Part 1 of a 2-part series. This article will cover the history of the fibromyalgia (FM) concept, current thinking on FM, and the epidemiology of the disease. Part 2 will appear in the November 2009 issue and will cover the role of pain processing in FM and potential treatment methods.
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Explore This IssueOctober 2009
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The Beginning of FM
Although there are clear descriptions of individuals with what we now call FM going back centuries in the medical literature, Sir William Gowers coined the term of “fibrositis,” which was considered a form of muscular rheumatism caused by inflammation of fibrous tissue overlying muscles.1 Although other terms such as “psychogenic rheumatism” were proposed and used in the mid-20th century, the term “fibrositis” remained the most widely used term to describe individuals with chronic widespread pain and no alternative explanation.
Several authors began to suggest that this term was a misnomer because there was no inflammation of the muscles. Moldofsky and colleagues performed seminal studies showing that individuals with fibrositis suffered from objective sleep disturbances, and showed that these same symptoms could be induced in healthy individuals deprived of sleep.2-5 Hudson and colleagues were arguably the first investigators to note the strong familial tendency to develop FM, and proposed that this condition is a variant of depression, coining the term “affective spectrum disorder.”6,7 In parallel during this period, Yunus and colleagues similarly began to note the high frequency of associated functional somatic syndromes, such as irritable bowel syndrome (IBS) and headache, with FM, again steering the focus away from skeletal muscle.8 Nonetheless, the theories positing a pathophysiologic role of skeletal muscle took time to fade, persisting into the mid-1990s.9-11
Just as spastic colitis became IBS, temporomandibular joint syndrome became temporomandibular disorder when it was recognized that the problem was not in the joint; chronic Epstein-Barr virus (EBV) syndrome became chronic fatigue syndrome (CFS) when it was realized that this syndrome occurs commonly after many viral illnesses and without infection with this pathogen; and fibrositis became FM.
It had also become clear that FM is not just FM. There is now significant evidence that FM is part of a much larger continuum that has been called many things, including functional somatic syndromes, medically unexplained symptoms, chronic multisymptom illnesses, somatoform disorders, and, perhaps most appropriately, central sensitivity syndromes (CSS). Yunus et al showed FM to be associated with tension-type headache, migraine, and IBS. Together with primary dysmenorrheal, these entities were depicted by Yunus in a Venn diagram in 1984, emphasizing the epidemiological and clinical overlap between the syndromes.8 In this article, the more recent term, CSS as proposed by Yunus, is used, because I feel that this represents the best nosological term at present for these syndromes.12 (See Table 1, above.)
TABLE 1: Clinical Syndromes Currently Considered Parts of the CSS Spectrum
- Chronic fatigue syndrome
- Irritable bowel syndrome and other functional gastrointestinal disorders
- Temporomandibular joint disorder
- Restless legs syndrome and periodic limb movements in sleep
- Idiopathic low back pain
- Multiple chemical sensitivity
- Primary dysmenorrhea
- Headache (tension > migraine, mixed)
- Interstitial cystitis/chronic prostatitis/painful bladder syndrome
- Chronic pelvic pain and endometriosis
- Myofascial pain syndrome/regional soft tissue pain syndrome
There is also a clear overlap between the CSS disorders and a variety of psychiatric disorders. This overlap likely occurs at least in part because the same neurotransmitters (albeit in different brain regions) are operative in psychiatric conditions. The presence of co-morbid psychiatric disturbances is somewhat more common in individuals with CSS seen in tertiary care settings than primary care settings.13,14 Figure 1 (below) demonstrates the overlap between FM, CFS, and a variety of regional pain syndromes, as well as psychiatric disorders,and shows that the common underlying pathophysiological mechanism seen in most individuals with FM, and large subsets of individuals with these other syndromes, is central nervous system (CNS) pain or sensory amplification.