Treatment of Posttraumatic Stress Disorder: A Review

ARIEH Y. SHALEV, MD, OMER BONNE, MD, AND SPENCER ETH, MD

This article analyzes the literature on the treatment of posttraumatic stress disorder (PTSD). It briefly exposes
the theoretical basis for each treatment modality and extensively examines pharmacological, behavioral,
cognitive, and psychodynamic therapies, as well as group and family therapies, hypnosis, inpatient treatment,
and rehabilitation. Articles were identified by scanning Medline and PsychLit for all papers in English
reporting treatment of PTSD. Anecdotal case reports were, then, excluded. Eighty one articles were identified
and categorized as either biological or psychological, with the latter category further divided into behavioral,
cognitive, psychodynamic, and other treatment modalities. Information regarding the type of trauma, the
sample studied, the treatment method, and the results of the treatment has been extracted from each article
and is presented briefly. A synthesis of findings in each area is provided. Most studies explored a single
treatment modality (e.g., pharmacological, behavioral). The cumulated evidence from these studies suggests
that several treatment protocols reduce PTSD symptoms and improve the patient's quality of life. The
magnitude of the results, however, is often limited, and remission is rarely achieved. Given the shortcoming
of unidemnsional treatment of PTSD, it is suggested that combining biological, psychological, and psycho-
social treatment may yield better results. It is further argued that rehabilitative goals should replace curative
techniques in those patients with chronic PTSD. A framework for identifying targets for each treatment
modality is presented.
Key words: biopsychosocial framework, posttraumatic stress disorder.

INTRODUCTION acting or feeling as if the traumatic event were

During the past 300 years, a variety of terms have
been applied to the mental sequelae of severe
trauma, including: Nostalgia, Soldier's Heart, Rail-
way Spine, Shell Shock, Combat Neurosis, and Com-
bat Fatigue. Each of these names reflected a theoret-
ical view of the cause of mental trauma (e.g.,
homesickness, mechanical impact, exhaustion, men-
tal conflict] and its nature (neurosis, dysregulated
circulation]. The current appellation, posttraumatic
stress disorder (PTSD) (l), points to our current
belief in stress as a cause of mental disorders.
In its most recent definition (1), PTSD is a perva-
sive anxiety disorder that follows exposure to stress-
ful events. DSM-IV diagnostic criteria for PTSD (l)
include: a) exposure or confrontation with a trau-
matic event accompanied by intense fear, helpless-
ness, or horror; b) persistent reexperiencing of the
traumatic event, expressed by at least one of the
following: recurrent and intrusive distressing recol-
lections of the event, recurrent distressing dreams,
From the Center for Traumatic Stress, Hadassah University
Hospital, Jerusalem, Israel.
Address reprint requests to: Arieh Y. Shalev, MD, Center for
Traumatic Stress, Department of Psychiatry, Hadassah University
Hospital, P.O. Box 12000, Jerusalem, 91120, Israel.
Received for publication January 17, 1995; revision received
August 10, 1995.
recurring, distress on exposure to cues that symbol-
ize or resemble an aspect of the event, and physio-
logical reactivity on exposure to cues that symbolize
or resemble the trauma; c) avoidance of stimuli
associated with the trauma and numbing of general
responsiveness, expressed by: efforts to avoid
thoughts, feelings, or conversations associated with
the trauma, efforts to avoid activities, places, or
people that arouse recollections of the trauma, in-
ability to recall an important aspect of the trauma,
markedly diminished interest in previously signifi-
cant activities, feeling of detachment or estrange-
ment from others, restricted range of affect, and
sense of a foreshortened future (three symptoms
required]; and d] persistent symptoms of increased
arousal, such as difficulty falling or staying asleep,
irritability or outbursts of anger, difficulty concen-
trating, hypervigilance, or exaggerated startle re-
sponse (two symptoms required). The duration of
the disturbance must exceed 1 month, and it should
be associated with significant distress or impair-
ment.
Several features of PTSD attest to its inherent
complexity: a) Instances of recovery from PTSD
regularly occur during the first year of its course (2),
and 15 to 25% of the survivors of severe traumatic
events may suffer from a chronic PTSD (3, 4); b)
PTSD is among the few disorders for which DSM-IV
specifies a cause (i.e., the traumatic event). Yet, this
requirement implicitly equates common incidents,

Psychosomatic Medicine 58:165-182 (1996) 165

0033-31 74/96/5802-0165S03.00/0
Copyright © 1996 by the American Psychosomatic Society

such as road traffic accidents, with prolonged war
exposure or colossal atrocities, such as the Holo-
caust; c) classified among the anxiety disorders,
PTSD has also been considered for inclusion among
the dissociative disorders or as part of a separate
category of "stress disorders" (5); and d) the core
clinical features of PTSD, namely reexperiencing
and avoidance, closely resemble those observed dur-
ing normal grief (6-8) thereby suggesting that PTSD
symptoms may reflect an attempt to deal with the
meaning of the trauma and the associated loss. Yet, a
strong component of learned conditioning seems to
underlay PTSD, and behavioral interventions effec-
tively ameliorate both avoidance and intrusion
symptoms in PTSD (9-11). Finally, neurobiological
research (12) offers pertinent insights into the patho-
physiology and pathogenesis of this "psychogenic"
disorder.
Unlike other disorders, such as major depression,
obsessive compulsive disorder (OCD), schizophre-
nia, or phobias, for which one treatment modality
has emerged as being uniquely effective (e.g., anti-
depressants, specific serotonin reuptake inhibitors
(SSRIs), neuroleptics, and desensitization, respec-
tively), PTSD has no such prominent treatment.
Given its complexity and given the lack of specific
therapy, one may argue that a reasonable approach to
the treatment of PTSD involves a multi-dimensional
model. Discontent with the therapeutic results of
unidimensional treatment approaches (13, 15) fur-
ther supports this argument. Barlow (15) proposed
one such complex model of PTSD, which includes
consideration of the role of biological and psycho-
logical vulnerabilities, negative life events, fear reac-
tions, perceptions of control, social support, and
coping strategies.
In a previous article (16), we proposed, on a basis
of clinical vignettes, a four-level model based on
Engel's (17) "biopsychosocial" paradigm. The bio-
logical level of this model refers to alterations in
neuronal functioning that may be expressed, in af-
fected individuals, as a result of their traumatic
exposure. The psychological-behavioral level in-
volves conditioned fear responses acquired during
the trauma and reinforced thereafter. The next level
incorporates altered networks of meanings as re-
flected in profound changes in self-concept and
interpersonal relations that follow trauma. Finally,
the social level includes real and symbolic interac-
tions between the individuals and the society that
are involved in the acquisition and maintenance of
the trauma, as well as the healing from trauma.
Although each of these four interacting levels is a
potential target of a specific treatment approach, we
166
A. Y. SHALEV et al.
have argued that a combined treatment approach,
addressing several of these layers, is particularly
appropriate for PTSD.
This article expands the multi-level paradigm by
critically reviewing the main explanatory models of
PTSD and the related literature on treatment of the
disorder. We also examine the idea that the neuro-
biological imprint of psychic trauma may become
indelible, such that rehabilitation rather than the
curative approach is often indicated.
THE BIOLOGICAL APPROACH TO PTSD
Biological Formulation and Research
Research into the psychobiology of PTSD has
followed two paths. The first consists of a search for
commonalties among biological findings in PTSD
and those in other mental disorders, and the second
involves a quest for specific attributes of PTSD.
Similarities Between PTSD and Other Mental
Disorders
Comorbid panic disorder was found in 13 to 19%
of PTSD patients (18, 19). In other PTSD patients,
sudden arousal on exposure to cues reminding the
patient of the trauma bears phenomenological re-
semblance to panic anxiety (20). Further, anxiety,
dissociation, and flashbacks can be elicited in PTSD
patients by experimental procedures that provoke
panic attacks in patients with panic disorder (e.g.,
administration of yohimbine or lactate) (20, 21).
Theoretical formulations based on this analogy as-
sign a role to the locus ceruleus-norepinephrine
(LC-NE) "alarm" system in PTSD (12, 21) and predict
a positive effect of anti-panic medication on PTSD
symptoms.
Major depression is frequently co-diagnosed in
PTSD patients (22, 23). Depressive symptoms resem-
ble DSM-IV PTSD symptoms of "diminished inter-
est," "restricted range of affect," and "sense of fore-
shortened future." Treatment modalities based on
that relationship involve antidepressants and MAO
inhibitors.
Specific Biological Attributes of PTSD
Among the "specific" models of PTSD are: a)
dysregulation of opioid neuromodulation, b) im-
printing and consolidation of traumatic memories,
and c) hypothalamic-pituitary-adrenal (HPA) axis
dysregulation.
Psychosomatic Medicine 58:165-182 (1996)
TREATMENT OF POSTTRAUMATIC STRESS DISORDER: A REVIEW
During stress, opioid neuromodulation is responsi-
ble for phenomena such as stress-induced analgesia
and amnesia (24). The "opioid" model of PTSD (24)
further expands the role of opioides into the chronic
condition, suggesting that the presence of distressful
and repetitive behavior in PTSD, such as self-inflicted
pain, reexposure to danger, or emergence of distressful
recollection of the trauma, is due to an inappropriate
release of endogenous opioides during adversity. Par-
tial support for this view was provided by a study
showing that naloxone, an opiate antagonist, reverses
stress-induced analgesia in PTSD (25).
The memory imprinting model assumes that the
"etching" of traumatic experiences into a neuronal
network plays a major role in the etiology of the
disorder. Earlier formulations (26, 27) theorized that
stress hormones, secreted during the traumatic
event, may mediate the consolidation of traumatic
memories. A recent observation (28) suggests, in-
deed, that inhibition of beta-adrenergic transmission
by propranolol, during exposure to distressful and
neutral audio-visual narratives, reduces the number
of distressful items remembered. The relevance of
these findings to conditions of extreme stress re-
quires further study.
Emotional memory is of particular interest in
PTSD. In a series of animal studies, LeDoux (29)
showed that the acquisition of fear conditioning is
mediated by a dual neuronal pathway that involves a
subcortical path, which includes the sensory thala-
mus and the lateral and central nuclei of the amyg-
dala, and b a thalamocortical path, involving the
sensory cortex and similarly leading to the amyg-
dala. Lesions to the cortical pathway, however, did
not interfere with the acquisition of conditioned
fear. Moreover, such lesions prevented the extinc-
tion of fear conditioning thereby suggesting that, in
the absence of cortical inhibition, emotional memo-
ries may be stored "forever" at subcortical levels of
the brain. Clinical features of PTSD (e.g., reactivation
of recovered PTSD patients on exposure to new
traumata or in aged veterans, delayed onset of PTSD
(e.g., 30-32)) are consistent with the concept of
indelible memory: harnessed, but never deleted.
Successful treatment of PTSD, accordingly, may not
involve an eradication of traumatic memories but
rather an enhanced control over previously acquired
fear responses.
A variation on the memory imprinting theme is the
kindling model of PTSD (33). By analogy with the
acquisition of kindled seizures in animals, this model
postulates that the repeated processing of distressful
recollections progressively decreases the threshold for
neuronal transmission of similar signals up to the point
Psychosomatic Medicine 58:165-182 (1996)
of inducing an irreversible cycle of spontaneous repe-
titions. Animal studies have shown that such a process
involves a cascade of functional and structural modi-
fications (e.g., early and late gene expression, new
protein synthesis, neuronal sprouting) leading to irre-
versible modifications of synaptic conductivity (33).
Important to note, this model extends the time
interval for "traumatic imprinting" into the postex-
posure period. It implies that intense arousal, paired
with external or internal cues of the trauma, during a
critical period after the event induces neuronal
changes that may later be expressed as PTSD. An
association between secondary stressors (i.e., those
that follow the impact phase of traumatic events)
and long term psychopathology is also predicted by
this model. Interventions aimed at reducing hyper-
arousal among recent trauma survivors (e.g., by com-
forting the patient or preventing further distress or
by pharmacological agents) may, therefore, operate
as secondary prevention.
Studies of the HPA axis have shown a decreased
epinephrine/cortisol ratio, elevated urinary cat-
echolamines, and an increased dexamethsone sup-
pression in PTSD (e.g., 34-36). Findings of en-
hanced feedback sensitivity of the HPA axis in PTSD
are opposed to those observed in depression. Re-
cently, elevated levels of serum-free triiodothyro-
nine, thyroxin-binding globulin, and total thyroxin
levels were found in PTSD (37), although findings of
decreased thyroid function were reported in survi-
vors of prolonged traumatization (38).
Animal research suggests that dopaminergic brain
systems could be involved in PTSD (12). Preadmin-
istration of the dopamine agents, for example, pre-
vents the acquisition of escape deficit (an equivalent
of chronic surrender) after inescapable shock (39).
Yehuda et al. (40) found an elevated urinary excre-
tion of dopamine in PTSD, which correlated with
PTSD symptom severity. This line of research has
not been followed, and the effect of neuroleptics has
not been studied systematically in PTSD.
Finally, findings of increased 5HT2 receptor affinity
and a decreased number of platelet-binding sites in
PTSD (41) imply that serotonergic neurotransmission
may play a role in PTSD. Preliminary evidence (42)
suggests that pretreatment paroxetine binding predicts
the clinical responses to SSRIs in PTSD patients.
Biological Treatment of PTSD
Reports of pharmacotherapy of PTSD include all
of the families of psychotropic agents (43-45). Table
1 summarizes the results of these reports.
167
 A. Y. SHALEV et al.

TABLE 1. Pharmacological Treatment of PTSD

Design, Time,
Drug (Dose in mg/day) Population N Results/Conclusion
Instruments

Antidepressants
Hogben and Phenelzine (45-57) OT Veterans 5 Decreased frequency of nightmares, flash-
Cornfield, 1981 backs startle reactions, violence
(61)
Burstein, 1984 Imipramine (50-350) OT Road accidents 10 Improved sleep, decreased intrusions
(62)
Falcon et al , Misc. tricyclics (200) OT Veterans 17 "Marked improvement in 82% of Ss."
1985 (63) Chart review and
CGI
Bleich et al., Amitriptyline (140) OT Veterans w/ 25 Improved sleep, memory, concentration.
1986 (64) Doxepine (100) Ma- Chart review recent (8-10 Decreased frequency of nightmares
protiline (150) Clomi- months) PTSD
pramine (150)
Shestazki et al., Phenelzine (45-75) vs. CT, RA, PC, CO Misc. trauma 13 No difference between the active drug
1987 (46) placebo 5-weeks, CGI, and placebo (significant decrease in
HAM-A, HAM-D, PTSD and anxiety in both).
IES
Kauffman et al. Desipramine (150-200) OT Misc. trauma 8 Significant decrease in depressive Sx.
1987(65) 4 weeks BDI,
HAM-D
Davidson et al., Phenelzine (45-60) OT Veterans 10 Improved PTSD Sx
1987 (66) 4 weeks CGI, IES
Frank et al., 1988 Phenelzine (71) CT, RA, PC Veterans 34 Phenelzine and imipramine superior to
(67) Imipramine (240) vs. 8 weeks SADS, placebo. IES intrusion improved but not
Placebo SCID-PTSD, IES, avoidance.
DEPR
Kinzie and Clonidine (0.2-6) and OT Refugees 9 Significant (16-pt) decrease of HAM-D
Leung, 1989 imipramine (50-100) HAM-D 12-19 Scores. Some improvement of intrusion,
(56) months nightmares and startle reactions
Reist et al., 1989 Desipramine (200) DB, PC, CO Veterans 18 Improvement in "some symptoms of de-
(47) 4 weeks BDI, pression," no change in anxiety and
HAM-D, IES PTSD Sx
Davidson et al., Amitriptyline (50-300) DB, PC Misc. PTSD 40 Significant effect on depression on Week
1990 (48) vs. placebo 4 and 8 weeks 4. Additional effect on anxiety, CGI, and
HAM-D, HAM-A, IES on Week 8
CGI, IES
Shay, 1992(53) Fluoxetine (20-80) OT Veterans 26 Reduced explosives, improved mood and
>12 months clini- insomnia in 16 (61%) patients
cal impression
Kosten et al., Phenelzine (60-79) RA, PC Veterans 19 44% improvement with phenelzine and
1991 (68) Imipramine (50-300) 8 weeks 23 25% with imipramine on Week 5. Im-
Placebo IES 18 proved intrusion but not avoidance or
depression
Nagy et al., 1993 Fluoxetine (20-80) OT Veterans 19 Significant reduction in PTSD Sx, mostly
(52) 10 weeks after 6 weeks, 50% reduction in fre-
CAPS quency of panic attacks, 30% drop out
due to side effects (anxiety)
Davidson et al., Amitriptyline (160) DB, PC War veterans 55 Significant effect on depression and CGI,
1993 (49) 4 and 8 weeks trend toward improvement in PTSD Sx.
CGI, HAM-D, IES Combat intensity predicts IES response
Van der Kolk et Fluoxetine (20) vs. pla- DB, PC War veterans and 23 Reduction in arousal numbing and depres-
al., 1994(51) cebo 5 weeks CAPS, civilian PTSD 24 sion. No significant effect on intrusion,
HAM-D dissociation or hostility. Better results in
DES, Host recent civilian PTSD, 27% drop out.
Kline, et al., 1994 Sertraline (98.5) OT Veterans with 19 Significantly reduced dysphoria, irritabil-
(54) 3 months BDI, mild but resis- ity, and anger in 12 (63%) Ss, although
IES, SANX, CGI tant depression nine (47%) still had insomnia
Benzodiazepines
Braun et a l , Alprazolam vs. placebo DB, PC, CO Misc. PTSD 10 Significant improvement in anxiety
1990(13) (2.5-6) 5 weeks, PTSD Sx, no effect on intrusion or avoidance,
Scale IES, HAM-A, 4 1 % dropout (7/17)
HAM-D

168 Psychosomatic Medicine 58:165-182 (1996)

TREATMENT OF POSTTRAUMATIC STRESS DISORDER: A REVIEW

TABLE 1. Continued
Design, Time,
Drug (Dose in mg/day) Population N Results/Conclusion
Instruments
Risse et al., 1990 Alprazolam (2.9) OT: discontinuation Veterans 8 Severe withdrawal symptoms on discon-
(58) tinuation
Loewenstein et Clonazepam (1-6) OT PTSD and MPD 5 Improved sleep, nightmares, flashbacks,
al. 1988 (57) and panic attacks
Mood stabilizers and others
Kitchner and Lithium (low doses) OT, Clinical obser- Veterans 4 Reduced anger, irritability, anxiely, and
Creenstein (300-600) vation insomnia
1985 (70)
Lipper et al., Carbamazepine OT Veterans 10 Improved CGI Scores. Reduced intensity
1986(59) (577-780) 6 weeks HAM-A, and frequency of nightmares, flashbacks,
HAM-D, SCL90, and intrusion Sx. No effect on avoid-
PMS, CGI ance
Wolf et al., 1988 Carbamazepine (not OT Veterans 10 Improved impulse control, violent behav-
(70) specified) ior, and anger
Brophy, 1991 Cyproheptadine (16-24) CR Veterans 4 Stopped nightmares
(71) anc/TCA Few days
Fesler, 1991 (60) Valproate (250-2000) OT 10.6 months Veterans 14 Improved hyperarousal and hyperreactivity
PTSD scale
Wells et al., 1991 Buspirone (35-90) CR Misc. PTSD 3 Improved anxiety, insomnia, flashbacks,
(72) and depression
Design: CO, Cross-over; CR, case report; DB, double blind; OT, open trial; PC, placebo controlled; RA, random assignment, TCA, tryciclic
antidepressants. Instruments- CAPS, clinician-administered PTSD scale; CGI, Clinical Global Impression; DEPR, Raskin Depression Scale; DES,
Dissociation Experience Scale; HAM-A, Hamilton Anxiety Scale; HAM-D, Hamilton Depression Scale; Host, Buss Durkee Hostility Inventory; IES,
Impact of Events Scale; PMS, Profile of Mood States; SADS, Structured Interview for Affective Disorders and Schizophrenia; SCL-90, Derogatis'
Symptoms Checklist 90. Diagnoses: MPD, multiple personality disorder.

Studies of antidepressants (46-73) suggest that
these drugs sometimes improve PTSD symptoms of
intrusion and avoidance as well as depression, in-
somnia, and anxiety. The magnitude of the therapeu-
tic response, however, is far less than that obtained
in major depression or panic disorder in that no
study has shown full remission of PTSD symptoms,
as is often the case in the major depression or panic
disorder. Moreover placebo-controlled, double-blind
studies (46-48) and an open trial (50) failed to
demonstrate a major effect of antidepressants on
PTSD symptoms of intrusion and avoidance. Recent
studies of fluoxetine, sertraline, and paroxetine (51-
54) suggest that SSRIs may ameliorate these symp-
toms to some extent. Van der Kolk's controlled study
(49) has further shown that survivors of recent trau-
mata (e.g., sexual abuse) benefit from fluoxetine
more than Vietnam veterans, in whom fluoxetine did
not reduce dissociation, hostility, or intrusion. Other
studies imply that the effect of antidepressants on
PTSD may be enhanced by lithium (55) and
clonidine (56).
Studies of benzodiazepines have produced mixed
results. One controlled investigation (13) failed to
show a specific effect of alprazolam on PTSD symp-
toms of intrusion and avoidance, despite a modest
effect on anxiety. An open study of clonazepam (57)
describes, however, improved sleep and reduction
in nightmares, flashbacks, and panic attacks. Severe
withdrawal symptoms have been described in PTSD
patients treated with alprazolam (58) whereas clon-
azepam has not been shown to cause severe with-
drawal.
Mood stabilizers such as lithium, sodium val-
proate, and carbamazepine have been studied in
open trials. The results indicate that these drugs
reduce irritability and improve impulse control in
PTSD (59, 60). By virtue of their "anti-kindling"
effects, clonidine, carbamazepine, and valproate
have been touted as particularly promising in PTSD.
However, among anti-kindling products, one must
distinguish those that prevent the acquisition of
kindled seizures (e.g., clonidine) from those that
inhibit acquired kindled seizures (e.g., carbamaz-
epine, valproate). The former may be considered for
early preventive treatment of PTSD, and the latter
may be useful in chronic PTSD.
Pharmacological studies of PTSD have numerous
shortcomings. As shown in Table 1, there are few
controlled studies, and the results of these studies
are inconsistent. Most of the research has been
conducted on male combat veterans with chronic
PTSD. The length of potential remissions and the
rate of relapse have not been studied. Comorbid

Psychosomatic Medicine 58:165-182 (1996) 169


personality disorders may create difficulties in com-
pliance with treatment regimen in PTSD. Finally, the
effect of early pharmacological intervention should
be further examined.
Commentators (43, 45) have opined that pharma-
cological treatment of PTSD may require prolonged
periods before being effective. In an 8-week study,
Davidson et al. (48) showed, in fact, that symptoms
of anxiety, intrusion, and avoidance continue to
improve between Week 4 and Week 8. Despite such
improvement, however, the authors found no evi-
dence for drug effects on the structured interview for
PTSD. Furthermore, 64% of the amitriptyline group
and 72% of controls still met diagnostic criteria for
PTSD on completion of the study.
As suggested by previous reviewers (e.g., 45),
pharmacotherapy alone is rarely sufficient to cure
PTSD. Many PTSD patients, however, find their
symptoms intolerable, and some seek relief by self-
medicating with alcohol or illicit drugs or by engag-
ing in life-threatening behavior, including suicide
(73). The relief provided from prescribed medication
may reduce the tendency of PTSD patients to self-
medicate, as well as the risk of violent behavior and
suicide. Furthermore, symptom relief provided by
medication may facilitate participation in psycho-
therapy (16, 45, 60).
THE PSYCHOLOGICAL APPROACH TO PTSD
The Behavioral Model
The core behavioral conceptualization of PTSD
identifies classic conditioning as the mechanism
linking the symptoms of PTSD to the precipitating
trauma. Subjects who originally react to a traumatic
event (unconditioned stimulus (UCS)) with fear and
arousal (unconditioned response (UCR)) will, ac-
cording to this model, continue to show the same
"conditioned" response (CR) to cues (conditioned
stimuli (CS)) that have been paired with the stressful
exposure.
Contrary to simple conditioning, however, the
learned response (CR) in PTSD does not extinguish
over time. To explain the lack of spontaneous extinc-
tion over time, Mowrer's (74) two-factor model was
applied to PTSD (75). In this model, the initial
"simple" conditioning (resulting in avoidance of
cues immediately present during the trauma, such as
combat sounds) is followed by operant conditioning,
in which avoidance of a variety of internal and
external cues that are loosely associated with the
trauma (such as any memory of combat or any sound
with similar properties) is rewarded by reduction in
170
A. Y. SHALEV et al.
distress. The reinforcement of such avoidance would
prevent the extinction of the conditioned response
over time and expand the avoidant behavior to
secondary and tertiary cues. Psychophysiological
studies showing increased responses to cues remi-
niscent of the trauma have provided the necessary
experimental support for the emotional conditioning
construct (76, 77).
Foa and colleagues' cognitive-behavioral model
(10, 78, 79) integrates the meaning attributed to the
trauma by the subject with conditioning. These au-
thors considered the possibility that the perception
of controllability and predictability and the subse-
quent attributions of threat are central to the devel-
opment of the conditioned responses involved in
PTSD. Such perceptions of the trauma should be
addressed in therapy along with desensitization or
flooding.
Behavior Therapy. Interventions based on behav-
ioral theory are designed to undo CR to CS that have
been paired with the trauma. Behavior therapy pro-
ceeds either by gradual (desensitization) or by mas-
sive (flooding) re-exposure to the CS. Another dis-
tinction is between live exposure (i.e., to real objects
and situations) and imaginal exposure.
Four controlled studies indicated that flooding
may reduce PTSD symptoms. Keane et al. (80) found
a significant effect of flooding on reexperiencing,
anxiety, and depression. Boudewyns and Hyer (81)
showed that flooding positively affected adjustment
in Vietnam veterans. Boudewyns and Hyer (82) also
indicated that clinical improvement, regardless of
treatment modality, is associated with a reduction in
physiological responses to traumatic imagery. Coo-
per and Clum (83) described a positive interaction
between flooding and interpersonal treatment. Foa et
al. (84) compared a treatment condition combining
behavioral and cognitive techniques, the stress inoc-
ulation therapy (SIT), with prolonged exposure (PE),
counseling, and waiting list control. PE had greater
efficacy in reducing PTSD symptoms at the 3.5-
month follow-up. Other open studies are summa-
rized in Table 2 (85, 86).
Contrasting with the above, Pitman et al. (14)
reported an exacerbation of depression and panic
anxiety, increased alcohol consumption, and mobi-
lization of negative appraisal during flooding ther-
apy. In 50 Vietnam veterans, Hyer et al. (87) simi-
larly reported that 17 of 20 subscales of the Millon
Clinical Multiaxial Inventory worsened after 5
weeks of exposure to revivified Vietnam experience.
Imaginal desensitization has been the object of
three controlled trials (11, 88, 89) and several open
studies (90-92). The treatment condition in Penis-
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TREATMENT OF POSTTRAUMATIC STRESS DISORDER: A REVIEW

TABLE 2. Psychological Treatment of PTSD

Design, Outcome
Treatment Modality Treatment Population N Results and Conclusions
Measures
Behavior therapy
Imaginal exposure
Flooding
Fairbank and Keane, Flooding CR War veterans 2 Extinction along thematic cues but not
1982(85) Clinical observation on anxiety related to other traumatic
events
McCaffrey and Fair- Combined relax- CR Road accident 2 Decrease in PTSD Symptoms
bank, 1985 (86) ation, flooding, Clinical observation
and in vivo expo-
sure
Keane et al., 1989 Flooding vs. waiting CT Veterans 24 "Statistically and clinically meaningful"
(80) list 6-month follow-up BDI, improvement in reexperiencing, anxi-
ZDS, MMPI-PTSD, ety and depression. No effect on
SANX, PTSD-Checklist, numbing and social avoidance
Social Adjustment Scale
Cooper and Clum, Flooding and stan- CT Vietnam vet- 14 Flooding increased the effectiveness of
1989(83) dard treatment vs. 3-month follow-up BDI, erans interpersonal treatment on re-experi-
standard treat- Vietnam Experience encing and sleep disturbances but
ment alone (14 Questionnaire had no effect on depression, anxiety,
sessions) or violence-proneness
Boudewyns et al., Direct therapeutic CT War veterans 58 More Ss treated with DTE identified as
1990(82) exposure (DTE, 3-month follow-up Vet- treatment successes
flooding) vs. erans Adjustment Scale
counseling
Boudewyns and Direct therapeutic CT War veterans 51 No difference between treatment condi-
Hyer, 1990 (81) exposure vs. Physiological responses tions. Reduced physiological re-
counseling to mental imagery, self- sponses predicts good outcome
reported anxiety across treatment conditions
Pitman et al., 1991 Flooding in OT War veterans 15 Exacerbation of depression, alcoholism,
(14) imagery Self-reported changes, panic attacks, negative appraisal, and
IES, SANX anger in six cases
Desensitization
Peniston 1986 (88) Desensitization as- CT War veterans 16 Reduction in nightmares, flashbacks,
sisted by biofeed- Subject's report muscle tension, and readmissions rate
back vs. no treat- in the active treatment group
ment (N= 8)
Brom et al., 1989 Compared desensi- CT Misc. trauma 11 Clinically significant improvement in
(89) tization, hypno- SCL-90, IES, SANX, per- 2 60% of treated and 26% of the un-
therapy, psy- sonality scale treated groups. No difference be-
chodynamic tween treatment modalities. Age, lo-
therapy, and wait- cus of control anger, and
ing-list control discontentment predict outcome
Richards and Rose, In vivo exposure vs. CR Misc. trauma 4 Exposure improved phobias. Imaginal
1991 (90) imaginal exposure Clinical assessment flooding improved dysphona and
phobic symptoms
Shalevetal., 1992 Desensitization CR Misc. nonmili- 4 Reduced physiological responses to
(91) Physiological response tary trauma specific recollections addressed in
to mental imagery therapy
Vaughan and Tarrier, Image habituation OT Misc. trauma 10 Six Ss improved, two moderate, and
1992(92) training Self-rating of anxiety two minimal improvement
and image intensity
Richards et al., 1994 Compared imaginal CT Misc. trauma 14 In both protocols, 75-80% improve-
(11) (N = 7) and live IES, BDI, CHQ, Work ment in measures of PTSD and 65%-
exposure (N = 7) and Social Adjustment 70% in depression, fear, CHQ, and
Scale, PTSD checklist, Social adjustment. More improvement
12-month follow-up in phobic avoidance in live exposure
Live Exposure
Solomon et al., 1992 Military fitness and CT War veterans 80 Worsening in PTSD Sx, general psychi-
(93) training program PTSD Sx, IES, SCL-90, atric symptomatology, and social
vs. no treatment PAIS, PSE functioning in participants of the pro-
gram

Psychosomatic Medicine 58:165-182 (1996) 171


Treatment Modality
Scurfield et al., 1992
(94)
Cognitive therapy
Resick et al., 1988(98)
Foa etal., 1991 (84)
Resick and Schnicke,
1992 (97)
Psychodynamic therapy
Foreman and Marmar,
1985 (108)
Hendin etal., 1986 (112)
Lindy et al., 1988 (111)
Lansky 1991 (113)
Marmar, 1991 (114)
Lindy et al., 1992 (115)
Group therapy
Walker, 1983 (117)
McWhirter and Liebman,
1988 (118)
Brockway, 1987 (119)
Fischman and Ross, 1990
(120)
Koller et al., 1992 (121)
172
A. Y. SHALEV et al.
TABLE 2. Continued
Design, Outcome
Population N Results and Conclusions
Measures
Helicopter ride OT War veterans 45 Increase in in-flight reactions, post-
therapy Attitude survey and flight intrusive and painful mem-
clinical observations ories. Improved peer group
bonding and desensitization
Compared stress CT Rape victims 37 No difference between type of
inoculation, asser- Modified fear survey, treatment at 3 and 6 months fol-
tion training, and SCL-90-R, Self-Expres- low-up. Significant improvement
supportive psy- sion Scale, Self-Concept across measures
chotherapy Scale, IES, Fear Target
scale
Compared stress CT Rape victims 45 All active treatment conditions
inoculation train- PTSD Sx, rape-related produced improvement. SIT >
ing (SIT), pro- distress, anxiety, and SC and WL immediately after
longed exposure depression treatment; PE > all others on
(PE), supportive 3.5-month follow-up
counseling (SC),
and wait-list (WL)
Cognitive process- CT Sexual assault 19 Improved PTSD Sx and depression
ing therapy vs. 3- and 6-month fol- in the active treatment group
waiting list con- low-up maintained for 6 months
trol
Time-limited dy- CR War veterans 6 Provided guidelines for manage-
namic psycho- Clinical assessment ment of initially poor therapeutic
therapy alliances
Dynamic psycho- CR War veterans 3 Emphasized understanding of the
therapy Clinical assessment origin and the adaptive function
of reliving experiences in PTSD
Intensive psychoan- OT War veterans 21 Showed reduction in general psy-
alytic psychother- Clinical rating; SCL-90; chiatric symptoms and intrusion,
apy IES no effect on avoidance
Psychoanalytic psy- CR War veterans 2 Discussed traditional and new ap-
Clinical observation
chotherapy proaches to interpreting trau-
matic nightmares
Brief dynamic psy- CR Chronic PTSD 3 Focus on self-concept, working
chotherapy Clinical observation alliance, and counter transfer-
ence
Psychodynamic CR Military and civil- 4 Offered insight into somatization,
psychotherapy Clinical observation ian trauma repetition, and working alliance
in the treatment of PTSD
Compared rap CR War veterans Discussed trust, personal integra-
groups with tradi- Clinical observation tion, and survival guilt
tional group ther-
apy
Anger control group CR War veterans Offered a model for anger reduc-
Clinical observation tion
Croup treatment of CR War veterans Dreams, a "direct road back to the
combat night- Clinical observation trauma," transformed into a ther-
mares apeutic tool when deciphered
empathically in the company of
peers
Time-limited group CR Survivors of Emphasized the relationship be-
treatment Clinical observation torture tween individual's experience
and sociopolitical factors
Psychodynamic CR Vietnam veterans Topics: traumatic experiences, pre-
group therapy: Four 16-week sequen- and postwar adaptation. Empha-
tial segments sized timely integration and
working through
Psychosomatic Medicine 58:165-182 (1996)
TREATMENT OF POSTTRAUMATIC STRESS DISORDER: A REVIEW

TABLE 2. Continued
Design, Outcome
Treatment Modality Treatment Population N Results and Conclusions
Measures
Hypnosis and suggestive
techniques
Kingsbury, 1988 (131) Hypnosis CR Car accidents 2 Clinical improvement
Clinical observation
Hickling et al., 1986 (132) Relaxation and CR Misc. trauma 6 Improved anxiety, depression, EMC,
biofeedback train- Clinical observation and clinical ratings
ing
Spiegel, 1988 (127), 1990 Hypnosis/split- CR Sexual assault 3 Illustrated the use of hypnosis in PTSD
(130) screen technique Clinical observation
Inpatient treatment
Perconte 1989 (135) Partial hospitaliza- FU War veterans 10 Initial treatment gains (32-52% on
tion SCL-90, 55% response SCL) eroded on 15-month follow-up
rate! but some improvement remains (15-
28%)
Scurfield etal., 1990 Inpatient program OT War veterans 86 Positive changes in self-esteem, inter-
(136) for PTSD MISS, IES, MMPI-PTSD, personal relationships, numbing, and
Sx checklist arousal. Minor (7%) reduction in
Avoidance and Intrusion SX, No
change in MMPI-PTSD scores
Funari et al., 1991 (134) Specialized inpa- OT War veterans 36 Decrease in PTSD-related anxiety and
tient treatment 140 days MCMI scores dysthymia and in schizoid, avoiding,
program and passive aggressive traits
Perconte and Crigger, Predictors of relapse FU War veterans 45 Alcohol consumption, smaller program
1991(136) after inpatient SCL-90 MMPI-PTSD, participation, and higher MMPI and
treatment Clinical evaluation SCL-90 scores predict relapse
Rehabilitation
Crunertet al., 1992 (137) Graded work OT Work-related 51 88-92% return to work, 8 1 % working
exposure Return to work (%) hand injury full time at 6-month follow-up, De-
creased work avoidance in patients
with flashbacks
Combined approach
Shalev etal., 1993 (16) Desensitization and CR Misc. nonmili- 4 Offered a hierarchical model for com-
interpersonal ther- Physiological responses tary trauma bining treatment techniques
apy to mental imagery, IES
McFarlane, 1989 (139) Combined therapy CR Misc. nonmili- 56 Stressed the need to consider sepa-
Clinical observation tary trauma rately disturbed attention and
arousal, traumatic preoccupation so-
cial, and occupational functioning
Design. CR, case report; CT, controlled trial; FU, follow-up; OT, open trial; Instruments: BDI, Beck Depression Inventory; CHQ, General Health
Questionnaire; IES, Impact of Events Scale; MCMI, Millon Clinical Multiaxial Inventory; MISS, Mississippi Rating Scale for Combat-Related PTSD;
MMPI-PTSD, MMPI PTSD subscale; PAIS, Psychological Adjustment to Illness Scale; PSE, Perceived Self-Efficacy Questionnaire; SANX,
Spielberger's State-Trait Anxiety Inventory; SCL-90, Derogatis' Symptoms checklist 90; ZDS, Zung Depression Scale.

ton's controlled study (88) was associated with re-
duction in nightmares, flashbacks, muscle tension,
and readmission rates. Brom et al. (89) compared
desensitization with brief dynamic therapy, hypno-
sis, and waiting list controls. All active treatments
produced measurable improvement. In a recent
study, Richards et al. (11) randomly assigned 14
civilian PTSD patients to either four sessions of
imaginal exposure followed by four sessions of live
exposure or the opposite sequence. Treatment ses-
sions were followed by self-exposure homework
assignment. Both protocols and both treatment mo-
dalities effectively reduced symptoms of PTSD, de-
pression, fear, and general health, as well as work
and social adjustment. The resulting improvement
was of significant magnitude, reaching up to 60 to
85% of initial target behavior. Live exposure yielded
more improvement on phobic avoidance. A fol-
low-up evaluation, conducted 12 months later [N =
11), showed further improvement in most areas
In many patients, PTSD is the result of exposure to
complex events, such as wars, torture, or captivity.
Desensitization, however, is often limited to the
results of a single event (e.g., a particular combat, a
rape). The capacity of PTSD patients to extend their
response to behavioral treatment to other traumata

Psychosomatic Medicine 58:165-182 (1996) 173


has been questioned. Two studies (85, 91) evaluated
physiological responses to mental imagery of the
trauma before and after behavior therapy and
showed that desensitization of one traumatic inci-
dent does not extend to other traumatic incidents
engendered by the same event. The usefulness of
behavior therapy in survivors of prolonged trauma-
tization requires, therefore, further studies.
A comprehensive study of live exposure (93) has
assessed the effects of a complex rehabilitation and
training program conducted by the Israel Defense
Force 4 years after the 1982 Lebanon war in an effort
to change the pervasive course of PTSD in veterans
of that war. The program included a month-long
exposure to military cues (e.g., rifle range, artillery
fire) within a military milieu along with cognitive,
behavioral, and supportive interventions. The study
compared 40 participants of the program with 40
PTSD controls who did not participate using mea-
sures of PTSD, general psychiatric symptomatology,
self-efficacy, and social and psychological adjust-
ment. Within-individual changes, induced by the
program, were also evaluated. The results showed
that, immediately and 9 months after the program,
participants in the program fared worse than con-
trols and worse than their own initial scores. In
another direct reexposure study, Scurfield et al. (94)
used a "helicopter ride therapy" with Vietnam vet-
erans with PTSD. That exposure was similarly asso-
ciated with intrusive painful memories and "in-
flight reactions," but it improved group cohesion
and provided a degree of desensitization. Contrast-
ing with the rather negative results reported above
are positive results of two studies (e.g., 11) that
addressed subjects with more recent PTSD.
Overall, studies of behavioral treatment in PTSD
report a significant but partial improvement. Clearly,
an undoing of a "conditioned response" is insuffi-
cient, thereby suggesting that the pathophysiology of
PTSD encompasses more than learned conditioning.
Moreover, direct exposure and flooding may result
in reactivation and worsening of symptoms and
behavior.
Cognitive Formulations of PTSD
The cognitive view of PTSD (79, 95, 96) postulates
that basic assumptions that normally underlie one's
expectations, appraisal, and behavior may be re-
vealed as inaccurate, insufficient, or inadequate by
traumatic experiences. Such critical events may then
lead to dysfunctional thinking and therefore to de-
pression, anxiety, and PTSD.
174
A. Y. SHALEV et al.
Cognitive psychology (e.g., 79) suggests that
knowledge acquired throughout life is represented
in memory in the form of knowledge structures (alias
schemata) and that such structures inspire the en-
coding and the interpretation of new information.
Cognitive schemata allow smooth adaptation to
changing reality while preserving one's personal
perspective and values. In healthy individuals, cog-
nitive schemata can be modified by progressive
assimilation of new experiences.
Traumatic events, in contrast, may be followed by
a breach in previously held assumptions such that
the novelty of the event sharply contrasts with pre-
vious schemata and can neither be adapted to nor be
assimilated. For example, belief in one's personal
strength may be replaced by a sense of extreme
vulnerability. Belief in one's capacity to reasonably
predict reality may turn into fearful expectation of
indiscriminate harm. Finally, preexisting negative
self-schemata can be reinforced by trauma. Janoff
and Bulman (95) proposed that victimization specif-
ically violates the assumptions that the world is
benevolent and meaningful and that the self is wor-
thy.
Appraisal of the world as eminently dangerous
and of oneself as everlastingly incompetent and
vulnerable interferes with recovery from trauma.
Cognitive therapists explore and challenge such in-
adequate schemata, discourage their generalization
to the patients' whole life, and foster the re-building
of a viable sense of personal worth, competence, and
safety.
Cognitive Therapy. Three controlled studies
looked at the effect of cognitive techniques in sub-
jects who had suffered from either rape or sexual
assault and showed that these techniques are fol-
lowed by a significant improvements. In the above
mentioned study by Foa et al. (84), the stress inocu-
lation technique produced a significant reduction of
PTSD symptoms immediately after treatment. Resick
and Shenicke (97) compared group cognitive pro-
cessing therapy, which comprised of education, ex-
posure, and cognitive components, with waiting list
control. Subjects in the treatment group improved in
measures of depression and maintained the im-
provement for 6 months. Finally, Resick et al. (98)
compared three treatment conditions (stress inocu-
lation, assertion training, and supportive psycho-
therapy) in 37 rape victims. All three treatment
conditions reduced symptoms of distress, avoid-
ance, and intrusion and improved self-expression
and self-concept. The results were maintained 3 and
6 months after treatment.
Psychosomatic Medicine 58:165-182 (1996)
TREATMENT OF POSTTRAUMATIC STRESS DISORDER: A REVIEW
Psychodynamic Formulations of PTSD
Psychodynamic formulations of PTSD and of its
predecessor, the "Traumatic Neurosis," are complex
and multifaceted. Two generic metaphors have been
advanced, including damage to a component of the
mental apparatus and incomplete processing of trau-
matic experiences.
The Metaphor of Damage to the Mental
Apparatus
Commenting on the repetitive and distressful
nightmares of patients with traumatic neurosis,
Freud (99) suggested that war trauma creates a
breach in a hypothetical "stimulus barrier" that
normally protects the mental apparatus from exces-
sive amounts of "excitation." As a result of this
structural impairment, the mental apparatus
abruptly modifies its operational rules by relaxing
the domination of homeostasis-based dynamics ex-
emplified by the "pleasure principle." Instead, the
psyche becomes subjugated to a hypothetical "repe-
tition compulsion": a "primitive" and more "biolog-
ical" set of functional rules. Individuals with trau-
matic neuroses, accordingly, are captive of the
dynamics of a ceaseless repetition compulsion.
The essence of this forgotten, yet most powerful,
insight of Freud's formulation is that the repetitive
phenomena, in traumatic neuroses, do not necessar-
ily contribute to self-healing and may often express a
posttraumatic surrender of the psychic apparatus to
a new and dysfunctional set of rules.
Recent structural formulations metaphorically re-
iterate Freud's original stance. At the heart of these
formulations is the appraisal that extreme trauma
alters the rules of mental functioning rather than
injects new content to old conflicts. In today's par-
lance, this alteration is referred to as "traumatized
self" (100,101) or "collapse of structures" (102). The
practical implication of such formulations is the
recognition that the self-healing capacity of PTSD
patients is impaired. Consequently, the therapy of
PTSD should include ego-supportive maneuvers,
address vulnerability in character structure, and
involve the therapist in the role of participant rather
than neutral observer.
{Crystal's (103) description, in survivors of massive
trauma, of "loss of affective modulation" is another
variation on the theme of "psychic damage." Krystal
argued that the fact of psychological surrender, typ-
ical to situations of prolonged subjugation to ex-
treme adversity, leads to a permanent impairment of
the survivor's affective life (e.g., inability to respond
Psychosomatic Medicine 58:165-182 (1996)
to subtle affective cues). This impairment resembles
alexithymia, a mental condition in which the person
is unable to recognize and use internal states of
affect. Research has confirmed the presence of alexi-
thymic traits in war veterans with PTSD (e.g., 104,
105).
McCann and Pearlman's (96) constructivist self-
development model offers a bridge between self- and
cognitive psychology. According to this model, three
aspects of the self are affected by trauma: a) self-
capacities, or the ability to tolerate intense affect and
regulate self-esteem; b) cognitive schemata, or beliefs
and expectations about self and others; and c) intru-
sive trauma memories and related distressing affect.
The Metaphor of Unresolved Mental Processing
of the Event
This psychodynamic model stems from the para-
digm of loss, mourning, and grief. Relating to the
similarities between symptoms of intrusion and
avoidance observed in posttraumatic individuals
and those defined by Freud (6) and described by
Lindemann (7) in the early phase of normal grief,
Horowitz (8) hypothesized that the "stress response
syndrome," an early equivalent of PTSD, results
from incomplete mental processing of the traumatic
event.
From a practical point of view, this concept sug-
gests that PTSD might resolve if the patient is en-
couraged to work through these conflicts. Such is the
main thrust of traditional psychodynamic psycho-
therapy of trauma-related disorders. However, the
experience of extreme arousal and panic associated
with the reactivation of traumatic memories, the
advent of dissociative reactions during psychody-
namic exploration of the trauma, and the extent of
psychic avoidance observed in some PTSD patients
complicates explorative techniques in many cases.
Psychodynamic Psychotherapy
Borrowing Lindy's definition (106), psychody-
namic psychotherapy specifically addresses the
meaning of trauma-related symptoms and behavior
and the meaning of the traumatic event. The analytic
psychotherapist hopes that insight regarding the
meaning of symptoms, both conscious and uncon-
scious, can help the patient master inner experiences
and repair and restore the integrity of life. In their
review of the field, Marmar et al. (107) emphasize
the importance of establishing a therapeutic alliance
and the intrinsic difficulty of that task. Handling
175

transference and counter transference reactions,
both related to the enduring effect of traumatization,
is emphasized by several authors (108-110).
Most of the literature on psychodynamic therapy
for PTSD consists of case reports and addresses
theoretical and technical aspects of the treatment.
The abovementioned controlled study by Brom et al.
(89) compared brief dynamic psychotherapy with
hypnotherapy, desensitization, and a waiting list
control. All active treatment groups improved signif-
icantly. In a well documented treatment project
(111), 21 Vietnam veterans with PTSD participated
in individual psychoanalytic psychotherapy for 1
year. Decreases in intrusive phenomena and depres-
sion were recorded in those patients who completed
their treatment. Other reports (112-115) are summa-
rized in Table 2.
OTHER TREATMENT MODALITIES AND
TECHNIQUES
Group Therapy
Historically, the "rap" groups that followed the
Vietnam war preceded many other therapies of trau-
matized combat veterans (116). The rap group ses-
sions consisted of disclosure of common experi-
ences, validation of feelings, and sharing of
existential distress among fellow veterans. In fact,
PTSD patients often perceive their life experiences
as fundamentally different from and incomprehen-
sible by nonvictims. Alienation, isolation, helpless-
ness, and mistrust are major psychological compo-
nents of PTSD, along with restricted affect,
emotional dyscontrol, irritability, and depression.
These features reduce PTSD patients' interpersonal
and social competence. Group therapies have, there-
fore, a major role in the comprehensive psychiatric
treatment of PTSD.
Despite the above information, data concerning
the efficacy of group therapy are mostly descriptive.
A few of the numerous studies of group therapies in
PTSD are summarized in Table 2 (117-121). Com-
mon denominators of all group approaches to PTSD
are attempts to reverse isolation and to reduce help-
lessness and alienation. Most authors also under-
score the need to: establish an effective working
alliance, facilitate disclosure, and enhance commu-
nication and mutual support among group members.
More specific goals have been set according to the
theoretical orientation and to the type of trauma.
Self-awareness and integration are emphasized by
cognitive group therapists (e.g., 122), and working
through traumatic experiences is typical of psy-
176
A. Y. SHALEV et al.
chodynamic groups (119, 121). Anger control (118)
and empathic understanding of combat nightmares
(119) are other specific goals.
Family Therapy
The impact of PTSD extends beyond individual
patients to affect their spouses, children, and the
larger network of relatives, friends, and co-workers.
Intimate family and social relationships may all
suffer as a result of inappropriate interactions with
persons exhibiting PTSD (123, 124). In particular,
isolation, hypervigilance, irritability, and a propen-
sity for loss of impulse control can contribute to a
deterioration of interpersonal functioning. Expres-
sion of violence, fear, suspiciousness, or tension
within families of PTSD patients may extend to
future generations. Family members' reactions may
reciprocally exacerbate the patient's condition.
Family therapy offers the opportunity to confer
benefits on both the identified patient and the family
(125). Most of the published literature on family and
couple therapy in PTSD, however, consists of anec-
dotal reports and theoretical formulation. Because of
the excessive divorce rate in Vietnam veterans and
other PTSD patients, couple therapy may be essen-
tial to salvage precarious marital ties (125). A recent
program involved the application of behavioral fam-
ily therapy, developed initially for use in schizo-
phrenics, to PTSD patients and their spouses (126).
Empirical studies are required to assess and docu-
ment the immediate and long term effect of family
therapy in PTSD.
Hypnosis
Hypnotic induction and other suggestive tech-
niques have been widely used in the treatment of
combat stress reactions (e.g., 128). Studies indicate
that Vietnam veterans with PTSD are more hypno-
tizable than normal controls (129-132). In a study by
Brom et al. (90), hypnotherapy was more effective
than waiting list control in improving avoidance and
distress in PTSD patients. Our own clinical experi-
ence indicates that some PTSD patients resist hyp-
notic suggestion, often as a way to remain in control,
and others respond to hypnotic induction by devel-
oping severe dissociative states (16). Hypnosis,
therefore, must be used with care and only as a
component of an overall treatment plan.
Psychosomatic Medicine 58:165-182 (1996)
TREATMENT OF POSTTRAUMATIC STRESS DISORDER: A REVIEW
Inpatient Treatment
Some PTSD patients, generally those with high
levels of symptomatology, may require hospitaliza-
tion, often in response to depression, substance
dependence, violence, or suicidal behavior. Four
studies of inpatient programs have been reported
(133-136), and two studies evaluated behavioral
treatment during the hospitalization of Vietnam vet-
erans with chronic PTSD. The programs included a
variety of interventions, such as group and milieu
therapy, individual therapy, counseling, behavior
therapy, and pharmacotherapy. The length of stay
varied among the studies, reaching up to 140 days
(135). Positive changes in self-esteem, interpersonal
relations, and symptoms of numbing and arousal
have been reported by Scurfield et al. (134). How-
ever, in a 12- to 26-month follow-up study of PTSD
inpatients released from hospital treatment, Per-
conte (136) showed that symptomatic relapse was
the rule. Some improvement (e.g., in employment
status) may, nevertheless, persist. Inpatient treat-
ment, therefore, does not markedly affect the course
of PTSD but may effectively address crises and
comorbidity.
Vocational Rehabilitation
Data concerning the chronic course of PTSD along
with the limited effectiveness of current treatments
strongly suggest that rehabilitation should be a major
approach to this disorder. Grunert et al.'s study of
graded work exposure (137) showed that efforts to
implement specific rehabilitation programs can be
very productive; 90% of 51 patients with PTSD after
work-related hand injuries returned to work, often
with a new employer, and about 84% were still
working 6 months later. Moreover, among subjects
who suffered from flashbacks, 73% successfully re-
turned to work. The presence of such flashbacks had
previously been associated with a 90% failure to
return to work.
At this point in time, however, the literature on
rehabilitation of PTSD patients is scarce. Data con-
cerning specific impairments related to PTSD, such
as short term memory deficit (e.g., 138), stimulus
sensitivity, reduced attention span, are unavailable.
Systematic delineation of such impairments is an
important step toward implementing rational reha-
bilitation programs for PTSD patients.
Psychosomatic Medicine 58:165-182 (1996)
DISCUSSION
As attested by this review, efforts to treat PTSD
have been extensive, reflecting the wide recognition
by clinician and researchers of the disorder's valid-
ity and the associated distress and dysfunction.
Having started with series of anecdotal reports, treat-
ment studies are becoming more sophisticated, in-
volving controlled designs and larger samples of
patients. On the other hand, and in the absence of
accepted pathophysiological theory, almost any
treatment modality, including ones that have not
been covered in this review, could be implemented
and assessed in PTSD. This heterogeneity, as well as
the feeling that "everything goes," is not serving the
field well.
Several assessment tools were widely used across
studies (e.g., the IES, MMPI), enabling comparisons
among them and with our experience. However,
despite the large number of studies, the inclusion of
survivors of a variety of events, the difficulties in
identifying control groups, and the heterogeneity in
initial symptom severity and in the duration of PTSD
before treatment clearly indicate that the lessons
learned from these studies are still preliminary.
Most studies reported substantial alleviation of
suffering, but many still had the mark of pioneering
enthusiasm and lacked self-critique. In controlled
studies, the effect size was often limited, and symp-
toms of depression, detachment, and anxiety im-
proved more than those of intrusion and avoidance.
No study claimed to have achieved durable remis-
sion in chronic PTSD, thereby reflecting many clini-
cians' belief that the disorder is rather unresponsive
to any form of treatment. Altogether, the cumulated
evidence suggests that patients with PTSD can ex-
pect to receive substantial help from therapists but
probably not a definite cure.
Given these limitations, several indications
emerge from reading the available data. First, evi-
dence tends to support the superior effectiveness of
early treatment, whether pharmacotherapy or cogni-
tive-behavioral therapy. Second, some success had
been documented in almost every treatment modal-
ity, and such partial improvement can often be of
great significance for the patient. Third, no agree-
ment has emerged as to a hierarchy of applying
treatment modalities in PTSD. Finally, evidence of
synergetic effects of pharmacotherapy and psycho-
therapy has been reported (61) in up to 70% of the
patients (64). The following paragraphs attempt to
translate these indications into practical guidelines
Rather than orienting the clinician toward a spe-
cific treatment modality, the diagnosis of PTSD
177

suggests that several treatment approaches could be
successfully combined. Within PTSD, therefore, the
clinician must identify the current sources of dis-
tress and dysfunction and evaluate their accessibil-
ity to treatment.
Particular PTSD symptoms may point the thera-
pist toward appropriate levels of impairment (16,
139). The presence of conditioned emotional re-
sponses is reflected by: efforts to avoid thoughts,
feelings, or conversations associated with the trau-
ma; efforts to avoid activities, places, or people that
arouse recollections of the trauma; intense psycho-
logical distress at exposure to cues evoking the
traumatic event; and physiological reactivity upon
exposure to such cues. Altered networks of meaning
are often reflected in profound changes in the pa-
tients' life trajectory, self-concept, sense of security,
and appraisal of others. Symptomatic behavior re-
lated to these changes is reflected in the DSM-IV
criteria of feelings of detachment or estrangement
from others, markedly diminished interest in signif-
icant activities, restricted range of affects, and a
sense of a foreshortened future. The degree to which
such symptoms reflect comorbid depression should
be weighed. Other DSM-IV criteria (i.e., inability to
recall an important aspect of the trauma, acting or
feeling as if the traumatic event were recurring) may
reflect the preferential use of the defense mecha-
nisms of denial, dissociation, or repression. Symp-
toms reflecting dysregulation of arousal are those
included in the "D" criteria of DSM-IV: hypervigi-
lance, exaggerated startle response, irritability, diffi-
culty concentrating, and sleep disturbances.
In evaluating the accessibility of these symptoms
to treatment, one must consider first that PTSD
symptoms may reflect different mental processes at
successive phases of the disorder. While perhaps
indicating a normal healing process in the early
stages of the disorder, recurrent and intrusive recol-
lections of the trauma may "age" with time and come
to represent an obsessively repetitive dysfunction of
memory. Attempts to explore, elaborate, and work
through these memories at later stages may often
aggravate rather than cure. Conditioned fear re-
sponses may, similarly, become indelible and
thereby inaccessible to eradication through desensi-
tization or flooding.
A second important principle is to evaluate the
extent to which one level of impairment interferes
with attempts to address other levels. Making a
hierarchical decision, in the proposed multi-level
model, involves knowing where to start, as in the
following examples.
Not every PTSD patient is extremely aroused.
178
A. Y. SHALEV et al.
Those who are, however, and those who have devel-
oped a pattern of dissociative responses to any
reminder of the trauma are poor candidates for
therapy that requires exploration, exposure, or any
additional demand. Treatment aimed at reducing the
underlying arousal or at better controlling dissocia-
tive responses should precede, in such patients, the
more explorative approaches. Treatment of severe
depression, insomnia, or alcohol or substance abuse
may take precedence at some stages of the disorder
over social and interpersonal rehabilitation. Patients
who are extremely avoidant of memories of the
trauma may better respond to interpersonal therapy
once their sensitivity to recalling the trauma is
addressed. The treatment of these patients could
start by imagery desensitization. Marital disputes
and work pressures often aggravate, to a critical
point, the patient's irritability and emotional dys-
control. Couple therapy and intervention in the work
place may be preferred, as a first step, in such
subjects. Finally, each PTSD patient has a unique
rhythm of developing trust, of sharing, and of forging
a therapeutic alliance.
As a final note, one should remember that, to some
extent, the imprint is indelible and hence immutable
by current methods. The evidence provided by this
review shows that attempts to cure chronic PTSD by
reversing its "etiological" mechanisms should be
reconsidered and replaced by more realistic goals
(e.g., vocational rehabilitation, family counseling,
and control of adverse health practices). Defining the
parameters of the disability associated with PTSD
and assessing the effect of combined treatment pro-
grams are important challenges for the future.
The authors thank Ms. Sarah Freedman for her
valuable work in reviewing and editing this manu-
script.
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