Journal of Traumatic Stress April 2014, 27, 175–181

PTSD Symptoms and Pain in Canadian Military Veterans: The Mediating Roles of Anxiety, Depression, and Alcohol Use Kara C. Irwin,1 Candace Konnert,1 May Wong,2 and Thomas A. O’Neill1 1

Department of Psychology, University of Calgary, Calgary, Alberta, Canada 2 Carewest Operational Stress Injury Clinic, Calgary, Alberta, Canada

Symptoms of posttraumatic stress disorder (PTSD) and pain are often comorbid among veterans. The purpose of this study was to investigate to what extent symptoms of anxiety, depression, and alcohol use mediated the relationship between PTSD symptoms and pain among 113 treated male Canadian veterans. Measures of PTSD, pain, anxiety symptoms, depression symptoms, and alcohol use were collected as part of the initial assessment. The bootstrapped resampling analyses were consistent with the hypothesis of mediation for anxiety and depression, but not alcohol use. The confidence intervals did not include zero and the indirect effect of PTSD on pain through anxiety was .04, CI [.03, .07]. The indirect effect of PTSD on pain through depression was .04, CI [.02, .07]. These findings suggest that PTSD and pain symptoms among veterans may be related through the underlying symptoms of anxiety and depression, thus emphasizing the importance of targeting anxiety and depression symptoms when treating comorbid PTSD and pain patients.

Posttraumatic stress disorder (PTSD) and pain are common among veterans who experience difficulties with the transition to civilian life. A recent survey of 1,072 Canadian veterans indicated that 80.3% of New Veterans Charter clients reported that pain or discomfort were always present and 42.5% had a diagnosis of PTSD (Thompson et al., 2011). Beckham et al. (1997) found that among their sample of 129 Vietnam veterans in an outpatient PTSD clinic, 80% reported chronic pain. Similarly, Otis et al. (2010) reported that 49% of their sample of 149 US veterans in a psychology pain management program also met criteria for PTSD. Although this study comprised primarily male veterans, the comorbidity of PTSD and pain symptoms has also been reported among female veterans. Asmundson, Wright, and Stein (2004) found that women with PTSD reported significantly more pain when compared to women with subsyndromal PTSD or no PTSD. This pattern of comorbidity can increase symptom severity of either or both conditions (Asmundson & Taylor, 2006). There is emerging evidence that the relationship between PTSD and pain is not just correlational in nature. The first longitudinal study to investigate this indicated that among 824 trauma patients, the relationship between acute pain at baseline and pain at 12-month follow-up was mediated by arousal symptoms at 3 months (Liedl et al., 2010).

Thus, arousal appears to play an important causal role in the maintenance of pain over time. Both PTSD and pain are highly comorbid with other mental health problems among veterans, including other anxiety disorders, depression, and substance abuse. Thompson et al. (2011) reported that among New Veterans Charter clients reporting pain or discomfort (always or recurring), 48.4% also experienced a mood disorder. Using structured diagnostic interviews, Orsillo et al. (1996) found that among 311 male Vietnam veterans with PTSD, 82% met criteria for another Axis I disorder, most often an anxiety (46%) or mood (68%) disorder. In the National Vietnam Veterans Readjustment Study, one of the largest to date, veterans with PTSD were two to six times more likely to abuse alcohol or drugs, compared to those without PTSD (Kulka et al., 1990). A variety of theoretical models have been proposed to account for the comorbidity of PTSD and pain (see review by Otis, Keane, & Kerns, 2003). In one of the models, Sharp and Harvey (2001) proposed a number of cognitive, affective, and behavioral factors by which PTSD and chronic pain are mutually maintained, including general anxiety, factors related to depression (e.g., negative attentional biases, fatigue, and lethargy), and reduced adaptive coping due to the cognitive demands of PTSD and pain symptoms. The most common maladaptive coping strategy that is discussed in the literature is avoidance, as described in the fear-avoidance model (Norton & Asmundson, 2003). In this model, avoidance is a central process underlying both pain and PTSD. In chronic pain, avoidance is most often related to activities that may be perceived by the individual as exacerbating pain, which in turn leads to further functional

Correspondence concerning this article should be addressed to Candace Konnert, Department of Psychology, University of Calgary, 2500 University Drive NW, Calgary, Alberta, Canada. E-mail: [email protected] C 2014 International Society for Traumatic Stress Studies. View Copyright  this article online at wileyonlinelibrary.com DOI: 10.1002/jts.21897

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disability and poor coping self-efficacy. In PTSD, avoidance is related to a fear of reexperiencing thoughts and feelings associated with the traumatic event. This pattern of avoiding behavior prevents individuals from effectively processing the traumatic event to a cohesive episode and narrative, resulting in fragmented memories and other symptoms seen in PTSD. Investigating potential mediators is important for theory development and a more complete understanding of the relationship between comorbid PTSD and pain. Anxiety and depression have been proposed as mediators given that they share significant symptom overlap with PTSD and pain across physiological (e.g., hyperarousal), cognitive (e.g., attentional biases), and behavioral (e.g., avoidance) domains, and additionally may share common vulnerability factors such as anxiety sensitivity (Asmundson, Coons, Taylor, & Katz, 2002). Theoretically, Sharp and Harvey (2001) denote that anxiety sensitivity for those with comorbid PTSD and pain may additionally fuel a vulnerability to misinterpret and catastrophize the physical sensations associated with pain and arousal. The fatigue, lethargy, and reduced activity levels associated with depression may contribute to increased disability and lack of exposure to and emotional processing of trauma related stimuli (Sharp & Harvey, 2001). Clinically, clients presenting chronic pain and comorbid mental health conditions are among the most challenging to treat due to their complex presentations. To date, there is limited evidence that existing treatments for PTSD and pain are efficacious for clients with comorbid pain and PTSD (Beck & Clapp, 2011). If depression and anxiety symptoms are mediators, targeting these symptoms may have significant collateral benefits for pain and PTSD. Although these theories identify possible underlying factors to explain the relationship between PTSD and pain, there has been limited empirical research supporting these potential mediators. To date, only one study has investigated depression as a mediator between PTSD and pain. Poundja, Fikretoglu, and Brunet (2006) reported that among their sample of 130 male veterans with PTSD, 69.2% reported severe pain on the Brief Pain Inventory whereas 17.7% and 10% reported moderate or mild pain, respectively. Mediation analyses indicated that 89.5% of the effect of PTSD on pain was through depression. In a related study, Jakupcak et al. (2006) investigated anxiety sensitivity and depression as mediators between PTSD and the more general category of somatic symptoms, which included pain and other cardiopulmonary symptoms (e.g., racing heart, shortness of breath). Among 45 male veterans who were inpatients at a PTSD Evaluation and Brief Treatment Unit, PTSD symptoms were positively and significantly correlated with anxiety sensitivity, depression symptoms, and somatic symptoms. When anxiety sensitivity and depression symptoms were entered into the regression analyses, however, PTSD symptoms no longer accounted for the major proportion of variance in somatic complaints. These results are consistent with those of Asmundson, Stein, and McCreary (2002) who reported that PTSD symptoms indirectly influenced health status through depression.

Given the significant comorbidity between PTSD and substance abuse (Kulka et al., 1990), alcohol use may be an additional and important mediator to investigate. Two studies have investigated alcohol use as a mediator among veterans; however, somatic symptoms were the focus in both studies rather than pain per se. Using structural equation modeling, Vasterling et al. (2008) tested the hypothesis that health risk behaviors, including alcohol consumption, would mediate PTSD and somatic symptoms in 800 US army soldiers who had been deployed to Iraq. The statistical model revealed no evidence that alcohol consumption mediated PTSD and somatic symptoms. A limitation of this study, however, is that alcohol consumption was assessed using a screening instrument that simply asked about the average number of alcoholic drinks consumed per week in the last month rather than using a measure with sound psychometric properties to assess for alcohol use. Asmundson et al. (2002) also tested alcohol use as an indirect path from PTSD to somatic symptoms among 1,187 formerly deployed Canadian male peacekeepers. Alcohol use, as assessed by frequency and quantity of use as well as occasions of heavy drinking, did not account for poorer health outcomes, over and above the contribution of PTSD symptoms. The current study is designed to extend the research literature in two ways. First, most mediational studies have focused on somatic complaints (of which pain was a component) as the outcome variable. Researchers have suggested that there may be unique relationships between PTSD and various components of physical health (e.g., pain, somatic complaints) and that pain is different from other indices of health (Poundja et al., 2006). Beckham et al. (1997) reported that veterans with more PTSD reexperiencing symptoms had higher levels of pain. Thus, the experience of pain may serve as a reminder of the original trauma, leading to memories of the event, heightened levels of arousal, and an avoidance response (Otis, Pincus, & Keane, 2006). Second, this study is the first of which we are aware to investigate these variables in veterans, who experience pain as more severe, chronic, and related to higher functional impairment when compared to the general population (Crosby, Colestro, Ventura, & Graham, 2006; Keane, Weathers, & Taft, 2006). To summarize, the literature suggests possible mediating roles of anxiety, depression and substance use on the relationship between symptoms of posttraumatic stress and pain. Based on the research of Poundja et al. (2006), we hypothesized that depression would mediate the relationship between PTSD and pain. Given the limited empirical evidence on the role of anxiety and alcohol use in the relationship between PTSD and pain, there were no specific hypotheses regarding their mediating influences. Method Participants and Procedure Participants were male veterans undergoing an initial assessment at the Carewest Operational Stress Injury (OSI) Clinic in

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

Mediators of PTSD Symptoms and Pain in Veterans

Table 1 Demographic and Military Characteristics of Participants Variable Highest level of educationa Less than high school High school diploma College diploma University degree Other Employment previous 6 monthsb Unemployed Sporadic employment Regular employment Student Retired Marital statusc Single Common law Married Divorced Separated Widowed Release from militaryd Voluntary honorable Medical Administrative reasons Retired Resigned Years since injurye ࣘ4 5–14 15–24 25–34 ࣙ35

n

%

19 46 9 9 17

19.0 46.0 9.0 9.0 17.0

36 8 48 1 14

33.6 7.5 44.9 0.9 13.1

17 9 62 17 5 1

15.3 8.1 55.9 15.3 4.5 0.9

20 45 19 12 2

20.4 45.9 19.4 12.2 2.0

9 30 23 10 14

10.5 34.9 26.7 11.6 16.3

Note. N = 113. Percentages may not total 100% due to rounding error. Missing data: a 13, b 6, c 2, d 15, e 27.

Calgary, Alberta, Canada. The Calgary OSI Clinic is one of 10 clinics in Canada that provide specialized assessment and treatment to veterans, Canadian Forces members, the Royal Canadian Mounted Police, and their families. Of the 220 clients assessed, 15 (6.8%) female clients were excluded due to small numbers, 31 (14.1%) were nonveterans (Royal Canadian Mounted Police or active duty military clients), and 61 (27.7%) did not complete measures of PTSD and pain. These exclusionary criteria resulted in 113 participants. The study was approved by the University of Calgary Conjoint Faculty Research Ethics Board. Table 1 presents demographic and military characteristics for the sample. Mean age was 48.14 years (SD = 14.44, range = 22–87 years). As indicated in Table 1, most had at least a high school education (81.0%), were engaged in regular employment (44.9%) or unemployed (33.6%), and were married (55.9%).

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The majority of veterans had served in the Army (81.7%), with a rank of Corporal (35.1%), Master Corporal (17.6%), or Warrant Officer (12.2%). Participants were deployed an average of 2.32 times (SD = 1.37) and 45.9% received a medical release. All veterans in this sample experienced an operational stress injury related to service, most often 5 to 14 (34.9%) or 15 to 24 (26.7%) years ago. Measures Symptoms of posttraumatic stress were assessed using the Detailed Assessment of Posttraumatic Stress (DAPS), a 104-item self-report measure based on a 5-point scale; higher scores indicate more severe symptoms (Briere, 2001). The DAPS has an internal consistency of .83. and convergent validities of .73 with the Posttraumatic Stress Disorder Checklist and .78 with the Clinician Administered PTSD Scale (McFall, Smith, Roszell, Tarver, & Malas, 1990). When compared with the Clinician Administered PTSD Scale for diagnostic utility, it yielded a sensitivity of .88 and a specificity of .86 (McFall et al., 1990). Pain was assessed using the Brief Pain Inventory, a self-report measure of pain intensity and pain interference (BPI; Cleeland, 1989). Internal consistency estimates were .85 for intensity and .88 for interference (Tan, Jensen, Thornby, & Shanti, 2004). For veterans, cut points for pain severity are as follows: mild (1–3), moderate (4–7), and severe (8–10; Tan, Jensen, Thornby, Rintala, & Anderson, 2008). Anxiety symptoms were assessed using the Beck Anxiety Inventory (BAI), a 21-item measure with ratings from 0 to 3 (Beck, Epstein, Brown, & Steer, 1988). Higher scores indicate more anxiety symptomatology. Internal consistency was .94 and it has a 2-factor solution representing cognitive and somatic symptoms (Fydrich, Dowdall, & Chambless, 1992; Hewitt, & Norton, 1993). Depression was assessed using the Beck Depression Inventory-II (BDI-II), a 21-item measure with ratings from 0 to 3 (Beck, Steer, & Brown, 1996). Higher scores indicate more depressive symptomatology. Internal consistency was .91 and factor analysis revealed two distinct factors (cognitiveaffective and somatic-vegetative symptoms; Dozois, Dobson, & Ahnberg, 1998). Alcohol use (intake, dependence, and adverse consequences) was assessed with the Alcohol Use Disorders Identification Test (AUDIT), a 10-item measure with ratings from 0 to 4 (Saunders, Aasland, Babor, de la Fuente, & Grant, 1993). A score of 8 or above indicates a potential alcohol problem (Saunders et al., 1993). A meta-analysis indicated a median sensitivity of .86, a median specificity of .89, and internal consistencies in the mid .80s (Reinert, & Allen, 2002). Data Analysis The mediating variables examined were anxiety symptoms (BAI), depression symptoms (BDI-II), and alcohol use (AUDIT). The significance of the mediated effect can be tested using a number of procedures. One promising approach involves the

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Table 2 Descriptive Statistics and Pearson Correlations Variable 1. DAPS 2. BPI 3. BAI 4. BDI 5. AUDIT

Results

α

M

SD

1

2

3

4

.96 .97 .88 .91 .74

87.10 4.42 18.44 25.78 8.18

19.80 2.90 9.67 11.15 8.50

– .23* .50** .52** .05

– .48** .51** -.12

– .60** .12

– .07

Note. N = 113. DAPS = Detailed Assessment of Posttraumatic Stress; BPI = Brief Pain Inventory; BAI = Beck Anxiety Inventory; BDI = Beck Depression Inventory; AUDIT = Alcohol Use Disorders Identification Test. *p < .05. **p < .001.

bootstrapping method, for which Preacher and Hayes (2004) offered an SPSS macro that estimates parameters and significance levels involving mediation. Recent simulation studies support the accuracy and power to detect mediation effects using this approach (e.g., Williams & MacKinnon, 2008). The macro estimates the 95% confidence interval (CI) of the indirect effect of the exogenous predictor (i.e., PTSD) on the final criterion (i.e., pain). It does this by comparing the observed indirect effect against a bootstrapped distribution constructed from 1,000 parallel data sets. Each simulated parallel data set is constructed by sampling randomly from the observed data set with replacement. If the CI does not include zero, the indirect (mediated) effect is significantly different than zero (Hayes, 2009; Preacher & Hayes, 2008).

Table 2 provides internal consistency reliabilities (Cronbach’s αs), descriptive statistics and Pearson correlations for measures of PTSD, pain, anxiety, depression, and alcohol use. Internal consistency reliabilities were good to excellent, with the exception of the AUDIT, which was acceptable. Average ratings for PTSD symptoms were in the moderate to severe range, whereas average ratings for pain severity, anxiety, and depression were in the moderate range. Approximately 40% of the sample was above the cutoff for potential alcohol misuse. Figure 1 contains unstandardized path coefficients involving the direct effects of PTSD on the proposed mediator variables, and the direct effects of the proposed mediator variables on pain. Using the bootstrapping methods advanced by Preacher and Hayes (2004), the test of anxiety as a mediator of the relationship between PTSD and pain was supported. Specifically, the CIs did not include zero and the magnitude of the indirect effect of PTSD on pain through anxiety was .04, 95% CI [.03, .07]. The findings are consistent with a mediational effect for depression .04, 95% CI [.02, .07]. Finally, the test of mediation involving alcohol use was .00, which was small and not significant, 95% CI [−.01, .00].

Discussion The results of this study support the theory speculating that anxiety and depression symptoms mediate the relationship between PTSD symptoms and pain. Findings were not supportive

Figure 1. Anxiety, depression, and alcohol use as mediators in the relationship between posttraumatic stress disorder (PTSD) and pain. Unstandardized path coefficients marked with an asterisk are associated with bootstrap confidence intervals that do not include zero and are considered significant (p < .05). Journal of Traumatic Stress DOI 10.1002/jts. Published on behalf of the International Society for Traumatic Stress Studies.

Mediators of PTSD Symptoms and Pain in Veterans

of alcohol use as a potential mediator between the relationship of PTSD symptoms and pain, consistent with studies that investigated alcohol use as a mediator between PTSD symptoms and general health status (Asmundson et al., 2002; Vesterling et al., 2008). This study replicates the findings of previous research using the AUDIT (Saunders et al., 1993), a more comprehensive measure with strong psychometric properties. The lack of support for the mediational effect of alcohol use may be related to the relatively low rates of problematic alcohol use in this sample. Overall, 61.1% of respondents scored below the cutoff, and the mean value was 8.23 out of a potential score of 40. Similar, low frequencies of alcohol consumption were reported by Asmundson et al. (2002) and Vasterling et al. (2008). Future studies should examine the mediating influence of alcohol use among veteran samples with a broader representation of participants with drinking problems. The theoretical model proposed by Sharp and Harvey (2001) identifies several distinct processes that may explain the mutual maintenance of PTSD and pain, including attentional biases, anxiety sensitivity, avoidant coping style, and reduced levels of activity. These processes play a prominent role in theories of anxiety and depression and are the focus of attention in empirically supported treatments. Key components of cognitive–behavioral treatments for anxiety and depression including exposure, behavioral activation, and cognitive restructuring may be particularly beneficial for those with comorbid PTSD and pain. For instance, Alschuler and Otis (2012) reported that patients with comorbid pain and PTSD engaged in more catastrophic thinking and had more negative beliefs when compared to veterans with pain alone. Thus, it may be particularly beneficial to focus on cognitive restructuring for those with comorbid PTSD and pain to shift such cognitive tendencies. These commonalities across disorders suggest that anxiety and depression may mediate the relationship between pain and PTSD through shared underlying factors and future research should investigate these further. Numerous authors have noted the need for research on the assessment and treatment of comorbid pain and PTSD, particularly given that the prevalence of chronic pain in the military is expected to increase significantly over the next 10 years due to the greater physical demands associated with deployment (Beck & Clapp, 2011; McCreary, Moore, Vriend, Peterson, & Gatchel, 2011). If, as theory suggests, PTSD and pain are mutually maintained, treating only one disorder will likely result in high rates of relapse and poorer long-term outcomes for clients. These are complex clients who may not respond well to the traditional delivery of evidence-based assessments and treatments for specific disorders, and the evaluation of integrated treatments for comorbid PTSD and pain is in its infancy (McCreary et al., 2011; Otis, Keane, Kerns, Monson, & Scioli, 2009). There is a lack of clarity, however, around how these interventions should be modified when PTSD and pain are comorbid. For example, if anxiety sensitivity is the focus of treatment, should interoceptive exposure be modified when pain is present (Asmundson & Taylor, 2006)?

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On a positive note, the results of this study suggest that treatment targeting anxiety and depression may serve to undermine the relationship between PTSD and pain, breaking the cycle of mutual maintenance suggested by Sharp and Harvey (2001) and reducing symptoms of both conditions. There is considerable overlap between empirically supported psychosocial treatments for pain, PTSD, other anxiety disorders, and depression with a focus on exposure, cognitive restructuring, and psychoeducation. If, however, as the results of this study suggest, treating anxiety and depression has collateral beneficial effects on PTSD and pain, this increases the range of treatment alternatives for breaking the PTSD and pain cycle. For example, a recent meta-analysis provides strong evidence for the efficacy of mindfulness and acceptance-based interventions in reducing symptoms of anxiety and depression (Vøllestad, Nielsen, & Nielsen, 2012). Thus, emerging and promising treatments for anxiety and depression may also be useful in targeting PTSD and pain. These findings should be considered in the context of a number of limitations. First, female veterans were excluded from the study. Although there is evidence to suggest that PTSD and pain frequently co-occur in female veterans (Asmundson et al., 2004), the mediational effects reported in this study as well as in other studies including only male veterans (Poundja et al., 2006) are limited to this specific population and may be different in female veterans. Second, because the data were collected as part of an initial OSIC assessment and not specifically for this study, a more global measure of anxiety (the BAI) was used rather than one designed to assess anxiety sensitivity, the theoretical construct identified in the mutual maintenance model. Having said that, many of the items on the BAI are similar to those found on measures of anxiety sensitivity, such as the Bodily Sensations Questionnaire (Chambless, Caputo, Bright, & Gallagher, 1984), focusing on physiological and autonomic arousal symptoms. Third, this study examined alcohol use, however, given previous rates of cannabis use (Goldman et al., 2010) and opioid misuse (Seal et al., 2012) in this population, these substances should also be investigated as possible mediators. Fourth, all measures were self-report with their inherent biases, which in this population and setting, could conceivably involve either underreporting symptoms due to perceived stigma or overreporting in cases where decisions about future benefits are pending. Finally, data used in this study were cross sectional. Without temporal ordering of the variables as in a longitudinal design, causal relationships cannot be determined (Kraemer, Kiernan, Essex, & Kupfer, 2008). It remains unclear if symptoms of posttraumatic stress occur before pain, and the temporal sequencing of anxiety and depression in the relationship is unknown. In conclusion, the comorbidity of PTSD and pain among veterans is widely recognized and the results of the current study support possible mediating influences of anxiety and depression symptoms in this relationship. Clearly, these are potential areas for intervention in integrated treatment programs for patients presenting comorbid PTSD and pain. Theoretically and

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clinically, further research would benefit from more attention to the underlying processes that account for these comorbidities. This could inform more targeted interventions for veterans with PTSD and pain.

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

PTSD symptoms and pain in Canadian military veterans: the mediating roles of anxiety, depression, and alcohol use.

Symptoms of posttraumatic stress disorder (PTSD) and pain are often comorbid among veterans. The purpose of this study was to investigate to what exte...
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