Aggression and Violent Behavior, Vol. 5, No. 1, pp.

79–97, 2000
Copyright  1999 Elsevier Science Ltd
Printed in the USA. All rights reserved
1359-1789/00/$–see front matter
PII S1359-1789(98)00021-4

COGNITIVE BEHAVIORAL THERAPY OF

VIOLENCE-RELATED POSTTRAUMATIC
STRESS DISORDER

Richard A. Bryant
University of New South Wales

ABSTRACT. Posttraumatic stress disorder (PTSD) represents the most common psychiat-
ric condition following exposure to violence. Although an increasing number of cognitive
behavioral therapy (CBT) studies point to efficacy of this approach in ameliorating PTSD
following violence, the methodological rigor of many studies has not been optimal. Further,
a significant proportion of traumatized individuals does not benefit from CBT. This article
reviews CBT outcome studies, discusses the methodological limitations of CBT studies for
PTSD, and offers suggestions for future research. This review highlights the need for more
systematic studies of components of CBT with a range of trauma populations to delineate
the parameters of effective CBT for individuals with PTSD.  1999 Elsevier Science Ltd.
All rights reserved.
KEY WORDS. Posttraumatic stress disorder, cognitive behavior therapy, treatment

THE PSYCHOLOGICAL SEQUELAE of assault have been well documented in recent

years (Foa & Riggs, 1995). The most common psychiatric condition to develop following
sexual and nonsexual assault is posttraumatic stress disorder (PTSD). Although this
potentially debilitating condition is reportedly common following assault, controlled stud-
ies of treatment for this disorder have only recently been conducted. The purpose of this
review is to summarize the current knowledge of cognitive behavioral treatments of PTSD,
to highlight the limitations of previous research, and to discuss the directions of future
study of treating violence-related PTSD.

DEFINITION OF PTSD
PTSD was introduced into psychiatric nomenclature in the third edition of the Diagnostic
and Statistical Manual of Mental Disorders (DSM-III-R; American Psychiatric Association,
1980). The definition of PTSD has undergone a number of revisions, and is currently

Correspondence should be addressed to Richard A. Bryant, School of Psychology, University of New

South Wales, NSW, 2052, Australia; E-mail: r.bryant@unsw.edu.au

79
80 R. A. Bryant

defined by DSM-IV (American Psychiatric Association, 1994). To satisfy criteria for PTSD,
one must initially have been exposed to a traumatic event. In defining a trauma, DSM-IV
stipulates that: “the person experienced, witnessed, or was confronted with an event or
events that involve actual or threatened death or serious injury; or a threat to the physical
integrity of himself or herself or others.” It should be noted that DSM-IV includes assault
and exposure to violence in its examples of precipitating traumatic events, and that
epidemiological studies indicate that violent assault represents one of the most common
precipitants of PTSD (Resnick, Kilpatrick, Dansky, Saunders, & Best, 1993). The individ-
ual must also respond to this trauma with “intense, fear, helplessness, or horror.” This
second component of the stressor definition places significant emphasis on the subjective
response to an event, and acknowledges that the personal reaction to a trauma plays a
crucial role in determining the development of PTSD.
DSM-IV divides PTSD symptoms into three clusters. To satisfy the reexperiencing
cluster of symptoms, one must suffer either intrusive memories, nightmares, a sense of
reliving the trauma, or psychological or physiological distress when reminded of the
trauma. To satisfy the avoidance cluster of symptoms, one must suffer at least three of
the following symptoms: persistent avoidance of thoughts, feelings, and reminders of the
trauma, inability to recall some aspect of the trauma, withdrawal from others and normal
activities, or emotional numbing. Finally, to satisfy the arousal cluster one must experience
at least two of the following symptoms: insomnia, irritability, difficulty concentrating,
hypervigilence, or heightened startle response. These symptoms must cause marked im-
pairment to one’s functioning, and persist for at least one month after the trauma. The
disorder is considered “chronic” if the symptoms persist for more than three months post-
trauma.
DSM-IV also introduced a new diagnosis, acute stress disorder, (ASD), to describe
acute trauma reactions that occur in the initial month following a trauma. A major rationale
for inclusion of ASD was that it could provide a diagnosis to identify those individuals
whom subsequently develop chronic PTSD (Koopman, Classen, Cardena, & Spiegel,
1995). Acute stress disorder (ASD) is conceptually similar to PTSD and shares many of
the same symptoms (for a review, see Bryant & Harvey, 1997). The major distinction
between ASD and PTSD is the former’s emphasis on dissociative symptoms. In addition
to requiring the individual to suffer reexperiencing, avoidance, and arousal symptoms, the
ASD criteria stipulates that the individual suffers at least three of five possible dissociative
symptoms. These include numbing, reduced awareness of their surroundings, derealization,
depersonalization, and dissociative amnesia. These symptoms may occur either at the
time of the trauma or during the subsequent month. Justification for the emphasis on
dissociative symptoms is that they are considered predictive of longer term psychopathol-
ogy (Koopman, Classen, & Spiegel, 1994). To suffer ASD one must display these symptoms
at least 2 days after the trauma but after a month the diagnosis is no longer applicable;
at this time the diagnosis of PTSD should be considered. The potential utility of the ASD
diagnosis is that it provides an opportunity to identify those individuals soon after their
assault who are likely to develop ongoing PTSD, and provide early treatment to facili-
tate recovery.

INCIDENCE OF PTSD FOLLOWING ASSAULT

Two well-controlled studies have been conducted on the incidence and course of PTSD
following assault (Riggs, Rothbaum, & Foa, 1995; Rothbaum, Foa, Riggs, Murdock, &
Walsh, 1992). Each study prospectively assessed sexual and nonsexual assault victims
 Posttraumatic Stress Disorder 81

during the initial 3 months following the assault. In terms of rape victims, 94% met criteria
for PTSD approximately 1 week following the assault, 65% met criteria 1 month after
the assault, and 47% met criteria 3 months after the rape (Rothbaum et al., 1992). A
similar pattern was observed for the victims of nonsexual assault, in that 76% met criteria
for PTSD approximately 2 weeks posttrauma, 42% met criteria one month posttrauma,
and 22% met criteria 3 months after the assault (Riggs et al., 1995). These findings
converge on the conclusion that at least half of assault victims who initially develop PTSD
symptoms will remit within the initial three months. Importantly, these studies also indicate
that a significant proportion of sexual and nonsexual assault victims continues to experience
chronic PTSD.
There is significant interest in early identification of victims of assault who will develop
chronic PTSD. The finding that many victims remit without therapy suggests that it is
not appropriate to provide formal intervention to all victims of assault who display initial
PTSD symptoms. If those individuals who are at risk of chronic PTSD individuals could
be identified at an initial stage, perhaps early intervention could prevent the subsequent
development of PTSD. In this context, it is interesting to note that Rothbaum et al. (1992)
compared the initial responses of rape victims who either did or did not develop chronic
PTSD. Those victims who did suffer long-term PTSD differed from the others in their
greater symptomatology soon after the trauma and their failure to make clinical gains
after the initial month following the rape. This pattern was interpreted as evidence for
the need for therapy for individuals who continue to experience PTSD after the initial 6
weeks posttrauma (Foa & Riggs, 1995).
As noted above, one promising means to identify trauma victims who are at risk of
developing longer term PTSD is the diagnosis of ASD. To date there are no studies of
the incidence and course of ASD following assault. In a prospective study of ASD following
motor vehicle accidents (MVA), however, Harvey and Bryant (1998) reported that 78%
of MVA survivors who met criteria for ASD still suffered PTSD 6 months posttrauma.
Considering the evidence that at least half of people who suffer PTSD symptoms shortly
after a trauma remit within 3 months, this diagnosis appears to be a potentially better
means to identify victims of assault shortly after the trauma who will develop longer term
PTSD. Although the ASD diagnosis has yet to be thoroughly validated with assault
victims, this diagnosis points to exciting opportunities to treat traumatized assault victims
before PTSD becomes entrenched.

THEORETICAL ISSUES
Most cognitive behavioral treatments of PTSD are related to variants of information-
processing theories of trauma response. Foa and Kozak (1986) adapted Lang’s (1977)
theory that fear is represented in cognitive networks of mental representations of fear-
related stimuli, responses, and meanings. According to Foa and Kozak (1986), trauma
can result in the formation of threat-oriented schema that serve to maintain a range of
PTSD symptoms. It is proposed that the constant activation of fear networks in PTSD
can account for hypervigilence to danger, intrusive thoughts of the trauma, and distorted
beliefs about trauma-related issues (Litz & Keane, 1989). On the basis of this theory, it
is proposed that symptom reduction can be achieved by satisfying two conditions. Specifi-
cally, the fear network must be activated and the associated erroneous beliefs need to be
corrected. There is increasing evidence that persistent PTSD is associated with inadequate
activation and accessibility of the fear network. For example, one recent study demon-
strated that inability to access specific memories of one’s trauma several weeks after the
82 R. A. Bryant

trauma predicted severity of posttraumatic stress disorder 6 months posttrauma (Harvey,

Bryant, & Dang, 1998).
A primary rationale for exposure therapies is that maintaining the heightened state of
anxiety that is experienced during proximity to the fearful stimulus will result in habitua-
tion. In the context of PTSD, the rationale of exposure to traumatic memories has been
extended to incorporate the modification of beliefs. Specifically, it has been proposed
that exposure to feared stimuli or memories leads to symptom reduction because: (a)
reminders of the trauma objectively do not harm the individual, (b) recalling the trauma
does not involve reliving the threat, (c) there is habituation because anxiety subsides over
time whilst remaining in proximity to the feared stimuli, and (d) the experience of anxiety
does not result in the feared loss of control (Jaycox & Foa, 1996). In this sense it is argued
that exposure leads to improvement because of two associated, but distinct, processes.
First, there is habituation of anxiety, and second there is learning that the exposure does
not lead to renewed threat.

OUTCOME STUDIES
Systematic Desensitization
Some of the earliest studies to apply behavioral principles to trauma victims focused on
systematic desensitization. This procedure, developed by Wolpe (1958), couples imagina-
tion of the feared stimulus with relaxation, and typically requires the individual to master
feared scenes in a hierarchically graded regime. Frank and colleagues investigated the
efficacy of systematic desensitization in a series of studies with female rape victims
(Frank & Stewart, 1983, 1984). In these studies systematic desensitization involved imagi-
nation of the traumatic scenarios combined with positive scenes. Participants received 14
sessions, and in 75% of cases the participants voluntarily initiated in vivo exposure exer-
cises. These studies concluded that treatment led to reduced fear and improved social
adjustment. The conclusions that can be drawn from these studies are limited, however,
because there were no control groups, PTSD measures were not employed, and because
a proportion of participants were treated in the acute trauma phase some improvement
may be attributed to natural adjustment. Caution about the utility of systematic desensitiza-
tion is also indicated by a report by Becker and Abel (1981) that indicated only very
modest symptom reduction for rape-related anxiety.

Exposure Therapies
Exposure therapies may take the form of either imaginal or in vivo exposure. Whereas
in vivo exposure requires the individual to remain in close proximity to actual stimuli
(e.g., the street on which individual was assaulted), imaginal exposure has the individual
imagine feared events or memories of the trauma. Although many treatment programs
utilize these two forms of exposure interchangeably, the focus in recent years has been
on imaginal exposure. This development has occurred because a primary target symptom
in the treatment of PTSD is intrusive memories. A common treatment of traumatic
memories is to direct the individual to focus attention on their memories in a way that
encourages them to engage fully with the distress associated with these recollections. This
form of prolonged exposure typically requires the individual to maintain this focus for at
least 45 minutes, by which time it is assumed that habituation may have occurred. Although
there are numerous case studies that have supported the use of exposure (e.g., Keane &
 Posttraumatic Stress Disorder 83

Kaloupek, 1982), this review will focus on controlled outcome studies of individuals who
developed PTSD following assault or violence.
In one of the first studies, Keane, Fairbank, Caddell, and Zimering (1989) randomly
allocated Vietnam veterans to either flooding (imaginal exposure) or to a wait-list control
group. Exposure treatment included relaxation training, rehearsal with benign imagery,
and imaginal exposure of traumatic memories. This study reported marked improvements
for the exposure treatment, including greater reductions in reported fear, depression, and
reexperiencing symptoms than the control group. Cooper and Clum (1989) provided
veterans with PTSD with either a standard treatment program (psychological/pharmaco-
logical) or the standard treatment combined with imaginal flooding. The veterans who
received imaginal flooding reported greater reductions in nightmares and anxiety. Boude-
wyns and colleagues (Boudewyns & Hyer, 1990; Boudewyns, Hyer, Woods, Harrison, &
McCrame, 1990) reported two studies of inpatient veterans who in addition to the regular
inpatient treatment program received either direct therapeutic exposure (either imaginal
or in vivo exposure) or traditional individual counseling. In both studies there was greater
reported improvement on general psychological functioning (specific PTSD symptoms
were not reported). Although each of these studies point to the potential efficacy of
exposure relative to more traditional treatment procedures, it must be noted that each
lacked blind posttreatment assessments of outcome. Absence of independent posttreat-
ment assessment raises significant concerns over the extent to which posttreatment mea-
sures may reflect expectancy bias. As Foa and Meadows (1997) note in their criteria of
gold standard practices for PTSD outcome studies, blind assessments are essential if
results are to be deemed reliable indicators of the effectiveness of any treatment procedure.
More rigorous investigation of the efficacy of exposure was conducted by Foa, Roth-
baum, Riggs, and Murdock (1991). This study randomly assigned female victims of sexual
or nonsexual assault to either prolonged exposure (PE), stress inoculation training (SIT),
supportive counseling, or a wait-list control group. This study provided participants with
9 twice-weekly sessions, and included blind assessments at posttreatment and 3-months
follow-up. Whereas SIT resulted in greater gains than SC or wait-list control at posttreat-
ment, the PE condition led to greater reduction in PTSD symptoms at follow-up. Interpre-
ting these results in terms of network theory, the authors claimed that whereas SIT led
to short-term symptom reduction, PE resulted in longer term benefits because the fear
networks were activated and modified.
In summary, there is increasing evidence that imaginal exposure is effective in reducing
PTSD symptoms. It needs to be noted, however, that in well-controlled studies efficacy
of PE has been limited. For example, Foa et al. (1991) reported that at follow-up 45%
of patients treated with exposure still satisfied criteria for PTSD, and 44% did not achieve
clinically significant gains. Similarly, in a later study Foa and colleagues reported that at
follow-up only 75% of patients who received PE and 50% of those who received PE and
SIT achieved good end-state functioning (cited in Foa & Meadows, 1997). These findings
indicate that whereas PE is beneficial for many individuals, a significant proportion of
individuals with PTSD will require alternative approaches.

In Vivo Versus Imaginal Exposure

As noted above, there has been a tendency in treatment studies to regard in vivo and
imaginal exposure similarly. Further, previous studies have often included in vivo exposure
as an optional adjunct to imaginal exposure (e.g., Foa et al., 1991) or as a spontaneous
addition to imaginal exposure initiated by participants (e.g., Frank et al., 1988). This
tendency appears unfortunate because there is convergent evidence that cognitive expo-
84 R. A. Bryant

sure treatments may lack optimal efficacy in treating the avoidance symptoms of PTSD
(Frueh, Turner, & Beidel, 1995; S. D. Solomon, Gerrity, & Muff, 1992). For example,
Keane et al. (1989) found that imaginal exposure resulted in decreased intrusive and
arousal PTSD symptoms but did not reduce avoidance and numbing. In contrast, studies
that have provided in vivo desensitization to traumatized individuals have reported signifi-
cant gains in terms of reduced avoidance symptomatology relative to control groups (e.g.,
Brom, Kleber, & Defares, 1989). Further, Foa et al. (1991) included in vivo exposure as
one homework activity in their PE treatment, and found significant decreases in avoidance
behavior. This finding is consistent with proposals that in vivo exposure is the optimal
treatment for reducing avoidance behavior in anxiety states (Marks, 1987).
Although in vivo exposure has been more extensively employed with combat-related
PTSD, the results have not been encouraging (Frueh et al., 1995). The Koach project,
which exposed soldiers to feared stimuli, resulted in poorer outcomes than controls (Z.
Solomon et al., 1992). This failure was attributed, among other factors, to inappropriate
provision of in vivo exposure strategies (Bleich, Shalev, Shoham, Solomon, & Kotler,
1992). This project highlighted the need for exposure studies to strictly define and adhere
to appropriate parameters of exposure regimes. Previous studies have not adequately
compared the relative efficacies of imaginal and in vivo exposure treatments, and accord-
ingly there is a lack of direction for the most appropriate means to reduce avoidance
behavior in PTSD. In an initial study of imaginal and in vivo exposure, Richards, Lovell,
and Marks (1994) found that in vivo exposure was more effective than imaginal exposure
in reducing avoidance. Conclusions from this study are limited, however, by the lack of
control groups. Accordingly, there is a marked need for investigation of the role of in
vivo exposure to supplement gains that may be initiated by imaginal exposure.

The Role of Cognitive Therapy

Cognitive therapy for PTSD is based on Beck’s (1972) theory that distorted beliefs about
one’s self and the world lead to heightened anxiety and depressive reactions. In the
context of PTSD, it is proposed that people may develop exaggerated beliefs about threats,
vulnerability, or worthlessness following a trauma (Foa & Riggs, 1993). This proposition
has been validated by a recent study that demonstrated that individuals with ASD exagger-
ated both the probability of future negative events and the negative consequences of
these events more than traumatized controls (Warda & Bryant, 1998). Cognitive therapy
aims to identify erroneous beliefs, and teaches individuals to modify their thoughts within
a more realistic framework. Despite the importance of cognitive therapy in a range of
anxiety and depressive disorders (Beck, Rush, Shaw, & Emery, 1979), there has been
relatively little systematic research on the efficacy of cognitive therapy in treating PTSD.
One reason for this appears to be the de facto role that it often plays in imaginal exposure
treatments. Numerous studies have included cognitive therapy as an adjunct to PE (Foa,
Hearst-Ikeda, & Perry, 1995; Foa et al., 1991; Resick & Schicke, 1992a), but these designs
have not allowed the differential influences of exposure and cognitive therapy to be
evaluated. For example, Resick and Schicke (1992b) have specifically proposed cognitive
processing therapy (CPT) as a structured combination of imaginal exposure and cognitive
therapy that is based on five major cognitive themes that they suggest are central to rape
victims’ cognitive schema. In an initial comparison of CPT and wait-list controls, they
reported that mean symptom reduction on the SCL-90 was 40% compared to 1.5% for
wait-list controls. This study was hampered, however, by the lack of blind evaluations
and specific PTSD measures. These authors increased this initial sample in a subsequently
reported study that included 54 female rape victims (Resnick & Schicke, 1992b). They
 Posttraumatic Stress Disorder 85

reported that whereas 96% of the sample initially met criteria for PTSD, 88% of those
who received CPT were not diagnosed following treatment. Although these studies point
to the efficacy of CPT, they do delineate the relative contributions of exposure and
cognitive therapy.
In the series of studies with female rape victims conducted by Frank and colleagues that
was described earlier, systematic desensitization was investigated with cognitive therapy
(Frank et al., 1988; Frank & Stewart, 1983, 1984). Although these two treatments were
not directly compared, a subsequent comparison of treatment gains indicated that the
two treatments resulted in comparable benefits (Turner & Frank, 1981). In their later
study, Frank et al. (1988) studied 84 participants who were randomly provided with
systematic desensitization or cognitive therapy. The latter comprised self-monitoring,
graded task assignments that minimized avoidance behaviors, and identification and chal-
lenging of cognitive errors. This study concluded that there were no significant differences
between participants who received either of the treatment programs, and that both led
to clinical gains. Conclusions that can be drawn from this series of studies are limited,
however, because there were no control groups and the cognitive therapy included behav-
ioral components that extended beyond the domain of cognitive therapy.
There are both theoretical and applied issues that need to be clarified by differentiating
the benefits of cognitive therapy and PE. It has been proposed by information processing
theories that PE facilitates recovery because it both promotes habituation to the anxiety-
laden stimuli that is not being avoided and permits cognitive restructuring as one learns
that fear-based beliefs are not reality-based (Jaycox & Foa, 1996). Our understanding of
the theoretical framework for trauma recovery could be enhanced by firmer understanding
of the differential roles that habituation and cognitive restructuring play in this therapeutic
process. From an applied perspective, there is a need to assess the extent to which
traumatized individuals require active cognitive therapy to supplement PE in order to
modify threat-based cognitive distortions. There are currently several projects underway
that are investigating the additive benefits of cognitive therapy in association with PE.
As will be discussed below, there are indications that specific types of trauma survivors
may be more responsive to cognitive therapy than exposure-based therapies, and future
work also need to identify the utility of cognitive therapy with particular types of
PTSD presentation.

Eye Movement Desensitization and Reprocessing

One popular variant of imaginal exposure is eye movement desensitization and reprocess-
ing (EMDR), which requires the patient to focus attention on a traumatic memory while
simultaneously visually tracking the therapist’s finger as it is moved across their visual
field (Shapiro, 1995). Although this technique has been the focus of much debate (see
Tolin, Montgomery, Kleinknecht, & Lohr, 1996), many case studies have attested to its
success in reducing distress associated with traumatic memories (see Lohr, Kleinknecht,
Tolin, & Barrett, 1996). In terms of controlled studies, the evidence for EMDR is mixed,
and is hindered somewhat by the presence of methodological problems in most studies
conducted to date. In a study that compared EMDR to a control condition, Jensen (1994)
found that although the EMDR group reported lower SUDS (subjective units of distress)
ratings than the control group, the groups did not differ in PTSD symptoms. Vaughan
and Tarrier (1994) reported that EMDR was comparably effective in reducing PTSD
symptoms to both anxiety management and repeated presentations of traumatic stimuli.
Although Wilson, Tinker, and Becker (1995) found that EMDR led to greater reductions
in PTSD-related symptoms than a wait-list control, this study was flawed by the reliance
86 R. A. Bryant

on self-report data and ambiguity about pretreatment severity levels. In combination,

these studies are limited in their inferences about the utility of EMDR because they lack
adequate methodological rigor.
More recently, Pitman and colleagues compared EMDR with EMDR minus the eye
movement component with veterans suffering PTSD (Pitman et al., 1996). The finding
that both groups showed symptom reduction suggests that exposure or nonspecific therapy
factors were more critical to therapy gains than eye movement itself. Rothbaum (1995)
has reported that in a study of rape victims EMDR obtained greater symptom reduction
than a wait-list control at both posttreatment and 3-month follow-up. These findings
indicate that whilst EMDR has potential as a treatment for PTSD, its efficacy relative to
more standard exposure therapies has yet to be demonstrated. The procedural similarities
between EMDR and other imaginal exposure therapies highlights the need for future
studies of EMDR to compare EMDR with other exposure therapies, monitor treatment
adherence, index expectancy factors, and ensure independent and objective outcome
measures are conducted.

Anxiety Management Techniques

Numerous studies have treated PTSD on the basis that it is primarily an anxiety disorder
that is mediated by inadequate skills to manage the symptoms of anxiety. That is, this
approach addresses management of the anxiety response rather than cognitions that
contribute to the anxiety. The most common anxiety management program employed in
PTSD is Meichenbaum’s (1975) stress inoculation training (SIT), which includes psycho-
education, relaxation skills, thought stopping, and self-talk.
Efficacy of SIT with rape victims was suggested by several early studies. Veronen and
Kilpatrick (1982) provided 15 female rape victims who displayed persistent anxiety and
avoidance symptoms 3 months posttrauma with 20 sessions of SIT. They reported marked
symptom reduction in fear, avoidance, and depression, and these gains were largely
maintained at 3-month follow-up. Conclusions of this study were limited, however, by the
lack of control groups, inadequate information concerning minimal severity for inclusion in
the study, and the omission of assessment of all PTSD symptoms. In a subsequent study
by the same authors, rape victims were offered either 10 sessions of SIT, peer counseling,
or systematic desensitization (Veronen & Kilpatrick, 1983). Most women declined therapy
and, of the 15 who accepted, 11 chose SIT, 3 chose peer counseling, and none chose
desensitization. Although no comparative analyses were viable in this study, posttreatment
results pointed to the efficacy of SIT in reducing rape-related anxiety and depression.
In a better controlled study, Resick and colleagues compared six 2-hour sessions of
either SIT, assertiveness training, supportive counseling, or a wait-list condition with rape
victims (Resick, Jordan, Girelli, Hutter, & Marhoefer-Dvorak, 1988). They found that all
treatments were comparably effective at posttreatment, and that gains were maintained
at 6-months follow-up on fear measures. It should be noted that this program modified
the SIT to include in vivo exposure to avoided stimuli. Inferences drawn from this study
are restricted, however, by the lack of strict inclusion criteria; that is, participants were
required to have been raped at least three months prior to the study and to suffer rape-
related fear and anxiety. Accordingly, the relevance of these findings to PTSD symptoms
is uncertain.
As described earlier, Foa et al. (1991) compared SIT with PE, supportive counseling,
and a wait-list condition with rape victims who had chronic PTSD. In this study SIT
comprised education, breathing retaining and muscle relaxation, thought stopping, cogni-
tive restructuring, modeling, and role-plays. Whereas SIT was the most effective treatment
 Posttraumatic Stress Disorder 87

at posttreatment, its efficacy relative to PE was diminished at 3-month follow-up. These

authors subsequently replicated this study in a design that compared PE, SIT, the combina-
tion of PE and SIT, and a wait-list control condition (cited in Foa & Meadows, 1997).
Somewhat surprisingly, PTSD severity at follow-up assessment (M 5 10 months) was
reduced by 66% after PE, 52% after SIT, and 48% after the combined exposure and SIT
program. This result has been attributed to the shorter time allocated to PE and SIT in
the combined treatment group relative to those who received only PE or SIT (Foa &
Meadows, 1997).

TREATMENTS OF ACUTE STRESS DISORDER

Considering that ASD was only introduced into DSM-IV in 1994, it is not surprising that
there are few treatment studies relevant to ASD. Although there are reports of crisis
intervention in the initial month(s) after a trauma being beneficial (e.g., Brom, Kleber, &
Hofman, 1993; Viney, Clark, Bunn, & Benjamin, 1985), these are not well-controlled
studies, do not utilize CBT in a structured manner, and have not adequately indexed PTSD
symptoms. Kilpatrick and Veronen (1983) reported on a brief behavioral intervention that
was provided to rape victims immediately after the assault. Fifteen victims were randomly
assigned to repeated assessments, delayed assessment, or the active intervention. The
intervention comprised a 4- to 6-hour treatment program aimed to prevent phobic reactions
as well as other PTSD symptoms. Therapy involved imaginal reliving of the trauma,
education about psychological responses to trauma, cognitive restructuring, and anxiety
management. This study indicated that the brief intervention was not more effective than
the repeated assessments. This negative finding needs to be interpreted, however, with
recognition of the small sample sizes, the lack of rigorous application of exposure, and
questions concerning the degree of pathology experienced after the rape. Further, inclusion
criteria and the time frame of this study may involve a possible confound in that it is
difficult to exclude the role of natural recovery in participants’ responses (Kilpatrick &
Calhoun, 1988).
Foa and colleagues recently reported on a brief cognitive behavioral treatment program
provided to sexual and nonsexual assault victims shortly after the assault (Foa, Riggs, &
Gershuny, 1995). This study compared CBT, which included PE, anxiety management,
in vivo exposure, and cognitive therapy, with matched participants who received repeated
assessments. Each participant received four treatment sessions, and then received assess-
ment by blind assessors at 2 months posttreatment and 5 months follow-up. Whereas
10% of the CBT group met criteria for PTSD at 2 months, 70% of the control group met
criteria; there were no differences between groups at five months, although the CBT
group was less depressed.
It needs to recognized, however, that the Foa et al. (1995) study did not include
participants who satisfied criteria for ASD, and accordingly it did not test the capacity
of CBT to assist individuals who met the more stringent criteria for ASD. In this context,
Bryant and colleagues have recently reported that CBT, comprising the same components
as employed by Foa et al. (1995), was effective in treating ASD in survivors of motor
vehicle and industrial accidents (Bryant, Harvey, Sackville, Dang, & Basten, in press).
Specifically, whereas CBT resulted in 10% of participants having PTSD at 6 months
posttrauma, 70% of those who received supportive counseling had PTSD 6 months later.
Although the study of treating ASD has only commenced, the early indicators suggest
that chronic PTSD may be prevented by providing early and brief CBT programs to those
trauma survivors who are most at risk of developing chronic PTSD. This proposal needs
88 R. A. Bryant

to be qualified, however, by recognizing the need for replication of early intervention

studies with a range of trauma populations. For example, there is evidence that early
intervention with bereaved individuals may not be effective (Polak, Egan, Vandebergh, &
Williams, 1975). Accordingly, future research needs to establish the parameters of benefi-
cial early CBT following trauma.

LIMITATIONS OF COGNITIVE BEHAVIOR THERAPY

Detrimental Effects of Exposure Therapies
There is increasing evidence that exposure-based therapies may not only be nonbeneficial
for some PTSD sufferers but may even be detrimental. Kilpatrick and colleagues (Kil-
patrick, Veronen, & Best, 1985; Kilpatrick, Veronen, & Resick, 1982) have criticized
flooding for sexual assault survivors because: (a) in aiming to reduce anxiety it may focus
on symptom change rather than modifying irrational thoughts, (b) it may contribute
to excessive noncompliance with therapy because of its distressing nature, (c) it may
inappropriately reduce anxiety to nonconsensual sex, and (d) it does not directly teach
coping strategies. Although each of these points has been countered by various authors
(Foa & Meadows, 1996; Rychtarick, Silverman, Van Landingham, & Prue, 1984), there
is some evidence that exposure-based therapies may not be appropriate for all PTSD
sufferers. Pitman and colleagues (Pitman et al., 1991) reported that they ceased a study that
employed flooding because of the significant adverse effects it had upon their participants.
Similarly, Vaughan and Tarrier (1992) reported that one of their sample of seven partici-
pants suffered a marked deterioration following exposure. This is consistent with clinical
experience from our current study on exposure with assault victims, where a small but
significant number of participants experienced increased PTSD and depressive symptoms
following exposure. These initial indications point to the need for close scrutiny of factors
that predispose one to adverse reactions to PE.

Anger
Anger is a common response in PTSD (Goenjian, 1993). Victims of assault frequently
feel frustrated by the trauma they have suffered, and there is currently little empirical
or theoretical direction for optimal management of this presentation. As noted earlier,
exposure-based therapies assume that individuals will experience elevated anxiety during
anxiety, and this response will promote habituation. The predominance of anger, however,
may impede activation of the fear network because it reduces the level of anxiety that is
experienced. Consistent with this proposal, Riggs et al. (1995) found that assault victims
who had higher state anger levels within 2 weeks of the trauma were more likely to have
higher PTSD scores one month later. Further, self-reported anger levels prior to treatment
were conversely associated with improvement, and facial expressions of fear, rather than
anger, during the initial exposure session in therapy were strongly correlated with therapeu-
tic gain (Foa et al., 1995; Jaycox, Perry, Freshman, Stafford, & Foa, 1995). These findings
indicate that more research is required that evaluates the efficacies of components of
CBT in treating PTSD patients who present with severe anger.

Dissociation
Activation of the fear network can also be impeded by dissociative mechanisms, such as
emotional numbing (Foa & Hearst-Ikeda, 1996), as well as more effortful cognitive avoid-
 Posttraumatic Stress Disorder 89

ance strategies (Ehlers & Steil, 1995). This problem may be more prevalent (a) in ASD
than PTSD because of the stronger dissociative responses reported in this acute reaction
(Harvey & Bryant, 1998) and (b) in very severe or prolonged traumas in which dissociative
reactions are more prevalent (Zatzick, Marmar, Weiss, & Metzler, 1994). No treatment
studies to date have investigated techniques to effectively manage this potential obstacle.
Several writers have suggested that hypnosis may serve to minimize the dissociative barrier
between the mental representations of the trauma and their associated affect (Spiegel &
Classen, 1995). This proposition argues that because hypnosis involves dissociative mecha-
nisms, and it can engage people’s attention in a very focused way, it may represent a
more effective technique than nonhypnotic strategies. To answer this question, we are
currently conducting a treatment study of assault victims who meet criteria for ASD in
which participants receive either CBT or CBT with hypnosis. Further research will be
required to determine the utility of adapting hypnosis as an adjunct to exposure-based ther-
apies.

Extreme Anxiety
Recent commentaries have also noted that exposure-based therapies can be impeded by
a participant’s excessive anxiety (Jaycox et al., 1995). It is proposed that exposure can
retraumatize the individual because the experience is perceived as overwhelming. Relat-
edly, there is evidence that exposure may not be successful if the individual’s memories
of the trauma are characterized by mental defeat or lack of mastery over the situation
(Ehlers et al., 1998). It is possible that simply activating traumatic memories in a way
that heightens the individual’s sense of anxiety and helplessness may further compound
the posttraumatic stress reaction. The aforementioned reports of participants who have
apparently suffered increased symptoms following exposure (Pitman et al., 1991; Vaughan &
Tarrier, 1992) support this possibility. Considering the maxim that a major goal of therapy
is to do no harm, it is imperative that future studies delineate factors that contraindicate
use of exposure (see Litz, Blake, Gerardi, & Keane, 1990). In this context it is important
for better understanding of the role of cognitive therapy in exposure because successful
response to exposure for individuals with maladaptive perceptions of the trauma may
require cognitive therapy in conjunction with exposure.

MEASUREMENT ISSUES
Comorbidity
There is strong evidence that many people who develop PTSD will also suffer comorbid
disorders. Depression, substance abuse, and anxiety disorders are among the common
comorbid diagnoses in the PTSD population (Davidson & Fairbank, 1993; Davidson,
Hughes, & Blazer, 1991; Keane & Wolfe, 1990). Further, there is evidence of elevated
rates of personality disorders (Faustman & White, 1989; Southwick, Yehuda, & Giller,
1993) among PTSD populations. Most cognitive behavioral treatment studies have focused
predominantly on reduction of PTSD symptoms. As discussed above, the rationale for
CBT of PTSD is essentially to habituate anxiety and modify threat-related cognitive
schema. Accordingly, relatively little attention has been directed to the influence of CBT
on comorbid conditions.
Several studies have indexed depressive symptoms, and found that exposure treatments
have resulted in reduced depressive symptoms (Bryant et al., in press; Foa et al., 1991).
It has been proposed that posttraumatic depression is frequently secondary to PTSD
90 R. A. Bryant

symptoms and that resolution of PTSD may lead to reduced depression (Nishith, Hearst,
Mueser, & Foa, 1995). This proposal has been demonstrated in a controlled case study
(Nishith et al., 1995), but there are currently no outcome studies to inform us of the merit
of CBT of PTSD on major depressive episodes. Considering the evidence supporting the
use of cognitive therapy for managing depression (Beck et al., 1979), future treatment
studies of PTSD need to evaluate the relative contributions of exposure and cognitive
therapy on comorbid depression.
Bereavement is a common condition in the posttraumatic reaction (Horowitz, 1993).
There are currently no controlled outcome studies of PTSD and bereavement. This is a
surprising omission from the literature considering the increasing evidence that posttrau-
matic stress and grief interact in many instances (Goenjian et al., 1995). Further, some
commentators suggest that the reexperiencing and numbing symptoms of PTSD are best
understood in the context of bereavement rather than anxiety disorders (Horowitz,
Weiss, & Marmar, 1987). Recent conceptualizations of bereavement have suggested that
both cognitive therapy and exposure techniques may be applicable to pathological grief
reactions (Kavanagh, 1990). There is a need for controlled studies to index the utility of
CBT in cases of PTSD that involve bereavement issues.
Similarly, there is a lack of research to guide appropriate management of substance abuse
in victims of assault who suffer from PTSD. Substance abuse is a common posttraumatic
response (Keane & Wolfe, 1990; Kulka et al., 1990), and it is conceptualized as a form
of avoidance behavior that assists management of distressing intrusive symptoms (Keane,
Gerardi, Lyons, & Wolfe, 1988). Considering that exposure based therapies typically
heighten distress and activate fear networks that include unwanted intrusions, it is possible
that this form of therapy may aggravate substance abuse. Considering that many PTSD
patients present with substance abuse, there is a need for outcome studies to guide the
optimal management of substance abuse during exposure-based treatments.

Long-Term Outcomes
A major limitation of many treatment studies is the relatively short periods of time in
which follow-up assessments are completed. Most studies include follow-up assessments
of 6 months (Bryant et al., in press; Foa et al., 1991). There is evidence that therapeutic
outcomes can differ from posttreatment assessments to follow-up assessments. For exam-
ple, Foa et al. (1991) found that whereas SIT was more effective at posttreatment, PE
had a superior effect at follow-up. This pattern underscores the possibility that therapeutic
techniques may mediate outcome differentially in the short-term and long-term. Further,
there is evidence that the course of PTSD can be influenced by ongoing stresses (Bryant &
Harvey, 1995c; Z. Solomon, Mikulincer, & Flum, 1988) and the use of specific coping
strategies (Bryant & Harvey, 1995a; Z. Solomon et al., 1988). Different therapeutic inter-
ventions may influence these posttrauma factors in ways that contribute to improved
functioning. Longer term follow-up assessments, including 2- and 3-year follow-ups, may
increase our understanding of the role of these interventions in long-term adjustment
to trauma.

Attrition Rates
There is increasing recognition that exposure-based therapies can result in significant
drop-out rates during treatment. Numerous studies have alluded to the difficulties that
many PTSD participants have in managing the distress elicited by exposure (Ehlers et
al., 1998; Pitman et al., 1991; Vaughan & Tarrier, 1992). Further, studies that have given
participants a treatment choice have reported that most participants decline the opportu-
 Posttraumatic Stress Disorder 91

nity to receive treatments that involve some form of exposure (Veronen & Kilpatrick,
1983). These reports indicate that whereas exposure may be useful for a significant propor-
tion of participants who complete treatment, there is a need for treatment studies to report
the proportion of participants who: (a) decline treatment because it involves exposure, (b)
drop out of exposure treatment programs, and (c) do not comply with exposure exercises or
homework. Acknowledgement of these rates, rather than restricting attention to compliant
participants, will permit more accurate assessment of the utility of exposure in PTSD.
Further, there is a need for future studies to index covert avoidance strategies that
participants may use to minimize anxiety during exposure. Studies of other anxiety disor-
ders in which exposure techniques are commonly employed, such as obsessive compulsive
disorder (Riggs & Foa, 1993) and generalized anxiety disorder (Brown, O’Leary, &
Barlow, 1993), have noted the need for factors that minimize the efficacy of exposure to
be monitored and removed.

SPECIFIC POPULATIONS
In recent years there has been increasing awareness that PTSD needs to be studied in
specific trauma populations. The aforementioned studies of PTSD following sexual and
nonsexual assault (Riggs et al., 1995; Rothbaum et al., 1992) indicate that the recovery
process is not identical following these related, but distinct, types of trauma. Further,
Riggs et al. (1995) found different recovery rates for females and males following nonsexual
assault. Specifically, whereas 70% of females and 50% of males satisfied PTSD criteria
(excluding the duration criterion) an average of 19 days posttrauma, this rate decreased
to 21% for females and 0% for males 4 months posttrauma. Accordingly, treatment
studies need to take into account the specific clinical needs that are associated with
different types of trauma.

Chronic PTSD
There is now strong agreement that many chronic PTSD populations are resistant to
psychological treatments (for reviews, see Frueh et al., 1995). Numerous studies have
indicated the failure of CBT to effectively reduce PTSD in chronic veteran populations.
Pitman and colleagues have reported that exposure therapy resulted in modest reduction
of PTSD (Pitman et al., 1996). These authors suggested that whereas this form of therapy
may be useful for individuals who have recently suffered a trauma, it may not be sufficient
for people who have developed long-term adjustment problems that have compounded
their PTSD. In Frueh et al.’s (1995) review of exposure-based treatment studies of combat-
related PTSD (Boudewyns & Hyer, 1990; Boudewyns et al., 1990; Cooper & Clum, 1989;
Keane et al., 1989), it was noted that whereas exposure was associated with reductions
in intrusive symptoms and psychophysiological indicators, the designs and measures used
in these studies did not allow any comparison between exposure and other CBT strategies.
At this stage there appears to be justification for not generalizing findings from treatment
studies of shorter term PTSD to more chronic populations. There is increasing evidence
that Vietnam veterans have complex comorbidity issues that may require more comprehen-
sive treatment programs that extend beyond exposure to traumatic memories and specifi-
cally address multifaceted adjustment issues. Accordingly, recent approaches to treating
more chronic PTSD populations have suggested that therapy separately addresses “first
generation” symptoms (e.g., reexperiencing symptoms) and “second generation” symp-
toms (e.g., social dysfunction) because the long-term adjustment problems that develop
92 R. A. Bryant

in the years posttrauma require distinct therapeutic approaches (Johnson, Feldman, South-
wick, & Charney, 1994).

Children
Despite the extensive literature on problems arising from childhood abuse, there is a
dearth of well-controlled treatment studies of this population (see Finkelhor & Berliner,
1995). A major obstacle to treatment studies in the past has been the difficulty in identifying
target symptoms that are to be treated. Recent work indicates that childhood abuse does
not lead to a definitive constellation of symptoms but can result in a wide range of
disorders (Kendall-Tackett, Williams, & Finkelhor, 1993). Accordingly, this population
represents a very heterogeneous group. There are also important developmental issues
that prevent generalizing from one age group to another. For example, one should not
provide a treatment to 5-year-old and 12-year-old children who have been abused, and
assume that similar processes are occurring in response to the treatment. There is a need
to tailor and evaluate treatments for each developmental stage. In terms of PTSD, there
appears to be some critical differences in the presentation of PTSD in children and adults
(McNally, 1991). For example, the prevalence of intrusive memories in adult PTSD may
not occur as much in children (Hopkins & King, 1994). Accordingly, it may not be
appropriate to assume that exposure-based therapies will function in a similar way with
childhood PTSD as it has been shown to with adults.
There is also the need to distinguish between acute and longer term childhood traumas.
Much of the work that has documented PTSD in children has focused on acute traumas
(e.g., Pynoos et al., 1987). It would be erroneous, however, to assume that a single
trauma is comparable to long-term abuse suffered within the context of intrafamily abuse.
Relatedly, treatment studies of PTSD in children need to address the role of family and
environment in a way that may not be as applicable with adults. There is evidence that
the effects of childhood abuse can be strongly influenced by the family environment in
which it occurred (Nash, Hulsey, Sexton, Harralson, & Lambert, 1993). For example,
family cohesion (Conte & Schuerman, 1987), maternal distress (Deblinger, McLeer, &
Henry, 1990), and help-seeking behavior (Waterman, 1993) are strong predictors of recov-
ery following abuse. Treatment studies need to account for the role of familial influence
on recovery. Moreover, initial evidence indicates that treatments that include parental
involvement may result in different therapy outcomes than those that only treat the abused
child (Deblinger, 1994). Treatment of PTSD in traumatized children may also need to
take into account the long-term effects of the trauma that may only be observed at
subsequent developmental stages (Briere, 1992). This possibility points to the need for
long-term follow-up of treated children. One study has reported that deterioration follow-
ing abuse was most likely in children with fewest initial symptoms (Gomez-Schwartz,
Horowitz, Cardarelli, & Sauzier, 1990). Accordingly, treatment studies also need to identify
the timing of intervention because onset of symptoms may occur either in the acute stage
or at later stages. In a recent review of treatment studies of abused children, Finkelhor
and Berliner (1995) concluded that “because enough appropriate studies have not been
done, the effectiveness of sexual abuse treatment has not yet been proven” (p. 1415).
The utility of cognitive behavior therapies are also not adequately tested in the context
of childhood PTSD. Future research needs to systematically evaluate CBT in children
following acute and longer term traumas, and apply strict experimental rigor to permit
firm inferences about the components of CBT that may be effective, the suitability of
CBT at different developmental states, and the long-term outcomes of CBT.
 Posttraumatic Stress Disorder 93

Traumatically Brain Injured Individuals

There is now increasing evidence that individuals who sustain a traumatic brain injury
(TBI) in the course of their trauma develop a pattern of PTSD that is not identical to
those who do not sustain a brain injury (Bryant, 1996; Bryant & Harvey, 1995b). Although
it has often been argued that the impaired consciousness associated with TBI precludes
traumatic memories being encoded and contributing to a PTSD reaction (Sbordone &
Liter, 1995), controlled studies indicate that mild TBI can result in similar levels of PTSD
as those without brain injury (Bryant & Harvey, 1998). There is evidence, however, that
TBI patients may present with a different profile of PTSD than non-TBI patients. For
example, TBI patients may not suffer the same level of intrusive recollections as other
trauma victims (Bryant & Harvey, 1995b). Further, the cognitive deficits that often accom-
pany TBI (Jennett & Teasdale, 1981), and the problems associated with postconcussive
symptomatology (Bohnen & Jolles, 1992) suggests that treatment needs may be different
for this group. Outcome studies that evaluate CBT programs for PTSD following different
levels of brain injury are required before we can conclude that exposure based therapies
are applicable to this population.

SUMMARY
This review has indicated that there are a number of important directions for future
research of treating PTSD following violence. Most importantly, there is a need to delineate
the reasons why exposure-based therapies result in only half of treatment participants
enjoying good end-state functioning. Considering the heterogeneity of PTSD presentations
following violent traumas (Foa et al., 1995), it is not surprising that a single intervention
is not equally effective for all people. The finding that imaginal exposure may have less
positive effects upon persistent avoidance behavior (Frueh et al., 1995; S. Solomon et al.,
1992) suggests that this component should be more closely investigated. Further, evidence
that particular coping strategies employed in the posttrauma period may influence PTSD
development (Harvey et al., 1998; Valentiner, Foa, Riggs, & Gershuny, 1996) indicates
that future studies need to take into account individual differences among PTSD samples.
The role of cognitive therapy needs to be clarified, and its contribution to successful
response to exposure evaluated. Finally, there is also a need for future treatment studies
to employ larger sample sizes to allow analysis of factors that predict positive and negative
responses to treatment. Refining exposure techniques on the basis of rigorous research
will provide an empirically driven framework for defining optimal components of CBT
for appropriate PTSD sufferers.

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