Patients typically present with chronic, widespread body pain and almost always have accompanying comorbid symptoms such as fatigue, memory difficulties, and sleep and mood difficulties
Physical examination is typically normal but there is often diffuse tenderness, which may be assessed by counting the number of tender points or by palpating several areas of the body.
Many therapies have been shown to be beneficial. Non-pharmacological therapies include patient education, exercise, and cognitive behavioural approaches. Pharmacological therapies include tricyclics, gabapentinoids, and serotonin-norepinephrine (noradrenaline) reuptake inhibitors. Patients often fare better when several different types of treatment are used together.
Even though practitioners may have a problem recognising fibromyalgia as a discrete disorder, they should understand the diagnostic and therapeutic importance of 'centralisation' of pain as exemplified by a typical fibromyalgia patient. When a patient with any chronic pain state develops evidence of centralisation of pain, it is likely that treatments that work well for acute pain or pain primarily due to nociceptive input (NSAIDs, opioids, anti-inflammatories, immunosuppressives, injections, surgical procedures) will be less effective.
Fibromyalgia is a chronic pain syndrome diagnosed by the presence of widespread body pain (front and back, right and left, both sides of the diaphragm) for at least 3 months in addition to tenderness (digital palpation at an approximate force of 4 kg) of at least 11 out of 18 designated tender point sites as defined by the American College of Rheumatology 1990 classification criteria.  Criteria have been established that do not require performing a tender point count.  These criteria comprise adding up the number of body sites of pain, as well as the presence and severity of frequent comorbid symptoms such as fatigue, memory problems, and sleep disturbances. Although there is not likely to be any single cause, substantial evidence suggests that this is in part a central nervous system-driven pain amplification syndrome.
Professor of Medicine
Division of Rheumatology
University of Michigan Health System
DJC has received consulting fees from Pfizer, Eli Lilly, Nuvo, Cerephex, Tonix, Abbott, Forest Laboratories, Johnson & Johnson, Merck, Perdue Pharmaceudicals, Zynerba, Astellas Pharmaceuticals, Williams & Connolly LLP, and Theravance; he has received research grant support from Pfizer, Cypress Biosciences, Forest Laboratories, Merck, Novo, and Cerephex. DJC is an author of a number of references cited in this monograph.
Dr Daniel J. Clauw would like to gratefully acknowledge Dr Lisa Ware Corbin, a previous contributor to this monograph. LWC declares that she has no competing interests.
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