What have we learnt from triggering migraine?

This review presents what we have learnt from triggering migraine.

Experimental studies have shown that glyceryl trinitrate (GTN), calcitonin gene-related peptide (CGRP), pituitary adenylate cyclase activating polypeptide-38 (PACAP38) and prostaglandin I2 (PGI2) induce migraine-like attacks in migraine suffers indistinguishable from their spontaneous attacks. These studies point to two key pathways to play an important role in migraine pathophysiology: cyclic guanosine monophosphate (cGMP) and cyclic adenosine monophosphate (cAMP). At present, no valid experimental model exists to reproduce aura episodes in migraine with aura patients. Familiar hemiplegic migraine patients seem to be less sensitive to GTN and CGRP provocation compared with common types of migraine. Advances in recent imaging studies suggest neuronal mechanisms to be behind migraine attacks. The experimental headache models have resulted in development and an ongoing search of new migraine targets.

Human models of migraine offer unique possibilities to study mechanisms responsible for different migraine subtypes and to explore the mechanisms of action of existing and future antimigraine drugs. Adding advanced imaging techniques to the models may lead to a better understanding of the complex events that constitutes a migraine attack and thereby more targeted ways of intervention.