[Neurophysiology of visual aura in migraine].

Visual processing in migraine has been targeted because the visual symptoms that are commonly associated with attack, either in the form of aura or other more subtle symptoms, indicate that the visual pathways are involved in migrainous pathophysiology. The visual aura of the migraine attack has been explained by the cortical spreading depression (CSD) of Leão, neuroelectric event beginning in the occipital cortex and propagating into contiguous brain region. Clinical observations suggest that hyperexcitability occurs not only during the attack, typically in the form of photophobia, but also between attacks. Numerous human neuroimaging, neurophysiological and psychophysical studies have identified differences in cortical visual processing in migraine. The possibility of imaging the typical visual aura with BOLD functional MRI has revealed multiple neurovascular events in the occipital cortex within a single attack that closely resemble CSD. As transient synchronized neuronal excitation precedes CSD, changes in cortical excitability underlie the migraine attack. Independent evidence for altered neuronal excitability in migraineurs between attacks emerges from visual evoked potentials (VEPs) and transcranial magnetic stimulation (TMS), recordings of cortical potentials and psychophysics. Recently, both TMS and psycho-physical studies measuring visual performance in migraineurs have used measures which presumably measure primary visual (V1) and visual association cortex. Our VEP and blink reflex study showed that migraine patients exhibiting allodynia might show central sensitization of braistem trigeminal neuron and had contrast modulation dysfunction during the cortical visual processing of V1 and visual association cortex in-between attacks. In pathophysiology of migraine, these neurophysiological and psychophysical studies indicate that abnormal visual and trigeminal hyperexcitability might persist between migraine attacks. The influence of migraine on cortical neural processing is likely to extend beyond V1 and abnormal cortical activity might lead to CSD when enhanced activation coincides with other factors.