Cerebrovascular changes in migraine: secondary manifestations of a circulating humoral agent?

The cerebrovascular concomitants of migraine, initial vasoconstrictriction succeeded by vasodilatation, have long been considered the primary event in the pathogenesis of headache. In recent years, certain physicochemical concomitants of the attack have been identified, all involving blood platelets: these include hyperaggregability, decrease 5-hydroxytryptamine concentration and decreased monoamine oxidase activity. These changes may represent the response to a circulating humoral agent, deriving perhaps from the pulmonary vascular bed. The agent may not only bring about nonspecific damage of the kind described but be responsible for the cerebrovascular changes and stimulation of pain receptors characteristic of the disease. This circulating humoral agent may belong to the prostaglandin family.