Blackout

BLACKOUT THE CAUSES AND SYMPTOMS OF PTSD COMPILED AND DESIGNED BY MAT T WELNACK

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OVERVIEW 2

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BLACKOUT THE CAUSES AND SYMPTOMS OF PTSD

BLACKOUT THE CAUSES AND SYMPTOMS OF PTSD COMPILED AND DESIGNED BY MAT T WELNACK

BLACKOUT: THE CAUSES AND SYMPTOMS OF PTSD Book design copyright Š2010 by Matt Welnack Published by Matt Welnack for course number GR.601, Elements of Typography, taught online by Carolina de Bartolo in Spring 2010 at Academy of Art University, San Francisco, CA. Printed at Pagdett Printing, Dallas, TX. Bound at The Key Printing and Binding, Oakland, CA. All rights reserved.

DEDICATION

This book is dedicated to my loving and supporting wife Kathleen. Thank you for your faithful encouragement and unending patience.

CONTENTS 1

OVERVIEW

2

POST-TRAUMATIC STRESS DISORDER:

3

THE ETIOLOGY OF COMBAT-RELATED

4

MORPHINE USE AFTER

5

PTSD AND DEPRESSION AFTER TRAUMA: UNDERSTANDING COMORBIDITY

76

6

APPROACHES TO TREATMENT

92

08

ACQUISITION, RECOGNITION, COURSE AND TREATMENT

POST-TRAUMATIC STRESS DISORDERS

COMBAT INJURY IN IRAQ

22

40

66

1

OVERVIEW

Post-traumatic stress disorder (PTSD) is an anxiety disorder that can occur following the experience or witnessing of a traumatic event. xyxyxyx xyxxyx xyxyx xyxyxyx xyxyx yxyxyxx yxxyyx xyx xy xyx yx yx xy xyx yx yx yx xy xy xyx yx yx xy xyx yx yx xy xyx yx yx xy A traumatic event is a life-threatening event such as military combat, natural disasters, terrorist incidents, serious accidents, or physical or sexual assault in adult or childhood. Most survivors of trauma return to normal given a little time. However, some people will have stress reactions that do not go away on their own, or may even get worse over time. These individuals may develop PTSD. People with PTSD experience three different kinds of symptoms. The first set of symptoms involves reliving the trauma in some way such as becoming upset when confronted with a traumatic reminder or thinking about the trauma when you are trying to do something else. The second set of symptoms involves either staying away from places or people that remind you of the trauma, isolating from other people, or feeling numb.

The third set of symptoms includes things such as feeling on guard, irritable, startling easily. In addition to the symptoms described above, we now know that there are clear biological changes that are associated with PTSD. It is complicated by the fact that people with PTSD often may develop additional disorders such as depression, substance abuse, problems of memory and cognition, and other problems of physical and mental health. These problems may lead to impairment of the person’s ability to function in social or family life, including occupational instability, marital problems and family problems. PTSD can be treated with with psychotherapy (“talk” therapy) and medicines such as antidepressants. Early treatment is important.

CHAP TER ONE 9

A BRIEF HISTORY OF THE PTSD DIAGNOSIS The risk of exposure to trauma has been a part of the human condition since we evolved as a species. Attacks by sabertooth tigers or twenty-first century terrorists have probably produced similar psychological sequelae in the survivors of such violence. Shakespeare’s Henry IV appears to meet many, if not all, of the diagnostic criteria for post-traumatic stress disorder (PTSD), as have other heroes and heroines throughout the world’s literature. The history of the development of the PTSD concept is described by Trimble.

In 1980, the American Psychiatric Association added PTSD to the third edition of its Diagnostic and Statistical Manual of Mental Disorders (DSM-III) nosologic classification scheme. Although controversial when first introduced, the PTSD diagnosis has filled an important gap in psychiatric theory and practice. From an historical perspective, the significant change ushered in by the PTSD concept was the stipulation that the etiological agent was outside the individual (i.e., a traumatic event) rather than an inherent individual weakness (i.e., a traumatic neurosis). The key to understanding the scientific basis and clinical expression of PTSD is the concept of “trauma.”

In its initial DSM-III formulation, a traumatic event was conceptualized as a catastrophic stressor that was outside the range of usual human experience. The framers of the original PTSD diagnosis had in mind events such as war, torture, rape, the Nazi Holocaust, the atomic bombings of Hiroshima and Nagasaki, natural disasters (such as earthquakes, hurricanes, and volcano eruptions), and human-made disasters (such as factory explosions, airplane crashes, and automobile accidents). They considered traumatic events to be clearly different from the very painful stressors that constitute the normal vicissitudes of life such as divorce, failure, rejection, serious illness, financial reverses, and the like. (By this logic, adverse psychological responses to such “ordinary stressors” would, in DSM-III terms, be characterized as Adjustment Disorders rather than PTSD.) This dichotomization between traumatic and other stressors was based on the assumption that, although most individuals have the ability to cope with ordinary stress, their adaptive capacities are likely to be overwhelmed when confronted by a traumatic stressor.

PTSD is unique among psychiatric diagnoses because of the great importance placed upon the etiological agent, the traumatic stressor. In fact, one cannot make a PTSD diagnosis unless the patient has actually met the “stressor criterion,” which means that he or she has been exposed to an historical event that is considered traumatic. Clinical experience with the PTSD diagnosis has shown, however, that there are individual differences regarding the capacity to cope with catastrophic stress. Therefore, while

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some people exposed to traumatic events do not develop PTSD, others go on to develop the full-blown syndrome. Such observations have prompted the recognition that trauma is not an external phenomenon that can be completely objectified. Like pain, the traumatic experience is filtered through cognitive and emotional processes before it can be appraised as an extreme threat. Because of individual differences in this process, different people appear to have different trauma thresholds, some more protected from and some more vulnerable to developing clinical symptoms after exposure to extremely stressful situations. Although there is currently a renewed interest in subjective aspects of traumatic exposure, it must be emphasized that events such as rape, torture, genocide, and severe war zone stress are experienced as traumatic events by nearly everyone.

The DSM-III diagnostic criteria for PTSD were revised in DSM-III-R (1987), DSM-IV (1994), and DSM-IV-TR (2000). A very similar syndrome is classified in ICD-10 (The ICD-10 Classification of Mental and Behavioural Disorders: Clinical Descriptions and Diagnostic Guidelines). Diagnostic criteria for PTSD include a history of exposure to a traumatic event and symptoms from each of three symptom clusters: intrusive recollections, avoidant/ numbing symptoms, and hyper-arousal symptoms. A fifth criterion concerns duration of symptoms. One important finding, which was not apparent when PTSD was first proposed as a diagnosis in 1980, is that it is relatively common. Recent data from the national comorbidity survey indicates PTSD prevalence rates are 5% and 10% respectively among American men and women. Rates of PTSD are much higher in postconflict settings such as Algeria (37%), Cambodia (28%), Ethiopia (16%), and Gaza (18%).

CRITERIA FOR A PTSD DIAGNOSIS As noted above, the “A” stressor criterion specifies that a person has been exposed to a catastrophic event involving actual or threatened death or injury, or a threat to the physical integrity of him/herself or others. During this traumatic exposure, the survivor’s subjective response was marked by intense fear, helplessness, or horror.

The “B”, or intrusive recollection, criterion includes symptoms that are perhaps the most distinctive and readily identifiable symptoms of PTSD. For individuals with PTSD, the traumatic event remains, sometimes for decades or a lifetime, a dominating psychological experience that retains its power to evoke panic, terror, dread, grief, or despair. These emotions manifest in daytime fantasies, traumatic nightmares, and psychotic reenactments known as PTSD flashbacks. Furthermore, trauma-related stimuli that trigger recollections of the original event have the power to evoke mental images, emotional responses, and psychological reactions associ-

CHAP TER ONE 11

ated with the trauma. Researchers can use this phenomenon to reproduce PTSD symptoms in the laboratory by exposing affected individuals to auditory or visual trauma-related stimuli.

The “C”, or avoidant/numbing, criterion consists of symptoms that reflect behavioral, cognitive, or emotional strategies PTSD patients use in an attempt to reduce the likelihood that they will expose themselves to traumarelated stimuli. PTSD patients also use these strategies in an attempt to minimize the intensity of their psychological response if they are exposed to such stimuli. Behavioral strategies include avoiding any situation in which they perceive a risk of confronting trauma-related stimuli. In its extreme manifestation, avoidant behavior may superficially resemble agoraphobia because the PTSD individual is afraid to leave the house for fear of confronting reminders of the traumatic event(s). Dissociation and psychogenic amnesia are included among the avoidant/numbing symptoms and involve the individuals cutting off the conscious experience of traumabased memories and feelings. Finally, since individuals with PTSD cannot tolerate strong emotions, especially those associated with the traumatic experience, they separate the cognitive from the emotional aspects of psychological experience and perceive only the former. Such “psychic numbing” is an emotional anesthesia that makes it extremely difficult for people with PTSD to participate in meaningful interpersonal relationships.

Symptoms included in the “D”, or hyper-arousal, criterion most closely resemble those seen in panic and generalized anxiety disorders. While symptoms such as insomnia and irritability are generic anxiety symptoms, hyper-vigilance and startle are more characteristic of PTSD. The hypervigilance in PTSD may sometimes become so intense as to appear like frank paranoia. The startle response has a unique neurobiological substrate and may actually be the most pathognomonic PTSD symptom.

The “E”, or duration, criterion specifies how long symptoms must persist in order to qualify for the (chronic or delayed) PTSD diagnosis. In DSM-III, the mandatory duration was six months. In DSM-III-R, the duration was shortened to one month, which it has remained.

The “F”, or functional significance, criterion specifies that the survivor must experience significant social, occupational, or other distress as a result of these symptoms.

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ASSESSING PTSD Since 1980, there has been a great deal of attention devoted to the development of instruments for assessing PTSD. Keane and associates, working with Vietnam war-zone veterans, have developed both psychometric and psychophysiologic assessment techniques that have proven to be both valid and reliable.

Other investigators have modified such assessment instruments and used them with natural disaster victims, rape/incest survivors, and other traumatized individuals.

These assessment techniques have been used in the epidemiological studies mentioned above and in other research protocols.

Neurobiological research indicates that PTSD may be associated with stable neurobiological alterations in both the central and autonomic nervous systems. Psychophysiological alterations associated with PTSD include hyper-arousal of the sympathetic nervous system, increased sensitivity and augmentation of the acousticstartle eye blink reflex, and sleep abnormalities. Neuropharmacologic and neuroendocrine abnormalities have been detected in most brain mechanisms that have evolved for coping, adaptation, and preservation of the species. These include the noradrenergic, hypothalamicpituitary-adrenocortical, serotonergic, glutamatergic, thyroid, endogenous opioid, and other systems.

Structural brain imaging suggests reduce volume of the hippocam-

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CASCADE MODEL OF PTSD

Excessive catecholamines at time of the trauma.

Inappropriate pairing of memories and distress.

Traumatic reminders would be distressing. Distress would provoke traumatic memories.

Further pairing of distress with more non-specific stimuli.

Further habituation and extinction.

If exposure to traumatic reminders results in distress and more stimuli are traumatic reminders.

Survivor will find him/herself frequently anxious.

Anxiety may be associated with increased CRF release.

Result in continued, sustained, alterations of the HPA axis.

Other behavioral consequences (e.g. personality).

pus and anterior cingulated. Functional brain imaging suggests excessive amygdala activity and reduced activation of the prefrontal cortex.

Longitudinal research has shown that PTSD can become a chronic psychiatric disorder and can persist for decades and sometimes for a lifetime.

Patients with chronic PTSD often exhibit a longitudinal course marked by remissions and relapses. There is also a delayed variant of PTSD in which individuals exposed to a traumatic event do not exhibit the PTSD syndrome until months or years afterward. Usually, the immediate precipitant is a situation that resembles the original trauma in a significant way (for example, a war veteran whose child is deployed to a war zone or a rape survivor who is sexually harassed or assaulted years later).

If an individual meets diagnostic criteria for PTSD, it is likely that he or she will meet DSM-IV-TR criteria for one or more additional diagnoses. Most of-

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ten, these comorbid diagnoses include major affective disorders, dysthymia, alcohol or substance abuse disorders, anxiety disorders, or personality disorders. There is a legitimate question whether the high rate of diagnostic comorbidity seen with PTSD is an artifact of our current decision-making rules for the PTSD diagnosis since there are not exclusionary criteria in DSM-III-R. In any case, high rates of comorbidity complicate treatment decisions concerning patients with PTSD since the clinician must decide whether to treat the comorbid disorders concurrently or sequentially.

Although PTSD continues to be classified as an anxiety disorder, areas of disagreement about its nosology and phenomenology remain. Questions about the syndrome itself include: what is the clinical course of untreated PTSD; are there different subtypes of PTSD; what is the distinction between traumatic simple phobia and PTSD; and what is the clinical phenomenology of prolonged and repeated trauma? With regard to the latter, Herman has argued that the current PTSD formulation fails to characterize the major symptoms of PTSD commonly seen in victims of prolonged, repeated interpersonal violence such as domestic or sexual abuse and political torture. She has proposed an alternative diagnostic formulation that emphasizes multiple symptoms, excessive somatization, dissociation, changes in affect, pathological changes in relationships, and pathological changes in identity.

PTSD has also been criticized from the perspective of cross-cultural psychology and medical anthropology, especially with respect to refugees, asylum seekers, and political torture victims from non-Western regions.

Clinicians and researchers working with such survivors argue that since PTSD has usually been diagnosed by clinicians from Western industrialized nations working with patients from a similar background, the diagnosis does not accurately reflect the clinical picture of traumatized individuals from non-Western traditional societies and cultures. Major gaps remain in our understanding of the effects of ethnicity and culture on the clinical phenomenology of post-traumatic syndromes. We have only just begun to apply vigorous ethnocultural research strategies to delineate possible differences between Western and non-Western societies regarding the psychological impact of traumatic exposure and the clinical manifestations of such exposure.

TREATMENT FOR PTSD The many therapeutic approaches offered to PTSD patients are presented in Foa, Keane, and Friedman’s comprehensive book on treatment. The most successful interventions are cognitive-behavioral therapy (CBT) and medication. Excellent results have been obtained with some CBT combi-

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nations of exposure therapy and cognitive restructuring, especially with female victims of childhood or adult sexual trauma. Sertraline (Zoloft) and paroxetine (Paxil) are selective serotonin reuptake inhibitors (SSRI) that are the first medications to have received FDA approval as indicated treatments for PTSD. Success has also been reported with Eye Movement Desensitization and Reprocessing (EMDR), although rigorous scientific data are lacking and it is unclear whether this approach is as effective as CBT. A frequent therapeutic option for mildly to moderately affected PTSD patients is group therapy, although empirical support for this is sparse. In such a setting, the PTSD patient can discuss traumatic memories, PTSD symptoms, and functional deficits with others who have had similar experiences. This approach has been most successful with war veterans, rape/incest victims, and natural disaster survivors. It is important that therapeutic goals be realistic because, in some cases, PTSD is a chronic and severely debilitating psychiatric disorder that is refractory to current available treatments. The hope remains, however, that our growing knowledge about PTSD will enable us to design interventions that are more effective for all patients afflicted with this disorder.

There is great interest in rapid interventions for acutely traumatized individuals, especially with respect to civilian disasters, military deployments, and emergency personnel (medical personnel, police, and firefighters).

This has become a major policy and public health issue since the massive traumatization caused by the September 11 terrorist attacks on the World Trade Center, Hurricane Katrina, the Asian Tsunami, and the current wars in Iraq or Afghanistan. Currently, there is controversy about which interventions work best during the immediate aftermath of a trauma. Research on critical incident stress debriefing (CISD), an intervention used widely, has brought disappointing results with respect to its efficacy to attenuate post-traumatic distress or to forestall the later development of PTSD. The National Center for PTSD and the National Center for Child Traumatic Stress have recently developed an alternative early intervention, Psychological First Aid, that is available online. Promising results have been shown with brief cognitive-behavioral therapy.

HOW DOES PTSD DEVELOP? All people with PTSD have lived through a traumatic event that caused them to fear for their lives, see horrible things, and feel helpless. Strong emotions caused by the event create changes in the brain that may result in PTSD. Most people who go through a traumatic event have some symptoms at the beginning. Yet only some will develop PTSD. It isn’t clear why some

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All people with PTSD have lived through a traumatic event that caused them to fear for their lives, see horrible things, and feel helpless.

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people develop PTSD and others don’t. How likely you are to get PTSD depends on many things. These include: » How intense the trauma was or how long it lasted » If you lost someone you were close to or were hurt » How close you were to the event » How strong your reaction was » How much you felt in control of events » How much help and support you got after the event Many people who develop PTSD get better at some time. But about 1 out of 3 people with PTSD may continue to have some symptoms. Even if you continue to have symptoms, treatment can help you cope. Your symptoms don’t have to interfere with your everyday activities, work, and relationships.

WHAT ARE OTHER COMMON PROBLEMS? People with PTSD may also have other problems. These include: » Drinking or drug problems » Feelings of hopelessness, shame, or despair » Employment problems » Relationships problems including divorce and violence » Physical symptoms CHILDREN AND PTSD Children can have PTSD too. They may have the symptoms described above or other symptoms depending on how old they are. As children get older their symptoms are more like those of adults. » Young children may become upset if their parents are not close by, have trouble sleeping, or suddenly have trouble with toilet training or going to the bathroom » Children who are in the first few years of elementary school (ages 6 to 9) may act out the trauma through play, drawings, or stories. They may complain of physical problems or become more irritable or aggressive.

They also may develop fears and anxiety that don’t seem to be caused by the traumatic event.

WHAT TREATMENTS ARE AVAILABLE? When you have PTSD, dealing with the past can be hard. Instead of telling others how you feel, you may keep your feelings bottled up. But treatment can help you get better. There are good treatments available for PTSD.

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Cognitive-behavioral therapy (CBT) is one type of counseling. It appears to be the most effective type of counseling for PTSD. There are different types of cognitive behavioral therapies such as cognitive therapy and exposure therapy. A similar kind of therapy called EMDR, or eye movement desensitization and reprocessing, is also used for PTSD. Medications can be effective too. A type of drug known as a selective serotonin reuptake inhibitor (SSRI), which is also used for depression, is effective for PTSD. After a trauma, people may go though a wide range of normal responses.

Such reactions may be experienced not only by people who experienced the trauma first-hand, but by those who have witnessed or heard about the trauma, or been involved with those immediately affected. Many reactions can be triggered by persons, places, or things associated with the trauma.

Some reactions may appear totally unrelated.

People are usually surprised that reactions to trauma can last longer than they expected. It may take weeks, months, and in some cases, many years to fully regain equilibrium. Many people will get through this period with the help and support of family and friends. But sometimes friends and family may push people to “get over it” before they’re ready. Let them know that such responses are not helpful for you right now, though you appreciate that they are trying to help. Many people find that individual, group, or family counseling are helpful, and in particular, EMDR is a phenomenally rapid and wonderful therapeutic method. Either way, the key word is connection—ask for help, support, understanding, and opportunities to talk.

The Chinese character for crisis is a combination of two words—danger and opportunity. People who fully engage in recovery from trauma discover unexpected benefits. As they gradually heal their wounds, survivors find that they are also developing inner strength, compassion for others, increasing self-awareness, and often the most surprising—a greater ability to experience joy and serenity than ever before.

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2

POST-TRAUMATIC STRESS DISORDER: ACQUISITION, RECOGNITION, COURSE, AND TREATMENT Jonathan R.T. Davidson, MD, Dan J. Stein, MD, PhD, Arieh Y. Shalev, MD and Rachel Yehuda, PhD

Post-traumatic stress disorder has been recognized as a distinct psychiatric disorder since the introduction of the Diagnostic and Statistical Manual of Mental Disorders (DSM-III) in 1980. xyxy xyxyxyx yxyx xyxyx yxyx xyxyyx xyxyxy xyx xyxyxy xyxyxy xxyxyyx xyxyyx xyx xyxyyx According to this classification, a diagnosis of PTSD required exposure to a recognizable stressor that would evoke symptoms of distress in almost everyone. This definition was modified some years later to emphasize the requirement of avoidance phenomena, which consist of deliberate efforts to avoid thoughts, feelings, activities, and situations that aroused recollections of the trauma. xxxy xyxyx xyx xyxyx x xyyxyx xyxyx xyxyxy xyxyxy xxyyxyxy xyxyxy xyxyxyx xyxyyx x xyxyxyx xyxyxy xxyyxyxyxyx xyxyx xyyxyxx xyxyx xyxyx xyxyxyx xyxyyx xyxyxyx xyxyxyx yx xyxyxyxy xyxyxy xyx xyxyxy xy. The avoidance of recollection of the traumatic stressor only served to emphasize the fundamental importance in the development of PTSD of exposure to an extreme, life-threatening stressor. Changes to the definition of PTSD that were brought about in the DSM-IV included redefining the traumatic event. This had to involve actual or threatened death or serious injury or a threat to the physical integrity to self or others. In addition, the person experiencing the event had to respond with intense fear, helplessness, or horror. Clinically significant distress and impairment in social, occupational, or other important areas of functioning with a minimum duration of 1 month were further requirements. This definition of PTSD now encompasses the concept of “vicarious traumatization” (being confronted by serious injury to others), which has significance for emergency services and rescue workers.

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INTRODUCTION Post-traumatic stress disorder (PTSD) is a chronic and disabling psychiatric disorder associated with a significant degree of morbidity. Lifetime prevalence rates in the community have been estimated at 1.3%–7.8%. However, as might be expected, a higher lifetime PTSD prevalence of around 30% has been reported for Vietnam veterans and female victims of rape in retrospective epidemiological studies. The risk of developing PTSD has been shown to vary according to the type of trauma. In common with many other psychiatric disorders, a higher prevalence of PTSD occurs in women than in men.

Post-traumatic stress disorder has been recognized as a distinct psychiatric disorder since the introduction of the Diagnostic and Statistical Manual of Mental Disorders (DSM-III) in 1980. According to this classification, a diagnosis of PTSD required exposure to a recognizable stressor that would evoke symptoms of distress in almost everyone. This definition was modified some years later to emphasize the requirement of avoidance phenomena, which consist of deliberate efforts to avoid thoughts, feelings, activities, and situations that aroused recollections of the trauma. The avoidance of recollection of the traumatic stressor only served to emphasize the fundamental importance in the development of PTSD of exposure to an extreme, life-threatening stressor. Changes to the definition of PTSD that were brought about in the DSM-IV included redefining the traumatic event. This had to involve actual or threatened death or serious injury or a threat to the physical integrity to self or others. In addition, the person experiencing the event had to respond with intense fear, helplessness, or horror. Clinically significant distress and impairment in social, occupational, or other important areas of functioning with a minimum duration of 1 month were further requirements. This definition of PTSD now encompasses the concept of “vicarious traumatization” (being confronted by serious injury to others), which has significance for emergency services and rescue workers.

Post-traumatic stress disorder frequently follows a chronic course and can be associated with recurrences related to exposure to multiple traumas.

In addition, PTSD is frequently comorbid with other psychiatric conditions such as anxiety disorders, depression, and substance abuse.

THE COURSE OF PTSD When faced with a traumatic experience, a large majority of the population will have a brief acute response to stress and will not develop any longlasting pathologic sequelae, whereas a smaller proportion will experience persistent PTSD, either alone or in combination with major depression.

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RATE OF PTSD SYMPTOMS IN RAPE VICTIMS 100

94%

80

60 47%

42%

40 25–15% 20

0

Trauma Event

3 9 months

[Undefined Time]

Years later

Previous vulnerability to depressive or anxiety disorders increases the likelihood that PTSD will develop. Indeed, both vulnerability and protective factors will affect the individual in the transitional phase from the acute stress response. In this critical stage, the acute reaction will stabilize in some individuals, whereas there is progressive decompensation in others.

Pathological Development Some of the symptoms of PTSD are considered to be reflections of the adaptive mental processes involved in the assimilation and integration of new information that results from exposure to trauma.

This equates to PTSD symptoms representing part of a normal survival instinct in individuals exposed to trauma, and the pathologic development of PTSD only follows if the response that leads to resolution of the trauma is disrupted in some way. The main conclusion of biological research into PTSD is that exposure to one or more traumatic events triggers a chain of mental and biological events, which ultimately lead to prolonged PTSD. An examination of the longitudinal course of PTSD in a study of rape victims showed that 94% of rape survivors had all the clinical symptoms of PTSD one week after the traumatic event, thereby suggesting that such a clinical picture probably constitutes a normal reaction. At 3 and 9 months after the event, the proportion of rape victims expressing symptoms of PTSD declines to 15%–25%. Following this period, the curve remains horizontal, indicating that PTSD is an unremitting and chronic disorder that can last for any length of time. In the National Comorbidity Study (NCS), median dura-

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tion of PTSD associated with worst lifetime trauma was 3 years for those receiving treatment and 5 years for those who did not receive treatment.

However, this estimate does not take into account the real possibility that people may experience PTSD more than once in their lives. Indeed, a great many people report exposure to multiple traumas over a life course. Data from the NCS which used DSM-III-R criteria showed that 60.7% of men and 51.2% of women reported exposure to at least one lifetime traumatic event. DSM-IV criteria for PTSD expand the set of stressful experiences to include sudden death of a close friend, or loved one, or diagnosis of a life-threatening illness. Results from a community epidemiologic survey in the USA that used DSM-IV criteria reported that 90% of respondents had exposure to at least one lifetime traumatic event.

PHYSIOLOGICAL RESPONSES It has been reported that nonphysically injured trauma survivors admitted to the emergency room, who subsequently went on to develop PTSD, had higher heart rates at the emergency department (mean=95.5 beats per minute, SD=13.9, versus mean=83.3 beats per minute, SD=10.9) (t=4.4, P<0.001) and 1 week later (mean=77.8 beats per minute, SD=11.9, versus mean=72.0 beats per minute, SD=9.5) (t=2.25, P<0.03), but not after 1 and 4 months. Similarly, in a study of trauma survivors, the physiologic response of heart rate, skin conductance and electromyography (frontalis) to mental imagery recorded a short time following the trauma has been shown to differentiate between those who go on to develop PTSD and those who do not. The importance of such physiologic responses is clear, since our clinical experience indicates that PTSD patients can re-access their trauma memories as often as 100 times a day and elicit these physiologic reactions each time. PTSD patients possibly continue to reinforce the initial impact of the trauma by reactivating it in this way. PTSD patients have also been reported to differentiate from normal survivors by poor habituation of skin conductance to a repetition of loud startling noises.

Traumatized non-PTSD and anxious groups showed normal habituation by contrast. This may represent a primary defect of the central nervous system that continues to identify and classify the loud tones as threatening in people with PTSD. Patients, therefore, continue to react, rather than rejecting the noises as redundant information and stopping the reaction to them. In a prospective study of 239 trauma survivors, the auditory startle response of all the trauma survivors is normal at 1 week. The response of those patients who go on to develop PTSD becomes abnormal between 1 and 4 months after the trauma, suggesting that this is the critical period during which the central nervous system adapts its response to ambiguous stimuli (such as loud noises) and determines whether PTSD develops.

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EXPOSURE TO TRAUMA AND CONDITIONAL PROBABILITY OF PTSD First Follow-up VARIABLE

Number of Respondents 1

Second Follow-up Exposed, %

PTSD among exposed, %

Number of Respondents 1

Exposed, %

PTSD among exposed, %

Prior exposure/PTSD

92

42.4

18.0

105

60.0

19.1

Prior exposure/no PTSD

294

33.3

12.2

386

41.5

6.3

No prior exposure

604

24.0

8.3

419

27.4

6.1

Male

613

28.4

13.8

575

38.1

11.0

Female

377

28.7

6.5

338

35.5

4.2

White

797

25.2

9.0

740

34.1

7.9

Black

193

42.0

16.1

173

50.3

10.3

College

289

22.2

9.4

269

34.2

7.6

Some college

701

31.1

11.5

644

38.4

8.9

MDD

112

42.9

20.8

163

46.6

15.8

No MDD

877

26.7

9.0

745

35.2

6.5

Anxiety disorders

237

32.9

19.2

300

41.3

12.1

No anxiety

753

27.1

7.8

610

35.3

6.5

SUD

261

28.0

15.1

277

36.5

9.9

No SUD

729

28.7

9.6

636

37.4

8.0

TOTAL

990

11.0

913

SEX

RACE

EDUCATION

PRE-EXISTING DISORDERS

28.5

37.1

8.6

1 Some variables do not add to the total because of missing data Abbreviations: MDD, major depressive disorder; PTSD, post-traumatic stress disorder; SUD, substance use disorder

CHAP TER T WO 27

Post-traumatic stress disorder frequently follows a chronic course and can be associated with recurrences related to exposure to multiple traumas.

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LIFETIME PREVALENCE OF EXPOSURE TO TRAUMA AND RISK OF PTSD

TRAUMA

Lifetime prevalence (%)

PTSD risk (%)

Male1

Male1

Female2

Female2

Life-threatening accident

25.0

13.8

6.3

8.8

Threatened with weapon

19.0

6.8

1.9

32.6

Physical attack

11.1

6.9

1.8

21.3

Rape

0.7

9.2

65.0

45.9

1 N=2,812 2 N=3,065

There are two important questions for the clinician to address when trying to recognize the vulnerable patients that will develop PTSD: 1) Why does trauma lead to PTSD for them rather than some other psychiatric disorder or no disorder at all? 2) What are the risk factors for determining these patients? The acute stress response is universal and nonpredictive of PTSD. Moreover, as mentioned, patients who develop PTSD fail to show a remission of these acute symptoms and show abnormally increased heart rates several days after the trauma as well as other abnormal physiologic responses such as the increased startle response. It would therefore appear that PTSD might develop as a failure of the body to reverse the acute stress response.

DELAYED AND CHRONIC FORMS OF PTSD The onset of PTSD can be delayed for years. In a large study by Solomon looking at individuals who presented for treatment within 6 years of the Lebanon war, 10% were considered delayed onset, 40% were delayed helpseeking, 33% were exacerbation of subclinical PTSD, 13% were reactivation of recovered PTSD, and the remaining 4% had other psychiatric disorders.

This is confirmed in the study by Shalev where 5.1% of patients were truly delayed onset PTSD and the rest were mainly PTSD patients who recovered and were then reactivated by another event.

Most cases of PTSD recover within 1 year, and after 6 years recovery without treatment is unlikely. However, up to 40% of patients with PTSD have a chronic condition. Chronic PTSD is prolonged and may be unremitting, and subject to reactivation upon exposure to stressors. In addition, it can be disabling and associated with substantial comorbidity. The risk of developing secondary comorbid disorders is related to a number of factors, including

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ENHANCED SUPPRESSION OF CORTISOL FOLLOWING LOW-DOSE DEXAMETHASONE By study author and number Average control Yehuda (38) Yehuda (39) Goenjian (40) Stein (41) Kellner (42)

60

80

100

PERCENTAGE OF CORTISOL SUPPRESSION

the severity of the trauma, gender, family history, past history, and the complexity of the PTSD reaction. Chronic PTSD is linked with abuse of alcohol, drugs, and medication. It is also associated with mortality from suicide.

The frequency of comorbid disorders with PTSD is shown for male and females in. The percentages of individuals with PTSD who have at least one other lifetime disorder is 88.0% for men and 79.0% for women. The major comorbid disorder seen with PTSD is depression, occurring in 47.9% of men and 48.5% of women. Other comorbid disorders include dysthymia, specific phobia and generalized anxiety disorder.

DISABILITY ASSOCIATED WITH PTSD The chronic form of PTSD is often debilitating. The disability associated with PTSD includes work impairment, change in life trajectories, impaired social relations, marital instability and perpetuation of violence. This not only represents a burden to the individual but to society as well.

In a study based on the analysis of the NCS data, which examined the effects of mental disorders on work impairment, work loss (defined as missing a full day of work), and work cut back (either missing part of a day or working less efficiently than usual) during the previous month was 0.8 days/month and 2.8 days/month, respectively. The amount of work im-

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pairment associated with PTSD was the same as that associated with major depression but less than that associated with panic disorder.

In the NCS data, among those with PTSD, there is an increased risk of making suicide plans (odds ratio [OR]=2.4; 95% confidence interval [CI]=1.7â&#x20AC;&#x201C;3.3) and an increased risk of attempting suicide (OR=6; 95% CI=3.4â&#x20AC;&#x201C;10.7) for patients suffering from PTSD. In addition, marital instability, unemployment, and increased use of outpatient care contribute greatly to the burden to society. The NCS analyses showed that the most extreme adverse effects of traumatic events were associated with complex ongoing traumas that occurred in childhood, such as parental violence, alcoholism, or depression. Such experiences interfere with lifelong patterns of interpersonal relationships and the process of mastering basic educational skills.

In the study by Stein, patients with PTSD reported significantly more functional impairment than patients without mental disorders. In addition, patients with PTSD made greater use of healthcare resources than non-mentally-ill patients and encountered considerable functional impairment.

A study of the quality of life with PTSD reported greater impairment at baseline for subjects with PTSD relative to those with major depression and obsessive-compulsive disorder on several domains of the

CHAP TER T WO 31

36-item Short-Form Health Survey. Similarly, in a study of PTSD among civilians, significant impairment was associated with PTSD as seen on the Sheehan Disability Scale, which measures the total work, family and social/leisure disability and the Vulnerability to the Effects of Stress Scale.

RECOGNITION OF PATIENTS WITH PTSD By definition, the patient with PTSD must have experienced a traumatic event before the onset of the disorder. The symptoms of PTSD revolve around reliving the traumatic experience, and include recurrent and intrusive thoughts and/or dreams of the trauma, difficulty in falling or staying asleep, irritability, hypervigilance, and avoidance of stimuli associated with the trauma.

Many patients, however, fail to seek medical help as they do not recognize that they have a problem. Certainly, the most commonly reported reason for not being in treatment among the 62% of PTSD cases in the NCS study was that they did not have a problem. Even those with quite severe impairment cited this reason. This failure to seek help is not only a question of lack of information or ability to perceive that they have a problem, but is representative of avoidance of trauma or addressing traumatic recollections. Those who recognized their need for help give a number of other reasons for being in treatment. Most commonly these were expense of treatment, uncertainty about where to go for help, thinking the problem will get better by itself, and wanting to solve the problem on oneâ&#x20AC;&#x2122;s own.

Others reasons included the stigma, fear of forced hospitalization, language barriers, and dissatisfaction with the services.

Among the general population in the United States, it is estimated that 38% of people with PTSD are treated in any given year. The majority of these patients (28% of cases and 75% of those in treatment) are seen by the medical practitioners, while others are seen by the human services personnel or self-help groups. Only 22% of those with PTSD (38% of those in treatment) are seen by mental health professionals (psychiatrist, clinical psychologists, or other).

Patients with PTSD who present in primary care are likely to present with somatic symptoms such as pain associated with increased onset of arterial, lower gastrointestinal, dermatologic, and musculoskeletal disorders.

Similarly, they also report numerous sleep disturbances. In a study of 1,832 subjects with PTSD from an urban general population, sleep disturbances also affected about 70% of the PTSD subjects. Violent or injurious behaviors during sleep, sleep paralysis, sleep talking, and hypnagogic and hypnopompic hallucinations were more frequently reported in respondents with PTSD.

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FREQUENCY OF COMORBID DISORDERS WITH PTSD IN MEN AND WOMEN 47.9

Major depression

48.5 21.4

Dysthymia

23.3 16.8

Generalized anxiety disorder

15.0 31.4

Simple phobia

29.0 51.9

Alcohol abuse

27.9 43.5

Substance abuse

26.9 88.0

At least one lifetime disorder

79.0

0

20 MEN

40

60

80

100

WOMEN

In a study of patients with irritable bowel syndrome, 18 of 50 patients (36%) were diagnosed with PTSD. Irritable bowel syndrome patients with a history of trauma were more likely to have other comorbid psychiatric diagnoses as well.

In a study to determine the relationship between a history of PTSD and somatization of symptoms, a history of PTSD was associated with significantly more symptoms in each of the somatic symptom groups, except pain. In addition, persons with PTSD were more likely to report each of the symptoms of somatization, compared to those with other psychiatric disorders. Prospectively, baseline history of PTSD signaled an increased risk of pain (OR=2.1) and conversion symptoms (OR=2.3) in the follow-up interval, relative to those with no disorder.

Chronic PTSD is linked with abuse of alcohol, drugs, and medication. In common with many other anxiety disorders, PTSD is often complicated by secondary depression (60%â&#x20AC;&#x201C;80% of patients), particularly if the condition has not been treated. Patients will therefore present in either primary

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or secondary care with comorbid depression, which complicates the recognition of PTSD per se, and prevents the primary diagnosis from being made. Despite some of the symptoms of PTSD being shared with major depression, the clinician should be alerted by the presence of intrusive recollections and pervasive avoidance of a trauma. In addition, when PTSD is complicated by secondary depression, the symptom profile tends to differ from that of major depression, with less psychomotor retardation or agitation. In the study of PTSD in the primary care medical setting by Stein, 11.8% of primary care attendees met diagnostic criteria for either full or partial PTSD. Comorbidity with major depression (61% of cases of PTSD) and generalized anxiety disorder (39%) was common, but less so with social phobia (17%) and panic disorder (6%). Substance use disorder comorbidity (22%) was also fairly common.

Patients who suffer from the effects of chronic interpersonal violence are more likely to have chronic PTSD, and the symptom profile is likely to be more complex and often involves severe forms of dissociation not found in more typical cases of PTSD. The profile is so distinct it has been argued for the creation of a separate diagnosis to characterize this response known as “complex PTSD” or “disorders of extreme stress not otherwise specified.” Although this diagnosis is not included in DSM-IV due to the fact that the vast majority of patients with this symptom cluster also meet criteria for PTSD, it is nonetheless clear that a complex PTSD subtype exists. This subtype is more chronic and disabling than other cases of PTSD, and it is particularly common among patients who were exposed at an early age to chronic traumatic interpersonal violence.

CORTISOL LEVELS ASSOCIATED WITH PTSD Sensory input from a traumatic event is transmitted to the amygdala, and following cortical input leads to activation of four simultaneous types of response. The first response is the activation of the startle response through the reticularis pontis caudalis. The second response, via the sympathetic nervous system, consists of a release of adrenaline to increase heart rate, blood pressure, blood flow, and increase of glucose to the muscles. This increase in adrenaline is also relevant for the formation of memory. Suppression of the parasympathetic nervous system, which occurs in order to shut down any responses that might compete with the sympathetic nervous system (e.g., digestion, tissue repair, ovulation), constitutes the third response and is independent of the sympathetic nervous system. Finally, in the fourth response, through the hypothalamicpituitary-adrenal (HPA) axis, the hippocampus and amygdala activate the hypothalamus, which releases corticotrophin release factor (CRF), which in turn activates the pituitary gland to release adrenocorticotrophin hor-

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mone. This then stimulates the adrenal gland to release cortisol. The cortisol levels, which are proportional in magnitude to the levels of the stressor, inhibit the sympathetic nervous system, and via a negative feedback inhibition also attenuate the HPA axis.

In healthy individuals, circulating catecholamines and cortisol return to normal within hours. In the long term, exposure to a subsequent stressor (sensitization) can occur and create an exaggerated stress response, but baseline hormone levels will not indicate whether previous stressful events have occurred. However, in individuals with chronic PTSD, both baseline CRF and cortisol levels are decreased. There is also increased sympathetic nervous system activation to trauma, enhanced startle response to both neutral and trauma-related cues, and evidence of decreased parasympathetic nervous system activity. This has led to the view that PTSD may represent an extension of the normal stress response. One hypothesis proposed to explain this is that there are insufficient cortisol levels at the time of the trauma in some individuals, such that the other biologic reactions are not inhibited, and a prolonged activation of some of the stress responses occurs.

In support of this, the cortisol levels found in the aftermath of a motor vehicle accident in patients who went on to develop PTSD were found to be lower than in those who remained well or in those who suffered from depression. A further study of cortisol levels taken in the emergency room from victims in the aftermath of a rape showed lower levels of cortisol in those who had suffered a previous assault than in those with no previous assault. Therefore, prior trauma is definitely a risk for developing PTSD, along with the more common risks such as exposure to trauma, avoidant personality, genetic or familial factors, and cognitive variables such as IQ and education. Studies to isolate which of these variables are particular risk factors for developing PTSD are difficult to design. However, one group of patients that have been shown to be a high-risk group for developing PTSD are the children of Holocaust survivors. Further study of this group showed that only the children of parents who developed PTSD during the Holocaust were at risk of PTSD themselves when faced with trauma. Children with PTSD whose parents had PTSD have low cortisol levels, while Holocaust children with no PTSD (and no parental PTSD) have normal cortisol levels. Interestingly, children with no trauma or PTSD but whose parents had PTSD also had low cortisol levels, indicating that the low cortisol may be related to factors that predate the trauma.

In short, low cortisol levels may be related to risk for PTSD. The most likely explanation for this low cortisol before trauma is that the cortisol receptors in the pituitary are oversensitive, leading to a greater negative feedback inhibition, which results in lower cortisol levels. This increased receptor sensitivity in PTSD has been successfully demonstrated using a low-dose dexamethasone suppression test, which repeatedly showed an enhanced suppression of cortisol in PTSD patients.

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Therefore, under acute stress, this enhanced negative feedback could result in a premature shut down of the HPA axis, which would prevent the damping down of the sympathetic nervous system. This would lead to a cascade of consequences as detailed in. If this cascade model for PTSD is correct, then possible areas for intervention that may help the patient with PTSD become apparent, such as: reduction of nonspecific arousal, reduction of memory-related distress, cognitive restructuring to avoid forming new associations and stimulus generalizations, cognitive restructuring to correct already formed negative associations, addressing any number of the cascade of alterations that have occurred since the trauma.

TREATMENT OF PTSD Appropriate treatment of PTSD is essential to reduce symptoms and increase both the functioning and quality of life of the patient. Early intervention is particularly crucial in order to help prevent the development of secondary chronic morbidity.

There are five main treatment goals when treating PTSD: reducing the core symptoms, improving stress resilience, improving quality of life, reducing disability and reducing comorbidity.

A number of treatment outcome studies for PTSD have focused on cognitive-behavioral therapy programs, which include variants of

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exposure therapy, anxiety management and cognitive therapy. More recently, eye movement and desensitization therapy has been employed.

Pharmacological treatments are being studied. Both kinds of treatment are effective.

Psychosocial treatment Psychosocial treatment of PTSD has shown some promising results and, when effective, has been associated with low relapse rates. Of the existing treatments, exposure therapy has the strongest evidence of efficacy in different populations of trauma victims with PTSD. However, a minority of patients failed to show sufficient gains with this therapy. Anxiety management techniques have also been shown to be effective in the treatment of PTSD after rape, although not widely studied.

Cognitive therapy has also been seen to be effective in rape victims. More recently, a study of different victim populations with a history of PTSD of at least 6 monthsâ&#x20AC;&#x2122; duration studied the treatment effect of prolonged exposure alone; cognitive restructuring alone; combined prolonged exposure and cognitive restructuring; or relaxation without prolonged exposure or cognitive restructuring. The study showed that both prolonged exposure and cognitive restructuring were each therapeutic on their own, were not mutually enhancing when combined, and were each superior to relaxation.

Interestingly, this lack of advantage for combining different types of psychosocial treatments was also found in a study by Foa Studies attempting to examine augmentation of exposure therapy outcome with the addition of cognitive restructuring do not show any additional benefit over exposure therapy alone. No studies have examined the relative efficacy of pharmacotherapy and cognitive-behavioral therapy, and whether combination of the two will augment the efficacy of each.

Eye movement and desensitization reprocessing (EMDR) is a relatively new therapy for PTSD that consists of a form of exposure accompanied by saccadic eye movements. In EMDR, the therapist asks the patient to visualize images about the trauma, while inducing eye movements by asking the patient to track rapid side-to-side movement of the therapistâ&#x20AC;&#x2122;s finger.

A cognitive therapy component is also included by asking patients to replace negative thoughts with positive ones. There have been several studies of the efficacy of EMDR in the treatment of PTSD, although most have not been well controlled.

Successful treatment of PTSD with regard to the patient will involve attitude to treatment, capacity to tolerate distress, availability of support, and extent of comorbidity. To determine the real benefit of psychosocial treatments for PTSD, further large, well-controlled studies that compare the benefits of specific techniques are required.

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PHARMACOTHERAPY The principal goals of pharmacotherapy are reducing PTSD symptoms, improving resilience to stress and quality of life, and reducing disability and comorbidity. Reducing comorbidity is particularly important since patients rarely present with pure PTSD. There are three main classes of drugs that have demonstrated efficacy in the treatment of PTSD: tricyclic antidepressants (TCAs) such as amitriptyline and imipramine, monoamine oxidase inhibitors (MAOIs) such as phenelzine, and SSRIs such as sertraline, paroxetine, and fluoxetine. In addition, a variety of other drugs show promise including antiadrenergics, anticonvulsants and antidepressants (lamotrigine, nefazodone, clonidine).

There is considerable evidence from placebo-controlled trials that TCAs and MAOIs are effective in reducing symptoms of PTSD. There is also preliminary evidence from open-label studies of carbamazepine, valproic acid, and from a small double-blind trial of lamotrigine, that anticonvulsants can produce benefit in PTSD. More recently, placebo-controlled studies have shown that the SSRIs sertraline and paroxetine are effective in decreasing symptoms of PTSD, and considerable interest has centered on these new data. Similarly, there have been positive placebo-controlled trials for fluoxetine, however results in USA combat veterans were not as positive as for the general PTSD population. A European study found benefit for fluoxetine in predominantly combat veterans, with relapse prevention effects in maintenance treatment.

In the 12-week, double-blind study of sertraline in 187 psychiatric outpatients with DSM-III-R PTSD, sertraline treatment yielded a significantly greater improvement than placebo in mean change from baseline for Clinician-Administered PTSD Scale Part 2 (CAPS-2) total score (P=0.02). In addition, sertraline was significantly better than placebo for the symptom clusters avoidance/numbing (P=0.02) and arousal (P=0.03), but not on reexperiencing/intrusion (P=0.14). In this study, however, 73% of the population was female and 61.5% had suffered physical or sexual assault. Further studies of sertraline are required to demonstrate its efficacy in both genders and across all trauma types. A relapse-prevention study found the risk of relapse to be significantly less with sertraline than with placebo after 9 months of treatment.

In a 5-week double-blind, randomized, placebo-controlled study of fluoxetine in 64 patients (22 women and 42 men) (31 veteran and 33 nonveterans), fluoxetine significantly reduced overall PTSD symptomatology as assessed by total CAPS score. However, the difference in PTSD symptom

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reduction occurred primarily in the subscales “numbing” (for the nonveteran group) and “arousal.” Fluoxetine was an effective antidepressant in the total sample as measured by the Hamilton Depression Rating Scale (HAM-D). However, these improvements in depression did not predict improvement in PTSD score. While there was substantial improvement in depression (HAM-D) in the veteran sample (P= 0.005), there were no meaningful changes in numbing symptoms (P=0.70). Conversely, the nonveteran sample had a modest improvement in depression (HAM-D, P=0.04), but there was a substantial improvement in numbing (P=0.002). In general, nonveteran patients responded much better than veteran patients, which is probably reflective of the higher level of symptomatology in the veterans. In another double-blind, randomized, placebo-controlled study in 53 civilians over a 12-week period, fluoxetine (up to 60 mg/day) significantly reduced overall PTSD symptomatology as assessed by the Duke Global Severity Rating for PTSD, the Structured Interview for PTSD, and the Davidson Trauma Scale (DTS). Vulnerability to the effects of stress also responded well to fluoxetine.

In the 12-week, open-label study with paroxetine that was conducted in 19 civilians with DSM-III-R PTSD, patients showed significantly reduced mean PTSD symptom scores for both the DTS score (P<0.0001) and the Impact of Event Scale score (P<0.0001). In addition, there were significant improvements in all symptom clusters for both scales. Interestingly, cumulative childhood trauma scores were significantly and negatively correlated with treatment response on the total DTS score (r=0.52, P<0.03). Since the study by Marshall, there has been a series of large clinical trials with paroxetine in PTSD. The clinical program involved 1,180 patients with a DSM-IV diagnosis of PTSD, and demonstrated that paroxetine relieves the symptoms of PTSD, significantly reducing mean change from baseline in CAPS-2 total score and Clinical Global Impression global improvement scale.

In addition, it significantly reduced the CAPS-2 score for reexperiencing/ intrusion (P<0.001), avoidance/numbing (P<0.001), and arousal (P<0.001) compared with placebo. This new data, which was generated in 12-week, double-blind, randomized, fixed- or flexible-dose studies also confirmed that treatment benefit with paroxetine (20–50 mg/day) was observed across all trauma types and in both genders.

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3

THE ETIOLOGY OF COMBAT-RELATED POST-TRAUMATIC STRESS DISORDERS Jim Goodwin, PsyD

Most Vietnam veterans have adjusted well to life back in the United States, following their wartime experiences. That’s a tribute to these veterans who faced a difficult homecoming to say the least. However, a very large number of veterans haven’t made it all the way home from the war in Southeast Asia. By conservative estimates, at least half a million Vietnam veterans still lead lives plagued by serious, war-related readjustment problems. Such problems crop up in a number of ways, varying from veteran to veteran. Flashbacks to combat... feelings of alienation or anger...depression, loneliness and an inability to get close to others...sometimes drug or alcohol problems...perhaps even suicidal feelings. The litany goes on. In its efforts to help these veterans, the 700,000-member Disabled American Veterans (DAV) funded the Forgotten Warrior Project research on Vietnam veterans by John P. Wilson, PhD at Cleveland State University. That research resulted in formation of the DAV Vietnam Veterans Outreach Program to provide counseling to these veterans in 1978. With 70 outreach offices across the United States, this DAV program served as a model for the Veterans Administration (VA) Operation Outreach program for Vietnam era veterans, which was established approximately a year later. Clinically, the readjustment problems these veterans suffer were designated as Post-Traumatic Stress Disorders in the American Psychiatric Association’s Diagnostic & Statistical Manual III (DSM III). Counseling psychologists working with Vietnam veterans in the DAV and VA outreach programs emphasize that these disorders are not mental illnesses. Rather, they are delayed reactions to the stress these veterans—particularly combat veterans— underwent during the war in Southeast Asia.

CHAP TER THREE 41

THE EVOLUTION OF POST-TRAUMATIC STRESS DISORDER It was not until World War I that specific clinical syndromes came to be associated with combat duty. In prior wars, it was assumed that such casualties were merely manifestations of poor discipline and cowardice.

However, with the protracted artillery barrages commonplace during “The Great War,” the concept evolved that the high air pressure of the exploding shells caused actual physiological damage, precipitating the numerous symptoms that were subsequently labeled “shell shock.” By the end of the war, further evolution accounted for the syndrome being labeled a “war neurosis.”

During the early years of World War II, psychiatric casualties had increased some 300 percent when compared with World War I, even though the preinduction psychiatric rejection rate was three to four times higher than World War I. At one point in the war, the number of men being discharged from the service for psychiatric reasons exceeded the total number of men being newly drafted.

During the Korean War, the approach to combat stress became even more pragmatic. Due to the work of Albert Glass, individual breakdowns in combat effectiveness were dealt with in a very situational manner. Clinicians provided immediate onsite treatment to affected individuals, always with the expectation that the combatant would return to duty as soon as possible. The results were gratifying. During World War II, 23 percent of the evacuations were for psychiatric reasons. But in Korea, psychiatric evacuations dropped to only six percent. It finally became clear that the situational stresses of the combatant were the primary factors leading to psychological casualty.

Surprisingly, with American involvement in the Vietnam War, psychological battlefield casualties evolved in a new direction. What was expected from past war experiences—and what was prepared for—did not materialize.

Battlefield psychological breakdown was at an all-time low, 12 per one thousand. It was decided that use of preventative measured learned in Korea and some added situational manipulation which will be discussed later had solved the age-old problem of psychological breakdown in combat.

As the war continued for a number of years, some interesting additional trends were noted. Although the behavior of some combatants in Vietnam undermined fighting efficiency, the symptoms presented rare but very well documented phenomenon of World War II began to be reobserved.

After the end of World War II, some men suffering from acute combat reaction, as well as some of their peers with no such symptoms at war’s end,

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WORLD WAR II VETERANS One in 20 soldiers suffer from PTSD symptoms

began to complain of common symptoms. These included intense anxiety, battle dreams, depression, explosive aggressive behavior and problems with interpersonal relationships, to name a few.

A similar trend was once more observed in Vietnam veterans as the war wore on. Both those who experienced acute combat reaction and many who did not began to complain of the above symptoms long after their combatant role had ceased. What was so unusual was the large numbers of veterans being affected after Vietnam. The pattern of neuropsychiatric disorder for combatants of World War II and Korea was quite different than for Vietnam. For both World War II and the Korean War, the incidence of neuropsychiatric disorder among combatants increased as the intensity of the wars increased. As these wars wore down, there was a corresponding decrease in these disorders until the incidence closely resembled the particular prewar periods. The prolonged or delayed symptoms noticed during the postwar periods were noted to be somewhat obscure and few in numbers; therefore, no great significance was attached to them. As the war in Vietnam progressed in intensity, there was no corresponding increase in neuropsychiatric casualties among combatants. It was not until the early 1970s that neuropsychiatric disorders began to increase. With the end of direct American troop involvement in Vietnam in 1973, the number of veterans presenting neuropsychiatric disorders began to increase tremendously.

CHAP TER THREE 43

VIETNAM’S PREDISPOSING EFFECTS FOR PTSD When direct American troop involvement in Vietnam became a reality, military planners looked to previous war experiences to help alleviate the problem of psychological disorder in combat. By then it was an understood fact that those combatants with the most combat exposure suffered the highest incidence of breakdown. In Korea this knowledge resulted in use, to some extent, of a “point system.” After accumulating so many points, an individual was rotated home, regardless of the progress of the war. This was further refined in Vietnam, the outcome being the DEROS (date of expected return from overseas) system. Every individual serving in Vietnam, except general officers, knew before leaving the United States when he or she was scheduled to return. The tour lasted 12 months for everyone except the Marines who, known for their one-upmanship, did a 13-month tour. DEROS promised the combatant a way out of the war other than as a physical or psychological casualty.

The advantages were clear: there would not be an endless period of protracted combat with the prospect of becoming a psychological casualty as the only hope for return to the United States without wounds. Rather, if a combatant could just hold together for the 12 or 13 months, he would be rotated to the United States; and, once home, he would leave the war far behind.

The disadvantages to DEROS were not as clear, and some time elapsed before they were noticed. DEROS was a very personal thing; each individual was rotated on his own with his own specific date. This meant that tours in Vietnam were solitary, individual episodes. It was rare, after the first few years of the war, that whole units were sent to the war zone simultaneously. Bourne said it best: “The war becomes a highly individualized and encapsulated event for each man. His war begins the day he arrives in the country, and ends the day he leaves.” Bourne further states, “He feels no continuity with those who precede or follow him: He even feels apart from those who are with him but rotating on a different schedule.”

Because of this very individual aspect of the war, unit morale, unit cohesion and unit identification suffered tremendously. Many studies from past wars point to the concept of how unit integrity acts as a buffer for the individual against the overwhelming stresses of combat. Many of the veterans of World War II spent weeks or months with their units returning on ships from all over the world. During the long trip home, these men had the closeness and emotional support of one another to rework the especially traumatic episodes they had experienced together. The epitaph for the Vietnam veteran, however, was a solitary plane ride home with

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complete strangers and a head full of grief, conflict, confusion and joy.

For every Vietnam combatant, the DEROS date became a fantasy that on a specific day all problems would cease as he flew swiftly back to the United States. The combatants believed that neither they as individuals nor the United States as a society had changed in their absence.

Hundreds of thousands of men lived this fantasy from day to day.

The universal popularity of shorttimer calendars is evidence of this.

A short-timer was a GI who was finishing his tour overseas. The calendars intricately marked off the days remaining of his overseas tour in all manner of designs with 365 spaces to fill in to complete the final design and mark that final day. The GIs overtly displayed these calendars to one another. Those with the shortest time left in the country were praised by others and would lead their peers on a fantasy excursion of how wonderful and carefree life would be as soon as they returned home. For many, this became an almost daily ritual. For those who may have been struggling with a psychological breakdown due to the stresses of combat, the DEROS fantasy served as a major prophylactic to actual overt symptoms of acute combat reaction. For these veterans, it was a hard-fought struggle to hold on until their time came due.

The vast majority of veterans did hold on as evidenced by the low neuropsychiatric casualty rates during the war (The Presidentâ&#x20AC;&#x2122;s

CHAP TER THREE 45

Studies from past wars point to the concept of how unit integrity acts as a buffer against the overwhelming stresses of combat.

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Commission on Mental Health, 1978). Rates of acute combat reaction or acute post-traumatic stress disorder were significantly lowered relative to the two previous wars. As a result, many combatants, who in previous wars might have become psychological statistics, held on somewhat tenuously until the end of their tours in Vietnam.

The struggle for most was an uphill battle. Those motivators that keep the combatant fighting—unit espirit de corps, small group solidarity and an ideological belief that this was the good fight—were not present in Vietnam. Unit espirit was effectively slashed by the DEROS system. Complete strangers, often GIs who were strangers even to a specific unit’s specialty, were transferred into units whenever individual rotations were completed.

Veterans who had finally reached a level of proficiency had also reached their DEROS date and were rotated. Green troops or “fucking new guys” with almost no experience in combat were thrown into their places. These FNGs were essentially avoided by the unit, at least until after a few months of experience; “short timers” did not want to get themselves killed by relying on inexperienced replacements. Needless to say, the unit culture or espirit was often lost in the lack of communication with the endless leavings and arrivals.

There were other unique aspects of group dynamics in Vietnam. Seasoned troops would stick together, often forming very close small groups for short periods, a normal combat experience noted in previous wars. Some groups formed along racial lines due to lack of unit cohesion within combat outfits. As a seasoned veteran got down to his last two months in Vietnam, he was struck by a strange malady known as the “short timer’s syndrome.” He would be withdrawn from the field and, if logistically possible, would be settled into a comparatively safe setting for the rest of his tour. His buddies would be left behind in the field without his skills, and he would be left with mixed feelings of joy and guilt. Interestingly, it was rare that a veteran ever wrote to his buddies still in Vietnam once he returned home. It has been an even rarer experience for two or more to get together following the war. This is a strong contrast to the endless reunions of World War II veterans. Feelings of guilt about leaving one’s buddies to whatever unknown fate in Vietnam apparently proved so strong that many veterans were often too frightened to attempt to find out what happened to those left behind.

Another factor unique to the Vietnam War was that the ideological basis for the war was very difficult to grasp. In World War II, the United States was very clearly threatened by a uniformed and easily recognizable foe. In Vietnam, it was quite the opposite. It appeared that the whole country was hostile to American forces. The enemy was rarely uniformed, and American

CHAP TER THREE 47

troops were often forced to kill women and children combatants. There were no real lines of demarcation, and just about any area was subject to attack.

Most American forces had been trained to fight in conventional warfare, in which other human beings are confronted and a block of land is either acquired or lost in the fray. However, in Vietnam, surprise firing devices such as booby traps accounted for a large number of casualties with the human foe rarely sighted. A block of land might be secured but not held. A unit would pull out to another conflict in the vicinity; and, if it wished to return to the same block of land, it would once again have to fight to take that land. It was an endless war with rarely seen foes and no ground gains, just a constant flow of troops in and out of the country. The only observable outcome was an interminable production of maimed, crippled bodies and countless corpses. Some were so disfigured it was hard to tell if they were Vietnamese or American, but they were all dead. The rage that such conditions generated was widespread among American troops. It manifested itself in violence and mistrust toward the Vietnamese, toward the authorities, and toward the society that sent these men to Vietnam and then would not support them.

Rather than a war with a just ideological basis, Vietnam became a private war of survival for every American individual involved.

What was especially problematic was that this was Americaâ&#x20AC;&#x2122;s first teenage war. The age of the average combatant was close to 20. According to Wilson, this period for most adolescents involves a psychosocial moratorium, during which the individual takes some time to establish a more stable and enduring personality structure and sense of self. Unfortunately for the adolescents who fought the war, the role of combatant versus survivor, as well as the many ambiguous and conflicting values associated with these roles, let to a clear disruption of this moratorium and to the many subsequent problems that followed for the young veterans.

Many men, who had either used drugs to deal with the overwhelming stresses of combat or developed other behavioral symptoms of similar stress-related etiology, were not recognized as struggling with acute combat reaction or post-traumatic stress disorder, acute subtype. Rather, their immediate behavior had proven to be problematic to the military, and they were offered an immediate resolution in the form of administrative discharges, often with diagnoses of character disorders.

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DISTRIBUTION OF INJURY AMONG INJURED SOLDIERS ACCORDING TO PTSD STATUS Improvised explosive device

No PTSD

Gunshot

PTSD

Mortar

Rocket-propelled grenade

Other grenade

Fragments from blast

Motor vehicle crash

Blunt trauma 0

10 PTSD

NO PTSD

20

30

40

50

Data are from the Navy-Marine Corps Combat Trauma Registry Expeditionary Medical Encounter Database.

The administrative discharge proved to be another method to temporarily repress any further overt symptoms. It provided yet another means of ending the stress without becoming an actual physical or psychological casualty. It, therefore, served to lower the actual incidence of psychological breakdown, as did the DEROS. Eventually, this widely used practice came to be questioned, and it was recognized that it had been used as a convenient way to eliminate many individuals who had major psychological problems dating from their combat service.

When the veteran finally returned home, his fantasy about his DEROS date was replaced by a rather harsh reality. As previously stated, World War II vets took weeks, sometimes months, to return home with their buddies.

Vietnam vets returned home alone. Many made the transition from rice paddy to Southern California in less than 36 hours. The civilian population of the World War II era had been treated to movies about the struggles

CHAP TER THREE 49

of readjustment for veterans (i.e. The Man In The Grey Flannel Suit, The Best Years of Our Lives, Pride of The Marines) to prepare them to help the veteran. The civilian population of the Vietnam era was treated to the horrors of the war on the six oâ&#x20AC;&#x2122;clock news. They were tired and numb to the whole experience. Some were even fighting mad, and many veterans came home to witness this fact. Some World War II veterans came home to victory parades. Vietnam veterans returned in defeat and witnessed anti-war marches and protests. For World War II veterans, resort hotels were taken over and made into redistribution stations to which veterans could bring their wives and devote two weeks to the initial homecoming. For Vietnam veterans, there were screaming anti-war crowds and locked military bases where they were processed back into civilian life in two or three days.

Those veterans who were struggling to make it back home finally did. However, they had drastically changed, and their world would never seem the

50 BL ACKOUT

same. Their fantasies were just that: fantasy. What they had experienced in Vietnam and on their return to their homes in the United States would leave an indelible mark that many may never erase.

THE CATALYSTS OF POST-TRAUMATIC STRESS DISORDERS FOR VIETNAM COMBAT VETERANS More than 8.5 million individuals served in the U.S. Armed Forces during the Vietnam era, 1964-1973. Approximately 2.8 million served in Southeast Asia. Of the latter number, almost one million saw active combat or were exposed to hostile, life-threatening situations. It is this writerâ&#x20AC;&#x2122;s opinion that the vast majority of Vietnam era veterans have had a much more problematic readjustment to civilian life than did their World War II and Korean War counterparts. This was due to the issues already discussed in this chapter, as well as to the state of the economy and the inadequacy of the GI Bill in the early 1970s. In addition, the combat veterans of Vietnam, many of whom immediately tried to become assimilated back into the peacetime culture, discovered that their outlook and feelings about their relationships and future life experiences had changed immensely. According to the fantasy, all was to be well again when they returned from Vietnam. The reality for many was quite different.

A number of studies point out that those veterans subjected to more extensive combat show more problematic symptoms during the period of readjustment. The usual pattern has been that of a combat veteran in Vietnam who held on until his DEROS date. He was largely asymptomatic at the point of his rotation back to the United States for the reasons previously discussed; on his return home, the joy of surviving continued to suppress any problematic symptoms. However, after a year or more, the veteran would begin to notice some changes in his outlook. But, because there was a time limit of one year after which the Veterans Administration would not recognize neuropsychiatric problems as service-connected, the veteran was unable to get service-connected disability compensation.

Treatment from the VA was very difficult to obtain. The veteran began to feel depressed, distrustful, cynical and restless. He experienced problems with sleep and with his temper. Strangely, he became somewhat obsessed with his combat experiences in Vietnam. He would also begin to question why he survived when others did not.

For approximately 500,000 veterans of the combat in Southeast Asia, this problematic outlook has become a chronic lifestyle affecting not only the veterans but countless millions of persons who are in contact with these veterans. The symptoms described below are experienced by all Vietnam combat veterans to varying degrees. However, for some with the most ex-

CHAP TER THREE 51

DISTRIBUTION OF CLINICAL CHARACTERISTICS IN INJURED MILITARY PERSONNEL ACCORDING TO PTSD STATUS 1

CHARACTERISTIC

PTSD (N=243)

No PTSD (N=453)

Age—Yr.

24.1±5.9

24.3±5.2

Male sex—no./total no. (%)

199/204 (98)

4 45/449 (99)

<9

176/242 (73)

276/452 (61)

10–16

49/242 (20)

122/452 (27)

>16

17/242 (7)

5 4/452 (12)

Amputation—no. (%)

4 (2)

24 (5)

Mild traumatic brain injury—no. (%)

28 (12)

41 (9)

Glasgow Coma Scale score 3

14.6±1.8

14.7±1.6

Injury Severity Score 2—no./total no. (%)

1 D ata are from the Navy-Marine Corps Combat Trauma Registry Expeditionary Medical Encounter Database 2 The Injury Severity Score provides an assessment of overall severity for patients with multiple injuries. The range of scores is 0–75, with 75 indicating the greatest overall severity of injuries.

3 The Glasgow Coma Scale is an indicator of consciousness ranging from 3 to 15, with 3 signifying deep unconsciousness and 15 normal mental status.

tensive combat histories and other variables which have yet to be enumerated, Vietnam-related problems have persisted in disrupting all areas of life experience. According to Wilson, the number of veterans experiencing these symptoms will climb until 1985, based on his belief of Erickson’s psychosocial developmental stages and how far along in these stages most combat veterans will be by 1985. Furthermore, without any intervention, what was once a reaction to a traumatic episode may for many become an almost unchangeable personality characteristic.

THE SYMPTOMS OF PTSD Chronic and/or Delayed Depression The vast majority of the Vietnam combat veterans I have interviewed are depressed. Many have been continually depressed since their experiences in Vietnam. They have the classic symptoms of sleep disturbance, psychomotor retardation, feelings of worthless-

52 BL ACKOUT

ness, difficulty in concentrating, etc. Many of these veterans have weapons in their possession, and they are no strangers to death. In treatment, it is especially important to find out if the veteran keeps a weapon in close proximity, because the possibility of suicide is always present.

When recalling various combat episodes during an interview, the veteran with a post-traumatic stress disorder almost invariably cries. He usually has had one or more episodes in which one of his buddies was killed. When asked how he handled these death when in Vietnam, he will often answer, “in the shortest amount of time possible.” Due to circumstances of war, extended grieving on the battlefield is very unproductive and could become a liability. Hence, grief was handled as quickly as possible, allowing little or no time for the grieving process. Many men reported feeling numb when this happened. When asked how they are now dealing with the deaths of their buddies in Vietnam, they invariably answer that they are not. They feel depressed; “How can I tell my wife, she’d never understand?” they ask.

“How can anyone who hasn’t been there understand?”

Accompanying the depression is a very well developed sense of helplessness about one’s condition. Vietnam-style combat held no final resolution of conflict for anyone. Regardless of how one might respond,t he overall outcome seemed to be just an endless production of casualties with no perceivable goals attained. Regardless of how well one worked, sweated, bled and even died, the outcome was the same. Our GIs gained no ground; they were constantly rocketed or mortared. They found little support from their “friends and neighbors” back home, the people in whose name so many were drafted into military service. They felt helpless. They returned to the United States, trying to put together some positive resolution of this episode in their lives, but the atmosphere at home was hopeless.

Many veterans report becoming extremely isolated when they are especially depressed. Substance abuse is often exaggerated during depressive periods. Self medication was an easily learned coping response in Vietnam; alcohol appears to be the drug of choice.

Isolation Combat veterans have few friends. Many veterans who witnessed traumatic experiences complain of feeling like old men in young men’s bodies. They feel isolated and distant from their peers. The veterans feel that most of their non-veteran peers would rather not hear what the combat experience was like; therefore, they feel rejected. Much of what many of these veterans had done during the war would seem like horrible crimes to their civilian peers. But, in the reality faced by Vietnam combatants, such actions were frequently the only means of survival.

CHAP TER THREE 53

Many veterans find it difficult to forget the lack of positive support they received from the American public during the war. This was especially brought home to them on the return from the combat zone to the United States.

Many were met by screaming crowds and the media calling them “depraved fiends” and “psychopathic killers.” Many personally confronted hostility from friends and family, as well as strangers. After their return home, some veterans found that the only defense was to search for a safe place. These veterans found themselves crisscrossing the continent, always searching for that place where they might feel accepted. Many veterans cling to the hope that they can move away from their problems. It is not unusual to interview a veteran who, either alone or with his family, has effectively isolated himself from others by repeatedly moving from one geographical location to another. The stress on his family is immense. The fantasy of living the life of a hermit plays a central role in many veterans’ daydreams.

Many admit to extended periods of isolation in the mountains, on the road, or just behind a closed door in the city. Some veterans have actually taken a weapon and attempted to live off the land.

It is not rare to find a combat veteran who has not had a social contact with a woman for years—other than with a prostitute, which is an accepted military procedure in the combat setting. If the veteran does marry, his wife will often complain about the isolation he imposes on the marital situation.

The veteran will often stay in the house and avoid any interactions with others. He also resents any interactions that his spouse may initiate. Many times, the wife is the source of financial stability.

Rage The veterans’ rage is frightening to them and to others around them.

For no apparent reason, many will strike out at whomever is near. Frequently, this includes their wives and children. Some of these veterans can be quite violent. This behavior generally frightens the veterans, apparently leading many to question their sanity; they are horrified at their behavior.

However, regardless of their afterthoughts, the rage reactions occur with frightening frequency.

Often veterans will recount episodes in which they became inebriated and had fantasies that they were surrounded or confronted by enemy Vietnamese. This can prove to be an especially frightening situation when others confront the veteran forcibly. For many combat veterans, it is once again a life-and-death struggle, a fight for survival.

Some veterans have been able to sublimate their rage, breaking inanimate objects or putting fists through walls. Many of them display bruises and cuts on their hands. Often, when these veterans feel the rage emerging, they

54 BL ACKOUT

will immediately leave the scene before somebody or something gets hurt; subsequently, they drive about aimlessly. Quite often, their behavior behind the wheel reflects their mood. A number of veterans have described to me the verbal catharsis they’ve achieved in explosions of expletives directed at any other drivers who may wrong them.

There are many reasons for the rage.

Military training equated rage with masculine identity in the performance of military duty. Whether one was in combat or not, the military experience stirred up more resentment and rage than most had ever felt. Finally, when combat in Vietnam was experienced, the combatants were often left with wild, violent impulses and no one upon whom to level them. The nature of guerrilla warfare—with its use of such tactics as booby trap land mines and surprise ambushes with the enemy’s quick retreat—left the combatants feeling like time bombs; the veterans wanted to fight back, but their antagonists had long since disappeared. Often they unleashed their rage at indiscriminate targets for want of more suitable targets.

On return from Vietnam, the rage that had been tapped in combat was displaced against those in authority. It was directed against those the veterans felt were responsible for getting them involved in the war in the first place—and against those who would not support the veterans while they were

CHAP TER THREE 55

in Vietnam or when they returned home. Fantasies of retaliation against political leaders, the military services, the Veterans Administration and anti-war protesters were present in the minds of many of these Vietnam combat veterans.

Along with the rage at authority figures from the Vietnam era, these veterans today often feel a generalized distrust of anyone in authority and the “system” in the present era. Many combat veterans with stress disorders have a long history of constantly changing their jobs. It is not unusual to interview a veteran who has had 30 to 40 jobs during the past 10 years.

One veteran I interviewed had nearly 80 jobs in a 10-year span. The rationale quite often given by the veterans is that they became bored or the work was beneath them. However, after I made some extended searches into their work backgrounds, it became apparent that they felt deep distrust for their employers and coworkers; they felt used and exploited; at times, such was the case. Many have had some uncomfortable confrontations with their employers and job peers, and many have been fired or have resigned on their own.

Avoidance of Feelings: Alienation The spouses of many of the veterans I have interviewed complain that the men are cold, uncaring individuals. Indeed the veterans themselves will recount episodes in which they did not feel anything when they witnessed the death of a buddy in combat or the more recent death of a close family relative. They are often somewhat troubled by these responses to tragedy; but, on the whole, they would rather deal with tragedy in their own detached way. What becomes especially problematic for these veterans, however, is an inability to experience the joys of life.

They often describe themselves as being emotionally dead.

The evolution of this emotional deadness began for Vietnam veterans when they first entered military boot camp. There they learned that the Vietnamese were not to be labeled as people but as “gooks, dinks, slopes, zipperheads and slants.” This dehumanization gradually generalized to the whole Vietnam experience. The American combatants themselves became “grunts,” the Viet Cong became “Victor Charlie,” and both groups were either “KIA” (killed in action) or “WIA” (wounded in action). Often, many “slopes” would get “zapped” (killed) by a “Cobra” (gunship), and the “grunts” would retreat by “Shithook” (evacuation by a Chinook helicopter); the jungle would be sown by “Puff the Magic Dragon” (a C-47 gunship with rapid-firing mini-gattling guns).

The pseudonyms served to blunt the anguish and the horror of the reality of combat. In conjunction with this almost surreal aspect of the fighting, psychic numbing furthered the coping and survival ability of the combat-

56 BL ACKOUT

ants by effectively knocking the aspect of feelings out of their cognitive abilities. This defense mechanism of survivors of traumatic experiences dulls an individual’s awareness of the death and destruction about him. It is a dynamic survival mechanism, helping one to pass through a period of trauma without becoming caught up in its tendrils. Psychic numbing only becomes nonproductive when the period of trauma is passed, and the individual is still numb to the affect around him.

Many veterans find it extremely uncomfortable to feel love and compassion for others. To do this, they would have to thaw their numb reactions to the death and horror that surrounded them in Vietnam. Some veterans I’ve interview actually believe that if they once again allow themselves to feel, they may never stop crying or may completely lose control of themselves; what they mean by this is unknown to them. Therefore, many of these veterans go through life with an impaired capacity to love and care for others. they have no feeling of direction or purpose in life. They are not sure why they even exist.

Survival Guilt When others have died and some have not, the survivors often ask, “How is it that I survived when others more worthy than I did not?” Survival guilt is an especially guilt-invoking symptom. It is not based on anything hypothetical. Rather, it is based on the harshest of realities, the actual death of comrades and the struggle of the survivor to live. Often the survivor has had to compromise himself or the life of someone else in order to live. The guilt that such an act invokes or guilt over simply surviving may eventually end in self-destructive behavior by the survivor.

Many veterans, who have survived when comrades were lost in surprise ambushes, protracted battles or even normal battlefield attrition, exhibit self-destructive behavior. It is common for them to recount the combat death of someone they held in esteem; and, invariably, the questions comes up, “Why wasn’t it me?” It is not unusual for these men to set themselves up for hopeless physical fights with insurmountable odds. “I don’t know why, but I always pick the biggest guy,” said the veteran in the transcript at the beginning of this chapter. Shatan notes that some of these men become involved in repeated single-car accidents. This writer interviewed one surviving veteran, whose company suffered over 80% casualties in one ambush. The veteran had had three single-car accidents during the previous week, two the day before he came in for the interview.

He was wondering if he were trying to kill himself.

I have also found that those veterans who suffer the most painful survival guilt are primarily those who served as corpsmen or medics. These unfortunate veterans were trained for a few months to render first aid on the

CHAP TER THREE 57

actual field of battle. The services they individually performed were heroic.

With a bare amount of medical knowledge and large amounts of courage and determination, they saved countless lives. However, many of the men they tried to save died. Many of these casualties were beyond all medical help, yet many corpsmen and medics suffer extremely painful memories to this day, blaming their â&#x20AC;&#x153;incompetenceâ&#x20AC;? for these deaths.

Another less destructive trend that I have noticed exists among a small number of Vietnam combat veterans who have become compulsive blood donors. One very isolated and alienated individual I interviewed actually drives some 80 miles round-trip once every other month to make his donation. His military history reveals that he was one of 13 men out of a 60-man platoon who survived the Battle of Hue. He was the only survivor who was not wounded. This veteran and similar vets talk openly about their guilt, and they find some relief today in giving their blood that others may live.

Anxiety Reactions Many Vietnam veterans describe themselves as very vigilant human beings; their autonomic senses are tuned to anything out of the ordinary. A loud discharge will cause many of them to start. A few will actually take such evasive action as falling to their knees or to the ground. Many veterans become very uncomfortable when people walk closely behind them. One veteran described his discomfort when people drive directly behind him. He would pull off the road, letting others pass, when they got within a few car lengths of him.

Some veterans are uncomfortable when standing out in the open. Many are uneasy when sitting with others behind them, often opting to sit up against something solid, such as a wall. The bigger the object is, the better.

Many combat veterans are most comfortable when sitting in the corner in a room, where they can see everyone about them.

Sleep Disturbance and Nightmares Few veterans struggling with posttraumatic stress disorders find the hours immediately before sleep very comfortable. In fact, many will stay awake as long as possible. They will often have a drink or smoke marijuana to dull any uncomfortable cognition that may enter during this vulnerable time period. Many report that they have nothing to occupy their minds at the end of the dayâ&#x20AC;&#x2122;s activities, and their thoughts wander. For many of them, it is a trip back to the battle zone. Very often they will watch TV late into the mornings.

Finally, with sleep, many veterans report having dreams about being shot at or being pursued and left with an empty weapon, unable to run anymore.

Recurrent dreams of specific traumatic episodes are frequently reported. It is not unusual for a veteran to reexperience, night after night, the death

58 BL ACKOUT

of a close friend or a death that he caused as a combatant. Dreams of everyday, common experiences in Vietnam are also frequently reported. For many, just the fear that they might actually be back in Vietnam is very disquieting.

Some veterans report being unable to remember their specific dreams, yet they feel dread about them.

Wives and partners report that the men sleep fitfully, and some call out in agitation. A very few actually grab their partners and attempt to do them harm before they have fully awakened. Finally, maintaining sleep has proven to be a problem for many of these veterans. They report waking up often during the night for no apparent reason. Many rise quite early in the morning, still feeling very tired.

Intrusive Thoughts Traumatic memories of the battlefield and other less affect-laden combat experiences often play a role in the daytime cognitions of combat veterans. Frequently, these veterans report replaying especially problematic combat experiences over and over again.

Many search for possible alternative outcomes to what actually happened in Vietnam. Many castigate themselves for what they might have done to change the situation, suffering subsequent guilt feelings today because they were unable to do so in combat. The vast majority report that these thoughts are very uncomfortable, yet they are unable to put them to rest.

CHAP TER THREE 59

Many of the obsessive episodes are triggered by common, everyday experiences that remind the veteran of the war zone: helicopters flying overhead, the smell of urine (corpses have no muscle tone, and the bladder evacuates at the moment of death), the smell of diesel fuel (the commodes and latrines contained diesel fuel and were burned when filled with human excrement), green tree lines (these were searched for any irregularity which often meant the presence of enemy movement), the sound of popcorn popping (the sound is very close to that of small arms gunfire in the distance), any loud noise, a rainy day and finally the sight of refugees.

A few combat veterans find the memories invoked by some of these and other stimuli so uncomfortable that they will actually go out of their way to avoid them. When exposed to one of the above or similar stimuli, a very small number of combat veterans undergo a short period of time in a dissociative-like state in which they actually reexperience past events in Vietnam. These flashbacks can last anywhere from a few seconds to a few hours. One veteran described an episode to me in which he had seen some armed men and felt he was back in Vietnam. The armed men were police officers. Not having a weapon to protect himself and others, he grabbed a passerby and forcefully sheltered this person in his home to protect him from what he felt were the â&#x20AC;&#x153;gooks.â&#x20AC;?

Such experiences among Vietnam veterans are rare, but not as uncommon as many may believe. Many veterans report flashback episodes that last only a few seconds. For many, the sound of a helicopter flying overhead is a cue to forget reality for a few seconds and remember Vietnam, reexperiencing

PHYSIOLOGICAL RESPONSES TO TRAUMA-RELATED MENTAL IMAGING

Heart rate

0

3

6

9

12

BEATS PER MINUTE

SURVIVORS WITHOUT PTSD

60 BL ACKOUT

SURVIVORS WITH PTSD

15

feelings they had there. It is especially troublesome for those veterans who are still “numb” and specifically attempting to avoid these feelings. For others, it is just a constant reminder of their time in Vietnam, something they will never forget.

Referrals For Help As already discussed, post-traumatic stress disorders result in widely varying degrees of impairment. When a single veteran (whether bachelor or divorced) with the disorder requests help, he is referred to a group of other combat veterans. The reasons are twofold.

First, the veteran is usually quite isolated and has lost many of his social skills. He has few contacts with other human beings. The group provides a microcosm in which he can again learn how to interact with other people.

It also helps remove the fear, prevalent among these veterans, that each individual veteran is the only individual with these symptoms. In addition, many of the veterans form close support groups of their own outside the therapy sessions; they telephone each other and help each other through particularly problematic episodes.

Second, the most basic rationale for group treatment of these veterans is that it finally provides the veteran with that “long boat ride home” with other veterans who have had similar experiences. It provides a forum in which veterans troubled by their combat experiences can work their feelings through with other veterans who have had similar conflicts. In addition, the present symptoms of the disorder are all quite similar, and there is more reinforcement in working through these symptoms with one’s peers than in doing it alone.

The group situation is appropriate for most degrees of the symptoms presented. The especially isolated individuals will often be quite frightened of the initial group session. When challenged by questioning the strength that brought them to the initial interview, however, they will usually respond by following through with the group. Those with severely homicidal or suicidal symptoms are best handled in a more crisis-oriented, one-toone setting until the crisis is resolved. I refer these veterans to an appropriate emergency team, with the expectation directly shared with the veteran that he will join the group as soon as the crisis has abated.

Veterans who are presently married or living with a partner present a somewhat different picture. Their relationships with their partners are almost invariably problematic. Frequently, a violent, explosive episode at home created the crisis that brought the veteran in for counseling in the first place. When such is the case or there is a history of battering of the partner, it is extremely important to refer the veteran and his partner to a family disturbance counseling center. The consequences of this contin-

CHAP TER THREE 61

ued behavior are obvious. In addition, a referral for the veteran to a group with other combat veterans is appropriate. The partner of the veteran may find some understanding of her plight and additional support from a womanâ&#x20AC;&#x2122;s group created specifically for partners of Vietnam combat veterans.

Other veterans who are married or living with a partner may not be experiencing so serious a problem.

However, the partners are often detached from one another; they just seem to live under the same roof, period. Referral of the veteran to a combat veterans group and referral of the partner to a partners of Vietnam veterans group is important.

Some veterans and their partners will jointly attend the screening session. Both are troubled by what has been happening and often want to enter marital therapy together immediately. In my experience, the veteran finds it extremely difficult in the beginning of therapy to deal with interactional aspects with his partner when other past interactions with traumatic overtones overshadow the present. When these traumatic experiences do surface, the partner is often unable to relate. Therefore, it is much more beneficial, in my opinion, to allow the veteran time with other combat veterans in a group. In the meantime, suggest a womanâ&#x20AC;&#x2122;s support group for partners of Vietnam veterans for the spouse. Here she would receive additional support as well as an understanding of PTSD.

62 BL ACKOUT

WAR-ZONE-RELATED STRESS REACTIONS Traumas are events in which a person has the feeling that he or she may die or be seriously injured or harmed, or events in which he or she witnesses such things happening to others. Traumatic events are of course common in the war zone, but they are common in the civilian world too, so that in addition to war zone experiences, many military personnel will have experienced one or more traumatic events in their civilian lives.

When they are happening, traumas often create feelings of intense fear, helplessness, or horror. Often in the days and weeks that follow trauma, there are longer-lasting stress reactions that can be surprising, distressing, and difficult to understand. By understanding their traumatic stress reactions better, Iraq War veterans can become less fearful of them and better able to cope with them. Traumatic war experiences often cause many of the following kinds of (often temporary) reactions in Veterans.

Unwanted remembering or re-experiencing Almost all Veterans experience difficulty controlling distressing memories of war. Although these memories are upsetting, on the positive side, the memories provide an opportunity for the person to make sense of what happened and gain mastery over the event.

Physical activation or arousal The bodyâ&#x20AC;&#x2122;s fight-or-flight reaction to a lifethreatening situation continues long after the event is over. It is upsetting to feel like your body is overreacting or out of control. However, on the positive side, these fight-or-flight reactions help prepare a person in a dangerous situation for quick response and emergency action.

Shutting down: Emotional numbing When overwhelmed by strong emotions, the body and mind sometimes react by shutting down and becoming numb. As a result, veterans may have difficulty experiencing loving feelings or feeling some emotions, especially when upset by traumatic memories.

Like many of the other reactions to trauma, this emotional numbing reaction is not something the veteran is doing on purpose.

Active avoidance of trauma-related thoughts and feelings Painful memories and physical sensations of fear can be frightening, so it is only natural to try to find ways to prevent them from happening. One way that most veterans do this is by avoiding anything people, places, conversations, thoughts, emotions and feelings, physical sensations that might act as a reminder of the trauma. This can be very helpful if it is used once in a while (e.g., avoiding upsetting news or television programs). But when avoidance is used too much, it can have two big negative effects.

CHAP TER THREE 63

RESPONSE TO TRICYCLIC ANTIDEPRESSANTS IN COMBAT-RELATED PTSD

Amitriptyline Placebo Imipramine Placebo 0

20

40

60

80

100

PERCENTAGE OF RESPONDERS

First, it can reduce veterans abilities to live their lives and enjoy themselves, because they can become isolated and limited in where they go and what they do. Second, avoiding thoughts and emotions connected with the trauma may reduce veterans abilities to recover from it. It is through thinking about what happened, and particularly through talking about it with trusted others, that survivors may best deal with what has happened.

By constantly avoiding thoughts, feelings, and discussions about the trauma, this potentially helpful process can be short-circuited.

Depression Most persons who have been traumatized experience depression. Feelings of depression then lead a person to think very negatively and feel hopeless. There is a sense of having lost things: oneâ&#x20AC;&#x2122;s previous self, a sense of optimism and hope, self-esteem, and self-confidence. With time, and sometimes with the help of counseling, the trauma survivor can regain self-esteem, self-confidence, and hope. It is important to let others know about feelings of depression and, of course, about any suicidal thoughts and feelings, which are sometimes a part of feeling depressed.

Self-blame, guilt, and shame Many veterans, in trying to make sense of their traumatic war experiences, blame themselves or feel guilty in some way. They may feel bad about some thing(s) they did or didnâ&#x20AC;&#x2122;t do in the war zone. Feelings of guilt or self-blame cause much distress and can prevent a person from reaching out for help.

Interpersonal problems Not surprisingly, the many changes noted above can affect relationships with other people. Trauma may cause difficulties between a veteran and his or her partner, family, friends, or co-workers.

64 BL ACKOUT

Particularly in close relationships, the emotional numbing and feeling of disconnection that are common after traumatic events may create distress and drive a wedge between the survivor and his or her family or close friends. The survivor’s avoidance of different kinds of social activities may frustrate family members. Sometimes, this avoidance results in social isolation that hurts relationships.

Others may respond in ways that worsen the problem rather than help recovery. They may have difficulty understanding, become angry with the veteran, communicate poorly, and fail to provide support. Partners and families need to participate in treatment; by learning more about traumatic stress, they can often become more understanding of the veteran and feel more able to help. Some kinds of traumatic experiences (e.g., sexual assault) can make it hard to trust other people.

Physical symptoms and health problems Because many traumas result in physical injury, pain is often part of the experience of survivors. This physical pain often causes emotional distress, because in addition to causing pain and discomfort, the injury also reminds them of their trauma. Because traumas stress the body, they can sometimes affect physical health, and survivors may experience stress-related physical symptoms such as headaches, nausea or other stomach problems, and skin problems. The veteran with PTSD will need to care for his or her health, seek medical care when appropriate, and inform the doctor or nurse about his or her traumas, in order to limit the effects of the trauma.

Except for some help with an immediate crisis upon being first interviewed during the screening session, the combat veteran struggling with the symptoms of post-traumatic stress disorder, chronic and/or delayed, benefits most from group interaction with his combat peers. Throughout this paper I have emphasized the individual, solitary aspect of the war for each veteran. The aftermath of the war has followed in kind. Now, with the help from the DAV Vietnam Veterans Outreach Program and the VA’s Operation Outreach (Vet Center) program, models have been established for reintegrating troubled Vietnam veterans with themselves and their society. Helping the community to recognize the problem and directing the veteran to the specialized services of the community have given the veteran struggling with this disorder a means of “coming home.”

CHAP TER THREE 65

4

MORPHINE USE AFTER COMBAT INJURY IN IRAQ Troy Lisa Holbrook, PhD, Michael R. Galarneau, MS, Judy L. Dye, MS, RN, ANP, Kimberly Quinn, BSN, and Amber L. Dougherty, MPH

Post-traumatic stress disorder (PTSD) is a common adverse mental health outcome among seriously injured civilians and military personnel who are survivors of trauma. Pharmacotherapy in the aftermath of serious physical injury or exposure to traumatic events may be effective for the secondary prevention of PTSD. xyxyxy xxyxyxyx xyx xyx xyxyxy xyxyxyx xxy We identified 696 injured U.S. military personnel without serious traumatic brain injury from the Navyâ&#x20AC;&#x201C;Marine Corps Combat Trauma Registry Expeditionary Medical Encounter Database. Complete data on medications administered were available for all personnel selected. xyxyx xyxyxyxyx xyxyx xyxyx xyxyxyx yxyyxyxyxyx xxyxyxyxyyxx xyxyyxxyxyxyxy. The diagnosis of PTSD was obtained from the Career History Archival Medical and Personnel System and verified in a review of medical records. Among the 696 patients studied, 243 received a diagnosis of PTSD and 453 did not. The use of morphine during early resuscitation and trauma care was significantly associated with a lower risk of PTSD after injury. Among the patients in whom PTSD developed, 61% received morphine; among those in whom PTSD did not develop, 76% received morphine (odds ratio, 0.47; P<0.001). This association remained significant after adjustment for injury severity, age, mechanism of injury, status with respect to amputation, and selected injury-related clinical factors. xyxyxy xxyxyxyx xyxyx x xyy xyyxyxyx xyyxx yxxyxy xyxx yxyxyxyyx xxyxyyx xx xyyxyx x x xyxyxyxyxyx xyxyx xyxyx xxyyxyx xyxyx xyxyxyx xyxyxyx yxyxyx xyxyyxyxyxyxyx xyxyxyx x. Our findings suggest that the use of morphine during trauma care may reduce the risk of subsequent development of PTSD after serious injury.

CHAP TER FOUR 67

Post-traumatic stress disorder (PTSD) is an important and well-documented mental health outcome among seriously injured civilian and military survivors of trauma. Increasing recognition of the profound and prolonged detrimental effects on general health status and quality of life when PTSD develops in the aftermath of serious physical injury or exposure to traumatic events has made its prevention a focus of research on trauma-related outcomes. The secondary prevention of PTSD with pharmacotherapy in the aftermath of major trauma is a newly evolving and important area of research.

Current knowledge of the pathogenesis and neurobiology of PTSD provides a strong theoretical basis for the role of pharmacotherapy in the secondary prevention of PTSD after major trauma. The primary aim of pharmacotherapy is to decrease or impede memory consolidation and the associated conditioned response to fear after a person goes through a traumatic event. This strategy is based on the hypothesis that pharmacotherapeutic agents such as opiates, anxiolytics, and beta-adrenergic antagonists may be effective in preventing the onset of PTSD. However, few studies have examined the efficacy of psychotherapeutic medications in the secondary prevention of PTSD that develops in the aftermath of major trauma.

Saxe and colleagues reported a protective effect of morphine against the onset of PTSD in children with burn injuries. Studies of other putative psychotherapeutic agents, including benzodiazepines and propranolol, have yielded inconsistent results. Little is known about the effect of morphine administration as part of trauma care on the rates of PTSD among seriously injured adults.

The U.S. Navy–Marine Corps Combat Trauma Registry Expeditionary Medical Encounter Database (CTR EMED) is a comprehensive prospective clinical database designed to preserve clinical records of casualties incurred in the Iraq military theater both during and outside of battle. We examined the effect of morphine use during early resuscitation and trauma care on the risk of PTSD in injured military personnel, using data from the Navy–Marine Corps CTR EMED. METHODS Study Population We identified injured military personnel for the study from those who were brought to forward medical treatment facilities (i.e., facilities closest to the point of injury) with injuries incurred during the major combat or support phases of Operation Iraqi Freedom, defined here as the 36-month period from January 2004 through December 2006. Medical treatment facilities located throughout the U.S. Navy–Marine Corps area of responsibility in Iraq provide initial resuscitative treatment for U.S. Army, Navy, and Marine Corps personnel arriving directly from the point of

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injury, as well as damage-control surgery, additional medical assessment, and stabilization for patients in need of evacuation. During the period from January 2004 through December 2006, these facilities included battalion aid stations (considered level 1 medical treatment facilities), forward resuscitative surgical-system facilities (level 2), and two surgical companies (level 2).

INJURY-SPECIFIC DATA Clinical data were obtained from the Navy–Marine Corps CTR EMED. The registry contains information collected from medical encounter forms used at forward medical treatment facilities in Iraq and from clinical records retained at U.S. Army theater hospitals (level 3) and the American hospital (level 4) at Landstuhl Regional Medical Center in Germany. The encounter form, a modified version of the Army Theater Trauma Registry, captures demographic data, time of arrival at the treatment facility, detailed information on the mechanism of injury, and comprehensive treatment data, including medications administered during early resuscitation and trauma care, dosages, route of administration, and interval between arrival at the facility and initiation of treatment. Encounter forms are completed either on paper or electronically by health care providers in the Iraqi theater and are forwarded to the Navy–Marine Corps CTR EMED at the Naval Health Research Center. One purpose of the database is to analyze patterns of combat injury and casualty management from the point of injury through the rehabilitative outcome, with a particular emphasis on the clinical events occurring at or near the point of injury.

The severity of injuries is assessed by trained clinical staff at the Navy–Marine Corps CTR EMED with the use of the Abbreviated Injury Scale and the Injury Severity Score. For the Abbreviated Injury Scale, each injury is assigned to one of six categories based on body location (head, face, chest, abdomen, extremities and pelvis, and skin) and is assessed with respect to clinical severity on a scale of 1 (relatively minor) to 6 (currently untreatable). The Injury Severity Score, which is derived from the scores on the Abbreviated Injury Scale for individual injuries, provides an assessment of overall severity for patients with multiple injuries. The range of scores for the Injury Severity Score is 0 to 75, with 75 indicating the greatest overall severity of injuries.

Of the 790 injured military personnel identified for potential inclusion in the study, we excluded 60 because they had serious traumatic brain injury and 34 because clinical or medication-related data were not complete. The focus of this report is the 696 injured military personnel with complete medication-related data from the Navy–Marine Corps CTR EMED who did not sustain a serious traumatic brain injury. Complete medication-related data were defined as a CTR EMED patient record with medication data

CHAP TER FOUR 69

coded and entered in the medical record. A serious traumatic brain injury was defined as a head injury with a score of 3 or higher on the Abbreviated Injury Scale and a diagnostic code, based on the International Classification of Diseases, 9th Revision, Clinical Modification, of 800.0 to 801.9 (fractures of the vault or base of the skull), 803.0 to 804.9 (fractures at other or unspecified skull sites and multiple fractures of the skull), 850.0 to 854.1 (intracranial injury, including concussion, contusion, laceration, and hemorrhage), or 873.0 to 873.9 (other open wounds of the head). The rationale for the exclusion of patients with serious traumatic brain injury was that the use of morphine in such patients would be both precluded and unwarranted under current Advanced Trauma Life Support protocols. Mild traumatic brain injury (defined as a score of 1 or 2 on the Abbreviated Injury Scale) and the score on the Glasgow Coma Scale on admission to the medical treatment facility were included as covariates in the analysis.

DATA ON PTSD Data was obtained on diagnoses of PTSD from the Career History Archival Medical and Personnel System and verified by reviewing medical records documented in the Department of Defense Medical Data Repository. The Career History Archival Medical and Personnel System, which is maintained by the Naval Health Research Center, contains personnel records from the Bureau of Naval Personnel and medical data from the Naval Medical Information Management Center. It includes information on all enlisted members on active duty in the U.S. Armed Forces since 1973. Assessments for PTSD were made from 1 to 24 months after the date of injury and were based on the diagnostic criteria detailed in the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV). Diagnoses were made by licensed, credentialed providers at both military treatment facilities and private clinics (with government reimbursement), with the use of inpatient and outpatient records.

RESULTS Characteristics of the patients The mean age was nearly identical in the group of 243 patients with PTSD and the group of 453 patients without PTSD. Of the 653 patients for whom data on sex were available, 99% were men. The Injury Severity Score for 90% of injuries was 16 or less; the remaining 10% of injuries, with a score of more than 16, were considered to be serious, and the rates of serious injury were somewhat higher in PTSDnegative patients (P<0.05). There were no marked or significant differences between PTSD-positive and PTSD-negative patients for the majority of selected clinical and resuscitation-related variables, including mild traumatic brain injury, score on the Glasgow Coma Scale, intubation, and

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ADJUSTED ODDS RATIOS FOR THE ASSOCIATION OF MORPHINE USE WITH THE RISK OF PTSD Models 1 and 2

.49

Morphine use

.66

1.03

Injury Severity Score

1.02

.40

Amputation

.42

.39

Rocket-propelled grenade

.46

.24

Fragments from blast

.30

1.14

Mild traumatic brain injury

1.03

0.0

0.2

0.4

0.6

0.8

1.0

1.2

ADJUSTED ODDS RATIO (95% CONFIDENCE INTERVAL)

chemical paralysis with anesthesia. The rate of amputation was higher among PTSD-negative patients (5%) than among PTSD-positive patients (2%), a difference that was small, although significant (P=0.03).

Mechanism of Injury For all major mechanisms of injury, there were no marked or significant differences according to PTSD status. Major mechanisms of injury for both PTSD-positive and PTSD-negative patients were improvised explosive devices, gunshots, grenades, mortar, and rocketpropelled grenades. Mechanisms of injury and clinical characteristics for all patients included in the analysis did not differ from those in the general patient population represented in the Navyâ&#x20AC;&#x201C;Marine Corps CTR EMED.

CHAP TER FOUR 71

The use of morphine was associated with a significantly reduced risk of PTSD development in injured military personnel.

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USE OF MORPHINE AND OTHER PSYCHOTROPIC MEDICATIONS Morphine use was common in both PTSD-positive and PTSD-negative injured military personnel (in 61% and 76%, respectively). All morphine administration was documented in medical treatment facilities designated as level 1 or level 2, and all morphine was given during resuscitation and trauma care. The transport time from the point of injury to the administration of morphine on arrival at a medical treatment facility was 1 hour or less in 71% of patients. In the study population, doses of morphine (morphine sulfate) were highly standardized, with the modal and median doses equal to 5 mg, and 55% of all morphine doses were between 2 and 5 mg. An additional 33% of doses were between 10 and 20 mg, and doses of more than 20 mg were used infrequently (accounting for only 12% of all doses). The route of administration was intravenous in 98% of patients. The use of other medications with psychotropic effects was uncommon. During resuscitation and trauma care, no patients received serotonin-reuptake inhibitors or beta-blockers.

ASSOCIATION BETWEEN MORPHINE USE AND RISK OF PTSD The use of morphine directly after injury, during resuscitation and early trauma care, was significantly associated with a reduced risk of PTSD (odds ratio, 0.47; P<0.001). This association remained significant and independent after adjustment for injury severity.

Morphine use was independently and significantly associated with a reduced risk of PTSD (odds ratio, 0.49; P<0.001). Sex was not a significant factor in the development of PTSD and was excluded from multivariate

UNADJUSTED AND ADJUSTED ODDS RATIOS FOR THE ASSOCIATION BETWEEN MORPHINE USE AND THE RISK OF PTSD

PTSD (N=243) Morphine use

147 (60)

No PTSD (N=453) 346 (76)

Unadjusted odds ratio (95% CI)

Odds ratio adjusted for ISS (95% CI)

.47 (.34â&#x20AC;&#x201C;.66)

.48 (.34-.68)

CI denotes confidence interval, and ISS Injury Severity Score

CHAP TER FOUR 73

analysis because of the small number of women in the study population.

Since the score on the Glasgow Coma Scale is a diagnostic measure of traumatic brain injury, it was incorporated into an alternative multivariate model (model 2), which did not materially alter the findings with respect to the effect of morphine use on the risk of PTSD (odds ratio, 0.66; P<0.05). Since intubation, use of chemical paralysis with anesthesia, and administration of benzodiazepines are closely correlated with one another, we also chose to enter each of these variables separately into multivariate models, controlling for the Injury Severity Score, status with respect to amputation, mechanism of injury, presence or absence of mild traumatic brain injury, and age (model 1). There was no indication that the protective effect of morphine use was dependent on the dose. PTSD was subsequently diagnosed in 40% of patients who received low doses of morphine (2 to 9 mg), 40% of those who received moderate doses (10 to 20 mg), and 23% of those who received high doses (>20 mg), with no significant difference in rates according to the dose.

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DISCUSSION Our study provides suggestive, observationally-derived evidence that the use of morphine in trauma care may be protective against the subsequent development of PTSD after serious injury. The use of morphine was associated with a significantly reduced risk of PTSD development in injured military personnel.

Very little is known about the effect of morphine use after serious physical injury on PTSD rates among adults. Our findings are supported by a preliminary study by Saxe and colleagues showing that morphine administration in a small sample of children with burn injuries had a significant protective effect against the development of PTSD symptoms at follow-up 6 months after hospitalization. Bryant and colleagues recently reported that the use of morphine had a significant protective effect against PTSD symptoms in injured adults. The results of the study by Bryant support our findings, although the investigators did not report a significant association between morphine use and a diagnosis of PTSDâ&#x20AC;&#x201D;the association was only with the severity of symptoms. However, the time frame of PTSD assessment in the study by Bryant was restricted to the first 3 months after injury, and this methodologic limitation may have accounted for the absence of a significant association with the onset of PTSD. Several reports have suggested that age, sex, and other, injury-related and clinical characteristics may also play an important role in the development of PTSD after serious injury. In our study, adjustment for age, mechanism of injury, and clinical characteristics such as the Injury Severity Score, amputation status, presence or absence of mild traumatic brain injury, score on the Glasgow Coma Scale, intubation status, and use or nonuse of benzodiazepines did not affect the strength of the protective association between morphine use after injury and the subsequent risk of PTSD. Bryant and colleagues did find that patients with mild traumatic brain injury were at increased risk for the onset of PTSD, but this difference in the results of the two studies may be due to differences in the definitions of mild traumatic brain injury and in the methods used for the assessment of PTSD. More research is needed to determine the potential role of the mechanism of injury, Injury Severity Score, and aspects of resuscitation and clinical treatment in the onset of PTSD after serious injury.

CHAP TER FOUR 75

5

PTSD AND DEPRESSION AFTER TRAUMA: UNDERSTANDING COMORBIDITY Meaghan L. O’Donnell, PhD, Mark Creamer, PhD and Phillipa Pattison, PhD

xxyxyx xyxyxyxyxy xyxyxyx xyx xyx yxyxyx x Post-traumatic stress disorder (PTSD) and major depression occur frequently following traumatic exposure, both as separate disorders and concurrently. This raises the question of whether PTSD and depression are separate disorders in the aftermath of trauma or part of a single general traumatic stress construct. xyxyx xyxyx xyxy xyx xyx xyxyxyx yx xyxyx xyx xyxyxyxyx yxxyx yxxyxyx xxyxyx xyx xyxyx xyxyx yx xyx yx This study aimed to explore the relationships among PTSD, depression, and comorbid PTSD/depression following traumatic injury.

A group of 363 injury survivors was assessed just prior to discharge from hospital and 3 and 12 months postinjury. Canonical correlations were used to examine the relationship between PTSD and depression symptom severity and a set of predictor variables. Multinomial logistic regression was used to identify whether the diagnostic categories of PTSD, depression, and comorbid PTSD/depression were associated with different groups of predictors. The majority of psychopathology in the aftermath of trauma was best conceptualized as a general traumatic stress factor, suggesting that when PTSD and depression occur together, they reflect a shared vulnerability with similar predictive variables. xyxy xyxy xyxyxyx xyxyx xxyxyxyxyxyx xyxyxyxyxyx xyxyxyxyx xyx xyx yxyxxxxxxxxxxx However, there was also evidence that in a minority of cases at 3 months, depression occurs independently from PTSD and was predicted by a different combination of variables. While PTSD and comorbid PTSD/depression are indistinguishable, the findings support the existence of depression as a separate construct in the acute, but not the chronic, aftermath of trauma.

CHAP TER FIVE 77

INTRODUCTION It is now well established that post-traumatic stress disorder (PTSD) develops in a significant minority of individuals following exposure to a traumatic experience. PTSD, however, is not the only psychiatric condition that may develop in the aftermath of trauma. On the contrary, comorbidity is the norm rather than the exception. Breslau, for example, found that 83% of her PTSD sample met criteria for at least one other psychiatric disorder, compared with 44% of those without PTSD. The National Comorbidity Survey reported that 88% of men and 79% of women with chronic PTSD met criteria for at least one other psychiatric diagnosis. A comparable Australian study found that another axis I disorder was present over the past 12 months in 85% of male subjects with PTSD and in 80% of female subjects.

In each of those studies, major depression was found to be one of the most prevalent conditions occurring concurrently with PTSD. Several possible causal pathways may explain this association between PTSD and major depression following traumatic exposure. There is evidence that preexisting major depression may render individuals more vulnerable to PTSD in the aftermath of trauma and, conversely, the presence of PTSD may increase the risk for first onset of major depression. These findings— that each disorder seems to increase susceptibility for the other—suggest the possibility of a shared vulnerability for both disorders. In support of this hypothesis is the finding that many risk factors—such as a history of depression, event severity, childhood abuse, and female gender—are risk factors for both PTSD and major depression. Taken together, these findings suggest that comorbid PTSD and depression in the aftermath of trauma may best be conceptualized as a single general traumatic stress construct.

Another possibility is that PTSD and major depression in the aftermath of trauma are separate constructs. An analysis of several different symptom measures following trauma, for example, found that a two-factor model of PTSD and depression provided the best account of the data. The authors argued that if PTSD and major depression together constituted a general psychiatric response to trauma, a single factor would provide the best fit of the data.

If PTSD and depression are, indeed, separate constructs, and exposure to traumatic events independently increases the risk for both, higher rates of depression would be expected in individuals exposed to trauma who did not develop PTSD when compared with individuals with no exposure to trauma. Regrettably, few attempts have been made to systematically examine the psychiatric impact of traumatic events in the absence of PTSD. Several studies of accident victims, however, have reported a high

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incidence of depression at 12 months posttrauma among individuals with no diagnosis of PTSD. Similarly, Shalev found that 29% of trauma survivors with major depression did not have comorbid PTSD and concluded that major depression and PTSD may be independent sequelae of traumatic events. This conclusion, however, is at odds with the findings of Breslau and her colleagues. They found that risk for major depression following trauma only increased in the subset of individuals who developed PTSD; depression did not increase in those who were exposed to trauma but did not develop PTSD. Breslau concluded that the data do not support the hypothesis that PTSD and major depression in trauma victims are influenced by separate vulnerabilities.

The purpose of the current study was to investigate these issues in a population of severely injured trauma survivors. Specifically, we aimed to determine predictors of symptom severity and categorical diagnosis for each condition and their combination (PTSD, depression, and comorbid PTSD/ depression). If PTSD and depression following trauma are, indeed, different constructs, then their symptom severity and diagnostic group should be a function of differential groups of predictors.

PARTICIPANTS A total of 363 consecutive admissions to a level 1 trauma service participated in the current study (88% participation rate). Criteria for inclusion were a physical injury requiring hospitalization for greater than 24 hours, age between 18 and 70, and either no brain injury or mild traumatic brain injury. Written consent was obtained from all participants following a description of the study. Of the 363 participants who completed the intake assessment, 337 completed the 3-month follow-up, 307 completed the 12-month follow-up, and 301 completed all three assessments.

The majority of participants were male (75%), and the average age was 36 years (SD=13.43). Participants spent an average of 10.13 days (SD=9.64) in the trauma center, with 31% requiring an intensive care unit (ICU) admission. The majority of injuries were caused by motor vehicle accidents (74%).

Slightly over half of the participants (56%) met criteria for a mild traumatic brain injury, and 47% were discharged to a rehabilitation facility (rather than being discharged home). These findings were generally consistent with the total population of admissions to the trauma service for the same time period, suggesting that the current sample was representative.

CHAP TER FIVE 79

ASSESSMENT OF PTSD AND DEPRESSION The aim of this study was to explore the relationship between PTSD, depression, and comorbid PTSD/depression, with the interest being more on distinct or overlapping constructs than on the presence or absence of a diagnosis per se. Thus, a decision was taken to include subsyndromal PTSD and minor depression. This overcame the potential problem caused by individuals meeting criteria for PTSD who also had significantly elevated depression levels but did not meet diagnostic criteria for major depression.

By including minor depression, these participants were classified in the comorbid category rather than the PTSD only group.

PTSD was diagnosed by using the Clinician-Administered PTSD Scale for DSM-IV, one of the most widely used structured clinical interviews for diagnosing PTSD. Participants were deemed to have subsyndromal PTSD if they met criteria for the reexperiencing symptom cluster and either the avoidance or arousal symptom clusters. Frequency and intensity scores were summed to obtain a total PTSD severity score.

Depression was diagnosed using the Structured Clinical Interview for DSMIV (SCID). Minor depression was defined according to DSM-IV criteria (the presence of either depressed mood or loss of interest and a total of two to four depressive symptoms). Depression severity was obtained using the Beck Depression Inventory, a widely used, 21-item, self-report scale. Individuals in the comorbid PTSD/depression group met criteria (full or subsyndromal) for both PTSD and depression.

ASSESSMENT OF PREDICTOR VARIABLES Variables selected to predict psychopathology in this study were grouped into four categories: trauma characteristics, individual characteristics, cognitive vulnerabilities, and acute stress responses. Trauma characteristics included length of time in hospital, admission to ICU, and discharge destination (rehabilitation facility or home). The severity of an individualâ&#x20AC;&#x2122;s injuries was measured with the Injury Severity Score, and the presence or absence of a mild traumatic brain injury was noted. Assessment of objective stressor intensity was recorded by using the severity of event scale, which comprises eight items corresponding to major generic stress dimensions.

Individual characteristics included age, gender, and employment status.

Problematic pretrauma alcohol use was assessed with the Alcohol Use Disorders Identification Test. Psychiatric history was measured by using a semistructured interview that asked about past diagnosable psychiatric conditions, psychiatric hospital admissions, and past psychiatric treat-

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PREVALENCE OF FULL AND SUBSYMDROMAL PTSD AND COMORBID PTSD/DEPRESSION 3 months (N=337) DIAGNOSIS

12 months (N=307)

N

%

N

%

251

74

244

79

Full

13

4

13

4

Full and subsymdromal

39

12

26

8

No diagnosis PTSD

COMORBID PTSD/DEPRESSION Full

16

5

19

6

Full and subsymdromal

31

9

22

7

ment. Trauma history was assessed with questions from the PTSD module of the Composite International Diagnostic Interview.

Three post-traumatic cognitive appraisal questions were asked. These assessed perceived control in the hospital (“How much control do you feel you have over what happens to you whilst in hospital?”), anticipated effect of injury (“How much do you think your injuries will affect your life [e.g., work, leisure, relationships] over the next 12 months?”), and anxiety about injury (“How anxious does this, the effect of the injury, make you feel?”).

Each of these questions was rated on a 5-point Likert scale.

The acute stress response included measures of reexperiencing, avoidance, and arousal assessed by using the relevant symptom clusters of the Clinician-Administered PTSD Scale.

PROCEDURE Initial assessments were conducted in the hospital shortly before discharge (a mean of 8 days postinjury). At the time of assessment, patients were hemodynamically stable, relatively pain free, and a minimum of 24 hours post-opioid analgesia.

CHAP TER FIVE 81

Recent data from the national comorbidity survey indicates PTSD prevalence rates are 5% and 10% respectively among American men and women.

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Participants had follow-up assessments 3 and 12 months postinjury.

These assessments were conducted by means of a telephone interview.

Thirty percent of all interviews were audiotaped, with one-third of these being randomly selected for interrater reliability. Agreement on the absence or presence of a Clinician-Administered PTSD Scale diagnosis was 100%, while agreement on the presence/absence of a SCID diagnosis of depression was 98%.

STATISTICAL ANALYSIS Analyses were conducted with SPSS 11.0. Canonical correlation was used to examine the relationship between symptom severity and predictor variables.

A canonical correlation analysis creates a pair of weighted sums (canonical variates) from each group of variables that are maximally correlated. Subsequent pairs of canonical variates are created that are maximally correlated with one another, subject to the condition that they are uncorrelated with earlier canonical variates. In this analysis, if PTSD and depression are separate constructs, predicted by different combinations of predictor variables, it would be expected that two pairs of canonical variates would have substantial correlations. In one pair, PTSD would be expected to load highly onto one variate and the predictors of PTSD onto the corresponding variate. In the other pair, depression should load highly onto one variate and the predictors of depression onto the corresponding variate. If PTSD and depression are best represented as a single construct, a pair of variates should show a substantial correlation, with both loading highly onto one variate in the pair and most of the predictor variables loading highly on the other variate.

CHANGES IN DIAGNOSTIC STATUS FROM 3 TO 12 MONTHS POST-INJURY Among subjects (N=301) admitted to a Level 1 trauma service 12-month diagnosis

No diagnosis 3-month diagnosis

PTSD

Depression

Comorbid PTSD/ Depression

N

%

N

%

N

%

N

%

No diagnosis

208

69

9

3

9

3

5

2

PTSD

12

4

11

4

3

1

6

2

Comorbid PTSD/depression

10

3

5

2

1

0

9

3

CHAP TER FIVE 83

Multinomial logistic regression was used to identify whether diagnostic categories were associated with differential groups of predictors. If PTSD and depression in the aftermath of trauma are, indeed, different constructs, it is reasonable to hypothesize that variables predicting a categorical diagnosis of PTSD would be different from those predicting a categorical diagnosis of depression. In order to examine this hypothesis, the four diagnostic groups (no diagnosis, PTSD alone, depression alone, and comorbid PTSD/depression) were used as a categorical dependent variable in a series of multinomial logistic regression analyses. Multinomial logistic regression was used because the dependent variable (diagnosis) had more than two categories. In examining whether the predictor variables could differentially predict specific diagnoses, a set of comparisons among categories was conducted. First, participants with PTSD, depression, and comorbid PTSD/depression were compared with partici-

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CANONICAL CORRELATIONS OF PSYCHOPATHOLOGY (PTSD AND DEPRESSION) AND PREDICTOR VARIABLES AT 3 AND 12 MONTHS 3 months (N=337)

12 months (N=307)

General traumatic stress variate

Depression without PTSD variate

General traumatic stress variate

PTSD

0.96

–0.28

0.99

Depression

0.89

0.46

0.82

PREDICTOR VARIABLES EVENT CHARACTERISTICS Days in the hospital

0.06

0.52

0.12

Injury severity score

0.05

0.43

0.10

ICU admission

0.04

0.41

0.06

Mild traumatic brain injury

0.29

0.11

0.14

INDIVIDUAL CHARACTERISTICS Alcohol use pretrauma

–0.02

0.33

–0.09

Psychiatric history

0.39

–0.11

0.42

Traumatic life events

0.36

–0.12

0.35

Gender

0.18

–0.38

0.18

COGNITIVE APPRAISALS Anticipated effect of injury

0.48

0.15

0.53

Anxiety about injury

0.53

–0.05

0.56

Dissociation

0.49

0.07

0.37

Reexperiencing

0.64

–0.32

0.54

Avoidance

0.51

–0.45

0.41

Arousal

0.78

0.05

0.71

Depression

0.76

0.32

0.73

ACUTE RESPONSES

CHAP TER FIVE 85

pants with no diagnosis, with the aim of identifying predictor variables for each diagnosis relative to no diagnosis. The second set of comparisons compared PTSD and depression with comorbid PTSD/ depression. Predictor variables aimed to differentiate participants with PTSD from those with comorbid PTSD/depression and to differentiate participants with depression from those with comorbid PTSD/ depression. The final comparison was between PTSD and depression, with the aim of identifying variables that would differentiate between individuals with PTSD alone and those with depression alone.

If PTSD and depression are, indeed, independent constructs, and if comorbid PTSD/depression is simply the conjunction of these two diagnoses, then it would be reasonable to expect that 1) PTSD and depression would be predicted by different variables and 2) comorbid PTSD/ depression would share predictors with both PTSD and depression. On the other hand, if PTSD and depression in the aftermath are the same construct, it would be reasonable to expect little difference between the predictors of PTSD, depression, and comorbid PTSD/depression.

In order to reduce the number of predictor variables in the analysis, two backwards elimination multinomial logistic regressions were conducted, one for diagnosis at 3 months and one for diagnosis at 12 months. Backwards elimination allows the removal of variables that

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fail to make a significant independent contribution to the prediction. Variables with contributions that were significant at a level of 0.10 or less at both time points were removed from the analysis. The 10 predictor variables that remained were used in all subsequent regression analyses.

RESULTS Prevalence and Course of Psychopathology Table 1 shows the proportion of participants meeting full criteria for PTSD alone, depression alone, and both diagnoses 3 and 12 months postinjury and the proportion when those meeting subsyndromal criteria for the conditions were included. A total of 15% of participants met full criteria for one of the above diagnoses at 3 months, compared with 14% at 12 months. Inclusion of subsyndromal cases increased these prevalence rates to 26% at 3 months and 21% at 12 months. It is interesting that inclusion of subsyndromal cases actually reduced the prevalence of depression alone at 3 months. This anomaly occurred because many participants with depression also had subsyndromal PTSD and, therefore, were moved to the comorbid group. Full plus subsyndromal criteria at 3 and 12 months are used for all subsequent analyses.

Diagnosis status change over time reveals considerable changes between 3 and 12 months postinjury. While the majority of participants (69%) remained free from a diagnosis (full or subsyndromal) across time, the proportion of those with a diagnosis at 3 months who no longer met criteria at 12 months was 49%. Around 10% of those who were free from disorder at 3 months had developed a diagnosis by 12 months. Of those who had a diagnosis at both 3 and 12 months, only 58% maintained the same diagnosis across time.

The majority (63%) of individuals with PTSD (full or subsyndromal) at 3 months continued to meet criteria for one of the three diagnoses (PTSD, depression, or comorbid PTSD/depression) at 12 months. Similarly, the majority (60%) of those with comorbid PTSD/depression at 3 months also had a diagnosis of some kind at 12 months. However, this was not the case for depression: 92% of those with a diagnosis of depression at 3 months recorded no diagnosis at 12 months.

Prediction of Severity Canonical correlation was used to examine the relationship between symptom severity and the predictor variables. At 3 months postinjury, two pairs of canonical variates reached significance.

The first canonical correlation was 0.71 (2=193.62, df=46, p<0.001). Since both PTSD and depression severity loaded highly onto this variate (0.96 and 0.89, respectively), it is best conceptualized as a general traumatic stress construct. A second canonical correlation was significant: 0.48 (2=51.10,

CHAP TER FIVE 87

df=22, p<0.001). Depression severity loaded positively onto this variate (0.46), while PTSD severity loaded negatively (â&#x20AC;&#x201C;0.28) suggesting that high score on this construct represents depression in the absence of PTSD. By 12 months postinjury, only one pair of canonical variates was significant (0.69; 2=141.27, df=46, p<0.001). Both PTSD and depression severity scores loaded highly onto this variate (0.99 and 0.82, respectively), again suggesting a construct of general traumatic stress.

Predicting Diagnoses Multinomial logistic regression was used to examine differences in predictors between 1) participants with PTSD, depression, and comorbid PTSD/depression compared with participants with no diagnosis; 2) participants with PTSD or depression alone compared with those with comorbid PTSD/depression; and 3) participants with PTSD compared with those with depression.

A combination of eight variables was able to differentiate PTSD alone from no diagnosis at 3 months postinjury. Seven of these eight variables also differentiated between comorbid PTSD/depression and no diagnosis, suggesting that PTSD alone and comorbid PTSD/depression may be the same construct in the aftermath of trauma. Only two variables, however, significantly differentiated depression from no diagnosis, adding support to the proposition generated by the canonical correlations that depression in the absence of PTSD symptoms may be a distinct construct at 3 months posttrauma. Consistent with that hypothesis, no variables differentiated PTSD alone from comorbid PTSD/depression, but five variables were able to differentiate depression alone from comorbid PTSD/depression. Finally, three variables differentiated PTSD alone from depression alone. Also in line with findings from the canonical correlation, the pattern at 12 months is less consistent, suggesting that depression may no longer exist independently from a more general traumatic stress construct.

DISCUSSION These data shed interesting light on the prevalence between PTSD, depression, and comorbid PTSD and depression in the aftermath of trauma, as well as on the relationships between these constructs. In this population of severely injured trauma survivors, full diagnostic criteria were met in almost equal numbers for each of the three diagnostic categories at 3 months (4%, 6%, and 5%) and 12 months (4%, 4%, and 6%). The addition of subsyndromal cases increased these figures considerably in PTSD (threefold) and comorbid PTSD/depression (twofold), highlighting the importance in both research and clinical settings of considering these cases that do not quite meet full diagnostic criteria.

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A surprising degree of movement between diagnostic categories was evident from 3 to 12 months postinjury. In particular, the finding that half of those with a diagnosis at both time points changed diagnostic categories between 3 and 12 months highlights the complex interaction and overlap between these diagnoses. The pattern of change across time was similar for the PTSD and comorbid groups, with comparable proportions of participants recovering, maintaining their diagnosis, or changing diagnostic categories.

Of importance, however, is that those with depression showed a different pattern: the majority of participants with a single depression diagnosis at 3 months had recovered by 12 months. The group with depression at 12 months comprised mainly individuals with no diagnosis at 3 months. Consistent with findings from subsequent analyses, these data suggest that there may be characteristics about depression at 3 months posttrauma that differentiate it from PTSD and comorbid PTSD/depression. In contrast, the degree of movement between the PTSD and comorbid groups across time suggests a strong similarity and overlapping of constructs.

It was apparent from the canonical correlations that most of the variance in psychopathology at both 3 and 12 months postinjury is accounted for by a construct of general traumatic stress within which PTSD and depression are indistinguishable. With the exception of mild traumatic brain injury, the predictors of this general distress are consistent at both time points. They comprise a combination of event characteristics (event severity, discharge destination), individual characteristics (past psychiatric and trauma history), negative cognitive appraisals about the injury and its potential impact, and high levels of PTSD symptoms, depression, and dissociation over the first week posttrauma. However, it appears that at 3 months, depression is differentially related and is predicted by different variables to those that are correlated with more general distress. These predictors, again, include a combination of event characteristics (days in the hospital, Injury Severity Score, ICU admission), individual characteristics (high pre-trauma alcohol use, male gender), and acute responses (low levels of reexperiencing and avoidance symptoms coupled with high acute depression). Although explaining only 15% of the variance, this second canonical variate is important, perhaps describing a construct of brief reactive depression that has resolved by the first anniversary of the traumatic event. Certainly, by 12 months, depression as an independent construct had disappeared and only one canonical variate was apparent, characterizing a more general chronic traumatic stress reaction.

Similar findings were apparent in terms of predicting a categorical diagnosis.

At 3 months postinjury, a pattern emerged that was consistent with the canonical correlations. A combination of variables was able to differentiate PTSD alone from no diagnosis, including event characteristics (ICU admis-

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sion, event severity), individual characteristics (prior psychiatric and trauma history), cognitive appraisals (anxiety about the potential impact of the injury), and acute responses (reexperiencing, arousal, and depression). With the exception of ICU admission, exactly the same combination of variables differentiated between comorbid PTSD/depression and no diagnosis. This suggests that PTSD alone and comorbid PTSD/depression are one and the same constructâ&#x20AC;&#x201D;akin to the general traumatic stress variate identified in the canonical correlation and largely predicted by the same variables. On the other hand, depression alone was not differentiated from no diagnosis by these predictors; only prior psychiatric history and prior alcohol use were able to differentiate depression alone from no diagnosis. Consistent with these findings, no variables were able to differentiate PTSD alone from comorbid PTSD/depression. Several variables, however, including discharge home (rather than to a rehabilitation facility), prior alcohol use, negative predictions about the effects of injury, and a low level of reexperiencing symptoms, were able to differentiate depression alone from comorbid PTSD/depression. Finally, three variables (event severity, prior alcohol use, and reexperiencing symptoms) were able to differentiate PTSD alone from depression alone.

It is not surprising that the picture at 12 months is somewhat less clear.

Although some similarity remains between predictors differentiating between PTSD alone and no diagnosis and between comorbid PTSD/depression and no diagnosis, the pattern is less consistent, and there is little to suggest that depression still exists as a separate construct.

Taken together, these findings generate an intriguing model. First, it is clear that the bulk of psychopathology in the aftermath of trauma is best conceptualized as a general traumatic stress factor. Consistent with the conclusion of Breslau et al, it would seem that the PTSD and depression symptoms that constitute this factor are part of a shared vulnerability and thus have the same predictive variables. PTSD and comorbid PTSD/depression are effectively one and the same thing. The data suggest that depressive symptoms are often integral to PTSD and that to separate depression out as a distinct disorder when it occurs with PTSD is a somewhat arbitrary distinction. However, there is also evidence to suggest that, in the first few months following trauma, depression may exist as a separate and independent entity, with its own unique set of predictors and its own unique course of recovery with a good prognosis. By 12 months posttrauma, as the psychopathology becomes more chronic, it also becomes less well differentiated and it is no longer possible to identify a unique construct of depression. Rather, all of the psychopathology is best explained by a more general chronic traumatic stress factor that is characterized by mixed PTSD and depressive symptoms.

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CHAP TER FIVE 91

6

APPROACHES TO TREATMENT Bessel A. van der Kolk, MD, Onno van der Hart, PhD and Jennifer Burbridge, MA

Lack of predictability and controllability are the central issues for the development and maintenance of PTSD. xyxyxy xyxyx yxyxyxyx xyyxyxxyyx xyxyx yxyxy xyxx yxyxyxyxyx xyxyyx xyxyxxyyxyxyxyxyxyxyxy xy xyxy The combination of intrusive and numbing symptoms has been consistently noted over the past century, and forms the basis of our understanding of the nature of PTSD. What distinguishes people who develop post-traumatic stress disorder from people who are merely temporarily overwhelmed is that people who develop PTSD become “stuck” on the trauma, keep re-living it in thoughts, feelings, or images. xyyxy yxxxyxyxyxyxyxyxyx xyxyx Evidence during the past decade supports the notion it is the intrusive reliving, rather than the traumatic event itself that is responsible for the complex biobehavioral change that we call PTSD. Once they become dominated by intrusions of the trauma, traumatized individuals begin organizing their lives around avoiding having them. xyxyxy xxyxyxyxyxyxyxyxyxyx xxyxyxyxyxy xxyxyxy xxyxyxyxyxyx xyx xyxyxy xxyxyxyx xyxyx xyxyxyx xyxyx xyxxyx yxyx xyxy xyxyxyxyxyxyxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx xxxxxxxxxxxx xx Avoidance may take many different forms: keeping away from reminders, ingesting drugs or alcohol that numb awareness of distressing emotional states, or utilizing dissociating to keep unpleasant experiences from conscious awareness. The helplessness, conditioned hyperarousal, and other trauma-related changes may permanently change how a person deals with stress, alter his/her self-concept and interfere with the view of the world as a basically safe and predictable place. xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx

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A relative sense of safety and predictability are preconditions for effective planning and personal action. Freud described how, in order to function properly, people need to be able to define their needs, anticipate how to meet them and plan for appropriate action. In order to do this, people need to be able to mentally entertain a range of options, without resorting to action. He called this capacity: “thought as experimental action.” Traumatized people seem to lose this essential capacity and have difficulty turning inwards to utilize their emotions as guides for action. Instead, their internal world becomes a danger zone and they seem to spend their energies on not thinking and planning.

The therapeutic relationship with these patients tends to be extraordinarily complex. It confronts all participants with intense emotional experiences, forcing them to explore the darkest corners of the mind, and to face the entire spectrum of human glory and degradation. The devastating effects of trauma on affect modulation, attention, perception, and the giving and taking of pleasure bring us face to face with the full destructive impact of traumatic stress to dominate, use and control others.

THE ROLE OF MEMORY AND DISSOCIATION Pierre Janet first described how the central issue in trauma is dissociation: memories of what has happened cannot be integrated into one’s general experiential schemes and ore split off from the rest of personal experience. Physiological hyperarousal seems to be a central precondition for dissociation to occur. Lack of integration on a schematic level causes the experience to be stored as affect states or as somatosensory elements of the trauma, which return into consciousness when reminders activate customary response patterns: physical sensations (such as panic attacks), visual images (such as flashbacks and nightmares), obsessive ruminations, or behavioral reenactments of elements of the trauma.

Most studies of people who develop PTSD find significant dissociative symptomatology The most extreme form of post-traumatic dissociation is seen in patients who suffer from Dissociative Identity Disorder.

Janet first described how traumatized people become “attached” (Freud would later use the term “fixated”) to the trauma: “unable to integrate traumatic memories, they seem to have lost their capacity to assimilate new experiences as well. It is as if their personality definitely stopped at a certain point and cannot enlarge any more by the addition or assimilation of new elements.” This suggests that traumatized people are prone to revert to earlier modes of cognitive processing of information when faced with new stresses.

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Since the core problem in PTSD consists of a failure to integrate an upsetting experience into autobiographical memory, the goal of treatment is find a way in which people can acknowledge the reality of what has happened without having to re-experience the trauma all over again. For this to occur merely uncovering memories is not enough: they need to be modified and transformed, i.e. reconstructed into neutral or meaningful narratives.

PTSD AS A BIOLOGICALLY-BASED DISORDER Abram Kardiner introduced the notion that “traumatic neuroses” are “physioneuroses” and that patients with PTSD remain on constant alert for environmental threat: “(t)he subject acts as if the original traumatic situation were still in existence and engages in protective devices which failed on the original occasion...” In PTSD, the physiological state of chronic overarousal is accompanied by difficulties in attention and concentration, as well as distortions in information processing, including narrowing of attention onto sources of potential challenge or threat. It appears that for traumatized people all emotions become angerous. While the function of their hyperarousal is to prepare them for some form of action in the face of threat, it does not build up specific skills and feelings of mastery and control, because the anticipated action is not specific.

Over the past few years it has become increasingly evident that the intensity of the initial somatic response to a potentially traumatic experience is the most significant predictor of long term outcome. If the stress is sufficiently overwhelming, the resulting trauma sets up a conditional emotional response in which the body continues to go into a fight, flight, or freeze responses at the least provocation: traumatized people keep experiencing life as a continuation of the trauma, and remain in a state of constant alert for its return. Many traumatized people who have consciously put the trauma behind them continue to experience anxiety and increased physical arousal when exposed to situations that remind them of the trauma, or even to unexpected events such as loud noises, and go into fight/flight reactions, without necessarily being aware of the origin of these extreme behaviors.

Though the biological underpinnings of response to trauma are extremely complex, forty years of research on humans and other mammals have demonstrated that trauma (particularly trauma early in the life cycle) has long term effects on the neurochemical response to stress, including the magnitude of the catecholamine response, the duration and extent of the cortisol response, as well as a number of other biological systems, such as the serotonin and endogenous opioid system.

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THE SYMPTOMATOLOGY OF PTSD While post-traumatic stress has been recognized in the poetry of Homer, Shakespeare and Goethe, psychiatry has consistently recognized its existence only since 1980 when PTSD was introduced into the DSM III. Since that time, there has been a growing literature documenting the post-traumatic symptoms of hyperarousal, hyper-reactivity to stimuli reminiscent of the trauma, avoidance and emotional numbing in a large variety of traumatized populations, including war veterans, children who have experienced physical or sexual assaults, women who have been battered and raped, people exposed to natural disasters, refugees and political prisoners.

Regardless of the origin of the terror, the central nervous system (CNS) reacts consistently to overwhelming, threatening, and uncontrollable experiences with conditioned emotional responses. For example, rape victims may respond to conditioned stimuli, such as the approach by an unknown man, as if they were about to be raped again, and experience panic.

Intrusive Re-experiencing Remembrance and intrusion of the trauma is expressed on many different levels, ranging from flashbacks, affective states, somatic sensations, nightmares, interpersonal re-enactments, including transference repetitions, character styles, and pervasive life themes. Laub and Auerhahn organized the different forms of knowing along a continuum according to the distance from the traumatic experience, each form also progressively represents a consciously deeper and more integrated â&#x20AC;&#x2DC;level of knowing.â&#x20AC;&#x2122; The different forms of remembering trauma range from 1) not knowing; 2) fugue states (in which events are relived in an altered

EFFECTS OF OPEN-LABEL PAROXETINE IN PTSD

Baseline Week 6 Week 12 0

10

20

30

40

SCORE ON DAVIDSON TRAUMA SCALE

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50

60

70

80

state of consciousness); 3) retention of the experience as compartmentalized, undigested fragments of perceptions that break into consciousness (with no conscious meaning or relation to oneself); 4) transference phenomena (wherein the traumatic legacy is lived out as oneâ&#x20AC;&#x2122;s inevitable fate); 5) its partial, hesitant expression as an overpowering narrative; 6) the experience of compelling, identity-defining and pervasive life themes (both conscious and unconscious); 7) its organization as a witnessed narrative.

These various forms of knowing are not mutually exclusive.

Autonomic hyperarousal While people with PTSD tend to deal with their environment by emotional constriction, their bodies continue to react to certain physical and emotional stimuli as if there were a continuing threat of annihilation.

Conditioned autonomic arousal to traumarelated stimuli has consistently been shown to occur in a variety of traumatized populations.

Autonomic arousal, which serves the essential function of alerting the organism to potential danger seems to loose that function in traumatized people: the easy triggering of somatic stress reactions causes people with PTSD to be unable to rely on bodily sensations to warn them against impending threat. Instead, the persistent warning signals loose their functions of signals of impending danger, and cease to alert the organism to take appropriate action.

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The key element of the psychotherapy of people with PTSD is the integration of the alien, the unacceptable, the terrifying, the incomprehensible.

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Numbing of responsiveness Aware of their difficulties in controlling their emotions, traumatized people seem to spend their energies on avoiding of distressing internal sensations, instead of attending to the demands of the environment. In addition, they lose satisfaction in matters that previously gave them a sense of satisfaction and may feel “dead to the world”. This emotional numbing may be expressed as depression, as anhedonia and lack of motivation, as psychosomatic reactions, or as dissociative states. In contrast with the intrusive PTSD symptoms, which occur in response to outside stimuli, numbing is part of these patients’ baseline functioning. In children, numbing has been observed among elementary school children attacked by a sniper, among witnesses to parental assault or murder, and among victims of physical or sexual abuse. They become less involved in playful social interactions, and often are withdrawn and isolated. After being traumatized, many people stop feeling pleasure from exploration and involvement in activities, and they feel that they just “go through the motions” of everyday living. Emotional numbness also gets in the way of resolving the trauma in psychotherapy: they give up on recovery and it keeps them from being able to imagine a future for themselves.

Intense emotional reactions and sleep problems The loss of neuromodulation that is at the core of PTSD leads to loss of affect regulation. Traumatized people go immediately from stimulus to response without being able to first figure out what makes them so upset. They tend to experience intense fear, anxiety, anger and panic in response to even minor stimuli.

This makes them either overreact and intimidate others, or to shut down and freeze. Both adults and children with such hyperarousal will experience sleep problems, both because they are unable to still themselves sufficiently to go to sleep, and because they are fearful of having traumatic nightmares. Many traumatized people report dream-interruption insomnia: they wake themselves up as soon as they start having a dream, for fear that this dream will turn into a trauma-related nightmare. They also are liable to exhibit hypervigilance, exaggerated startle response and restlessness.

Memory disturbances and dissociation Increased autonomic arousal not only interferes with psychological comfort, anxiety itself also may trigger memories of previous traumatic experiences. The administration of lactate, which stimulates the physiological arousal system, elicits flashbacks and panic attacks in people with PTSD. Yohimbine injections (which stimulate NE release from the Locus Coeruleus) are able to induce flashbacks in Vietnam veterans with PTSD. Any arousing situation may trigger memories of long-ago traumatic experiences and precipitate reactions that are irrelevant to present demands.

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In addition to hyperamnesia and intrusive memories, chronically traumatized people, particularly children may develop amnestic syndromes related to the traumatic event. During the stage of life that children, in a stageappropriate way, try on different identities in their daily play activities, children who are exposed to prolonged and severe trauma may be capable of organizing whole personality fragments in order to cope with traumatic experiences. In the long term, this may give rise to the syndrome of Dissociative Identity Disorder, which may occurs in about 4% of psychiatric inpatients in the USA. Psychosomatic reactions Chronic anxiety and emotional numbing also get in the way of learning to identify and articulate internal states and wishes.

People traumatized as children frequently suffer from alexithymiaâ&#x20AC;&#x201D;an inability to translate somatic sensations into basic feelings, such as anger, happiness or fear. This failure to translate somatic states into words and symbols causes them to experience emotions simply as physical problems.

This naturally plays havoc with intimate and trusting interpersonal communications. These people have somatization disorders and relate to the world through their bodies. They experience distress in terms of physical organs, rather than as psychological states.

PRINCIPLES OF TREATMENT The treatment of PTSD has three principal components: 1) processing and coming to terms with the horrifying, overwhelming experience, 2) controlling and mastering physiological and biological stress reactions, 3) re-establishing secure social connections and interpersonal efficacy.

The aim of these therapies is to help the traumatized individual to move from being dominated and haunted by the past to being present in the here and now, capable of responding to current exigencies with his or her fullest potential. Thus, the trauma needs to be placed in the larger perspective of a personâ&#x20AC;&#x2122;s life, as a relatively isolated historical event, or series of events, that occurred at a particular time, and in a particular place, and that can be expected to not recur if the traumatized individual takes charge of his or her life. Tragically, many traumatized people are involved in situations of ongoing trauma, in which they have little or no personal control over what happens to them. However, even under those circumstances, learning how to properly assess what is going on and planning oneâ&#x20AC;&#x2122;s responses still can be expected to have significant psychological benefits.

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RESPONSE TO PAROXETINE IN PTSD: MULTICENTER TRIALS

PLACEBO

Study 648

20–50 mg/day

PLACEBO

Study 651

20 mg/day 40 mg/day

0

–5

–10

–15

–20

–25

–30

–35

–40

U N A D J U S T E D M E A N C H A N G E F RO M B A S E L I N E I N C A P S -2 T O TA L S C O R E

ACUTE TRAUMA Immediately after the trauma, the emphasis needs to be on self-regulation and on rebuilding. This means the re-establishment of a sense of security and predictability, and active engagement in adaptive action. Only a limited proportion of people who are traumatized develop PTSD. Most traumatized people seem to be able to successfully negotiate these initial adaptive phases without succumbing to the long term progression of their acute stress reaction into PTSD. For them, the trauma becomes merely a terrible experience that happened to them some time in their past. It is quite unclear whether talking about what has happened is always useful in preventing the development of PTSD. Some surprising findings have come out of careful Critical Incidence Stress Debriefing research: the few controlled studies that have examined the preventative effect of debriefing immediately following exposure to a traumatic event have suggested a poorer outcome following debriefing as compared with no intervention.

Give the paucity of controlled studies, we are left with the clinical impression that the initial response to trauma consists of reconnecting with ordinary supportive networks, and of engaging activities that re-establish a sense of mastery. It is obvious that the role of mental health professionals in these initial recuperative efforts is quite limited.

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THE NEED FOR PHASE ORIENTED TREATMENT Trauma needs to be treated differently at different phases of peopleâ&#x20AC;&#x2122;s lives following the trauma, and at the different stages of the disorder PTSD. Treatments that may be effective at some stages of treatment might not be effective at others. For example, on a pharmacological level, initial management with drugs that decrease autonomic arousal will decrease nightmares and flashback, promote sleep, and are likely to prevent the kindling effects that are thought to underlie the long-term establishment of PTSD symptomatology. These same drugs, once the Disorder has been established have, at best, a palliative function, and serotonin re-uptake blockers, which seem to have little immediate benefit, can be immensely helpful in allowing people to attend to current asks, and not to dwell on past fears, interpretations, and fixations. In this context, it is interesting to note that Foa found that in the initial stages of treatment of rape victims Stress Inoculation Training turned out to be as effective a treatment of PTSD as was Prolonged Imaginal Exposure. However, on follow-up, imaginal flooding had superior results to stress inoculation. If there are differential effects of therapeutic modalities within a four month time frame, it is likely that there would be differential effects over longer time spans. It is likely that some forms of therapy might be effective at some stages, but have

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negative outcomes at other phases of the illness. Another instance is abreaction. It appears that abreaction as a treatment is most effective early in the course of the illness, and that its effectiveness decreases over time.

For example, exposure therapy using “flooding” techniques have been found to worsen the symptoms of some patients, particularly in those in whom the focal trauma was decades earlier. When intrusions of fragments of the trauma are the predominant symptom, exposure and desensitization may be what is most required. At a later stage of the progression of the disorder, when people have organized their entire lives around avoidance of triggers of the trauma, and approach other people as potential triggers of traumatic intrusions, helplessness, suspicion, anger, and interpersonal problems may dominate the symptom picture. When that is the case, primary attention needs to be paid to stabilization in the social realm.

PSYCHOTHERAPEUTIC INTERVENTIONS The key element of the psychotherapy of people with PTSD—as perhaps for all psychotherapy—is the integration of the alien, the unacceptable, the terrifying, the incomprehensible. Life events initially experienced as alien, as if imposed from outside upon passive victims, must come to be “personalized” affectively as integrated aspects of one’s history and life experiences. The massive defenses, initially established as emergency protective measures, must gradually relax their grip upon the psyche, so that dissociated aspects of experience do not continue to intrude into one’s life experience and thereby threaten to retraumatize an already traumatized victim.

Psychotherapy must address two fundamental aspects of PTSD: the deconditioning of anxiety, and the pervasive effects that trauma has on the way victims views themselves and the world. In only the simplest cases will it be sufficient to decondition the anxiety associated with the trauma. In the vast majority of patients, both aspects will have to be treated, which means the use of a combination of procedures for Reconditioning anxiety, for changing beliefs, and for developing a cognitive system that somehow allows a person to continue to cope effectively in a world that now is known to be capable of great destructiveness.

Stabilization In the treatment of simple cases of PTSD, it is perhaps possible to move quickly, to activating the traumatic memory. In more complex cases, it should be part of a more encompassing treatment model, which must include careful preparation, with an eye on providing the patient with a capacity to feel safe while accessing traumatic material. For the past century, psychotherapeutic clinicians have basically adopted a phase-oriented model that consists of reintegration and rehabilitation. In the first phase the foundation is laid that enables patient to deal with the challenge

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of confronting the trauma. The patient is helped with establishing more stability and safety in daily life, including social support, stress inoculation, ways of controlling symptoms and ways of containing intrusive memories.

Psychopharmacological management often is an integral part of stabilization.

The identification of feelings by verbalizing somatic states The function of emotions is to alert people to the occurrence, significance, and nature of subjectively significant events. Ordinarily, emotions are de-activated when schemas and situations have been realigned (e.g., by taking action that conforms situations to schemas, or by amending schemas to better fit situations). Thus, emotions function as signals to readjust one’s expectations of the world and to take adaptive action. Krystal first noted that in people with PTSD emotions seem to loose much of their alerting function: a dissociation is set up between emotional arousal and goal-directed action. Traumatized people lose their capacity to interpret the meaning of their emotional arousal, which thus becomes irrelevant is a current signal.

Unable to interpret the meaning of their emotional arousal, feelings themselves become endowed with a negative valence: because no release can be found in adaptive action, emotions merely become reminders of one’s inability to affect the outcome of one’s life. Hence, aside from the concrete, usually visual, reminders of the trauma, feelings in general come to be experienced as traumatic reminders, and are to be avoided.

Unable to neutralize affects with adaptive action, traumatized people tend to experience their affects as somatic states: either through their smooth, or striated musculature. Thus, people with PTSD tend to somatize or to discharge their emotions with actions that are irrelevant to the stimulus that precipitated the emotion: with aggressive actions against self or others. When the disorganizing intrusions can be understood as failures of integration of traumatic experiences into the totality of one’s life, the psychotherapist is in a position to recognize seemingly overwhelming affective experiences as actual reliving of past terror. One’s natural proclivity in psychotherapy is to help the patient avoid experiencing undue pain; yet the patient’s affective experiences are part and parcel of healing and integration. The psychotherapist who understands the nature of trauma can aid the process of integration by staying with the patient through his suffering, by providing a perspective that the suffering is meaningful and bearable, and by helping in the mastery of trauma through putting the experience into symbolic, communicable form, such as words, thoughts, and feelings. The patient’s “repeating” the trauma in action is the forerunner to his “remembering” and symbolizing it in words, which in turn is the precursor accompaniment to his “working it through” in emotional experience.

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Deconditioning of traumatic memories and responses This consists of: (a) controlled activation of the traumatic memories, and (b) corrections of faulty traumatic beliefs.

The critical issue is to introduce the capacity to flexibly remember the trauma. In order for this to occur, some new information that is incompatible to the traumatic memory must be introduced. The most important new information is probably the fact that the patient is able to confront the traumatic memory by a trusted therapist in a safe environment. In order to help the patient regulate emotional arousal, secure attachment may be even more important than evoking the traumatic memories. Therefore, it is important for the patient to establish and maintain an emotional connection with the therapist. While behavioral therapists speak about exposure-procedures, which are either systematic desensitization procedures or implosive therapy or flooding procedures, they neglect to write about the intensely personal element in all psychotherapeutic procedures, which is a critical element in the success of effective treatment. So, while these clinicians and researchers almost exclusively present their data about decreases of fear or anxiety through controlled exposure to (a) the stimulus components (environmental cues), (b) the response components (e.g. motoric actions, heart pounding), and the meaning elements of the traumatic memory, their results are most likely heavily

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affected by their personal investment in the well-being of their patients, which is communicated and translated into a subjective sense of safety.

According to Foa & Kozak two conditions are required for anxiety reduction in the treatment of PTSD: 1) a person must attend to fear-relevant information in a manner that will activate his/her own fear memory. As long as the fear is not experienced, the fear structure cannot be modified. 2) in order to form a new, non-fear structure, some of the information that evoked the fear must be absent in the new context in which the fear is being provoked.

Exposure to information consistent with a fear memory would be expected to strengthen the fear (i.e., sensitize and thereby increase the likelihood of developing PTSD). Hence the critical issue in treatment is to expose the patient to an experience that contains elements that are sufficiently similar to an existing traumatic memory in order to activate it, and at the same time for it to be an experience that contains aspects that are incompatible enough to change it (for example experiencing a traumatic memory in a safe and controllable environment, being able to evoke a traumatic image, without feeling overwhelmed by the associated emotions).

There are at least two significant problems with this exposure technique: 1) Because excessive arousal interferes with the acquisition of new information, excessive arousal impedes habituation. When that occurs, the fear structure will not be corrected, but instead, will be confirmed: instead of promoting habituation, it accidentally fosters sensitization. 2) An additional serious obstacle to effective treatment is that the strong response elements in the PTSD structure may promote avoidance: strong fear and discomfort motivates people who suffer from PTSD to avoid or escape confrontation with situations that remind him/her of the trauma, in order to overcome the intrusive, sensorimotor elements of the trauma, a person must transform the traumatic (non-verbal) memory into a personal narrative, in which the trauma is experienced as a historical event that is part of a personâ&#x20AC;&#x2122;s autobiography. This entails being able to tell the story of the shocking event without reexperiencing it. It is generally assumed that once all relevant elements of the total traumatic experience have been identified and thoroughly and deeply examined and experienced in the therapy, successful synthesis will take place. The work by Resick & Schnicke supports the notion that exposure of all elements of the trauma, and their associated shifts in perception of self and others does lead to successful resolution of trauma-related symptomatology.

Traumatic experiences are not only processed by means of currently existing mental schemes, but they may also activate latent self-concepts and views of relationships that were formed earlier in life. This activation of latent schemes is particularly relevant for people with prior his-

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tories of trauma, even in those who subsequently have been able to make a successful adaptation.

When trauma activates these earlier self-schemas, these will compete and co-exist with more mature schemes in explaining cause and effect relationships in regards to the trauma. These different, and often competing mental schemes then will determine the psychological organization of the traumatic experience.

Psychotherapy needs to specifically address how the trauma has affected people’s sense of self-efficacy, their capacity for trust and intimacy, their ability to negotiate their personal needs, and their ability to feel empathy for other people.

GROUP PSYCHOTHERAPY Emotional attachment is the primary protection against being traumatized: people have always gathered in communities and organizations to help them deal with outside challenges: we seek close emotional relationships with others in order to help us anticipate, meet and integrate difficult experiences. Contemporary research has shown that as long as the social support network remains intact, people are relatively well protected against even catastrophic stresses. For young children, the family usually is a very effective source of protection against traumatization, and most children are amazingly resilient as long as they have a caregiverwho is emotionally and physically available. Mature people also rely on their families, colleagues and friends to provide such

CONDITIONAL RISK FOR PTSD BY VARIABLE Percentage

AOR1 (95% CI)

SEX Female

13.0

Male

6.2

2.01 (1.23–3.29) 1.00

EDUCATION < High school

7.2

0.90 (0.29–2.74)

High school

9.1

1.25 (0.57–2.73)

Some college

12.4

1.82 (0.87–3.84)

Four-year college

5.5

1.00

� $25,000

11.7

0.98 (0.41–2.37)

$25,000–34,999

9.6

0.85 (0.32–2.27)

$35,000–49,999

9.5

1.01 (0.41–2.49)

$50,000–74,999

6.1

0.64 (0.26–1.59)

≥ $75,000

8.5

1.00

Divorced/widowed

14.1

1.82 (0.90–3.69)

Never married

10.1

1.23 (0.63–2.40)

7.3

1.00

HOUSEHOLD INCOME

MARITAL STATUS

Married

1 AOR indicates adjusted odds ratio, derived from logistic regression model in which PTSD is the dependent variable and all listed variables are the independent variables; CI, confidence interval

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a trauma membrane. In recognition of this need for affiliation as a protection against trauma, it has become widely accepted that the central issue in acute crisis intervention is the provision and restoration of social support.

However, curiously, research has not supported the efficacy of standardized Stress Debriefing interventions following trauma.

The task of group therapy and community interventions is to help victims regain a sense of safety and of mastery. After an acute trauma, fellow victims often provide the most effective short-term bond because the shared history of trauma can form the nucleus of retrieving a sense of communality.

Regardless of the nature of the trauma, or the structure of the group, the aim of group therapy is to help people actively attend to the requirements of the moment, without undue intrusions from past perceptions and experiences. Group therapy is widely regarded as a treatment of choice for pa-

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tients with trauma histories. It has been used for victims of interpersonal violence natural disasters, childhood sexual abuse, rape, spouse battering, concentration camps and war trauma. In a group of people who have gone through similar experiences, most traumatized people eventually are able to find the appropriate words to express what has happened to them. As was observed almost fifty years ago: “by working out their problems in a small group they should be able to face the larger group, i.e., their world, in an easier manner.”

There are many levels of trauma-related group psychotherapies, with different degrees of emphasis on stabilization, memory retrieval, bonding, negotiation of interpersonal differences, and support. However, to varying degrees, the purpose of all trauma related groups is to 1) stabilize psychological and physiological reactions to the trauma, 2) to explore and validate perceptions and emotions, 3) to retrieve memories, 4) to understand the effects of past experience on current affects and behaviors and 5) to learn new ways of coping with interpersonal stress.

PSYCHOPHARMACOLOGICAL TREATMENT While it is widely recognized that PTSD is a “physioneurosis”, i.e. that it is based on psychological manifestations of biological changes, systematic psycho-pharmacological studies of PTSD are scarce and almost entirely limited to tricyclic antidepressants and MAO inhibitors. As of July, 1994, a total of only 134 patients with PTSD had been studied in double-blind placebo controlled studies. The treatment effects of the psychotropic agents examined in these systematic studies have been quite modest. In addition, in open studies and clinical reports, usefulness has been claimed for benzodiazepines, lithium carbonate, carbamazepine, clonidine and beta adrenergic blockers, but their efficacy has not been confirmed in double-blind, placebo controlled studies.

Three double-blind trials of tricyclic antidepressants have been published, two of which demonstrated some improvement in PTSD symptoms. Davidson, studying in-patient and out-patient veterans of World War II and Vietnam, showed that amitriptyline caused a decrease in overall PTSD, primarily by decreasing avoidant symptoms. In two reports of essentially the same sample, Frank, Kosten and their collaborators found that imipramine was more effective than placebo in out-patient Vietnam veterans, particularly decreasing intrusive symptoms. On the other hand, Reist found no significant difference between desipramine and placebo in a four week crossover trial. All three studies report a lack of placebo response in war veterans with chronic PTSD.

CHAP TER SIX 109

INDEX A

D

G

Abbreviated Injury Scale, 23, 25 Acoustic-startle eye blink reflex, 38 Acute combat reaction, 75, 78–82 Acute stress response, 73 Acute trauma, 69–78 Addictive behavior, 32, 35, 37–40 Adjustment disorders, 10 Advanced Trauma Life Support protocol, 61 Agoraphobia, 29 Alcoholism, 25, 57, 58 Alcohol Use Disorders Identification Test, 56 Albert Glass, 91 Anxiety disorders, 29, 53–55 Anxiety reactions, 30 Army Theater Trauma Registry, 70 Avoidance, 16, 19, 61, 62

Davidson Trauma Scale, 80 Delayed depression, 42, 67–68 Delayed onset PTSD, 23, 25 Department of Defense Medical Data Repository, 75 Depression, 39, 42, 67, 95 DEROS, 62–64 Diagnostic and Statistical Manual of Mental Disorders, 10 Disabled American Veterans, 66 Disability associated with PTSD, 37 Dissociation, 11 Dissociative identity disorder, 11–13 DSM III, 10, 23 DSM-IV-TR, 10, 12–15, 56, 83 DSM-IV, 10, 13 Duke Global Severity Rating, 71 Duration criterion, 19 Dysregulation, 102 Dysthymia, 39

Generalized anxiety disorders, 38–40 Glasgow Coma Scale, 103 Grief, 13, 57, 60 Group Psychotherapy, 96 Guerrilla warfare, 80

E

ICU admission, 80, 85–87, 91 Injury Severity Score, 107 Impact of Event Scale, 105 Interpersonal relationships, 28–31 Intrusive recollection, 27 Intrusive thoughts, 27–30 Iraq War, 23 Isolation, 74–76

B Battle of Hue, 55 Benzodiazepine, 95–97

C Catecholamines, 88 Central nervous system, 19, 41–44 Chemical paralysis, 101 Chi-square analysis, 103 Clinical Global Impression, 99 Cognitive variables, 14–17 Comorbidity, 79–85, 89, 93, 97 Composite International Diagnostic Interview, 107 Conditioned autonomic arousal, 33 Conversion symptoms, 64 Corticotrophin release factor, 98 Cortisol, 95, 97 Critical Incidence Stress Debriefing, 44

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Early intervention, 32 Electromyography, 69 Erickson’s psychosocial developmental stages, 38 Excessive somatization, 103

F Family therapy, 93–95 Flashbacks, 14, 84 Flooding technique, 92 Forced hospitalization, 16, 18, 30 Forgotten Warrior Project, 75 Frank paranoia, 85 Functional significance, 78

H Habituation, 28 Hamilton Depression Rating Scale, 104 Holocaust survivors, 27 Hurricane Katrina, 20, 26 Hyper-arousal, 15 Hyper-vigilance, 15, 16 Hypnagogic and hypnopompic hallucinations, 69, 76 Hypothalamic-pituitary-adrenal axis, 99

I

L Learned survival technique, 40–43 Learning difficulties, 25 Lebanon war, 30 Longitudinal research, 81

M

R

T

Major affective disorders, 36, 59 MAO inhibitors, 100–102 Medical anthropology, 19, 37, 103 Memory, 35 Morphine, 48–54, 59, 88, 90 Multinomial logistic regression, 95 Musculoskeletal disorders, 54

Rage, 14, 18 Rape victims, 33,40 Readjustment, 87–90 Redistribution stations, 51 Restitutive experience, 73

Transference phenomena, 98 Traumatic brain injury, 56, 90, 102, 105 Traumatic nightmares, 26 Treatment cognitive-behavioral therapy (CBT), 62 cognitive restructuring, 64 Eye Movement Desensitization and Reprocessing (EMDR), 83 exposure therapy, 66 group therapy, 81 medication, 63 paroxetine (Paxil), 75 Sertraline (Zoloft), 75 Selective serotonin reuptake inhibitors (SSRI), 75 Tricyclic antidepressants, 47, 49–53

N National Center for PTSD, 17, 20–23 National Comorbidity Study, 64 Naval Health Research Center, 68, 70 Neurochemical response to stress, 24 Neuroendocrine abnormalities, 106 Neuromodulation, 24–28 Neuropsychiatric casualties, 51 Neuropsychiatric disorder, 11, 23, 51

P Panic disorder, 13, 22, 72–77 Parasympathetic nervous system, 72 Pathological development, 35 Personality disorders, 15, 19, 36–40 Pharmacotherapy, 100 Pheneizine sulfate, 102 Physiological responses, 61 Physioneurosis, 68 Pierre Janet, 58 Prediction of Symptom Severity, 107 Prolonged Imaginal Exposure, 35 Propranolol, 107 Psychogenic amnesia, 75 Psychological first aid, 76, 98 Psychophysiological alterations, 58 Psychosocial treatment, 79 Psychotic reenactments, 68–71 Psychotropic medications, 99–105 PTSD prevalence, 67

S Secondary chronic morbidity, 69–72 Serotonin-reuptake inhibitors, 96 Sexual assault, 39, 61 Sheehan Disability Scale, 107 Situational manipulation, 43, 46, 55 Skin conductance, 81 Sleep abnormalities, 19 Sleep disturbance and nightmares, 20 Sleep paralysis, 20 Social support, 74, 82 Somatosensory, 91, 95 Stabilization, 66 Startle response, 23 Stimulus components, 56 Stressor criterion, 14–18 Stress inoculation, 53 Stress inoculation training, 53 Stress resilience, 75 Structural brain imaging, 22 Structured Clinical Interview, 101 Subclinical PTSD, 83 Substance abuse disorders, 13–15 Survival guilt, 74 Sympathetic nervous system, 67

V Veterans Administration, 71 Vicarious traumatization, 82–84 Vietnam Veterans Outreach Program, 71 Vietnam War, 72–75, 79 Vulnerability to the Effects of Stress Scale, 89

W War neurosis, 88 Work loss, 19, 25 World War I, 89 World War II, 89–92

Y Yohimbine injections, 100

INDEX 111

COLOPHON This book was set in Klavika. Designed by Eric Olson of Process Type Foundry in Minnesota and released in 2004, this sans serif reflects both humanist and geometric influences.

OVERVIEW 113

114 BL ACKOUT

OVERVIEW 115

BLACKOUT THE CAUSES AND SYMPTOMS OF PTSD COMPILED AND DESIGNED BY MAT T WELNACK

Post-traumatic stress disorder (PTSD) is an anxiety disorder that can occur following the experience or witnessing of a traumatic event. A traumatic event is a life-threatening event such as military combat, natural disasters, terrorist incidents, serious accidents, or physical or sexual assault in adult or childhood. Most survivors of trauma return to normal given a little time.

Some people will have stress reactions that do not go away on their own, or may even get worse over time. These individuals may develop PTSD.

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