An evaluation of competing models for the structure of PTSD ...

C 2010) Journal of Traumatic Stress, Vol. 23, No. 5, October 2010, pp. 631–638 (

An Evaluation of Competing Models for the Structure of PTSD Symptoms Using External Measures of Comorbidity Mark W. Miller, Erika J. Wolf, Kelly M. Harrington, Timothy A. Brown, Danny G. Kaloupek, and Terence M. Keane National Center for PTSD, VA Boston Healthcare System and Boston University School of Medicine Research on the structure of posttraumatic stress disorder (PTSD) symptoms has yielded support for two 4-factor models: the King (King, Leskin, King, & Weathers, 1998) and Simms/Watson models (Simms, Watson, & Doebbeling, 2002). This study evaluated them using data drawn from 1,128 Vietnam veterans by comparing associations with a latent internalizing comorbidity variable and five scales from the MMPI-2 Restructured Clinical (RC) Scales (Tellegen et al., 2003). The Simms/Watson dysphoria factor failed to show evidence of superior convergent or discriminant validity in association with external measures relative to the numbing or hyperarousal factors of the King model. Findings raise questions about proposals to abandon the distinction between numbing and hyperarousal symptoms in favor of a dysphoria-based model.

Posttraumatic stress disorder (PTSD) has been the source of considerable controversy since its initial appearance in the Diagnostic and Statistical Manual of Mental Disorders-Third Edition (DSM ; American Psychiatric Association, 1980). One longstanding concern involves the discriminant validity and specificity of its symptoms, particularly those listed under Criteria C (avoidance and numbing) and D (hyperarousal). Critics have noted that several of these symptoms appear in the diagnostic criteria for other disorders and have questioned the specificity of their relationship to trauma exposure (McNally, 1992; Rosen & Lilienfeld, 2008; Spitzer, First, & Wakefield, 2007). These concerns are underscored by results of studies suggesting that measures of PTSD discriminate poorly between PTSD and other anxiety disorders

(Engelhard, Arntz, & van den Hout, 2007) and that many depressed patients with no history of trauma display all of the other DSM-IV criteria for PTSD (Bodkin, Pope, Detke, & Hudson, 2007). Clinical and epidemiological studies suggest that the majority of individuals with PTSD meet criteria for another Axis I diagnosis, which raises additional questions about the factors that cause and maintain PTSD comorbidity (e.g., Brown, Campbell, Lehman, Grisham, & Mancill, 2001; Kessler, Sonnega, Bromet, Hughes, & Nelson, 1995; Kulka et al., 1990). Contemporary structural models of psychiatric diagnostic comorbidity suggest that the co-occurrence of PTSD symptoms with other anxiety disorders and the unipolar mood disorders may be the manifestation of a common vulnerability to a broad spectrum of psychopathology, referred to here as the internalizing disorders, but known also as the “emotional” or “distress” disorders (Brown & Barlow, 2009; Clark, 2005; Clark & Watson, 2006; Krueger, 1999). According to these models, individual disorders in this class contain both unique and common elements. The unique component consists of symptoms that distinguish individual disorders from one another. The common component, often termed negative emotionality or negative affectivity, is conceptualized as a temperament-based individual difference factor. It is thought to confer risk for the development of internalizing psychopathology and to be responsible for the high co-occurrence among disorders in this class (cf. Clark & Watson, 2006; Miller, 2003; Mineka, Watson, & Clark, 1998; Tellegen, 1985; Watson, 2005; Zinbarg & Barlow, 1996). Recent studies suggest that many of the PTSD numbing and hyperarousal symptoms cohere together and align conceptually with

Mark W. Miller, National Center for PTSD, VA Boston Healthcare System & Department of Psychiatry, Boston University School of Medicine; Erika J. Wolf, National Center for PTSD, VA Boston Healthcare System & Department of Psychology, Boston University; Kelly M. Harrington, National Center for PTSD, VA Boston Healthcare System & Department of Psychiatry, Boston University School of Medicine; Timothy A. Brown, Department of Psychology, Boston University; Danny G. Kaloupek, National Center for PTSD, VA Boston Healthcare System & Department of Psychiatry, Boston University School of Medicine; Terence M. Keane, National Center for PTSD, VA Boston Healthcare System & Department of Psychiatry, Boston University School of Medicine. This research was supported, in part, by the VA Cooperative Studies Program of the Veterans Health Administration under designation CS-334, a VA Merit Review grant to Mark W. Miller, a National Institute of Mental Health grant to Mark W. Miller (5RO1MH079806), and a National Institute of Mental Health grant (5F31MH074267) to Erika J. Wolf. Correspondence concerning this article should be addressed to: Mark W. Miller, National Center for PTSD (116B-2), VA Boston Healthcare System, 150 South Huntington Avenue, Boston, MA 02130. E-mail: [email protected]. Published 2010. This article is a US Government work and is in the public domain in the USA. View this article online at wileyonlinelibrary.com DOI: 10.1002/jts.20559

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this common factor (Baschnagel, O’Connor, Colder, & Hawk, 2005; Elklit & Shevlin, 2007; Palmieri, Weathers, Difede, & King, 2007; Simms et al., 2002; Watson, 2005). In the first of these studies, Simms et al. (2002) performed confirmatory factor analyses (CFA) of PTSD symptom data drawn from a large sample of Gulf War veterans and found a best-fitting solution comprised of four factors that they termed intrusions, avoidance, hyperarousal, and dysphoria. The defining feature of this model (henceforth referred to as the Simms/Watson model) was a broad factor defined by eight traditional markers of numbing and hyperarousal including impaired trauma recollection, loss of interest, detachment, restricted affect, sense of foreshortened future, sleep disturbance, anger/irritability, and impaired concentration (symptoms C3–C7 and D1–D3) that the authors termed dysphoria. The remaining symptoms loaded on a five-item intrusion factor defined by the reexperiencing symptoms (B1–B5), a two-item avoidance factor defined by the effortful avoidance symptoms (C1 and C2), and a two-item hyperarousal factor defined by hypervigilance and exaggerated startle (D4 and D5). The next best fitting factor solution in the Simms et al. (2002) study—referred to here as the King model—was comprised of reexperiencing (B1–B5), effortful avoidance (C1 and C2), numbing (C3–C7) and hyperarousal (D1–D5) factors (c.f., King et al., 1998). Prior to the Simms et al. study, the majority of published CFA studies on the structure of PTSD had shown the superiority of the King model relative to 1-, 2-, or 3-factor alternatives and there was a degree of a consensus among authorities in the field that it provided the best fit to the 17 DSM-IV symptoms (for reviews, see Elklit & Shevlin, 2007; Palmieri, Weathers, et al., 2007). Since then, however, investigators who have compared fit indices for the two 4-factor models have found evidence for the superiority of the Simms/Watson model in some (Baschnagel et al., 2005; Krause, Kaltman, Goodman, & Dutton, 2007; Palmieri, Weathers, et al., 2007), but not all datasets (McWilliams, Cox, & Asmundson, 2005; Palmieri & Fitzgerald, 2005; Palmieri, Marshall, & Schell, 2007). For example, Palmieri, Weathers, et al. (2007) reported that the Simms/Watson model provided the best fit to data from a self-report checklist, whereas the King model provided the best fit to data derived from a structured clinician-administered interview. Overall, however, differences in fit statistics between the two models have been subtle with variability across studies linked to specific sample characteristics and/or the individual PTSD measures employed. The conceptual appeal of the Simms/Watson model is the consonance with structural models of comorbidity that it aims to achieve by separating symptoms hypothesized to be specific to PTSD (i.e., the intrusion, avoidance, hyperarousal factors) from common ones (dysphoria). Unfortunately, few studies have evaluated the extent to which the model actually achieves this goal. This question can be addressed by evaluating the convergent and discriminant validity of the alternative models relative to external criteria. Simms et al. (2002) approached this by examining corre-

lations between the sum of items in each factor of their model and external measures of other psychopathology. They found the dysphoria factor to be most highly correlated with external measures of depression and generalized anxiety, but they did not directly compare their model with the King model in terms of their differential relations with these or other external variables. To our knowledge, only one published study to date has performed this type of analysis. Palmieri, Weathers, et al. (2007) compared the differential relationships between the two models and external measures of depression, anger, and global symptom severity. Support for the convergent validity of the Simms/Watson dysphoria factor was provided by evidence that correlations with the comorbidity measures were generally slightly higher for dysphoria than for either the numbing or hyperarousal scales of the King model though these differences were not tested statistically. Evaluating the validity of the two models on the basis of the existing literature is also complicated by the fact that only two prior studies have compared the two models using a clinicianadministered PTSD assessment (i.e., Elhai, Ford, Ruggiero, & Frueh, 2009; Palmieri, Weathers et al., 2007). The others were based on self-report measures of PTSD (Baschnagel et al., 2005; Krause et al., 2007; Palmieri & Fitzgerald, 2005) or a checklist administered by lay interviewers (McWilliams et al., 2005). Furthermore, samples used in prior studies have generally been characterized by low base rates of PTSD. For example, the Simms et al. (2002) study was based on PTSD Checklist (PCL; Weathers, Litz, Herman, Huska & Keane, 1993) data obtained from a military sample in which only 22% of participants reported exposure to a combat stressor that would satisfy PTSD Criterion A. Moreover, in that study, the mean PCL score for cases with Criterion A exposure was more than two standard deviations below the cutoff of 50 recommended for diagnosing PTSD in veterans (cf., Forbes, Creamer, & Biddle, 2001).

MODEL RELATIONS TO EXTERNAL MEASURES OF COMORBIDITY The primary aim of this study was to evaluate the convergent and discriminant validity of the two leading models for the structure of PTSD symptoms in relation to (a) a latent variable based on clinician-determined diagnoses of the internalizing spectrum, and (b) select scales from the MMPI-2 Restructured Clinical Scales (RCSs; Tellegen et al., 2003), namely, Demoralization (RCd), Low Positive Emotions (RC2), Antisocial Behavior (RC4), Dysfunctional Negative Emotions (RC7), and Hypomanic Activation (RC9). The internalizing factor corresponds conceptually to the latent dimension of psychopathology that the Simms/Watson dysphoria factor purports to capture. Similarly, the Demoralization, Dysfunctional Negative Emotions, and Low Positive Emotionality scales were selected on the basis of their hypothesized relations to the PTSD factors and relevant structural models of

Journal of Traumatic Stress DOI 10.1002/jts. Published on behalf of the International Society for Traumatic Stress Studies.

Competing Models for the Structure of PTSD Symptoms the internalizing disorders. The first two assess facets of negative emotionality, with Demoralization reflecting unpleasant affective valence (e.g., depressed mood, generalized distress) and Dysfunctional Negative Emotions relating more strongly to negative arousal (e.g., fear and anxiety). Low Positive Emotions, on the other hand, reflects the loss of pleasure associated with depression (Tellegen et al., 2003; Tellegen et al., 2006). Recent research has shown these scales to correlate highly with trait measures of negative emotionality and with symptoms of generalized distress, anxiety, fear, and depression (i.e., Demoralization with generalized distress, Dysfunctional Negative Emotions with anxiety and fear, Low Positive Emotions with depression; Sellbom & Ben-Porath, 2005; Sellbom, Ben-Porath, & Graham, 2006; Sellbom, Graham, & Schenk, 2006; Simms, Casillas, Clark, Watson, & Doebbeling, 2005; Tellegen et al., 2003; Tellegen et al., 2006; Wolf et al., 2008). The Antisocial Behavior and Hypomanic Activation scales were included as indices of discriminant validity. Though these scales may be elevated in a subset of individuals with an externalizing form of PTSD (Miller, Kaloupek, Dillon, & Keane, 2004), the constructs that they were designed to measure have no clear theoretical relationship to the PTSD symptom factors of either model. Specific hypotheses were advanced to evaluate the convergent and discriminant validity of the two models:

1. If the Simms/Watson dysphoria factor captures symptom variance related to general (i.e., non-PTSD specific) distress better than either the numbing or hyperarousal factor of the King model, then we should find stronger correlations between dysphoria and a latent variable representing the common component of disorders of the internalizing spectrum relative to the strength of these associations for the numbing and hyperarousal factors of the King model. 2. For the same reason, we expected to observe stronger associations between the Simms/Watson dysphoria factor and both Demoralization and Dysfunctional Negative Emotions than between either the King numbing or hyperarousal factor and these two RC scales. 3. Given prior evidence for an association between the King numbing symptoms and specific deficits in the capacity to experience positive emotions (Litz & Gray, 2002), we hypothesized that the King numbing factor would evidence stronger associations with Low Positive Emotions than would the considerably broader Simms/Watson dysphoria factor. 4. Finally, the two models were not expected to differ in terms of their relations to the Antisocial Behavior and Hypomanic Activation scales. Both models were expected to show evidence of discriminant validity relative to these scales, i.e., significantly lower associations with them compared to the other RC scales.

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METHOD Participants Participants were 1,128 male veterans who served in the Vietnam Theater of operations between August 1964 and May 1975. The sample included a high base rate of individuals with current or lifetime diagnoses of PTSD (i.e., 629 current and 166 lifetime, comprising a total of 70% of the sample). The remaining 333 had no history of PTSD that met the diagnostic-threshold for the disorder. Participants were recruited from 15 VA sites for a study examining the psychophysiological assessment of PTSD (see Keane et al., 1998 for details; Litz & Gray, 2002). In total, 2,115 participants were screened for the study and 1,461 met eligibility criteria. Of these, 1,325 provided data on all or some of the measures included in the original study design; 168 of these participants were excluded from this study due to inconsistent responding on the MMPI-2 (see below). An additional 29 participants were omitted due to missing data on greater than 20% of the PTSD items on the Structured Clinical Interview for DSM-III-R (SCID; Spitzer, Williams, Gibbon, & First, 1989). No participants were omitted due to missing data on the MMPI-2 or the dichotomous SCID diagnoses. Of the final sample of 1,128, 70% identified themselves as Caucasian/White, 18% as African American/Black, 8% as Hispanic, 2% were American Indian/Alaskan Native, and 2% Asian/Pacific Islander. The average age of participants at the time of the assessment was 43 years (SD = 4 years).

Measures The MMPI-2 (Butcher, Dahlstrom, Graham, Tellegen, & Kaemmer, 1989) is a 567-item true–false inventory that assesses a broad range of self-reported psychopathology. Data were examined for invalid response profiles with individuals excluded from analysis if Infrequency (F ) > 100 and Infrequency-Psychopathology (F [ p]) > 80, or True Response Inconsistency (TRIN) > 100, or Variable Response Inconsistency (VRIN) > 80 (Arbisi & Ben-Porath, 1995), consistent with prior studies from this dataset (Miller et al., 2004; Miller, Vogt, Mozley, Kaloupek, & Keane, 2006; Wolf et al., 2008). Raw scores, corrected for measurement error, for the five RC scales were examined as indicators of the external validity of the two 4-factor PTSD models. The SCID was administered by doctoral-level clinicians to assess current and lifetime PTSD, major depressive disorder, social phobia, panic disorder, and obsessive–compulsive disorder according to the DSM-III-R (American Psychiatric Association, 1987) criteria. All items on the PTSD module were administered and skip-out rules were not followed for this module. Items on the PTSD module are categorical in nature and range from 1 to 3. One hundred twenty-eight of the interviews were audio-recorded and scored by a secondary rater to evaluate interrater reliability. Kappa for the PTSD diagnosis (current or past vs. never) was .73,


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and coefficient alpha estimate for the total PTSD symptom count was .93. Kappas for the diagnoses that contributed to the internalizing latent variable were as follows: panic disorder, κ = .65; obsessive–compulsive disorder, κ = .60; major depressive disorder, κ = .55; and social phobia, κ = .37.

Data Analysis Data analyses were performed with the Mplus statistical software, version 5.2 (Muthén & Muthén, 1998–2007) using the mean and variance-adjusted weighted least squares (WLSMV) estimator due to the categorical nature of the SCID PTSD items. With the use of this estimator, the PTSD item factor loadings are probit coefficients based on the estimated polycoric correlation matrix while correlations between latent variables in the model are equivalent to standard linear regression coefficients as the latent variables underlying categorical indicators are continuous. Participants with missing data were included in analyses (aside from, as previously described, subjects with > 20% of missing data on the SCID PTSD items) as the WLSMV estimator invokes a four-step procedure to model such cases directly, building on direct maximum likelihood estimation. Analyses were based on current PTSD symptoms. We first compared the fit of the King and Simms/Watson models using fit statistics from the absolute (χ 2 ) parsimony (root mean square error of approximation [RMSEA]), and comparative-fit (TuckerLewis index [TLI], and comparative fit index [CFI]) classes of indices and applied cutoff guidelines recommended by Hu and Bentler (1999) and Kline (2005) to determine the acceptability of each model. Specifically, RMSEA values less than .06 were considered an indication of good model fit. CFI and TLI values ≥ .90 and ≥ .95 were considered as indicators of adequate and good model fit, respectively. Second, we examined the construct validity of the two 4factor PTSD models using structural equation modeling by computing correlations between the PTSD factors of the King and Simms/Watson models and the selected MMPI-2 RC scales. The RC scales were modeled as single indicators of their respective constructs with measurement error specified based on an estimate of the internal consistency (coefficient alpha) for each variable.1 In separate structural equation models, we further evaluated the construct validity of the two PTSD models by comparing the correlations between the PTSD factors of the two models and a latent variable reflecting internalizing psychopathology. This latent variable was indicated by dichotomous SCID-derived current diagnoses on major depression (the marker indicator), panic dis-

Table 1. Model Fit for King and Simms/Watson Models and for Models Incorporating External Correlates Model King alone Simms/Watson alone King with RC scales Simms/Watson with RC scales King with internalizing Simms/Watson with internalizing

The coefficient alpha values for the MMPI-2 scales that were used to adjust for measurement error in these analyses were obtained from a prior investigation using the same sample (Wolf et al., 2008) with the same research sample. See Brown (2006) for more information about adjusting for measurement error in SEMs with single indicators.

df

CFI

TLI

RMSEA

257.48 300.45 332.87 365.83

85 84 111 111

.98 .97 .96 .95

1.00 .99 .99 .99

.04 .05 .04 .05

260.75 298.94

120 120

.99 .98

1.00 .99

.03 .04

Note. df = degrees of freedom; RMSEA = root mean square error of approximation; TLI = Tucker-Lewis index; CFI = comparative fit index; RC = restructured clinical. All χ 2 values are statistically significant at p < .001.

order, social phobia, and obsessive–compulsive disorder. Indicator loadings on the internalizing latent variable are probit coefficients. Third, the statistical significance of the difference in the magnitude of pairs of correlations between the two models was examined by computing Fisher’s z-tests to compare independent correlations. All p-values reported for the z and t-statistics are two-tailed.

RESULTS Model Fit As shown in Table 1, the King and Simms/Watson models both yielded fit statistics that were consistent with good model fit and were roughly equivalent with one another, though with a slight advantage for the King model.2 To examine differential patterns of associations between the two PTSD models and the RC scales (modeled as single indicators corrected for measurement error) and comorbid internalizing disorders, four additional models were evaluated: one for each PTSD model in which the RC scales were included as correlates of the PTSD symptom factors and one for each PTSD model in which the internalizing factor was modeled as a correlate of the PTSD symptom factors. The fit of these measurement models is shown in Table 1. All models yielded good fit statistics that were approximately equivalent for the King and Simms/Watson models (see Table 1). All diagnostic indicators loaded significantly on the latent internalizing variable at the p < .001 level (standardized loading for major depression = .64, for panic disorder = .59, for obsessive–compulsive disorder = .50, 2

1

χ2

The completely standardized indicator loadings and unreliability are available upon request. We also examined fit statistics for 1, 2, and 3-factor solutions as described by Palmieri et al. (2007). As in the vast majority of prior studies, results showed that the two 4-factor models provided better fit to the data than their simpler alternatives. These analyses and results were omitted in the interest of space but are available from the first author.


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Table 2. Relationships Between the PTSD Factors and Their External Correlates

1. Reexperiencing 2. Avoidance 3. King numbing 4. Simms/Watson dysphoria 5. King hyperarousal 6. Simms/Watson hyperarousal 7. RCd 8. RC2 9. RC4 10.RC7 11.RC9 12. Internalizing

1

2

3

4

5

6

7

8

9

10

11

12

– .78 .86 .90 .92 .87 .58 .52 .31 .57 .37 .80

– .73 .74 .72 .70 .47 .47 .23 .52 .24 .66

– NA .91 NA .67 .64 .37 .60 .33 .79

– NA .90 .69 .66 .38 .64 .36 .86

– NA .65 .60 .40 .65 .40 .87

– .56 .50 .38 .60 .38 .76

– .86 .52 .90 .45 NA

– .31 .68 .08 NA

– .53 .61 NA

– .66 NA

– NA

–

Note. PTSD = posttraumatic stress disorder; RCd = Demoralization; RC2 = Low Positive Emotions; RC4 = Antisocial Behavior; RC7 = Dysfunctional Negative Emotions; RC9 = Hypomanic Activation. Correlations between factors that were modeled in separate structural equation models (e.g., emotional numbing and dysphoria, internalizing and the RC scales) cannot be computed and are reflected as NA in the table. All correlations were statistically significant at the p < .05 level.

and for social phobia = .37; standard error for these indicators was .05, .06, .08, and .06, respectively).

Convergent and Discriminant Validity To evaluate the convergent and discriminant validity of the two models, we compared patterns of association between the PTSD symptom factors of the King and Simms/Watson models with the internalizing latent variable and the RC scales. Table 2 contains a matrix of correlations among the PTSD symptom factors, the internalizing factor, and the RC scales, adjusted for measurement error. To address our first study hypothesis, that the Simms/Watson dysphoria factor captures symptom variance related to general distress better than either the numbing or hyperarousal factor of the King model, we compared the relative associations of these three PTSD factors with internalizing. Results of between-model analyses showed no significant difference between the strength of the Simms/Watson dysphoria factor correlation with internalizing relative to that of the King hyperarousal factor (r s = .86 and .87, respectively), z < 1. The Simms/Watson dysphoria factor was more strongly associated with internalizing (r = .86) relative to the King emotional numbing factor (r = .79), z = 5.26, p < .001. Our second hypothesis was that stronger associations would be observed between the Simms/Watson dysphoria factor and the RC Demoralization and Dysfunctional Negative Emotions scales than between either the King numbing or King hyperarousal factors and these two RC scales. Again, contrary to prediction, betweenmodel analyses showed no significant difference in strengths of association with Demoralization between the King numbing and Simms/Watson dysphoria factors (r s = .67 and .69, respectively), z < 1, or in the strength of association with Demoralization be-

tween the Simms/Watson dysphoria and King hyperarousal factors (r s = .69 and .65, respectively), z = 1.72, ns. Similarly, the association between the Simms/Watson dysphoria factor and Dysfunctional Negative Emotions (r = .64) was equivalent to both the association between the King numbing factor and Dysfunctional Negative Emotions (r = .60), z = 1.54, ns, and to the relationship between the King hyperarousal factor and Dysfunctional Negative Emotions (r = .65), z < 1. Our third hypothesis was that the King numbing factor would evidence stronger associations with Low Positive Emotions than would the Simms/Watson dysphoria factor. Contrary to prediction, analyses revealed no difference in the strength of association between the King emotional numbing factor and Low Positive Emotions and the Simms/Watson dysphoria factor and this RC scale (r s = .64 and .66), z < 1. Finally, all PTSD factors from both models evidenced discriminant validity with respect to their associations with the Antisocial Behavior and Hypomanic Activation scales in that these associations were greatly attenuated relative to their associations with Demoralization and Dysfunctional Negative Emotions. Specifically, the Simms/Watson dysphoria factor correlated with RC4 (r = .38) and RC9 (r = .36) equivalently to the King Emotional Numbing factor with RC4 and RC9 (r = .37, z = .28, p = .78 and r = .33, z = .81, p = .42, respectively). Similarly, the two hyperarousal factors showed equivalent patterns of association with RC4 and RC9 (both r s for King hyperarousal factor = .40 versus both r s for Simms/Watson hyperarousal factor = .38), zs < 1.

DISCUSSION Research on the factor structure of PTSD symptoms has primarily yielded support for two alternative models, referred to here as


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the King (King et al., 1998) and Simms/Watson models (Simms et al., 2002). Until recently, the majority of published studies in this area had provided support for the King model and there was a degree of a consensus among authorities in the field that it provided the best fit to the 17 DSM-IV symptoms of PTSD. More recently, the Simms/Watson model has attracted attention because it purports to capture, on one factor, the general symptoms of distress/dysphoria thought to be common to all of the internalizing or emotional disorders. In doing so, it aims to distinguish common dysphoria symptoms (C3–C7) from ones that are thematically linked to trauma (B1–5, C1–2) or do not appear in other DSMIV diagnoses (D4 and D5). In this respect, the Simms/Watson model is compatible with proposals to improve the discriminant validity of PTSD by distinguishing (or potentially eliminating) symptoms that are not unique to the diagnosis (e.g., Spitzer et al., 2007). The primary goal of this study was to evaluate whether the Simms/Watson model accomplishes this aim. We approached this question by developing hypotheses, derived from Simms et al.’s (2002) work, about model relations to external convergent and discriminant validity measures and testing them using data drawn from a large and carefully assessed sample of veterans with a high prevalence of PTSD. Results suggested that the Simms/Watson Dysphoria factor failed to show improved associations with any of the external measures examined relative to the numbing or hyperarousal factors of the King model. The strongest test of study hypotheses involved the comparison of model associations with a latent variable representing the common variance shared by major depressive disorder, social phobia, panic disorder, and obsessive–compulsive disorder (i.e., an Internalizing factor). We hypothesized that if the Simms/Watson model captures symptom variance related to general distress better than the King model, then we would find stronger correlations between dysphoria and internalizing relative to the strength of these associations for both of the King factors. Analyses showed no significant advantage for the Simms/Watson dysphoria factor compared to the King hyperarousal factor in terms of their respective associations with internalizing comorbidity. Similarly, when we compared the two models with respect to their associations with the Demoralization, Low Positive Emotions, and Dysfunctional Negative Emotions RC scales, we also found no significant improvement in variance accounted for by the Simms/Watson dysphoria factor relative to the more strongly associated of the two King factors. At the same time, we also found no evidence to support our hypothesis that the King numbing factor would evidence stronger associations with Low Positive Emotions than would the Simms/Watson dysphoria factor. Thus, results provided no evidence that the Simms/Watson dysphoria factor captures symptom variance related to general distress better than the numbing and hyperarousal factors of the King model and the models were also equivalent in the prediction of positive emotional deficits. These findings are consistent with results of another recent study that tested assumptions of the Simms/Watson model

and found that the dysphoria symptoms were no more strongly correlated than other PTSD symptoms with separate measures of general distress (Marshall, Schell, & Miles, 2010). This conclusion should be weighed in light of study limitations including its exclusive focus on male military veterans, which leaves unaddressed the extent to which results generalize to women and civilian samples. The study was also limited by the absence of symptom- or item-level data for comorbid diagnoses, which otherwise would have allowed us to examine directly the construct overlap between depression, for example, and the PTSD symptom factors of the two models. Notable strengths of the study that arguably mitigate these weakness include (a) a large sample with a high base rate of individuals with PTSD (i.e., 70% met criteria for lifetime or current PTSD); (b) current symptom data based on a gold-standard structured interview administered by clinicians; and (c) the use of latent variables (as well as single indicators adjusted for measurement error) in analyses that examined external correlates in relation to the two primary models of interest. Results of this study have implications for proposed revisions to the PTSD diagnosis in future editions of the DSM and ICD classification system. Though the Simms et al. (2002) model is conceptually appealing from a comorbidity theory standpoint and may provide excellent fit to the data in many samples, evidence for its incremental external validity relative to the King model is scant. In contrast, the theoretical and empirical distinction between numbing and hyperarousal has guided clinical and neurobiological research on PTSD since DSM-III. There is evidence for the clinical utility of this distinction and the putative neurobiological mechanisms underlying these separate factors. Absent clearer, more compelling evidence for the external validity and psychometric superiority of an alternative model, it would seem imprudent to discard 30 years of research based on the distinction between numbing and hyperarousal.

REFERENCES American Psychiatric Association. (1980). Diagnostic and statistical manual of mental disorders (3rd ed.). Washington, DC: Author. American Psychiatric Association. (1987). Diagnostic and statistical manual of mental disorders (3rd ed., rev.). Washington, DC: Author. Arbisi, P. A., & Ben-Porath, Y. S. (1995). An MMPI-2 infrequent response scale for use with psychopathological populations: The Infrequency-Psychopathology Scale, F(p). Psychological Assessment, 7, 424–431. Baschnagel, J. S., O’Connor, R. M., Colder, C. R., & Hawk, L. W., Jr. (2005). Factor structure of posttraumatic stress among Western New York undergraduates following the September 11th terrorist attack on the World Trade Center. Journal of Traumatic Stress, 18, 677–684. Bodkin, J. A., Pope, H. G., Detke, M. J., & Hudson, J. I. (2007). Is PTSD caused by traumatic stress? Journal of Anxiety Disorders, 21, 176–182. Brown, T. A. (2006). Confirmatory factor analysis for applied research. New York: Guilford Press. Brown, T. A., & Barlow, D. H. (2009). A proposal for a dimensional classification system based on the shared features of the DSM-IV anxiety and mood disorders:


Competing Models for the Structure of PTSD Symptoms Implications for assessment and treatment. Psychological Assessment, 21, 256– 271. Brown, T. A., Campbell, L. A., Lehman, C. L., Grisham, J. R., & Mancill, R. B. (2001). Current and lifetime comorbidity of the DSM-IV anxiety and mood disorders in a large clinical sample. Journal of Abnormal Psychology, 110, 585–599. Butcher, J. N., Dahlstrom, W. G., Graham, J. R., Tellegen, A. M., & Kaemmer, B. (1989). MMPI-2: Manual for administration and scoring. Minneapolis, MN: University of Minnesota Press. Clark, L. A. (2005). Temperament as a unifying basis for personality and psychopathology. Journal of Abnormal Psychology, 114, 505– 521. Clark, L. A., & Watson, D. (2006). Distress and fear disorders: An alternative empirically based taxonomy of the “mood” and “anxiety” disorders. British Journal of Psychiatry, 189, 481–483. Elhai, J. D., Ford, J. D., Ruggiero, K. J., & Frueh, B. C. (2009). Diagnostic alterations for posttraumatic stress disorder: Examining data from the National Comorbidity Survey Replication and National Survey of Adolescents. Psychological Medicine, 39, 1957–1966. Elklit, A., & Shevlin, M. (2007). The structure of PTSD symptoms: A test of alternative models using confirmatory factor analysis. British Journal of Clinical Psychology, 46, 299–313. Engelhard, I. M., Arntz, A., & van den Hout, M. A. (2007). Low specificity of symptoms on the post-traumatic stress disorder (PTSD) symptom scale: A comparison of individuals with PTSD, individuals with other anxiety disorders and individuals without psychopathology. British Journal of Clinical Psychology, 46, 449–456. Forbes, D., Creamer, M., & Biddle, D. (2001). The validity of the PTSD Checklist as a measure of symptomatic change in combat-related PTSD. Behaviour Research and Therapy, 39, 977–986. 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. Keane, T. M., Kolb, L. C., Kaloupek, D. G., Orr, S. P., Blanchard, E. B., Thomas, R. G., et al. (1998). Utility of psychophysiological measurement in the diagnosis of posttraumatic stress disorder: Results from a Department of Veterans Affairs Cooperative Study. Journal of Consulting and Clinical Psychology, 66, 914– 923. Kessler, R. C., Sonnega, A., Bromet, E., Hughes, M., & Nelson, C. B. (1995). Posttraumatic stress disorder in the National Comorbidity Survey. Archives of General Psychiatry, 52, 1048–1060. King, D. W., Leskin, G. A., King, L. A., & Weathers, F. W. (1998). Confirmatory factor analysis of the clinician-administered PTSD Scale: Evidence for the dimensionality of posttraumatic stress disorder. Psychological Assessment, 10, 90–96. Kline, R. B. (2005). Principles and practice of structural equation modeling (2nd ed.). New York: Guilford Press. Krause, E. D., Kaltman, S., Goodman, L. A., & Dutton, M. A. (2007). Longitudinal factor structure of posttraumatic stress symptoms related to intimate partner violence. Psychological Assessment, 19, 165–175. Krueger, R. F. (1999). The structure of common mental disorders. Archives of General Psychiatry, 56, 921–926. Kulka, R. A., Schlenger, W. E., Fairbank, J. A., Hough, R. L., Jordan, B. K., Marmar, C. R., et al. (1990). Trauma and the Vietnam War generation: Report on the findings from the National Vietnam Veterans Readjustment Study. New York: Brunner/Mazel. Litz, B. T., & Gray, M. J. (2002). Emotional numbing in posttraumatic stress disorder: Current and future research directions. Australian and New Zealand Journal of Psychiatry, 36, 198–204.

637

Marshall, G. N., Schell, T. L., & Miles, J. N. V. (2010). All PTSD symptoms are highly associated with general distress: Ramifications for the dysphoria symptom cluster. Journal of Abnormal Psychology, 119, 126–135. McNally, R. J. (1992). Psychopathology of posttraumatic stress disorder (PTSD): Boundaries of the syndrome. In M. Basoglu (Ed.), Torture and its consequences: Current treatment approaches (pp. 229–252). Cambridge: Cambridge University Press. McWilliams, L. A., Cox, B. J., & Asmundson, G. J. (2005). Symptom structure of posttraumatic stress disorder in a nationally representative sample. Journal of Anxiety Disorders, 19, 626–641. Miller, M. W. (2003). Personality and the etiology and expression of PTSD: A three-factor model perspective. Clinical Psychology: Science and Practice, 10, 373–393. Miller, M. W., Kaloupek, D. G., Dillon, A. L., & Keane, T. M. (2004). Externalizing and internalizing subtypes of combat-related PTSD: A replication and extension using the PSY-5 scales. Journal of Abnormal Psychology, 113, 636–645. Miller, M. W., Vogt, D. S., Mozley, S. L., Kaloupek, D. G., & Keane, T. M. (2006). PTSD and substance-related problems: The mediating roles of disconstraint and negative emotionality. Journal of Abnormal Psychology, 115, 369– 379. Mineka, S., Watson, D., & Clark, L. A. (1998). Comorbidity of anxiety and unipolar mood disorders. Annual Review of Psychology, 49, 377–412. Muthén, L. K., & Muthén, B. O. (1998–2007). Mplus user’s guide (4th ed.). Los Angeles: Author. Palmieri, P. A., & Fitzgerald, L. F. (2005). Confirmatory factor analysis of posttraumatic stress symptoms in sexually harassed women. Journal of Traumatic Stress, 18, 657–666. Palmieri, P. A., Marshall, G. N., & Schell, T. L. (2007). Confirmatory factor analysis of posttraumatic stress symptoms in Cambodian refugees. Journal of Traumatic Stress, 20, 207–216. Palmieri, P. A., Weathers, F. W., Difede, J., & King, D. W. (2007). Confirmatory factor analysis of the PTSD Checklist and the Clinician-Administered PTSD Scale in disaster workers exposed to the World Trade Center ground zero. Journal of Abnormal Psychology, 116, 329–341. Rosen, G. M., & Lilienfeld, S. O. (2008). Posttraumatic stress disorder: An empirical evaluation of core assumptions. Clinical Psychology Review, 28, 837– 868. Sellbom, M., & Ben-Porath, Y. S. (2005). Mapping the MMPI-2 Restructured Clinical Scales onto normal personality traits: Evidence of construct validity. Journal of Personality Assessment, 85, 179–187. Sellbom, M., Ben-Porath, Y. S., & Graham, J. R. (2006). Correlates of the MMPI-2 Restructured Clinical (RC) Scales in a college counseling setting. Journal of Personality Assessment, 86, 88–99. Sellbom, M., Graham, J. R., & Schenk, P. W. (2006). Incremental validity of the MMPI-2 Restructured Clinical (RC) Scales in a private practice sample. Journal of Personality Assessment, 86, 196–205. Simms, L. J., Casillas, A., Clark, L. A., Watson, D., & Doebbeling, B. N. (2005). Psychometric evaluation of the Restructured Clinical Scales of the MMPI-2. Psychological Assessment, 17, 345–358. Simms, L. J., Watson, D., & Doebbeling, B. N. (2002). Confirmatory factor analyses of posttraumatic stress symptoms in deployed and nondeployed veterans of the Gulf War. Journal of Abnormal Psychology, 111, 637–647. Spitzer, R. L., First, M. B., & Wakefield, J. C. (2007). Saving PTSD from itself in DSM-V. Journal of Anxiety Disorders, 21, 233–241. Spitzer, R. L., Williams, J. B. W., Gibbon, M., & First, M. D. (1989). Structured Clinical Interview for DSM-III-R, Patient Version (SCID-P). New York: New York State Psychiatric Institute.


638

Miller et al.

Tellegen, A. (1985). Structures of mood and personality and their relevance to assessing anxiety, with an emphasis on self-report. In A. H. Tuma & J. D. Maser (Eds.), Anxiety and the anxiety disorders (pp. 681–706). Hillsdale, NJ: Erlbaum. Tellegen, A., Ben-Porath, Y. S., McNulty, J. L., Arbisi, P. A., Graham, J. R., & Kaemmer, B. (2003). The MMPI-2 Restructured Clinical (RC) Scales: Development, validation, and interpretation. Minneapolis, MN: University of Minnesota Press. Tellegen, A., Ben-Porath, Y. S., Sellbom, M., Arbisi, P. A., McNulty, J. L., & Graham, J. R. (2006). Further evidence on the validity of the MMPI-2 Restructured Clinical (RC) Scales: Addressing questions raised by Rogers, Sewell, Harrison, and Jordan and Nichols. Journal of Personality Assessment, 87, 148– 171.

Watson, D. (2005). Rethinking the mood and anxiety disorders: A quantitative hierarchical model for DSM-V. Journal of Abnormal Psychology, 114, 522–536. Weathers, F. W., Litz, B. T., Herman, D. S., Huska, J. A., & Keane, T. M. (1993, October). The PTSD Checklist (PCL): Reliability, validity, and diagnostic utility. Paper presented at the Annual Convention of the International Society for Traumatic Stress Studies, San Antonio, TX. Wolf, E. J., Miller, M. W., Orazem, R. O., Weierich, M. R., Castillo, D. T., Milford, J., et al. (2008). The MMPI-2 Restructured Clinical Scales in the assessment of posttraumatic stress disorder and comorbid disorders. Psychological Assessment, 20, 327–340. Zinbarg, R. E., & Barlow, D. H. (1996). Structure of anxiety and the anxiety disorders: A hierarchical model. Journal of Abnormal Psychology, 105, 181–193.


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