Abstract
About 30 years ago, the hypothesis that serotonin (5-hydroxytryptamine) was important to the pathogenesis of migraine caused great excitement. Methysergide had been found to antagonize certain peripheral actions of 5-hydroxytryptamine and had been introduced as the first drug capable of preventing or reducing the intensity and frequency of migraine attacks.1 Subsequent studies revealed that platelet levels of 5-hydroxytryptamine fall consistently at the onset of headache and that migrainous episodes may be triggered by drugs releasing 5-hydroxytryptamine.2 Such changes in circulating levels proved to be pharmacologically trivial, however, and interest in the humoral role of 5-hydroxytryptamine in migraine declin d. Today, . . .