CILR

www.elsevier.com/locate/cabp Cognitive and Behavioral Practice 13 (2006) 8–16

Addressing Shared Vulnerability for Comorbid PTSD and Chronic Pain: A Cognitive-Behavioral Perspective

Gordon J.G. Asmundson and Heather D. Hadjistavropolous, University of Regina, Saskatchewan

Posttraumatic stress disorder (PTSD) frequently co-occurs with other conditions and symptoms that can complicate assessment and

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treatment. Of these, chronic musculoskeletal pain and related avoidance behaviors are amongst the most common and, unfortunately, the most often overlooked. In this paper we discuss issues that warrant consideration in developing and implementing a treatment plan that may maximize chances of successful outcome for GH, a patient with PTSD and chronic pain. Assessment strategies used in arriving at a case formulation are presented and, based on the emerging state-of-the-art, a tentative cognitive-behavioral treatment program targeting shared vulnerability for PTSD and chronic musculoskeletal pain is presented. Issues pertinent to anticipated treatment outcome are also discussed.

IT IS COMMON for patients with posttraumatic stressdisorder (PTSD) to present with a number of co- occurring somatic and mental health problems. These often include increased reporting of physical symptoms and physical health problems (Sareen, Cox, Clara, & Asmundson, 2005) as well as increased alcohol consump- tion and depressed mood (for reviews, see Resnick, Acierno, & Kilpatrick, 1997; Schnurr & Jankowski, 1999). Chronic musculoskeletal pain also frequently co- occurs with PTSD (in 50% to 80% of military or paramilitary personnel with PTSD and 20% to 30% of community dwellers with PTSD) and, although a signif- icant complicating factor, it is often overlooked in treatment planning and delivery (Asmundson et al., 2002; McWilliams et al., 2003). Road traffic collisions (RTCs), work-related injury, and service in combat and emergency rooms appear to be the most common events precipitating the development of PTSD accompanied by chronic pain (Asmundson et al., 1998; Beckham et al., 1997; Blanchard & Hickling, 2004; Taylor & Koch, 1995). Research suggests that people with comorbid PTSD and chronic pain, compared to those with only one of these conditions, have greater distress and impairment (Bryant et al., 1999). Various models, discussed in more detail below, have been proposed to explain the high comor- bidity between PTSD and chronic pain and can be useful in the process of assessment and treatment planning.

The purpose of this paper is to comment on the case of GH, a 40-year-old single male who developed PTSD,

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chronic pain, mild depression, and cued panic attacks subsequent to an RTC 9 months ago. Below we critique aspects of Wald and Taylor’s case conceptualization as well as their choice of assessment instruments. We also describe the approach we would recommend for assessment as well as our case conceptualization, adjuvant assessment strate- gies that might be considered, our tentative treatment plan, and the anticipated outcome for GH.

Getting Started

We believe that assessment is, in large part, a conceptually driven process. This means that theory should be at the foundation of any decisions regarding what is important to assess in any given case. The information gleaned from assessment is then used to develop the case formulation and, on this basis, the treatment plan. Cognitive-behavior therapists are fortu- nate in that they have fairly well developed theories regarding a large number of psychopathologies; however, there are often challenges in finding a starting point when a patient presents with multiple or comorbid complaints. This can make it difficult to identify which theoretical position or positions to choose as the basis for laying the foundation and, consequently, which of the presenting problems to focus on. GH represents one such challenge.

Based on the background information provided for GH—information that would often be available through review of the patient’s accident and post-accident medical history or on initial screening (as appears the case for GH)—there are several potential starting points. First, he was in a significant RTC in which he sustained a potential head trauma. Second, he sustained mild injury to other parts of his body and at 9 months post-accident was still

9Case Conference Response: Addressing Shared Vulnerability

bothered by pain in his neck and back. Third, he missed 6 weeks of work before returning part-time but was not involved in litigation related to the RTC. Finally, he reported irritability with others and difficulty concen- trating. An immediate challenge in GH’s case is determining whether to focus on issues related to the potential head trauma and GH’s report that a neuropsy- chologist said he had “mild, sustained, brain damage”— something that might explain his irritability and concen- tration difficulties—or to turn attention elsewhere.

We concur with Wald and Taylor’s decision to forgo further neuropsychological assessment. As they note, the observed deficits would likely be mild. The American Congress of Rehabilitation Medicine (1993) defines mild traumatic brain injury as an injury that results in anterograde amnesia of less than 24 hours. GH had anterograde amnesia for approximately 1 hour after regaining consciousness (the duration of which was not stated). The observed deficits would also be difficult to interpret given overlap with symptoms of PTSD and, indeed, with chronic pain. That is, the irritability and concentration difficulties may be symptomatic of these other conditions. Delaying assessment and treatment of other presenting problems in order to obtain additional neuropsychological screening does not seem warranted in this case. This leaves for consideration the primary issues of PTSD and chronic pain.

As noted at the outset of this paper, it is common for patients with PTSD to also present with chronic pain. The latter can complicate treatment of the former if overlooked in assessment and treatment planning (Asmundson et al., 2002; Wald, Taylor, & Fedoroff, 2004). Armed with knowledge of emerging cognitive- behavioral theories regarding the relationship between PTSD and chronic pain, the cognitive-behavioral ther- apist will have a strong foundation on which to base assessment, case conceptualization, and treatment planning for these potentially complicated cases. What are these theories? Wald and Taylor mention the theory of mutual maintenance (Asmundson et al., 2002; Sharp & Harvey, 2001) and use it as a foundation for assessment and case conceptualization. In essence, this theory posits that certain components of PTSD (e.g., physiological arousal, numbing of affect, behavioral avoidance) maintain or exacerbate symptoms of pain through increased muscle tension, inactivity, and the like and, similarly, that certain components of chronic pain (e.g., nociception, catastrophizing, behavioral avoidance) maintain or exacerbate symptoms of PTSD by serving as a persistent reminder of trauma.

A related theory is that of shared vulnerability (Asmundson et al., 2002). This theory holds that there are individual difference factors, possibly genetically determined, that predispose people to develop both

PTSD and chronic pain. Of several potential constructs that appear to denote these individual difference factors (see review by Turk, 2002), anxiety sensitivity appears most promising. Anxiety sensitivity is defined as the fear of anxiety-related bodily sensations based on the belief that they may have harmful cognitive, somatic, or social consequences and is believed to amplify the intensity of fear and anxiety responses (Reiss & McNally, 1985; Taylor, 1999). Anxiety sensitivity, as measured by the Anxiety Sensitivity Index (ASI; Peterson & Reiss, 1992), has been shown to be elevated in patients with PTSD (Taylor, Koch, & McNally, 1992) as well as in patients with chronic pain who present with significant function- al limitations (see review by Asmundson et al., 2000). Accumulating evidence supports the hypothesis that high levels of anxiety sensitivity increase the risk of pain- related avoidance and disability following physical injury (Asmundson & Taylor, 1996). There is also evidence that anxiety sensitivity may be genetically determined (Jang et al., 1999; Stein, Jang, & Livesley, 1999). Collectively, these finding suggest that people with high levels of anxiety sensitivity are prone to respond to traumatic stressors involving painful physical injury with more intense emotional reactions, such as fear that increases the likelihood of developing co-occurring PTSD and persistent pain-related problems (also see Turk, 2002). We will consider both the mutual maintenance and shared vulnerability theories as a foundation for further discussion of GH as both hold important implications for assessment, case conceptualization, and treatment planning.

Initial Assessment

Wald and Taylor present a comprehensive and well- planned assessment of GH. Their approach is to be commended on several grounds. It is conceptually grounded and based, in part, on the current state-of- the-art regarding cognitive-behavioral approaches to PTSD and its overlap with chronic pain (i.e., mutual maintenance theory). The use of both a general and specific structured clinical interview provides invaluable information regarding GH’s most salient problems as well as those that might have been otherwise overlooked. Indeed, while the Clinician Administered PTSD Scale (CAPS; Blake et al., 1997) provided rich detail on his PTSD symptoms, the addition of the Structured Clinical Interview for DSM-IV (SCID-IV; First et al., 1996) to the assessment package allowed for systematic identification and detailing of GH’s co-occurring problems with depression, panic attacks, and mild pain (in all cases at levels or in ways that didn’t warrant additional DSM-IV diagnoses). It also allowed other potential diagnoses that might impact on treatment planning (e.g., substance abuse) to be conclusively ruled out.

10 Asmundson & Hadjistavropolous

Although not always a standard part of clinical assessment, supplementing the clinical interview with self-report information allowed Wald and Taylor to further corroborate information collected during the clinical interview and to glean additional details regarding GH’s most salient problems. The addition of the Posttraumatic Stress Severity Scale (PTSS; Foa, 1995) and the Posttrau- matic Cognitions Inventory (PCI; Foa et al., 1999) revealed important additional information regarding the severity of GH’s symptoms and the strength of specific anger-, guilt-, and blame-related beliefs that he held. The inclusion of the Beck Depression Inventory (BDI; Beck & Steer, 1987) and the Beck Anxiety Inventory (BAI; Beck & Steer, 1993) confirm that, despite not meeting diagnostic criteria for a depressive or other anxiety disorder, GH had significant depressive and general anxiety symptoms at initial assessment. Use of several pain measures revealed additional information regarding pain severity and its impact on GH’s daily functioning.

This assessment package, with one exception, is conceptually rooted within the mutual maintenance theory. We are pleased, despite the theoretical disconnect with our formulation of the mutual maintenance theory (although see Sharp & Harvey, 2001), that Wald and Taylor included the Anxiety Sensitivity Index in their self-report package. This measure revealed an exceptionally elevated score (at 2.5 standard deviations above the mean of healthy controls and 1 standard deviation above the mean for patientswithPTSD),suggestingthatGHheldstrongbeliefs that his anxiety-related sensations signaled extreme personal danger and that he was prone to significant emotional reactions to fear and anxiety. This high score is also consistent with GH being at risk for and developing pain-related avoidance (and chronic pain). The signifi- cance of this to our case conceptualization and treatment plan will become apparent in subsequent sections.

Adjuvant Assessment Strategies

Are there areas of the assessment package that Wald and Taylor might have strengthened? As noted above, their assessment was generally comprehensive and well planned. There are very few areas to be critical of, and we would proceed in a very similar manner. The only thing that we would do differently is buttress the assessment of GH’s pain and perhaps his accident- related fear. For the latter we would use the Accident Fear Questionnaire (AFQ; Kuch, Cox, & Direnfeld, 1995), a short self-report measure comprising a 10-item accident profile and a 10-item phobic avoidance subscale with excellent psychometric properties and screening characteristics (Asmundson et al., 1999).

Key dimensions of pain that warrant consideration in any comprehensive assessment package include pain severity or intensity, pain location and distribution,

attitudes and beliefs about pain and its effects, ways of coping with pain, pain-specific emotional distress (i.e., fear, anxiety, mood changes), and functional abilities and limitations (Asmundson, 2002; Tait, 1999). The interview and two self-report measures of pain selected by Wald and Taylor clearly assess several of these key dimensions and, thus, are good choices for inclusion. Indeed, from the interview we learn that GH’s pain is located in his neck and back, fluctuates in severity from mild to moderate, has persisted for approximately 9 months, is aggravated by stress, and is associated with frustration and avoidance behaviors. The Multidimensional Pain Inventory (MPI; Kerns, Turk, & Rudy, 1985), in addition to assessing impact on functional abilities and limitations, allows for assessment of cognitive, affective, and behavioral factors associated with pain. The MPI revealed that GH had mild pain that affected his functioning and social interactions to a moderate degree, but did not keep him from a number of other activities. The MPI and Brief Pain Inventory (Cleeland, 1989) do not, however, provide the richness of detail regarding attitudes and beliefs about pain, ways of coping with pain, and pain-specific behaviors and emotional distress that can be gleaned from other measures.

There are numerous additional self-report measures that would permit a more detailed evaluation of these pain dimensions and the manner in which they affect GH’s overall disability. We would have added three pain measures to GH’s assessment package. Our top choices for this case, based on evidence of strong psychometric properties and clinical utility, include the Pain Catastro- phizing Scale (Sullivan, Bishop, & Pivik, 1995), the Chronic Pain Coping Inventory (Jensen et al., 1995), and the Pain Anxiety Symptom Scale (McCracken et al., 1992). These measures and their relevance to assessing GH are described below.

Pain Catastrophizing Scale (PCS)

The PCS (Sullivan et al., 1995) consists of 13 items describing different thoughts and feelings that people may have when they are experiencing pain. Items are rated on a 5-point Likert scale ranging from 0 (not at all) to 4 (all the time) and yield a total score and three subscale scores assessing rumination (e.g., “I can’t stop thinking about how much it hurts”), magnification (e.g., “I worry that something serious may happen”), and helplessness (e.g., “There is nothing I can do to reduce the intensity of the pain”). The PCS and its subscales have excellent psychometric properties (Sullivan et al., 1995). GH experiences pain in many situations, including those for which he can identify triggers (e.g., driving, working at the computer, physical activity, when stressed) and those where he cannot (e.g., when relaxing at home). Given that catastrophizing interferes with efficacy of coping

11Case Conference Response: Addressing Shared Vulnerability

strategies and thereby contributes to heightened levels of pain and disability (Sullivan et al., 1998), detailed knowledge of how GH is interpreting his pain would aid in treatment planning.

Chronic Pain Coping Inventory (CPCI) The CPCI (Jensen et al., 1995) is a 65-item self-report

measure of cognitive and behavioral coping strategies that patients use when they are experiencing pain or are attempting to prevent pain. Eight coping strategies— positive coping self-statements, guarding, resting, asking for assistance, seeking social support, relaxation, task persistence, and exercising—are assessed. Items depict how frequently each of these coping strategies are used in the previous week and, as such, are measured on an 8- point scale expressed in number of days. Recent studies suggest that the CPCI provides a comprehensive and psychometrically sound assessment of pain-specific coping (Hadjistavropoulos, MacLeod, & Asmundson, 1999). Romano, Jensen, and Turner (2003) have recently published an abbreviated form of the CPCI, which comprises 42 instead of 65 items. Since the abbreviated CPCI has psychometric properties that are comparable to the original (Romano et al., 2003), it can be substituted in situations where assessment time is a consideration. We would use the CPCI for several reasons. One of GH’s treatment goals is a desire to be pain free. He perceived himself as having some degree of control over his pain, primarily through use of medication, physiotherapy, massage therapy, frequent rest, and avoidance of certain physical activities such as outdoor work. Systematic assessment with the CPCI would add to our understanding of his ways of coping with his painful physical injury and would also assist with outcome evaluation following treatment.

Pain Anxiety Symptoms Scale (PASS)

The PASS (McCracken et al., 1992) is a 40-item scale that was designed to address four specific facets of pain- specific anxiety that correspond closely to multiple response modalities identified in the three-system model of fear (Hugdahl, 1981; Lang, 1968): (1) fearful appraisals of pain (e.g., “Pain sensations are terrifying”); (2) cognitive anxiety/interference related to pain (e.g., “I find it hard to concentrate when I hurt”); (3) physiological symptoms arising from pain (e.g., “Pain seems to cause my heart to pound or race”); and, (4) escape/avoidance behavior in response to activities that are associated with pain (e.g., “I try to avoid activities that cause pain”). Items are measured on a 6-point Likert scale that is anchored by descriptive phrases (0 = never, 5 = always). Psychometric properties are excellent (Asmundson & Larsen, 2000). The measure is

useful in assessing patients presenting with pain because of its focus on pain-specific anxiety responses that, with strong associations with depression and pain-related disability (McCracken et al., 1992), are important targets for treatment (Vlaeyen & Linton, 2000; Vlaeyen et al., 2004). The PASS is also available in a short form (PASS- 20) comprising 20 items. The PASS-20 assesses the same four facets of pain-specific anxiety as the longer version and initial studies suggest that psychometric properties are preserved (Coons et al., 2004; McCracken & Dhingra, 2002). Given the length of GH’s current assessment package we would recommend use of the PASS-20 to determine the degree of overlap between pain-specific and PTSD-related catastrophic cognitions, avoidance behaviors, and hyperarousal. His treatment may need to be tailored to address elevations on specific subscales where overlap with PTSD symptoms is limited.

Diagnosis and Case Conceptualization

An important product of any assessment is obtaining a clear picture of the patient’s primary diagnosis and associated presenting problems. We concur with Wald and Taylor’s conclusion that GH presents with a primary problem of PTSD and that this is significantly compli- cated by mild to moderate chronic pain associated with functional limitations. Armed with this information, the cognitive-behavior therapist can develop a working model of the case based on factors contributing to the primary presenting problem. Below we present our case formulation for GH organized by predisposing (or vulnerability) factors, precipitating (or triggering and exacerbating) factors, perpetuating (or maintenance) factors, protective factors, and general considerations related to co-morbid PTSD and pain.

Predisposing Factors

As noted above, anxiety sensitivity has been identified as a potential vulnerability factor for PTSD and chronic pain as well as their comorbid presentation. GH presents with an exceedingly elevated score on the ASI. It is probable that elevated levels of pre-accident anxiety sensitivity led GH to have a more severe emotional reaction to both his RTC and the pain associated with his injuries. Unfortunately, we do not know what level of anxiety sensitivity GH had pre-accident. It is equally possible that the RTC served to elevate his anxiety sensitivity (i.e., to make him more fearful of arousal- related somatic sensations associated with his accident) and thereby exacerbate his emotional response to post- accident events (e.g., difficulties with concentration, cued panic attacks, experiences with pain). It is noteworthy that GH reported that he had always felt the need to be strong and in control of his emotions. This suggests that he may have had elevated pre-

12 Asmundson & Hadjistavropolous

accident anxiety sensitivity. Regardless, it appears that anxiety sensitivity is a critical predisposing factor and possibly an important precipitating factor (see below) for GH.

Lack of social support has also been identified as a vulnerability factor for PTSD (Brewin, Andrews, & Valentine, 2000). From the information provided, it is unclear what the nature of GH’s social network was at the time of his RTC and in the post-accident period prior to his transfer to Canada. It seems that, although he did not have a current significant relationship, he may have had a core of family and friends. This would have been protective; however, with his transfer, GH appears to have become socially isolated. Social support considera- tions are discussed in more detail below. Other predis- posing factors implicated in PTSD, such as the experience of previous trauma and evidence of prior psychopathol- ogy (Breslau et al., 1991), are not evident in this case.

Precipitating Factors

The primary precipitating factor in this case was involvement in the RTC and GH’s fearful response to it. Although he suffered amnesia (anterograde and retro- grade) for the accident itself, he exhibited a marked fear response (characterized by nightmares, intrusive images, reactivity to accident-related stimuli) within 24 hours post- accident with worsening over the following month. Moreover, GH was inactive post-accident and had completely avoided cycling ever since. He also found that pain prevented him from participating in sports, doing outdoor work, and participating in social functions. His collective lack of activity likely promoted physical deconditioning and muscle weakening which, in turn, likely contributed to aggravation of his pain and pain- related avoidance behavior over time (Verbunt et al., 2003). As noted above, anxiety sensitivity may have also played a role in exacerbating both his PTSD and pain symptoms.

Perpetuating Factors

We have already discussed in general terms how the symptoms of PSTD and chronic pain can be mutually maintaining. It is likely that GH’s PTSD symptoms are serving to maintain (or even exacerbate) his pain and pain-related cognitions and behaviors and, conversely, that his experiences with pain are feeding his PTSD symptoms. For example, his experiences with chronic pain in his neck and back may serve as regular reminders of his accident, leading to his daily intrusive thoughts, frequent nightmares, avoidance of stimuli and situations associated with the accident, and his marked sleep disruption. Conversely, his reexperiencing and avoidance symptoms likely contribute to perpetual muscle tension

and, together with poor sleep, maintain his pain and pain- related cognitions and behaviors. There are other secondary factors that are likely serving as perpetuating factors. For example, his cued panic attacks very likely contribute to his continuing avoidance of stimuli and activities that he associates with the accident and, at the same time, promote muscular tension that leads to pain. Likewise, his angry and depressive ruminations about the accident may, in turn, perpetuate both his PTSD and the severity and limiting nature of the pain symptoms. We do not specifically address anger and depression in our tentative treatment plan and would do so only if they remained significant at posttreatment.

Protective Factors

Protective factors are not always present. There is little evidence that GH has any protective factors that would reduce his PTSD or pain symptoms. It has been suggested that the development of PTSD requires conscious recollections of the traumatic event (Mayou, Bryant, & Duthie, 1993; Sbordone & Liter, 1995); that is, loss of consciousness during a traumatic event should protect against the development of significant posttraumatic stress symptoms. Most studies do not support this position (for review, see Bryant, 2001) and, important to this case, GH developed PTSD despite his temporary loss of consciousness and associated amnesia for the event. His loss of consciousness was not protective. Social support may be another important factor in protecting against development and exacerbation of PTSD as well as persistent pain problems. However, based on the infor- mation provided by Wald and Taylor, it appears that GH is socially isolated—he is not in a relationship, has no immediate family living near him, and, having just relocated from another country within the past 6 months, appears to have developed few friends. If the provisional treatment plan did not progress as anticipated we would further assess GH’s social support network and consider it in a revised treatment plan (see, for example, Tarrier & Humphreys, 2004).

General Considerations Despite GH having PTSD symptoms at the severe end

of the spectrum (see Wald & Taylor’s Table 1, this issue) and complicated by chronic pain, it is apparent from additional information provided by Wald and Taylor that there are several points of optimism that can be drawn upon in treatment and need to be generally considered in conceptualizing the case. First, with respect to the accident, GH was not wearing reflective clothing, was cycling in dim overcast light, and did not have lights on his bike. Discussion of these factors may assist GH in reducing his feelings of guilt and improving

13Case Conference Response: Addressing Shared Vulnerability

his sense that he could prevent this type of accident in the future. Second, GH is described as being open and pleasant. Finally, he is described as having above- average intelligence, being a high achiever and highly motivated. These latter points suggest that there will be few difficulties with developing and fostering a sound therapeutic relationship with GH, his under- standing of psychoeducational components of treat- ment, his understanding of therapist-guided and homework assignments, and his motivation for partic- ipating in treatment through to fruition.

Tentative Treatment Plan

Our tentative treatment plan is a direct extension of the above case formulation and is geared toward assisting GH to tackle his most salient problems (i.e., PTSD and pain). Cognitive-behavioral therapies are amongst the most effective for both PTSD (Taylor et al., 2003; van Etten & Taylor, 1998) and chronic pain (Hadjistavropoulos & de Williams, 2004; Morley et al., 1999). Our tentative treatment plan incorporates aspects of both. Moreover, because of the shared relevance of anxiety sensitivity in PTSD and pain, and since treating anxiety sensitivity may improve treatment of both PTSD (Taylor, 2004) and chronic pain (Asmundson, 1999), our plan draws heavily on techni- ques that reduce anxiety sensitivity. The plan, as outlined below, addresses all of GH’s stated treatment goals (i.e., to be less sensitive to things, to be less anxious with driving and cycling, to no longer have terrifying RTC-related nightmares, to be more relaxed), with the exception of his desire to be pain-free. Because this latter goal is unrealistic, we would provide education adapted from cognitive-behavioral pain management techniques to help GH reframe this goal. For example, rather than seeking to be pain-free, he might alter the goal such that his focus is not viewing pain as something that signals physical catastrophe. Our adjuvant assess- ments would assist in clarifying how specifically to reframe this goal. We tentatively recommend 15 to 18 weekly appointments for GH, each lasting 60 to 90 minutes. Each appointment would include daily homework exercises related to the session and to be practiced each day prior to the subsequent appoint- ment. Anxiety and pain severity ratings would be taken repeatedly before and after treatment and homework exercises. Likewise, the preassessment battery (supple- mented by our adjuvant self-report measures) would be readministered midtreatment and at the second-to-last appointment. These measures would be used to assess session-by-session and overall progress in treatment.

Concurrent with the tentative treatment plan out- lined below, we would recommend that GH schedule exercise and fitness training, designed by a physiother-

apist or exercise therapist familiar with chronic pain, to promote pacing, resumption of previous activity levels, and physical reconditioning. This is particularly impor- tant for GH in order to counter the effects of pain- promoting deconditioning that has occurred as a result of his recent inactivity and avoidance behavior. We would also recommend a work site visit by an occupa- tional therapist to explore ergonomic problems that may be contributing to his pain. We would also recommend that GH have his medication reviewed by a physician with specialized knowledge in chronic pain. Emerging evidence suggests that propranolol, a beta blocker that is sometimes used for analgesic purposes, may also be effective in alleviating PTSD symptoms (Pitman et al., 2002).

The primary elements of our tentative treatment plan are as follows:

• Psychoeducation regarding PTSD and pain (1 to 2 sessions). This would include explanation of the shared vulnerability hypothesis and the role that anxiety sensitivity plays in GH’s symptom profile.

• Relaxation training, as described by Taylor and Asmundson (2004), including release-only relaxation and rapid relaxation as well as diaphragmatic breathing (3 sessions). This training serves several purposes. First, it provides GH with skills that may help in controlling muscle tension and associated pain that may arise and interfere with other treatment components described below. Second, it provides him with skills that can be used in everyday living to aid his goal of becoming more relaxed. We would forgo tense-release relaxation in order to minimize the potential of triggering pain from muscle tension and spasms. If necessary, attention diver- sion methods (see Fernandez & Turk, 1989) would be incorporated as a means of addressing lingering pain-related catastrophic cognitions. Cognitive restructuring would also be used to address GH’s beliefs about pain, teaching the identification of catastrophizing cognitions and strategies to chal- lenge and change them. GH, for instance, holds the belief that he has been permanently changed for the worse and that his life has been destroyed by the trauma. Further strategies for pain treat- ment may be required, depending on the results of the adjuvant pain assessment instruments we recommended.

• Interoceptive exposure exercises designed to reduce elevated anxiety sensitivity (3 to 4 sessions). In short, this entails consideration of medical contraindications fol- lowed by selection and practice of a number of exercises designed to promote increasingly distres- sing arousal-related bodily sensations (see Taylor,

14 Asmundson & Hadjistavropolous

2000). During these sessions, cognitions relevant to anxiety sensations (e.g., concentration difficulties indicate that he is going crazy, feeling that it is important to stay in control of his emotions) would also be discussed and challenged as necessary. The primary purpose of this set of exercises is to lower GH’s level of anxiety sensitivity and thereby reduce the overall severity of his symptoms, improve chances of success with subsequent treatment components, and, relative to his goals, aid in making him “less sensitive to things” (or, more accurately, to be less concerned about the personal and social conse- quences of arousal-related sensations). Secondarily, these exercises may also diminish the probability that GH will experience panic when faced with RTC- related stimuli.

• Imaginal exposure to trauma-related stimuli (4 sessions). GH experienced anterograde and retrograde amne- sia for the RTC; however, he does report intrusive images about the accident as well as distressing nightmares. Our approach to imaginal exposure entails having GH verbally recite his RTC-related recollections and associated nightmares followed by formation of an associated hierarchy (from least to most distressing) and graded exposure along the hierarchy. These exercises, combined with the in vivo exposure exercises described below, address a number of PTSD-related symptoms (e.g., intrusions, nightmares) that GH reports as particularly distres- sing. These sessions may also need to address some of GH’s specific dysfunctional cognitions (e.g., “You can never know who will harm you,” “I have to be especially careful because you never know what can happen next,” “The world is a dangerous place”). GH will be encouraged to identify these thought patterns and implement alternative positive cogni- tions (“There are many strategies that can be used to reduce danger”).

• In vivo exposure to trauma-related stimuli and situations (3 to 4 sessions). GH has remained avoidant of numerous activities. Combined with the scheduling of exercise and fitness training, the interoceptive exposure exercise described above may reduce some of this avoidance (e.g., for riding a bike). However, as needed, graded in vivo exposure exercises would be used to address lingering avoidance of driving, riding as a passenger, crossing busy streets, and the like.

• Review of successes and relapse prevention strategies (1 session). Relapse prevention would consist of identi- fication of vulnerable states or situations and preparation to deal effectively with them. Strategies for regaining control of unexpected spikes in anxiety sensitivity would also be covered.

Anticipated Outcome

As noted by Wald and Taylor, the co-occurrence of PTSD and pain can complicate treatment and diminish the likelihood of successful outcome. GH has a number of factors that suggest poor prognosis. These include the report of potential mild traumatic brain injury, minimal social support, severe PTSD symptoms in three of the four symptom domains (i.e., severe reexperiencing, avoidance, and numbing along with moderate hyperarousal), trau- ma-related guilt and anger, strongly held dysfunctional beliefs about himself, and strongly held negative beliefs about the world. He also brings several strengths that may serve him well in treatment. For example, he is open and personable, is motivated to not let the RTC ruin his life, has a strong interest in psychological treatment, has no history of psychiatric problems, is not abusing substances, and his pain, although present and persistent, is not reported as severe. All things considered, we are optimistic that GH and patients with similar symptom profiles will benefit from treatment and be successful in maintaining treatment gains, particularly where that treatment is designed with a component that specifically targets the shared vulnerability for PTSD and pain.

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Preparation of this article was supported by New Emerging Team Grant PTS–63186 from the Canadian Institutes of Health Research (CIHR) Institute of Neurosciences, Mental Health and Addiction. Dr. Asmund- son is supported by a CIHR Investigator Award.

Address correspondence to Gordon J. G. Asmundson, Anxiety and Illness Behaviours Laboratory, University of Regina, Regina, Saskatch- ewan, Canada S4S 0A2; e-mail: gordon.asmundso [email protected].

Received: February 14, 2005 Accepted: March 31, 2005 Available online 21 February 2006