What triggers your aura migraines

causes

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"Viszera" is Latin and, according to Duden, means the "organs located inside the skull, chest, abdominal and pelvic cavities". Pain that arises on or in these organs is also called "gut pain" or, medically, "visceral pain" for short. Based on this definition, it is actually already clear what it is about: For example the pain of appendicitis, biliary or intestinal colic, pleurisy or even a heart attack.

The visceral pain has three typical characteristics in common: They often radiate into distant skin areas or muscles, they lead to an excessive sensitivity to pain in the affected organ system and / or the skin area into which the pain radiates, and visceral pain is particularly common with vegetative symptoms such as sweating, paleness, rise in blood pressure, muscle tension, nausea and / or vomiting.

We find these signs, for example, in an acute heart attack: The severe and devastating pain in the heart behind the sternum often radiates into the shoulders (especially the left) and left arm. But the pain can also be localized in the lower jaw, in the upper abdomen or on the back between the shoulder blades. The organ itself, as well as the affected skin areas, are more sensitive to pain, the complexion is pale gray and pale. There is often nausea and vomiting, cold sweats on the forehead and upper lip, and there may even be a sudden breakdown in the circulatory system.

Qualities of Migraine Pain

Although brain tissue is injured to a greater or lesser extent in every brain operation, anesthesia is in principle not necessary. Reason: The brain tissue is insensitive to pain. Given the bestial pain in the head with migraines, this statement seems strange to say the least. Apparently something happens during a migraine attack that makes the otherwise pain-insensitive structures of the brain extremely sensitive. We will still try to narrow down this “something” in the following sections.

But this is first and foremost about pain and its qualities. Until recently, migraines were referred to as deep pain. Today we know that the term “intestinal pain” is far more applicable to migraines. Because it is also true of migraine pain that it is often difficult to localize and that it radiates into distant areas - in migraines mostly into the neck muscles. In addition, it has been shown that migraine pain can be accompanied by numerous vegetative symptoms: nausea and vomiting, sensitivity to light and noise, pale skin, freezing, shivering, tremors and much more.

Migraines as a circulatory disorder?

There are several reasons why changes in the blood flow to the brain - i.e. too much or too little pressure in the blood vessels - can be assumed to be the cause of migraines:

  • The migraine headache is throbbing and increases with each pulse.
  • Headaches also occur with other disorders of the blood vessels in the brain - e.g. stroke, high blood pressure or inflammation of the blood vessels.
  • The brain itself is not sensitive to pain. But the blood vessels of the brain do.
  • Certain agents, the so-called triptans, which influence the size of the cerebral vessels and thus the blood flow, can effectively stop a migraine attack.
  • During the aura phase, there is a reduced blood flow in the cerebral cortex in the area of ​​the back of the head. The interesting thing: This area is responsible for vision, among other things. And as you have already learned, most of the aura symptoms are of a visual nature.

Concomitant phenomenon, not cause

At first glance, the connections between changes in blood flow in the brain and migraines are entirely plausible: each of the five points in itself is absolutely correct. But the conclusion that migraine is a purely vascular disease (in the blood vessels) is unlikely.

Let's take a closer look at point 5. There is no question that there is the aforementioned reduced blood flow during the aura. It has been proven by numerous procedures. But if we look at the course of the cerebral blood flow in different forms of migraine - with aura, without aura - we immediately see that this cannot be the explanation for the migraine itself. Because with migraines without aura there is no change in blood flow in the head. The migraine pain can consequently have nothing to do with the blood circulation, even if points 1 to 4 above seem to be strong indicators.

But what about the aura? Is it at least triggered by the changes in blood flow? Not even that is clear. Whether or not it can be responsible for this depends on how bad the blood supply is in the affected area of ​​the brain. If it is actually 50 percent - as the supporters of the so-called vascular hypothesis claim - there would be an oxygen deficiency for the brain cells, which could well lead to the aura symptoms. If, on the other hand, the blood flow drops by a maximum of 25 percent - as the proponents of the neurogenic (caused by nerves) hypothesis assume, this would not be sufficient to explain the effects.

No matter how the discussion ends in the end: Changes in the width of the veins in the brain alone are out of the question as the primary cause of migraines. Regardless of the strength of the changes in blood flow, we should only consider them as accompanying symptoms.

Migraines as inflammation?

If we have injured ourselves on a thorn while gardening and foreign objects such as bacteria may have penetrated the wound or if we have lain in the sun for too long without protection, the typical signs of inflammation show up: the affected area reddens and swells , gets hot and hurts.

In both cases (thorn, sunburn), body tissue is injured and the inflammatory response that follows is nothing more than the body's normal way of repairing the injury. In the process, messenger substances (so-called inflammation mediators) are released, which ensure a stronger blood flow in the area (reddening), make the blood vessels more permeable, so that more immune cells and tissue fluid can escape (swelling), accelerate the metabolism at the site of the event (heat ) and increase the sensitivity to pain. It is therefore a sensible process that on the one hand creates the conditions for the necessary repairs and at the same time warns us through the pain to put even more strain on the injured area.

Special case of neurogenic inflammation

An inflammatory reaction can, however, also be triggered by nerves - hence the term “neurogenic inflammation” - without tissue damage or infection with bacteria being present. In this case, increased nerve activity triggers the release of the inflammatory messenger substances. As with any other inflammation, these cause an increased blood flow in the blood vessels of the meninges, make the veins more permeable and increase the sensitivity to pain in the area. Applied to migraines, the neurogenic inflammation model can explain why the blood vessels in the brain are so sensitive to pain that the pain intensifies with every pulse beat.

Partial explanation yes, cause no

What is certain is that neurogenic inflammation is an important mechanism for the body to ward off damage. However, it is not certain whether it actually plays an important role in migraines. The concept of neurogenic inflammation, however, offers meaningful explanations for some aspects of migraines, which is why they actually have a high priority in modern migraine models. The cause of migraines in the sense of a factor X, which gives us the answer to all open questions, is certainly not neurogenic inflammation.

Brain under high voltage

Sudden changes in the normal rhythm of life are particularly effective triggers for migraine attacks. It appears that these changes cause a temporary disruption of the normal flow of information. It is a particular merit of the Belgian migraine researcher Jean Schoenen and his colleagues to have made this special willingness to change stimulus processing visible through laboratory measurements in 1984. It is a special derivation of the brain waves, an electro-encephalography (EEG), during which the patient has to pay attention to and react to certain stimuli.

Get ready to accelerate

What is examined under laboratory conditions is well known to us from everyday life: a car driver has to stop at a red light. He has no idea how long the traffic light has been red and therefore does not know exactly when the yellow phase will come. He therefore stays in a phase of medium readiness and carefully observes whether the traffic light changes. As soon as the traffic light shows yellow, the driver knows that after a few seconds green will follow and he then has to let go of the clutch and accelerate. The driver is now particularly focused, prepares himself internally for his task and carries it out immediately after switching to green. The brain must be particularly active during the phase of increased readiness immediately before the action is carried out: It must plan the action in advance so that it can be performed immediately, and it must take into account an internal clock in order to be able to estimate the time between the yellow and green phases .

Migraine sufferers think differently

This particular willingness can now be made visible in the EEG. Of course, you don't set up traffic lights in the laboratory. But the principle is the same. The usual procedure is, for example, that the patient connected to the EEG puts on headphones and locked glasses with built-in lights. The patient is told that, for example, three seconds after a cue (e.g. a short click) is heard in the headphones, the lamp in the glasses lights up. As soon as this light signal comes, the patient should press a button.

In order to get meaningful results, this process is usually repeated at least 30 times. The pause between the individual measurements is of different length, so that the patient never knows exactly when the next cue will come. The individual measurements are averaged with the help of a computer, and the level of the electrical voltage shift in the EEG can be determined very precisely on the basis of the mean values.

It turns out that the brain of migraineurs reacts differently to such tasks than the brain of healthy people or people with other types of headache. There are two abnormalities:

  • The voltage shift in the EEG - i.e. the zigzag lines on the paper or monitor - is significantly greater than in other people.
  • While the voltage shift becomes increasingly smaller in healthy people after several measurements, it remains high in migraine patients.

These measurements are important evidence that the brain of migraine sufferers evidently reacts particularly actively to stimuli. But not only that: While in healthy people the attention decreases more and more when the stimulus is repeated several times, the brain of the migraine patient remains constantly in maximum readiness. Apparently, the brain cannot “switch off” and is in the truest sense of the word constantly under “high voltage”. Interestingly, successful treatment of patients with medication to prevent migraines - so-called beta-blockers - can normalize this altered electrical behavior in the brain.

Practical: Modern model of the development of migraines

Migraine researchers have accumulated a great deal of knowledge over the past 100 years. The many individual findings - in addition to numerous others, the facts already mentioned on vascular theory, neurogenic inflammation and the excessive activity of the brain in migraine sufferers - are astonishing. However, this accumulation of knowledge also poses a major problem: the large amount of data makes it increasingly difficult to understand what is happening.

What is certain is that it is not a single factor that causes migraines. But I would like to offer you a theory that incorporates as much of the data found as possible. Although many of the assumptions of this migraine theory are not yet backed up in detail by research data, this model can relate a number of individual findings to one another in a meaningful way. I call it the "neurological-behavioral migraine theory".

The beginning of the migraine attack

According to this migraine theory, migraine patients have an innate peculiarity of stimulus processing in the brain - they are constantly under "high voltage". If certain triggering factors (so-called trigger factors) are added too quickly, too suddenly, too long or too intensely, a cascade of physiological changes, some of which take place simultaneously, is set in motion in migraine sufferers, which ultimately make up the migraine attack. The trigger factors are, so to speak, the drop that brings the barrel to overflow.

Which trigger factors are decisive in the respective situation can only be predicted in a small number of patients. For example, external stimuli such as stress, noise, irregularities in the sleep-wake cycle or daily routine, as well as certain foods come into question. Internal factors can also trigger an attack: changes in hormonal levels, hunger or changes in metabolism, for example due to medication.

Inundation with neurotransmitters

The basically increased activity of the brain plus trigger factor (s) now leads to a sudden and excessive activation in the brain. Far too many neurotransmitters are released within a very short time, especially the mood-regulating hormone ("happiness hormone") serotonin and other exciting neurotransmitters. The brain misinterprets the excessive release of messenger substances as the body's reaction to poisoning. The logical consequence is the activation of protective reflexes in the form of nausea and vomiting. However, these are biologically ineffective, since the excessive activation of the messenger substances was ultimately not initiated by a real poisoning via food intake, but by the excessive processing of stimuli and the excessive concentration of the nerve messenger substances in the brain cannot be eliminated by vomiting. Senseless nausea, nausea and vomiting are the result.

The emergence of the aura symptoms

At the same time, the excessively released excitatory neurotransmitters can trigger a so-called “spreading depression” - in a region of the cerebrum that is responsible for processing sensory impressions. "Spreading Depression" means something like "spreading dampening (of nerve cells)". It is she who can produce the aura symptoms in the migraine sufferer. The respective brain cells are initially overexcited and then fall into a state of reduced activity. This disturbance of the nerve cells and the associated reduced blood flow spreads over the brain area at a speed of three to six millimeters per minute. This is exactly the speed that the aura symptoms also show as they spread. The nerve cells on the spreading front always fire like mad, only to fall into a state of lethargy after the front has advanced. This is most noticeable in the form of the aura that is characterized by abnormal sensations: The aura begins, for example, with a tingling sensation in the fingertips. The tingling sensation wanders up the arm to the tongue over the course of 30 to 60 minutes and takes the path that is marked out by the disturbed brain cells in the cerebral cortex. After the tingling sensation, numbness often remains that corresponds to the subdued excitation of the brain cells and, like the other aura symptoms, eventually disappears.

The pain sets in

The spreading depression disrupts the electrolyte concentrations (for example of the mineral magnesium) in and between the cells. The result is that neighboring pain receptors are excited and are thereby enabled to convey pain. It takes about 30 to 60 minutes for inflammatory messenger substances to be released and cause neurogenic inflammation in the area of ​​the blood vessels in the meninges. Because the inflammation spreads in the blood vessels - and therefore also the sensitivity to pain - the consequences of the inflammation add up both spatially and temporally: the migraine pain typically spreads across different areas of the head and increases in intensity over time.

This lasts until the body's compensation mechanisms take effect. This includes the breakdown of the nerve messenger substances released in the initial phase and the activation of the body's own pain defense systems.It can take several hours, in individual cases up to three days, until these mechanisms are able to compensate for the dysregulation in the central nervous system.

With or without aura?

Which mechanisms lead to a migraine with or without aura have not yet been clearly established. One possible explanation is that the processes described in migraines with aura initially run much faster and thus lead to relevant blood flow changes in the central nervous system, which can be held responsible for the development of the aura. In migraines without aura, on the other hand, a very slow, only gradually developing mechanism could be set in motion, the disturbance of which does not lead to a noticeable change in the blood flow, but then also releases the inflammatory neurotransmitters and induces pain in the area of ​​the blood vessels lead in the meninges.

Radio interference in the brain

The messenger substances released too much at the beginning of the attack must of course also be broken down again. However, the rapid breakdown of these messenger substances leads to a phase of messenger substance exhaustion - the stores of the important nerve messenger substances are initially empty and have to be replenished. But without messenger substances, no or no correct conduction of stimuli in the brain. Consequence: The global information processing in the brain is disturbed.

The brain stem is also affected

The result of the inflammation induced by the excessive release of neurotransmitters is also an activation of the nerve centers of the brain stem. This means that areas of the body can also be included in the experience of pain that were initially not involved. These include in particular the shoulder and neck muscles as well as areas of the skull that are not directly affected by the neurogenic inflammation.

This sensory overuse could also explain the fact that normally non-painful stimuli are experienced as extremely obnoxious during the migraine attack, especially in the form of light and noise oversensitivity. Therapeutic maneuvers, such as massages, heat applications or trigger point injections in the area of ​​the head and neck muscles, can reduce the permanent subliminal stimulus influence in the brainstem and thus be experienced as pleasant by the migraineurs without, however, changing the persistence of the migraine attack. The influence of mental mechanisms on migraines - in particular cognitions, emotions, abilities to act actively on stimuli (e.g. coping with stress), and mental relaxation - can be understood by activating the body's own pain control systems.