What makes UpToDate so powerful?

  • over 11000 topics
  • 22 specialties
  • 5,700 physician authors
  • evidence-based recommendations
See more sample topics
Find Patient Print
0 Find synonyms

Find synonyms Find exact match

Posttraumatic stress disorder in adults: Epidemiology, pathophysiology, clinical manifestations, course, assessment, and diagnosis
Official reprint from UpToDate®
www.uptodate.com ©2018 UpToDate, Inc. and/or its affiliates. All Rights Reserved.
The content on the UpToDate website is not intended nor recommended as a substitute for medical advice, diagnosis, or treatment. Always seek the advice of your own physician or other qualified health care professional regarding any medical questions or conditions. The use of this website is governed by the UpToDate Terms of Use ©2018 UpToDate, Inc.
Posttraumatic stress disorder in adults: Epidemiology, pathophysiology, clinical manifestations, course, assessment, and diagnosis
View in Chinese
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Dec 2017. | This topic last updated: Nov 02, 2017.

INTRODUCTION — Posttraumatic stress disorder (PTSD) has been described as "the complex somatic, cognitive, affective, and behavioral effects of psychological trauma" [1]. PTSD is characterized by intrusive thoughts, nightmares and flashbacks of past traumatic events, avoidance of reminders of trauma, hypervigilance, and sleep disturbance, all of which lead to considerable social, occupational, and interpersonal dysfunction.

The diagnosis of PTSD can be challenging because of the heterogeneity of the presentation and resistance on the part of the patient to discuss past trauma. Another complicating factor is that traumatic events are associated with a range of other psychopathology including depression and anxiety disorders. Patients exposed to multiple traumatic events may be mistakenly diagnosed with PTSD rather than another primary disorder.

The epidemiology, pathophysiology, clinical manifestations, course, and diagnosis of PTSD are discussed here. Pharmacotherapy and psychotherapy of PTSD are discussed separately. The epidemiology, pathophysiology, clinical manifestations, diagnosis, and treatment of acute stress disorder are also discussed separately. (See "Pharmacotherapy for posttraumatic stress disorder in adults" and "Psychotherapy for posttraumatic stress disorder in adults" and "Dissociative aspects of posttraumatic stress disorder: Epidemiology, clinical manifestations, assessment, and diagnosis" and "Acute stress disorder in adults: Epidemiology, pathogenesis, clinical manifestations, course, and diagnosis" and "Treatment of acute stress disorder in adults".)

EPIDEMIOLOGY — Many different types of trauma have been found to result in PTSD, including those listed below. Many of these events are common, resulting in a large number of affected individuals. An analysis from a survey of a large, representative community-based sample in 24 countries estimated the conditional probability of PTSD for 29 types of traumatic events [2]:

Sexual relationship violence – 33 percent (eg, rape, childhood sexual abuse, intimate partner violence).

Interpersonal-network traumatic experiences – 30 percent (eg, unexpected death of a loved one, life-threatening illness of a child, other traumatic event of a loved one).

Interpersonal violence – 12 percent (eg, childhood physical abuse or witnessing interpersonal violence, physical assault, or being threatened by violence).

Exposure to organized violence – 3 percent (eg, refugee, kidnapped, civilian in war zone).

Participation in organized violence – 11 percent (eg, combat exposure, witnessing death/serious injury or discovered dead bodies, accidentally or purposefully caused death or serious injury).

Other life-threatening traumatic events – 12 percent (eg, life-threatening motor vehicle collision, natural disaster, toxic chemical exposure).

Prevalence and susceptibility — The lifetime prevalence of PTSD ranges from 6.1 to 9.2 percent in national samples of the general adult population in the United States and Canada [3-6], with one-year prevalence rates of 3.5 to 4.7 percent [6,7]. As an example, in a United States sample of 5692 respondents, 82.7 percent were exposed to severe and potentially traumatic events, and 8.3 percent of the trauma exposed were diagnosed with lifetime PTSD. Further, among patients from a community primary care clinic, 65 percent reported a history of exposure to severe, potentially traumatic events; 12 percent went on to develop PTSD [5,8].

Lower prevalence rates, however, have been found outside of North America:

A World Health Organization study found a lifetime prevalence of PTSD in upper-middle income and lower-middle income countries of 2.3 and 2.1 percent respectively [5].

A national sample of 10,641 Australians found a lifetime prevalence of PTSD of 1.0 percent [9].

The higher rates of PTSD in North American samples compared with other countries are not well understood [8]. The likelihood of developing PTSD and the presentation of the disorder appear to be affected by a number of individual and societal factors discussed below [10-12].

Individual pretrauma risk factors for developing PTSD after a traumatic event include gender; age at trauma; race; lower education; lower socioeconomic status; being separated, divorced, or widowed; previous trauma; general childhood adversity; personal and family psychiatric history; reported childhood abuse; poor social support; and initial severity of reaction to the traumatic event [4,13-16].

The frequency with which PTSD occurs after a traumatic event has been found to be influenced by characteristics of the individual and the inciting event [17]. Intentional trauma has been found to have a greater association with PTSD than traumatic events that were unintentional/nonassaultive [2,18]. Women are four times more likely to develop PTSD than men, after adjusting for exposure to traumatic events [13]. The rates of PTSD are similar among men and women after events such as accidents (6.3 versus 8.8 percent), natural disasters (3.7 versus 5.4 percent), and sudden death of a loved one (12.6 versus 16.2 percent). The incidence of PTSD after rape is higher in men compared with women (65 versus 46 percent), even though women are more than 10 times as likely as men to be raped. The rate of PTSD is lower in men compared with women after events such as molestation (12.2 versus 26.5 percent) and physical assault (1.8 versus 21.3 percent).

Higher rates of PTSD have been found in population subgroups in the United States compared with the general population, including Native Americans living on reservations and refugees from countries where traumatic stress was endemic. In two large samples of Native Americans, lifetime prevalence of PTSD ranged from 14.2 to 16.1 percent [19]. In a systematic review of 19 studies of mental disorders among Native Americans in the United States, Canada, and Latin America, indigenous peoples had 1.4 greater odds of lifetime PTSD compared with nonindigenous [20]. Among Cambodian refugees, two decades after resettling in the United States, 62 percent met criteria for PTSD in the previous year [21].

Sexual assault — Sexual assault is the most frequent type of trauma experienced by women with PTSD [22,23]. In a nationally representative sample of 4008 women in the United States, the lifetime prevalence of PTSD was 12.3 percent. Of the women who had a history of PTSD, 32 percent had been raped and 31 percent experienced a sexual assault other than rape [22]. (See "Evaluation and management of adult and adolescent sexual assault victims".)

Mass conflict and displacement — A meta-analysis of 145 studies of 64,332 refugees and other conflict-affected individuals internationally found a mean PTSD prevalence rate of 30.6 percent (95% CI 26.3-35.2) [24]. Factors associated with higher PTSD rates included reported torture, cumulative exposure to potentially traumatic events, shorter time since conflict, and the assessed level of political terror.

Combat — PTSD occurring after combat injury appears to be strongly correlated with the extent of injury and with the occurrence and severity of traumatic brain injury [25]. PTSD typically develops over several months. Examples of study findings include:

The prevalence of PTSD was 4.2 percent at one month and 12.2 percent by four months postinjury in a study of soldiers hospitalized for war-related injuries [26]. Soldiers with a high severity of physical problems a month after injury were at greater risk of PTSD six months later, compared with those with lower physical problem severity (odds ratio 7.0, 95% CI 3.1-16.0). Almost one-half of soldiers with war-related mild traumatic brain injury (concussion syndrome) met criteria for PTSD.

In a study of 8621 deployed British military personnel [27], factors associated with a higher risk of developing PTSD included:

Experiencing a combat role in war (compared with deployment without combat)

Childhood adversity

Having left the service

Serious accident

A higher military rank was associated with a lower risk of developing PTSD.

In Canada, the prevalence of PTSD among Regular Force members who deployed in support of the mission in Afghanistan was 7.7 percent, compared with 3.2 percent of Regular Force personnel who did not deploy [28].

Experiencing traumatic brain injury during military deployment was a strong predictor of subsequent PTSD symptoms in a prospective, longitudinal study of 1648 United States Marine servicemen deployed in Iraq or Afghanistan [29,30]. Subjects were assessed prior to a seven-month deployment and again three to six months following their return to the United States.

Myocardial infarction — A meta-analysis of 24 observational studies including 2383 patients who experienced an acute coronary syndrome (ACS; ie, a myocardial infarction or unstable angina) found a prevalence rate of ACS-induced PTSD of 12 percent (95% CI 9-16 percent) [31]. Data from three studies of 609 patients that met quality criteria for the meta-analysis found that patients experiencing ACS-induced PTSD had a twofold risk of subsequent mortality or ACS recurrence (risk ratio = 2; 95% CI 1.69–2.37) compared with ACS patients who did not experience PTSD symptoms. (See "Overview of the non-acute management of ST elevation myocardial infarction" and "Overview of the non-acute management of unstable angina and non-ST elevation myocardial infarction".)

Stroke — Although less extensive than the literature on PTSD and acute coronary syndrome, there is a growing literature suggesting that up to one in four cases of stroke or transient ischemic attack may be associated with PTSD [32,33].

Intensive-care unit stay — A 2008 systematic analysis of 15 studies found the prevalence of PTSD in patients who survived intensive care unit (ICU) hospitalization to be approximately 20 percent [34]. A 2015 meta-analysis found pooled prevalences of clinically important PTSD symptoms after ICU discharge of 24 percent one to six months later and 22 percent 7 to 12 months later [35]. Risk factors for PTSD symptoms were benzodiazepine use, early memories of frightening ICU experiences, and pre-ICU comorbid psychopathology. Neither the severity of critical illness nor length of ICU stay were predictors of PTSD. PTSD symptoms were associated with poorer quality of life. (See "Overview of inpatient management in the adult trauma patient".)

Severity of physical injury — There has been some work suggesting that self-perceived fear of death during the traumatic event has been associated with PTSD [36]. Multiple studies have shown that a high heart rate (>95 beats per minute) at first presentation to emergency department is a risk factor for PTSD among those with physical injury [37]. Acute high levels of pain have been linked to PTSD among patients with severe physical injury [38]. There is a substantial body of evidence that PTSD and pain are often comorbid through mutual maintenance [39].

PATHOPHYSIOLOGY — While much of the pathophysiology of PTSD is unclear, interesting research findings are accruing. Studies using magnetic resonance imaging scans have shown that there is decreased volume of the hippocampus, left amygdala, and anterior cingulate cortex in patients with PTSD compared with matched controls [40,41]. Other reports have demonstrated increased central norepinephrine levels with down-regulated central adrenergic receptors [42], chronically decreased glucocorticoid levels with up-regulation of their receptors (possibly accounting for the anecdotal finding that there are more autoimmune diseases in these patients), and hemispheric lateralization in which there is a relative failure of left hemispheric function (possibly accounting for confusion related to time sequence of traumatic events) [43].

Researchers suspect that genetics may contribute to an individual's susceptibility to PTSD through an interaction with environmental factors [44,45]. However, research studies on the genetics of PTSD have generally been small and findings have been inconclusive [46]. As an example of a potential gene-environment interaction, the presence of one of four polymorphisms at the stress-related gene FKBP5 was found to be associated with an increased risk for PTSD in patients with a history of child abuse, but not in patients without history of child abuse [47].

Previous exposure to trauma appears to increase the risk of developing PTSD with subsequent traumatic events [48]. The mechanism by which this "sensitization" occurs is unclear. A study of severely injured accident victims who were healthy before experiencing trauma found that the incidence of PTSD was low [49].

CLINICAL MANIFESTATIONS — Most individuals who experience trauma react to some degree when experiencing reminders of the trauma. Patients with PTSD, however, experience marked cognitive, affective, and behavioral responses to stimuli, leading to flashbacks, severe anxiety, and fleeing or combative behavior. These individuals compensate for such intense arousal by attempting to avoid experiences that may begin to elicit symptoms; this can result in emotional numbing, diminished interest in everyday activities, and, in the extreme, may result in detachment from others.

There are important distinguishing characteristics of PTSD symptoms in patients who experienced most of their trauma in childhood (eg, physical and sexual abuse) [1]. Compared with controls, these individuals often show greater difficulty with affect regulation (eg, unmodulated anger), and often demonstrate more dissociation, somatic symptoms, self-destructive behavior, and suicidal behavior.

Co-occurring conditions

Psychiatric – Psychiatric comorbidity is high in patients with PTSD. The National Comorbidity Survey data suggest that 16 percent have one coexisting psychiatric disorder, 17 percent have two psychiatric disorders, and 50 percent have three or more [18]. Depressive disorders, anxiety disorders, and substance abuse are two to four times more prevalent in patients with PTSD; substance abuse is often due to the patient's attempts to self-medicate symptoms [4,18]. Approximately 20 percent of people with PTSD have reported use of alcohol or other substances to reduce tension [50].

Patients with PTSD have been found to have increased rates of co-occurring borderline personality disorder and antisocial personality disorder compared with the general population. PTSD was associated with increased odds of having lifetime and past-year antisocial personality disorder (odds ratios range from 1.8 to 3.3) in a nationally representative United States sample [6,51]. It can be difficult in some cases for clinicians to differentiate PTSD symptoms in patients presenting with borderline personality disorder (BPD). A large United States sample demonstrated that 24 percent of patients with PTSD had a diagnosis of BPD. Compared with people who had PTSD alone or BPD alone, those with comorbid PTSD and BPD had more comorbidity, increased likelihood of suicide attempts, and high levels of traumatic events in childhood [52].

Studies suggest that somatic symptoms are as much as 90 times more likely in patients with PTSD than in patients without the disorder [53]. (See "Somatization: Epidemiology, pathogenesis, clinical features, medical evaluation, and diagnosis".)

Medical – Research evidence suggests that exposure to traumatic events and PTSD are associated with a range of physical health conditions including bone and joint, neurologic, cardiovascular, respiratory, and metabolic disease (odds ratios ranging from 1.5 to 3.0) [54-56].

As an example, in a population-based study of 3171 community respondents, PTSD was associated with increased risks for angina (odds ratio 2.4, 95% CI 1.3-4.5), heart failure (odds ratio 3.4, 95% CI 1.9-6.0), bronchitis, asthma, liver, and peripheral artery disease (odds ratio range = 2.5, 3.1) after adjusting for sociodemographic factors, smoking, body mass index, blood pressure, depression, and alcohol use disorders [54].

Other studies have found that PTSD is associated with higher rates of:

Autoimmune and endocrine disorders [57]

Obesity [58], food addiction [59], and type II diabetes [60] in women

Alzheimer’s and vascular dementia (modest associations) [61]

A systematic review found associations between PTSD and possible biological markers of accelerated aging, as well as with earlier mortality (average hazard ratio 1.29) [62].

Traumatic brain injury (TBI) and PTSD have high rates of co-occurrence among civilians and, particularly, among soldiers with combat-related TBI [63]. As an example, 11 percent of American soldiers returning from combat in Iraq and Afghanistan were reported to screen positive for PTSD in 2008. Among returning soldiers with mild TBI, 62 percent screened positive for PTSD [64]. A study in United States soldiers demonstrated that deployment-related TBI was independently associated with an increased risk for PTSD during the one-year follow-up period [30].

COURSE — Most individuals who develop PTSD experience its onset within a few months of the traumatic event. However, epidemiologic studies have found that approximately 25 percent experience a delayed onset after six months or more [65].

PTSD is commonly a chronic condition, with only one-third of patients recovering at one-year follow-up and one-third still symptomatic ten years after the exposure to the trauma [18].

Functioning — Individuals with one or more PTSD symptoms are more likely to experience occupational problems, have poorer social supports, and have more disability than controls [66]. PTSD may increase the risk for attempted suicide [67,68]. Individuals with PTSD have higher rates of problems in intimate relationships, including marital difficulties, compared with people without PTSD [66,69].

Individual psychotherapy has been found to improve overall psychosocial functioning [70]. Accumulating evidence suggests that cognitive-behavioral conjoint therapy for individuals with PTSD and their partners is an effective strategy for reducing PTSD symptom severity and increasing intimate relationship satisfaction [71]. (See "Psychotherapy for posttraumatic stress disorder in adults", section on 'Couples therapy'.)

SCREENING — Soldiers, veterans, and traumatically injured civilians should be systematically screened for PTSD; however, screening is likely to lead to better clinical outcomes only when coupled with high quality mental health services [72]. Primary care patients presenting with new anxiety, fear, or insomnia should be screened for PTSD and a history of trauma [73]. Others in which PTSD would be a diagnostic consideration include patients with anxiety symptoms, social isolation, increased substance abuse (alcohol and/or tobacco), or attempts at distraction through excessive work. (See "Pharmacotherapy for posttraumatic stress disorder in adults" and "Psychotherapy for posttraumatic stress disorder in adults".)

ASSESSMENT — Patients with possible PTSD should receive a comprehensive psychiatric assessment. Examples of questions a clinician can ask to elicit symptoms of PTSD are provided below.

How do you feel when you recall the event?

Do you experience dreams or flashbacks about it?

Do you find yourself avoiding people or activities you associate with the event?

Do you find yourself forgetting occurrences from that period?

Do you find yourself looking carefully around when you are in a public place?

Patients need to be asked specific questions about their traumatic experience(s) to differentiate PTSD from other psychiatric disorders. These questions should be asked with sensitivity. Patients are often reluctant to discuss past traumatic events because of guilt, embarrassment, or discomfort inherent in revisiting painful memories.

Patients may minimize their symptoms of PTSD. Some patients may feel that past trauma has little or no effect on present symptoms. Military personnel in the United States have been reported to be reluctant to disclose PTSD symptoms due to stigmatization and fear of professional repercussions [74].

Patients diagnosed with PTSD should also be assessed for suicidal or parasuicidal ideation or acts and co-occurring psychiatric conditions, substance use disorders, and medical conditions.

Assessment tools — The four-item Primary Care PTSD screening tool has demonstrated good reliability and validity (table 1) [75].

The PTSD checklist (PCL-5), a 20-item self-report measure, can be used to screen patients for PTSD and monitor the severity of symptoms over time [76,77]. A single version of the PCL-5 replaced separate versions for civilian and military populations. The psychometric properties of the PCL-5 show high rates of sensitivity and specificity. A score of 38 (out of a maximum score of 80) is associated with a diagnosis of PTSD (table 2).

The Clinician-Administered PTSD Scale (CAPS) is a 30-item, structured interview that can be used to make diagnoses of PTSD in the past week, past month, or lifetime, as well as to assess the severity of PTSD symptoms.

DIAGNOSIS — A diagnosis of PTSD is made for patients older than age six years who meet all of the following DSM-5 criteria [78]:

A. Exposure to actual or threatened death, serious injury, or sexual violence in one (or more) of the following ways:

1. Directly experiencing the traumatic event(s).

2. Witnessing, in person, the event(s) as it occurred to others.

3. Learning that the traumatic event(s) occurred to a close family member or close friend. In cases of actual or threatened death of a family member or friend, the event(s) must have been violent or accidental.

4. Experiencing repeated or extreme exposure to aversive details of the traumatic event(s) (eg, first responders collecting human remains; police officers repeatedly exposed to details of child abuse).

Note: Criterion A4 does not apply to exposure through electronic media, television, movies, or pictures, unless this exposure is work related.

B. Presence of one (or more) of the following intrusion symptoms associated with the traumatic event(s), beginning after the traumatic event(s) occurred:

1. Recurrent, involuntary, and intrusive distressing memories of the traumatic event(s).

Note: In children older than six years, repetitive play may occur in which themes or aspects of the traumatic event(s) are expressed.

2. Recurrent distressing dreams in which the content and/or affect of the dream are related to the traumatic event(s).

Note: In children, there may be frightening dreams without recognizable content.

3. Dissociative reactions (eg, flashbacks) in which the individual feels or acts as if the traumatic event(s) were recurring. (Such reactions may occur on a continuum, with the most extreme expression being a complete loss of awareness of present surroundings.)

Note: In children, trauma-specific reenactment may occur in play.

4. Intense or prolonged psychological distress at exposure to internal or external cues that symbolize or resemble an aspect of the traumatic event(s).

5. Marked physiological reactions to internal or external cues that symbolize or resemble an aspect of the traumatic event(s).

C. Persistent avoidance of stimuli associated with the traumatic event(s), beginning after the traumatic event(s) occurred, as evidenced by one or both of the following:

1. Avoidance of or efforts to avoid distressing memories, thoughts, or feelings about or closely associated with the traumatic event(s).

2. Avoidance of or efforts to avoid external reminders (people, places, conversations, activities, objects, situations) that arouse distressing memories, thoughts, or feelings about or closely associated with the traumatic event(s).

D. Negative alterations in cognitions and mood associated with the traumatic event(s), beginning or worsening after the traumatic event(s) occurred, as evidenced by two (or more) of the following:

1. Inability to remember an important aspect of the traumatic event(s) (typically due to dissociative amnesia and not to other factors such as head injury, alcohol, or drugs).

2. Persistent and exaggerated negative beliefs or expectations about oneself, others, or the world, for example:

-"I am bad''

-"No one can be trusted''

-"The world is completely dangerous"

-"My whole nervous system is permanently ruined"

3. Persistent, distorted cognitions about the cause or consequences of the traumatic event(s) that lead the individual to blame himself/herself or others.

4. Persistent negative emotional state (eg, fear, horror, anger, guilt, or shame).

5. Markedly diminished interest or participation in significant activities.

6. Feelings of detachment or estrangement from others.

7. Persistent inability to experience positive emotions (eg, inability to experience happiness, satisfaction, or loving feelings).

E. Marked alterations in arousal and reactivity associated with the traumatic event(s), beginning or worsening after the traumatic event(s) occurred, as evidenced by two (or more) of the following:

1. Irritable behavior and angry outbursts (with little or no provocation) typically expressed as verbal or physical aggression toward people or objects.

2. Reckless or self-destructive behavior.

3. Hypervigilance.

4. Exaggerated startle response.

5. Problems with concentration.

6. Sleep disturbance (eg, difficulty falling or staying asleep or restless sleep).

F. Duration of the disturbance (Criteria B, C, D, and E) is more than one month.

G. The disturbance causes clinically significant distress or impairment in social, occupational, or other important areas of functioning.

H. The disturbance is not attributable to the physiological effects of a substance (eg, medication, alcohol) or another medical condition.

Subtypes — Specify whether presentation of disorder is:

With dissociative symptoms — The individual's symptoms meet the criteria for posttraumatic stress disorder, and in addition, in response to the stressor, the individual experiences persistent or recurrent symptoms of either of the following:

1. Depersonalization – Persistent or recurrent experiences of feeling detached from, and as if one were an outside observer of, one's mental processes or body (eg, feeling as though one were in a dream; feeling a sense of unreality of self or body or of time moving slowly).

2. Derealization – Persistent or recurrent experiences of unreality of surroundings (eg, the world around the individual is experienced as unreal, dreamlike, distant, or distorted).

Note: To use this subtype, the dissociative symptoms must not be attributable to the physiologic effects of a substance (eg, blackouts, behavior during alcohol intoxication) or another medical condition (eg, complex partial seizures).

With delayed expression — If the full diagnostic criteria are not met until at least six months after the event (although the onset and expression of some symptoms may be immediate).

Revisions to diagnostic criteria for PTSD from DSM-IV to DSM-5 include [78,79]:

The stressor criterion (Criterion A) in DSM-5 requires being explicit as to whether the traumatic events were experienced directly, witnessed, or experienced indirectly.

The criterion regarding the patient’s subjective reaction to the traumatic event (Criterion A2) in DSM-IV was eliminated in DSM-5.

The categories of presenting symptoms were revised to intrusion, negative alterations in mood and cognitions, avoidance, and arousal.

Two new symptoms were added to criteria E (marked alterations in arousal and reactivity associated with traumatic event(s), including irritable behavior and angry outbursts and reckless or self-destructive behavior).

Differentiating acute stress disorder — Individuals presenting with symptoms of posttraumatic stress and functional impairment after a highly traumatic event are diagnosed as having acute stress disorder (ASD) for the first 30 days following the event. Most people recover completely within this period. For those who remain symptomatic (at the threshold established by DSM-5 criteria) after 30 days, their diagnosis is then reclassified as PTSD. (See "Acute stress disorder in adults: Epidemiology, pathogenesis, clinical manifestations, course, and diagnosis".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, “The Basics” and “Beyond the Basics.” The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on “patient info” and the keyword(s) of interest.)

Basics topic (see "Patient education: Post-traumatic stress disorder (The Basics)")


The one-year prevalence of DSM-IV posttraumatic stress disorder (PTSD) has been found to range from 1 to 6 percent in the general adult population samples across the world. (See 'Epidemiology' above.)

Many different types of trauma can result in PTSD, including military combat, sexual or physical assault, disasters, childhood sexual abuse, sudden death of a loved one, severe physical injury or sudden-onset medical illness, and intensive care unit hospitalization. (See 'Epidemiology' above.)

The pathophysiology of PTSD is not well understood. However, differences in neuroanatomy, neurotransmitters, and brain functioning have been found in individuals with the disorder. (See 'Pathophysiology' above.)

Individuals with PTSD experience marked cognitive, affective, and behavioral responses to stimuli reminding them of trauma they experienced, eg, flashbacks, severe anxiety, and fleeing or combative behavior. They compensate for this intense arousal through avoidance, emotional numbing, and diminished interest in people and activities. (See 'Clinical manifestations' above.)

PTSD is commonly accompanied by comorbid psychiatric conditions, including depression, substance use disorders, and somatic symptoms. (See 'Co-occurring conditions' above.)

Military, veterans, indigenous, and refugee groups and traumatically injured civilians should be systematically screened for PTSD; however, screening is only effective when coupled with high quality mental health services [72]. Primary care patients presenting with new anxiety, fear, or insomnia should be screened for PTSD and a history of trauma [73]. (See 'Screening' above.)

The four-item Primary Care PTSD measure and the Posttraumatic Stress Disorder Checklist have demonstrated good reliability and validity for screening for PTSD.

Diagnostic criteria for PTSD include: experiencing or witnessing a severe, traumatic event resulting in symptoms in each of four categories (intrusion, negative alteration in mood and cognitions, avoidance, and arousal); social or occupational impairment; and symptoms and impairment lasting at least one month after the trauma. (See 'Diagnosis' above.)

A diagnosis of PTSD is made only after a month has passed since the traumatic event. Prior to that time, patients with PTSD-like symptoms and functional impairment are diagnosed with acute stress disorder. (See 'Diagnosis' above and "Acute stress disorder in adults: Epidemiology, pathogenesis, clinical manifestations, course, and diagnosis".)

ACKNOWLEDGMENT — We are saddened by the death of Wayne Katon, MD, who passed away in March 2015. UpToDate wishes to acknowledge Dr. Katon's past work as an author for this topic. We would also like to acknowledge Paul Ciechanowski, MD, who contributed to earlier versions of this topic.

Use of UpToDate is subject to the  Subscription and License Agreement.


  1. van der Kolk BA, Pelcovitz D, Roth S, et al. Dissociation, somatization, and affect dysregulation: the complexity of adaptation of trauma. Am J Psychiatry 1996; 153:83.
  2. Kessler RC, Rose S, Koenen KC, et al. How well can post-traumatic stress disorder be predicted from pre-trauma risk factors? An exploratory study in the WHO World Mental Health Surveys. World Psychiatry 2014; 13:265.
  3. Kessler RC, Berglund P, Demler O, et al. Lifetime prevalence and age-of-onset distributions of DSM-IV disorders in the National Comorbidity Survey Replication. Arch Gen Psychiatry 2005; 62:593.
  4. Van Ameringen M, Mancini C, Patterson B, Boyle MH. Post-traumatic stress disorder in Canada. CNS Neurosci Ther 2008; 14:171.
  5. Koenen KC, Ratanatharathorn A, Ng L, et al. Posttraumatic stress disorder in the World Mental Health Surveys. Psychol Med 2017; 47:2260.
  6. Goldstein RB, Smith SM, Chou SP, et al. The epidemiology of DSM-5 posttraumatic stress disorder in the United States: results from the National Epidemiologic Survey on Alcohol and Related Conditions-III. Soc Psychiatry Psychiatr Epidemiol 2016; 51:1137.
  7. Kessler RC, Chiu WT, Demler O, et al. Prevalence, severity, and comorbidity of 12-month DSM-IV disorders in the National Comorbidity Survey Replication. Arch Gen Psychiatry 2005; 62:617.
  8. Stein MB, McQuaid JR, Pedrelli P, et al. Posttraumatic stress disorder in the primary care medical setting. Gen Hosp Psychiatry 2000; 22:261.
  9. Creamer M, Burgess P, McFarlane AC. Post-traumatic stress disorder: findings from the Australian National Survey of Mental Health and Well-being. Psychol Med 2001; 31:1237.
  10. Stein DJ, Seedat S, Iversen A, Wessely S. Post-traumatic stress disorder: medicine and politics. Lancet 2007; 369:139.
  11. Kroll J. Posttraumatic symptoms and the complexity of responses to trauma. JAMA 2003; 290:667.
  12. Sareen J, Erickson J, Medved MI, et al. Risk factors for post-injury mental health problems. Depress Anxiety 2013; 30:321.
  13. Vieweg WV, Julius DA, Fernandez A, et al. Posttraumatic stress disorder: clinical features, pathophysiology, and treatment. Am J Med 2006; 119:383.
  14. Liebschutz J, Saitz R, Brower V, et al. PTSD in urban primary care: high prevalence and low physician recognition. J Gen Intern Med 2007; 22:719.
  15. Bisson JI. Post-traumatic stress disorder. BMJ 2007; 334:789.
  16. Brewin CR, Andrews B, Valentine JD. Meta-analysis of risk factors for posttraumatic stress disorder in trauma-exposed adults. J Consult Clin Psychol 2000; 68:748.
  17. Yehuda R. Post-traumatic stress disorder. N Engl J Med 2002; 346:108.
  18. Kessler RC, Sonnega A, Bromet E, et al. Posttraumatic stress disorder in the National Comorbidity Survey. Arch Gen Psychiatry 1995; 52:1048.
  19. Beals J, Manson SM, Whitesell NR, et al. Prevalence of DSM-IV disorders and attendant help-seeking in 2 American Indian reservation populations. Arch Gen Psychiatry 2005; 62:99.
  20. Kisely S, Alichniewicz KK, Black EB, et al. The prevalence of depression and anxiety disorders in indigenous people of the Americas: A systematic review and meta-analysis. J Psychiatr Res 2017; 84:137.
  21. Marshall GN, Schell TL, Elliott MN, et al. Mental health of Cambodian refugees 2 decades after resettlement in the United States. JAMA 2005; 294:571.
  22. Resnick HS, Kilpatrick DG, Dansky BS, et al. Prevalence of civilian trauma and posttraumatic stress disorder in a representative national sample of women. J Consult Clin Psychol 1993; 61:984.
  23. Chivers-Wilson KA. Sexual assault and posttraumatic stress disorder: a review of the biological, psychological and sociological factors and treatments. Mcgill J Med 2006; 9:111.
  24. Steel Z, Chey T, Silove D, et al. Association of torture and other potentially traumatic events with mental health outcomes among populations exposed to mass conflict and displacement: a systematic review and meta-analysis. JAMA 2009; 302:537.
  25. Grieger TA, Cozza SJ, Ursano RJ, et al. Posttraumatic stress disorder and depression in battle-injured soldiers. Am J Psychiatry 2006; 163:1777.
  26. Hoge CW, McGurk D, Thomas JL, et al. Mild traumatic brain injury in U.S. Soldiers returning from Iraq. N Engl J Med 2008; 358:453.
  27. Jones M, Sundin J, Goodwin L, et al. What explains post-traumatic stress disorder (PTSD) in UK service personnel: deployment or something else? Psychol Med 2013; 43:1703.
  28. Patten SB. Mental Health in the Canadian Armed Forces: New Data, New Answers, and New Questions. Can J Psychiatry 2016; 61:4S.
  29. Yurgil KA, Barkauskas DA, Vasterling JJ, et al. Association between traumatic brain injury and risk of posttraumatic stress disorder in active-duty Marines. JAMA Psychiatry 2014; 71:149.
  30. Stein MB, Kessler RC, Heeringa SG, et al. Prospective longitudinal evaluation of the effect of deployment-acquired traumatic brain injury on posttraumatic stress and related disorders: results from the Army Study to Assess Risk and Resilience in Servicemembers (Army STARRS). Am J Psychiatry 2015; 172:1101.
  31. Edmondson D, Richardson S, Falzon L, et al. Posttraumatic stress disorder prevalence and risk of recurrence in acute coronary syndrome patients: a meta-analytic review. PLoS One 2012; 7:e38915.
  32. Edmondson D, Richardson S, Fausett JK, et al. Prevalence of PTSD in Survivors of Stroke and Transient Ischemic Attack: A Meta-Analytic Review. PLoS One 2013; 8:e66435.
  33. Garton AL, Sisti JA, Gupta VP, et al. Poststroke post-traumatic stress disorder: A review. Stroke 2017; 48:507.
  34. Davydow DS, Gifford JM, Desai SV, et al. Posttraumatic stress disorder in general intensive care unit survivors: a systematic review. Gen Hosp Psychiatry 2008; 30:421.
  35. Parker AM, Sricharoenchai T, Raparla S, et al. Posttraumatic stress disorder in critical illness survivors: a metaanalysis. Crit Care Med 2015; 43:1121.
  36. Holbrook TL, Hoyt DB, Stein MB, Sieber WJ. Perceived threat to life predicts posttraumatic stress disorder after major trauma: risk factors and functional outcome. J Trauma 2001; 51:287.
  37. Zatzick DF, Russo J, Pitman RK, et al. Reevaluating the association between emergency department heart rate and the development of posttraumatic stress disorder: A public health approach. Biol Psychiatry 2005; 57:91.
  38. Norman SB, Stein MB, Dimsdale JE, Hoyt DB. Pain in the aftermath of trauma is a risk factor for post-traumatic stress disorder. Psychol Med 2008; 38:533.
  39. Asmundson GJ, Coons MJ, Taylor S, Katz J. PTSD and the experience of pain: research and clinical implications of shared vulnerability and mutual maintenance models. Can J Psychiatry 2002; 47:930.
  40. Bremner JD, Randall P, Scott TM, et al. MRI-based measurement of hippocampal volume in patients with combat-related posttraumatic stress disorder. Am J Psychiatry 1995; 152:973.
  41. Karl A, Schaefer M, Malta LS, et al. A meta-analysis of structural brain abnormalities in PTSD. Neurosci Biobehav Rev 2006; 30:1004.
  42. Geracioti TD Jr, Baker DG, Ekhator NN, et al. CSF norepinephrine concentrations in posttraumatic stress disorder. Am J Psychiatry 2001; 158:1227.
  43. van der Kolk BA. The psychobiology of posttraumatic stress disorder. J Clin Psychiatry 1997; 58 Suppl 9:16.
  44. Kilpatrick DG, Koenen KC, Ruggiero KJ, et al. The serotonin transporter genotype and social support and moderation of posttraumatic stress disorder and depression in hurricane-exposed adults. Am J Psychiatry 2007; 164:1693.
  45. Tian Y, Liu H, Guse L, et al. Association of Genetic Factors and Gene-Environment Interactions With Risk of Developing Posttraumatic Stress Disorder in a Case-Control Study. Biol Res Nurs 2015; 17:364.
  46. Broekman BF, Olff M, Boer F. The genetic background to PTSD. Neurosci Biobehav Rev 2007; 31:348.
  47. Binder EB, Bradley RG, Liu W, et al. Association of FKBP5 polymorphisms and childhood abuse with risk of posttraumatic stress disorder symptoms in adults. JAMA 2008; 299:1291.
  48. Breslau N, Chilcoat HD, Kessler RC, Davis GC. Previous exposure to trauma and PTSD effects of subsequent trauma: results from the Detroit Area Survey of Trauma. Am J Psychiatry 1999; 156:902.
  49. Schnyder U, Moergeli H, Klaghofer R, Buddeberg C. Incidence and prediction of posttraumatic stress disorder symptoms in severely injured accident victims. Am J Psychiatry 2001; 158:594.
  50. Leeies M, Pagura J, Sareen J, Bolton JM. The use of alcohol and drugs to self-medicate symptoms of posttraumatic stress disorder. Depress Anxiety 2010; 27:731.
  51. Sareen J, Stein MB, Cox BJ, Hassard ST. Understanding comorbidity of anxiety disorders with antisocial behavior: findings from two large community surveys. J Nerv Ment Dis 2004; 192:178.
  52. Pagura J, Stein MB, Bolton JM, et al. Comorbidity of borderline personality disorder and posttraumatic stress disorder in the U.S. population. J Psychiatr Res 2010; 44:1190.
  53. Davidson JR, Hughes D, Blazer DG, George LK. Post-traumatic stress disorder in the community: an epidemiological study. Psychol Med 1991; 21:713.
  54. Spitzer C, Barnow S, Völzke H, et al. Trauma, posttraumatic stress disorder, and physical illness: findings from the general population. Psychosom Med 2009; 71:1012.
  55. Gradus JL, Farkas DK, Svensson E, et al. Posttraumatic stress disorder and cancer risk: a nationwide cohort study. Eur J Epidemiol 2015; 30:563.
  56. Husarewycz MN, El-Gabalawy R, Logsetty S, Sareen J. The association between number and type of traumatic life experiences and physical conditions in a nationally representative sample. Gen Hosp Psychiatry 2014; 36:26.
  57. O'Donovan A, Cohen BE, Seal KH, et al. Elevated risk for autoimmune disorders in iraq and afghanistan veterans with posttraumatic stress disorder. Biol Psychiatry 2015; 77:365.
  58. Dedert EA, Calhoun PS, Watkins LL, et al. Posttraumatic stress disorder, cardiovascular, and metabolic disease: a review of the evidence. Ann Behav Med 2010; 39:61.
  59. Mason SM, Flint AJ, Roberts AL, et al. Posttraumatic stress disorder symptoms and food addiction in women by timing and type of trauma exposure. JAMA Psychiatry 2014; 71:1271.
  60. Roberts AL, Agnew-Blais JC, Spiegelman D, et al. Posttraumatic stress disorder and incidence of type 2 diabetes mellitus in a sample of women: a 22-year longitudinal study. JAMA Psychiatry 2015; 72:203.
  61. Greenberg MS, Tanev K, Marin MF, Pitman RK. Stress, PTSD, and dementia. Alzheimers Dement 2014; 10:S155.
  62. Lohr JB, Palmer BW, Eidt CA, et al. Is Post-Traumatic Stress Disorder Associated with Premature Senescence? A Review of the Literature. Am J Geriatr Psychiatry 2015; 23:709.
  63. Halbauer JD, Ashford JW, Zeitzer JM, et al. Neuropsychiatric diagnosis and management of chronic sequelae of war-related mild to moderate traumatic brain injury. J Rehabil Res Dev 2009; 46:757.
  64. Schneiderman AI, Braver ER, Kang HK. Understanding sequelae of injury mechanisms and mild traumatic brain injury incurred during the conflicts in Iraq and Afghanistan: persistent postconcussive symptoms and posttraumatic stress disorder. Am J Epidemiol 2008; 167:1446.
  65. Smid GE, Mooren TT, van der Mast RC, et al. Delayed posttraumatic stress disorder: systematic review, meta-analysis, and meta-regression analysis of prospective studies. J Clin Psychiatry 2009; 70:1572.
  66. Solomon SD, Davidson JR. Trauma: prevalence, impairment, service use, and cost. J Clin Psychiatry 1997; 58 Suppl 9:5.
  67. Wilcox HC, Storr CL, Breslau N. Posttraumatic stress disorder and suicide attempts in a community sample of urban american young adults. Arch Gen Psychiatry 2009; 66:305.
  68. Bernal M, Haro JM, Bernert S, et al. Risk factors for suicidality in Europe: results from the ESEMED study. J Affect Disord 2007; 101:27.
  69. Taft CT, Watkins LE, Stafford J, et al. Posttraumatic stress disorder and intimate relationship problems: a meta-analysis. J Consult Clin Psychol 2011; 79:22.
  70. Schnurr PP, Hayes AF, Lunney CA, et al. Longitudinal analysis of the relationship between symptoms and quality of life in veterans treated for posttraumatic stress disorder. J Consult Clin Psychol 2006; 74:707.
  71. Monson CM, Fredman SJ, Macdonald A, et al. Effect of cognitive-behavioral couple therapy for PTSD: a randomized controlled trial. JAMA 2012; 308:700.
  72. Zatzick D, Roy-Byrne P, Russo J, et al. A randomized effectiveness trial of stepped collaborative care for acutely injured trauma survivors. Arch Gen Psychiatry 2004; 61:498.
  73. Wilson JF. Posttraumatic stress disorder needs to be recognized in primary care. Ann Intern Med 2007; 146:617.
  74. Hoge CW, Castro CA, Messer SC, et al. Combat duty in Iraq and Afghanistan, mental health problems, and barriers to care. N Engl J Med 2004; 351:13.
  75. Spoont MR, Williams JW Jr, Kehle-Forbes S, et al. Does This Patient Have Posttraumatic Stress Disorder?: Rational Clinical Examination Systematic Review. JAMA 2015; 314:501.
  76. Weathers FW, Juska JA, Keane TM. The PTSD checklist - civilian version. Boston National Center for PTSD. Boston Veterans Affairs Medical Center 1991.
  77. Blevins CA, Weathers FW, Davis MT, et al. The Posttraumatic Stress Disorder Checklist for DSM-5 (PCL-5): Development and Initial Psychometric Evaluation. J Trauma Stress 2015; 28:489.
  78. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), American Psychiatric Association, Arlington 2013.
  79. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision, American Psychiatric Association, Washington DC 2000.
Topic 500 Version 27.0

All topics are updated as new information becomes available. Our peer review process typically takes one to six weeks depending on the issue.