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Migraine is a disorder of altered brain excitability, as can be readily observed from the clinical symptoms. The photophobia, hyperalgesia, and allodynia that often accompany headache are amplifications or distortions of normal sensations. More dramatically, the positive features of the migraine aura represent aberrant brain activity apparently unrelated to any stimulus in the environment.
Research in humans supports the clinical data. Electroencephalography, magnetoencephalography, evoked potentials, and transcranial magnetic stimulation all show evidence of either increased response to stimuli or decreased habituation to repetitive stimuli, consistent with increased brain excitability in migraine.1 Functional imaging has shown waves of perfusion change in the occipital lobe consistent with cortical spreading depression, the massive depolarization thought to underlie the migraine aura.2,3
Perhaps because of the more dramatic symptoms, most of our evidence for increased excitability comes from migraine with aura. What can be said about migraine without aura, which accounts for the majority of migraine patients, and the majority of headaches even in patients with aura?
In the current issue of Neurology®, Denuelle et al.4 quite literally shed some light on this question. They show that the occipital cortex responds differently to light during an attack compared to attack-free …
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