Migraine with and without aura: symptoms and treatment

Oh gods, gods, why are you punishing me? Yes, no doubt! It’s her, her again, the invincible, terrible disease of hemicrania, which makes half your head hurt. There is no remedy for it, there is no salvation. I’ll try not to move my head.. This is exactly how Pontius Pilate describes his headache in the immortal work of M.A. Bulgakov. The main character is so afraid of pain that he “cowardly thinks about death.” Unfortunately, not every person suffering from this illness finds his Yeshua Ha-Nozri, who, as we remember, not only recognized the illness, but was also able to heal it. But this is a literary work, and we will try to analyze this disease from the point of view of modern medicine.

What does migraine with aura mean?

Migraine with aura is a disorder characterized by recurrent episodes of reversible local neurological symptoms (aura), usually increasing over 5-20 minutes and lasting no more than 60 minutes.

“Aura” is a term by which doctors mean the following:

• Visual impairment
  . These can be lines, lights, spots, flickering. In severe cases, loss of vision. All manifestations are reversible.
• Sensory perception disorders
  . It seems that goosebumps are crawling all over the body, the person feels tingling, and there may be areas of numbness. All this is also reversible.
• Speech disorders
  , which also go away along with the attack.

In 73% of migraine attacks with aura, the headache begins not after the end of the aura, but during the aura itself and can be accompanied by other migraine symptoms - nausea (51%), photophobia (88%) and phonophobia (73%) i Morozova O.G. Migraine: new international criteria for diagnosis and principles of therapy based on evidence-based medicine and our own clinical experience / O.G. Morozova // International Neurological Journal. — 2021. — No. 3 (81). — pp. 131-138. . It happens that a panic migraine develops. Its complications are fear, anxiety, etc.

Migraines with and without aura are the same. A person usually feels a throbbing pain in one side of the head. Often it is concentrated in the eyeball. The pain intensifies with movement, sound and light stimuli. It can last from 4 hours to 3 days. At this time, it is impossible to lead a normal lifestyle. A person wants to be left alone in a dark and cool room, freeze, hide under the blanket. Typically, patients describe the pain as “bursting,” “splitting,” “about to burst,” “every sound like a hammer on the head.” And even after an attack, the consequences persist. The person is apathetic, tired and overwhelmed. It takes more than one day to recover.

And first a little history

The French word “migraine” (migraine) came to us from Latin; this disease was also called hemicrania (hemicrania - “half of the head”). The first written references to migraine symptoms are found in the cuneiform tables of the ancient Sumerians, which are more than 7,000 years old. Perhaps our ancestors suffered from migraines back in the Neolithic. Attempts to treat this particular disease can explain some of the skulls with traces of trepanation. Most likely, the ancient Homo sapiens tried to “release the evil spirit” that, in their opinion, was lodged in the skull. Migraine was well known to the healers of Ancient Egypt - papyri with recipes for its treatment have survived to this day. The first detailed description of a disease with severe headache, very similar to migraine, was made by the ancient Greek physician Aretaeus of Cappadocia in his book “On Acute and Chronic Diseases.” This healer called the disease heterocrania (heterokrania - another, alien head). He also compiled the first detailed classification of migraines and described several cases of death due to migraines, which, most likely, were actually cerebral hemorrhages. Celsus, a physician who worked in the 1st century BC, believed that the disease lasts throughout life, but does not threaten it. He put forward the (incorrect) theory that migraine attacks are usually accompanied by fever. There are also mentions of migraine in Hippocrates and Avicenna (in the “Canon of Medical Science”). However, the name given by the ancient Roman physician Claudius Galen has survived to this day - hemicrania. Galen thereby emphasized one of the distinctive features of this disease - the localization of pain in only one half of the head. The Greek physician Eginat identified factors that provoke migraine attacks, such as noise, shouting, bright light, strong smelling substances, and drinking wine. In the 4th century AD, Caelius Aurelian drew attention to the fact that migraine pain can be localized in the depths of the eye socket and radiate to the back of the head. In the 6th century AD, Alexander of Tralles pointed out the difference between migraine (hemicrania) and other headaches (cephalgia). At the same time, he believed that the source of headaches were disorders of the gastrointestinal tract and proposed replacing bloodletting, which was practiced to treat the disease, with enemas. With the advent of the Middle Ages, difficult times came for migraine sufferers. They were accused of having connections with the devil, and they tried to “drive out the possessing demons” with torture and torment. Only in the 16th century did scientists and doctors return to this problem. Various theories have been put forward about the origin of hemicrania and methods of its treatment. The disease was associated either with visual impairment or with lesions of the digestive system. Until the end of the 19th century, the main methods of treatment were bloodletting (6 ounces at a time, equivalent to 150 grams) and emetics. The period of the late 19th and early 20th centuries was characterized by a surge of activity in the study of migraine. For example, Flatau (Polish neurologist), in his monograph, which most fully describes the then ideas about migraine, provides references to more than 470 works on this problem. Among the great and famous people, Julius Caesar, Calvin, Linnaeus, Pascal, Beethoven, Darwin, Marx, Nobel, Heine, Edgar Allan Poe, Maupassant, Wagner, Chopin, Tchaikovsky, Nietzsche, Freud suffered from migraines.

Differences from migraine without aura

Migraine without aura is called “classic”. Approximately 80% of patients suffer from it. A migraine without an aura manifests itself as throbbing pain at one point. It is not preceded by any visual, auditory or sensory impairment. Sometimes people don’t even realize that it’s a migraine, but think that they just have a headache. For this reason, patients do not go to the doctor, which is fraught with consequences.

You have migraine without aura if the following symptoms are present:

• 5 episodes of pain.
• The attacks last from 4 to 72 hours if you do not take medication.
• The pain throbs and is concentrated on one side of the head. The forehead, neck, and then the face or back of the head may hurt.
• With any physical activity the pain gets worse.
• There may be nausea, fear of light, sounds, voices.

What are the characteristics of migraine with aura?

About 20% of patients experience an aura. But only a few say that it occurs with every attack. The most common symptom of an aura is visual disturbances. Less commonly – sensory organ disorders (tingling, numbness, goosebumps). Aura symptoms are divided into positive and negative. In the first case, something is felt, and in the second, the fields of vision disappear or the hands go numb. Another property of the aura is dynamism. That is, a gradual increase in symptoms, and then their gradual decline. Usually the aura is replaced by a headache, but sometimes the aura appears on its own.

Migraine with aura is characterized by the following symptoms:

• Two episodes of migraine without aura.
• The presence of an aura for 1 hour or more before pain occurs. In this case, the following neurological symptoms appear - one or more:
• visual disturbances – photophobia, blinking, black spots in the field of vision, flickering arches, lines, zigzags, incorrect perception of objects in the field of vision;
• sound disorders, mainly intolerance to any sounds;
• speech problems;
• sensory disturbances – tingling, burning, numbness, etc.;
• impairment of motor abilities, such as sudden weakening of muscles on one side of the body.

Clinical picture

Clinically, a migraine attack without aura consists of three phases: prodrome, migraine attack, postdrome. Symptoms of the prodrome usually develop several hours before a migraine attack and include increased sensitivity or, on the contrary, decreased perception, irritability, tearfulness, excessive yawning, addiction to special foods (most often sweet), drowsiness, swelling. A migraine headache is one-sided, often pulsating, worsens with physical activity, and is accompanied by nausea and repeated vomiting. “Painful” behavior is typical: the patient tries to go to bed, retire to a darkened room, cover his head with a scarf or towel, and avoids bright light and noise. Upon objective examination, patients are asthenized, emotionally tense, and in some, a swollen temporal artery is detected on the affected side. Often patients try to compress the temporal artery, as a temporary cessation of blood flow reduces the throbbing pain. There are no focal changes in the neurological status, but quite often on the side of the headache there is pronounced pain in the muscles of the neck and skull, and tension during palpation. With migraine with aura, a prodrome can also occur, but most often the first phase is an aura, the clinical picture of which depends on the localization of the pathological process. In 90% of patients, it manifests itself in the form of visual disturbances, usually in the form of lightning and zigzags, flashes, sparks, combined with flickering spiral-like contours or scotomas. Sensory disorders - paresthesia - are in second place in terms of frequency of occurrence; first, the hand is usually involved in this process, then numbness spreads to the face and tongue (the so-called spreading cortical depression occurs, combined with regional oligemia). The aura symptoms regress completely after 20–30 minutes (up to 60 minutes), and before the attack there is usually a “free” interval without headache, which lasts no more than an hour, then a migraine attack develops. After the end of the attack, a postdromal period begins, lasting for 24 hours. Patients feel fatigue, muscle pain, swelling, frequent urination, and euphoria. Scientific American 299, 56 - 63 (2008) Ophthalmoplegic migraine is characterized To make a diagnosis of “Migraine with aura,” the patient must meet at least two criteria from points 1 and 2, and criteria 3 and 4 are also mandatory.

1. The aura must have at least one of the following characteristics:
   Visual disturbances that occur after the aura (flashes, dots, lines, circles before the eyes)
2. Tactile sensations that disappear after the aura (tingling, numbness)
3. Speech disturbances completely disappear after the aura
4. There are at least 2 symptoms in the aura:
   Visual and tactile symptoms are always the same before attacks
5. Aura symptoms develop gradually
6. The duration of each symptom is 5-60 minutes
7. Headache attacks meet the criteria for migraine.
8. The symptoms are not related to other diseases.

Retinal migraine is a very rare disease, which is a paroxysmal bilateral visual impairment in the form of scotoma or loss of visual fields, which lasts 10–15 minutes. Visual disturbances alternate with attacks of migraine without aura or migraine with ophthalmic aura.

Causes of migraine

The mechanisms of migraine development are not fully understood. A predisposing factor in the development of the disease is hereditarily determined dysfunction of vasomotor regulation. Approximately 70% of migraine patients have close relatives with a history of migraine-like headaches i Morozova O.G. Migraine: modern ideas about classification, diagnosis, therapy and prevention (part I) / O.G. Morozova // Emergency Medicine. - 2012. - No. 4 (43). — P. 32-41. .

There are two groups of factors that influence the course of migraine: those that worsen the course of migraine as a whole and those that provoke an attack.

Factors that worsen the course of migraine . In a patient with migraine, factors such as emotional stress, frequent consumption of alcoholic beverages, and other environmental influences can cause a long-term (over several months or years) worsening of the disease in the form of an increase in the frequency and/or intensity of attacks.

In patients with migraine, precipitating factors increase the likelihood of attacks; their effects usually appear within less than 48 hours. Despite the fact that migraine triggers have been well studied in a number of epidemiological studies (for example, the influence of menstruation i Koreshkina M.I. Modern aspects of diagnosis and treatment of migraine / M.I. Koreshkina // Neurology, neuropsychiatry, psychosomatics. - 2013. - P. 92-96.) and clinical (the effect of aspartame, chocolate, etc.) studies, in each individual case it is not always easy to establish a direct causal relationship between the provocateur and a migraine attack.

Factors provoking migraine paroxysms (migraine triggers) i Morozova O.G. Migraine: modern ideas about classification, diagnosis, therapy and prevention (part I) / O.G. Morozova // Emergency Medicine. - 2012. - No. 4 (43). — P. 32-41. :

• dietary: hunger, irregular nutrition, some foods (chocolate, cheese, nuts, alcohol (red wine), creams, yogurt, chicken liver, avocado, citrus fruits, bananas, concentrated soups, fried pork, sausages, pizza, coffee, cola, tea);
• hormonal: menstruation, ovulation, estrogen replacement therapy, oral contraceptives;
• psychological: emotional stress, anxiety,
• depression, fatigue;
• weather changes;
• exercise stress;
• lack or excess of night sleep;
• stuffiness, odors (smell of perfume);
• visual stimuli (flickering or bright light);
• cold;
• noise;
• staying on top.

Pathogenesis

Scientific American 299, 56 - 63 (2008) The pathophysiology of migraine has always remained mysterious, so by the end of the 20th century, three directions in its pathogenesis had emerged. All of them have received experimental and clinical confirmation. The first direction is based on the assumption: attacks are associated with narrowing or expansion of intra- and extracranial arteries. This is one of the initial theories. She suggests that migraines are caused by sudden constriction of intracranial vessels, causing cerebral ischemia and resulting aura. Following this, expansion of the extracranial blood vessels occurs, which causes headaches (Wolf, 1930). the shunt theory was proposed (G. Hake, 1960s). The headache was explained by the fact that during an attack, blood tends to pass from the artery directly into the vein through the arteriovenous shunt, bypassing the intracranial capillaries. This causes cerebral ischemia, which is the main cause of headaches. The platelet theory suggests that migraine is caused by a primary platelet disorder. When platelets stick together, a significant amount of the neurotransmitter 5-hydroxytryptamine (5-HT) is released. This theory is proven by the fact that platelets of migraine patients have a more pronounced ability to stick together than those of healthy people, and are more sensitive to factors that provoke the release of 5-HT. The second direction explains pain by a discharge arising in the trigger zone of the midbrain (possibly in the serotonergic dorsal raphe nuclei of the brainstem). Recent positron emission studies have shown that the dorsal region near the midbrain aqueduct is activated during migraine. This activity is not reduced even by sumatriptan, even if it reduces migraine pain. These areas of the brain contain serotonin-, norepinephrine-, endorphin- and GABAergic systems. It is assumed that the triggering factor for migraine is the disturbance of this particular complex of neurophysiological interactions in this area. A sharp release of serotonin leads to vasoconstriction of blood vessels (prodromal period), however, 5-HT is quickly processed and removed from the blood, which leads to vasodilation and the development of a headache attack. Therefore, a number of researchers (Vein A.M. et al.; Gtsbel H.) believe that migraine is a primary neurogenic cerebral dysfunction with the presence of genetically determined brain stem failure, severe cortical hyperactivity with periodically occurring dysfunction of the hypothalamus. Finally, the third direction is associated with the excitation of neurons of the trigeminal nucleus in the brain stem (the so-called trigeminovascular system). The axons of these neurons terminate in the arterial walls and release vasoactive neuropeptides. (M. Moskowitz et al., 1989). According to this theory, the source of headaches are the cranial vessels and vessels of the dura mater, which have trigeminal innervation and are under the control of the mid-stem structures of the brain. During a spontaneous migraine attack, the brain stem structures located near the aqueduct of Sylvius, in the area of ​​the locus coeruleus and the reticular formation, are activated, which are a kind of generator of a migraine attack. This leads to antidromic activation of the trigeminal-vascular system with the release of neuropeptides into the vascular wall (substance P, a neuropeptide associated with the gene that controls calcitonin), causing their dilatation, increased permeability and, as a consequence, the development of neurogenic inflammation in it. Aseptic neurogenic inflammation activates the nociceptive terminals of the afferent fibers of the trigeminal nerve located in the vascular wall, leading to the formation of a feeling of pain at the level of the central nervous system. As already mentioned, special attention is currently paid to serotonin as a key link in the pathogenesis of migraine. It is assumed that it is the triggering factor for the development of migraine, and the attack itself can occur through any of these mechanisms or a combination of them. The serotonin theory is also confirmed by the fact that during a migraine attack:

• The content of 5-HT in platelets drops sharply (by 30-40%)
• There is an increased content of serotonin metabolic products in the urine
• Migraine attacks can be provoked by taking reserpine, which promotes the release of 5-HT
• Known anti-migraine drugs (ergotamine) interact with 5-HT receptors
• Intravenous serotonin may relieve migraine attacks.

Types and symptoms of migraine auras

Let's look at the main types of auras and how they manifest themselves.

Visual or ophthalmological

This aura is called “classical”. With it, visual images appear - flashes of light, curved or straight lines, flickering objects, white or golden figures, spherical images, etc.

Symptoms develop over 5-30 minutes. Positive ones can be replaced by negative ones. The duration of the aura can reach 1 hour. The image usually appears in the center of the visual field. It gradually increases and moves to the periphery. A scotoma remains behind him

– dark, “blind” area. During the aura or within an hour after its appearance, pain occurs. When the attack ends, any disturbances go away without consequences.

Retinal

With such an aura, scotomas or blindness in one eye occur. Symptoms persist for up to 1 hour. The headache comes after scotomas in about an hour, but can also occur before them. This is a rare type of aura. There is an assumption that the symptoms appear due to spasm of the central retinal artery. In most patients, retinal migraine attacks alternate with migraine attacks with or without classic aura.

Auditory

Auditory auras are hallucinations with sound. Ringing in the ears may occur, and patients sometimes hear music or voices. Doctors associate this aura with epileptic activity in the cerebral cortex, in its temporal region.

Speech

It manifests itself as a speech disorder because it affects the speech centers of the brain. Before an attack of pain, for a few minutes, no more, it is difficult or impossible for a person to speak. He can rearrange syllables in words, letters, repeat the same thing. At the same time, the consciousness is absolutely pure.

Vestibular

This is an aura in the form of movement disorders - dizziness. A fairly common phenomenon that can be hidden or obvious. In the second case, a person “sicks” even with small loads. In the first, violations can only be detected within the framework of an examination. According to the ICD, 2 forms of vestibular migraine are distinguished:

• Basilar
  - occurs rarely, mainly in teenage girls. The attack begins with visual disturbances, followed by dizziness, tinnitus, sensory disturbances, etc. Then, in 25% of cases, confusion occurs. Neurological symptoms persist for 20-30 minutes, then pain in the back of the head occurs. Without treatment, throbbing pain may persist for 2-3 days.
• Paroxysmal dizziness of younger children
  (benign). Occurs in children 1-4 years old. It manifests itself as short – from a few seconds to a few minutes – attacks of dizziness. The child loses stability, becomes anxious, and vomits. He may turn pale and sweat profusely. No headache. Attacks may recur over several months or years.

Vegetative

Often such auras are manifested by a feeling of heat, chills, cold, trembling; the face and neck may turn red or pale. Goosebumps may appear, and hairs may even rise on the skin. During an attack, the size of the pupil may change, and asymmetrically. Usually such an attack is part of a complex attack, and not an independent phenomenon.

Pathophysiology of aura in migraine

The aura is probably caused by cortical spreading - a “brain storm”. It is a wave of intense nerve cell activity that moves across an unusually large area of ​​the cortex (the folded outer layer of the brain) - and especially in the areas responsible for vision. COURTESY OF DAVID W. DODICK (Dodick); UNIVERSITY OF CALIFORNIA, IRVINE, MEDICAL CENTER (Gargus); TAMI TOLPA (brain illustrations); COURTESY OF NOUCHINE HADJIKHANI (brain scans); MIGRAINE ACTION ASSOCIATION AND BOEHRINGER INGELHEIM (aura art) Scientific American 299, 56 - 63 (2008) Following the hyperexcitability phase, there comes a period of relatively long inhibition of nerve cells, during which neurons are in a state of “suspended activity”, when they cannot be excited. If we look at this in more detail, then: neural activity is controlled by precisely synchronized flows of sodium, potassium and calcium ions across the membrane of the nerve cell through ion channels and pumps, providing the resting cell with large amounts of potassium and small amounts of sodium and calcium. The neuron “discharges” and releases neurotransmitters when the flow of sodium and calcium ions rushes through the opening channels and depolarizes the membrane, as a result of which its inner surface becomes positively charged relative to the outer one. After this, the cells hyperpolarize for a short time: allowing potassium ions to rush outward, they now acquire a strong negative charge from the inside relative to the outer surface. The hyperpolarization closes the sodium and potassium channels, and soon after its discharge the neuron returns to a resting state. However, after intense stimulation, neurons may remain overly hyperpolarized or inhibited for a long time. The phase of hyperexcitability and subsequent inhibition, which characterize cortical spreading depression, may explain those changes in blood flow that were detected before the onset of migraine pain. When neurons are active and firing, they require a lot of energy and therefore a lot of blood (during this stage, blood flow increases up to 300%). This is precisely the picture that experts observed on tomograms of patients experiencing aura. However, later, during inhibition, silent neurons need less blood (the level decreases to normal).

Diagnosis of migraine with aura

The diagnosis is made by a neurologist, and it is he who should be contacted with such a problem as soon as possible. The doctor must rule out cysts, tumors, encephalitis and vascular pathologies that cause similar symptoms. Therefore, a neurological examination, CT or MRI of the brain is performed, and the patient is sent for a consultation with an ophthalmologist for examination and determination of visual fields.

An EEG (electroencephalography) is required, which provides information about the functional activity and characteristics of the brain biorhythm of a particular patient. Based on the EEG results, the doctor then selects medications for therapy.

Diagnostics

Diagnosis of migraine includes a thorough collection of complaints and medical history. Often, characteristic complaints, as well as the absence of objective neurological disorders, allow a diagnosis to be made.

However, occasionally it is necessary to clarify the diagnosis and exclude focal brain lesions, hydrocephalus and other pathological conditions. In such cases, they resort to neuroimaging research methods (MRI, MSCT, etc.), neurophysiological research (EEG, REG, polysomnography), and the general clinical minimum.

Features of migraine manifestations in children and pregnant women

In childhood, the peculiarity of an attack is its short duration, from 30 minutes to several hours, and bilateral pain. It becomes one-sided in adolescence. Most often, children experience pain in the temples, forehead, and periorbital area. The nature of the pain is also not the same as in adults. The pain is squeezing, pounding, slightly throbbing. Children describe the latter extremely rarely.

It is difficult for a child to talk about his feelings, so the intensity of pain is assessed using VAS - a visual analogue scale with points from 0 to 10. Scales with emoticons can be used - from smiling to crying.

During pregnancy, migraines can occur even in those who have not previously suffered from them. In 25% of cases it is migraine with aura. It is much more difficult to tolerate, and there is almost nothing to eliminate the pain due to the delicate position. The approved drugs - No-Shpa, Citramon or Paracetamol - do not help. During pregnancy, aura most often manifests itself as photophobia, withdrawal, intolerance to sounds and strong odors, very severe nausea and the urge to vomit. The main causes of pain during pregnancy:

• consumption of “dangerous” foods – cheese, chocolate, citrus fruits;
• lack of water in the body;
• constant lack of sleep because the stomach makes it very uncomfortable to sleep;
• stress, frequent worries;
• large weight gain;
• violation of metabolic processes.

How to treat migraine with aura and how to relieve pain effectively and quickly

Since it is almost impossible to avoid an attack if there is a trigger, you need to know ways to improve the condition, because migraine is not a death sentence.

The final diagnosis is made by a neurologist. He will tell you what to do, how to treat the disease, how to increase the intervals between attacks.

Treatment for migraines is based on eliminating the pain and making it happen as little as possible or go away altogether. NSAIDs or specific medications, most often triptans, may be used. Intravenous infusion therapy is also used to treat migraines. The effectiveness of pain relief is directly proportional to the time of taking the drugs. You can stop an attack when it has just begun. Unfortunately, many people miss this moment with the thought “what if it doesn’t hurt.” However, at the peak of an attack, the tablets have almost no effect, because with migraine gastrostasis in the intestines, the absorption of any substances is very difficult.

Alternative ways to alleviate the condition are physical activity, exercise therapy, physiotherapy, and psychotherapy. Massage of the collar area is especially useful, because muscle spasm in this area can provoke an attack. Recently, migraines have been successfully treated with injections of botulinum toxin type A. The injections make remission last longer, and in some cases relieve pain for a very long time.

Treatment of migraines using traditional medicine

Many traditional medicine methods can provide relief from pain.

Ginger root

Ginger has the ability to block prostaglandins, thereby reducing the severity of pain. The same principle applies to most NSPVs. Ginger tea is prepared at home. Ginger root is crushed, then added to boiling water and simmered for 10 minutes over low heat. Next, the tea is filtered and drunk plain or with lemon and honey.

Chamomile

Has an anti-inflammatory and calming effect. You need to take two tablespoons of chamomile in a glass of water and cook the mixture for 5 minutes over low heat. Next, you need to strain the broth and drink it plain or with lemon and honey.

Lavender

Lavender oil is used for inhalation. The solution is prepared as follows: a teaspoon of oil is diluted in three glasses of boiling water. Breathe over the resulting solution for 15 minutes. Lavender oil can be mixed with peppermint oil and apply the mixture to the temples, gently massaging it a little. It is best to combine massage and inhalation.

Treatment and prevention

Unfortunately, treating migraine is a rather long and expensive process. It should be said that the indication for hospitalization in a neurological hospital is only diagnosed complicated migraine and the presence of migraine status (duration of severe pain more than 72 hours); other cases are treated on an outpatient basis. In an outpatient setting, you can use the complex effects of drug and non-drug therapy, normalization of the daily routine and lifestyle modification. Among the drugs used for migraine are vascular drugs, drugs that affect the serotonin system, non-steroidal anti-inflammatory drugs, and antiepileptic drugs.

Non-drug methods of therapy include massage of the collar area and scalp, as well as some physiotherapy. Electrosleep is very effective, as it significantly reduces the frequency of attacks.

Normalizing the daily routine consists, first of all, of maintaining a strict sleep schedule, excluding lack of sleep, as well as excessively long periods of sleep. Among the general recommendations, it should be noted the need to exclude a number of foods from the diet (primarily alcohol), as well as regular exercise therapy.

More detailed information about migraine medications, dosages, treatment regimens, and general recommendations can be found in the following article (read the article!).

What happens if migraine is left untreated?

Migraine is not a harmless disease. The disease is identified by the World Health Organization as a risk factor for cerebral strokes. Numerous epidemiological studies have revealed correlations between migraine and stroke, especially in young women suffering from migraine with aura i Ashina M. Vascular changes have a primary role im migraine / M. Ashina // Cephalalgia. - 2012. - 32. - 5. - P. 428-430. . Migraine is associated with a 16-fold increase in the risk of stroke in pregnancy and the overall risk of cardiovascular events in women. Migraine can be a risk factor not only for stroke, but also for “silent” heart attacks and damage to the white matter of the brain. These changes most often occur in women suffering from migraine with aura, and are associated with severe and frequent migraine attacks i Hadjikhani N. Mechanism of migraine aura revealed by functional MRI in the visual cortex / N. Hadjikhani // Proc. Natl. Acad. Sci USA. - 2001. - 98. - P. 4687-4692. .

You shouldn’t treat the attacks as “survived and are fine”, you need to see a doctor and get treatment.

Migraine prevention

Prevention involves taking the medicine daily for a certain period of time. Which one is prescribed by a neurologist individually. This medicine will act not on the symptoms, but on the cause of the disease, preventing attacks from developing. However, drug prevention is not indicated for everyone. It is prescribed if:

• number of attacks – up to 8 per month or 2 per week;
• Even specific anti-migraine medications - Zomig, Relpax and other triptans - hardly help the patient;
• Triptans and analgesics cannot be taken due to contraindications;
• The patient has hemiplegic migraine, a rare hereditary disease that leads to stroke.

Migraine classification ICD-10

Migraine is coded G43: Diseases of the nervous system => Episodic and paroxysmal disorders => Migraine.

Etiology of the disease

Hereditary factors play a significant role in the occurrence of migraine, and the risk of developing the disease in children with a hereditary burden on the paternal side is 30%, and on the maternal side - 72%. If both spouses suffer from migraine, then the likelihood of it occurring in their children is 80-90%. About 20 mutations have been found in various loci that are in one way or another associated with this disease. At the same time, genetic preconditions are more significant for migraine with aura than for attacks without it. There are also factors that provoke an attack (but it can begin without them). These include, for example: - stress, nervous and physical stress, - food factors (cheese, chocolate, nuts, fish), alcoholic drinks (most often beer and red wine, champagne), - taking hormonal contraceptives, - sleep (lack of , oddly enough, an excess), including changes in time zones, - weather factors (changes in weather, changes in climatic conditions).

Sources:

1. Ashina M. Vascular changes have a primary role in migraine / M. Ashina // Cephalalgia. - 2012. - 32. - 5. - P. 428-430.
2. Hadjikhani N. Mechanism of migraine aura revealed by functional MRI in the visual cortex / N. Hadjikhani // Proc. Natl. Acad. Sci USA. - 2001. - 98. - P. 4687-4692.
3. Esin O.R. Migraine: Basic principles of treatment and prevention / O.R. Esin [et al.] // Clinician. - 2011. - No. 4. - P. 10-16.
4. Koreshkina M.I. Modern aspects of diagnosis and treatment of migraine / M.I. Koreshkina // Neurology, neuropsychiatry, psychosomatics. - 2013. - pp. 92-96.
5. Morozova O.G. Migraine: new international criteria for diagnosis and principles of therapy based on evidence-based medicine and our own clinical experience / O.G. Morozova // International Neurological Journal. — 2021. — No. 3 (81). — pp. 131-138.
6. Morozova O.G. Migraine: modern ideas about classification, diagnosis, therapy and prevention (part I) / O.G. Morozova // Emergency Medicine. - 2012. - No. 4 (43). — P. 32-41.

Treatment

So, treatment includes preventing an attack and stopping it. Basic goals :

• Reduce the frequency and severity of attacks, disability
• Reduce the use of poorly tolerated, ineffective, or unwanted pharmacotherapies for the treatment of acute pain
• Improve quality of life
• Avoid escalation of acute headache when discontinuing medications
• Teach and empower patients to manage their disease to enhance
• personal control of migraines
• Reduce headache-related distress and psychological symptoms

To begin with, all patients are given general recommendations for effective treatment of migraine:

• Compliance with work and rest schedules, avoiding stress and excessive overload
• Maintaining a sleep schedule and avoiding excess sleep on weekends, since excessive sleep often causes “weekend migraines”
• Regularity of meals, avoidance of dietary errors, especially those that are suspected as provocateurs of headache attacks
• Avoiding alcohol, especially red wine and beer
• Limiting intake of coffee and strong tea
• Limiting the use of simple and combined analgesics (no more than twice a week), which is associated with a high risk of developing “reverse headaches”
• Avoiding excessive late-night exercise, especially prolonged sitting with the head bent
• Elimination of possible migraine triggers specific to a particular patient (bright flickering light or light flashes, sudden loud sounds, strong odors)

Analgesics and NSAIDs are used to relieve a migraine attack.

Scientific American 299, 56 – 63 (2008) doi:10.1038/scientificamerican0808-56 The most acceptable and frequently used agent is acetylsalicylic acid. Its action is aimed at blocking the conduction of pain impulses by suppressing the synthesis of pain modulators (prostaglandins, kinins, etc.); the antiplatelet properties of the drug, which help improve capillary blood flow, are also important. Aspirin is prescribed in the first minutes or hours of an attack, no later than 2 hours later, 500–1000 mg per day. For severe attacks, combined analgesics are prescribed solpadeine, etc. Contraindications to the use of these drugs are the presence of gastrointestinal diseases, a tendency to bleeding, and individual intolerance. In second place in terms of frequency of use are ergot preparations, which have a powerful vasoconstrictor effect on the smooth muscles of the artery walls. They prevent neurogenic inflammation and have dopaminergic and adrenergic effects. Drugs in this group are highly effective (75% of attacks are stopped within 20–45 minutes). Example - Ergotamine tartrate 0.01 under the tongue, no more than 3 tablets per day. Fewer side effects occur with combination drugs containing ergotamine and caffeine. At the beginning of an attack, take 1-2 tablets, but no more than 6 tablets per day. Selective serotonin First generation drugs are used: sumatriptan (imigran), 50–100 mg orally; II generation drugs: zolmitriptan (zomig) - 2.5 mg orally, naratriptan (naramig) - 2.5 mg, rizatriptan (maxalt) - 5 mg; III generation drugs - eletriptan (relpax) - 40 mg, etc. Relpax has maximum selectivity to 5-HT/VD receptors, which ensures high efficiency and a minimum number of side effects. Migraine status is Apply:

• prednisolone 40–60 mg or dexamethasone 4–8 mg IV bolus,
• ergotamine IV drip,
• neuroleptics (cerucal, raglan, melipramine),
• tranquilizers.

In this case, the use of periosteal and intraosseous blockades is especially indicated. During the interictal period the following are used:

• β-blockers (anaprilin, atenolol, etc.),
• calcium channel blockers (verapamil, nifedipine),
• antidepressants (amitriptyline, Coaxil, Prozac, etc.),
• serotonin antagonists (metisegrid, peritol, etc.).

In older patients, nootropic and vascular drugs have a good effect. The use of muscle relaxants (sirdalud, mydocalm, etc.) is also effective; it is recommended to include anticonvulsants in treatment - carbamazepine, gabapentin. Drug therapy is selected individually for the patient. Long-term observation is required to keep the number of attacks to a minimum. Author: Denis Dokuchaev Translation of pictures from Scientific American: Georgy Borisov and Boris Lee References

1. Clinical guidelines for the diagnosis and treatment of patients with migraine from the American Academy of Neurology
2. Migraine: clinical picture, diagnosis, treatment, E. L. Sokov, L. E. Kornilova
3. Neurology national guide, 2015 Gusev, Konovalov
4. Migraine. Stepanchenkov
5. Principles of migraine treatment G.R. Tabeeva
6. Modern approaches to the diagnosis and treatment of migraine B.S. Frolov, V.I. Kurpatov.
7. Migraine and epilepsy. Yu.E. Azimova, G.R. Tabeeva
8. Why Migraines Strike David W. Dodick & J. Jay Gargus Scientific American 299, 56 – 63 (2008) doi:10.1038/scientificamerican0808-56