Understanding Comorbid Posttraumatic Stress Disorder and Chronic Pain: Current Treatments and Future Directions
It is crucial for providers, researchers, and consumers to understand chronic pain through a comprehensive model that accounts for both the complexity of the pain experience and the complicated changes in the pain experience and phenotype with in the context of trauma. Early theories of pain, which are covered later in this chapter, failed to adequately account for pain complexity and are insufficient to guide diagnosis, understanding, and treatment of trauma-related pain (i.e., pain and comorbid posttraumatic stress disorder [PTSD]). The first part of this chapter will describe the evolution of understanding pain from unidimensional Cartesian models to more complex models that culminated in the predominant contemporary biopsychosocial model. The biopsychosocial model accurately acknowledges that the experience of pain cannot be explained solely through the physical experience and that the physical experience is affected by factors seemingly unrelated to one’s physical pain. Hence, any proposed explanatory models of chronic pain comorbidity must also acknowledge this fact. Finally, the chapter will explore existing treatments for comorbid pain and PTSD (both pharmacological and nonpharmacological) and will offer suggestions on future directions for research and clinical care that may guide ongoing efforts to effectively treat these complex patient populations.
Prevalence of Chronic Pain and Posttraumatic Stress Disorder
Up to 40% of adults in the United States experience chronic pain, defined as persistent pain lasting for at least 6 months, with costs estimated at $560 billion. Chronic pain may occur within several contexts, including musculoskeletal injury, cancer, and traumatic events. Indeed, pain is highly comorbid with PTSD, a disorder characterized by avoidance, hypervigilance, negative cognitions and affect, and intrusive symptoms (e.g., flashbacks). Moreover, those with chronic pain are more likely to endorse PTSD symptoms than their counterparts without chronic pain. , Military populations are particularly susceptible to this comorbidity and are more likely to be diagnosed with PTSD and/or chronic pain compared with the civilian population. , With advancements in battlefield technology, and medicine more generally, current military personnel have a better chance at surviving than those in the Vietnam era; nevertheless, physical and mental health conditions persist beyond their time of service. Similarly, civilians who have experienced a traumatic event are also more likely to survive due to advancements in medicine. Therefore it is pertinent to examine the current state of the science as it relates to how these two common health conditions (i.e., chronic pain and PTSD) are understood and treated, the historical context from which this thinking evolved, and the innovations that may lie ahead.
Historical and Modern Perspectives of Pain Treatment
In order to understand current pharmacologic treatments for pain, it is important to place these treatments within the context, evolution, and acquired knowledge of earlier biomedical models dating back to Descartes. Descartes viewed pain as one of the principal perceptual and physical bodily experiences that test the existence of the body. He believed that pain was a disturbance passed through nerve fibers throughout the body until it reached the brain and was evidence that the mind and body are dualistic mechanisms responding in tandem to specific stimuli such as temperature and pain. Not only did this promote thought from philosophers, it also subsequently led scientists to attempt to locate pain nerve fibers within the body that transferred pain sensations. Descartes’ theory, also now known as the specificity theory , was essential in promoting research related to specific functions of nerve pathways to the brain in response to pain. The two-step process consists of the (1) body integrating a pain signal into one bodily sensation and (2) traveling to the brain where it is mechanically perceived. This influenced the practice of medicinal usage, whereby practitioners pursued physical pain treatments, such as herb usage for analgesic effects or physicians severing specific pain nerve fibers to prevent pain signals from reaching the brain.
Descartes’ specificity theory was further developed by physician Charles Bell in his influential essay, the Idea of a New Anatomy of the Brain , which ultimately led to the discovery of the central nervous system (CNS). The CNS provides a direct relationship between a stimulus and the sensation of pain via sensory receptors known as “nociceptors.” Nociceptive pain reception occurs when noxious stimuli are sensed by pain receptors, or nociceptors, located in the skin and then transmitted via electric signals to higher brain centers for processing. , , ,
The relationship between nociception and pain is complex because the inputs involved are beyond biological nociception. Opposition of Descartes’ specificity theory of pain has led to other historical pain conceptualizations, including the intensity theory of pain and the pattern theory of pain . The intensity theory of pain hypothesizes that the experience of pain is the result of a significant intensity or threshold being reached. This led neurologists and physiologists in the 1800s to formulate the theory that the intensity of pain is directly related to the amount of associated tissue injury. After a certain threshold, an increased painful sensory input would summate and transmit in the spinal cord (i.e., CNS) and then to the brain. Researchers during this time theorized that this central summation generated impulse sensations that were interpreted as pain for the individual only when the number of intense responding fibers and their discharge frequency exceeded a certain threshold that then determined the perceptual response to the nociceptive (sensory) input. , , ,
Modern theories of pain foretold the most utilized theoretical perspective to date, the biopsychosocial model. The gate control theory sought to combine and support the main principles of the specificity, intensity, and pattern theories of pain. Melzack and Wall theorized that there is a mechanistic gate in the spinal cord, specifically in the dorsal horn, that controls the transmission of sensory information in the spinal cord and to the brain. This mechanism is controlled by the activity in the large and small fibers. Large fibers inhibit or close the gate, whereas small fibers enable or open the gate. When nociceptive pain, tissue injury, or pain information reaches a certain threshold that exceeds the inhibition of the gate, this opens the gate and activates the pathways that lead to the experience of pain and pain-related behaviors (e.g., taking hand away from fire). Therefore this theory provided a neural basis and reconciled the earlier biomedical models of pain (i.e., specificity, intensity, and pattern theories of pain). This also laid the foundation for pain research and pain mechanisms in the 20th century. However, Melzack and Wall (1965) acknowledged that a more comprehensive model was needed to consider the emotional and cognitive effects of pain and their effects on pain-related behavior when an individual is experiencing pain. , ,
The need for a more comprehensive pain model led Melzack to create the neuromatrix theory of pain, which attempted to explain the nature of pain, and is based on prominent pain biomedical models. Melzack (in 2001) proposed that pain is a complex experience that is shaped by unique neurosignatures within the brain’s neural network, which he coined as the body-self neuromatrix. , This network assimilates cognitive evaluation, sensory-discriminative, and motivational-affective networks and posits that the output patterns of the neuromatrix engage perceptual, behavioral, and homeostatic systems within the body and mind in response to an injury and/or chronic physical and cognitive stress. Melzack’s theory was formulated on pain syndromes that had no organic injury such as phantom limb pain and nonspecific low-back pain. Preceding biomedical models dating back to Descartes did not hold true to the assumption that there must be tissue damage in order for pain to occur. Similarly, according to Melzack’s neuromatrix model, pain could have no correlation with tissue damage and can be the product of multiple parts of the CNS working together to generate a painful experience (e.g., fibromyalgia). This theory provided a comprehensive explanation of pain by integrating tenets from the specificity theory with affective and pattern-response theories to formulate the neuromatrix theory of pain , with the experience of pain being the result of an interplay of these various neural networks. Melzack and Casey encouraged medical professionals to move away from a sensory-dominant approach (e.g., surgical, pharmacologic) and treat chronic pain with a more multidisciplinary/multimodal (including pharmacologic and nonpharmacologic approaches) biopsychosocial approach. , , This multimodal theory contributed to a biopsychosocial model for evaluating and treating pain.
Recent movement toward a biopsychosocial approach for treating chronic pain views an individual as an integrated “whole person” whose mind and body are interconnected and manifest dynamic interactions between biological, psychologic, and social components of their painful experience. The biopsychosocial model of pain is well supported by research and has expanded upon the biological mediators of chronic pain, elucidating the role of maladaptive stress responses via the hypothalamic-pituitary-adrenal (HPA) axis. Chronic pain dysregulates the HPA axis activity, and thus cortisol levels, which in turn is associated with differences in pain intensity, pain thresholds, and anxiety levels.
Pain, Cognitions, and Affect
Psychological components of the pain experience, such as pain catastrophizing (“an exaggerated negative mental set brought to bear during actual or anticipated painful experience” ), fear-avoidance, and negative affect, have been recognized as common aspects of the chronic pain experience within the fear-avoidance model of pain. , Social factors such as solicitous and punishing responses from marital partners, lower perceived level of social support, and lower socioeconomic status negatively impact self-reported pain intensity and disability level. Moreover, there are cultural norms surrounding appropriate expressions of pain, and they may influence pain tolerance and the perceived pain intensity ratings of others. Lethem and colleagues contended that ultimately there are two options when experiencing a fear: “confrontation” or “avoidance.” The central premise of the fear-avoidance model is that confrontation diminishes fear over time, whereas avoidance maintains or exacerbates the fear response.
Mood affects how individuals view pain and is considered an integral component of the fear-avoidance model. A review of the literature paints a picture indicating chronic pain comorbidity should be expected within clinical settings. Depression and anxiety disorders, PTSD, substance abuse, suicidality, and sexual abuse have all been linked to chronic pain. Prevalence rates of depressive disorders vary by chronic pain disorder, with 4%–12% prevalence rates among those with neuropathic disorders and 21%–83% prevalence rates among those with fibromyalgia. Temporomandibular joint (TMJ) disorder prevalence rates for comorbid depressive disorders are also notably high: 16%–65%. Anxiety disorders, when including PTSD, are as high as 65% for TMJ, 60% for fibromyalgia, 51% for abdominal pain, and 45% for migraine headache. Examining PTSD specifically, nearly a quarter of individuals with chronic pain have comorbid PTSD. Fibromyalgia also appears to have the highest range of prevalence rates for substance use disorders (up to 25%), with spinal chronic pain up to 14%, and arthritis up to 12%. Opioid use disorder, specifically, has been reported in up to 43% with chronic pain.
Mental health comorbidities associated with chronic pain not only affect mood and exacerbation of pain-related disability , but also the perception of pain. A meta-analysis examining depression and pain perception showed that, overall, individuals with depression have a higher pain threshold (i.e., the moment pain is felt). , However, the method by which pain is induced is also predictive, with ischemic methods resulting in lower pain threshold. No overall differences emerged in pain tolerance or pain ratings across those with and without depression. Finally, comorbid PTSD and chronic pain has higher pain thresholds and pain sensitivity (i.e., the same stimuli feel more painful for those with comorbid chronic pain and PTSD). Anxiety, depression, and other mood disorders have the potential to affect how one experiences pain, linking these psychosocial processes to the pain experience. Viewing pain as a problem only related to physical symptoms with an organic cause does not fully capture the pain phenomenon. Thus, treatments only focusing on pain sensations have limited effectiveness.
Treating Chronic Pain
Taking a biopsychosocial perspective is increasingly shown to be essential in effectively treating and managing chronic pain. The primary aim of biopsychosocial treatment is not to reduce pain intensity, but instead to focus on restoring and optimizing an individual’s ability to function in their daily lives while reducing long-term reliance on pharmacologic interventions. Biopsychosocial pain management can involve medication, psychotherapeutic interventions, physical therapy, stimulatory analgesia and neuromodulation, interventional procedures and surgery, and functional restoration programs. Within the biopsychosocial perspective, the emphasis of chronic pain treatment shifts from efforts to cure the pain or symptoms to efforts of improving functioning and quality of life through better management. This perspective allows for the implementation of an interdisciplinary approach toward the treatment of chronic pain, wherein the treatment team consists of a coordinating multidisciplinary group of individuals who are treating the patient under one treatment plan. This collaborative group may consist of a physician, nurse, psychologist, physical therapist, and occupational therapist. Within this team, each member has a specific role. These roles include (but are not limited to) the following: physicians are in charge of the medical aspects of treatment; nurses monitor the patient after treatments; psychologists provide cognitive behavioral psychosocial interventions; physical therapists engage the patient in treatment focused on movement; and occupational therapists engage the patient around work-related factors. By using an interdisciplinary approach, the entirety of the person is treated. For patients, much of the time may be spent in psychosocial interventions, which include a variety of interventions and techniques.
Psychological treatments for chronic pain often consist of several components. Many chronic pain interventions utilize cognitive behavioral techniques that improve pain-related outcomes. , Cognitive behavior therapies (CBTs) focus on modifying problematic thoughts (e.g., automatic thoughts related to self-efficacy), emotions (e.g., an irrational fear of re-injury), and behaviors (e.g., sedentary behaviors) to reduce pain-related disability and intensity. A more recent iteration of CBT is acceptance and commitment therapy (ACT), which Hayes et al. explain as focusing on mindfulness, valued actions, and acceptance of difficult thoughts, emotions, and/or circumstances. ACT and other acceptance-based interventions, such as mindfulness, is efficacious in treating chronic pain, with randomized controlled trials (RCTs) of acceptance-based interventions for pain resulting in significant improvements in pain and physical well-being. , However, when mindfulness and mindfulness-based stress reduction (MBSR) were systematically examined, mixed results emerged. An early meta-analysis examining MBSR to active controls showed a medium and statistically significant effect size for mental health variables. A meta-analysis showed that MBSR for chronic pain, compared to usual care, resulted in significant differences in the short term, but not long term, regarding pain intensity, and also showed nonsignificant effects when comparing MBSR to active treatment groups in both the short term and long term. Short-term effects of MBSR, compared to usual care, on pain-related disability approached significance but was nonsignificant regarding long-term effects. Short-term effects and long-term effects of MBSR compared to active treatment were nonsignificant. Another meta-analysis that looked at both mindfulness and MBSR interventions also showed nonsignificant effects for mindfulness-based cognitive therapy and MBSR (although the MBSR effect size approached significance) and significant effects for other mindfulness interventions. Taking publication bias into consideration, the authors state that effects of mindfulness meditation are “low overall for both short and long term.” Discrepant results may be due to the periods in which these meta-analyses were conducted, the heterogeneity of results leading to large confidence intervals, and/or how mindfulness was defined. Because mindfulness may support self-efficacy and can be taught in a relatively brief time-frame, the available research, although equivocal, supports the use of mindfulness-based interventions for chronic pain.
Explaining the Chronic Pain and Posttraumatic Stress Disorder Comorbidity
As far back as 2001, researchers have attempted to coalesce the available research in order to explain the relationship between chronic pain and PTSD. During this time, the shared vulnerability and mutual maintenance models of comorbidity , began their ascent as prominent heuristics through which to view the co-occurring disorders. Both acknowledge the role of psychological and social variables, while not ignoring the biological contributions, through the biopsychosocial model. Nevertheless, there is a great deal that has yet to be determined about how these disorders are linked.
Shared Vulnerability: Anxiety Sensitivity
One of the earliest models of pain and PTSD comorbidity was based on observations of hypervigilance associated with both conditions that created a mutual vulnerability for the comorbidity. Viewing chronic pain and PTSD from a shared vulnerability perspective highlights a diathesis related to anxiety sensitivity (AS) and genetic predispositions. AS refers to how people think about their bodily sensations, as they relate to how manageable the thoughts are (e.g., “It is an impossibility to control my thoughts about my disorders.”), whether the sensations have potential social consequences (e.g., “I may be unwelcome if people see me limping.”), and whether the sensations have potential physical consequences (e.g., “If this pain continues, my leg will probably be amputated.”). , Separate lines of research show that individuals with chronic pain and PTSD symptoms have increased levels of AS. Within a chronic pain context, AS predicts increased opioid dependence, severity, and misuse, stress, and disordered eating. Within a PTSD context, AS is implicated in emotion dysregulation, symptoms of obsessive-compulsive disorder , and decreased distress tolerance. Sensations within the body prime mental representations of what may occur; when these mental representations occur within a comorbid context (such as chronic pain and PTSD), they may have compounding detrimental consequences. In other words, among those who have comorbid PTSD and chronic pain, any reminder of physical pain or trauma may be associated with increased levels of anxiety and attention to the symptoms compared with those who have one or none of the disorders.
Among a comorbid PTSD and chronic pain population, AS plays an important role in symptom manifestation and evidence supports its inclusion within a stress-diathesis model of chronic pain and PTSD. , Among those with musculoskeletal pain, AS was elevated if they had been through a traumatic experience and exhibited symptoms of PTSD, compared with those who did not exhibit these symptoms. Separately, AS and PTSD symptoms predict emotional distress and interact with each other, whereby emotional distress worsens among those with musculoskeletal pain. This suggests that heightened anxiety around physical symptoms may worsen the effect of PTSD on one’s physical pain-related distress. Among those with chronic pain, AS is a significant predictor of PTSD symptoms above and beyond one’s history of trauma, highlighting how thoughts related to the pain experience and bodily sensations may play a role in PTSD.
Hyperarousal symptoms of PTSD are often characterized via their physiologic manifestations, relating this symptom cluster to AS. Indeed, both hyperarousal and numbing symptoms are significantly related to AS among individuals diagnosed with chronic musculoskeletal back pain. Among prisoners of war, hyperarousal longitudinally mediates the relationship between captivity and AS and between captivity and pain catastrophizing. Nevertheless, the long-term implications of AS are unclear, as AS predicts initial, but not later, neuropathic pain among those who received treatment in a trauma center.
Shared Vulnerability: Genetic Cause
Within the shared vulnerability model, genetic vulnerabilities play a prominent role, highlighting the biological component of the biopsychosocial model. Decades of research on the stress-vulnerability model shows that genetic predispositions play a role in both physical and mental health. Approximately 30%–40% of the variance in PTSD is heritable. Much of the genetic architecture underlying the risk for PTSD appears to overlap with vulnerabilities for depression and anxiety. It is quite possible that there are multiple genetic architectures underlying PTSD, which may explain the difficulties in the replication of findings by genome-wide association studies.
At this time, there are few well-supported genetic markers of both PTSD and chronic pain. However, the current research of genetic markers of stress (HPA axis) and inflammation for PTSD and chronic pain supports overlap of these disorders. FK506 binding protein 5 (FKBP5) polymorphisms provide one of the most promising gene candidates for PTSD vulnerability. High expression of FKBP5 is linked to greater glucocorticoid receptor sensitivity and lower basal cortisol levels, and low basal cortisol levels are thought to be a vulnerability factor for developing PTSD after a traumatic event. In an epigenetic study, Blacker and colleagues found that FKBP5 methylation increased in nonresponders to PTSD treatment and decreased in responders to treatment. The direction of methylation related to PTSD appears to be allele-specific, with the methylation or demethylation associated with greater severity of PTSD dependent on the exact allele being modified.
There is even less known about genetic and epigenetic involvement in chronic pain. Variants of the FKBP5 gene are associated with chronic pain development after trauma exposure, and the stress response microRNA (miRNA) 320a is linked to the development of chronic pain after car accidents.
Both the HPA axis and the immune system are involved in PTSD and chronic pain, further substantiating a fundamental biological link between the two conditions. Expression of immune system genes is associated with the presence of PTSD and upregulation of immune system genes is associated with greater intrusion symptoms of PTSD. Polymorphisms of immune system genes have been implicated as vulnerabilities for PTSD. , Studies of stress hormones and inflammatory markers support genetic findings of altered immune and HPA axis regulation in PTSD. Interestingly, many of the miRNAs associated with PTSD are involved in the regulation of stress and proinflammatory responses implicated in chronic pain. Indeed, there are several miRNAs associated with pain sensitization, inflammation, and stress responses. , Further studies are still needed to conclusively elucidate specific shared markers for underlying vulnerability.
Mutual Maintenance Model
The mutual maintenance model of the chronic pain and PTSD comorbidity incorporates all three factors of the tripartite biopsychosocial model, weaving an intricate tale of biological predispositions, affective and cognitive components, and social aspects of the pain experience into one explanatory model. The model hypothesizes that the unique comorbidity associated with chronic pain and PTSD is due to each disorder influencing the other (i.e., mutually maintaining). The mutual maintenance model highlights seven different cognitive and emotional processes that form a shared mechanism of comorbidity: attentional biases, AS, reminders of traumatic experiences, avoidance, negative affect and decreased physical activity, negative perceptions of illness, and the inability to use effective coping strategies. Despite the considerable attention paid to the chronic pain and PTSD comorbidity, research has marginally progressed from its original formulation of nearly 20 years ago.
As established earlier in this chapter, those with chronic pain are prone toward hypervigilance related to pain sensations, similar to how those with PTSD are prone toward hypervigilance related to potentially dangerous internal or external stimuli related to their traumatic experiences. These attentional biases are often measured in a laboratory setting utilizing a Stroop task, an experimental paradigm whereby participants are presented with a word in a specific color. The more time an individual takes to name the color of the word, the more attention is being placed on the word itself. For instance, it would be expected that those with chronic pain would take longer to name a color of the word “pain” versus “chair.” Similarly, reasoning biases are biases related to probability—for instance, believing it is more probable than it actually is to experience pain and/or a traumatic experience. More recent research suggests that those with chronic pain and PTSD become more focused on pain and trauma-related cues than those with chronic pain but without PTSD, providing evidence that it does not matter if the stimulus is pain- or trauma-related. Indeed, there may be a generalization of hypervigilance occurring within this comorbidity. Individuals with chronic pain are acutely aware of pain sensations that occur, and those with PTSD are threatened by reminders of the trauma. When both disorders play a significant role, hypervigilance then becomes focused on both trauma reminders and pain sensations.
Intrusive reminders of the traumatic experience have long been hypothesized to play an important role in maintaining the chronic pain/PTSD comorbidity. , Those with pain are more likely to endorse a PTSD diagnosis, and PTSD-related negative cognitions are associated with pain severity above and beyond PTSD symptoms and alcohol use among veterans with comorbid PTSD and alcohol use disorder. When individuals experience a pain sensation, this may result in intrusive thoughts about the traumatic experience, thus serving as a reminder for both the pain and the trauma. Conversely, reminders of the trauma may result in individuals becoming focused on the body part(s) associated with the trauma, thus provoking a physical pain response. When the pain sensations or reminders of the traumatic events come to mind, engagement in activities that promote wellness and recovery decreases. The interplay between the experience of pain and PTSD symptoms results in experiences that individuals with PTSD and chronic pain want to avoid. Of course, avoidance of thoughts, emotions, and behaviors comes with its own complications.
Avoidance is considered one of the main contributors to the onset and exacerbation of chronic pain and PTSD. It has been linked to increased pain-related disability and PTSD symptoms and is considered a driving force behind the chronic pain and PTSD comorbidity. , , Individuals with chronic pain prefer to avoid painful experiences, and individuals with PTSD prefer to avoid reminders of trauma, cues that may be internal or external. When facial expressions are used as stimuli, veterans with chronic pain show an attentional bias away from painful expressions and toward happy faces, compared to controls. Nevertheless, little has been done to qualitatively define the purpose of pain-related avoidance, and research designed to better understand these goals is needed. Theoretic and empirical perspectives point toward focusing on goal cognitions and better understanding what is most meaningful to an individual. , Avoidance of emotionally or physically painful stimuli may eventually result in decreased engagement with one’s community and social activities, resulting in adverse clinical outcomes, because these activities are mechanisms by which individuals maintain their identity (i.e., Who am I?) and sense of self-worth. Consequences of decreased engagement in meaningful activities within this comorbidity have yet to be fully explored.
Negative Affect and Decreased Physical Activity
Negative affect is common in those with comorbid chronic pain and PTSD. Research shows how symptoms of depression mediate the relationship between PTSD symptoms and pain, indicating the depressive experience, whether endogenous or from inactivity, is associated with increased pain in the context of PTSD. Social isolation and a lack of desire for increased activity levels (both putative mechanisms for poor outcomes in chronic pain and PTSD) have been linked to depression. , Although negative affect has long been hypothesized as an influencing component of chronic pain, it has only recently been established as an integral part of PTSD symptomology.
Anxiety Sensitivity and Negative Perceptions of Illness
AS (which has already been discussed as part of the shared vulnerability perspective of the chronic pain and PTSD comorbidity) and perceptions of pain are closely linked, and both play a role within the mutual maintenance model. Perception of one’s pain refers to how sensitive individuals are to the experience of pain. Although pain sensitivity has been proposed as a mutually maintaining component of the PTSD and chronic pain comorbidity, research around this assertion is still developing. For patients with chronic pain and those with comorbid PTSD, there is an increase in one’s pain threshold and pain sensitivity. Interestingly, those with PTSD and without chronic pain exhibit decreased pain sensitivity, , although these results may be due to the differences in pain thresholds among those with PTSD. More research within the comorbid population is indicated.
Finally, Sharp and Harvey implicate (in)effective coping strategies as a mutually maintaining factor of the comorbidity, explaining that cognitive processes, such as pain catastrophizing, prevent individuals from effectively coping with their chronic pain. Increased pain catastrophizing and decreased self-efficacy is endorsed among those with comorbid PTSD and chronic pain, compared with those with chronic pain only. Among military personnel with chronic pain, PTSD symptoms are associated with decreased pain acceptance, increased fear avoidance, and increased catastrophizing. Moreover, those with comorbid chronic pain and PTSD experience increased healthcare utilization compared with those with just one of the disorders, indicating that the coping strategies being used are ineffective and/or do not lead to decreased need for medical care and pharmacological and nonpharmacological pain management treatment.
Common Pharmacologic Targets of Chronic Pain/Posttraumatic Stress Disorder Comorbidity
There is some overlap between the pharmacological interventions recommended for chronic pain and PTSD, further substantiating an underlying process that may mutually maintain both conditions. Common treatments for chronic pain include acetaminophen, nonsteroidal antiinflammatory drugs, tricyclic antidepressants, serotonin and norepinephrine reuptake inhibitors (SNRIs), anticonvulsants, opioids, and muscle relaxants. A couple selective serotonin reuptake inhibitors (SSRIs) are approved by the US Food and Drug Administration (FDA) for PTSD, but research shows mixed effectiveness of SSRIs for PTSD symptoms. Research indicates that an SNRI, venlafaxine, may be more effective in reducing symptoms of PTSD compared with SSRIs. There is also evidence that noradrenaline, which is increased by SNRIs, has anti-inflammatory and neuroprotective roles in chronic pain.
Medications for PTSD may or may not be prescribed directly after a traumatic experience. There is some research indicating that glucocorticoids used immediately after a traumatic event reduce the risk of developing PTSD. Holbrook and colleagues found postinjury use of opioids was linked to lower rates of PTSD after severe injuries; however, the exact mechanisms for lower PTSD rates (whether biological or psychological) are unknown. Although benzodiazepines are frequently prescribed to individuals with PTSD, they may increase the risk of suppressed breathing when taken with opioids. Concurrent use of benzodiazepines and opioids predicts problematic opioid use. ,
Although controversial, there is increasing interest in cannabinoid compounds (including cannabidiol [CBD] and Δ 9 -tetrahydrocannabinol [THC]), because these compounds have accumulated some support for benefit in separate studies of chronic pain and PTSD. Indeed, the endocannabinoid system is currently under investigation for both chronic pain and PTSD and the pain and PTSD comorbidity. In an observational study of self-administered cannabis, investigators identified a 3-point decrease in pain using a 0–10 visual analogue scale after cannabis use. Unfortunately, the outcomes of the study were limited (e.g., the duration of reduced pain was not reported) and more work is needed to substantiate a benefit of causal cannabis use for pain. The author did specify, however, that THC potency, not CBD potency, was the strongest predictor of pain reduction. Cannabinoids have been shown to enhance fear extinction, exhibit anxiolytic effects, and reduce inflammation, all of which are potentially relevant to both PTSD and chronic pain. Much more information is needed to endorse cannabinoids as the recommended treatment for either condition, and both CBD and THC derivatives are regulated by the FDA in the United States. Epidiolex (a form of CBD), Marinol (a form of THC), Syndros (a form of THC), and Cesamet (structurally similar to THC) have limited approved treatment uses. To date, there are no FDA-approved cannabinoids for the treatment of chronic pain, and there is still a lack of high-quality research regarding safety and effectiveness of cannabinoids.
Nonpharmacological Targets of Chronic Pain and Posttraumatic Stress Disorder Comorbidity
Nonpharmacological treatment approaches for addressing the chronic pain and PTSD comorbidity are still in their infancy, with only a handful of clinical trials providing a guideline for clinicians. Overall, treatment recommendations include the following: psychoeducation related to PTSD and chronic pain symptoms, treatments related to how these symptoms are associated with each other, decreasing avoidance, decreasing attentional biases and arousal, and increasing positive mood and acceptance.
The most common treatments for chronic pain and PTSD, separately, are built upon the foundations of CBT techniques and the biopsychosocial model. In PTSD treatment, avoidance and maladaptive thinking patterns are often targeted. Similarly, maladaptive coping strategies (e.g., pain nonacceptance and catastrophizing) are often targeted in chronic pain treatment using an integrated biopsychosocial model. Current treatments designed to decrease symptoms within the chronic pain and PTSD comorbidity often pull from these approaches. When treatments do not necessarily target the chronic pain and PTSD comorbidity but assess outcomes related to both disorders, moderate effects for PTSD and small effects for pain outcomes emerge, which shows psychological interventions can provide benefit for both of these comorbid conditions. ACT is a third-wave CBT intervention that focuses on valued actions, acceptance, and cognitive flexibility. A recent meta-analysis revealed that ACT for chronic pain results in small effect sizes for improvements in functioning, quality of life, and pain intensity. It found a moderate effect size for anxiety and large effect sizes for pain acceptance and comorbid depression. Another meta-analysis found similar results with a smaller effect size for depression when ACT was used for chronic pain. In veterans with chronic pain and PTSD, clinically significant reductions in PTSD symptoms and improved pain outcomes were observed after treatment with ACT.
Targeting the chronic pain and PTSD comorbidity, Otis et al. developed a treatment that included elements from cognitive processing therapy and CBT for pain, producing mixed results. The treatment included goal-setting, meaning-making, and exposure. Although the small trial (of six total individuals) resulted in three individuals dropping out of treatment, those who stayed in treatment endorsed a decrease in pain-related disability and PTSD symptoms. In a study focused on chronic PTSD symptoms, Beck et al. implemented a CBT group therapy protocol, wherein 80% of individuals endorsed chronic pain in the sample. Although the sample size was small, medium to large effect sizes were found after treatment for PTSD and pain-related disability. Nevertheless, one-third of the sample subjects dropped out, and only 29% of the treatment group endorsed what the authors called “high end-state functioning,” defined as minimal PTSD and depression scores. Finally, a trauma-focused CBT intervention, which included psychoeducation, exposure, cognitive restructuring, and relaxation techniques, resulted in significant decreases in both PTSD and pain-related disability in the treatment group compared with the waitlist control.
With such a complicated population, wherein treatments for even one of the two disorders remain to be completely understood, nontraditional approaches offer a compelling and holistic alternative that has been tested with some success. Somatic reexperiencing, which focuses on bodily sensations related to traumatic experiences, combined with exercise, was implemented in a RCT for comorbid chronic pain and PTSD. Although the treatment resulted in a decrease in PTSD symptoms, pain-related disability remained unchanged, indicating more was needed to address the symptoms of pain. Other treatments have been more successful in concurrently treating pain symptoms and PTSD, including eye movement desensitization and reprocessing (EMDR) therapy and accelerated response therapy, a therapy that utilizes eye movements, along with imaginal exposure and rescripting.
Modification of Pain Management Delivery Pathways
Chronic pain and PTSD are notably complex, and both clinicians and researchers confronting this problem understand that the strongest treatments are likely to include multiple modalities. Indeed, some of the strongest work in chronic pain management focuses on interdisciplinary models of care that include medical, physical, and psychological interventions meaningfully integrated into a unified conceptual model of care ( see Functional Restoration). Complex PTSD also responds well to intensive outpatient treatment that mimics interdisciplinary pain management through a strong focus on both functional and psychologic treatments (see Massed Prolonged Exposure). Although effective, these high-intensity treatments are notoriously difficult to implement, so large medical systems have begun to explore care systems designed to organize different treatments for pain and PTSD using existing but disconnected clinical resources. By organizing existing treatments and increasing communication between providers, health systems hope to better address the comorbid pain and PTSD complexity and obtain better outcomes. For example, the Department of Veterans’ Affairs has established a stepped care model of pain management that encourages routine assessment of PTSD and recommendations for referral to evidence-based care for pain-suffering veterans who screen positive for PTSD. The Defense Health Agency (DHA) has begun to implement a comprehensive pain management pathway that includes components for both pain and PTSD treatment organized under a comprehensive system of care. Research on pain and PTSD comorbidity has begun to shift toward pragmatic studies of these integrated systems, offering perhaps the strongest potential for effectively addressing this comorbidity. Future studies should capitalize on nascent health systems and clinical informatics resources to enhance this endeavor.
Research on interventions for either chronic pain or PTSD has grown for decades, and more needs to be done to strengthen and refine interventions for each of these conditions. Unfortunately, few studies have examined treatments designed to effectively address both conditions concordantly. This lack of research attention is particularly disturbing in light of the growing recognition of high comorbidity rates between these conditions and the well-demonstrated complexity of the pain-PTSD phenotype. Initial models explaining the chronic pain and PTSD comorbidity have provided invaluable insight toward better understanding how and why these disorders seem to be so difficult to treat. For one, treating PTSD or chronic pain alone comes with its own problems: attrition rates are high; individuals fail to respond to treatment; and, each disorder has a multifaceted symptom profile affecting many aspects of individuals’ lives (e.g., social and physical functioning). In one sense, the comorbidity is like any other, wherein common thoughts, emotions, and behaviors maintain the disorders. In a more complicated sense, each disorder challenges patients in finding alternative ways of being in the world. One’s assumptions about a fair and just world are disrupted; interpretations of bodily sensations that once seemed harmless are now terrifying; enjoyable and meaningful activities may no longer be possible; and the feedback received from others that imply acceptance and commonality may now be altered. If a more thorough understanding is to be attained and treatments are to be improved, methodological considerations and novel mechanisms will need to be addressed.
Much emphasis has been placed on the “mutually maintaining” components of this comorbidity. For instance, intrusive thoughts related to a traumatic experience may trigger thoughts of pain, increasing pain severity. Certainly, analyses comparing those with comorbid chronic pain and PTSD with other groups are able to show between-group effects of certain symptom profiles. Although these studies provide insight into these symptoms, they fail to show causality and leave other confounding variables as possible explanations. In addition, cross-sectional studies provide data at one time point, essentially providing a snapshot of symptoms with little context. Even longitudinal designs, including RCTs, often measure participants using self-report data at only a few time points, resulting in insufficient data for truly understanding the causal moment-by -moment symptom presentations that are hypothesized to maintain the comorbidity.
Ecological momentary assessment (EMA) offers a potentially more informative way to understand pain and PTSD comorbidity (compared with longitudinal RCTs). EMA is a technologic advancement within the field of longitudinal research, whereby participants receive a notification on an electronic device (e.g., a smartphone) instructing them to answer several items about their symptoms, condition, or functioning at that moment. This can be done at several points during the day, providing rich data on momentary emotional and physical states. Despite the hypothesized role of mutually maintaining symptoms, only one study using these methods within this population has been published. Pacella et al. assessed 67 individuals who were admitted into an emergency room for various types of injuries (e.g., motor vehicle accident or fall). Each day, they received five text messages asking them about PTSD symptoms, pain, and social support. EMA was carried out for 14 days, wherein pain severity significantly decreased across the time of the study. Moreover, daily changes in hyperarousal (and, to a marginal degree, avoidance) were predictive of pain severity. Studies such as this would provide ecological data related to a variety of psychosocial variables known to be associated with the chronic pain and PTSD comorbidity. New technology may also provide biological data on a moment-by-moment basis.
Technology allowing for wearable devices to monitor biomarkers of pain and PTSD have skyrocketed in recent years. Activity trackers, such as Fitbit or Apple Watch, are able to monitor heart rate and the number of steps an individual has taken, including the intensity of those steps. Use of wearable devices has grown, in part, through improvements in sensor design resulting in strong reliability and validity for biomarkers such as activity and heart rate. Smart shirts are available that measure heart rate, temperature, blood pressure, and respiration and have the potential to provide a clearer picture of CNS responses to life stressors compared with what could be gleaned from wristwatch devices. Knowing the HPA axis is a primary common factor between PTSD and chronic pain, gathering real-time biological data associated with pain severity may be highly impactful. Research could focus on attaining pain severity levels when there is evidence of an increase in heart rate or respiration. Causal directionality could be assessed, and interventions could target these moments in an attempt to shape behavior and internal responses to external stimuli. For instance, it may be that a trauma reminder results in a response from the sympathetic nervous system, whereby one’s heart rate increases, and thoughts of the reminder become acutely salient. Awareness of these moments, made possible due to wearable technology and real-time data, provides feedback to patients that now is the time they should use mindfulness techniques, breathing exercises, or another skill learned in therapy.
The Role of Identity
The biopsychosocial model attempts to incorporate most or all aspects of an individual into treatment. Yet, somehow the self and issues related to identity, changing social roles, and other losses are often left out of consideration. Nevertheless, theoretical work has shown how issues of identity play a role in pain-related disability, and a focus on valued goals may be an important pathway toward patient improvement. , Among individuals with pain, tension related to met and/or unmet goals has been associated with fear of pain and pain severity. , Individuals with chronic pain struggle to meet the demands of community and social engagements, behaviors that provide individuals with a sense of meaning and purpose. Similarly, those who recover from PTSD engage in social activities and are an active member of their family, both of which provide individuals with a coherent sense of self, identity, and sense of meaning and purpose.
A recent advancement in the PTSD literature is the study of moral injury, which essentially amounts to an injury to the sense of self. Moral injury is defined as the effect of participating in an event or events that is incompatible with one’s internal moral code: values, worldviews, and culturally derived beliefs have somehow not been maintained. Moral injury may occur, for example, when a member of the armed services is forced to harm someone else for survival, thus acting outside the realm of previously held ethical boundaries. These values and ethics are the more tangible manifestations of one’s identity, and when these are disrupted, negative consequences can emerge.
A patient with comorbid PTSD and chronic pain struggles on two fronts: an identity that has been disrupted and limited resources to engage in behaviors and cognitions that enable a coherent identity to re-emerge. A coherent identity has been linked to a bevy of positive outcomes, including less emotional distress, avoidance, depression and anxiety symptoms, and social anxiety, and serves as a means to buffer against existential concerns. ,
However, current treatments for the chronic pain and PTSD comorbidity do not adequately focus on developing a coherent sense of self or cultivating a “true self” that is always there despite changing social roles and physical abilities. Although ACT may touch on these subjects, the focus of ACT consists of defining one’s values already in place and acting on them. Individuals with comorbid chronic pain and PTSD have experienced abrupt changes in multiple aspects of their lives, and additional work may be needed in order to answer the question of “Who am I?” Future treatments that specifically target identity disturbances may be beneficial to many patients, particularly those who struggle to complete traditional treatments that target avoidance, such as cognitive processing therapy or prolonged exposure therapy.
Researchers may find it beneficial to examine treatment approaches outside the confines of trauma and chronic pain. For instance, dialectical behavior therapy (DBT), a third-wave CBT that incorporates mindfulness and cognitive dialectics, is highly effective for the treatment of borderline personality disorder, a disorder characterized, in part, by an unstable sense of self. Indeed, research implicates identity disturbances as a factor of opioid misuse above and beyond pain severity and interference within a chronic pain sample. Incorporating elements of DBT into a treatment approach for this comorbidity may be highly beneficial for reducing opioid misuse and pain-related disability.
Identity is but one component of the sociocultural buffer that prevents existential concerns from becoming an issue. When a traumatic event occurs, those with increased PTSD symptoms endorse increased death thoughts and death anxiety, an inability to utilize self-affirmation strategies, and negative biases in coping strategies. Traumatic events disrupt cognitions that allow individuals to believe that the world is a just, safe, trustworthy, and meaningful place (e.g., just-world theory). , , It is not a far leap to assume that similar internal events happen in those with chronic pain. Indeed, existential concerns appear to play a unique role within chronic pain populations, in whom these concerns have broad implications related to pain intensity, pain disability, life satisfaction, and depression. Treatment with an existential focus has been shown to be effective in decreasing pain-related disability, especially for those with higher spirituality/religiosity. Treatment approaches that target moral injury, identity, meaning, and valued goals, when combined with other CBT techniques and pharmacotherapy, may be particularly beneficial in reducing disability, as well as symptoms of PTSD. It remains to be seen not only if patients would find these treatments more rewarding and beneficial, but also whether they can be readily translated into short-term treatments implemented as adjunct therapies within primary care or pain clinics.
This chapter characterized the epidemiology, cause, maintaining factors, current treatments, and future directions of the unique comorbidity between chronic pain and PTSD. Within either a chronic pain or PTSD sample, rates of having the other disorder are high, particularly in military personnel and those who are more vulnerable at developing this comorbid condition. Various genetic, cognitive, and emotional components appear to play a role in how these disorders are developed and maintained. The shared vulnerability model posits that AS and genetic predispositions (particularly as they relate to the HPA axis and stress response) make it more likely that certain individuals will develop this comorbidity. Similarly, it appears these disorders are mutually maintained by individuals avoiding physical and psychological pain, being more attuned to their experiences as they relate to chronic pain and PTSD, having negative affective and cognitive responses to these experiences, being constantly reminded of the pain and/or traumatic event, and being unable to effectively cope with the pain and/or PTSD symptoms. Since these theoretical models have been introduced, little progress has been made in how to best understand and treat this comorbidity. Recent technological advances have allowed for the possibility to gain causal and moment-by-moment knowledge (e.g., EMA) of how these disorders interact. Finally, the role of identity within this comorbidity has yet to be fully explored and offers a promising novel target of change that encompasses many aspects of both the shared vulnerability and mutual maintenance models.