Mindfulness-Based Cognitive Therapy for Chronic Pain

A Clinical Manual and Guide

Melissa A. Day

• Publisher: Wiley-Blackwell
• Year: 2017
• Print ISBN: 9781119257905, 9781119257615
• eBook ISBN: 9781119257646
• Edition: 1
• Topic: Medicine
• Subtopic: Anesthesiology & Pain Management

This unique new guide integrates recent advances in the biopsychosocial understanding of chronic pain with state-of-the-art cognitive therapy and mindfulness techniques to offer a fresh, highly-effective MBCT approach to helping individuals manage chronic pain.

• There is intense interest from clinicians, researchers and patients alike in mindfulness-based therapeutic techniques, and the integration of mindfulness theory and practice with CBT
• Provides everything a therapist needs to integrate MBCT into their practice and optimize its delivery, including a manualized 8-session program and guidance on how to teach MBCT skills
• Features case studies and real-world examples that help practitioners to avoid common pitfalls and optimize the delivery of MBCT for chronic pain for their own individual clients
• Features links to guided meditations, client and therapist handouts and other powerful tools

Part I
Chronic Pain

1
Defining Chronic Pain and its Territory

At some point in our lives nearly all of us have experienced pain. What I call “bare bones pain” is adaptive and is as essential to our everyday existence as being able to see, hear, touch, taste, and smell. Pain is our most profound teacher, claiming our attention, implanting itself in memory, readily recalled at a hint of danger. Rare individuals born with a congenital insensitivity to pain experience an abnormal amount of injuries and infections due to their inability to perceive and respond appropriately to painful stimuli and usually die young (Melzack & Wall, 1982). Most of the time when we experience pain, it naturally diminishes as the source (i.e., the injury in whatever form) heals. However, in some instances, pain persists beyond the normal or expected healing time, may arise with or without an identifiable “cause,” is unamenable to traditional biomedical treatment options, and it becomes chronic. Along with the territory of chronic pain often comes depressed mood, stress, loss of gainful employment, relationship strain, and a host of other compounding circumstances—the pain is no longer “bare bones.”

The International Association for the Study of Pain (IASP), the world’s largest interdisciplinary forum devoted to science, clinical practice, and education in the field of pain defines pain as: “An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage” (IASP Taxonomy, 1994, Part III, p. 3). Inclusion of the terms “unpleasant” and “emotional” in this definition clearly delineates psychology as integral in the experience of both acute and chronic pain. While there are a variety of taxonomies used to distinguish acute vs. chronic pain, the most common is a temporal profile. Depending on the type of pain and the various definitions, “chronic” is rather arbitrarily demarcated typically as pain experienced at least half of the days of the past 3 or 6 months (IASP Subcommittee on Taxonomy, 1986; NIH, 2011). For pain arising primarily from a specific injury, this 3‐ or 6‐month time frame refers to the time that extends past the “normal” expected healing process from the initial injury (IASP Taxonomy, 1994); however, it often proves exceedingly difficult to determine the end of the healing process (Apkarian, Baliki, & Geha, 2009). Therefore, many have argued that such a taxonomy for classifying chronic pain is inadequate (Apkarian, Hashmi, & Baliki, 2011), and instead, some researchers have focused efforts on identifying brain maps and biomarkers for differentiating acute from chronic pain. However, one aspect from the various definitions that is now widely agreed upon is that chronic pain is inherently biopsychosocial in nature as opposed to simply a biomedical phenomenon that can be explained purely in terms of the amount of tissue damage (which was the popular view held right up until the 20th century). In using the MBCT approach to treat pain, it is first helpful to hold a working understanding of such historical perspectives, as well as to be familiar with (and to be able to explain to patients) the current knowledge base of each aspect that makes up the experience of pain: the biological, psychological or human experience, and social factors. Keeping in mind, though, that although these shared features of the experience of pain are common, in reality our experience of pain is deeply personal.

A Historical Perspective of Pain

The Biopsychosocial Model: Pain ≠ Just Broken Bones and Tissue Damage

Traditionally pain has been understood from a biomedical perspective that has equated the amount of pain experienced to the amount of underlying tissue damage in a 1:1 relationship. The biomedical model originated from the 17th century with Descartes’ mind–body dualism philosophy, and dominated illness and pain conceptualization for almost 300 years, right up until approximately mid‐way through the last century. Pain was described purely in reductionistic, mechanistic, physical terms and the brain was considered to play a passive, receptive role of pain signals; psychosocial factors were considered essentially irrelevant. However, Beecher, who served as a physician in the US Army during the Second World War, provided one of the most famous early documented examples of evidence refuting the biomedical perspective (Beecher, 1946). Of the civilians and soldiers that Beecher treated who had experienced compound fractures, penetrating wounds to the abdomen, lost limbs or other intensely painful injuries, Beecher noticed that the majority of the soldiers (as many as 75%) reported no to moderate pain, and required far less pain medication than the civilians with comparable injuries. Beecher documented that the differentiating factor seemed to be the meaning that the civilians and soldiers were attributing to the injury. To the soldiers, this was their ticket home—they were evacuated and returned to the US for recuperation; to the civilians on the other hand, they were to leave the hospital to return to their war‐torn homeland, and to likely a loss of wages due to an inability to return to work.

Other research began to accumulate supporting Beecher’s observations. As one eloquent research example, Jensen and colleagues (Jensen et al., 1994) conducted a magnetic resonance imaging (MRI) study examining the lumbar spines of asymptomatic individuals (i.e., people with no pain, or history of pain) and found that only 36% had normal intervertebral discs at all levels, while the firm majority (64%) had bulges of at least one (and typically more) lumbar disc. In another study, Keefe and colleagues demonstrated that coping strategies were more predictive of self‐reported osteoarthritic knee pain than X‐ray evidence of the disease (Keefe et al., 1987). Other everyday examples of where the level of injury doesn’t necessarily map on to the amount of pain experienced include when we see athletes playing through a game with a severe injury, maybe we hear on the news about a parent running through fire to rescue their child from a burning house, and yogis during deep meditation will not feel pain.

These observations and empirical findings, and a plethora of findings from other studies, called in to question the very foundation that the biomedical model was built upon, and clearly showed that “verifiable” tissue damage is a poor indicator of pain, and that the brain plays a dynamic, central role in pain processing and perception. Thus, mounting dissatisfaction with the biomedical models’ account for illness and pain culminated in a tipping point when Engel (1977) formally challenged this prevailing conceptualization and proposed the integrated biopsychosocial model. The biopsychosocial model redefined illness (including but not specific to pain) as an entity not entirely subsumed under the biological sphere. Instead, manifest illness development, maintenance, and progression were viewed as the result of the convergence of a multitude of internal and external, biological, psychological, emotional, social, and behavioral influences. The shifted emphasis in Engel’s approach—away from the purely physical realm—aligned perfectly with Melzack and Wall’s (1965) “Gate Control Theory,” and together these two models fueled a zeitgeist in the way pain was assessed and treated.

The Neuromatrix Model of Pain

The Gate Control Theory—now known as the Neuromatrix Model of Pain—is often delivered as an educational component of psychological pain treatments (including MBCT, as you shall see) to convey the rationale to clients as to why psychological treatments work for real pain, so it is worth spending some time here to go over it in detail. In essence, this revolutionary theory proposed by Melzack and Wall was the first to formally hypothesize that the brain plays an active, dynamic role in the interpretive processes of the sensory experience of pain (Melzack, 2001, 2005; Melzack & Wall, 1965, 1982). This theory is in stark contrast to the biomedical conceptualization, where the brain was considered a passive recipient of pain signals from a peripheral pain generator (i.e., the identified “source” of injury/pain). The Gate Control Theory represented, for the first time, a conceptualization of pain that took into account the unique and highly interconnected role of neurophysiological pathways, thoughts, emotions, and behavior in determining the experience we call “pain.” The original theory described how descending (inhibitory or excitatory) signals from the brain were the stimulus that opened or closed a gating mechanism in the spinal column, and that this mechanism ultimately controlled the amount of pain signals that could reach the brain. Specifically, the theory proposed that if the “gates” are narrowed or closed (i.e., if descending inhibitory signals from the brain predominate), fewer pain signals are processed in the brain and less pain is experienced; however, if the gates are wide open (i.e., if descending excitatory signals from the brain predominate) more pain signals are processed in the brain and the felt experience of pain is amplified.

The Gate Control Theory and the subsequent Neuromatrix Model paved the way for an ensuing body of neuroimaging research. Through the use of technology such as functional MRI, studies have conclusively demonstrated that critical pain pathways travel through brain areas closely interconnected with cognitive and emotional activity (e.g., the thalamus, anterior cingulated cortex, and limbic system), and Melzack and Wall were the first to emphasize that this neuromatrix had the capacity to inhibit or enhance the sensory flow of painful stimuli. This important research on pain in the brain has demonstrated that psychological processes can actually shape the way painful stimuli are interpreted by the brain and thereby provides convincing evidence that psychological interventions for the treatment of chronic pain hold tremendous potential.

Models of Stress

As I touched on in the Introduction, living with daily pain as a persistent companion is typically stressful, and stress in turn makes pain worse. Thus, an integral component in many pain treatments is learning to manage stress more effectively. Stress has become a popular term that is a catchphrase for a multiplicity of situations, pressures, and experiences—what one person experiences as stress though, another person might see as the environment in which to thrive. The term “stress” historically has origins in the field of physics, where it describes the force that produces a strain to bend or break an object; however, the way we typically use the word “stress” today was first coined by Seyle in the 1950s (Selye, 1956). Seyle was ...

Table of contents

• Cover
• Title Page
• Table of Contents
• Foreword
• Acknowledgments
• About the Companion Website
• Introduction
• Part I: Chronic Pain
• Part II: MBCT for Chronic Pain
• Conclusion
• Index
• End User License Agreement