New research points to the cause of migraines

How brain activity can cause the most intense headaches - migraines - is a common problem that has long puzzled scientists. A recent study in mice has shown that spinal fluid content may be the cause of this condition.

Accordingly, a new study published in the journal Science on July 4 has provided clues about the neurological phenomena that cause migraines. Scientists found that a brief 'blackout' - when nerve activity momentarily stops - abruptly changed the content of cerebrospinal fluid, the clear fluid that surrounds the brain and spinal cord living. This altered fluid content travels through a previously unknown gap in the anatomy to nerves in the skull, where it activates pain receptors and inflammation, causing pain. head.

' This is a new discovery in the way we study the origins of headaches ,' said Dr. Gregory Dussor from the University of Texas. ' Headaches may simply be a general warning sign for many unusual things happening inside the brain. In this case, pain is an agent of self-protection, it warns your body that it needs to rest, recover or simply sleep '.

The brain does not know pain on its own

In fact, our brain itself has absolutely no pain receptors. Instead, headaches come from areas outside the brain in the peripheral nervous system. But how the brain, which is not directly linked to the peripheral nervous system, can activate the nerves that cause headaches is not well understood, making treatment of this type of condition difficult. .

To dig deeper for answers, scientists conducted research in mice on a specific type of headache, called auditory migraine. The results showed that a third of people with migraines experienced a pre-headache episode, marked by symptoms such as nausea, vomiting, sensitivity to light and numbness. This phenomenon can last five minutes to an hour. During that process, the brain experiences a brief 'blackout' called cortical spreading depression (CSD), which occurs when nerve cell activity stops for a short period of time.

Further research into migraines shows that headaches occur when molecules in the cerebrospinal fluid flow out of the brain and activate nerves in the meninges, the layer that protects the brain and spinal cord.

Scientists wanted to discover whether similar leaks in cerebrospinal fluid activate the trigeminal nerve. The nerve branches connect to each other in the trigeminal ganglion at the base of the skull, which is a center that relays sensory information between the face and jaw to the brain, and also contains pain receptors and inflammatory proteins. .

Nerve bundles

The research team bred mice with CSD and analyzed their movements and cerebrospinal fluid content. During CSD, they found that the concentration of certain proteins in the cerebrospinal fluid dropped to less than half the normal level. Levels of other proteins more than doubled, including the pain-transmitting protein CGRP, which is a target of migraine drugs.

The researchers also discovered a previously unknown gap in the protective layers surrounding the trigeminal ganglion, allowing cerebrospinal fluid to flood into these neurons. So they tested whether spinal fluid with different protein concentrations would activate the trigeminal nerve in control mice.

Cerebrospinal fluid collected immediately after CSD increased the activity of trigeminal neurons - suggesting that headaches may be triggered from pain signals sent from these stimulated cells . However, cerebrospinal fluid collected 2.5 hours after CSD did not have the same effect.

Anything released into the cerebrospinal fluid is degraded. So it's a short-term phenomenon.

More research will be needed in the future to discover why proteins in the spinal fluid that affect the trigeminal ganglion cause headaches but not other types of pain. ' This will raise a lot of interesting questions, and will probably become the driving force of many new research projects '.