It is increasingly accepted among medical and mental health care providers that cognitions and emotions play a significant role in the perception of chronic pain and resulting disability. Though this seems an obvious point, it is a major leap considering that, as recently as 40 years ago, the primary thought was that all pain perception is directly related to the severity of injury (i.e., the worse it looks the worse it must be), as pain was believed to exist only in the presence of identifiable, causal, pathophysiology. This archaic, dualistic Cartesian style of thinking has since evolved considerably (Turk, 1996). In the 1950s, both (Bonica, 1953) and Engel (1959) described psychological factors as important contributors to the pain experience. Melzack, a leader in the exploration of the etiology behind the perception and experience of pain, made an important early contribution to its understanding. In 1965, Melzack and Wall (1965) proposed the gate control theory of pain, which solidified the involvement of the central nervous system (CNS) as an essential component in the perception and processing of pain. The gate control theory of pain served to provide a scientific understanding of how brain-generated experiences, such as emotion, affected pain perception. This theory effectively narrowed the gap between the mental and physical health fields by tying together nociception and emotional experience. Following this, a proliferation of research arose aimed at identification of specific psychological and social factors believed to play a key role in the development, maintenance and perception of pain. Specifically, Gatchel and Epker (1999) and Turk (1996) discussed at length the various contributions of behavioral, affective, and cognitive factors, as well as psychosocial risk factors for pain. In sum, their research has served to further refute the previous dualistic view of pain-that pain patients were either legitimate medical patients with "real" physical etiology or that they were psychiatric patients whose pain experience was "all in their head." Despite the incorrect assumption that chronic pain is an inherently psychological problem, chronic pain patients do have a higher prevalence of psychiatric disorders, such as depression and personality disorders, relative to the general population (Gatchel, Polatin, Mayer, & Garcy, 1994; Kinney, Gatchel, Polatin, Fogarty, & Mayer, 1993; Polatin, Kinney, Gatchel, Lillo, & Mayer, 1993). Specifically, Kinney et al. (1993) found that, among 200 chronic low back pain patients who were assessed with the Structured Clinical Interview for the Diagnostic and Statistical Manual of Mental Disorders-III-Revised, 70% met lifetime diagnostic criteria for Axis I disorders and 51% met criteria for Axis II diagnoses. In addition to significant psychiatric distress, patients with chronic pain often have a number of additional risk factors for increased difficulty in obtaining maximal treatment gains. Specific factors identified in the literature include: a patient's reliance on passive coping strategies (e.g., catastrophizing, hoping and praying, M. J. L. Sullivan et al., 2001) versus active ones (trying to distract oneself by getting together with friends or working on a hobby, etc., Truchon & Fillion, 2000); the presence of psychological distress, which is a barrier for positive patient outcomes through reduced treatment compliance (Proctor, Gatchel, & Robinson, 2000; Riley et al., 1999); vulnerability to stress-related increases in pain (e.g., as measured by elevations of certain Minnesota Multiphasic Personality Inventory (MMPI) profiles such as the "conversion V", Proctor et al., 2000); and depression (Proctor et al., 2000). Gatchel (1996) has further described the complex interplay of pain, psychopathology, and personality in the form of a three-stage model of the progression from acute to subacute to chronic pain and disability. His model describes the emotional deconditioning that occurs over the progression of injury and illness. Specifically, in Stage 1, patients react to the pain stimulus with emotionality such as fear and anxiety. In Stage 2, pain extends past the normal expected duration of healing and patients begin to demonstrate psychosocial distress. This display of distress will likely depend on patients' premorbid personality characteristics and current stressors. In Stage 3, assumption of the "sick role" occurs when patients solely focus on the pain and resulting limitations. At this stage, they are unable to effectively cope and problem-solve appropriate pain management solutions without therapeutic assistance. The above theories and models fit nicely with the currently well-accepted biopsychosocial model of pain, which has been relied upon heavily in the field of rehabilitation since the 1980's. Schultz (2000) traces the etiology of the biopsychosocial model 50 years ago to a meeting of the World Health Organization (WHO) in which health was defined as a multifaceted combination of biological/physical, emotional/psychological, and social well-being, as opposed to a mere absence of biological organic pathology. Thus, the WHO functionally recognized that health and, conversely, disability are defined by a complex interaction among a variety of factors. Further, Belar and Deardorff (1999) recount evidence dating back to the 1700s of individuals recognizing an interaction between the body and mind. The growing amount of evidence supporting a mind-body interaction eventually led to a model of pain and disability which, instead of exclusively focusing on either psychosocial or physical etiologies, conceptualizes pain and disability as a consequence of the interaction among biological, psychological and social phenomena. This model is a multifaceted model that considers biological, psychological, and social aspects (Crichton & Morley, 2002; Gatchel, 1996; Wright & Gatchel, 2002). Not only do these multiple factors contribute to the etiology of disability, they have a reciprocal effect of intensifying and perpetuating each other and, consequently, impacting the duration and intensity of pain and disability symptomatology (Crichton & Morley, 2002). Within the biopsychosocial model, the patient is treated as a "whole" person, not just a body part or painful condition. Consequently, the treatment goals are aimed not exclusively at relieving the pain, but rather more importantly on improving the individual's quality of life and restoring his or her full functioning in physical, occupational, emotional, and social domains. Also, Kwan, Ferrari, and Friel (2001) stress that the biopsychosocial model of disability addresses all aspects of disability, including consideration of possible patient motivators such as secondary and tertiary gains. To date, the biopsychosocial model remains one of the most comprehensive ways of conceptualizing and treating chronic pain (Mayer, Gatchel, & Evans, 2002). Though the biopsychosocial model is widely accepted and serves as the basis for the majority of interdisciplinary chronic pain treatment programs, scientific research of the mind-body relationship is ever evolving. Most recently, Melzack (1999) has built upon his previous gate control theory of pain and developed the neuromatrix model of pain. This model grew out of Melzack's work with patients who continued to experience pain following spinal cord resection (i.e., as in phantom limb pain). His new model proposes a complex interaction of neural inputs from within and outside of the brain. This latest model, the neuromatrix model, accounts for genetic contributions to the perception of pain, as well as the individual's recent past and present experience, and sensory inputs. To address the multifactorial contributors to pain, including physical, psychological, and social phenomena, the most widely accepted and utilized method is the cognitive-behavioral therapeutic approach. Within the cognitive-behavioral model, patients are educated about the mind-body connection and then instructed in techniques to manage pain and related stress and disability for the purpose of increasing function despite pain. The key components of this approach are described below.
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