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.