Despite abundant evidence for persisting and sometimes disabling psychological sequelae of exposure to extreme stressors, the evolution of posttraumatic stress disorder (PTSD) as a modern diagnosis was relatively recent. PTSD-like disorders were described in the U.S. Civil War (DaCosta's Syndrome, Irritable Heart of Soldiers), associated with railroad accidents in the late nineteenth century (Railway Spine), following World Wars I and II (Shell Shock, Traumatic Neurosis, Neurasthenia, Survivor Syndrome).
In the 1950s and 1960s, debate revolved around the issue of whether there was anything unique about the psychiatric symptoms that emerged following extreme stress relative to psychiatric symptoms that were expressed in the context of the stresses of everyday life. Thus, the diagnosis of Gross Stress Reaction appeared in the initial Diagnostic and Statistical Manual of Mental Disorders (DSM), but was excluded from DSM-II. In 1980, in the wake of the collection of a compelling body of clinical research on soldiers of the Vietnam War, studies of victims of physical and sexual assault, and victims of natural disasters, the American Psychiatric Association introduced PTSD diagnostic criteria in a form that is fundamentally similar to current diagnostic schema. Unlike other anxiety disorders, PTSD is predicated on the occurrence of at least one discrete external event, namely a precipitating trauma. DSM-III defined a trauma as “experiencing an event that is outside the range of usual human experience.” However, subsequent epidemiologic studies found that traumatic events are common, that greater than half of the population experienced trauma sometime during their life, and that even witnessing trauma could be predictive of PTSD. The DSM-IV-TR now stipulates two sub-criteria—one objective, one subjective—to meet formal diagnosis of PTSD: (A1) 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 physical integrity of self or others; and (A2) the person's response involved fear, helplessness, or horror. The change in the definition of a traumatic event from DSM-III to DSM-IV resulted in higher rates of PTSD in a number of epidemiologic studies. The fiscal year 2005 report from the Veterans Benefits Administration indicated that PTSD was the costliest diagnosis for the VA, and the third most frequently claimed disability, comprising 4.2% of all claims.
Data from the largest mental health epidemiological study to date indicate a majority of Americans have had exposure to at least one potentially traumatic (Criterion A) event. The National Comorbidity Study (NCS) surveyed 5877 Americans (2812 men and 3065 women) aged 15–54 years, and reported that 60.7% of men and 51.2% of women reported experiencing at least one extremely stressful event in their lifetime. Of those who had experienced at least one of these events, the majority of men (56.3%) and a significant percentage of women (48.6%) reported experiencing multiple extremely stressful events.
The prevalence of exposure to extreme stress has also been examined within specific populations such as inner-city residents, women, and combat veterans. For example, in a sample of 4008 American women, 69% of respondents had experienced at least one of these events in their life. Other studies have found extreme stress exposure rates as high as 92.2% for men and 87.1% for women living in inner-city metropolitan areas.
The prevalence of exposure to extreme stressors has recently received increased attention in the United States in the wake of terrorist attacks on civilians and military combat operations in Iraq and Afghanistan. When 3671 U.S. Army and Marine Corps personnel were surveyed 3–4 months after their return from Iraq or Afghanistan, prevalence of life-threatening combat engagement was significantly higher for troops deployed to Iraq compared to Afghanistan: 30% of soldiers from Afghanistan reported “seeing dead or seriously injured or killed Americans,” whereas 70% of Iraq veterans endorsed having these experiences; 12% of veterans from Afghanistan reported “handling or uncovering human remains,” while over half of all Iraq veterans surveyed (54%) had firsthand experience with war dead.
Despite the ubiquity of extremely stressful life events, only a minority of survivors develop PTSD. For example, the National Vietnam Veterans Readjustment Study (NVVRS) compiled data from 3016 subjects, comprising 1632 Vietnam theater veterans, 716 veterans from the Vietnam era who did not serve in-theater, and a civilian (n = 668) cohort (Kulka, Schlenger, Fairbank, Hough, Jordan, Marmar, and Weiss, 1990). Lifetime prevalence for PTSD was 31% for males, and 27% for female veterans; incidence rates 20–25 years after the war were 15% and 9%, respectively. Overall, these findings indicate that a majority of Vietnam veterans did not suffer from chronic maladjustment or PTSD even though most combat-experienced soldiers in this study endured repeated and sustained extreme stress. Recent reanalysis of the NVVRS has adjusted original prevalence rates of PTSD in Vietnam veterans from 30.9% to 18.7% lifetime, and 15.2–9.1% current (Dohrenwend et al., 2006). In comparison, lifetime prevalence of PTSD among adult Americans in the NCS was 7.8%, despite a 60.6% exposure rate for men and 51.2% for women. Among current active-duty combat veterans rates of PTSD were concordant with the difference in combat exposure, with 12.5% of Iraq veterans, and 6.2% of Afghanistan veterans meeting PTSD criteria.
Rates of PTSD vary depending on the nature of trauma. For example, rape results in high rates of PTSD in both men (65%) and women (46%), while automobile accidents have been associated with lower rates of PTSD (men, 25%; women, 13.8%). Prevalence rates for PTSD have been as disparate as 20% for wounded combat veterans and 3% for veterans who were not wounded.
Multiple psychological, biological, and environmental factors appear to be involved in the etiology of PTSD. In attempting to understand neural and behavioral mechanisms that contribute to the etiology of PTSD, investigators have highlighted four features of PTSD.
Fear Conditioning and Learning
The Two-Factor model (Mowrer, 1947) is a combination of classical (Pavlovian) and operant (reinforcement) conditioning. Classical conditioning is the process of pairing together, or associating, two stimuli: the traumatic event (unconditioned stimulus, UCS) and associated sensory stimuli (conditioned stimuli, CS). As a result of this pairing, the formerly neutral CS now elicits the same fear response (conditioned response, CR) (and autonomic arousal) as the UCS.
In cases of PTSD, there may be modality specific (i.e., classical conditioning), as well as polymodal (i.e., contextual conditioning), stimuli paired with the CR. Moreover, behavioral neuroscience research has shown that classical and contextual conditioning are partially mediated by different brain regions. Classical conditioning is known to involve thalamo–amygdala pathways, whereas contextual conditioning occurs via input to the hippocampus and amygdala from higher cortical areas. In the case of contextual conditioning, multiple and often complex environmental stimuli that are present during exposure to the feared stimulus (UCS) become associated. For example, after exposure to a roadside Improvised Explosive Device (IED) in Iraq, a veteran while driving in the United States may experience fear and autonomic arousal when exposed to modality specific (e.g., a loud muffler backfire) or contextual (e.g., hot dirt road, trash in the median, and smell of diesel fuel) stimuli, each of which were previously neutral.
According to the classical conditioning model, a learned CR in PTSD should become extinct over time in the absence of exposure to the original trauma (UCS). However, avoidance or escape thoughts and behaviors often produce a welcome mitigation in anxious arousal, thereby creating a powerful reinforcement (operant conditioning) of continued avoidance. The unintended consequence for the sufferer of PTSD is that new learning (extinction of fear-based arousal) is inhibited.
Although a stimulus (S) → response (R) model sufficiently explains the acquisition of fear-based conditioning, it is inadequate in that a stimulus does not always produce the same response. For example, the S → R model does not account for the fact that two people can experience the same exact trauma, yet have different reactions. To account for the variability in responses to a stimulus, the S → R model has been modified to the S → O → R model (Eysenck, 1967), where response to a given stimulus is dependent on the nature of the organism. A major component in an information processing model is the appraisal of trauma-related information. Appraisal of a trauma comprises multiple information processing domains including perceived predictability of the event, controllability of the trauma, intensity of emotions, valence of emotions, and personal meaning assigned to the experience. For example, individuals who assign greater positive meaning to stressful events typically exhibit more adaptive responses.
The processing of trauma-related emotions is particularly relevant to avoidance and intrusive memories. According to the Emotion Processing Theory (Foa and Kozack, 1986), memories of traumatic events are stored, along with associated (i.e., conditioned) cues, in information networks called “fear structures.” The individual with PTSD avoids encountering or thinking about the trauma, or its cues, in an attempt to avoid activation of the associative network of trauma-related memories. Intrusive memories are believed to occur as a result of implicit exposure to one or more cues that activate the fear structure.
A number of neurobiological models have been proposed as an attempt to explain PTSD or specific aspects of PTSD. Prominent among these models are those involving genetic polymorphisms related to stress vulnerability (e.g., polymorphisms of the serotonin transporter gene). Additionally, several models involve detrimental changes to fear, learning, and memory circuits. For example, mammalian learning is known to be optimized by a high degree of neuroplasticity in excitatory inputs to the amygdala from the medial PFC, hippocampus, and thalamus. However, these circuits are also vulnerable to maladaptive alterations secondary to chronic or acute stress, further changing neuromodulation of learning and memory circuits. Such alterations then result in heightened sensitization to stress, enhanced encoding and consolidation of emotional memory, increased fear conditionability, cortical inhibition of limbic activity, and reduced capacity for extinction. Neurobiological vulnerabilities may also be responsible for certain structural abnormalities (e.g., reduced hippocampal volume); although it is uncertain whether these abnormalities are the cause or consequence of PTSD.
Several factors have been identified with increased risk for PTSD. Individual risk factors for PTSD include gender (female), history of prior trauma (i.e., childhood sexual abuse), and a family history of anxiety disorders. For example, data indicate women are twice as likely as men to develop PTSD. However, although several studies do in fact reveal higher rates of PTSD for women, it is necessary to interpret these results within the context of differences in types of trauma to which men and women are most commonly exposed. A review of PTSD research conducted since 1991 did find distinctions in exposure to trauma and PTSD between men and women (Hidalgo and Davidson, 2000). Results suggest that although men are at higher risk of exposure to traumatic events, women are more at risk for developing PTSD. Moreover, men experienced more physical assault and life-threatening traumas, whereas women experienced more sexual assault and childhood parental neglect.
Certain dimensions of personality are also implicated as risk factors for PTSD. In particular, individuals with a stable and consistent pattern of experiencing negative emotionality (NEM) may be more vulnerable to PTSD following exposure to an extreme stressor. NEM is a disposition characterized by anxiety, emotional lability, poor interpersonal interactions, and overall negative mood. A related personality construct is neuroticism, which is defined by a high degree of negative affect, and increased acquisition of fear through conditioning. Longitudinal studies of combat veterans pre- and postdeployment have revealed NEM as a significant predictor of both PTSD development and severity. Conversely, positive emotionality (PEM) is hypothesized as a personality factor that moderates the relationship between NEM and PTSD.
Aspects of the trauma and the way it was experienced are also risk factors for PTSD; in general, the greater the intensity of the trauma, the greater the CR and prevalence of PTSD. Factors that contribute to the intensity of the traumatic response and PTSD include duration of the trauma, predictability and controllability of the event, failed attempts to avoid injury, perceived sense of failure, actual loss, proximity to the traumatic event and degree of peritraumatic arousal and dissociation. A survey of 1008 adult survivors of the September 11 World Trade Center attacks found that 7.5% reported symptoms consistent with a diagnosis of PTSD; however, higher rates of PTSD (20%) were found within the larger sample for those living closer to the World Trade Center (Galea, Ahern, Resnick, Kilpatrick, Bucuvalas, Gold, and Vlahov, 2002).
Given that not all individuals exposed to the same traumatic event will develop PTSD, it becomes vital to understand what it is about those individuals who do well under stress and are able to recover from trauma? In contrast to traditional investigations that seek to determine the causes and catalysts for psychopathology, resilience research, particularly within the field of trauma studies, attempts to explain why some individuals are relatively resistant to the negative impact of trauma, recover rapidly after traumatic exposure, or experience positive growth in response to trauma. Resilience to stress has been investigated from neurobiological (Charney, 2004) and psychosocial perspectives (Southwick, Vythilingam, and Charney, 2005).
Neurobiological Resilience Factors
Numerous genetic factors, developmental influences, brain regions, endocrine and neurotransmitter systems appear to be associated with resilience to stress. Among the neurobiological factors that recently have received attention are: sympathetic nervous system activity that responds robustly to stress but that returns to baseline rapidly perhaps secondary to regulation by neuropeptide Y (NPY) and galanin; capacity to contain the corticotrophin-releasing factor (CRF) response to stress perhaps in association with DHEA, NPY and a host of other regulators; a durable dopamine-mediated reward system that might allow traumatized individuals to remain optimistic and hopeful even in the context of extreme or chronic stress; amygdalae that do not overreact to the environment; hippocampi that provide sufficient inhibition to the hypothalamic-pituitary-adrenal axis (HPA axis); and ample cortical executive and inhibitory capacity.
Elevated levels of plasma NPY have been found in humans following extreme stressors such as military survival training. Moreover, higher levels of NPY have been correlated with better performance during simulated prisoner of war training with Special Forces soldiers. Lower baseline and yohimbine-stimulated levels of NPY have been found in combat veterans with a current diagnosis of PTSD, but other studies of combat-related PTSD and female victims of sexual assault (Seedat, Stein, Kennedy, and Hauger, 2003) have yielded mixed results, suggesting that low levels of NPY are not associated with PTSD, but rather exposure to trauma.
Other neurophysiological factors associated with improved performance under extreme stress and the ability to physically and mentally recover following trauma are low vagal tone and increased heart rate variability (Morgan, Aikins, Steffian, Hazlett, and Southwick, 2007).
A traditional view of resilience is that people who have a stronger constitution are more functional under all circumstances. An alternative view is that people are biased by their genotypes to function best at certain levels of arousal, e.g., COMT gene polymorphism. Under resting conditions, the less functional variant (higher dopamine in PFC) functions better with respect to PFC-related cognitive function, but with stress, the less functional variant is overstimulated and functions more poorly than the other group. The people with higher functioning COMT (less dopamine) are “sluggish” under normal conditions but function more optimally relative to their peers under conditions of high stress.
Psychosocial Resilience Factors
Resilience to stress has been correlated with optimism, humor, social support, and an active instead of avoidant coping-style. Research has also identified openness-to-change and extroversion as positive predictors of growth following traumatic experiences. Two closely related constructs associated with resilience are cognitive flexibility and emotion regulation. Cognitive flexibility, marked by the ability to reframe problems and extract personal meaning from stressful situations, has been associated with reappraisal of events as less threatening and a greater sense of self-efficacy in the face of challenge. Moreover, there is some evidence to suggest that resilience is not a static or stable dimension, but is responsive to therapeutic and pharmacological augmentation.
Clearly, resilience to stress is associated with a complex set of interactions between neurobiological and psychosocial factors. For example, Kaufman et al. (2004) studied the effects of social support networks in children who were at risk genetically (s/s allele of the 5-HTTLPR serotonin transporter gene promoter polymorphism) and environmentally (documented history of maltreatment) revealed that strength of social support networks and positive social relationships moderated the risk for depression above and beyond genetic vulnerabilities and early exposure to overwhelming stress.
A study of 4042 Vietnam era twin pairs indicates that vulnerability to PTSD has a significant genetic component. After controlling for variability in combat exposure, genetic concordance accounted for 13–30% of the variance in reexperiencing symptoms (Cluster B), 30–34% of the variance in avoidance symptoms (Cluster C), and 28–32% of the variance in the (Cluster D) hyperarousal symptoms.
Studies of probands with anxiety disorders and other twin studies indicate that PTSD symptoms are moderately heritable. Increasingly, evidence suggests that PTSD is caused by a complex interaction between genetic vulnerabilities to stress and the nature of the stressor. Given the inherent difficulty in isolating environmental stressors, experimentally controlling for extraneous variables during traumatic events, and the unlikelihood of identifying a single PTSD gene, there is growing interest in endophenotypes.
In monozygotic twins discordant for service in Vietnam, premorbid NSS scores can predict PTSD when coupled with exposure to the stress of combat (Gurvits et al., 2006). However, a longitudinal study, also of co-twins discordant for combat exposure in Vietnam, found that degree of combat stress, not a genetic vulnerability, was the strongest predictor of persistence of PTSD symptoms 30 years after exposure (Roy-Byrne, Arguelles, Vitek, Goldberg, Keane, True, and Pitman, 2004). Results from psychophysiological research similarly suggest that not all PTSD symptoms are genetically determined. For example, a study of (n = 50) monozygotic twin pairs discordant for combat exposure in Vietnam showed that the noncombat exposed co-twin failed to demonstrate increased heart rate in response to startling tones. The fact an increased heart rate response to startling tones was evident in the combat exposed group, but not their co-twins, suggests that some aspect of autonomic reactivity is not related to genetic factors.
PTSD is characterized by a constellation of reexperiencing, avoidance, and hyperarousal symptoms. Most pathognomonic among these three symptom clusters are episodes of reexperiencing (i.e., flashbacks, nightmares, and intrusive memories). Such memories are rarely, if ever, wanted, and intrude against the will, sometimes for years or even a lifetime. Individuals with PTSD typically try to avoid these memories, both cognitively and behaviorally, and often rearrange their lives around avoiding potential reminders of the trauma that trigger remembrance.
In addition to cognitive and behavioral avoidance, PTSD is marked by significant avoidance of emotional arousal (i.e., emotional numbing); indeed, of the three symptom clusters, avoidance and emotional numbing are most predictive of a PTSD diagnosis and can have debilitating effects on psychosocial function. For instance, evaluation of survivors of the Oklahoma city bombing has shown that Cluster C (avoidance and numbing) symptoms were pivotal to the diagnosis of PTSD, whereas Clusters B (re-experiencing) and D (arousal) were not significantly associated with diagnosis. Of the survivors who met diagnostic criteria for Cluster C, 96% had a diagnosis of PTSD; however, of those who met Cluster B or Cluster D criteria, only 40% and 39% were diagnosed with PTSD, respectively. Conversely, for those individuals who did not receive a diagnosis of PTSD, only 2% met Cluster C criteria, whereas 70% and 73% met criteria for Clusters B and D, respectively.
Some individuals with PTSD experience amnesia for aspects of the traumatic event. This inability to recall certain trauma-related memories, despite hyperaccessibility of other trauma memories, may be explained in part by selective attention, dissociation, or extreme arousal, which can compromise encoding and consolidation of memory at the time of trauma. Likewise, degree of dissociation has been found to be highly predictive of PTSD following life-threatening trauma. Emotional numbing can be difficult to identify clinically since it is not necessarily manifest as flat affect, but rather as a restricted range of affect, and marked detachment from others. In this regard, collateral reporting sources (e.g., family members, significant others) are often integral to an accurate diagnostic assessment. Moreover, emotional numbing can often appear as indifference toward future plans and general apathy about setting goals such as getting married, owning a home, need for a healthy lifestyle, or career advancement.
Insomnia is a major problem for many trauma survivors with PTSD. They often describe difficulty falling asleep and staying asleep secondary to hypervigilance and/or fear of having nightmares. It is not uncommon for vivid nightmares to violently awaken survivors from their sleep.
A number of psychophysiological findings, characteristic of autonomic reactivity, help to differentiate individuals with current PTSD from those with a past diagnosis of PTSD or no history of PTSD. Increased heart rate reactivity to trauma-related stimuli (e.g., imagery, narratives) has been found in individuals with PTSD. Such cardiac-reactivity appears to be relatively specific to PTSD, as comparison studies including veterans with anxiety disorders other than PTSD have not shown similar increases in heart-rate. Moreover, cardiac reactivity in PTSD does not appear to be a generalized autonomic response to indiscriminate stressors, but rather is associated with trauma specific cues (Orr, Metzger, and Pitman, 2002). PTSD has also been identified by exaggerated startle response, as measured by EMG “eyeblink,” increased skin conductance (SC) magnitudes (e.g., galvanic skin response) and slower SC habituation, and increased conditionability to aversive (laboratory shock) stimuli.
Information processing biases in PTSD have been studied using various cognitive paradigms. Although some trends in information processing bias have emerged, conclusive results in PTSD have been elusive. For example, individuals with PTSD have demonstrated an attentional bias for threat-related words during the color-naming portion of the Stroop task. Namely, compared to control samples, individuals show an increased latency in naming trauma or emotion words. While this is a robust finding, it is not clear how such results should be interpreted. It remains unclear whether an increased latency for naming trauma words is due to more rapid encoding in individuals with PTSD. Alternatively, those with PTSD may attempt to inhibit (i.e., avoidance) processing of emotionally aversive stimuli.
There is tentative support for biases in judgment showing that individuals with PTSD interpret ambiguous sentences and words (e.g., homographs) as threatening. Memory biases in PTSD have been less consistently demonstrated. In particular, there is some evidence for a mood-congruent memory effect in PTSD, to wit, individuals with PTSD demonstrate a memory advantage for trauma-related information. However, it remains unclear whether this explicit memory bias is the result of recall advantages inherent in personally salient information, or whether the advantages are due to true mood congruency between internal affective state and emotional valence assigned to the remembered material. Support for implicit memory biases in PTSD, based on implicit priming (i.e., below perceptual awareness threshold) and word stem completion task paradigms, is also limited.
Biases in forgetting, in particular thought suppression and cognitive avoidance, have been explored as an explanation for the inconsistent memory findings in PTSD. It has been hypothesized that individuals with PTSD will attempt to suppress or avoid recall of trauma-related memories. In fact, some studies have indicated a bias away from anxiety-provoking information, suggesting there is an implicit or strategic effort to avoid aversive thoughts and memories. However, evidence that individuals with PTSD engage in cognitive avoidance strategies or thought suppression during recall of trauma-related information is tentative.
Individuals with PTSD demonstrate a range of cognitive abnormalities, particularly in the areas of attention, concentration, learning, and memory (Vasterling and Brewin, 2005). Additionally, PTSD is associated with lower full-scale IQ; however, reliance on estimates of premorbid intellectual functioning makes causal inferences difficult. Individuals with PTSD show deficits in working memory and sustained attention, but not on tasks of executive set switching. Of note, cognitive deficits in these domains occur with threat-neutral, nontrauma-related stimuli. Similarly, PTSD research with emotionally neutral list-learning tasks has revealed retrieval deficits for newly learned information. That deficits occurred for free recall of recently learned information, but not during recognition trials, suggests that such impairments are not due to encoding impairments, but rather indicate a problem with consolidation of new information into long-term storage. Neuropsychological domains that predominantly remain intact include visuospatial functioning, language, and psychomotor performance.
Multiple neurobiological alterations or abnormalities have been associated with PTSD. The most extensively studied alterations have involved the HPA axis and the sympathetic nervous system. Alterations in the HPA axis in PTSD include (i) elevated resting cerebrospinal fluid levels of CRF; (ii) alterations in 24-hour urine excretion of cortisol, 24-hour plasma cortisol levels, lymphocyte glucocorticoid receptor number, cortisol response to dexamethasone, adrenocorticotropic hormone (ACTH) response to CRF, b-endorphin and ACTH response to metryapone; and (iii) adrenal androgen abnormalities.
Alterations in sympathetic nervous system reactivity include exaggerated increases in heart rate, blood pressure, norepinephrine, and epinephrine in response to traumatic reminders administered in the laboratory; elevated 24-hour plasma norepinephrine; elevated 24-hour urine excretion of norepinephrine and epinephrine, reduced platelet adrenergic receptor number; increased subjective, behavioral, physiological, and biochemical (increased plasma methoxyhydroxyphenylglycol) responses to intravenous yohimbine (an α2-adrenoreceptor antagonist); blunted response to clonidine; and altered yohimbine-induced cerebral blood flow. Alterations in sympathetic nervous system reactivity may contribute to symptoms of reexperiencing and hyperarousal. Neurocognitive and brain imaging studies comparing individuals with PTSD and individuals without psychiatric disorders have reported that subjects with PTSD show biased attention to negative and potentially dangerous information, reductions in hippocampal volume and function, exaggerated amygdala responses to stressful cues, and stress-induced reduction in PFC metabolism.
Positron Emission Tomography (PET) of individuals with PTSD has shown increased activity of the right hemisphere amygdaloid complex during rehearsals of the precipitant trauma. Other research has indicated bilateral hippocampal volume reduction in PTSD, hypothesized to be secondary to the deteriorating effects of glucocorticoids on pyramidal cells in the CA1 and CA2 regions. Moreover, functional magnetic resonance imaging (fMRI) studies of PTSD have shown a positive correlation between symptom severity and reduced hippocampal activity during tests of learning and memory (See Etiology).
PTSD can occur from very early childhood to late in life. Onset of PTSD symptoms most commonly occurs within 3 months following trauma exposure, although symptom manifestation has been known to be delayed for years after the trauma. The course of PTSD is variable, with distinctions sometimes made among chronic, intermittent, residual, and reactivated types. Despite variation in course, epidemiologic studies suggest that the majority of symptoms do attenuate with time. For example, the NCS indicated that PTSD resolve in 6 years for approximately 60% of cases. Follow-up research on 2752 New York city residents 6 months after the terrorist attacks revealed a marked decline in the rates of PTSD from 7.5% to 0.6% (Galea, Vlahov, Resnick, Ahern, Susser, Gold, Bucuvalas and Kilpatrick, 2003). However, it may be that some symptoms are more likely to decrease than others over time. A study of Israeli military personnel over a 2-year period found that symptoms of reexperiencing and intrusive memories decreased, but avoidance and emotional numbing symptoms increased. Although recovery occurs within 3 months in approximately half of those diagnosed with PTSD, for those who do not recover within 3 months PTSD is often chronic and markedly detrimental to physical, social, occupational, and interpersonal functioning.
Moreover, PTSD can be complicated by recurrent exposure to trauma or trauma-associated cues that trigger reactivation of symptoms.
A variety of rating scales have been developed for the assessment of PTSD, the nature of certain traumas, and specific responses to trauma. Many of these measures have been validated for use in diagnostic and treatment settings.
Combat Experiences Scale (CES)
The CES is an assessment of exposure to stereotypical warfare experiences such as firing a weapon, being fired on (by enemy or friendly fire), witnessing injury and death, and going on special missions and patrols that involve such experiences. The CES, standardized in a Persian Gulf War sample, was developed as contemporary version of the Vietnam era Combat Exposure Scale.
Posttraumatic Stress Checklist (PCL)
The PCL is a 17-item assessment of PTSD symptom severity developed by the National Center for PTSD. The military version of the PCL is keyed to stressful military experiences, and corresponds to 17 items directly adapted from the DSM-IV PTSD criteria. Psychometric data were obtained from veterans of the Vietnam War as well as the Persian Gulf War.
Posttraumatic Diagnostic Scale (PDS)
The PDS is a 49-item measure of PTSD symptom severity and frequency according to the DSM-IV criteria. Symptom severity is anchored to an individual's ‘most upsetting traumatic event.’ The PDS is distinct from other PTSD assessments in that it also assesses features Criteria A (trauma) and Criteria F (functioning).
Clinician Administered Scales
Clinician Administered PTSD Scale (CAPS)
The CAPS is a structured clinical interview measuring the frequency and intensity of the 17 DSM-IV symptoms of PTSD and 8 associated symptoms. The CAPS also contains five global rating questions regarding the impact of symptoms on social and occupational functioning, improvement since previous assessment, and overall validity and severity of reported symptoms.
Structured Clinical Interview for DSM Disorders (SCID)
The SCID is a clinician-based structured interview designed to assess the majority of Axis I and Axis II disorders. The PTSD portion of the SCID is found in Module F—Anxiety Disorders. Several versions of the SCID are available for use dependent on the setting (e.g. research, clinical, and nonpatient populations). The SCID is also available in several different languages.
Mississippi Scale for PTSD
The scale consists of 39 self-report items derived from the Diagnostic and Statistical Manual of Mental Disorders III-R criteria for PTSD. The first version of the Mississippi Scale contained 35 items, based on the unrevised DSM-III criteria for PTSD. The four added items (items 36–39) assess reexperiencing, psychogenic amnesia, hypervigilance, and increased arousal symptomatology.
Impact of Events Scale (IES)
The IES is a 22-item self-report measure of reaction to stressful events. The IES was created for the study of bereaved individuals, and was then adopted for studying the psychological impact of trauma.
Trauma Symptom Inventory (TSI)
The TSI is a 100-item evaluation of acute and chronic symptomatology from a wide variety of traumas, including rape, combat experiences, major accidents, natural disasters, as well as childhood abuse. The various scales of the TSI assess a wide range of psychological impacts. These include not only symptoms typically associated with PTSD or acute stress disorder (ASD), but also those intra- and interpersonal difficulties often associated with more chronic psychological trauma. The TSI does not generate DSM-IV diagnoses; instead, it is intended to evaluate the relative level of various forms of posttraumatic distress.
Differential Diagnosis (Including Comorbid Conditions)
Symptoms that arise from an event that is stressful, but not of the life-threatening nature and intensity of Criterion A events for PTSD, fall under the rubric of AD.
Acute Stress Disorder (ASD)
ASD is differentiated from PTSD on two criteria. The first is that ASD symptoms must occur within 4 weeks of the traumatic event, whereas PTSD may have a delayed onset. The second distinction is that ASD symptoms must remit within 4 weeks of their initial presentation; symptoms that last beyond 4 weeks may indicate PTSD.
Obsessive-Compulsive Disorder (OCD)
OCD and PTSD have overlapping symptoms of intrusive thoughts. However, unwanted thoughts in PTSD are distinct in that they are circumscribed to trauma-related events and memories. Although intrusive thoughts in OCD are often distressing, they are not specific to a traumatic event.
Delusions and hallucinations, characteristic of psychotic episodes, are distinct from those that occur during PTSD flashbacks. According to diagnostic criteria, persistent reexperiencing of the trauma may include hallucinations and illusions about specific life-threatening events. Such flashbacks may seem, at the time, real to the individual with PTSD. However, conclusion of the PTSD flashback is frequently followed by an acknowledgment that the event was not really reoccurring although it felt like it at the time. In contrast, by their nature, delusions and hallucinations are indistinguishable from reality for the person experiencing psychosis.
An emerging literature on the comorbidity of Axis II disorders with anxiety spectrum disorders requires an understanding of personality disorders that frequently co-occur with PTSD. Both retrospective and longitudinal research have identified significant correlations between PTSD and some Axis II disorders. In particular, there is a close relationship between PTSD and borderline personality disorder (BPD). Longitudinal research documented that a diagnosis of PTSD, rather than a history of mere trauma exposure, was the strongest predictor of features of BPD. Among the Axis II features most closely associated with PTSD: Frantic efforts to avoid abandonment; rejection of help; inappropriate anger; general impulsiveness.
PTSD diagnostic evaluations rely predominantly, if not exclusively, on self-report measures. An accurate diagnosis of PTSD can be complicated by the fact that, by definition, it requires an identifiable (Criterion A1) event. As such, issues of secondary gain and remuneration for personal damages make PTSD especially open to legal scrutiny of potential malingering. Thus, ruling out feigned symptoms through collateral reporting sources and psychometrically sound measures is a fundamental component of differential diagnosis for PTSD.
Epidemiological studies indicate that PTSD is rarely a sole diagnosis. In both the NCS and the NVVRS, 50–88% of individuals with a diagnosis of PTSD also had at least one concomitant disorder. In the NVVRS, 99% of those who received a diagnosis of PTSD had at least one other comorbid diagnosis in their lifetime. The most prevalent comorbid diagnoses with PTSD are major depressive disorder (MDD) and alcohol abuse. Although MDD tends to occur equally in males and females as a comorbid diagnosis, alcohol abuse is more frequently found among males with PTSD. Anxiety spectrum disorders such as specific phobias, social phobia, generalized anxiety disorder (GAD), and agoraphobia frequently co-occur with PTSD. Results from the NCS also revealed high comorbidity rates for anti-social personality disorder (43% male and 15% female). Other studies of Axis II disorders and PTSD have been limited by sample size, but reveal notable trends. Among these studies, high PTSD comorbidity rates have been found in BPD and paranoid personality disorder.
Empirically validated interventions specifically for PTSD are in their nascency, and have evolved from treatments showing success in the larger set of anxiety spectrum disorders. Prominent among current treatment modalities are cognitive–behavioral therapy (CBT) and selective serotonin reuptake inhibitors (SSRIs). Additionally, treatment combining medication and therapy is often optimal.
Selective Serotonin Reuptake Inhibitors (SSRIs)
Serotonin is implicated in PTSD, as well as a variety of other mood and anxiety disorders that are frequently comorbid with PTSD (e.g., depression, anxiety, impulsivity, substance abuse). Several selective serotonin reuptake inhibitors (SSRIs) have been studied in the treatment of PTSD (Friedman, 2002): sertraline, paroxetine, fluoxetine, and fluvoxamine. Randomized clinical trials (RCTs) have shown SSRIs to be efficacious in treating symptoms in all three PTSD clusters (i.e., reexperiencing, avoidance and numbing, hyperarousal), as well as in treating symptoms associated with PTSD such as impulsivity, depression, suicidal thoughts, obsessive thinking, and substance abuse. To date, sertraline and paroxetine are the only two medications approved by the U.S. Food and Drug Administration for the treatment of PTSD.
Monoamine Oxidase Inhibitors (MAOIs)
MAOIs have been found especially effective in reducing PTSD symptoms of reexperiencing and sleep disturbance; however, avoidance and hyperarousal symptoms have been largely unaffected. Moreover, RCTs involving MAOIs have been limited because of potential side effects, particularly in patients with comorbid substance abuse disorders.
Tricyclic Antidepressants (TCAs)
Imipramine, amitriptyline, and desipramine, among the most effective TCAs for depression and other anxiety disorders, have not received sufficient study in the treatment of PTSD. In the relatively few trials that have been conducted, TCAs have appeared to be most helpful for re-experiencing symptoms.
Similar to MAOIs, antiadrenergic agents (e.g., clonidine, guanfacine, and propranolol) reduce reexperiencing and hyperarousal symptoms in PTSD. A pilot study (Pitman et al., 2002) suggests propanolol may alter consolidation of trauma memories, thereby inhibiting trauma conditioning immediately following acute exposure. However, replication of this finding is pending in several RCTs.
As with other anxiety disorders, the long-term risks of prescribing benzodiazepines for PTSD may outweigh their immediate anxiolytic benefits. The short half-life of some benzodiazepines can facilitate medication tolerance and dependence, and also serve as a powerful reinforcement for avoidance and numbing coping mechanisms. Moreover, benzodiazepines often become a safety signal and a significant obstacle to exposure treatments, therein prohibiting extinction learning in CBT. Despite their widespread use for many anxiety disorders, benzodiazepines have not been found efficacious in treating PTSD.
Cognitive–Behavioral Therapy (CBT)
Although cognitive–behavioral approaches were developed specifically for PTSD, CBT has become the preferred treatment modality given growing treatment outcome data demonstrating its success with other anxiety disorders. CBT comprises several variations, all of which have a goal of fear extinction and improved coping through conditioning and modifying thoughts.
Exposure therapy involves reexposing the traumatized individual to sensory stimuli associated with the traumatic event. Exposure can take the form of mental imagery, pictures, role playing, virtual reality, or reinstatement of physiological arousal cues through interoceptive exercises (i.e., sweating, hyperventilation, increased heart and respiratory rates, etc.). The duration of exposure varies, and can be as short as a few seconds, or as long as 90 minutes (e.g., Prolonged Exposure [PE] therapy). In hierarchical reexposure, trauma cues are introduced systematically, starting with the least threatening stimuli, gradually increasing to exercises of greater intensity as desensitization is achieved. Systematic desensitization (SD) occurs over a period of several weeks, though some approaches immediately escalate to the most extreme stressors (e.g., flooding therapy). In either approach, the key to successful exposure therapy is controlling avoidance behaviors, and ensuring a positive outcome at the conclusion of each exposure trial. A positive outcome is imperative for each exposure to facilitate extinction of the original feared cue through learning new associations (i.e., cue = positive or tolerable outcome).
Stress Inoculation Training (SIT)
The principle goal of SIT is to reduce fear reactions that foster operant avoidance and prohibit extinction learning. This goal is accomplished through a three-stage process involving psychoeducation (conditioning theory and psychobiology of fear), cognitive skills training (reframing and relaxation techniques), and application (scenarios, roleplaying, or in vivo exposures).
CT for PTSD focuses on thoughts and beliefs about the trauma and its associated cues. Targeted thoughts include “the likelihood the trauma will reoccur,” “how the individual has responded to trauma,” and “what certain reactions to trauma exposure might mean.” Individuals are encouraged to identify assumptions and automatic beliefs about the traumatic event (e.g., “I can't handle this,” “I’m going crazy,” or “PTSD will ruin my life forever”). Individuals then learn to challenge those assumptions through alternative hypothesis generation and reality testing. Other cognitive skills involve learning how to change perspectives (i.e., cognitive reframing or restructuring), decatastrophizing, and relaxation techniques.
Cognitive Processing Therapy (CPT)
CPT was developed to address the broader range of emotions other than fear that frequently accompany PTSD in victims of rape and crime: anger, guilt, sadness, and shame (Resick and Schnike, 1992). CPT focuses on memories of the traumatic event, exploring associated intense emotions. Trauma memories are explored through use of diaries and narrative scripts about their trauma, and individuals are encouraged to articulate personal meaning of the traumatic event. Memories of the trauma are reconstructed in narrative format, incorporating as much sensory stimuli into the description as possible. These narratives are then to be read on a daily basis for several weeks. Therapy sessions involve discussion of the trauma narrative, and examination of irrational thoughts and unpleasant emotions evoked by remembering. Support for CPT continues to grow, due in part to recent comparison studies that highlight larger treatment effect sizes compared to medication. For example, following a 12-session course of CPT in Vietnam combat veterans, 40% of the intention to treat sample no longer met diagnostic criteria for PTSD, a result that was independent of service-connected disability status (Monson et al., 2007).
Eye-Movement Desensitization and Reprocessing (EMDR)
EMDR is a controversial technique, not regarding its efficacy, but rather its theoretical underpinnings. EMDR was unintentionally discovered when its originator (Shapiro, 1995) noticed that focusing visual attention on wave movements of tree leaves in the wind provided relief from unpleasant rumination. From this observation, EMDR has evolved as a repetitive lateral eye-movement exercise that facilitates cognitive processing of trauma-related thoughts. EMDR is conducted by the therapist waving the tip of the index finger rapidly back-and-forth in front of the patient's eyes. The finger tip is held 30–35 cm from the patient's face at a rate of 2 waves per second, for a total of 24 waves. Following each eye-movement trial, the patient is instructed first to attempt to block out the memory, take a relaxing breath, and then return to the memory. Each sequence of EMDR is followed by subjective appraisals of distress precipitated by the memory; the sequence is repeated until subject distress decreases to zero.