The pathophysiology of migraine

Abstract

The knowledge of the pathophysiology of migraine has advanced to a great extent, particularly over the last 15 years. New genetic data, involving mutations in the CACNL1A4 gene on chromosome 19p13.1 encoding the a1 subunit of the brain specific P/Q-type calcium channel, the role of neuropeptides such as CGRP, NK1 and SP, the influence of NO as a key molecule in migraine, the development of experimental models including the plasma extravasation model developed by Moskowitz’ group and the use of advanced neuroimaging techniques (PET, MR and MEG) are some of the recent achievements. New anti-migraine drugs are on the way, developed according to the new pathophysiological knowledge. Leão's spreading depression remains as one of the most important neurophysiological phenomena in migraine. It activates the trigeminovascular system, induces CGRP-mediated vasodilation and provokes the expression of c-fos in the trigeminal nucleus caudalis. The migrainous pain does not seem to be produced by vasodilation, so classifying headaches in “vascular” and “non-vascular” is no longer appropriate.