[Mechanisms and genetics of migraine]

Migraine is the most frequent primary headache disorder. It is a neurovascular disorder in which the primary abnormality is thought to be a neuronal excitability underlined by a complex genetic susceptibility. Epidemiogenetic studies have shown that migraine without aura and migraine with aura are polygenic conditions. The three known migraine genes have been identified by the study of the unique monogenic variety of migraine, i.e. familial hemiplegic migraine. These genes all encode ion transporters: the P/Q type calcium channel, a calcium/potassium ATPase and a sodium channel. According to the latter hypothesis about the mechanisms of migraine attacks, poorly known triggers initiate a cortical wave of depolarisation that is responsible for the transient aura symptoms. This cortical spreading depression induces several biochemical changes which, by diffusion through the extracellular space, stimulate the trigeminovascular fibres. These fibres release vasoactive neuropeptides that initiate the neurogenic inflammation. Trigeminovascular fibres transmit nociceptive information centrally via the brainstem. The trigeminovascular fibres also activate the parasympathetic system that is responsible for the persistence of vasodilation in meningeal vessels.