Mécanisme et fonctionnement de la migraine

Mechanism and functioning of migraine

Aug 16, 2021

How a migraine works, from triggers to headache

We are going through this article to explain to you simply the mechanism of migraine . Sometimes we have to take a few shortcuts to simplify understanding. However, you will find additional articles to allow you to go further. Also keep in mind that the way migraine works has changed a lot in the last 10 years and continues to change. There is still a large part of darkness where scientific research has not provided an answer. Here are the basics to understand how migraine works . Find out how to relieve migraine naturally

Several phases of migraine that involve a succession of different mechanisms

Migraine evolves according to four phases which are: prodromes, migraine aura, headache and postdromes.

The prodromal (or premonitory) phase is the first phase described in the migraine attack. It can start a few hours or a few days before the next phases. 30 to 40% of migraine patients experience this phase through several symptoms. These are: aphasia (language disorder), digestive disorder (diarrhea or constipation), difficulty concentrating , increased frequency of urination, increased appetite, mood change (irritability or depression…), or intense fatigue . This list is not exhaustive and some patients may still experience many other symptoms.

The migraine aura is felt by approximately 20 to 30% of patients . These are symptoms that indicate a disturbance in the nervous system . In the majority of cases, these are visual signs, in which case we speak of ophthalmic migraine or migraine with typical aura. However, other signs may be associated, such as motor or sensory disorders . A patient sometimes had migraines with aura and sometimes migraines without.

The headache phase is the phase where the described pain in the head. In general this phase that we consider as migraine. It is the consequence of an inflammatory phenomenon at the level of the envelope which surrounds the brain: the meninges. Indeed it is not the brain that hurts directly, it is not innervated and is unable to feel pain.

The last phase of postdromes has exactly the same signs as the very first phase of prodromes.

MRI of the brain on a tablet with a red area illustrating pain

The mechanism of migraine headache

It all starts with the triggering factors . Depending on the patient they can be very different. These can be environmental variations, stress, hormones, overeating, sleep disturbances , etc. each patient knows their triggers for a migraine.

Triggers to the hypothalamus

By various mechanisms, these triggering factors are integrated into the brain and particularly at the level of an area called the hypothalamus. To learn more about the integration of triggers in the brain, we invite you to read the article on the role of TRP receptors . The hypothalamus therefore integrates a multitude of information that it then retransmits to different areas of the brain . We know that in the migraine patient, the hypothalamus has an increased activity . He's like super excited all the time. This state of excitement is found even between seizures . Therefore, in the migraine patient the hypothalamus needs constancy. Any variations that are a little too great can lead to a phase of intense hyperactivity. Now we believe today that it is the key element in the triggering of migraine attacks. As the hypothalamus integrates a multitude of different information, this explains the great diversity of triggering factors.

From the hypothalamus to massive hyperactivity of neurons

When the hypothalamus enters a phase of hyperactivity, the patient can experience a whole host of disorders which are usually regulated by the latter. Feelings of fatigue, hunger, irritability, etc. found in the prodrome phase . This is hyperactivity will lead to several consequences. First, it will stimulate certain areas of the brain where neurons can be observed to be highly excited and then enter a phase of silence . One of the areas most affected by this phenomenon is the visual area . This explains why the majority of migraine auras are visual. The hyperactivity of these neurons in the visual area is felt by the patient by flickering, hatched lines, etc. in the field of view. If other tunes are affected, the symptoms may be different. This is the case of language air for speech disorders, motor areas for movement disorders, etc. So far, the patient may experience these “overactive brain” symptoms, but still has not started the headache phase. So he doesn't have a headache yet.

The beginning of the pain phase

This cerebral hyperactivity results in a particular behavior of the neurons, namely a phase of excitation followed by a phase of silence. In scientific jargon, we speak of depolarization of neurons and then repolarization. As this phenomenon progresses gradually to extend to other areas of the brain (we said that it generally begins in the visual area), we speak of cortical invasive depression . This invasive cortical depression will lead to a massive release of protons which will stimulate the pain receptors at the level of the envelope of the brain, that is to say the meninges. This is the very beginning of the headache phase: migraine pain sets in.

Maintaining the pain phase: the trigeminal system

To feel pain somewhere, a nerve must travel from the area of ​​pain to the brain . If, for example, you suffer from leg pain, it is your sciatic nerve that sends the information back to the spinal cord and then to the brain. In migraine, in the case of a headache, it's exactly the same thing. It is necessary to have a nerve that starts from the envelope of the brain and then is integrated into the brain itself . This nerve in question is the trigeminal nerve . It is a cranial nerve which innervates the meninges, but which also takes part in the sensitivity of the face. Basically, your whole head is sensory innervated by this nerve . photo credit: sawakinom

When we talk about the massive proton release, which will stimulate the pain receptors at the level of the envelope of the brain , it is about the stimulation of the trigeminal nerve at the level of the meninges. This will integrate the pain and then bring it up into the brain. This is the moment when the patient is able to feel and describe the pain (it is strong or light, to the right or to the left, pulsating or diffuse, etc.). On the other hand, the trigeminal nerve will participate in the massive release of pro-inflammatory substances , that is to say, which will promote the maintenance of pain. These are essentially CGRP, substance P, interleukins, etc.
If we dwell for a minute on CGRP (peptide linked to the calcitonin genes), it promotes inflammation, but it is also a powerful vasodilator. That is to say, it will cause dilation of the blood vessels. However, this dilation of blood vessels was noticed a very long time ago, when the first researchers studied migraine. It is for this reason that it has long been thought that migraine was the consequence of a dilation of the blood vessels. Now you understand that this is only an associated effect and not the cause of the migraine. New treatments for chronic migraine have been put on the market, these are CGRP inhibitors (antibodies directed against CGRP or its receptor). We have devoted an article to these promising new treatments.

The return to the postdromes

Gradually, the homeostasis of the body will take over . That is to say the return to equilibrium. The pain will gradually fade between 4 to 72 hours . This is the end of the headache and the patient is in the postdrome phase. All of this brain activity, along with the pain, will leave the patient in a state of extreme fatigue . It sometimes takes several days to recover from it and without being immune to a new migraine attack .

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