Synonyms in a broader sense
migraine attack, seizure-like headache, hemicrania, hemicrania, unilateral headache, migraine attack, unilateral headache
Definition
Migraine is usually a pulsating headache that occurs in attacks and has a hemiplegic character. The pain usually begins on one side of the forehead, temple and eye. In almost all cases the headache attack is preceded by a so-called aura.
This is a visual disturbance that manifests itself through flickering or jagged light or loss of field of vision. In many cases the headache is accompanied by symptoms such as vomiting and dizziness. Headaches with nausea or headaches with abdominal pain also often occur together.
EpidemiologyGender Distribution
Large studies have shown that about 10% of the Central European population suffer from migraine. The female sex is more frequently affected with a distribution of 2:1. The first onset of hemiplegic headache usually occurs in puberty or early adolescence, with girls and boys being affected about equally frequently in childhood.
The first occurrence of migraine almost always occurs between the ages of 10 and 30. A first occurrence after the age of 50 is rare and must always be examined for alternative causes of headache. The pathogenesis of migraine is ultimately and conclusively unclear.
There are currently various more or less reliable approaches to the development of migraine. It is known that the human brain has no pain receptors. Pain is caused exclusively by the meninges (dura mater = hard meninges and pia mater = soft meninges), which surround the brain and spinal cord, and their blood vessels (arteries and veins).
Many migraine attacks begin in the morning hours from sleep. A disturbance of the sleep – awake – rhythm can lead to migraine. An important substance in this sleep-wake rhythm is the messenger substance serotonin (5 HT or 5-hydroxytryptamine).
This messenger substance can be released by alcohol, especially red wine from the storage site, the blood platelets (thrombocytes) and provoke a seizure. Other food-related triggers are said to be chocolate via the ingredient phenylatyalmin or cheese via tyramine. Furthermore, the “stress hormones” adrenalin and noradrenalin have an important influence on the development.
Both hormones regulate the vascular width of the brain vessels. One theory of migraine development describes a temporally and locally limited circulatory disorder of the brain. This leads to a narrowing of the blood vessels of the brain and the meninges, which can lead to neurological symptoms.
This circulatory disorder can be detected with highly specific examinations such as positron emission tomography (PET). The frequent detection of a circulatory disorder in the posterior part of the brain leads to the assumption that there is a so-called migraine center. The circulatory disorder can typically be detected before the actual migraine and coincides with the phase of the aura (see below).
Another theory describes a temporary permeability of the vessel walls for blood components into the brain environment, which activates the body’s own degradation system (macrophages). This vascular permeability is caused by extreme vasodilatation, which follows the phase of vasoconstriction. In the course of these degradation processes, a localized inflammatory reaction occurs around the blood vessels of the meninges.
Since the meninges are very sensitive to pain, the severe headache develops, which is therefore partly perceived in a pulse-synchronous manner. This means that the pulse beat causes a throbbing pain. This form of inflammation is sometimes also called neurogenic inflammation.
It seems to be certain that there is a disturbance of a certain calcium channel (PQ – calcium channel) of the brain. Through the exchange of calcium ions inside and outside the cell, a voltage can be generated, which enables brain cells to “communicate” with other brain cells. A disturbance of the calcium channel leads to a disturbance of communication with the following neurological symptoms and headaches.
An aura can be detected in approximately every 5th -10th migraine patient (10 – 20%). These are neurological failures of the eye 10 – 60 minutes before the actual migraine attack begins. In exceptional cases, it can last for several hours.The cause should be a temporal and local circulatory disturbance of the brain. Typical neurological symptoms of the aura are
- Blurred blurred vision (flicker scotoma)
- Visual field failures, which means that parts of the field of vision are blinded by the eye, which is often not directly noticed, because the brain replaces the failed parts
- Double images
- Emotional disorders
- Speech disorder
- Partial to hemiplegia and numbness (
