Concluding Remarks

Abstract

One of the most well-known pathophysiological phenomena in migraine is cerebral ischemia, possibly induced by vasospasm with consequent prodromic focal symptoms, followed by a reactive vasodilation associated with the pain. From a neuropharmacological point of view, the role of serotonin as a mediator of vasospasm has long dominated the scientific field, and antiserotonin drugs have, for almost as long, governed the therapeutic field. More recent approaches have implicated platelet aggregability, focal cerebral hypoxia and opioid neuropeptides in the genesis of migraine. Here I shall attempt to review the different aspects that, even though controversial, summarize the situation as it stands at the end of 1984.