The ACR preliminary diagnostic criteria for fibromyalgia and measurement of symptom severity.
(Arthritis Care Res. 2010;62:600–610.)
Abstract
Objective: To develop simple, practical criteria for clinical diagnosis of fibromyalgia that are suitable for use in primary and specialty care and that do not require a tender point examination, and to provide a severity scale for characteristic fibromyalgia symptoms.
Methods: We performed a multicenter study of 829 previously diagnosed fibromyalgia patients and controls using physician physical and interview examinations, including a widespread pain index (WPI), a measure of the number of painful body regions. Random forest and recursive partitioning analyses were used to guide the development of a case definition of fibromyalgia, to develop criteria, and to construct a symptom severity (SS) scale.
Results: Approximately 25% of fibromyalgia patients did not satisfy the American College of Rheumatology (ACR) 1990 classification criteria at the time of the study. The most important diagnostic variables were WPI and categorical scales for cognitive symptoms, unrefreshed sleep, fatigue, and number of somatic symptoms. The categorical scales were summed to create an SS scale. We combined the SS scale and the WPI to recommend a new case definition of fibromyalgia: (WPI ≥7 AND SS ≥5) OR (WPI 3–6 AND SS ≥9).
Conclusion: This simple clinical case definition of fibromyalgia correctly classifies 88.1% of cases classified by the ACR classification criteria, and does not require a physical or tender point examination. The SS scale enables assessment of fibromyalgia symptom severity in persons with current or previous fibromyalgia, and in those to whom the criteria have not been applied. It will be especially useful in the longitudinal evaluation of patients with marked symptom variability.
Functional magnetic resonance imaging evidence of augmented pain processing in fibromyalgia.
(Arthritis Rheum. 2002;46:1333–1343.)
Abstract
Objective: To use functional magnetic resonance imaging (fMRI) to evaluate the pattern of cerebral activation during the application of painful pressure and determine whether this pattern is augmented in patients with fibromyalgia (FM) compared with controls.
Methods: Pressure was applied to the left thumbnail beds of 16 right-handed patients with FM and 16 right-handed matched controls. Each FM patient underwent fMRI while moderately painful pressure was being applied. The functional activation patterns in FM patients were compared with those in controls, who were tested under two conditions: the “stimulus pressure control” condition, during which they received an amount of pressure similar to that delivered to patients, and the “subjective pain control” condition, during which the intensity of stimulation was increased to deliver a subjective level of pain similar to that experienced by patients.
Results: Stimulation with adequate pressure to cause similar pain in both groups resulted in 19 regions of increased regional cerebral blood flow in healthy controls and 12 significant regions in patients. Increased fMRI signal occurred in 7 regions common to both groups, and decreased signal was observed in 1 common region. In contrast, stimulation of controls with the same amount of pressure that caused pain in patients resulted in only 2 regions of increased signal, neither of which coincided with a region of activation in patients. Statistical comparison of the patient and control groups receiving similar stimulus pressures revealed 13 regions of greater activation in the patient group. In contrast, similar stimulus pressures produced only 1 region of greater activation in the control group.
Conclusion: The fact that comparable subjectively painful conditions resulted in activation patterns that were similar in patients and controls, whereas similar pressures resulted in no common regions of activation and greater effects in patients, supports the hypothesis that FM is characterized by cortical or subcortical augmentation of pain processing.
Association of concomitant fibromyalgia with worse disease activity score in 28 joints, health assessment questionnaire, and short form 36 scores in patients with rheumatoid arthritis.
(Arthritis Care Res. 2009;61:794–800.)
Abstract
Objective: To study the association of the presence of fibromyalgia (FM) with the Disease Activity Score in 28 joints (DAS28), the Health Assessment Questionnaire (HAQ), and the Medical Outcomes Study Short Form 36 (SF-36) health survey in patients with rheumatoid arthritis (RA).
Methods: A total of 270 outpatients with RA were enrolled in a prospective cross-sectional study. The patients underwent clinical evaluation and application of the HAQ and SF-36 questionnaires. Disease activity was evaluated using the DAS28 score. FM and RA diagnoses were made according to ACR criteria.
Results: The overall prevalence of FM was 13.4%. This group of patients had a higher prevalence of female sex, older mean age, higher functional class, and longer morning stiffness than patients with only RA. Mean ± SD DAS28 scores were significantly higher in patients with RA and FM (5.36 ± 0.99) than in patients with RA only (4.03 ± 1.39; p <0.001). In a multivariable linear regression analysis, FM was an important predictor of the DAS28 score, even after adjusting for the erythrocyte sedimentation rate, number of swollen joints, functional class, number of disease-modifying antirheumatic drugs currently in use, current dose of steroids, and articular erosions. HAQ and SF-36 scores were also worse in patients with RA and associated FM.
Conclusion: FM is related to worse scores on the DAS28, HAQ, and SF-36 in patients with RA. The presence of FM may have major implications in the interpretation of the DAS28 score because it is related to higher scores independently of objective evidence of RA activity.
Report of the ACR Pain Management Task Force.
(Arthritis Care Res. 2009;62: 590–599.)
Introduction
Pain is the most common symptom of patients with rheumatic disorders and can occur in both inflammatory and noninflammatory conditions. As a complex phenomenon with a strong subjective component, pain can be influenced by the nature of the underlying disease, personal predisposition (biologic and psychological), as well as environmental and psychosocial factors that impact the pain experience. In the management of patients with musculoskeletal disease, therefore, the characterization of pain (e.g., its onset, duration periodicity, and impact on functioning) is important in establishing the diagnosis and developing a comprehensive treatment plan to reduce pain and to improve quality of life.
Although rheumatologists diagnose and treat pain, they do not characterize themselves as “pain physicians.” Rather, in their professional identity, many rheumatologists consider themselves more narrowly as subspecialists who treat musculoskeletal disorders that have a component of acute and chronic nonmalignant pain. Furthermore, rheumatologists have traditionally approached pain from the perspective of the proximal causes of pain such as tissue injury and inflammation, and have concentrated therapy on reducing inflammation either locally or systemically. The therapies used have been predominantly pharmacologic and include nonsteroidal antiinflammatory drugs (NSAIDs), disease-modifying agents including biologics, and corticosteroids. Although commonly recommended, nonpharmacologic psychosocial interventions such as cognitive-behavioral therapy or body-based therapies including exercise are generally considered less effective by rheumatologists despite evidence that such approaches can be highly efficacious depending on the setting or disease.
For most conditions treated by rheumatologists, the etiology of pain has been conceptualized primarily in the context of events in peripheral tissue. As a result, rheumatologists have relied heavily on pharmacologic therapies directed at the immune system to control symptoms, especially in inflammatory disease. Correspondingly, for patients with major or irreversible tissue damage, whether arising in inflammatory or noninflammatory disease, surgery has been the mainstay of treatment, with pharmacologic therapy used as a transition until a definitive operation is performed. Given this approach, events in the central nervous systems contributing to the experience of pain have received less attention in treatment, with additional analgesic, psychosocial, or interventional therapies receiving neither extensive investigation nor widespread or appropriate use. This approach may limit the utilization of newer and multidisciplinary approaches to pain management in the care of patients with rheumatic disease as well as the conduct of cutting-edge pain research by rheumatologists.
To increase the understanding of a rheumatologist’s role in pain management and the place of pain in the rheumatology research agenda, the Executive Committee of the American College of Rheumatology (ACR) established a task force whose goal was to consider these issues both at present and in the future as the field develops. This task force conducted literature reviews and practitioner surveys, and held face-to-face and telephone meetings to gauge the impact of a greater focus on pain management on practice, training, and education. At the heart of this task force’s inquiry are the following types of questions: Are rheumatology health care providers optimally treating their patients’ pain? How can rheumatologists and allied health professionals become better informed regarding the new research and clinical opportunities for pain management? What is the approach to patients with inflammatory disease who have responded to disease-modifying antirheumatic drugs (DMARDs) and/or a biologic agent but nevertheless have ongoing pain? What is the role of psychosocial and other nonpharmacologic interventions in the management of musculoskeletal pain?
The relevance of these issues is highlighted by a recent study of European rheumatoid arthritis (RA) patients indicating that two-thirds reported inadequate pain control. Indeed, despite advances in the management of rheumatic diseases, many patients believe that their physicians focus on the treatment of the underlying musculoskeletal disease and are not concerned with relieving pain itself. Although some patients may have this impression, the ACR, in its position statement on pain management in rheumatic diseases, nevertheless affirms that effective pain and symptom management is an ethical obligation of all health care providers and organizations.
The intent of the initiative is not to remake rheumatologists as pain specialists in general, but rather to increase their skill and expertise in the management of pain as it relates to a specific group of painful disorders. The goal of this report is to summarize the salient issues in treatment, research, and training considered by the task force to establish the foundation for ACR initiatives to enhance the effectiveness of rheumatologists and rheumatology health professionals in the diagnosis and management of pain associated with rheumatic diseases to improve patient outcomes.
Catastrophizing and pain in arthritis, fibromyalgia, and other rheumatic diseases.
(Arthritis Rheum. 2006;55:325–332.)
Abstract
Objective: Pain is among the most frequently reported, bothersome, and disabling symptoms described by patients with osteoarthritis, rheumatoid arthritis, fibromyalgia, and other musculoskeletal conditions. This review describes a growing body of literature relating catastrophizing, a set of cognitive and emotional processes encompassing magnification of pain-related stimuli, feelings of helplessness, and a generally pessimistic orientation, to the experience of pain and pain-related sequelae across several rheumatic diseases.
Methods: We reviewed published articles in which pain-related catastrophizing was assessed in the context of one or more rheumatic conditions. Because much of the available information on catastrophizing is derived from the more general chronic pain literature, seminal studies in other disease states were also considered.
Results: Catastrophizing is positively related, in both cross-sectional and prospective studies across different musculoskeletal conditions, to the reported severity of pain, affective distress, muscle and joint tenderness, pain-related disability, poor outcomes of pain treatment, and, potentially, to inflammatory disease activity. Moreover, these associations generally persist after controlling for symptoms of depression. There appear to be multiple mechanisms by which catastrophizing exerts its harmful effects, from maladaptive influences on the social environment to direct amplification of the central nervous system’s processing of pain.
Conclusion: Catastrophizing is a critically important variable in understanding the experience of pain in rheumatologic disorders as well as other chronic pain conditions. Pain-related catastrophizing may be an important target for both psychosocial and pharmacologic treatment of pain.
Evidence of augmented central pain processing in idiopathic chronic low back pain.
(Arthritis Rheum. 2004;50:613–623.)
Abstract
Objective: For many individuals with chronic low back pain (CLBP), there is no identifiable cause. In other idiopathic chronic pain conditions, sensory testing and functional magnetic resonance imaging (fMRI) have identified the occurrence of generalized increased pain sensitivity, hyperalgesia, and altered brain processing, suggesting central augmentation of pain processing in such conditions. We compared the results of both of these methods as applied to patients with idiopathic CLBP (n=11), patients with widespread pain (fibromyalgia; n=16), and healthy control subjects (n=11).
Methods: Patients with CLBP had low back pain persisting for at least 12 months that was unexplained by MRI/radiographic changes. Experimental pain testing was performed at a neutral site (thumbnail) to assess the pressure-pain threshold in all subjects. For fMRI studies, stimuli of equal pressure (2 kg) and of equal subjective pain intensity (slightly intense pain) were applied to this same site.
Results: Despite low numbers of tender points in the CLBP group, experimental pain testing revealed hyperalgesia in this group as well as in the fibromyalgia group; the pressure required to produce slightly intense pain was significantly higher in the controls (5.6 kg) than in the patients with CLBP (3.9 kg) (P=0.03) or the patients with fibromyalgia (3.5 kg) (P=0.006). When equal amounts of pressure were applied to the three groups, fMRI detected five common regions of neuronal activation in pain-related cortical areas in the CLBP and fibromyalgia groups (in the contralateral primary and secondary [S2] somatosensory cortices, inferior parietal lobule, cerebellum, and ipsilateral S2). This same stimulus resulted in only a single activation in controls (in the contralateral S2 somatosensory cortex). When subjects in the three groups received stimuli that evoked subjectively equal pain, fMRI revealed common neuronal activations in all three groups.
Conclusion: At equal levels of pressure, patients with CLBP or fibromyalgia experienced significantly more pain and showed more extensive, common patterns of neuronal activation in pain-related cortical areas. When stimuli that elicited equally painful responses were applied (requiring significantly lower pressure in both patient groups as compared with the control group), neuronal activations were similar among the three groups. These findings are consistent with the occurrence of augmented central pain processing in patients with idiopathic CLBP.
Chronic low back pain (CLBP) is one of the most common and expensive musculoskeletal disorders in developed countries. Back pain in general affects 70–85% of all people at some time in their lives, but 90% of affected individuals recover, typically within 12 weeks. Recovery after 12 weeks is slow and uncertain, and this subset of patients with CLBP accounts for major expenses in the health care and disability systems.
Despite the magnitude of the problem, little is known about the precise cause of CLBP. There is often a mismatch between objective findings and symptoms. Despite advances in imaging, in most patients, it is impossible to determine whether identifiable structural or mechanical abnormalities are responsible for the symptoms. Moreover, even when anatomic abnormalities are detected, the significance is unclear, since bulging disks or annular tears are found in high percentages of asymptomatic individuals. This mismatch between anatomic abnormalities and symptoms has led to studies of the psychosocial factors that may contribute to CLBP. These studies suggest that increasing age, female sex, lower levels of formal education, depression, stress, job dissatisfaction, and disability/compensation issues may play some role in expression of symptoms and in chronicity. However, all of the known anatomic, demographic, and psychosocial factors that might cause CLBP do not explain the symptoms in a significant number of subjects. These individuals are sometimes referred to as having “idiopathic” or “nonspecific” CLBP.
Pain in other idiopathic chronic pain conditions, such as irritable bowel syndrome and fibromyalgia syndrome (FMS), appears to result from abnormalities in pain processing rather than from damage or inflammation of peripheral structures. A common finding in these and other “central” or “non-nociceptive” pain syndromes is increased tenderness to pressure, which can be classified as mechanical hyperalgesia (i.e., increased pain in response to normally painful stimuli) and/or mechanical allodynia (i.e., pain in response to normally nonpainful stimuli). These abnormalities are found even in the absence of any identifiable psychological or behavioral factors, thus implicating central mechanisms that exacerbate pain (e.g., “wind-up”) or that attenuate pathways that begin in the brain stem and normally inhibit the ascending transmission of pain-related activity.
The finding of augmented stimulation-evoked pain, assessed by patient self-report, has recently been corroborated by functional brain imaging techniques that allow the visualization of structures that are potentially involved in pain processing. These methods infer increased neural activity from highly localized increases in regional cerebral blood flow that are produced in response to anticipated metabolic demands. These methods can involve infusion of radioactive tracers or, in the case of functional magnetic resonance imaging (fMRI), the magnetic character of the level of oxygen in the blood is used as an indirect, intrinsic tracer. Functional imaging studies have shown that painful stimulation produces increased neural activity in structures involved in the processing of sensation, movement, cognition, and emotion. Functional imaging studies in chronic pain states that are characterized by hyperalgesia/allodynia have corroborated patients’ self-reports of mechanical hyperalgesia, identifying objective evidence of augmented responses to pressure stimuli (such as in the viscera and periphery in irritable bowel syndrome and FMS, respectively).
In a recent cross-sectional study of CLBP, we demonstrated that a simple laboratory measure of pressure-pain sensitivity was the best correlate of pain and functional status, exceeding the predictive value of any other demographic, psychological, or radiographic variable. In the present study, we have expanded on this work and performed both experimental pain testing and functional imaging in a cohort of patients with CLBP. This particular cohort was specifically identified to have idiopathic CLBP, i.e., individuals without evidence of any anatomic abnormalities on MRI or plain radiographs that could explain these symptoms. These patients were compared with both a normal healthy control group and a cohort of individuals with FMS.