Chapter 28: Posttraumatic Stress Disorder PDF

Barry University Library Access Provided by: Current Diagnosis & Treatment: Psychiatry, 4th Edition Chapter 28: Posttraumatic Stress Disorder and Acute Stress Disorder...

Barry University Library Access Provided by: Current Diagnosis & Treatment: Psychiatry, 4th Edition Chapter 28: Posttraumatic Stress Disorder and Acute Stress Disorder Douglas C. Johnson; John H. Krystal; Steven M. Southwick† †Deceased POSTTRAUMATIC STRESS DISORDER General Considerations It has long been known that traumatic events can have profound effects on memories, cognitions, emotions, and behaviors. However, 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 is relatively recent. PTSD­like disorders were described in the U.S. Civil War (DaCosta’s syndrome, irritable heart of soldiers), following railroad accidents in the late nineteenth century (Railway Spine), and as the tragic consequence of World Wars I and II (shell shock, traumatic neurosis, neurasthenia, and 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 DSM­II. In 1980, in the wake 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 schemata. Unlike other disorders, PTSD is predicated on the occurrence of at least one discrete external event, namely a precipitating trauma. DSM­III 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 DSM­IV­TR stipulated two subcriteria—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 DSM­III to DSM­IV resulted in higher rates of PTSD in a number of epidemiologic studies. Critical work on effective therapies, incidence, and cost of PTSD to society are generally based on studies of American military veterans. The fiscal year 2005 report from the Department of Veterans Affairs (VA)n indicated that PTSD was the costliest diagnosis for the VA, and the third most frequently claimed disability, making up 4.2% of all claims. The DSM­5 removed subcriterion A2, rendering individual response to traumatic events irrelevant to diagnosis. Moreover, with DSM­5 and DSM­5­5TR, PTSD is no longer considered an anxiety disorder and is listed under a new category of Stress and Trauma­Related Disorders. A. Epidemiology 1. Extreme stress exposure A majority of Americans have been 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 (Kessler et al, 1995). Of those who had experienced at least one of these events, 56.3% of men and 48.6% of women reported experiencing multiple extremely stressful events. The prevalence of exposure to extreme stress has also been examined within specific populations such as women, inner­city residents, and combat veterans. For example, in a sample of 4008 American women, 69% of respondents reported at least one traumatic event in her life (Resnick et al, 1993); in the city of Detroit reported rates of traumatic exposure were 92.2% for men and 87.1% for women (Breslau et al, 1998); and among U.S. Army and Marine Corps personnel serving in Iraq, 70% endorsed “seeing dead or seriously wounded or killed Americans” (Hoge et al, 2004). Downloaded 2025­2­16 5:21 P Your IP is Chapter 28: Posttraumatic Stress Disorder and Acute Stress Disorder, Douglas C. Johnson; John H. Krystal; Steven M. Southwick† Page 1 / 18 2. Prevalence ©2025 McGrawrates of PTSD Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility In the NCS, 7.8% of Americans met DSM­III criteria for lifetime PTSD despite a 60.6% exposure rate for men and 51.2% for women (Kessler et al, 1995). of women reported experiencing multiple extremely stressful events. Barry University Library The prevalence of exposure to extreme stress has also been examined within specific populations such as women, inner­city residents, andby: Access Provided combat veterans. For example, in a sample of 4008 American women, 69% of respondents reported at least one traumatic event in her life (Resnick et al, 1993); in the city of Detroit reported rates of traumatic exposure were 92.2% for men and 87.1% for women (Breslau et al, 1998); and among U.S. Army and Marine Corps personnel serving in Iraq, 70% endorsed “seeing dead or seriously wounded or killed Americans” (Hoge et al, 2004). 2. Prevalence rates of PTSD In the NCS, 7.8% of Americans met DSM­III criteria for lifetime PTSD despite a 60.6% exposure rate for men and 51.2% for women (Kessler et al, 1995). Similar rates were reported in the National Epidemiologic Survey on Alcohol and Related Conditions, where 6.4% of 34,653 Americans met DSM­IV criteria for lifetime PTSD with an additional 6.6% meeting criteria for lifetime partial PTSD (Pietrzak et al, 2011). As part of the National Comorbidity Survey Replication, lifetime morbid risk for PTSD (i.e., the percentage of Americans who already have a lifetime history of PTSD plus those who do not have a lifetime history of PTSD but who are expected to develop PTSD at some point in their life) has been estimated at 10.1% (Kessler et al, 2012). 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%), whereas automobile accidents have been associated with lower rates of PTSD (men, 25%; women, 13.8%) (Kessler et al, 1995). Regarding rates of PTSD among veterans of war, the National Vietnam Veterans Readjustment Study (NVVRS) found that 18.7% of Vietnam veterans met lifetime and 9.1% current criteria for PTSD (Dohrenwend et al, 2006). More recently the Institute of Medicine estimated prevalence of PTSD to be between 13% and 20% among U.S. soldiers who served in Iraq and Afghanistan (IOM, 2012). B. Etiology 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 at least four features of PTSD. 1. Fear conditioning and learning The Two­Factor 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 modality­specific (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 in Iraq, a veteran while driving in the United States may experience fear and autonomic arousal when exposed to modality­specific (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. Sounds, sights, smells, time of day or year (i.e., anniversary reaction), or other ordinarily neutral stimuli that are present during the frightening event may later trigger fear and physiological arousal. Typically, fear­conditioned memories extinguish over time if survivors systematically expose themselves to fear­inducing stimuli while in a safe environment. Gradually, the brain learns that these stimuli are no longer dangerous. However, when trauma survivors knowingly or unknowingly avoid traumatic thoughts, triggers, or reminders in order to avoid feeling anxious or afraid, they no longer have the opportunity to extinguish these fear­ conditioned memories. Although avoidance generally reduces anxious arousal in the short run, it also creates a powerful reinforcement for continued avoidance with the unintended consequence of perpetuating trauma­related psychopathology. 2. Information processing Although a stimulus (S) → response (R) model sufficiently explains the acquisition of fear­based conditioning, it is inadequate in that a stimulus does not always produce the same response. Models that involve the processing of information and emotions typically emphasize the role of appraisal or interpretation of trauma­related information/experiences. Individuals are more likely to appraise a situation as threatening or out of their control, and thus are more likely to develop trauma­related psychopathology, when they believe that they do not possess the personal capabilities or external resources to meet the demands of the situation. On the other hand, individuals are more likely to appraise a situation as a challenge when they believe they can successfully deal with it. Whether an individual appraises a stressful situation as a challenge or a threat depends on numerous factors including personality, cognitive, behavioral and emotion regulation skills, prior experiences of success or failure in stressful situations, personal Downloaded 2025­2­16 5:21 P Your IP is meaning of the Chapter 28: event, and quality Posttraumatic Stressand degreeand Disorder of social Acutesupport, among other Stress Disorder, factors Douglas C. (Southwick & Charney, Johnson; John 2012). H. Krystal; Steven M. Southwick† Page 2 / 18 ©2025 McGraw Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility The processing of trauma­related emotions is particularly relevant to avoidance and intrusive memories. According to the Emotion Processing Theory (Foa & Kozack, 1986), memories of traumatic events are stored, along with associated (i.e., conditioned) cues, in information networks called “fear not always produce the same response. Models that involve the processing of information and emotions typically emphasize the role of appraisal or Barry interpretation of trauma­related information/experiences. Individuals are more likely to appraise a situation as threatening or out University of their Library control, and thus are more likely to develop trauma­related psychopathology, when they believe that they do not possess the personal capabilities or external Access Provided by: resources to meet the demands of the situation. On the other hand, individuals are more likely to appraise a situation as a challenge when they believe they can successfully deal with it. Whether an individual appraises a stressful situation as a challenge or a threat depends on numerous factors including personality, cognitive, behavioral and emotion regulation skills, prior experiences of success or failure in stressful situations, personal meaning of the event, and quality and degree of social support, among other factors (Southwick & Charney, 2012). The processing of trauma­related emotions is particularly relevant to avoidance and intrusive memories. According to the Emotion Processing Theory (Foa & 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 trauma­related memories. Intrusive memories are believed to occur as a result of implicit exposure to one or more cues that activate the fear structure. 3. Neurobiological systems A number of neurobiological models have been proposed to explain PTSD or specific aspects of PTSD. Examples include the role of genetic polymorphisms related to stress vulnerability (e.g., polymorphisms of the serotonin transporter gene), sensitization of neurobiological systems (e.g., noradrenergic system) involved in the stress response, exaggerated fear conditioning, overconsolidation of emotional memories, insufficient cortical inhibition of limbic activity, reduced capacity to extinguish fear­conditioned memories, and poor regulation of hypothalamic–pituitary–adrenal (HPA) axis and sympathetic nervous system responses to stress. In one of the most comprehensive causal neurobiological models of PTSD, Admon, Milad, and Hendler (2013) propose that preexisting hyperactivity of the amygdala and dorsal anterior cingulate cortex (dACC) is associated with exaggerated fear responses and with increased likelihood of developing PTSD. They further speculate that traumatic exposure may cause alterations to areas of the medial prefrontal cortex (mPFC) and to structural and functional connections between the mPFC and the hippocampus, resulting in an acquired reduction in capacity to inhibit/regulate the fear response. Currently, it is uncertain to what degree neurobiological alterations are either the cause or consequence of PTSD. C. Risk Some people are more likely to develop PTSD than others when exposed to traumatic events. Risk for developing PTSD is likely increased by a variety of genetic, neurobiological, and psychosocial factors. Psychosocial risk factors have typically been classified as pretraumatic, peritraumatic, and posttraumatic (Brewin et al, 2000; Ozer et al, 2003). Common pretraumatic risk factors that have been identified in published research, meta­analyses, and literature reviews include female gender, younger age, lower education, lower intelligence, negative emotionality (i.e., disposition characterized by anxiety, emotional lability, poor interpersonal interactions, and overall negative mood), past history of trauma (e.g., childhood sexual or physical abuse), and past individual or family psychiatric history. Commonly identified peritraumatic factors include high degree of traumatic exposure, pronounced dissociation, and excessive peritraumatic physiological activation (e.g., panic attack). For example, a survey of 1008 adult survivors of the September 11, 2001, 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 et al, 2002). Finally, posttrauma risk factors have included dysfunctional coping strategies (e.g., avoidance), low social support, and subsequent exposure to additional stressors and traumatic events. D. Resilience Given that not all individuals exposed to the same traumatic event will develop PTSD, it becomes vital to understand what is different about those individuals who do well under stress and are able to recover from the stress of 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 et al, 2005; Southwick and Charney, 2012). 1. Neurobiological resilience factors Numerous genetic factors, developmental influences, brain regions, and 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 corticotropin­releasing 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; an Downloaded amygdala that2025­2­16 5:21 P Your does not overreact IPenvironment; to the is a hippocampus that provides sufficient inhibition to the HPA axis and that accurately Chapter 28: Posttraumatic Stress Disorder and Acute Stress Disorder, Douglas C. Johnson; John H. Krystal; Steven M. Southwick† Page 3 / 18 differentiates cues for danger and safety; and ample cortical ©2025 McGraw Hill. All Rights Reserved. Terms of Use Privacyexecutive and inhibitory Policy Notice capacity. Accessibility Elevated levels of plasma NPY have been found in humans following extreme stressors such as military survival training. Moreover, higher levels of NPY Numerous genetic factors, developmental influences, brain regions, and endocrine and neurotransmitter systems appear to beBarry University associated with Library resilience to stress. Among the neurobiological factors that recently have received attention are sympathetic nervous system activity that responds Access Provided by: robustly to stress but that returns to baseline rapidly, perhaps secondary to regulation by neuropeptide Y (NPY) and galanin; capacity to contain the corticotropin­releasing 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; an amygdala that does not overreact to the environment; a hippocampus that provides sufficient inhibition to the HPA axis and that accurately differentiates cues for danger and safety; 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. In contrast, lower baseline and yohimbine­stimulated levels of NPY have been found in combat veterans with a current diagnosis of PTSD, but other studies of combat­related PTSD and female victims of sexual assault (Seedat et al, 2003) have yielded mixed results. Other neurophysiological factors associated with an adaptive response to extreme stress and the ability to physically and mentally recover following trauma are high vagal tone and increased heart rate variability (HRV). HRV is vagally mediated, with efferent projections to heart and lungs, and afferents involved in regulation of blood pressure. Thus, HRV is a measure of the balance between sympathetic and parasympathetic signals and represents overall flexibility to anticipate, respond to, and recover from stress. Higher resting­state HRV is characterized by parasympathetic dominance. A recent meta­analysis of fMRI studies reported a relationship between HRV and activation in prefrontal (mPFC, dACC) and limbic (amygdala) regions (Thayer et al, 2012). In terms of function, higher HRV is associated with increased working memory capacity, greater emotion regulation, and enhanced response inhibition. 2. Psychosocial resilience factors Resilience to stress has been correlated with optimism, humor, social support, and an active rather than 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 self­efficacy 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 intervention. 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 5­HTTLPR serotonin transporter gene promoter polymorphism) and environmentally (documented history of maltreatment) and found that strength of social support networks and positive social relationships moderated the risk for depression independent of genetic vulnerabilities and early exposure to overwhelming stress. E. Genetics Data from twin studies suggest that risk for PTSD is moderately heritable. A study of 4042 Vietnam­era 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 (True et al, 1993). Proneness to exposure to traumatic events may also be influenced by familial nongenetic factors. To date, using a candidate gene approach where genes are selected for analysis based on known underlying molecular pathways, specific genes associated with PTSD have been linked to dopaminergic, serotonergic, noradrenergic, and HPA axis systems. However, in many cases results have been inconsistent or have not been replicated. One of the most promising approaches for studying genetic contributions to risk for PTSD involves genome­wide association studies (GWAS) where the entire genome is analyzed in relation to PTSD. For example, in a series of recent GWAS, Xie and colleagues (2013) reported a significant association between TLL1 rs6812849 and PTSD among European Americans. TLL1rs6812849 is a protein implicated in promoting neurogenesis, which is known to be inhibited by stress. Recent research in epigenetics has shown that a host of external and internal stimuli, such as social support, fear, and stress, can trigger biochemical reactions that can affect gene expression by either “turning on” or “turning off” genes. This rapidly growing field shows great promise in advancing the understanding of stress vulnerability and stress resilience (Nestler, 2012). Clinical Findings A. Signs and Symptoms PTSD diagnostic criteria were revised in DSM­5 to more closely reflect published clinical evidence. In DSM­5, PTSD was moved from the Anxiety Disorders group into a new category of Trauma and Stressor­Related Disorders that also includes Acute Stress Disorder (ASD) and Adjustment Downloaded 2025­2­16 5:21 P Your IP is Disorders. Chapter 28:Criterion A2 was Stress Posttraumatic dropped from DSM­5 Disorder because and Acute response Stress to trauma Disorder, (i.e.,C.fear, Douglas helplessness, Johnson; John H.and horror) Krystal; has been Steven shown to be a Page M. Southwick† poor 4 / 18 predictor ©2025 of subsequent McGraw PTSD diagnosis Hill. All Rights or symptom Reserved. Terms of severity (Pereda Use Privacy & Forero, Policy 2012). Notice In addition, PTSD symptom clusters were revised from three Accessibility criteria (reexperiencing, avoidance, and hyperarousal) in DSM­IV to four criteria (intrusion, avoidance, negative affect, and hyperarousal) in DSM­5. Most pathognomonic among these four symptom clusters are episodes of reexperiencing (i.e., flashbacks, nightmares, and intrusive memories). Such Clinical Findings Barry University Library Access Provided by: A. Signs and Symptoms PTSD diagnostic criteria were revised in DSM­5 to more closely reflect published clinical evidence. In DSM­5, PTSD was moved from the Anxiety Disorders group into a new category of Trauma and Stressor­Related Disorders that also includes Acute Stress Disorder (ASD) and Adjustment Disorders. Criterion A2 was dropped from DSM­5 because response to trauma (i.e., fear, helplessness, and horror) has been shown to be a poor predictor of subsequent PTSD diagnosis or symptom severity (Pereda & Forero, 2012). In addition, PTSD symptom clusters were revised from three criteria (reexperiencing, avoidance, and hyperarousal) in DSM­IV to four criteria (intrusion, avoidance, negative affect, and hyperarousal) in DSM­5. Most pathognomonic among these four 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, avoidance and emotional numbing often have debilitating effects on psychosocial function. Some individuals with PTSD experience amnesia for aspects of the traumatic event. This inability to recall certain trauma­related 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 predictive of PTSD following life­ threatening trauma. Emotional numbing can be difficult to identify clinically because 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. B. Specific Behavioral or Physioiogical Findings (Laboratory Findings) 1. Physiological Exaggerated physiological reactivity has been described among traumatized individuals for centuries. In fact, in the 1940s, PTSD was referred to as “physioneurosis” because unlike other “neuroses,” it appeared to have a profound underlying physiological basis. More recently, in a meta­analysis of more than 1000 adults, Pole (2007) found that PTSD was associated with higher resting arousal as well as larger responses to startling sounds, standardized trauma cues, and personal trauma memories compared to individuals without PTSD. One of the most reliable correlates of PTSD was elevated heart rate, which has been shown to prospectively predict PTSD. Such cardiac reactivity may 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 trauma­specific cues (Orr et al, 2002). 2. Cognitive Information­processing biases in PTSD have been studied using various cognitive paradigms. Studies of attentional bias using a dot­probe task and eye tracking indicate that PTSD is associated with increased attention toward trauma­related cues and difficulty disengaging from threat­related words. Emotion regulation and response inhibition have been studied using the emotional Stroop task. The “Stroop effect” is demonstrated by the increased response time needed to inhibit a prepotent (i.e., overlearned) response. The emotional Stroop is a variation of the traditional color­word naming task, but substitutes trauma­related words (e.g., insurgent, amputate) for color words. Relative to age­ and education­matched civilian and military controls, veterans of OEF/OIF took longer to respond and were less accurate for combat words (Ashley et al, 2013). Moreover, there were no group differences in response times for noncombat words. Rather than global information processing inefficiencies, these results suggest that individuals with PTSD have a unique processing bias for threat­related information. 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 mood­congruent memory effect in PTSD, to wit, individuals with PTSD demonstrate a memory advantage for trauma­related 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, Downloaded in particular 2025­2­16 thought 5:21 P Your suppression and cognitive avoidance, have been explored as an explanation for the inconsistent memory IP is Chapter 28: findings in Posttraumatic PTSD. It has beenStress Disorderthat hypothesized andindividuals Acute Stress withDisorder, PTSD willDouglas attempt C. Johnson;or to suppress John H.recall avoid Krystal; of trauma­related memories. Page Steven M. Southwick† 5 / 18 In fact, ©2025 McGraw Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility some studies have indicated a bias away from anxiety­provoking information, suggesting that 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 trauma­related information is tentative. effect in PTSD, to wit, individuals with PTSD demonstrate a memory advantage for trauma­related information. However, it remains unclear whether Barry University Library this explicit memory bias is the result of recall advantages inherent in personally salient information, or whether the advantages are due to true mood Access Provided by: 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 trauma­related memories. In fact, some studies have indicated a bias away from anxiety­provoking information, suggesting that 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 trauma­related information is tentative. 3. Neuropsychological Individuals with PTSD demonstrate a range of cognitive abnormalities, particularly in the areas of attention (simple, divided, and sustained), concentration, learning, and memory (Vasterling & Brewin, 2005). Combat­related PTSD is also associated with decreased (i.e., quicker) reaction time on stimulus recognition tests. In addition, PTSD is associated with lower full­scale IQ; however, reliance on estimates of premorbid intellectual functioning makes causal inferences difficult. A study of deployed and nondeployed Gulf War–era veterans (N = 2189) showed differences in rates of neuropsychological impairment. After adjusting for academic achievement, age, and rank, 3.7% of deployed veterans had definite impairments in sustained attention, and 2.6% had definite impairments in motor speed. In contrast, 1.7% and 1.4% of nondeployed veterans had definite impairments in sustained attention and motor speed, respectively (Toomey et al, 2009). In a recent comprehensive review of prospective, longitudinal, twin, and cross­sectional studies of executive function, Aupperle and colleagues (2012) report that PTSD is characterized by deficits in executive function, including attention and working memory, sustained attention, and inhibitory functions, as well as flexibility, switching, and planning. Although PTSD has been associated with enhanced attention to threat­relevant stimuli, it has also been associated with dysfunction in ability to subsequently inhibit or disengage from these stimuli. The authors speculate that these deficits might exacerbate reexperiencing and arousal symptoms, which in turn may increase avoidance of arousing stimuli. There is some evidence to suggest that subtle deficits in executive function may predate trauma in some individuals and thus increase the risk of developing PTSD. Performance of individuals with PTSD on tasks of executive set­switching has been mixed, with some studies showing relative inefficiencies, whereas others show that individuals with PTSD are within normal limits. Of note, cognitive deficits in these domains occur with threat­neutral, nontrauma stimuli. Relative to non­PTSD combat­exposed and nondeployed personnel, individuals with PTSD have been shown to experience increased combat­ related thought intrusions during a neutral thought suppression task. Moreover, the neutral thought suppression task was more difficult for individuals with PTSD as measured by physiologic indicators of effort and stress (e.g., galvanic skin conductance; Aikins et al, 2009). Similarly, PTSD research with emotionally neutral list­learning tasks has revealed retrieval deficits for newly learned information. That occurrence of deficits in 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 long­term storage. Neuropsychological domains that appear to remain intact include visuospatial functioning, language, and psychomotor performance. 4. Psychobiological 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 (1) elevated resting cerebrospinal fluid levels of CRF; (2) alterations in 24­hour urine excretion of cortisol, 24­hour plasma cortisol levels, lymphocyte glucocorticoid receptor number, cortisol response to dexamethasone, adrenocorticotropic hormone (ACTH) response to CRF, and β­endorphin and ACTH response to metyrapone; and (3) adrenal androgen abnormalities. Alterations in sympathetic nervous system reactivity include exaggerated increases in heart rate, blood pressure, and epinephrine in response to traumatic reminders administered in the laboratory; elevated 24­hour plasma norepinephrine; elevated 24­hour 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 α2­adrenoreceptor antagonist); blunted response to clonidine; and altered yohimbine­induced 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 stress­induced reduction in PFC metabolism. C. Neuroimaging Downloaded 2025­2­16 PTSD is associated 5:21 P Your with alterations IP is brain structure and function. Consistent with animal research, studies in humans have reported smaller in both Chapter 28: Posttraumatic Stress Disorder and Acute Stress Disorder, Douglas C. Johnson; John H. Krystal; Steven M. Southwick† Page 6 / 18 bilateral volume and reduced neuronal density of the hippocampus, smaller volume in prefrontal cortical brain regions including the ventral medial ©2025 McGraw Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility prefrontal cortex (vmPFC) and the anterior cingulate cortex, and alterations in white matter tract integrity in the cingulum bundle among subjects with PTSD compared to controls. In response to trauma­related stimuli, functional neuroimaging studies have found exaggerated activation of the hyperarousal. Neurocognitive and brain imaging studies comparing individuals with PTSD and individuals without psychiatric disorders have reported Barry University that subjects with PTSD show biased attention to negative and potentially dangerous information, reductions in hippocampal volume Library and function, exaggerated amygdala responses to stressful cues, and stress­induced reduction in PFC metabolism. Access Provided by: C. Neuroimaging PTSD is associated with alterations in both brain structure and function. Consistent with animal research, studies in humans have reported smaller bilateral volume and reduced neuronal density of the hippocampus, smaller volume in prefrontal cortical brain regions including the ventral medial prefrontal cortex (vmPFC) and the anterior cingulate cortex, and alterations in white matter tract integrity in the cingulum bundle among subjects with PTSD compared to controls. In response to trauma­related stimuli, functional neuroimaging studies have found exaggerated activation of the amygdala, dACC, and insula, as well as decreased activation of areas of the vmPFC among subjects with PTSD compared to controls. Taken together these findings have lead researchers to propose a neurocircuitry model of PTSD that includes overactivation of areas of the brain involved in detection and response to fear and internal body states including arousal (i.e., amygdala, anterior cingulate cortex, insula) in conjunction with decreased activation of brain regions that inhibit negative emotional states and that facilitate extinction of fear (i.e., vmPFC). In addition, evidence suggests that abnormalities reported in hippocampal structure and function may affect memory as well as ability to differentiate safe versus dangerous contextual cues. Currently there is debate about the temporal relationship between brain structure and function and the development of PTSD. Evidence suggests that structural and functional differences represent both vulnerability factors and maladaptation to trauma. For example, studies of individuals with PTSD and their non–trauma­exposed cotwins suggest that reduced hippocampal volume may be a premorbid risk factor as well as a result of trauma exposure (Kitayama et al, 2005; Gilbertson et al, 2002). Similarly, increased resting­state metabolic activity in the dACC of non–trauma­exposed twins has been associated with symptom severity in combat­exposed cotwins with PTSD (Shin et al, 2009), whereas reduced functional connectivity between hippocampus and vmPFC may be the result of exposure to acute stress (e.g., Admon et al, 2013). Finally, there is emerging evidence that reduction of PTSD symptoms is associated with increased vmPFC activation (Hughes & Shin, 2011). D. Course of Illness The course of PTSD is variable. PTSD can occur from very early childhood to late in life. Onset of PTSD symptoms commonly occurs within 3 months following trauma exposure, although symptom manifestation can be delayed for years after the trauma. Common trajectories of PTSD symptoms include chronic elevation, chronic subsyndromal, delayed onset, recovery, and resilience/resistant (Pietrzak et al, 2013). Despite variation in course, epidemiologic studies suggest that the majority of symptoms do attenuate with time. For example, the NCS indicated that PTSD resolves in 6 years in approximately 60% of cases. However, it may be that some symptoms are more likely to decrease than others over time. A study of Israeli military personnel over a 2­year period found that symptoms of reexperiencing and intrusive memories decreased, whereas avoidance and emotional numbing symptoms increased (Solomon & Mikulincer, 1992). Although recovery occurs in most of those diagnosed with PTSD, for those who do not recover PTSD is often markedly detrimental to physical, social, occupational, and interpersonal functioning. Moreover, PTSD can be complicated by recurrent exposure to trauma or trauma­associated cues that trigger reactivation of symptoms. E. Psychological Testing A variety of rating scales have been developed for the assessment of PTSD, the nature of certain traumas, and specific responses to stress. Some of these measures have been validated for use in diagnostic and treatment settings; however, some researchers have recommended that reliance solely on self­report checklist should be avoided when possible, especially in cases involving differential diagnosis. For example, in a study of individuals with traumatic brain injury (TBI) (n = 34), 44–59% of participants were diagnosed with PTSD based on self­report questionnaires. In contrast, when a structured clinical interview was used, only 3% were determined to meet DSM­IV­TR criteria for PTSD (Sumpter & McMillan, 2005). 1. Self­report measures i. 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 a contemporary version of the Vietnam era Combat Exposure Scale. ii. PTSD Checklist for DSM­5­TR (PCL­5) The PCL is a 20­item assessment of PTSD symptom severity developed by the National Center for PTSD. Items correspond to 20 PTSD symptom criteria directly adapted from the DSM­5. The PCL­5 can be used for screening, presumptive diagnosis, and monitoring symptom change during and after treatment. The self­report rating scale for each item is 0 (not at all) to 4 (extremely), with total scores ranging from 0 to 80. The increase in number of Downloaded 2025­2­16 5:21 P Your IP is items and28: Chapter change in rating scale Posttraumatic means Stress that and Disorder scores on the Acute PCL­5 Stress do not correspond Disorder, Douglas C.toJohnson; scores onJohn the DSM­IV version H. Krystal; of the Steven M.PCL and should be Southwick† Page 7 / 18 ©2025 McGraw interpreted Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility separately. iii. Posttraumatic Diagnostic Scale (PDS) ii. PTSD Checklist for DSM­5­TR (PCL­5) Barry University Library Access Provided by: The PCL is a 20­item assessment of PTSD symptom severity developed by the National Center for PTSD. Items correspond to 20 PTSD symptom criteria directly adapted from the DSM­5. The PCL­5 can be used for screening, presumptive diagnosis, and monitoring symptom change during and after treatment. The self­report rating scale for each item is 0 (not at all) to 4 (extremely), with total scores ranging from 0 to 80. The increase in number of items and change in rating scale means that scores on the PCL­5 do not correspond to scores on the DSM­IV version of the PCL and should be interpreted separately. iii. Posttraumatic Diagnostic Scale (PDS) The PDS is a 49­item measure of PTSD symptom severity and frequency according to the DSM­IV 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). iv. Davidson Trauma Scale (DTS) The DTS assesses each of 17 PTSD symptoms corresponding to DSM­IV­TR criteria. Symptom frequency and intensity are assessed separately for each symptom on a 5­point Likert scale. Frequency scores range from 0 (not at all) to 4 (every day). Intensity scores range from 0 (not at all) to 4 (extremely distressing). v. Perceived Stress Scale (PSS) The PSS is one of the most widely used measures of subjective experiences of stress. The PSS assesses the individual perceptions of stress over the last 30 days across three dimensions: uncontrollability, unpredictability, and overwhelming nature. vi. Connor­Davidson Resilience Scale (CD­RISC) The CD­RISC is a 25­item self­report scale assessing stress coping ability. The scale comprises five factors that broadly correspond to tenacity, tolerance of negative affect, acceptance of change, perceived control, and spirituality. The CD­RISC has several potential applications, including identifying individuals at risk for stress­related psychopathology, and as a treatment outcome variable. vii. Response to Stressful Experiences Scale (RSES) The RSES is a 22­item measure that assesses how individual typically responds to stressful life events. The scale comprises five protective factors: (1) meaning­making and restoration, (2) active­coping, (3) cognitive flexibility, (4) spirituality, and (5) self­efficacy. The RSES asks respondents, “During and after life’s most stressful events, I tend to…. “ Responses are measured on a 5­point Likert scale ranging from 0 (not at all like me) to 4 (exactly like me). viii. Deployment Risk and Resilience Inventory­2 (DRRI­2) The DRRI­2 is a suite of 17 measures designed to assess psychosocial factors associated with vulnerability to stress before, during, and after military deployment. The DRRI­2 was developed in a national sample of veterans from Operation Enduring Freedom (OEF) and Operation Iraqi Freedom (OIF) (Vogt et al, 2013). Psychosocial factors assessed by the DRRI­2 include unit cohesion, perceived social support, training and readiness, combat exposure, aftermath of battle, and family stressors. 2. Clinician­administered scales i. Clinician­Administered PTSD Scale for DSM­5­TR (CAPS­5) The CAPS is a 30­item structured clinical interview measuring the frequency and intensity of the DSM­5 symptoms of PTSD (Weathers et al, 2013). The CAPS­5 comprises standardized questions and probes for each of the 20 DSM­5 symptom criteria. Additional questions assess onset and duration of symptoms, social and occupational functioning, change over time, response validity, and overall symptom severity. There are also specifications for diagnosis of depersonalization and derealization subtypes. The CAPS­5 can be used to make a current (past month) diagnosis of PTSD, make a lifetime diagnosis of PTSD, and assess PTSD symptoms over the last week. ii. Structured Clinical Interview for DSM Disorders (SCID) Downloaded 2025­2­16 5:21structured The SCID is a clinician­based P Your IPinterview is designed to assess the majority of mental health disorders. The PTSD portion of the SCID is found in Chapter 28: Posttraumatic Stress Disorder and Acute Stress Disorder, Douglas C. Johnson; John H. Krystal; Steven M. Southwick† Page 8 / 18 Module F—Anxiety Disorders. Several versions of the SCID are available for use dependent on the setting (e.g., research, clinical, and nonpatient ©2025 McGraw Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility populations). symptoms, social and occupational functioning, change over time, response validity, and overall symptom severity. There are also specifications for diagnosis of depersonalization and derealization subtypes. The CAPS­5 can be used to make a current (past month) diagnosis ofBarry University PTSD, Library make a lifetime diagnosis of PTSD, and assess PTSD symptoms over the last week. Access Provided by: ii. Structured Clinical Interview for DSM Disorders (SCID) The SCID is a clinician­based structured interview designed to assess the majority of mental health 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). TheSCID is also available in several different languages. A new DSM 5 version was scheduled to be released in October 2014. It can reliably be used with DSM­5­TR. iii. Mississippi Scale for PTSD The scale consists of 39 self­report items derived from the Diagnostic and Statistical Manual of Mental Disorders III­R criteria for PTSD. The first version of the Mississippi Scale contained 35 items, based on the unrevised DSM­III criteria for PTSD. The four added items (items 36–39) assess reexperiencing, psychogenic amnesia, hypervigilance, and increased arousal symptomatology. iv. Impact of Events Scale (IES) The IES is a 22­item self­report 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. v. Trauma Symptom Inventory (TSI) The TSI is a 100­item evaluation of acute and chronic symptomatology from a wide variety of traumas, including rape, combat experiences, major accidents, and 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 ASD but also those intra­ and interpersonal difficulties often associated with more chronic psychological trauma. The TSI does not generate DSM­IV diagnoses; instead, it is intended to evaluate the relative level of various forms of posttraumatic distress. vi. Morel Emotional Numbing Test (MENT) The MENT is currently the only clinician­administered tool developed specifically to detect symptom exaggeration in PTSD. The MENT is a 60­item forced choice recognition test and requires the respondent to match various facial expressions with a label that correctly identifies the expressed emotion. Each item comprises one correct response and one foil. Several published studies support the reliability and validity of the MENT in distinguishing individuals with PTSD from individuals feigning PTSD­related cognitive impairment (Messer & Fremouw, 2007; Morel, 1998, 2008). Differential Diagnosis (Including Comorbid Conditions) 1. Major or mild neurocognitive disorder (NCD) due to traumatic brain injury (TBI) PTSD and TBI frequently co­occur as a result of trauma, and symptom overlap can make differential diagnosis challenging, particularly in cases of mild TBI. Individuals who have suffered a closed head injury can experience difficulties with attention and concentration, sleep disturbance, posttraumatic amnesia, and negative affect, all of which are also symptoms of PTSD. In cases where head injury was sustained during a life­threatening trauma, formal neuropsychological testing and a structured clinical interview of symptoms can inform differential diagnosis. In cases of potential PTSD and/or NCD due to mild TBI, attention should be given to clinical indicators unique to each condition, such as avoidance and reexperiencing in PTSD, or loss of consciousness, neurological soft signs (i.e., Glasgow Coma Score), and cognitive slowing in mild TBI. 2. Adjustment disorder (AD) Symptoms that arise from an event that is stressful, but not of the life­threatening nature and intensity of Criterion A events for PTSD, fall under the rubric of AD. 3. 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 Downloaded 2025­2­16 5:21 P Your IP is weeks may Chapter 28:indicate PTSD. Stress Disorder and Acute Stress Disorder, Douglas C. Johnson; John H. Krystal; Steven M. Southwick† Page 9 / 18 Posttraumatic ©2025 McGraw Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility 4. Obsessive–compulsive disorder (OCD) rubric of AD. Barry University Library Access Provided by: 3. 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. 4. 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 trauma­related events and memories. Although intrusive thoughts in OCD are often distressing, they are not specific to a traumatic event. 5. Psychotic disorders 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 life­threatening 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. 6. Personality disorders An emerging literature on the comorbidity of personality disorders with anxiety spectrum disorders requires an understanding of personality disorders that frequently co­occur with PTSD. Retrospective and longitudinal research has identified significant correlations between PTSD and some personality 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 personality disorder features most closely associated with PTSD are frantic efforts to avoid abandonment, rejection of help, inappropriate anger, and general impulsiveness. 7. Malingering PTSD diagnostic evaluations often rely on self­report measures. An accurate diagnosis of PTSD can be complicated by the fact that, by definition, it requires an identifiable (Criterion A) 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. 8. Comorbidity 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, and agoraphobia frequently co­occur with PTSD. Results from the NCS also revealed high comorbidity rates for antisocial personality disorder (43% male and 15% female). Other studies of personality 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. Treatment A. Psychopharmacologic Interventions Psychoactive medications play an important role in the treatment of PTSD. A large study of veterans (N = 247,297) diagnosed with PTSD showed that 80% were provided prescriptions for psychotropic medications. Of those prescribed medications for management of PTSD symptoms, 89% were prescribed antidepressants, 61% received anxiolytics, and 34% received antipsychotics (Mohamed & Rosenheck, 2008). Selective serotonin reuptake inhibitors (SSRIs) are generally considered first­line medications for the treatment of PTSD (VA/DOD Treatment Guidelines, 2010; Watts et al, 2013). Currently, sertraline and paroxetine are the only two medications that have been approved by the U.S. Food and Downloaded 2025­2­16 Drug Administration 5:21 for the P Your IP treatment is of PTSD. Fluoxetine, another SSRI, and venlafaxine, a serotonin–norepinephrine reuptake inhibitor, have also Chapter 28: Posttraumatic Stress Disorder and Acute Stress Disorder, Douglas C. Johnson; John H. Krystal; Steven M. Southwick† Page 10 / 18 demonstrated efficacy in placebo­controlled trials. SSRIs have been shown to reduce symptoms of all PTSD symptom clusters as well as comorbid ©2025 McGraw Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility mood and anxiety symptoms. There is evidence to suggest that some individuals with PTSD can continue to experience additional symptom reduction when SSRIs are continued beyond 12 weeks. Psychoactive medications play an important role in the treatment of PTSD. A large study of veterans (N = 247,297) diagnosed with PTSD showed that Barry University Library 80% were provided prescriptions for psychotropic medications. Of those prescribed medications for management of PTSD symptoms, 89% were Access Provided by: prescribed antidepressants, 61% received anxiolytics, and 34% received antipsychotics (Mohamed & Rosenheck, 2008). Selective serotonin reuptake inhibitors (SSRIs) are generally considered first­line medications for the treatment of PTSD (VA/DOD Treatment Guidelines, 2010; Watts et al, 2013). Currently, sertraline and paroxetine are the only two medications that have been approved by the U.S. Food and Drug Administration for the treatment of PTSD. Fluoxetine, another SSRI, and venlafaxine, a serotonin–norepinephrine reuptake inhibitor, have also demonstrated efficacy in placebo­controlled trials. SSRIs have been shown to reduce symptoms of all PTSD symptom clusters as well as comorbid mood and anxiety symptoms. There is evidence to suggest that some individuals with PTSD can continue to experience additional symptom reduction when SSRIs are continued beyond 12 weeks. The investigation and clinical use of monoamine oxidase inhibitors (MAOIs) for the treatment of PTSD has been limited because of potential side effects, particularly in patients with comorbid substance abuse disorders. Although results have been inconsistent in open trials, in a well­designed randomized controlled trial (RCT) involving Vietnam veterans with PTSD, those treated with phenelzine demonstrated significant improvement in reexperiencing and arousal symptoms (Kosten et al, 1991). Tricyclic antidepressants appear to be as effective as MAOIs or SSRIs in treating PTSD. However, like MAOIs, they generally have a more adverse side effect profile than SSRIs. In a recent RCT, desipramine was as effective as sertraline in treating veterans with PTSD and comorbid alcohol dependence (Petrakis et al, 2012). Prazosin, an adrenergic agent that blocks alpha­1 receptors, has been shown in several RCTs to improve sleep and reduce nightmares in PTSD. In a recent 15­week RTC involving 67 active­duty combat veterans with PTSD, prazosin was found to be effective in reducing traumatic nightmares and other symptoms of arousal as well as improving global functioning (Raskind et al, 2013). Medications that have not shown consistent positive effects for the treatment of PTSD include atypical antipsychotics (e.g., risperidone), anticonvulsants (e.g., valproate), and benzodiazepines. In fact, there is some evidence to suggest that the prolonged use of benzodiazepines immediately following traumatic exposure may increase the likelihood of developing symptoms of PTSD, perhaps by interfering with extinction and/or the cognitive processing of traumatic memories. In general, RCTs for psychotropic medications have reported small to moderate effect sizes for the treatment of PTSD. The use of pharmacological agents to prevent the development of PTSD is a topic of great interest (Kearns et al, 2012). Based on preclinical findings, it has been hypothesized that a number of agents might reduce or prevent the likelihood of developing PTSD. Examples include the use of adrenergic agents (e.g., propranolol) and opiates (e.g., morphine) to block encoding/consolidation/reconsolidation of traumatic memories, CRF antagonists to suppress sympathetic and HPA­axis responses to stress, glucocorticoids to downregulate supersensitive glucocorticoid receptors, and antidepressants (e.g., imipramine). Psychotropic medications are often prescribed in combination with cognitive–behavioral psychotherapies, which have been shown to be more effective than medications for the treatment of PTSD. There is a great need for more effective pharmacologic treatments for PTSD. The medications that are currently approved were not developed to address specific neurobiological alterations seen in PTSD. It is anticipated that pharmacological interventions specifically designed to address underlying pathophysiological alterations in PTSD will enhance treatment efficacy. It is also possible that matching an individual to a specific pharmacologic treatment will enhance efficacy, because biological profiles or subtypes might differ among individuals with PTSD. B. Psychotherapeutic Interventions Several psychotherapeutic techniques have been shown to be effective in treating PTSD. A recent meta­analysis of 137 treatment comparisons showed cognitive therapy, exposure therapy, and eye­movement desensitization and reprocessing (EMDR) were among the most effective (Watts et al, 2013). Results also indicate that no single therapy is consistently most effective, and some therapies may not be effective for PTSD. 1. Cognitive–behavioral therapy (CBT) Although cognitive–behavioral approaches were not 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. i. Exposure therapy 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 Downloaded 2025­2­16 5:21 P Your IP is threatening Chapter 28:stimuli, gradually Posttraumatic increasing Stress to exercises Disorder and Acuteof Stress greaterDisorder, intensity Douglas as desensitization C. Johnson; John H. Systematic is achieved. desensitization Krystal; Steven (SD) occurs M. Southwick† Page over a 11 / 18 period ©2025 of several Hill. McGraw weeks, thoughReserved. All Rights some approaches Termsimmediately escalate of Use Privacy to the Policy most extreme Notice stressors (e.g., flooding therapy). In either approach, the Accessibility 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 = i. Exposure therapy Barry University Library Exposure therapy involves reexposing the traumatized individual to sensory stimuli associated with the traumatic event. Exposure can Access take by: Provided 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). ii. 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 three­stage process involving psychoeducation (conditioning theory and psychobiology of fear), cognitive skills training (reframing and relaxation techniques), and application (scenarios, roleplaying, or in vivo exposures). iii. Cognitive therapy (CT) 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. iv. 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 & Schnike, 1992). CPT focuses on memories of the traumatic event and exploring associated intense emotions. Trauma memories are explored through the 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 many 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 12­session course of CPT in Vietnam combat veterans, 40% of the intention­to­treat sample no longer met diagnostic criteria for PTSD, a result that was independent of service­ connected disability status (Monson et al, 2007). v. Mindfulness based cognitive therapy (MBCT) MBCT is a mindfulness­based therapeutic approach that incorporates components of CPT. It is focused on promoting an individual to attain a “decentered” perspective (i.e., thoughts are not facts) (Boyd et al, 2017). This enables individuals with PTSD to better distinguish fear from their current reality. 2. Eye­movement 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, 1996) 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 eye­movement 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 eye­movement 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. 3. Mindfulness­based treatments Since its introduction into Western psychology in the 1980s and 1990s, mindfulness has grown exponentially in its use within the field. Mindfulness­ Downloaded 2025­2­16is 5:21 based stress reduction P Your used a commonly IP is treatment approach. One model of treatment may consist of 8 weeks of 2­ to 2.5­hour group sessions. The Chapter 28: Posttraumatic Stress Disorder approach may use mindfulness meditation and andyoga. Acute Stress The Disorder, program Douglas encourages C. Johnson; John nonjudgmental H. Krystal; of and acceptance Steven M. Southwick† thoughts Page 12 / 18 as they occur in the ©2025 McGraw Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility present (Boyd et Al, 2017). Several theoretical models have been proposed as to how mindfulness affects brain function and reduces the symptomatology of PTSD. Although 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 Barry University Library subjective appraisals of distress precipitated by the memory; the sequence is repeated until subject distress decreases to zero. Access Provided by: 3. Mindfulness­based treatments Since its introduction into Western psychology in the 1980s and 1990s, mindfulness has grown exponentially in its use within the field. Mindfulness­ based stress reduction is a commonly used treatment approach. One model of treatment may consist of 8 weeks of 2­ to 2.5­hour group sessions. The approach may use mindfulness meditation and yoga. The program encourages nonjudgmental and acceptance of thoughts as they occur in the present (Boyd et Al, 2017). Several theoretical models have been proposed as to how mindfulness affects brain function and reduces the symptomatology of PTSD. Although mindfulness­based approaches have utility in treating PTSD, more work is needed for them to become first­line approaches. (Boyd et.al 2017) Complications/Adverse Outcomes of Treatment The primary complication to psychotherapy for PTSD, especially for cognitive–behavioral­based approaches, is avoidance. Behavioral avoidance can take the form of missed therapy appointments, incomplete treatment homework, or failure to engage trauma cues during in vivo exposures. Cognitive avoidance can also complicate treatment if it is persistent. Sometimes individuals who appear to engage exposure exercises behaviorally may be covertly dissociating from the experience in an effort to attenuate arousal and full exposure to the trauma cue. Avoidance may also take the form of self­medication through the use of alcohol and substance abuse. A complication that has received limited attention is the potential impediment that benzodiazepines present to exposure therapies. The short half­life (i.e., fast action) of some benzodiazepines is a powerful reinforcement to individuals with PTSD who are averse to autonomic arousal. A heavy reliance on benzodiazepines or alcohol interferes with new learning (i.e., extinction conditioning) that is pivotal for extinguishing maladaptive associations with trauma cues. Additional impediments to treatment include sleep irregularities that make new learning more difficult, as well as psychosocial dysfunction that often accompanies chronic, untreated PTSD. Prognosis The fact that most individuals with PTSD get better over time does not lessen its psychosocial and functional impact, as subclinical symptom levels can have profound negative consequences. However, the evolution of several promising therapies for PTSD (see section Treatment) suggests that even the most difficult cases are treatable. As is the treatability for those who have strong support networks, fewer comorbid diagnoses, and fully engage in empirically validated treatments. In contrast, individuals with complex PTSD resulting from multiple childhood traumas, poor interpersonal support networks, personality disorders, comorbid substance abuse, and diminished cognitive resources are less likely to recover. Admon R, Leykin D, Lubin G, et al. Stress­induced reduction in hippocampal volume and connectivity with the ventromedial prefrontal cortex are related to maladaptive response to stressful military service. Hum Brain Mapp. 2013;34(11):2808–2816. [PubMed: 22807242] Admon R, Milad MR, Hendler T. A causal model of post­traumatic stress disorder: disentangling predisposed from acquired neural abnormalities. Trends Cogn Sci. 2013;17(7):337–347. [PubMed: 23768722] Aikins DE, Johnson DC, Borelli JL, et al. Thought suppression failures in combat PTSD: a cognitive load hypothesis. Behav Res Ther. 2009;47(9):744– 751. [PubMed: 19586619] American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders , 4th ed. Washington, DC: American Psychiatric Association; 1994. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders , 4th ed, text revision. Washington, DC: American Psychiatric Association; 2000. American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders , 5th ed. Washington, DC: American Psychiatric Association; 2013. Ashley V, Honzel N, Larsen J, et al. Attentional bias for trauma­related words: exaggerated emotional Stroop effect in Afghanistan and Iraq war veterans with PTSD. BMC Psychiatry. 2013;13:86. [PubMed: 23496805] Aupperle RL, Melrose AL, Stein MB, et al. Executive function and PTSD: disengaging from trauma. Neuropharmacology. 2012;62(2):686–694. [PubMed: 21349277] Downloaded 2025­2­16 Baker DG, Ekhator 5:21 P Your NN, Kasckow IP al. JW, et is Higher levels of basal serial CSF cortisol in combat veterans with posttraumatic stress disorder. Am J Chapter 28: Posttraumatic Stress Disorder and Acute Stress Disorder, Douglas C. Johnson; John H. Krystal; Steven M. Southwick† Page 13 / 18 Psychiatry. 2005;162:992–994. [PubMed: 15863803] ©2025 McGraw Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility Boyd J, Lanius R, McKinnon C. Mindfulnes­based treatments for posttraumatic stress disorder: a review of the treatment literature and Ashley V, Honzel N, Larsen J, et al. 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