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Biennial Review of Pain

Ronald Melzack Award Lecture: Putting the brain to work in cognitive behavioral therapy for chronic pain

Thorn, Beverly E.

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doi: 10.1097/j.pain.0000000000001839
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1. Introduction

Biomedical treatments for chronic pain have not been uniformly effective and sometimes have caused harm.38,40,76 As a result, international guidelines have proliferated for treating chronic pain using nonpharmaceutical, noninvasive, biopsychosocial therapies.3,24,37,68,94 In current practice, however, clinics delivering unimodal biomedical interventions are flourishing (and such treatments are increasingly provided even in developing countries).5,7 Meanwhile, interdisciplinary pain treatment programs, despite their superiority over unimodal treatments,25,39,87 have steadily declined. Based on US Medicare reimbursement data available over 20 years ago, when laminectomy surgery costs were approximately $30,000 USD, a standardized efficacious 10-session group cognitive behavioral therapy (CBT) approach costs 168 times less than spinal surgery.9 More recent data report skyrocketing costs for spinal surgeries, some of which bill out at over $400,000 USD for the surgery alone.38 Meanwhile, biopsychosocial pain treatments continue to be poorly reimbursed (if at all) and are not widely available in the United States or internationally.

Many health care practitioners are not familiar with biopsychosocial therapies such as CBT and may view psychosocial treatments as only appropriate for those with mental illness. Moreover, some practitioners may hold the erroneous belief that chronic pain is an expression of mental hurt and generated psychologically. Furthermore, practitioners may not know that treatments based on a biopsychosocial model have a biological outcome. However, a wealth of evidence supports that biopsychosocial treatments are conceptually and empirically linked to our current understanding of pain neurophysiology. For example, there is growing evidence that CBT can reverse some of the neuronal changes associated with chronic pain, including post-treatment increases in the prefrontal and posterior parietal cortex (areas believed to be associated with pain appraisal) and decreases in somatosensory cortex (perhaps reflecting reductions in the perception of pain severity).72 A randomized controlled trial of CBT compared with pain education reported post-CBT decreases in connectivity between the limbic system (emotions) and other areas of the brain, and enhanced connectivity between prefrontal cortices (cognition) and other regions of the brain.74

Treatments using the biopsychosocial model do not ignore the biological, nor do they advocate refraining from appropriately assessing and treating ongoing tissue damage. However, treating patients with pain as if all pain is related to ongoing tissue damage that must be located and repaired (a biomedical model) has led to the false impression that hurt = harm and that “real” pain is detectable with a biomedical marker and correctable with the right biomedical intervention. The net result is that, at least in the United States, health care costs are out of control, there is an opioid epidemic, and patients have unrealistic expectations of being pain-free. Many of our patients do not know that they can harness the power of their thoughts, emotions, and behaviors to help themselves manage their chronic pain, thus increasing function and quality of life despite pain.

In this review, which is written as part of the 2020 IASP Ronald Melzack Lecture Award, I revisit Melzack and Wall's gate control model of pain54 as a biopsychosocial construct and explore its more recent clinical applications in specific kinds of pain education56,79,83 and cognitive-behavioral therapy (CBT).79,83 Although it is acknowledged that we have advanced our understanding beyond the original gate control theory to more fully appreciate the role of the brain in pain, I will discuss the applicability of using this very basic framework for patients. I describe recent research using a simplified gate control schematic as a treatment rationale for pain education and CBT with low-income, multiply disadvantaged patients,83 using the gate control model as a launching point to discuss the cognitive aspects of CBT (and pain education). Targeting a cognitive model of pain (thoughts influence emotions and behavior), I provide examples of how psychosocial health care providers work alongside patients to train them in skills to work with their thoughts, to motivate patients, and to help them implement pain self-management behaviors. Moving into a brief examination of treatment mechanism (mediation and moderation), I will conclude with the argument that effective psychosocial interventions share more commonalities than sometimes acknowledged, and that these treatments can be used to help patients self-manage their pain, and perhaps to change health care cultures.

2. Gate control model briefly revisited

More than 50 years ago, Melzack and Wall54 proposed that a neural gate in the spinal cord could modulate pain signals coming from the periphery and going to the brain. Today, this is common knowledge in the pain research world, but in 1965, we were still operating under the 16th century Cartesian notion that nociceptors in the periphery had a direct line to the brain (through spinal cord). Thus, pain signals, activated by noxious stimuli, rang a bell in the pain center of the brain. Presumably, the more nociceptors that were activated (ie, the stronger the stimulus), the louder the bell rang. It is now clear that there is not a one-to-one correspondence between tissue damage and pain, and that one's experience of pain does not necessarily indicate ongoing tissue damage. However, there is still an alarming amount of adherence to a strict biomedical model of pain within a variety of cultures and in many health care systems around the world. What was revolutionary about the gate control model was the idea that the brain could monitor and modulate the activity of the spinal cord transmission neurons. Specifically implicated were brain-mediated cognitive and affective factors as part of the neural process of pain perception and part of the descending “central control” of the spinal cord gating system.

Although it is now established that neural mechanisms are more complex than that originally proposed by Melzack and Wall,52–54 the general concepts remain, that a gating mechanism in the spinal cord excites or inhibits information flow to the brain, and that there are descending central control mechanisms that increase or decrease the sensitivity of the nociceptive system through this gating mechanism—possibly, through multiple gates and multiple systems.8,86 The perception of pain is influenced by signals received from the periphery but driven by what the central nervous system does with those signals.

3. Gate control model used clinically

Educating patients about how pain is processed in the brain (including elements of the gate control/neuromatrix model) is considered to be of increasing importance as reflected in international pain management guidelines and its inclusion in many current biopsychosocial treatment approaches. Lorimer Moseley and colleagues have promoted pain neurophysiology education (PNE) for patients with chronic pain,11,51,55,57,58,60,73 and there is a growing literature examining its efficacy. Systematic reviews and recent clinical trials report differing levels of support for the “neuroeducation” approach, particularly as a unimodal treatment, but there is strong support for the rationale of explaining pain processing in the brain when working with individuals in pain.15,46,85,95,96 Of note, one such review reported that multisession cognitive behavioral therapy (CBT) preceded by PNE produced better longer-term outcomes compared with neurophysiology education alone.15 Another clinical trial reports that hypnosis enhances the effect of PNE in patients with low back pain, and a very recent paper suggests combining PNE with motivational interviewing techniques may bolster its effects.61,70 Thus, PNE may not be enough.

In past and current psychosocial research, pain education alone has sometimes been used as an attention control condition.31,88 Although there are multiple approaches to a pain education intervention, and reported efficacy is variable,2,63 there is likely an important distinction between pathophysiology education (which provides a biomedical explanation of disc pathology, for example) and a biopsychosocial approach. The latter typically includes pain self-management education, often provides some measure of neurophysiology education, and usually emphasizes the importance of cognitions and emotions.29,34,49,79,82–84,90 Psychosocial pain education could be considered a therapeutic strategy if it is formulated to enhance patient understanding of their condition, help them reconceptualize pain and pain management as multi-dimensional rather than solely determined by tissue pathology, and provide a rationale for engaging in pain self-management. A key point is that for pain education to be effective, it must provide the rationale (and likely, the motivation) to engage in known pain self-management behaviors. In either case, behaviors must change for pain self-management to be effective. For example, if patients learn about the importance of maintaining physical activity despite chronic pain, physical activity must actually be implemented to effectively reduce pain-related interference in daily activities.

Figure 1.
Figure 1.:
Gate control diagram: Patient handout used to convey the concepts of the brain as a filter of so-called pain signals, emphasizing cognitive and affective mediation, and illustrating descending inhibitory (or excitatory) mechanisms.79,80

While there is growing emphasis on the importance of patient education in chronic pain management,37,59,66,68 patients in general practice rarely receive comprehensive biopsychosocial education as part of their treatment and likely would not understand it unless provided in a userfriendly (jargon-free, practical) way. Considering that 49% of those in developed nations (52% in the United States) have basic or below basic reading skills (basic skills translate to reading at the fourth-fifth grade levels),69 pain education, of necessity, must be simplified.

4. Simplified pain education and cognitive behavioral therapy

Cognitive behavioral therapy is well established as an efficacious treatment for chronic pain,1,30,36,97 but with moderate overall effect sizes.28 In current CBT approaches, educating the patient about pain is infused into the skill-training aspects. Our clinical research team has incorporated into our treatment approach, a simplified discussion of pain as a perception that is filtered by the brain, emphasizing the capacity of the brain to “open” or “close” a pain gate to process more or fewer pain signals. See Figure 1 for the illustration we use to facilitate this discussion. This is an adaptation of more complex neurophysiology pain education approaches,11,12 and it serves as our treatment rationale for psychosocial pain management, specifically, cognitive behavioral therapy.32,79 We emphasize the following specific points: First, contrary to what is typically understood, pain is not a sensation but a perceptual experience in the brain that involves many filters. Second, the brain processes the sensation of pain by filtering so-called pain signals through multiple sites involved in memory, emotion, and thought processes. Third, the brain monitors so-called pain signals coming into the spinal cord and, based on what is happening in the filtering sites, can enhance those incoming pain signals (“open the gate”), ultimately making the brain more sensitive to pain, or diminish the strength of the signal (“close the gate”). In essence, we use a simplified version of the original gate control model, retaining the general concepts, providing our own simplified illustration, and avoiding reference to complex neurophysiological terminology (eg, interneurons, calcium channels, central sensitization, and descending inhibition).

In previous research,82 our laboratory evaluated 2 group-administered psychosocial pain treatments in patients receiving care at low-income US health care settings. Both the cognitive behavioral therapy (CBT) and pain education (EDU) conditions included our above-described simplified gate control theory. These treatments were adapted to decrease the literacy demands of patient materials and reduce the cognitive demands of the interventions. For example, the reading levels of patient written materials were lowered from 10th grade (in original format80) to fifth grade, and key illustrations were used to help emphasize certain points. Furthermore, during the treatment groups, jargon and multisyllabic words were avoided, interactive teaching methods were used, and cotherapists provided one-on-one assistance when it seemed that group members were struggling with a concept.42 Both CBT and EDU were provided in 10 weekly 90-minute group discussion sessions with 5 to 7 participants. Both treatments emphasized therapeutic alliance, group discussion, and group affiliation, and both treatments used a biopsychosocial model to provide useable information about pain, the brain, and pain self-management. CBT, additionally, involved active skill-building exercises (with homework), whereas EDU did not include skills training. Study results revealed moderate treatment effects on pain severity, and pain interference in daily functioning for both interventions, with no significant differences between treatments. EDU was better tolerated than CBT, producing fewer dropouts. Although these findings suggested that literacy-adapted CBT and EDU may both be efficacious in this population, the trial was underpowered to reliably detect differences between conditions and lacked a usual medical care (UC) comparison group, preventing evaluation of whether these therapies could augment existing medical practices.

Following additional simplifications in the CBT treatment protocol to enhance retention (eg, removed written homework requirements, provided CDs of session summaries to patients, additional simplifications of patient workbooks79), we conducted a randomized controlled comparative efficacy trial powered to detect differences between conditions (290 participants, again at low-income US clinics) and added a usual medical care condition.83 Both CBT and EDU included our simplified “gate control” education as a treatment rationale and matching of the interventions with regard to format. The participant sample represented those with multiple disadvantages, often with the triple disparity of low income, low primary literacy, and minority status (African American). Study completion rate (83%) showed no differences across conditions, suggesting that the additional adaptations made to CBT enhanced its acceptability. Similar to the earlier study,82 both CBT and EDU (but not the usual care condition) produced significant pre- to post-treatment decreases in mean pain intensity and pain interference, with treatment gains mostly maintained at 6-month follow-up. Comparisons of effect sizes/confidence intervals, clinically meaningful improvement rates (defined as 30% or greater improvement26), and minimally important change criteria,26 showed CBT having small clinical advantages over EDU on pain intensity and physical function.83 In terms of potential harms/adverse events, 28 of all 290 participants sought emergency department treatment at some point during the trial (mostly temporary pain exacerbations). Six participants were hospitalized overnight for non pain-related reasons (eg, asthma). No events were determined to be caused by participation in the trial.83 Both CBT and EDU showed clear advantages over and above usual medical care, answering in the affirmative that these therapies can be used to augment existing medical practices.

The unique aspect of the CBT treatment compared with EDU in the above studies is that, in addition to simplified pain neurophysiology and relevant pain self-management information, patients receiving CBT are provided with structured, guided training, and hands-on practice in a variety of pain self-management skills, including relaxation techniques for stress management, activity pacing, assertiveness training, cognitive restructuring, and emotional disclosure. Each of the skill-oriented techniques taught during the CBT program are referred to as “gate closers”79 to enhance the connection for the patient between the use of cognitive behavioral skills and the descending pain inhibitory mechanisms first proposed in the gate control model. See Table 1 for a session-by-session breakdown of our CBT protocol as well as a comparison with the EDU protocol. Of note, this CBT program is based on an original protocol developed over decades79,80 and supported in empirical studies.82–84

Table 1
Table 1:
Session content in cognitive behavioral therapy and pain education protocols used in Thorn et al. (2018).79–81

5. The importance of thoughts and examples of psychosocial pain intervention techniques targeting them

Both CBT and EDU in the above protocols emphasize the importance of thoughts as a key process in pain-self management. An adaptation of the transactional model of stress45 is used to provide a cognitive model of pain,80 which (simplified) is referred to as the “Think → Feel → Act” model. Traditional cognitive therapy6 delineates categories of thought processes and targets each category therapeutically. Below is a brief description of the categories, with examples of therapeutic techniques used.

5.1. Judgments about stressors

Pain is stressful, as are many life challenges associated with chronic pain. An important component of the stress reaction is one's judgment regarding the stressor. For example, the thought that a pain flare-up signals ongoing tissue damage (ie, hurt = harm) is a judgment about the pain. Pain directs one's attention and is therefore compelling and interrupts function, especially if deemed to be a threat. As Eccleston (2018, pg s17) put it, for the person with chronic pain, “The lived experience …is to be in a state of defensive alert, of being urged to escape and avoid harm.”28 One example of a clinical application using primary appraisals is to teach patients to examine their initial judgments of a situation and determine whether they are viewing it as a threat, a loss, or a challenge.79,80 Focusing one's attention on the judgment of the stressor (and not necessarily the stressor itself) allows them to consider working on their interpretation, often parsing out aspects that are indeed a challenge instead of a threat/loss. Another example of a clinical application of judging pain is that represented by the fear of movement/(reinjury) model and the subsequent clinical application of in vivo exposure to overcome judgments of hurt = harm.17,91,92 Using graded exposure to physical movement, patients learn that appropriately paced physical activity using proper body mechanics does not create injury or pain exacerbations. Thus, they are able to change their judgment that physical activity causes injury to the body.

5.2. Judgments about coping options

Many of our thoughts throughout the day arise somewhat spontaneously and provide a running commentary of environmental events. These “automatic thoughts” often occur in response to or in anticipation of pain. Examples of negative automatic thoughts might be “No one believes my pain is real” and “I won't be able to work much longer because of my pain.”79

Catastrophic thinking (a negative mental set about pain or potential pain) has been an imperfect, albeit robust, construct in the pain literature for decades. In hundreds of studies, catastrophizing has emerged as both a predictor of poor adjustment to pain and a specific target of intervention. An example of a catastrophizing thought taken from the well-known Pain Catastrophizing Scale77 and included (slightly altered) in the Patient-Reported Outcomes Measurement Information System Roadmap Initiative item bank for pain catastrophizing (PROMIS)4,13 is “I keep thinking about how much it hurts.” Classic cognitive therapy techniques such as cognitive restructuring exercises have frequently been used to (effectively) reduce catastrophizing and other negative pain-related thinking.79 In cognitive restructuring, patients are guided to become aware of negative thoughts that work against them and then examine whether the thought is true, partly true, or partly false. They are then trained how to come up with a more realistic, helpful, and less negative thought to “close the pain gate.” It is important to note that other techniques not targeting catastrophizing thoughts per se, such as (but not limited to) mindfulness-based therapies20 and acceptance and commitment therapies,33 have also reported decreases in pain catastrophizing after treatment.93

5.3. Acquired “rules” for self and others

Beliefs about the cause of pain and how it should be treated develop over time and are heavily influenced by cultural and social expectations. An example of such a belief is “a competent doctor who cares should find the source of the pain and fix it.” Patients with pain also develop “rules” about how they should be as a person with pain, such as “a man should work and provide for his family.”79 Helping patients recognizes the implicit “rules” they hold for themselves and others, and guiding them to assess whether these rules work for or against them can give them a sense of agency over a previously unrecognized cognitive process.79,80 An example of a potential clinical application of an acquired belief involves the concept of perceived injustice after injury leading to chronic pain. A patient might have the belief that “The guy responsible for this accident should be given a life sentence for taking away my life.” Therapeutic techniques that decrease anger, reduce overly harsh judgment, and increase a sense of forgiveness have all been suggested as ways of reducing perceived injustice.50,62,67,78 Possibly, these techniques function to increase one's acceptance that one has a chronic condition and a willingness to engage in activities despite pain. Acceptance and commitment therapy, mindfulness, and positive psychology techniques specifically target reduced judgment and increased forgiveness and have also been shown to increase pain acceptance after treatment.41,65

5.4. Deepest beliefs: identity

In classic cognitive therapy, one's core beliefs are underlying views about the self, interacting between life events and one's temperament.6 One's identity is often thought of as uniform and invariant, although others have suggested that we have a number of identities, often competing with each other and acting in concert with the social, cultural, and even with the internal (biological) environment.28,43 Beck and others have suggested that one's core identity includes both positive and negative aspects of one's view of themselves.6 When environmental circumstances are perceived as “positive,” more positive beliefs about the self are activated; conversely, when circumstances are perceived as “negative,” one tends to devalue oneself and hold on to negative self-constructs. Core beliefs and negative self-identity are also considered to be the most difficult to change among the types of cognitions already discussed. An example of an unhelpful core belief that may be activated with chronic pain is “I am damaged goods.”79 Unfortunately, as pain becomes more chronic, the person with pain likely comes to develop an identity as a “disabled chronic pain patient.” This belief functions to set the individual with pain up for passivity, a “sick person” role, withdrawal, and helplessness, and the downward spiral continues.

An example of a technique that could be used to examine and possibly change negative self-identity is emotional disclosure.64,71 Written emotional disclosure exercises have been used therapeutically with a variety of patients, including those with chronic pain,48 and focus on teaching patients to write about (or sometimes audio record) previously undisclosed, negative, unresolved experiences. Recently, Mark Lumley and colleagues have expanded the application of written disclosure exercises to a treatment program termed emotional awareness and expression therapy (EAET).47 A large well-controlled trial in fibromyalgia patients comparing EAET with CBT (and an educational control) found approximately equivalent results between EAET and CBT (except that a greater percentage of EAET participants achieved >50% pain reduction), with both superior to education. Thus, EAET, in addition to more traditional cognitive therapy techniques, may hold value in helping patients consider and modify negative personal identities.

6. The movement towards identifying mechanisms and targeting those that are critical

Colleagues and I have suggested that psychosocial pain management may engage several therapeutic processes: changing what we think, that is, cognitive content; changing how we think (ie, cognitive processes), working with our emotions (ie, mood states); and changing our actions to manage pain (ie, behavior).21,23,81 I would argue that although traditional cognitive therapy has been previously criticized as shortsighted or superficial by targeting a change in one's thought content (using the emblematic cognitive therapy techniques referred to as cognitive restructuring), it is possible, and even likely that techniques emphasizing cognitions also change how one thinks (ie, alter one's relationship to their thoughts by learning to observe one's ever-changing thoughts without being emotionally overcome by them).20,79 In fact, it is quite possible that cognitive therapy techniques such as cognitive restructuring exercises do not require a change in cognitive content but instead alert individuals to their process of thinking. As such, cognitive restructuring, and other classically “cognitive” therapy exercises, may have important similarities to therapies sometimes referred to as “third wave” CBT: acceptance and commitment therapy (ACT) and mindfulness-based therapies.

Although different therapeutic techniques are applied, and different theorized mechanisms of change are hypothesized, there is more evidence to suggest shared, rather than treatment-specific therapeutic mediators across treatments. Consider pain catastrophizing, for example. Significant reductions in pain catastrophizing have been found with biopsychosocial pain education,82,83 CBT, mindfulness-based stress reduction, and mindfulness-based cognitive therapy,14,23,82,83 ACT,16 and even physical exercise,44,75 yoga,18,44 and Tai Chi.35 Most of these treatments do not target changing cognitive content (eg, mindfulness-based stress reduction and ACT), and some (eg, physical exercise) do not target cognitions at all.

Planning treatment research that assesses mechanisms is necessary, but difficult, and results are often complex, likely reflecting reciprocal relationships between changes in hypothesized mechanism and crucial outcomes. For example, in a post hoc crossed lagged analysis of both the CBT and EDU data from our most recent RCT described above,83 we found that early changes in cognitions predicted late-treatment changes in pain intensity and interference in daily activities due to pain for both EDU and CBT. However, early changes in pain outcomes also predicted later treatment changes in cognitions.10 Because EDU did not involve skills training or cognitive restructuring, and considering the above research reporting that a wide variety of treatments show reductions in catastrophizing after treatment, it seems likely that cognitive therapy per se is not the key procedure for cognitive change. However, cognitive change (content or process), perhaps regardless of how it is brought about, seems to be an important piece of the mechanism puzzle.

Given the few outcome differences between CBT and EDU in our study, one might conclude that EDU, which takes less cognitive effort on the part of therapist or patient and requires fewer resources on cash-strapped health care systems, might be a “good enough” option. In fact, Vlaeyen and colleagues made this argument after finding that pain education plus group cognitive therapy compared with pain education plus group discussion provided few differences in critical outcomes, although cognitive therapy was more expensive to administer.34,90 It is interesting to note that these researchers also speculated that poor compliance, difficulty completing homework, and lack of individual support may have decreased the overall efficacy of the cognitive therapy program. This latter comment may speak to the importance of simplifying our psychosocial treatments.

Another approach to disentangling treatment mechanisms is to move beyond examining average outcomes between or across treatment groups and to examine moderators of treatment efficacy. That is, do differences among patients predict whether they will get more or less benefit out of a particular treatment? (ie, heterogeneity of treatment effects). In another post hoc analysis of the comparative efficacy trial conducted by our group,83 we looked at common demographic and potential cognitive moderators of treatment outcome differences across conditions. As expected, few meaningful moderation effects were found in the usual medical care condition. Interestingly, neither sex nor minority status moderated differences between any of the conditions. However, those patients with lower education, literacy, and working memory benefitted more from CBT than EDU.27 We believe this unexpected effect can be attributed to our team's multiyear effort to simplify our CBT patient materials and therapeutic process, removing the requirement for written homework, and providing enhanced individual support within the structure of the group for those with lower literacy levels. Thus, it seems that those with higher literacy and cognitive skills were able to take the biopsychosocial pain education information and apply it to their daily lives, whereas those with lower literacy and cognitive function benefited more from the structure and support provided by specific skills training without the burden of written homework. This interpretation has some support from the qualitative analysis of post-treatment interviews in our earlier trial,22 in which some EDU participants said they were able to “take the information and run with it,” while some CBT participants commented that specific training and practice (eg, behavioral pacing) was useful in helping them engage in pain self-management behaviors.

7. Future directions and conclusion

The research findings reported above hold potential promise for implementing biopsychosocial treatments in many low-income settings and developing nations with patients previously believed to be inappropriate for a cognitively oriented approach. CBT is believed to require abstract reasoning, comfort with reading and writing, and written homework compliance. It is important to underscore that our results suggest that those with lower reading and cognitive function did better with the structure of CBT (as simplified), while higher functioning individuals benefitted from either simplified EDU or CBT. Our findings suggest that simplifying our psychosocial techniques would reach a wider swath of individuals than the typically more privileged highly educated or wealthy nations. Furthermore, the structure and guidance provided by simplified CBT skills training seem to be a better option than EDU when limited educational attainment and literacy are concerns. An important caveat is that both CBT and EDU as delivered in our trial relied heavily on motivational approaches through strong therapeutic alliance and group coherence to provide an accepting and collaborative learning environment. This emphasis, including a treatment rationale that is understandable and makes sense, likely instilled positive outcome expectancy. Furthermore, both treatments involved multiple sessions (10) over the same number of weeks with adequate time provided for interactive learning and discussion (90 minutes). Patients received culturally tailored and literacy-adapted workbooks and audio CDs to facilitate comprehension. Efforts are underway to adapt and administer the CBT protocol to disadvantaged populations in Australia89 and similar efforts to adapt and simplify related treatments (eg, pain neuropsychology education) are being tested in Nepal.73

In conclusion, I would argue that all pain is brain-mediated, and therefore, all pain is organic. I think it is unlikely that a biomarker for objective pain will be found despite the field's tenacity to identify one19 because such a search suggests that some pain is real and some is not. Assessing and treating only one aspect of pain (ie, tissue damage) have likely led to iatrogenic harm and much suffering. Furthermore, our patients (and society in general) have been trained to expect that pain can be eradicated by medical professionals. Patients have had little access to pain self-management training, nor have they been given relevant, useful (and user-friendly) information about the brain—the seat of this perception we call pain. This review highlighted some biopsychosocial interventions that conceptualize pain using a cognitive model, offering unique research assessing the impact of simplifying our message and our psychosocial treatments. Continuing interdisciplinary collaboration in research and treatment will always be in the best interest of our patients.

Conflict of interest statement

B.E. Thorn is a consultant on grants awarded by the National Institutes of Health and on an ongoing PCORI award. She receives book royalties from Guilford Publications and has received consultation fees from Pittsburgh Veteran's Administration and travel reimbursement from the National Register of Health Care Providers in Psychology.

Acknowledgements

The author thanks Dr. Melissa Day for comments on earlier drafts of this manuscript and Ms. Andrea Newman for citation preparation. The author thanks her patients and students over the past 40 years. The author posthumously thanks Ronald Melzack for sharing his ideas and research and moving them forward.

References

[1]. Aggarwal VR, Lovell K, Peters S, Javidi H, Joughin A, Goldthorpe J. Psychosocial interventions for the management of chronic orofacial pain. Cochrane Database Syst Rev 2011:CD008456.
[2]. Ainpradub K, Sitthipornvorakul E, Janwantanakul P, van der Beek AJ. Effect of education on non-specific neck and low back pain: a meta-analysis of randomized controlled trials. Man Ther 2016;22:31–41.
[3]. Almeida M, Saragiotto B, Richards B, Maher CG. Primary care management of non-specific low back pain: key messages from recent clinical guidelines. Med J Aust 2018;208:272–5.
[4]. Amtmann D, Bamer AM, Kim J, Chung H, Salem R. People with multiple sclerosis report significantly worse symptoms and health related quality of life than the US general population as measured by PROMIS and NeuroQoL outcome measures. Disabil Health J 2018;11:99–107.
[5]. Bajracharya S, Singh M, Singh G, Shrestha B. Clinico-epidemiological study of spinal injuries in a predominantly rural population of eastern Nepal: a 10 years' analysis. Indian J Orthop 2007;41:286–9.
[6]. Beck AT. Cognitive therapy and the emotional disorders. Oxford: International Universities Press, 1976.
[7]. Bhattarai S, Chhetri HP, Alam K, Thapa P. A study on factors affecting low back pain and safety and efficacy of nsaids in acute low back pain in a tertiary care hospital of Western Nepal. J Clin Diagn Res 2013;7:2752–8.
[8]. Braz J, Solorzano C, Wang X, Basbaum A. Transmitting pain and itch messages: a contemporary view of the spinal cord circuits that generate gate control. Neuron 2014;82:522–36.
[9]. Bruns D, Mueller K, Warren PA. Biopsychosocial law, health care reform, and the control of medical inflation in Colorado. Rehabil Psychol 2012;57:81–97.
[10]. Burns J, Van Dyke B, Newman A, Morais C, Thorn B. CBT and pain education for people with chronic pain: tests of treatment mechanisms. J Consul Clin Psychol.
[11]. Butler D, Moseley GL. Explain Pain. 2nd ed. Adelaide: NOI Group Publications, 2013.
[12]. Catley MJ, O'Connell NE, Moseley GL. How good is the neurophysiology of pain questionnaire? A rasch analysis of psychometric properties. J Pain 2013;14:818–27.
[13]. Cella D, Yount S, Rothrock N, Gershon R, Cook K, Reeve B, Ader D, Fries JF, Bruce B, Rose M. The patient-reported outcomes measurement information system (PROMIS): progress of an NIH roadmap cooperative group during its first two years. Med Care 2007;45:S3–S11.
[14]. Cherkin DC, Sherman KJ, Balderson BH, Cook AJ, Anderson ML, Hawkes RJ, Hansen KE, Turner JA. Effect of mindfulness-based stress reduction vs cognitive behavioral therapy or usual care on back pain and functional limitations in adults with chronic low back pain. JAMA 2016;315:1240.
[15]. Clarke CL, Ryan CG, Martin DJ. Pain neurophysiology education for the management of individuals with chronic low back pain: a systematic review and meta-analysis. Man Ther 2011;16:544–9.
[16]. Craner JR, Lake ES, Bancroft KA, George LL. Treatment outcomes and mechanisms for an ACT-based 10-week interdisciplinary chronic pain rehabilitation program. Pain Pract 2020;20:44–54.
[17]. Crombez G, Eccleston C, Van Damme S, Vlaeyen JWS, Karoly P. Fear-avoidance model of chronic pain: the next generation. Clin J Pain 2012;28:475–83.
[18]. Curtis K, Osadchuk A, Katz J. An eight-week yoga intervention is associated with improvements in pain, psychological functioning and mindfulness, and changes in cortisol levels in women with fibromyalgia. J Pain Res 2011;4:189–201.
[19]. Davis KD, Flor H, Greely HT, Iannetti GD, MacKey S, Ploner M, Pustilnik A, Tracey I, Treede RD, Wager TD. Brain imaging tests for chronic pain: medical, legal and ethical issues and recommendations. Nat Rev Neurol 2017;13:624–38.
[20]. Day MA. Mindfulness-based cognitive therapy for chronic pain: a clinical manual and guide. Chichester: Wiley, 2017.
[21]. Day MA, Jensen MP, Ehde DM, Thorn BE. Toward a theoretical model for mindfulness-based pain management. J Pain 2014;15:691–703.
[22]. Day MA, Thorn BE, Kapoor S. A qualitative analysis of a randomized controlled trial comparing a cognitive-behavioral treatment with education. J Pain 2011;12:941–52.
[23]. Day MA, Thorn BE, Ward LC, Rubin N, Hickman SD, Scogin F, Kilgo GR. Mindfulness-based cognitive therapy for the treatment of headache pain: a pilot study. Clin J Pain 2014;30:152–61.
[24]. Department of Veterans Affairs, Department of Defense. Opioid therapy for chronic pain work group. VA/DoD clinical practice guideline for opioid therapy for chronic pain. 2017. Available at: www.healthquality.va.gov/guidelines/Pain/cot. Accessed August 2, 2017.
[25]. Dorflinger LM, Ruser C, Sellinger J, Edens EL, Kerns RD, Becker WC. Integrating interdisciplinary pain management into primary care: development and implementation of a novel clinical program. Pain Med 2014;15:2046–54.
[26]. Dworkin RH, Turk DC, Wyrwich KW, Beaton D, Cleeland CS, Farrar JT, Haythornthwaite JA, Jensen MP, Kerns RD, Ader DN, Brandenburg N, Burke LB, Cella D, Chandler J, Cowan P, Dimitrova R, Dionne R, Hertz S, Jadad AR, Katz NP, Kehlet H, Kramer LD, Manning DC, McCormick C, McDermott MP, McQuay HJ, Patel S, Porter L, Quessy S, Rappaport BA, Rauschkolb C, Revicki DA, Rothman M, Schmader KE, Stacey BR, Stauffer JW, von Stein T, White RE, Witter J, Zavisic S. Interpreting the clinical importance of treatment outcomes in chronic pain clinical trials: IMMPACT recommendations. J Pain 2008;9:105–21.
[27]. Van Dyke BP, Newman AK, Moraís CA, Burns JW, Eyer JC, Thorn BE. Heterogeneity of treatment effects in a randomized trial of literacy-adapted group cognitive-behavioral therapy, pain psychoeducation, and usual medical care for multiply disadvantaged patients with chronic pain. J Pain 2019;20:1236–48.
[28]. Eccleston C. Chronic pain as embodied defence: implications for current and future psychological treatments. PAIN 2018;159:S17–23.
[29]. Ehde D, Jensen M, Engel J, Hanley M, Raichle K, Osborne T. Education intervention therapist manual: project II: role of catastrophizing in chronic pain. Seattle: University of Washington, 2005.
[30]. Ehde DM, Dillworth TM, Turner JA. Cognitive-behavioral therapy for individuals with chronic pain: efficacy, innovations, and directions for research. Am Psychol 2014;69:153–66.
[31]. Ersek M, Turner JA, Cain KC, Kemp CA. Chronic pain self-management for older adults: a randomized controlled trial [ISRCTN11899548]. BMC Geriatr 2004;4:1–11.
[32]. Eyer J, Thorn B. The LAMP study: a randomized controlled behavioral trial of psychosocial treatments for chronic pain in individuals with financial disadvantage. J Health Psychol 2015:1–12.
[33]. Feliu-Soler A, Montesinos F, Gutiérrez-Martínez O, Scott W, McCracken LM, Luciano JV. Current status of acceptance and commitment therapy for chronic pain: a narrative review. J Pain Res 2018;11:2145–59.
[34]. Goossens MEJB, Rutten-van Mölken MPMH, Leidl RM, Bos SGPM, Vlaeyen JWS, Teeken-Gruben NJG. Cognitive-educational treatment of fibromyalgia: a randomized clinical trial. II. Economic evaluation. J Rheumatol 1996;23:1246–54.
[35]. Hall AM, Kamper SJ, Emsley R, Maher CG. Does pain-catastrophising mediate the effect of tai chi on treatment outcomes for people with low back pain? Complement. Ther Med 2016;25:61–6.
[36]. Hoffman BM, Papas RK, Chatkoff DK, Kerns RD. Meta-analysis of psychological interventions for chronic low back pain. Heal Psychol 2007;26:1–9.
[37]. Institute of Medicine. Relieving pain in America: A blueprint for transforming prevention, care, education, and research. Washington, D.C.: National Academies Press, 2011.
[38]. Jain NB, Ayers GD, Fan R, Kuhn JE, Baumgarten KM, Matzkin E, Higgins LD. Predictors of pain and functional outcomes after operative treatment for rotator cuff tears. J Shoulder Elbow Surg 2018;27:1393–400.
[39]. Kamper SJ, Apeldoorn AT, Chiarotto A, Smeets RJ, Ostelo RW, Guzman J, van Tulder MW. Multidisciplinary biopsychosocial rehabilitation for chronic low back pain. Cochrane Database Syst Rev 2014:CD000963.
[40]. Kolodny A, Courtwright DT, Hwang CS, Kreiner P, Eadie JL, Clark TW, Alexander GC. The prescription opioid and heroin crisis: a public health approach to an epidemic of addiction. Annu Rev Public Health 2015;36:559–74.
[41]. Kratz AL, Murphy J, Kalpakjian CZ, Chen P. Medicate or meditate? Greater pain acceptance is related to lower pain medication use in persons with chronic pain and spinal cord injury. Clin J Pain 2018;34:357–65.
[42]. Kuhajda MC, Thorn BE, Gaskins SW, Day MA, Cabbil CM. Literacy and cultural adaptations for cognitive behavioral therapy in a rural pain population. Transl Behav Med 2011;1:216–23.
[43]. Lackoff G, Johnson M. Metaphors we live by. Chicago: University of Chicago Press, 1980.
[44]. Lazaridou A, Koulouris A, Devine JK, Haack M, Jamison RN, Edwards RR, Schreiber KL. Impact of daily yoga-based exercise on pain, catastrophizing, and sleep amongst individuals with fibromyalgia. J Pain Res 2019;12:2915–23.
[45]. Lazarus RS, Folkman S. Stress, appraisal, and coping. New York: Springer, 1984.
[46]. Louw A, Diener I, Butler DS, Puentedura EJ. The effect of neuroscience education on pain, disability, anxiety, and stress in chronic musculoskeletal pain. Arch Phys Med Rehabil 2011;92:2041–56.
[47]. Lumley MA, Schubiner H, Lockhart NA, Kidwell KM, Harte SE, Clauw DJ, Williams DA. Emotional awareness and expression therapy, cognitive behavioral therapy, and education for fibromyalgia: a cluster-randomized controlled trial. PAIN 2017;158:2354–63.
[48]. Lumley MA, Sklar ER, Carty JN. Emotional disclosure interventions for chronic pain: from the laboratory to the clinic. Transl Behav Med 2012;2:73–81.
[49]. Martínez MP, Sánchez AI, Miró E, Medina A, Lami MJ. The relationship between the fear-avoidance model of pain and personality traits in fibromyalgia patients. J Clin Psychol Med Settings 2011;18:380–91.
[50]. McParland J, Hezseltine L, Serpell M, Eccleston C, Stenner P. An investigation of constructions of justice and injustice in chronic pain: a Q-methodology approach. J Health Psychol 2011;16:873–83.
[51]. Meeus M, Nijs J, Van Oosterwijck J, Van Alsenoy V, Truijen S. Pain physiology education improves pain beliefs in patients with chronic fatigue syndrome compared with pacing and self-management education: a double-blind randomized controlled trial. Arch Phys Med Rehabil 2010;91:1153–9.
[52]. Melzack R. From the gate to the neuromatrix. PAIN 1999(suppl 6):S121–6.
[53]. Melzack R. Pain: past, present and future. Can J Exp Psychol 1993;47:615–29.
[54]. Melzack R, Wall PD. Pain mechanisms: a new theory. Science 1965;150:971–9.
[55]. Moseley GL. Evidence for a direct relationship between cognitive and physical change during an education intervention in people with chronic low back pain. Eur J Pain 2004;8:39–45.
[56]. Moseley GL. Innovative treatments for back pain. PAIN 2017;158:S2–S10.
[57]. Moseley GL. Whole of community pain education for back pain. Why does first-line care get almost no attention and what exactly are we waiting for? Br J Sports Med 2019;53:588–9.
[58]. Moseley GL, Nicholas MK, Hodges PW. A randomized controlled trial of intensive neurophysiology education in chronic low back pain. Clin J Pain 2004;20:324–30.
[59]. National Pain Strategy outlines actions for improving pain care|HHS.gov. Available at: https://www.hhs.gov/ash/about-ash/news/2016/national-pain-strategy-outlines-actions-improving-pain-care/index.html. Accessed January 11, 2020.
[60]. Nijs J, Paul van Wilgen C, Van Oosterwijck J, van Ittersum M, Meeus M. How to explain central sensitization to patients with “unexplained” chronic musculoskeletal pain: practice guidelines. Man Ther 2011;16:413–18.
[61]. Nijs J, Wijma AJ, Willaert W, Huysmans E, Mintken P, Smeets R, Goossens M, van Wilgen CP, van Bogaert W, Louw A, Cleland J, Donaldson M. Integrating Motivational interviewing in pain neuroscience education for people with chronic pain: a practical guide for clinicians. Phys Ther 2020:pii: pzaa021.
[62]. Offenbaecher M, Dezutter J, Kohls N, Sigl C, Vallejo MA, Rivera J, Bauerdorf F, Schelling J, Vincent A, Hirsch JK, Sirois FM, Webb JR, Toussaint LL. Struggling with adversities of life. Clin J Pain 2017;33:528–34.
[63]. Van Oosterwijck J, Meeus M, Paul L, De Schryver M, Pascal A, Lambrecht L, Nijs J. Pain physiology education improves health status and endogenous pain inhibition in fibromyalgia: a double-blind randomized controlled trial. Clin J Pain 2013;29:873–82.
[64]. Pennebaker JW, Beall SK. Confronting a Traumatic Event. Toward an understanding of inhibition and disease. J Abnorm Psychol 1986;95:274–81.
[65]. Peters ML, Smeets E, Feijge M, Van Breukelen G, Andersson G, Buhrman M, Linton SJ. Happy despite pain: a randomized controlled trial of an 8-week internet-delivered positive psychology intervention for enhancing well-being in patients with chronic pain. Clin J Pain 2017;33:962–75.
[66]. Promotion O of DP and H. Arthritis, osteoporosis, and chronic back conditions. Healthy People 2020. Available at: https://www.healthypeople.gov/2020/topics-objectives/topic/Arthritis-Osteoporosis-and-Chronic-Back-Conditions. Accessed January 11, 2020.
[67]. Purdie F, Morley S. Compassion and chronic pain. PAIN 2016;157:2625–7.
[68]. Qaseem A, Wilt TJ, McLean RM, Forciea MA. Noninvasive treatments for acute, subacute, and chronic low back pain: a clinical practice guideline from the American College of Physicians. Ann Intern Med 2017;166:514–30.
[69]. Rampey BD, Finnegan R, Goodman M, Mohadjer L, Krenzke T, Hogan J, Provasnik S. Skills of U.S. unemployed, young, and older adults in sharper focus: results from the program for the international assessment of adult competencies (PIAAC) 2012/2014. First Look. U.S. Department of Education, Washington, DC: National Center for Education Statistics, 2012.
[70]. Rizzo RRN, Medeiros FC, Pires LG, Pimenta RM, McAuley JH, Jensen MP, Costa LOP. Hypnosis enhances the effects of pain education in patients with chronic nonspecific low back pain: a randomized controlled trial. J Pain 2018;19:1103.e1–1103.e9.
[71]. Schwartz GE, Kline JP. Repression, emotional disclosure, and health: theoretical, empirical, and clinical considerations. In: Pennebaker JW, editor. Emotion, disclosure, & health. Washington, DC: American Psychological Association, 1995.
[72]. Seminowicz DA, Shpaner M, Keaser ML, Krauthamer GM, Mantegna J, Dumas JA, Newhouse PA, Filippi CG, Keefe FJ, Naylor MR. Cognitive-behavioral therapy increases prefrontal cortex gray matter in patients with chronic pain. J Pain 2013;14:1573–84.
[73]. Sharma S, Jensen MP, Moseley GL, Abbott JH. Results of a feasibility randomised clinical trial on Pain Education for low back pain in Nepal: the Pain Education in Nepal-low back pain (PEN-LBP) feasibility trial. BMJ Open 2019;9:e026874.
[74]. Shpaner M, Kelly C, Lieberman G, Perelman H, Davis M, Keefe FJ, Naylor MR. Unlearning chronic pain: a randomized controlled trial to investigate changes in intrinsic brain connectivity following cognitive behavioral therapy. Neuroimage Clin 2014;5:365–76.
[75]. Smeets RJEM, Vlaeyen JWS, Kester ADM, Knottnerus JA. Reduction of pain catastrophizing mediates the outcome of both physical and cognitive-behavioral treatment in chronic low back pain. J Pain 2006;7:261–71.
[76]. Street JT, Lenehan BJ, Dipaola CP, Boyd MD, Kwon BK, Paquette SJ, Dvorak MFS, Rampersaud YR, Fisher CG. Morbidity and mortality of major adult spinal surgery. A prospective cohort analysis of 942 consecutive patients. Spine J 2012;12:22–34.
[77]. Sullivan MJL, Bishop SR, Pivik J. The pain catastrophizing Scale: development and validation. Psychol Assess 1995;7:524–32.
[78]. Sullivan MJL, Scott W, Trost Z. Perceived injustice: a risk factor for problematic pain outcomes. Clin J Pain 2012;28:484–8.
[79]. Thorn BE. Cognitive therapy for chronic pain, second edition: a step-by-step guide. New York, NY: The Guilford Press, 2017.
[80]. Thorn BE. Cognitive therapy for chronic pain: a step-by-step guide. New York, NY: Guilford Press, 2004.
[81]. Thorn BE, Burns JW. Common and specific treatment mechanisms in psychosocial pain interventions: the need for a new research agenda. PAIN 2011;152:705–6.
[82]. Thorn BE, Day MA, Burns J, Kuhajda MC, Gaskins SW, Sweeney K, McConley R, Ward LC, Cabbil C. Randomized trial of group cognitive behavioral therapy compared with a pain education control for low-literacy rural people with chronic pain. PAIN 2011;152:2710–20.
[83]. Thorn BE, Eyer JC, Van Dyke BP, Torres CA, Burns JW, Kim M, Newman AK, Campbell LC, Anderson B, Block PR, Bobrow BJ, Brooks R, Burton TT, Cheavens JS, DeMonte CM, DeMonte WD, Edwards CS, Jeong M, Mulla MM, Penn T, Smith LJ, Tucker DH. Literacy-adapted cognitive behavioral therapy versus education for chronic pain at low-income clinics. Ann Intern Med 2018;168:471.
[84]. Thorn BE, Pence LB, Ward LC, Kilgo G, Clements KL, Cross TH, Davis AM, Tsui PW. A randomized clinical trial of targeted cognitive behavioral treatment to reduce catastrophizing in chronic headache sufferers. J Pain 2007;8:938–49.
[85]. Traeger AC, Lee H, Hübscher M, Skinner IW, Moseley GL, Nicholas MK, Henschke N, Refshauge KM, Blyth FM, Main CJ, Hush JM, Lo S, McAuley JH. Effect of intensive patient education vs placebo patient education on outcomes in patients with acute low back pain: a randomized clinical trial. JAMA Neurol 2019;76:161–9.
[86]. Treede RD. Gain control mechanisms in the nociceptive system. PAIN 2016;157:1199–204.
[87]. Turk DC, Audette J, Levy RM, Mackey SC, Stanos S. Assessment and treatment of psychosocial comorbidities in patients with neuropathic pain. Mayo Clin Proc 2010;85.
[88]. Turner JA, Mancl L, Aaron LA. Short- and long-term efficacy of brief cognitive-behavioral therapy for patients with chronic temporomandibular disorder pain: a randomized, controlled trial. PAIN 2006;121:181–94.
[89]. UQ Researchers: Dr. Melissa Day. Univ. Queensl. Available at: https://resarchers.uq.edu.au/researcher/11740. Accessed July 2, 2020.
[90]. Vlaeyen JW, Teeken-Gruben NJ, Goossens ME, Rutten-van Mölken MP, Pelt RA, van Eek H, Heuts PH. Cognitive-educational treatment of fibromyalgia: a randomized clinical trial. I. Clinical effects. J Rheumatol 1996;23:1237–45.
[91]. Vlaeyen JWS, De Jong J, Geilen M, Heuts PHTG, Van Breukelen G. The treatment of fear of movement/(re)injury in chronic low back pain: further evidence on the effectiveness of exposure in vivo. Clin J Pain 2002;18:251–61.
[92]. Vlaeyen JWS, Linton SJ. Fear-avoidance model of chronic musculoskeletal pain: 12 years on. PAIN 2012;153:1144–7.
[93]. Vowles KE, McCracken LM, Eccleston C. Processes of change in treatment for chronic pain: the contributions of pain, acceptance, and catastrophizing. Eur J Pain 2007;11:779–87.
[94]. Van Wambeke P, Desomer A, Ailiet L, Berquin A, Dumoulin C, Depreitere B, Dewachter J, Dolphens M, Forget P, Fraselle V, Hans G, Hoste D, Mahieu G, Michielsen J, Nielens H, Orban T, Parlevliet T, Simons E, Tobbackx Y, Van Zundert J, Vanderstraeten J, Vanschaeybroek P, Vlaeyen J, Jonckheer P. Low back pain and radicular pain: assessment and management. Brussels: KCE Report, 2017.
[95]. Watson JA, Ryan CG, Cooper L, Ellington D, Whittle R, Lavender M, Dixon J, Atkinson G, Cooper K, Martin DJ. Pain neuroscience education for adults with chronic musculoskeletal pain: a mixed-methods systematic review and meta-analysis. J Pain 2019;20:1140.e1–1140.e22.
[96]. Werner EL, Storheim K, Lochting I, Wisloff T, Grotle M. Cognitive patient education for low back pain in primary care: a cluster randomized controlled trial and cost-effectiveness analysis. Spine (Phila Pa 1976) 2016;41:455–62.
[97]. Williams ACdC, Eccleston C, Morley S. Psychological therapies for the management of chronic pain (excluding headache) in adults. Cochrane Database Syst Rev 2012;11:CD007407.
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