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The classical vascular mechanism of migraine attacks demonstrated by Wolff — intracranial vasoconstriction during the prodromal stage and passive vasodilatation of extracranial arteries during the painful phase — has been confirmed by modern methods. Arterial distension is, however, not sufficient to explain the origin of the pain: to give rise to an acute migraineous pain, it must be associated with a lowered pain threshold of the receptors situated in the wall of the affected vessels. A number of humoral factors — plasmakinin, serotonin, histamine — intervene in the chain of events that culminates in migraine headache.
At the start of the attack, the blood platelets release serotonin, the mast cells in the affected area release histamine and proteolytic enzymes that split plasmakininogens to form plas-makinins. Free serotonin and histamine increase capillary permeability and favor transudation of plasmakinin into the vessel walls andperivascular tissues. The combined effect of serotonin and plasmakinin on the vessel wall receptors reduces their pain threshold. On the other hand, the bulk of the released serotonin is excreted as 5-HIAA, and plasma serotonin falls. Since serotonin has a constricting effect on the extracranial arteries and a dilating one on the capillaries, the fall in its plasma level induces hypotonia of these arteries and capillary constriction, which results in a passive distension of the arterial walls. The two factors necessary for the production of pain are thus present: a low pain threshold and vascular distension. In addition to these three main humoral mediators, the part played by tyramine in migraine of alimentary origin, the precipitating effect of estrogen decrease in mentrual migraine and the hypothetical role of prostaglan-dins and prolactin are discussed.
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