Scientists have found a new communication pathway in the brain that could be key to stopping migraines. This pathway links different nerve centers within the brain, skull, and the rest of the body. The discovery may lead to new treatments that prevent migraines or reduce their migraine pain.
Researchers have been trying to figure out where migraines start in the brain and how these painful headaches cause other symptoms like nausea and vomiting. For one-third of migraine sufferers, the headache is preceded by an aura, a visual disturbance caused by abnormal brain activity. However, how this activity inside the brain affects pain receptors outside the brain has not been clear.
The brain is protected by a barrier called the blood-brain barrier, which keeps harmful substances out of the central nervous system (CNS). The spinal cord has a similar protective barrier. A key nerve hub that links the CNS to the rest of the body’s nerves is the trigeminal ganglion. This cluster of nerves, located at the base of the skull, has been implicated in migraines and headaches and transmits sensory information from the face and jaws to the brain.
Previously, researchers thought the trigeminal ganglion was outside the blood-brain barrier, making it easier to target with drugs. However, this also meant it was not exposed to the cerebrospinal fluid (CSF) that surrounds the brain and spinal cord.
A new study in mice revealed that CSF carries signaling molecules directly to the trigeminal ganglion, bypassing a slower, known route. This fluid enters the trigeminal ganglion and activates pain-sensing neurons, which could explain why migraines are often one-sided.
University of Copenhagen biologist Martin Kaag Rasmussen and his team conducted experiments showing that CSF from the visual cortex of the brain (where migraine auras often start) flows to the trigeminal ganglion. The fluid quickly enters the ganglion, which lacks a protective sheath, allowing molecules to penetrate the nerves.
The study found that after a migraine aura, the CSF contained molecules like CGRP (calcitonin gene-related peptide), which activate trigeminal ganglion nerves and cause pain. However, the CSF composition normalizes quickly, indicating other processes might drive the headache in later phases.
While there are differences between mice and humans, the researchers hope this discovery will lead to new drug targets for patients who do not respond well to current migraine therapies. Their findings suggest that CSF is not just a waste-clearing fluid but also an important signal carrier in the brain.
Neuroscientists Andrew Russo and Jeffrey Iliff, in a perspective accompanying the study, wrote that this new mechanism links the central and peripheral nervous systems and could lead to new migraine treatments.
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