[The role of serotonin in the pathophysiology of migraine]

Of the many factors that have been implicated in the pathophysiology of migraine, none seems to have a better claim than serotonin (5-hydroxytryptamine, 5-HT). The evidence for this is: 5-HT concentrations in blood increase during the prodromal (aura) phase and subsequently, decrease to subnormal levels in the headache phase; migraine attacks may be triggered, in susceptible, subjects, by reserpine which depletes body serotonin; migraine attacks may be triggered, in susceptible subjects, by reserpine which depletes body serotonin; migraine attacks may be relieved by intravenous injection of 5-HT; medications known to affect 5-HT concentrations have been shown to be efficacious in both aborting (agonists of 5-HT1 receptors) and preventing (antagonists of 5-HT2 receptors) migraine attacks. Since most of 5-HT in blood is stored in the platelets, attention of many investigators focused on the platelet function abnormalities. The positive findings provoked some of them to hypothesise that migraine is a primarily platelet disorder. Advances in the understanding of the role of 5-HT in migraine and the pharmacology of this amine have now resulted in the development of a highly selective 5-HT1 -like receptor agonist which selectively constricts cranial blood vessels and inhibits neurogenically-mediated plasma protein extravasation in the dura mater.