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Chronic Post-Traumatic Stress Disorders

Chapter 16

CHRONIC POST-TRAUMATIC STRESS

DISORDER

FRANKLIN D. JONES, M.D., F.A.P.A.*

INTRODUCTION

History

Proposed Nomenclature for the Military

ETIOLOGY

Biological Models of PTSD

A Biopsychosocial Model of Etiology

PTSD PRESENTATIONS

TREATMENT

Psychotherapy

Pharmacotherapy

PTSD AMONG PRISONERS OF WAR

Precaptivity Training

Captivity Adaptation

Postcaptivity Recovery

SUMMARY AND CONCLUSION

*Colonel (ret), Medical Corps, U.S. Army; Clinical Professor, Uniformed Services University of the Health Sciences, Bethesda, Maryland; Past

President and Secretary and currently Honorary President of the Military Section, World Psychiatric Association; formerly Psychiatry and

Neurology Consultant, Office of The Surgeon General, U.S. Army
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David N. Fairrington Long Binh 1968

David N. Fairrington was a member of the U.S. Army Artist Team #6 and was in Vietnam from February

through June of 1968. In this striking visual presentation from that conflict, Fairrington captures the essence

of every soldier’s worst nightmare—carrying the body of his dead buddy and fearing that he himself may

be the body being carried. Post-traumatic stress disorder is a complex of symptoms most often predominated by flashbacks and repetitive nightmares of this nature.

Art: Courtesy of US Center of Military History, Washington, DC.
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Chronic Post-Traumatic Stress Disorders

INTRODUCTION

Post-traumatic stress disorders (PTSDs) comprise

the majority of stress disorders associated with the

trauma of combat, either of the acute, chronic, or

delayed type. Combat fatigue may be considered a

form of acute PTSD in its original understanding.

Chapter 1, Psychiatric Lessons of War, describes

this in greater detail. The chronic and delayed

forms of PTSD have assumed considerable importance as sequelae of combat in Vietnam and in the

1982 Lebanon War.1 The specific criteria for a diagnosis of PTSD, as delineated by the American Psychiatric Association’s descriptive and nontheoretical

Diagnostic and Statistical Manual, Fourth Edition

(DSM-IV),2 are presented in Exhibit 16-1.

History

Modern theories of PTSD begin with the 19th

century concept of traumatic neurosis. Railway

accidents from the middle of the century had seen

the development of increasing litigation by injured

persons suffering from pain and paralysis. The new

specialty of neurology initially attributed these apparent neurological deficits to spinal cord injury;

however, clinical and autopsy evidence began to

accumulate, revealing little correspondence between

tissue destruction (usually absent) and degree of

disability. It was recognized that “railway spine”

was a functional disorder. Charcot’s3 demonstrations of the production of paralysis and other symptoms in “hysterical” women suggested to Freud in

1893 a psychological etiology of hysteria. Charcot

retained his belief in a neurological cause of hysteria and its manifestations. This was the prevailing

idea. In 1889 Charcot’s student, Oppenheim,4 coined

the term “traumatic neurosis” to describe what he

thought was a “molecular derangement” of nerve

tissue. Initially Freud accepted this idea, postulating with Breuer in their classic work, Studies in

Hysteria,

5 an organic “hypnoid state” that made one

vulnerable to hysterical symptoms when stimulated by a traumatic event. Freud believed that the

traumatic event in hysteria was sexual. Later, when

evidence accumulated that cast doubt on the presence of actual sexual trauma, he postulated that a

fantasized sexual trauma could produce hysteria.6

Later Freud attributed war neuroses to conflicts in

ego structures (ego, id, superego) and instinctual

drives (libido, destrudo).7

The idea that psychological trauma could produce apparent physical disabilities became generally recognized, especially with the appearance of

numerous “shell shock” casualties of World War I.

The pendulum swung from considering those with

traumatic neuroses as neurological cases to considering them to be of purely psychological causation.

Eventually traumatic neurosis was mostly subsumed

under conversion or somatoform disorders but a

large group, whose symptoms took the form of

mood and behavioral disturbances, did not fit this

categorization.

The first edition of the American Psychiatric Association Diagnostic and Statistical Manual of Mental Disorders published in 1952 (DSM-I)8 included

combat reactions under Gross Stress Reaction that

corresponded in the International Statistical Classification9 1948 revision to Acute Situational Maladjustment. In DSM-I Gross Stress Reaction was to be

reserved for “conditions of great or unusual stress”

in which “a normal personality may utilize established patterns of reaction to deal with overwhelming fear.”8(p40) These were differentiated from neurosis and psychosis on the basis of “clinical history,

reversibility of reaction, and its transient character.”8(p40) In terms of prognosis the following was

stated: “When promptly and adequately treated,

the condition may clear rapidly. It is also possible

that the reaction may progress to one of the neurotic

reactions. If the reaction persists, this term is to be

regarded as a temporary diagnosis to be used only

until a more definitive diagnosis is established.”8(p40)

The diagnosis was stated to be “justified only in

situations in which the individual has been exposed

to severe physical demands or extreme emotional

stress, such as in combat or in civilian catastrophe

(fire, earthquake, explosion, etc.).”8(p40) In many

instances this diagnosis applied to previously more

or less “normal persons who have experienced intolerable stress.”8(p40)

The second edition of the Diagnostic and Statistical Manual (DSM-II, 1968)10 substituted the term

Adjustment Reaction of Adult Life for Gross Stress

Reaction. This was in the general category of Transient Situational Disturbances, which were defined

as follows:

This major category is reserved for more or less

transient disorders of any severity (including those
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EXHIBIT 16-1

APA DIAGNOSTIC CRITERIA FOR DSM-IV 309.81 POST-TRAUMATIC STRESS DISORDER

Reprinted with permission from American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 4th

ed. (DSM-IV). Washington, DC: APA; 1994: 427–429.

Exhibit 16-1 is not shown because the copyright permission granted to the Borden Institute, TMM,

does not allow the Borden Institute to grant permission to other users and/or does not include usage

in electronic media. The current user must apply to the publisher named in the figure legend for

permission to use this illustration in any type of publication media.
413

Chronic Post-Traumatic Stress Disorders

of psychotic proportions) that occur in individuals

without any apparent underlying mental disorders

and that represent an acute reaction from overwhelming environmental stress.10(pp48–49)

It is further stated in terms of prognosis that, “If

the patient has good adaptive capacity, his symptoms

usually recede as the stress diminishes” (author’s emphasis). If, however, the symptoms persist after the

stress is removed, the diagnosis of another mental

disorder is indicated.”10(p49)

This is a most unfortunate change because one

gains the impression that therapy should be aimed

at removing the individual from the stressful environment; in fact, a brief respite from the stressors is

needed, but removal too far produces chronic symptoms, and the object of treatment is rapid return to the

high-stress environment. Furthermore, it implies that

outcome is dependent only on the individual’s innate

adaptive capacity rather than requiring therapeutic

interventions to permit that adaptive capacity to recover. Contrast this impression with that given in

DSM-I: “When promptly and adequately treated,

the condition may clear rapidly.”8(p40)

In the third edition of the Diagnostic and Statistical Manual (DSM-III),11 published in 1980, the

clinician may place the combat stress reaction in the

Adjustment Disorder category specifying the presentation (depressed mood, anxious mood, etc.) or

may choose the Post-Traumatic Stress Disorder category. In the former, outcome as in DSM-II is stated

to be dependent on removing the stressor: “It is

assumed that the disturbance will eventually remit

after the stressor ceases.”11(p299)

Post-Traumatic Stress Disorder, among other criteria, lists “a recognizable stressor that would evoke

significant symptoms of distress in almost everyone.”11(p238) By dividing these disorders into acute

(duration of symptoms or onset of symptoms, less

than 6 mo following the onset of the traumatic event),

chronic (duration of symptoms 6 mo or more) and

delayed (onset at least 6 mo after the traumatic event),

the impression is given that one is dealing with a

lengthy disturbance due to psychological trauma.

In DSM III-R,12 the 1987 revision of DSM-III, and

DSM-IV,2 the 1994 edition, there is a requirement

for symptoms to last longer than a month. Presumably this was intended to make a distinction from

transient adjustment disorders; however, this requirement introduces an unnecessary disjunction

to the clinical and theoretical understanding of PTSD

as an exaggeration of normal responses to psychic

trauma. It does underscore the fact that the

eventuation of chronic symptoms suggests perhaps

persistent biological changes.

DSM-IV adds a new category, Acute Stress Disorder, for similar symptoms that occur during or

soon after the trauma, last for at least 2 days, and

cause clinically significant distress or impairment.

If this persists beyond 4 weeks, it becomes Acute

PTSD. This category corresponds reasonably well

to those stress (battle fatigue) casualties who require “restoration” at medical holding facilities

(clearing stations) for 2 to 3 days. It also covers

those who require “reconditioning” for 7 to 14 days

(or up to 4 wks) further to the rear. The DSM-IV also

notes that “some symptomatology following exposure to extreme stress is ubiquitous and often does

not require any diagnosis.” This could apply to

those battle fatigued service members who can remain in their own small unit or be given 1 to 2 days

of rest in a nonmedical support element, or who

recover and return to duty with only 24 to 36 hours

of treatment at a forward medical (clearing) company. The DSM-IV has also shortened the onset

time of chronic PTSD to 3 months post-trauma,

although “delayed onset” is still after 6 months.

In summary, DSM-I, having been published

shortly after the Korean conflict and based in large

part on the U.S. Army nomenclature growing out of

World War II experience, retained the correct concept for battle fatigue, which was placed under

Gross Stress Reaction. In fact, the description of

Gross Stress Reaction was almost an exact reiteration of that for Combat Exhaustion given in TB Med

203, the War Department Technical Bulletin, Nomenclature and Method of Recording Diagnoses,

published 19 October 1945.13 DSM-I was heavily

influenced by the psychobiology of Adolf Meyer

and the experiences of World War II psychiatrists.14

DSM-II, however, was published in 1967, over 15

years after the end of the Korean conflict, the last

conflict in which large numbers of battle fatigue

casualties were seen. The Vietnam conflict was in

its early stages; however, very few battle fatigue

cases were produced primarily because of the lowintensity nature of combat and other factors.15,16

Consequently the treatment lessons implicit in labeling did not have an urgent, emotional reality to

the authors of DSM-II.

The authors of DSM-III were well aware of the

effect of labeling as can be seen in the use of

“schizophreniform” instead of “schizophrenia” but

lack of familiarity with battle fatigue cases again led

to a failure to understand the treatment implications of the labels involved.
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414

Some of the thought involved might have been

due in part to the need to view Vietnam veterans as

having been damaged by their experiences in

Vietnam and as appropriate recipients of psychiatric care. Such concern might have led to the acceptance of post-traumatic stress disorder (PTSD)

and delayed post-traumatic stress disorder (DPTSD)

for a larger cohort of behaviors (such as addictive and aggressive acts) than had previously been

considered as sequelae of psychological trauma.

Unfortunately, such labels hold potential untoward consequences for the perception, diagnosis,

and treatment of the varied stress disorders that can

be generated in combat and that are amenable to

rapid intervention, very brief therapy, and quick

restoration to duty. DPTSD must be seen as a

special case that undoubtedly involves more complex historical factors both pre- and post-combat

than the usual stress responses to the trauma of

combat.

The DSM-IV category of Acute Stress Disorder

helps to restore a distinction between the transitory

reactions to extreme stress and more persistent

symptoms, “Acute” may also have fewer negative

connotations than DSM-I’s use of “Gross,” although

“gross” does imply more than a trivial response.

Proposed Nomenclature for the Military

The following guidance was given when the author was Psychiatry and Neurology Consultant to

the U.S. Army Surgeon General. It encapsulates

ideas on proper nomenclature for combat psychiatric casualties, drawing from the Manual of International Statistical Classification of Diseases, Injuries and

Causes of Death9 (also known as ICD-9):

Psychiatric combat casualties consist of a unique

group of military patients for whom the diagnosis

has strong possibilities for adversely affecting recovery. The term “battle fatigue” is ideal in that it

suggests a nearly normal response, is relatively

nonspecific in allowing for labeling of the great

variety of symptom syndromes known to occur,

and most importantly conveys an expectancy of

rapid resolution. The disadvantage is that many

psychiatric casualties occur so soon in combat that

fatigue cannot reasonably be presumed to be a

factor. Policy will be that patients in whom fatigue

can reasonably be considered a factor will continue

to be diagnosed as battle fatigue while those in

whom fatigue cannot be so considered will be diagnosed transient battle reaction. Both terms should

be considered roughly equivalent, should be treated

similarly and will be coded with ICD-9 number

308.4 (mixed disorders as reaction to stress). Avoidance of technical terms that could be regarded as

diagnoses (eg, “anxiety,” “conversion,” “paralysis”) is desirable. Two examples follow:

1. Unwounded soldier presenting with tremor,

tachycardia, sweating, paralysis of right arm,

and glove anesthesia of right hand ten minutes after observing a friend killed in the

first hour of battle:

(Axis I) 308.4 Transient battle reaction manifested by numbness and weakness of right

arm and hand, sweating, and rapid pulse.

2. Unwounded soldier developing fatigue,

tremor, tachycardia, sweating, paralysis of

right arm, and glove anesthesia of right hand

following 36 hours of sustained combat exposure.

(Axis I) 308.4 Battle fatigue manifested by

fatigue, numbness and weakness of right

arm and hand, sweating, and rapid pulse.

Subsequently, in current doctrine, the distinction between battle fatigue and transient battle reaction was abandoned. The rationale is that fatigue,

by definition, is impaired performance due to doing

something too long or too hard. As S.L.A. Marshall

observed, fatigue or exhaustion can be brought on

very rapidly by extreme fear. Anticipatory anxiety,

as well as physiologic strain can bring on battle

fatigue even before the battle starts. Therefore, the

one term, battle fatigue, suffices. As operations

other than war, such as disaster relief or peacekeeping in high stress conditions have increased

while combat has decreased, the terms “contingency fatigue” and “conflict fatigue” have also been

proposed.

ETIOLOGY

Psychiatric theories of etiology generally derive

from the cultural or scientific zeitgeist. Ancient

Egyptian healers, noting almost exclusive incidence

of hysteria in women and being well-versed in

anatomy, assumed that the multiple somatic symptoms of hysteria were due to migration of the uterus,

a theory that held sway until the medieval Catholic

Church, emphasizing the conflict between Satan

and God, attributed hysteria to possession by evil

spirits. After Isaac Newton revolutionized science

with his theory of universal gravitation, Anton

Mesmer began treating hysteria with magnets
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Chronic Post-Traumatic Stress Disorders

thought to have effects similar to planetary bodies.

In a contest with the renowned exorcist Father

Gassner, Mesmer demonstrated the superiority of

his “scientific” approach over the older theory of

possession.17

Likewise, in an era in which the intelligentsia

accepted Charles Darwin’s concepts of the evolution of increasingly complex structure and behavior

based on the survival of animals with the best instincts, Freud saw various neuroses as resulting

from instinctual drives clashing with reality. Thus,

those with hysteria suffered from unfulfilled sexual

wishes and those with obsessions and compulsions

suffered from expressions of or defenses against

anal eroticism and aggression. In this view, psychological trauma could cause anxiety symptoms due

to the activation of unacceptable sexual and aggressive wishes. While temperament varied, the psychological conflict was considered paramount. Until

the late 1970s psychological explanations of PTSD

etiology, usually based on psychoanalytic or learning theories, predominated.

Gradually, perhaps presaged by the Watson-Crick

discovery of the molecular structure of DNA, biological explanations of causality in mental disorders have gained hegemony. The concept of hysteria has almost disappeared except as a cluster of

personality traits; and obsessive-compulsive disorders are viewed by many as the survival in some

persons of instinctual grooming and other social

behaviors of our mammalian ancestors, often best

treated with medications.18 Concerning PTSD, this

biological supremacy has emphasized the physiological and neural aspects.

Biological Models of PTSD

Patients with chronic PTSD present with “positive” symptoms such as anxiety, tachycardia, muscle

tension, shortness of breath, insomnia, irritability,

and exaggerated startle response, which have been

postulated as arising from conditioned autonomic

activation to innocuous stimuli.19–23 PTSD is also

characterized by “negative” symptoms such as diminished interest in formerly significant activities,

interpersonal detachment, restricted affective range,

and a feeling of foreshortened future. These symptoms have been likened to the animal model of

learned helplessness.24

Biological models of PTSD have emphasized the

role of noradrenergic systems in the brain (primarily the locus ceruleus and its projections), which

are activated by situations of alarm or trauma, the

fight-flight reaction of Cannon.25 Such “trauma

centers” in the brain could be conditioned by threatening environmental events or stimuli associated

with threat (conditioned fear stimuli) to respond to

innocuous situations with PTSD symptoms.26

Drugs that inhibit noradrenergic brain systems

have been used to treat stress symptoms including

those of PTSD. These include clonidine, β-adrenergic blocking agents (propranolol), antidepressants

(which downregulate β-adrenergic receptors), and

benzodiazepines (GABA facilitators).26 Many substances abused by persons with PTSD may be attempts at self-treatment because they share the ability to inhibit noradrenergic systems, at least

temporarily. These include alcohol, benzodiazepines, barbiturates, and opiates.26 The effectiveness of serotonergic attenuating agents (such as

buspirone, a partial mixed serotonin 1A/1B receptor agonist) in treating anxiety disorders suggests

serotonergic excess theories of anxiety as well.

Stress-mediated changes in neuronal structures

of lower animals suggest that PTSD could be associated with fundamental and long-lasting modifications, including alterations in neuronal structure

and gene expression.26 Treatment, therefore, must

often be intensive and prolonged and preventive

measures should be the first approach.

While traumas cannot be prevented in conflicts,

it is noteworthy that not all those exposed to severe

traumas develop PTSD. In animal experiments of

inescapable shock or stress (ie, the learned helplessness model of PTSD and depression)27 those animals that could gain control over stress presentation and the severity, duration, and repetition of the

aversive stimulus did not develop learned helplessness. The presence of a supportive peer and previous escape experience have protective effects in

animals though biological and social vulnerabilities are factors.26

Studies also revealed that animals given antidepressants, clonidine, and benzodiazepines did not

develop learned helplessness when exposed to inescapable stress.27 Substances often abused by PTSD

sufferers (stimulants, barbiturates, ethanol, and

chronic use of benzodiazepines) were ineffective in

reversing learned helplessness once it developed;

however, antidepressants, clonidine, and buspirone,

had a normalizing effect in animal studies.26

In summary, while older theories emphasized

psychological trauma or conflict and conditioning

aspects of PTSD etiology, more recent investigators

have emphasized lasting neuronal changes and behavior in traumatized animals, postulating a

hyperadrenergic state with hypercortisolism and

physiological arousal to innocuous stimuli that re-
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416

semble the original stressor. Others28,29 have pointed

out the aspect of repetition of the trauma manifested by intrusive thoughts, nightmares, and even

hallucinations, thus implicating memory systems

as paramount. The author has emphasized a multifactorial etiology or biopsychosocial model of

chronic PTSD.30

A Biopsychosocial Model of Etiology

Chronic PTSD symptoms develop in those with social

and biological predispositions in whom the stressor is

meaningful when social supports are inadequate and the

symptoms are maintained because of subsequent inadvertent reinforcement of the maladaptive behaviors.

Following both World War I and World War II,

large numbers of combat veterans were treated in

Veterans Administration hospitals for chronic “war

neuroses.” Many of these former soldiers had broken in combat and had been evacuated, never to

rejoin their comrades. In many such soldiers a

dynamic was set up that produced increasing disability. The dynamic developed as follows: (a) the

soldier was conflicted over almost instinctual

urgings to leave the combat arena to secure personal survival, battling with his own concepts of

duty, honor, and responsibility to his comrades

requiring him to remain in combat, (b) medical

symptoms developed offering an honorable route

out of combat, (c) the symptoms were accepted as a

legitimate reason for leaving and the soldier was

evacuated, (d) the soldier experienced guilt for abandoning his comrades because at some level he did

not accept the legitimacy of his symptoms, (e) the

symptoms became strengthened and exaggerated

because of the soldier’s need to prove to others and

himself that he was really disabled and legitimately

left combat, and finally, (f) any reproach either from

internal guilt or from external doubt as to the medical necessity for his symptoms resulted in further

strengthening of the symptoms.

Such a dynamic would explain the development,

progression, and persistence of symptoms in the

improperly treated acute post-traumatic stress casualty who becomes chronically disabled; but how

can one explain the development of delayed PTSD

symptoms, often occurring years after combat exposure? Such cases suggest that the dynamic described may represent only a special case of a more

pervasive condition. Based on his study of psychiatric casualties in the 1973 Yom Kippur War and the

1982 Israel-Lebanon War, Belenky31 has postulated

that psychiatric casualties form a spectrum ranging

from immediate (“battle shock”) through acute

(“combat fatigue”) to late (chronic and delayed

PTSD) combat stress reactions. In each case the

etiopathogenic element is combat stress. The distinctions are based on certain intrinsic (personality,

prior adjustment) and extrinsic (degree and quality

of trauma, presence of ameliorating influences)

factors. This conceptualization complements

Marlowe’s battle ecologies scheme, with the latter

focusing on environmental factors (combat intensity).32

In Belenky’s conceptualization, delayed PTSD

results from the traumatic process itself, depending

on degree of trauma, and develops somewhat independently of subsequent events. The author’s view

of the development of delayed PTSD is slightly

different. While he agrees that a psychologically

traumatic event will result in PTSD symptomatology, he would emphasize the contingent nature of

the maintenance of, or delayed appearance of,

disabling symptoms. As with the dynamic described earlier, acute post-traumatic symptoms are

maintained and become chronic by their reinforcing value in preventing guilt or admonishment for

the soldier’s evasion of combat responsibilities. This

has sometimes occurred because of improper or

absent treatment.

The delayed PTSD syndrome, however, has a

slightly different history. In these cases the soldier

has experienced a traumatic event with variable

degrees of subsequent symptoms that eventually

disappear and may not even be remembered. Often, these soldiers performed without obvious impairment at the time, perhaps by denying fear or

grief. After a symptom-free interval, the former

combatant again experiences environmental stress.

Such stress may or may not resemble the stress of

combat; however, it evokes anxiety symptoms that

usually are similar to those of combat. This similarity evokes memories of combat trauma and even

produces in some instances reaction patterns similar to combat. These symptoms are reinforced in a

variety of ways, including the concern of friends,

justification for acting out otherwise unacceptable

feelings, sustaining the patients’ indignation over

being abused by society, and monetary reinforcement (Veterans Administration [VA] pension).

Within the past decade the belief has developed

that delayed and chronic PTSD are more common

following unpopular conflicts. This belief is based

on experience with U.S. veterans of the Vietnam

conflict and more recently with Israeli veterans of

the 1982 Lebanon War. In the Vietnam instance,

estimates as high as 700,000 or 25% of Vietnam

veterans were given as suffering from chronic
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Chronic Post-Traumatic Stress Disorders

PTSD.33,34 Other estimates as high as 60% of combat

veterans have been given.35 A more accurate figure

for Vietnam appears to be 17%,36 less than the 25%

psychiatric disabilities given for World War II veterans. In the Lebanon instance studies37 have revealed that two thirds of Israeli psychiatric casualties have been of the chronic or delayed PTSD type.

This is exaggerated because all Lebanon War veterans reporting to a mental health facility were labeled as suffering from PTSD even though they had

prior psychiatric diagnoses including manic-depressive disorder.38

Despite the possible exaggeration of PTSD prevalence, some relationship between unpopular wars

and chronic and delayed PTSD seems to exist.

Goodwin33 has identified the following variables as

producing chronic PTSD in Vietnam veterans: it

was a teenage war (average age 20 for combatants);

there was a fixed tour (unrealistic expectations after

return to states); the ideological basis of the war was

unclear (saving the corrupt South Vietnamese “democracy” from the North Vietnamese, not Soviet or

Chinese Communists); the enemy was hard to identify (sometimes the enemy appeared to be civilians—including women and children); there was

widespread use of illicit drugs (especially heroin

and cannabis); tranquilizing drugs were first used

in combat (may have suppressed symptoms of

stress); administrative discharges were frequent

(often for drug abuse) and were only temporary

solutions to stress; and the rapid return to the United

States did not allow for decompression, with the

returnee often being met with a hostile or indifferent homecoming. This may be a reflection of the

lack of societal support for wars of this type. They

are frequently ambiguous with a large percentage

of the population indifferent or hostile to the war.

Such wars are usually prolonged beyond the expectations of the initiators of combat and the patience

of the populations, and they often include actions

against civilians.

PTSD can be conceptualized as a special case of a

broader mechanism by which the mental apparatus

handles aversive stimuli. Freud’s postulate, described shortly after World War I, of a repetition

compulsion in which the organism replays the psychic trauma in an attempt to gain mastery, may play

a role, especially with the early symptoms.7 This

replaying may take the form of dreams or nightmares, recurrent memories, or even hallucinatory

“flashbacks” of the traumatic event. The sufferer

may be preoccupied with “if only I had (or hadn’t...)”

thoughts. Other mechanisms such as positive reinforcement (secondary gain in Freud’s model) seem

more important in the chronic maintenance of symptoms. The emergence of delayed symptoms may be

explained on the basis of an association between the

current situation and an aspect of the traumatic

situation. Ullmann and Krasner39 have used the

term “redintegration” for such evocation of behavior more appropriate to an earlier life event. Whatever the theory of causation, PTSD symptoms appear to be relatively universal given a severe enough

stressor; however, it is not the presence of symptoms but the psychological purposes they serve that

determines the degree of disability.

PTSD PRESENTATIONS

Diagnosis, treatment, and prevention of PTSD

will be considered in the context of the following

cases, which illustrate some of the features of chronic

and delayed PTSD. Diagnosis, treatment, and prevention of acute PTSD have already been described

in Chapter 1, Psychiatric Lessons of War, and Chapter 2, Traditional Warfare Combat Stress Casualties, in terms of combat fatigue or combat stress

reactions. The following two cases, known to the

author, illustrate some of the features of chronic and

delayed post-traumatic stress, ranging from normal

memories which are not a disorder to disabling PTSD.

Case Study 1: Just Bad Dreams

June K., now 60 years old, has never sought mental

health care despite mild, chronic post-traumatic stress

symptoms. Typically she develops nightmares after seeing a war movie or when undergoing unusual psychological stress such as the death of a family member. The

nightmares awaken her and her husband who reassures

her; then she falls asleep without further incident.

The psychic trauma that she experienced occurred at

the age of 18 when she was captured by the North

Koreans when they invaded Seoul in 1951. From a

prominent South Korean family, she and her parents and

siblings had been targeted for capture, torture, and death.

Knowing this, the family had dispersed throughout Seoul.

June K., the oldest child, had found work under an assumed name in order to buy food for her family (forced

rationing and use of North Korean money prevented

purchase of food with family resources). She was turned

in to the North Koreans by a collaborator who had recognized her from newspaper photographs. After several

days’ captivity, which included occasional beatings, she

escaped when the compound was bombed by U.S. planes.
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418

She hid for several weeks until Seoul was recaptured by

UN forces.

June K. served as a laboratory technician with U.S.

forces until the war ended; then she came to the United

States on a Fulbright Scholarship. Other than rare nightmares about her war experiences, there are no other

symptoms and no apparent secondary gains.

Comment: This person exhibits typical mild chronic

post-traumatic stress symptoms that do not appear to

serve any adaptive role in her current functioning. Her

symptoms are evoked by associations with the traumatic

event.

Case Study 2: The Assassination Witness

While the author was consulting in the psychiatric unit

of a military hospital in an Arabic country in 1985, he

interviewed a 54-year-old army major, formerly a Warrant

Officer, with 32 years of active duty. The major was

married with five children. He dated the onset of his

symptoms to an incident several years earlier when he

was present at the assassination of the leader of his

government, having been invited by his oldest son to see

him march in the parade.

Sitting near the leader, he initially thought that the firing

of weapons was part of the normal demonstration of

support for him. When he recognized the hostile nature of

the firing, which killed the head of state, the patient ran in

a panic about 3 miles, collapsing at the gate to his military

unit. He stated that ever since that time he has had

headaches, nightmares, and giddiness. Physical exams

and neurological studies revealed no apparent physical

basis for his symptoms.

The symptoms persisted roughly a year at which time

he was admitted to a hospital where he remained for

another year. In the hospital he was found to be severely

depressed but not suicidal. He also had severe anxiety,

trembling, elevated heart rate, complaints of irritability,

and dreams of airplanes bombing. He had also become

angry with his oldest son, who had urged him to attend

the ceremony. On one occasion he had even started

choking him. Psychometrics revealed that he had average intelligence and neurotic symptoms, primarily a depressive disorder with hysterical personality. He was

treated with thioridazine, lorazepam, and psychotherapy.

His request for a medical separation from the military was

denied.

Past history revealed that he had similar symptoms in

the 1956 Arab-Israeli War when, as an officer candidate at

the military academy, he was in a building that was

bombed, causing it to collapse. He remained terrified

underneath his bed for hours until he was dug out. Shortly

thereafter, a bullet from a second air raid narrowly missed

him. Afterwards he collected bullets as souvenirs. He had

a period of nightmares and anxiety following these episodes, but this did not persist beyond a few weeks.

A decade later he was an advisor to the Yemen Army

during their civil war. He stated that for a period of about

6 months he was constantly panicked. Several of his

fellow soldiers were ambushed and their bodies mutilated; however, he did not witness these episodes. He felt

isolated, alone among foreigners. A psychiatrist who

served at about the same time verified that such incidents

did occur but that the biggest problem was material

deprivation in an inhospitable climate. Following that tour

he again developed symptoms of anxiety and nightmares

that lasted for several months, but then they dissipated

and he experienced no particular problems until the assassination.

Currently, the patient appeared as a middle-aged man

with gray hair who was anxious and sweating profusely

while recounting his symptomatology. He presented my

fellow psychiatrists, some of whom had treated him, with

a letter that detailed his current complaints. He could not

tell us why he had persistent symptoms after the assassination, but did not after the barracks bombings in 1956

and after his Yemen tour. He did not participate in the

1967 or the 1973 wars with Israel.

The following were the patient’s complaints: giddiness,

especially when walking, with a tendency to be worse on

the right side; tinnitus leading to irritability and sometimes

violent actions toward his wife or children; numbness or

tingling in his scalp, “like I had a helmet on”; general

paresthesias all over the body; sleep disturbances (early

morning awakening, fatigue after having nightmares, and

frightening awakenings). During the day he often felt

tense as if his “head were full of blood” and as if the blood

in his head were “boiling.” He stated that he would

become irritable if in crowds or if he heard loud noises,

especially shooting. He also stated that he had profuse

sweating of the right hand. He described sexual difficulties (impotence for the past 3 years); pessimistic outlook

(that he hadn’t achieved anything in his life); withdrawal

and suspiciousness of other people; impulsiveness, depression, and sadness (in contrast to formerly being

friendly and energetic); anorexia with mild weight loss;

and smelling something burning. (The author’s colleagues

pointed out that this is a common symptom among PTSD

sufferers who were exposed to napalm or burning flesh in

various wars; however, this patient was not exposed to

those conditions, so the etiology of this symptom is obscure. Perhaps it may have been modeled after the

symptoms of other PTSD patients on the wards; such

“contagion” of symptoms among suggestible battle fatigue cases is common.)

During the interview the patient was very energetic and

animated, sweating profusely at times when recalling his

symptoms; but, at the same time he seemed to derive

some relief or even pleasure from sharing those symptoms and his suffering. His physician said that this patient,

despite the diagnosis on psychological testing of a hysterical personality, actually had many features of an obsessivecompulsive personality (having been meticulously clean,

very organized, very attentive to details, and somewhat

rigid in interpersonal relationships).

Etiologically, this patient appeared to have all of the

elements of a post-traumatic stress disorder: a severe

stressor (the assassination in which he could have been
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Chronic Post-Traumatic Stress Disorders

killed) and recreation of this and earlier traumas in nightmares and perhaps the smelling of something burning

(which could have been reminiscent of the gun powder at

the time of the assassination—an intrusion of the trauma

into the present). He also displayed the explosive irritability and aggressiveness as well as the withdrawal from

social contact that are often found in PTSD. The irritability

in the presence of loud noises, particularly the firing of

weapons, has some components of a startle reaction.

In terms of treatment, group psychotherapy should be

considered in this case although the lack of patients with

PTSD symptoms from the assassination episode would

weaken this approach. Usually group therapy works best

when all group members have been exposed to a similar

stressful situation.

Past individual psychotherapy apparently had focused

on ventilation and supportive treatment. It had also

emphasized work because he was denied compensation

and a medical separation. Such an emphasis on “here

and now” issues is desirable.

Comment: This patient exhibited a plethora of symptoms that, while typical of chronic PTSD, are seldom all

found in one person. His symptoms appear to serve a

current adaptive role in his functioning in making him a

focus of attention and sympathy and excusing him from

some military duties. Pharmacotherapy in such cases is

often quite rewarding. The patient had received some

anxiety relief from the thioridazine and lorazepam; however, he continued to be troubled by a multiplicity of

symptoms. Recent studies have shown that the use of

benzodiazepines beyond a few months may actually be

countertherapeutic due to the development of tolerance

effects.40 He had not yet been treated with antidepressants, particularly monoamine oxidase inhibitors (MAOI)

or the tricyclics. Although the mechanism of action of

these agents is unknown (their effectiveness might be

related to suppression of dreaming or REM (rapid eye

movement) sleep (and thus nightmares), due to a general

antidepressant effect or due to a specific anxiolytic action

related to downregulation of β-adrenergic or serotonin 1-

A receptors), these antidepressants often produce dramatic relief of symptoms. The author recommended a trial

of phenelzine (a hydralazine-type MAOI—Nardil) in a

dose of up to 90 mg per day. If there were problems with

his use of MAOI, perhaps dietary restrictions not being

enforceable, or other problems such as hypotension, then

a trial with a tricyclic, probably imipramine, was recommended. At the time, selective serotonin reuptake inhibitors (SSRI) were not available. Currently, a trial of an

SSRI might be helpful.

The following case, provided by Dean A. Inouye,

M.D., reveals an aspect of personality, alexithymia,

that may play a role in chronic PTSD. Alexithymia

(literally “inability to read emotions”) was described

as a characteristic of some patients who appear

unable to properly interpret emotions in themselves

and others.41

Case Study 3: Chronic PTSD and Alexithymia

First sergeant (1SG) MC is a 43-year-old married white

male with 22 years of service, self-referred for feelings of

distress following his involvement in a shooting incident.

In July 1991, 1SG MC and a security officer had attempted

to evict an occupant from the company barracks. The

occupant produced a gun and, without warning, shot 1SG

MC in the chest and killed the security officer. The patient

underwent surgery, which revealed no injury to vital structures. His post-operative course was unremarkable.

Past medical history revealed that the patient experienced three injuries during his two tours as a medic in the

Republic of Vietnam: 1969, gunshot wound to right thigh;

1970, fragment wounds to right leg and head; 1971, burns

to right hand and head. He had no other significant past

medical history or current medications. He rarely used

alcohol and denied use of tobacco or caffeine. He had no

known drug allergies.

Social history revealed that he was adopted in infancy

with a fraternal twin brother into an upper middle class

family. He was close to both parents, did well in school,

graduating from high school. He had no behavior problems

and joined the Army at age 20 after 2 years of business

college, “because I always wanted to.” His military history

was exemplary with many awards and citations.

Course: The patient first presented to outpatient psychiatry 1 month after his injury, complaining of rumination

about the shooting incident, decreased appetite, and

early insomnia with multiple awakenings, which he stated

was “no different than when I was shot in Vietnam.” He

appeared anxious but his mental status exam was otherwise unremarkable. He was given a diagnosis of adjustment disorder with mixed emotional features. He was

briefly tried on lorazepam (Ativan) 1 to 2 mg at bedtime to

improve the insomnia. The medication was discontinued

when the patient terminated treatment after three visits.

The patient returned to psychiatry 6 months after his

injury complaining of rumination with depressed mood,

pan-insomnia, increased appetite with 22 lb weight gain,

lack of energy and initiative, pervasive anxiety, sudden

crying spells and angry outbursts, decreased self-esteem

and social withdrawal, and a feeling of loss of control of his

emotions.

He had experienced the death of friends during the war

but denied survivor guilt. After returning from Vietnam he

had complained of prominent generalized anxiety; pronounced startle reaction without hypervigilance; pan-insomnia with multiple awakenings; nightmares of battle

scenes and ambush; difficulty concentrating; angry outbursts; fear of flying in helicopters but no vivid recollections while awake. He received no specific treatment for

his symptoms except diazepam (Valium). His symptoms

gradually abated after a few years although he continued

to have occasional nightmares. He believed that his

present PTSD symptoms were worse than those after the

Vietnam conflict. He was anxious and tearful during his

exam. He was given a provisional diagnosis of posttraumatic stress disorder. He was started on doxepin
War Psychiatry

420

(Sinequon) 25 mg at bedtime to improve his anxiety and

insomnia. Six weeks later, his treatment was terminated

due to his unwillingness to attend his appointments.

The patient returned to psychiatry a year after his

injury, 3 weeks before the anniversary date of the shooting incident. He complained of vivid recollections and

nightmares of the shooting event, hypervigilance and

easy startle, fear of situations similar to the shooting

event, difficulty falling and remaining asleep with multiple

awakenings, generalized irritability with occasional explosive anger, decreased concentration, and thoughts of

death. He denied feelings of guilt over his survival. He

expressed ambivalence about “coming for help” and fear

of becoming a patient in the hospital. On exam, he was

restless, with labile affect, and was frequently tearful.

During all interviews he was remarkably without insight

and unable to verbalize his feelings. His diagnosis of

post-traumatic stress disorder was confirmed. He was

given an additional diagnosis of alexithymia. He was

started on fluoxetine (Prozac) 20 mg tablets once a day

and clonazepam (Klonopin) 0.5 mg tablets three times a

day to improve his anxiety and insomnia. The patient was

placed on buspirone (BuSpar) 15mg per day, later increased to 30 mg per day.

He experienced a marked increase in his symptoms

during the anniversary week of the shooting. After that,

his anxiety decreased slightly and he experienced occasional nights of improved sleep, with fewer awakenings.

He complained of mild daytime sedation and the buspirone

was discontinued. His PTSD symptoms, in general,

remained unchanged. In October 1992, buspirone 5 mg

tablets three times a day was reintroduced to improve

anxiety, with the goal to discontinue clonazepam and

morning drowsiness. He reported gradually decreasing

anxiety and improved sleep. However, his anxiety was

often markedly worse on weekends and he continued to

have two to three awakenings per night.

The patient continued on the above medications with

clonazepam reduced to 0.5 mg at bedtime. After 2 months

on the medication regimen, the patient reported significantly decreased anxiety, improved feeling of control, and

improved sleep quality with fewer awakenings. On exam,

his restlessness and lability of affect were improved. His

other PTSD symptoms were unchanged and he could not

do his work satisfactorily. He was therefore presented to

a medical evaluation board (MEB) for separation from the

military.

Comment: This soldier had continued to experience

difficulties at work and he anticipated difficulties working

in a foreign country after impending retirement. The

symptoms may have represented an attempt to delay

retirement and hold on to his U.S. Army identity. They

may also have been an attempt to convey his feelings of

disability for compensation purposes.

These case studies suggest that varying degrees

of symptoms will follow a traumatic event. Whether

they become disabling depends on the use to which

they are put. In some circumstances, they can be

highly adaptive. The Arabian major, for instance,

trapped for 6 more years in a job that he did not

enjoy with little chance of promotion, would have

gained not only an exit from the army but also

additional money for a disability separation. Furthermore, his possible envy and anger toward his

upwardly mobile officer son could be justified by

making him responsible for the major’s current

distress. June K., however, does not utilize her

symptoms for current conflicts, having other adaptive mechanisms.

1SG MC functioned adequately until the time

approached for his retirement from the military

with the turmoil and uncertainties of a civilian life

in a foreign country. The symptoms kept him his

military identity and allowed him to express his

distress in an acceptable manner, a common finding

in alexithymic persons who cannot express feelings

directly but do so with symptoms, usually physical.

One of the main methods of preventing chronic

PTSD is by preventing (or properly treating) acute

post-traumatic stress symptoms.42,43 An important

element in preventing acute post-traumatic stress

(combat breakdown) is the presence of cohesive

units or social support during the stressful event.

Stretch44 has shown that social support following the

stressful event is also important in preventing or

attenuating symptoms of chronic or delayed PTSD.

He found, for example, that soldiers who remained

in the U.S. Army (which is socially supportive of the

combat role) following combat in Vietnam had significantly less symptomatology than controls who

left the military following assignment in Vietnam.

It is possible, of course, that self-selection accounted

for some differences (with those more prone to

PTSD disaffiliating themselves from the military);

however, other studies45 reinforce the importance

of social support in the prevention of PTSD.

TREATMENT

The treatment of chronic PTSD, like its etiology,

involves multiple modalities including emotional

conditioning, cognitive restructuring, and pharmacological interventions.46

Psychotherapy

Individual therapy is often too intense for both

patient and therapist, and group therapy with peers
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Chronic Post-Traumatic Stress Disorders

is usually preferable. While some “debriefing”

(abreaction and ventilation) of the original traumatic events must be expected, it is important to

prevent these sessions from becoming “stuck in the

past,” endlessly reiterating old guilts and grudges

and trying to outdo others’ stories. Here, and in

individual therapy if it is undertaken, the focus is

on current issues as in Glasser’s reality therapy

approach.47 It is usually clear to an objective observer what reinforcements are maintaining the

symptoms. To help clarify this area and intervene

in diminishing this reinforcement, family and other

interested parties may need to be interviewed individually and conjointly. This may also reveal that

the patient has minimized significant alcohol or

other substance abuse. When substance dependency is clearly established, an intervention and

referral for detoxification and rehabilitation in a

specialized program is indicated. Self-help groups

such as Alcoholics Anonymous (AA), Narcotics

Anonymous (NA), and Cocaine Anonymous (CA)

should play a prominent part in the treatment.

Deconditioning by teaching the evocation of the

relaxation response48 can help alleviate not only the

heightened tension of the hyperadrenergic state but

also the tendency to use substances for relaxation.

Exercise programs can also be beneficial in this respect.

Pharmacotherapy

Since the early descriptions of barbiturate treatment of combat stress casualties of World War II,49 a

variety of medications have been used to treat acute

and chronic PTSD symptoms. The first relatively

effective use was reported in an uncontrolled study of

five war veterans utilizing phenelzine.50 Subsequent

studies have validated the usefulness of MAOIs and

tricyclic antidepressants (TCAs) in the treatment of

some PTSD patients, particularly when complemented

with psychosocial therapies.51–54 More recently, the

SSRIs may be useful for some of these patients.

Most reports have emphasized the presence of

concurrent disorders with PTSD, particularly substance abuse, depressive disorders, and personality

disorders.52,54 These concurrent disorders often require different approaches and may prevent effective pharmacotherapy of PTSD symptoms.

For the different PTSD symptoms themselves,

different medications may vary in efficacy. Antidepressants appear to improve intrusive symptoms

(such as recurrent intrusive recollections, nightmares, and panic episodes) but may be less effective

with avoidant symptoms (such as withdrawal, emotional numbing).54 Intrusive symptoms as well as

hostility and feelings of violence were improved

by the tricyclic anticonvulsant carbamazepine

(Tegretol) in 70% of Vietnam veteran inpatients in a

study by Lipper and others.55 Again, improvement

in the avoidant symptoms was somewhat less. In

view of carbamazepine’s antikindling effect, this

suggests that PTSD symptoms may arise from the

effect of trauma in evoking repeated strong emotions, which result in neuronal irritability and inappropriate activation as postulated by Post et al56 in

the pathophysiology of certain mood disorders and

borderline personality disorders. Antikindling

agents such as valproic acid (Depa-kene) and

clonazepam appear useful as alternatives to lithium

and carbamazepine.

Other medications that have been helpful with

some PTSD patients include the antihypertensive

drugs, clonidine and propranolol, both of which

inhibit noradrenergic activity though by different

mechanisms.57 While benzodiazepines would seem

useful in anxiety symptoms of PTSD, they have not

been systematically studied, probably because of

their high abuse potential in this population. Preliminary reports of lithium therapy by Davidson et

al54 reveal encouraging results in diminishing explosiveness, irritability, mood swings, and impulsive behavior, as well as in reducing nightmares

and improving sleep. Carbamazepine, valproic acid,

and clonazepam appear similarly useful in these

symptoms.

At this time, careful assessment and treatment of

concurrent conditions and clinical trials with a variety

of medications along with psychosocial interventions

are warranted for most chronic PTSD patients.

PTSD can occur following any severe stressor;

however, prisoners of war represent a special case

in which the stressors tend to be chronic as well as

severe. They merit special consideration for study

and proposed interventions since the entire group

suffers similar status and deprivation stressors.

PTSD AMONG PRISONERS OF WAR

Prisoners of war (POWs) frequently develop

symptoms of chronic PTSD (see Chapter 17, The

Prisoner of War). POWs do not necessarily develop

psychiatric disorders; however, follow-up studies

of POWs during World War II, the Korean conflict,

and the Vietnam conflict indicate an increased risk
War Psychiatry

422

of such disorders.58–60 The risk is greatly influenced

by the conditions of captivity. Holocaust victims

almost universally suffered from PTSD.61 Soldiers

incarcerated by the Japanese during World War II

and by the North Koreans (and brainwashed by the

Chinese) during the Korean conflict have had increased rates of depressive, anxiety, and psychosomatic disorders, as well as suicide. Conditions of

captivity were often excessively harsh with many

deaths from malnutrition, infections, and exposure.

Soldiers who had surrendered to the Japanese

were treated with absolute contempt because they

had violated the samurai warrior code of Bushido,

which required the fighting man to die in combat,

commit hara kiri (suicide by disembowelment), or

request execution by the less favored method of

decapitation.62 Undoubtedly, brain syndromes

caused by malnutrition exacerbated the chronic posttraumatic stress disorders arising from captivity.

During the Korean conflict, captive Americans

were not only exposed to malnutrition, disease, and

harsh camp conditions but also to a calculated psychological offensive aimed at breaking them that

came to be called brainwashing. Crude coercive

measures involving Pavlovian conditioning, both

aversive and positive, with sleep deprivation, physical and psychological torture, and rewards for “acceptable” behavior (such as denouncing capitalism

and American “imperialism,” and admitting to using chemical and biological warfare) were used in

conjunction with sophisticated social manipulation.

Officers were separated from enlisted ranks to destroy the influence of leadership. Cohesion was

destroyed by rewarding selected soldiers for informing on their fellows. Rewards of food, clothing, and medication might mean the difference between survival and death during the cold Korean

winters. Information was carefully controlled; only

adverse news (such as race riots in the United States)

was presented to the POWs.

Critics of the POWs, not taking into account this

new form of psychological warfare and hearing

American soldiers denounce America or confess to

fabricated war crimes, accused them of lacking willpower and indicted American child-rearing practices as producing psychological weaklings. Such

criticisms were even extended to those who died of

malnutrition, exposure, and illness; they were accused of having “give-up-itis,” moral strength so

weak that they would die rather than try to live in

adverse circumstances.63

Based on his interviews with 20 randomly selected repatriates at the end of the Korean conflict

and the work of colleagues who interviewed 300

men, Schein,64 a researcher at Walter Reed Army

Institute of Research, described what was probably

the most extensive attempt to destroy unit cohesion

and realign social viewpoints ever perpetrated

against U.S. prisoners of war. The men were segregated according to race and ethnicity. Military rank

was disregarded and the Chinese captors randomly

selected small unit leaders. Informers were actively

solicited and given special treatment, some of it life

sustaining, such as adequate food while others were

starving. Such favors were sometimes given

noncollaborating soldiers to destroy confidence in

them. POWs soon felt that they could not trust

anyone. Signed confessions of germ warfare or

other war crimes by U.S. forces were solicited and

shown to POWs to attack the moral position of the

United States. No group association was allowed

other than Chinese-orchestrated self-criticism or

propaganda lectures. Mail was censored so that

only bad news was transmitted. Similarly, all news

was from communist sources—press, radio, magazines, and movies. Race riots and criminal acts in

the United States were highly publicized.

The postcaptivity evaluations revealed that the

communists had little success in changing beliefs

and attitudes; however, in producing collaboration

they had been much more successful with about

10% to 15% of the men chronically collaborating in

giving pro-communist lectures, broadcasting propaganda, giving false confessions, informing on

fellow POWs, and so forth. Some attempted to

obstruct the communists and they were generally

transferred elsewhere. A few developed severe

apathy, quit eating, and died. The most common

response was neither collaboration nor obstruction

of the communists but what the men called “playing it cool”; that is, physical and emotional withdrawal from the whole environment, developing an

attitude of watching and waiting rather than hoping and planning.

Schein concluded, “Ultimately that which sustains humans is their personality integration born

out of secure and stable group identifications.”64(p30)

Long-term follow-up has revealed that while many

POWs improved, symptoms were often life-long.65–67

Following the Korean conflict, there was a great

deal of media attention focused on the behavior of

Korean-era POWs and measures that might be taken

for the physical and psychological survival of the

POW. In 1955, President Eisenhower issued the

Code of Conduct68 (Figure 16-1) that reaffirmed the

basic tenets of resisting the enemy as much as possible and attempting to escape when feasible. It was

and is believed that these guidelines actually pro-
423

Chronic Post-Traumatic Stress Disorders

THE CODE OF CONDUCT

Article 1

I am an American fighting man. I serve in the

forces which guard my country and our way of life.

I am prepared to give my life in their defense.

Article 2

I will never surrender of my own free will. If in

command, I will never surrender my men while

they still have the means to resist.

Article 3

If I am captured, I will continue to resist by all means

available. I will make every effort to escape and aid others to

escape. I will accept neither parole nor special favors from

the enemy.

Article 4

If I become a prisoner of war, I will keep faith

with my fellow prisoners. I will give no information or take part in any action which might be

harmful to my comrades. If I am senior, I will

take command. If not, I will obey the lawful

orders of those appointed over me and will back

them up in every way.

Article 5

When questioned, should I become a prisoner of

war, I am required to give name, rank, service number, and

date of birth. I will evade answering further questions to the

utmost of my ability. I will make no oral or written statements

disloyal to my country and its allies or harmful to their cause.

Article 6

I will never forget that I am an American fighting man, responsible for my actions, and dedicated to the principles which made

 my country free. I will trust in my God and in the United States of America.

tect the soldier from undue guilt associated with

giving in under a less stringent code. More recently, forced “confessions” and denunciations of

America are ignored because they are obtained by

coercion.

Most of the American POWs of the Vietnam

conflict were aviation officers shot down over North

Vietnam. They had succeeded in the rigorous selection and training process for aviation pilots. Not

surprisingly, these highly intelligent men invented

ingenious methods of resisting the enemy, communicating among themselves even though usually

placed in solitary confinement, and strengthening

their mental defenses. They often practiced regular

physical exercise, meditation, and “mental exercises” such as remembering books, mentally building a home, and writing journals though deprived

of writing materials. Follow-up studies conducted

after their release revealed that they were healthier

than matched controls in all physiological systems

other than dental and mental health. They tended

to suffer more psychological problems than the

controls but the differences were slight.

The relatively small number of POWs who had

been captured in South Vietnam consisted primarily of ground troops whose experiences were similar to those captured by the Japanese and North

Koreans. Their postcaptivity adjustment resembled

that of the World War II and Korean conflict POWs

(ie, increased morbidity).

An understanding of and techniques for handling captivity stress have been developed69–72 based

on the experiences of POWs from World War II, the

Korean and Vietnam conflicts as well as other groups

Fig 16-1. Code of Conduct for Members of the Armed Forces of the United States. After the Korean conflict, it was

realized that coercive “brainwashing” could cause even the most patriotic soldier to be induced to make statements

denouncing his country. The code was originally issued by Executive Order 10631 on 17 August 1955 by President

Dwight D. Eisenhower and was amended by Executive Order 12017 on 3 November 1977 by President Jimmy Carter.

Each soldier is given a copy. Data source: Department of the Army, Code of Conduct/Survival, Evasion, Resistance, and

Escape (SERE) Training. Washington, DC: DA, 10 December 1985. Army Regulation 350-30.
War Psychiatry

424

(USS Pueblo crew members captured by North Korea and the U.S. Embassy personnel taken hostage

in Iran). These can be considered in three phases:

(1) precaptivity training; (2) captivity adaptation;

and (3) postcaptivity recovery.

Precaptivity Training

Precaptivity training is needed for anyone likely

to become captive, including military personnel,

embassy staff, and others. This should involve

learning the expected responses to phases of captivity and methods of adapting optimally to them, and

realistic role-playing for purposes of familiarization and desensitization. Generally such training

will have survival value. While 30% of American

prisoners of the Japanese and North Koreans died

in captivity, only 15% of American POWs in North

Vietnam died. Although demographic differences

(higher education, older, and mostly officers in the

Vietnam POW population) and a less hostile climate were predominantly responsible for fewer

deaths, soldiers who became POWs in Vietnam had

been given captivity training.71

Captivity Adaptation

Captivity adaptation generally occurs in certain

stages, which have been described by Rahe and

Genender72 as follows:

Stage 1: Startle/Panic—First Seconds to Minutes

Captivity typically occurs as an abrupt transition

from normal daily activities to a situation of forceful, often brutal subjugation, a situation that cannot

be assimilated quickly. Captors are excitable and

have an increased likelihood of killing the captives

at this point, producing paralyzing fear, stunned

dissociation, or panic flights in captives. Feelings of

defenselessness and confusion usually follow actual capture. Successful coping involves rapidly

controlling these emotions. This may be facilitated

by conscious attempts to count the captors, to memorize their features, and to focus on details of the

situation.

Stage 2: Disbelief—First Minutes to Hours

Denial in the form of thinking, “This can’t

be happening” or “I’m dreaming,” may occur.

Captives often believe that they will be rescued

quickly and are disappointed when this does not

occur. Captors engage in various dehumanizing

activities such as stripping clothing and personal

items, binding, blindfolding, beating, and photographing prisoners for propaganda purposes. Similarly, “confessions” may be extorted by torture for

propaganda value. Captives usually cope best by

turning their attention inward—thinking of loved

ones, home, and freedom—because psychological

dissociation from the painful situation is adaptive

in this setting.

Stage 3: Hypervigilance—First Hours to Days

The emergence of increased alertness to environmental cues can be useful—attempting to keep track

of time, mileage, turns of the vehicle; however,

guards are usually highly attentive to possible escape attempts at this time. Generally some form of

interrogation will begin with emphasis on intelligence gathering. Hypervigilance can be useful in

helping the captive withhold desired intelligence, in

orienting to a 24-hour cycle, in assessing the captors,

and in possibly eliciting the sympathy of guards

who may assist the captive in obtaining reading and

writing materials and other basic amenities.

Stage 4: Resistance/Compliance—First Days to

Weeks

As the captors attempt to coerce the captives into

cooperating, the resistance/compliance stage begins. Interrogations change from intelligence gathering to exploitation with coercive demands for

“confessions” of “crimes” or enforced public appearances, often in degrading conditions. Given

sufficient physical and psychological torture, virtually anyone can be forced to cooperate with his

captors. The degree of cooperation depends on the

severity of torture inflicted and the captive’s commitment to resist.

The techniques used by captors derive from those

used by the Czarist Russian and Stalinist secret

police and the state police of Nazi Germany, with

refinements added by the Communist Chinese and

North Koreans. They include intimidating arrest;

imprisonments of indeterminate length; physical,

social, and nutritional deprivation; disturbances of

body rhythms; physical and sensory isolation; stressful (often brutal) interrogations; unpredictable responses from guards and inquisitors; prolonged

fear of death; and attempts to “reeducate” the captive. Settings are usually cramped, filthy, pestridden, uncomfortably cold or hot, with poor lighting and ventilation. Communication with fellow

captives, or even guards, is prohibited.
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Chronic Post-Traumatic Stress Disorders

Coping in these circumstances involves attempts

to keep physically fit, to give the captors just enough

information (preferably hard to validate and requiring lengthy time) to prevent severe torture, and

attempts to communicate with fellow captives.

Religious faith, prayer, meditation, and thoughts of

loved ones also play an important role in coping.

Stage 5: Depression—First Weeks to Months

As the extent of his losses (freedom, family,

friends, fortune, and possibly future) becomes apparent, the captive may become depressed. The captive

may show the classical signs and symptoms of depression, including anorexia, retarded speech and

movements, insomnia, fatigue, guilt, self-condemnation, and suicidal thoughts or attempts. Coping

is greatly aided by a strong support group, hence

the need to establish communication. The captive

can use his own intelligence to fight boredom, composing stories and poems, mentally constructing

buildings, solving mathematical problems, etc.

Captor behavior at this time is primarily custodial.

Stage 6: Gradual Acceptance—First Months to Years

The captive realizes that his captivity may be

prolonged and that he must make more productive

use of his time if he is to survive. Custodial behavior by captors is usually maintained although “reeducation” efforts may continue. Coping behavior

by captives involves living from day to day, taking

each day as it comes, and attempting to maintain

physical and mental stamina. Group support, if

available, is extremely sustaining. Best is group

creative work such as crafts, sports, and possibly

escape planning.

Postcaptivity Recovery

Rahe and Genender72 have described six stages of

recovery from captivity as follows:

Stage 1. Brief Euphoria—First Seconds to Minutes

The period of elevated spirits of a released captive is usually short-lived. The captive is often

mistrustful that the return from captivity may be

another false hope. Celebrations may fall flat.

Stage 2: Hyperarousal—First Minutes to Hours

In contrast to the understimulation of the later

stages of captivity, the released captive is overwhelmed by stimuli and mentally slowed, causing

a “punch-drunk” appearance. Often sleep-deprived

on their transition to freedom, the former captives

may be confused and exhausted.

Postcaptivity management optimally includes

a period of from several days to a week of “decompression.” The ex-captive needs protection from

the very intrusive media and even from

relatives, because he may make remarks that he

will later regret. For example, persons still influenced by the “Stockholm Syndrome” (identification with the captors) upon release have made

statements favoring the aims of their captors

and detrimental to the national interests of their

country.

During this decompression time, thorough physical examination and correction of medical problems

(eg, infections, infestations, dental care) can be

accomplished. Rest and restoration of physiological deficits (sleep, food, fluids) are important

just as with combat stress cases. In addition to

physical restoration, the principles of proximity

and immediacy indicate rapid return to the

precaptivity milieu after decompression and positive expectancy. Psychiatric examination must be

carefully conducted to avoid an expectation of mental illness, which can lead to a chronic “compensation neurosis.” A positive expectation that the excaptive will soon return to work is important. The

psychiatric examination should be both diagnostic

and therapeutic, allowing ventilation while providing reassurance.

Stage 3: Compliance/Resistance—First Hours to

Days

Captives initially on release are likely to comply

with most requests, having been conditioned to do

so by their captors. As they regain feelings of

individual power and capability, captives will begin to resist activities that appear to have little

relevance to their own needs, for example, appointments, psychological testing, and intelligence debriefing. Treatment plans should take into account

this emerging independence by allowing free time,

the wearing of clothing other than hospital pajamas, time for group meetings with fellow captives,

etc. Group cohesion can be fostered by having excaptives eat together and engage in group “rap

sessions.” As with Marshall’s73 technique of debriefing troops after a battle, the reconstruction of

events and correction of misperceptions can be

highly therapeutic. Finally, follow-up reunions

may be helpful.
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426

Stage 4: Denial—First Days to Weeks

After an initial candidness about their problems

adjusting to freedom, captives are likely to enter a

phase of denying that their captivity has produced

significant emotional or physical problems. While

these statements should not be challenged directly,

they should not be taken at face value. Arrangements for ongoing follow-up evaluations and treatment should be made, often through liaison with

family members.

Stage 5: Restitution—First Weeks to Months

Attempts at restitution may take a variety of

forms, such as gross obesity from overeating, problems with emotional control, and isolation to avoid

overstimulation. Employers may attempt restitution by granting long vacations from work when, in

actuality, return to a work routine generally helps

the ex-captive reestablish feelings of self-worth.

The family may attempt restitution by providing all

the love and attention they could not show during

the captivity. Captives may have difficulty interpreting nonverbal behaviors and the affective content of language. Families should be told to expect

disconcerting responses, including crude table manners, and bathroom and sleeping habits acquired in

captivity. They should also be told to expect and

even encourage the ex-captive to recount his captivity experience because it seems to serve a therapeutic abreactive purpose.

Stage 6: Gradual Readjustment—First Months to

Years

Follow-up studies of American POWs from Korea and from World War II Japanese prisons, in both

circumstances experiences being extremely severe,

revealed increased rates of infectious, cardiovascular, degenerative, and psychiatric disorders and

accidental deaths compared to control subjects over

the next 25 to 30 years.72 Depending on the severity

of circumstances and the individual’s coping skills,

some psychological scarring and premature physical disability is likely for the duration of the exPOW’s life. Ongoing follow-up for significantly

traumatized individuals may prevent or attenuate

disability, but some degree of post-traumatic stress

symptoms is inevitable.

SUMMARY AND CONCLUSION

Post-traumatic stress disorder has come to epitomize the blaming and legalistic tendency in modern

American society. It is given currency to explain

the most outrageous behavior from Vietnam veterans’ trafficking in cocaine and narcotics and

robbing banks to a sexually promiscuous

woman’s attributing her behavior to trauma on a

San Francisco cable car. Despite these unlikely

extensions of the PTSD concept, a core of solid data

exists suggesting psychic trauma as underlying

much of nonbiologically generated mental illness.

Such apparently disparate conditions as multiple

personality disorders, panic disorders, and

psychogenic depressions may result from early

physical and sexual abuse. Psychic trauma occurring in older persons may lead to the development

of a constellation of symptoms and behaviors that

are termed PTSD. It is often unclear as to who is

most responsible for these symptoms, the traumatized person or the original stressor. Attorneys

make a living persuading juries and judges one way

or the other.

The traumatized person’s best hope is to accept

responsibility for his symptoms and to develop

coping methods to neutralize them. This should be

the aim of psychiatric treatment.

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