Pain medicine training: Module 9

Abstract
Fibromyalgia is characterized by widespread pain and tenderness, and has a significant familial component. The etiology of fibromyalgia remains unclear, but genetic factors seem to have a significant role, and are influenced by environmental factors. Research over the past two decades has demonstrated that genetic polymorphisms in the serotoninergic, dopaminergic and catecholaminergic systems of pain transmission and processing are involved in the etiology of fibromyalgia, but additional candidates continue to emerge. Fibromyalgia is thought to belong to the group of affective spectrum disorders, which include related psychiatric and medical disorders. As the concept of affective spectrum disorders continues to evolve, progress in the understanding of the genetic basis of related functional disorders, such as irritable bowel syndrome and post-traumatic-stress disorder, is aiding our understanding of the genetic basis of fibromyalgia.

Abstract
Objective: To address how health professionals may inadvertently contribute to the stigmatization of patients with chronic pain.

Setting: Formulation and implementation of the Australian National Pain Strategy.

Design: Review of current concepts of stereotyping and stigma, consideration of their relationship to empathy, and how they might impinge upon the clinical encounter.

Findings: The extinction of empathy, which we refer to as "negative empathy," can overwhelm health professionals, allowing the entry of negative community stereotypes of chronic pain sufferers and add to their stigmatization. Prevailing dualistic frames of reference encourage this process.

Conclusion: Greater awareness by health professionals of their own potential, often inadvertent, contribution to the stigmatization of their patients with chronic pain may serve as a basis for an expanded model of clinical engagement.

Abstract
Objective: The discovery of neuroplastic phenomena such as central sensitization of nociception has challenged pain theory to evolve, to encompass unpredictable and unlikely chronic pain states, and to cope with the emerging complexity of the brain. Recently, the proposition that chronic pain is a disease in its own right has gained currency, based upon functional and structural changes in the brain constituting a distinctive pathology. Proponents have expanded the theory to identify "eudynia" ("good" pain) and "maldynia" ("bad" pain).

Methods: A critical examination of the proposition that chronic pain is a disease was conducted within the framework of evolution of pain medicine theory.

Results: Three dominant theories were identified: specificity theory (the "hard-wired" nervous system); neuroplasticity theory (the "soft-wired" nervous system); and pain-as-a-disease. The progression from specificity theory to neuroplasticity theory was based upon empirical evidence and conceptual clarity. The latter theory confronts the uncertainty and the unpredictability of pain, and offers explanations for conditions where ongoing noxious input is not discernible. However, not only does pain-as-a-disease elevate the neurophysiological mechanisms underlying the experience of chronic pain to the status of a disease, but also it conceives of pain as a "thing" that is itself capable of producing an effect. This reasoning is found to be faulty on two grounds: the confusion of pain as a symptom, a cause, and a pathology; and the fallacy that can arise when an interpretation is claimed to be a truth.

Conclusions: The proposition that chronic pain is a disease cannot be supported on clinical and pathological grounds, as well as in terms of ways of knowing. The promulgation of "good" and "bad" pain has the potential to obstruct necessary dialogue for advancing the science and treatment of pain. We suggest a way forward to resolve this impasse.

Abstract
Unlike acute pain that warns us of injury or disease, chronic or persistent pain serves no adaptive purpose. Though there is no agreed on definition of chronic pain, it is commonly referred to as pain that is without biological value, lasting longer than the typical healing time, not responsive to treatments based on specific remedies, and of a duration greater than 6 months. Chronic pain that is severe and intractable has detrimental consequences, including psychological distress, job loss, social isolation, and, not surprisingly, it is highly comorbid with depression and anxiety. Historically, pain without an apparent anatomical or neurophysiological origin was labelled as psychopathological. This approach is damaging to the patient and provider alike. It pollutes the therapeutic relationship by introducing an element of mutual distrust as well as implicit, if not explicit, blame. It is demoralizing to the patient who feels at fault, disbelieved, and alone. Moreover, many medically unexplained pains are now understood to involve an interplay between peripheral and central neurophysiological mechanisms that have gone awry. The new Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, somatic symptom disorder overpsychologizes people with chronic pain; it has low sensitivity and specificity, and it contributes to misdiagnosis, as well as unnecessary stigma. Adjustment disorder remains the most appropriate, accurate, and acceptable diagnosis for people who are overly concerned about their pain.

Abstract
Objective: The study aimed to seek a unifying biological basis for the phenomena encompassed in fibromyalgia syndrome (chronic widespread pain and associated morbidities).

Setting: While much progress has been made in the last decade in understanding chronic widespread pain, its pathogenesis remains stubbornly obscure and its treatment difficult. Two themes are gaining currency in the field: that chronic widespread pain is the result of central sensitization of nociception, and that chronic pain is somehow related to activation of a global stress response.

Design: In this article we merge these two ideas within the perspective of evolutionary biology to generate a hypothesis about the critical molecular pathway involved in chronic stress response activation, namely substance P and its preferred receptor, neurokinin-1 (NK-1R), which has many empirically testable implications.

Conclusion: Drawing on diverse findings in neurobiology, immunology, physiology, and comparative biology, we suggest that the form of central sensitization that leads to the profound phenomenological features of chronic widespread pain is part of a whole-organism stress response, which is evolutionarily conserved, following a general pattern found in the simplest living systems.

Abstract
Objective: To identify whether the biopsychosocial framework of illness has overcome the limitations of the biomedical model of disease when applied in the practice of pain medicine.

Design: Critical review of the literature concerning the application of biopsychosocial models to the praxis of pain medicine and the concepts of living systems.

Results: The biopsychosocial model of illness, formulated by Engel in 1977, has generated the International Association for the Study of Pain (IASP) definition of pain, two major conceptual frameworks in pain medicine, and three putative explanatory models for pain. However, in the absence of a theory that seeks to understand the lived experience of pain as an emergent and unpredictable phenomenon, these progeny of the biopsychosocial model have been caught in circular argument and have been unable to overcome biomedical reductionism or the perpetuation of body-mind dualism. In particular, the implication that pain can be a "thing" separate and distinct from the body bears little relationship to the lived experience of pain. Such marginalizing results when an observer attempts to reduce the experience of the pain of another person.

Conclusions: The self-referentiality of living systems (through their qualities of autopoiesis, noncentrality and negentropy) sees pain "emerge" in unpredictable ways that defy any lineal reduction of the lived experience to any particular "thing." Pain therefore constitutes an aporia, a space and presence that defies us access to its secrets. We suggest a project in which pain may be apprehended in the clinical encounter, through the engagement of two autonomous self-referential beings in the intersubjective or so-called third space, from which new therapeutic possibilities can arise.

Abstract
We review the concept and importance of functional somatic symptoms and syndromes such as irritable bowel syndrome and chronic fatigue syndrome. On the basis of a literature review, we conclude that a substantial overlap exists between the individual syndromes and that the similarities between them outweigh the differences. Similarities are apparent in case definition, reported symptoms, and in non-symptom association such as patients' sex, outlook, and response to treatment. We conclude that the existing definitions of these syndromes in terms of specific symptoms is of limited value; instead we believe a dimensional classification is likely to be more productive.

Abstract
Central sensitivity syndromes (CSS) include fibromyalgia syndrome (FMS), irritable bowel syndrome, temporomandibular disorder, restless legs syndrome, chronic fatigue syndrome, and other similar chronic painful conditions that are based on central sensitization (CS). CSS are mutually associated. In this paper, prevalence of FMS among other members of CSS has been described. An important recent recognition is an increased prevalence of FMS in other chronic pain conditions with structural pathology, for example, rheumatoid arthritis, systemic lupus, ankylosing spondylitis, osteoarthritis, diabetes mellitus, and inflammatory bowel disease. Diagnosis and proper management of FMS among these diseases are of crucial importance so that unwarranted use of such medications as corticosteroids can be avoided, since FMS often occurs when RA or SLE is relatively mild.