I think most of us have experienced a migraine at one point in our lives. It’s a headache that can cause severe throbbing pain or a pulsing sensation, usually on one side of the head. Migraine attacks can last for hours to days, and the pain can be so bad that it interferes with your daily activities. In some cases, people can also become sensitive to light, sound, smell, and touch or experience nausea and vomiting. Usually, everyone just takes a painkiller and calls it a day, but sometimes, that won’t be enough. That’s why there is ongoing research about what the mechanism of migraine pain actually is.
CGRP (calcitonin gene-related peptide) is a small protein typically responsible for pain transmission in neurons and is known to be elevated in the tissue surrounding the brain during a migraine attack. Scientists have discovered that this protein’s increase also affects the brain's lymphatic vessels, which facilitate the removal of cerebrospinal fluid in order to create a pathway for immune cells to do their job. If this process fails, it can directly contribute to migraine pain.
Even when this is what the research points to, the exact mechanism still needs further investigation and the proper links between migraine, CGRP, and meningeal lymphatic vessels need to be established. It’s also a question of how this process will differ with and without the use of the medications so far approved to treat migraine attacks.
Resources:
N. P. Nelson-Maney, et al. (2024) Meningeal lymphatic CGRP signaling governs pain via cerebrospinal fluid efflux and neuroinflammation in migraine models
J.-L. Thomas, et al. (2024) Meningeal lymphatic vessel dysfunction driven by CGRP signaling causes migraine-like pain in mice
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