Chronic Opioid Use in Fibromyalgia Syndrome

A Clinical Review

Jacob T. Painter, PharmD, MBA, PhD; Leslie J. Crofford, MD


J Clin Rheumatol. 2013;19(2):72-77. 

In This Article

FM and Its Relation to Other Disorders

The understanding of FM has developed greatly since the early 20th century when Sir William Gowers assigned the term fibrositis to dispersed muscular pain seen in clinic. "Fibromyalgia" did not appear in the nomenclature until the mid-1970s,[14] and this shift in terminology represented the growing understanding that the clinical presentation represented pain, but not inflammation of the fibrous tissue. The etiology of FM involves both genetic vulnerability and environmental triggers. Fibromyalgia aggregates strongly in families, with first-degree relatives bearing an 8-fold increased risk of developing the syndrome.[15] Recent evidence suggests that FM patients may have inherited tendencies toward various nociceptive and analgesic pathway abnormalities, measured as pain sensitivity, predisposing them to development of chronic pain symptoms.[16] Although genetics do play an important role in the etiology of FM, environmental factors, especially exposure to stressors such as physical trauma or mechanical derangement, chronic inflammation, certain infections, and emotional stress, are also considered contributors to its development.[17]

It is becoming increasingly evident that disordered central pain processing is key to the development of FM.[18] As research methods advance, possible deficiencies in γ-aminobutyric acid–ergic, aminergic, or cannabinoid signaling are being identified.[16] Research has shown that FM patients have augmented pain response profiles when exposed to either pressure[19] or thermal[20] stimuli. This can be measured both subjectively and objectively using techniques such as functional magnetic resonance imaging.[21] The current understanding of FM is that of altered pain physiology such that normal or innocuous sensory afferent input received by normal neural pathways is perceived as noxious when represented in the pain processing regions of the brain. Fibromyalgia and related disorders are identified by symptoms, suffering, and disability.[22]

Other pain amplification or central pain syndromes include irritable bowel syndrome, temporomandibular disorder, and vulvodynia. Each of these syndromes is characterized by pain without an identifiable peripheral cause.[18] All of these and other pain amplification syndromes, as well as major depressive disorder and generalized anxiety disorder, are found to coaggregate with FM.[15,23,24] From a clinical perspective, pain amplification syndromes are recognized as variable pain descriptions (eg, burning, throbbing, stabbing) that are difficult to precisely localize and tend to move from site to site. There is a strong association with a personal or family history of pain and a history of associated neuropsychiatric symptoms.

Chronic musculoskeletal pain, including mechanical derangements, degenerative disorders, and inflammatory conditions, is present in 10% to 12% of the general population.[25] Some of these individuals with chronic pain also meet the clinical criteria for FM.[26] Fibromyalgia is present in approximately 5% of women[27] and 1.6% of men[28] in the general population. Fibromyalgia in the population occurs along a spectrum where at one end pain and tenderness are the exclusive symptoms, and at the other, pain is accompanied by significant psychological and cognitive detriment.[29] This spectrum is multidimensional, and patients may exhibit severe pain symptoms exclusively or have moderate pain but suffer from numerous other associated symptoms. The identification of central pain amplification as an important mechanism underlying FM suggests that chronic use of opioids, associated with changes in the central nervous system that may facilitate hyperalgesia, is particularly problematic for this group of patients (Table 1).