Posttraumatic Stress Disorder
DSM-IV-TR Diagnostic Criteria
The person has been exposed to a traumatic event in which both of the following were present:
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 person’s response involved intense fear, helplessness, or horror
Note: In children, this may be expressed instead by disorganized or agitated behavior.
The traumatic event is persistently re-experienced in one (or more) of the following ways:
Recurrent and intrusive distressing recollections of the event, including images, thoughts, or perceptions
Note: In young children, repetitive play may occur in which themes or aspects of the trauma are expressed.
Recurrent distressing dreams of the event
Note: In children, there may be frightening dreams without recognizable content.
Acting or feeling as if the traumatic event were recurring (includes a sense of reliving the experience, illusions, hallucinations, and dissociative flashback episodes, including those that occur on awakening or when intoxicated)
Note: In young children, trauma-specific reenactment may occur.
Intense psychological distress at exposure to internal or external cues that symbolize or resemble an aspect of the traumatic event
Physiological reactivity on exposure to internal or external cues that symbolize or resemble an aspect of the traumatic event
Persistent avoidance of stimuli associated with the trauma and numbing of general responsiveness (not present before the trauma), as indicated by three (or more) of the following:
Efforts to avoid thoughts, feelings, or conversations associated with the trauma
Efforts to avoid activities, places, or people that arouse recollections of the trauma
Inability to recall an important aspect of the trauma
Markedly diminished interest or participation in significant activities
Feeling of detachment or estrangement from others
Restricted range of affect (e.g., unable to have loving feelings)
Sense of foreshortened future (e.g., does not expect to have a career, marriage, children, or a normal life span)
Persistent symptoms of increased arousal (not present before the trauma), as indicated by two (or more) of the following:
Difficulty falling or staying asleep
Irritability or outbursts of anger
Difficulty concentrating
Hypervigilance
Exaggerated startle response
Duration of the disturbance (symptoms in Criteria B, C, and D) is more than 1 month.
The disturbance causes clinically significant distress or impairment in social, occupational, or other important areas of functioning.
(Reprinted, with permission, from Diagnostic and Statistical Manual of Mental Disorders, 4th edn., Text Revision. Washington DC: American Psychiatric Association, 2000.)
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.
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).
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.
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.
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