Causes of migraine

Previously, the cause of migraine was considered primarily vascular pathology. Indeed, during a migraine attack, expansion of the vessels of the dura mater, in the innervation of which the trigeminal nerve fibers (the so-called trigeminovascular fibers) participate. In turn, the vasodilation and sensation of pain during a migraine attack are secondary and are caused by the isolation of painful neuropeptides-vasodilators from the endings of triheminovascular fibers, the most important of them being the peptide associated with the calcitonin gene (CGRP) and neurokinin A. Thus, activation of the trigeminovascular system - The most important mechanism that triggers a migraine attack. According to the latest data, the mechanism of such activation is associated with the fact that migraine patients have an increased sensitivity (sensitization) of trigeminovascular fibers, on the one hand, and an increased excitability of the cerebral cortex, on the other.

Migraine provokers play an important role in activating the trigeminovascular system and "triggering" a migraine attack, the most frequent of them being emotional stress, weather change, menstruation, hunger and physical overexertion.

More often the attack does not occur during the stress, but after the resolution of a stressful situation. As a reason migraine can play a violation of the rhythm of sleep and wakefulness, and seizures can be triggered by lack of sleep, and excessive sleep ("migraine weekend"). Some foods: alcohol (especially red wine and champagne), chocolate, citrus fruits, some sorts of cheese, products containing yeast - can also trigger a migraine attack. The provoking effect of some products is explained by the content of tyramine and phenylethylamine in them. Migraine provokers include vasodilator drugs, noise, stuffiness, bright and flashing light.

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Migraine risk factors

• Hormonal changes
• Nutritional factors
• Menstruation
• Pregnancy
• Climax
• Contraceptives / hormone replacement therapy
• Hunger
• Alcohol
• Nutritional supplements
• Products (chocolate cheese, nuts, citrus, etc.)
• Physical factors
• Environmental factors
• Exercise stress
• Lack of sleep
• Excess sleep
• Stress / relaxation
• Anxiety
• Meteofactors
• Bright light
• Smells
• Stuffiness

The most common risk factors for developing migraine attacks (triggers)

Risk factors
Hormonal	Menstruation, ovulation, oral contraceptives, hormone replacement therapy
Dietary	Alcohol (dry red wine, champagne, beer); food rich in nitrites; monosodium glutamate; aspartame; chocolate; cocoa; nuts; eggs; celery; seasoned cheese; missed meal
Psychogenic	Stress, post-stress period (weekend or vacation), anxiety, anxiety, depression
Conflict	Bright light, sparkling lights, visual stimulation, fluorescent lighting, smells, weather changes
Related to sleep	Lack of sleep,
A variety of	Craniocerebral injury, physical stress, overwork, chronic diseases
Medications	Nitroglycerin, histamine, reserpine, ranitidine, hydralazine, estrogen

Migraine pathogenesis

The pathogenesis of migraine is very complicated. If you previously thought that migraine is a pathological condition of the vessels of the head, then in recent years the emphasis has shifted to the brain itself. Primarily violated the metabolism of neurotransmitters in the brain, which triggers a cascade of pathological processes leading to paroxysm of intense headache. Familiar cases of migraine are well known, which is transmitted by an autosomal dominant type with a high penetrance of the gene, especially over the female line. Recently it was revealed that the family hemiplegic migraine is associated with a defect of the 19th chromosome (loci 4 and 13). Perhaps other variants of migraine are associated with other genes of the chromosome, which are responsible for the exchange of neurotransmitters.

Important role in the development of migraine attack is played by vasoactive biogenic amines - serotonin, catecholamines, histamine, peptide kinins, prostaglandins, etc. When migraine occurs, first of all, intensive release of serotonin from platelets. Serotonin narrows large arteries and veins, and also dilates capillaries, which creates conditions for slowing blood flow and developing cerebral ischemia. Before the phase of intense headache, intracerebral blood flow decreases, which is clinically manifested in various aura variants. If the blood flow in the vertebral-basilar basin, including the posterior cerebral artery, is reduced, then various visual disorders (photophobia, photopsy, hemianopsia, scotoma), phonophobia, dysarthria, vestibular and discordant disturbances arise as aura of migraine. When blood flow is reduced in the system of carotid arteries, there are clinical signs of dysphoria, speech disorders, movements (mono-, hemiparesis) or sensitivity (paresthesia, numbness, etc.). With prolonged vasospasm and irrigation of vegetative unmyelinated vasoactive fibers, neuropeptides, substance P and calcitonin, the gene-bound peptide, nitricinins, are released into the wall of the vessel, which increase the permeability of the wall and lead to its neurogenic aseptic inflammation. This is accompanied by edema of the vessel wall and its stretching. Free serotonin is excreted in the urine in unchanged form or in the form of metabolites, and at the height of the migraine attack its content falls, which increases the atony of the vessels of the head, increases the permeability of the vascular wall. Such changes in the vessels cause irritation of sensitive receptors of the trigeminal (trigeminal) nerve and the formation of a painful syndrome of the corresponding localization (eye socket, frontal-parietal-temporal region). The pain is not due to vasodilatation, but is a consequence of the excitation of the afferent fibers of the trigeminal nerve in the walls of the vessels. Vascular-trigeminal theory has been extensively studied in recent years. There is a hypothesis about the primary pathology of the platelet system. With migraine, increased platelet aggregation is detected. This aggregation is enhanced by a decrease in the activity of the enzyme MAO (monoamine oxidase), so seizures can be provoked by the use of products containing tyramine, which binds MAO. Tyramine also has an effect on the release of serotonin from platelets and norepinephrine of nerve endings, which further enhances vasoconstriction. Simultaneously, the metabolism of mast cells slows down in tissues and the secretion of histamine increases, which, like serotonin, strengthens the permeability of the vascular wall. This facilitates the passage through it of plasma-kinins - tissue hormones, in particular bradykinin, a significant content of which is found in the soft tissues surrounding the temporal artery (characteristic of throbbing pain). In the breakdown of platelets, also increases the level of prostaglandins, especially E1 and E2, which lead to a decrease in blood flow in the internal and increase blood flow in the external carotid artery. These processes contribute to reducing the pain threshold of the vessels. Prevalence of migraine attacks in women is known and their frequent connection with the menstrual cycle. The connection of migraine attacks with the level of plasma estrogen, which increase the serotonin content and reduce the pain threshold of the vascular wall, has been revealed. Changes in neurogenic regulation also lead to the expansion of arterio-venous shunts, which facilitates the "robbing" of the capillary network and ischemic hypoxia, blood overflow of venous vessels and excessive stretching. In patients with migraine, there is also a central adrenergic insufficiency, which is manifested by parasympathetic traits: arterial hypotension, vestibulopathy, peptic ulcer, constipation, allergic reactions, etc.

In general, the pathogenesis of migraine can reveal a combination of so-called nonspecific factors (mitochondrial insufficiency, brain excitability) and specific (vascular changes, the functioning of the trigemin-vascular system).

It should be noted that in a genesis, but rather in maintaining a vascular headache in migraine sufferers, a reflex tension of the muscles of the scalp and cervical corset (trapezoidal, nodular) plays a certain role in response to pain. This was confirmed when recording EMG from the trapezius muscles in patients with lateral migraines: the EMG oscillations on the patient side even outside the attack were almost 2 times greater than in the healthy one.

It is established that the debut and exacerbation of the disease is usually preceded by psychogenic factors; in the history the significant number of children's and actual psycho-traumatic situations is revealed. Patients are characterized by quite pronounced emotional and personal changes. The importance of the head in their conception of the body's own scheme is very high, and pain attacks occur at a time when there is a sense of threat to a certain level of aspiration, to its "ego-ideal." Pain in this case is the most acceptable social way of "protection". Detection of a pronounced psychovegetative syndrome in patients with migraine in combination with the endogenous and exogenously conditioned neurotransmitter disorders, ie the presence of a psychovegetative-endocrine-somatic link in the genesis of the disease, gives grounds to consider migraine as a psychosomatic disease.

Regarding the mechanism of the headache to the present, there is no satisfactory explanation: according to several authors, it is based on the inferiority of regional sympathetic innervation (possibly, genetically conditioned). Periodicity depends on the biorhythms of homeostasis with fluctuations in the level of vasoactive substances. The effect of external factors is mediated through changes in the humoral environment, as a result of which compensation is lost in the defective area of sympathetic innervation.

Of particular interest is the discussion of migraine and epilepsy. Common to these conditions, according to S. N. Davidenkov, is primarily paroxysmalism, sufficient stereotyping of attacks, sometimes postpristupnaya drowsiness. The results of the day EEG study were sometimes contradictory: from normal to detecting a kind of epileptiform activity. However, careful polygraph studies conducted at night not only failed to detect epileptic phenomena on the EEG (although sleep is a powerful physiological provoker of epileptic activity), but also revealed a tendency in these patients to intensify activating influences (lengthening of falling asleep, shortening of deep stages of sleep and increase superficial), which reflects an increase in activation in sleep and the presence of emotional tension. The appearance of nocturnal cephalalgia in patients with migraine seems to be associated with a fast phase of sleep, when, as is known, the maximum changes in autonomic regulation occur, the violation of which is inherent in migraine patients. This is manifested in the failure of compensation and the appearance of a cephalic attack.

It has also been shown that allergic conditions can only serve as a "trigger" and not a pathogenetic factor for migraine.

Migraine attacks are provoked by many factors: weather changes, geomagnetic influences, atmospheric pressure differences, violations of the working and rest regime (lack of sleep, excessive sleep), physical and mental overstrain, alcohol abuse, overheating, etc.

Migraine: what happens?

The main theories explaining the pathogenesis and causes of migraine are:

1. The vascular theory of migraine Wolff (1930). According to her, migraine is caused by an unexpected narrowing of the intracranial vessels, which provokes brain ischemia and aura. This is followed by the expansion of extracranial blood vessels, which causes a headache.
2. Trigeminal-vascular theory of migraine (M. Moskowitz et al., 1989). In accordance with this, with a spontaneous migraine attack, potentials arise in the brain stem structures, which triggers activation of the trigeminal-vascular system with the release into the wall of the cranial vessels of neuropeptides (substance P, neuropeptide associated with the gene controlling calcitonin), causing their dilatation, increased permeability and, as a consequence, the development of neurogenic inflammation in it. Aseptic neurogenic inflammation activates nociceptive terminals of the afferent fibers of the trigeminal nerve, located in the vascular wall, leading to the formation of a sensation of pain at the CNS level.
3. Serotonergic theory of migraine. It is known that serotonin (5-hydro-oxytryptamine) is significantly more than other transmitters, (ie, chemicals that interact between cells), is involved in the pathophysiology of migraine, and probably plays an initiating role in the development of migraine headache.

Migraines are divided into migraine with aura (classical) and migraine without an aura (simple). A simple migraine is observed more often - 80% of all migraine cases, with simple migraine pain occurs without precursors and usually increases more slowly. Classical migraines begin with visual or other symptoms.

In 1948, Wolff described three main diagnostic criteria for classic migraine:

1. Prodromal stage or aura, usually visual.
2. One-sided headache.
3. Nausea or vomiting.

At the present time, light and sound can be added to these signs, the presence of trigger factors, a hereditary history.

Among the clinical signs of migraine, visual impairment (visual field defects, photopsy, scintillating scotoma), sometimes aphasia, numbness, ringing in the ears, nausea and vomiting, photophobia, and occasionally temporary hemiparesis.

Characterized by family history and the relationship of seizures with any provoking factors - certain types of foods (chocolate, red wine), hunger, physical or emotional stress, menstruation.

Migraines with aura most often begin with visual symptoms in the form of flashes of light, blind spots (cattle) or hemianopsia (limitation of the field of vision). Migraine usually appears when the visual aura (lasting several minutes) ends or the intensity of its manifestations decreases. Other harbingers of the migraine attack are marked less frequently, but sometimes they follow each other: after the hemianopsia tingling in the face or limbs appears. For a migraine aura, a change in positive symptoms is negative (for example, scotoma followed by flashes of light, tingling with numbness). Characteristic for migraine dyspeptic phenomena occur at the height of the headache. Vomiting in most cases facilitates migraine or even interrupts the attack. During the attack, the tenderness of the head covers is also noted.