Posttraumatic stress disorder | |
---|---|
Art therapy project created by a U.S. Marine with posttraumatic stress disorder | |
Specialty | Psychiatry, clinical psychology |
Symptoms | Disturbing thoughts, feelings, or dreams related to the event; mental or physical distress to trauma-related cues; efforts to avoid trauma-related situations; increased fight-or-flight response |
Complications | Suicide |
Duration | > 1 month |
Causes | Exposure to a traumatic event |
Diagnostic method | Based on symptoms |
Treatment | Counseling, medication |
Medication | Selective serotonin reuptake inhibitor |
Frequency | 8.7% (lifetime risk); 3.5% (12-month risk) (USA) |
Posttraumatic stress disorder (PTSD) 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 an increase in the fight-or-flight response. 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. A person with PTSD is at a higher risk for suicide and intentional self-harm.
Most people who experience a traumatic event do 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 10 years of age. Diagnosis is based on the presence of specific symptoms following a traumatic event.
Prevention may be possible when counselling is targeted at those with early symptoms but is not effective when provided to all trauma-exposed individuals whether or not symptoms are present. The main treatments for people with PTSD are counselling (psychotherapy) and medication. Antidepressants of the selective serotonin reuptake inhibitor type are the first-line medications for PTSD and result in benefit in about half of people. Benefits from medication are less than those seen with counselling. It is not known whether using medications and counselling together has greater benefit than either method separately. 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, the condition 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 U.S. 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).
Signs and symptoms
Symptoms of PTSD generally begin within the first 3 months after the
inciting traumatic event, but may not begin until years later.
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, dissociative episodes of reliving
the trauma ("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). Some following a traumatic event experience posttraumatic growth.
Associated medical conditions
Trauma survivors often develop depression, anxiety disorders, and mood disorders in addition to PTSD.
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, when substance use disorders are comorbid with PTSD. Resolving these problems can bring about improvement in an individual's mental health status and anxiety levels.
In children and adolescents, there is a strong association
between emotional regulation difficulties (e.g. mood swings, anger
outbursts, temper tantrums) and post-traumatic stress symptoms, independent of age, gender, or type of trauma.
Risk factors
Persons considered at risk include combat military personnel, victims
of natural disasters, concentration camp survivors, and victims of
violent crime. Persons employed in occupations that expose them to
violence (such as soldiers) or disasters (such as emergency service workers) are also at risk.
Other occupations that are at higher risk include 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 hippocampus, the higher risk of PTSD.
Trauma
PTSD has been associated with a wide range of traumatic events. The
risk of developing PTSD after a traumatic event varies by trauma type and is highest following exposure to sexual violence (11.4%), particularly rape (19.0%).
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.
Motor vehicle collision survivors, both children and adults, are at an increased risk of PTSD. About 20% of children were diagnosed with PTSD following a road traffic accident, compared to 22% of adults.
Females were more likely to be diagnosed with PTSD following a road
traffic accident, whether the accident occurred during childhood or
adulthood.
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. On average, 16% of children exposed to a traumatic event develop PTSD, varying according to type of exposure and gender.
Similar to the adult population, risk factors for PTSD in children
include: female gender, exposure to disasters (natural or manmade),
negative coping behaviours, and/or lacking proper social support
systems.
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.
The risk of developing PTSD is increased in individuals who are exposed to physical abuse, physical assault, or kidnapping. Women who experience physical violence are more likely to develop PTSD than men.
Intimate partner 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. There is a strong association between the development of PTSD in mothers that experienced domestic violence during the perinatal period of their pregnancy.
Those who have experienced sexual assault or rape may develop symptoms of PTSD.
PTSD symptoms include re-experiencing the assault, avoiding things
associated with the assault, numbness, and increased anxiety and an
increased startle response.
The likelihood of sustained symptoms of PTSD is higher if the rapist
confined or restrained the person, if the person being raped believed
the rapist would kill him or her, the person who was raped was very
young or very old, and if the rapist was someone he or she knew. The
likelihood of sustained severe symptoms is also higher if people around
the survivor ignore (or are ignorant of) the rape or blame the rape
survivor.
Military service is a risk factor for developing PTSD.
Around 78% of people exposed to combat do not develop PTSD; in about
25% of military personnel who develop PTSD, its appearance is delayed.
Refugees are also at an increased risk for PTSD due to their
exposure to war, hardships, and traumatic events. The rates for PTSD
within refugee populations range from 4% to 86%.
While the stresses of war impact everyone involved, displaced persons
have been shown to be more affected than nondisplaced persons.
Unexpected death of a loved one
Sudden, unexpected death of a loved one is the most common traumatic event type reported in cross-national studies.
However, the majority of people who experience this type of event will
not go on to develop PTSD. An analysis from the WHO World Mental Health
Surveys found a 5.2% risk of developing PTSD after learning of the
unexpected death of a loved one.
Because of the high prevalence of this type of traumatic event,
unexpected death of a loved one accounts for approximately 20% of PTSD
cases worldwide.
Life-threatening illness
Medical conditions associated with an increased risk of PTSD include cancer, heart attack, and stroke. 22% of cancer survivors present with lifelong PTSD like symptoms. Intensive-care unit (ICU) hospitalization is also a risk factor for PTSD. Some women experience PTSD from their experiences related to breast cancer and mastectomy.
Loved ones of those who experience life-threatening illnesses are also
at risk for developing PTSD, such as parents of child with chronic
illnesses.
Women who experience miscarriage are at risk of PTSD. Those who experience subsequent miscarriages have an increased risk of PTSD compared to those experiencing only one. PTSD can also occur after childbirth and the risk increases if a woman has experienced trauma prior to the pregnancy.
Prevalence of PTSD following normal childbirth (that is, excluding
stillbirth or major complications) is estimated to be between 2.8 and
5.6% at 6 weeks postpartum, with rates dropping to 1.5% at 6 months postpartum. Symptoms of PTSD are common following childbirth, with prevalence of 24-30.1% at 6 weeks, dropping to 13.6% at 6 months. Emergency childbirth is also associated with PTSD. Some women experience PTSD from their experiences related to breast cancer and mastectomy.
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).
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.
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. 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 with clinical 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 contribute to symptoms: low levels can contribute to anhedonia, apathy, impaired attention, and motor deficits; high levels can contribute to psychosis, agitation, and restlessness.
Multiple studies described elevated concentrations of the thyroid hormone triiodothyronine in PTSD. This kind of type 2 allostatic adaptation may contribute to increased sensitivity to catecholamines and other stress mediators.
Hyperresponsiveness in the norepinephrine system can also 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 of corticotropin-releasing hormone, lower basal cortisol levels, and enhanced negative feedback suppression of the HPA axis by dexamethasone.
Neuroanatomy
A meta-analysis of structural MRI studies found an association with reduced total brain volume, intracranial volume, and volumes of the hippocampus, insula cortex, and anterior cingulate. Much of this research stems from PTSD in those exposed to the Vietnam War.
People with PTSD 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. During high stress, the hippocampus,
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.
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.
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.
While as a whole, amygdala hyperactivity is reported by meta analysis
of functional neuroimaging in PTSD, there is a large degree of
heterogeniety, more so than in social anxiety disorder or phobic
disorder. Comparing dorsal(roughly the CeA) and ventral(roughly the
BLA) clusters, hyperactivity is more robust in the ventral cluster,
while hypoactivity is evident in the dorsal cluster. The distinction
may explain the blunted emotions in PTSD(via desensitization in the CeA)
as well as the fear related component.
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 an air show plane crash in 1988 (Ramstein, Germany).
Diagnosis
PTSD can be difficult to diagnose, because of:
- the subjective nature of most of the diagnostic criteria (although this is true for many mental disorders);
- the potential for over-reporting, e.g., while seeking disability benefits, or when PTSD could be a mitigating factor at criminal sentencing;
- the potential for under-reporting, e.g., stigma, pride, fear that a PTSD diagnosis might preclude certain employment opportunities;
- symptom overlap with other mental disorders such as obsessive compulsive disorder and generalized anxiety disorder;
- association with other mental disorders such as major depressive disorder and generalized anxiety disorder;
- substance use disorders, which often produce some of the same signs and symptoms as PTSD; and
- substance use disorders can increase vulnerability to PTSD or exacerbate PTSD symptoms or both; and
- PTSD increases the risk for developing substance abuse disorders.
- the differential expression of symptoms culturally (specifically with respect to avoidance and numbing symptoms, distressing dreams, and somatic symptoms)
Screening and assessment
A number of screening instruments are used for screening adults for PTSD, such as the PTSD Checklist for DSM-5 (PCL-5) and the Primary Care PTSD Screen for DSM-5 (PC-PTSD-5).
There are also several screening and assessment instruments for
use with children and adolescents. These include the Child PTSD Symptom
Scale (CPSS), Child Trauma Screening Questionnaire, and UCLA Posttraumatic Stress Disorder Reaction Index for DSM-IV.
In addition, there are also screening and assessment instruments
for caregivers of very young children (six years of age and younger).
These include the Young Child PTSD Screen, the Young Child PTSD Checklist, and the Diagnostic Infant and Preschool Assessment.
Diagnostic and statistical manual
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 DSM-5
diagnostic criteria for PTSD include four symptom clusters:
re-experiencing, avoidance, negative alterations in cognition/mood, and
alterations in arousal and reactivity.
International classification of diseases
The International Classification of Diseases and Related Health
Problems 10 (ICD-10) classifies PTSD under "Reaction to severe stress,
and adjustment disorders."
The ICD-10 criteria for PTSD include re-experiencing, avoidance, and
either increased reactivity or inability to recall certain details
related to the event.
The ICD-11
diagnostic description for PTSD contains three components or symptom
groups (1) re-experiencing, (2) avoidance, and (3) heightened sense of
threat.
Another difference between the ICD-10 and ICD-11 PTSD diagnostic
formulations, ICD-11 no longer includes verbal thoughts about the
traumatic event as a symptom. There is a predicted lower rate of diagnosed PTSD using ICD-11 compared to ICD10 or DSM-5.
ICD-11 also proposes identifying a distinct group with complex
post-traumatic stress disorder (CPTSD), who have more often experienced
multiple and sustained traumas and have greater functional impairment
than those with PTSD.
Differential diagnosis
A diagnosis of PTSD requires that the person has been exposed to an
extreme, life-threatening stressor. 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.
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.
Obsessive compulsive disorder may be diagnosed for intrusive thoughts that are recurring but not related to a specific traumatic event.
In extreme cases of prolonged, repeated traumatization where there is no viable chance of escape, survivors may develop complex post-traumatic stress disorder.
This occurs as a result of layers of trauma rather than a single
traumatic event, and includes additional symptomatology, such as the
loss of a coherent sense of self.
Prevention
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 for acute stress (symptoms lasting less than one month). Some evidence supports the use of hydrocortisone for prevention in adults, although there is limited or no evidence supporting propranolol, escitalopram, temazepam, or gabapentin.
Psychological debriefing
Trauma-exposed individuals often receive treatment called psychological debriefing
in an effort to prevent PTSD, which consists of interviews that are
meant to allow individuals to directly confront the event and share
their feelings with the counselor and to help structure their memories
of the event. However, several meta-analyses find that psychological debriefing is unhelpful and is potentially harmful. This is true for both single-session debriefing and multiple session interventions. As of 2017 The American Psychological Association assessed psychological debriefing as No Research Support/Treatment is Potentially Harmful.
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.
Management
Reviews of studies have found that combination therapy (psychological
and pharmacotherapy) is no more effective than psychological therapy
alone.
Counselling
The approaches with the strongest evidence include behavioral and cognitive-behavioral therapies such as prolonged exposure therapy, cognitive processing therapy, and eye movement desensitization and reprocessing (EMDR).
In addition, brief eclectic psychotherapy (BEP), narrative exposure
therapy (NET), and written narrative exposure therapies also have a
evidence.
A meta-analytic comparison of EMDR and cognitive behavioral therapy
(CBT) 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. A meta-analysis in children and adolescent also found that EMDR was as efficacious as cognitive behavioral therapy.
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
CBT seeks to change the way a person 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 have endorsed the need for exposure. The U.S. 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 U.S. 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 and thus results should be
interpreted with caution pending further research. There was not enough evidence to know whether or not EMDR could eliminate PTSD in adults. In children and adolescents, a recent meta-analysis of randomized controlled trials using MetaNSUE
to avoid biases related to missing information found that EMDR was at
least as efficacious as CBT, and superior to waitlist or placebo. 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."
Interpersonal psychotherapy
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.
Medication
While many medications do not have enough evidence to support their
use, three (fluoxetine, paroxetine, and venlafaxine) have been shown to
have a small to modest benefit over placebo. With many medications, residual PTSD symptoms following treatment is the rule rather than the exception.
Antidepressants
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
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 can cause dissociation. 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. 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).
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.
Cannabinoids
Evidence as of 2017 is insufficient to determine if medical cannabis is useful for PTSD. However, use of cannabis or derived products is widespread among U.S. veterans with PTSD.
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. Currently, a handful of states permit the use of medical cannabis for the treatment of PTSD.
Other
Exercise, sport and physical activity
Physical activity can influence people's psychological 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 way a child relives traumatic events,
and that can be a symptom of trauma 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. Wounded Warrior Project partnered with the US Department of Veterans Affairs to create Warrior Care Network, a national health system of PTSD treatment centers.
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 2013, epidemiological rates have not changed significantly.
Most of the current reliable data regarding the epidemiology of PTSD is
based on DSM-IV criteria, as the DSM-5 was not introduced until 2013.
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.
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.
As of 2017, the cross-national lifetime prevalence of PTSD was 3.9%, based on a survey were 5.6% had been exposed to trauma.
The primary factor impacting treatment-seeking behavior, which can help
to mitigate PTSD development after trauma was income, while being
younger, female, and having less social status (less education, lower
individual income, and being unemployed) were all factors associated
with less treatment-seeking behaviour.
Region | Country | PTSD DALY rate, overall |
PTSD DALY rate, females |
PTSD DALY rate, males |
---|---|---|---|---|
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 (3.6%) to have PTSD at some point in their lives.
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. 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.
Military combat
The United States Department of Veterans Affairs estimates that 830,000 Vietnam War veterans suffered symptoms of PTSD. The National Vietnam Veterans' Readjustment Study
(NVVRS) found 15% of male and 9% of female Vietnam veterans had PTSD at
the time of the study. Life-time prevalence of PTSD was 31% for males
and 27% 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.
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.
As of 2013, rates of PTSD have been estimated at up to 20% for veterans returning from Iraq and Afghanistan. As of 2013 13% of veterans returning from Iraq were unemployed.
Man-made disasters
The September 11 attacks took the lives of nearly 3,000 people, leaving 6,000 injured. First responders (police and firefighters), emergency medical services, sanitation workers, and volunteers were all involved in the recovery efforts. The prevalence
of probable PTSD in these highly exposed populations was estimated
across multiple studies utilizing in-person, telephone, and online interviews and questionnaires.
Overall prevalence of PTSD was highest immediately following the
attacks and decreased over time. However, disparities were found among
the different types of recovery workers.
The rate of probable PTSD for first responders was lowest directly
after the attacks and increased from ranges of 4.8-7.8% to 7.4-16.5%
between the 5-6 year follow-up and a later assessment.
When comparing traditional responders to non-traditional responders
(volunteers), the probable PTSD prevalence 2.5 years after the initial
visit was greater in volunteers with estimates of 11.7% and 17.2%
respectively. Volunteer participation in tasks atypical to the defined occupational role was a significant risk factor for PTSD.
Other risk factors included exposure intensity, earlier start date,
duration of time spent on site, and constant, negative reminders of the
trauma.
Additional research has been performed to understand the social
consequences of the September 11 attacks. Alcohol consumption was
assessed in a cohort of World Trade Center workers using the cut-annoyed-guilty-eye (CAGE) questionnaire
for alcohol abuse. Almost 50% of World Trade Center workers who
self-identified as alcohol users reported drinking more during the
rescue efforts. Nearly a quarter of these individuals reported drinking more following the recovery.
If determined to have probable PTSD status, the risk of developing an
alcohol problem was double compared to those without psychological morbidity.
Social disability was also studied in this cohort as a social
consequence of the September 11 attacks. Defined by the disruption of
family, work, and social life, the risk of developing social disability
increased 17-fold when categorized as having probable PTSD.
Veterans
United States
The United States provides a range of benefits for veterans that the VA
has determined have PTSD, which developed during, or as a result of,
their military service. These benefits may include tax-free cash
payments, free or low-cost mental health treatment and other healthcare, vocational rehabilitation services, employment assistance, and independent living support.
Iraq
Young Iraqis have high rates of post-traumatic stress disorder due to the 2003 invasion of Iraq.
United Kingdom
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.
Canada
Veterans Affairs Canada
offers a new program that includes rehabilitation, financial benefits,
job placement, health benefits program, disability awards, peer support and family support.
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.
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". The diagnosis includes language which relates the condition to combat as well as to "civilian catastrophe".
A USAF study carried out in 1979 focused on individuals (civilian
and military) who had worked to recover or identify the remains of
those who died in Jonestown.
The bodies had been dead for several days, and a third of them had been
children. The study used the term "dysphoria" to describe PTSD-like
symptoms.
Early in 1978, the diagnosis term "post-traumatic stress
disorder" was first recommended in a working group finding presented to
the Committee of Reactive Disorders. The condition was described in the DSM-III (1980) as posttraumatic stress disorder. In the DSM-IV, the spelling "posttraumatic stress disorder" is used, while in the ICD-10, the spelling is "post-traumatic stress disorder".
The addition of the term to the DSM-III was greatly influenced by
the experiences and conditions of U.S. military veterans of the Vietnam War. 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.
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), written around 1597, represents an unusually accurate description of the symptom constellation of PTSD.
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."
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. Aspects of PTSD in soldiers of ancient Assyria
have been identified using written sources from 1300–600 BCE. These
Assyrian soldiers would undergo a three-year rotation of combat before
being allowed to return home, and were purported to have faced immense
challenges in reconciling their past actions in war with their civilian
lives. Connections between the actions of Viking berserkers and the hyperarousal of post-traumatic stress disorder have also been drawn.
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".
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."
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. This paved the way for a more comprehensive understanding of causes of PTSD.
After PTSD became an official psychiatric diagnosis with the publication of DSM-III (1980), the number of personal injury lawsuits (tort claims) asserting the plaintiff suffered from PTSD increased rapidly. However, triers of fact
(judges and juries) often regarded the PTSD diagnostic criteria as
imprecise, a view shared by legal scholars, trauma specialists, forensic psychologists, and forensic psychiatrists.
Professional discussions and debates in academic journals, at
conferences, and between thought leaders, led to a more clearly-defined
set of diagnostic criteria in DSM-IV, particularly the definition of a
"traumatic event".
The DSM-IV classified PTSD under anxiety disorders, but the DSM-5
created a new category called "Trauma- and Stressor-Related Disorders,"
in which PTSD is now classified.
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. 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.
Some at the Pentagon have used the terminology "PTSS" (syndrome
instead of disorder, to avoid connotation of stigma), or just "PTS".
The comedian George Carlin criticized the euphemism treadmill which led to progressive change of the way PTSD was referred to over the course of the 20th century, from "shell shock" in the First World War to the "battle fatigue" in the Second World War, to "operational exhaustion" in the Korean War, to the current "post-traumatic stress disorder", coined during the Vietnam War, which "added a hyphen" and which, he commented, "completely burie[s] [the pain] under jargon".
He also stated that the name given to the condition has had a direct
effect on the way veteran soldiers with PTSD were treated and perceived
by civilian populations over time.
Research
Most knowledge regarding PTSD comes from studies in high-income countries.
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.
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, examination of neuroendocrine and neuroimmune responses in plasma revealed a trend toward increase in corticosterone in PTSD and combination groups.
Stellate ganglion block is an experimental procedure for the treatment of PTSD.
Psychotherapy adjuncts
MDMA was used for psychedelic therapy for a variety of indications before its criminalization in the U.S. in 1985. In response to its criminalization, the Multidisciplinary Association for Psychedelic Studies
(MAPS) was founded as a nonprofit drug-development organization to
develop MDMA into a legal prescription drug for use as an adjunct in
psychotherapy.
The drug is hypothesized to facilitate psychotherapy by reducing fear,
thereby allowing people to reprocess and accept their traumatic memories
without becoming emotionally overwhelmed. In this treatment, people
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. People
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. The phase 2 clinical trials of the MDMA-Assisted Psychotherapy, was publicized at the end of November 2016. Preliminary results suggest MDMA-assisted psychotherapy might be effective. MAPS received FDA approval of a phase 3 trials.
Researchers are also investigating using D-cycloserine, hydrocortisone, and propranolol as add on therapy to more conventional exposure therapy.