Chronic fatigue syndrome has received considerable attention in lay and medical media. This syndrome reportedly leads to significant physical and psychological debility in a large segment of the population. Specific diagnostic and treatment regimens have been proposed and are being administered to patients. Yet, there remain few data which can validate the existence of the syndrome as distinct from a wide variety of other, largely psychiatric, disorders, and little understanding of its pathogenesis. The pilot feasibility study proposed in this application seeks to clarify and extend an understanding of the role of hypothalamic-pituitary-adrenal (HPA) axis dysregulation in the pathogenesis of this disorder. The overall objective of this protocol is to test the hyposthesis that patients with chronic fatigue syndrome manifest a characteristic neuroendocrine defect, namely, a reduction in adrenal glucocorticoid secretion mediated by a failure in the central release of corticotropin-releasing hormone (CRH). Specifically, we will confirm and extend our preliminary findings of impaired activation of the HPA axis in patients with chronic fatigue syndrome by examining the patterns of pulsatile secretion of ACTH during periods of maximal and minimal activity of the axis. The results of this proposal will be used to demonstrate the feasability of the pulsatility methodology and provide further pilot data which will enhance the likelihood for success of our federal grant application.
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