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BRIEF REPORT Emergency Department Predictors of Posttraumatic Stress Reduction for Trauma-Exposed Individuals With and Without an Early Intervention Matthew PriceUniversity of Vermont Megan Kearns Centers for Disease Control and Prevention and Emory University School of Medicine Debra Houry and Barbara O. Rothbaum Emory University School of Medicine Objective:Recent data have supported the use of an early exposure intervention to promote a reduction in acute stress and posttraumatic stress disorder (PTSD) symptoms after trauma exposure. The present study explored a comprehensive predictive model that included history of trauma exposure, dissociation at the time of the trauma and early intervention, and physiological responses (cortisol and heart rate) to determine which variables were most indicative of reduced PTSD symptoms for an early intervention or treatment as usual.Method:Participants (n 137) were randomly assigned to the early intervention condition (n 68) or assessment-only condition (n 69) while receiving care at the emergency department of a Level 1 trauma center. Follow-up assessments occurred at 4 and 12 weeks posttrauma.

Results:Findings suggested that dissociation at the time of the 1st treatment session was associated with reduced response to the early intervention. No other predictors were associated with treatment response.

For treatment as usual, cortisol levels at the time of acute care and dissociation at the time of the traumatic event were positively associated with PTSD symptoms.Conclusions:Dissociation at the time at which treatment starts may indicate poorer response to early intervention for PTSD. Similarly, dissociation at the time of the event was positively related to PTSD symptoms in those who received treatment as usual. Recent work has suggested exposure therapy administered shortly after a trauma can reduce subsequent posttraumatic stress disorder (PTSD) symptoms (Rothbaum et al., 2012). The variabil- ity in outcomes, however, highlights a need to identify predictors of response in order to target treatment to those at greatest risk and those most likely to benefit (Kearns, Ressler, Zatzick, & Roth- baum, 2012). The present study evaluated several variables theo- rized to predict response to an early intervention due to their enhancement of fear acquisition after a trauma (Craske et al.,2008). These variables include childhood trauma exposure, heart rate, cortisol levels, and dissociation.

Childhood trauma exposure is hypothesized to influence re- sponse to an adulthood trauma. Childhood exposure may establish fear pathways that are strengthened after exposure to subsequent stressful events (Clemmons, Walsh, DiLillo, & Messman-Moore, 2007). Indeed, childhood traumas are associated with more severe PTSD symptoms after an adulthood trauma (Nishith, Mechanic, & Resick, 2000). Those with such histories may be less likely to benefit from early intervention after an adulthood trauma as a result. Prior work is inconclusive on the influence of childhood trauma on treatment outcome in chronic PTSD samples, however.

Hembree, Street, Riggs, and Foa (2004)reported childhood trauma exposure was associated with reduced PTSD symptoms for pro- longed exposure (PE), whereasResick, Nishith, and Griffin (2003) did not find this association using PE or cognitive processing therapy (CPT).

The initial physiological response to trauma may also enhance fear acquisition. An elevated heart rate (HR) 1 week post-trauma was indicative of increased PTSD symptoms 4 months (Shalev et al., 1998), 6 months (Bryant, Harvey, Guthrie, & Moulds, 2000), and 2 years later (Bryant & Harvey, 2002). Similarly, posttrauma cortisol has been negatively related to increased PTSD symptoms (for a review seeDiGangi et al., 2013). Three studies suggested baseline cortisol was not predictive of symptom reduction during treatment (Gerardi, Rothbaum, Astin, & Kelley, 2010;Olff, de This article was published Online First February 3, 2014.

Matthew Price, Department of Psychology, University of Vermont; Megan Kearns, Centers for Disease Control and Prevention, and Depart- ment of Psychiatry and Behavioral Sciences, Emory University School of Medicine; Debra Houry, Department of Emergency Medicine, Emory University School of Medicine; Barbara O. Rothbaum, Department of Psychiatry and Behavioral Sciences, Emory University School of Medi- cine.

This work was supported by National Institute of Mental Health Grant R34MH083078 (principal investigator: Barbara O. Rothbaum) and Emory Center for Injury Control, Centers for Disease Control and Prevention Grant 5R49CE001494 (principal investigator: Debra Houry). The study was registered with clinicaltrials.gov (NCT00895518).

Correspondence concerning this article should be addressed to Matthew Price, Department of Psychology, University of Vermont, Burlington, VT 05405. E-mail:[email protected] This document is copyrighted by the American Psychological Association or one of its allied publishers.

This article is intended solely for the personal use of the individual user and is not to be disseminated broadly. Journal of Consulting and Clinical Psychology© 2014 American Psychological Association 2014, Vol. 82, No. 2, 336 –3410022-006X/14/$12.00 DOI:10.1037/a0035537 336 Vries, Güzelcan, Assies, & Gersons, 2007;Yehuda et al., 2009).

However, none of these studies examined the relation of physio- logical responses with an early intervention.

Last, increased peritraumatic dissociation, which involves a disruption of consciousness, memory, body awareness, and per- ception of the environment in response to intense emotional dis- tress, is associated with increased PTSD symptoms (Lanius et al., 2010). Recent work has posited that dissociation attenuates treat- ment response (Lanius, Brand, Vermetten, Frewen, & Spiegel, 2012). However, empirical work has not supported this hypothesis in PE (Hagenaars, van Minnen, & Hoogduin, 2010), CPT (Resick, Suvak, Johnides, Mitchell, & Iverson, 2012), or social skills with narrative storytelling therapy (Cloitre, Petkova, Wang, & Lu Las- sell, 2012). A potential explanation for the discrepancy between the theorized and empirical findings is the assessment of dissoci- ation. The above studies assessed dissociation over the past week or month, whereas dissociation at the time of treatment is posited to reduce response (Lanius et al., 2012).

No studies have examined these factors as predictors of re- sponse to an early intervention for PTSD. Four predictors were hypothesized to be associated with increased PTSD symptoms 4 and 12 weeks posttrauma among those who received an early intervention in the emergency department and those who received treatment as usual: (1) childhood trauma exposure, (2) increased HR, (3) reduced cortisol, and (4) increased peritraumatic dissoci- ation and dissociation at the start of treatment. Method Participants Participants were 137 individuals who presented at the emer- gency department (ED) after experiencing a Criterion A trauma according to theDiagnostic and Statistical Manual of Mental Disorders(4th ed.;DSM–IV;American Psychiatric Association, 1994). Participants had a mean age of 31.47 years (SD 11.65) and were mostly African American (78%) and female (65%), with 77% making less than $40,000 annually.

Measures Heart rate.Nurses obtained HR during the initial physical exam.

Salivary cortisol.Cortisol was obtained from a sample of 25–50 l of saliva and expressed using the high sensitivity salivary cortisol enzyme immunoassay (Salimetrics, State College, Penn- sylvania).

Standardized Trauma Interview (STI;Foa & Rothbaum, 2001).The STI is a 41-item interview on relevant aspects of trauma (interrater agreement 0.99). The STI was used to deter- mine if the trauma met Criterion A for a diagnosis of PTSD.

Childhood Trauma Questionnaire (CTQ;Bernstein, Fink, Handelsman, & Foote, 1994).The CTQ is a 25-item self-report scale that assesses negative childhood experiences and has excel- lent psychometric properties. CTQ total scores (range 25–125) offer a valid indicator of early trauma exposure (Scher, Stein,Asmundson, McCreary, & Forde, 2001). Internal consistency for the current study was excellent (0.93).

Immediate Stress Reaction Checklist (ISRC;Fein, Kassam- Adams, Vu, & Datner, 2001).The peritraumatic and postevent dissociation subscales of the ISRC were used to assess reactions at the time of the trauma (range 0 –36) and at the time of the assessment (range 0 –9). Internal consistency for the current study was good (0.86).

PTSD Symptom Scale, Interview Version (PSS-I;Foa, Riggs, Dancu, & Rothbaum, 1993).The PSS-I is a 17-item interview that corresponds to theDSM–IVPTSD symptoms.

Symptoms were rated on a 0 –3 scale, with total scores ranging from 0 to 51 (interrater agreement 0.99). Procedure Assessors with a minimum of a master’s degree were positioned in the ED of the largest Level One trauma center in Georgia from 7 a.m. to 7 p.m. daily. Patients who spoke English, did not have a loss of consciousness, and were alert and oriented were included in the study. After completing baseline measures (CTQ, ISRC sub- scales, HR, and Cortisol), patients were randomly assigned to receive a modified prolonged exposure intervention (INT) in the ED (n 68) or treatment as usual (TAU;n 69), which involved no additional intervention. Participants were assessed for PTSD symptoms 4 and 12 weeks posttrauma. The majority of participants completed the 4-week (TAU: 81%; INT: 66%) and 12-week (TAU: 72%; INT: 59%) evaluations. The hospital and university institutional review board approved this investigation.

Treatment.Treatment included three 60-min sessions across 3 weeks (1 per week). The first session began in the ED after the patient was medically stable. The remaining sessions occurred in the ED in a private space. The protocol was a modified version of PE (Foa, Hembree, & Rothbaum, 2007), and treatment was pro- vided by master’s- or doctoral-level clinicians. The first session included a presentation of the treatment rationale, 30 – 45 min of imaginal exposure followed by processing, identification of in vivo exposures to be completed as homework, and deep breathing skills. The session concluded with a review of normal trauma reactions and the assignment of three tasks for homework: (1) listening to an audiotaped recording of in-session imaginal expo- sure exercise, (2) in vivo exposures to reduce fear, and (3) sched- uling of self-care tasks such as engaging in social activities. The second and third sessions began with a review of the homework assigned during the previous sessions. These sessions included additional imaginal exposure with processing, the continued as- signment of imaginal and in vivo exposure, and self-care tasks for homework. Patients were encouraged to continue in vivo exposure and self-care tasks after the third session.

Data Analytic Plan Separate mixed effect models that included fixed effects for time, baseline cortisol, HR, peritraumatic dissociation, postevent dissociation, sexual assault, and child trauma history were used (Hox, 2010). PTSD symptoms served as the outcome. Time cor- responded to change from Week 4 to Week 12 and was coded as 1 and 0, respectively. Continuous predictors were group- mean-centered. A random intercept was included but not a random This document is copyrighted by the American Psychological Association or one of its allied publishers.

This article is intended solely for the personal use of the individual user and is not to be disseminated broadly. 337 EMERGENCY DEPARTMENT PREDICTORS OF PTSD REDUCTION slope. Missing data were handled with full information maximum- likelihood estimation. An intent-to-treat sample was used in that all participants who were enrolled in the study were included in the analyses and a Bonferonni correction of .025 was used.

Separate receiver operating characteristic (ROC) curves for the assessment and intervention conditions were used to identify cut- off points on significant predictors of Week 12 PTSD. PTSD status was derived from the PSS-I such that a diagnosis corresponded toa response of 2 or greater on one reexperiencing item, three avoidance items, and two hyperarousal items. Results Descriptive information and a correlation matrix are presented inTable 1andTable 2, respectively. Overall dropout rate was higher for INT (n 27, 59%) than for TAU (n 19, 41%), but Table 1 Descriptive Statistics for Intervention and Treatment as Usual Conditions at Week 4 and Week 12 Intervention Treatment as usual Week 4 (n 47) Week 12 (n 42) Week 4 (n 55) Week 12 (n 49) PTSD symptoms 19.19 (12.32) 15.97 (11.68) 23.03 (11.24) 19.03 (12.17) Baseline variables Baseline variables Peritraumatic dissociation 11.98 (5.29) 10.65 (4.74) Postevent dissociation 2.31 (1.83) 1.81 (1.67) Child trauma exposure 49.60 (20.98) 50.27 (20.79) Cortisol 0.15 (0.21) 0.15 (0.14) Heart rate 84.42 (16.41) 84.73 (19.20) Sexual assault (%) 41 30 Note.Values in parenthesis are standard deviations. Posttraumatic stress disorder (PTSD) was measured with the Posttraumatic Symptom Scale–Interview Version. Peritraumatic and postevent dissociation were measured with the Immediate Stress Reaction Checklist. Child trauma exposure was measuredwith the Child Trauma Questionnaire.

Table 2 Correlations for Intervention and Treatment as Usual Conditions at Week 4 and Week 12 Condition 1 2 3 4 5 6 Treatment as usual (Week 4) 1. PTSD symptoms 1.00 0.18 0.43 0.29 –0.10 0.03 2. Child trauma exposure 1.00 0.03 0.11 –0.29 –0.28 3. Peritraumatic dissociation 1.00 0.56 0.02 –0.07 4. Postevent dissociation 1.00 0.14 0.03 5. Cortisol1.00 0.28 6. Heart rate1.00 Treatment as usual (Week 12) 1. PTSD symptoms 1.00 0.19 0.38 0.25 –0.09 0.12 2. Child trauma exposure 1.00 0.03 0.11 –0.29 –0.28 3. Peritraumatic dissociation 1.00 0.56 0.02 –0.07 4. Postevent dissociation 1.00 0.14 0.03 5. Cortisol1.00 0.28 6. Heart rate1.00 Intervention (Week 4) 1. PTSD symptoms 1.00 0.28 0.37 0.43 0.07 0.01 2. Child trauma exposure 1.00 0.08 0.13 –0.11 –0.13 3. Peritraumatic dissociation 1.00 0.63 –0.03 0.04 4. Postevent dissociation 1.00 –0.09 –0.17 5. Cortisol1.00 0.14 6. Heart rate1.00 Intervention (Week 12) 1. PTSD symptoms 1.00 0.29 0.27 0.43 0.09 0.00 2. Child trauma exposure 1.00 0.08 0.13 –0.11 –0.13 3. Peritraumatic dissociation 1.00 0.63 –0.03 0.04 4. Postevent dissociation 1.00 –0.09 –0.17 5. Cortisol1.00 0.14 6. Heart rate1.00 Note.Posttraumatic stress disorder (PTSD) was measured with the Posttraumatic Symptom Scale–Interview Version. Child trauma exposure was measured with the Child Trauma Questionnaire. Peritraumatic and postevent dissociation were measured with the Immediate Stress Reaction Checklist. p .05. p .01. This document is copyrighted by the American Psychological Association or one of its allied publishers.

This article is intended solely for the personal use of the individual user and is not to be disseminated broadly. 338 PRICE, KEARNS, HOURY, AND ROTHBAUM the difference was not significant, 2(1) 1.92,p .167. Drop- outs did not differ on demographic variables of age, ethnicity, gender, or income (ps .07–.79). None of the predictor variables were associated with slope for both conditions. Removal of these variables did not significantly alter fit according to the change in the deviance statistic for the intervention, 2(6) 2.37,p .887, or the assessment, 2(6) 2.78,p .835, conditions.

For INT, PTSD significantly changed from Week 4 to Week 12 ( 10 3.58,p .015). Dissociation at the start of treatment was positively associated with PTSD at Week 12 ( 02 5.08,p .001). Baseline cortisol, child trauma history, peritraumatic disso- ciation, and HR were not related to Week 12 PTSD for INT (see Table 3). The total model accounted for 51% of the variance in Week 12 PTSD. For TAU, PTSD symptoms significantly changed from Week 4 to Week 12 ( 10 – 4.89,p .010). Baseline cortisol was negatively related to PTSD at Week 12 ( 04 –30.16, p .002), but child trauma history was not ( 03 0.14,p .030).

Peritraumatic dissociation was positively related to PTSD ( 01 0.95,p .003), yet postevent dissociation ( 02 – 0.07,p .958) and HR were not (seeTable 3). The model accounted for 68% of the variance in Week 12 PTSD.

Dissociation at the start of treatment for INT and peritraumatic dissociation for TAU were used to identify a cutoff point to predict PTSD status at Week 12 (seeFigure 1for ROC curves for dissociation as predictor of PTSD status). At Week 12, 26% (n 11) of INT and 47% (n 23) of TAU were classified as havingPTSD. For INT, dissociation at the start of treatment accounted for 73% of the area under the curve (p .025), which was classified as fair (Metz, 1978). The cutoff with the optimal balance of sensitivity (0.91) and specificity (0.57) was 2. This score correctly identified 56% of the sample who received the intervention who did not have PTSD at Week 12. For TAU, peritraumatic dissoci- ation accounted for 66% of the area under the curve (p .058), which was classified as poor. Discussion The high prevalence of trauma exposure coupled with chal- lenges in delivering universal prevention demonstrates a clear need for methods to identify those at greatest risk for PTSD and those most likely to benefit from specific interventions. The present study suggested sexual assault victims and those with reduced dissociation at the start of treatment benefited most from early treatment. Increased dissociation, childhood trauma exposure, and low salivary cortisol were associated with more severe PTSD symptoms in those who did not receive treatment.

High levels of dissociation at the start of treatment may interfere with treatment response through reduced acquisition of new inhib- itory learning (Lanius et al., 2012). Inhibitory learning is the acquisition of nonfearful learning during exposure and is the presumed mechanism by which exposure therapy is effective (Craske et al., 2008). Dissociation at the start of an early interven- Table 3 Parameters for Models of Predictors of PTSD Symptoms at Week 4 and Week 12 for Those in the Intervention Condition and Those in the Treatment as Usual Condition Variable Parameter (SE)p95% CI Standardized effect a Intervention Fixed effects Week 12 (intercept) 20.06 (2.53) .001 [15.11, 25.02] — Peritraumatic dissociation 0.37 (0.42) .373 [ 1.18, 0.44] 0.16 Postevent dissociation 5.08 (1.18) .001 [2.76, 7.39] 0.74 Child trauma exposure 0.17 (0.09) .057 [ 0.01, 0.34] 0.29 Cortisol 14.69 (15.09) .33 [ 14.89, 44.28] 0.25 Heart rate 0.04 (0.08) .611 [ 0.12, 0.20] 0.06 Sexual assault 11.32 (3.89) .004 [ 18.95, 3.68] 0.46 Week 4 to Week 12 change 3.58 (1.48) .015 [0.68, 6.47] 0.15 Random effect Intercept 55.98 (24.13) .020 [8.68, 103.27] Treatment as usual Fixed effects Week 12 (intercept) 17.80 (1.89) .001 [14.10, 21.50] 0.21 Peritraumatic dissociation 0.95 (0.32) .003 [0.62, 1.57] 0.37 Postevent dissociation 0.07 (1.25) .958 [ 2.52, 2.39] 0.01 Child trauma exposure 0.14 (0.06) .030 [0.01, 0.26] 0.24 Cortisol 30.16 (9.51) .002 [ 48.81, 11.52] 6.41 Heart rate 0.14 (0.08) .095 [ 0.02, 0.29] 0.20 Sexual assault 3.15 (3.31) .340 [ 3.33, 9.63] 0.12 Week 4 to Week 12 change 4.89 (1.89) .010 [1.19, 8.59] 0.21 Random effect Intercept 30.62 (17.70) .084 [ 4.08, 65.32] Note.Posttraumatic stress disorder (PTSD) was measured with the Posttraumatic Symptom Scale–Interview Version. Child trauma exposure was measured with the Child Trauma Questionnaire. Peritraumatic and postevent dissociation were measured with the Immediate Stress Reaction Checklist. CI confidence interval. aStandardized effects were calculated according to the recommendations ofHox (2010)and correspond to standardized unit changes in PTSD symptoms per 1 standardized unit change in the predictor. Absolute values are presented to facilitate interpretation. This document is copyrighted by the American Psychological Association or one of its allied publishers.

This article is intended solely for the personal use of the individual user and is not to be disseminated broadly. 339 EMERGENCY DEPARTMENT PREDICTORS OF PTSD REDUCTION tion may serve as a clinically useful indicator of treatment re- sponse. The current study suggested that a score of 2 or greater on the ISRC used in the current study could identify those who are less likely to respond. This finding should be considered prelim- inary, however, pending replication with other early interventions and traditional exposure therapy approaches.

The present study did not assess dissociation at subsequent treatment sessions, however. It is unclear if variation in dissocia- tion across treatment influences response or if dissociation at the start of treatment is predictive of outcomes. This distinction is important given that related research has shown that fluctuations in symptoms across sessions interfere with response to exposure therapy (Price & Anderson, 2011). Such findings would inform clinical practice in that elevated dissociation at the start of a given session would help the therapist plan a given session. The optimal course of treatment must also be explored to determine if a higher dose of exposure is needed or if use of alternative treatments (e.g., coping strategies) would be more beneficial.

Findings in the TAU condition corroborate prior research show- ing that a reduced cortisol reaction at the time of trauma exposure, indicative of a chronic stress response, and increased peritraumatic dissociation represent possible mechanisms of PTSD development (Ozer, Best, Lipsey, & Weiss, 2003). However, the measure of peritraumatic dissociation did not identify those at greatest risk for PTSD according to the ROC analysis. It is unclear if this was due to the measure used in the current study, the sample size, or the predictive utility of self-reported dissociation. Additional research on this topic is needed.

A limitation of the study was the assessment of PTSD only at 4 and 12 weeks posttrauma. Additional follow-up periods may haveprovided further insight into the relationship between the proposed risk factors and PTSD outcome over time. In addition, limited information is available about the participants’ experiences in the intervening hours between trauma exposure and enrollment in the study. Although this is a brief time frame (median 6.92;M 11.79 hr,SD 12.90) relative to other research on predictors of PTSD and early intervention, we believe it is a critical period for the formation of fear memories. Furthermore, the sample size was not sufficiently powered to detect small to medium effects in such models. Work with larger, noninferiority samples is needed to conclusively determine if these variables have clinically useful associations with early intervention response and PTSD risk. Last, the dropout rates and exclusion criteria may limit the generaliz- ability of the findings to all trauma-exposed individuals.

Despite these limitations, the findings of this study have impor- tant implications for future research on PTSD and early interven- tion. Screening for peritraumatic dissociation and low cortisol levels in recent trauma survivors could identify those at greatest risk and those who need further intervention. For those who receive early intervention and treatment, the present findings high- light the potentially interfering role of dissociation at the start of treatment. Additional work is needed to develop clinically useful screening tools from these measures. References American Psychiatric Association. (1994).Diagnostic and statistical man- ual of mental disorders(4th ed.). Washington, DC: Author.

Bernstein, D. P., Fink, L., Handelsman, L., & Foote, J. (1994). Initial reliability and validity of a new retrospective measure of child abuse and neglect.American Journal of Psychiatry, 151,1132–1136. Figure 1.Receiver operating characteristic (ROC) curves for intervention and assessment (treatment as usual) conditions using the respective dissociation variables as predictors of posttraumatic stress disorder diagnostic status at Week 12. The ROC curve for the intervention condition used postevent dissociation. The ROC curve for the assessment condition used peritraumatic dissociation. This document is copyrighted by the American Psychological Association or one of its allied publishers.

This article is intended solely for the personal use of the individual user and is not to be disseminated broadly. 340 PRICE, KEARNS, HOURY, AND ROTHBAUM Bryant, R. A., & Harvey, A. G. (2002). Delayed-onset posttraumatic stress disorder: A prospective evaluation.Australian and New Zealand Journal of Psychiatry, 36,205–209.doi:10.1046/j.1440-1614.2002.01009.x Bryant, R. A., Harvey, A. G., Guthrie, R. M., & Moulds, M. L. (2000). A prospective study of psychophysiological arousal, acute stress disorder, and posttraumatic stress disorder.Journal of Abnormal Psychology, 109, 341–344.doi:10.1037/0021-843X.109.2.341 Clemmons, J. C., Walsh, K., DiLillo, D., & Messman-Moore, T. L. (2007).

Unique and combined contributions of multiple child abuse types and abuse severity to adult trauma symptomatology.Child Maltreatment, 12(2), 172–181.doi:10.1177/1077559506298248 Cloitre, M., Petkova, E., Wang, J., & Lu Lassell, F. (2012). An examina- tion 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 Craske, M. G., Kircanski, K., Zelikowsky, M., Mystkowski, J., Chowd- hury, N., & Baker, A. (2008). Optimizing inhibitory learning during exposure therapy.Behaviour Research and Therapy, 46(1), 5–27.doi:

10.1016/j.brat.2007.10.003 DiGangi, J. A., Gomez, D., Mendoza, L., Jason, L. A., Keys, C. B., & Koenen, K. C. (2013). Pretrauma risk factors for posttraumatic stress disorder: A systematic review of the literature.Clinical Psychology Review, 33,728 –744.doi:10.1016/j.cpr.2013.05.002 Fein, J. A., Kassam-Adams, N., Vu, T., & Datner, E. M. (2001). Emer- gency department evaluation of acute stress disorder symptoms in vio- lently injured youths.Annals of Emergency Medicine, 38,391–396.

doi:10.1067/mem.2001.118225 Foa, E., Hembree, E., & Rothbaum, B. O. (2007).Prolonged exposure therapy for PTSD: Emotional processing of traumatic experiences ther- apist guide(1st ed.). New York, NY: Oxford University Press.

Foa, E. B., Riggs, D. S., Dancu, C. V., & Rothbaum, B. O. (1993).

Reliability and validity of a brief instrument for assessing post-traumatic stress disorder.Journal of Traumatic Stress, 6,459 – 473.doi:10.1002/ jts.2490060405 Foa, E. B., & Rothbaum, B. O. (2001).Treating the trauma of rape:

Cognitive-behavioral therapy for PTSD. New York, NY: Guilford Press.

Gerardi, M., Rothbaum, B. O., Astin, M. C., & Kelley, M. (2010). Cortisol response following exposure treatment for PTSD in rape victims.Jour- nal of Aggression, Maltreatment & Trauma, 19,349 –356.doi:10.1080/ 10926771003781297 Hagenaars, M. A., van Minnen, A., & Hoogduin, K. A. L. (2010). The impact of dissociation and depression on the efficacy of prolonged exposure treatment for PTSD.Behaviour Research and Therapy, 48(1), 19 –27.doi:10.1016/j.brat.2009.09.001 Hembree, E. A., Street, G. P., Riggs, D. S., & Foa, E. B. (2004). Do assault-related variables predict response to cognitive behavioral treat- ment for PTSD?Journal of Consulting and Clinical Psychology, 72, 531–534.doi:10.1037/0022-006X.72.3.531 Hox, J. (2010).Multilevel analysis: Techniques and applications(2nd ed.).

Sussex, England: Routledge.

Kearns, M. C., Ressler, K. J., Zatzick, D., & Rothbaum, B. O. (2012). Early interventions for PTSD: A review.Depression and Anxiety, 29,833– 842.doi:10.1002/da.21997 Lanius, R. A., Brand, B., Vermetten, E., Frewen, P. A., & Spiegel, D.

(2012). The dissociative subtype of posttraumatic 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.Amer- ican Journal of Psychiatry, 167,640 – 647.doi:10.1176/appi.ajp.2009 .09081168 Metz, C. E. (1978). Basic principles of ROC analysis.Seminars in Nuclear Medicine, 8,283–298.doi:10.1016/S0001-2998(78)80014-2 Nishith, P., Mechanic, M. B., & Resick, P. A. (2000). Prior interpersonal trauma: The contribution to current PTSD symptoms in female rape victims.Journal of Abnormal Psychology, 109,20 –25.doi:10.1037/ 0021-843X.109.1.20 Olff, M., de Vries, G.-J., Güzelcan, Y., Assies, J., & Gersons, B. P. R.

(2007). Changes in cortisol and DHEA plasma levels after psychother- apy for PTSD.Psychoneuroendocrinology, 32,619 – 626.doi:10.1016/ j.psyneuen.2007.04.001 Ozer, E. J., Best, S. R., Lipsey, T. L., & Weiss, D. S. (2003). Predictors of posttraumatic stress disorder and symptoms in adults: A meta-analysis.

Psychological Bulletin, 129,52–73.doi:10.1037/0033-2909.129.1.52 Price, M., & Anderson, P. L. (2011). The impact of cognitive behavioral therapy on post event processing among those with social anxiety disorder.Behaviour Research and Therapy, 49,132–137.doi:10.1016/ j.brat.2010.11.006 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 –342, 351–355.

Resick, P. A., Suvak, M. K., Johnides, B. D., Mitchell, K. S., & Iverson, K. M. (2012). The impact of dissociation on PTSD treatment cognitive processing therapy.Depression and Anxiety.doi:10.1002/da.21938 Rothbaum, B. O., Kearns, M. C., Price, M., Malcoun, E., Davis, M., Ressler, K. J.,...Houry, D. (2012). Early intervention may prevent the development of posttraumatic stress disorder: A randomized pilot civil- ian study with modified prolonged exposure.Biological Psychiatry, 72, 957–963.doi:10.1016/j.biopsych.2012.06.002 Scher, C. D., Stein, M. B., Asmundson, G. J., McCreary, D. R., & Forde, D. R. (2001). The Childhood Trauma Questionnaire in a community sample: Psychometric properties and normative data.Journal of Trau- matic Stress, 14,843– 857.doi:10.1023/A:1013058625719 Shalev, A. Y., Sahar, T., Freedman, S., Peri, T., Glick, N., Brandes, D.,...

Pitman, R. K. (1998). A prospective study of heart rate response fol- lowing trauma and the subsequent development of posttraumatic stress disorder.Archives of General Psychiatry, 55,553–559.doi:10.1001/ archpsyc.55.6.553 Yehuda, R., Bierer, L. M., Sarapas, C., Makotkine, I., Andrew, R., & Seckl, J. R. (2009). Cortisol metabolic predictors of response to psychotherapy for symptoms of PTSD in survivors of the World Trade Center attacks on September 11, 2001.Psychoneuroendocrinology, 34,1304 –1313.

doi:10.1016/j.psyneuen.2009.03.018 Received November 15, 2012 Revision received September 26, 2013 Accepted October 28, 2013 This document is copyrighted by the American Psychological Association or one of its allied publishers.

This article is intended solely for the personal use of the individual user and is not to be disseminated broadly. 341 EMERGENCY DEPARTMENT PREDICTORS OF PTSD REDUCTION