Fibromyalgia (FM) is a rheumatic disorder characterized by the presence of widespread musculoskeletal pain and the presence of tender points. Other symptoms, including fatigue, sleep disturbance, and neuropsychological complaints, contribute significantly to the morbidity associated with FM. One of the most prominent complaints in patients with FM is impaired cognitive ability. The notion that cognitive deficits are fundamental to FM is impaired cognitive ability. The notion that cognitive deficits are fundamental to FM has some credibility, as there is growing evidence that there are subtle but important cognitive deficits associated with Chronic Fatigue Syndrome (CFS), a related disorder, that cannot be explained by psychiatric symptoms. It is possible that cognitive defects in FM patients could result from single or multiple central nervous system perturbations associated with FM. In the present proposal, we will correlate cognitive function of FM patients with measures of neuroendocrine function. A basic thesis advanced is that FM patients may have both cognitive and neuroendocrine function similar to that of controls subjects who are 20 to 30 years older. Indeed, cognitive testing in patients with CFS reveals changes similar to those seen in subjects of advanced chronological age. In two experiments, FM patients will be compared to age-and education- matched controls, as well as to education-matched older adults. Neuroendocrine function will be measured as well, as will depression, pain, fatigue, and beliefs about memory function. This approach permits us to determine whether there are differences in cognitive function of fibromyalgia patients from others, and whether cognitive agins is a good model for understanding the cognitive effects of FM. In addition and perhaps more importantly, the integration of a cognitive approach with a neuroendocrine approach will allow us to determine what mechanisms account for the cognitive differences--neurochemical, psychiatric, or experience pain and fatigue. Knowing the mechanisms underlying observed cognitive deficits, rather than merely demonstrating that there are deficits, has important implications for treatment of the disorder as well as for understanding its etiology.
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