Fibromyalgia

Nicole Reams MD (Dr. Reams of the University of Michigan has no relevant financial relationships to disclose.)
James G Greene MD PhD, editor. (Dr. Greene of Emory University School of Medicine has no relevant financial relationships to disclose.)
Originally released December 3, 2014; expires December 3, 2017

This article includes discussion of fibromyalgia, chronic widespread pain, fibrositis, muscular rheumatism, myofascial pain syndrome, and trigger point syndrome. 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 skeletal muscle to various locations, including the chest, neck, and head (Travell 1968). At this time, patients were receiving trigger point injections with procaine for treatment of their pain. In the 1970s, Smythe laid the foundation of modern fibromyalgia syndrome by describing widespread pain and tender points (Reynolds 1983; Inanici and Yunus 2004).

The diagnostic criteria for fibromyalgia syndrome were originally published in 1990 and emphasized chronic widespread pain with a number of tender points (Wolfe et al 1990). Newer diagnostic criteria published in 2010 moved away from tender points and were more symptom-based, describing fibromyalgia as a widespread pain syndrome not dependent on specific trigger points for diagnosis (Wolfe et al 2011).

The content you are trying to view is available only to logged in, current MedLink Neurology subscribers.

If you are a subscriber, please log in.

If you are a former subscriber or have registered before, please log in first and then click select a Service Plan or contact Subscriber Services. Site license users, click the Site License Acces link on the Homepage at an authorized computer.

If you have never registered before, click Learn More about MedLink Neurology  or view available Service Plans.