There have been many attempts to explain the pathophysiological mechanism of migraine — for example, the platelet theory, the biogenic amine theory, or the vascular, vaso-neurogenic, and neural theories. There is still general agreement that the migraine aura is associated with a regional vasoconstriction, whilst the headache phase is accompanied by a localized vasodilatation of the cranial arteries. It is also a generally held concept that 5-hydroxytryptamine (5-HT, serotonin) is somehow involved in the pathogenesis of the disease. This chapter hypothesizes that the vasodilator phase of...

There have been many attempts to explain the pathophysiological mechanism of migraine — for example, the platelet theory, the biogenic amine theory, or the vascular, vaso-neurogenic, and neural theories. There is still general agreement that the migraine aura is associated with a regional vasoconstriction, whilst the headache phase is accompanied by a localized vasodilatation of the cranial arteries. It is also a generally held concept that 5-hydroxytryptamine (5-HT, serotonin) is somehow involved in the pathogenesis of the disease. This chapter hypothesizes that the vasodilator phase of migraine is mediated by two powerful vasorelaxants, which are generated by the endothelium, namely prostacyclin and the ‘endothelium-derived relaxing factor’ which has been identified as nitric oxide (NO).