Posttraumatic stress disorder (PTSD)[note 1] is a mental disorder that can develop after a person is exposed to a traumatic event, such as sexual assault, warfare, traffic collisions, or other threats on a person’s life. Symptoms may include disturbing thoughts, feelings, or dreams related to the events, mental or physical distress to trauma-related cues, attempts to avoid trauma-related cues, alterations in how a person thinks and feels, and increased arousal. These symptoms last for more than a month after the event. Young children are less likely to show distress but instead may express their memories through play. Those with PTSD are at a higher risk of suicide.
Most people who have experienced a traumatic event will not develop PTSD. People who experience interpersonal trauma (for example rape or child abuse) are more likely to develop PTSD, as compared to people who experience non-assault based trauma such as accidents and natural disasters. About half of people develop PTSD following rape. Children are less likely than adults to develop PTSD after trauma, especially if they are under ten years of age. Diagnosis is based on the presence of specific symptoms following a traumatic event.
Prevention may be possible when therapy is targeted at those with early symptoms but is not effective when carried out among all people following trauma. The main treatments for people with PTSD are counselling and medication. A number of different types of therapy may be useful. This may occur one-on-one or in a group. Antidepressants of the selective serotonin reuptake inhibitor type are the first-line medications for PTSD and result in benefit in about half of people. These benefits are less than those seen with therapy. It is unclear if using medications and therapy together has greater benefit. Other medications do not have enough evidence to support their use and in the case of benzodiazepines may worsen outcomes.
In the United States about 3.5% of adults have PTSD in a given year, and 9% of people develop it at some point in their life. In much of the rest of the world, rates during a given year are between 0.5% and 1%.Higher rates may occur in regions of armed conflict. It is more common in women than men. Symptoms of trauma-related mental disorders have been documented since at least the time of the ancient Greeks. During the World Wars study increased and it was known under various terms including “shell shock” and “combat neurosis”. The term “posttraumatic stress disorder” came into use in the 1970s in large part due to the diagnoses of US military veterans of the Vietnam War. 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).
PTSD was classified as an anxiety disorder in the DSM-IV, but has since been reclassified as a “trauma- and stressor-related disorder” in the 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. While it is common to have symptoms after any traumatic event, these must persist to a sufficient degree (i.e., causing dysfunction in life 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).
Persons considered at risk include, for example, combat military personnel, victims of natural disasters, concentration camp survivors, and victims of violent crime. Individuals frequently experience “survivor’s guilt” for remaining alive while others died. Causes of the symptoms of PTSD are the experiencing or witnessing of a stressor event involving death, serious injury or such threat to the self or others in a situation in which the individual felt intense fear, horror, or powerlessness. Persons employed in occupations that expose them to violence (such as soldiers) or disasters (such as emergency service workers) are also at risk. An extensive literature review identifies other occupations and professions that are at higher risk, including police officers, firefighters, ambulance personnel, health care professionals, train drivers, divers, journalists, and sailors, in addition to people who work at banks, post offices or in stores. The size of the hippocampus is inversely related to post-traumatic stress disorder and treatment success; the smaller the higher risk of PTSD.
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. Most people will experience at least one traumatizing event in their lifetime. Men are more likely to experience a traumatic event, but women are more likely to experience the kind of high-impact traumatic event that can lead to PTSD, such as interpersonal violence and sexual assault.
DSM-5 expanded the trauma definition to include some cases of indirect exposure such as repeated exposure to details of a traumatic event experienced by a loved one and work-related video exposure (e.g., “drone” pilots).
Posttraumatic stress reactions have not been studied as well in children and adolescents as adults. The rate of PTSD may be lower in children than adults, but in the absence of therapy, symptoms may continue for decades. One estimate suggests that the proportion of children and adolescents having PTSD in a non-wartorn population in a developed country may be 1% compared to 1.5% to 3% of adults, and much lower below the age of 10 years.
Predictor models have consistently found that childhood trauma, chronic adversity, and familial stressors increase risk for PTSD as well as risk for biological markers of risk for PTSD after a traumatic event in adulthood. Experiencing bullying as a child or an adult has been correlated with the development of PTSD. Peritraumatic dissociation in children is a predictive indicator of the development of PTSD later in life. This effect of childhood trauma, which is not well-understood, may be a marker for both traumatic experiences and attachment problems. Proximity to, duration of, and severity of the trauma make an impact, and interpersonal traumas cause more problems than impersonal ones.
Quasi-experimental studies have demonstrated a relationship between intrusive thoughts and intentional control responses such that suppression increases the frequency of unwanted intrusive thoughts. These results suggest that suppression of intrusive thoughts may be important in the development and maintenance of PTSD.
An individual that has been exposed to domestic violence is predisposed to the development of PTSD. However, being exposed to a traumatic experience does not automatically indicate that an individual will develop PTSD. There is a strong association between the development of PTSD in mothers that experienced domestic violence during the perinatal period of their pregnancy.
Early intervention appears to be a critical preventive measure. 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.
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).
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. PTSD can have numerous clinical and occupational effects. 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.
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.
PTSD is under-diagnosed in female veterans. Sexual assault in the military is a leading cause for female soldiers developing PTSD; a female soldier who is sexually assaulted while serving in the military is nine times more likely to develop PTSD than a female soldier who is not assaulted. A soldier’s assailant may be her colleague or superior officer, making it difficult for her to both report the crime and to avoid interacting with her assailant again. Until the Tailhook scandal drew attention to the problem, the role that sexual assault in the military plays in female veterans developing PTSD went largely unstudied.
Protective effects include social support, which also helps with recovery if PTSD develops. For more aggravating factors to recovery once home, see social alienation among returning war veterans.
There is evidence that susceptibility to PTSD is hereditary. Approximately 30% of the variance in PTSD is caused from genetics alone. For twin pairs exposed to combat in Vietnam, having a monozygotic (identical) twin with PTSD was associated with an increased risk of the co-twin’s having PTSD compared to twins that were dizygotic (non-identical twins). There is evidence that those with a genetically smaller hippocampus are more likely to develop PTSD following a traumatic event. Research has also found that PTSD shares many genetic influences common to other psychiatric disorders. Panic and generalized anxiety disorders and PTSD share 60% of the same genetic variance. Alcohol, nicotine, and drug dependence share greater than 40% genetic similarities.
Several biological indicators have been identified that are related to later PTSD development. Heightened startle responses and a smaller hippocampal volume have been identified as biomarkers for the risk of developing PTSD. Additionally, one study found that soldiers whose leukocytes had greater numbers of glucocorticoid receptors were more prone to developing PTSD after experiencing trauma.
Drug and substance abuse
Drug abuse and alcohol abuse commonly co-occur with PTSD. Recovery from posttraumatic stress disorder or other anxiety disorders may be hindered, or the condition worsened, by medication or substance use; resolving these problems can bring about improvement in an individual’s mental health status and anxiety levels.
PTSD symptoms may result when a traumatic event causes an over-reactive adrenaline response, which creates deep neurological patterns in the brain. These patterns can persist long after the event that triggered the fear, making an individual hyper-responsive to future fearful situations. During traumatic experiences the high levels of stress hormones secreted suppress hypothalamic activity that may be a major factor toward the development of PTSD.
PTSD causes biochemical changes in the brain and body, that differ from other psychiatric disorders such as major depression. Individuals diagnosed with PTSD respond more strongly to a dexamethasone suppression test than individuals diagnosed withclinical depression.
Most people with PTSD show a low secretion of cortisol and high secretion of catecholamines in urine, with a norepinephrine/cortisol ratio consequently higher than comparable non-diagnosed individuals. This is in contrast to the normative fight-or-flight response, in which both catecholamine and cortisol levels are elevated after exposure to a stressor.
Brain catecholamine levels are high, and corticotropin-releasing factor (CRF) concentrations are high. Together, these findings suggest abnormality in the hypothalamic-pituitary-adrenal (HPA) axis.
The maintenance of fear has been shown to include the HPA axis, the locus coeruleus–noradrenergic systems, and the connections between the limbic system and frontal cortex. The HPA axis that coordinates the hormonal response to stress, which activates the LC-noradrenergic system, is implicated in the over-consolidation of memories that occurs in the aftermath of trauma. This over-consolidation increases the likelihood of one’s developing PTSD. The amygdala is responsible for threat detection and the conditioned and unconditioned fear responses that are carried out as a response to a threat.
The HPA axis is responsible for coordinating the hormonal response to stress. Given the strong cortisol suppression to dexamethasone in PTSD, HPA axis abnormalities are likely predicated on strong negative feedback inhibition of cortisol, itself likely due to an increased sensitivity of glucocorticoid receptors. PTSD has been hypothesized to be a maladaptive learning pathway to fear response through a hypersensitive, hyperreactive, and hyperresponsive HPA axis.
Low cortisol levels may predispose individuals to PTSD: Following war trauma, Swedish soldiers serving in Bosnia and Herzegovina with low pre-service salivary cortisol levels had a higher risk of reacting with PTSD symptoms, following war trauma, than soldiers with normal pre-service levels. Because cortisol is normally important in restoring homeostasis after the stress response, it is thought that trauma survivors with low cortisol experience a poorly contained—that is, longer and more distressing—response, setting the stage for PTSD.
It is thought that the locus coeruleus-noradrenergic system mediates the over-consolidation of fear memory. High levels of cortisol reduce noradrenergic activity, and because people with PTSD tend to have reduced levels of cortisol, it has been proposed that individuals with PTSD cannot regulate the increased noradrenergic response to traumatic stress. Intrusive memories and conditioned fear responses are thought to be a result of the response to associated triggers. 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.
Other studies indicate that people that suffer from PTSD have chronically low levels of serotonin, which contributes to the commonly associated behavioral symptoms such as anxiety, ruminations, irritability, aggression, suicidality, and impulsivity. Serotonin also contributes to the stabilization of glucocorticoid production.
Dopamine levels in a person with PTSD can help contribute to the symptoms associated. Low levels of dopamine can contribute to anhedonia, apathy, impaired attention, and motor deficits. Increased levels of dopamine can cause psychosis, agitation, and restlessness.
Hyperresponsiveness in the norepinephrine system can be caused by continued exposure to high stress. Overactivation of norepinephrine receptors in the prefrontal cortex can be connected to the flashbacks and nightmares frequently experienced by those with PTSD. A decrease in other norepinephrine functions (awareness of the current environment) prevents the memory mechanisms in the brain from processing that the experience, and emotions the person is experiencing during a flashback are not associated with the current environment.
There is considerable controversy within the medical community regarding the neurobiology of PTSD. A 2012 review showed no clear relationship between cortisol levels and PTSD. The majority of reports indicate people with PTSD have elevated levels ofcorticotropin-releasing hormone, lower basal cortisol levels, and enhanced negative feedback suppression of the HPA axis by dexamethasone.
For example, a prospective study using the Vietnam Head Injury Study showed that damage to the prefrontal cortex may be protective against later development of PTSD. PTSD patients have 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.
The amygdala is strongly involved in forming emotional memories, especially fear-related memories. Neuroimaging studies in humans have revealed aspects of PTSD morphology and function. During high stress, thehippocampus, which is associated with placing memories in the correct context of space and time and memory recall, is suppressed. According to one theory this suppression may be the cause of the flashbacks that can affect people with PTSD. When someone with PTSD undergoes stimuli similar to the traumatic event, the body perceives the event as occurring again because the memory was never properly recorded in the person’s memory.[unreliable medical source?]
The amygdalocentric model of PTSD proposes that the amygdala is very much aroused and insufficiently controlled by the medial prefrontal cortex and the hippocampus, in particular during extinction. This is consistent with an interpretation of PTSD as a syndrome of deficient extinction ability.
A 2011 study found that fear extinction-induced IGF2/IGFBP7 signalling promotes the survival of hippocampal neurons in 2-3 week old newborn mice. This suggests that enhancing IGF2 signalling and adultneurogenesis might be suitable to treat diseases linked to excessive fear memory such as PTSD. Further animal and clinical research into the amygdala and fear conditioning may suggest additional treatments for the condition.
The 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.
In a 2007 study Vietnam War combat veterans with PTSD showed a 20% reduction in the volume of their hippocampus compared with veterans having suffered no such symptoms. This finding was not replicated in chronic PTSD patients traumatized at anair show plane crash in 1988 (Ramstein, Germany). A 2016 study strengthened theory that a smaller hippocampus increases the risk for post-traumatic stress disorder, and a larger hippocampus increases the likelihood efficacious treatment.
PTSD can be particularly difficult to diagnose, because numerous factors can lead to over-reporting (e.g., disability) and under-reporting (e.g., avoidance) symptoms, dysfunction and distress.
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. Primary Care PTSD Screen and PTSD Checklist are other screening tools.
The American Academy of Child and Adolescent Psychiatry practice parameters is a guidelines for the assessment and treatment of PTSD.
A revised form of the Impact of Events scale (IES-R) gives a total score ranging from 0 to 88. 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.
Diagnostic and statistical manual
Since the introduction of DSM-IV, the number of possible events that might be used to diagnose PTSD has increased; one study suggests that the increase is around 50%. Various scales to measure the severity and frequency of PTSD symptoms exist. Standardized screening tools such as Trauma Screening Questionnaire and PTSD Symptom Scale can be used to detect possible symptoms of posttraumatic stress disorder and suggest the need for a formal diagnostic assessment.
International classification of diseases
The diagnostic criteria for PTSD, stipulated in the International Statistical Classification of Diseases and Related Health Problems 10 (ICD-10), may be summarized as:
- Exposure to a stressful event or situation (either short or long lasting) of exceptionally threatening or catastrophic nature, which is likely to cause pervasive distress in almost anyone.
- Persistent remembering, or “reliving” the stressor by intrusive flashbacks, vivid memories, recurring dreams, or by experiencing distress when exposed to circumstances resembling or associated with the stressor.
- Actual or preferred avoidance of circumstances resembling or associated with the stressor (not present before exposure to the stressor).
- Either (1) or (2):
- Inability to recall, either partially or completely, some important aspects of the period of exposure to the stressor
- Persistent symptoms of increased psychological sensitivity and arousal (not present before exposure to the stressor) shown by any two of the following:
- difficulty in falling or staying asleep
- irritability or outbursts of anger
- difficulty in concentrating
- exaggerated startle response.
The International Statistical Classification of Diseases and Related Health Problems 10 diagnostic guidelines state: In general, this disorder should not be diagnosed unless there is evidence that it arose within 6 months of a traumatic event of exceptional severity. A “probable” diagnosis might still be possible if the delay between the event and the onset was longer than 6 months, provided that the clinical manifestations are typical and no alternative identification of the disorder (e.g., as an anxiety or obsessive-compulsive disorder or depressive episode) is plausible. In addition to evidence of trauma, there must be a repetitive, intrusive recollection or re-enactment of the event in memories, daytime imagery, or dreams. Conspicuous emotional detachment, numbing of feeling, and avoidance of stimuli that might arouse recollection of the trauma are often present but are not essential for the diagnosis. The autonomic disturbances, mood disorder, and behavioural abnormalities all contribute to the diagnosis but are not of prime importance. The late chronic sequelae of devastating stress, i.e. those manifest decades after the stressful experience, should be classified under F62.0.
A diagnosis of PTSD requires that the person has been exposed 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 partner being fired, or a spouse leaving. If any of the symptom pattern is present before the stressor, another diagnosis is required, such as brief psychotic disorder or major depressive disorder. Other differential diagnoses are schizophrenia or other disorders with psychotic features such as Psychotic disorders due to a general medical condition. Drug-induced psychotic disorders can be considered if substance abuse is involved.
The symptom pattern for acute stress disorder must occur and be resolved within four weeks of the trauma. If it lasts longer, and the symptom pattern fits that characteristic of PTSD, the diagnosis may be changed.
Modest benefits have been seen from early access to cognitive behavioral therapy. Critical incident stress management has been suggested as a means of preventing PTSD, but subsequent studies suggest the likelihood of its producing negative outcomes. A review “…did not find any evidence to support the use of an intervention offered to everyone”, and that “…multiple session interventions may result in worse outcome than no intervention for some individuals.” The World Health Organization recommends against the use of benzodiazepines and antidepressants in those having experienced trauma. Some evidence supports the use of hydrocortisone for prevention in adults, however there is limited or no evidence supportingpropranolol, escitalopram, temazepam, or gabapentin. Conversely, taking benzodiazepines after trauma is associated with a 2-5 times increased risk of developing PTSD and major depressive disorder.
Trauma-exposed individuals often receive treatment called psychological debriefing in an effort to prevent PTSD. Several meta-analyses; however, find that psychological debriefing is unhelpful and is potentially harmful. This is true for both single-session debriefing and multiple session interventions. The American Psychological Association judges the status of psychological debriefing as No Research Support/Treatment is Potentially Harmful.
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.
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.
Systematic reviews have found that combination therapy (psychological and pharmacotherapy) is no more effective than psychological therapy alone.
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.
The psychotherapy programs with the strongest demonstrated efficacy include cognitive behavioral programs, variants of exposure therapy, stress inoculation training (SIT), variants of cognitive therapy (CT), eye movement desensitization and reprocessing (EMDR), mindfulness-based meditation and many combinations of these procedures. EMDR and trauma-focused cognitive behavioral therapy (TFCBT) were recommended as first-line treatments for trauma victims in a 2007 review; however, “the evidence base [for EMDR] was not as strong as that for TFCBT … Furthermore, there was limited evidence that TFCBT and EMDR were superior to supportive/non-directive treatments, hence it is highly unlikely that their effectiveness is due to non-specific factors such as attention.” A meta-analytic comparison of EMDR and cognitive behavioral therapy found both protocols indistinguishable in terms of effectiveness in treating PTSD; however, “the contribution of the eye movement component in EMDR to treatment outcome” is unclear.
Furthermore, the availability of school-based therapy is particularly important for children with PTSD. Children with PTSD are far more likely to pursue treatment at school (because of its proximity and ease) than at a free clinic.
Cognitive behavioral therapy
Cognitive behavioral therapy (CBT) seeks to change the way a trauma victim feels and acts by changing the patterns of thinking or behavior, or both, responsible for negative emotions. CBT has been proven to be an effective treatment for PTSD and is currently considered the standard of care for PTSD by the United States Department of Defense. In CBT, individuals learn to identify thoughts that make them feel afraid or upset and replace them with less distressing thoughts. The goal is to understand how certain thoughts about events cause PTSD-related stress.
Recent research on contextually based third-generation behavior therapies suggests that they may produce results comparable to some of the better validated therapies. Many of these therapy methods have a significant element of exposure and have demonstrated success in treating the primary problems of PTSD and co-occurring depressive symptoms.
Exposure therapy is a type of cognitive behavioral therapy that involves assisting trauma survivors to re-experience distressing trauma-related memories and reminders in order to facilitate habituation and successful emotional processing of the trauma memory. Most exposure therapy programs include both imaginal confrontation with the traumatic memories and real-life exposure to trauma reminders; this therapy modality is well supported by clinical evidence. The success of exposure-based therapies has raised the question of whether exposure is a necessary ingredient in the treatment of PTSD. Some organizations[which?] have endorsed the need for exposure. The US Department of Veterans Affairs has been actively training mental health treatment staff in prolonged exposure therapy and Cognitive Processing Therapy in an effort to better treat US veterans with PTSD.
Eye movement desensitization and reprocessing
Eye movement desensitization and reprocessing (EMDR) is a form of psychotherapy developed and studied by Francine Shapiro. She had noticed that, when she was thinking about disturbing memories herself, her eyes were moving rapidly. When she brought her eye movements under control while thinking, the thoughts were less distressing.
In 2002, Shapiro and Maxfield published a theory of why this might work, called adaptive information processing. This theory proposes that eye movement can be used to facilitate emotional processing of memories, changing the person’s memory to attend to more adaptive information. The therapist initiates voluntary rapid eye movements while the person focuses on memories, feelings or thoughts about a particular trauma. The therapists uses hand movements to get the person to move their eyes backward and forward, but hand-tapping or tones can also be used. EMDR closely resembles cognitive behavior therapy as it combines exposure (re-visiting the traumatic event), working on cognitive processes and relaxation/self-monitoring.However, exposure by way of being asked to think about the experience rather than talk about it has been highlighted as one of the more important distinguishing elements of EMDR.
There have been multiple small controlled trials of four to eight weeks of EMDR in adults as well as children and adolescents. EMDR reduced PTSD symptoms enough in the short term that one in two adults no longer met the criteria for PTSD, but the number of people involved in these trials was small. There was not enough evidence to know whether or not EMDR could eliminate PTSD. There was some evidence that EMDR might prevent depression. There were no studies comparing EMDR to other psychological treatments or to medication. Adverse effects were largely unstudied. The benefits were greater for women with a history of sexual assault compared with people who had experienced other types of traumatizing events (such as accidents, physical assaults and war). There is a small amount of evidence that EMDR may improve re-experiencing symptoms in children and adolescents, but EMDR has not been shown to improve other PTSD symptoms, anxiety, or depression.
The eye movement component of the therapy may not be critical for benefit. As there has been no major, high quality randomized trial of EMDR with eye movements versus EMDR without eye movements, the controversy over effectiveness is likely to continue. Authors of a meta-analysis published in 2013 stated, “We found that people treated with eye movement therapy had greater improvement in their symptoms of post-traumatic stress disorder than people given therapy without eye movements….Secondly we found that that in laboratory studies the evidence concludes that thinking of upsetting memories and simultaneously doing a task that facilitates eye movements reduces the vividness and distress associated with the upsetting memories.”
Other approaches, in particular involving social supports, may also be important. An open trial of interpersonal psychotherapy reported high rates of remission from PTSD symptoms without using exposure. A current, NIMH-funded trial in New York City is now (and into 2013) comparing interpersonal psychotherapy, prolonged exposure therapy, and relaxation therapy.[full citation needed]
Selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs) may have some benefit for PTSD symptoms. Tricyclic antidepressants are equally effective but are less well tolerated. Evidence provides support for a small or modest improvement with sertraline, fluoxetine, paroxetine, and venlafaxine. Thus, these four medications are considered to be first-line medications for PTSD.
Benzodiazepines are not recommended for the treatment of PTSD due to a lack of evidence of benefit and risk of worsening PTSD symptoms. Some authors believe that the use of benzodiazepines is contraindicated for acute stress, as this group of drugs promotes dissociation and ulterior revivals. Nevertheless, some use benzodiazepines with caution for short-term anxiety and insomnia. 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. 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. 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. Due to a number 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. 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). “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.”
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.
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. Additionally, there are other treatments with stronger efficacy and less risks (e.g., psychotherapy, serotonergic antidepressants, adrenergic inhibitors).
- Exercise, sport and physical activity
Physical activity can influence people’s psychological wellbeing and physical health. The U.S. National Center for PTSD recommends moderate exercise as a way to distract from disturbing emotions, build self-esteem and increase feelings of being in control again. They recommend a discussion with a doctor before starting an exercise program.
- Play therapy for children
Play is thought to help children link their inner thoughts with their outer world, connecting real experiences with abstract thought. Repetitive play can also be one of the ways a child relives traumatic events, and that can be a symptom of traumatization in a child or young person. Although it is commonly used, there have not been enough studies comparing outcomes in groups of children receiving and not receiving play therapy, so the effects of play therapy are not yet understood.
- Military programs
Many veterans of the wars in Iraq and Afghanistan have faced significant physical, emotional, and relational disruptions. In response, the United States Marine Corps has instituted programs to assist them in re-adjusting to civilian life, especially in their relationships with spouses and loved ones, to help them communicate better and understand what the other has gone through. Walter Reed Army Institute of Research (WRAIR) developed the Battlemind program to assist service members avoid or ameliorate PTSD and related problems.
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