Changes in Posttraumatic Stress Disorder and

Journal of Consulting and Clinical Psychology 2012, Vol. 80, No. 6, 957–967

© 2012 American Psychological Association 0022-006X/12/$12.00 DOI: 10.1037/a0030485

Changes in Posttraumatic Stress Disorder and Depressive Symptoms During Cognitive Processing Therapy: Evidence for Concurrent Change Gabrielle I. Liverant

Michael K. Suvak

VA Boston Healthcare System, Brockton, Massachusetts, and Boston University School of Medicine

National Center for PTSD/VA Boston Healthcare System, Boston, Massachusetts

Suzanne L. Pineles

Patricia A. Resick

National Center for PTSD/VA Boston Healthcare System, Boston, Massachusetts, and Boston University School of Medicine

National Center for PTSD/VA Boston Healthcare System, Boston, Massachusetts, and Boston University

Objective: Trauma-focused psychotherapies reduce both posttraumatic stress disorder (PTSD) and cooccurring depression. However, little is known about the relationship between changes in PTSD and depression during treatment. This study examined the association between changes in PTSD and depression during the course of cognitive processing therapy (CPT) and its treatment components. Method: Data were drawn from a dismantling trial investigating the comparative efficacy of the components of CPT (Resick, Galovski, et al., 2008). One hundred twenty-six women (mean age ⫽ 36.14 years) from the original randomized intent-to-treat sample (N ⫽ 150) who attended at least 1 treatment session were included in this study. Participants diagnosed with PTSD were assigned to 1 of 3 treatment conditions: the full CPT protocol (n ⫽ 44), the cognitive therapy component of CPT (n ⫽ 39), and the written account component of CPT (n ⫽ 43). The majority of the sample self-identified as Caucasian (67%; 29% African American and 4% Other). Primary outcome measures included the Posttraumatic Diagnostic Scale and Beck Depression Inventory–II, administered at 8 time points (baseline, weekly throughout 6 weeks of treatment, and posttreatment). Results: Multilevel regression analyses were conducted to examine relationships between PTSD and depression during treatment. Results indicated that changes in PTSD and depression were strongly related. Multilevel mediation analyses revealed that changes in PTSD and depression occurred concurrently, with lagged analyses providing no evidence that changes in symptoms of 1 disorder preceded changes in the other. Conclusions: Results suggest that changes in PTSD and depression occur contemporaneously during CPT. Keywords: PTSD, depression, treatment, psychotherapy, cognitive processing therapy

Posttraumatic stress disorder (PTSD) and major depressive disorder (MDD) are debilitating mental disorders associated with substantial impairment in quality of life, work productivity, and social functioning (e.g., Kessler, 2000; Kessler et al., 2003; Savoca & Rosenheck, 2000; Simon, 2003; Walker et al., 2003). These disorders also co-occur at high rates following trauma exposure. Among individuals with PTSD, estimates of current comorbidity for MDD range from approximately 30% to 50% (e.g., Blanchard, Buckley, Hickling, & Taylor, 1998; Kessler, Sonnega, Bromet,

Hughes, & Nelson, 1995; Resick, Nishith, Weaver, Astin, & Feuer, 2002; Shalev et al., 1998). The common co-occurrence of PTSD with MDD appears to represent a more severe posttraumatic condition that is associated with increased symptom severity and suicidality (Gradus et al., 2010; Shalev et al., 1998) as well as decreased social and occupational functioning (e.g., Blanchard et al., 1998). Furthermore, the presence of co-occurring MDD has been associated with lower rates of posttraumatic symptom remission (e.g., Blanchard et al., 1998). Given the high rates, functional

This article was published Online First October 15, 2012. Gabrielle I. Liverant, Psychology Service, VA Boston Healthcare System, Brockton, Massachusetts, and Department of Psychiatry, Boston University School of Medicine; Michael K. Suvak, National Center for PTSD/VA Boston Healthcare System, Boston, Massachusetts; Suzanne L. Pineles, National Center for PTSD/VA Boston Healthcare System, Boston, Massachusetts, and Department of Psychiatry, Boston University School of Medicine; Patricia A. Resick, National Center for PTSD/VA Boston Healthcare System, Boston, Massachusetts, and Departments of Psychiatry and Psychology, Boston University. Michael Suvak is now at the Department of Psychology, Suffolk University, Boston, Massachusetts.

This research was supported by National Institute of Mental Health Grant 2-R01-MH51509 awarded to Patricia A. Resick at the University of Missouri–St. Louis. During work on this paper, Gabrielle I. Liverant was supported by a VA Career Development Award from the Department of Veterans Affairs. Additional support was provided to Suzanne L. Pineles through a VA Career Development Award from the Department of Veterans Affairs. Correspondence concerning this article should be addressed to Gabrielle I. Liverant, VA Boston Healthcare System–Brockton Campus (116A), 940 Belmont Street, Brockton, MA 02301-5596. E-mail: gabrielle.liverant@ va.gov 957

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impairment, and potential treatment implications associated with co-occurring depression among individuals with PTSD, it is important to further our understanding of the interrelationship of these two conditions following trauma. Notably, at the symptom level, PTSD and MDD share related diagnostic criteria, including emotional numbing/anhedonia, sleep disruption, and concentration problems (American Psychiatric Association, 2000; Franklin & Zimmerman, 2001). This symptom overlap has led to the investigation of the unique and shared components of these disorders using factor analytic techniques (Blanchard et al., 1998; Grant, Beck, Marques, Palyo, & Clapp, 2008). Overall, these cross-sectional studies have found strong relationships between latent PTSD and MDD factors, while still supporting the distinctiveness of the two disorder constructs (e.g., Grant et al., 2008; Simms, Watson, & Doebbeling, 2002). In several studies, researchers have attempted to identify the sequence of onset for PTSD and MDD following trauma exposure. However, findings have been mixed, with some studies suggesting that PTSD precedes the onset of MDD and others suggesting that MDD may precede and potentiate the onset of PTSD following trauma exposure (e.g., Breslau, Davis, Peterson, & Schultz, 1997, 2000; Shalev et al., 1998). In addition, two naturalistic studies have examined the direction of influence between PTSD and depression over time following trauma (Erickson, Wolfe, King, King, & Sharkansky, 2001; King, King, McArdle, Shalev, & Doron-Lamarca, 2009). Erickson et al. investigated the prospective relation between PTSD and depression symptoms in a sample of Gulf War veterans. Results showed reciprocal relationships between PTSD and depression over a 24-month period following the end of deployment. Similarly, King et al. examined the interrelationships between changes in PTSD and depression after trauma exposure in a reanalysis of prospective data following emergency room patients who had experienced a Criterion A event (original study; Shalev et al., 2008). Study findings supported strong effects for depression on subsequent changes in PTSD as well as effects for PTSD on subsequent change in depression. Although the results reviewed above have begun to characterize the naturalistic, dynamic interrelationship of change in PTSD and depression following trauma exposure, only one study has implemented sophisticated data analytic methods to examine the relationship between changes in PTSD and depression during traumafocused psychotherapy (Aderka, Foa, Applebaum, Shafran, & Gilboa-Schechtman, 2011). Analysis of pre- and posttreatment data from numerous clinical trials demonstrates that traumafocused psychotherapies decrease co-occurring depressive symptoms in addition to having primary effects on PTSD (e.g., Foa et al., 2005; Resick, Galovski, et al., 2008; Resick, Nishith, & Griffin, 2003; Resick et al., 2002). However, little is known about the temporal dynamics between PTSD and depression during the course of different psychotherapeutic treatments. Aderka et al. (2011) investigated the interrelationship of PTSD and depression symptoms during the course of prolonged exposure (PE) therapy among children and adolescents. Lagged multilevel mediation analysis indicated reciprocal relations between the two disorders during treatment. However, changes in PTSD symptoms accounted for 64% of change in depression symptoms, but changes in depression accounted for only 11% of change in PTSD symptoms. This suggests a more primary role for PTSD in mediating subsequent change in depression than for depression mediating

changes in PTSD. These findings have begun to elucidate the relationship between changes in PTSD and depression during exposure-based treatment among children. However, to date, no study has examined the relationships between these two disorders during cognitively based PTSD treatments or among adults. Additional studies are needed across PTSD treatments and populations to inform our understanding of the mechanisms of action for different PTSD interventions. Studies of this type will help us to improve existing treatments for the common co-occurrence of these two disorders (e.g., Aderka et al., 2011). Cognitive processing therapy (CPT) has been established as an effective treatment for PTSD among individuals who have experienced a wide range of trauma (Ahrens & Rexford, 2002; Chard, 2005; Monson et al., 2006; Resick et al., 2002, 2003; Schulz, Resick, Huber, & Griffin, 2006). CPT is a cognitive-behavioral treatment that incorporates both cognitive therapy and written trauma accounts (e.g., Resick, Monson, & Chard, 2008). Many of the cognitive techniques used in CPT are similar to procedures implemented in cognitive therapy for depression (Beck, 1976; Beck, Rush, Shaw, & Emery, 1979) except that CPT is a prescribed 12-session, trauma-focused protocol. CPT has been shown to reduce both primary PTSD symptoms and secondary symptoms of co-occurring depression (e.g., Resick et al., 2002; Resick et al., 2008). Thus, it may be particularly important to understand the sequencing and interrelationship of changes in PTSD and cooccurring depression during the course of this trauma treatment. The current study is a reanalysis of existing data from a dismantling study that examined the comparative efficacy of the different components of CPT: (a) the cognitive therapy component of CPT (CPT-C), (b) the written account component of CPT (WA), and (c) the original combined CPT protocol (CPT; Resick, Galovski, et al., 2008). Results from the original study suggest that all three treatment conditions resulted in significant improvements in both PTSD and co-occurring depression (Resick, Galovski, et al., 2008). Findings further showed that CPT-C produced significantly greater reductions than WA in PTSD symptoms. However, the full CPT protocol was not significantly different from either WA or CPT-C in the treatment of PTSD symptoms. No significant differences in depression were found between the three treatment conditions. However, there were trends for larger reductions in depression in the CPT-C versus WA conditions throughout treatment. In the current study, existing data from this original investigation (Resick, Galovski, et al., 2008) were reanalyzed to examine the interrelationship of changes in PTSD and depression symptoms during the course of trauma-focused psychotherapy.

Method Participants One hundred twenty-six women (44 CPT, 43 WA, 39 CPT-C) from Resick, Galovski, et al.’s (2008) original randomized intentto-treat (ITT) sample (N ⫽ 150) who attended at least one treatment session were included in this study. Although we appreciate the need to include the entire ITT sample in analyses to establish efficacy, our goal in the current study was to examine the relationship between symptoms of PTSD and depression during the course of treatment. Thus, we excluded the 24 ITT participants who completed the pretreatment assessment but did not attend any

CHANGES IN PTSD AND DEPRESSION DURING CPT

treatment sessions. A series of chi-squared analyses and t tests indicated that participants who started treatment did not differ from ITT participants who were randomized but did not attend any treatment sessions on income, highest education level completed, marital status, age, treatment condition, initial MDD diagnosis, initial PTSD symptoms, or initial depression symptoms. The only significant group difference to emerge was ethnicity; Caucasian participants were more likely than African American participants to start treatment, ␹2(4) ⫽ 13.94, p ⬍ .05. Participants were women who had experienced sexual or physical assault in childhood or adulthood, at least 3 months prior to enrollment, and who met diagnostic criteria for PTSD (American Psychiatric Association, 1994) during the initial assessment. Participants either were free from psychotropic medications or had been stabilized on their medication regimen for at least 3 months. Trial exclusion criteria included current psychosis, suicidal intent, illiteracy, and drug or alcohol dependence (Resick, Galovski, et al., 2008). Overall, these women (n ⫽ 126) were an average of 36.14 years of age (SD ⫽ 12.75) and had completed an average of 13.96 years of education (SD ⫽ 2.90). The majority of the sample selfidentified as Caucasian (67%; 29% African American and 4% Other). Most participants were single (47%; 22% married or cohabiting; 27% separated or divorced; 4% widowed). On average, the participants’ index trauma (i.e., the trauma that the participant identified as the worst and that was the initial focus of treatment) occurred 14.96 years before enrollment (SD ⫽ 14.68). At the pretreatment assessment, all participants met Diagnostic and Statistical Manual of Mental Disorders (4th ed.; DSM–IV; American Psychiatric Association, 1994) criteria for PTSD, 66 (52%) met criteria for current MDD, and 27 (21%) met criteria for panic disorder. Fifty-three (42%) of the sample were using psychotropic medication. A series of chi-squared analyses indicated that the frequency of these comorbid conditions and medication use did not vary as a function of treatment condition. Following a telephone screening procedure, potentially eligible participants were invited for an initial study visit, at which time they provided informed consent for participation and completed further assessment of eligibility. All study procedures were conducted in compliance with the University of Missouri Institutional Review Board. Secondary data analysis and data management for this project were conducted in compliance with the VA Boston Healthcare System’s Institutional Review Board.

Treatment As described above, participants were randomly assigned to treatment with CPT, CPT-C, or WA. All three treatments were scheduled to be completed within 6 weeks and were equated in total hours of therapy (i.e., 12 hr). However, they were delivered slightly differently. CPT and CPT-C consisted of twelve 60-min sessions conducted twice per week. WA consisted of two 60-min sessions in Week 1 followed by five weekly 2-hr sessions, for a total of seven sessions. Below are brief descriptions of the three treatments. (Please see Resick, Galovski, et al., 2008, for additional details on the treatment conditions.) CPT (Resick, 2001; Resick & Schnicke, 1993). CPT is a manualized cognitive-behavioral treatment for PTSD with a primary emphasis on cognitive interventions designed to help the

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client process the traumatic event(s). There are two primary components of this treatment: written trauma accounts and interventions focused on challenging cognitive distortions. Clients are asked to complete writing exercises describing their most traumatic event(s) and the current impact of the event(s). The clients read their accounts to the therapist in session and at home between sessions. Socratic questioning and worksheets are used to help the client challenge distorted cognitions related to the traumatic event. These worksheets build on each other, teaching cognitive challenging skills that culminate in the development of alternative, more balanced self-statements. Later sessions focus on correcting overgeneralized beliefs related to the themes of safety, trust, power/control, esteem, and intimacy. CPT-C. The CPT-C protocol is identical to the CPT protocol except the written account component is excluded. Sessions from the full protocol with written accounts are replaced with additional worksheets and in-session skills practice focusing on identifying and restructuring dysfunctional cognitions about traumatic events. WA. The WA protocol focuses on the written trauma accounts and excludes the cognitive therapy components of CPT. The first two 1-hr sessions of this treatment consist of psychoeducation, along with instruction regarding subjective units of distress (SUDS) and construction of trauma scripts. During the remaining five 2-hr sessions, the client writes alone in a room for 45– 60 min about her worst trauma. After the writing period, the therapist returns to the room and the client reads the account aloud to the therapist. The therapist does not engage in cognitive therapy or challenges but can direct the client to check on emotions, focus on “hot spots,” provide support, record SUDS ratings, and provide psychoeducation. Homework consists of reading the account daily and recording associated SUDs ratings.

Measures Clinician-Administered PTSD Scale (CAPS; Blake et al., 1990, 1995). This interview was used to assess for PTSD diagnosis during the baseline assessment. Interviewers were trained master’s-level clinicians who received ongoing supervision. Each interview was reviewed and discussed in a diagnostic consensus meeting. The interviews were audiotaped, and 31 of the interviews in Resick, Galovski, et al.’s (2008) RCT were rated by a second rater. Interrater reliability for PTSD diagnosis was excellent (␬ ⫽ 1.0). Structured Clinical Interview for DSM–IV Axis I Disorders—Patient Edition (SCID; First, Spitzer, Gibbon, & Williams, 1996). The SCID is a semistructured interview designed to assess DSM–IV Axis I disorders. In this study, modules assessing panic disorder, major depressive disorder, and substance abuse/dependence as well as the psychotic screen were administered during the baseline assessment. The interviewers who administered the CAPS also administered the SCID. SCID interview results were discussed in supervision and at a diagnostic consensus meeting. A random sample of 40 tapes from Resick, Galovski, et al.’s (2008) RCT was evaluated for diagnostic reliability. These values were also very good (␬ ⫽ 0.80 for MDD, ␬ ⫽ 1.00 for alcohol and substance dependence, ␬ ⫽ 0.75 for panic disorder). Beck Depression Inventory–II (BDI-II; Beck, Steer, & Brown, 1996). This 21-item self-report measure assesses severity of depressive symptoms. The BDI-II was administered during

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the baseline assessment, weekly during 6 weeks of treatment, and at posttreatment (totaling eight time points). The BDI-II has demonstrated excellent reliability and validity in outpatient samples (e.g., Beck, Steer, Ball, & Ranieri, 1996). The BDI-II demonstrated high internal consistency (e.g., ␣ ⫽ .90 for the baseline assessment) within the current study sample. Posttraumatic Diagnostic Scale (PDS; Foa, 1995). This 49item self-report measure assesses trauma history and all DSM–IV diagnostic criteria for PTSD. Participants rate the frequency of each symptom item on a 4-point scale ranging from 0 to 3. The PTSD severity score is calculated by summing the 17 items on the scale that assess PTSD symptoms. The 17 items of the PDS were administered at the same time points as the BDI-II. The PDS has demonstrated good reliability and validity within trauma samples (Foa, Cashman, Jaycox, & Perry, 1997). The PDS also demonstrated good internal consistency (e.g., ␣ ⫽ .86 for the baseline assessment) within the current study sample. A clinical cutoff of 18 on the PDS indicates a probable current diagnosis of chronic PTSD (Ehring, Kleim, Clark, Foa, & Ehlers, 2007).

regression coefficients produced by HLM. Because HLM does not produce standardized regression coefficients, we report the partial correlation coefficients (pr) as an indicator of effect size for each Level 1 coefficient. Kirk (1996) proposed .10, .24, and .37 for small, medium, and large effect sizes, respectively. HLM produces a log-likelihood-based goodness-of-fit statistic referred to as the deviance statistic. To examine the overall effects of treatment condition, we evaluated change in the deviance statistic, computed by subtracting the deviance statistic from the model with the treatment condition variables included from the deviance statistic from the model without these variables (⌬dev; which follows a chi-squared distribution with degrees of freedom equal to the difference between the number of parameters between the two models being compared; Raudenbush & Bryk, 2002). Two types of multilevel regression analyses were conducted to (a) examine the relationship between change over time in PTSD and change over time in depression and (b) examine the temporal dynamics of this relationship. To help facilitate interpretation of results, we provide procedures for each specific analysis prior to reporting the results.

Data Analysis Multilevel regression analyses were conducted to examine the relationship between change in PTSD and depression symptoms during the course of treatment (Singer & Willett, 2003; Suvak, Walling, Iverson, Taft, & Resick, 2009). Multilevel regression analysis was developed to analyze nested, or hierarchical, data structures (e.g., Raudenbush & Bryk, 2002). For longitudinal designs, multiple assessments are nested within individuals. The repeated-measures, or within-participants, component of multilevel models is often referred to as the Level 1 component of the analyses, and the component of the model referring to differences across participants is typically referred to as the Level 2 component. In the current study, the Level 1 variables were the repeated measures of PTSD (i.e., PDS) and depression (i.e., BDI-II), and the Level 2 predictor variables included treatment condition and pretreatment MDD diagnosis (as assessed by the SCID). The primary purpose of multilevel models when applied to longitudinal data is to simultaneously examine Level 1 (i.e., within-participants) associations and how these associations are distributed across Level 2 units (i.e., individuals). Multilevel regression offers a number of strengths that facilitate sophisticated and powerful examinations of change over time. Strengths of this approach include (a) capability of handling missing data and unbalanced designs (i.e., the number of assessment points and the timing of assessments can vary across subjects), (b) highly efficient and powerful estimation procedures that include all data points available, and (c) modeling flexibility that provides multiple options for how to model time and allows for the inclusion of continuous or categorical, time invariant or time varying, predictors and covariates. This modeling flexibility enables the sophisticated examination of the relationship among multiple variables over time. Thus, these analyses are well suited to examine mechanisms of change during the course of treatment. Hierarchical linear and nonlinear modeling software (HLM6; Raudenbush, Bryk, & Congdon, 2005) with full maximum likelihood estimation was used to conduct primary analyses. To evaluate the significance of Level 1 associations, we evaluated the

Results At the initial assessment, the mean PTSD (PDS) and depression (BDI-II) levels for the sample were 29.65 (SD ⫽ 9.30) and 26.82 (SD ⫽ 10.67), respectively. As expected, these two self-reports were strongly correlated (r ⫽ .61, p ⬍ .001) at the initial assessment.

Multilevel Mediational Analyses To examine how changes in depression were associated with changes in PTSD symptoms, we conducted a series of multilevel mediational analyses (Bauer, Preacher, & Gil, 2006; Kenny, Korchmaros, & Bolger, 2003). The mediation approach that we adopted investigated mediation of change, as opposed to mediation of treatment. In other words, we investigated factors that accounted for within-subject change during treatment and not factors that accounted for differences across treatment conditions. Thus, the predictor in our mediation models was time, as opposed to treatment condition. We examined the trajectory of each outcome variable (i.e., the association between time and PTSD and depression symptoms) with and without the proposed mediator (i.e., depression or PTSD) included as a time-varying covariate. (See Figures 1a and 1b for a schematic of this analytic approach.) The first set of meditational models examined whether changes in PTSD were associated with changes in depression by using mediation procedures to see if change in PTSD accounted for change in depression and vice versa. Mediation Model A examines whether reductions in depression due to treatment are accounted for by reductions in PTSD symptoms. The following findings would support this hypothesis: (a) a substantial reduction in the regression coefficient indicating the degree to which depression changes over time when PTSD is added as a timevarying covariate (which can be evaluated by comparing paths c and c= of Figures 1a and 1b), and (b) a significant indirect path from time (which is the predictor variable in growth curve analyses) to depression through PTSD. To evaluate whether reductions in PTSD are accounted for by reductions in depres-


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(a) Mediaon Model A Time

Depression

c

PTSD b

a

Time

Indices of mediation • a*b (95 CI) percent mediation • ab/(c’ + a*b + abcov)

Depression

c‘

(b) Mediaon Model B Time

PTSD

c

Depression b

a

Time

Indices of mediation • a*b (95 CI) percent mediation • ab/(c’ + a*b + abcov)

PTSD c‘

(c)Moderated-Mediaon

Moderator (Treatment Condition, Pre-Treatment MDD Diagnosis)

Outcome (PTSD, Depression)

Time c Moderator Mediator (Depression, PTSD)

(Treatment Condition, Pre-Treatment MDD Diagnosis)

Indices of mediation • a*b (95 CI)

a

b

Time c‘

Outcome (PTSD, Depression)

Figure 1. Schematic of mediation models. PTSD ⫽ posttraumatic stress disorder; CI ⫽ confidence interval; MDD ⫽ major depressive disorder.

sion symptoms, in Mediation Model B, PTSD was included as the outcome variable (in separate analyses) and depression was included as the mediator variable. This approach is increasingly being applied to data from randomized controlled trials to identify mechanisms of change and to test whether the proposed mediation model varies across different treatment conditions (e.g., Hofmann et al., 2007). Conceptually, multilevel mediation analyses are very similar to traditional cross-sectional mediation analyses. However, a few adjustments are needed to address the nested-data structure. For instance, because of the multilevel design, Paths a (predictor to mediator) and b (mediator to outcome when controlling for the predictor) vary across Level 1 units (i.e., participants) and can potentially covary. Estimates of the confidence interval

for the indirect effect (a*b) and estimates of percent mediation must take into account this potential covariation between Paths a and b (Bauer et al., 2006; Kenny et al., 2003). We used the multivariate approach described by Bauer et al. (2006) that simultaneously estimates Paths a and b in the same model and produces estimates of the covariation of these two paths. To produce confidence intervals and significance tests for indirect effects (i.e., a*b), we used the asymmetric distribution of products tests, as described by MacKinnon and colleagues (MacKinnon, Fritz, Williams, & Lockwood, 2007; MacKinnon, Lockwood, Hoffman, West, & Sheets, 2002), which can take into account the covariation between Paths a and b. To produce an estimate of the strength of the indirect effect or mediation, we computed the percentage of the total relationship between the predictor

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and the outcome (total effect ⫽ c= ⫹ ab ⫹ covariance of ab) that was accounted for by the indirect effect (ab ⫹ covariance of ab).1 Table 1 summarizes the results of the mediation analyses. Nonlagged mediation analyses. The Analysis 1 section of Table 1 provides the estimates for the initial mediation models examining the relationship between PTSD and depression over time. Mediation Models A and B both indicated that changes in PTSD and depression were substantially related to each other, with PTSD accounting for 81% of the reductions in depression and depression accounting for 55% of the reductions in PTSD. Importantly, the mediator in these initial mediation analyses was measured at the same time as the outcome. In other words, the data were not lagged (i.e., they were contemporaneous). Therefore, these initial mediation analyses do not address the directionality of the relationship between PTSD and depression over time. They merely indicate that changes occurring in depression during treatment are accounted for by changes in PTSD during that same time period, not a previous time period (and vice versa). Lagged mediation analyses. To evaluate the directionality of the relationship between PTSD and depression, we conducted lagged mediation analyses.2 The lagged mediation analyses were similar to the initial mediation analyses described above with one exception: The mediator variable was lagged (i.e., the mediator variable at Time T-1 was used to predict the outcome at Time T). The lagged mediation analyses tested the following possibilities: (a) changes in PTSD preceded changes in depression, (b) changes in depression preceded changes in PTSD, (c) PTSD and depression are reciprocally related across time, with changes in PTSD leading to later changes in depression and vice versa, or (d) the changes that occurred between the two variables occurred at the same time with no longitudinal influence of one variable on the other. The results of these analyses are depicted in the Analysis 2 section of Table 1. The most notable result of the lagged mediation analyses is that neither of the indirect paths was statistically significant, which supports possibility (d) described above. In sum, the nonlagged mediation analyses documented a significant association between change in PTSD and change in depression over time, and the lagged mediation analyses indicated that change in these two variables occurred concurrently.

Moderated-Mediation Analyses: Effects of Treatment Condition The next set of mediation analyses included treatment condition in the Level 2 component of the multilevel-mediation models to evaluate the possibility of moderated mediation (see Figure 1c for a depiction). Moderated mediation (e.g., Bauer et al., 2006; Hofmann et al., 2007; Tein, Sandler, MacKinnon, & Wolchik, 2004) occurs when a mediation model of interest varies significantly (either paths a, b, c, or c= of the mediation model or the overall strength of the indirect effect) as a function of a moderator variable. In this study, we included a dummycoded treatment variable in the Level 2 regression equations of the mediation models to examine whether Mediation Models A and B varied significantly as a function of treatment group. The regression intercepts of these Level 2 equations produce estimates of each of the mediation paths for the reference group

(i.e., treatment group coded as 0), and the regression coefficients for the dummy-coded variables produce estimates of the differences in each path between the two treatment conditions. Switching the coding of the dummy-coded variable allows one to estimate the paths for all groups. As summarized in the Analysis 3 and Analysis 4 sections of Table 1, the results indicated that the mediation models were largely consistent across the three treatment conditions. However, a few small but notable differences emerged across the treatments. The differences were found in Mediation Model B (changes in depression accounting for changes in PTSD) of the lagged analysis. (See the Analysis 4 section of Table 1.) Path b (i.e., the relationship between the mediator, or the lagged depression score, and the outcome) significantly differed between the CPT and CPT-C conditions (bdiff ⫽ 0.17, t ⫽ 2.25, p ⬍ .001, pr ⫽ .20), with the association being stronger for the CPT-C condition. In addition, the indirect path ab (ab ⫽ .12; 95% CI ⫽ ⫺.20, .38; 90% CI ⫽ ⫺.14, .34) did not approach statistical significance, with a percent mediation of approximately zero for participants receiving CPT,3 but the indirect path ab (ab ⫽ ⫺.30; 95% CI ⫽ ⫺.61, .05; 90% CI ⫽ ⫺.14, ⫺.01) approached statistical significance (i.e., the 90% CI did not include zero) with a percent mediation of approximately 7% for participants receiving CPT-C. Finally, Path c= (i.e., change over time in PTSD when controlling for depression) was significantly stronger for participants receiving CPT than for participants receiving CPT-C (bdiff ⫽ 1.20, t ⫽ 2.20, p ⬍ .05, pr ⫽ .20) or WA (bdiff ⫽ 7.41, t ⫽ 4.52, p ⬍ .001, pr ⫽ .19), with no difference between the CPT-C and WA conditions (bdiff ⫽ 0.08, t ⫽ 0.16, ns, pr ⫽ .02). When moderated mediation is evaluated, differences in each individual path of the mediation model as well as differences in the indirect effect across the moderator must be examined. The fact that two of the paths of the mediation model (i.e., b and c=) significantly differed across the CPT and CPT-C 1 The equation used to calculate percent mediation: 100 * (ab ⫹ covariance of ab)/(c= ⫹ ab ⫹ covariance of ab). 2 To be included in the lagged analyses, participants needed to have data available from at least two consecutive assessments. Twelve participants (5 CPT, 3 CPT-WA, and 4 CPT-CT) did not meet this requirement and were excluded from the lagged analyses. In addition, because the lagged analyses consisted of regressing the outcome at assessment t on the mediator at time t-1, the lagged analyses used assessments 2– 8 to estimate change in the outcome variable, but the nonlagged analyses used assessments 1– 8 to estimate change in the outcome. To confirm that any differences emerging between the nonlagged and lagged analyses were not due to the exclusion of participants and exclusion of the first assessment occasion, we reran all of the nonlagged analyses removing these 12 cases and the first assessment of the outcome. Removing these participants and data points minimally impacted the results of the nonlagged analyses. Results of these analyses are available upon request to the first author. However, because the original nonlagged analyses that included all participants and all available data points provide the most accurate estimates of change during treatment, we have presented the results of these analyses in this paper. 3 The calculation of the percent mediation estimates produced a few negative values (e.g., the percent mediation values for the CPT condition in the lagged-mediation models). Negative percent mediation values occurred when the indirect (a*b) path did not significantly differ from zero and was a function of the sign of the indirect path (although not significantly differing from zero), being opposite of the sign of the direct effect (i.e., c=). Because confidence intervals for these estimates included zero, the most prudent interpretation of the negative percent mediation values is that no evidence of mediation was produced by the models.

A B A B

A B A B A B A B A B A B A B A B A B A B

1 Overall nonlagged 2 Overall lagged

3a CPT nonlagged 3b WA nonlagged 3c CPT-C nonlagged 4a CPT lagged 4b WA lagged 4c CPT-C lagged 5a MDD ⫺ nonlagged 5b MDD ⫹ nonlagged 6a MDD ⫺ lagged 6b MDD ⫹ lagged

PTSD Dep PTSD Dep PTSD Dep PTSD Dep PTSD Dep PTSD Dep PTSD Dep PTSD Dep PTSD Dep PTSD Dep

PTSD Dep PTSD Dep

M Mediator

Dep PTSD Dep PTSD Dep PTSD Dep PTSD Dep PTSD Dep PTSD Dep PTSD Dep PTSD Dep PTSD Dep PTSD

Dep PTSD Dep PTSD

Y Outcome ⴚ0.43 ⴚ1.13 ⫺2.84 ⫺2.57 ⴚ0.56 ⴚ1.43 ⫺0.22 ⴚ0.94 ⴚ0.53 ⴚ0.98 ⴚ2.97 ⴚ3.61a ⴚ2.14 ⴚ2.50b ⴚ2.66 ⴚ2.50b ⴚ0.51 ⴚ1.16 ⴚ0.36 ⴚ1.10 ⫺2.44 ⫺2.68 ⫺2.44 ⫺3.02

Combined across conditions ⴚ2.53 0.69 ⴚ2.26 0.57 ⴚ2.74 0.04 ⴚ2.95 0.01 Each condition separately ⴚ2.78 0.68 ⴚ2.52 0.49 ⴚ2.12 0.68 ⴚ1.77 0.61 ⴚ2.68 0.70 ⴚ2.51 0.63 ⴚ3.51 ⫺0.02 ⴚ3.03 ⫺0.04a ⴚ2.60 0.02 ⴚ2.35 0.06 ⴚ2.80 0.02 ⴚ2.85 0.11b ⴚ2.51 0.68 ⴚ2.32 0.52 ⴚ2.55 0.69 ⴚ2.20 0.63 ⫺2.81 ⫺0.02 ⫺2.58 0.05 ⫺3.11 0.03 ⫺2.94 0.04

ⴚ2.52 ⴚ2.74 0.61 ⴚ2.11 0.63 ⴚ2.67 ⴚ3.03 ⴚ3.50 ⴚ2.35 ⴚ2.61 ⴚ2.85 ⴚ2.81 ⴚ2.32 ⴚ2.52 ⴚ2.20 ⴚ2.49 ⫺2.58 ⫺2.84 ⫺2.94 ⫺3.11

c= Change in Y controlling for M

ⴚ2.22 ⴚ2.51 ⴚ2.97 ⴚ2.74

B M predicting Y controlling for time

a Change in M

c Change in Y

0.12 ⫺0.20 ⫺0.57 ⫺0.78 ⫺0.33 ⫺0.22 ⫺0.43 ⫺0.39 ⫺0.10 ⫺0.84 0.36 0.36 ⫺0.33 ⫺0.52 ⫺0.10 ⫺0.22 ⫺0.45 ⫺0.05 ⫺0.13 ⫺0.83

⫺0.23 ⫺0.37 ⫺0.01 ⫺0.60

Cor ab Correlation of a and b

ⴚ1.91 [⫺2.46, ⫺1.40] ⴚ1.23 [⫺1.65, ⫺0.85] ⴚ1.44 [⫺2.68, ⫺0.52] ⴚ1.09 [⫺1.64, ⫺0.63] ⴚ1.88 [⫺2.50, ⫺1.33] ⴚ1.59 [⫺2.12, ⫺1.11] 0.07 [⫺0.65, 0.69] 0.12 [⫺0.20, 0.38] ⫺0.04 [⫺2.02, 1.83] ⫺0.14 [⫺0.40, 0.03] ⫺0.06 [⫺0.49, 0.33] ⫺0.30z [⫺0.62, 0.05] ⫺2.23 [⫺2.23, ⫺1.25] ⫺1.21 [⫺1.64, ⫺0.84] ⫺2.18 [⫺2.18, ⫺1.37] ⫺1.38 [⫺1.76, ⫺1.04] ⫺0.36 [⫺0.36, 0.39] ⫺0.12 [⫺0.31, 0.05] ⫺0.37 [⫺0.37, 0.20] ⫺0.12 [⫺0.39, 0.09]

ⴚ1.74 [⫺2.07, ⫺1.43] ⴚ1.30 [⫺1.59, ⫺1.04] ⫺0.12 [⫺0.27, 0.02] ⫺0.02 [⫺0.28, 0.20]

ab [95% CI] indirect effect

76.7 [70.5, 81.0] 47.5 [39.2, 54.5] 87.3 [73.1, 92.6] 57.7 [46.4, 66.2] 79.1 [73.4, 83.2] 63.0 [54.8, 69.3] ⫺10.6 [⫺43.5, 12.9] ⫺0.2 [⫺8.1, 7.9] 2.1 [⫺587.2, 48.7] 11.3 [5.7, 18.9] 5.3 [⫺9.9, 18.1] 7.4 [⫺6.2, 17.1] 78.2 [72.8, 82.1] 54.2 [46.2, 60.8] 83.15 [79.41, 85.94] 56.84 [50.10, 62.45] 7.53 [⫺6.23, 19.93] 4.74 [⫺1.45, 10.71] 3.94 [⫺7.78, 13.80] 7.91 [1.57, 15.10]

80.7 [83.2, 77.6] 55.3 [59.9, 50.1] 7.5 [⫺0.5, 15.35] 4.1 [⫺0.7, 8.58]

Percent mediation [95% CI]

Note. Bold type indicates p ⬍ .05; italic type indicates p ⬍ .10; c, a, b, and c= represent the paths of the mediation model as depicted in Figure 1; ab ⫽ the indirect effect; Cor ab ⫽ correlation between paths a and b; 95% CI ⫽ 95 percent confidence interval. Superscripts a and b denote statistically significant (p ⬍ .05) difference across treatment conditions; superscript z denotes p ⬍ .09. PTSD ⫽ symptoms of posttraumatic stress disorder as assessed by the Posttraumatic Diagnostic Scale; Dep ⫽ symptoms of depression as assessed by the Beck Depression Inventory–II; CPT ⫽ the cognitive processing therapy treatment condition that received the full CPT protocol; CPT-C ⫽ the treatment condition that received the cognitive component of CPT; WA ⫽ the treatment condition that received only the written accounts component of CPT; MDD ⫺ indicates participants who did not meet criteria for major depressive disorder at pretreatment; MDD ⫹ indicates participants who did meet criteria for major depressive disorder at pretreatment. Analyses 1 (nonlagged) and 2 (lagged) refer to the models examined across all participants (i.e., not including treatment condition or pretreatment MDD status in the model). Analyses 3 (nonlagged) and 4 (lagged) refer to the moderated mediation analyses and present the coefficients for each treatment condition. Analyses 5 (nonlagged) and 6 (lagged) refer to the moderated mediation analyses examining the impact of pretreatment MDD status and present the coefficients for those with and without a MDD diagnosis separately. In the Model column, “A” specifies the mediation model with depression as the outcome and PTSD as the mediator, and “B” specifies the mediation model with PTSD as the outcome and depression as the mediator.

Model

Analysis no.

Path/variable Description

Table 1 Summary of the Mediation Analyses


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conditions in combination with the finding that the indirect effect from time to PTSD through depression approached statistical significance for the CPT-C group, but did not for the CPT group, could suggest that the relationship between depression and PTSD during the course of therapy may be affected by treatment type, with depression accounting for changes in PTSD to a greater extent in more cognitively based psychotherapies. However, these results should be interpreted with caution because the indirect path only approached significance for the CPT-C condition.

Moderated-Mediation Analyses: Effects of Pretreatment MDD Diagnosis Finally, MDD diagnosis at pretreatment was examined as a moderator of the relationship between PTSD and depression during treatment using the moderated-mediation approach described above. The regression intercepts of the model examining PTSD and depression over time without mediators indicated that mean depression and PTSD levels at the pretreatment assessment were 31.78 (SD ⫽ 9.42) and 33.84 (SD ⫽ 8.52), respectively, for participants meeting criteria for MDD at the pretreatment assessment and 24.37 (SD ⫽ 8.98) and 27.11 (SD ⫽ 7.57) for participants not meeting criteria for MDD at the pretreatment assessment, with the differences between the groups reaching statistical significance for both outcomes (depression: bdiff ⫽ 7.41, t ⫽ 4.52, p ⬍ .001, pr ⫽ .38; PTSD: bdiff ⫽ 5.73, t ⫽ 3.99, p ⬍ .001, pr ⫽ .34). Although participants with MDD initially reported higher levels of symptoms, MDD status did not affect the mediation model (see the Analyses 5 and 6 sections of Table 1). None of the mediation paths significantly differed as a function of MDD status, and there was overlap in the 95% CIs for the indirect paths. This overlap suggested that the relationship between PTSD and depression during the course of treatment was not influenced by the presence of an initial diagnosis of MDD.

Discussion Multilevel mediation analyses revealed that changes in PTSD and depression occurred concurrently and provided no evidence of temporal precedence for changes in one of these variables over the other. In other words, no evidence was found to support changes in one disorder leading to subsequent changes in the other. Instead, this pattern of results suggests that a third factor (e.g., treatment) influenced change in both disorders simultaneously. Findings from this study add to the limited existing literature examining the interrelationship between changes in PTSD and depression during the course of trauma treatment. This investigation utilized a novel design, sample, and methods to examine the relationship between symptoms of the two disorders across different types of trauma-focused therapy. This study is the first to investigate the relationship between changes in PTSD and depression during trauma treatment among adults. In addition, this study was the first to explore the relationship between changes in PTSD and depression during the course of CPT and its treatment components. As mentioned previously, CPT is a cognitive therapy for PTSD that incorporates many techniques that were originally developed as part of Beck’s cognitive therapy for depression (e.g., Socratic questioning;

Beck et al., 1979). Given the similar therapeutic procedures found in CPT and cognitive therapies for depression, it is not surprising that both disorders improved concurrently, perhaps suggesting that CPT and its treatment components act on a common mechanism of change affecting both disorders. Findings from this study with CPT and its components deviated from results found in the one other study examining the relationship between PTSD and depression during trauma-focused psychotherapy (Aderka et al., 2011). In contrast to the current investigation, Aderka et al. (2011) found evidence of reciprocal change in PTSD and depression during the course of PE in children and adolescents. Their analyses identified a primary role for PTSD as the mediator, with changes in PTSD accounting for 64% of change in depression compared to changes in depression accounting for only 11% of change in PTSD. Of note, Aderka et al.’s results were found using a lagged model, which suggests that change in PTSD influenced subsequent change in depression. Instead, findings from the present study suggested contemporaneous change in PTSD and depression, with no evidence for changes in one disorder contributing to changes in the other. It is difficult to interpret the contradictory findings from these two studies examining CPT and PE (Aderka et al., 2011). For example, observed differences in the relationship between changes in PTSD and depression may have been influenced by distinct study populations (i.e., children and adolescents vs. adults) or differing design and assessment methods in the two studies. Another possibility is that the change may occur through different mechanisms in PE and CPT. Gallagher and Resick (2011) found that hopelessness, a symptom related to depression, improved more during CPT than PE. In CPT, changes in hopelessness predicted changes in PTSD symptoms during treatment. In contrast, in PE, PTSD symptoms were found to improve through habituation to exposures (as measured by changes in SUDS ratings), before and after accounting for level of hopelessness. Gallagher and Resick’s findings may suggest that CPT, a cognitive therapy, works in a different manner than PE (i.e., CPT works directly top down, and PE acts bottom up through extinction with an eventual effect on cognitions). The findings of the moderated mediation analyses did not support differences in the relationship between PTSD and depression in the more exposure-based, WA component of CPT. This finding differs from the results from the one existing investigation of relationships of change in PTSD and depression during PE (Aderka et al., 2011). This lack of moderated mediation may be due to low power associated with the size of the study sample. However, the WA condition in this dismantling trial also was not designed to be representative of exposure-based treatments for PTSD. Instead, the WA condition was designed to evaluate the effectiveness of this unique component of the CPT protocol. The WA condition consisted of repeated writing and reading of trauma accounts, which may function differently than the imaginal and in vivo exposure techniques used in PE (Foa, Hembree, & Rothbaum, 2007). In addition, research with the written disclosure paradigm suggests that the process of writing about a trauma may promote cognitive adaptation and organization in addition to producing exposure-based effects (e.g., Park & Blumberg, 2002; Pennebaker, 1997; Sloan & Marx, 2004; Smyth, True, & Souto, 2001). Thus, lack of a differential relationship between changes in PTSD and depression within the WA condition also could be due to greater


associated cognitive change with writing-based exposure techniques. Alternatively, it is possible that the WA condition provided a smaller dose of exposure than is included in PE (Foa et al., 2007), thereby attenuating any differential relationship between the two disorders that might be found with more exposure-based treatments. Interpretation of this study’s moderated mediation results is complicated by differences in efficacy and schedule of treatment administration across the three CPT components examined in the dismantling trial (Resick, Galovski, et al., 2008). This differentiation in PTSD treatment efficacy and scheduling cannot be eliminated as a factor that may have influenced findings related to the presence or absence of differences across WA, CPT, and CPT-C. Furthermore, our study sample included participants who completed at least one treatment session but may have attended differing numbers of treatment sessions. Thus, study results may have been affected by participants who received only a few sessions of treatment. In addition, as discussed above, low power in these analyses may have undermined our ability to find significant differences in the relationship of change between PTSD and depression across the treatment components. Overall, results from the moderated mediation analyses were mixed and may have been influenced by any or all of the factors reviewed above. As a result, these findings should be interpreted cautiously, and future studies with larger sample sizes are needed to clarify results. In sum, results from this investigation documented a significant association between changes in PTSD and depression during the course of CPT and its treatment components and suggested that changes in these two outcomes occurred at the same time. These findings diverged from the one existing study examining the relationship between changes in these disorders during PE (e.g., Aderka et al., 2011). This discrepancy is noteworthy. However, given the numerous differences between these studies and possible differences in mechanism of change, clear conclusions cannot be drawn regarding the presence of distinct relationships of change among PTSD and depression symptoms during different trauma-focused psychotherapies. Future research is needed to directly compare potential differences in these relationships during CPT and PE. This will provide a more complete conceptualization of the interrelationship of PTSD and depression during the course of different therapies. Future research in this area will enhance our understanding of the mechanisms of action for various PTSD interventions and improve current treatments for the common and debilitating co-occurrence of these two disorders (e.g., Blanchard et al., 1998; Kessler et al., 1995).

References Aderka, I. M., Foa, E. B., Applebaum, E., Shafran, N., & GilboaSchechtman, E. (2011). Direction of influence between posttraumatic and depressive symptoms during prolonged exposure therapy among children and adolescents. Journal of Consulting and Clinical Psychology, 79, 421– 425. doi:10.1037/a0023318 Ahrens, J., & Rexford, L. (2002). Cognitive processing therapy for incarcerated adolescents with PTSD. Journal of Aggression, Maltreatment & Trauma, 6, 201–216. doi:10.1300/J146v06n01_10 American Psychiatric Association. (1994). Diagnostic and statistical manual of mental disorders (4th ed.). Washington, DC: Author.

965

American Psychiatric Association. (2000). Diagnostic and statistical manual of mental disorders (4th ed., text rev.). Washington, DC: Author. Bauer, D. J., Preacher, K. J., & Gil, K. M. (2006). Conceptualizing and testing random indirect effects and moderated mediation in multilevel models: New procedures and recommendations. Psychological Methods, 11, 142–163. doi:10.1037/1082-989X.11.2.142 Beck, A. T. (1976). Cognitive therapy and the emotional disorders. New York, NY: International Universities Press. Beck, A. T., Rush, A. J., Shaw, B. F., & Emery, G. (1979). Cognitive therapy of depression. New York, NY: Guilford Press. Beck, A. T., Steer, R. A., Ball, R., & Ranieri, W. F. (1996). Comparison of Beck Depression Inventories–IA and –II in psychiatric outpatients. Journal of Personality Assessment, 67, 588 –597. doi:10.1207/ s15327752jpa6703_13 Beck, A. T., Steer, R. A., & Brown, G. K. (1996). Beck Depression Inventory manual (2nd ed.). San Antonio, TX: Psychological Corporation. Blake, D. D., Weathers, F. W., Nagy, L. M., Kaloupek, D. G., Gusman, F. D., Charney, D. S., & Keane, T. M. (1995). The development of a clinician-administered PTSD scale. Journal of Traumatic Stress, 8, 75–90. doi:10.1002/jts.2490080106 Blake, D. D., Weathers, F., Nagy, L. M., Kaloupek, D. G., Klauminzer, G., Charney, D. S., & Keane, T. M. (1990). A clinician rating scale for assessing current and lifetime PTSD: The CAPS-1. Behavior Therapist, 13, 187–188. Blanchard, E. B., Buckley, T. C., Hickling, E. J., & Taylor, A. E. (1998). Posttraumatic stress disorder and comorbid major depression: Is the correlation an illusion? Journal of Anxiety Disorders, 12, 21–37. doi: 10.1016/S0887-6185(97)00047-9 Breslau, N., Davis, G. C., Peterson, E. L., & Schultz, L. (1997). Psychiatric sequelae of posttraumatic stress disorder in women. Archives of General Psychiatry, 54, 81– 87. doi:10.1001/archpsyc.1997.01830130087016 Breslau, N., Davis, G. C., Peterson, E. L., & Schultz, L. R. (2000). A second look at comorbidity in victims of trauma: The posttraumatic stress disorder–major depression connection. Biological Psychiatry, 48, 902–909. doi:10.1016/S0006-3223(00)00933-1 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 Ehring, T., Kleim, B., Clark, D. M., Foa, E. B., & Ehlers, A. (2007). Screening for posttraumatic stress disorder: What combination of symptoms predicts best? Journal of Nervous and Mental Disease, 195, 1004 – 1012. doi:10.1097/NMD.0b013e31815c1999 Erickson, D. J., Wolfe, J., King, D. W., King, L. A., & Sharkansky, E. J. (2001). Posttraumatic stress disorder and depression symptomatology in a sample of Gulf War veterans: A prospective analysis. Journal of Consulting and Clinical Psychology, 69, 41– 49. doi:10.1037/0022006X.69.1.41 First, M. B., Spitzer, R. L., Gibbon, M., & Williams, J. (1996). Structured Clinical Interview for DSM–IV Axis I Disorders—Patient Edition (SCID-I/P, Version 2.0). New York: Biometrics Research Department, New York State Psychiatric Institute. Foa, E. B. (1995). Posttraumatic Stress Diagnostic Scale manual. Minneapolis, MN: National Computer Systems. Foa, E. B., Cashman, L., Jaycox, L., & Perry, K. (1997). The validation of a self-report measure of posttraumatic stress disorder: The Posttraumatic Diagnostic Scale. Psychological Assessment, 9, 445– 451. doi:10.1037/ 1040-3590.9.4.445 Foa, E. B., Hembree, E. A., Cahill, S. P., Rauch, S. M., Riggs, D. S., Feeny, N. C., & Yadin, E. (2005). Randomized trial of prolonged exposure for posttraumatic stress disorder with and without cognitive restructuring: Outcome at academic and community clinics. Journal of Consulting and Clinical Psychology, 73, 953–964. doi:10.1037/0022-006X.73.5.953

966


Foa, E. B., Hembree, E. A., & Rothbaum, B. (2007). Prolonged exposure therapy for PTSD: Emotional processing of traumatic experiences: Therapist guide. New York, NY: Oxford University Press. Franklin, C. L., & Zimmerman, M. (2001). Posttraumatic stress disorder and major depressive disorder: Investigating the role of overlapping symptoms in diagnostic comorbidity. Journal of Nervous and Mental Disease, 189, 548 –551. doi:10.1097/00005053-200108000-00008 Gallagher, M. W., & Resick, P. A. (2011). Mechanisms of change in cognitive processing therapy and prolonged exposure therapy for PTSD: Preliminary evidence for the differential effects of hopelessness and habituation. Cognitive Therapy and Research. Advance online publication. doi:10.1007/s10608-011-9423-6 Gradus, J. L., Qin, P., Lincoln, A. K., Miller, M., Lawler, E., Sorensen, H. T., & Lash, T. L. (2010). Posttraumatic stress disorder and completed suicide. American Journal of Epidemiology, 171, 721–727. doi:10.1093/ aje/kwp456 Grant, D. M., Beck, J., Marques, L., Palyo, S. A., & Clapp, J. D. (2008). The structure of distress following trauma: Posttraumatic stress disorder, major depressive disorder, and generalized anxiety disorder. Journal of Abnormal Psychology, 117, 662– 672. doi:10.1037/a0012591 Hofmann, S. G., Meuret, A. E., Rosenfield, D., Suvak, M. K., Barlow, D. H., Gorman, J. M., . . . Woods, S. W. (2007). Preliminary evidence for cognitive mediation during cognitive– behavioral therapy of panic disorder. Journal of Consulting and Clinical Psychology, 75, 374 –379. doi:10.1037/0022-006X.75.3.374 Kenny, D. A., Korchmaros, J. D., & Bolger, N. (2003). Lower level mediation in multilevel models. Psychological Methods, 8, 115–128. doi:10.1037/1082-989X.8.2.115 Kessler, R. C. (2000). Posttraumatic stress disorder: The burden to the individual and to society. Journal of Clinical Psychiatry, 61(Suppl. 5), 4 –12. Kessler, R. C., Berglund, P., Demler, O., Jin, R., Koretz, D., Merikangas, K. R., . . . Wang, P. S. (2003). The epidemiology of major depressive disorder: Results from the National Comorbidity Survey Replication (NCS-R). JAMA: Journal of the American Medical Association, 289, 3095–3105. doi:10.1001/jama.289.23.3095 Kessler, R. C., Sonnega, A., Bromet, E., Hughes, M., & Nelson, C. B. (1995). Posttraumatic stress disorder in the National Comorbidity Survey. Archives of General Psychiatry, 52, 1048 –1060. doi:10.1001/ archpsyc.1995.03950240066012 King, D. W., King, L. A., McArdle, J. J., Shalev, A. Y., & Doron-LaMarca, S. (2009). Sequential temporal dependencies in associations between symptoms of depression and posttraumatic stress disorder: An application of bivariate latent difference score structural equation modeling. Multivariate Behavioral Research, 44, 437– 464. doi:10.1080/ 00273170903103308 Kirk, R. E. (1996). Practical significance: A concept whose time has come. Educational and Psychological Measurement, 56, 746 –759. doi: 10.1177/0013164496056005002 MacKinnon, D. P., Fritz, M. S., Williams, J., & Lockwood, C. M. (2007). Distribution of the product confidence limits for the indirect effect: Program PRODLIN. Behavior Research Methods, 39, 384 –389. doi: 10.3758/BF03193007 MacKinnon, D. P., Lockwood, C. M., Hoffman, J. M., West, S. G., & Sheets, V. (2002). A comparison of methods to test mediation and other intervening variable effects. Psychological Methods, 7, 83–104. doi: 10.1037/1082-989X.7.1.83 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

Park, C. L., & Blumberg, C. (2002). Disclosing trauma through writing: Testing the meaning-making hypothesis. Cognitive Therapy and Research, 26, 597– 616. doi:10.1023/A:1020353109229 Pennebaker, J. W. (1997). Writing about emotional experiences as a therapeutic process. Psychological Science, 8, 162–166. doi:10.1111/j .1467-9280.1997.tb00403.x Raudenbush, S. W., & Bryk, A. S. (2002). Hierarchical linear models: Applications and data analysis methods (2nd ed.). Newbury Park, CA: Sage. Raudenbush, S. W., Bryk, A. S., & Congdon, R. (2005). HLM 6.0: Hierarchical linear modeling. Lincolnwood, IL: Scientific Software International. Resick, P. A. (2001). Cognitive therapy for posttraumatic stress disorder. Journal of Cognitive Psychotherapy, 15, 321–329. Resick, P. A., Galovski, T. E., Uhlmansiek, M., Scher, C. D., Clum, G. A., & Young-Xu, Y. (2008). A randomized clinical trial to dismantle components of cognitive processing therapy for posttraumatic stress disorder in female victims of interpersonal violence. Journal of Consulting and Clinical Psychology, 76, 243–258. doi:10.1037/0022-006X.76.2.243 Resick, P. A., Monson, C. M., & Chard, K. M. (2008). Cognitive processing therapy: Veteran/military version. Washington, DC: Department of Veterans Affairs. 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 Spectrums, 8, 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 treatment 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. K. (1993). Cognitive processing therapy for rape victims: A treatment manual. Thousand Oaks, CA: Sage. Savoca, E., & Rosenheck, R. (2000). The civilian labor market experiences of Vietnam-era veterans: The influence of psychiatric disorders. Journal of Mental Health Policy and Economics, 3, 199 –207. doi:10.1002/mhp .102 Schulz, P. M., Resick, P. A., Huber, L., & Griffin, M. G. (2006). The effectiveness of cognitive processing therapy for PTSD with refugees in a community setting. Cognitive and Behavioral Practice, 13, 322–331. doi:10.1016/j.cbpra.2006.04.011 Shalev, A. Y., Freedman, S., Peri, T., Brandes, D., Sahar, T., Orr, S. P., & Pitman, R. K. (1998). Prospective study of posttraumatic stress disorder and depression following trauma. American Journal of Psychiatry, 155, 630 – 637. Shalev, A. Y., Videlock, E. J., Peleg, T., Segman, R., Pitman, R. K., & Yehuda, R. (2008). Stress hormones and post-traumatic stress disorder in civilian trauma victims: A longitudinal study. Part I: HPA axis responses. International Journal of Neuropsychopharmacology, 11, 365– 372. doi:10.1017/S1461145707008127 Simms, L. J., Watson, D., & Doebbeling, B. N. (2002). Confirmatory factor analyses of posttraumatic stress symptoms in deployed and nondeployed veterans of the Gulf War. Journal of Abnormal Psychology, 111, 637– 647. doi:10.1037/0021-843X.111.4.637 Simon, G. E. (2003). Social and economic burden of mood disorders. Biological Psychiatry, 54, 208 –215. doi:10.1016/S00063223(03)00420-7 Singer, J. D., & Willett, J. B. (2003). Applied longitudinal data analysis: Modeling change and event occurrence. New York, NY: Oxford University Press. Sloan, D. M., & Marx, B. P. (2004). Taking pen to hand: Evaluating theories underlying the written disclosure paradigm. Clinical Psychology: Science and Practice, 11, 121–137. doi:10.1093/clipsy.bph062

CHANGES IN PTSD AND DEPRESSION DURING CPT Smyth, J., True, N., & Souto, J. (2001). Effects of writing about traumatic experiences: The necessity for narrative structuring. Journal of Social and Clinical Psychology, 20, 161–172. doi:10.1521/jscp.20.2.161.22266 Suvak, M. K., Walling, S. M., Iverson, K. M., Taft, C. T., & Resick, P. A. (2009). Multilevel regression analyses to investigate the relationship between two variables over time: Examining the longitudinal association between intrusion and avoidance. Journal of Traumatic Stress, 22, 622– 631. Tein, J.-Y., Sandler, I. N., MacKinnon, D. P., & Wolchik, S. A. (2004). How did it work? Who did it work for? Mediation in the context of a moderated prevention effect for children of divorce. Journal of Consult-

967

ing and Clinical Psychology, 72, 617– 624. doi:10.1037/0022-006X.72 .4.617 Walker, E. A., Katon, W., Russo, J., Ciechanowski, P., Newman, E., & Wagner, A. W. (2003). Health care costs associated with posttraumatic stress disorder symptoms in women. Archives of General Psychiatry, 60, 369 –374. doi:10.1001/archpsyc.60.4.369

Received June 15, 2011 Revision received July 24, 2012 Accepted July 25, 2012 䡲

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