Expert Answer: Migraine pathophysiology

What is the difference between the vascular and neurovascular theories pertaining to migraine pathophysiology?

When doctors talk about what’s causing migraine, they’ll mention things like the vascular hypothesis, the neural theory, and the neurovascular model. Although these medical words sound pretty impressive, the words hypothesis, theory, and model tell a very clear story—doctors don’t REALLY know what they’re talking about! Even the smartest doctor knows that we’re really just learning what’s causing migraine—that’s why we have theories rather than fact. Headache doctors spend a lot of time trying to decide what are all of the important factors that cause migraine. They know that once all of the factors have been uncovered, then we really WILL know what’s causing migraine. Today, however, we just have ideas—good ideas—but ideas and theories that are still changing and evolving as we learn more and more by studying migraineurs.

Migraine sufferers often notice the blood vessels at their temples become more prominent and tender during a migraine. And migraine pain is typically described as pulsing or throbbing. This led doctors to look to the blood vessels as the cause of migraine. The blood vessel or vascular theory of migraine really began in 1937 after Drs. Graham and Wolff published an article describing an incredible experiment they conducted. Using 14 patients with migraine, they showed that injecting the drug ergotamine decreased headache pain and caused pulsations in the temple arteries to decrease by half. They could then bring back both the blood vessel pulsing AND the headache by injecting these same people with another chemical called histamine. They were also able to decrease blood vessel pulsing and headache by injecting adrenaline. These experiments linked pulsing vessels with migraine pain, starting many decades of the theory that migraine was caused by abnormally reactive blood vessels.

As doctors did more experiments with migraine sufferers, they began to wonder if there was more to the story than just excited blood vessels. Some experts argued that migraine was really caused by abnormal brain activity or an excited nervous system. These doctors pointed to changes in levels of pain chemicals in the brain and other signs of abnormal nerve functioning in migraine sufferers. After years of very heated debate about which was really the problem, the blood vessels or the brain, Dr. Moskowitz, a doctor at working at Massachusetts General Hospital and Harvard Medical School, reported animal experiments that linked changes in blood vessels and changes in activity in nerves that cause head and face pain. His work suggested both sides were right—migraine sufferers have changes in brain chemicals that result in changes in migraine symptoms AND throbbing blood vessels. The changes in the blood vessels actually occur because nerve chemicals change and signal the blood vessels to expand and become more sensitive to throbbing. This important work was the beginning of today’s neurovascular model.

The neurovascular model is the reason that some migraine therapies (like the triptans) target chemicals in the brain like serotonin and others (like some anti-seizure drugs) work to reduce brain excitability. Once brain chemicals have been correctly balanced, the brain will stop sending migraine signals, like those signals triggering blood vessels to expand.

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