Running head: DISSOCIATION AND PTSD TREATMENT
1
Supplemental Materials
The Influence of the Dissociative Subtype of Posttraumatic Stress Disorder on Treatment
Efficacy in Female Veterans and Active Duty Service Members
by E. J. Wolf et al., 2015, Journal of Consulting & Clinical Psychology
http://dx.doi.org/10.1037/ccp0000036
The Influence of the Dissociative Subtype of Posttraumatic Stress Disorder
on Treatment Efficacy in Female Veterans and Active Duty Service Members
Erika J. Wolf
National Center for PTSD at VA Boston Healthcare System, Boston, MA
Boston University School of Medicine, Department of Psychiatry, Boston, MA
Carole A. Lunney
National Center for PTSD, White River Junction, VT
Paula P. Schnurr
National Center for PTSD, White River Junction, VT
Department of Psychiatry, Geisel School of Medicine at Dartmouth, Hanover, NH
Acknowledgements: The data reported in this article were drawn from grant CSP #494 from the
VA Cooperative Studies Program with support from the Department of Defense for CSP #494.
This work was also supported by a Career Development Award to Erika J. Wolf from the United
States (U.S.) Department of Veterans Affairs, Clinical Sciences Research and Development
Program. The contents of this manuscript do not represent the views of the U.S. Department of
Veterans Affairs, the Department of Defense, or the United States Government.
Corresponding Author (for publication): Paula P. Schnurr, National Center for PTSD (116D),
VA Medical Center, White River Junction, VT 05009. E-mail: paula.schnurr@dartmouth.edu
DISSOCIATION AND PTSD TREATMENT
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Abstract
Objective: A dissociative subtype of posttraumatic stress disorder (PTSD) was recently
added to the Diagnostic and Statistical Manual-5 (American Psychiatric Association, 2013) and
is thought to be associated with poor PTSD treatment response. Method: We used latent growth
curve modeling to examine data from a randomized controlled trial of Prolonged Exposure and
Present-Centered Therapy for PTSD in a sample of 284 female veterans and active duty service
members with PTSD to test the association between the dissociative subtype and treatment
response. Results: Individuals with the dissociative subtype (defined using latent profile
analysis) had a flatter slope (p = .008) compared to those with high PTSD symptoms and no
dissociation such that the former group showed, on average, a 9.75 (95% CI = -16.94 to -2.57)
lesser decrease in PTSD severity scores on the Clinician Administered PTSD Scale (Blake et al.,
1995) over the course of the trial. However, this effect was small in magnitude. Dissociative
symptoms decreased markedly among those with the subtype, though neither treatment explicitly
addressed such symptoms. There were no differences as a function of treatment type.
Conclusions: Results raise doubt about the common clinical perception that exposure therapy is
not effective or appropriate for individuals who have PTSD and dissociation and provide
empirical support for the use of exposure treatment for individuals with the dissociative subtype
of PTSD.
Public Health Significance. This study found that female veterans and active duty service
members with the dissociative subtype of posttraumatic stress disorder (PTSD) did not respond
as well to PTSD treatment with Prolonged Exposure or Present-Centered Therapy as did those
without the subtype. However, both PTSD and dissociation symptoms did improve markedly in
DISSOCIATION AND PTSD TREATMENT
the dissociative group, suggesting that the dissociative subtype is not a contraindication for the
use of empirically supported treatments for PTSD.
Keywords. Dissociative subtype, PTSD, latent growth curve, treatment response.
3
DISSOCIATION AND PTSD TREATMENT
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The Influence of the Dissociative Subtype of Posttraumatic Stress Disorder
on Treatment Efficacy in Female Veterans and Active Duty Service Members
The dissociative subtype of posttraumatic stress disorder (PTSD) was added to the 5th
edition of the Diagnostic and Statistical Manual (DSM-5, American Psychiatric Association
[APA], 2013) based on evidence that a discrete subgroup of approximately 15%-30% of
individuals with PTSD show marked symptoms of derealization and depersonalization. The
subtype is defined in the DSM as meeting full criteria for PTSD and showing comorbid and
“persistent or recurrent” symptoms of derealization (i.e., experiencing the world as unreal or
dreamlike) and/or depersonalization (i.e., feeling as if one’s physical body is disconnected from
the self; APA, 2013). The inclusion of the subtype in the DSM may yield new insight into the
understanding of the pathophysiology and treatment of the disorder. In particular, a precise
definition of dissociation in PTSD should help to reliably parse the heterogeneity in the
presentation of the disorder into more homogenous subgroups; this is important for studying the
etiology, course, and treatment of the disorder as unmeasured heterogeneity in the measurement
of PTSD would likely obscure such associations. The codification of the subtype may also aid in
clinical assessment, case conceptualization, and treatment planning as individuals with these low
prevalence but highly salient symptoms can be reliably identified. The subtype is thought to
negatively influence responses to exposure-based PTSD treatment (Lanius et al., 2010) because,
by definition, exposure therapy requires experiencing and processing of trauma-related emotions
and individuals who dissociate would not be expected to access and attend to trauma-related
emotions. Further, dissociation is often considered a contraindication for exposure-based
treatment for the disorder (Becker, Zayfert, & Anderson, 2004). Despite this perception, there is
only limited evidence to suggest that dissociation negatively influences response to exposure
DISSOCIATION AND PTSD TREATMENT
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therapy (Ehlers, Hackmann & Clark, 2006; Hagenaars, van Minnen, & Hoogduin, 2010;
Halvorsen, Stenmark, Neuner, & Nordahl, 2014; Price, Kearns, Houry, & Rothbaum, 2014). The
primary aim of this study was to examine if the dissociative subtype affects PTSD treatment
efficacy using data from a large, randomized controlled trial of Prolonged Exposure (PE) therapy
for PTSD in a sample of female veterans and active duty service members (Schnurr et al., 2007).
Psychometric research has provided strong and consistent evidence for the dissociative
subtype of PTSD. Specifically, Wolf, Miller et al. (2012) followed by Wolf, Lunney et al.
(2012) used latent profile analysis (LPA), a type of latent variable modeling which identifies
homogenous subgroups of individuals from a heterogeneous sample on the basis of an
unobserved (i.e., latent) characteristic, to evaluate the underlying structure of PTSD and
dissociative symptom comorbidity. They demonstrated that when symptoms of PTSD and
dissociation were submitted to the LPA, three clear classes emerged: a group defined by low or
moderate PTSD symptom severity and low scores on dissociation; a group defined by high
PTSD symptom severity and low scores on dissociation; and a group defined by equally high
PTSD symptom severity and comorbid high scores on dissociation, particularly on symptoms
reflecting derealization and depersonalization. This basic pattern of results has now been found
in male and female veterans and service members (Armour, Karstoft, & Richardson, 2014; Wolf,
Lunney et al., 2012; Wolf, Miller et al., 2012), trauma-exposed civilians, including sexual assault
survivors (Armour, Elklit, Lauterbach, & Elhai, 2014; Steuwe et al., 2012), and trauma-exposed
college students (Blevins et al., 2014), with subtype estimates ranging from approximately 15%30%. Additional research suggests that the subtype can be identified across many different
continents, countries, and cultures—an evaluation of symptoms of derealization and
depersonalization among individuals with PTSD using data from the World Mental Health
DISSOCIATION AND PTSD TREATMENT
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surveys found that approximately 15% of those with PTSD also exhibited these dissociative
symptoms (Stein et al., 2013).
Dissociation is theorized to negatively impact activation of the fear network (van
Minnen, Harned, Zoellner, & Mills, 2012), which is the presumed mechanism of action in
exposure-based treatments for PTSD, such as PE. This has led some investigators to hypothesize
that dissociation may negatively impact efficacy of exposure-based treatment (Lanius et al.,
2010) and this is consistent with research suggesting that 51% of clinicians consider dissociation
a contraindication for PE (Becker et al., 2004). Dissociation may also interfere with the efficacy
of cognitive and narrative therapies for PTSD, including Cognitive Processing Therapy, as
dissociation would be expected to impair the ability to generate, attend to, and retain restructured
trauma-related cognitions and may also interfere with access to trauma-related memories when
engaged in writing trauma narratives. However, the data do not support these hypotheses at
present. Rather, research to date suggests that there are either no effects of dissociation on
treatment responsiveness (exposure or cognitive therapy), or, at best, very subtle effects (Cloitre,
Petkova, Wang, & Lu, 2012; Ehlers et al., 2006; Hagenaars et al.,, 2010; Halvorsen et al., 2014;
Price et al.,2014; Resick, Suvak, Johnides, Mitchell, & Iverson, 2012). In one of the first studies
to systematically examine the effects of dissociation on PTSD treatment response, Hagenaars,
van Minnen, and Hoogduin (2010) reported no influence of dissociation on response to PE in a
sample of 71 Dutch participants with mixed trauma histories. Although individuals with high
levels of dissociation tended to have high levels of PTSD at pre and post-treatment, their rate of
symptom improvement did not differ as a function of baseline dissociation symptoms. There was
also no effect of dissociation on treatment drop-out. Similarly, Halvorsen, Stenmark, Neuner,
and Nordahl (2014) reported no effect of symptoms of derealization and depersonalization on
DISSOCIATION AND PTSD TREATMENT
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PTSD treatment response to Narrative Exposure Therapy or treatment as usual in a sample of 81
refugees and asylum-seekers with PTSD. Speckens, Ehlers, Hackmann and Clark (2006) also
found no effect of dissociation on the efficacy of imaginal reliving administered as part of one of
two randomized controlled trials of cognitive therapy for PTSD in a sample of 44 individuals
with PTSD secondary to a variety of trauma types.
To our knowledge, only three studies have provided modest evidence that dissociation is
associated with response to PTSD treatment, although not necessarily poor treatment response.
Cloitre, Petkova, Wang, and Lu (2012) analyzed data from a randomized controlled trial of Skills
Training in Affective and Interpersonal Regulation (STAIR) and Narrative Story Telling (NST)
in a sample of 104 women with childhood-abuse related PTSD. They found no overall effect of
baseline dissociation (including symptoms of derealization, depersonalization, and amnesia) on
change in PTSD symptoms in response to treatment. However, participants with high posttreatment dissociation who had completed the combined STAIR/NST treatment fared better
(showed greater PTSD symptom decline at three and six-month follow-ups) than did individuals
with high post-treatment dissociation who completed either of the other treatment conditions
(STAIR and supportive counseling or NST and supportive counseling). Neither the baseline nor
the post-treatment high dissociation groups differed from the baseline or post-treatment low
dissociation groups, respectively, on PTSD treatment response except that the group with high
baseline dissociation was less likely than the group with low baseline dissociation to drop out of
treatment.
Resick, Suvak, Johnides, Mitchell, and Iverson (2012) also reported a subtle effect of
dissociation on PTSD treatment response. They re-analyzed data from a randomized controlled
trial of Cognitive Processing Therapy (CPT) in 150 women with PTSD related to physical or
DISSOCIATION AND PTSD TREATMENT
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sexual abuse who received either the full course of CPT, a modified course of CPT which
included only the cognitive therapy without the written trauma account (CPT-C), or the written
trauma account only without cognitive therapy. They reported that there was no overall effect of
dissociation on PTSD symptom decline but when treatment type was taken into consideration,
individuals with high levels of dissociation showed faster PTSD symptom improvement if they
were assigned to the full CPT treatment as compared to CPT-C. Though the rate at which PTSD
symptoms changed differed as a function of treatment type and dissociation, there was no overall
difference in the amount of change over time—those with high dissociation symptoms in CPT or
CPT-C showed the same amount of change overall. As with Cloitre et al., (2012), the differences
reported by Resick et al. (2012) were among those with high levels of dissociation and not
between those with high versus low levels of dissociation.
Finally, Price, Kearns, Houry, and Rothbaum (2014) studied 137 individuals who were
assigned to either an exposure-based treatment or an assessment-only condition in the immediate
aftermath of trauma exposure and followed them for 12 weeks. They found dissociation at the
start of the exposure treatment was associated with greater PTSD symptom severity at the 12week follow-up (i.e., dissociation was associated with poorer PTSD treatment response); this
effect was not observed in the assessment-only condition. Further, dissociation explained a
majority of the variance in the presence/absence of the PTSD diagnosis at the 12-week followup. However, interpretation of these effects is made difficult because the investigators did not
measure baseline PTSD symptoms, and therefore could not adjust for baseline symptoms in the
analyses of 12-week follow-up symptoms. This makes it unclear if the effect was specific to
dissociative symptoms or perhaps driven by higher baseline PTSD symptoms in the group with
DISSOCIATION AND PTSD TREATMENT
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dissociation; high baseline PTSD symptoms would likely be related to high follow-up symptom
severity.
Some studies have also examined the reverse question—that is, do symptoms of
dissociation improve in response to PTSD treatment? Cloitre et al. (2012) demonstrated that
high dissociation symptoms at baseline tended to be associated with high dissociation symptoms
during and after PTSD treatment but also found that this effect was moderated by treatment type
such that those assigned to the double active treatment condition (STAIR/NST) had a faster rate
of dissociation symptom improvement as well as greater overall reductions in dissociation.
Resick et al. (2012) reported significant improvement in dissociation symptoms over time, which
did not differ as a function of treatment group, and Hagenaars et al. (2010) also reported that
dissociation symptoms improved with treatment. Thus, although the evidence for dissociation
negatively impacting PTSD symptom change in response to treatment is fairly weak, there is
stronger evidence for the notion that PTSD treatment ameliorates symptoms of dissociation.
One caveat to this line of work is that it is difficult to interpret null findings since these
may be a function of methodological and statistical factors or sample-specific associations in the
data. None of the studies reviewed above were designed for the purpose of evaluating predictors
of treatment response, which would require a randomized controlled trial to be adequately
powered to test dissociation X time or dissociation X time X treatment type interaction effects.
This is important, as interaction effects are typically small in magnitude and require large
samples to have sufficient power to observe. The majority of the studies to date have included
fairly small samples (with Resick et al., 2012, employing the largest sample at n = 150, divided
across 3 conditions). In addition, studies have not examined the effect of the dissociative
subtype specifically, and instead have tended to examine the effect of dissociation symptoms
DISSOCIATION AND PTSD TREATMENT
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generally (i.e., not limited to the symptoms of derealization and depersonalization which define
the subtype in DSM-5) on treatment response. Given these concerns, it remains unclear if
dissociation truly does not influence the efficacy of empirically supported PTSD treatment or if
the lack of a significant effect of dissociation on treatment response is simply due to limited
statistical power or how dissociation has been defined.
Aims and Hypotheses
The primary aim of this study was to examine if the dissociative subtype of PTSD was
associated with differential PTSD symptom response to treatment in a sample of female service
members and Veterans. A second aim was to evaluate how dissociative symptoms changed
among those with the subtype in response to PTSD treatment. We evaluated these aims in a
dataset that we have previously employed to test the latent structure of dissociation and PTSD.
Specifically, using data from a large, randomized clinical trial of PE versus Present-Centered
Therapy (PCT) for the treatment of PTSD among military women (Schnurr et al., 2007), we
previously conducted LPAs of the 17 DSM-IV (APA, 1994) PTSD symptoms and four items
indexing derealization and depersonalization, as measured at the baseline assessment for the
clinical trial (Wolf, Lunney et al., 2012). Approximately 30% of the sample was assigned to the
high PTSD and dissociative class in that study. To extend this work, we retained most likely
class assignment from the best fitting LPA solution (i.e., the moderate PTSD, high PTSD, or
high PTSD and high dissociation groups) and used class membership as a predictor of PTSD
symptoms and PTSD symptom change over time using latent growth curve modeling. We
hypothesized that the dissociative subtype would be associated with poorer response to treatment
as defined by less PTSD symptom improvement (i.e., a flatter slope) relative to the moderate and
high PTSD groups. Given concerns (van Minnen et al., 2012) that individuals who dissociate
DISSOCIATION AND PTSD TREATMENT
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may not be able to engage in and benefit from treatments grounded in emotional exposure and
processing (i.e., PE), we tested if treatment type (PE versus PCT) interacted with the subtype to
predict PTSD treatment response. As the literature is inconclusive regarding this, we did not
advance any specific hypotheses about this possible interaction. Based on the research to date
(Cloitre et al., 2012; Hagenaars et al., 2010; Resick et al., 2012), we hypothesized that
dissociative symptoms would improve among those with the subtype in response to PTSD
treatment and we also tested if this effect differed by treatment condition.
Method
Participants
Participants were 284 female veterans (n = 277) and active-duty service members (n = 7)
who participated in a multi-site (n = 12) randomized clinical trial of PE for PTSD (Schnurr et al.,
2007). Inclusion criteria were current PTSD according to DSM-IV criteria, a clear memory of
the index trauma, three or more months since trauma exposure, agreement to not receive other
psychotherapy for PTSD during the study, and (for those on psychoactive medication) a stable
regimen of at least 2 months. Exclusion criteria were substance dependence within the last 3
months; current psychotic symptoms, mania, or bipolar disorder; prominent current suicidal or
homicidal ideation; cognitive impairment; current involvement in a violent relationship; or selfmutilation within the past 6 months.
Mean age of participants was 44.79 (SD = 9.44, range 22–78). Just under a third of
participants (n = 90) were married or living as married. Almost half (45.4%, n = 129) selfidentified as a non-White minority. Most participants (89.1%, n = 253) had more than a high
school education. Almost 40% (n = 111) of participants were working full- or part-time and
22.7% (n = 63) had an approved VA PTSD service-connected disability. The overwhelming
DISSOCIATION AND PTSD TREATMENT
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majority of the sample had been exposed to sexual assault (93.0%). Data were available from
235 participants at immediate post-treatment, 232 participants at 3-month follow-up and from
229 participants at six-month follow-up. Participants were not removed from the study if they
missed an assessment.1
Measures
PTSD diagnosis and PTSD symptom severity were assessed using the ClinicianAdministered PTSD Scale (CAPS; Blake et al., 1995), the gold-standard structured clinical
interview for the assessment of PTSD. Each DSM-IV PTSD criterion is rated on frequency and
intensity scales that range from 0 to 4. For each PTSD symptom, severity is computed as the
sum of the frequency and intensity rating, and overall severity is calculated as the sum of
severity scores across all 17 symptoms. A diagnosis on the CAPS was indicated by a total
severity score of 45 or greater plus endorsement of the requisite DSM-IV PTSD symptom cluster
criteria (i.e., 1 reexperiencing symptom, 3 avoidance and numbing symptoms, and 2
hyperarousal symptoms) each at a frequency of 1 or greater and an intensity of 2 or greater
(Weathers, Ruscio, & Keane, 1999) . Inter-rater reliability for CAPS severity scores as
determined by having a second rater listen to the audiotape recordings of a randomly selected
12.5% of the interviews yielded an intraclass correlation coefficient of 0.92.
Dissociation was measured using four derealization and depersonalization items from the
Dissociation scale of the Trauma Symptom Inventory (TSI; Briere, 1995), a self-report
questionnaire that assesses PTSD symptoms and associated features experienced during the past
6 months on a scale from 0 (never) to 3 (often). A composite measure of dissociation was
computed by taking the mean of the following four TSI items: “feeling like you were outside of
your body”; “feeling like you were watching yourself from far away”; “feeling like things
DISSOCIATION AND PTSD TREATMENT
13
weren’t real”; and “feeling like you were in a dream.” These four items were used by Wolf,
Lunney et al. (2012) to define the dissociative subtype in the prior latent profile analysis of
PTSD and dissociation.
Procedure
At each site, an institutional review board approved the study protocol. Participants gave
written informed consent prior to enrollment. A master’s- or doctoral-level assessor, blinded to
treatment assignment, performed assessments before and after treatment and at 3- and 6-month
follow-up appointments. All therapy sessions were videotaped and reviewed by supervisors who
provided weekly phone supervision; group calls with master supervisors also were employed to
maintain treatment fidelity.
Participants were randomly assigned to either PE (n = 141) or PCT (n = 143). Both
therapies consisted of 10 weekly 90-minute sessions, conducted by a master’s- or doctoral-level
clinician experienced in treating women with PTSD. PE included education about common
reactions to trauma, imaginal exposure, homework (listening to a recording of the recounting
made during the therapy session and repeated in vivo exposure to safe situations the patient
avoided because of trauma-related fear), and discussion of thoughts and feelings related to
exposure exercises. PCT focused on current life problems as manifestations of PTSD. Initial
sessions focused on discussing and reviewing general daily difficulties; subsequent sessions
reviewed accomplishments made during therapy, and made plans for the future. No instructions
for exposure or cognitive restructuring were given. We have previously reported that there were
no significant trauma exposure or demographic differences among the treatment groups and no
site or therapist treatment effects; see Wolf, Lunney et al. (2012) for additional details about this
and the procedure, including response rates and attrition.
DISSOCIATION AND PTSD TREATMENT
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Data Analyses
We retained most likely class assignment in the Moderate PTSD, High PTSD, or High
PTSD and Dissociation classes from the latent profile analysis described in Wolf, Lunney et al.
(2012) for use as covariates in latent growth curve models examining PTSD and dissociation
symptom change over time as a function of latent class assignment. Specifically, we created two
dummy-coded variables (one reflecting membership in the Moderate PTSD class versus the High
PTSD and Dissociative class and one reflecting membership in the High PTSD class versus the
High PTSD and Dissociative class, with the latter as the reference group) and specified these two
variables as predictors of the latent intercept and slope factors included in the analysis. We have
previously demonstrated (see Wolf, Lunney et al., 2012) that these groups differed only with
respect to race (minority status) and not with respect to other demographic or trauma exposure
variables. Therefore, secondary analyses included minority status as covariate of latent class
membership. As the shape of change over time (e.g., linear or quadratic slope) was not a focus
of this research and because we did not expect the shape of change to be equivalent across all
assessment time points (spaced at 3 month intervals), we fixed the first and last slope loadings
(baseline and Month 6) and freely estimated those for the assessments at Months 0 and 3. In
subsequent analyses designed simply to obtain estimated means from the model at Months 0 and
3, we fixed the baseline and Month 0 (and, separately, the baseline and Month 3) loadings so as
to estimate change over these time points. We also examined the potential moderating effect of
treatment type on change in symptoms for each group by computing interaction terms (e.g.,
Moderate vs. High PTSD and Dissociation class X Treatment Type) and included these
interaction terms as additional predictors of the intercept and slope factors. These analyses were
conducted separately for the CAPS severity scores and the derealization/depersonalization item
DISSOCIATION AND PTSD TREATMENT
15
mean scores (on the same four items used to define the subtype in Wolf, Lunney et al., 2012) in
parallel analyses. We also examined if the groups differed in terms of loss or retention of PTSD
diagnosis over time using logistic regression and in terms of the amount of treatment received as
a function of class membership (and class membership X treatment type) using chi-square and
ANOVAs, as appropriate. For all analyses, we compared the dissociative class to the moderate
and high PTSD classes, though the primary comparison of interest was that between the
dissociative class and the high PTSD class because differences between these groups can be
attributed to dissociation. In contrast, the dissociative class differed substantially from the
moderate PTSD group on both dissociation and PTSD severity, making it impossible to
determine if group differences in treatment trajectory was a function of dissociation, PTSD
severity, or both. All latent variable analyses were conducted with the Mplus 7.0 statistical
modeling software (Muthén & Muthén, 2012) using maximum likelihood estimation. Missing
data were modeled directly; the maximum amount of missing data on variables submitted to the
analysis was 20.1%. Models were evaluated using the standard fit indices including overall
model χ2, root mean square error of approximation (RMSEA), standardized root mean square
residual (SRMR), comparative fit index (CFI), and Tucker-Lewis index (TLI) using the
guidelines recommended by Hu and Bentler (1999).
Results
Descriptive statistics (observed mean CAPS severity scores and SDs) for each class at
each time point as a function of treatment type are listed in Table 1. An initial latent growth
curve model that included treatment type by class assignment interaction terms as predictors of
the latent intercept and slope factors fit the data well, χ2 (13, n = 284) = 10.33, p = .67, RMSEA
< .001, 90% CI for RMSEA: < .001 = .05, CFI = 1.0, TLI = 1.01, SRMR = .02, but revealed no
DISSOCIATION AND PTSD TREATMENT
16
significant interactions between treatment type and latent class on the latent intercept or slope
factors (smallest p = .29; additional details available from the first author). Therefore, all
subsequent analyses collapsed across treatment type and did not include this variable as a
moderator of the class effects on the intercept and slope factors.
The second latent growth curve model, which included only the effects of group
membership on the latent slope and intercept factors, yielded a good fitting model, χ2 (7, n = 284)
= 3.78, p = .80, RMSEA < .001, 90% CI for RMSEA: < .001 = .05, CFI = 1.0, TLI = 1.01,
SRMR = .01, with the moderate and high PTSD groups, relative to the dissociative group (the
reference group) predicting the latent intercept variable. Specifically, the parameter estimates
suggested that the high PTSD group had a baseline CAPS severity score that was, on average,
5.05 points higher than the score for the dissociative class, 95% CI [1.29, 8.81], p = .009, and the
moderate PTSD group had a baseline CAPS severity score that was, on average, 20.49 points
below that of the dissociative class, 95% CI [-23.89, -17.10], p < .001.
There was also an effect of the high PTSD class (vs. the dissociative class) on the slope
factor: on average, CAPS severity scores decreased 9.75 points more from the first to the last
assessments for the high PTSD class relative to the dissociative class, 95% CI [-16.94, -2.57], p
= .008. In other words, class membership predicted the slope factor such that the rate of change
was more moderate in the dissociative class compared to the high PTSD class (see Figure 1 for
estimated means at each time point as a function of class membership).2 There was no slope
effect when comparing the moderate PTSD group to the dissociative group (unstandardized γ = 3.69, p = .26) nor was the baseline CAPS score associated with the subsequent rate of symptom
change (e.g., no slope by intercept effect; unstandardized γ = 24.74, p = .76). The mean baseline
CAPS score for the High PTSD and Dissociative class (i.e., the conditional intercept) was
DISSOCIATION AND PTSD TREATMENT
17
estimated as 85.09, 95% CI [82.49, 87.69], p < .001, and the mean rate of change for this group
(i.e., the conditional slope) from the first to last CAPS assessment was -18.71, 95% CI [-23.75, 13.68,] p < .001. The residual variance for the slope factor was significant (p < .001), suggesting
additional factors other than class assignment contributed to individual variability in the rate of
change over time; the residual variance in the intercept was not significant (p = .08).
Although the dissociative group had a slightly lower baseline CAPS severity score and
improved at a slower rate than the non-dissociative high PTSD class, there were no differences
between these two groups in the percentage of individuals who no longer met criteria for PTSD
at any of the post-treatment assessment points. Specifically, as listed in Table 2, immediately
following treatment, approximately 18% of those in the two high PTSD groups no longer met
criteria for the disorder, and approximately 44% of those in the moderate PTSD group no longer
met criteria for the disorder. Logistic regression analyses revealed an omnibus significant group
difference, χ2 (2, n = 235) = 18.19, p = .0001, and follow-up pairwise testing showed that this
was due to the difference between the two high PTSD groups compared with the moderate PTSD
group. The two high PTSD groups did not differ from each other, Wald χ2 (1, n = 235) = 0.02, p
= .89. In contrast, the moderate group differed from both the non-dissociative high PTSD group,
χ2 (1, n = 235) = 10.34, p = .0013, and the dissociative group, χ2 (1, n = 235) = 12.20, p = .0005.
This same pattern of results held at both the three- and six-month follow-up assessments as well
(see Table 2).
We next examined if individuals in the dissociative class had received less treatment than
those in the other classes, as this might potentially account for the more moderate rate of
symptom change compared to the high PTSD group as suggested by the results of the latent
growth curve model. There were no differences in the number of completed sessions of
DISSOCIATION AND PTSD TREATMENT
18
treatment as a function of group membership (moderate PTSD group: M = 7.91, SD = 3.53; high
PTSD group: M = 8.50, SD = 2.94; and dissociative group: M = 8.04, SD = 3.33); F (2, 281) =
0.78, p = .46. There was also no difference in the number of completed sessions as a function of
group membership by treatment type; F (2, 278) = 0.04, p = .96. There was no difference in the
proportion of participants who received any treatment at all (i.e., 1 or more sessions) as a
function of class membership (moderate group: 93.4%; high group: 94.9%; dissociative group:
94.1%); χ2 (2, 284) = 0.19, p = .91. Nor was there a class membership by treatment type effect
for the proportion of participants who received any treatment at all; χ2 (2, 284) = 0.95, p = .62.
Similarly, there were no group differences in the proportion of participants who completed
treatment (moderate group: 70.3%; high group: 74.4%; dissociative group: 68.2%); χ2 (2, 284) =
0.77, p = .68. There was no significant interaction between group membership and treatment
type on treatment completion; χ2 (2, 284) = 0.03, p = .99.
We then evaluated if the severity of derealization and depersonalization changed in
response to PTSD treatment. To do so, we ran the same type of latent growth curve model as we
did for CAPS severity scores, except that mean scores across the four derealization and
depersonalization items were the primary dependent variables. Descriptive statistics (observed
mean dissociation scores and SDs) for each class at each time point as a function of treatment
type are listed in Table 3. As with the model for CAPS severity, the initial model included a
term reflecting moderation of the effect of class assignment on the latent intercept and slope
variables as a function of treatment type. Although this yielded a good fitting model, χ2 (13, n =
284) = 16.00, p = .25 (RMSEA = .03, 90% CI for RMSEA: < .001 = .07, CFI = 1.0, TLI = .99,
SRMR = .02), there was no significant interaction between latent class assignment and treatment
DISSOCIATION AND PTSD TREATMENT
19
type on the slope or intercept factors (smallest p = .10; additional details available from first
author).
Given, this, we again collapsed across treatment type and eliminated the interaction term
and re-ran the latent growth curve model. This model fit the data well, χ2 (7, n = 284) = 12.40, p
= .09 (RMSEA = .05, 90% CI for RMSEA: < .001 = .10, CFI = .99, TLI = .99, SRMR = .03),
and revealed significant effects of the moderate and high PTSD classes (versus the dissociative
class) on the intercept factor (unstandardized γs = -1.66 and -1.45, respectively, both ps < .001,
95% CIs: -1.77 to -1.55 and -1.57 to -1.32, respectively). As would be expected, the former two
groups had lower baseline mean scores on the dissociation items relative to the dissociative class.
In addition, both group variables predicted the slope factor such that the moderate and high
PTSD groups had more positive slopes (unstandardized γs = 0.67 and 0.71, respectively, both ps
< .001, 95% CIs: 0.46 to 0.89 and 0.48 to 0.94, respectively) relative to the dissociative class,
indicating less dissociative symptom decline in these two groups.3 The baseline conditional
intercept estimate for the dissociative group was 1.95, 95% CI [1.86, 2.03], p < .001, and the
average rate of symptom decline (i.e., conditional slope) for this group was estimated at -0.52,
95% CI [-0.69, -0.36], p < .001, across the first to last assessment points. The slope and intercept
factors were not related to each other (r = -.04, p = .69). The residual variance for the slope
factor was significant (p = .005), suggesting additional variability in the rate of change over time
not accounted for by latent class membership; the residual variance for the intercept factor was
not significant (p = .213). Figure 2 shows the estimated means on the four-item dissociation
scale at each time point as a function of latent class assignment.
DISSOCIATION AND PTSD TREATMENT
20
Discussion
The primary aim of this study was to evaluate if the dissociative subtype of PTSD was
associated with a differential response to trauma-focused and non-trauma-focused PTSD
treatment in a sample of female active duty service members and Veterans. Using latent growth
curve models to analyze data from a randomized controlled trial of PE versus PCT, we found
that the rate of PTSD symptom change was slower (i.e., less steep) for individuals with the
dissociative subtype relative to individuals with high PTSD symptoms but without dissociation,
regardless of PTSD treatment type.
To our knowledge, this is the largest study to date to evaluate the effect of the
dissociative subtype on PTSD treatment response and the first to use latent class assignment to
the dissociative group as the moderator of treatment outcome. This was also the first time the
subtype has been shown to moderate overall PTSD treatment response; prior work has supported
subtle effects of dissociation on treatment response (Cloitre et al., 2012; Resick et al., 2012) but
no overall dissociation X time effects. On average, the high PTSD group had a 9.75 greater
decrease (i.e., steeper slope) in CAPS severity scores over the course of the study compared to
the dissociative group. The high PTSD group also had higher baseline PTSD symptoms so that
by the end of the follow-up period, the high PTSD group was estimated to have CAPS scores
that were just 4.7 points below that of the dissociative class (see Figure 1). Thus, although
dissociation was associated with lesser treatment response relative to the high PTSD group, the
magnitude of this effect was small and the clinical significance modest. The rate of change did
not differ between the dissociative group and the moderate PTSD class. In contrast to the
prevailing clinical perception (Becker et al., 2004), these findings suggest that presence of the
DISSOCIATION AND PTSD TREATMENT
21
dissociative subtype is not a contraindication for PE as individuals with the subtype can benefit
from exposure therapy.
Moreover, analyses focused on change in dissociative symptoms over time provided
support for the notion that PTSD treatment may yield marked reductions in dissociative
symptoms. Specifically, the dissociative group showed significant decreases in dissociative
symptoms (and more so than the other groups, presumably because of the dissociative group’s
higher baseline dissociative symptoms), though dissociation was still elevated in this group at the
six-month follow-up (see Figure 2). This is consistent with other work that suggests that
dissociative symptoms improve during the course of PTSD treatment (Cloitre et al., 2012;
Hagenaars et al., 2010; Resick et al., 2012). Our finding is notable given that neither
intervention evaluated in this trial was explicitly developed to treat dissociative symptoms, nor
did either treatment include dissociation-related content. More generally, our finding is
consistent with prior work showing that comorbid symptoms tend to improve when PTSD is
successfully treated. For example, cognitive behavioral therapies for PTSD have been shown to
ameliorate comorbid suicidal ideation (Gradus, Suvak, Wisco, Marx, & Resick, 2013),
depressive symptoms (Liverant, Suvak, Pineles, & Resick, 2012), disordered eating (Mitchell,
Wells, Mendes, & Resick, 2012), self-reported physical health problems (Galovski, Monson,
Bruce, & Resick, 2009; Shipherd, Clum, Suvak, & Resick, 2014), sexual dysfunction (Schnurr et
al., 2009), and alcohol use problems (Foa et al., 2013).
Results also speak to an ongoing question regarding whether individuals with PTSD and
comorbid symptoms of dissociation require a greater dose or different type of treatment to treat
symptoms. For example, Cloitre et al. (2012) suggested that individuals with PTSD and marked
symptoms of dissociation may preferentially benefit from phase-oriented treatment that includes
DISSOCIATION AND PTSD TREATMENT
22
skills training prior to written exposure therapy. In that study, individuals with relatively higher
post-treatment dissociation symptoms who had completed the STAIR/NST treatment arm
showed reduced PTSD symptoms at long-term follow-up compared to those with equally high
post-treatment dissociation who had completed one of the other treatment conditions. However,
complicating the interpretation of this is the fact that a phase-based treatment was the only
double active treatment condition in that study. It is possible that individuals who received
STAIR/NST fared better at long-term follow-up because they received a double dose of active
treatments compared to the groups who received a single dose of active treatment (i.e.,
supportive counseling plus either written exposure or skills training). It is unknown if those with
higher levels of post-treatment dissociation would have fared equally well if they had completed
two forms of exposure therapy, for example, without the skills training. Moreover, in that study,
the effect was not between those with high versus low levels of dissociation but rather between
those with somewhat higher post-treatment dissociation (i.e., scores of 1 or 2 on a 0-4 index)
who were assigned to different treatment arms, suggesting that those with the subtype did as well
as those without. Similarly, Resick et al. (2012) found that those with high baseline levels of
dissociation showed a faster decrease in PTSD symptoms if they completed CPT as opposed to
CPT-C, though follow-up PTSD symptom severity levels in this group was not dependent on
treatment assignment. Given this, and the results of our study, it would be premature to conclude
that individuals with the dissociative subtype require a different type of treatment or a greater
dose of therapy in order to achieve similar symptom reduction as those without the subtype.
Analyses also suggested that participants with the subtype were no more likely to drop
out from the treatment or to otherwise receive less treatment than those without the subtype,
regardless of treatment type. This suggests the intervention was tolerable to those with the
DISSOCIATION AND PTSD TREATMENT
23
dissociative subtype. Together with the results supporting both PTSD and dissociative symptom
improvement in response to treatment, this provides further support for the use of empirically
supported therapies for individuals with the subtype.
Implications for the Subtype
Our findings extend the literature concerning the importance of the subtype in the DSM-5
PTSD diagnostic criteria. The subtype may prove useful in treatment planning, case
conceptualization, and tracking an individual’s response to treatment. It would be reasonable to
provide psychoeducation regarding dissociation to those with the subtype, to ensure that
symptoms of dissociation do not endanger an individual’s safety, and to develop safety plans as
needed. Results also suggest the importance of assessing for the subtype in future PTSD
treatment trials. If the subtype is not quantified and its variance separated from that of PTSD,
then it is likely that unmeasured variability in the PTSD diagnosis will obscure the search for
effective treatment for the disorder. Moreover, the subtype is associated with greater functional
impairment (Stein et al., 2013), and it is unknown the extent to which impairment changes in
response to treatment; this raises the question of whether the subtype is associated with greater
cost to the individual and society even after treatment-related symptom reduction. This concern
is particularly relevant given our finding that dissociative symptoms were still elevated following
treatment among those with the subtype.
Prior work also suggests that the subtype is important for studying the biology of
PTSD—there is preliminary evidence that the symptoms of the subtype may be associated with
genetic variants that are independent of PTSD (Wolf et al., 2014) and individuals with the
subtype may have a differential pattern of brain activation in response to trauma cues than those
without (see Lanius et al., 2010, 2012). This suggests a possible distinct etiology and
DISSOCIATION AND PTSD TREATMENT
24
neurobiology of PTSD with versus without the subtype and failure to parse this heterogeneity
into more homogeneous phenotypes may hinder the search for risk factors, biomarkers, and
correlates of the disorder. Thus, together with the results of prior research, this study supports
the retention of the subtype in future revisions to the DSM.
Limitations
Results of this study need to be considered in light of their limitations. First, this study
included only female veterans and active duty service members undergoing PE and PCT. It is
unknown if results generalize to men, non-Veterans, or those engaged in other forms of PTSD
treatment. Second, it is possible that excluding individuals with active self-injury and suicidal
ideation from the treatment trial may have limited the severity of dissociative symptoms in the
sample; broader inclusion criteria might yield larger effects for dissociation on PTSD treatment
response. Third, our analyses focused on subtype by treatment type interactions on the rate of
change are essentially a two-way interaction and were likely under-powered and should be
interpreted with caution. Fourth, results are based on the DSM-IV definition of PTSD although
the dissociative subtype was not included in the diagnostic criteria until DSM-5 and it is unclear
if results generalize to the current definition of PTSD, though the strong correlation between the
two criteria sets (Miller et al., 2013) suggest that generalization across these versions of the DSM
is likely. Finally, given inconsistent findings in the literature and the fact that our significant
differences in slope from baseline to six-month follow-up were somewhat obscured by
differences in baseline symptoms between the high PTSD and dissociative, it will be important
for future work to attempt to replicate these results to continue to test the effects of the subtype
on PTSD treatment response.
Conclusions
DISSOCIATION AND PTSD TREATMENT
25
We found an effect of the dissociative subtype on PTSD treatment response such that
those with the subtype, while showing reductions in symptoms, did not show the same degree of
PTSD symptom remission as did those with high PTSD but without dissociation. However, this
effect was small and of modest clinical significance. In addition, symptoms of dissociation
improved in response to therapies that were not directly targeting such symptoms, albeit these
symptoms were still elevated throughout the study for those with the subtype at baseline.
Women with the subtype were no more or less likely to drop out of treatment, suggesting that
standard empirically supported therapies for PTSD, including exposure therapy, are tolerable to
this group. Results raise doubt about the common clinical perception that exposure-based
treatment is not effective or appropriate for individuals with PTSD and dissociation and provide
empirical support for the use of exposure treatment for individuals with the dissociative subtype
of PTSD.
DISSOCIATION AND PTSD TREATMENT
26
References
American Psychiatric Association. (1994). Diagnostic and statistical manual of mental disorders
(4th ed.). Washington, DC: Author.
American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders
(5th ed.). Arlington, VA: Author.
Armour, C., Elklit, A., Lauterbach, D., & Elhai, J. (2014). The DSM-5 dissociative-PTSD
subtype: Can levels of depression, anxiety, hostility, and sleeping difficulties differentiate
between dissociative-PTSD and PTSD in rape victims? Journal of Anxiety Disorders, 28,
418-426. doi:10.1016/j.janxdis.2013.12.008
Armour, C., Karstoft, K. I., & Richardson, J. D. (2014). The co-occurrence of PTSD and
dissociation: Differentiating severe PTSD from dissociative-PTSD. Social Psychiatry and
Psychiatric Epidemiology, 8, 1297-1306. doi:10.1007/s00127-014-0819-y
Becker, C. B., Zayfert, C., & Anderson, E. (2004). A survey of psychologists’ attitudes and
utilization of exposure therapy for PTSD. Behaviour Research and Therapy, 42, 277-292.
doi:10.1016/S0005-7967(03)00138-4
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
Blevins, C. A., Weathers, F. W., & Witte, T. K. (2014). Dissociation and posttraumatic stress
disorder: A latent profile analysis. Journal of Traumatic Stress, 27, 388-396.
doi:10.1002/jts.21933
Briere, J. (1995). Trauma Symptom Inventory Professional Manual. Odessa, FL: Psychological
Assessment Resources.
DISSOCIATION AND PTSD TREATMENT
27
Cloitre, M., Petkova, E., Wang, J., & Lu, F. (2012). An examination of the influence of a
sequential treatment on the course and impact of dissociation among women with PTSD
related to childhood abuse. Depression and Anxiety, 29, 709-717. doi:10.1002/da.21920
Farchione, T. J., Fairholme, C. P., Ellard, K. K., Bosseau, C. L., Thompson-Hollands, J., Carl, J.
R.,… Barlow, D. H. (2012). Unified protocol for transdiagnostic treatment of emotional
disorders: A randomized controlled trial. Behavior Therapy, 43, 666-678.
doi:10.1016/j.beth.2012.01.001
Foa, E. B., Yusko, D. A., McLean, C. P., Suvak, M. K., Bux, D. A., Jr., Oslin, D., & Volpicelli,
J. (2013). Concurrent naltrexone and prolonged exposure therapy for patients with
comorbid alcohol dependence and PTSD: A randomized clinical trial. Journal of the
American Medical Association, 310, 488–495. doi:10.1001/jama.2013.82681724275
Galovski, T. E., Monson, C., Bruce, S. E., & Resick, P. A. (2009). Does cognitive-behavioral
therapy for PTSD improve perceived health and sleep impairment? Journal of Traumatic
Stress, 22, 197-204. doi:10.1002/jts.20418
Gradus, J. L., Suvak, M. K., Wisco, B. E., Marx, B. P., & Resick, P. A. (2013). Treatment of
posttraumatic stress disorder reduces suicidal ideation. Depression and Anxiety, 30, 10461053. doi:10.1002/da.22117
Gros, D. F. (2014). Development and initial evaluation of Transdiagnostic Behavioral Therapy
(TBT) for veterans with affective disorders. Psychiatry Research, 220, 275-282.
doi:10.1016/j.psychres.2014.08.018
Hagenaars, M. A., van Minnen, A., & Hoogduin, K. L. (2010). The impact of dissociation and
depression on the efficacy of prolonged exposure treatment for PTSD. Behaviour
Research and Therapy, 48, 19-27. doi:10.1016/j.brat.2009.09.001
DISSOCIATION AND PTSD TREATMENT
28
Halvorsen, J. Ø., Stenmark, H., Neuner, F., & Nordahl, H. M. (2014). Does dissociation
moderate treatment outcomes of narrative exposure therapy for PTSD? A secondary
analysis from a randomized controlled clinical trial. Behaviour Research and Therapy,
57, 21-28. doi:10.1016/j.brat.2014.03.010
Hu, L. & Bentler, P.M. (1999). Cutoff criteria for fit indexes in covariance structure analysis:
Conventional criteria versus new alternatives. Structural Equation Modeling, 6, 1–55.
doi:10.1080/10705519909540118
Lanius, R. A., Brand, B., Vermetten, E. Frewen, P. A., & Spiegel, D. (2012). The dissociative
subtype of posttraumatic stress disorder: Rationale, clinical, and neurobiological
evidence, and implications. Depression and Anxiety, 29, 701-708. doi:10.1002/da.21889
Lanius, R. A., Vermetten, E., Loewenstein, R. J., Brand, B., Schmahl, C., Bremner, J. D.,
Spiegel, D. (2010). Emotion modulation in PTSD: clinical and neurobiological evidence
for a dissociative subtype. American Journal of Psychiatry, 167, 640-647.
doi:10.1176/appi.ajp.2009.09081168
Liverant, G. I., Suvak, M. K., Pineles, S. L., & Resick, P. A. (2012). Changes in posttraumatic
stress disorder and depressive symptoms during cognitive processing therapy: Evidence
for concurrent change. Journal of Consulting and Clinical Psychology, 80, 957-967.
doi:10.1037/a0030485
Miller, M. W., Wolf, E. J., Kilpatrick, D., Resnick, H., Marx, B., Holowka, D., Keane, T. M.,
Rosen, R. C, & Friedman, M. J. (2013). The prevalence and latent structure of proposed
DSM-5 posttraumatic stress disorder symptoms in US national and veteran samples.
Psychological Trauma: Theory, Research, Practice and Policy, 5, 501-512. doi:
10.1037/a0029730
DISSOCIATION AND PTSD TREATMENT
29
Mitchell, K. S., Wells, S. Y., Mendes, A., & Resick, P. A. (2012). Treatment improves
symptoms shared by PTSD and disordered eating. Journal of Traumatic Stress, 25, 535542. doi:10.1002/jts.21737
Muthén, L. K. & Muthén, B. O. (1998-2012). Mplus user’s guide (7th ed.). Los Angeles, CA:
Muthén & Muthén.
Price, M., Kearns, M., Houry, D., & Rothbaum, B. O. (2014). Emergency department predictors
of posttraumatic stress reduction for trauma-exposed individuals with and without an
early intervention. Journal of Consulting and Clinical Psychology, 82, 336-341.
doi:10.1037/a0035537
Resick, P. A., Suvak, M. K., Johnides, B. D., Mitchell, K. S., & Iverson, K. M. (2012). The
impact of dissociation on PTSD treatment with cognitive processing therapy. Depression
and Anxiety, 29, 718-730. doi:10.1002/da.21938
Schnurr, P. P., Friedman, M., Engel, C., Foa, E., Shea, M., Chow, B.,…Bernardy, N. (2005).
Issues in the design of multisite clinical trials of psychotherapy: VA Cooperative Study
No. 494 as an example. Contemporary Clinical Trials, 26, 626-636.
doi:10.1016/j.cct.2005.09.001
Schnurr, P. P., Friedman, M., Engel, C., Foa, E., Shea, M., Chow, B.,…Bernardy, N. (2007).
Cognitive behavioral therapy for posttraumatic stress disorder in women: A randomized
controlled trial. Journal of the American Medical Association, 297, 820–830.
doi:10.1001/jama.297.8.820
Schnurr, P. P., Lunney, C. A., Forshay, E., Thurston, V. L., Chow, B. K., Resick, P. A., &
Foa, E. B. (2009). Sexual function outcomes in women treated for posttraumatic stress
disorder. Journal of Women’s Health, 18, 1549–1557. doi:10.1089/jwh.2008.1165
DISSOCIATION AND PTSD TREATMENT
30
Shipherd, J. C., Clum, G., Suvak, M., & Resick, P. A. (2014). Treatment-related reductions in
PTSD and changes in physical health symptoms in women. Journal of Behavioral
Medicine, 37, 423-433. doi:10.1007/s10865-013-9500-2
Stein, D. J., Koenen, K. C., Friedman, M. J., Hill, E., McLaughlin, K. A., Petukhova, M., . . .
Kessler, R. C. (2013). Dissociation in posttraumatic stress disorder: Evidence from the
World Mental Health Surveys. Biological Psychiatry, 73, 302–312.
doi:10.1016/j.biopsych.2012.08.022
Speckens, A. E. M., Ehlers, A., Hackmann, A., & Clark, D. M. (2006). Changes in intrusive
memories associated with imaginal reliving in posttraumatic stress disorder. Journal of
Anxiety Disorders, 20, 328-341. doi:10.1016/j.janxdis.2005.02.004
Steuwe, C., Lanius, R. A., & Frewen, P. A. (2012). Evidence for a dissociative subtype of PTSD
by latent profile and confirmatory factor analyses in a civilian sample. Depression and
Anxiety, 29, 689-700. doi:10.1002/da.21944
van Minnen, A., Harned, M. S., Zoellner, L., & Mills, K. (2012). Examining potential
contraindications for prolonged exposure therapy for PTSD. European Journal of
Psychotraumatology, 3, 18805. doi:10.3402/ejpt.v3i0.18805
Weathers, F. W., Ruscio, A. M., & Keane, T. M. (1999). Psychometric properties of nine scoring
rules for the Clinician-Administered Posttraumatic Stress Disorder Scale. Psychological
Assessment, 11, 124–133. doi:10.1037//1040-3590.11.2.124
Wolf, E. J., Lunney, C. A., Miller, M. W., Resick, P. A., Friedman, M. J., & Schnurr, P. P.
(2012). The dissociative subtype of PTSD: A replication and extension. Depression and
Anxiety, 29, 679-688. doi:10.1002/da.21946
DISSOCIATION AND PTSD TREATMENT
31
Wolf, E. J., Miller, M. W., Reardon, A. F., Ryabchenko, K. A., Castillo, D., & Freund, R.
(2012). A latent class analysis of dissociation and PTSD: Evidence for a dissociative
subtype. Archives of General Psychiatry, 69, 698-705.
doi:10.1001/archgenpsychiatry.2011.1574
Wolf, E. J., Rasmusson, A. M., Mitchell, K. M., Logue, M. W., Baldwin, C. B., & Miller, M. W.
(2014). A genome-wide association study of clinical symptoms of dissociation in a
trauma-exposed sample. Depression and Anxiety, 31, 352-360. doi:10.1002/da.22260
DISSOCIATION AND PTSD TREATMENT
32
Footnotes
1
Additional participant descriptive characteristics, and details about the measures and
procedures, including inclusion/exclusion criteria, and response rates and attrition, are provided
in Schnurr et al. (2007).
2
We have previously reported (Wolf, Lunney et al., 2012) that the dissociative class did
not differ from the high PTSD group on demographic or trauma-related variables with the
exception of race, such that the moderate and high PTSD groups included a greater percentage of
women who self-reported as White (relative to identifying as a racial minority). Given this, we
conducted secondary analyses in which we included race (minority or non-minority) as a
covariate of group membership and re-ran the latent growth model. Results with respect to the
effect of the DS on the intercept and growth factors were unchanged from the primary results
reported in the text (details available from first author).
3
We also reexamined our latent growth curve model predicting change in dissociative
symptoms with race as a covariate of group membership (as footnote # 2). We again found that
results with respect to the slope and intercept effects were unchanged from that reported in the
text without this covariate (details available from first author).
DISSOCIATION AND PTSD TREATMENT
33
Table 1
Observed Mean CAPS Severity Scores (and SDs) by Group and Treatment Type at Each Assessment
Class
Baseline
PCT
Month 0
PE
PCT
Month 3
PE
Month 6
PCT
PE
PCT
PE
M (SD)
Moderate PTSD
High PTSD
High PTSD & Dissociation
64.75
64.44
51.25
36.72
47.59
37.00
45.63
36.91
(9.20)
(10.06)
(19.69)
(25.16)
(20.61)
(23.03)
(23.01)
(22.88)
91.03
89.21
64.26
67.93
62.33
60.90
61.06
63.57
(12.00)
(9.00)
(25.27)
(27.26)
(27.38)
(27.70)
(27.53)
(28.11)
83.98
86.21
70.62
66.83
65.25
65.69
65.00
64.40
(15.29)
(17.65)
(23.53)
(27.72)
(25.62)
(26.47)
(30.13)
(29.49)
Note. PCT = Present-Centered Therapy; PE = Prolonged Exposure; PTSD = posttraumatic stress disorder; M = mean; SD = standard
deviation.
DISSOCIATION AND PTSD TREATMENT
34
Table 2
Percentage of Individuals who no Longer Met Criteria for PTSD at Follow-up as a Function of
Class Assignment
% No Longer Meeting Criteria for PTSD
Follow-up Point
1. Moderate
2. High
3. High PTSD
PTSD
PTSD
& Dissociative
Omnibus Comparison
(n = 98)
(n = 64)
(n = 73)
χ2 (df = 2)
Month 0
43.88a
18.75b
17.81b
18.19***
Month 3
45.92a
24.19b
20.83b
14.50***
Month 6
50.53a
26.15b
26.09b
14.30***
Note. Sample size listed in the second row reflects the baseline sample size for each group.
Sample size at the immediate follow-up assessment (Month 0) was n = 98, 64, and 73 for groups
1,2, and 3, respectively. Sample size at Month 3 was n = 98, 62, and 72 for groups 1, 2, and 3,
respectively. Sample size Month 6 was n = 95, 65, and 69 for groups 1, 2, and 3, respectively.
For each follow-up, percentages sharing the same subscript are not significantly different from
each other (p > .05). PTSD = posttraumatic stress disorder.
***p < .001.
DISSOCIATION AND PTSD TREATMENT
35
Table 3
Observed Mean Dissociation Severity Scores (and SDs) by Group and Treatment Type at Each Assessment
Class
Baseline
PCT
Month 0
PE
PCT
Month 3
PE
Month 6
PCT
PE
PCT
PE
M (SD)
Moderate PTSD
High PTSD
High PTSD & Dissociation
0.30
0.27
0.47
0.30
0.48
0.38
0.55
0.31
(0.33)
(0.36)
(0.49)
(0.43)
(0.61)
(0.48)
(0.71)
(0.56)
0.49
0.50
0.71
0.78
0.64
0.74
0.41
0.75
(0.36)
(0.39)
(0.76)
(0.78)
(0.62)
(0.81)
(0.55)
(0.71)
1.92
1.97
1.53
1.47
1.54
1.47
1.42
1.22
(0.54)
(0.48)
(0.80)
(0.88)
(0.88)
(0.81)
(0.90)
(0.97)
Note. PCT = Present-Centered Therapy; PE = Prolonged Exposure; PTSD = posttraumatic stress disorder.
DISSOCIATION AND PTSD TREATMENT
Figure 1
The figure shows the estimated mean CAPS severity scores at pre-treatment and follow-up
assessments as a function of class assignment. PTSD = posttraumatic stress disorder; CAPS =
Clinician Administered PTSD Scale.
36
DISSOCIATION AND PTSD TREATMENT
37
Figure 2
The figure shows the estimated mean dissociation item severity scores at pre-treatment and
follow-up assessments as a function of class assignment. PTSD = posttraumatic stress disorder;
CAPS = Clinician Administered PTSD Scale.