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Photophobia: The Occipital Cortex Response to Bright Light during Migraine

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Photophobia: The Occipital Cortex Response to Bright Light during Migraine Empty Photophobia: The Occipital Cortex Response to Bright Light during Migraine

Post by Tee Thu Jun 09, 2011 11:15 pm

March 7, 2011

Photophobia, a term describing the worsening of migraine pain with bright light while in the midst of an attack and also an uncomfortable sense of glare when exposed to bright light between attacks, is a characteristic feature of migraine and an area of active research. In a landmark study published in Nature Neuroscience in 2010, scientists from Harvard identified a new pathway in the brain that is responsible for carrying this signal. More recently, researchers from France have built upon this understanding to investigate the changes in blood flow that occur in the occipital cortex, the area of the brain responsible for vision, during migraine attacks when a migraineur is presented with a bright light stimulus.

These authors exposed 8 individuals who had migraine without aura to a uniform light stimulus under three different clinical situations (untreated migraine 2-7 hours into the attack, migraine after treatment with sumatriptan and complete headache resolution, and also during an attack-free period) and measured changes in blood flow over the visual cortex using functional imaging studies. They first found the threshold level of light intensity that caused an increase in headache pain while a subject was in the midst of a migraine attack. The researchers then examined changes in blood flow over the visual cortex during a migraine attack, after treatment with sumatriptan, and also between migraine attacks when the individual was exposed to this same intensity of light. Increased blood flow is thought to be a marker of increased neuronal activity.

The authors made two important observations with this study: 1) the same intensity of light that worsened migraine headache pain while a subject was in the midst of an attack did not cause any discomfort after the migraine was successfully treated with sumatriptan or between migraine attacks; and 2) blood flow in the occipital cortex increased substantially when that individual was exposed to this light stimulus both during an untreated migraine and after pain resolution following treatment with sumatriptan, but not between attacks of migraine.

As blood flow was greatest with exposure to this light during an untreated migraine, the results suggest that pain is an important part of this response; however, given that there was still increased blood flow seen with this light stimulus after the headache was eliminated with sumatriptan, these findings imply that pain is not the only factor.

This study reinforces the concept that, similar to those with migraine with visual aura, the occipital cortex of those individuals who experience migraine without visual aura also appears to be hyperexcitable. In addition, the fact that there was increased activity even after the pain had resolved, appears to point again to the important role that brainstem control centers may play in migraine by rendering the occipital cortex more responsive to visual stimuli. Future research will continue to search for the generator(s) of migraine, to better understand how to best to prevent attacks and intervene earlier to terminate more effectively those attacks that do start.

Rashmi Halker, MD
Mayo Clinic, Phoenix, AZ
Tee
Tee
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