Introduction
Another recent application of the beta-blocker is migraine. In this case, beta-blockers are initially not used for the direct acute treatment of migraine, but for prevention. Especially for patients who suffer from strong and regular migraine attacks that recur at regular intervals, a preventive treatment with beta-blockers should be considered.
When beta-blockers are used for the treatment or prophylaxis of migraine, one makes use of the versatile effectiveness and the effect profile of beta-blockers. These would be, on the one hand, the effect which is also used for the treatment of high blood pressure and cardiac arrhythmia and which relates to heart rate reduction. Beta-blockers reduce the docking of adrenaline to the receptors by blocking the beta-receptors, which are also present in the heart muscle.
This lowers the heart rate and also blood pressure. Migraine patients usually complain of strong throbbing pain when the pain is of a painful character, mostly one-sided. So far, this pathomechanism has not yet been clearly clarified, but a close relationship between migraine pain and pulse is suspected. The throbbing migraine pain often has a pulse synchronisation.
We’re working beta blockers for migraines?
The idea behind the use of the beta-blocker is to reduce the heart rate. When the heart beats slower, the painful impulses are also “sent” more slowly. Blood pressure also has an effect on migraine pain.
For example, a strong pain stimulus in the area of the head leads to a slight increase in blood pressure (pain reaction of the body) even in non-blood pressure patients. This in turn leads to an increase in pain. A vicious circle begins.
Although the blood pressure of migraine patients is not extremely high and at some point stagnates in its rise, treatment to lower blood pressure has a positive effect on the sensation of pain. A further property of the beta-blocker is also used. Beta-blockers also have an effect on the transmission of stimuli to certain nerves by blocking receptors.
This is reduced after taking beta-blockers. In this case, the reduced transmission of the pain stimulus is mainly used. On the one hand, the reduced effect of adrenaline (due to blocked beta receptors) leads to a reduced pain sensation in the brain, on the other hand the actual pain transmission is also slowed down.
The sensation of pain takes place more slowly, more retarded and is no longer perceived so intensively. The side effect of the beta-blockers can be regarded as undesirable and disturbing on the one hand, and on the other hand as part of the actual treatment. Because beta-blockers, if taken initially, can also lead to fatigue and sedation.
Patients who are plagued by migraine pain often find this type of sedative effect pleasant and relaxing. A disadvantage is the dose-effect relationship of the beta-blocker. The body mimics beta receptors when the others that are present are regularly blocked.
It does this for this reason, so that the adrenergic substances can find a receptor and act despite the blockage. The more receptors are replicated, the lower the beta-blocker effect. When this habituation process occurs, one must usually increase the dose of beta-blocker to achieve the same effect.
Also for this reason the beta-blocker should not be discontinued abruptly, because the body would then react with an increased effect. This would most likely be noticeable by a rapid to racing pulse (so-called tachycardia) and also an increase in blood pressure. It is also important to pay close attention to how the pulse and blood pressure develop under a beta-receptor blockade.
Thus, if the blood pressure or pulse is too low, countermeasures must be taken quickly to avoid circulatory instability. There are numerous drugs that are counted among the beta-blockers. Not all of them are used in migraine treatment.
Despite their common structure, this is mainly due to the different bioavailabilities, i.e. flooding and outflow. Beta-blockers such as metoprolol and propanolol are used in the treatment of migraine, and here especially for the prophylaxis of new migraine attacks. Beta-blockers are not used for the acute treatment of migraine attacks.
The reason is that the effect of newly applied beta-blockers only occurs after a few days and is therefore not necessary for acute treatment. Especially if patients suffer from regular migraine attacks, the use of a beta-blocker should be considered. These include very severe migraine attacks and migraine attacks that occur several times a month.
In this case, treatment with metoprolol or propanolol should be started after appropriate neurological clarification. Initially an initial dose of 2.5 mg should be chosen. However, if the desired success is not achieved, the beta-blocker can also be increased to 5 mg. Every adjustment or change of the beta-blocker should be made under close monitoring of blood pressure and heart rate. If a migraine attack occurs despite the use of beta-blockers, the medication should not be discontinued but continued.
All articles in this series:
