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Gulf War and Health, Volume 6: Physiologic, Psychologic, and Psychosocial Effects of Deployment-Related Stress 5 POSTTRAUMATIC STRESS DISORDER Posttraumatic stress disorder (PTSD) is an anxiety disorder that is defined as resulting from exposure to a traumatic event. War-related traumatic events have been detailed in numerous studies (see Chapter 3). However, not everyone exposed to a war-zone trauma will develop PTSD, nor is the course of the disorder the same for everyone that does develop it. There are many factors that affect a person’s response to a traumatic event and there is much research being done to elucidate the biological mechanisms of PTSD. It is widely recognized that soldiers suffer psychologic consequences of combat (Jones 2006). The constellation of symptoms that has come to be known as PTSD was given other names in earlier wars. During the Civil War, “irritable heart” or “effort syndrome” featured shortness of breath, disturbed sleep, palpitations, and other symptoms. During World War I, effort syndrome was again diagnosed, as was “shell shock,” which was first described in British soldiers evacuated from the trenches in France. Marked by blindness, muteness, and amnesia, shell shock was initially thought to be the result of brain concussion from nearby shell explosions, but over time it became clear that effort syndrome and shell shock had psychologic origins (Hyams et al. 1996; Shephard 2001). During World War II, physicians identified an acute psychologic syndrome commonly found in soldiers, which they referred to as battle fatigue or combat exhaustion, so named to avoid stigma and to imply that soldiers would recover naturally with food and rest. Although the sheer number of psychiatric casualties was high, many of the troops were returned to combat after treatment near the front line (Grob 1994; Shephard 2001). Nevertheless, in 1942-1945, 850,000 active-duty U.S. soldiers were admitted to military hospitals for neuropsychiatric care (Starr 1982). A persistent and chronic form of battle fatigue was described among those veterans (Friedman et al. 1994; Grob 1994; Southwick et al. 1994). In World War II, Grinker and Spiegel (1945) described cases of “war neurosis” in members of combat aircrews. The primary symptoms of war neurosis were restlessness, irritability, aggression, fatigue, sleep difficulties, anxiety, startle reaction, tension, depression, personality changes, memory disturbances, tremors, difficulty in concentrating, alcoholism, preoccupation with combat experiences, decrease in appetite, psychosomatic symptoms, irrational fears, and suspiciousness. The experiences of World War II military psychiatrists were instrumental in spurring the profession into the modern era of psychiatric diagnosis. Military psychiatrists believed that psychiatric disorders among veterans of military combat were more pervasive and serious than had been anticipated before the war. They also believed, contrary to prevailing views, that psychological maladjustment could be triggered by external stress (Grob 1994). Their influence
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Gulf War and Health, Volume 6: Physiologic, Psychologic, and Psychosocial Effects of Deployment-Related Stress was felt in the first edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM), published in 1952 by the American Psychiatric Association (APA). After the Vietnam War, research demonstrated that many veterans, particularly those exposed to severe war-related trauma, and other traumatized populations such as Holocaust survivors, suffered from chronic psychologic problems that often resulted in social and occupational dysfunction. The strength of the evidence led to the formal recognition of PTSD as a psychiatric diagnosis in the third edition of DSM (DSM-III), published in 1980. Because the DSM-III provided a formal operational definition of PTSD, it presented a platform for large-scale studies of PTSD in Vietnam veterans and veterans of later wars. In the sections below, the committee discusses the diagnosis and clinical features of PTSD; its prevalence in military populations; the course of the disorder; the comorbidity of PTSD with other psychiatric disorders and associated disability of people who have PTSD; risk and protective factors for PTSD; and finally the neurobiology of PTSD. DIAGNOSIS AND CLINICAL FEATURES People who are exposed to traumatic events react to them in different ways; some experience temporary distress, and others will go on to develop PTSD or other psychiatric disorders, such as major depression. The criteria for PTSD are listed in the fourth edition of the DSM (DSM-IV-TR) (Box 5-1) and require that the person have experienced, witnessed, or been confronted with an event that involves actual or threatened death, serious injury, or a threat to the physical integrity of self or others and that the person have responded with intense fear, helplessness, or horror. Symptoms must persist for a month or more and include three symptom clusters: Re-experiencing—intrusive recollections of a traumatic event, such as flashbacks or nightmares. Avoidance/numbing—efforts to avoid reminders of the event and numbing of emotions. Hyperarousal—manifested by, for example, difficulty in sleeping or jumpiness. Finally, the person must have clinically significant distress or functional impairment resulting from the symptoms (APA 2000). Two terms are used to describe PTSD in this report: lifetime and current. In lifetime PTSD, the person has met the criteria for a diagnosis of PTSD at some point and may or may not be symptomatic at the time of the assessment. The meaning of current PTSD varies by study; it can mean that the person met the criteria for PTSD at the time of the assessment, within the preceding month, within the preceding 3 months, 6 months, even 12 months. The committee used the terminology and timeframe for PTSD as given in each study. Lifetime and current PTSD may or may not be related to combat or deployment experiences; when PTSD has been related to combat or deployment experiences, the committee has included this information in its discussion. PTSD should be assessed on the basis of a thorough diagnostic interview; structured or semistructured interviews, such as the Clinician-Administered PTSD Scale, the Structured Clinical Interview for DSM-IV (SCID), the Diagnostic Interview Schedule for DSM-IV (DIS-IV), and the Composite International Diagnostic Interview (CIDI) are examples of diagnostic
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Gulf War and Health, Volume 6: Physiologic, Psychologic, and Psychosocial Effects of Deployment-Related Stress interviews. However, many epidemiologic studies use screening instruments to assess the number and frequency of symptoms of PTSD, rather than a full diagnostic interview. Those screening instruments include the Department of Veterans Affairs (VA) Primary Care PTSD Screen, the PTSD Checklist (either military or civilian version), the Mississippi Scale for Combat-Related PTSD, and the Keane Scale of the Minnesota Multiphasic Personality Inventory (MMPI-PK). BOX 5-1 DSM-IV Diagnostic Criteria for Posttraumatic Stress Disorder The person has been exposed to a traumatic event in which both of the following were present: The person experienced, witnessed, or was confronted with an event or events that involved actual or threatened death or serious injury, or a threat to the physical integrity of self or others. The person’s response involved intense fear, helplessness, or horror. The traumatic event is persistently re-experienced in one (or more) of the following ways: Recurrent and intrusive distressing recollections of the event, including images, thoughts, and/or perceptions; Recurrent distressing dreams of the event; Acting or feeling as if the traumatic event were recurring (includes a sense of reliving the experience, illusions, hallucinations, and/or dissociative flashback episodes, including those that occur on awakening or when intoxicated); Intense psychological distress at exposure to internal or external cues that symbolize or resemble an aspect of the traumatic event; Physiological reactivity on exposure to internal or external cues that symbolize or resemble an aspect of the traumatic event. Persistent avoidance of stimuli associated with the trauma and numbing of general responsiveness (not present before the trauma), as indicated by at least three of the following: efforts to avoid thoughts, feelings, and/or conversations associated with the trauma; efforts to avoid activities, places, and/or people that arouse recollections of the trauma; inability to recall an important aspect of the trauma; markedly diminished interest or participation in significant activities; feeling of detachment or estrangement from others; restricted range of affect (e.g., inability to have loving feelings); sense of a foreshortened future (e.g., does not expect to have a career, marriage, children, or a normal life span). Persistent symptoms of increased arousal (not present before the trauma), as indicated by at least two of the following: difficulty falling or staying asleep; irritability or outbursts of anger; difficulty concentrating; hypervigilance; exaggerated startle response. Duration of the disturbance (symptoms in Criteria B, C, and D) is more than one (1) month. The disturbance causes clinically significant distress and/or impairment in social, occupational, and/or other important areas of functioning. SOURCE: Reprinted with permission from APA (2000).
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Gulf War and Health, Volume 6: Physiologic, Psychologic, and Psychosocial Effects of Deployment-Related Stress PREVALENCE The National Comorbidity Survey (NCS) conducted in 1990-1992 on a nationally representative sample of 5877 people, found the prevalence of lifetime PTSD to be 7.8% (5% in men and 10% in women) (Kessler et al. 1995). In the NCS replication conducted in 2001-2003 on 9282 people, Kessler et al. (2005b) found the prevalence of PTSD in the previous 12 months to be 3.5%. PTSD was assessed according to the World Health Organization World Mental Health Survey version of the CIDI. In a study of young adults in a health maintenance organization in an urban area, Breslau (2001a) estimated that about 8% of adults may experience lifetime PTSD, or about 15-24% of those who are exposed to traumatic events. Although women’s exposure to traumatic events is estimated to be somewhat less than that of men, twice as many women develop PTSD (Breslau 2001a). In a comparison group of 500 civilians in the National Vietnam Veterans Readjustment Study (NVVRS), Kulka et al. (1990) found that 1.2% of men and 0.3% of women had current (6-month) PTSD. Many people experience traumatic events. Some traumatic events are common and are associated with a relatively low prevalence of PTSD, such as the sudden death of a loved one; other, less common traumatic events, such as rape, are associated with a very high prevalence of PTSD (see Table 5-1). In the case of the 1995 Oklahoma City bombing, it was found that the postdisaster prevalence of PTSD was 34% among all cases identified in 4-8 months after the bombing (North et al. 1999). TABLE 5-1 Prevalence of Traumatic Events and PTSD in Men and Women Traumatic Event Prevalence of Event (%) Prevalence of Lifetime PTSD in Response to Event (%) Men Women Men Women Rape 0.7 9.2 65.0 45.9 Molestation 2.8 12.3 12.2 26.5 Physical assault 11.1 6.9 1.8 21.3 Accident 25.0 13.8 6.3 8.8 Natural disaster 18.9 15.2 3.7 5.4 Witnessed death or injury 40.1 18.6 9.1 2.8 Learned about a traumatic event 63.1 61.8 1.4 3.2 Sudden death of a loved one 61.1 59.0 12.6 16.2 SOURCE: Adapted with permission from Yehuda (2002). Combat is one of the most traumatic events a person can experience. Men who named combat as their “worst lifetime traumatic event” were found to be 7 times as likely to have PTSD than men naming other experiences (Prigerson et al. 2001). Nearly 30% of all cases of PTSD in the U.S. population are attributed to combat experience (Prigerson et al. 2002). Numerous studies in military populations have provided estimates of the prevalence of PTSD; some of those are discussed below.
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Gulf War and Health, Volume 6: Physiologic, Psychologic, and Psychosocial Effects of Deployment-Related Stress Operation Enduring Freedom and Operation Iraqi Freedom In U.S. combat troops deployed to Afghanistan and Iraq, the risk of having PTSD 3-4 months after their return was 6.2% for Army troops returning from Afghanistan (odds ratio [OR] 1.26, 95% confidence interval [CI] 0.97-1.64) and 12.9% for Army (OR 2.84, 95% CI 2.17-3.72) and 12.2% for Marines (OR 2.66, 95% CI 2.01-3.51) returning from Iraq. The risk of having PTSD before deployment was 5.0% for all the military personnel screened using the PTSD Checklist (Hoge et al. 2004). A year after their return from Iraq, 16.6% of the U.S. Army combat troops met the screening criteria for PTSD (Hoge et al. 2007). The Department of Defense conducted a mental-health survey of Army soldiers and Marines deployed in Iraq in 2003, 2004, and 2006. In 2003, 16% of the soldiers and Marines met the screening criteria for PTSD while deployed; in 2004, 14% met the criteria; and in 2006, 17% of soldiers and 14% of Marines met the criteria (MHAT 2006). Gulf War The effects of the 1991 Gulf War on Army active-duty, and reserve or National Guard units from Pennsylvania and Hawaii were studied about 2 years after the war (Stretch et al. 1996). Of the deployed active-duty and reserve or National Guard soldiers, 8% and 9.2%, respectively, had a symptom complex suggestive of PTSD; of the nondeployed active-duty and reserve or National Guard soldiers, only 1.3% and 2.1%, respectively, had such symptoms. In an earlier study of 11,000 active-duty Gulf War soldiers conducted 6-12 months after the war, current PTSD rates were 12.9-15.5% (Stretch et al. 1996). The lower rates in the Pennsylvania and Hawaiian troops were attributed to their military occupations—support activities—which may have resulted in less exposure to traumatic events than the active-duty Army soldiers who had engaged in combat. In a 1995-1997 survey of 9476 Gulf War-era veterans and 11,441 Gulf War-deployed veterans in all four services, Kang et al. (2003) found that 12.1% of deployed veterans and 4.3% of nondeployed veterans met the screening criteria for current PTSD using the PTSD Checklist (adjusted OR 3.1, 95% CI 2.7-3.4). The risk of PTSD increased with the severity of the stress, ranging from 3.3% in activated but nondeployed reserve personnel (minimal stress) to 22.6% in Gulf War-deployed veterans who had worn chemical protective gear, heard chemical alarms, been involved in direct combat duty, and witnessed deaths (maximal stress). In a followup to that study, Toomey et al. (2007) found that 6.2% of Gulf War-deployed veterans and 1.1% of nondeployed veterans had a diagnosis of war-related PTSD 10 years after the war (OR 5.78, 95% CI 2.62-12.74; adjusted for age, sex, ethnicity, duty type, service branch, and rank). Ikin et al. (2004) found that a decade after the Gulf War, 5.1% of Australian Gulf War veterans had PTSD (diagnosed with the CIDI), compared with 1.7% of nondeployed Australian veterans. Few of the Australian veterans experienced direct combat; rather, their stressors were associated with the threat of combat, anticipation of attack with biologic or chemical agents, and the discomfort and isolation of deployment. Similar risks for PTSD were seen in Canadian Gulf War-deployed and nondeployed veterans (Goss Gilroy Inc. 1998). A 1998-2001 mail survey of 23,358 UK Gulf War veterans also found increased self-reports of PTSD and associated symptoms compared with nondeployed military personnel (1.0% vs 0.4%, OR 2.4, 95% CI 1.8-3.1) (Simmons et al. 2004).
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Gulf War and Health, Volume 6: Physiologic, Psychologic, and Psychosocial Effects of Deployment-Related Stress Vietnam War The NVVRS assessed the readjustment to civilian life and the prevalence of PTSD and other psychiatric disorders in 3016 Vietnam veterans 15-20 years after the war (Kulka et al. 1990). It was estimated that 15.2% of all male Vietnam-theater veterans had current (6-month) combat-related PTSD and 30.9% had lifetime combat-related PTSD (the former value is equivalent to about 479,000 of the 3.14 million men who served in the Vietnam theater). Of the 7200 female veterans, it was estimated that 8.5% had current PTSD and 26.9% had lifetime PTSD. The prevalence of current PTSD (35.8%) was 4 times as high in men (7 times as high as in women) exposed to high levels of war-zone stress as in men exposed to low or moderate war-zone stress (8.5%); 2-3 times as high as in those with service-connected physical disabilities (wounded in combat), and twice as high as in men (5 times as high in women) with lifetime substance-abuse disorders (Schlenger et al. 1992). Exposure to war-zone stress was more predictive of PTSD in the NVVRS study than were predisposing factors (Keane 1998). Dohrenwend et al. (2006) reanalyzed the military records of 1200 male Vietnam-theater veterans from the NVVRS with a records-based military-history measure of exposure to war-zone stressors. Over 86% of the veterans with war-related PTSD described events that were personally life-threatening or involved witnessing death of or physical harm to others. A diagnosis of PTSD was based on the SCID. A dose-response relationship was established: fewer than 1% of low-exposed veterans had a diagnosis of current (as of 1988) war-related PTSD vs 28.1% of those in the high-exposure category. When adjusted for impairment of functioning and documentation of exposure to war-related traumatic events, the prevalence of lifetime and current war-related PTSD was 18.7% and 9.1%, respectively. The Vietnam Experience Study (VES) was conducted by the Centers for Disease Control and Prevention in 1984 on a random sample of 2490 Vietnam theater and 1972 era Army veterans via telephone interview. A subsample of the respondents received a physical examination by a clinician and were interviewed with the DIS for assessment of psychiatric disorders (CDC 1988). Lifetime and current (1-month) PTSD rates were 14.7% and 2.2%, respectively, in the theater veterans 13 years after the end of the war. PTSD prevalence in the era veterans was not given. Using the same dataset, but including noncombat PTSD with combat-related PTSD, Boscarino (1995) found the prevalence of current PTSD in theater and era veterans to be 12% and 2%, respectively. PTSD was positively associated with reported combat exposure (OR 2.42, p < 0.001). In an effort to reconcile the different prevalences of combat-related PTSD in Vietnam veterans reported in the NVVRS and the VES, Thompson et al. (2006) noted that the discrepancies could be minimized if the same definition of PTSD were applied to both studies. Rates determined with particularly broad and sensitive criteria were about 5 times those determined with more restrictive criteria. The authors concluded that consistent methods of diagnosis are needed to compare rates of PTSD in different studies of veteran populations. O’Toole et al. (1996) found the prevalence of lifetime PTSD to be 21% in Australian Vietnam veterans (diagnosed with the SCID) and 12% for current PTSD, 20-25 years after the war. World War II and Korean War Veterans of World War II and the Korean War who are participating in the Normative Aging Study, a long-term study established by the VA in Boston that has screened and tracked
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Gulf War and Health, Volume 6: Physiologic, Psychologic, and Psychosocial Effects of Deployment-Related Stress over 6000 men for a variety of health conditions since its inception in 1961, were screened for PTSD in 1990 (Spiro et al. 1994). The Mississippi Scale for Combat-Related PTSD was used to assess 809 World War II veterans (54% of whom experienced combat) and 401 Korean War veterans (19% of whom experienced combat); the Combat Exposure Scale and two additional questions on length of time in combat and exposure to combat outcomes were used to assess combat-exposure severity. The estimated prevalence of PTSD was 0.74% in World War II veterans (whether combat-exposed or not) and 0.25% in Korean War veterans (whether combat-exposed or not). On the basis of combat exposure of the World War II veterans, the estimated prevalence of PTSD increased from 0.94% in those with light to moderate exposure to 3.45% in those with moderate to heavy exposure. None of the 76 combat-exposed Korean War veterans screened positively for PTSD, although 0.31% of the Korean War veterans who were not exposed to combat did. Kang et al. (2006) compared the health status of 19,442 U.S. World War II prisoners of war with a randomly selected control group of 9728 veterans who had served in the military during World War II but had not been prisoners of war. On the basis of computerized VA inpatient medical records for 1990-2000 and outpatient medical records for 1997-2000 or computerized medical records from the Health Care Financing Administration, they found that 113 of the control group (1.16%) had a diagnosis of PTSD. PTSD had been diagnosed in 3254 (16.7%) of the POWs, 71% of whom had been interned in Europe. The study did not indicate whether the control group had been engaged in combat or where they had served during the war. Table 5-2 summarizes the prevalence or risk of PTSD in numerous studies of U.S. military personnel. Some of the difference in rates might be attributed to the definition of PTSD being used (DSM-III-R or DSM-IV-TR) and the instruments used to screen for or diagnose it. COURSE DSM-IV recognizes that the onset of PTSD may be acute, beginning within 6 months of exposure to the traumatic event, or delayed, beginning more than 6 months after the traumatic event. Symptoms typically begin shortly after exposure—even on the first day (North et al. 1999). The lag time between exposure and development of enough symptoms to meet the diagnostic criteria is variable and may be years (Bremner et al. 1996; Bryant and Harvey 2002; Carty et al. 2006; Gray et al. 2004; Green et al. 1990a; Op den Velde et al. 1996; Port et al. 2001; Ruzich et al. 2005). It is considered to be chronic by DSM-IV-TR criteria if symptoms persist for 3 months or longer. PTSD can be chronic with no remission, or it can be recurrent with periods of remission and recurrence (Friedman 2003). Of the veterans with PTSD in the NVVRS, Schnurr et al. (2003) found that PTSD resulted from traumatic experiences before their Vietnam deployment in 8%; for those with PTSD related to Vietnam, it began in 31% in the same year that they went to Vietnam; it began in 31% in the following year, it began in 32% within 2-5 years of entry into Vietnam, and it began in 6% even later. More than 40% of the veterans had symptoms that had persisted for more than 2 decades. Symptoms began earlier in men than in women. Among men, members of ethnic minority groups were slower to develop symptoms.
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Gulf War and Health, Volume 6: Physiologic, Psychologic, and Psychosocial Effects of Deployment-Related Stress TABLE 5-2 Estimated Prevalence of PTSD in U.S. Military Populations Population PTSD Prevalence How Measured When Assessed Reference OEF combat troops Current: predeployment 5%; 6% postdeployment (n = 1962) PTSD Checklist Army: 3-4 months after return from combat duty Hoge et al. 2004 OIF combat troops Current: 5% predeployment; 12-13% postdeployment Iraq (n = 1709) PTSD Checklist Army: 1 week before deployment and 3-4 months after return from combat duty Marines: 3-4 months after return from combat duty Hoge et al. 2004 Current: 14-17% (n = 1767) PTSD Checklist 9 months into deployment MHAT 2006 Gulf War veterans Current: 3.4% (n = 967) CIDI February 2000-October 2001 Fiedler et al. 2006 Current: Ft. Devens 5%, 8% (n = 148) New Orleans 7%, 8% (n = 58) (according to CAPS and Mississippi Scale, respectively) CAPS for 75% of subjects Ft. Devens cohort: initial survey within 5 days of return (spring 1991) and winter 1992/spring 1993 Proctor et al. 1998 Mississippi Scale for Desert Storm War Personnel for 99% of subjects New Orleans cohort: initial survey within 9 months of return in 1991 and summer 1994/fall 1995 Current: 12% (n = 11441) PTSD Checklist November 1995-1997 Kang et al. 2003 Lifetime: 6.2% (n = 1061) CAPS 10 years after war Toomey et al. 2007 Current: 8-9.2% (n = 1524) 17-item questionnaire based on DSM-III-R criteria Impact of Event Scale Brief Symptom Inventory 1.5-2 years after war Stretch et al. 1996 Vietnam veterans Current: 15% men (n = 1200), 8.5% women (n = 432) Lifetime: 30.6% men, 26.9% women Mississippi Scale for Combat-Related PTSD DIS MMPI PTSD Scale SCID 15 or more years after service Kulka et al. 1990 Current: 9.1% Lifetime: 18.7% (n = 1200) Military records Historical accounts Diagnostic histories of PTSD MMPI SCID 1988 for NVVRS Dohrenwend et al. 2006 Current: 2.2% Lifetime: 14.7% post deployment (n = 2490) DIS MMPI 11-12 years after Vietnam War; 15-20 years after Army service CDC 1988
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Gulf War and Health, Volume 6: Physiologic, Psychologic, and Psychosocial Effects of Deployment-Related Stress Population PTSD Prevalence How Measured When Assessed Reference Korean War veterans Current: 0.25% (n = 401) Mississippi Scale for Combat-Related PTSD Combat Exposure Scale Normative Aging Study cohort; questionnaires sent in 1990 Spiro et al. 1994 World War II veterans Current: 0.74% (n = 809) Mississippi Scale for Combat-Related PTSD Combat Exposure Scale Normative Aging Study cohort; questionnaires sent in 1990 Spiro et al. 1994 NOTE: CAPS = Clinician-Administered PTSD Scale, CIDI = Composite International Diagnostic Interview, DIS = Diagnostic Interview Schedule, MMPI = Minnesota Multiphasic Personality Inventory, OEF = Operation Enduring Freedom, OIF = Operation Iraqi Freedom, SCID = Structured Clinical Interview for DSM-IV. In a small study, Bremner et al. (1996) found that of 61 Vietnam veterans with combat-related PTSD, 0 (15%) developed PTSD during their combat tour and 38 (62%) met the criteria for PTSD within 2 years of the end of their combat tour, and 8 patients (13%) did not meet the full criteria for PTSD until 10 or more years after their tours ended. The first symptoms reported were typically in the hyperarousal cluster. Symptoms typically increased during the first few years and then leveled off. Increasing PTSD symptoms and symptom severity were observed Wolfe et al. (1999) in a larger cohort of 2119 male and 194 female Gulf War veterans screened for PTSD. Five days after their return from the gulf, 3% of the veterans (8% of women and 3% of men) exceeded the PTSD screening cutoff; at 18-24 months, the percentage of veterans exceeding the cutoff had more than doubled to 8% (16% of women and 7% of men). Similar results were seen in 84 National Guard troops (medical and military police units) returning from the Gulf War (Southwick et al. 1993b, 1995). Most of the PTSD symptoms reported at 2 years after deployment were present by 6 months, but symptom severity continued to increase. The hyperarousal symptom cluster was more prevalent than the intrusive-memories cluster, which was more prevalent than the avoidance-numbing cluster. PTSD symptom severity did not differ between the units or between the sexes. Those who were highly symptomatic at 6 months continued to be symptomatic at 2 years. In many cases, PTSD will remit naturally (McFarlane 1997). Most (60%) PTSD remissions in the general population occur within 1 year. More than one-third of cases do not remit, however, regardless of whether the person receives treatment (Connor and Butterfield 2003; Kessler et al. 1995). In the NCS, the median time to remission among people who ever sought professional treatment was 36 months, but it was 64 months for those who did not (Kessler et al. 1995). Factors associated with PTSD chronicity in the general population are a greater number of symptoms (especially numbing and arousal symptoms), comorbid alcohol abuse or other psychiatric or medical illness, being female, having a family history of antisocial behavior, and having a history of childhood trauma (Breslau 2001b). Marshall et al. (2006) found that NVVRS veterans with chronic war-related PTSD had more numbing symptoms and, to a lesser extent, more hyperarousal symptoms than veterans with PTSD in remission; re-experiencing symptoms did not appear to be related to PTSD chronicity.
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Gulf War and Health, Volume 6: Physiologic, Psychologic, and Psychosocial Effects of Deployment-Related Stress The above studies indicate that the development and course of PTSD are variable. Some people may have no or few symptoms of PTSD initially but develop more symptoms over time and others may rapidly develop symptoms that meet the full diagnostic criteria for PTSD. Some recover or experience a reduction in symptoms, others suffer longstanding PTSD symptoms (Friedman et al. 1994; Kulka et al. 1990; Schnurr et al. 2003), and still others will follow an episodic course. Even those who appear to have recovered entirely from PTSD may experience a recurrence of symptoms years later, especially if exposed to additional trauma or other important life events, such as the death of a spouse (Friedman et al. 1994). COMORBIDITY AND DISABILITY People with PTSD tend to report poor health and impaired function in many life activities. Several studies indicate that veterans with PTSD report more symptoms of adverse health and disability than do veterans without PTSD (see Chapter 6 for more information on symptom reporting). On examination, many people with PTSD are found to have other psychiatric disorders that increase the complexity of diagnosing PTSD. The presence of those additional psychiatric disorders may also play a role in the adverse health effects seen with PTSD. In Chapter 6, studies are assessed for the strength of the association between deployment to a war zone and PTSD; those studies are found in the section on psychiatric disorders. The body of evidence that addresses specific health effects that may occur in veterans with PTSD is also reviewed in Chapter 6 for each relevant health effect. The psychosocial effects seen in veterans with PTSD, including effects on family and employment, are considered in Chapter 7. Comorbidity In veteran and general population samples, PTSD frequently co-occurs with other psychiatric or substance-use disorders. In the NVVRS, male and female theater veterans with PTSD were 10-15 times more likely to have depression and dysthymia and 20 times more likely to have an anxiety disorder than their counterparts without PTSD (Kulka et al. 1990). Zatzick et al. (1997a) found that the risk of having PTSD was significantly greater in male NVVRS veterans with major depression (OR 17.6, 95% CI 6.5-47.4), alcohol abuse or dependence (OR 3.2, 95% CI 1.9-5.4), drug abuse or dependence (OR 7.4, 95% CI 2.2-24.5), or panic disorder (OR 22.6, 95% CI 3.1-163.5) that in those with the disorders. Among female veterans, PTSD was seen in 51% of those with major depression, 40.7% of those with alcohol abuse or dependence, and 70.1% of those with panic disorder (Zatzick et al. 1997b). High rates of comorbidity are also seen in the general population. In the NCS, 88.3% of men and 79.0% of women with PTSD had a life history of mood, anxiety, or substance-use disorders (Kessler et al. 1995). The temporal relationship between PTSD and other psychiatric and substance-use disorders is complex. Psychiatric comorbidity increases the likelihood of PTSD, as found in the NCS. However, PTSD also increases the likelihood of developing the other disorders (Schnurr et al. 2000a, 2002; Shalev et al. 1998). Trauma can also lead to the simultaneous development of PTSD and other psychiatric disorders, such as major depression (Shalev et al. 1998). For example, in a study of 262 World War II and Korean War prisoners of war (Engdahl et al. 1998), half of whom developed war-related PTSD, 66% of those with PTSD but only 34% of those without PTSD had another anxiety, mood, or substance-use disorder. The
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Gulf War and Health, Volume 6: Physiologic, Psychologic, and Psychosocial Effects of Deployment-Related Stress majority of the other disorders began in the same year as PTSD. Although the high rate of psychiatric and substance-use comorbidity can be partly explained by symptom overlap in DSM-IV, it does not diminish the diagnostic integrity of PTSD; rather, it suggests the importance of complete clinical evaluations to elucidate the full clinical picture of each patient. Disability PTSD can result in profound and long-term impairment of functioning and quality of life. This section considers the functional outcomes and disability that may occur in veterans with PTSD. Psychosocial effects and the impact of PTSD on family, friends, and others are discussed in Chapter 7. DSM-IV requires that a diagnosis of PTSD include “clinically significant distress and/or impairment in social, occupational, and/or other important areas of functioning” (APA 2000). Therefore, it is important to understand the distress and disability that may be associated with it. Zatzick et al. evaluated 1190 male and 432 female Vietnam veterans by using data from the NVVRS (1997a,b). Of the men, 242 (15.3%) were diagnosed with PTSD and more than 90% of those men reported having one or more of 30 chronic nonpsychiatric medical conditions within the preceding 12 months. Of the veterans with no nonpsychiatric medical disorders, less than 10% had PTSD, whereas of the 141 veterans reporting four or more medical disorders, 31.9% had PTSD. Among the women, 8.9% had PTSD diagnosed, of whom 70% reported having one or more of 37 chronic medical conditions within the preceding 12 months. PTSD was present in only 4.2% of the female veterans with no chronic medical conditions but in 19.1% of those reporting four or more medical conditions. Veterans with PTSD reported significantly (p < 0.05) more functional impairment than veterans without PTSD, including inability to work, fair or poor health, diminished well-being, current limitation in physical functioning, and more days in bed in the preceding 3 months. Dohrenwend et al. (2006) also reanalyzed the NVVRS data, including the Global Assessment of Functioning (GAF) scale that is traditionally used by VA to assess a veteran’s functional impairment. Of the sample of 260 veterans who had no diagnosis of PTSD or a diagnosis of past PTSD, 47% and 44%, respectively, were rated as having good functioning, although none of the veterans who had a diagnosis of current PTSD had good functioning in all GAF areas. Of those with current PTSD, 15% had only slight impairment, 41% had some difficulty, and 37% had moderate or serious impairment. The GAF scores were related to the severity of the PTSD. A study of 70 UK active-duty military personnel referred to a PTSD clinic found that a diagnosis of PTSD, major depression, or alcohol dependence did not predict disability in work, relationships, or social activities, although symptoms of depression accounted for much of any total functional impairment, particularly in family life (Neal et al. 2004). Bleich and Solomon (2004) found that in Israeli veterans, PTSD symptoms resulted in more impairment in occupational functioning than in interpersonal functioning or activities of daily living. World War II veterans 70-74 years old, who had PTSD as a result of their participation in secret military tests of mustard gas during the war were assessed for health-related disability (Schnurr et al. 2000b). As of 1996, compared with similarly exposed veterans without PTSD, veterans with PTSD had decreased functioning and increased impairment on all measures: physical function, social function, physical role impairment, emotional role impairment, lifetime disability, and current unemployment.
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Gulf War and Health, Volume 6: Physiologic, Psychologic, and Psychosocial Effects of Deployment-Related Stress Fontana A, Rosenheck R. 1994b. Traumatic war stressors and psychiatric symptoms among World War II, Korean, and Vietnam War veterans. Psychology and Aging 9(1):27-33. Fontana A, Rosenheck R, Horvath T. 1997. Social support and psychopathology in the war zone. Journal of Nervous and Mental Disease 185(11):675-681. Fontana A, Litz B, Rosenheck R. 2000. Impact of combat and sexual harassment on the severity of posttraumatic stress disorder among men and women peacekeepers in Somalia. Journal of Nervous and Mental Disease 188(3):163-169. Friedman M. 2003. Post Traumatic Stress Disorder. Kansas City, MO: Compact Clinicals. Friedman MJ. 2002. Future pharmacotheraphy for post-traumatic stress disorder: Prevention and treatment. Psychiatry Clinics of North America 25:427-441. Friedman MJ, Schnurr PP, McDonagh-Coyle A. 1994. Post-traumatic stress disorder in the military veteran. Psychiatry Clinics of North America 17(2):265-277. Friedman MJ, Schnurr PP, Sengupta A, Holmes T, Ashcraft M. 2004. The Hawaii Vietnam Veterans Project: Is minority status a risk factor for posttraumatic stress disorder? Journal of Nervous and Mental Disease 192(1):42-50. Gibbs MS. 1989. Factors in the victim that mediate between disaster and psychopathology: A review. Journal of Traumatic Stress 2(4):489-514. Gilbertson MW, Shenton ME, Ciszewski A, Kasai K, Lasko NB, Orr SP, Pitman RK. 2002. Smaller hippocampal volume predicts pathologic vulnerability to psychological trauma. Nature Neuroscience 5(11):1242-1247. Gill JM, Szanton SL, Page GG. 2005. Biological underpinnings of health alterations in women with PTSD: A sex disparity. Biological Research for Nursing 7(1):44-54. Gold SD, Marx BP, Soler-Baillo JM, Sloan DM. 2005. Is life stress more traumatic than traumatic stress? Journal of Anxiety Disorders 19(6):687-698. Goldberg J, True WR, Eisen SA, Henderson WG. 1990. A twin study of the effects of the Vietnam War on posttraumatic stress disorder. Journal of the American Medical Association 263(9):1227-1232. Goldzweig CL, Balekian TM, Rolon C, Yano EM, Shekelle PG. 2006. The state of women veterans’ health research: Results of a systematic literature review. Journal of General Internal Medicine 21(Suppl 3):S82-S92. Goss Gilroy Inc. 1998. Health Study of Canadian Forces Personnel Involved in the 1991 Conflict in the Persian Gulf. Ottawa, Canada: Goss Gilroy Inc. Department of National Defence. Gray MJ, Bolton EE, Litz BT. 2004. A longitudinal analysis of PTSD symptom course: Delayed-onset PTSD in Somalia peacekeepers. Journal of Consulting and Clinical Psychology 72(5):909-913. Green BL, Grace MC, Lindy JD, Gleser GC. 1990a. War stressors and symptom persistence in posttraumatic stress disorder. Journal of Anxiety Disorders 4(1):31-39. Green BL, Grace MC, Lindy JD, Gleser GC, Leonard A. 1990b. Risk factors for PTSD and other diagnoses in a general sample of Vietnam veterans. American Journal of Psychiatry 147(6):729-733.
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Gulf War and Health, Volume 6: Physiologic, Psychologic, and Psychosocial Effects of Deployment-Related Stress Grieger TA, Cozza SJ, Ursano RJ, Hoge C, Martinez PE, Engel CC, Wain HJ. 2006. Posttraumatic stress disorder and depression in battle-injured soldiers. American Journal of Psychiatry 163(10):1777-1783. Grillon C, Baas J. 2003. A review of the modulation of the startle reflex by affective states and its application in psychiatry. Clinical Neurophysiology 114:1557-1579. Grinker RR, Spiegel JP. 1945. Men Under Stress. Philadelphia, PA: Blakiston. Grob GN. 1994. The Mad Among Us: A History of the Care of America’s Mentally Ill. New York: Free Press. Habib KE, Weld KP, Rice KC, Pushkas J, Champoux M, Listwak S, Webster EL, Atkinson AJ, Schulkin J, Contoreggi C, Chrousos GP, McCann SM, Suomi SJ, Higley JD, Gold PW. 2000. Oral administration of a corticotropin-releasing hormone receptor antagonist significantly attenuates behavioral, neuroendocrine, and autonomic responses to stress in primates. Proceedings of the National Academy of Sciences of the United States of America 97(11):6079-6084. Herman J. 1992. Trauma and Recovery. New York: Basic Books. Hitchcock JM, Davis M. 1986. Lesions of the amygdala, but not of the cerebellum or red nucleus, block conditioned fear as measured with the potentiated startle paradigm. Behavioral Neuroscience 100:11-22. Hitchcock JM, Sananes CB, Davis M. 1989. Sensitization of the startle reflex by footshock: Blockade by lesions of the central nucleus of the amygdala or its efferent pathway to the brainstem. Behavioral Neuroscience 103:509-518. Hoge CW, Lesikar SE, Guevara R, Lange J, Brundage JF, Engel CC Jr., Messer SC, Orman DT. 2002. Mental disorders among U.S. military personnel in the 1990s: Association with high levels of health care utilization and early military attrition. American Journal of Psychiatry 159(9):1576-1583. Hoge CW, Castro CA, Messer SC, McGurk D, Cotting DI, Koffman RL. 2004. Combat duty in Iraq and Afghanistan, mental health problems, and barriers to care. New England Journal of Medicine 351(1):13-22. Hoge CW, Terhakopian A, Castro CA, Messer SC, Engel CC. 2007. Association of posttraumatic stress disorder with somatic symptoms, health care visits, and absenteeism among Iraq War veterans. American Journal of Psychiatry 164(1):150-153. Horrigan JP. 1996. Guanfacine for PTSD nightmares. Journal of the American Academy of Child Adolescent Psychiatry 35(8):975-976. Hyams KC, Wignall FS, Roswell R. 1996. War syndromes and their evaluation: From the U.S. Civil War to the Persian Gulf War. Annals of Internal Medicine 125(5):398-405. Ikin JF, Sim MR, Creamer MC, Forbes AB, McKenzie DP, Kelsall HL, Glass DC, McFarlane AC, Abramson MJ, Ittak P, Dwyer T, Blizzard L, Delaney KR, Horsley KW, Harrex WK, Schwarz H. 2004. War-related psychological stressors and risk of psychological disorders in Australian veterans of the 1991 Gulf War. British Journal of Psychiatry 185:116-126. Jennings PA, Aldwin CM, Levenson MR, Spiro A 3rd, Mroczek DK. 2006. Combat exposure, perceived benefits of military service, and wisdom in later life: Findings from the Normative Aging Study. Research on Aging 28(1):115-134.
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Gulf War and Health, Volume 6: Physiologic, Psychologic, and Psychosocial Effects of Deployment-Related Stress Jones E. 2006. Historical approaches to post-combat disorders. Philosophical Transactions of the Royal Society of London—Series B: Biological Sciences 361(1468):533-542. Kang H, Dalager N, Mahan C, Ishii E. 2005. The role of sexual assault on the risk of PTSD among Gulf War veterans. Annals of Epidemiology 15(3):191-195. Kang HK, Natelson BH, Mahan CM, Lee KY, Murphy FM. 2003. Post-traumatic stress disorder and chronic fatigue syndrome-like illness among Gulf War veterans: A population-based survey of 30,000 veterans. American Journal of Epidemiology 157(2):141-148. Kang HK, Bullman TA, Taylor JW. 2006. Risk of selected cardiovascular diseases and posttraumatic stress disorder among former World War II prisoners of war. Annals of Epidemiology 16(5):381-386. Kardiner A, Spiegel H. 1947. War Stress and Neurotic Illness. New York: Paul B. Hoeber. Keane TM. 1998. Psychological effects of military combat. In: Dohrenwend BP, editor. Adversity, Stress, and Psychopathology. Oxford, UK: Oxford University Press. Pp. 52-65. Kessler RC, Sonnega A, Bromet E, Hughes M, Nelson CB. 1995. Posttraumatic stress disorder in the National Comorbidity Survey. Archives of General Psychiatry 52(12):1048-1060. Kessler RC, Berglund P, Demler O, Jin R, Merikangas KR, Walters EE. 2005a. Lifetime prevalence and age-of-onset distributions of DSM-IV disorders in the National Comorbidity Survey Replication. Archives of General Psychiatry 62(6):593-602. Kessler RC, Chiu WT, Demler O, Merikangas KR, Walters EE. 2005b. Prevalence, severity, and comorbidity of 12-month DSM-IV disorders in the National Comorbidity Survey Replication. Archives of General Psychiatry 62(6):617-627. King DW, King LA, Foy DW, Keane TM, Fairbank JA. 1999. Posttraumatic stress disorder in a national sample of female and male Vietnam veterans: Risk factors, war-zone stressors, and resilience-recovery variables. Journal of Abnormal Psychology 108(1):164-170. Kinzie JD, Leung P. 1989. Clonidine in Cambodian patients with posttraumatic stress disorder. Journal of Nervous and Mental Disease 177(9):546-550. Koenen KC, Stellman JM, Stellman SD, Sommer JF Jr. 2003. Risk factors for course of posttraumatic stress disorder among Vietnam veterans: A 14-year follow-up of American Legionnaires. Journal of Consulting and Clinical Psychology 71(6):980-986. Kolb LC. 1987. A neuropsychological hypothesis explaining posttraumatic stress disorders. American Journal of Psychiatry 144(8):989-995. Koren D, Norman D, Cohen A, Berman J, Klein EM. 2005. Increased PTSD risk with combat-related injury: A matched comparison study of injured and uninjured soldiers experiencing the same combat events. American Journal of Psychiatry 162(2):276-282. Kosten TR, Mason JW, Giller EL, Ostroff RB, Harkness L. 1987. Sustained urinary norepinephrine and epinephrine elevation in post-traumatic stress disorder. Psychoneuroendocrinology 12(1):13-20. Kulka RA, Schlenger WE, Fairbank JA, Hough RL, Jordan BK, Marmar CR, Weiss DS. 1990. Trauma and the Vietnam War Generation: Report of Findings from the National Vietnam Veterans Readjustment Study. New York: Brunner/Mazel Publishers.
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Gulf War and Health, Volume 6: Physiologic, Psychologic, and Psychosocial Effects of Deployment-Related Stress Lapp KG, Bosworth HB, Strauss JL, Stechuchak KM, Horner RD, Calhoun PS, Meador KG, Lipper S, Butterfield MI. 2005. Lifetime sexual and physical victimization among male veterans with combat-related post-traumatic stress disorder. Military Medicine 170(9):787-790. LeDoux J. 1996. Emotional networks and motor control: A fearful view. Progress in Brain Research 107:437-446. Lee KA, Vaillant GE, Torrey WC, Elder GH. 1995. A 50-year prospective study of the psychological sequelae of World War II combat. American Journal of Psychiatry 152(4):516-522. Marsella AJ, Friedman MJ, Spain EH. 1993. Ethnocultural aspects of posttraumatic stress disorder. In: Oldham JM, Riba MB, Tasman A, editors. Review of Psychiatry. Washington, DC: American Psychiatric Press. Marshall RD, Turner JB, Lewis-Fernandez R, Koenan K, Neria Y, Dohrenwend BP. 2006. Symptom patterns associated with chronic PTSD in male veterans: New findings from the National Vietnam Veterans Readjustment Study. Journal of Nervous and Mental Disease 194(4):275-278. Mason JW, Giller EL, Kosten TR, Ostroff RB, Podd L. 1986. Urinary free-cortisol levels in posttraumatic stress disorder patients. Journal of Nervous and Mental Disease 174(3):145-149. McFall ME, Murburg MM, Ko GN, Veith RC. 1990. Autonomic responses to stress in Vietnam combat veterans with posttraumatic stress disorder. Biological Psychiatry 27(10):1165-1175. McFarlane AC. 1997. The prevalence and longitudinal course of PTSD. Implications for the neurobiological models of PTSD. Annals of the New York Academy of Sciences 821:10-23. Mellman TA, Kumar A, Kulick-Bell R, Kumar M, Nolan B. 1995a. Nocturnal/daytime urine noradrenergic measures and sleep in combat-related PTSD. Biological Psychiatry 38:174-179. Mellman TA, Kulick-Bell R, Ashlock L, Nolan B. 1995b. Sleep events among veterans with combat-related posttraumatic stress disorder. American Journal of Psychiatry 152:110-115. Mellman TA, Bustamante V, Fins AL, Pigeon WR, Nolan B. 2002. REM sleep and the early development of posttraumatic stress disorder. American Journal of Psychiatry 159:1696-1701. Metzger LJ, Orr SP, Berry NJ, Ahern CE, Lasko NB, Pitman RK. 1999. Physiologic reactivity to startling tones in women with posttraumatic stress disorder. Journal of Abnormal Psychology 108:347-352. MHAT (Mental Health Advisory Team). 2006. Mental Health Advisory Team (MHAT) IV Operation Iraqi Freedom 05-07: Final Report. [Washington, DC]: Office of the Surgeon Multinational Force-Iraq and Office of the Surgeon General United States Army Medical Command. [Online]. Available: http://www.armymedicine.army.mil/news/mhat/mhat_iv/MHAT_IV_Report_17NOV06.pdf. Murburg MM, McFall ME, Ko GN, Veith RC. 1994. Stress-induced alterations in plasma catecholamines and sympathetic nervous system funuction in PTSD. In: Murburg MM, editor. Catecholamine Function in Post-Traumatic Stress Disorder: Emerging Concepts. 1st Ed. Washington, DC: American Psychiatric Press. Pp. 189-202.
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Gulf War and Health, Volume 6: Physiologic, Psychologic, and Psychosocial Effects of Deployment-Related Stress Murdoch M, Polusny MA, Hodges J, Cowper D. 2006. The association between in-service sexual harassment and post-traumatic stress disorder among Department of Veterans Affairs disability applicants. Military Medicine 171(2):166-173. Myers KM, Davis M. 2007. Mechanisms of fear extinction. Molecular Psychiatry 12(2):120-150. Neal LA, Green G, Turner MA. 2004. Post-traumatic stress and disability. British Journal of Psychiatry 184:247-250. Neeleman J, Ormel J, Bijl RV. 2001. The distribution of psychiatric and somatic ill health: Associations with personality and socioeconomic status. Psychosomatic Medicine 63(2):239-247. North CS. 1995. Human response to violent trauma. Balliere’s Clinical Psychiatry 1:225-245. North CS, Smith EM, Spitznagel EL. 1994. Posttraumatic stress disorder in survivors of a mass shooting. American Journal of Psychiatry 151(1):82-88. North CS, Nixon SJ, Shariat S, Mallonee S, McMillen C, Spitznagel EL, Smith EM. 1999. Psychiatric disorders among survivors of the Oklahoma City bombing. Journal of the American Medical Association 282(8):755-762. North CS, Spitznagel EL, Smith EM. 2001. A prospective study of coping after exposure to a mass murder episode. Annals of Clinical Psychiatry 13(2):81-87. Op den Velde W, Hovens JE, Aarts PG, Frey-Wouters E, Falger PR, Van Duijn H, De Groen JH. 1996. Prevalence and course of posttraumatic stress disorder in Dutch veterans of the civilian resistance during World War II: An overview. Psychological Reports 78(2):519-529. Orr SP, Claiborn JM, Altman B, Forgue DF, de Jong JB, Pitman RK, Herz LR. 1990. Psychometric profile of posttraumatic stress disorder, anxious, and healthy Vietnam veterans: Correlations with psychophysiologic responses. Journal of Consulting Clinical Psychology 58(3):329-335. O’Toole BI, Marshall RP, Grayson DA, Schureck RJ, Dobson M, French M, Pulvertaft B, Meldrum L, Bolton J, Vennard J. 1996. The Australian Vietnam Veterans Health Study: III. Psychological health of Australian Vietnam veterans and its relationship to combat. International Journal of Epidemiology 25(2):331-340. Ozer EJ, Best SR, Lipsey TL, Weiss DS. 2003. Predictors of posttraumatic stress disorder and symptoms in adults: A meta-analysis. Psychological Bulletin 129(1):52-73. Perry BD. 1994. Neurobiological squeal of childhood trauma: Post-traumatic stress disorder in children. In: Murburg M, editor. Catecholamine Function in Post Traumatic Stress Disorder: Emerging Concepts. Washington, DC: American Psychiatric Press. Pp. 253-276. Perry BD, Giller EL Jr., Southwick SM. 1987. Altered platelet alpha 2-adrenergic binding sites in posttraumatic stress disorder. American Journal of Psychiatry 144(11):1511-1512. Pitman RK, Orr SP. 1990. Twenty-four hour urinary cortisol and catecholamine excretion in combat-related posttraumatic stress disorder. Biological Psychiatry 27(2):245-247. Pitman RK, Altman B, Macklin ML. 1989. Prevalence of posttraumatic stress disorder in wounded Vietnam veterans. American Journal of Psychiatry 46(5):667-669. Pitman RK, Sanders KM, Zusman RM, Healy AR, Cheema F, Lasko NB, Cahill L, Orr SP. 2002. Pilot study of secondary prevention of posttraumatic stress disorder with propranolol. Biological Psychiatry 51(2):189-192.
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Gulf War and Health, Volume 6: Physiologic, Psychologic, and Psychosocial Effects of Deployment-Related Stress Port CL, Engdahl B, Frazier P. 2001. A longitudinal and retrospective study of PTSD among older prisoners of war. American Journal of Psychiatry 158(9):1474-1479. Prigerson HG, Maciejewski PK, Rosenheck RA. 2001. Combat trauma: Trauma with highest risk of delayed onset and unresolved posttraumatic stress disorder symptoms, unemployment, and abuse among men. Journal of Nervous and Mental Disease 189(2):99-108. Prigerson HG, Maciejewski PK, Rosenheck RA. 2002. Population attributable fractions of psychiatric disorders and behavioral outcomes associated with combat exposure among U.S. men. American Journal of Public Health 92(1):59-63. Prins A, Kaloupek DG, Keane TM. 1995. Psychophysiological evidence for autonomic arousal and startle in traumatized adult populations. In: Friedman MJ, Charney DS, Deutch AY, editors. Neurobiological and Clinical Consequences of Stress: From Normal Adaptation to PTSD. Philadelphia, PA: Lippincott-Raven. Pp. 291-314. Proctor SP, Heeren T, White RF, Wolfe J, Borgos MS, Davis JD, Pepper L, Clapp R, Sutker PB, Vasterling JJ, Ozonoff D. 1998. Health status of Persian Gulf War veterans: Self-reported symptoms, environmental exposures and the effect of stress. International Journal of Epidemiology 27(6):1000-1010. Raskind MA, Thompson C, Petrie EC, Dobie DJ, Rein RJ, Hoff DJ, McFall ME, Peskind ER. 2002. Prazosin reduces nightmares in combat veterans with posttraumatic stress disorder. Journal of Clinical Psychiatry 63(7):565-568. Raskind MA, Peskind ER, Kanter ED, Petrie EC, Radant A, Thompson CE, Dobie DJ, Hoff D, Rein RJ, Straits-Troster K, Thomas RJ, McFall MM. 2003. Reduction of nightmares and other PTSD symptoms in combat veterans by prazosin: A placebo-controlled study. American Journal of Psychiatry 160:371-373. Raskind MA, Peskind ER, Hof DJ, Hart KL, Homes HA, Warren D, Schofer J, O’Connell J, Taylor F, Gross C, Rohde K, McFall ME. 2007. A parallel group placebo controlled study of prazosin for trauma nightmares and sleep disturbances in combat veterans with posttraumatic stress disorder. Biological Psychiatry 61:928-934. Regehr C, Hemsworth D, Hill J. 2001. Individual predictors of posttraumatic distress: A structural equation model. Canadian Journal of Psychiatry 46(2):156-161. Resnick HS, Yehuda R, Acierno R. 1997. Acute post-rape plasma cortisol, alcohol use, and PTSD symptom profile among recent rape victims. Annals of the New York Academy of Sciences 821:433-436. Ross RJ, Ball WA, Sullivan KA, Caroff SN. 1989. Sleep disturbance as the hallmark of posttraumatic stress disorder. American Journal of Psychiatry 146:697-707. Ross RJ, Ball WA, Dinges DF, Kribbs NB, Morrison AR, Silver SM, Mulvaney FD. 1994. Motor dysfunction during sleep in posttraumatic stress disorder. Sleep 17:723-732. Rothbaum B, Foa E, Riggs D, Murdock T, Walsh W. 1992. A prospective examination of posttraumatic stress disorder in rape. Journal of Traumatic Stress 5:455-475. Roy-Byrne P, Arguelles L, Vitek ME, Goldberg J, Keane TM, True WR, Pitman RK. 2004. Persistence and change of PTSD symptomatology—a longitudinal co-twin control analysis of the Vietnam Era Twin Registry. Social Psychiatry and Psychiatric Epidemiology 39(9):681-685.
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Gulf War and Health, Volume 6: Physiologic, Psychologic, and Psychosocial Effects of Deployment-Related Stress Ruzich MJ, Looi JC, Robertson MD. 2005. Delayed onset of posttraumatic stress disorder among male combat veterans: A case series. American Journal of Geriatric Psychiatry 13(5):424-427. Seal KH, Bertenthal D, Miner CR, Sen S, Marmar C. 2007. Bringing the war back home: Mental health disorders among 103,788 U.S. veterans returning from Iraq and Afghanistan seen at Department of Veterans Affairs facilities. Archives of Internal Medicine 167:476-482. Schelling G, Briegel J, Roozendaal B, Stoll C, Rothenhausler HB, Kapfhammer HP. 2001. The effect of stress doses of hydrocortisone during septic shock on posttraumatic stress disorder in survivors. Biological Psychiatry 50(12):978-985. Schelling G, Roozendaal B, Krauseneck T, Schmoelz M, DE Quervain D, Briegel J. 2006. Efficacy of hydrocortisone in preventing posttraumatic stress disorder following critical illness and major surgery. Annals of the New York Academy of Sciences 1071:46-53. Schlenger WE, Kulka RA, Fairbank JA, Hough RL. 1992. The prevalence of post-traumatic stress disorder in the Vietnam generation: A multimethod, multisource assessment of psychiatric disorder. Journal of Traumatic Stress 5(3):333-363. Schnurr PP, Spiro A, Paris AH. 2000a. Physician-diagnosed medical disorders in relation to PTSD symptoms in older male military veterans. Health Psychology 19(1):91-97. Schnurr PP, Ford JD, Friedman MJ, Green BL, Dain BJ, Sengupta A. 2000b. Predictors and outcomes of posttraumatic stress disorder in World War II veterans exposed to mustard gas. Journal of Consulting and Clinical Psychology 68(2):258-268. Schnurr PP, Friedman MJ, Bernardy NC. 2002. Research on posttraumatic stress disorder: Epidemiology, pathophysiology, and assessment. Journal of Clinical Psychology 58(8):877-889. Schnurr PP, Lunney CA, Sengupta A, Waelde LC. 2003. A descriptive analysis of PTSD chronicity in Vietnam veterans. Journal of Traumatic Stress 16(6):545-553. Schnurr PP, Lunney CA, Sengupta A. 2004. Risk factors for the development versus maintenance of posttraumatic stress disorder. Journal of Traumatic Stress 17(2):85-95. Shalev AY, Freedman S, Peri T, Brandes D, Sahar T, Orr SP, Pitman RK. 1998. Prospective study of posttraumatic stress disorder and depression following trauma. American Journal of Psychiatry 155(5):630-637. Shephard B. 2001. A War of Nerves: Soldiers and Psychiatrists in the Twentieth Century. Cambridge, MA: Harvard University Press. Simmons R, Maconochie N, Doyle P. 2004. Self-reported ill health in male UK Gulf War veterans: A retrospective cohort study. BMC Public Health 4(1):27. Slusarcick AL, Ursano RJ, Dinneen MP, Fullerton CS. 2001. Factors associated with depression on a hospital ship deployed during the Persian Gulf War. Military Medicine 166(3):248-252. Smith MA, Davidson J, Ritchie JC, Kudler H. 1989. The corticotropin-releasing hormone test in patients with posttraumatic stress disorder. Biological Psychiatry 26(4):349-355. Solomon SD, Smith EM, Robins N, Fischbach RL. 1987. Social involvement as a mediator of disaster-induced stress. Journal of Applied Social Psychology 17(12):1092-1112. Southwick S, Friedman MJ. 2001. Neurolobiological models of posttraumatic stress disorder. In: Gerrity E, Keane TM, Tuma F, editors. The Mental Health Consequences of Torture. New York: Kluwer. Pp. 73-87.
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Gulf War and Health, Volume 6: Physiologic, Psychologic, and Psychosocial Effects of Deployment-Related Stress Yehuda R, Southwick SM, Giller EL Jr. 1992b. Exposure to atrocities and severity of chronic posttraumatic stress disorder in Vietnam combat veterans. American Journal of Psychiatry 149(3):333-336. Yehuda R, Teicher MH, Giller EL. 1995. Lack of significant cortisol and growth hormone changes in Israeli civilians during the Gulf War. American Journal of Psychiatry 152(4):652-653. Yehuda R, Halligan SL, Grossman R, Golier JA, Wong C. 2002. The cortisol and glucocorticoid receptor response to low dose dexamethasone administration in aging combat veterans and Holocaust survivors with and without posttraumatic stress disorder. Biological Psychiatry 52(5):393-403. Yehuda R, Golier JA, Yang RK, Tischler L. 2004. Enhanced sensitivity to glucocorticoids in peripheral mononuclear leukocytes in posttraumatic stress disorder. Biological Psychiatry 55(11):1110-1116. Zatzick DF, Marmar CR, Weiss DS, Browner WS, Metzler TJ, Golding JM, Stewart A, Schlenger WE, Wells KB. 1997a. Posttraumatic stress disorder and functioning and quality of life outcomes in a nationally representative sample of male Vietnam veterans. American Journal of Psychiatry 154(12):1690-1695. Zatzick DF, Weiss DS, Marmar CR, Metzler TJ, Wells K, Golding JM, Stewart A, Schlenger WE, Browner WS. 1997b. Post-traumatic stress disorder and functioning and quality of life outcomes in female Vietnam veterans. Military Medicine 162(10):661-665.
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