Posttraumatic stress disorder

Posttraumatic stress disorder
Art therapy project created by a U.S. Marine with posttraumatic stress disorder
Classification and external resources
Specialty	Psychiatry
ICD-10	F43.1
ICD-9-CM	309.81
DiseasesDB	33846
MedlinePlus	000925
eMedicine	med/1900
Patient UK	Posttraumatic stress disorder
MeSH	D013313

Posttraumatic stress disorder (PTSD)^{[note 1]} is a mental disorder that can develop after a person is exposed to one or more traumatic events, such as sexual assault, warfare, traffic collisions, terrorism or other threats on a person's life.^[1] Symptoms include disturbing thoughts or feelings related to past traumas intruding on the present, avoidance of trauma-related cues, alterations in how a person thinks and feels about themselves and the world, and hyperarousal, persisting for more than a month after a traumatic event.^[1]

Most people who have experienced a traumatizing event will not develop PTSD.^[2] People who experience interpersonal trauma (e.g., sexual assault, child abuse) are more likely to develop PTSD, as opposed to people who experience non-assault based trauma such as accidents and natural disasters.^[3] Children are less likely than adults to develop PTSD after trauma, especially if they are under ten years of age.^[2]

Psychotherapy is the "gold standard" of treatment for PTSD. Various psychotherapies are evidence-based for PTSD, including prolonged exposure, cognitive processing therapy, eye movement desensitization and reprocessing, cognitive restructuring therapy, trauma-focused cognitive behavioral therapy, brief eclectic psychotherapy, narrative therapy, and stress inoculation training.^[4][5] Therapists generally meet one-on-one with individuals with PTSD, but frequently group therapy or more intensive settings (e.g., inpatient, residential) are also beneficial. Serotonergic antidepressants (such as fluoxetine and paroxetine, which are the only medications FDA approved for PTSD) are the first-line pharmacologic agents used for PTSD, but medications are best used to augment psychotherapy as they rarely result in recovery from PTSD, alone.^[4][6][7][8] Most other medications do not have enough evidence to support their use, may only improve symptoms a small amount without resulting in functional recovery, or, in the case of benzodiazepines, have actually been found to worsen and prolong PTSD, including inhibiting the benefits of psychotherapy.^[9][10]

The term "posttraumatic stress disorder" was coined in the early 1970s in large part due to the suffering of US military veterans of the Vietnam War.^[11] It was officially recognized by the American Psychiatric Association in 1980 in the third edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-III).^[12] Trauma-related mental disorders have been documented since at least the 17th century, and became more commonly recognized during the World Wars under various terms including "shell shock," "combat fatigue," and "war neurosis." ^[13][14]

Classification

Posttraumatic stress disorder was classified as an anxiety disorder in the DSM-IV, but has since been reclassified as a "trauma- and stressor-related disorder" in DSM-5. The characteristic symptoms are not present before exposure to the traumatic event. In the typical case, the individual with PTSD persistently avoids trauma-related thoughts and emotions, and discussion of the traumatic event, and may even have amnesia of the event. However, the event is commonly relived by the individual through intrusive, recurrent recollections, flashbacks, and nightmares.^[15] While it is common to have symptoms after any traumatic event, these must persist to a sufficient degree (i.e., causing dysfunction in life and/or clinical levels of distress) for longer than one month after the trauma to be classified as PTSD (clinically significant dysfunction or distress for less than one month after the trauma may be acute stress disorder).^{[1][16][17][18]}

Risk factors

Persons considered at risk include, for example, combat military personnel, victims of natural disasters, concentration camp survivors, and victims of violent crime. Individuals frequently experience "survivor's guilt" for remaining alive while others died. Causes of the symptoms of PTSD are the experiencing or witnessing of a stressor event involving death, serious injury or such threat to the self or others in a situation in which the individual felt intense fear, horror, or powerlessness.^[20] Persons employed in occupations that expose them to violence (such as soldiers) or disasters (such as emergency service workers) are also at risk.^[20]

Trauma

PTSD is believed to be caused by the experience of a wide range of traumatic events and, in particular if the trauma is extreme, can occur in persons with no predisposing conditions.^[21][22] Most people will experience at least one traumatizing event in their lifetime.^[23] Men are more likely to experience a traumatic event, but women are more likely to experience the kind of high-impact traumatic event that can lead to PTSD, such as interpersonal violence and sexual assault.^[2]

Posttraumatic stress reactions have not been studied as well in children and adolescents as adults.^[2] The rate of PTSD may be lower in children than adults, but in the absence of therapy, symptoms may continue for decades.^[2] One estimate suggests that the proportion of children and adolescents having PTSD in a non-wartorn population in a developed country may be 1% compared to 1.5% to 3% of adults, and much lower below the age of 10 years.^[2]

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] Children or adults may develop PTSD symptoms by experiencing bullying.^[27] Peritraumatic dissociation in children is a predictive indicator of the development of PTSD later in life.^[28] This effect of childhood trauma, which is not well-understood, may be a marker for both traumatic experiences and attachment problems.^[29][30] Proximity to, duration of, and severity of the trauma make an impact, and interpersonal traumas cause more problems than impersonal ones.^[31]

Quasi-experimental studies have demonstrated a relationship between intrusive thoughts and intentional control responses such that suppression increases the frequency of unwanted intrusive thoughts. These results suggest that suppression of intrusive thoughts may be important in the development and maintenance of PTSD.^[32]

Foster care

Adults who were in foster care as children have a higher rate of PTSD.

Domestic violence

An individual that has been exposed to domestic violence is predisposed to the development of PTSD. However, being exposed to a traumatic experience does not automatically indicate that an individual will develop PTSD.^[16] There is a strong association between the development of PTSD in mothers that experienced domestic violence during the perinatal period of their pregnancy.^[33]

Military experience

Early intervention appears to be a critical preventive measure.^[34] Studies have shown that soldiers prepared for the potential of a traumatic experience are more prepared to deal with the stress of a traumatic experience and therefore less likely to develop PTSD.^[16]

Among American troops in Vietnam a greater portion of women experienced high levels of war-zone stress compared to theater men—39.9 percent versus 23.5 percent. The key to this fact is that the vast majority (6,250 or 83.3%) of the women who served in the war zone were nurses who dealt almost daily with death. Black veterans had nearly 2.5 fold the risk of developing war zone-related PTSD as compared to white/other veterans. Hispanics had more than three times the risk. But the most revealing fact, theater veterans injured or wounded in combat had nearly four times the risk of developing PTSD compared to those not injured/wounded according to two key studies—the August 2014 National Vietnam Veterans Longitudinal Study (NVVLS). Paired with the late 1980s National Vietnam Veterans Readjustment Study (NVVRS).^[35]

The long-term medical consequence of PTSD among male veterans who served in the Vietnam War was that they were almost twice as likely to die in the quarter of a century between the two key studies than those who did not have PTSD. It was also found those with PTSD were more likely to die of chronic conditions such as cancer, nervous system disorders, and musculoskeletal problems. The etiology of this relationship is not certain other than lingering stress from combat such as nightmares, intrusive memories, and hyper-vigilance are aggravating factors contributing to psychological and physiological illnesses.^[35]

The racial similarity between Hispanic and Vietnamese soldiers, and the discrimination Hispanic soldiers faced from their own military, made it difficult for Hispanic soldiers to dehumanize their enemy. Hispanic veterans who reported experiencing racial discrimination during their service displayed more symptoms of PTSD than Hispanic veterans who did not.^[36]

PTSD is under-diagnosed in female veterans.^[37] Sexual assault in the military is a leading cause for female soldiers developing PTSD; a female soldier who is sexually assaulted while serving in the military is nine times more likely to develop PTSD than a female soldier who is not assaulted. A soldier's assailant may be her colleague or superior officer, making it difficult for her to both report the crime and to avoid interacting with her assailant again.^[38] Until the Tailhook scandal drew attention to the problem, the role that sexual assault in the military plays in female veterans developing PTSD went largely unstudied.^[39]

Protective effects include social support, which also helps with recovery if PTSD develops.^[40][41] For more aggravating factors to recovery once home, see social alienation among returning war veterans.

Pre-trauma Factors

Several biological indicators have been identified that are related to later PTSD development. Heightened startle responses and a smaller hippocampal volume have been identified as biomarkers for the risk of developing PTSD.^[42] Additionally, one study found that soldiers whose leukocytes had greater numbers of glucocorticoid receptors were more prone to developing PTSD after experiencing trauma.^[42]

Genetics

There is evidence that susceptibility to PTSD is hereditary. Approximately 30% of the variance in PTSD is caused from genetics alone. For twin pairs exposed to combat in Vietnam, having a monozygotic (identical) twin with PTSD was associated with an increased risk of the co-twin's having PTSD compared to twins that were dizygotic (non-identical twins).^[43] There is evidence that those with a genetically smaller hippocampus are more likely to develop PTSD following a traumatic event. Research has also found that PTSD shares many genetic influences common to other psychiatric disorders. Panic and generalized anxiety disorders and PTSD share 60% of the same genetic variance. Alcohol, nicotine, and drug dependence share greater than 40% genetic similarities.^[28]

Post-trauma Factors

Drug and substance abuse

Drug abuse and alcohol abuse commonly co-occur with PTSD.^[44] 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.^[45][46]

Pathophysiology

Neuroendocrinology

PTSD symptoms may result when a traumatic event causes an over-reactive adrenaline response, which creates deep neurological patterns in the brain. These patterns can persist long after the event that triggered the fear, making an individual hyper-responsive to future fearful situations.^[16][47] During traumatic experiences the high levels of stress hormones secreted suppress hypothalamic activity that may be a major factor toward the development of PTSD.^[48]

PTSD causes biochemical changes in the brain and body, that differ from other psychiatric disorders such as major depression. Individuals diagnosed with PTSD respond more strongly to a dexamethasone suppression test than individuals diagnosed with clinical depression.^[49][50]

In addition, most people with PTSD also show a low secretion of cortisol and high secretion of catecholamines in urine,^[51] with a norepinephrine/cortisol ratio consequently higher than comparable non-diagnosed individuals.^[52] 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.^[53]

Brain catecholamine levels are high,^[54] and corticotropin-releasing factor (CRF) concentrations are high.^[55][56] Together, these findings suggest abnormality in the hypothalamic-pituitary-adrenal (HPA) axis.

The HPA axis is responsible for coordinating the hormonal response to stress.^[28] 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.^[57]

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.^[58]

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.^[59] Because cortisol is normally important in restoring homeostasis after the stress response, it is thought that trauma survivors with low cortisol experience a poorly contained—that is, longer and more distressing—response, setting the stage for PTSD.

Other studies indicate that people that suffer from PTSD have chronically low levels of serotonin, which contributes to the commonly associated behavioral symptoms such as anxiety, ruminations, irritability, aggression, suicidality, and impulsivity.^[60] Serotonin also contributes to the stabilization of glucocorticoid production.

Dopamine levels in a person with PTSD can help contribute to the symptoms associated. Low levels of dopamine can contribute to anhedonia, apathy, impaired attention, and motor deficits. Increased levels of dopamine can cause psychosis, agitation, and restlessness.^[60]

Hyperresponsiveness in the norepinephrine system can be caused by continued exposure to high stress. Overactivation of norepinephrine receptors in the prefrontal cortex can be connected to the flashbacks and nightmares frequently experienced by those with PTSD. A decrease in other norepinephrine functions (awareness of the current environment) prevents the memory mechanisms in the brain from processing that the experience, and emotions the person is experiencing during a flashback are not associated with the current environment.^[60]

However, there is considerable controversy within the medical community regarding the neurobiology of PTSD. A review of existing studies on this subject showed no clear relationship between cortisol levels and PTSD. However, the majority of reports indicate people with PTSD have elevated levels of corticotropin-releasing hormone, lower basal cortisol levels, and enhanced negative feedback suppression of the HPA axis by dexamethasone.^[28][61]

Neuroanatomy

Three areas of the brain in which function may be altered in PTSD have been identified: the prefrontal cortex, amygdala, and hippocampus. Much of this research has utilised PTSD victims from the Vietnam War. For example, a prospective study using the Vietnam Head Injury Study showed that damage to the prefrontal cortex may actually be protective against later development of PTSD.^[63] In a study by Gurvits et al., combat veterans of the Vietnam War with PTSD showed a 20% reduction in the volume of their hippocampus compared with veterans having suffered no such symptoms.^[64] This finding could not be replicated in chronic PTSD patients traumatized at an air show plane crash in 1988 (Ramstein, Germany).^[65]

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.^[66] However, during high stress times the hippocampus, which is associated with the ability to place memories in the correct context of space and time, and with the ability to recall the memory, is suppressed. This suppression is hypothesized to be the cause of the flashbacks that often affect people with PTSD. When someone with PTSD undergoes stimuli similar to the traumatic event, the body perceives the event as occurring again because the memory was never properly recorded in the person's memory.^[28][67]

The amygdalocentric model of PTSD proposes that it is associated with hyperarousal of the amygdala and insufficient top-down control by the medial prefrontal cortex and the hippocampus in particular during extinction.^[68] This is consistent with an interpretation of PTSD as a syndrome of deficient extinction ability.^[68][69] A study at the European Neuroscience Institute-Goettingen (Germany) found that fear extinction-induced IGF2/IGFBP7 signalling promotes the survival of 17–19-day-old newborn hippocampal neurons. This suggests that therapeutic strategies that enhance IGF2 signalling and adult neurogenesis might be suitable to treat diseases linked to excessive fear memory such as PTSD.^[70] Further animal and clinical research into the amygdala and fear conditioning may suggest additional treatments for the condition.

The maintenance of the fear involved with PTSD has been shown to include the HPA axis, the locus coeruleus-noradrenergic systems, and the connections between the limbic system and frontal cortex. The HPA axis that coordinates the hormonal response to stress,^[71] which activates the LC-noradrenergic system, is implicated in the over-consolidation of memories that occurs in the aftermath of trauma.^[72] This over-consolidation increases the likelihood of one's developing PTSD. The amygdala is responsible for threat detection and the conditioned and unconditioned fear responses that are carried out as a response to a threat.^[28]

The LC-noradrenergic system has been hypothesized to mediate the over-consolidation of fear memory in PTSD. High levels of cortisol reduce noradrenergic activity, and because people with PTSD tend to have reduced levels of cortisol, it is proposed that individuals with PTSD fail to regulate the increased noradrenergic response to traumatic stress.^[73] It is thought that the intrusive memories and conditioned fear responses to associated triggers is a result of this response. Neuropeptide Y has been reported to reduce the release of norepinephrine and has been demonstrated to have anxiolytic properties in animal models. Studies have shown people with PTSD demonstrate reduced levels of NPY, possibly indicating their increased anxiety levels.^[28]

The basolateral nucleus (BLA) of the amygdala is responsible for the comparison and development of associations between unconditioned and conditioned responses to stimuli, which results in the fear conditioning present in PTSD. The BLA activates the central nucleus (CeA) of the amygdala, which elaborates the fear response, (including behavioral response to threat and elevated startle response). Descending inhibitory inputs from the medial prefrontal cortex (mPFC) regulate the transmission from the BLA to the CeA, which is hypothesized to play a role in the extinction of conditioned fear responses.^[28]

Studies have also shown that PTSD patients show hypoactiviation or decreased brain activity in the dorsal and rostral anterior cingulate cortices and the ventromedial prefrontal cortex, areas linked to the experience and regulation of emotion.^[74]

Diagnosis

Screening and assessment

A number of screening instruments, including the UCLA PTSD Index for DSM-IV, which have good reliability and validity, are used for the screening of PTSD for children and young adults.^[75] Primary Care PTSD Screen and PTSD Checklist are other screening tools.^[76]

The American Academy of Child and Adolescent Psychiatry practice parameters is a guidelines for the assessment and treatment of PTSD.^[77]

A revised form of the Impact of Events scale (IES-R) gives a total score ranging from 0 to 88.^[78] A score of 24 or more confers a clinical concern for PTSD, and a score of 33 is suggested to represent the best cutoff for a probable diagnosis of PTSD.^[79]

Diagnostic and statistical manual

Since the introduction of DSM-IV, the number of possible events that might be used to diagnose PTSD has increased; one study suggests that the increase is around 50%.^[80] Various scales to measure the severity and frequency of PTSD symptoms exist.^[81][82] Standardized screening tools such as Trauma Screening Questionnaire^[83] and PTSD Symptom Scale^[84] can be used to detect possible symptoms of posttraumatic stress disorder and suggest the need for a formal diagnostic assessment.

In DSM-5, published in May, 2013, PTSD is classified as a trauma- and stress-related disorder.^[1]

International classification of diseases

The diagnostic criteria for PTSD, stipulated in the International Statistical Classification of Diseases and Related Health Problems 10 (ICD-10), may be summarized as:^[85]

• Exposure to a stressful event or situation (either short or long lasting) of exceptionally threatening or catastrophic nature, which is likely to cause pervasive distress in almost anyone.
• Persistent remembering, or "reliving" the stressor by intrusive flash backs, vivid memories, recurring dreams, or by experiencing distress when exposed to circumstances resembling or associated with the stressor.
• Actual or preferred avoidance of circumstances resembling or associated with the stressor (not present before exposure to the stressor).
• Either (1) or (2):

1. Inability to recall, either partially or completely, some important aspects of the period of exposure to the stressor
2. Persistent symptoms of increased psychological sensitivity and arousal (not present before exposure to the stressor) shown by any two of the following:

• difficulty in falling or staying asleep
• irritability or outbursts of anger
• difficulty in concentrating
• hyper-vigilance
• exaggerated startle response.

The International Statistical Classification of Diseases and Related Health Problems 10 diagnostic guidelines state:^[85] In general, this disorder should not be diagnosed unless there is evidence that it arose within 6 months of a traumatic event of exceptional severity. A "probable" diagnosis might still be possible if the delay between the event and the onset was longer than 6 months, provided that the clinical manifestations are typical and no alternative identification of the disorder (e.g., as an anxiety or obsessive-compulsive disorder or depressive episode) is plausible. In addition to evidence of trauma, there must be a repetitive, intrusive recollection or re-enactment of the event in memories, daytime imagery, or dreams. Conspicuous emotional detachment, numbing of feeling, and avoidance of stimuli that might arouse recollection of the trauma are often present but are not essential for the diagnosis. The autonomic disturbances, mood disorder, and behavioural abnormalities all contribute to the diagnosis but are not of prime importance. The late chronic sequelae of devastating stress, i.e. those manifest decades after the stressful experience, should be classified under F62.0.

Differential diagnosis

A diagnosis of PTSD requires exposure to an extreme stressor such as one that is life-threatening. Any stressor can result in a diagnosis of adjustment disorder and it is an appropriate diagnosis for a stressor and a symptom pattern that does not meet the criteria for PTSD, for example a stressor like a partner being fired, or a spouse leaving. If any of the symptom pattern is present before the stressor, another diagnosis is required, such as brief psychotic disorder or major depressive disorder. Other differential diagnoses are schizophrenia or other disorders with psychotic features such as Psychotic disorders due to a general medical condition. Drug-induced psychotic disorders can be considered if substance abuse is involved.^[15]

The symptom pattern for acute stress disorder must occur and be resolved within four weeks of the trauma. If it lasts longer, and the symptom pattern fits that characteristic of PTSD, the diagnosis may be changed.^[15]

Obsessive compulsive disorder may be diagnosed for intrusive thoughts that are recurring but not related to a specific traumatic event.^[15]

Malingering should be considered if a financial and/or legal advantage is a possibility.

Prevention

Modest benefits have been seen from early access to cognitive behavioral therapy.^[86] Critical incident stress management has been suggested as a means of preventing PTSD, but subsequent studies suggest the likelihood of its producing negative outcomes.^[87][88] A review "...did not find any evidence to support the use of an intervention offered to everyone", and that "...multiple session interventions may result in worse outcome than no intervention for some individuals."^[89] The World Health Organization recommends against the use of benzodiazepines and antidepressants in those having experienced trauma.^[90] Some evidence supports the use of hydrocortisone for prevention in adults, however there is limited or no evidence supporting propranolol, escitalopram, temazepam, or gabapentin.^[91] Conversely, taking benzodiazepines after trauma is associated with a 2-5 times increased risk of developing PTSD and major depressive disorder.^[9]

Psychological debriefing

Trauma-exposed individuals often receive treatment called psychological debriefing in an effort to prevent PTSD.^[86] Several meta-analyses; however, find that psychological debriefing is unhelpful and is potentially harmful.^[86][92][93] This is true for both single-session debriefing and multiple session interventions.^[89] The American Psychological Association judges the status of psychological debriefing as No Research Support/Treatment is Potentially Harmful.^[94]

Psychological debriefing was; however, the most often used preventive measure, partly because of the relative ease with which this treatment can be given to individuals directly following an event. It consists of interviews that are meant to allow individuals to directly confront the event and share their feelings with the counselor and to help structure their memories of the event.^[86]

Risk-targeted interventions

Risk-targeted interventions are those that attempt to mitigate specific formative information or events. It can target modeling normal behaviors, instruction on a task, or giving information on the event.^[95][96]

Management

Psychotherapy

Many forms of psychotherapy have been found to be efficacious for trauma-related problems such as PTSD. Basic counseling practices common to many treatments for PTSD include education about the condition, and provision of safety and support.^[16][84]

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),^[97] mindfulness-based meditation^[98] and many combinations of these procedures.^[99] EMDR and trauma-focused cognitive behavioral therapy (TFCBT) were recommended as first-line treatments for trauma victims in a 2007 review; however, "the evidence base [for EMDR] was not as strong as that for TFCBT ... Furthermore, there was limited evidence that TFCBT and EMDR were superior to supportive/non-directive treatments, hence it is highly unlikely that their effectiveness is due to non-specific factors such as attention."^[100] 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.^[101]

Cognitive behavioral therapy

Cognitive behavioral therapy (CBT) seeks to change the way a trauma victim feels and acts by changing the patterns of thinking or behavior, or both, responsible for negative emotions. CBT has been proven to be an effective treatment for PTSD and is currently considered the standard of care for PTSD by the United States Department of Defense.^[102] In CBT, individuals learn to identify thoughts that make them feel afraid or upset and replace them with less distressing thoughts. The goal is to understand how certain thoughts about events cause PTSD-related stress.

Recent research on contextually based third-generation behavior therapies suggests that they may produce results comparable to some of the better validated therapies.^[103] Many of these therapy methods have a significant element of exposure^[102] and have demonstrated success in treating the primary problems of PTSD and co-occurring depressive symptoms.^[104]

Exposure therapy is a type of cognitive behavioral therapy^[105] that involves assisting trauma survivors to re-experience distressing trauma-related memories and reminders in order to facilitate habituation and successful emotional processing of the trauma memory. Most exposure therapy programs include both imaginal confrontation with the traumatic memories and real-life exposure to trauma reminders; this therapy modality is well supported by clinical evidence. The success of exposure-based therapies has raised the question of whether exposure is a necessary ingredient in the treatment of PTSD.^[106] Some organizations have endorsed the need for exposure.^[107][108] The US Department of Veterans Affairs has been actively training mental health treatment staff in prolonged exposure therapy^[109] and Cognitive Processing Therapy^[110] in an effort to better treat US veterans with PTSD.

Eye movement desensitization and reprocessing

Eye movement desensitization and reprocessing (EMDR) is a form of psychotherapy developed and studied by Francine Shapiro.^[111] She had noticed that, when she was thinking about disturbing memories herself, her eyes were moving rapidly. When she brought her eye movements under control while thinking, the thoughts were less distressing.^[111]

In 2002, Shapiro and Maxfield published a theory of why this might work, called adaptive information processing.^[112] This theory proposes that eye movement can be used to facilitate emotional processing of memories, changing the person's memory to attend to more adaptive information.^[113] The therapist initiates voluntary rapid eye movements while the person focuses on memories, feelings or thoughts about a particular trauma.^[2][114] The therapists uses hand movements to get the person to move their eyes backward and forward, but hand-tapping or tones can also be used.^[2] EMDR closely resembles cognitive behavior therapy as it combines exposure (re-visiting the traumatic event), working on cognitive processes and relaxation/self-monitoring.^[2] However, exposure by way of being asked to think about the experience rather than talk about it has been highlighted as one of the more important distinguishing elements of EMDR.^[115]

There have been multiple small controlled trials of four to eight weeks of EMDR in adults^[116] as well as children and adolescents.^[114] EMDR reduced PTSD symptoms enough in the short term that one in two adults no longer met the criteria for PTSD, but the number of people involved in these trials was small.^[116] There was not enough evidence to know whether or not EMDR could eliminate PTSD.^[116] There was some evidence that EMDR might prevent depression.^[116] There were no studies comparing EMDR to other psychological treatments or to medication.^[116] Adverse effects were largely unstudied.^[116] The benefits were greater for women with a history of sexual assault compared with people who had experienced other types of traumatizing events (such as accidents, physical assaults and war). There is a small amount of evidence that EMDR may improve re-experiencing symptoms in children and adolescents, but EMDR has not been shown to improve other PTSD symptoms, anxiety, or depression.^[114]

The eye movement component of the therapy may not be critical for benefit.^[2][113] As there has been no major, high quality randomized trial of EMDR with eye movements versus EMDR without eye movements, the controversy over effectiveness is likely to continue.^[115] Authors of a meta-analysis published in 2013 stated, "We found that people treated with eye movement therapy had greater improvement in their symptoms of post-traumatic stress disorder than people given therapy without eye movements….Secondly we found that that in laboratory studies the evidence concludes that thinking of upsetting memories and simultaneously doing a task that facilitates eye movements reduces the vividness and distress associated with the upsetting memories."^[97]

Interpersonal psychotherapy

Other approaches, in particular involving social supports,^[40][41] may also be important. An open trial of interpersonal psychotherapy^[117] reported high rates of remission from PTSD symptoms without using exposure.^[118] A current, NIMH-funded trial in New York City is now (and into 2013) comparing interpersonal psychotherapy, prolonged exposure therapy, and relaxation therapy.^{[119][120][121]}

Medication

Most medications do not have enough evidence to support their use.^[10] With many medications, residual symptoms following treatment is the rule rather than the exception.^[122]

Antidepressants

Selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs) may have some benefit for PTSD symptoms.^[10][123] Tricyclic antidepressants are equally effective but are less well tolerated.^[124] Evidence provides support for a small or modest improvement with sertraline, fluoxetine, paroxetine, and venlafaxine.^[10][125] Thus, these four medications are considered to be first-line medications for PTSD.^[123][126]

Benzodiazepines

Benzodiazepines (the most commonly prescribed including alprazolam, clonazepam, lorazepam, and diazepam) are not recommended for the treatment of PTSD due to a lack of evidence of benefit and risk of worsening PTSD symptoms.^[9][127] Some authors believe that the use of benzodiazepines is contraindicated for acute stress, as this group of drugs promotes dissociation and ulterior revivals.^[128] Nevertheless, some use benzodiazepines with caution for short-term anxiety and insomnia.^{[129][130][131]} While benzodiazepines can alleviate acute anxiety, there is no consistent evidence that they can stop the development of PTSD and may actually increase the risk of developing PTSD 2-5 times.^[9] Additionally, benzodiazepines may reduce the effectiveness of psychotherapeutic interventions, and there is some evidence that benzodiazepines may actually contribute to the development and chronification of PTSD. For those who already have PTSD, benzodiazepines may worsen and prolong the course of illness, by worsening psychotherapy outcomes, and causing or exacerbating aggression, depression (including suicidality), and substance use.^[9] Other drawbacks include the risk of developing a benzodiazepine dependence, tolerance (i.e., short-term benefits wearing off with time), and withdrawal syndrome; additionally, individuals with PTSD (even those without a history of alcohol or drug misuse) are at an increased risk of abusing benzodiazepines.^{[9][126][132]} Due to a plethora of other treatments with greater efficacy for PTSD and less risks (e.g., prolonged exposure, cognitive processing therapy, eye movement desensitization and reprocessing, cognitive restructuring therapy, trauma-focused cognitive behavioral therapy, brief eclectic psychotherapy, narrative therapy, stress inoculation training, serotonergic antidepressants, adrenergic inhibitors, antipsychotics, and even anticonvulsants), benzodiazepines should be considered relatively contraindicated until all other treatment options are exhausted.^[4][5][9] For those who argue that benzodiazepines should be used sooner in the most severe cases, the adverse risk of disinhibition (associated with suicidality, aggression and crimes) and clinical risks of delaying or inhibiting definitive efficacious treatments, make other alternative treatments preferable (e.g., inpatient, residential, partial hospitalization, intensive outpatient, dialectic behavior therapy; and other fast-acting sedating medications such as trazodone, mirtazapine, amitripytline, doxepin, prazosin, propranolol, guanfacine, clonidine, quetiapine, olanzapine, valproate, gabapentin).^[4][7][8] "PTSD recovery should denote improved functioning (e.g. healthy relationships, employment), not simply sedation.... For years, sedatives were the only thing we had in our armamentarium for PTSD. Now, we have many more tools and our patients – whether survivors of assault, combat or any other trauma – deserve those treatments that have proven to be safer and more effective."^[9]

Glucocorticoids

Glucocorticoids may be useful for short-term therapy to protect against neurodegeneration caused by the extended stress response that characterizes PTSD, but long-term use may actually promote neurodegeneration.^[133]

Cannabinoids

The cannabinoid nabilone is sometimes used off-label for nightmares in PTSD. Although some short-term benefit was shown, adverse effects are common and it has not been adequately studied to determine efficacy.^[134] Additionally, there are other treatments with stronger efficacy and less risks (e.g., psychotherapy, serotonergic antidepressants, adrenergic inhibitors).

Other

Exercise, sport and physical activity

Physical activity can have an impact on people's psychological wellbeing^[135] and physical health.^[136] The U.S. National Center for PTSD recommends moderate exercise as a way to distract from disturbing emotions, build self-esteem and increase feelings of being in control again. They recommend a discussion with a doctor before starting an exercise program.^[137]

Play therapy for children

Play is thought to help children link their inner thoughts with their outer world, connecting real experiences with abstract thought.^[138] Repetitive play can also be one of the ways a child relives traumatic events, and that can be a symptom of traumatization in a child or young person.^[139] Although it is commonly used, there have not been enough studies comparing outcomes in groups of children receiving and not receiving play therapy, so the effects of play therapy are not yet understood.^[2][138]

Military programs

Many veterans of the wars in Iraq and Afghanistan have faced significant physical, emotional, and relational disruptions. In response, the United States Marine Corps has instituted programs to assist them in re-adjusting to civilian life, especially in their relationships with spouses and loved ones, to help them communicate better and understand what the other has gone through.^[140] Walter Reed Army Institute of Research (WRAIR) developed the Battlemind program to assist service members avoid or ameliorate PTSD and related problems.

Epidemiology

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.^[142]

The United Nations' World Health Organization publishes estimates of PTSD impact for each of its member states; the latest data available are for 2004. Considering only the 25 most populated countries ranked by overall age-standardized Disability-Adjusted Life Year (DALY) rate, the top half of the ranked list is dominated by Asian/Pacific countries, the US, and Egypt.^[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, 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	Vietnam	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 States

The National Comorbidity Survey Replication has estimated that the lifetime prevalence of PTSD among adult Americans is 6.8%, with women (9.7%) more than twice as likely as men^[60] (3.6%) to have PTSD at some point in their lives.^[146] More than 60% of men and more than 60% of women experience at least one traumatic event in their life. The most frequently reported traumatic events by men are rape, combat, and childhood neglect or physical abuse. Women most frequently report instances of rape, sexual molestation, physical attack, being threatened with a weapon and childhood physical abuse.^[60] 88% of men and 79% of women with lifetime PTSD have at least one comorbid psychiatric disorder. Major depressive disorder, 48% of men and 49% of women, and lifetime alcohol abuse or dependence, 51.9% of men and 27.9% of women, are the most common comorbid disorders.^[147]

The United States Department of Veterans Affairs estimates that 830,000 Vietnam War veterans suffered symptoms of PTSD.^[148] The National Vietnam Veterans' Readjustment Study (NVVRS) found 15.2% of male and 8.5% of female Vietnam veterans 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.^[149]

A 2011 study from Georgia State University and San Diego State University found that rates of PTSD diagnosis increased significantly when troops were stationed in combat zones, had tours of longer than a year, experienced combat, or were injured. Military personnel serving in combat zones were 12.1 percentage points more likely to receive a PTSD diagnosis than their active-duty counterparts in non-combat zones. Those serving more than 12 months in a combat zone were 14.3 percentage points more likely to be diagnosed with PTSD than those having served less than one year. Experiencing an enemy firefight was associated a 18.3 percentage point increase in the probability of PTSD, while being wounded or injured in combat was associated a 23.9 percentage point increase in the likelihood of a PTSD diagnosis. For the 2.16 million U.S. troops deployed in combat zones between 2001 and 2010, the total estimated two-year costs of treatment for combat-related PTSD are between $1.54 billion and $2.69 billion.^[150]

As of 2013, rates of PTSD have been estimated at up to 20% for veterans returning from Iraq and Afghanistan.^[23] As of 2013 13% of veterans returning from Iraq were unemployed.^[151]

Society and culture

United States—veterans

Other countries—veterans

In the UK, there are various charities and service organisations dedicated to aiding veterans in readjusting to civilian life. The Royal British Legion and the more recently established Help for Heroes are two of Britain's more high-profile veterans' organisations which have actively advocated for veterans over the years. There has been some controversy that the NHS has not done enough in tackling mental health issues and is instead "dumping" veterans on charities such as Combat Stress.^[152][153]

Veterans Affairs Canada offers a new program that includes rehabilitation, financial benefits, job placement, health benefits program, disability awards, peer support^{[154][155][156]} and family support.^[157]

History

The 1952 edition of the DSM-I includes a diagnosis of "gross stress reaction", which has similarities to the modern definition and understanding of PTSD.^[158] Gross stress reaction is defined as a “normal personality [utilizing] established patterns of reaction to deal with overwhelming fear” as a response to “conditions of great stress”.^[159] The diagnosis includes language which relates the condition to combat as well as to “civilian catastrophe”.^[159]

Early in 1978, the term was used in a working group finding presented to the Committee of Reactive Disorders.^[160] The condition was added to the DSM-III, which was being developed in the 1980s, as posttraumatic stress disorder.^[158][160] In the DSM-IV, the spelling "posttraumatic stress disorder" is used, while in the ICD-10, the spelling is "post-traumatic stress disorder".^[161]

The addition of the term to the DSM-III was greatly influenced by the experiences and conditions of US military veterans of the Vietnam War.^[11] Due to its association with the war in Vietnam, PTSD has become synonymous with many historical war-time diagnoses such as railway spine, stress syndrome, nostalgia, soldier's heart, shell shock, battle fatigue, combat stress reaction, or traumatic war neurosis.^[162][163] Some of these terms date back to the 19th century, which is indicative of the universal nature of the condition. In a similar vein, psychiatrist Jonathan Shay has proposed that Lady Percy's soliloquy in the William Shakespeare play Henry IV, Part 1 (act 2, scene 3, lines 40–62^[164]), written around 1597, represents an unusually accurate description of the symptom constellation of PTSD.^[165]

The correlations between combat and PTSD are undeniable; according to Stéphane Audoin-Rouzeau and Annette Becker, "One-tenth of mobilized American men were hospitalized for mental disturbances between 1942 and 1945, and, after thirty-five days of uninterrupted combat, 98% of them manifested psychiatric disturbances in varying degrees."^[166] In fact, much of the available published research regarding PTSD is based on studies done on veterans of the war in Vietnam. A study based on personal letters from soldiers of the 18th-century Prussian Army concludes that combatants may have had PTSD.^[167]

The researchers from the Grady Trauma Project highlight the tendency people have to focus on the combat side of PTSD: “less public awareness has focused on civilian PTSD, which results from trauma exposure that is not combat related... “ and “much of the research on civilian PTSD has focused on the sequelae of a single, disastrous event, such as the Oklahoma City bombing, September 11th attacks, and Hurricane Katrina”.^[168] Disparity in the focus of PTSD research affects the already popular perception of the exclusive interconnectedness of combat and PTSD. This is misleading when it comes to understanding the implications and extent of PTSD as a neurological disorder. Dating back to the definition of Gross stress reaction in the DSM-I, civilian experience of catastrophic or high stress events is included as a cause of PTSD in medical literature. The 2014 National Comorbidity Survey reports that “the traumas most commonly associated with PTSD are combat exposure and witnessing among men and rape and sexual molestation among women.”^[169] Because of the initial overt focus on PTSD as a combat related disorder when it was first fleshed out in the years following the war in Vietnam, in 1975 Ann Wolbert Burgess and Lynda Lytle Holmstrom defined Rape trauma syndrome, RTS, in order to draw attention to the striking similarities between the experiences of soldiers returning from war and of rape victims.^[170] This paved the way for a more comprehensive understanding of causes of PTSD.

Terminology

The Diagnostic and Statistical Manual of Mental Disorders does not hyphenate 'post' and 'traumatic', thus, the DSM-5 lists the disorder as posttraumatic stress disorder. However, many scientific journal articles and other scholarly publications do hyphenate the name of the disorder, viz., post-traumatic stress disorder.^[171] Dictionaries also differ with regard to the preferred spelling of the disorder with the Collins English Dictionary - Complete and Unabridged using the hyphenated spelling, and the American Heritage Dictionary of the English Language, Fifth Edition and the Random House Kernerman Webster's College Dictionary giving the non-hyphenated spelling.^[172]

Research

To recapitulate some of the neurological and neurobehavioral symptoms experienced by the veteran population of recent conflicts in Iraq and Afghanistan, researchers at the Roskamp Institute and the James A Haley Veteran’s Hospital (Tampa) have developed an animal model to study the consequences of mild traumatic brain injury (mTBI) and PTSD.^[173] In the laboratory, the researchers exposed mice to a repeated session of unpredictable stressor (i.e. predator odor while restrained), and physical trauma in the form of inescapable foot-shock, and this was also combined with a mTBI. In this study, PTSD animals demonstrated recall of traumatic memories, anxiety, and an impaired social behavior, while animals subject to both mTBI and PTSD had a pattern of disinhibitory-like behavior. mTBI abrogated both contextual fear and impairments in social behavior seen in PTSD animals. In comparison with other animal studies,^[173][174] examination of neuroendocrine and neuroimmune responses in plasma revealed a trend toward increase in corticosterone in PTSD and combination groups.

Psychotherapy adjuncts

MDMA was used for psychedelic therapy for a variety of indications before its criminalization in the US in 1985. In response to its criminalization, the Multidisciplinary Association for Psychedelic Studies was founded as a nonprofit drug-development organization to develop MDMA into a legal prescription drug for use as an adjunct in psychotherapy.^[175] The drug is hypothesized to facilitate psychotherapy by reducing fear, thereby allowing patients to reprocess and accept their traumatic memories without becoming emotionally overwhelmed. In this treatment, patients participate in an extended psychotherapy session during the acute activity of the drug, and then spend the night at the treatment facility. In the sessions with the drug, therapists are not directive and support the patients in exploring their inner experiences. Patients participate in standard psychotherapy sessions before the drug-assisted sessions, as well as after the drug-assisted psychotherapy to help them integrate their experiences with the drug.^[176] Preliminary results suggest MDMA-assisted psychotherapy might be effective for individuals who have not responded favorably to other treatments. Future research employing larger sample sizes and an appropriate placebo condition, i.e., one in which subjects cannot discern if they are in the experimental or control condition, will increase confidence in the results of initial research.^[177][178]

Clinical research is also investigating using D-cycloserine, hydrocortisone, and propranolol as adjuncts to more conventional exposure therapy.^[178]

Notes

References

External links

Wikimedia Commons has media related to Posttraumatic stress disorder.

• Posttraumatic stress disorder at DMOZ
• Resources for the public from VA National PTSD Center
• Resources for professionals from VA National PTSD Center
• Post Traumatic Stress Disorder Information Resource from The University of Queensland School of Medicine
• Resources for Parents of Children with PTSD from The Children's Hospital of Philadelphia
• AACAP practice parameters for assessment and treatment for PTSD

Mental and behavioral disorders (F 290–319)   Neurological/symptomatic Dementia Mild cognitive impairment Alzheimer's disease Vascular dementia Pick's disease Creutzfeldt–Jakob disease Huntington's disease Parkinson's disease AIDS dementia complex Frontotemporal dementia Sundowning Wandering Autism spectrum Autism Asperger syndrome Savant syndrome PDD-NOS High-functioning autism Other Delirium Post-concussion syndrome Organic brain syndrome   Psychoactive substances, substance abuse, drug abuse and substance-related disorders Intoxication/Drug overdose Physical dependence Substance dependence Rebound effect Double rebound Withdrawal   Schizophrenia, schizotypal and delusional Psychosis Schizoaffective disorder Schizophreniform disorder Brief reactive psychosis Schizophrenia Disorganized schizophrenia Delusional disorder Folie à deux   Mood (affective) Mania Bipolar disorder (Bipolar I Bipolar II Cyclothymia Bipolar NOS) Depression (Major depressive disorder Dysthymia Seasonal affective disorder Atypical depression Melancholic depression)   Neurotic, stress-related and somatoform Anxiety disorder Phobia Agoraphobia Social anxiety Social phobia (Anthropophobia) Specific phobia (Claustrophobia) Specific social phobia Other Panic disorder Panic attack Generalized anxiety disorder OCD stress (Acute stress reaction PTSD) Adjustment disorder Adjustment disorder with depressed mood Somatoform disorder Somatization disorder Body dysmorphic disorder Hypochondriasis Nosophobia Da Costa's syndrome Psychalgia Conversion disorder (Ganser syndrome Globus pharyngis) Neurasthenia Mass psychogenic illness Dissociative disorder Dissociative identity disorder Psychogenic amnesia Fugue state Depersonalization disorder   Physiological/physical behavioral Eating disorder Anorexia nervosa Bulimia nervosa Rumination syndrome NOS Nonorganic sleep disorders (Nonorganic hypersomnia Nonorganic insomnia) Parasomnia (REM sleep behavior disorder Night terror Nightmare) Sexual dysfunction sexual desire (Hypoactive sexual desire disorder Hypersexuality) sexual arousal (Female sexual arousal disorder) Erectile dysfunction orgasm (Anorgasmia Delayed ejaculation Premature ejaculation Sexual anhedonia) pain (Vaginismus Dyspareunia) Postnatal Postpartum depression Postnatal psychosis   Adult personality and behavior Gender dysphoria Sexual maturation disorder Ego-dystonic sexual orientation Sexual relationship disorder Paraphilia (Voyeurism Fetishism) Other Personality disorder Impulse control disorder (Kleptomania Trichotillomania Pyromania Dermatillomania) Body-focused repetitive behavior Factitious disorder (Münchausen syndrome)   Disorders typically diagnosed in childhood Intellectual disability X-linked intellectual disability (Lujan-Fryns syndrome) Psychological development (developmental disabilities) Specific Pervasive Autism spectrum disorders Emotional and behavioral ADHD Conduct disorder (ODD) Emotional/behavioral disorder (Separation anxiety disorder) social functioning (Selective mutism RAD DAD) Tic disorder (Tourette syndrome) Speech (Stuttering Cluttering) Movement disorder (Stereotypic)   Symptoms and uncategorized Catatonia False pregnancy Intermittent explosive disorder Psychomotor agitation Stereotypy Psychogenic non-epileptic seizures Klüver-Bucy syndrome

Trauma Principles Polytrauma Major trauma Traumatology Triage Resuscitation Trauma triad of death Assessment Clinical prediction rules Revised Trauma Score Injury Severity Score Abbreviated Injury Scale NACA score Investigations Diagnostic peritoneal lavage Focused assessment with sonography for trauma Management Principles Advanced trauma life support Trauma surgery Trauma center Trauma team Damage control surgery Early appropriate care Procedures Resuscitative thoracotomy Pathophysiology Injury MSK Bone fracture Joint dislocation Degloving Soft tissue injury Resp Flail chest Pneumothorax Hemothorax Diaphragmatic rupture Pulmonary contusion Cardio Internal bleeding Thoracic aorta injury Cardiac tamponade GI Blunt kidney trauma Ruptured spleen Neuro Penetrating head injury Traumatic brain injury Intracranial hemorrhage Mechanism Blast injury Blunt trauma Burn Penetrating trauma Crush injury Stab wound Ballistic trauma Electrocution Region Abdominal trauma Chest trauma Facial trauma Head injury Spinal cord injury Demographic Geriatric trauma Pediatric trauma Sequelae Posttraumatic stress disorder Wound healing Acute lung injury Crush syndrome Rhabdomyolysis Compartment syndrome Contracture Volkmann's contracture Fat embolism Chronic traumatic encephalopathy

Authority control GND: 4361388-3 NDL: 01000003