| Diseasesdb | 33846 |
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| Medlineplus | 000925 |
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| Emedicinesubj | med |
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| Emedicinetopic | 1900 |
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| Meshid | D013313 |
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Posttraumatic stress disorder (also known as post-traumatic stress disorder or PTSD) is a severe anxiety disorder that can develop after exposure to any event that results in psychological trauma. It has three sub-forms: acute, chronic, and delayed-onset.
Causes
Psychological trauma
PTSD is believed to be caused by either
physical trauma or
psychological trauma, or more frequently a combination of both.
Traumatic events that may cause PTSD symptoms to develop include violent assault, kidnapping, sexual assault, torture, being a hostage, prisoner of war or concentration camp victim, experiencing a disaster, violent automobile accidents or getting a diagnosis of a life-threatening illness. Preliminary research suggests that child abuse may interact with mutations in a stress-related gene to increase the risk of PTSD in adults.
Multiple studies show that parental PTSD and other posttraumatic disturbances in parental psychological functioning can, despite a traumatized parent's best efforts, interfere with their response to their child as well as their child's response to trauma. Parents with violence-related PTSD may, for example, inadvertently expose their children to developmentally inappropriate violent media due to their need to manage their own emotional dysregulation. Clinical findings indicate that a failure to provide adequate treatment to children after they suffer a traumatic experience, depending on their vulnerability and the severity of the trauma, will ultimately lead to PTSD symptoms in adulthood.
Neuroendocrinology
PTSD symptoms may result when a traumatic event causes an overactive adrenaline response, which creates deep neurological patterns in the brain. These patterns can persist long after the event that triggered the fear, making an individual hyper-responsive to future fearful situations.
PTSD displays biochemical changes in the brain and body that differ from other psychiatric disorders such as major depression. Individuals diagnosed with PTSD respond more strongly to a dexamethasone suppression test than individuals diagnosed with clinical depression.
In addition, most people with PTSD also show a low secretion of cortisol and high secretion of catecholamines in urine, with a norepinephrine/cortisol ratio consequently higher than comparable non-diagnosed individuals. 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 low, and corticotropin-releasing factor (CRF) concentrations are high. Together, these findings suggest abnormality in the hypothalamic-pituitary-adrenal (HPA) axis.
Given the strong cortisol suppression to dexamethasone in PTSD, HPA axis abnormalities are likely predicated on strong negative feedback inhibition of cortisol, itself likely due to an increased sensitivity of glucocorticoid receptors. Some researchers have associated the response to stress in PTSD with long-term exposure to high levels of norepinephrine and low levels of cortisol, a pattern associated with improved learning in animals.
Translating this reaction to human conditions gives a pathophysiological explanation for PTSD by a maladaptive learning pathway to fear response through a hypersensitive, hyperreactive and hyperresponsive HPA axis.
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.
However, there is considerable controversy within the medical community regarding the neurobiology of PTSD. A review of existing studies on this subject showed no clear relationship between cortisol levels and PTSD. Only a slight majority have found a decrease in cortisol levels while others have found no effect or even an increase.
Neuroanatomy
Three areas of the brain whose function may be altered in PTSD have been identified: the
prefrontal cortex,
amygdala and
hippocampus. Much of this research has utilised PTSD victims from the Vietnam War. For example, a prospective study using the Vietnam Head Injury Study showed that damage to the prefrontal cortex may actually be protective against later development of PTSD. In a study by Gurvits et al., combat veterans of the
Vietnam War with PTSD showed a 20% reduction in the volume of their
hippocampus compared with veterans who suffered no such symptoms. This finding could not be replicated in chronic PTSD patients traumatized at an air show plane crash in 1988 (Ramstein, Germany).
In human studies, the amygdala has been shown to be strongly involved in the formation of emotional memories, especially fear-related memories. Neuroimaging studies in humans have revealed both morphological and functional aspects of PTSD.
The amygdalocentric model of PTSD proposes that it is associated with hyperarousal of the amygdala and insufficient top-down control by the medial prefrontal cortex and the hippocampus particularly during extinction. This is consistent with an interpretation of PTSD as a syndrome of deficient extinction ability. Further animal and clinical research into the amygdala and fear conditioning may suggest additional treatments for the condition.
Genetics
There is evidence that susceptibility to PTSD is hereditary. For twin pairs exposed to combat in Vietnam, having a monozygotic (identical) twin with PTSD was associated with an increased risk of the co-twin having PTSD compared to twins that were dizygotic (non-identical twins).
Recently, it has been found that several single-nucleotide polymorphisms (SNPs) in FK506 binding protein 5 (FKBP5) interact with childhood trauma to predict severity of adult PTSD. These findings suggest that individuals with these SNPs who are abused as children are more susceptible to PTSD as adults.
This is particularly interesting given that FKBP5 SNPs have previously been associated with peritraumatic dissociation (that is, dissociation at the time of the trauma), which has itself been shown to be predictive of PTSD. Furthermore, FKBP5 may be less expressed in those with current PTSD. Another recent study found a single SNP in a putative estrogen response element on ADCYAP1R1 (encodes pituitary adenylate cyclase-activating polypeptide type I receptor or PAC1) to predict PTSD diagnosis and symptoms in females. Incidentally, this SNP is also associated with fear discrimination. The study suggests that perturbations in the PACAP-PAC1 pathway are involved in abnormal stress responses underlying PTSD.
Risk factors
Although most people (50-90%) encounter trauma over a lifetime, only about 8% develop full PTSD. 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 also make an impact; and interpersonal traumas cause more problems than impersonal ones.
Military experience
Schnurr, Lunney, and Sengupta Other research also indicates the protective effects of social support in averting PTSD or facilitating recovery if it develops.
In one study (Dubner and Motta, 1999), 60% of children in foster care who had experienced sexual abuse had PTSD, and 42% of those who had been physically abused fulfilled the PTSD criteria. PTSD was also found in 18% of the children who were not abused. These children may have developed PTSD due to witnessing violence in the home, or as a result of real or perceived parental abandonment.
Diagnosis
Criteria
The diagnostic criteria for PTSD, stipulated in the
Diagnostic and Statistical Manual of Mental Disorders IV (Text Revision) (DSM-IV-TR), may be summarized as:
A: Exposure to a traumatic event
This must have involved
both (a) loss of "physical integrity", or risk of serious injury or death, to self or others, and (b) a response to the event that involved intense fear, horror or helplessness (or in children, the response must involve disorganized or agitated behavior). (The
DSM-IV-TR criterion differs substantially from the previous DSM-III-R stressor criterion, which specified the traumatic event should be of a type that would cause "significant symptoms of distress in almost anyone," and that the event was "outside the range of usual human experience.")
B: Persistent re-experiencing
One or more of these must be present in the victim:
flashback memories, recurring distressing dreams, subjective re-experiencing of the traumatic event(s), or intense negative psychological or physiological response to any objective or subjective reminder of the traumatic event(s).
C: Persistent avoidance and emotional numbing
This involves a sufficient level of:
avoidance of stimuli associated with the trauma, such as certain thoughts or feelings, or talking about the event(s);
avoidance of behaviors, places, or people that might lead to distressing memories;
inability to recall major parts of the trauma(s), or decreased involvement in significant life activities;
decreased capacity (down to complete inability) to feel certain feelings;
an expectation that one's future will be somehow constrained in ways not normal to other people.
D: Persistent symptoms of increased arousal not present before
These are all physiological response issues, such as difficulty falling or staying asleep, or problems with anger, concentration, or
hypervigilance.
E: Duration of symptoms for more than 1 month
If all other criteria are present, but 30 days have not elapsed, the individual is diagnosed with
Acute stress disorder.
F: Significant impairment
The symptoms reported must lead to "clinically significant distress or impairment" of major domains of life activity, such as social relations, occupational activities, or other "important areas of functioning".
Assessment
Since the introduction of
DSM-IV, the number of possible events which might be used to diagnose PTSD has increased; one study suggests that the increase is around 50%. Various scales exist to measure the severity and frequency of PTSD symptoms. 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.
Research-based alternative symptom group conceptualizations
Emerging
factor analytic research suggests that PTSD symptoms group empirically into four clusters, not the three currently described in the
Diagnostic and Statistical Manual of Mental Disorders. One model supported by this research divides the traditional avoidance symptoms into a cluster of numbing symptoms (such as loss of interest and feeling emotionally numb) and a cluster of behavioral avoidance symptoms (such as avoiding reminders of the trauma). An alternative model adds a fourth cluster of dysphoric symptoms. These include symptoms of emotional numbing, as well as anger, sleep disturbance, and difficulty concentrating (traditionally grouped under the hyperarousal cluster).
DSM-5 proposed diagnostic criteria changes
In preparation for the May 2013
release of the
DSM-5, the fifth version of the
American Psychiatric Association's diagnostic manual, draft diagnostic criteria was released for public comment, followed by a two-year period of field testing. Proposed changes to the criteria include:
Criterion A (prior exposure to traumatic events) is more specifically stated, and evaluation of an individual's emotional response at the time (current criterion A2) is dropped.
Several items in Criterion B (intrusion symptoms) are rewritten to add or augment certain distinctions now considered important.
Special consideration is given to developmentally appropriate criteria for use with children and adolescents. This is especially evident in the restated Criterion B - intrusion symptoms. Development of age-specific criteria for diagnosis of PTSD is ongoing at this time.
Criterion C (avoidance and numbing) has been split into "C" and "D":
* Criterion C (new version) now focuses solely on avoidance of behaviors or physical or temporal reminders of the traumatic experience(s). What were formerly two symptoms are now three, due to slight changes in descriptions.
* New Criterion D focuses on negative alterations in cognition and mood associated with the traumatic event(s), and contains two new symptoms, one expanded symptom, and four largely unchanged symptoms specified in the previous criteria.
Criterion E (formerly "D"), which focuses on increased arousal and reactivity, contains one modestly revised, one entirely new, and four unchanged symptoms.
Criterion F (formerly "E") still requires duration of symptoms to have been at least one month.
Criterion G (formerly "F") stipulates symptom impact ("disturbance") in the same way as before.
The "acute" vs "delayed" distinction is dropped; the "delayed" specifier is considered appropriate if clinical symptom onset is no sooner than 6 months after the traumatic event(s).
"Developmental trauma disorder", a proposed new diagnosis, was still under discussion at the time of the draft publication.
Public policy response
,
Washington, D.C.]]
In recent history, catastrophes (by human means or not) such as the 2004 Indian Ocean tsunami may have caused PTSD in many survivors and rescue workers. Today relief workers from organizations such as the Red Cross and the Salvation Army provide counseling after major disasters as part of their standard procedures to curb severe cases of posttraumatic stress disorder.
United States
A review of the provision of compensation to veterans for PTSD by the United States Department of Veterans Affairs began in 2005 after the VA had noted a 30% increase in PTSD claims in recent years. This led to a backlash from veterans'-rights groups, and to some highly publicized suicides by veterans who feared losing their benefits, which in some cases constituted their only income. In response, on November 10, 2005, the Secretary of Veterans Affairs announced that "the Department of Veterans Affairs (VA) will not review the files of 72,000 veterans currently receiving disability compensation for posttraumatic stress disorder..."
The diagnosis of PTSD in U.S. military veterans has been a subject of some controversy due to uncertainties in objectively diagnosing PTSD in those who may have been exposed to trauma, and due to this diagnosis' association with some incidence of compensation-seeking behavior.
Many veterans of the wars in Iraq and Afghanistan returning home have faced significant physical, emotional and relational disruptions. In response, the United States Marine Corps has instituted programs to assist them in re-adjusting to civilian life, especially in their relationships with spouses and loved ones, to help them communicate better and understand what the other has gone through. Walter Reed Army Institute of Research (WRAIR) developed the Battlemind program to assist service members avoid or ameliorate PTSD and related problems.
Other countries
In the UK, there has been some controversy that National Health Service is dumping veterans on service charities like
Combat Stress.
Veterans Affairs Canada offers a new program that includes rehabilitation, financial benefits, job placement, health benefits program, disability awards and family support.
Management
Prevention and early intervention strategies
Modest benefits have been seen from early access to cognitive behavioral therapy, as well as from some medications such as
propranolol.
Critical incident stress management has been suggested as a means of preventing PTSD but subsequent studies suggest the likelihood of its producing
iatrogenic outcomes. A review of multiple studies confirmed the finding of no benefit to trauma survivors from single-session early-response interventions, as well as a failure of blanket multiple-session prevention interventions to yield a benefit to all participants (some were even harmed).
Early detection
The ability to prescreen individuals would be of great help in getting treatment to those who are at risk of PTSD prior to development of the syndrome. Several biological indicators have been identified that are related to later PTSD development. First, Delhanty found that higher response times and a smaller
hippocampal volume were identified as linked to later PTSD development. However, both of these indicators are relatively difficult to test for and need specialized tests and or equipment to identify. A blood biomarker is much easier to test for. Van Zuiden et al. found just such a biomarker when testing U.S. Army soldiers prior to deployment. They found that soldiers with more glucocorticoid receptors (GR) were more likely to be diagnosed with PTSD six months after deployment. However, higher GR levels have not been identified as a cause of PTSD, and may instead be an intermediator, or even an indicator that the individual has previously experienced traumatic events. There is a great deal of overlap between high GR levels and those who later are diagnosed with and without PTSD. Thus, the identification of high GR is simply a vulnerability indicator at this time.
Delhanty for example were able to identify that the forensic exam given to victims after a rape was associated with PTSD.
Finally, global treatments attempt to avoid the problems of early detection by simply treating everyone involved. However, many studies
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), and many combinations of these procedures. A 2010 review disagrees that these treatments have proven efficacy, and points out methodological flaws in the studies and previous meta-analyses.
EMDR or trauma-focused cognitive behavioral therapy (TFCBT) was recommended as first-line treatments for trauma victims in a 2007 review; however, "the evidence base [for EMDR] was not as strong as that for TFCBT ... Furthermore, there was limited evidence that TFCBT and EMDR were superior to supportive/non-directive treatments, hence it is highly unlikely that their effectiveness is due to non-specific factors such as attention." 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.
Behavioral and Cognitive Behavioral therapy
Cognitive Behavioral Therapy (CBT) seeks to change the way a trauma victim feels and acts by changing the patterns of thinking and/or behavior responsible for negative emotions. CBT have been proven to be an effective treatment for
PTSD, and is currently considered the standard of care for PTSD by the
United States Department of Defense In CBT, individuals learn to identify thoughts that make them feel afraid or upset, and replace them with less distressing thoughts. The goal is to understand how certain thoughts about cause PTSD-related stress.
Recent research on contextually based third-generation behavior therapies suggests that they may produce results comparable to some of the better validated therapies. 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. Indeed, the success of exposure-based therapies has raised the question of whether exposure is a necessary ingredient in the treatment of PTSD. Some organizations have endorsed the need for exposure. 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 specifically targeted as a treatment for PTSD. Based on the evidence of controlled research, the
American Psychiatric Association and the United States Department of Veterans Affairs and Department of Defense have placed EMDR in the highest category of effectiveness and research support in the treatment of trauma. Several international bodies have made similar recommendations. However, some reviewers no longer believe that the eye movements assist in recovery, proposing instead that the review of and engagement with memories, processing of cognitions, and rehearsal of coping skills are the psychotherapeutically effective components of the procedure.
Interpersonal psychotherapy
Other approaches, particularly 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
A variety of medications has shown adjunctive benefit in reducing PTSD symptoms, but "there is no clear drug treatment for PTSD". Positive symptoms (re-experiencing, hypervigilance, increased arousal) generally respond better to medication than negative symptoms (avoidance, withdrawal), and it is recommended that any drug trial last for at least 6–8 weeks. SSRIs for which there are data to support use include:
citalopram,
escitalopram,
fluoxetine,
paroxetine, and
sertraline.
Among the anti-depressants described in this section, bupropion and venlafaxine have the lowest patient drop-out rates. Sertraline, fluoxetine, and nefazodone have a modestly higher drop-out rate (~15%), and the heterocyclics and paroxetine have the highest rates (~20%+). Where drop-out is caused or feared because of medication side-effects, it should be remembered that most patients do not experience such side-effects.
Alpha-adrenergic antagonists. Prazosin ("Minipress"), in a small study of combat veterans, has shown substantial benefit in relieving or reducing nightmares. Clonidine ("Catapres") can be helpful with startle, hyperarousal, and general autonomic hyperexcitability. as well as mood or aggression. Topiramate ("Topamax") Valproic acid ("Depakene") and has shown reduction of symptoms of irritability, aggression, and impulsiveness, and in reducing flashbacks. Nefazodone ("Serzone") can be effective with sleep disturbance symptoms, and with secondary depression, anxiety, and sexual dysfunction symptoms. hyperarousal, and sleep disturbance.
Glucocorticoids. Additionally, post-stress high dose corticosterone administration was recently found to reduce 'PTSD-like' behaviors in a rat model of PTSD. In this study, corticosterone impaired memory performance, suggesting that it may reduce risk for PTSD by interfering with consolidation of traumatic memories. The neurodegenerative effects of the glucocorticoids, however, may prove this treatment counterproductive.
Heterocyclic / Tricyclic anti-depressants anti-depressants. Amitriptyline ("Elavil") has shown benefit for positive distress symptoms, and for avoidance, and Imipramine ("Tofranil") has shown benefit for intrusive symptoms. and Israel.
Symptom prevention: potentially useful medication classes
Some medications have shown benefit in preventing PTSD or reducing its incidence, when given in close proximity to a traumatic event. These medications include:
Alpha-adrenergic antagonists. Anecdotal report of success in using clonidine ("Catapres") to reduce traumatic stress symptoms suggests that it may have benefit in preventing PTSD.
Beta blockers. Propranolol ("Inderal"), similarly to clonidine, may be useful if there are significant symptoms of "over-arousal". These may inhibit the formation of traumatic memories by blocking adrenaline's effects on the amygdala.
Glucocorticoids. There is some evidence suggesting that administering glucocorticoids immediately after a traumatic experience may help prevent PTSD. Several studies have shown that individuals who receive high doses of hydrocortisone for treatment of septic shock, or following surgery, have a lower incidence and fewer symptoms of PTSD.
Opiates. In a retrospective analysis of combat injury field data for US troops in Iraq, it was found that those who received morphine in the early stages of their treatment had a significantly lower rate of subsequent PTSD, when compared with those who did not receive morphine at that time.
Medications by symptom group affected
Medications can affect one or more of the symptoms, in one or more of the three major symptom classes
Some medications can also help with symptoms which may occur secondary to PTSD.
Benzodiazepines are risky in several ways. They can be especially addictive when PTSD is present, and this is especially true with the fast-acting ones. Dis-inhibition upon initiation of treatment is another risk with this medication class. Finally, termination of the drug can be especially difficult.]]
There is debate over the rates of PTSD found in populations, but despite changes in diagnosis and the criteria used to define PTSD between 1997 and 2007, epidemiological rates have not changed significantly.
International PTSD rates
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 USA, 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.
{| class="wikitable" border="1"
|+ Age-standardized Disability-adjusted life year (DALY) rates for PTSD, per 100,000 inhabitants, in 25 most populous countries, The National Vietnam Veterans' Readjustment Study (NVVRS) found 15.2% of male and 8.5% of female Vietnam Vets to suffer from current PTSD at the time of the study. Life-Time prevalence of PTSD was 30.9% for males and 26.9% for females. In a reanalysis of the NVVRS data, along with analysis of the data from the Matsunaga Vietnam Veterans Project, Schnurr, Lunney, Sengupta, and Waelde found that, contrary to the initial analysis of the NVVRS data, a large majority of Vietnam veterans suffered from PTSD symptoms (but not the disorder itself). Four out of five reported recent symptoms when interviewed 20–25 years after Vietnam. and wild elephants suffering from posttraumatic stress reactions, the latter from seeing members of their herd shot by hunters. Service dogs used overseas in the military have been said to develop posttraumatic stress after witnessing war.
History
Earliest reports
Reports of battle-associated stress reactions appear as early as the 6th century BC/BCE. One of the first descriptions of PTSD was made by the Greek historian
Herodotus. In 490 BC/BCE he described, during the
Battle of Marathon, an Athenian soldier who suffered no injury from war but became permanently blind after witnessing the death of a fellow soldier.
Modern recognition in military settings
In the early 19th century military medical doctors started diagnosing soldiers with "exhaustion" after the stress of battle. This "exhaustion" was characterized by mental shutdown due to individual or group trauma. Soldiers during the 19th century were not supposed to be scared or show any fear in the midst of battle. The only treatment for this "exhaustion" was to bring the afflicted to the back for a bit then send them back into battle. During the intense and frequently repeated stress, the soldiers became fatigued as a part of their body's natural shock reaction.
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."
Although PTSD-like symptoms have also been recognized in combat veterans of many military conflicts since, the modern understanding of PTSD dates from the 1970s, largely as a result of the problems that were still being experienced by US military veterans of the war in Vietnam.
Early in 1978, the term was used in a working group finding presented to the Committee of Reactive Disorders.[ The term was formally recognized in 1980.][ (In the authoritative DSM-IV, the spelling "posttraumatic stress disorder" is used. Elsewhere, "posttraumatic" is often rendered as two words — "post-traumatic stress disorder" or "post traumatic stress disorder" — especially in less formal writing on the subject.)
]
See also
References
External links
Management of PTSD in adults and children by the National Institute for Health and Clinical Excellence (UK)
Practice guidelines from the American Psychiatric Association
Post Traumatic Stress Disorder Information Resource from The University of Queensland School of Medicine
Resources for Parents of Children with PTSD from The Children's Hospital of Philadelphia
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