Post-Traumatic Stress Disorder

Technical detailed article about post-traumatic stress disorder (PTSD).

Topics covered:

  • Introduction
  • What makes a stressor traumatic?
  • Clinical features
  • Classification
  • Diagnosis and differential diagnosis
    • Diagnostic criteria in ICD-10 and DSM-IV
    • Differential diagnoses
    • Ongoing research on symptom criteria
    • Assessment instruments
  • Epidemiology
    • How common are traumatic events in the population?
    • What types of trauma are associated with high PTSD rates?
    • What proportion of people develop PTSD in response to a traumatic stressor?
    • How prevalent is PTSD in the population?
    • Partial PTSD
    • Comorbidity of PTSD with other disorders and symptoms
    • Summary of main findings from epidemiological studies
  • Aetiology
    • Psychological processes
    • Biological processes
  • Course and prognosis
    • Time course of symptoms
    • Factors that influence the risk of developing PTSD
    • Factors affecting recovery from trauma
  • Treatment of PTSD
    • Psychological treatments
    • Pharmacological treatments
  • Advice on management
    • Diagnosing PTSD
    • Choice of treatment
    • Special problems in the management of PTSD patients
  • References


Clinicians have long noted that traumatic events can lead to severe psychological disturbance. At the end of the nineteenth and the beginning of the twentieth centuries, railway disasters, the World Wars, and the Holocaust prompted systematic descriptions of the symptoms associated with traumatic stress reactions. These include the spontaneous re-experiencing of aspects of the traumatic events, startle responses, irritability, impairment in concentration and memory, disturbed sleep, distressing dreams, depression, phobias, guilt, psychic numbing, and multiple somatic symptoms. A variety of labels were used to describe these reactions including ‘fright neurosis', ‘combat/war neurosis', ‘shell-shock', ‘survivor syndrome', and ‘nuclearism'. (1,2 and 3)

Whether the traumatic event can be considered a major cause of these psychological symptoms, has been the subject of considerable debate. Charcot, Janet, Freud, and Breuer suggested that hysterical symptoms were caused by psychological trauma, but their views were not widely accepted. The dominant view was that a traumatic event in itself was not a sufficient cause of post-trauma symptoms, and experts searched for other causes. Many suspected an organic cause. For example, damage to the spinal cord was suggested as the cause of the ‘railway spine syndrome', microsections of exploded bombs entering the brain as the cause of ‘shell shock', and starvation and brain damage as causes of the chronic psychological difficulties of concentration camp survivors. Others doubted the validity of the symptom reports and suggested that malingering and compensation-seeking (‘compensation neurosis') was the major cause in most cases. Finally, the psychological symptoms were attributed to pre-existing psychological dysfunction. The predominant view was that reactions to traumatic events are transient, and that therefore only people with unstable personalities, pre-existing neurotic conflicts, or mental illness would develop chronic symptoms. (1,2 and 3)

It was the recognition of the long-standing psychological problems of many war veterans, especially Vietnam veterans, that changed this view and convinced clinicians and researchers that even people with sound personalities can develop clinically significant psychological symptoms if they are exposed to horrific stressors. This prompted the introduction of post-traumatic stress disorder (PTSD) as a diagnostic category in DSM-III. (4) It was thus recognized that traumatic events such as combat, rape, man-made or natural disasters give rise to a characteristic pattern of psychological symptoms. The diagnostic criteria specified the experience of a traumatic event as a necessary condition for the diagnosis. ICD-10 (5) emphasized the causal role of traumatic stressors in producing psychological dysfunction even more clearly, in that a specific group of disorders, ‘reaction to severe stress, and adjustment disorders', was created. These disorders are ‘thought to arise always as a direct consequence of the acute severe stress or continued trauma. The stressful the primary and overriding causal factor, and the disorder would not have occurred without its impact.'

What makes a stressor traumatic?

In everyday language, many upsetting situations are described as ‘traumatic', for example divorce, loss of job, or failing an examination. However, a field study designed to establish what kinds of stressors lead to the characteristic symptoms of PTSD, showed that only 0.4 per cent of a community sample developed the characteristic symptoms of PTSD in response to such ‘low magnitude' stressors. (6) Thus, in diagnosing PTSD, it appeared necessary to employ a strict definition of what constitutes a traumatic stressor.

Few people would contest that horrific events such as rape or bombings are traumatic. In an attempt to capture the essence of these stressors, the authors of DSM-IIIR required a traumatic stressor to be ‘outside the range of usual human experience' and that it ‘would be markedly distressing to almost anyone'. (7) However, epidemiological studies showed that stressors that can lead to PTSD are actually quite common, for example road traffic accidents (8) or sexual assault.(9) Thus, the DSM-IIIR definition appeared too restrictive.

ICD-10 uses a broader definition and characterizes traumatic stressors by their exceptional severity and the distress they would cause for the average person ‘a stressful event or situation...of an exceptionally threatening of catastrophic nature, which is likely to cause pervasive distress in almost anyone'. (5) Thus, the ICD-10 diagnosis refers to a common-sense understanding of which situations are likely to be extremely distressing.

In contrast, the authors of DSM-IV(10) attempted a specific definition. On the basis of research findings that threat to life or physical integrity during the event is one of the most consistent predictors of PTSD, (11) DSM-IV requires that the person ‘experienced, witnessed, or was confronted with an event or events that involved actual or threatened death or serious injury, or a threat to the physical integrity of self or others'. The authors of DSM-IV made a further important step, in that they moved away from a purely situational definition and included the person's subjective response to the situation as an additional criterion, requiring that the ‘person's response involved intense fear, helplessness, or horror' (or disorganized or agitated behaviour in the case of children). (10) The latter criterion takes into account that there is a large interindividual variability in the psychological response to the same situation.

The stressor criterion of DSM-IV is still under debate. Recent research suggests that both components of the definition may require extension. First, it may be necessary to include further possible emotional responses to traumatic stressors. There is accumulating evidence that emotional numbing during traumatic events is predictive of PTSD. (12) Furthermore, it has been established that perpetrators of violent crime sometimes develop PTSD. Witnessing or participating in war-related crimes such as torturing or killing prisoners of war and civilians and mutilation of corpses is more closely linked to PTSD in Vietnam veterans than the threat of death associated with combat. (13) The psychological state of the perpetrators during the events that later lead to PTSD has not been studied in detail, but it is doubtful that they would meet the current DSM-IV definition. More likely, feelings of shame or guilt that were experienced at the time or subsequently, may be predictive of PTSD in this group.

Second, the emphasis on threat to life or physical integrity may omit important dimensions of subgroups of traumatic events. The threat to the perception of oneself as an autonomous human being may be a relevant dimension of traumatic events that involve intentional harm by other people. (14) Mental defeat, the perceived loss of all autonomy, was related to PTSD in political prisoners and assault victims, (14,15) independent of other indicators of trauma severity including threat to life and perceived helplessness.

Clinical features

The most characteristic symptoms of PTSD are the re-experiencing symptoms. Patients involuntarily re-experience aspects of the traumatic event in a very vivid and distressing way. This includes: flashbacks in which the person acts or feels as if the event were recurring; nightmares; and intrusive images or other sensory impressions from the event. For example, a women who was assaulted kept seeing the eyes of the perpetrator looking through the letterbox before he broke into her house, and a man involved in a severe car crash at night kept hearing the sound of the impact. Despite these vivid memory fragments, intentional recall of the event is often poor and disorganized, and some patients have amnesia for parts of the event.

Reminders of the trauma arouse intense distress and/or physiological reactions and are consequently avoided, including conversations about the event. Patients try to push memories of the event out of their mind and avoid thinking about the event in detail, particularly about its worst moments. On the other hand, many ruminate excessively about questions that prevent them from coming to terms with the event, for example about why the event happened to them, about how it could have been prevented, or about how they could take revenge.

The patients emotional state ranges from intense fear, anger, sadness, guilt, or shame to emotional numbness. They often describe feeling detached from other people and give up previously significant activities. Various symptoms of hyperarousal include hypervigilance, exaggerated startle responses, irritability, difficulty concentrating, and sleep problems.


ICD-10 (5) classifies PTSD (F43.1) among the reactions to severe stress and adjustment disorders (F43) that are primarily caused by stressful events. DSM-IV (10) classifies PTSD (309.81) among the anxiety disorders because symptom patterns, psychophysiological responses, family studies, and the efficacy of exposure treatment and serotonergic drugs suggested a relationship with other anxiety disorders. However, some of the symptoms would also suggest a relationship with dissociative disorders (e.g. amnesia) or depression (e.g. loss of interest). (16,17)

Diagnosis and differential diagnosis

Diagnostic criteria in ICD-10 and DSM-IV

Table 1 compares the diagnostic criteria of ICD-10 and DSM-IV. (10) ICD-10 research diagnostic criteria, (18) as well as diagnostic guidelines, (5) are included. The diagnostic systems agree on the core symptoms of PTSD—re-experiencing, avoidance, emotional numbing, and hyperarousal—but differ in the weight assigned to them.

  • DSM-IV puts a stronger emphasis on the avoidance/numbing cluster of symptoms by requiring a minimum of three of these symptoms. Although emotional numbing is listed prominently in the ICD-10 diagnostic guidelines, it was not included in the ICD-10 research diagnostic criteria. As a consequence, patients that meet ICD-10 criteria may not fulfil the criteria for a DSM-IV PTSD diagnosis if they have too few of the numbing symptoms. They would be diagnosed as having an adjustment disorder according to DSM-IV.
  • The ICD-10 research diagnostic criteria require the patient to either suffer from psychogenic amnesia or hyperarousal symptoms. Thus, in contrast to DSM-IV, a patient could be diagnosed as having PTSD in the absence of hyperarousal symptoms if amnesia is present.
  • DSM-IV states two additional criteria that are not included in ICD-10. First, it requires a minimum symptom duration of 1 month because acute stress disorder would be diagnosed before 4 weeks have elapsed. Second, it requires that the symptoms cause significant distress or impaired functioning.

Thus, although the diagnostic systems largely agree on the type of symptoms that characterize PTSD, DSM-IV criteria are stricter. A recent large-scale study (19) found a prevalence of ICD-10 PTSD of 6.9 per cent, and a prevalence of DSM-IV PTSD of 3 per cent. The concordance between the diagnostic systems was only 35 per cent. The concordance could have been increased to 56 per cent if ICD-10 included a criterion of emotional numbing and if the DSM-IV disability criterion was dropped.

Differential diagnoses

Distinguishing features include the following:

  • the type of stressor (adjustment disorders, enduring personality change)
  • the symptom pattern (adjustment disorders, enduring personality change)
  • the duration of the symptoms (acute stress disorder, acute stress reaction)
  • the question of whether the avoidance, numbing, and hyperarousal symptoms were present before the traumatic event occurred (other anxiety or depressive disorders)
  • the nature of the intrusive cognitions and perceptual disturbances (obsessive–compulsive disorder, psychotic symptoms, substance-induced symptoms).

Prolonged repeated trauma, such as captivity or repeated childhood sexual abuse, may lead to a more complex pattern of symptoms, ‘complex PTSD', that is characterized by somatization, dissociation, affect dysregulation, poor impulse control, self-destructive behaviour, and pathological patterns of relationships. (20) It was debated whether to include a category ‘disorders of extreme stress not otherwise specified' ( DESNOS) into DSM-IV to accommodate these cases, but the decision was not to include it. (16) In ICD-10, the diagnosis ‘Enduring personality changes after catastrophic experience' covers such long-standing consequences of enduring trauma.

Furthermore, it is currently being debated whether an additional diagnostic category ‘traumatic grief' should be included into the psychiatric classification system. (21,22)

Ongoing research on symptom criteria

Recent research has questioned the symptom clusters of DSM-IV. In particular, it emerges that it may be preferable to assess the emotional numbing symptoms separately from the avoidance symptoms, because these symptoms do not load on the same factor in factor analyses and may have different underlying mechanisms. Furthermore, it may be preferable to include severity criteria for the symptoms rather than relying on counting the presence of symptoms. (23)

Assessment instruments

Several semistructured interviews assess the DSM-IV criteria for PTSD. The Structured Clinical Interview for DSM-IV ( SCID) (24) allows one to establish the diagnosis of PTSD. The Clinician Administered PTSD Scale (CAPS) (25) nd the Anxiety Disorders Interview Schedule for DSM-IV (ADIS-IV)(26) provide measures of symptom severity as well as establishing the diagnosis of PTSD.

The most widely used self-report measure of PTSD symptoms used to be the Impact of Event Scale. (27) The original scale contained two scales, an intrusion and an avoidance scale. It has recently been expanded to include an additional hyperarousal scale ( IES-R). (28) The IES-R does not cover all the symptoms of PTSD specified in DSM-IV. This is why new measures that are modelled on the DSM-IV criteria are now commonly used in research studies, for example the Post-traumatic Stress Diagnostic Scale (PDS). (29)


The available epidemiological data so far stem mainly from studies conducted in the United States. It remains to be investigated whether these data replicate in other countries. The prevalence of PTSD may be low in some societies such as Iceland or Hong Kong. One has to bear in mind that the society and natural environment set conditions for exposure to traumatic events. For example, in the last decades, people in developing countries have had a much greater exposure to war and natural disasters than people in industrialized Western societies. (30)

How common are traumatic events in the population?

In a large representative United States' sample, Kessler et al. (31) found that 60.7 per cent of the men and 51.2 per cent of the women had experienced at least one traumatic event meeting DSM-IIIR criteria in their lifetime. The most common types of trauma were witnessing someone being killed or severely injured, accidents, and being involved in a fire, flood, or natural disaster. Using DSM-IV criteria, Stein et al. (32) found a lifetime exposure to serious traumatic events of 81.3 per cent for men, and 74.2 per cent for women. Sudden death of a loved person was one of the most frequent traumatic stressors (DSM-IV criteria). (33)

What types of trauma are associated with high PTSD rates?

PTSD rates depend on the type of traumatic event. Rape was associated with the highest PTSD rates in several studies. For example, 65 per cent of the men and 46 per cent of the women who had been raped met PTSD criteria in the Kessler et al. (31) study. Other traumatic events associated with high PTSD rates included combat exposure, childhood neglect and physical abuse, sexual molestation; and for women only, physical attack and being threatened with a weapon, kidnapped, or held hostage. Accidents, witnessing death or injury, and fire or natural disasters were associated with relatively low lifetime PTSD rates of less than 10 per cent. (31) Other research has shown high PTSD rates for torture victims, (34) survivors of the Holocaust, (35) and prisoners of war. (36)

The emphasis in DSM-IV on threat to life or physical integrity has led to increasing awareness that medical illness and treatment can lead to PTSD. (37) Waking up during anaesthesia, especially if the patient experienced pain, is an example for such a traumatic event. Epidemiological data for this subgroup of PTSD patients are largely lacking.

What proportion of people develop PTSD in response to a traumatic stressor?

Kessler et al. (31) found that the risk of developing PTSD after a traumatic event is 8.1 per cent for men, and 20.4 per cent for women. For young urban populations, higher risks have been reported; Breslau et al. found an overall risk of 23.6 per cent, (38) a risk of 13 per cent for men and 30.2 per cent for women.(39)

The figures reported in these studies may be influenced by two types of biases that have opposite effects on probability estimates. First, Breslau et al. (33) have pointed out that previous studies overestimated the PTSD-risk imposed by traumatic events because participants reported on the worst trauma that they had experienced. When the symptoms induced by a traumatic event that was randomly selected from the ones that a person had experienced were assessed, the conditional risk of PTSD following exposure to trauma was found to be 9.2 per cent, using DSM-IV criteria.

Second, the retrospective methodology used in the epidemiological studies may have led to underestimation of PTSD rates due to selective recall. For example, the prevalence of PTSD 3 months after road traffic accidents was found to be around 20 per cent in prospective longitudinal studies, (40,41) whereas the retrospective studies found prevalences below 10 per cent.

How prevalent is PTSD in the population?

Kessler et al. (31) estimated that the lifetime prevalence of PTSD is 7.8 per cent, using DSM-IIIR criteria. Women had a higher prevalence than men (10.4 versus 5.0 per cent). This was due to both a greater exposure to high-impact trauma (rape, sexual molestation, childhood neglect, and childhood physical abuse) and a greater likelihood of developing PTSD when exposed to a traumatic event. Other studies using DSM-IIIR criteria have yielded similarly high prevalence rates. (9,39) A recent study used DSM-IV criteria and found a past-month PTSD prevalence of 2.7 per cent for women and 1.2 per cent for men. (32)

Earlier studies using DSM-III criteria had reported lower lifetime prevalences of about 1 per cent. (42,43) Besides differences in procedures and sampling methods, the low PTSD prevalence in these earlier studies may be due to the use of an interview schedule with low sensitivity in detecting PTSD. (44) In particular, the interview asked global questions about the occurrence of traumatic events and lacked the repeated probing for specific events or event categories that seems to be necessary in eliciting relevant experiences.

Partial PTSD

Several studies have found substantial levels of distress and disability for traumatized people who met some, but not all, of the PTSD criteria specified in DSM-IV. (32) These people may be at greater risk of developing the full PTSD syndrome than people with fewer symptoms. (40,41)

Comorbidity of PTSD with other disorders and symptoms

PTSD shows a substantial comorbidity with affective disorders, other anxiety disorders, substance-use disorders, and somatization. In the study by Kessler et al., (31) 88.3 per cent of the men and 78.1 per cent of the women with PTSD had comorbid psychiatric diagnoses. Studies of veterans with PTSD have also indicated an enhanced level of problems in family and marital adjustment and violent behaviour, (45) and heavy smoking.(46) Furthermore, reports of poor health and increased rates of various diseases, in particular infectious and nervous system diseases, are associated with PTSD. (47)

Is PTSD primary or secondary to the comorbid diagnoses? There is, as yet, little research into this question. The retrospective accounts obtained by Kessler et al. (31) suggested that PTSD was primary to comorbid affective or substance-use disorders in the majority of cases, and PTSD was primary to comorbid anxiety disorders in about half of the cases. Similarly, Breslau et al. (39) found that PTSD increased the risks for first-onset major depression and alcohol-use disorder. Conversely, pre-existing major depression also increased vulnerability to the PTSD-inducing effects of traumatic events and risk for exposure to traumatic events. A prospective study confirmed that PTSD increased the risk of subsequent pain, conversion symptoms, and somatization symptoms.(48)

Most of the comorbidity research has concentrated on the nature of the relationship between PTSD and alcohol or drug abuse. A recent longitudinal study (49) of 1007 adults showed that PTSD led to an increased risk of drug abuse or dependence, whereas exposure to traumatic events in the absence of PTSD did not increase the risk. Consistent with the interpretation that drug-use disorders are usually secondary to PTSD, there was no evidence that pre-existing drug abuse or dependence influenced the risk of PTSD after traumatic exposure. Similarly, the majority of studies have found that PTSD precedes the development of alcohol-abuse problems. There are probably several mechanisms for this relationship. In the short term, alcohol is used to self-medicate the symptoms of PTSD, but paradoxically intoxication and withdrawal symptoms may intensify the symptoms in the long term. (50)

Longitudinal studies have produced conflicting findings on whether drug use increases the risk of exposure to traumatic events. (49) However, other studies have suggested that alcohol abuse may increase the likelihood of traumatization because of its association with violence and accidents. (51)

Summary of main findings from epidemiological studies

  • The majority of people will experience at least one traumatic event in their lifetime.
  • In assessing PTSD history, interviewers should probe for specific events.
  • Assault, in particular sexual assault, and combat have a higher impact than accidents and disasters. (31,32)
  • If the frequency and impact of traumatic events are considered together, sudden unexpected death of a loved one (33) and road traffic accidents(8) can be considered important causes of PTSD in Western industrialized societies.
  • Men tend to experience more traumatic events than women, but women experience higher impact events. (31,32)
  • Women are at least twice as likely to develop PTSD in response to a traumatic event than men. This enhanced risk is not explained by differences in the type of traumatic event. The estimated lifetime prevalence for women is approximately 10 to 12 per cent, and for men 5 to 6 per cent. (9,31,38,39)
  • Comorbid depression and substance-use disorders appear to be secondary to PTSD in the majority of cases.


There is no single accepted theory of PTSD. Theoretical explanations have focused on psychological and biological mechanisms that are not mutually exclusive.

Psychological processes

Fear conditioning

Mowrer's two-factor conditioning theory of phobias has been applied to PTSD. (52,53 and 54) It is suggested that through classical (Pavlovian) conditioning, stimuli that were present at the time of the trauma (unconditioned stimulus) become associated with fear and arousal responses. Subsequently, the conditioned stimuli trigger similar (conditioned) responses when presented on their own. Through stimulus generalization and higher-order conditioning, a wide variety of stimuli become triggers of distress in the aftermath of trauma. Quite naturally, the person will try to avoid the conditioned stimuli and the associated distress. The avoidance behaviour is negatively reinforced (operant or instrumental conditioning) because it leads to a reduction in psychological and physical discomfort. In the long term, however, avoidance prevents extinction of the conditioned fear responses to reminders of the traumatic event, and thus maintains the problem.

Appraisals of the traumatic event and its sequelae

A traumatic event threatens the person's view of the world, the self, and the future. Several theorists propose that this threat to basic inner models is at the core of PTSD, or of responses to trauma in general. Horowitz (21) explained re-experiencing symptoms as the result of a slow process that helps the traumatized person to adjust their inner models (schemas) of the self and the world to the traumatic experience. Until this process is completed, the information related to the traumatic event is thought to be held in active memory and thus intrudes into consciousness. Similarly, Janoff-Bulman (55) proposed that traumatic events ‘shatter' previously held beliefs (e.g. ‘The world is a safe place'), and that post-trauma adjustment requires rebuilding basic beliefs about the self and the world. However, PTSD is quite often associated with a confirmation of previously held negative beliefs rather than a shattering of positive beliefs (e.g. ‘Bad things always happen to me') (50,56,57) so that recovery requires the modification of these beliefs.

The persistence of PTSD symptoms has been explained by individual differences in the appraisal of the traumatic event: that is to say, in what personal meaning it has for them.(56,58,59) Some people are able to see the trauma as a time-limited terrible experience that does not necessarily have negative implications for the future, and may also be able to find some element of personal growth in it. These people are likely to recover quickly. Individuals with persistent PTSD are characterized by excessively negative appraisals of the event. The nature of predominant emotional responses in PTSD depends on the particular appraisals; for example, appraisals concerning danger lead to fear (‘Nowhere is safe'), appraisals concerning others violating personal rules lead to anger (‘Others have not treated me fairly'), appraisals concerning responsibility for the traumatic event lead to guilt or shame (‘It was my fault', ‘I did something despicable'), and appraisals concerning loss lead to sadness (‘My life will never be the same again'). (58) Such appraisals distinguished between traumatized individuals with and without PTSD. (60)

Negative appraisals involved in maintaining PTSD do not only concern the traumatic event itself, but also its sequelae such as the initial PTSD symptoms or responses of other people in the aftermath of the traumatic event. (58,61,62) In line with this hypothesis, negative interpretations of intrusive recollections (e.g. ‘I am going mad') after road traffic accidents were one of the most important predictors of PTSD at 1 year after the event. (41) Perceived negative responses from other people in the aftermath of trauma predicted PTSD in studies of assault and torture victims. (14,15)

Nature of trauma memories

PTSD patients have relatively poor intentional recall of the traumatic event. Their narratives of the event tend to be fragmented and disorganized. (63) With successful treatment, the narratives become elaborated and organized. (64) These observations have led to the hypothesis that insufficient elaboration of the event and its meaning leads to the re-experiencing symptoms of PTSD. (58) Autobiographical memories are normally organized in a way that prevents triggering of very vivid and emotional re-experiencing of an event. Recall is driven by themes and personal time periods, and it is relatively abstract. (65) Ehlers and Clark (58) suggested that re-experiencing in PTSD occurs because the trauma memory is inadequately linked to its context in time, place, and other autobiographical memories. Stimuli that resemble those present during the traumatic event can thus trigger vivid memories and strong emotional responses that are experienced as if the event was happening right now.

Foa and colleagues (56,62) suggested that PTSD is characterized by a pathological network in memory that is particularly large and easily triggered. It contains many stimulus propositions that are erroneously linked to danger, causing fear responses to harmless stimuli associated with the traumatic event in memory. In addition, the person's reactions during the trauma are linked to the belief that the self is incompetent. Activation of components of the trauma memory (for instance, by confrontation to a reminder, by similar bodily sensations, or by thinking about the event) will activate the whole network, including the emotional responses that the person had during the traumatic event.

Brewin and colleagues (66) have proposed that the symptoms of PTSD can only be explained if one assumes several levels of representation of the traumatic event, for example verbally accessible memory and memory that is triggered by situation-specific cues. PTSD is thought to be characterized by easily accessible situationally specific memories.

Patients with PTSD may not only have deficits in their autobiographical memories of the traumatic event, but the organization of the autobiographical memory base in general may be affected. (58) Patients with PTSD have difficulty retrieving specific autobiographical memories and exhibit overgeneral memories, similar to depressed patients. (6) These memory deficits may be linked to poor problem-solving and enhanced stress responses to everyday stressors, a sense of foreshortened future (because the overgeneral memory of the past makes it difficult to envisage a future), and more frequent stimulus-driven retrieval of memories of the traumatic event leading to re-experiencing symptoms.

Behaviours that maintain PTSD symptoms

Whereas many people will recover from initial PTSD symptoms, some do not get better. This has led researchers to specify possible maintaining behaviours. These include avoidance of reminders, suppression of thoughts and memories connected to the event, rumination, safety behaviours, dissociation, and the use of alcohol or drugs. Ehlers and Clark(58) suggested that these behaviours and cognitive strategies maintain PTSD in three ways. First, some behaviours directly lead to increases in symptoms; for example, thought suppression leads to paradoxical increases in intrusion frequency. Second, other behaviours prevent changes in the problematic appraisals; for example, constantly checking one's rear mirror (a safety behaviour) after a car accident prevents change in the appraisal that another accident will happen if one does not check the mirror. Third, other behaviours prevent elaboration of the trauma memory and its link to other experiences. For example, avoiding thinking about the event prevents people from incorporating the fact that they did not die into the trauma memory, and they thus continue to re-experience the fear of dying they originally experienced during the event. Several studies have found that avoidance, safety behaviours, thought suppression, and rumination predict maintenance of PTSD. (15,41)

Some of the cognitive processes that maintain PTSD symptoms are not intentional. Patients with PTSD have an unintentional attentional bias to stimuli that are reminiscent of the traumatic event. (6) Involuntary selective attention to reminders may be one of the reasons why these patients have frequent re-experiencing symptoms. Rumination is often described by the patient as unintentional. In particular, patients have problems stopping ruminating once they have started. Rumination may represent a cognitive habit that started as an intentional strategy employed to solve problems and that became more automatic with time.

Biological processes

A number of biological factors have been linked to PTSD symptoms. They have the effect that they make people with PTSD hyper-responsive to stressful stimuli, especially stimuli that are reminiscent of the trauma. (67)

Chronic stress reaction

Patients with PTSD show several abnormalities that are consistent with a chronic stress reaction or an enhanced reactivity to minor stressors. There is evidence for a chronically enhanced secretion of adrenaline (epinephrine) and noradrenaline (norepinephrine). In psychophysiological studies, patients with PTSD showed enhanced startle responses and higher baseline heart rates and blood pressure than traumatized controls without PTSD. However, these responses may, in part, reflect anticipatory anxiety related to the expectation of trauma cues. Patients with PTSD exhibit greater physiological reactivity to trauma cues (e.g. sounds, pictures, or guided imagery) than control subjects without PTSD. (6)

Hypothalamic–pituitary–adrenal axis abnormalities

Patients with current PTSD show abnormally low levels of cortisol compared to normal controls and traumatized individuals without current PTSD. In addition, PTSD patients have an increased number of lymphocyte glucocorticoid receptors. When given a low dose of dexamethasone, PTSD patients exhibit hypersuppression of cortisol. Thus, patients with PTSD show a very different pattern of hypothalamic–pituitary–adrenal response than patients with major depression. The pattern of findings suggests that the hypothalamic–pituitary–adrenal axis in PTSD is characterized by enhanced negative feedback. (68) There may also be a downregulation of corticotrophin-releasing factor receptors at the anterior pituitary due to chronic increases in this factor. (69) Overall, the pattern of findings suggests that, in PTSD, the hypothalamic–pituitary–adrenal axis is set to produce large responses to further stressors.

Neuroendocrinological abnormalities

Several neurotransmitter systems seem to be dysregulated in PTSD. (53) Research suggests a sensitization of the noradrenergic system, in particular, a downregulation of a2-adrenergic receptors, in a subgroup of PTSD patients. (70) The downregulation of the a2-adrenergic receptors is thought to lead to enhanced locus coeruleus activity and increased levels of noradrenaline. This could cause the symptoms of autonomic hyperarousal and re-experiencing (through the effects on b-adrenergic receptors in the amygdalae and cortical structures). Yohimbine (which blocks the a2-receptors) provokes flashbacks and panic attacks in a substantial subgroup of PTSD patients.

Another subgroup of PTSD seems to be characterized by a sensitized serotonergic system. They respond to meta-chlorophenylpiperazine with panic attacks and PTSD symptoms such as flashbacks. (70) In animals, serotonin depletion has been linked to hyperirritability and inability to modulate arousal. These effects parallel the hyperarousal symptoms in PTSD. Serotonin controls the function of the septohippocampal behavioural inhibition system. Sensitization of this system will lead to a impaired distinction between reward, punishment, novelty and frustrative non-reward with the consequence that the behavioural inhibition system can be activated by mild everyday stressors. (67)

Endogenous opiates have been suspected to mediate the symptoms of emotional numbing and amnesia. In the animal model, uncontrollable stress leads to the secretion of endogenous opiates that induce analgesia. Patients with PTSD show conditioned secretion of endorphins and analgesia when confronted with reminders of the traumatic event. (67)

Veterans with PTSD show enhanced levels of corticotrophin-releasing factor (CRF) in their cerebrospinal fluid compared to normal controls. (69) Intraventricular administration of CRF has been shown to lead to enhanced plasma adrenaline and noradrenaline concentrations and anxiety and fear-related behaviours in animals, and it is thus thought that the enhanced CRF levels could cause these symptoms in PTSD patients.

The dopaminergic, g-aminobutyric acid, and N -methyl-D-aspartate systems have also been implicated in PTSD, but the evidence for these hypotheses is sparse at this stage.

Thyroid function

Some studies have found an increased levels of thyroid hormones in patients with PTSD. These are correlated with the severity of hyperarousal symptoms. (67)


Magnetic resonance imaging studies have shown a reduced hippocampal volume in veterans and women with a history of childhood sexual abuse. This line of research was prompted by animal studies showing that high levels of cortisol seen during stress are associated with damage to the hippocampus. (71) Disturbances of hippocampal function may lead to enhanced reactivity to stimulation, and may be involved in the deficits in autobiographical memory observed in PTSD patients. (6) It remains unclear whether the decreased hippocampal volume is a risk factor for the development of PTSD or a consequence of chronic PTSD.

It has been suggested that PTSD is characterized by dysfunctions in the amygdalae or the areas that project to them (the hippocampus, septum, and prefrontal cortex), leading to problems in the extinction of fear responses to reminders of the traumatic event. (53) Animal studies established that conditioned fear responses could only be extinguished if the cortex was intact. (72) Consistent with possible deficits in cortical control, positron emission tomography studies have shown a relative decrease in middle temporal blood flow (and several adjacent medial prefrontal areas) in patients with PTSD relative to controls when they imagined the traumatic event or were presented with reminders of it. The middle temporal cortex plays a role in the extinction of fear through inhibition of amygdala function. At the same time, PTSD patients showed increased blood flow in the limbic regions (parahippocampus and cingulate). (71)

Animal models of PTSD

There are biological and psychological parallels between the animal model of inescapable shock and exposure to a traumatic event. The uncontrollability of an aversive event seems to make it particularly traumatic. (73) Inescapable shock leads to changes in the noradrenergic system, the HPA axis, and endogenous opiates that parallel findings in PTSD patients. (53)

However, these effects are usually only observed after repeated exposure to inescapable shock, whereas one traumatic event can be sufficient in inducing PTSD. This is why some authors have suggested that the animal model of kindling or behavioural sensitization is more appropriate in explaining PTSD. Kindling refers to a process whereby intermittent subconvulsive electrical stimulation of the limbic system eventually has the effect that the animal will respond with a seizure to a stimulus that previously was subthreshold. Post et al. (74) have suggested that the repeated re-experiencing of the traumatic event may constitute a kindling process, to the effect that PTSD symptoms become more easily triggered with time. Similarly, previous exposure to stressors may sensitize people to respond with PTSD symptoms to a traumatic event.

Animal models suggest that the massive secretion of neurohormones at the time of the trauma, in particular noradrenaline and vasopressin, leads to overconsolidation (long-term potentiation) of the trauma memory. This would have the effect that the conditioned fear responses are particularly difficult to extinguish and that stimuli that resemble those present during trauma are particularly likely to trigger intrusive memories, distress, and/or the corresponding physiological responses. (67)

Genetic factors

Twin studies have found a higher concordance of PTSD among monozygotic than dizygotic twins. There is also an increased prevalence of psychiatric disorders, especially anxiety disorders, affective disorders, sociopathy, and/or substance abuse, among family members of people with PTSD. (75)

Course and prognosis

Time course of symptoms

For the vast majority of PTSD cases, symptoms begin immediately after the traumatic event. Delayed onset is found in a minority (11 per cent or less) of the cases. (6)

A series of prospective longitudinal studies suggest that a large proportion of people who initially develop PTSD recover within the first year after a traumatic event. For example, a study of rape victims found that 94 per cent met PTSD criteria (with the exception of the symptom duration criterion) in the 2 weeks after the trauma, and 65 per cent, 47 per cent, and 42 per cent at 1, 3, and 6 months, respectively. (76) Across different studies, it can be estimated that about 50 per cent of those with initial PTSD symptoms will recover during the first year. Long-term outcome depends on initial symptom severity. People with high initial PTSD severity were more likely to remain symptomatic at follow-up than those with low initial symptom severity. (41)

The substantial rate of initial recovery does not imply, however, that PTSD in general has a good prognosis. A substantial proportion of traumatized individuals will suffer long-standing morbidity after a traumatic event. Retrospective studies suggest that about one-third of people who develop PTSD after a traumatic event will not recover for many years. (31)

Factors that influence the risk of developing PTSD

Demographic variables and pretrauma personality

Women are at greater risk of developing PTSD than men, and black and Hispanic people are at greater risk than Caucasians. (8,31,39,77) As yet, the mechanisms of these relationships remain unclear.

A personal or family history of psychiatric disorders, especially mood and anxiety disorders, increases the risk of PTSD. (38,39,75,78) Previous traumatic experiences, in particular childhood sexual or physical abuse, (38,79,80) childhood separation from parents, (39) and family instability (80) are also associated with a higher risk of PTSD.

Among the personality variables predicting PTSD are low intelligence, (81) neuroticism, (38,78) low self-esteem, (82) external locus of control, (83) and pre-existing negative beliefs about the self and the world. (15) Political activism appears to be protective in torture survivors. (84)

Stressor variables

PTSD risk depends on the severity of the stressor. Prolonged and repeated trauma, exposure to the grotesque aftermath of violence, events that involve intentional harm by another person and abusive violence, and events that involve harm to children are particularly likely to lead to PTSD. (11,59,85,86) Injury severity is only a weak predictor of PTSD. Long-term health problems and loss of function may play a greater role in maintaining PTSD. (41,85) There are some reports that unconsciousness during a traumatic event may decrease the risk of PTSD, (87) but other studies have found small associations in the opposite direction. (41) Psychological responses during trauma PTSD risk depends on the degree of psychological distress the traumatic event caused. The psychological impact of the trauma depends on the perceived threat to life, (11) the perceived loss of control (helplessness), (88) causal attributions (89) and the perceived threat to one's autonomy (mental defeat). (14) Among the psychological responses predicting PTSD are feelings of anger, guilt, or shame (90,91) and dissociation and numbing. (92,93)

Factors affecting recovery from trauma

Recovery environment

Recovery is facilitated by social support and the absence of negative responses from others after the event. (15,83,94,95) Further stressful or traumatic life events impede recovery from PTSD. (95,96 and 97) This includes the stress caused by long-lasting negative effects of the event on health and personal appearance, financial difficulties, disruptions in everyday life, and ongoing litigation. (41,87,96)

Psychological processes

Excessively negative appraisals of the traumatic event impede recovery (e.g. ‘Nowhere is safe', ‘I cannot trust anyone', ‘I am inadequate'). (15,57,60) If individuals interpret their initial PTSD symptoms as signs that they are going mad or losing control, or as signs of a permanent change for the worse, they are less likely to recover. (15,41)

If individuals engage in behaviours or cognitive coping styles that prevent them from ‘working through' and accepting the trauma, they are less likely to recover. Such maladaptive behaviours include avoidance, not talking about the experience, safety behaviours, denial, thought suppression, and rumination. (15,41,83,94,98)

Treatment of PTSD

Several psychological and pharmacological treatments are effective in PTSD. The effect sizes (Cohen's d statistic) given below are taken from a recent meta-analysis of 61 treatment-outcome trials. (99) The difference between the pre- and post-treatment scores is divided by the pooled standard deviation of the pre- and post-treatment scores. An effect size d = 1 means that the treatment led to improvement by one standard deviation. In interpreting the effect sizes, one has to bear in mind that PTSD patients in pill-placebo or waiting-list conditions also showed some improvement. Mean effect sizes for these conditions were d = 0.77 and d = 0.75 for observer-rated PTSD symptoms, and d = 0.51 and d = 0.44 for self-rated PTSD symptoms.

Psychological treatments

Cognitive-behavioural therapy

Cognitive-behavioural treatments are effective in the treatment of PTSD. The meta-analysis (99) reported mean effect sizes of d = 1.89 for observer-rated and d = 1.27 for self-rated PTSD symptoms. This analysis included several versions of cognitive-behavioural therapy that are described below.


All versions of cognitive-behavioural therapy include some form of education about the symptoms of PTSD and treatment rationales. Common reactions to trauma are explained to normalize the patient's PTSD symptoms. The therapists explains the necessity of confronting the memory of the traumatic event and of giving up behaviours that maintain the problem such as avoidance and safety behaviours. Self-monitoring of symptoms Most cognitive-behavioural therapy treatments include some form of self-monitoring that may in itself be therapeutic. Tarrier et al. (100) found that 4 weeks of systematic self-monitoring of intrusive symptoms led to considerable and stable improvement in about 10 per cent of the cases studied.


Exposure treatment comprises two components. (62) In imaginal exposure, patients are asked to relive the traumatic event in their imagination, including their thoughts and feelings at the time. This is repeated until the reliving no longer evokes high levels of distress. In vivo exposure involves confronting (safe) situations that patients avoid because they remind them of the trauma (e.g. going to the site of the traumatic event, driving again after a road traffic accident). Exposure is repeated until the patient no longer responds with high levels of distress. There are probably several mechanisms for the efficacy of exposure treatment. (58,62) First, patients realize that exposure does not lead to a feared outcome (for example, going to the site of an accident will not mean that another accident will happen; thinking about the trauma will not make them go mad) and thus helps in correcting dysfunctional beliefs about danger of the world and the meaning of PTSD symptoms. Second, the repeated reliving of the event helps them to create an organized memory and facilitates the distinction that intrusive thoughts and images are memories rather than something happening right now.

Exposure treatment is superior to supportive psychotherapy and relaxation treatment. (101,102) Whereas exposure treatment is effective in the majority of cases, a minority of patients become worse.(100) In particular, exposure treatment does not appear suitable for patients whose traumatic memories are about being perpetrators rather than victims. (101) It may also have limits in treating survivors of complex and prolonged traumatic events such as torture, war, or captivity. (103)

Cognitive therapy/restructuring

Cognitive therapy identifies and modifies excessively negative appraisals of the traumatic event and/or its sequelae. (57,104) Methods include discussion of the evidence for and against the appraisals, identification of thinking errors, challenging of appraisals with behavioural tests, and imagery modification. Recent studies have shown that cognitive therapy is effective on its own, without additional exposure treatment. (100,102) When verbal challenging of dysfunctional beliefs was used as an additional treatment after a session of imaginal exposure, it did not lead to additional treatment gains. (102)

Anxiety management (stress inoculation)

The goal of this treatment is to teach the patient a set of skills that will help them cope with stress. Examples include relaxation training, training in slow abdominal breathing, thought stopping of unwanted thoughts, assertiveness training, and training in positive thinking. (59) Anxiety management is more effective than supportive psychotherapy. In the long term it appears to be somewhat less effective than exposure treatment. (101) Relaxation treatment alone is less effective than exposure and cognitive therapy in the short and long term. (102)

Anger management

An anger management programme for PTSD patients with severe anger reactions is more effective in reducing anger than routine clinical care. (105)

Eye-movement desensitization reprocessing

This is a relatively new and controversial treatment. (106) The patient is instructed to focus on a trauma-related image and its accompanying feelings, sensations, and thoughts, while visually tracking the therapist's fingers as they move back and forth in front of the patient's eyes. After a set of approximately 24 eye movements, cognitive and emotional reactions are discussed with the therapist. Coping statements are also introduced while the scene is being imagined. A series of studies have established that eye-movement desensitization reprocessing is effective, at least for self-rated PTSD symptoms. Mean effect sizes were d = 0.69 for observer-rated and d = 1.24 for self-rated PTSD symptoms. For self-rated symptoms, eye-movement desensitization reprocessing effect sizes were larger than those of control conditions. The mechanism of treatment is not yet understood. Recent studies have shown that the eye movements are not a necessary component of the treatment. (99)

Psychodynamic therapy

The treatment focuses on understanding the meaning of the traumatic event in the context of the patient's previous experiences, personality, and attitudes. The goal of the treatment is to work through and resolve an unconscious conflict which the traumatic event is thought to have provoked. One controlled study of psychodynamic therapy showed an effect size of d = 0.90 for self-rated PTSD symptoms. (99) Psychodynamic therapy was more effective than the waiting-list condition in that study. Further uncontrolled reports indicated that psychodynamic therapy may be effective. (101,103) More studies are needed to evaluate whether this holds up in controlled studies.


The patient is given instructions to induce a state of highly focused attention, a reduced awareness of peripheral stimuli, and a heightened suggestibility. The goal of this treatment is to enhance control over trauma-related emotional distress and hyperarousal symptoms and to facilitate the recollection of details of the traumatic event. One controlled study of hypnotherapy showed an effect size of d = 0.94 for self-rated PTSD symptoms.(99) Hypnotherapy was more effective than the waiting-list condition in that study. halev et al. (103) raise concerns about the use of hypnotherapy in the treatment of PTSD as it may induce dissociative states.

Pharmacological treatments

Selective serotonin-reuptake inhibitors (SSRIs)

SSRIs (sertraline, fluvoxamine, fluoxetine) are effective in the treatment of PTSD symptoms. (107) They affect all the PTSD symptoms, including the avoidance, numbing, and hyperarousal symptoms. (108) The meta-analysis showed mean effect sizes of d = 1.43 for observer-rated and d = 1.38 for self-rated PTSD symptoms. (99) Across studies, the SSRIs were more effective than all other drug therapies. SSRIs are an attractive choice because they reduce alcohol consumption; a relevant finding given the high comorbidity of PTSD with substance abuse or dependency. (108) Despite the overall impressive effects, SSRIs may not be effective in all populations of PTSD patients. One study showed that fluoxetine was significantly superior to placebo in civilians in a trauma clinic, but not in combat veterans in a Veterans Administration Hospital. (107)

Monoamine oxidase inhibitors (MAOIs)

Phenelzine has shown good effects on re-experiencing symptoms and insomnia, but weak effects on avoidance, numbing, and hyperarousal symptoms. (108) However, the meta-analysis did not find the MAOIs to be significantly more effective than control conditions such as a pill placebo or a waiting list. (99) Effect sizes were d = 0.92 for observer-rated and d = 0.61 for self-rated PTSD symptoms. Some studies may have underestimated the MAOI effects because of an inadequate length of treatment. (108) Thus, MAOIs such as phenelzine may be useful in the treatment of PTSD, but cannot be considered among the first-choice treatments because of the risks of hypertensive crisis and the necessary dietary restrictions. (107) The development and evaluation of reversible inhibitors of monoamine oxidase type A such as moclobemide for the treatment of PTSD appears promising. (107,108)

Tricyclic antidepressants

Evidence for the efficacy of tricyclic antidepressants is mixed. If at all, they seem to be effective in less severe cases of PTSD. (107) These agents seem to mainly affect the re-experiencing rather than the avoidance, numbing, and hyperarousal symptoms of PTSD. (108) The mean effect sizes across studies were not significantly greater than for pill-placebo or waiting-list controls, (99) d = 0.86 for observer-rated and d = 0.54 for self-rated PTSD symptoms. Some of the studies may have failed to find a drug effect because the treatment length was insufficient. (107) Two trials of combat veterans administered amitriptyline or imipramine for 8 weeks found that 35 per cent more patients improved with the tricyclic antidepressant than with placebo. However, treatment was less effective the more severe the symptoms were and the greater the combat exposure had been.


Anticonvulsants (carbamazepine, valproate) have shown promising effects in preliminary studies, but have not yet been widely investigated. (108) Effect sizes in a study of carbamazepine were d = 1.45 for observer-rated and d = 0.93 for self-rated PTSD symptoms. (99) It has been estimated that about 65 per cent of PTSD patients respond to anticonvulsant therapy. (107)


Benzodiazepines do not appear to be effective in the treatment of PTSD. They do not affect the re-experiencing, avoidance, and numbing symptoms, although they may show some effects on insomnia, irritability, and general anxiety and arousal symptoms. (108) The effect sizes in one study were d = 0.54 for observer-rated and d = 0.49 for self-rated PTSD symptoms,(99) and these were not different from pill-placebo or waiting-list controls. In addition to the poor efficacy, caution is warranted with short-acting benzodiazepines such as alprazolam. They may pose a particular problem with PTSD patients because they may cause a rebound syndrome upon discontinuation including anxiety, sleep disturbance, nightmares, and rage reactions. (107)

Antiadrenergic agents

Although adrenergic dysregulation is associated with chronic PTSD, antiadrenergic agents have received little attention as a treatment option. Several case reports and open trials found positive effects of propanolol or clonidine on PTSD symptoms. (108) It remains to be investigated whether these results hold up in controlled trials.

Advice on management

Diagnosing PTSD

In diagnosing PTSD, clinicians need to ascertain that patients experienced a traumatic event and that they involuntarily re-experience the event. In addition, patients will show symptoms of hyperarousal, avoidance, and emotional numbing. Self-report instruments such as the Post-traumatic Stress Diagnostic Scale (29) or semistructured interviews such as the Clinician Administered PTSD Scale (25) are useful in assessing the symptom pattern. The DSM-IV criterion of a minimum of three avoidance or numbing symptoms appears too strict for clinical purposes. It does not appear justified to withhold treatment if the patient is distressed by the PTSD symptoms but fails to meet this criterion.

Choice of treatment

The best treatment options of PTSD to date are cognitive-behavioural treatments and SSRIs. Effect sizes of these treatments are comparable. Psychological treatments have the advantage of lower drop-out rates. The meta-analysis found that, across studies, 14 per cent of the patients dropped out of psychological treatments, compared with 36 per cent for the SSRIs. (99) An additional advantage of cognitive-behavioural treatments is their established long-term effectiveness. Treatment gains are maintained during follow-up. (99,109) In contrast, long-term follow-up studies are lacking for pharmacological treatments, so that it is not known whether treatment-effects are maintained when medications are withdrawn or when they are continued for long periods. The advantage of SSRIs compared to cognitive-behavioural treatment is that they are more readily available.

Recent expert consensus guidelines concluded that cognitive-behavioural treatments are the treatment of choice for PTSD. For very severe or special cases (e.g. geriatric patients) the combination of these psychological treatments with pharmacotherapy is recommended as an alternative to psychological treatment alone. (110)

Special considerations may apply to subgroups of PTSD patients. The efficacy of psychological treatments in patients with comorbid substance dependence remains to be established. It has been suggested that SSRIs are particularly useful for these patients, (108) but controlled trials are lacking.

Special problems in the management of PTSD patients

Avoidance is one of the main symptoms of PTSD, and it can thus take years for the patient to seek help for this condition. It is important for clinicians to bear in mind that even those who seek help may find it hard to talk about the traumatic experience, and may show signs of avoidance such as irregular attendance or failure to disclose the worst moments of the trauma initially. Therapeutic techniques to deal with this problem include empathy, gradual encouragement, and giving the patient control over the timing and mode of working through the experience (e.g. writing, talking into a tape recorder, reliving with the support of the therapist).

One of the requirements for change is that the patient feels safe. Therapists therefore have to make sure that they establish a good relationship with the patient, and that the therapeutic setting or their behaviour does not remind the patient of the traumatic event. Sometimes support in changing living circumstances may be necessary if they prevent the patient from being safe (e.g. moving house if assaulted by a neighbour).

Patients with PTSD often suffer from poor sleep and concentration, and find it painful to face reminders of the trauma. For these reasons, they have difficulty in dealing with the aftermath of traumatic events such as legal procedures and continuing treatment for physical injuries, including the long delays that this usually involves. Such ongoing stressors impede recovery, and patients may therefore benefit from problem-solving and practical advice. 


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