2

History, Diagnostic Criteria, and Epidemiology

This chapter provides an overview of the epidemiology of posttrau-matic stress disorder (PTSD). It begins with a brief history of the disorder in the American military, which is followed by a discussion of its diagnostic criteria. The remainder of the chapter presents factors associated with trauma and PTSD, first in the general population and then in military and veteran populations, with an emphasis on combat as the traumatic event that triggered the development of PTSD. Although other traumatic events—such as the terrorist attacks of September 11, 2001, and Hurricane Katrina—have increased knowledge about PTSD, this chapter does not focus on civilian populations or nonmilitary related trauma. The chapter concludes with special epidemiologic considerations regarding PTSD in military populations and their implications for screening, diagnosis, and treatment.

HISTORY OF PTSD

Prior to the codifying of PTSD by the American Psychiatric Association (APA) as a distinct mental health disorder in 1980 (APA, 1980), characteristic symptoms of PTSD had been recognized and documented in the 19th century in civilians involved in catastrophic events, such as railway collisions, and in American soldiers fighting in the Civil War (Birmes et al., 2003; Jones, 2006; Welke, 2001). Many Civil War soldiers had diagnoses of nostalgia or melancholia, characterized by lethargy, withdrawal, and “excessive emotionality” (Birmes et al., 2003). Others had diagnoses of exhaustion, effort syndrome, or heart conditions variously called “irritable



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2 History, Diagnostic Criteria, and Epidemiology T his chapter provides an overview of the epidemiology of posttrau- matic stress disorder (PTSD). It begins with a brief history of the disorder in the American military, which is followed by a discussion of its diagnostic criteria. The remainder of the chapter presents factors as- sociated with trauma and PTSD, first in the general population and then in military and veteran populations, with an emphasis on combat as the traumatic event that triggered the development of PTSD. Although other traumatic events—such as the terrorist attacks of September 11, 2001, and Hurricane Katrina—have increased knowledge about PTSD, this chapter does not focus on civilian populations or nonmilitary related trauma. The chapter concludes with special epidemiologic considerations regarding PTSD in military populations and their implications for screening, diagno- sis, and treatment. HISTORY OF PTSD Prior to the codifying of PTSD by the American Psychiatric Association (APA) as a distinct mental health disorder in 1980 (APA, 1980), charac- teristic symptoms of PTSD had been recognized and documented in the 19th century in civilians involved in catastrophic events, such as railway collisions, and in American soldiers fighting in the Civil War (Birmes et al., 2003; Jones, 2006; Welke, 2001). Many Civil War soldiers had diagnoses of nostalgia or melancholia, characterized by lethargy, withdrawal, and “excessive emotionality” (Birmes et al., 2003). Others had diagnoses of exhaustion, effort syndrome, or heart conditions variously called “irritable 25

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26 PTSD IN MILITARY AND VETERAN POPULATIONS heart,” “soldier’s heart,” and “cardiac muscular exhaustion.” Many medi- cal professionals and surgeons at the time believed that those conditions arose from the heavy packs that soldiers carried, insufficient time for new recruits to acclimatize to the military lifestyle, homesickness, and, as one army surgeon stated, poorly motivated soldiers who had unrealistic expec- tations of war (Jones, 2006). For much of the 20th century, psychologic conditions and impairments in military personnel were not accorded high medical priority because of the high fatality rates from disease, infection, and accidental injuries during war. During World War I, shell shock and disordered action of the heart were commonly diagnosed in combat veterans (Jones, 2006). Symptoms of shell shock included tremors, tics, fatigue, memory loss, difficulty in sleep- ing, nightmares, and poor concentration—similar to many of the symptoms associated with PTSD. What is now known as delayed-onset PTSD was termed old-sergeant syndrome during the era of the world wars, when after prolonged combat, experienced soldiers were no longer able to cope with the constant threats of death or serious injury (Shephard, 2000). Stemming from the World War I definition of shell shock, other common diagnoses of soldiers during World War II included exhaustion, battle exhaustion, fly- ing syndrome, war neurosis, cardiac neurosis, and psychoneurosis (Jones, 2006). It was not until after the Vietnam War that research and methodical documentation of what was then termed combat fatigue began to accelerate in response to the many veterans suffering from chronic psychologic prob- lems that resulted in social and occupational dysfunction (IOM, 2008a). The National Vietnam Veterans Readjustment Survey (NVVRS) was one of the first large-scale studies to examine PTSD and other combat-related psychologic issues in a veteran population (Kulka, 1990). The NVVRS helped to illuminate PTSD as a signature wound of the Vietnam War and resulted in greater recognition of PTSD as a mental health disorder. The findings contributed to the formal recognition of PTSD as a distinct dis- order by the APA and later refining of the characteristic symptoms and diagnostic criteria. DIAGNOSTIC CRITERIA FOR PTSD Since 1980, PTSD has been the focus of much epidemiologic and clinical research, which in turn has led to modifications in the defining diagnostic criteria for PTSD. The current diagnostic criteria, taken from the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edi- tion, Text Revision (DSM-IV-TR), can be found in Box 2-1 (APA, 2000). The Department of Defense (DoD) and the Department of Veterans Affairs

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27 HISTORY, DIAGNOSTIC CRITERIA, AND EPIDEMIOLOGY BOX 2-1 DSM-IV-TR Diagnostic Criteria for Posttraumatic Stress Disorder 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 the physical integrity of self or others A2. The person’s response involved intense fear, helplessness, or horror B. Re-experiencing Symptoms (requires one or more of): B1. Intrusive recollections B2. Distressing nightmares B3. Acting/feeling as though event were recurring (flashbacks) B4. Psychological distress when exposed to traumatic reminders B5. Physiological reactivity when exposed to traumatic reminders C. Avoidant/Numbing Symptoms (requires three or more of): C1. Avoidance of thoughts, feelings, or conversations associated with the stressor C2. Avoidance of activities, places, or people associated with the stressor C3. Inability to recall important aspects of traumatic event C4. Diminished interest in significant activities C5. Detachment from others C6. Restricted range of affect C7. Sense of foreshortened future D. Hyperarousal Symptoms (requires two or more of): D1. Sleep problems D2. Irritability D3. Concentration problems D4. Hypervigilance D5. Exaggerated startle response E. Duration of the disturbance is at least 1 month Acute—when the duration of symptoms is less than 3 months Chronic—when symptoms last 3 months or longer With Delayed Onset—at least 6 months have elapsed between the traumatic event and onset of symptoms F. Requires significant distress or functional impairment SOURCE: American Psychiatric Association (2000) with permission. (VA) both use these criteria in diagnosing the condition in service members and veterans. PTSD is unique among psychiatric disorders in that it is linked to a spe- cific trigger: a traumatic event (Criterion A1). Traumatic events known to

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28 PTSD IN MILITARY AND VETERAN POPULATIONS trigger PTSD include combat, natural and accidental disasters (for example, tsunamis, earthquakes, and vehicle and airplane crashes), and victimization or abuse (for example, sexual assault, armed robbery, and torture) (Basile et al., 2004; Harrison and Kinner, 1998; Hoge et al., 2004; Neria et al., 2007; Punamaki et al., 2010). PTSD may be of acute, chronic, or delayed onset. In acute PTSD, symptoms develop immediately or soon after experiencing a traumatic event and persist longer than a month but less than 3 months. If symptom duration is longer than 3 months, a person has chronic PTSD. In delayed-onset PTSD, a person does not express symptoms for months or even years after the traumatic event (APA, 2000). The condition is con- sidered partial or subthreshold PTSD if a person does not meet the full diag- nostic criteria—exposure to a traumatic event and at least six symptoms: at least one B criterion of re-experiencing, at least three C criteria of numbing or avoidance, and at least two D criteria of hyperarousal—or if symptoms are not in the correct distribution. Changes to the diagnostic criteria for PTSD proposed for the next version of the DSM are shown in Box 2-2. BOX 2-2 Proposed Changes in Diagnostic Criteria for PTSD in DSM-5 Research on PTSD and acute stress reactions has progressed, and diagnostic criteria are expected to change to reflect the updated version of DSM-5. One of the changes affects Criterion A1: it is proposed to expand it from experiencing or witnessing threatened or actual death or serious injury to oneself or others to include learning about such an event that happened to a relative or close friend and to include first responders or others who are continuously exposed to or experience details of traumatic events (Friedman et al., 2010). Because of the characteristics of the statistical association and predictive value of experiencing intense fear, helplessness, or horror during the event and onset of PTSD (Brewin et al., 2000a) and because some persons—for example, military personnel, who are trained to not have an emotional response during such an event—it has been proposed that Criterion A2 be eliminated (Friedman et al., 2010). Other proposed changes for PTSD in DSM-5 include replacing the current three-pronged model with a four-pronged model. In the proposed model, Criterion B would become “Intrusion Symptoms,” Criterion C “Persistent Avoidance,” Cri- terion D “Alterations in Cognition and Mood,” and Criterion E “Hyperarousal and Reactivity Symptoms.” Although all 17 symptoms of DSM-IV would be kept in the proposed DSM-5, some of them would be revised or regrouped (such as includ- ing anger and aggressive behavior with irritability), and three symptoms would be added: erroneous self-blame or other blame regarding the cause or consequences of trauma, pervasive negative emotional states, and reckless and self-destructive behavior. The final proposed change in DSM-5 is to omit the distinction between acute and chronic PTSD. There is no proposal to include cases of subthreshold, or subsyndromal, PTSD as a distinct disorder in DSM-5 (Friedman et al., 2010).

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29 HISTORY, DIAGNOSTIC CRITERIA, AND EPIDEMIOLOGY EPIDEMIOLOGY OF PTSD IN THE GENERAL POPULATION This section begins with a brief discussion of factors associated with the experience of trauma in the general population, inasmuch as this is a main criterion in the diagnosis of PTSD, before considering the epidemiology of PTSD in the general population. The next major section deals with trauma and epidemiology specific to military and veteran populations. Men are more likely than women to experience potential traumatic events overall, although the types of traumatic events differ by sex (Tolin and Foa, 2006). Studies assessing the role of race and ethnicity have had mixed results but have found that whites have higher risks of exposure to any traumatic event than Hispanics and blacks (Noris, 1992; Roberts et al., 2011). Other factors found to be associated with increased risk of ex- periencing traumatic events include lower education attainment (less than a 4-year college degree), lower annual income (less than $25,000), and nonheterosexual orientation (Breslau et al., 1998; Roberts et al., 2010). Three prospective studies have documented that externalizing behavioral problems (for example, difficult temperament and antisocial behavior) in early childhood increase the risk of traumatic-event exposure—particularly assaultive violence—over a lifetime (Breslau et al., 2006; Koenen et al., 2007; Storr et al., 2007). Trauma type and severity are central determinants of the risk of devel- opment of PTSD. Experiencing physical injuries (penetrating and assault), viewing the event as a true threat to one’s life, and suffering major losses are all associated with a higher risk of PTSD (Holbrook et al., 2001; Ozer et al., 2003). The occurrence of dissociation itself during a traumatic event does not appear to predict development of PTSD as much as dissociation that persists after the event (Panasetis and Bryant, 2003) or the experience of perievent emotional reactions (Galea et al., 2003). As recognized by the VA/ DoD Clinical Practice Guideline for Management of Post-Traumatic Stress (2010), lack of social support, trauma severity, and ongoing life stress in- crease the risk of PTSD. Lack or loss of social support (for example, spouse, friends, or family) after a traumatic event and ongoing life stress—including loss of employment, financial strain, and disability—have been associated with increased risk of PTSD (Brewin et al., 2000a; Ozer et al., 2003). Several large, nationally representative surveys have provided estimates of the prevalence of PTSD in the general population. The National Comor- bidity Survey (NCS), conducted from 1990 to 1992, was one of the first large-scale surveys to examine the distribution of and factors associated with psychiatric disorders in the United States. Using a structured diag- nostic interview, the NCS found that the lifetime prevalence of PTSD was 7.8% overall (Kessler et al., 1995). In the National Comorbidity Survey– Replication (NCS–R) conducted 10 years after the original, the prevalence

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30 PTSD IN MILITARY AND VETERAN POPULATIONS of lifetime PTSD was estimated to be 6.8% overall and that of current (12-month) PTSD 3.6% overall (Kessler et al., 2005). The 2004–2005 Na- tional Epidemiologic Survey on Alcohol and Related Conditions estimated lifetime prevalence of PTSD to be 7.3% overall (Roberts et al., 2011). Sex and trauma type are two risk factors associated with PTSD (protec- tive factors are discussed in Chapter 5). PTSD prevalence has consistently been shown to differ by sex in the civilian population (Kessler et al., 1995, 2005; Tolin and Foa, 2006). The original NCS found PTSD prevalence to be twice as great in women as in men, and the NCS–R estimated it to be 2.7 times greater in women than in men (Harvard Medical School, 2007b; Kessler et al., 1995). The type of trauma experienced may lead to the dis- crepancy between the sexes. For example, Tolin and Foa (2006) found no sex differences associated with PTSD in persons who experienced assaultive violence or nonsexual child abuse or neglect, but there were marked differ- ences between men and women who experienced combat, accidents, and disasters. Men were more likely to report having experienced a traumatic event over their lifetimes, but women were more likely to meet criteria for PTSD (Tolin and Foa, 2006), have PTSD symptoms four times as long as men (48 months vs. 12 months) (Breslau et al., 1998), have a poorer quality of life if they have PTSD (Holbrook et al., 2001; Seedat et al., 2005), and develop more comorbid psychiatric disorders (Seedat et al., 2005). There is some evidence on the effect of race and ethnicity on the devel- opment of PTSD although findings are inconsistent among studies. Results from the 2004–2005 wave of the National Epidemiologic Survey on Alcohol and Related Conditions showed that whites were more likely to have expe- rienced any trauma, and lifetime prevalence of PTSD was highest in blacks and lowest in Asians. Even after adjustment for characteristics related to trauma, the risk of PTSD was significantly higher in blacks and lower in Asians than in whites in the sample (Roberts et al., 2011). Marshall et al. (2009) found that in a sample of survivors of physical trauma, Hispanic whites reported greater symptoms related to cognitive and sensory percep- tion (for example, hypervigilance and emotional reactivity) and overall symptom severity than non-Hispanic whites. Other work has shown that Hispanic whites are more likely to report PTSD after a traumatic event than are non-Hispanic whites (Galea et al., 2004). In a study of adults 18–45 years old in the Detroit area, Breslau et al. (1998) found that nonwhites were not at higher risk for PTSD than whites. PTSD can affect people of any age. In the NCS–R, people were divided into four cohorts: 18–29, 30–44, 45–59, and older than 59 years old. The highest lifetime and 12-month prevalences of PTSD were in the group 45–59 years old (9.2% and 5.3%, respectively), and the lowest preva- lences (2.8% and 1.0%, respectively) were in the group over 59 years old (Harvard Medical School, 2007a,b). Results from the earlier NCS showed

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31 HISTORY, DIAGNOSTIC CRITERIA, AND EPIDEMIOLOGY a different distribution of lifetime prevalence of PTSD by age group. The lowest prevalence was in men 15–24 years old (2.8%) and women 45–54 years old (8.7%) (Kessler et al., 1995). However, most of those studies ex- amined the association between current age of the participants and PTSD symptoms or diagnostic threshold, and the strength of association between age and development of PTSD is unknown. Prevalence estimates of PTSD by age groups may also be confounded by historical events, such as the Vietnam War. Sexual orientation has been associated with risk of PTSD. The National Epidemiologic Survey of Alcohol and Related Conditions found that the risk of PTSD was significantly higher in lesbians and gays, bisexuals, and heterosexuals with any same-sex partners than it was in the heterosexual reference group. After adjusting for demographic factors, the higher risk of PTSD was largely explained by nonheterosexuals’ greater exposure to violence, exposure to more potentially traumatic events, and earlier age at trauma exposure (Roberts et al., 2010). Cognitive reserve—individual differences in brain structure and function that are thought to provide resilience against damage from neuropathology— is thought to be one important etiologic factor in the development and se- verity of PTSD and other neuropsychiatric disorders (Barnett et al., 2006). Intelligence quotient (IQ), a marker of cognitive reserve, has been shown to be inversely related to risk of PTSD and other psychiatric disorders (Batty et al., 2005; Walker et al., 2002). In a 17-year prospective study of randomly selected newborns in southeastern Michigan, Breslau et al. (2006) found that children who at the age of 6 years had an IQ of greater than 115 had a decreased conditional risk of PTSD after trauma exposure; however, the risk increased for children that experienced anxiety disorders and whom teachers rated as high for externalizing problems. Overall, the authors found that high IQ (115 or higher) protected exposed persons from developing PTSD in this cohort (Breslau et al., 2006). Similarly, Koenen et al. (2007) examined the association between early childhood neurocognitive factors and risk of PTSD in a New Zealand birth cohort that was followed through the age of 32 years. The authors found that IQ assessed at the age of 5 years was inversely associated with risk for developing PTSD by the age of 32 years. No associations were found between PTSD and other neurodevelopmental factors assessed in the co- hort, suggesting that the IQ–PTSD association was not a marker of broader neurodevelopmental deficits. The findings on the strength of association between family psychiatric history and PTSD are mixed. In one analysis of NCS data, after controlling for previous traumatic events, parental mental health disorders were associ- ated with increased risk of PTSD in both men and women (Bromet et al., 1998). Although Breslau et al. (1991) found statistically significant associa-

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32 PTSD IN MILITARY AND VETERAN POPULATIONS tions between PTSD after a traumatic event and family psychiatric history of depression, anxiety, and psychosis, a meta-analysis of risk factors for PTSD did not find this association in either civilian or military population studies (Brewin et al., 2000b). A family history of psychiatric disorders may be indicative of adverse family environment, which may increase the risk of experiencing a traumatic event, such as abuse, during childhood (Breslau et al., 1995; Brewin et al., 2000b). A positive association was found be- tween reported family history of psychopathologic conditions and higher rates of PTSD symptoms or diagnosis, but the strength of this relationship differed by the type of traumatic experience of the target event (stronger after noncombat interpersonal violence than after combat exposure) and method of PTSD assessment (stronger when symptoms were determined in interviews than in self-reports) (Ozer et al., 2003). In a study that followed a New Zealand birth cohort and assessed for PTSD at the age of 26 years and again at the age of 32 years, maternal depression before the age of 11 years was associated with increased risk of PTSD through the age of 32 years (Koenen et al., 2007). Family and twin studies of PTSD have produced two major findings. First, PTSD has a genetic component. Modern genetic studies of PTSD be- gan with the observation that relatives of probands (persons serving as in- dex cases in genetic investigations of families) who had PTSD had a higher risk of the disorder than relatives of similarly trauma-exposed controls who did not develop PTSD. Twin studies established that genetic influences ex- plain much of the vulnerability to PTSD, from about 30% in male Vietnam veterans (True et al., 1993) to 72% in young women (Sartor et al., 2011), even after genetic influences on trauma exposure are accounted for. Second, both family and twin studies suggest that there is strong overlap for genetic influences on PTSD and those of other mental disorders including major depression, generalized anxiety disorder, and alcohol and drug dependence. For example, in a sample of Vietnam veterans, common genetic influences explained 63% of the major depression–PTSD comorbidity and 58% ge- netic variance in PTSD (Koenen et al., 2008a). Other studies using the Vietnam Era Twin Registry found genetic influences of generalized anxiety disorder and panic disorder symptoms (Chantarujikapong et al., 2001), alcohol dependence and drug dependence (Xian et al., 2000), and nicotine dependence (Koenen et al., 2005b) account for a substantial proportion of the genetic variance for PTSD. Those results suggest that most of the genes that affect the risk of PTSD also influence the risk of these psychiatric dis- orders and vice versa. A more complete discussion of genetic influences on PTSD is found in Chapter 3. Several prospective studies have implicated pretrauma psychopathology in increasing the risk of PTSD. In a cohort of randomly selected newborns in southeastern Michigan followed for 17 years, children who at the age of

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33 HISTORY, DIAGNOSTIC CRITERIA, AND EPIDEMIOLOGY 6 years were rated as having externalizing problems above the normal range were more likely to develop PTSD than children who were rated as normal externalizers; young adults who had received a diagnosis of any anxiety disorder at the age of 6 years were significantly more likely to develop PTSD than those who had not (Breslau et al., 2006). Another prospective study in a cohort of children of similar age entering first grade over a 2-year period and followed for 15 years, those who in first grade were categorized as highly anxious or having depressive mood were at higher risk for PTSD among those exposed to traumatic events than their peers who did not have these psychologic problems; exhibiting aggressive or disruptive behaviors, concentration problems, and low social interaction were not found to be associated with increased risk of PTSD in this cohort (Storr et al., 2007). A third prospective study, which followed a New Zealand birth cohort and assessed for trauma exposure and PTSD at the ages of 26 and 32 years, found several childhood risk factors to be associated with PTSD. Childhood temperament ratings were made at the ages of 3 and 5 years, and behavior ratings were made by teachers biannually from the ages of 5 through 11 years. Children who had difficult temperaments or antisocial behavior and who were unpopular were statistically more likely to develop PTSD than their peers who did not have these characteristics. Antisocial behavior as- sessed before the age of 11 years predicted development of PTSD at the age of 26 years and at the age of 32 years. Childhood poverty and high levels of internalizing symptoms in mothers were also associated with development of PTSD (Koenen et al., 2007). Childhood abuse may have an effect on the development of PTSD. A meta-analysis that considered nine studies suggests that abuse during child- hood is a risk factor for PTSD (Brewin et al., 2000b). Desai et al. (2002) found that physical or sexual childhood victimization or both increased the risk of adult victimization by an intimate partner. This aligns with NCS findings that women who experienced physical abuse during childhood had the highest risk of lifetime PTSD (Kessler et al., 1995). In addition to pretrauma psychopathology or childhood abuse, prior trauma has been shown to increase the risk of PTSD. Ozer et al. (2003) found a significant association between a history of prior trauma and PTSD symptoms or diagnosis. Persons who experienced a traumatic event before the target stressor reported higher levels of PTSD symptoms on the average than persons who did not. Prior trauma was more strongly associated with PTSD in connection with traumatic experiences of noncombat interpersonal violence than with combat exposures (Ozer et al., 2003). However, more recent data from prospective studies offer evidence against the hypothesis that prior trauma alone increases the risk of PTSD. Using a random sample from a large health maintenance organization in southeastern Michigan, Breslau et al. (2008) found that prior experience of trauma does not neces-

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34 PTSD IN MILITARY AND VETERAN POPULATIONS sarily increase the risk of PTSD in response to a subsequent trauma. Only those persons who developed PTSD in response to a prior trauma had an increased risk of PTSD after a later trauma. A follow-up study on assaultive violence found that it was the development of prior PTSD after a trauma that was predictive of the development of current PTSD after a later trauma (Breslau and Peterson, 2010). Trajectory of PTSD The course of PTSD may remit with time, with steepest remission in the first 12 months after diagnosis. In a nonrandomized, observational, retrospective analysis based on the NCS, the median time until diagnostic criteria were no longer met in those who received treatment was 36 months compared with 64 months in those who did not receive treatment (Kessler et al., 1995). However, approximately one-third of PTSD cases do not remit even after many years of treatment. A prospective study of PTSD in rape victims found that half recovered spontaneously, with the steepest declines from the first to the fourth assessment (mean, 35 days after the assault), whereas victims who had a diagnosis of PTSD 2 months or more after the trauma (rape) were unlikely to recover without treatment (Rothbaum et al., 1992). Other studies have shown remission of PTSD after particular trau- matic events, such as disasters, in the first 6 months after exposure to the event (Galea and Resnick, 2005). Although PTSD is triggered by the initial exposure to a traumatic event, several studies have shown that exposure to ongoing stressors and other traumatic events throughout life contributes to the persistence of PTSD in the general population (Galea et al., 2008). Few studies have investigated the chronicity of PTSD, most conducted before some current therapies were available; therefore, they are rela- tively dated. Two similarly designed prospective observational studies of people who had diagnosed PTSD and who were seeking care in tertiary care psychiatric practices (Zlotnick et al., 1999) or primary care practices (Zlotnick et al., 2004) had similar findings. Over the 5-year follow-up of the 54 persons in the tertiary care study, the probability of experiencing full remission was 18%. Chronicity of PTSD was associated with a history of alcohol abuse or dependence and childhood trauma (Zlotnick et al., 1999). In the primary care study, the authors considered full and partial remission separately. The findings were similar to those of the tertiary care study: over the 2-year follow-up of the 84 primary care subjects, the probability of full remission was 18% and the probability of partial remission 69%. Both full remission and partial remission were associated with fewer co- morbid anxiety disorders and a smaller degree of psychosocial impairment. The authors also evaluated the type, dose, and duration of treatment. The treatment was not randomized, but there was no association between the

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35 HISTORY, DIAGNOSTIC CRITERIA, AND EPIDEMIOLOGY use of selective serotonin reuptake inhibitors or serotonin norepinephrine reuptake inhibitors and PTSD status at any point during the follow-up period (Zlotnick et al., 2004). Men who reported combat as their worst trauma in the NCS were more likely to have lifetime PTSD, delayed onset of PTSD symptoms, and unresolved PTSD symptoms than men who named other types of trauma as their worst (Prigerson et al., 2001). Veterans enrolled in the NVVRS who had ever had full or partial PTSD reported they had experienced symptoms 63% of the time during the preceding 5 years (data collected between 1994–1996); 55% reported having symptoms every month, and 17% re- ported having no symptoms. In the 3 months before assessment, 78% had been symptomatic (Schnurr et al., 2003). PTSD is associated with several adverse outcomes, including lower quality of life, work-related impairment, and medical illness throughout its course (Marshall et al., 2001; Resnick and Rosenheck, 2008; Zatzick et al., 1997). Several studies have shown an adverse effect of PTSD on physical health (Weiss et al., 2011), and others have found that exposure to a traumatic event increases the risk of adverse physical health, includ- ing many of the leading causes of premature death, such as cardiovascular disease and stroke (Boscarino, 2008; Cohen et al., 2009, 2010; Dirkzwager et al., 2007; Dong et al., 2004; Kubzansky et al., 2007, 2009). The asso- ciations are thought to be mediated in part by health behaviors, such as smoking, alcohol use, and physical inactivity (Breslau et al., 2003; Dobie et al., 2004). Because it would be unethical to expose humans to major trauma experimentally, randomized studies of the trajectory of PTSD are not feasible. The only available studies of trajectory of PTSD are natural history and observational studies, so the inference of findings to the general populaton is limited, and this makes it difficult to project future care and treatment needs. Comorbidities of PTSD People who have PTSD often have co-occurring psychologic disorders, such as depressive disorders, substance dependence, panic disorder, agora- phobia, generalized anxiety disorder, social phobia, bipolar disorder, and somatization (APA, 2000). People who have diagnoses of more than one mental health disorder have greater impairment than those who have a single diagnosis (IOM, 2008b). Those additional disorders can precede or present simultaneously with PTSD, and they may also resolve before, after, or simultaneously with PTSD. A prospective study that used data from a New Zealand birth cohort found that 96.3% of all adults who at the age of 32 years had a diagnosis of PTSD in the preceding year and 93.5% of those meeting criteria for lifetime diagnosis of PTSD at the age of 26 years

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48 PTSD IN MILITARY AND VETERAN POPULATIONS physical health are unlikely to join the armed forces or to complete basic training, and the same should be true of people who have poor mental health. If such people are not medically discharged early in their military ca- reers, they may be excluded from some deployments (Wilson et al., 2009). Subthreshold PTSD As discussed earlier in this chapter, DSM-IV lists 17 symptoms of PTSD, at least 6 of which are required—in the correct distribution (one re-experiencing, three numbing or avoidance, and two hyperarousal)—for a diagnosis of PTSD. However, several studies have indicated that even sub- threshold PTSD is impairing and that people who have it may benefit from treatment (Grubaugh et al., 2005; Marshall et al., 2001; Stein et al., 1997; Zlotnick et al., 2002). If the purpose of diagnosing PTSD and treating it is to regain and maintain functioning, then it is clear that any symptoms that are potentially attributable to prior trauma and are accompanied by functional impairment warrant treatment. Subthreshold PTSD may also be a signal of other pathologic conditions, such as depression or an additional anxiety disorder, in that there is overlap in the defining symptoms of these conditions. Subthreshold symptoms have potential implications for screen- ing, level of functioning, degree of distress, and treatment. A full discussion of the implications of subthreshold PTSD is beyond the scope of this report, but it merits mention as a subject of further inquiry. Compensation Issues and Secondary Gain PTSD in military and veteran populations is complicated by concerns about malingering and attempts to receive the diagnosis for secondary gain. This issue has become particularly important in military populations inasmuch as its presence is formally recognized as making someone eligible for DoD and VA benefits. Thus, a diagnosis of PTSD is problematic in both active-duty and veteran populations, and can lead to underreporting (for example, to remain in one’s position) or to overreporting (for example, to gain benefits or to be excused from duty). A previous Institute of Medicine report on PTSD compensation and military service (IOM, 2007) noted that, apart from problems with the current procedures for assigning a disability rating to PTSD, other considerations include “barriers or disincentives to recovery, the effect of disability compensation on recovery, and the advis- ability of periodic re-examination of PTSD compensation beneficiaries.” Although that committee found that compensation does not appear to serve as a disincentive to seeking treatment, periodic re-examinations for veterans who have a PTSD service-connected disability were regarded as inappropri- ate because research on misreporting and exaggeration of symptoms had

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49 HISTORY, DIAGNOSTIC CRITERIA, AND EPIDEMIOLOGY not found evidence supporting a singling out of PTSD (IOM, 2007). This is an important and complicated issue, and the present committee will re- consider it if any new literature becomes available during phase 2. SUMMARY PTSD is prevalent in the general population in which it has a lifetime prevalence of about 8% in adults, but military and veteran populations are exposed to many more traumatic events than the general population, and service members who have served in OEF and OIF have a lifetime PTSD prevalence of 13% to 20%. Many factors increase a service mem- ber’s risk of PTSD, some demographic—such as age; sex; prior exposure to trauma, particularly sexual assault and childhood maltreatment; lower education attainment; and lower IQ—and some combat-specific—such as killing someone, seeing someone killed, and being in an explosion or being badly injured. PTSD is often comorbid with other psychologic or medical conditions, such as depression, substance use (particularly alcohol use) disorder, and traumatic brain injury. Special considerations in the diagno- sis of and treatment for PTSD in military and veteran populations include subthreshold PTSD, underreporting and overreporting of PTSD symptoms, the role of stigma in seeking care for PTSD, the healthy warrior effect, and compensation. The next chapter provides a discussion of the biologic basis of and factors that affect the development of PTSD. REFERENCES APA (American Psychiatric Association). 1980. DSM-III: Diagnostic and statistical manual of mental disorders. 3rd ed. Washington, DC: American Psychiatric Association. APA. 2000. Diagnostic and statistical manual of mental disorders, fourth edition, text revision (DSM-IV-TR). Washington, DC: American Psychiatric Association. Arrighi, H. M., and I. Hertzpicciotto. 1994. The evolving concept of the healthy worker sur- vivor effect. Epidemiology 5(2):189-196. Barnett, J. H., C. H. Salmond, P. B. Jones, and B. J. Sahakian. 2006. Cognitive reserve in neuropsychiatry. Psychological Medicine 36(8):1053-1064. Basile, K. C., I. Arias, S. Desai, and M. P. Thompson. 2004. The differential association of intimate partner physical, sexual, psychological, and stalking violence and posttraumatic stress symptoms in a nationally representative sample of women. Journal of Traumatic Stress 17(5):413-421. Batty, G. D., E. L. Mortensen, and M. Osler. 2005. Childhood IQ in relation to later psychi- atric disorder: Evidence from a Danish birth cohort study. British Journal of Psychiatry 187:180-181. Birmes, P., L. Hatton, A. Brunet, and L. Schmitt. 2003. Early historical literature for post- traumatic symptomatology. Stress and Health 19(1):17-26. Boscarino, J. A. 2008. A prospective study of PTSD and early-age heart disease mortality among Vietnam veterans: Implications for surveillance and prevention. Psychosomatic Medicine 70(6):668-676.

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