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Posttraumatic stress disorder
Classification and external resources
ICD-10 F43.1
ICD-9 309.81
DiseasesDB 33846
MedlinePlus 000925
eMedicine med/1900
MeSH D013313

Posttraumatic stress disorder (also known as post-traumatic stress disorder or 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 acute stress response.

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-9) require that the symptoms last more than one month and cause significant impairment in social, occupational, or other important areas of functioning.[1]

ClassificationEdit

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. These persisting posttraumatic stress symptoms cause significant disruptions of one or more important areas of life function.[4] It has three sub-forms: acute, chronic, and delayed-onset.[5]

CausesEdit

Psychological traumaEdit

PTSD is believed to be caused by either physical trauma or psychological trauma, or more frequently a combination of both.[1] According to Atkinson et al. (2000)[citation needed] PTSD is more likely to be caused by physical or psychological trauma caused by humans such as rape, war or terrorist attack than trauma caused by natural disasters. Possible sources of trauma include experiencing or witnessing childhood or adult physical, emotional or sexual abuse.[1] In addition, experiencing or witnessing an event perceived as life-threatening such as physical assault, adult experiences of sexual assault, accidents, drug addiction, illnesses, medical complications, or employment in occupations exposed to war (such as soldiers) or disaster (such as emergency service workers).[citation needed]

Traumatic events that may cause PTSD symptoms to develop include violent assault, kidnapping, sexual assault, 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 or adults may develop PTSD symptoms by experiencing bullying or mobbing.[6][7] Preliminary research suggests that child abuse may interact with mutations in a stress-related gene to increase the risk of PTSD in adults.[8][unreliable medical source?][9][unreliable medical source?][10]

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.[unreliable medical source?][11][unreliable medical source?][12] 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.[unreliable medical source?][13] 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.[14]

NeuroendocrinologyEdit

PTSD symptoms may result when a traumatic event causes an overactive 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.[15][Full citation needed][unreliable source?]

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.[16][17]

In addition, most people with PTSD also show a low secretion of cortisol and high secretion of catecholamines in urine, with a norepinephrine/cortisol ratio consequently higher than comparable non-diagnosed individuals.[18] 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.[19]

Brain catecholamine levels are low,[20] and corticotropin-releasing factor (CRF) concentrations are high.[21][22] 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.[23] 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.[24]

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.[25] 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.[26]

NeuroanatomyEdit

File:PTSD stress brain.gif

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 conflicts. 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.[28] 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.[29] This finding could not be replicated in chronic PTSD patients traumatized at an air show plane crash in 1988 (Ramstein, Germany).[30][31]

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.[citation needed]

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.[32] This is consistent with an interpretation of PTSD as a syndrome of deficient extinction ability.[32][33] Further animal and clinical research into the amygdala and fear conditioning may suggest additional treatments for the condition.

GeneticsEdit

There is evidence that susceptibility to PTSD is hereditary. 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).[34]

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.[35][36] 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),[37] which has itself been shown to be predictive of PTSD.[38][39] Furthermore, FKBP5 may be less expressed in those with current PTSD.[40]

Risk and protective factors for PTSD developmentEdit

Although most people (50-90%) encounter trauma over a lifetime,[41][42] only about 8% develop full PTSD.[41] Vulnerability to PTSD presumably stems from an interaction of biological diathesis, early childhood developmental experiences, and trauma severity.[citation needed]

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.[43][44][45][46] This effect of childhood trauma, which is not well understood, may be a marker for both traumatic experiences and attachment problems.[47][48] Proximity to, duration of, and severity of the trauma also make an impact; and interpersonal traumas cause more problems than impersonal ones.[49]

Military experienceEdit

Schnurr, Lunney, and Sengupta[39] 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.[50] Other research also indicates the protective effects of social support in averting and recovery from PTSD.[51][52]

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.[citation needed]

Foster careEdit

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 percent of those in the study meet the diagnostic criteria for PTSD as compared to 12-13 percent of Iraq war veterans and 15 percent of Vietnam war veterans, and a rate of 4 percent in the general population. The recovery rate for foster home alumni was 28.2% as opposed to 47% in the general population.[53][54]

In one study (Dubner and Motta, 1999),[55] 60% of children in foster care who had experienced sexual abuse had PTSD, and 42% of those who had been physically abused fulfilled 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.

DiagnosisEdit

CriteriaEdit

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][56]

A: Exposure to a traumatic eventEdit

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."[57])

B: Persistent re-experiencingEdit

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 numbingEdit

This involves a sufficient level of:

  • avoidance of stimuli associated with the trauma, such as certain thoughts or feelings, or talking about the event(s);
  • avoidance of behaviors, places, or people that might lead to distressing memories;
  • inability to recall major parts of the trauma(s), or decreased involvement in significant life activities;
  • decreased capacity (down to complete inability) to feel certain feelings;
  • an expectation that one's future will be somehow constrained in ways not normal to other people.

D: Persistent symptoms of increased arousal not present beforeEdit

These are all physiological response issues, such as difficulty falling or staying asleep, or problems with anger, concentration, or hypervigilance.

E: Duration of symptoms for more than 1 monthEdit

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

F. Significant impairmentEdit

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".[58]

AssessmentEdit

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%.[59] Various scales exist to measure the severity and frequency of PTSD symptoms.[60][61]

Research-based alternative symptom group conceptualizationsEdit

Emerging factor analytic research[62] suggests that PTSD symptoms group empirically into four clusters, not the three currently described in the Diagnostic and Statistical Manual of Mental Disorders[dated info]. 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).[63] 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).[64][65]

DSM-5 proposed diagnostic criteria changesEdit

In preparation for the May 2013[66] release of the DSM-5,[67] the fifth version of the American Psychiatric Association's diagnostic manual, draft diagnostic criteria was released for public comment, followed by a two-year period of field testing.[68] Proposed changes to the criteria include:[69][dated info]

  • Criterion A (prior exposure to traumatic events) is more specifically stated, and evaluation of an individual's emotional response at the time (current criterion A2) is dropped.
  • Several items in Criterion B (intrusion symptoms) are rewritten to add or augment certain distinctions now considered important.
  • Special consideration is given to developmentally appropriate criteria for use with children and adolescents. This is especially evident in the restated Criterion B - intrusion symptoms. Development of age-specific criteria for diagnosis of PTSD is ongoing at this time.
  • Criterion C (avoidance and numbing) has been split into "C" and "D":
    • Criterion C (new version) now focuses solely on avoidance of behaviors or physical or temporal reminders of the traumatic experience(s). What were formerly two symptoms are now three, due to slight changes in descriptions.
    • New Criterion D focuses on negative alterations in cognition and mood associated with the traumatic event(s), and contains two new symptoms, one expanded symptom, and four largely unchanged symptoms specified in the previous criteria.
  • Criterion E (formerly "D"), which focuses on increased arousal and reactivity, contains one modestly revised, one entirely new, and four unchanged symptoms.
  • Criterion F (formerly "E") still requires duration of symptoms to have been at least one month.
  • Criterion G (formerly "F") stipulates symptom impact ("disturbance") in the same way as before.
  • The "acute" vs "delayed" distinction is dropped; the "delayed" specifier is considered appropriate if clinical symptom onset is no sooner than 6 months after the traumatic event(s).

"Developmental trauma disorder", a proposed new diagnosis, was still under discussion at the time of the draft publication.[70][dated info]

PreventionEdit

File:Vietnam War Memorial Washington DC Maya Lin-editA.jpg

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 StatesEdit

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.[71]

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. 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..."[72][Full citation needed]

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.[73]

Many 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.[74] Walter Reed Army Institute of Research (WRAIR) developed the Battlemind program to assist service members avoid or ameliorate PTSD and related problems.

Other countriesEdit

In the UK, there has been some controversy that National Health Service is dumping veterans on service charities like Combat Stress.[75][76][77]

Veterans Affairs Canada offers a new program that includes rehabilitation, financial benefits, job placement, health benefits program, disability awards and family support.[78]

ManagementEdit

Prevention and early intervention strategiesEdit

Modest benefits have been from early access to cognitive behavioral therapy, as well as from some medications such as propranolol.[79] Critical incident stress management has also been suggested as a means of preventing PTSD but subsequent studies suggested iatrogenic effects[80][81] and later studies both confirmed harm and failed to demonstrate any benefits.[citation needed]

Psychotherapeutic interventionsEdit

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.[82][Full citation needed]

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),[not in citation given][Need quotation to verify] and many combinations of these procedures.[83][84] A 2010 review disagrees that these treatments have proven efficacy, and points out methodological flaws in the studies and previous meta-analyses.[85]

EMDR or trauma-focused cognitive behavioral therapy (TFCBT) was 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."[86] 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.[87]

Behavioral and Cognitive Behavioral therapyEdit

Cognitive Behavioral Therapy (CBT) seeks to change the way a trauma victim feels and acts by changing the patterns of thinking and/or behavior responsible for negative emotions. CBT have 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[88] 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 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.[89] Many of these therapy methods have a significant element of exposure,[90] and have demonstrated success in treating the primary problems of PTSD and co-occurring depressive symptoms.[91]

Exposure therapy is a type of cognitive behavioral therapy[92] 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. Indeed, the success of exposure-based therapies has raised the question of whether exposure is a necessary ingredient in the treatment of PTSD.[93] Some organizations have endorsed the need for exposure.[94][95] The US Department of Veterans Affairs has been actively training mental health treatment staff in Prolonged Exposure Therapy[96] and Cognitive Processing Therapy[97] in an effort to better treat US Veterans with PTSD.

Eye movement desensitization and reprocessingEdit

Eye movement desensitization and reprocessing (EMDR) is specifically targeted as a treatment for PTSD.[98] Based on the evidence of controlled research, the American Psychiatric Association[not in citation given][99] and the United States Department of Veterans Affairs and Department of Defense[not in citation given][100] have placed EMDR in the highest category of effectiveness and research support in the treatment of trauma. Several international bodies have made similar recommendations.[101] 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.[85][102][neutrality is disputed]

Interpersonal psychotherapyEdit

Other approaches, particularly involving social supports,[51][52] may also be important. An open trial of interpersonal psychotherapy[103] reported high rates of remission from PTSD symptoms without using exposure.[104] A current, NIMH-funded trial in New York City is now comparing interpersonal psychotherapy, prolonged exposure therapy, and relaxation therapy.[105][Full citation needed][dated info]

MedicationEdit

Symptom prevention: potentially useful medication classesEdit

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[106] 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.[107]

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.[108][109][110]

Opiates. In a retrospective analysis of combat injury field data for US troops in Iraq, it was found that those who received morphine in the early stages of their treatment had a significantly lower rate of subsequent PTSD, when compared with those who did not receive morphine at that time.[111]

Symptom management: potentially useful medication classesEdit

A variety of medications has shown adjunctive benefit in reducing PTSD symptoms,[112] but "there is no clear drug treatment for PTSD".[113] 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.[113] Among the anti-depressants described below, 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%+).[114] 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.[115]

Alpha-adrenergic agonists. Prazosin ("Minipress"), in a small study of combat veterans, has shown substantial benefit in relieving or reducing nightmares.[116] Clonidine ("Catapres") can be helpful with startle, hyperarousal, and general autonomic hyperexcitability.[117]

Anti-convulsants, mood stabilizers, anti-aggression agents. Carbamazepine ("Tegretol") has likely benefit in reducing arousal symptoms involving noxious affect,[118] as well as mood or aggression.[119] Topiramate ("Topamax")[116] has been effective in achieving major reductions in flashbacks and nightmares, and no reduction of effect was seen over time.[116] Zolpidem ("Ambien") has also proven useful in treating sleep disturbances.[117]

Lamotrigine ("Lamictal") may be useful in reducing reexperiencing symptoms, as well as avoidance and emotional numbing.[116][120][121][122] Valproic acid ("Depakene") and has shown reduction of symptoms of irritability, aggression, and impulsiveness, and in reducing flashbacks.[117] Similarly, lithium carbonate has worked to control mood and aggressions (but not anxiety) symptoms.[119] Buspirone ("BuSpar") has an effect similar to that of lithium, with the additional benefit of working to reduce hyperarousal symptoms.[117]

Antipsychotics. Risperidone can be used to help with dissociation, mood issues, and aggression.[123]

Atypical antidepressants.[124] Nefazodone ("Serzone") can be effective with sleep disturbance symptoms, and with secondary depression, anxiety, and sexual dysfunction symptoms.[118] Trazodone ("Desyrel") can also reduce or eliminate problems with disturbed sleep, and with anger and anxiety.[118]

Beta blockers. Propranolol ("Inderal") has demonstrated possibilities in reducing hyperarousal symptoms, including sleep disturbances.[107][117]

Benzodiazepines. These can be used with caution for short-term anxiety relief,[123][125] hyperarousal, and sleep disturbance.[117] 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 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.[126][127]

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.[128] The neurodegenerative effects of the glucocorticoids, however, may prove this treatment counterproductive.[129]

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.[118]

Monoamine-oxidase inhibitors (MAOs). Phenelzine ("Nardil") has for some time been observed to be effective with hyperarousal and depression, and is especially effective with nightmares.[118]

SSRIs (selective serotonin reuptake inhibitors). SSRIs are considered to be a first-line drug treatment.[126][130] SSRIs for which there are data to support use include: citalopram, escitalopram,[131] fluoxetine,[118] fluvoxamine,[132] paroxetine,[133] and sertraline.[118][134]

Miscellaneous other medications. Clinical trials evaluating methylenedioxymethamphetamine (MDMA, "Ecstasy") in conjunction with psychotherapy are being conducted in Switzerland[135] and Israel.[136]

Medications by symptom group affectedEdit

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:[123][125][137]

Symptom class Symptom Medication
Reexperiencing
  intrusive recall amitriptyline; fluoxetine; imipramine; lamotrigine; sertraline
intrusive reexperiencing amitriptyline; fluoxetine; imipramine; nefazodone; sertraline (women only); topiramate;
sleep disturbance, nightmares benzodiazepines; carbamazepine; clonidine; nefazodone; phenelzine; prazosin; topiramate; trazodone; zolpidem
dissociative recall risperidone
intense psychological distress (anger, anxiety) when exposed to reminders of traumatic event(s) benzodiazepines; buspirone; carbamazepine; lithium (not for anxiety); nefazodone; trazodone
Avoidance
  avoidance amitriptyline; fluoxetine; lamotrigine; nefazodone; sertraline
feelings of detachment or estrangement from others amitriptyline; risperidone
restricted range of affect (numbing) amitriptyline; lamotrigine; sertraline (women only)
Hyperarousal
  general hyperarousal amitriptyline; nefazodone; phenelzine; sertraline (women only)
sleep disturbance, nightmares benzodiazepines; carbamazepine; clonidine; nefazodone; phenelzine; trazodone; zolpidem
irritability, anger (and impulsiveness) carbamazepine; nefazodone; valproic acid
anger buspirone; fluoxetine; lithium; trazodone
aggression risperidone
exaggerated startle response; general autonomic hyperexcitability benzodiazepines; buspirone; carbamazepine; clonidine; propranolol; valproic acid

Some medications can also help with symptoms which may occur secondary to PTSD.[137]

Secondary symptom Medication
depression nefazodone; phenelzine
dream content distortions nefazodone
relapse of symptoms carbamazepine;
self-mutilation clonidine; buprenorphine
sexual function reduction nefazodone
sleep hours reduction nefazodone

Medication and self-medication issues and risks with PTSDEdit

Alcohol abuse and drug abuse commonly co-occurs with PTSD.[116] 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.[138][139]

Benzodiazepines are risky in several ways. They can be especially addictive when PTSD is present, and this is especially true with the fast-acting ones. Dis-inhibition upon initiation of treatment is another risk with this medication class. Finally, termination of the drug can be especially difficult.[140] Recovery from benzodiazepine abuse or dependence tends to take a lot longer than recovery from alcohol abuse or dependence, but people can regain their previous good health. PTSD symptoms may temporarily worsen however, during alcohol withdrawal or benzodiazepine withdrawal.[138]

Yohimbine (not considered specifically appropriate for PTSD) increases arousal by increasing release of endogenous norepinephrine, and can worsen PTSD symptoms.[140]

EpidemiologyEdit

File:Post-traumatic stress disorder world map - DALY - WHO2004.svg

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 ratesEdit

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,[142] 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.[143] 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.[144][145]

Age-standardized Disability-adjusted life year (DALY) rates for PTSD, per 100,000 inhabitants, in 25 most populous countries,[142] ranked by overall rate (2004)
Region Country PTSD DALY rate,
overall
[143] PTSD DALY rate,
females
[144] PTSD DALY rate,
males[145]
Asia / Pacific Thailand 59 86 30
Asia / Pacific Indonesia 58 86 30
Asia / Pacific Philippines 58 86 30
Americas USA 58 86 30
Asia / Pacific Bangladesh 57 85 29
Africa Egypt 56 83 30
Asia / Pacific India 56 85 29
Asia / Pacific Iran 56 83 30
Asia / Pacific Pakistan 56 85 29
Asia / Pacific Japan 55 80 31
Asia / Pacific Myanmar 55 81 30
Europe Turkey 55 81 30
Asia / Pacific Viet Nam 55 80 30
Europe France 54 80 28
Europe Germany 54 80 28
Europe Italy 54 80 28
Asia / Pacific Russian Federation 54 78 30
Europe United Kingdom 54 80 28
Africa Nigeria 53 76 29
Africa Dem. Republ. of Congo 52 76 28
Africa Ethiopia 52 76 28
Africa South Africa 52 76 28
Asia / Pacific China 51 76 28
Americas Mexico 46 60 30
Americas Brazil 45 60 30

United StatesEdit

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 (5%) to have PTSD at some point in their lives.[41]

The United States Department of Veterans Affairs estimates that 830,000 Vietnam War veterans suffered symptoms of PTSD.[146] 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.[50]

In other speciesEdit

There have been reports of captive[147] and wild[148] 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[149] to develop posttraumatic stress after witnessing war.

HistoryEdit

Earliest reportsEdit

Reports of battle-associated stress reactions appear as early as the 6th century BC/BCE.[150] One of the first descriptions of PTSD was made by the Greek historian Herodotus. In 490 BC/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.[151]

Modern recognition in military settingsEdit

File:Statue Three Servicemen Vietnam Veterans Memorial-editA.png

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. As in the present time, soldiers during the 19th century were not supposed to be scared or show any fear in the midst of battle. The only treatment for this "exhaustion" was to bring the afflicted to the back for a bit then send them back into battle. During the intense and frequently repeated stress, the soldiers became fatigued as a part of their body's natural shock reaction.[152][Full citation needed]

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.[153]

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.[150]

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

TerminologyEdit

The term post-traumatic stress disorder or PTSD was coined in the mid 1970s.[150] Early in 1978, the term was used in a working group finding presented to the Committee of Reactive Disorders.[71] The term was formally recognized in 1980.[150] (In the authoritative DSM-IV, 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.)

See alsoEdit

ReferencesEdit

  1. 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 American Psychiatric Association (1994). Diagnostic and statistical manual of mental disorders: DSM-IV. Washington, DC: American Psychiatric Association. ISBN 0890420610.
  2. Satcher D et al. (1999). "Chapter 4.2". Mental Health: A Report of the Surgeon General. Surgeon General of the United States. http://www.surgeongeneral.gov/library/mentalhealth/chapter4/sec2.html.
  3. 3.0 3.1 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. http://publications.cpa-apc.org/media.php?mid=490. Retrieved 2008-03-12.
  4. Kaplan, HI; Sadock, BJ, Grebb, JA (1994). Kaplan and Sadock's synopsis of psychiatry: Behavioral sciences, clinical psychiatry, 7th ed.. Baltimore: Williams & Williams. pp. 606–609.
  5. Satcher D et al. (1999). "Chapter 4". Mental Health: A Report of the Surgeon General. Surgeon General of the United States. http://www.surgeongeneral.gov/library/mentalhealth/toc.html#chapter4.
  6. Kelleher I, Harley M, Lynch F, Arseneault L, Fitzpatrick C, Cannon M (November 2008). "Associations between childhood trauma, bullying and psychotic symptoms among a school-based adolescent sample". Br J Psychiatry 193 (5): 378–82. doi:10.1192/bjp.bp.108.049536. PMID 18978317.
  7. ["Are they really out to get your patient?" http://www.innovations-training.com/0804CP_Article4.pdf] Current Psychiatry Volume 8 Number 4
  8. Binder EB, Bradley RG, Liu W, et al. (March 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. PMC 2441757. PMID 18349090.
  9. [unreliable medical source?]Peggy Peck, Executive Editor (2008-03-09). "Genes May Affect Lifelong Impact of Child Abuse". MedPage Today. http://www.medpagetoday.com/Genetics/GeneticTesting/dh/8824.
  10. [unreliable medical source?]Constance Holden (2008-03-18). "Seeds of PTSD Planted in Childhood". ScienceNOW Daily News. http://sciencenow.sciencemag.org/cgi/content/full/2008/318/2?etoc.
  11. [unreliable medical source?]Schechter DS, Coates SW, Kaminer T, et al. (2008). "Distorted maternal mental representations and atypical behavior in a clinical sample of violence-exposed mothers and their toddlers". J Trauma Dissociation 9 (2): 123–47. doi:10.1080/15299730802045666. PMC 2577290. PMID 18985165.
  12. [unreliable medical source?]Schechter DS, Zygmunt A, Coates SW, et al. (September 2007). "Caregiver traumatization adversely impacts young children's mental representations on the MacArthur Story Stem Battery". Attach Hum Dev 9 (3): 187–205. doi:10.1080/14616730701453762. PMC 2078523. PMID 18007959.
  13. [unreliable medical source?] Schechter DS, Gross A, Willheim E, et al. (December 2009). "Is maternal PTSD associated with greater exposure of very young children to violent media?". J Trauma Stress 22 (6): 658–62. doi:10.1002/jts.20472. PMC 2798921. PMID 19924819.
  14. Clarke, C. et. al. 2007. Childhood and Adulthood Psychological Ill Health as Predictors of Midlife and Anxiety disorders. Archives of General Psychiatry. 64. pp668-678
  15. PBS Series "The Secret Life of the Brain Episode 4, 2001
  16. Yehuda R, Halligan SL, Golier JA, Grossman R, Bierer LM (2004). "Effects of trauma exposure on the cortisol response to dexamethasone administration in PTSD and major depressive disorder". Psychoneuroendocrinology 29 (3): 389–404. doi:10.1016/S0306-4530(03)00052-0. PMID 14644068.
  17. Yehuda R, Halligan SL, Grossman R, Golier JA, Wong C (2002). "The cortisol and glucocorticoid receptor response to low dose dexamethasone administration in aging combat veterans and holocaust survivors with and without posttraumatic stress disorder". Biol Psychiatry 52 (5): 393–403. doi:10.1016/S0006-3223(02)01357-4. PMID 12242055.
  18. 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.
  19. [unreliable medical source?]Bohnen N, Nicolson N, Sulon J, Jolles J (1991). "Coping style, trait anxiety and cortisol reactivity during mental stress". J Psychosom Res 35 (2-3): 141–7. doi:10.1016/0022-3999(91)90068-Y. PMID 2046048.
  20. Geracioti TD Jr, Baker DG, Ekhator NN, West SA, Hill KK, Bruce AB, Schmidt D, Rounds-Kugler B, Yehuda R, Keck PE Jr, Kasckow JW (2001). "CSF norepinephrine concentrations in posttraumatic stress disorder". Am J Psychiatry 158 (8): 1227–1230. doi:10.1176/appi.ajp.158.8.1227. PMID 11481155.
  21. [unreliable medical source?]Sautter FJ, Bissette G, Wiley J, et al. (December 2003). "Corticotropin-releasing factor in posttraumatic stress disorder (PTSD) with secondary psychotic symptoms, nonpsychotic PTSD, and healthy control subjects". Biol. Psychiatry 54 (12): 1382–8. doi:10.1016/S0006-3223(03)00571-7. PMID 14675802.
  22. [unreliable medical source?]de Kloet CS, Vermetten E, Geuze E, et al. (2008). "Elevated plasma corticotrophin-releasing hormone levels in veterans with posttraumatic stress disorder". Prog. Brain Res. 167: 287–91. doi:10.1016/S0079-6123(07)67025-3. PMID 18037027.[unreliable medical source?]
  23. Yehuda R (2001). "Biology of posttraumatic stress disorder". J Clin Psychiatry 62 Suppl 17: 41–6. PMID 11495096.
  24. Yehuda R (2002). "Clinical relevance of biologic findings in PTSD". Psychiatr Q 73 (2): 123–33. doi:10.1023/A:1015055711424. PMID 12025720.
  25. 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.
  26. 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.
  27. "NIMH · Post Traumatic Stress Disorder Research Fact Sheet". National Institutes of Health. http://www.nimh.nih.gov/health/publications/post-traumatic-stress-disorder-research-fact-sheet/index.shtml.
  28. [unreliable medical source?] [|Newton, Philip]. "From Mouse to Man; the Anatomy of Posttraumatic Stress Disorder". http://www.psychologytoday.com/blog/mouse-man/200901/the-anatomy-post-traumatic-stress-disorder. Retrieved 20 December 2009.
  29. Carlson, Neil R. (2007). Physiology of Behavior (9 ed.). Pearson Education, Inc.
  30. Jatzko A, Rothenhöfer S, Schmitt A, Gaser C, Demiracka T, Weber-Fahr W, Wessa M, Magnotta V, Braus DF. (2006). Hippocampal volume in chronic posttraumatic stress disorder (PTSD): MRI study using two different evaluation methods. Journal of Affective Disorders. 94: 121-126.
  31. http://dbm.neuro.uni-jena.de/pdf-files/Jatzko-JAD06.pdf
  32. 32.0 32.1 Milad MR, Pitman RK, Ellis CB, Gold AL, Shin LM, Lasko NB, Zeidan MA, Handwerger K, Orr SP, Rauch SL. (2009). Neurobiological basis of failure to recall extinction memory in posttraumatic stress disorder. Biol Psychiatry. 66(12):1075-82. PMID 19748076
  33. Stein MB, Paulus MP. (2009). Imbalance of approach and avoidance: the yin and yang of anxiety disorders. Biol Psychiatry. 66(12):1072-4. Template:Doi PMID 19944792
  34. 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.
  35. http://www.psychologytoday.com/blog/mouse-man/200811/gene-anxiety-depression-and-posttraumatic-stress-disorder-fkbp5
  36. 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. PMC 2441757. PMID 18349090.
  37. 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.
  38. 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.
  39. 39.0 39.1 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.
  40. Yehuda R, Cai G, Golier JA, Sarapas C, Galea S, Ising M, Rein T, Schmeidler J, Müller-Myhsok B, Holsboer F, Buxbaum JD (24 April 2009 [Epub ahead of print]). "Gene expression patterns associated with posttraumatic stress disorder following exposure to the World Trade Center attacks.". Biol Psychiatry 66 (7): 708–11. doi:10.1016/j.biopsych.2009.02.034. PMID 19393990.
  41. 41.0 41.1 41.2 Kessler RC, Sonnega A, Bromet E, Hughes M, Nelson CB (December 1995). "Posttraumatic stress disorder in the National Comorbidity Survey". Arch Gen Psychiatry 52 (12): 1048–60. PMID 7492257.
  42. Breslau N, Kessler RC, Chilcoat HD, Schultz LR, Davis GC, Andreski P (July 1998). "Trauma and posttraumatic stress disorder in the community: the 1996 Detroit Area Survey of Trauma". Arch Gen Psychiatry 55 (7): 626–32. doi:10.1001/archpsyc.55.7.626. PMID 9672053. http://archpsyc.ama-assn.org/cgi/pmidlookup?view=long&pmid=9672053.
  43. Koenen KC, Moffitt TE, Poulton R, Martin J, Caspi A (February 2007). "Early childhood factors associated with the development of post-traumatic stress disorder: results from a longitudinal birth cohort". Psychol Med 37 (2): 181–92. doi:10.1017/S0033291706009019. PMC 2254221. PMID 17052377.
  44. Lapp KG, Bosworth HB, Strauss JL, et al. (September 2005). "Lifetime sexual and physical victimization among male veterans with combat-related post-traumatic stress disorder". Mil Med 170 (9): 787–90. PMID 16261985.
  45. Otte C, Neylan TC, Pole N, et al. (January 2005). "Association between childhood trauma and catecholamine response to psychological stress in police academy recruits". Biol. Psychiatry 57 (1): 27–32. doi:10.1016/j.biopsych.2004.10.009. PMID 15607297.
  46. Resnick HS, Yehuda R, Pitman RK, Foy DW (November 1995). "Effect of previous trauma on acute plasma cortisol level following rape". Am J Psychiatry 152 (11): 1675–7. PMID 7485635. http://ajp.psychiatryonline.org/cgi/pmidlookup?view=long&pmid=7485635.
  47. Laor N, Wolmer L, Mayes LC, et al. (May 1996). "Israeli preschoolers under Scud missile attacks. A developmental perspective on risk-modifying factors". Arch Gen Psychiatry 53 (5): 416–23. PMID 8624185.
  48. Laor N, Wolmer L, Mayes LC, Gershon A, Weizman R, Cohen DJ (March 1997). "Israeli preschool children under Scuds: a 30-month follow-up". J Am Acad Child Adolesc Psychiatry 36 (3): 349–56. doi:10.1097/00004583-199703000-00013. PMID 9055515. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0890-8567&volume=36&issue=3&spage=349.
  49. Janoff-Bulman R: Shattered Assumptions: Toward a New Psychology of Trauma. New York: Free Press, 1992.
  50. 50.0 50.1 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].
  51. 51.0 51.1 Brewin CR, Andrews B, Valentine JD (October 2000). "Meta-analysis of risk factors for posttraumatic stress disorder in trauma-exposed adults". J Consult Clin Psychol 68 (5): 748–66. doi:10.1037/0022-006X.68.5.748. PMID 11068961. http://content.apa.org/journals/ccp/68/5/748.
  52. 52.0 52.1 Ozer EJ, Best SR, Lipsey TL, Weiss DS (January 2003). "Predictors of posttraumatic stress disorder and symptoms in adults: a meta-analysis". Psychol Bull 129 (1): 52–73. doi:10.1037/0033-2909.129.1.52. PMID 12555794. http://content.apa.org/journals/bul/129/1/52.
  53. Template:Cite press release
  54. Casey Family Programs (2005). "Assessing the Effects of Foster Care: Mental Health Outcomes from the Casey National Alumni Study". http://www.casey.org/Resources/Publications/pdf/CaseyNationalAlumniStudy_MentalHealth.pdf
  55. Dubner AE, Motta RW. Sexually and physically abused foster care children and posttraumatic stress disorder. J Consult Clin Psychol. 1999 Jun;67(3):367-73.PMID 10369057
  56. "NIMH · What are the symptoms of PTSD?". National Institute of Mental Health. http://www.nimh.nih.gov/health/publications/post-traumatic-stress-disorder-ptsd/what-are-the-symptoms-of-ptsd.shtml.
  57. American Psychiatric Association (1987). Diagnostic and Statistical Manual of Mental Disorders: DSM-III-R. ISBN 0890420181.
  58. American Psychiatric Association (1994). Diagnostic and statistical manual of mental disorders, quick reference. Washington, D.C.: American Psychiatric Association. p. 211. ISBN 0-89042-063-7.
  59. 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.
  60. Blake DD, Weathers FW, Nagy LM, et al. (January 1995). "The development of a Clinician-Administered PTSD Scale". J Trauma Stress 8 (1): 75–90. doi:10.1002/jts.2490080106. PMID 7712061.
  61. Foa E: The Post Traumatic Diagnostic Scale Manual. Minneapolis, NCS, 1995.
  62. Pietrzak RH, Southwick SM (June). "The importance of four-factor emotional numbing and dysphoria models in PTSD.". Am J Psychiatry 166 (6): 726–727. doi:10.1176/appi.ajp.2009.09010032. PMID 19487403.
  63. King DW, Leskin GA, King LA, Weathers FW (June). "Confirmatory factor analysis of the clinician-administered PTSD Scale: Evidence for the dimensionality of posttraumatic stress disorder.". Psychol Assess 10 (2): 90–96. doi:10.1037/1040-3590.10.2.90.
  64. Ask E, Mark S (Sep). "The structure of PTSD symptoms: A test of alternative models using confirmatory factor analysis.". Br J Clin Psychol 46 (3): 299–313. doi:10.1348/014466506X171540. PMID 17535523.
  65. Palmieri PA, Weathers FW, Difede J, King DW (May). "Confirmatory factor analysis of the PTSD Checklist and the Clinician-Administered PTSD Scale in disaster workers exposed to the World Trade Center Ground Zero.". J Abnorm Psychol 116 (2): 329–341. doi:10.1037/0021-843X.116.2.329. PMID 17516765.
  66. "Timeline". http://www.dsm5.org/about/Pages/Timeline.aspx. Retrieved 2010-04-22.
  67. American Psychiatric Association (2010-03-09). "APA Modifies DSM Naming Convention to Reflect Publication Changes". http://www.dsm5.org/Newsroom/Documents/DSM-Name-Change.pdf. Retrieved 2010-06-11.
  68. Gever, J (10 February 2010). "DSM-V Draft Promises Big Changes in Some Psychiatric Diagnoses". http://www.medpagetoday.com/Psychiatry/GeneralPsychiatry/18399. Retrieved 10 February 2010.
  69. "309.81 Posttraumatic Stress Disorder: Proposed Revision". American Psychiatric Association. 2010. http://www.dsm5.org/ProposedRevisions/Pages/proposedrevision.aspx?rid=165. Retrieved 2010-03-20.
  70. "Conditions Proposed by Outside Sources". http://www.dsm5.org/ProposedRevisions/Pages/ConditionsProposedbyOutsideSources.aspx. Retrieved 11 February 2010.
  71. 71.0 71.1 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.; on-line.
  72. United States Department of Veteran Affairs.
  73. Vedantam, Shankar (2005-12-27). "A Political Debate On Stress Disorder: As Claims Rise, VA Takes Stock". Washington Post. http://www.washingtonpost.com/wp-dyn/content/article/2005/12/26/AR2005122600792.html. Retrieved 2008-03-12.
  74. "Marine Corps Offers Yoga, Massages to Marriages Strained by War". Fox News. Associated Press. 2008-04-02. http://www.foxnews.com/story/0,2933,344991,00.html. Retrieved 2008-04-03.
  75. Dixon, Laura (February 28, 2009). "Lance Corporal Johnson Beharry accuses Government of neglecting soldiers". London: Times Online. http://www.timesonline.co.uk/tol/news/politics/article5819059.ece. Retrieved 2009-08-29.
  76. "British troops in Afghanistan face mental health timebomb 'on the scale of Vietnam' | Mail Online". Dailymail.co.uk. http://www.dailymail.co.uk/news/article-1158350/Troops-face-mental-trauma-scale-Vietnam.html. Retrieved 2009-08-29.
  77. "UK | Full interview: L/Cpl Johnson Beharry". BBC News. 2009-02-28. http://news.bbc.co.uk/1/hi/uk/7916852.stm. Retrieved 2009-08-29.
  78. "The New Veterans Charter for CF Veterans and their Families". Vac-Acc.Gc.Ca. 2006-07-12. http://www.vac-acc.gc.ca/clients/sub.cfm?source=Forces/nvc&CFID=9295860&CFTOKEN=39698927. Retrieved 2009-08-29.
  79. 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.
  80. Carlier, IVE; Lamberts RD; van Uchelen AJ; Gersons BPR (1998). "Disaster-related post-traumatic stress in police officers: A field study of the impact of debriefing". Stress Medicine 14 (3): 143–8. doi:10.1002/(SICI)1099-1700(199807)14:3<143::AID-SMI770>3.0.CO;2-S. http://doi.apa.org/?uid=1998-10258-001.
  81. 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.
  82. Foa 1997.
  83. 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.
  84. Brom D, Kleber RJ, Defares PB (October 1989). "Brief psychotherapy for posttraumatic stress disorders". J Consult Clin Psychol 57 (5): 607–12. doi:10.1037/0022-006X.57.5.607. PMID 2571625. http://content.apa.org/journals/ccp/57/5/607.
  85. 85.0 85.1 Ehlers A, Bisson J, Clark DM, et al. (March 2010). "Do all psychological treatments really work the same in posttraumatic stress disorder?". Clin Psychol Rev 30 (2): 269–76. doi:10.1016/j.cpr.2009.12.001. PMC 2852651. PMID 20051310.
  86. Bisson JI, Ehlers A, Matthews R, Pilling S, Richards D, Turner S (2007). "Psychological treatments for chronic post-traumatic stress disorder. Systematic review and meta-analysis". The British Journal of Psychiatry : the journal of mental science 190: 97–104. doi:10.1192/bjp.bp.106.021402. PMID 17267924. http://bjp.rcpsych.org/cgi/content/full/190/2/97.
  87. 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.
  88. Hassija, C.M. & Gray, M.J. (2007). Behavioral Interventions for Trauma and Posttraumatic Stress Disorder. International Journal of Behavioral Consultation and Therapy, 3(2),166-175. BAO
  89. Mulick, P.S., Landes, S. & Kanter, J.W. (2005) Contextual Behavior Therapies in the Treatment of PTSD: A Review. International Journal of Behavioral Consultation and Therapy, 1(3), 223-228 [2]
  90. Hassija, C.M. & Gray, M.J. (2007). Behavioral Interventions for Trauma and Posttraumatic Stress Disorder. International Journal of Behavioral Consultation and Therapy, 3(2), 166-175. [3]
  91. Mulick, P.S., and Naugle, A.E. (2009). Behavioral Activation in the Treatment of Comorbid Posttraumatic Stress Disorder and Major Depressive Disorder. International Journal of Behavioral Consultation and Therapy, 5(2), 330-339. [4]
  92. Grohol, JM. "What is Exposure Therapy?". http://psychcentral.com/lib/2009/what-is-exposure-therapy/. Retrieved 2010-07-14.
  93. Joseph, JS; Gray, M.J. (2008). BAO "Exposure Therapy for Posttraumatic Stress Disorder". Journal of Behavior Analysis of Offender and Victim: Treatment and Prevention 1 (4): 69–80. http://www.baojournal.com BAO. Retrieved 2010-05-10.
  94. Ursano RJ, Bell C, Eth S, et al. (November 2004). "Practice guideline for the treatment of patients with acute stress disorder and posttraumatic stress disorder". Am J Psychiatry 161 (11 Suppl): 3–31. doi:10.1176/appi.ajp.161.1.3. PMID 15617511.
  95. Committee on Treatment of Posttraumatic Stress Disorder, Institute of Medicine: Treatment of Posttraumatic Stress Disorder: An Assessment of the Evidence. Washington, D.C.: National Academies Press, 2008 ISBN 0-309-10926-4.
  96. "Prolonged Exposure Therapy". 2009-09-29. http://www.ptsd.va.gov/public/pages/prolonged-exposure-therapy.asp. Retrieved 2010-07-14.
  97. Karlin, B. E., Ruzek, J. I. Chard, K. M., Eftekhari, A., Monson, C. M., Hembree, E. A., Resick, P. A., Foa, E. B. (2010). Dissemination of evidence-based psychological treatments for posttraumatic stress disorder in the Veterans Health Administration. Journal of Traumatic Stress, 23, 663-673.
  98. 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.
  99. "Practice Guideline for the treatment of patients with acute stress disorder and posttraumatic stress disorder". Arlington, VA: American Psychiatric Association. 2004. http://www.guideline.gov/summary/summary.aspx?doc_id=5954.
  100. VA/DoD clinical practice guideline for the management of post-traumatic stress. Washington, DC: Department of Veteran Affairs & United States Department of Defense. June 2008. Archived from the original on 2008-06-29. http://web.archive.org/web/20080629095323/http://www.oqp.med.va.gov/cpg/PTSD/PTSD_cpg/frameset.htm.
  101. See
  102. Australian guidelines for the treatment of adults with acute stress disorder and post traumatic stress disorder. Melbourne, Victoria: Australian Centre for Posttraumatic Mental Health. 2007. ISBN 9780975224663. http://www.acpmh.unimelb.edu.au/resources/resources-guidelines.html#1.
  103. Weissman MM, Markowitz JC, Klerman GL: Clinician’s Quick Guide to Interpersonal Psychotherapy. New York: Oxford University Press, 2007.
  104. Bleiberg KL, Markowitz JC (January 2005). "A pilot study of interpersonal psychotherapy for posttraumatic stress disorder". Am J Psychiatry 162 (1): 181–3. doi:10.1176/appi.ajp.162.1.181. PMID 15625219.
  105. http://www.columbiatrauma.org/
  106. {Khoshnu, E (October 2006). "Clonidine for Treatment of PTSD". Clinical Psychiatry News 34 (10): 22. http://www.clinicalpsychiatrynews.com/article/S0270-6644%2806%2971796-9/fulltext. Retrieved 9 February 2010.
  107. 107.0 107.1 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.
  108. Schelling G, Roozendaal B, Krauseneck T, Schmoelz M, DE Quervain D, Briegel J. (2006). "Efficacy of hydrocortisone in preventing posttraumatic stress disorder following critical illness and major surgery.". Ann N Y Acad Sci 1071: 46–53. doi:10.1196/annals.1364.005. PMID 16891561.
  109. Weis F, Kilger E, Roozendaal B, de Quervain DJ, Lamm P, Schmidt M, Schmölz M, Briegel J, Schelling G. (2006). "Stress doses of hydrocortisone reduce chronic stress symptoms and improve health-related quality of life in high-risk patients after cardiac surgery: a randomized study.". J Thorac Cardiovasc Surg 131 (2): 277–282. doi:10.1016/j.jtcvs.2005.07.063. PMID 16434254.
  110. Schelling G, Kilger E, Roozendaal B, de Quervain DJ, Briegel J, Dagge A, Rothenhäusler HB, Krauseneck T, Nollert G, Kapfhammer HP. (2004). "Stress doses of hydrocortisone, traumatic memories, and symptoms of posttraumatic stress disorder in patients after cardiac surgery: a randomized study.". Biol Psychiatry 55 (6): 627–633. doi:10.1016/j.biopsych.2003.09.014. PMID 15013832.
  111. Holbrook, T.L., et al.; Galarneau, MR; Dye, JL; Quinn, K; Dougherty, AL (2010-01-14). "Morphine use after combat injury in Iraq and post-traumatic stress disorder.". N Engl J Med 362 (110): 110–7. doi:10.1056/NEJMoa0903326. PMID 20071700. http://content.nejm.org/cgi/content/full/362/2/110. Retrieved 2009-02-05.
  112. Maxmen, J. S.; Ward, N. G. (1995). Essential psychopathology and its treatment, 2nd ed., revised for DSM-IV (second ed.). New York: W. W. Norton. p. 280. ISBN 0-393-70173-5.
  113. 113.0 113.1 Maxmen, J. S.; Ward, N. G. (2002). Psychotropic drugs: fast facts (third ed.). New York: W. W. Norton. p. 346. ISBN 0-393-70301-0.
  114. Maxmen, J. S.; Ward, N. G. (1995). Essential psychopathology and its treatment, 2nd ed., revised for DSM-IV (second ed.). New York: W. W. Norton. p. 104. ISBN 0-393-70173-5.
  115. Maxmen, J. S.; Ward, N. G. (1995). Essential psychopathology and its treatment, 2nd ed., revised for DSM-IV (second ed.). New York: W. W. Norton. p. 175. ISBN 0-393-70173-5.
  116. 116.0 116.1 116.2 116.3 116.4 Maxmen, J. S.; Ward, N. G. (2002). Psychotropic drugs: fast facts (third ed.). New York: W. W. Norton. p. 348. ISBN 0-393-70301-0.
  117. 117.0 117.1 117.2 117.3 117.4 117.5 Maxmen, J. S.; Ward, N. G. (2002). Psychotropic drugs: fast facts (third ed.). New York: W. W. Norton. p. 349. ISBN 0-393-70301-0.
  118. 118.0 118.1 118.2 118.3 118.4 118.5 118.6 Maxmen, J. S.; Ward, N. G. (2002). Psychotropic drugs: fast facts (third ed.). New York: W. W. Norton. p. 347. ISBN 0-393-70301-0.
  119. 119.0 119.1 Lacy CF, Armstrong LL et al. (2008). Drug Information Handbook. Lexi-Comp. pp. 260, 934.
  120. "Lamotrigine FAQ". http://www.psycom.net/depression.central.lamotrigine.html. Retrieved 2007-05-01.
  121. SSRIs versus Non-SSRIs in Post-traumatic Stress Disorder, Department of Psychiatry and Behavioral Sciences, Montefiore Medical Center, Albert Einstein College of Medicine.
  122. Hertzberg MA, Butterfield MI, Feldman ME, et al. (May 1999). "A preliminary study of lamotrigine for the treatment of posttraumatic stress disorder". Biol. Psychiatry 45 (9): 1226–9. doi:10.1016/S0006-3223(99)00011-6. PMID 10331117. http://linkinghub.elsevier.com/retrieve/pii/S0006-3223(99)00011-6.
  123. 123.0 123.1 123.2 Kapfhammer, HP. (Dec 2008). "[Therapeutic possibilities after traumatic experiences]". Psychiatr Danub 20 (4): 532–45. PMID 19011595.
  124. Maxmen, J. S.; Ward, N. G. (1995). Essential psychopathology and its treatment, 2nd ed., revised for DSM-IV (second ed.). New York: W. W. Norton. p. 95. ISBN 0-393-70173-5.
  125. 125.0 125.1 Reist, C (2005). Post-traumatic Stress Disorder. Compendia, Build ID: F000005, published by Epocrates.com
  126. 126.0 126.1 Berger, W.; Mendlowicz, MV.; Marques-Portella, C.; Kinrys, G.; Fontenelle, LF.; Marmar, CR.; Figueira, I. (Mar 2009). "Pharmacologic alternatives to antidepressants in posttraumatic stress disorder: a systematic review.". Prog Neuropsychopharmacol Biol Psychiatry 33 (2): 169–80. doi:10.1016/j.pnpbp.2008.12.004. PMC 2720612. PMID 19141307.
  127. Martényi, F. (Mar 2005). "[Three paradigms in the treatment of posttraumatic stress disorder]". Neuropsychopharmacol Hung 7 (1): 11–21. PMID 16167463.
  128. Cohen H, Matar MA, Buskila D, Kaplan Z, Zohar J. (2008). "Early post-stressor intervention with high-dose corticosterone attenuates posttraumatic stress response in an animal model of posttraumatic stress disorder.". Biol Psychiatry 64 (8): 708–717. doi:10.1016/j.biopsych.2008.05.025. PMID 18635156.
  129. Sapolsky RM, Romero LM, Munck AU. (2000). "How do glucocorticoids influence stress responses? Integrating permissive, suppressive, stimulatory, and preparative actions.". Endocr Review 21 (1): 55–89. doi:10.1210/er.21.1.55. PMID 10696570.
  130. Cooper, J.; Carty, J.; Creamer, M. (Aug 2005). "Pharmacotherapy for posttraumatic stress disorder: empirical review and clinical recommendations.". Aust N Z J Psychiatry 39 (8): 674–82. doi:10.1111/j.1440-1614.2005.01651.x. PMID 16050921.
  131. Yehuda R (2000). "Biology of posttraumatic stress disorder". J Clin Psychiatry 61 (Suppl 7): 14–21. PMID 10795605.
  132. Marshall RD, Beebe KL, Oldham M, Zaninelli R (December 2001). "Efficacy and safety of paroxetine treatment for chronic PTSD: a fixed-dose, placebo-controlled study". Am J Psychiatry 158 (12): 1982–8. doi:10.1176/appi.ajp.158.12.1982. PMID 11729013. http://ajp.psychiatryonline.org/cgi/pmidlookup?view=long&pmid=11729013.
  133. Brady K, Pearlstein T, Asnis GM, et al. (April 2000). "Efficacy and safety of sertraline treatment of posttraumatic stress disorder: a randomized controlled trial". JAMA 283 (14): 1837–44. doi:10.1001/jama.283.14.1837. PMID 10770145. http://jama.ama-assn.org/cgi/pmidlookup?view=long&pmid=10770145.
  134. Davidson JR, Rothbaum BO, van der Kolk BA, Sikes CR, Farfel GM (May 2001). "Multicenter, double-blind comparison of sertraline and placebo in the treatment of posttraumatic stress disorder". Arch Gen Psychiatry 58 (5): 485–92. doi:10.1001/archpsyc.58.5.485. PMID 11343529. http://archpsyc.ama-assn.org/cgi/pmidlookup?view=long&pmid=11343529.
  135. "Study of 3,4-Methylenedioxymethamphetamine-Assisted Psychotherapy in People With Posttraumatic Stress Disorder". ClinicalTrials.gov. U.S. National Institutes of Health. February 2009. http://clinicaltrials.gov/ct2/show/NCT00353938. Retrieved on June 17, 2009.
  136. "Randomized Placebo-Controlled Study of MDMA-Assisted Psychotherapy in People With PTSD - Israel". ClinicalTrials.gov. U.S. National Institutes of Health. February 2009. http://clinicaltrials.gov/ct2/show/NCT00402298. Retrieved on June 17, 2009.
  137. 137.0 137.1 Maxmen, J. S.; Ward, N. G. (2002). Psychotropic drugs: fast facts (third ed.). New York: W. W. Norton. pp. 347–349. ISBN 0-393-70301-0.
  138. 138.0 138.1 Cohen SI (February 1995). "Alcohol and benzodiazepines generate anxiety, panic and phobias". J R Soc Med 88 (2): 73–77. PMC 1295099. PMID 7769598.
  139. Spates, R. & Souza (2007). Treatment of PTSD and Substance Abuse Comorbidity. The Behavior Analyst Today, 9(1), 11-26 [5]
  140. 140.0 140.1 Maxmen, J. S.; Ward, N. G. (2002). Psychotropic drugs: fast facts (third ed.). New York: W. W. Norton. p. 348. ISBN 0-393-70301-0.
  141. "Mortality and Burden of Disease Estimates for WHO Member States in 2004". World Health Organization. http://www.who.int/entity/healthinfo/global_burden_disease/gbddeathdalycountryestimates2004.xls.
  142. 142.0 142.1 List of countries by population
  143. 143.0 143.1 "Mortality and Burden of Disease Estimates for WHO Member States: Persons, all ages (2004)" (xls). World Health Organization. 2004. http://www.who.int/entity/healthinfo/global_burden_disease/gbddeathdalycountryestimates2004.xls. Retrieved 2009-11-12.
  144. 144.0 144.1 "Mortality and Burden of Disease Estimates for WHO Member States: Females, all ages (2004)" (xls). World Health Organization. 2004. http://www.who.int/entity/healthinfo/global_burden_disease/gbddeathdalycountryestimates_female_2004.xls. Retrieved 2009-11-12.
  145. 145.0 145.1 "Mortality and Burden of Disease Estimates for WHO Member States: Males, all ages (2004)" (xls). World Health Organization. 2004. http://www.who.int/entity/healthinfo/global_burden_disease/gbddeathdalycountryestimates_male_2004.xls. Retrieved 2009-11-12.
  146. The War's Costs . Digital History.
  147. Bradshaw, G.A.; Lindner, L. (no date). "Post-Traumatic Stress and Elephants in Captivity". http://www.elephants.com/ptsd/Bradshaw&Lindner_PTSD-rev.pdf. Retrieved 2010-01-01.
  148. Bradshaw, G.A.; Schore, A. N., Brown, J.L., Poole, J.H., & Moss, C.J. (2005-02-24). "Elephant breakdown". Nature 423. http://www.elephants.com/media/Elephant_breakdown_2005.pdf. Retrieved 2010-01-01.
  149. Associated Press (2010-08-03). "PTSD Victims Include Military Dogs, Too". http://www.cbsnews.com/stories/2010/08/03/national/main6739176.shtml.
  150. 150.0 150.1 150.2 150.3 When trauma tips you over: PTSD Part 1 All in the Mind, Australian Broadcasting Commission, 9 October 2004.
  151. Swartz' Textbook of Physical Diagnosis: History and Examination.
  152. [6]
  153. World War One --- A New Kind of War | Part II, From 14 - 18 Understanding the Great War, by Stéphane Audoin-Rouzeau, Annette Becker

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