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Pathogenesis of fibromyalgia

INTRODUCTION

Fibromyalgia is a chronic pain disorder with unknown etiology and unclear pathophysiology [1,2].

There is no evidence that a single event "causes" fibromyalgia. Rather, many physical and/or emotional stressors may trigger or aggravate symptoms. These have included certain infections, such as a viral illness or Lyme disease as well as emotional or physical trauma [1-3].

The diagnosis is currently based upon the presence of widespread musculoskeletal pain and excess tenderness in at least 11 of 18 predefined anatomic sites (figure 1). A detailed description of the clinical manifestations of fibromyalgia and an approach to the diagnosis of fibromyalgia in adults and children are presented separately. (See "Clinical manifestations and diagnosis of fibromyalgia in adults" and "Clinical manifestations and diagnosis of fibromyalgia in children and adolescents".)

Fibromyalgia is only one of many causes of widespread pain. A discussion of the differential diagnosis of fibromyalgia and the broad differential diagnosis is presented separately. (See "Differential diagnosis of fibromyalgia".)

PATHOGENESIS

Fibromyalgia is currently considered to be a disorder of pain regulation, classified often under the term central sensitization [1,2,4]. During much of the 20th century, fibromyalgia was thought to be a muscle disease. However, controlled trials found no evidence for significant pathologic or biochemical muscle abnormalities [1-5]. As an example, measures of muscle function, including force generation and lactate production during exercise, and muscle pain following exertion are remarkably similar in women with fibromyalgia (FMS) and sedentary female controls [6,7]. Most investigators now believe that any muscle pathology is secondary to pain and inactivity rather than primary in nature [1,5-7].

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