Cognitive Behaviour Therapy

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A meta-analytic review of cognitive processing

therapy for adults with posttraumatic stress
disorder

Gordon J. G. Asmundson, Audur S. Thorisdottir, Jacob W. Roden-Foreman,

Scarlett O. Baird, Sara M. Witcraft, Aliza T. Stein, Jasper A. J. Smits & Mark B
Powers

To cite this article: Gordon J. G. Asmundson, Audur S. Thorisdottir, Jacob W. Roden-Foreman,

Scarlett O. Baird, Sara M. Witcraft, Aliza T. Stein, Jasper A. J. Smits & Mark B Powers (2019) A
meta-analytic review of cognitive processing therapy for adults with posttraumatic stress disorder,
Cognitive Behaviour Therapy, 48:1, 1-14, DOI: 10.1080/16506073.2018.1522371

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COGNITIVE BEHAVIOUR THERAPY
2019, VOL. 48, NO. 1, 1–14
https://doi.org/10.1080/16506073.2018.1522371

A meta-analytic review of cognitive processing therapy for

adults with posttraumatic stress disorder
Gordon J. G. Asmundsona, Audur S. Thorisdottir a, Jacob W. Roden-Foreman b
,
Scarlett O. Baird c, Sara M. Witcraft d, Aliza T. Stein c, Jasper A. J. Smits c
and Mark B Powers b,c
a
Department of Psychology, University of Regina, Regina, Saskatchewan, Canada; bDivision of Trauma,
Critical Care, Acute Care Surgery, Baylor University Medical Center at Dallas, Dallas, TX, USA; cDepartment
of Psychology, University of Texas at Austin, Austin, TX, USA; dDepartment of Psychology, The University of
Mississippi, University, MS, USA

ABSTRACT ARTICLE HISTORY

Numerous studies have demonstrated the efficacy of cognitive pro- Received 22 July 2018
cessing therapy (CPT) for treating posttraumatic stress disorder Accepted 7 September 2018
(PTSD). Two prior meta-analyses of studies are available but used KEYWORDS
approaches that limit conclusions that can be drawn regarding the Meta-analysis; cognitive
impact of CPT on PTSD outcomes. The current meta-analysis processing therapy;
reviewed outcomes of trials that tested the efficacy of CPT for PTSD posttraumatic stress
in adults and evaluated potential moderators of outcomes. All pub- disorder; review; CPT
lished trials comparing CPT against an inactive control condition (i.e.
psychological placebo or wait-list) or other active treatment for PTSD
in adults were included, resulting in 11 studies with a total of 1130
participants. CPT outperformed inactive control conditions on PTSD
outcome measures at posttreatment (mean Hedges’ g = 1.24) and
follow-up (mean Hedges’ g = 0.90). The average CPT-treated partici-
pant fared better than 89% of those in inactive control conditions at
posttreatment and 82% at follow-up. Results also showed that CPT
outperformed inactive control conditions on non-PTSD outcome
measures at posttreatment and follow-up and that CPT outper-
formed other active treatments at posttreatment but not at follow-
up. Effect sizes of CPT on PTSD symptoms were not significantly
moderated by participant age, number of treatment sessions, total
sample size, length of follow-up, or group versus individual treat-
ment; but, older studies had larger effect sizes and percent female sex
moderated the effect of CPT on non-PTSD outcomes. These meta-
analytic findings indicate that CPT is an effective PTSD treatment with
lasting benefits across a range of outcomes.

Introduction
Posttraumatic stress disorder (PTSD) is a common and costly condition that can
develop following exposure to a traumatic event. PTSD often follows a chronic
course wherein the frequency and severity of symptoms fluctuate over time depend-
ing on a range of factors, including the degree of exposure to subsequent stressors,

CONTACT Gordon J. G. Asmundson Gordon.Asmundson@uregina.ca Department of Psychology, University of

Regina, Regina, Saskatchewan S4S 0A2, Canada
© Swedish Association for Behaviour Therapy
2 G. J. G. ASMUNDSON ET AL.

which can amplify or exacerbate symptoms (Taylor, 2017). Individuals with PTSD
are at increased risk for developing other psychiatric disorders (e.g. anxiety dis-
orders, depressive disorders, substance-use disorders; American Psychiatric
Association [APA], 2013) as well as diminished physical health (Asmundson,
Coons, Taylor, & Katz, 2002), a variety of general medical conditions (Sareen,
Cox, Clara, & Asmundson, 2005), and suicidal behavior (Sareen et al., 2007).
Approximately 10% of the general population will experience PTSD during their
lifetime (Seedat & Stein, 2001); however, lifetime prevalence rates of PTSD exceed
50% in certain at-risk groups (e.g. deployed military, first responders, inner city
inhabitants; APA, 2013). There are, fortunately, numerous evidence-based treat-
ments for PTSD, including pharmacotherapy (for review, see Stein, Isper, &
Seedat, 2006) and various forms of trauma-focused psychotherapy (for reviews, see
Bradley, Greene, Russ, Dutra, & Westen, 2005; Cusack et al., 2016; Kline, Cooper,
Rytwinski, & Feeny, 2018; Olthuis et al., 2016; Van Etten & Taylor, 1998).
One form of trauma-focused psychotherapy with evidence for its efficacy and
effectiveness is cognitive processing therapy (CPT; Resick & Schnicke, 1992).
Indeed, CPT is one of four psychological treatments for PTSD that is considered to
have strong research support by The US Department of Veterans Affairs and
Department of Defense (2017) and Division 12 of the APA (2017). Other treatments
with strong research support include cognitive behavior therapy, cognitive therapy,
and prolonged exposure. CPT is a manualized therapy—originally designed for
trauma associated with sexual assault (Resick & Schnicke, 1992) and later adapted
for other trauma types (e.g. combat trauma; Monson et al., 2006)—typically compris-
ing twelve 60–90 min sessions once or twice per week with a focus on trauma
memories and reducing distress via written exposures and cognitive restructuring
around themes of safety, trust, power/control, esteem, and intimacy. More specifically,
CPT focuses on helping patients understand and reconceptualize their trauma by
modifying maladaptive appraisals, or “stuck-points” (e.g. believing that other people
should not be trusted, assuming personal blame for the death of others), that disrupt
recovery through promotion of avoidance behaviors and secondary emotional
responses (e.g. guilt, shame).
There have been only two meta-analyses focusing specifically on CPT (Holliday,
Holder, & Suris, 2018; Lenz, Bruijn, Serman, & Bailey, 2014). These meta-analyses show
that CPT reduces trauma-related distress; but, both used approaches that limit the
conclusions that can be drawn regarding the impact of CPT on PTSD outcomes. Lenz
et al. (2014) meta-analyzed 11 studies assessing CPT, grouping together trials with adult
and youth participants and including at least one trial that did not use CPT (i.e. Hinton
et al., 2004). Holliday et al. (2018) analyzed pre- to posttreatment effects of CPT on
negative cognitions in nine studies using a single-arm meta-analysis, an approach not
requiring or analyzing data from control conditions. While a recent meta-analysis of
psychological treatments for adults with PTSD (Cusack et al., 2016) showed that CPT
had large effects for trauma-related distress, it included only four randomized con-
trolled trials (i.e. Chard, 2005; Forbes et al., 2012; Monson et al., 2006; Resick, Nishith,
Weaver, Astin, & Feuer, 2002) and did not include an assessment of moderator
variables (e.g. mean age, year of publication, length of follow-up). The purposes of
the present meta-analysis were to address the need for a comprehensive systematic
 COGNITIVE BEHAVIOUR THERAPY 3

review of the posttreatment and follow-up outcomes of trials testing the efficacy of CPT
for PTSD in adults and to evaluate possible moderator variables.
We derived several hypotheses based on the extant literature: (1) CPT will out-
perform inactive control conditions (i.e. psychological placebo or wait-list) on PTSD
outcome measures at posttreatment; (2) CPT will outperform inactive control con-
ditions on non-PTSD outcome measures (i.e. measures of depression and anxiety) at
posttreatment; (3) CPT will outperform inactive control conditions on PTSD out-
come measures at follow-up; and (4) CPT will outperform inactive control condi-
tions on non-PTSD outcome measures at follow-up. Additionally, although we did
not expect CPT to outperform other active treatments (e.g. prolonged exposure,
written exposure therapy) on PTSD outcomes, these were compared on an explora-
tory basis. Possible moderator variables included in our analyses were mean age,
percent female sex, number of treatment sessions, year of publication, total sample
size, length of follow-up, and group versus individual treatment delivery.

Materials and methods

Inclusion and exclusion criteria
Inclusion criteria were as follows: (a) participants met full Diagnostic and Statistical
Manual (DSM) IV, DSM-IV-TR, or DSM-5 criteria for PTSD or surpassed evidence-
based clinical cutoff scores on a psychometrically sound clinician-rated or self-report
measure of PTSD symptoms; (b) participants were adults (18–65 years); (c) trial used
random assignment; (d) trial compared CPT to an adequate control condition (e.g.
wait-list control, psychological placebo) or other active treatment for PTSD; (e)
treatments focused on PTSD rather than comorbid conditions (e.g. substance use);
and (f) PTSD severity was assessed using psychometrically sound clinician-rated or
self-report measures. Treatments were classified as CPT if they were based on the
format described by Resick and Schnicke (1992) and included both cognitive therapy
(e.g. identify and challenge maladaptive trauma-related beliefs) and written trauma
accounts. Exclusion criteria were as follows: (a) single case studies; (b) studies focused
on acute stress disorder; (c) studies with insufficient data, unless authors were able to
provide the data; and (d) studies focused on prevention. Also, in order to avoid issues
of conflation and ensure statistical independence of the samples, studies that pre-
sented secondary analyses of data from original trials meeting the inclusion criteria
noted above were excluded (e.g. Resick, Nishith, & Griffin, 2003; Resick, Williams,
Suvak, Monson, & Gradus, 2012). No restrictions were made based on type of trauma
or duration of PTSD symptoms.

Search methods
A comprehensive search for trials meeting the above inclusion criteria was conducted in
PsycINFO, PubMed, Embase, Scopus, clinicaltrials.gov, and the Cochrane Central
Register of Controlled Trials up to July 2018. The searches included the following
terms: “cognitive processing therapy” or “CPT;” “posttraumatic,” “post-traumatic,”
“posttraumatic stress disorder,” “post-traumatic stress disorder,” or “PTSD;” “clinical
4 G. J. G. ASMUNDSON ET AL.

trial”, “random,” “randomly,” “randomize,” “randomise,” “randomized,” or “rando-

mised;” and “placebo” or “control group.” These terms were searched as key words,
title, abstract, and medical subject headings. We also examined citation maps and used
“cited by” search tools (Moher, Liberati, Tetzlaff, & Altman, 2009). Three independent
investigators conducted the literature searches and extracted the data from the identi-
fied studies. Inconsistencies were discussed and resolved by consensus, and data entry
was cross-checked for accuracy.

Data collection
We collected data on treatment conditions, number of treatment sessions, sample
characteristics, year of publication, and length of follow-up. As shown in Table 1,
PTSD-relevant outcomes were clinician-rated or self-rated PTSD symptoms and non-
PTSD outcomes were self-report measures of depression and anxiety. Inactive control
conditions included psychological placebo or wait-list. Psychological placebo treatments
were defined as treatments that were not designed to specifically target symptoms of
PTSD, such as relaxation. Wait-list was defined as time-limited conditions where
participants did not receive any treatment. The two types of inactive controls were
collapsed based on conceptual similarity and earlier analyses showing no significant
differences between the groups for any outcome (all p ≥ 0.295). Active treatments were
defined as treatments that involved theory and/or empirically based components for
alleviating PTSD symptoms.

Study quality ratings

A modified version of the brief quality assessment guideline of Jadad et al. (1996) was
used to rate the quality of the included trials. Jadad et al. proposed three criteria for
quality assessment: (1) random assignment to condition, (2) double-blinding, and (3)
description of withdrawals and dropouts. Criterion 2 was deemed not applicable to our
assessment as trial participants cannot remain blind to their psychological treatment
condition.

Data analysis
The software Comprehensive Meta-Analysis (Borenstein & Rothstein, 1999) was used
for synthesizing and analyzing the data. For each trial, between-group effect sizes
were calculated for PTSD and non-PTSD outcome measures. In the presence of
multiple measurements of the same outcome at the same time point (e.g. posttreat-
ment PTSD assessed using two measures), the mean effect size was used. Similarly,
we used the mean effect size across all follow-ups if a trial had multiple follow-up
measurements.
Effect sizes were calculated using Hedges’ g (Rosenthal, 1991) according to the
following formula:
T  X
X C
g¼
SP
 COGNITIVE BEHAVIOUR THERAPY 5

Table 1. Trials included in the meta-analysis.

% Full PTSD
% Sample PTSD No. of Follow-up outcome Non-PTSD
Trial Conditions N Female population criteria sessions (months) measures outcome
Bass et al. CPT, PSYC 313a 100 Community 98 12 6 HTQ HSCL-25
(2013) PL
Butollo CPT, TX1 141 66 Community 100 15–24 6 IES-R, PDS –
et al.
(2016)
Chard CPT, WL 71 100 Community 100 17 12 CAPS, BDI
(2005) MPSS
Forbes CPT, PSYC 59 3 Military 100 12 3 CAPS, PCL BDI-II,
et al. PL STAI-S
(2012)
Galovski CPT, WL 100 69 Community 100 4–18 – CAPS, PDS BDI-II
et al.
(2012)
Maxwell CPT, TX2 18 81 Community 100 6–12 3 CAPS, BDI
et al. MPSS-
(2016) SR
Monson CPT, WL 60 11 Military 100 12 1 CAPS, PCL BDI, STAI
et al.
(2006)
Resick et al. CPT, TX3, 121 100 Community 100 12 9 CAPS-SI, BDI
(2002) WL PSS-SR
Resick et al. CPT, PSYC 108 7 Military 100 12 12 PCL-S, BDI-II
(2015) PL PSS-I
Sloan et al. CPT, TX4 126 48 Military 100 5–12 9 CAPS-5 –
(2018)
Surís et al. CPT, PSYC 86 85 Military 100 12 6 CAPS, PCL QIDS
(2013) PL
BDI-II: Beck Depression Inventory II; CAPS: Clinical Administered PTSD Scale; HTQ: The Harvard Trauma Questionnaire;
HSCL-25: The Hopkins Symptom Checklist; IES-R: Impact of Event Scale—Revised; MPSS: Modified PTSD Symptom
Scale; PCL: The PTSD Checklist; PCL-S: The PTSD Checklist: Stressor Specific Version; PSYCH PL: psychological placebo;
PSS: PTSD Symptom Scale; PSS-I: PTSD Symptom Scale-Interview; STAI: The Spielberger State-Trait Anxiety Inventory;
TX1: dialogical exposure therapy; TX2: memory specific training; TX3: prolonged exposure therapy; TX4: written
exposure therapy; QUIDS: The Quick Inventory of Depressive Symptomatology.
a
The number of participants at follow-up.

where X T is the mean of the treatment group, X

 C is the mean of the comparison group,
and SP is the pooled standard deviation. Weighted estimators were assigned in all
calculations of effect sizes to improve the precision of estimation for smaller sample
sizes (Hedges & Olkin, 1985). Mean effect sizes were computed using the following
formula:
P
wj gj
g ¼ P
wj

where wj is the weight for each study and gj is the effect size for each study. Mean effect
sizes were calculated with random effects models, which allow for heterogeneity of effects
(e.g. effect sizes may vary between studies based on sample characteristics and the
implementation of the intervention; Borenstein, Hedges, Higgins, & Rothstein, 2010).
Effect sizes were interpreted using Cohen’s conventional values of effects ranging from
small (0.2) to large (0.8; Cohen, 1988). The mean effect size is equivalent to a Z-score that
can be used to describe the magnitude of the difference in terms of comparison percen-
tiles; for example, a mean effect size of 1.96 means that the average participant in the
active intervention group improved more than 97.5% of those in the control condition.
6 G. J. G. ASMUNDSON ET AL.

Heterogeneity was measured using I2, Q, and tau statistics. I2 describes the percen-
tage of variation across study results that is not due to chance. In line with Higgins,
Thompson, Deeks, and Altman (2003), I2 of 25% was considered low, 50% moderate,
and 75% high heterogeneity. Q is the weighted sum of the squared differences between
the effects of a study and the pooled effect across studies in the meta-analysis. Finally,
tau is the standard deviation of the estimated true effect size. Significant heterogeneity
indicates that effect sizes were inconsistent across the meta-analyzed studies, which
supports the use of random effects models over fixed effects models and suggests that
moderator variables may influence effect sizes (Fletcher, 2007).
Restricted maximum likelihood meta-regressions were used to test the relationships
between moderator variables and effect sizes. Moderator analyses are presented with
intercepts (B0), which represent the mean effect size after controlling for the moderator,
the slope for moderator effect (B), and the R2 analogue, which is the proportion of
between-study variance explained by the moderator. Possible moderators included
mean age, percent female sex, number of treatment sessions, year of publication, total
sample size, length of follow-up, and group versus individual treatment delivery.
The problem of selective publication in the scientific literature (i.e. “the file drawer
problem”), which refers to a tendency to publish significant results but not nonsigni-
ficant ones, is a concern to any meta-analysis and may lead to inflated effect size
estimates (Rosenthal, 1991). Several methods have been proposed to address publica-
tion bias in meta-analyses, including funnel plots, which depict the relationship
between studies’ sample sizes and effect sizes. Duval and Tweedie’s trim and fill method
and Egger’s (1997) regression test were used to quantify funnel plot interpretations. The
trim and fill method identifies potentially missing studies by finding studies with effect
sizes significantly departing from the mean effect size, then imputing studies that
counteract them. Egger’s regression test uses studies’ precision (1/standard error) to
predict their standardized effects; the intercept (B0) represents the amount of bias and
is tested using a one-sided p-value. Lastly, Rosenthal’s fail-safe N (Rosenthal, 1979;
Borenstein, Hedges, Higgings, & Rothstein, 2009) indicates the number of studies with
no significant effect needed to raise the p-value for the mean effect size above 0.05. A
fail-safe N greater than the file drawer N (5k + 10, where k is the number of studies) is
considered robust.

Results
Search results and study quality
The search produced 344 potential articles, 333 of which were excluded for various
reasons (e.g. duplicates, did not meet inclusion criteria). Eleven studies with a total
of 1130 participants met criteria for inclusion and were retained for the meta-
analysis. As shown in Table 1, four of the 11 studies compared CPT to active
treatment (Butollo, Karl, König, & Rosner, 2016; Maxwell et al., 2016; Resick et al.,
2002; Sloan, Marx, Lee, & Resick, 2018), four studies utilized psychological placebo
control (Bass et al., 2013; Forbes et al., 2012; Resick et al., 2015; Surís, Link-Malcolm,
Chard, Ahn, & North, 2013), and four used wait-list comparison (Chard, 2005;
Galovski, Blain, Mott, Elwood, & Houle, 2012; Monson et al., 2006; Resick et al.,
 COGNITIVE BEHAVIOUR THERAPY 7

2002). Active treatments included dialogical exposure therapy, memory specific

training, prolonged exposure, and written exposure therapy (see column 2 in
Table 1). All but one of the trials included participants who met diagnostic criteria
for PTSD. The one exception (Bass et al., 2013) enrolled members of various
Kongoian villages based on meeting self-reported PTSD symptom severity cutoffs
indicative of a probable PTSD diagnosis; however, in that study, four women from
one village who did not meet the symptom severity criteria were included in the
analyses. While these four women had a history of sexual assault and received
treatment, there is no information on how close their scores were to the cutoff
and what the rationale was for including them in the analysis. All trials met criteria 1
(random assignment to condition) and 3 (description of withdrawals and dropouts)
of the quality assessment guidelines of Jadad et al. (1996).

Hypothesis 1: CPT will outperform inactive control conditions on PTSD outcome

measures at posttreatment.

This analysis included eight studies (Bass et al., 2013; Chard, 2005; Forbes et al., 2012;
Galovski et al., 2012; Monson et al., 2006; Resick et al., 2002, 2015; Surís et al., 2013) with
841 participants. As shown in Figure 1, CPT outperformed the inactive control condi-
tions, showing a large effect (mean Hedges’ g = 1.24 [95% CI = 0.80–1.67], z = 5.57,
p < 0.001) where the average CPT-treated participant fared better than approximately
89% of those in the inactive control conditions. The effect was significantly heterogeneous
(Q(df = 7) = 55.29, p < 0.001). Tau indicated that the standard deviation of the underlying
true effect across studies was 0.58 (95% CI = 0.41–1.49), and I2 indicated high hetero-
geneity, with 87.34% (95% CI = 77.21–97.84%) of the variance in the observed effects
reflecting variance in the true effect. Percent female sex (B0 = 0.63 [95% CI = −0.13–1.40],
p = 0.104; B = 0.01 [95% CI = 0.00–0.02], p = 0.062, R2 analogue = 0.28) was the only
moderator to approach a significant effect. Other moderators showed no significant effect
(all p > 0.148). The funnel plot for this analysis showed some indication of publication
bias, with smaller studies generally reporting larger effects. Trim and fill analysis showed
no evidence of missing studies with effects below the mean effect but indicated one
missing study with an effect larger than the overall mean. Incorporating this study
resulted in an imputed mean effect of g = 1.38 (95% CI = 0.89–1.88). Similarly, Egger’s
regression test indicated a nonsignificant potential for publication bias (B0 = 5.22 [95%
CI = −1.89–12.32], t(df = 6) = 1.80, one-sided p = 0.061). At 443, the fail-safe N for this
analysis was substantially higher than the file drawer N of 50, indicating that these meta-
analytic results are quite robust to publication bias.

Hypothesis 2: CPT will outperform inactive control conditions on non-PTSD outcome

measures at posttreatment.

This analysis also included eight studies (Bass et al., 2013; Chard, 2005; Forbes et al.,
2012; Galovski et al., 2012; Monson et al., 2006; Resick et al., 2002, 2015; Surís et al., 2013)
with 838 participants. CPT outperformed the inactive control conditions with a large effect
size (mean Hedges’ g = 1.01 [95% CI = 0.72–1.29], z = 6.93, p < 0.001). Thus, the average
CPT-treated participant fared better than approximately 84% of controls. The effect was
8 G. J. G. ASMUNDSON ET AL.

Figure 1. Forest plot of effect sizes (Hedges’ g) comparing CPT versus inactive controls at posttreat-
ment on PTSD outcome measures. Positive values favor CPT while negative values favor inactive
controls.

significantly heterogeneous (Q(df = 7) = 24.74, p < 0.001; tau = 0.34 [95% CI = 0.19–1.00];
I2 = 71.71% [95% CI = 44.50–95.59%]). Two variables were found to be significant
moderators: percent female sex (B0 = 0.53 [95% CI = 0.12–0.94], z = 2.56, p = 0.011;
B = 0.01 [95% CI = 0.00–0.01], z = 2.65, p = 0.008; R2 analogue = 0.66) and number of
sessions (B0 = −1.31 [95% CI = −3.28–0.66], z = −1.30, p = 0.194; B = 0.18 [95% CI = 0.03–
0.33], z = 2.31, p = 0.021; R2 analogue = 0.47). All other moderators showed no significant
effect (all p > 0.197). Trim and fill analysis indicated two missing studies with an effect
larger than the overall mean. Incorporating these resulted in an imputed mean effect of
g = 1.17 (95% CI = 0.86–1.49). Egger’s regression test indicated no significant publication
bias (B0 = 1.08 [95% CI = −5.46–7.62], t(df = 6) = 0.41, one-sided p = 0.350). At 349, the
fail-safe N for this analysis was substantially higher than the file drawer N of 50, indicating
that these meta-analytic results are robust.

Hypothesis 3: CPT will outperform inactive control conditions on PTSD outcome

measures at follow-up.

This analysis included six studies (Bass et al., 2013; Forbes et al., 2012; Monson et al.,
2006; Resick et al., 2002, 2015; Surís et al., 2013) with 689 participants. CPT out-
performed inactive control conditions on PTSD measures across follow-ups, showing a
moderate-to-large effect (mean Hedges’ g = 0.90 [95% CI = 0.57–1.23], z = 5.36,
p < 0.001). The average CPT-treated participant fared better than approximately 82%
of controls. The effect was significantly heterogeneous (Q(df = 5) = 17.94, p = 0.003;
tau = 0.34 [95% CI = 0.15–1.11]; I2 = 72.12% [95% CI = 33.03–96.47%]). None of the
 COGNITIVE BEHAVIOUR THERAPY 9

moderators showed a significant effect (all p > 0.109). Trim and fill analysis indicated no
missing studies. Egger’s regression test indicated no significant publication bias
(B0 = 1.07 [95% CI = −5.84–7.99], t(df = 4) = 0.43, one-sided p = 0.344). At 163, the
fail-safe N for this analysis was substantially higher than the file drawer N of 40,
indicating that these meta-analytic results are robust.

Hypothesis 4: CPT will outperform inactive control conditions on non-PTSD outcome

measures at follow-up.

This analysis also included six studies (Bass et al., 2013; Forbes et al., 2012; Monson
et al., 2006; Resick et al., 2002, 2015; Surís et al., 2013) with 689 participants. CPT
outperformed the inactive control conditions with a moderate-to-large effect (mean
Hedges’ g = 0.82 [95% CI = 0.48–1.16], z = 4.68, p < 0.001). Thus, the average CPT-
treated participant fared better than approximately 79% of controls. The effect was
significantly heterogeneous (Q(df = 5) = 19.99, p < 0.001; tau = 0.36 [95% CI = 0.18–
1.19]; I2 = 74.99% [95% CI = 42.75–96.98%]). Percent female sex was a significant
moderator (B0 = 0.41 [95% CI = −0.05–0.88], z = 1.75, p = 0.080; B = 0.01 [95%
CI = 0.00–0.01], z = 2.20, p = 0.028; R2 analogue = 0.57). None of the other variables
were significant moderators (all p ≥ 0.654). Trim and fill analysis indicated one missing
study with an effect larger than the mean, which resulted in an imputed mean effect of
g = 0.91 (95% CI = 0.58–1.25). Egger’s regression test indicated no significant publica-
tion bias (B0 = −1.83 [95% CI = −9.32–5.67], t(df = 4) = 0.68, one-sided p = 0.268). At
146, the fail-safe N for this analysis was substantially higher than the file drawer N of 40,
indicating that these meta-analytic results are robust.

CPT versus active controls

Four studies (Butollo et al., 2016; Maxwell et al., 2016; Resick et al., 2002; Sloan et al., 2018)
with 407 participants compared CPT to an active control at posttreatment on PTSD
measures. As shown by Figure 2, participants receiving CPT fared significantly better
than those receiving another active treatment at posttreatment, although the size of the
effect was small to moderate (Hedges’ g = 0.26 [95% CI = 0.04–0.48], z = 2.34, p = 0.019),
with no significant heterogeneity (Q(df = 3) = 3.64, p = 0.303; tau = 0.10 [95% CI = 0.00–
0.75]; I2 = 17.58% [95% CI = 0.00–93.02%]). Given the lack of significant heterogeneity and
the small number of studies, moderator analyses were not conducted. Trim and fill analyses
indicated one missing study with an effect larger than the mean, resulting in an imputed
effect size of g = 0.27 (95% CI = 0.08–0.46). Egger’s regression test indicated no significant
publication bias (B0 = −0.39 [95% CI = −9.71–8.94], t(df = 2) = 0.18, one-sided p = 0.437).
The fail-safe N for this analysis (3) was substantially lower than the file drawer N of 25,
indicating that these meta-analytic results are not robust.
The same four studies compared CPT to an active control at follow-up. Participants
receiving CPT did not significantly differ from those receiving another active treatment
across follow-ups (Hedges’ g = 0.17 [95% CI = −0.02–0.37], z = 1.77, p = 0.077); this
effect was not significantly heterogeneous (Q(df = 3) = 0.86, p = 0.835; tau = 0.00 [95%
CI = 0.00–0.34]; I2 = 0.00% [95% CI = 0.00–72.76%]). Trim and fill analyses indicated
one missing study with an effect larger than the mean, resulting in an imputed effect
10 G. J. G. ASMUNDSON ET AL.

Figure 2. Forest plot of effect sizes (Hedges’ g) comparing CPT versus active controls at posttreat-
ment on PTSD outcome measures. Positive values favor CPT while negative values favor inactive
controls.

size of g = 0.18 (95% CI = −0.01–0.37). Egger’s regression test indicated no significant

publication bias (B0 = −0.36 [95% CI = −4.78–4.06], t(df = 2) = 0.35, one-sided
p = 0.379). The fail-safe N was applicable as there was no significant effect.

Discussion
Despite being the most studied of the anxiety-related disorders (Asmundson &
Asmundson, 2018; McNally, 2018), and despite the availability of a variety of evi-
dence-based treatments (for reviews, see Cusack et al., 2016; Kline et al., 2018;
Olthuis et al., 2016), PTSD remains a challenge to treat successfully. CPT is one of
four psychological treatments for PTSD considered to have strong research support
(APA, 2017; The US Department of Veterans Affairs and Department of Defense,
2017). This study used meta-analysis to assess the outcomes of 11 trials designed to
test the efficacy of CPT for PTSD in adults and considered posttreatment effects as well
as sample- and study-specific moderators of outcome.
Overall, results supported our hypotheses. CPT outperformed inactive control con-
ditions (i.e. waitlist and psychological placebo) on measures of PTSD symptoms at
posttreatment and follow-up, with respective effect sizes of 1.24 and 0.90. CPT also
performed better on non-PTSD outcome measures at posttreatment and follow-up,
with respective effect sizes of 1.01 and 0.82. These results were robust and unlikely to be
attributable to publication bias. In comparison to other types of active treatment for
PTSD used in these trials—dialogical exposure therapy, memory-specific training,
prolonged exposure, and written exposure therapy—individuals who received CPT
 COGNITIVE BEHAVIOUR THERAPY 11

had significantly better outcomes at posttreatment. The size of the effect was, however,
small to moderate (Hedges’ g of 0.26), did not remain significant at follow-up, and the
meta-analytic results were not robust. In line with the published recommendations of
evidence-based treatment for PTSD (APA, 2017; The US Department of Veterans
Affairs and Department of Defense, 2017) and preliminary meta-analytic findings
(Cusack et al., 2016), our results indicate that CPT is an effective treatment for PTSD
that has lasting benefits across a range of outcomes.
Our finding that CPT outperformed other active treatments at posttreatment, with
small-to-moderate effect sizes, is in contrast to previously published meta-analytic
research showing that prolonged exposure did not outperform other types of active
treatments for PTSD (Powers, Halpern, Ferenschak, Gillihan, & Foa, 2010), including
CPT. It is noteworthy, however, that these findings were not robust, were based on data
from only four trials, and that only one of these trials included an active treatment from
amongst those endorsed with strong empirical support for PTSD (i.e. prolonged
exposure therapy, Resick et al., 2002). The other trials used various other active
treatments based on exposure principles or gestalt theory for which evidence is less
robust. As previously noted by Cusack et al. (2016), additional research is needed to
systematically compare the outcomes of various active PTSD treatments.
Moderation analyses consistently revealed percent female sex to influence the effect
size of CPT treatment such that studies with higher proportions of female participants
generally reported larger effect sizes. This may indicate that CPT is more effective for
females than males. Since the moderation analyses are based on aggregated data,
however, such an interpretation may not be accurate (Petkova, Tarpey, Huang, &
Deng, 2013). Further analysis of participant-level data (i.e. non-aggregated data) will
be needed to confirm and elucidate this finding.
These findings need to be considered in the context of several limitations. Most
notably, this meta-analysis is limited by the number of trials that evaluated CPT against
active treatments for PTSD; thus, conclusions regarding differential efficacy of CPT
versus other active treatments on posttreatment outcomes are tentative. As there were
no studies utilizing pharmacological treatment meeting study criteria, we are unable to
draw conclusions about the relative efficacy of CPT versus pharmacotherapy for PTSD.
Likewise, as we included only trials utilizing adult participants, conclusions may not
generalize to youths. It is also noteworthy that follow-up analyses included fewer studies
and participants than posttreatment analyses and were based on follow-up periods that
ranged from 1 to 12 months. Finally, we did not include a comprehensive assessment of
study quality; as such, we did not test for variability in study quality as a moderator.
To conclude, this meta-analysis indicates that CPT is an effective treatment for PTSD
that has lasting benefits across a range of outcomes; indeed, it outperformed inactive
control conditions for both PTSD-specific and non-PTSD (i.e. depression and anxiety)
outcomes at posttreatment and follow-up, and outperformed other active treatments,
albeit with small to moderate effect sizes, at posttreatment. While additional research is
needed to directly compare CPT against other active treatments for PTSD, both
psychological and pharmacological, the results of this meta-analysis support prior
indications (APA, 2017; The US Department of Veterans Affairs and Department of
Defense, 2017) that CPT is a primary level psychological treatment for PTSD.
12 G. J. G. ASMUNDSON ET AL.

Disclosure statement
Dr. Asmundson is the Editor-in-Chief of the Journal of Anxiety Disorders and Clinical Psychology
Review. He receives financial support through grants from the Canadian Institutes of Health
Research, payments for his editorial work on the aforementioned journals, and royalties from
various book publishers. Dr. Smits receives support from the National Institutes of Health, the
Cancer Prevention and Research Institute of Texas, and has been paid as a consultant for
Microtransponder, Inc. and Aptinyx, Inc.

ORCID
Audur S. Thorisdottir http://orcid.org/0000-0002-2209-148X
Jacob W. Roden-Foreman http://orcid.org/0000-0002-8338-397X
Scarlett O. Baird http://orcid.org/0000-0002-0820-9269
Sara M. Witcraft http://orcid.org/0000-0001-8890-0465
Aliza T. Stein http://orcid.org/0000-0002-0542-9864
Jasper A. J. Smits http://orcid.org/0000-0001-7128-9807
Mark B Powers http://orcid.org/0000-0001-7898-073X

References
American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders
(5th ed. ed.). Washington, DC: Author.
American Psychological Association. (July, 2017). Clinical practice guideline for the treatment of
posttraumatic stress disorder. Retrieved from http://www.apa.org/ptsd-guideline/treatments/
index.aspx
Asmundson, G. J. G., & Asmundson, A. J. N. (2018). Are anxiety disorders publications
continuing on a trajectory of growth? A look at Boschen’s (2008) predictions and beyond.
Journal or Anxiety Disorders, 56, 1–4. doi:10.1016/j.janxdis.2018.05.003
Asmundson, G. J. G., Coons, M. J., Taylor, S., & Katz, J. (2002). PTSD and the experience of
pain: Research and clinical implications of shared vulnerability and mutual maintenance
model. The Canadian Journal of Psychiatry, 47, 930–937. doi:10.1177/070674370204701004
Bass, J. K., Annan, J., Murray, S. M., Kaysen, D., Griffiths, S., Cetinoglu, T., & Bolton, P. A.
(2013). Controlled trial of psychotherapy for Congolese survivors of sexual violence. The New
England Journal of Medicine, 368, 2182–2191. doi:10.1056/NEJMoa1211853
Borenstein, M., Hedges, L. V., Higgins, J. P. T., & Rothstein, H. R. (2009). Introduction to meta-
analysis. United Kingdom: John Wiley & Sons Ltd.
Borenstein, M., Hedges, L. V., Higgins, J. P. T., & Rothstein, H. R. (2010). A basic introduction to
fixed-effect and random-effects models for meta-analysis. Research Synthesis Methods, 1(97–
111). doi:10.1002/jrsm.12
Borenstein, M., & Rothstein, H. (1999). Comprehensive meta-analysis: A computer program for
research synthesis. Version 1.0 23 [Computer Software]. Biostat: Englewood Cliffs.
Bradley, R., Greene, J., Russ, E., Dutra, L., & Westen, D. (2005). A multidimensional meta-
analysis of psychotherapy for PTSD. American Journal of Psychiatry, 162, 214–227.
doi:10.1176/appi.ajp.162.2.214
Butollo, W., Karl, R., König, J., & Rosner, R. (2016). A randomized controlled clinical trial of
dialogical exposure therapy versus cognitive processing therapy for adult outpatients suffering
from PTSD after type 1 trauma in adulthood. Psychotherapy and Psychosomatics, 85, 16–26.
doi:10.1159/000440726
Chard, K. M. (2005). An evaluation of cognitive processing therapy for the treatment of
posttraumatic stress disorder related to childhood sexual abuse. Journal of Consulting and
Clinical Psychology, 73, 965–971. doi:10.1037/0022-006X.73.5.965
 COGNITIVE BEHAVIOUR THERAPY 13

Cohen, J. (1988). Statistical power analysis for the behavioral sciences (2nd ed.). Hillsdale, NJ:
Lawrence Erlbaum Associates.
Cusack, K., Jonas, D. E., Forneris, C. A., Wines, C., Sonis, J., Cook Middleton, J., & Gaynes, B. N.
(2016). Psychological treatments for adults with posttraumatic stress disorder: A systematic
review and meta-analysis. Clinical Psychology Review, 43, 128–141. doi:10.1016/j.
cpr.2015.10.003
Egger, M. (1997). Bias in meta-analysis detected by a simple, graphical test. BMJ, 13, 629–634.
doi:10.1136/bmj.315.7109.629
Fletcher, J. (2007). What is heterogeneity and is it important? BMJ: British Medical Journal, 334
(7584), 94–96. doi:10.1136/bmj.39057.406644.68
Forbes, D., Lloyd, D., Nixon, R. D. V., Elliott, P., Varker, T., Perry, D., & Creamer, M. (2012). A
multisite randomized controlled effectiveness trial of cognitive processing therapy for military-
related posttraumatic stress disorder. Journal of Anxiety Disorders, 26, 442–452. doi:10.1016/j.
janxdis.2012.01.006
Galovski, T. E., Blain, L. M., Mott, J. M., Elwood, L., & Houle, T. (2012). Manualized therapy for
PTSD: Flexing the structure of cognitive processing therapy. Journal of Consulting and Clinical
Psychology, 80, 968–981. doi:10.1037/a0030600
Hedges, L. V., & Olkin, I. (1985). Statistical methods for meta-analysis. Orlando, FL: Academic.
Higgins, J. P. T., Thompson, S. G., Deeks, J. J., & Altman, D. G. (2003). Measuring inconsistency
in meta-analyses. BMJ: British Medical Journal, 327, 557–560. doi:10.1136/bmj.327.7414.557
Hinton, D. E., Pham, T., Tran, M., Safren, S. A., Otto, M. W., & Pollack, M. H. (2004). CBT for
Vietnameses refugees with treatment-resistant PTSD and panic attacks: A pilot study. Journal
of Trauatic Stress, 17, 429–433. doi:10.1023/B:JOTS.0000048956.03529.fa
Holliday, R., Holder, N., & Suris, A. (2018). A single-arm meta-analysis of cognitive processing
therapy in addressing trauma-related negative cognitions. Journal of Aggression, Maltreatment
& Trauma. doi:10.1080/10926771.2018.1429511
Jadad, A. R., Moore, R. A., Carroll, D., Jenkinson, C., Reynolds, D. J. M., Gavaghan, D. J., &
McQuay, H. J. (1996). Assessing the quality of reports of randomized clinical trials: Is blinding
necessary? Controlled Clinical Trials, 17(1), 1–12.
Kline, A. C., Cooper, A. A., Rytwinski, N. K., & Feeny, N. C. (2018). Long-etrm efficacy of
psychotherapy for posttraumatic stress disorder: A meta-analysis or randomized controlled
trials. Clinical Psychology Review, 59, 30–40. doi:10.1016/j.cpr.2017.10.009
Lenz, S., Bruijn, B., Serman, N. S., & Bailey, L. (2014). Effectiveness of cognitive processing
therapy for treating posttraumatic stress disorder. Journal of Mental Health Counseling, 36,
360–376. doi:10.17744/mehc.36.4.1360805271967kvq
Maxwell, K., Callahan, J. L., Holtz, P., Janis, B. M., Gerber, M. M., & Connor, D. R. (2016).
Comparative study of group treatments for posttraumatic stress disorder. Psychotherapy, 53,
433–445. doi:10.1037/pst0000032
McNally, R. J. (2018). Posttraumatic stress disorder as a growth industry: Comment on asmund-
son and asmundson (2018). Journal of Anxiety Disorders, 56, 14–16. doi:10.1016/j.
janxdis.2018.03.008
Moher, D., Liberati, A., Tetzlaff, J., & Altman, D. G. (2009). Preferred reporting items for
systematic reviews and meta-analyses: The PRISMA statement. PLoS Medicine, 6(7),
e1000097. doi:10.1371/journal.pmed1000097
Monson, C. M., Schnurr, P. P., Resick, P. A., Friedman, M. J., Young-Xu, Y., & Stevens, S. P. (2006).
Cognitive processing therapy for veterans with military-related posttraumatic stress disorder.
Journal of Consulting and Clinical Psychology, 74, 898–907. doi:10.1037/0022-006X.74.5.898
Olthuis, J. V., Woznet, L., Asmundson, G. J. G., Cramm, H., Lingley-Pottie, P., & McGrath, P. J.
(2016).Distance-delivered interventions for PTSD: A systematic review and meta-analysis.
Journal of Anxiety Disorders, 44, 9–26. doi:10.1016/j.janxdis.2016.09.010.
Petkova, E., Tarpey, T., Huang, L., & Deng, L. (2013). Interpreting meta-regression: Application
to recent controversies in antidepressants’ efficacy. Statistics in Medicine, 32(17), 2875–2892.
doi:10.1002/sim.5766
14 G. J. G. ASMUNDSON ET AL.

Powers, M. B., Halpern, J. M., Ferenschak, M. P., Gillihan, S. J., & Foa, E. B. (2010). A meta-
analytic review of prolonged exposure for posttraumatic stress disorder. Clinical Psychology
Review, 30, 635–641. doi:10.1016/j.cpr.2010.04.007
Resick, P. A., Nishith, P., & Griffin, M. G. (2003). How well does cognitive-behavioral therapy
treat symptoms of complex PTSD? An examination of child sexual abuse survivors within a
clinical trial. CNS Spectr, 8(5), 340–355.
Resick, P. A., Nishith, P., Weaver, T. L., Astin, M. C., & Feuer, C. A. (2002). A comparison of
cognitive-processing therapy with prolonged exposure and a waiting condition for the treat-
ment of chronic posttraumatic stress disorder in female rape victims. Journal of Consulting
and Clinical Psychology, 70, 867–879. doi:10.1037//0022-006x.70.4.867
Resick, P. A., & Schnicke, M. A. (1992). Cognitive processing therapy for sexual assault victims.
Journal of Consulting and Clinical Psychology, 60, 748–756. doi:10.1037//0022-006x.60.5.748
Resick, P. A., & Schnicke, M. K. (1993). Cognitive processing therapy for rape victims: A treatment
manual. Newbury Park, CA: Sage.
Resick, P. A., Wachen, J. S., Mintz, J., Young-McCaughan, S., Roache, J. D., Wachen, J. S., &
Borah, A. M. (2015). A randomized clinical trial of group cognitive processing therapy
compared with group present-centered therapy for PTSD among active duty military person-
nel. Journal of Consulting and Clinical Psychology, 83, 1058–1068. doi:10.1037/ccp0000016
Resick, P. A., Williams, L. F., Suvak, M. K., Monson, C. M., & Gradus, J. L. (2012). Long-term
outcomes of cognitive-behavioral treatments for posttraumatic stress disorder among female rape
survivors. Journal of Consulting and Clinical Psychology, 80, 201–210. doi:10.1037/a0026602
Rosenthal, R. (1979). The file drawer problem and tolerance for null results. Psychological
Bulletin, 86, 638–641. doi:10.1037/0033-2909.86.3.638
Rosenthal, R. (1991). Meta-analytic procedures for social research. London, UK: Sage.
Sareen, J., Cox, B. J., Clara, I., & Asmundson, G. J. G. (2005). The relationship between anxiety
disorders and physical disorders in the U.S national comorbidity survey. Depression and
Anxiety, 21, 193–202. doi:10.1002/da.20072
Sareen, J., Cox, B. J., Stein, M. B., Afifi, T. O., Fleet, C., & Asmundson, G. J. G. (2007). Physical
and mental comorbidity, disability, and suicidal behaviour associated with posttraumatic stress
disorder in a large community sample. Psychosomatic Medicine, 69, 242–248. doi:10.1097/
PSY.0b013e31803146d8
Seedat, S., & Stein, M. B. (2001). Post-traumatic stress disorder: A review of recent findings.
Current Psychiatry Reports, 3, 288–294. doi:10.1007/s11920-001-0021-2
Sloan, D. M., Marx, B. P., Lee, D. J., & Resick, P. A. (2018). A brief exposure-based treatment vs
cognitive processing therapy for posttraumatic stress disorder: A randomized noninferiority
clinical trial. JAMA Psychiatry, 75, 233–239. doi:10.1001/jamapsychiatry.2017.4249
Stein, D. J., Isper, J. C., & Seedat, S. (2006). Pharmacotherapy for post traumatic stress disorder
(PTSD). Cohrane Database Systematic Reviews, 1. doi:10.1002/14651858.CD002795.pub2
Surís, A., Link-Malcolm, J., Chard, K., Ahn, C., & North, C. (2013). A randomized clinical trial of
cognitive processing therapy for veterans with PTSD related to military sexual trauma. Journal
of Traumatic Stress, 26, 28–37. doi:10.1002/jts.21765
Taylor, S. (2017). Clinician’s guide to PTSD: A cognitive-behavioral approach (2nd ed.). New
York: Guilford Press.
The US Department of Veterans Affairs and Department of Defense. (2017). VA/DOD clinical
practice guideline for the management of posttraumatic stress disorder and acute stress disorder.
Washington DC. Retrieved from https://www.healthquality.va.gov/guidelines/MH/ptsd/
VADoDPTSDCPGFinal012418.pdf
Van Etten, M. L., & Taylor, S. (1998). Comparative efficacy of treatments for post-traumatic
stress disorder: A meta-analysis. Clinical Psychology and Psychotherapy, 5, 126–144.
doi:10.1002/(SICI)1099-0879(199809)5:3<126::AID-CPP153>3.0.CO;2-H