Structural abnormalities in brains of migraine sufferers


Researchers from Harvard Medical School have found structural abnormalities in the brains of migraine sufferers which provide an anatomical basis for some of the visual disturbances experienced by people with the condition.

In PLoS Medicine, Granziera et al report on a study which uses hi-resolution functional magnetic resonance imaging (fMRI) to show that the thickness of two regions of visual cortex, MT+ and V3A, are significantly thicker in migraine sufferers than in healthy people.

The study also revealed anatomical alterations in the superior colliculus (SC) and lateral geniculate nucleus (LGN), two subcortical regions in the visual pathway. MT+ and V3A are involved in motion processing, and the SC and LGN are also involved in various aspects of visual processing.

Migraine is a widespread disorder, affecting an estimated 6-8% of men and 15-25% of women, but its causes are a mystery. A migraine is an intense and disabling headache, which is experienced periodically and is often accompanied by nausea and hypersensitivity to light and sound. It has been suggested that behavioural, environmental, dietary or hormonal triggers can lead to the development of a migraine. Between 20-30% of migraine sufferers also experience aura, or visual disturbances such as the perception of flashing lights or zig-zags. These phenomena normally appear gradually over 5-20 minutes, and precede a migraine.

The theory that migraines are caused by abnormalities in cerebral blood flow has now been discredited, and current thinking has it that cortical spreading depression (CSD) is responsible for the condition. In CSD, a slow, self-propagating wave of depolarization inhibits activity first in the source cortical area then in adjacent ones. In theory, this results in the release of inflammatory mediators which irritate the roots of the cranial nerves (particularly the trigeminal nerve).

The anatomical differences found by Granziera and her colleagues were observed in patients who suffer from migraines with aura and in those who suffer from migraine without aura, providing some evidence for a common pathophysiology for both types. The findings contradict the assumption that migraine is caused by abnormal brain function without underlying changes in structure; give weight to previous suggestions that the V3A region is a source of CSD in migraine; and may also provide clinicians with a non-invasive marker for migraine.

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