For a billion people worldwide, the symptoms can be devastating: throbbing headache, nausea, blurred vision and tiredness that can take days. But how the brain activity triggers this severe headache - migraines - has long spent a puzzle.

A study 1 on mice, published in science on July 4, now provides information on the neurological events that trigger migraines. It suggests that a short brain failure - when the neural activity comes to a standstill - temporarily changes the content of the liquor cerebrospinalis, the clear liquid that surrounds the brain and the spinal cord. This changed fluid is to be transported to nerves in the skull by a previously unknown gap in the anatomy, where it activates pain and inflammatory receptors and causes a headache.

"This work is a rethink of how we see the origin of the headache," says Gregory Dussor, a neurologist at the University of Texas in Dallas in Richardson. "A headache could simply be a general warning signal that many things happen in the brain that are not normal."

"Migraine is actually protective in this regard. The pain is protective because he tells the person to rest and relax and sleep," says co -author Maiken Nedergaard, a neurologist at the University of Copenhagen.

painless brain

The brain itself has no pain receptors; The sensation of headaches comes from areas outside the brain that lies in the peripheral nervous system. But how the brain, which is not directly connected to the peripheral nervous system, nerves activated to cause headaches is badly understood what it makes difficult to treat.

scientists who worked with a mouse model of a certain type of headache, the so -called auricular migraines, set out to research this. A third of the migraine patients experience a phase of their headache, which is known as aura and has symptoms such as nausea, vomiting, sensitivity to light and numbness. It can take five minutes to an hour. During the aura, the brain experiences depression called cortical spread (CSD) when the neural activity exposes for a short time.

Studies of migraines suggest that the headache occurs when molecules flow out of the brain in the cerebrospinal cerebrospinalis and activate nerves in the meninges, the layers that protect the brain and the spinal cord.

Nedergaard's team wanted to explore whether there are similar leaks in the Cerebrospinal Cerebrospinalis, which activate the trigeminal nerve that runs through the face and skull. The nerve branches combine in the trigeminal ganglion on the skull base. This is a hub for forwarding sensory information between the face and jaw to the brain and contains receptors for pain and inflammatory proteins.

nerve bundle

The authors breeded mice that CSDs experienced and analyzed the movement and content of their liquor cerebrospinalis. During a CSD, they found that the concentrations of some proteins in the liquid sank to less than half of their usual values. The values ​​of other proteins doubled, including the pain-transmitting protein CGRP, which is a goal of migraine medication.

The researchers also discovered a previously unknown gap in the protective layers around the trigeminal ganglion, which enables the Cerebrospinal Cerebrospinalis to flow into these nerve cells. They therefore tested whether spinal cord fluids with different protein concentrations on the trigeminal nerves had a effect on control mice.

The liquid collected shortly after a CSD increased the activity of the trigeminal nerve cells - which indicates that headaches could be triggered from pain signals from these activated cells. The liquid that was collected for 2.5 hours after CSDS did not have the same effect.

"Whatever is released in the Cerebrospinal Cerebrospinalis is broken down. So it is a short -term phenomenon," says Nedergaard.

"" It really shows this beautiful potential interaction in how a change in the brain can affect the periphery. There can be an exchange between these two components of the nervous system, and we should be more aware of it, "says Philip Holland, a neurologist at King’s College London.

Dussor suggests that future studies should investigate why the proteins in the spinal cord fluids that hit the trigeminal ganglion, cause headaches and no other pain type. "This will raise a lot of interesting questions in the industry and probably be the starting point for many new research projects."