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Brain 'Blackout' Linked to Migraine Aura

Rat study reveals new target for treating painful headache

THURSDAY, Jan. 31, 2002 (HealthDayNews) -- For 20 percent of migraine sufferers, the onset of this excruciating headache is heralded by an "aura," where images of flashing lights or shifting shapes cloud their vision.

Now, new research suggests this warning sign may correspond with a pattern of depressed brain cell activity that sweeps across the cortex like a rolling blackout, and it may be linked to the painful migraine that follows.

It's the first study to suggest that brain activity is behind migraines, and experts say it may point to new ways to interrupt the cascade of events leading to this agonizing form of headache. HealthDay first reported this discovery last October when the researchers presented their findings at the annual meeting of the American Neurological Association.

Migraine affects about 28 million Americans, 75 percent of whom are women. Besides the extreme, often throbbing, pain that is frequently centered in one area of the head, patients can experience nausea, vomiting and extreme sensitivity to light and sound. The aura usually lasts 20 to 30 minutes, and the headache follows within an hour.

Stress, emotion and sleep disturbances are all thought to play a role in increasing the risk of migraine, but the brain's contribution to this condition has remained poorly understood.

The idea that a migraine aura is linked to depressed brain cell activity first surfaced in 1944, when a study suggested the aura moves across a person's visual field at a speed matching the spread of the depressed activity across the cortex.

Now, Harvard researchers report in the February issue of Nature Medicine that in a study of brain activity in rats, this phenomenon, called cortical spreading depression (CSD), triggers activity in the trigeminal nerves, which send motor signals to the head. That, in turn, causes inflammation of the pain-sensitive meninges, which is believed responsible for the trademark pain of migraine.

"When we were able to trigger these CSDs, then you could see very clearly the footprints and the fingerprints of the pain system," says senior investigator Dr. Michael A. Moskowitz, a professor of neurology. "We think it's a direct irritation of the pain-transmitting fibers from the surface of the brain, triggered by this electrical, biochemical event that's slowly spreading across the visual cortex."

When the trigeminal system is irritated, he says, a reflex pathway dilates a main meningeal blood vessel.

However, what triggers CSD in humans is not yet understood.

Dr. Constantino Iadecola, a professor of neurology and neuroscience at Cornell University's Weill Medical College in New York, says there is some speculation migraines with visual auras might be triggered by visual input.

Moskowitz says people with migraines who don't experience visual auras may have other triggers, while Iadecola says the CSD may be affecting a part of the brain that doesn't produce obvious symptoms.

Triptans, the most commonly used drugs for migraines, try to block irritation of the trigeminal nerve, while other drugs such as valproic acid or Neurontin (gabapentin) aim to suppress abnormal brain cell activity in the cortex.

Iadecola, who wrote an accompanying commentary, says drugs that block a receptor called NMDA, which plays a critical role in CSD, could be a useful therapy for migraines. However, such treatments are still in development, he says, with many compounds causing severe side effects.

What To Do: For general information about migraine, check out the National Institute of Neurological Disorders and Stroke or the National Headache Foundation. You can read about women and migraine from the American Council for Headache Education.

SOURCES: Interviews with Michael A. Moskowitz, M.D., professor, neurology, Harvard Medical School, Boston; Constantino Iadecola, M.D., professor, Division of Neurobiology, Department of Neurology and Neuroscience, Weill Medical College, Cornell University, New York City; February 2002 Nature Medicine
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