Abstract

Fibromyalgia is a chronic pain syndrome. Neuman and Buskila noted that fibromyalgia afflicts approximately 5% of women and 1.6% of men. The diagnosis of fibromyalgia is primarily based on chronic widespread pain that has (1) pain on both sides of the body, (2) is above and below the waist, (3) should involve the axial skeleton, and (4) must have been present for more than 3 months. Physical examination must include at least 11 of 18 tender points. In clinical practice, nearly half the population may have fewer tender points. A new proposed fibromyalgia syndrome also includes sleep deficits, daytime fatigue, and altered cognition/mood as a part of the syndrome. Comorbid psychiatric disorders are common in fibromyalgia. Arnold et al. reported that 75% of patients with fibromyalgia have a mood disorder, 60% have an anxiety disorder, and 26% have a substance use disorder. A clearly defined causative explanation for fibromyalgia has eluded investigators. One of the earliest explanations for fibromyalgia looked at the most obvious source—muscle. However, this theory was disproved quickly, leading to more central explanations. The two most accepted evidence-based theories include: neuropeptide abnormalities (involving entities such as Substance P, serotonin, and endogenous opioids); and neuroendocrine defects (including the hypothalamo-pituitary adrenal [HPA], hypothalamo-pituitary gonadal [HPG], hypothalamo-pituitary-thyroid, and the growth hormone axes). Endorphins play a significant role in pain perception. Hence, it is not surprising that a number of investigators have looked at perturbations of endorphin function as a possible explanation for fibromyalgia. Vaeroy et al. observed that CSF -endorphin levels are either normal or lowered in individuals with fibromyalgia. The authors concluded that other endogenous opioids (such as proenkephalin and prodynorphin) may

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