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  • Updated 02.10.2024
  • Released 12.03.2014
  • Expires For CME 02.10.2027




This article depicts the history, etiology, epidemiology, pathophysiology, and management of fibromyalgia. The article includes a description of the development of clinically useful diagnostic criteria as well as a summary of the evolving understanding of pathophysiologic mechanisms of this chronic pain disorder and management modalities.

Key points

• Fibromyalgia syndrome is a chronic generalized primary pain disorder.

• Fibromyalgia is best understood by central sensitization to pain.

• Fibromyalgia is a clinical diagnosis based on patients’ self-reports of widespread, functionally limiting pain, with tenderness of muscles, tendons, and ligaments, after the exclusion of another disease accounting for all symptoms by history taking and physical exam.

• Fibromyalgia can be a comorbid condition of inflammatory rheumatic diseases, such as rheumatoid arthritis; a comorbid disease does not rule out fibromyalgia.

• Multidisciplinary care, including patient education, pharmacologic and nonpharmacologic methods, and improving patients’ self-efficacy, is the most appropriate approach for managing fibromyalgia.

Historical note and terminology

Fibromyalgia syndrome is a recognized clinical entity with accepted diagnostic criteria. Its name and the understanding of disease mechanisms have developed over time. In the nineteenth century, physicians used the term “muscular rheumatism” to refer to a condition characterized by pain and stiffness of the muscles and soft tissues. This entity was described as “recurrent pain in the fleshy parts” and “pulling, tearing, shooting, sticking” pains with stiffness and immobility of the affected parts (22). However, “muscular rheumatism” is a too broad, imprecise umbrella term for fibromyalgia; the term is sometimes also used for localized noninflammatory conditions and for polymyalgia rheumatica.

In 1904, Sir William Gowers coined the term “fibrositis,” referring to a chronic pain syndrome that was thought to be due to focal nodules and inflammatory exudates in rheumatic muscle. This term and initial hypotheses about the pathology of this disorder have since been abandoned. Shortly thereafter, several physicians began to describe fibromyalgia based on tender points (rather than nodules), which were affected by physical activity, weather, and emotions. These points were commonly found near origins or insertions of muscle. For centuries, scientists had understood the disease as a muscle disorder; however, patients also described symptoms of hyperalgesia and allodynia, so central nervous involvement came to mind. In 1920, Lindstedt introduced the idea of central sensitization, describing muscular rheumatism as “a pathologic increase in the general sensitivity of the nervous system” felt to be secondary to sensory reflex phenomenon.

In the late 1930s, the term “trigger point” was introduced to refer to radiating pain or referred pain that could be produced from stimulation of a local area, the trigger point. In 1942, the term “myofascial pain syndrome” was introduced based on work by Janet Travell that described pain referred from “trigger points” in skeletal muscles to various locations, including the chest, neck, and head (48). Myofascial pain syndrome is now recognized as distinct from fibromyalgia. In the 1970s, Smythe laid the foundation of fibromyalgia syndrome as it is seen now, by describing widespread pain and tender points (41; 26). Because definite etiological structural lesions of the nervous system had not been identified, fibromyalgia was excluded from the diagnosis of neuropathic pain in 2011. However, small fiber pathology is observed in approximately 50% of people with fibromyalgia (20). This small fiber pathology may be a specific feature of fibromyalgia, not a comorbid small fiber neuropathy, as the clinical phenotype of small fiber pathology in fibromyalgia seems distinct from that of small fiber neuropathy (50).

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