Fibromyalgia

K K Jain MD (Dr. Jain is a consultant in neurology and has no relevant financial relationships to disclose.)
Originally released December 3, 2014; last updated June 2, 2017; expires June 2, 2020

This article includes discussion of fibromyalgia, chronic widespread pain, fibrositis, and muscular rheumatism. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.

Overview

In this article, the author discusses the history, etiology, epidemiology, pathophysiology, and management of fibromyalgia. The article includes an explanation of the evolving understanding of the pathophysiology of this chronic pain disorder as well as the development of clinically useful diagnostic criteria.

Key points

 

• Fibromyalgia syndrome is a chronic pain disorder.

 

• Fibromyalgia is best understood by central sensitization to pain.

 

• Fibromyalgia is a clinical diagnosis and is based on patients' self-report of widespread, functionally limiting pain.

 

• Multidisciplinary care, including pharmacologic and nonpharmacologic methods, and improving patients' self-efficacy is the most effective approach for treatment of fibromyalgia.

Historical note and terminology

Fibromyalgia syndrome is now a recognized clinical entity with accepted diagnostic criteria; however, its name and the understanding of the underlying disease process have developed over time. In the eighteenth 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 (Hadler 1986).

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 this entity based on tender points or nerve points in muscle, rather than nodules, which were affected by physical activity, weather, and emotions. These nerve points were thought to be areas of poor neural network communication and contained fibrous tissue or focal cell necrosis. These points were found to be more common in some areas of the body and more common near origins or insertions of muscle. For centuries, scientists had understood the disease as a disorder of muscle; however, patients described radiating pain, so nerve involvement was questioned. 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” or “trigger zone” was introduced and referred to radiating pain or referred pain that could be produced from stimulation of a local area. 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 (Travell 1968). Myofascial pain syndrome is now recognized as distinct from fibromyalgia. In the 1970s, Smythe laid the foundation of modern fibromyalgia syndrome by describing widespread pain and tender points (Reynolds 1983; Inanici and Yunus 2004).

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