Fibromyalgia: where are we a decade after the American College of Rheumatology classification criteria were developed?

The American College of Rheumatology (ACR) published classification criteria for fibromyalgia (FM) in 1990 (1). These criteria allow investigators around the world to investigate mechanisms of symptom expression in FM with assurance that research subjects share the presence of chronic widespread pain and evidence of altered pain processing, as demonstrated by the presence of tender points. With publication of the classification criteria, the ACR assumed a leadership position in research into basic mechanisms underlying FM symptoms and management of patients with FM. What progress has been made in the decade since the ACR classification criteria were developed? A strength of the criteria from a research standpoint is that FM patients meeting the ACR classification criteria are at the extreme end of the spectrum of pain and tenderness. As a result, a number of studies have demonstrated important alterations in pain processing in FM. These studies use subjective ratings of experimental pain paradigms as well as objective demonstration of an altered central representation of painful stimuli. Petzke et al demonstrated that patients with FM had low mechanical and thermal pain thresholds regardless of whether the stimulus was presented in a predictable, ascending manner (as with tender point determinations or dolorimetery) or randomly (2). These data suggest that, compared with healthy individuals, FM patients do not rate pain stimuli higher because of psychological hypervigilance or “expectancy.” Staud et al showed that patients with FM exhibit altered temporal summation of pain stimuli administered as a thermal stimulus to skin or as a mechanical stimulus to muscle (3,4). The results of these studies suggest a parallel between the human condition of FM and the “wind-up” phenomenon that leads to hyperalgesia and has been extensively studied in animal models (5). Other data corroborating the veracity of FM patients’ descriptions of pain have been collected using paradigms that are not dependent on subjective reports by patients. For example, Lorenz et al demonstrated altered laser-evoked potentials as objective representation of the central nervous system (CNS) response to cutaneous stimulation (6). Patients with FM were shown by Mountz et al and by Cianfrini et al to have reduced thalamic blood flow under resting conditions (a finding observed in other chronic pain states) and altered responses to mechanical pain stimuli (7,8). Finally, Grant et al demonstrated that increased blood flow to brain regions known to receive pain input correlates with the intensity of perceived pain rather than the absolute level of the stimulus (9). All these data arguably complement the most consistent biologic finding supporting aberrant central pain transmission in FM—the 3-fold higher concentrations of substance P in cerebrospinal fluid (CSF) of FM patients compared with those in the CSF of normal controls (10–13). Taken together, the data on pain processing in FM demonstrate that the central representation of pain correlates with patient reports of pain, and that purely behavioral or psychological factors are not primarily responsible for the pain and tenderness seen in FM. The ACR classification criteria focus only on pain, however, and disregard other important FM symptoms, including fatigue, cognitive disturbance, sleep disturbance, and psychological distress. If one takes a more general view of FM that includes these symptoms and commonly associated syndromes (e.g., chronic fatigue syndrome, irritable bowel syndrome, and depression), then the ACR criteria fail to capture the essence of the FM syndrome. When research subjects are identified using the ACR criteria, there is greater variability Leslie J. Crofford, MD: University of Michigan, Ann Arbor; Daniel J. Clauw, MD: University of Michigan, Ann Arbor, and Georgetown University, Washington, DC. Address correspondence and reprint requests to Leslie J. Crofford, MD, Room 5510A, MSRB-I, 1150 West Medical Center Drive, Ann Arbor, MI 48109-0680. E-mail: crofford@umich.edu. Submitted for publication November 27, 2001; accepted December 5, 2001.