Journal of Consulting and Clinical Psychology Copyright 2002 by the American Psychological Association, Inc.

2002, Vol. 70, No. 4, 1022–1028 0022-006X/02/$5.00 DOI: 10.1037//0022-006X.70.4.1022

Does Imaginal Exposure Exacerbate PTSD Symptoms?

Edna B. Foa, Lori A. Zoellner, Norah C. Feeny, Elizabeth A. Hembree, and Jennifer Alvarez-Conrad
University of Pennsylvania

Symptom exacerbation (i.e., treatment side effects) has often been neglected in the psychotherapy
literature. Although prolonged exposure has gained empirical support for the treatment of chronic
posttraumatic stress disorder (PTSD), some have expressed concern that imaginal exposure, a component
of this therapy, may cause symptom exacerbation, leading to inferior outcome or dropout. In the present
study, symptom exacerbation was examined in 76 women with chronic PTSD. To define a “reliable”
exacerbation, we used a method incorporating the standard deviation and test–retest reliability of each
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outcome measure. Only a minority of participants exhibited reliable symptom exacerbation. Individuals
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who reported symptom exacerbation benefited comparably from treatment. Further, symptom exacerba-
tion was unrelated to dropout. Thus, although a minority of individuals experienced a temporary
symptom exacerbation, this exacerbation was unrelated to outcome.

Over the past two decades, imaginal exposure has gained in-
creasing attention as a treatment for chronic posttraumatic stress
disorder (PTSD). Imaginal exposure, or reliving, involves repeated
recounting of the traumatic experience, an intervention that has
been shown to promote habituation of pathological anxiety (e.g.,
Foa & Chambless, 1978; Levin, Cook, & Lang, 1982). Imaginal
exposure was first used to treat PTSD in combat veterans (e.g.,
Cooper & Clum, 1989; Keane, Fairbank, Caddell, & Zimering,
1989). Veterans with PTSD treated with imaginal exposure, then
termed imaginal flooding, improved relative to wait-list control
and standard treatment, respectively, although the magnitude of
their improvement was moderate. Several other studies in veterans
have reported similar results (e.g., Boudewyns & Hyer, 1990;
Boudewyns, Hyer, Woods, Harrison, & McCranie, 1990).
Despite this success, trauma experts have been reluctant to use
imaginal exposure with victims of traumatic events other than
combat, in particular sexual assault victims, for fear of “retrauma-
tizing” them and increasing their suffering. Specifically, Kilpatrick
and Best (1984) suggested that high levels of anxiety induced
through imaginal exposure may be construed as negative experi-
Edna B. Foa, Lori A. Zoellner, Norah C. Feeny, Elizabeth A. Hembree,
and Jennifer Alvarez-Conrad, Center for the Treatment and Study of
Anxiety, Department of Psychiatry, University of Pennsylvania.
Lori A. Zoellner is now at the Department of Psychology, University of
Washington. Norah C. Feeny is now at the Department of Psychiatry, Case
Western Reserve University.
Preparation of this article was supported by Grant MH42173 to Edna B.
Foa from the National Institute of Mental Health. We thank Lisa Jaycox,
Elizabeth Meadows, Constance Dancu, Lee Fitzgibbons, Jane Folk, and
Elna Yadin, who recruited, entered, or treated some of the clients in this
study. We also express our appreciation to Grant Devilly for his thoughtful
comments on an earlier version of this article, particularly in relation to
defining reliable exacerbation.
Correspondence concerning this article should be addressed to Edna B.
Foa, Center for the Treatment and Study of Anxiety, University of Penn-
sylvania, 3535 Market Street, Philadelphia, Pennsylvania 19104. Email:
foa@mail.med.upenn.edu
ences by victims, who may, as a result, develop an aversion to
coming to therapy. They further posited that after treatment, sexual
assault victims may exhibit higher levels of distress than they did
before treatment and may be less likely to enter treatment in the
future.
Kilpatrick and Best’s (1984) assertions were not supported by
studies that evaluated the efficacy of prolonged exposure therapy,
in which imaginal exposure occupies a central role, with assault-
related PTSD. Indeed, among female victims of sexual and non-
sexual assault with chronic PTSD, prolonged exposure has con-
sistently yielded significant reductions of PTSD, depression, and
anxiety symptoms compared with control conditions (Foa, Roth-
baum, Riggs, & Murdock, 1991; Foa et al., 1999). Furthermore,
comparable results have been found using prolonged exposure
with victims of various traumas (e.g., Devilly & Spence, 1999;
Marks, Lovell, Noshirvani, Livanou, & Thrasher, 1998).
Despite the accumulating evidence for the efficacy of prolonged
exposure therapy, concerns about the possible exacerbation of
PTSD and anxiety symptoms during or following this treatment
have persisted. Recently, Tarrier et al. (1999) found both cognitive
therapy and imaginal exposure equally effective interventions for
chronic PTSD. In their discussion, however, they asserted that “a
significantly greater number of patients receiving IE worsened
over treatment. However, this effect disappeared by follow-up”
(Tarrier et al., 1999, p. 17). For further discussion of Tarrier et al.’s
claim regarding worsening of symptoms following exposure, see
Devilly and Foa (2001).
Imaginal exposure has been hypothesized to increase not only
PTSD and anxiety but also other pathological signs. In a descrip-
tion of six cases, Pitman et al. (1991) proposed that imaginal
exposure can exacerbate feelings of guilt, self-blame, and failure.
They further suggested that although imaginal exposure may
heighten awareness of these emotions and cognitions, it may not be
effective in resolving these posttrauma negative appraisals. In
another article, Pitman, Orr, Altman, et al. (1996) asserted that in
comparison with flooding (i.e., exposure), eye movement desen-
sitization and reprocessing (EMDR) was “less anxiety provoking
for patients (as well as therapists), better tolerated, and preductive

1022
 SYMPTOM EXACERBATION AND EXPOSURE
of fewer adverse consequences” (Pitman, Orr, Altman, & Longpre,
1996, p. 428). These conclusions were drawn despite the fact that
although examined in separate studies, EMDR and flooding pro-
duced comparable outcomes. For further discussion of these is-
sues, see Cahill and Frueh (1997).
In summary, many well-controlled studies have documented the
efficacy and efficiency of prolonged exposure therapy in reducing
PTSD and related pathology, such as depression and anxiety (see
Foa & Rothbaum, 1998, for a review). However, the question
remains to what extent, if at all, this therapy is associated with
symptom exacerbation. In the present study, we sought to examine
this question by analyzing biweekly assessments of PTSD, depres-
sion, and anxiety conducted over the course of treatment. In this
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way, symptoms were monitored prior to the onset of imaginal
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exposure and during several weeks of imaginal exposure. We
addressed three main questions: (a) Is the onset of imaginal expo-
sure associated with an exacerbation of PTSD or anxiety symp-
toms? (b) Is the onset of imaginal exposure associated with an
increase in depression symptoms? and (c) Do patients who show
an exacerbation in these symptoms fail to improve in treatment or
drop out of treatment?
In exploring these questions, a key issue becomes how to
operationally define clinically significant exacerbation. Notably,
the issue of how to define clinically significant improvement has
received much attention (e.g., Jacobson, Roberts, Berns, &
McGlinchey, 1999; Jacobson & Truax, 1991), whereas less con-
sideration has been given to the issue of how to determine symp-
tom worsening or exacerbation. To carefully assess possible symp-
tom exacerbation, we used multiple measures (i.e., PTSD severity,
depression, anxiety) and conservative criteria for exacerbation.
Clinically, symptoms fluctuate from one assessment to another,
and this fluctuation reflects both “true” and error variance. How-
ever, clinically significant symptom exacerbation implies deterio-
ration beyond error variability. To measure reliable, clinically
meaningful deterioration, we took into account both the standard
deviation and the test–retest reliability of each of our measures,
using a method based on the standard error of measurement (see
Devilly & Foa, 2001). To determine a cutoff score defining reli-
able exacerbation, we considered two types of samples: psychiatric
and nonclinical samples. The former samples typically yield larger
standard deviations than the latter and thus would produce higher
cutoff scores, which in turn would lead to the classification of a
smaller number of participants as “significantly deteriorated.” In
the present study, we opted to use the more conservative alterna-
tive (i.e., a higher number of people classified as deteriorated) by
using values derived from normal samples.
Method
Participants
Participants were female victims of sexual and nonsexual assault with a
primary diagnosis of chronic PTSD, with minimum symptom duration of 3
months. This cutoff point for chronic PTSD was derived from the Diag-
nostic and Statistical Manual of Mental Disorders (4th ed., DSM–IV;
American Psychiatric Association, 1994) criteria. Participants were re-
cruited for a larger PTSD treatment outcome study through referrals from
medical professionals, local victim assistance agencies, and media adver-
tisements. Eligibility for the study was determined in the initial evaluation
1023
conducted by experienced clinicians, which included the PTSD Symptom
Scale—Interview Version (PSS–I; Foa, Riggs, Dancu, & Rothbaum, 1993)
and the Structured Clinical Interview for DSM–IV Axis I Disorders—
Patient Edition (SCID–I/P, Version 2; First, Spitzer, Gibbon, & Williams,
1995). Women who were assaulted by an intimate partner with whom they
had an ongoing relationship and those with primary diagnoses of organic
mental disorder, schizophrenia, bipolar disorder, or current alcohol or drug
dependence were excluded from the study. All participants were inter-
viewed at the Center for the Treatment and Study of Anxiety or at Women
Organized Against Rape (WOAR) in urban Philadelphia, Pennsylvania. Of
all women who were seen for an intake evaluation, about 16% were not
eligible for the study, most often because either PTSD was not the primary
diagnosis or they did not meet PTSD diagnostic criteria. An additional 11%
were eligible but declined participation or did not follow through with
entering the program. The remaining women entered the study. The present
investigation included all available participants (N ⫽ 76) from the larger,
ongoing outcome study, who were randomized to an active treatment
condition (i.e., were not randomized to wait list) and whose data had been
entered and verified for accuracy.
Participants ranged in age from 17 to 57 years (M ⫽ 32.78, SD ⫽ 10.46).
A total of 35.5% were African American, 2.6% Asian, 56.6% Caucasian,
and 5.3% Hispanic. Of the women, 69.7% were victims of a sexual
assault, 19.7% of nonsexual assault, and 10.5% of childhood sexual assault.
The average time since assault was almost 7 years (6.86 years), with a
range of 3 months to 39 years. Sixty-three percent of the women were
single, 23.2% married or cohabiting, and 13.7% separated or divorced. A
total of 26.1% had a high school education or less, 46.6% had some
technical school or college education, and 27.3% had a college education.
Of the participants, 32.4% reported a total income of over $30,000 per
year, 46.5% between $10,000 and $30,000, and 21.1% below $10,000 per
year.
Measures
PSS–I. The PSS–I is a 17-item interview assessing the severity of each
of the DSM–IV PTSD symptoms during the past 2 weeks and ascertaining
PTSD diagnostic status. Each symptom is rated on a 4-point scale ranging
from 0 (not at all) to 3 (very much). Subscale scores are calculated by
summing items in each of the PTSD symptom clusters: reexperiencing,
avoidance, and arousal. Foa et al. (1993) found high internal consistency
(␣ ⫽ .85), moderate to high correlations with other measures of psycho-
pathology, high test–retest reliability (r ⫽ .80), and high interrater reli-
ability (k ⫽ .91). For the present study, internal consistency based on
Cronbach’s alpha was .80. A randomly selected 10% sample of the inter-
views conducted with the participants in this investigation were indepen-
dently rated by another evaluator. The interrater reliability was high (k ⫽
.94). The data for treatment outcome were derived from the PSS–I.
Standardized Assault Interview (SAI; Rothbaum, Foa, Riggs, Murdock,
& Walsh, 1992). The SAI is a 136-item semistructured interview, which
gathers information regarding demographic variables, previous victimiza-
tion history, assault characteristics, and interactions with the legal system.
In regard to previous victimization history, the SAI assesses the presence
of other Criterion A traumas, in either adulthood or childhood, on the basis
of the DSM–IV (American Psychiatric Association, 1994). In regard to the
index assault-related characteristics, the SAI specifically assesses the time
since assault, perception of life threat during the assault, and injury during
the assault. An earlier version of this interview measure reported an
interrater reliability of .90. Demographic information, time since assault,
and assault type were derived from this interview.
PTSD Symptom Scale—Self-Report (PSS–SR; Foa et al., 1993). The
PSS–SR consists of 17 questions that correspond to PTSD symptoms from
the Diagnostic and Statistical Manual of Mental Disorders (3rd ed., rev.,
DSM–III–R; American Psychiatric Association, 1987), each rated on a
scale ranging from 0 to 3 for frequency and severity. The PSS–SR has been
 1024 FOA, ZOELLNER, FEENY, HEMBREE, AND ALVAREZ-CONRAD
found to be internally consistent (␣ ⫽ .91) and stable over a period of one
month (r ⫽ .74). Subscales assessing reexperiencing, avoidance, and
arousal are also internally consistent and stable. Higher scores on this
measure indicate more severe symptoms. The data regarding symptom
change following introduction of imaginal exposure were derived from the
PSS–SR.
Beck Anxiety Inventory (BAI; Beck, Epstein, Brown, & Steer, 1988).
The BAI is a 21-item inventory measure for trait anxiety. It has good
internal consistency, acceptable reliability, and acceptable convergent and
discriminant validity (Fydrich, Dowdall, & Chambless, 1992; Hewitt &
Norton, 1993).
Beck Depression Inventory (BDI; Beck, Ward, Mendelson, Mock, &
Erbaugh, 1961). The BDI is a 21-item inventory used to assess depres-
sion, with items rated on a 0 to 3 scale. This instrument has moderate to
good internal consistency, with alpha ranging between .58 to .93.
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Procedure
Independent evaluations were conducted by interviewers blind to treat-
ment assignment. Evaluations were conducted before and after treatment,
which consisted of either 9 or 12 therapy sessions. Number of sessions was
determined on the basis of a participant’s response to treatment by Session
8: For those who obtained 70% or greater reduction in self-reported PTSD
symptoms, treatment terminated at Session 9; for the remainder, therapy
was extended to 12 sessions.
Independent evaluations. As part of a treatment study for chronic
PTSD, trained female evaluators that had either a master’s or a PhD degree
in psychology and had extensive training in instrument administration
interviewed participants. The pretreatment interview included the PSS–I.
After their eligibility was ascertained, participants were given a series of
self-report measures. These included the BDI, the PSS–SR, and the BAI.
Participants returned the self-report measures at their first treatment ses-
sion, within 2 weeks of the initial evaluation. Participants were reimbursed
$50 for the initial interview and completion of the self-report question-
naires. During the first treatment session, the therapist administered the
assault interview (SAI). Posttreatment evaluations were conducted within 2
weeks of treatment completion and included the PSS–I, PSS–SR, BDI,
and BAI. Participants were reimbursed a total of $100 for completion
of treatment, posttreatment evaluation, and posttreatment self-report
questionnaires.
Biweekly assessments. In addition to the pre- and posttreatment eval-
uations, participants completed self-report measures prior to treatment
sessions for every 2 weeks during the active treatment phase. All self-
report questionnaires (i.e., PSS–SR, BDI, and BAI) were completed im-
mediately before Sessions 2, 4, 6, and 8 (and 10, if treatment consisted
of 12 sessions). These self-report measures were rated for the previous
2-week period and provided the indexes of change in PTSD, anxiety, and
depression symptoms that were used to determine presence or absence of
exacerbation.
Treatment. Participants were randomly assigned to weekly sessions of
treatment by prolonged imaginal and in vivo exposure alone (PE; n ⫽ 41,
53.9%) or by prolonged imaginal and in vivo exposure combined with
cognitive restructuring (PE/CR; n ⫽ 35, 46.1%), or were assigned to a
9-week wait list followed by treatment (not included in the present inves-
tigation). Individual treatment was conducted by female master’s- and
PhD-level therapists who received ongoing supervision and followed man-
uals that specified precise treatment guidelines for each session. Treatment
sessions were 90 –120 min in length. Data from both treatment completers
(n ⫽ 64, 84.2%) and treatment dropouts (n ⫽ 12, 15.8%) were included in
the analyses.
For the PE condition, Sessions 1 and 2 were devoted to information
gathering, presentation of treatment rationale, construction of in vivo
exposure hierarchy, and initiation of in vivo homework. Imaginal exposure
to the traumatic memory was begun in Session 3 and consisted of reliving
the traumatic event in imagination and describing the memory in the
present tense. The assault memory was repeated if necessary to allow total
reliving of 45– 60 min in duration. Imaginal exposure was repeated in all
subsequent treatment sessions for 30 – 45 min. The exposure was tape-
recorded, and participants were instructed to listen to the tape daily at
home. Additional homework included in vivo exposure to objectively safe
situations that caused anxiety or were avoided. The procedure in the PE/CR
treatment was identical, except that cognitive restructuring was introduced
in Session 3, and imaginal exposure in Session 4. All subsequent sessions
included 30 – 45 min of imaginal exposure and 15–25 min of cognitive
restructuring. For a detailed description of treatments, see Foa and Roth-
baum (1998). Because imaginal exposure in the PE/CR condition was not
initiated until the fourth treatment session, any symptom exacerbation in
the PE/CR condition between Week 2 and Week 4 would not be related to
the onset of imaginal exposure. Thus, PE/CR treatment provided a control
condition to PE treatment, where imaginal exposure was introduced at
Week 3, and consequently, the Week 4 assessment would reflect the effects
of this treatment component.
Results
The Impact of Initial Imaginal Exposure on Symptom
Exacerbation: A Comparison of PE and PE/CR
For our initial analysis, we operationally defined a symptom
exacerbation (i.e., reliable deterioration) from Week 2 to Week 4,
using data obtained from a normal sample on 2-week test–retest
reliability and standard error of measurement for each of the three
measures (Devilly & Foa, 2001). The 2-week test–retest reliability
of the PSS–SR is .83 and the standard deviation is 10.54 in a
non-PTSD sample (Foa, Cashman, Jaycox, & Perry, 1997). There-
fore, the standard error of measurement at any time point for the
scale would be SE ⫽10.54公(1 ⫺ .83), yielding 4.35. The standard
error of the difference between two administrations of a scale
would be calculated using 公2(SE2). Thus, for the PSS–SR, the
standard error of the differences between two administrations
would be calculated as 公2(4.322). Thus, reliable exacerbation for
the PSS–SR would be defined as an increase of greater than 6.15.
For the BAI, the standard deviation for a normal sample is 9.6 and
test–retest is .62 (Creamer, Foran, & Bell, 1995). Thus, reliable
exacerbation would be defined as an increase of greater than 8.37.
For the BDI, the standard deviation for a normal sample is 6.82
and test–retest reliability is .78 (Oliver & Simmons, 1985). Thus,
reliable exacerbation would be defined as an increase of greater
than 4.53 for depression (BDI). For our main chi-square analyses,
power to detect medium effects with an alpha of .05 ranged from
.64 to .71 depending on sample size, and power to detect large
effects with an alpha of .05 ranged from .97 to .99, depending on
sample size (Cohen, 1988).
As described earlier, for the PE condition, the first imaginal
exposure occurred at Week 3, and therefore symptom exacerbation
at Week 4 could be attributable to the initiation of imaginal
exposure; for the PE/CR condition, the first imaginal exposure
occurred at Week 4, and therefore symptom exacerbation at
Week 4 would be attributable to other sources. To examine
whether undergoing the first imaginal exposure was associated
with an increase in symptoms from Week 2 to Week 4, we
conducted chi-square analyses, comparing the PE and PE/CR
conditions. The majority of individuals in the PE condition
 SYMPTOM EXACERBATION AND EXPOSURE
(84.6%, n ⫽ 33) and in the PE/CR condition (97.1%, n ⫽ 33) did
not exhibit an exacerbation of PTSD symptoms (PSS–SR) upon
initiation of imaginal exposure. However, for those who did ex-
hibit an exacerbation in PTSD symptoms at Week 4, 85.7% (n ⫽
6) were in the PE condition and 14.3% (n ⫽ 1) were in the PE/CR
condition, ␹2(N ⫽ 73) ⫽ 3.24, p ⫽ .07, C ⫽ .21.1 Thus, if an
exacerbation did occur, it tended to be associated with initiation of
imaginal exposure, though this difference did not reach
significance.
For general anxiety (BAI), the majority of individuals in the PE
condition (71.8%, n ⫽ 28) and in the PE/CR condition (91.2%,
n ⫽ 31) did not exhibit an exacerbation upon the initiation of
imaginal exposure. However, of the individuals who reported an
exacerbation in anxiety symptoms, 78.6% (n ⫽ 11) were in the PE
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condition and 21.4% (n ⫽ 3) were in the PE/CR condition, ␹2(N ⫽
73) ⫽ 4.40, p ⬍ .05, C ⫽ .24. Thus, there was a relationship
between initiation of imaginal exposure and exacerbation in anx-
iety symptoms.
Finally, for depression (BDI), a similar pattern emerged. The
majority of individuals in the PE condition (87.2%, n ⫽ 34) and in
the PE/CR condition (97.1%, n ⫽ 33) did not exhibit an exacer-
bation of depressive symptoms upon initiation of imaginal expo-
sure. However, for those who did exhibit exacerbation in depres-
sive symptoms at Week 4, 83.3% (n ⫽ 5) were in the PE condition
and 16.7% (n ⫽ 1) were in the PE/CR condition, ␹2(N ⫽
73) ⫽ 2.35, p ⫽ .13. Thus, if an exacerbation did occur, it tended
to be associated with initiation of imaginal exposure, though this
difference did not reach significance.
The Relationship Between Symptom Exacerbation and
Improvement: Posttreatment Comparison
To examine the impact of initial imaginal exposure on symptom
exacerbation across both the PE/CR and the PE conditions, we
calculated symptom change from Week 2 to Week 6 for all
participants. Extending the analyses to Week 6 was necessary in
order to include the PE/CR condition, as imaginal exposure was
instituted at Week 4, after the assessment had been conducted.
Thus, assessment of exacerbation was examined over three ses-
sions of imaginal exposure for the PE group and over two sessions
of imaginal exposure for the PE/CR group. Overall, 10.5% (n ⫽ 8)
reported an exacerbation in PTSD symptoms. For individuals who
reported an exacerbation in PTSD symptoms (PSS–SR), the in-
crease ranged from 7 to 17 points (M ⫽ 9.50, SD ⫽ 4.07). A total
of 21.1% (n ⫽ 16) reported an exacerbation in anxiety symptoms
(BAI), ranging from 9 to 34 (M ⫽ 17.46, SD ⫽ 8.41). Fi-
nally, 9.2% (n ⫽ 7) reported an exacerbation in depression symp-
toms (BDI), ranging from 5 to 16 (M ⫽ 8.58, SD ⫽ 3.98). Thus,
only a minority of women reported an exacerbation in symptoms;
an increase in general anxiety was the most common form of
exacerbation.
Overall, 20 participants out of 76 reported a reliable exacerba-
tion of PTSD, anxiety, or depression symptoms. Because of the
overlap in participants reporting an exacerbation, we conducted
subsequent analyses combining exacerbation groups, in which
reliable exacerbation was defined as a reliable exacerbation on any
of the three measures.
1025
We next examined the hypothesis that individuals who experi-
enced an exacerbation would fail to improve in treatment. To do
this, we compared posttreatment scores for individuals who expe-
rienced an exacerbation with those who did not experience an
exacerbation. Means and standard deviations can be seen in Ta-
ble 1. Posttreatment scores did not differ between individuals who
experienced an exacerbation and those who did not, on either
PTSD severity or general anxiety: for PSS–SR, t(57) ⫽ 1.41, p ⫽
.17; for BAI, t(59) ⫽ 1.42, p ⫽ .16. There was a trend toward
posttreatment scores differing on depression (BDI), t(59) ⫽ 1.83,
p ⫽ .07, partial ␩2 ⫽ .05, with the exacerbation group reporting
slightly higher depression scores. Finally, the presence of PTSD
diagnosis, measured through clinician interview with the PSS–I, at
posttreatment was compared between individuals who experienced
an exacerbation and those who did not. Overall, 68.3% of all
participants no longer met PTSD diagnostic criteria. There was no
reliable difference between groups in rate of PTSD diagnosis at
posttreatment, ␹2(N ⫽ 60) ⫽ 0.34, p ⫽ 0.55.
Exacerbation of Symptoms and Posttreatment End-State
Functioning
To further examine the relationship between symptom exacer-
bation and response to treatment, we generated a composite index
for clinically significant improvement (i.e., good end-state func-
tioning) and compared symptom exacerbation in those with good
and poor end-state functioning (for rationale, see Foa et al., 1999).
Participants were categorized as attaining good end-state function-
ing if their severity score was 15 or below on the PSS–I and 10 or
below on both the BDI and the BAI.
Overall, 57.4% of all participants obtained good end-state func-
tioning. A total of 52.9% (n ⫽ 9) of those with symptom exacer-
bation and 59.1% (n ⫽ 26) of those without exacerbation obtained
good end-state functioning, ␹2(N ⫽ 61) ⫽ 0.19, p ⫽ .66. Thus,
individuals who experienced an exacerbation of symptoms did not
benefit from treatment less than those without such an
exacerbation.
Symptom Exacerbation and Treatment Dropout
Twelve participants (15.8%) dropped out of treatment before
Session 9, with 1 participant dropping out after Week 2, 6 partic-
ipants dropping out between Weeks 4 and 6, and 5 participants
dropping out between Weeks 6 and 8. To examine whether par-
ticipants who showed symptom exacerbation were more likely to
drop out of treatment, we conducted a chi-square analysis. For
individuals who showed an exacerbation in symptoms, 15% (n ⫽
3) dropped out of treatment compared with 16.7% (n ⫽ 9) among
individuals who did not show such exacerbation, ␹2(N ⫽
74) ⫽ 0.03, p ⫽ .86. Thus, individuals who dropped out of
treatment were not more likely to show symptom exacerbation.
1
Pearson’s coefficient of contingency, C, was used as a measure of
effect size for chi-square analyses (Cohen, 1988).
 1026 FOA, ZOELLNER, FEENY, HEMBREE, AND ALVAREZ-CONRAD

Table 1 apy often leads to exacerbation of trauma-related symptoms, a high

Means and Standard Deviations Across Treatment Sessions rate of dropout, and reduced benefits from treatment. Our results
for Individuals Reporting No Exacerbation or suggest that a minority of participants receiving treatment for
Exacerbation of Symptoms chronic PTSD do show reliable, albeit on average small, increases
in symptoms after the introduction of imaginal exposure: 10.5%
PSS–SR BAI BDI reported an increase in PTSD symptoms, 21.1% in anxiety,
Time M SD M SD M SD
and 9.2% in depression. One week after the first imaginal exposure
in the PE condition (at the Week 4 assessment), more individuals
Pretreatment in that condition reported exacerbation in anxiety symptoms than
No increase 33.21 8.85 24.18 11.35 24.55 8.27 in the PE/CR condition, where the first imaginal exposure occurred
Increase 29.90 7.00 22.52 11.21 23.64 9.70
after the Week 4 assessment. This comparison suggests that the
Week 2
No increase 28.94 10.45 21.86 11.79 22.56 9.18 introduction of imaginal exposure may be associated with a tem-
Increase 24.76 7.86 15.40 11.16 17.99 7.94 porary increase in general anxiety symptoms.
Week 4
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The suggestion that symptom exacerbation may impede re-

No increase 24.13 10.16 18.05 11.93 17.55 8.90
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sponse to treatment (e.g., Kilpatrick & Best, 1984) did not receive
Increase 28.55 8.00 26.08 14.33 18.83 6.49
Week 6 support in the present study. Individuals reporting initial symptom
No increase 19.58 12.16 14.19 13.30 13.36 8.73 exacerbation on PTSD, anxiety, or depression benefited from
Increase 22.44 8.04 21.78 15.55 15.22 7.26 treatment as much as those who did not report such an exacerba-
Week 8 tion. It is important to note that even individuals who occupied the
No increase 16.76 11.89 13.75 13.65 12.71 10.19
upper range of symptom exacerbation benefited from treatment.
Increase 20.29 12.51 15.28 10.74 15.82 10.49
Posttreatment The contention that imaginal exposure encourages premature treat-
No increase 9.09 8.28 6.84 9.35 7.11 7.31 ment termination did not gain support from our data either, as 6 of
Increase 14.13 14.52 11.18 9.57 11.85 9.60 the noncompleters (50%) terminated therapy between Weeks 4
and 6, and 5 (42%) did so between Weeks 6 and 8, well after the
Note. PSS–SR ⫽ PTSD Symptom Scale—Self-Report; BAI ⫽ Beck
Anxiety Inventory; BDI ⫽ Beck Depression Inventory; PTSD ⫽ posttrau- introduction of imaginal exposure. Moreover, the number of treat-
matic stress disorder. ment completers (those who completed 9 or 12 sessions) who
reported symptom exacerbation did not differ from that of non-
completers. Overall, the present results do not support the concern
Post Hoc Analyses: Individuals With High Exacerbation (e.g., Kilpatrick & Best, 1984; Pitman et al., 1991) that prolonged
of Symptoms exposure therapy leads to general symptom exacerbation, which in
Although no differences in response to treatment and dropout turn encourages dropouts and hampers response to treatment for
rates were obtained between those with and those without symp- PTSD.
tom exacerbation, it is possible that only extreme symptom exac- In summary, prolonged exposure therapy has gained more em-
erbation has an impact on response to treatment. To explore this pirical support for its efficacy than any other treatment for PTSD
post hoc hypothesis, we examined the symptom reduction from (see Foa & Meadows, 1997, for a review), and some studies even
pre- to posttreatment in individuals who reported an exacerbation suggest that it is the most efficient treatment for this disorder (as
of two times greater than the established cutoff on either PTSD cited in Hembree & Foa, 2000). However, enthusiasm for this
severity (⬎ 12.3), anxiety (⬎ 16.74), or depression (⬎ 9.06). Six treatment has been tempered by concerns about its safety. The
participants met this criterion: 1 for PTSD severity and for anxi- results of the present study are reassuring about the tolerability of
ety, 4 for anxiety only, and 1 for depression only. Of those 6, 1 exposure treatment for clients with chronic PTSD. Indeed, our
(16.7%) dropped out of treatment. Four out of the 5 treatment results indicate that clinicians need not abandon the use of expo-
completers exhibited symptom reduction: Case A reported a de- sure when clients report temporary symptom worsening. As noted
crease in PTSD symptoms (PSS–SR) from 38 to 11, in anxiety above, although exposure therapy does not jeopardize patients’
symptoms (BAI) from 28 to 2, and in depressive symptoms (BDI) welfare, the introduction of imaginal exposure may cause a tem-
from 29 to 14; Case B reported a decrease in PTSD symptoms porary increase in anxiety symptoms for a small minority of
from 25 to 8, in anxiety from 11 to 4, and in depression from 16 patients. Given this finding, clinicians would be well advised to
to 5; Case C reported a decrease in PTSD symptoms from 47 to 40, inform patients about this possibility at the outset of treatment and
in anxiety symptoms from 40 to 28, and in depression from 47 to to reassure them about the transient nature of such increases.
22; Case D reported a decrease in PTSD symptoms from 26 to 11 Several caveats regarding these findings should be noted. First,
and reported increases in anxiety symptoms from 11 to 14 and in the sample in the present study was limited to female assault
depression from 14 to 23; and finally, Case E reported a decrease victims, and so the generalizability to other trauma populations is
in PTSD symptoms from 30 to 6, in anxiety symptoms from 33 unknown. Second, the therapists in this study were highly experi-
to 7, and in depression from 22 to 6. enced in treating female assault victims and in managing anxiety in
the context of imaginal exposure. Indeed, some researchers have
suggested (e.g., Dreessen & Arntz, 1998) that many therapeutic
Discussion
complications may be overcome by a skilled therapist and that,
In this article, we examined the assertion that imaginal exposure therefore, such complications do not necessarily influence treat-
to traumatic memories in the context of prolonged exposure ther- ment outcome. Thus, the generalizability of the present results to
 SYMPTOM EXACERBATION AND EXPOSURE
therapists less experienced with the treatment of chronic PTSD is
also unknown. Third, because the cell sizes were small for some of
our comparisons, there may not have been enough power to detect
small to medium-size effects on individual self-report measures.
However, in this study, we were primarily interested in examining
whether large differences (i.e., clients worsening significantly and
showing evidence of an inability to tolerate or benefit from expo-
sure) existed between those who did and those who did not show
symptom exacerbation. Across analyses, power was sufficient to
detect such large, clinically significant effects.
The method by which we operationalized reliable exacerbation
is novel and thus has not been validated in comparison with other
methods for determining clinically significant deterioration. Al-
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.
though we selected a relatively sensitive, or conservative, method
This document is copyrighted by the American Psychological Association or one of its allied publishers.
of detecting deterioration, other definitions may yield different
results. The study of treatment deterioration warrants additional
attention. Future research should include a weekly measure of
symptoms of interest, which would allow for a higher resolution of
symptom patterns over time. Although we failed to find a rela-
tionship between symptom exacerbation and benefit from treat-
ment, the examination of predictors of symptom increase may shed
light on individual variables and response to treatment.
References
American Psychiatric Association. (1987). Diagnostic and statistical man-
ual of mental disorders (3rd ed., rev.). Washington, DC: Author.
American Psychiatric Association. (1994). Diagnostic and statistical man-
ual of mental disorders (4th ed.). Washington, DC: Author.
Beck, A. T., Epstein, N., Brown, G., & Steer, R. A. (1988). An inventory
for measuring clinical anxiety: Psychometric properties. Journal of
Consulting and Clinical Psychology, 56, 893– 897.
Beck, A. T., Ward, C. H., Mendelson, M., Mock, J., & Erbaugh, J. (1961).
An inventory for measuring depression. Archives of General Psychia-
try, 4, 561–571.
Boudewyns, P. A., & Hyer, L. (1990). Physiological response to combat
memories and preliminary treatment outcome in Vietnam veterans:
PTSD patients treated with direct therapeutic exposure. Behavior Ther-
apy, 21, 63– 87.
Boudewyns, P. A., Hyer, L., Woods, M. G., Harrison, W. R., & McCranie,
E. (1990). PTSD among Vietnam veterans: An early look at treatment
outcome using direct therapeutic exposure. Journal of Traumatic
Stress, 3, 359 –368.
Cahill, S. P., & Frueh, B. C. (1997). Flooding versus eye movement
desensitization and reprocessing therapy: Relative efficacy has yet to be
investigated—Comment on Pitman et al. (1996). Comprehensive Psy-
chiatry, 38, 300 –303.
Cohen, J. (1988). Statistical power analyses for the behavioral sciences
(2nd ed.). Hillsdale, NJ: Erlbaum.
Cooper, N. A., & Clum, G. A. (1989). Imaginal flooding as a supplemen-
tary treatment for PTSD in combat veterans: A controlled study. Behav-
ior Therapy, 3, 381–391.
Creamer, M., Foran, J., & Bell, R. (1995). The Beck Anxiety Inventory in
a non-clinical sample. Behavior Research & Therapy, 33, 477– 485.
Devilly, G. J., & Foa, E. B. (2001). Comments on Tarrier et al.’s study and
the investigation of exposure and cognitive therapy. Journal of Consult-
ing and Clinical Psychology, 69, 114 –116.
Devilly, G. J., & Spence, S. H. (1999). The relative efficacy and treatment
distress of EMDR and a cognitive– behavior trauma protocol in the
amelioration of posttraumatic stress disorder. Journal of Anxiety Disor-
ders, 13, 131–157.
1027
Dreessen, L., & Arntz, A. (1998). The impact of personality disorders on
treatment outcome of anxiety disorders: Best-evidence synthesis. Behav-
iour Research & Therapy, 36, 483–504.
First, M. B., Spitzer, R. L., Gibbon, M., & Williams, J. B. (1995).
Structured clinical interview for DSM–IV Axis I disorders—patient
edition (SCID–I/P, Version 2). New York: New York State Psychiatric
Institute, Biometrics Research Department.
Foa, E. B., Cashman, L., Jaycox, L., & Perry, K. (1997). The validation of
a self-report measure of PTSD: The Posttraumatic Diagnostic Scale.
Psychological Assessment, 9, 445– 451.
Foa, E. B., & Chambless, D. L. (1978). Habituation of subjective anxiety
during flooding in imagery. Behaviour Research and Therapy, 16,
391–399.
Foa, E. B., Dancu, C. V., Hembree, E. A., Jaycox, L. H., Meadows, E. A.,
& Street, G. P. (1999). A comparison of exposure therapy, stress
inoculation training, and their combination for reducing posttraumatic
stress disorder in female assault victims. Journal of Consulting and
Clinical Psychology, 67, 194 –200.
Foa, E. B., & Meadows, E. A. (1997). Psychosocial treatments for post-
traumatic stress disorder: A critical review. In J. Spence, J. M. Darley,
& D. J. Foss (Eds.), Annual review of psychology (Vol. 48, pp. 449 –
480). Palo Alto, CA: Annual Reviews.
Foa, E. B., Riggs, D. S., Dancu, C. V., & Rothbaum, B. O. (1993).
Reliability and validity of a brief instrument for assessing post-traumatic
stress disorder. Journal of Traumatic Stress, 6, 459 – 473.
Foa, E. B., & Rothbaum, B. O. (1998). Treating the trauma of rape. New
York: Guilford Press.
Foa, E. B., Rothbaum, B. O., Riggs, D., & Murdock, T. (1991). Treatment
of post-traumatic stress disorder in rape victims: A comparison between
cognitive– behavioral procedures and counseling. Journal of Consulting
and Clinical Psychology, 59, 715–723.
Fydrich, T., Dowdall, D., & Chambless, D. L. (1992). Reliability and
validity of the Beck Anxiety Inventory. Journal of Anxiety Disorders, 6,
55– 61.
Hembree, E., & Foa, E. B. (2000). PTSD: Psychological factors and
psychosocial interventions. Journal of Clinical Psychiatry, 61(Suppl. 7),
33–39.
Hewitt, P. L., & Norton, R. (1993). The Beck Anxiety Inventory: A
psychometric analysis. Psychological Assessment, 5, 408 – 412.
Jacobson, N. S., Roberts, L. J., Berns, S. B., & McGlinchey, J. B. (1999).
Methods for defining and determining the clinical significance of treat-
ment effects: Description, application, and alternatives. Journal of Con-
sulting and Clinical Psychology, 67, 300 –307.
Jacobson, N. S., & Truax, P. (1991). Clinical significance: A statistical
approach to defining meaningful change in psychotherapy research.
Journal of Consulting and Clinical Psychology, 59, 12–19.
Keane, T. M., Fairbank, J. A., Caddell, J. M., & Zimering, R. T. (1989).
Implosive (flooding) therapy reduces symptoms of PTSD in Vietnam
combat veterans. Behavior Therapy, 20, 245–260.
Kilpatrick, D. G., & Best, C. L. (1984). Some cautionary remarks on
treating sexual assault victims with implosion. Behavior Therapy, 15,
421– 423.
Levin, D. N., Cook, E. W., & Lang, P. J. (1982). Fear imagery and fear
behavior: Psychophysiological analysis of clients receiving treatment for
anxiety disorder. Psychophysiology, 19, 571–572.
Marks, I., Lovell, K., Noshirvani, H., Livanou, M., & Thrasher, S. (1998).
Treatment of posttraumatic stress disorder by exposure and/or cognitive
restructuring: A controlled study. Archives of General Psychiatry, 55,
317–325.
Oliver, J. M., & Simmons, M. E. (1985). Affective disorders and depres-
sion as measured by the diagnostic interview schedule and the Beck
Depression Inventory in an unselected adult population. Journal of
Clinical Psychology, 41, 469 – 477.
 1028 FOA, ZOELLNER, FEENY, HEMBREE, AND ALVAREZ-CONRAD
Pitman, R. K., Altman, B., Greenwald, E., Longpre, R. E., Macklin, M. L.,
Poire, R. E., & Steketee, G. S. (1991). Psychiatric complication during
flooding therapy for posttraumatic stress disorder. Journal of Clinical
Psychiatry, 52, 17–20.
Pitman, R. K., Orr, S. P., Altman, B., & Longpre, R. E. (1996). Emotional
processing during eye movement desensitization and reprocessing ther-
apy of Vietnam veterans with chronic posttraumatic stress. Comprehen-
sive Psychiatry, 37, 419 – 429.
Pitman, R. K., Orr, S. P., Altman, B., Longpre, R. E., Poire, R. E., &
Macklin, M. L. (1996). Emotional processing and outcome of imaginal
flooding therapy in Vietnam veterans with chronic posttraumatic stress
disorder. Comprehensive Psychiatry, 37, 409 – 418.
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.
This document is copyrighted by the American Psychological Association or one of its allied publishers.
Rothbaum, B. O., Foa, E. B., Riggs, D. S., Murdock, T., & Walsh, W.
(1992). A prospective examination of post-traumatic stress disorder in
rape victims. Journal of Traumatic Stress, 5, 455– 475.
Tarrier, N., Pilgrim, H., Sommerfield, C., Fragher, B., Reynolds, M.,
Graham, E., & Barrowclough, C. (1999). A randomized trial of cognitive
therapy and imaginal exposure in the treatment of chronic posttraumatic
stress disorder. Journal of Consulting and Clinical Psychology, 67,
13–18.
Received October 2, 2000
Revision received December 29, 2001
Accepted January 7, 2002 䡲