Abstract
Migraine is characterized by symptoms related to cortical hyperexcitability such as photophobia, phonophobia, osmophobia and allodynia. One-third of migraineurs experience aura, whose neurophysiological substrate is thought to be cortical spreading depression (CSD). Functional magnetic resonance imaging (MRI) has shown the migraine aura to be characterized by cerebral hyperactivity/hyperperfusion followed by hypometabolism/hypoperfusion spreading along the occipital cortex with the same spatiotemporal organization as the experimentally triggered CSD. The link between migraine aura and headache remains undetermined. Neuroimaging studies have failed to show a leakage of the blood-brain barrier, which was suspected to occur during CSD and to cause the stimulation of trigeminal nociceptive receptors. However, recent studies have highlighted the involvement of neuroglial inflammation and other studies have suggested that a common central network plays a role in the link between CSD and migraine pain. Finally, MRI has made it possible to study the contribution of metabolites such as glutamic acid, γ-amino-butyric acid and sodium in the pathophysiology of hyperexcitability in migraine.
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