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The discovery of a feedback system that’s active during a migraine headache has researchers at the University of Iowa questioning some of the traditional theories about migraine headaches.

The team found that inflammatory agents released during a migraine seem to signal certain nerve cells (neurons) in your brain to increase production of a neuropeptide, calcitonin gene-related peptide, or CGRP. One result of CGRP’s presence is to stimulate your brain tissue to release more inflammatory agents. The new inflammatory agents send more signals to the neurons to release more CGRP, the cycle continues, and so does your migraine.

At present, the most effective migraine medication on the market is sumatriptan, which provides relief for 50 to 75 percent of the people who use it. Even though scientists know it works, they don’t understand why or how.

While studying the drug, the Iowa researchers discovered that sumatriptan keeps calcium levels high in the neurons. In most cases, a high-calcium level also means a high level of neuropeptides in the affected neurons. However, when the participants took sumatriptan, CGRP didn’t increase, which may be one reason why this drug works so well against migraines. If the CGRP doesn’t increase, then the inflammatory agent-CGRP cycle described earlier is broken.

Interestingly, the same signal (calcium release) can give two different reactions depending on the strength and duration of the signal. A short, fast burst of calcium causes an increase in the CGRP, which continues the cycle and your headache. However, if the calcium increase is a slow, steady rise, it actually lessens the amount of CGRP that is released. Researchers believe it is this second type of calcium increase that sumatriptan brings about.

As a follow-up to this study, researchers will look for the exact mechanism for the initial release of CGRP, with the hope that blocking this action would divert the migraine.