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 tricyclic antidepressants, gabapentinoids, and serotonin-noradrenaline (norepinephrine) 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.
The 1990 American College of Rheumatology criteria for the classification of fibromyalgia required that an individual had widespread 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. Subsequent criteria do not require a tender point examination by performing a tender point count, and focus on identifying widespread pain in combination with fatigue and memory and sleep difficulties. 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.
History and exam
Daniel J. Clauw, MD
Professor of Anesthesiology, Medicine, and Psychiatry
University of Michigan Health System
DJC has received consulting fees from Pfizer, Eli Lilly, Nuvo, Cerephex, Tonix, Abbott, Forest Laboratories, Johnson & Johnson, Merck, Purdue Pharma, Zynerba, Astellas Pharmaceuticals, Williams & Connolly LLP, and Aptinyx; he has received research grant support from Pfizer, Cypress Biosciences, Forest Laboratories, Merck, Novo, Cerephex, and Aptinyx. DJC is an author of a number of references cited in this topic.
Dr Daniel J. Clauw would like to gratefully acknowledge Dr Lisa Ware Corbin, a previous contributor to this topic.
LWC declares that she has no competing interests.
Don Goldenberg, MD
Emeritus Professor of Medicine
Tufts University School of Medicine
DG declares that he has no competing interests.
Robert Bennett, MD
Professor of Medicine and Nursing Research
Oregon Health & Science University
RB declares that he has no competing interests.
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