BACKGROUND: Photophobia is an abnormal sensitivity to light experienced by migraineurs during attacks. The pathophysiology of photophobia is poorly understood. Nevertheless, 2 facts appear to have a link with photophobia: visual cortex hyperexcitability on the one hand and interactions between visual pathway and trigeminal nociception on the other. METHODS: We used H(2)(15)O PET to study photophobia induced by continuous luminous stimulation covering the whole visual field in 8 migraineurs during spontaneous migraine attacks, after headache relief by sumatriptan and during attack-free interval. The intensity of the luminous stimulation provoking photophobia with subsequent headache enhancement was specifically determined for each patient. RESULTS: We found that low luminous stimulation (median of 240 Cd/m(2)) activated the visual cortex during migraine attacks and after headache relief but not during the attack-free interval. The visual cortex activation was statistically stronger during migraine headache than after pain relief. CONCLUSION: 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.
BACKGROUND:Photophobia is an abnormal sensitivity to light experienced by migraineurs during attacks. The pathophysiology of photophobia is poorly understood. Nevertheless, 2 facts appear to have a link with photophobia: visual cortex hyperexcitability on the one hand and interactions between visual pathway and trigeminal nociception on the other. METHODS: We used H(2)(15)O PET to study photophobia induced by continuous luminous stimulation covering the whole visual field in 8 migraineurs during spontaneous migraine attacks, after headache relief by sumatriptan and during attack-free interval. The intensity of the luminous stimulation provoking photophobia with subsequent headache enhancement was specifically determined for each patient. RESULTS: We found that low luminous stimulation (median of 240 Cd/m(2)) activated the visual cortex during migraine attacks and after headache relief but not during the attack-free interval. The visual cortex activation was statistically stronger during migraineheadache than after pain relief. CONCLUSION: 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.
Authors: Mohammad S Asghar; Adam E Hansen; Henrik B W Larsson; Jes Olesen; Messoud Ashina Journal: J Headache Pain Date: 2012-01-14 Impact factor: 7.277