Hypothalamic activity, long suspected by clinical and experimental arguments as a possible trigger for migraine, is demonstrated for the first time during spontaneous attacks.

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These findings suggest that ictal photophobia is linked with a visual cortex hyperexcitability. The mechanism of this cortical hyperexcitability could not be explained only by trigeminal nociception because it persisted after headache relief. We hypothesize that modulation of cortical excitability during migraine attack could be under brainstem nuclei control.