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The migraine attack is characterized by alterations in sensory perception, such as photophobia or allodynia, which have in common an uncomfortable amplification of the percept. It is not known how these changes arise. We evaluated the ability of cortical spreading depression (CSD), the proposed mechanism of the migraine aura, to shape the cortical activity that underlies sensory perception. We measured forepaw- and hindpaw-evoked sensory responses in rat, before and after CSD, using multielectrode array recordings and two-dimensional optical spectroscopy. CSD significantly altered cortical sensory processing on a timescale compatible with the duration of the migraine attack. Both electrophysiological and hemodynamic maps had a reduced surface area (were sharpened) after CSD. Electrophysiological responses were potentiated at the receptive field center but suppressed in surround regions. Finally, the normal adaptation of sensory-evoked responses was attenuated at the receptive field center. In summary, we show that CSD induces changes in the evoked cortical response that are consistent with known mechanisms of cortical plasticity. These mechanisms provide a novel neurobiological substrate to explain the sensory alterations of the migraine attack.

Cortical Sensory Plasticity in a Model of Migraine with Aura