Most people think MIGRAINE = BAD HEADACHE. But that’s not true…

The headache of migraine is often such a profound part of the experience that is all most people think about. But there are many other (non-headache) migraine symptoms, including heightened senses (of light, sound, and smell), a sense of disequilibrium or imbalance, and nausea. All of these symptoms are just as much migraine as the headache. In fact, you can even have migraine WITHOUT headache!

So what is migraine?

We used to think migraine was simply a stretching of the arteries in the head – known as the vascular theory of migraine. But as imaging techniques developed and we were better able to measure blood vessel caliber during migraine attacks it became apparent that, while changes in the caliber of the blood vessels in the brain can occur during a migraine attack, these changes are not necessary for migraine to occur.

As the vascular theory of migraine fell out of favor, the neurologic theory of migraine took over. With new imaging modalities available, not only were we able to measure changes in blood vessel caliber, we were also able to observe changes in the activity of the brain during attacks. This lead to the hypothesis that migraine is a disease of the nervous system – known as the neural hypothesis of migraine. To focus just on the changes occurring in the nervous system during migraine is to ignore the changes that occur in the blood vessels.

We now understand migraine as a neuro-vascular condition; recognizing there are changes in both the vascular and neurologic systems. What we don’t know is how these systems interact with each other.

Where Does it Come From? 

The current theory of migraine can be broken down into three steps:

Step 1. Cortical spreading depression (CSD)

CSD is a phenomena that occurs in people with migraine. It consists of a slow moving wave that spreads across the brain at a rate of 2-6 mm/minute. As the wave moves across the brain, the area in front of the wave experiences increased activity and the area behind the wave experiences prolonged decreased activity. CSD has eloquently been shown to be the source of migraine “aura” (usually a visual disturbance prior to the headache phase of migraine).

Step 2. Dural inflammation

Brain tissue is not pain sensitive, but the dura (the protective layer around the brain) is. The current theory proposes this wave of CSD triggers the release of inflammatory molecules that move to the surface of the brain and trigger inflammation of the pain-sensitive dura.

Step 3. Pain processing

Pain sensors (called nociceptors) in the dura then send their nerves through the trigeminal nerve into the brain stem, then up to the thalamus where they are relayed to other areas of the brain to be interpreted as pain.

While there are many scientific studies that support various aspects of this theory, there are also reasons to question it. For example, only one third of people with migraine experience aura; aura can occur during or even after the headache phase of migraine; and inflammation of the dura has not been observed with brain imaging in people with migraine.

As you can see, there is much to learn about where migraine comes from. We at the University of Vermont Headache Clinic are conducting a study investigating this relationship.

If you have migraine with attacks that affect just one side of your head at a time, and are interested in finding out more about our One-Sided Migraine Research Study, click here.

Adam S. Sprouse-Blum, MD, is a family medicine physician at the University of Vermont Medical Center and Assistant Professor at the Robert Larner, MD, College of Medicine at the University of Vermont.

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