social Support List (SSL) were employed to assess PTSD symptomatology, AA, and OSS respectively. Data was analyzed using Multiple Dimensional Scaling. On the projected space, variables that have strong correlations have shorter distances between them than variables with lower correlations. On the MDS screen, the securely attached group (A) was further away from PTSD than the insecurely attached while individuals who received OSS were further away from PTSD than those who did not. Overall, the securely attached group was furthest from PTSD. On the one side, individuals characterized by secure attachment and/or high OSS are less likely to develop PTSD. On the other side, individuals characterized by insecure attachment and/or low OSS are more likely to develop PTSD following a TE. Following a TE, insecurely attached adults (B, C, & D) and low OSS-rated individuals are at a greater risk of developing PTSD in comparison to securely attached adults (A) and high OSS-rated individuals respectively.

Mediators: Experiential Avoidance and Forgiveness

In this study PTSD is conceptualized as an inability to integrate traumatic material such as nightmares, flashbacks, and thoughts into one’s experiential and memory systems because of their distressing nature. Experiential avoidance (EA) is the product of a survivor’s (1) unwillingness to experience personal events such as emotions and thoughts, and (2) action to alter the experiences or their frequencies or context in which they emerge.[37] According to many researchers, forgiveness, which does not equal forgetting, involves a reduction of negative feelings towards the aggressor.[38] According to Enright,[39] forgiveness involves four phases. During phase 1, the survivor fully experiences injury pains and negative emotions caused by the TE. Once fully experienced, the emotions and pain can be understood and confronted. In phase 2, the survivor recognizes the fact that an over-dwelling on these emotions and pain can only exacerbate suffering. Phase 3 demands alterations of a survivor’s appraisals of the aggressor. An attempt is made to place the event in the context of the aggressor’s life. This phase also requires an acceptance of the pain. In the last phase, the survivor experiences positive emotions that come with forgiving the aggressor, accepting the pain, and finding meaning in the suffering. Given that TE are often interpersonal where one individual intentionally harms another as in rape and intimate partner violence, forgiveness can serve as a mediator when a survivor allows himself or herself to experience injuries and pain, to understand and accept the pain and suffering, and to work through the traumatic materials without significant avoidance from them.

To test for mediation the study collected data from a college representative sample of 1,014. Of these, 229 met the inclusion Criterion A (which had to be of an interpersonal nature) for PTSD. Over 95% of the participants were below the age of 24. Interpersonal TE or critical incidences were assessed using the Traumatic Life Events Questionnaire (TLEQ) that yielded a total count of interpersonal TE. EA was assessed through three psychometric measures: Acceptance and Action Questionnaire – AAQ,[40] Toronto Alexithymia Scale – TAS-20,[41] and White Bear Thought Suppression Inventory – WBSI.[42] To measure forgiveness, the study utilized the Enright Forgiveness Inventory – EFI.[43] Lastly, PTSD was assessed in terms of the number of PTSD symptoms using the Distressing Events Questionnaire – DEQ.[44]

Each separate pathway in the models above produced a significant association. The direct effects of the ITE on PTSD symptomatology were significantly reduced after the introduction of the suspected mediator(s) in each model based on structural equation modeling and the McKinnon analysis.[45] The combination of experiential avoidance and forgiveness in the same mediation pathway led to a greater significant reduction of the direct effect of ITE on PTSD. In other words, a combination of EA and forgiveness yields a more powerful mediation effect, albeit in a non-additive form.

See also: Psychological resilience

Diagnosis

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

A. Exposure to a traumatic event
B. Persistent reexperience (e.g. flashbacks, nightmares)
C. Persistent avoidance of stimuli associated with the trauma (e.g. inability to talk about things even related to the experience, avoidance of things and discussions that trigger flashbacks and reexperiencing symptoms fear of losing control)
D. Persistent symptoms of increased arousal (e.g. difficulty falling or staying asleep, anger and hypervigilance)
E. Duration of symptoms more than 1 month
F. Significant impairment in social, occupational, or other important areas of functioning (e.g. problems with work and relationships.)

Notably, criterion A (the "stressor") consists of two parts, both of which must apply for a diagnosis of PTSD. The first (A1) requires that "the person experienced, witnessed, or was confronted with an event or events that involved actual or threatened death or serious injury, or a threat to the physical integrity of self or others." The second (A2) requires that "the person’s response involved intense fear, helplessness, or horror." 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." Since the introduction of DSM-IV, the number of possible PTSD traumas has increased and one study suggests that the increase is around 50%.[46] Various scales exist to measure the severity and frequency of PTSD symptoms.[47][48]

Treatment

Many forms of psychotherapy have been advocated for trauma-related problems such as PTSD. Basic counseling for PTSD includes education about the condition and provision of safety and support.[49] Cognitive therapy shows good results,[50] and group therapy may be helpful in reducing isolation and social stigma.[51] The psychotherapy programs with the strongest demonstrated efficacy include psychodynamic therapy, cognitive behavioral programs, variants of exposure therapy, stress inoculation training (SIT), variants of cognitive therapy (CT), eye movement desensitization and reprocessing (EMDR), and many combinations of these procedures.[52][53] Exposure involves assisting trauma survivors to therapeutically confront 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.

Indeed, the success of exposure-based therapies has raised the question of whether exposure is a necessary ingredient in the treatment of PTSD. Some organizations have endorsed the need for exposure.[54][55] Yet other approaches, particularly involving social supports,[56][57] may also be important. A recent open trial of interpersonal psychotherapy[58] reported high rates of remission from PTSD symptoms without using exposure.[59] A randomized controlled trial funded by the National Institute of Mental Health is currently comparing exposure-based psychotherapy to interpersonal psychotherapy at the New York State Psychiatric Institute (www.columbiatrauma.org; 212 543-6747).

Critical incident stress management

Early intervention after a traumatic incident,[60] known as Critical Incident Stress Management (CISM) is used to attempt to reduce traumatic effects of an incident, and potentially prevent a full-blown occurrence of PTSD. However, recent studies regarding CISM seem to indicate iatrogenic effects.[61][62] Six studies have formally looked at the effect of CISM, four finding no benefit for preventing PTSD, and the other two studies indicating that CISM actually made things worse. Hence this is not a recommended treatment. Some benefit was found from being connected early to cognitive behavioral therapy, or for some medications such as propranolol. Effects of all these prevention strategies was modest.[63]

Eye movement desensitization and reprocessing

Eye Movement Desensitization and Reprocessing (EMDR) is specifically targeted as a treatment for PTSD.[64] Research on EMDR is largely supported by those with the copyright for EMDR and third-party studies of its effectiveness are lacking, but a meta-analytic comparison of EMDR and cognitive behavioral therapy found both protocols indistinguishable in terms of effectiveness in treating PTSD.[65]

Medication

Medications have shown benefit in reducing PTSD symptoms, but rarely achieve complete remission. Standard medication therapy useful in treating PTSD includes SSRIs (selective serotonin reuptake inhibitors) and TCAs (tricyclic antidepressants). Tricyclics tend to be associated with greater side effects and lesser improvement of the three PTSD symptom clusters than SSRIs. SSRIs for which there are data to support use include: citalopram, escitalopram, fluvoxamine, paroxetine and sertraline.[66][67][68][69]

There are data to support the use of "autonomic medicines" such Propranolol (beta blocker) and Clonidine (alpha-adrenergic agonist) if there are significant symptoms of "over-arousal". These may inhibit the formation of traumatic memories by blocking adrenaline's effects on the amygdala, has been used in an attempt to reduce the impact of traumatic events.[70] or they may simply demonstrate to the patient that the symptoms can be controlled thereby assisting with "self efficacy" and helping the patient remain calmer. There is also data to support the use of mood-stabilizers such lithium carbonate, divalproex sodium and carbemazepine if there is significant uncontrolled mood or aggression. Risperidone is used to help with dissociation, mood and aggression, and benzodiazepines are used for short-term anxiety relief.[71]

MDMA

While MDMA had its first exposure to the psychiatric community in the 1960s, gaining a reputation for its communication enhancing qualities, it hasn't been until recent years that formal studies have been carried out. The US Food and Drug Administration (FDA) recently approved a clinical protocol that combines the drug MDMA with talk therapy sessions.[72] Funded by the non-profit Multidisciplinary Association for Psychedelic Studies (MAPS),[73] the studies are taking place in South Carolina under the supervision and direction of Dr. Michael Mithoefer. Other PTSD/MDMA research include a pilot study in Switzerland, co-sponsored by MAPS and the Swiss Medical Association for Psycholytic Therapy (SAePT),[74] and another study approved in Israel to investigate MDMA as a tool in the psychotherapeutic treatment of crime and terrorism-related PTSD.[75]

There are several features of MDMA that make it an excellent candidate for treating PTSD in psychotherapy. The effects of MDMA are such that activity in the left amygdala,[76] responsible for fear and anxiety, decreases in rats. This makes it a promising candidate as a tool in psychotherapy, allowing the patient to explore and examine their trauma (and accompanying emotions) without the fear and retraumatization encountered without drug. Ordinarily incapacitated by the resurgence of emotions (fear, shame, anger) attached to the trauma, subjects are rendered capable of approaching their trauma in a new and constructive way. Further helpful in treating PTSD, is the new capacity to experience empathy and compassion for both others and the self.[77]

Combination therapies

PTSD is commonly treated using a combination of psychotherapy (cognitive-behavioral therapy, group therapy, and exposure therapy are popular) and medications such as antidepressants (e.g. SSRIs such as fluoxetine and sertraline, SNRI's such as venlafaxine, NaSSA's such as mirtazapine and tricyclic antidepressant such as amitriptyline[78]) or atypical antipsychotic drugs (such as quetiapine and olanzapine).[79] Recently the anticonvulsant lamotrigine has been reported to be useful in treating some people with PTSD.[80][81][82] Geodon (ziprasidone) is one of the most effective treatments shown to work 89% of the time in PTSD patients.[83] Geodon works by blocking two of the fight-or-flight chemicals (catecholamines): norepinephrine (noradrenaline) and dopamine.[84] Carrot of Hope has been promoting the benefits of combining Geodon with the beta-adrenergic blocker propranolol to create a PTSD cocktail. Since propranolol works by blocking the third catecholamine, epinephrine (adrenaline),[85] the combination of the two medicines work to block all three fight-or-flight chemicals. Propranolol (40 mg) has been commonly prescribed off-label for stage fright in the late 1970s.[86][87] The television show 60 Minutes featured propranolol where low doses (10-20 mg) used in research have been shown to stop panic attacks and reduce the impact of traumatic memories. As propranolol lasts in the system for 4 hours, the study dosages are typically given 4 times a day to cover a 16 hour span.[88] Alpha-adrenergic blocker prazosin has also shown impressive effects in PTSD patients, curbing brain damage and reducing nightmares.[89][90] Unlike propranolol, prazosin acts on norepinephrine[91] and, therefore, is contraindicated for use with Geodon.

Other techniques

Attachment- and relationship-based treatments are also often used.[92][93] In these cases, the treatment of complex trauma often requires a multi-modal approach. Medical Marijuana is also used for treatment of PTSD [citation needed]. Yoga Nidra has been used to help soldiers cope with the symptoms of PTSD.[94]

Epidemiology

PTSD may be experienced following any traumatic experience, or series of experiences that satisfy the criteria and that do not allow the victim to readily recuperate from the detrimental effects of stress. The National Comorbidity Survey Report provided the following information about PTSD in the general adult population: The estimated lifetime prevalence of PTSD among adult Americans is 7.8%, with women (10.4%) twice as likely as men (5%) to have PTSD at some point in their lives.[citation needed]

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. Four out of five reported recent symptoms when interviewed 20-25 years after Vietnam.[31]

In recent history, catastrophes (by human means or not) such as the Indian Ocean Tsunami Disaster 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 post-traumatic stress disorder.

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.[2]

History

Earliest reports

Reports of battle-associated stress appear as early as the 6th century BC.[95] 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 Vietnam veterans.[95] One of the first descriptions of PTSD was made by the Greek historian Herodotus. In 490 BCE he described, during the Battle of Marathon, an Athenian soldier who suffered no injury from war but became permanently blind after witnessing the death of a fellow soldier.[96]

The term post-traumatic stress disorder or PTSD was coined in the mid 1970s.[95] Early in 1978, the term was used in a working group finding presented to the Committee of Reactive Disorders.[97] The term was formally recognized in 1980.[95] (In the DSM-IV, which is considered authoritative, the spelling "posttraumatic stress disorder" is used. Elsewhere, "posttraumatic" is often rendered as two words — "post-traumatic stress disorder" or "post traumatic stress disorder" — especially in less formal writing on the subject.)

Veterans and politics

The diagnosis was removed from the DSM-II, which resulted in the inability of Vietnam veterans to receive benefits for this condition. 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.[97]

In the United States, the provision of compensation to veterans for PTSD is under review by the Department of Veterans Affairs (VA). The review was begun in 2005 after the VA had noted a 30% increase in PTSD claims in recent years. The VA undertook the review because of budget concerns and apparent inconsistencies in the awarding of compensation by different rating offices.

This led to a backlash from veterans'-rights groups, and to some highly-publicized suicides by veterans who feared losing their benefits, 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 post-traumatic stress disorder..."[98]

The diagnosis of PTSD has been a subject of some controversy due to uncertainties in objectively diagnosing PTSD in those who may have been exposed to trauma, and due to this diagnosis' association with some incidence of compensation-seeking behavior.[99]

The social stigma of PTSD may result in under-representation of the disorder in military personnel, emergency service workers and in societies where the specific trauma-causing event is stigmatized (e.g. sexual assault).[2]

Many US veterans of the wars in Iraq and Afghanistan returning home 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.[93] Similarly, Walter Reed Army Institute of Research (WRAIR) developed the Battlemind program to assist servicemembers avoid or ameliorate PTSD and related problems.

Canadian veterans

Veterans Affairs Canada is a new program including rehabilitation, financial benefits, job placement, health benefits program, disability awards and family support.[100]

Cultural references

In recent decades, with the concept of trauma and PTSD in particular becoming just as much a cultural phenomenon as a medical or legal one, artists have engaged the issue in their work. Many movies, such as First Blood, Birdy, Coming Home, The Deer Hunter, Born on the Fourth of July, and Heaven & Earth deal with PTSD. It is an especially popular subject amongst "war veteran" films, often portraying Vietnam war veterans suffering from extreme PTSD and having difficulties adjusting to civilian life.

In more recent work, an example is that of Krzysztof Wodiczko who teaches at MIT and who is known for interviewing people and then projecting these interviews onto large public buildings.[101] Wodiczko aims to bring trauma not merely into public discourse but to have it contest the presumed stability of cherished urban monuments. His work has brought to life issues such as homelessness, rape, and violence. Other artists who engage the issue of trauma are Everlyn Nicodemus of Tanzania and Milica Tomic of Serbia.[102]

George Carlin comments on the various incarnations of PTSD terminology on his 1990 album Parental Advisory: Explicit Lyrics. He traces the progression of what he views as euphemisms, which followed "shell shock" in World War I, "battle fatigue" in World War II, "operational exhaustion" in the Korean War, and finally PTSD, a clinical, hyphenated term, in the Vietnam War. "The pain is completely buried under jargon. Post-traumatic stress disorder. I'll bet you if we'd have still been calling it shell shock, some of those Viet Nam veterans might have gotten the attention they needed at the time." <ref>George Carlin - Parental Advisory Explicit Lyrics</ref

The second season (12/2000) Christmas episode of The West Wing (Noel), dealt with PTSD as seen through the eyes of Deputy White House Chief Of Staff Josh Lyman, who was nearly killed in an assassination attempt several months earlier. He spends the day with a psychotherapist trying to get to the root of why he spontaneously and inexplicably put his hand through his apartment window, causing a slash wound he has to lie about.

See also

References

  1. ^ a b c d e f g h American Psychiatric Association (1994). Diagnostic and statistical manual of mental disorders: DSM-IV. Washington, DC: American Psychiatric Association. ISBN 0890420610.; on-line
  2. ^ a b c Brunet A, Akerib V, Birmes P (2007). "Don't throw out the baby with the bathwater (PTSD is not overdiagnosed)" (pdf). Can J Psychiatry. 52 (8): 501–2, discussion 503. PMID 17955912. Retrieved 2008-03-12.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  3. ^ David Satcher; et al. (1999). "Chapter 4.2". Mental Health: A Report of the Surgeon General. {{cite book}}: Explicit use of et al. in: |author= (help)
  4. ^ Brown, Scheflin and Hammond (1998). Memory, Trauma Treatment, And the Law. New York, NY: W. W. Norton. ISBN 0-393-70254-5.
  5. ^ Binder, MD. PhD, E. B. (2008). "Association of FKBP5 Polymorphisms and Childhood Abuse With Risk of Posttraumatic Stress Disorder Symptoms in Adults". JAMA. 299 (11): 1291–1305. doi:10.1001/jama.299.11.1291. PMID 18349090. Retrieved 2008-03-31. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  6. ^ Template:Cite article
  7. ^ Template:Cite article
  8. ^ 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. doi:10.1097/00005053-198808000-00008. PMID 3404142.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  9. ^ Sautter FJ, Bisette G, Wiley J, Manguno-Mire G, Schoenbachler B, Myers L, Johnson JE, Cerbone A, Malaspina D (2003). "Corticotropin-releasing factor in posttraumatic stress disorder with secondary psychotic symptoms, nonpsychotic PTSD, and healthy control subjects". Biol Psychiatry. 54 (12): 1382–8. doi:10.1016/S0006-3223(03)00571-7. PMID 14675802.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  10. ^ 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. 167: 287–91. PMID 18037027.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  11. ^ Yehuda R (2001). "Biology of posttraumatic stress disorder". J Clin Psychiatry. 62 Suppl 17: 41–6. PMID 11495096.
  12. ^ Yehuda R (2002). "Clinical relevance of biologic findings in PTSD". Psychiatr Q. 73 (2): 123–33. doi:10.1023/A:1015055711424. PMID 12025720.
  13. ^ 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. doi:10.1016/S0006-3223(01)01253-7. PMID 11750895.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  14. ^ 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. doi:10.1016/j.biopsych.2003.12.021. PMID 15110738.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  15. ^ Carlson, Neil R. (2007). Physiology of Behavior (9 ed.). Pearson Education, Inc.
  16. ^ True WR, Rice J, Eisen SA; et al. (1993). "A twin study of genetic and environmental contributions to liability for posttraumatic stress symptoms". Arch. Gen. Psychiatry. 50 (4): 257–64. PMID 8466386. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  17. ^ Binder EB, Bradley RG, Liu W; et al. (2008). "Association of FKBP5 polymorphisms and childhood abuse with risk of posttraumatic stress disorder symptoms in adults". JAMA. 299 (11): 1291–305. doi:10.1001/jama.299.11.1291. PMID 18349090. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  18. ^ Koenen KC, Saxe G, Purcell S; et al. (2005). "Polymorphisms in FKBP5 are associated with peritraumatic dissociation in medically injured children". Mol Psychiatry. 10 (12): 1058–9. doi:10.1038/sj.mp.4001727. PMID 16088328. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  19. ^ Birmes P, Brunet A, Carreras D; et al. (2003). "The predictive power of peritraumatic dissociation and acute stress symptoms for posttraumatic stress symptoms: a three-month prospective study". Am J Psychiatry. 160 (7): 1337–9. doi:10.1176/appi.ajp.160.7.1337. PMID 12832251. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  20. ^ Schnurr PP, Lunney CA, Sengupta A (2004). "Risk factors for the development versus maintenance of posttraumatic stress disorder". J Trauma Stress. 17 (2): 85–95. doi:10.1023/B:JOTS.0000022614.21794.f4. PMID 15141781.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  21. ^ Kessler RC, Sonnega A, Bromet E, Hughes M, Nelson CB: Posttraumatic stress disorder in the National Comorbidity Survey. Arch Gen Psychiatry 1995;52:1048-1060
  22. ^ Breslau N, Kessler RC, Chilcoat HD, Schultz LR, Davis GC, Andreski P: Trauma and posttraumatic stress disorder in the community: the 1996 Detroit Area Survey of Trauma. Arch Gen Psychiatry 1998;55:626-632
  23. ^ Kessler RC, Sonnega A, Bromet E, Hughes M, Nelson CB: Posttraumatic stress disorder in the National Comorbidity Survey. Arch Gen Psychiatry 1995;52:1048-1060
  24. ^ Koenen KC, Moffitt TE, Poulton R, Martin J, Caspi A: Early childhood factors associated with the development of post-traumatic stress disorder: results from a longitudinal birth cohort. Psychol Med 2007 37:181-92
  25. ^ Lapp KG, Bosworth HB, Strauss JL, Stechuchak KM, Horner RD, Calhoun PS, Meador KG, Lipper S, Butterfield MI: Lifetime sexual and physical victimization among male veterans with combat-related post-traumatic stress disorder. Mil Med 2005;170:787-90
  26. ^ Otte C, Neylan TC, Pole N, Metzler T, Best S, Henn-Haase C, Yehuda R, Marmar CR: Association between childhood trauma and catecholamine response to psychological stress in police academy recruits. Biol Psychiatry 2005;57:27-32
  27. ^ Resnick HS, Yehuda R, Pitman RK, Foy DW: Effect of previous trauma on acute plasma cortisol level following rape. Am J Psychiatry 1995;152:1675-1677
  28. ^ Laor N, Wolmer L, Mayes LC, Golomb A, Silverberg DS, Weitzman R, Cohen DJ: Israeli preschoolers under Scud missile attacks: A developmental perspective on risk-modifying factors. Arch Gen Psych 1996;53:416-23
  29. ^ Laor N, Wolmer L, Mayes LC, Gershon A, Weitzman R, Cohen DJ: Israeli preschool children under Scuds: a 30-month follow-up. JAACAP 1997;36:349-56
  30. ^ Janoff-Bulman R: Shattered Assumptions: Toward a New Psychology of Trauma. New York: Free Press, 1992
  31. ^ a b Jennifer L. Price, Ph.D.: Findings from the National Vietnam Veterans' Readjustment Study - Factsheet. National Center for PTSD. United States Department of Veterans Affairs [1]
  32. ^ Brewin CR, Andrews B, Valentine JD: Meta-analysis of risk factors for posttraumatic stress disorder in trauma-exposed adults. J Consult Clin Psychology 2000;68:748-766
  33. ^ Ozer EJ, Best SR, Lipsey TL, Weiss DS: Predictors of posttraumatic stress disorder and symptoms in adults: a meta-analysis. Psychol Bull 2003;129:52-73
  34. ^ Baron, R., & Kenny, D. (1986). The moderator–mediator variable distinction in social psychological research: Conceptual, strategic, and statistical considerations. Journal of Personality and Social Psychology, 51, 1173–1182.
  35. ^ a b Declercq, F., & Palmans, V. (2006). Two subjective factors as moderators between critical incidents and the occurrence of post traumatic stress disorders: ‘Adult attachment’ and ‘perception of social support.’ The British Psychological Society, 79, 323-337.
  36. ^ Bartholomew, K., & Horowitz, L. (1991). Attachment styles among young adults: A test of a four-category model. Journal of Personality and Social Psychology, 61, 226-244.
  37. ^ Hayes, S., Wilson, K., Gifford, E., Follette, V., & Strosahl, K. (1996). Experiential avoidance and behavioral disorders: A functional dimensional approach to diagnosis and treatment. Journal of Consulting and Clinical Psychology, 64(6), 1152–1168.
  38. ^ McCullough, M., & Witvliet, C. (2002). The psychology of forgiveness. In C. Snyder & S. Lopez (Eds.), Handbook of positive psychology (pp. 446–458). London: Oxford University Press.
  39. ^ Enright, R. (2001). Forgiveness is a choice: A step-by-step process for resolving anger and restoring hope. Washington, DC: American Psychological Association.
  40. ^ Hayes, S., Strosahl, K., Wilson, K., Bissett, R., Pistorello, J., Toarmino, D. et al., (2004). The Acceptance and Action Questionnaire (AAQ) as a measure of experiential avoidance. Manuscript submitted for publication.
  41. ^ Bagby, R., Parker, J. & Taylor, J. (1994). The twenty–item Toronto Alexithymia Scale: I. Item selection and cross–validation of the factor structure. Journal of Psychosomatic Research, 38, 23–32.
  42. ^ Wegner, D., & Zanakos, S. (1994). Chronic thought suppression. Journal of Personality, 62, 615–640.
  43. ^ Enright, R., & Fitzgibbons, R. (2000). Helping clients forgive: An empirical guide to resolving anger and restoring hope. Washington, DC: American Psychological Association.
  44. ^ Kubany, E., Leisen, M., Kaplan, A., & Kelly, M. (2000). Validation of a brief measure of Posttraumatic Stress Disorder: The Distressing Event Questionnaire (DEQ). Psychological Assessment, 12(2), 197–209.
  45. ^ MacKinnon, D., Warsi, G., & Dwyer, J. (1995). A simulation study of mediated effect measures. Multivariate Behavioral Research, 30, 41–62.
  46. ^ Breslau N, Kessler RC (2001). "The stressor criterion in DSM-IV posttraumatic stress disorder: an empirical investigation". Biol. Psychiatry. 50 (9): 699–704. doi:10.1016/S0006-3223(01)01167-2. PMID 11704077.
  47. ^ Blake DD, Weather FW, Nagy LM, Kaloupek DG, Gusman FD, Charney DS, Keane TM: The development of a clinician-administered PTSD scale. J Traumatic Stress 1995;8:75-90
  48. ^ Foa E: The Post Traumatic Diagnostic Scale Manual. Minneapolis, NCS, 1995
  49. ^ Foa 1997
  50. ^ Resick 2002
  51. ^ Foy 2002
  52. ^ Cahill, S. P., & Foa, E. B. (2004). A glass half empty or half full? Where we are and directions for future research in the treatment of PTSD. In S. Taylor (ed.), Advances in the Treatment of Posttraumatic Stress Disorder: Cognitive-behavioral perspectives (pp. 267-313) New York: Springer.
  53. ^ Brom, D (1989). "Brief psychotherapy for posttraumatic stress disorders". J Consult Clin Psychol. 57 (5): 607–12. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  54. ^ American Psychiatric Association: Practice guideline for the treatment of patients with acute stress disorder and posttraumatic stress disorder. Am J Psychiatry 2004;161:11(suppl)
  55. ^ 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 -10: 0-309-10926-4
  56. ^ Brewin CR, Andrews B, Valentine JD: Meta-analysis of risk factors for posttraumatic stress disorder in trauma-exposed adults. J Consult Clin Psychology 2000;68:748-766
  57. ^ Ozer EJ, Best SR, Lipsey TL, Weiss DS: Predictors of posttraumatic stress disorder and symptoms in adults: a meta-analysis. Psychol Bull 2003;129:52-73
  58. ^ Weissman MM, Markowitz JC, Klerman GL: Clinician’s Quick Guide to Interpersonal Psychotherapy. New York: Oxford University Press, 2007
  59. ^ Bleiberg KL, Markowitz JC: Interpersonal psychotherapy for posttraumatic stress disorder. Am J Psychiatry 2005;162-181-183
  60. ^ Brown, Asa Don Ph.D., "The effects of childhood trauma on adult perception and worldview", Capella University, 2008, 152 pages; AAT 3297512
  61. ^ Carlier, IVE (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. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  62. ^ 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: 589–93. doi:10.1192/bjp.176.6.589. PMID 10974967.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  63. ^ 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. doi:10.1177/0145445506295057. PMID 17179532.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  64. ^ Devilly GJ, Spence SH (1999). "The relative efficacy and treatment distress of EMDR and a cognitive-behavior trauma treatment protocol in the amelioration of posttraumatic stress disorder". J Anxiety Disord. 13 (1–2): 131–57. doi:10.1016/S0887-6185(98)00044-9. PMID 10225505.
  65. ^ 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. doi:10.1017/S0033291706007963. PMID 16740177.
  66. ^ Yehuda, R. (2000), Biology of posttraumatic stress disorder. Journal of Clinical Psychiatry, 61 (7): 14-21
  67. ^ Marshall RD, Beebe KL, Oldham M, Zaninelli R: Efficacy and safety of paroxetine treatment for chronic PTSD: a fixed dose, placebo controlled study. Am J Psychiatry December 2001;158:1982 1988
  68. ^ Brady K, Pearlstein T, Asnis GM, Baker D, Rothbaum B, Sikes CR, Farfel GM: Efficacy and safety of sertraline treatment of posttraumatic stress disorder: a randomized controlled trial. JAMA 2000;283:1837-1844
  69. ^ Davidson JRT, Rothbaum BO, van der Kolk BA, Sikes CR, Farfel GM: Multicenter, double-blind comparison of sertraline and placebo in the treatment of posttraumatic stress disorder. Arch Gen Psychiatry 2001;58:485-492
  70. ^ Pitman RK, Sanders KM, Zusman RM; et al. (2002). "Pilot study of secondary prevention of posttraumatic stress disorder with propranolol". Biol. Psychiatry. 51 (2): 189–92. doi:10.1016/S0006-3223(01)01279-3. PMID 11822998. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  71. ^ Reist C (2005) Post-traumatic Stress Disorder. Compendia, Build ID: F000005, published by Epocrates.com
  72. ^ MAPS FDA and IRB approved MDMA/PTSD protocol
  73. ^ [www.maps.org]
  74. ^ http://www.maps.org/mdma/swissmdmaptsd/protocol280507.pdf
  75. ^ MDMA-assisted Psychotherapy in Twelve People with War and Terrorism-related PTSD
  76. ^ http://www.maps.org/research/mdma/ptsd_study/treatment-manual/053005/intro.html
  77. ^ Ecstasy is the Key to Treating PTSD
  78. ^ National Institute for Clinical Excellence: The Treatment of PTSD in Adults and Children
  79. ^ Schatzberg, Alan F. (2007). Manual of Clinical Psychopharmacology. American Psychiatric Pub, Inc. ISBN 1585623172. {{cite book}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  80. ^ "Lamotrigine FAQ". Retrieved 2007-05-01.
  81. ^ SSRIs versus Non-SSRIs in Post-traumatic Stress Disorder, Department of Psychiatry and Behavioral Sciences, Montefiore Medical Center, Albert Einstein College of Medicine
  82. ^ A preliminary study of lamotrigine for the treatment of posttraumatic stress disorder, Biol Psychiatry May 1, 1999;45(9):1226-9
  83. ^ ZIPRASIDONE TREATMENT FOR POSTTRAUMATIC STRESS DISORDER: 128 CASES
  84. ^ "Geodon pharmacology FAQ". Retrieved 2008-07-24.
  85. ^ "Propranolol pharmacology FAQ". Retrieved 2008-07-24.
  86. ^ Brantigan, CO (January 1982). Effect of Beta Blockade and Beta Stimulation on Stage Fright. American Journal of Medicine. pp. 88–94. {{cite book}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)CS1 maint: year (link)
  87. ^ Gates, GA (Nov-December 1985). Effect of Beta Blockade on Singing Performance. Ann Otol Rhinol Laryngol. pp. 570–4. {{cite book}}: Check date values in: |year= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)CS1 maint: year (link)
  88. ^ "A Pill to Calm Traumatic Memories FAQ". Retrieved 2008-07-24.
  89. ^ "Prazosin curbs brain damage from PTSD FAQ". Retrieved 2008-07-24.
  90. ^ "Prazosin drug helps post-traumatic stress nightmares FAQ". Retrieved 2008-07-24.
  91. ^ "Prazosin pharmacology FAQ". Retrieved 2008-07-24.
  92. ^ Johnson, Susan (2005). Emotionally Focused Couple Therapy with Trauma Survivors: Strengthening Attachment Bonds (Guilford Family Therapy Series). New York: The Guilford Press. ISBN 1-59385-165-0.
  93. ^ a b ""Marine Corps Offers Yoga, Massages to Marriages Strained by War"". Associated Press. 2008-04-02. Retrieved 2008-04-03.
  94. ^ Eileen Rivers, Washington Post, Tuesday, May 6, 2008; Page HE01
  95. ^ a b c d When trauma tips you over: PTSD Part 1 All in the Mind, Australian Broadcasting Commission, 9 October 2004
  96. ^ Swartz' Textbook of Physical Diagnosis: History and Examination
  97. ^ a b Shalev, Arieh Y.; Yehuda, Rachel; Alexander C. McFarlane (2000). International handbook of human response to trauma. New York: Kluwer Academic/Plenum Press. ISBN 0-306-46095-5.{{cite book}}: CS1 maint: multiple names: authors list (link); on-line
  98. ^ United States Department of Veteran Affairs
  99. ^ Vedantam, Shankar (2005-12-27). "A Political Debate On Stress Disorder: As Claims Rise, VA Takes Stock". The Washington Post. Retrieved 2008-03-12.
  100. ^ VAC-ACC.GC.CA
  101. ^ Mark Jarzombek, "The Post-traumatic Turn and the Art of Walid Ra'ad and Krzysztof Wodiczko: from Theory to Trope and Beyond," in Trauma and Visuality, Saltzman, Lisa and Eric Rosenberg, editors (University Press of New England, 2006)
  102. ^ Elizabeth Cowie, "Perceiving Memory and Tales of the Other: the work of Milica Tomic," Camera Austria, no. [?], pp. 14-16.
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