This subproject is one of many research subprojects utilizing theresources provided by a Center grant funded by NIH/NCRR. The subproject andinvestigator (PI) may have received primary funding from another NIH source,and thus could be represented in other CRISP entries. The institution listed isfor the Center, which is not necessarily the institution for the investigator.This is a study to learn more about the pathogenesis of cyclic vomiting syndrome (CVS) and of migraine headaches, specifically those with nausea and/or emesis. Animal data suggest that corticotropin-releasing factor (CRF) may play a role. The study hypothesis is that systemic CRF levels and hypothalamic-pituitary-adrenal (HPA) axis activity are heightened during systemic episodes. CRF has a -well-established role if inducing gastric stasis and vomiting in animals and its resulting behavioral, autonomic, endocrine effects resemble those clinical features seen in CVS. The model of CRF-induced emeses may explain the antiemetic utility of dexamethasone during chemotherapy-induced vomiting and migraine headaches. ACTH, cortisol and catecholamine levels will serve as indicators of HPA axis activation. The study objectives are firstly to demonstrate or refute this hypothesis and secondly, to evaluate the effect of dexamethasone on CRF axis activity and on clinical symptoms under three conditions including: 1) when well (i.e. in between epsidoes), 2) during acute episodes of cyclic vomiting or migraine headaches (treated with saline placebo), and, 3) during acute episodes of cyclic vomiting or migraine headaches in which CRF is suppressed by dexamethasone. Subjects with migraine headaches will receive ketorolac under both 2) and 3).
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