Causes of migraine

Previously, vascular pathology was considered as the cause of migraine. Indeed, during a migraine attack, there is a dilation of the vessels of the dura mater, in the innervation of which the fibers of the trigeminal nerve (the so-called trigeminovascular fibers) participate. In turn, vasodilation and the sensation of pain during a migraine attack are secondary and are caused by the release of pain neuropeptides-vasodilators from the endings of trigeminovascular fibers, the most important of which are the peptide associated with the calcitonin gene (CGRP) and neurokinin A. Thus, activation of the trigeminovascular system is 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 increased sensitivity (sensitization) of trigeminovascular fibers, on the one hand, and increased excitability of the cerebral cortex, on the other.

An important role in the activation of the trigeminovascular system and the “launch” of a migraine attack is played by migraine triggers, the most common of which are emotional stress, weather changes, menstruation, hunger and physical overexertion.

Most often, an attack occurs not during the stress itself, but after the stressful situation has resolved. Migraine can be caused by a disturbance in the sleep-wake rhythm, and attacks can be provoked by both lack of sleep and excess sleep ("weekend migraine"). Some foods: alcohol (especially red wine and champagne), chocolate, citrus fruits, some types 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. Migraine triggers include vasodilators, noise, stuffiness, bright and flashing lights.

[ 1 ], [ 2 ]

Risk factors for developing migraine

• Hormonal changes
• Nutritional factors
• Menstruation
• Pregnancy
• Climax
• Contraceptives/hormone replacement therapy
• Hunger
• Alcohol
• Food additives
• Products (chocolate, cheese, nuts, citrus, etc.)
• Physical factors
• Environmental factors
• Physical activity
• Lack of sleep
• Excessive sleep
• Stress/relaxation
• Anxiety
• Meteorological factors
• 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 wines, champagne, beer); foods rich in nitrites; monosodium glutamate; aspartame; chocolate; cocoa; nuts; eggs; celery; aged cheese; skipping meals
Psychogenic	Stress, post-stress period (weekend or vacation), anxiety, worry, depression
Wednesday	Bright lights, flashing lights, visual stimulation, fluorescent lighting, odors, weather changes
Sleep related	Lack of sleep, oversleeping
Various	Traumatic brain injury, physical stress, fatigue, chronic diseases
Medicines	Nitroglycerin, histamine, reserpine, ranitidine, hydralazine, estrogen

Pathogenesis of migraine

The pathogenesis of migraine is very complex. If earlier it was 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. Initially, the metabolism of neurotransmitters in the brain is disrupted, which triggers a cascade of pathological processes leading to a paroxysm of intense headache. Familial cases of migraine are well known, which is transmitted by an autosomal dominant type with high penetrance of the gene, especially in the female line. Recently, it was found that familial hemiplegic migraine is associated with a defect of the 19th chromosome (loci 4 and 13). Perhaps other types of migraine are associated with other genes of the chromosome responsible for the exchange of neurotransmitters.

Vasoactive biogenic amines play an important role in the development of a migraine attack - serotonin, catecholamines, histamine, peptide kinins, prostaglandins, etc. During a migraine, first of all, there is an intensive release of serotonin from platelets. Serotonin narrows large arteries and veins, and also dilates capillaries, which creates conditions for slowing down blood flow and developing cerebral ischemia. Before the phase of intense headache, intracerebral blood flow decreases, which is clinically manifested in various types of aura. If blood flow in the vertebrobasilar basin, including the posterior cerebral artery, is reduced, then various visual disorders (photophobia, photopsia, hemianopsia, scotoma), phonophobia, dysarthria, vestibular and discoordination disorders occur as a migraine aura. With the reduction of blood flow in the carotid artery system, clinical signs of dysphoria, speech disorder, movement disorders (mono-, hemiparesis) or sensitivity (paresthesia, numbness, etc.) appear. With prolonged vascular spasm and irritation of vegetative unmyelinated vasoactive fibers, neuropeptides are released into the vessel wall - substance P and calcitonin gene-related peptide, nitrokinins, 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 unchanged or as metabolites, and at the height of a migraine attack its content drops, which increases the atony of the head vessels, increases the permeability of the vascular wall. Such changes in the vessels cause irritation of the sensory receptors of the trigeminal nerve and the formation of pain syndrome in the corresponding localization (eye socket, frontal-parietal-temporal region). The pain is not caused by vasodilation, but is a consequence of excitation of the afferent fibers of the trigeminal nerve in the walls of the vessels. The vascular-trigeminal theory has been widely studied in recent years. There is a hypothesis about the primary pathology of the platelet system. Increased platelet aggregation is detected in migraine. This aggregation increases with a decrease in the activity of the MAO (monoamine oxidase) enzyme, so attacks can be provoked by eating foods containing tyramine, which binds MAO. Tyramine also affects the release of serotonin from platelets and norepinephrine from nerve endings, which further increases vasoconstriction. At the same time, the metabolism of mast cells slows down in the tissues and the release of histamine increases, which, like serotonin, increases the permeability of the vascular wall. This facilitates the passage of plasmokinins - tissue hormones, in particular bradykinin, a significant content of which is also found in the soft tissues surrounding the temporal artery (characterized by pulsating pain). With the breakdown of platelets, the level of prostaglandins also increases, especially E1 and E2,which lead to a decrease in blood flow in the internal and an increase in blood flow in the external carotid artery. These processes contribute to a decrease in the pain threshold of the vessels. It is known that migraine attacks predominate in women and are often associated with the menstrual cycle. A connection has been found between migraine attacks and the level of plasma estrogens, which contribute to an increase in serotonin content and a decrease in the pain threshold of the vascular wall. Changes in neurogenic regulation also lead to the expansion of arteriovenous shunts, which contributes to the "stealing" of the capillary network and ischemic hypoxia, overflow of blood in the venous vessels and their excessive stretching. Patients with migraine also have central adrenergic insufficiency, which is manifested by parasympathetic features: arterial hypotension, vestibulopathy, peptic ulcer, constipation, allergic reactions, etc.

In general, in the pathogenesis of migraine, a combination of so-called non-specific factors (mitochondrial insufficiency, brain excitability) and specific factors (vascular changes, functioning of the trigeminvascular system) can be identified.

It should be noted that in the genesis, or rather in the maintenance of vascular headache in migraine patients, a certain role is played by reflex tension of the scalp and cervical corset muscles (trapezius, sternocleidomastoid) in response to pain. This was confirmed when recording EMG from the trapezius muscles in patients with lateralized migraines: EMG oscillations on the affected side, even outside of an attack, were almost 2 times greater than on the healthy side.

It has been established that the debut and exacerbation of the disease are usually preceded by psychogenic factors; a significant number of childhood and current psychotraumatic situations are revealed in the anamnesis. Patients are characterized by fairly pronounced emotional and personality changes. The significance of the head in their idea of their own body scheme is very high, and attacks of pain occur at the moment when a feeling of a threat to a certain level of claims, their "ego-ideal" appears. Pain in this case is the most acceptable social way of "defense". The detection of a pronounced psychovegetative syndrome in migraine patients in combination with the above-described endogenously and exogenously conditioned neurotransmitter disorders, i.e. the presence of a psychovegetative-endocrine-somatic link in the genesis of the disease, gives grounds to consider migraine as a psychosomatic disease.

There is no satisfactory explanation for the mechanism of cluster headache to date: according to a number of authors, it is based on the inadequacy of regional sympathetic innervation (possibly genetically determined). The periodicity depends on the biorhythms of homeostasis with fluctuations in the level of vasoactive substances. The action of external factors is mediated through changes in the humoral environment, as a result of which compensation in the defective area of sympathetic innervation is disrupted.

Of particular interest is the discussion of migraine and epilepsy. According to S. N. Davidenkov, these conditions have in common, first of all, paroxysmal nature, sufficiently stereotypical attacks, and sometimes post-attack drowsiness. The results of daytime EEG studies were sometimes contradictory: from normal to the detection of some semblance of epileptiform activity. However, careful polygraphic studies conducted at night not only failed to detect epileptic phenomena on the EEG (although sleep is a powerful physiological provocateur of epileptic activity), but also revealed a tendency in these patients to increase activating influences (lengthening the time to fall asleep, shortening the deep stages of sleep and increasing the superficial ones), which reflects an increase in activation during sleep and the presence of emotional tension. The occurrence of nighttime cephalgia in migraine patients is apparently associated with the rapid sleep phase, when, as is known, maximum changes in vegetative regulation occur, the disruption of which is initially inherent in migraine patients. This is manifested by a breakdown in compensation and the occurrence of a cephalgic attack.

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

Migraine attacks are provoked by many factors: weather changes, geomagnetic influences, changes in atmospheric pressure, disruptions in work and rest schedules (lack of sleep, excessive sleep), physical and mental overexertion, alcohol abuse, overheating, etc.

Migraine: What's Happening?

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

1. Wolff's vascular theory of migraine (1930). According to it, migraine is caused by an unexpected narrowing of intracranial vessels, which provokes cerebral ischemia and aura. This is followed by an expansion of extracranial blood vessels, which causes headache.
2. Trigeminal-vascular theory of migraine (M. Moskowitz et al., 1989). According to it, during a spontaneous attack of migraine, potentials arise in the brain stem structures, which causes activation of the trigeminal-vascular system with the release of neuropeptides (substance P, a neuropeptide associated with the gene controlling calcitonin) into the wall of cranial vessels, causing their dilation, 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.
3. Serotonergic theory of migraine. It is known that serotonin (5-hydroxytryptamine) is significantly more involved in the pathophysiology of migraine than other transmitters (i.e. chemical substances that carry out interactions between cells), and probably plays an initiating role in the development of migraine headache.

Migraine is divided into migraine with aura (classic) and migraine without aura (simple). Simple migraine is observed more often - 80% of all cases of migraine, with simple migraine the pain occurs without warning signs and usually increases more slowly. Classic migraine begins with visual or other symptoms.

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

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

Nowadays, these symptoms can be supplemented by photophobia and phonophobia, the presence of trigger factors, and a hereditary history.

Among the clinical signs of migraine, visual disturbances (visual field defects, photopsia, flickering scotoma) are described; sometimes aphasia, numbness, tinnitus, nausea and vomiting, photophobia, and occasionally temporary hemiparesis occur.

A family history and a connection between attacks and some provoking factors are typical - certain types of food (chocolate, red wine), hunger, physical or emotional stress, menstruation.

Migraine with aura most often begins with visual symptoms in the form of flashes of light, blind spots (scotoma) or hemianopsia (limitation of the visual field). Migraine usually appears when the visual aura (lasting several minutes) ends or its intensity decreases. Other precursors of a migraine attack are noted much less often, but sometimes they follow one another: hemianopsia is followed by tingling in the face or limbs. Migraine aura is characterized by a change in positive symptoms to negative ones (for example, flashes of light are followed by scotoma, tingling by numbness). Dyspeptic symptoms characteristic of migraine occur at the height of the headache. Vomiting in most cases relieves migraine or even interrupts the attack. During the attack, pain in the scalp is also noted.