Fibromyalgia syndrome (FMS) is a chronic pain syndrome characterized by diffuse musculoskeletal pain. In quantitative sensory testing studies, FMS patients display alterations in heat, cold, and mechanical sensitivity. Genetic studies support a key role for the biogenic amine system, and single nucleotide polymorphisms have been identified in serotonin and dopamine transporter and receptor genes of FMS patients. The pathophysiology of fibromyalgia includes contributions from both the ascending and descending somatosensory systems, and decreased central nervous system inhibition of peripheral nociceptive signalling. Three drugs have been approved for the treatment of FMS: Lyrica® (pregablin), Cymbalta® (duloxetine), and Savella® (milnacipran). These drugs were originally developed for indications other than FMS, and were later approved for FMS after successful clinical trials. One hurdle in the development of drugs specifically for FMS is the availability of preclinical animal models of the disease. Recently, several rodent models have been described with potential for translation to the human pain syndrome. In this review, we discuss recent developments toward understanding the pathophysiology of FMS, currently available pharmacologic therapy, ongoing clinical trials, and potential animal models of FMS.
Keywords: Central dysfunction, chronic widespread pain, etiology, usculoskeletal, pathophysiology, pharmacologic therapy, potential models, Fibromyalgia syndrome (FMS), quantitative sensory testing studies, dopamine transporter and receptor genes, fibromyalgia, somatosensory systems, human pain syndrome
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