Pharmacologic Treatment of Migraine

Abstract

The vascular theory of migraine proposed by Wolff, attributing migrainous symptoms to paroxysmal constriction and dilation of the cranial vasculature, held sway for over four decades and even now remains embraced by many clinicians and the lay public. Recent investigations, however, suggest that this proposed mechanism is untenable; although changes in blood vessel caliber and blood flow do occur in some patients during some attacks, they are not required for the production of migrainous symptoms and appear to be largely epiphenomena, occurring subsequent (and consequent) to another primary process. Evidence is mounting that migraine may result from a pathologic alteration of neurotransmission within the brain stem and trigeminovascular system, and one of the neurotransmitters primarily involved is serotonin. This has led to an explosion of interest in therapeutic agents which influence serotoninergic receptors, and the astounding success enjoyed by the first of these agents to be utilized clinically (sumatriptan and dihydroergotamine) and their offspring suggests that our understanding of this common and vexing problem will increase and be paralleled by the identification of yet more specific and effective treatment intervention.