Abstract

The aetiology of migraine headaches has been the source of a great deal of conjecture, and debate continues over its origin as a vascular or brain disorder, as well as the role of vasoactive substances in its genesis. Abnormal platelet aggregation associated with the release of vasoactive substances has been observed in migraine (Deshmukh & Meyer 1977). In addition, prostaglandins have been shown to playa role in acute migraine attacks (Amano & Meyer 1982; Rabey et al. 1976; Vardi et al. 1979). Recently, a trend has developed toward the study of non-steroidal anti-inflammatory drugs (NSAIDs) in various headache models, including migraine . Studies have confirmed the usefulness of these agents in migraine and vascular-related headaches such as chronic paroxysmal hemicrania (Sjaastad et al. 1979), cluster headache variant (Medina & Diamond 1981), and exertional headaches (Diamond & Medina 1982). The NSAIDs are prostaglandin inhibitors, and although they differ widely in chemical structure there is a uniform decrease in prostaglandin synthesis by the inhibition of cyclooxygenase. This action may serve as an index of the potency of the NSAIDs (Boghen & Desaulniers 1983).

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