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Relationship between migraine and stroke

History of a relationship study between the pathologies

The relationship between migraine and stroke was noticed for the first time by Fere in 1881. He made one of the earliest and most comprehensive descriptions of 12 patients who suffered from a classical migraine case combined with sensorimotor disorders and permanent speech disorders. Based on these initial and latter studies conducted by the researcher, it was suggested that the cause of stroke in patients who also suffered from migraine is a spasm of the cerebral vessels.

Pathomorphological studies of fatal cases of cerebral infarction in patients with migraine, did not reveal the presence of morphological markers of a stroke. As a result of this, doctors explained these disorders by the cerebral vasospasm. There was no connection found between permanent neurologic disorders and morphological changes (in particular, angiographic changes) in patients with migraine.

More than half a century later - in the mid-1950s - scientists suggested that repetitive regular attacks of severe migraine could locally damage brain arteries. This can lead to thromboembolic stroke or arterial dissection in the interictal migraine period. A hypothesis has been formulated to explain the origin of persistent neurological disorders in migraine. It was the hypothesis of local vascular disorders that occur during the vasodilator phase of a migraine attack.

In the past 50 years, clinical studies have been conducted, which showed convincing evidence of the relationship between cerebral infarction and migraine. These verified cases were conducted by using computed tomography (CT), angiography, MRI and positron emission tomography.

Kaul and co-authors were among the first ones to angiographically demonstrate the occlusion of the main trunk and branches of the posterior cerebral artery in patients with migraine. This was followed by such symptoms as spontaneous pain, hemiparesis, hemianopia, dysphasia and transient amnesia. This deficiency appeared during the migraine attack in all patients described by the authors of the study.

Vasospasm associated with migraine was first documented arteriographically in 1964. A 40-year old patient suffered from a left-sided hemianopia with numbness on the left half of the body. This was followed by a right-sided hemicranial pulsating pain. The angiography showed a weak filling of the intracranial carotid system when neurological defect most prevalent. During the headache, which developed later on, the authors noted a complete restoration of the filling of the internal carotid artery. Later on, these observations were repeatedly proved by evidence in similar studies.

The widespread use of CT scanning began in the mid-1970s. It has verified changes similar to a cerebral infarction in patients with migraine. A series of CT studies on migraine patients showed a prevalence of these morphological changes ranging from 34% to 71% - regardless of the presence of a neurological defect. Cases on 94 patients with recurrent migraine pain were published. In 6 patients, changes similar to the infarction were found. In 4 cases, doctors noted a decrease in the density of brain matter in the region of the occipital cortex and defects in the vision. Edema of the brain tissue - especially where periventricular white matter is - was found in 6 other patients.

Some time later the doctors managed to conduct a CT scan of several migraine patients during a migraine attack. The image obtained showed the presence of low density zones in the posterior parts of the brain. These zones completely regressed when the headache disappeared. Interestingly enough, morphological changes were localized in the posterior basin of the circulation in most cases.

Modern understanding of the problem

Introduction of MRI into clinical practice significantly optimized studies about the connection between stroke and migraine. The main advantage of MRI over CT scan was that MRI was able to differentiate migraine-associated strokes from strokes that are were not associated with migraine. For the researchers, the most interesting studies conducted by MRI observations are the detection of the presence of white matter damage in patients with migraine. This damage is detected in about 30% of routine MRI studies. This damage is found in 12% of cases in clinically healthy people. In a number of studies, such changes were most often observed in migraine subtypes. These subtypes were associated with neurological manifestations of the aura. A meta-analysis of seven MRI studies comparing frequency of these migraine disorders with its prevalence in the population, showed that migraine patients have an increased risk of developing white matter damage. The risk is on average 3.9 times higher than in non-migraine patients.

Regardless of connection between migraine and cerebrovascular disorders, repetitive episodes of headache in migraine patients can cause complications associated with either disruption in the functioning of certain CNS structures, or with permanent changes in them. One example of such complications are deposits of iron in patients with migraine which are not associated with heme. They are located in areas of the brain stem that correspond to the gray matter.

Currently, migraine is considered to be a risk factor for subclinical brain damage. Presence of infarctions in the posterior vascular pool is higher in migraine patients. The damage to the deep white matter is greater as compared to the control group of non-migraine patients of the corresponding age. The highest risk of cerebellar infarction is ascribed to migraine with aura. Migraine in general is also considered a risk factor for deep damage of white brain substance.

Prevention of stroke in patients with migraine

Currently, the prevention of stroke is achieved by taking medications that have modulatory and neurotrophic properties. These medications improve the plasticity of the nerve tissue. They also normalize metabolic processes in the peripheral and central nervous systems. Drugs of combined action (the ones that normalize both microcirculation and metabolism) include Vasobral. It is known for treating cerebrovascular diseases and preventing migraine.

This medicine includes a-dihydroergocryptin (blocks a1- and a2-adrenoreceptors) and caffeine which has a stimulating effect on serotonergic and dopaminergic receptors of the central nervous system). Vasobral produces antihypoxic, neuroprotective and vasoactive effects. It decreases the aggregation of erythrocytes and platelets, improves metabolic processes and blood circulation in the brain and increases resistance of brain tissues to hypoxia. All this produces a good preventive effect both for migraine and cerebrovascular pathologies.


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