Northwestern State Medical University named after I. I. Mechnikov

Department of Neurology named after Academician S.N. Davidenkova

Topic: “Headache. Migraine. Etiopathogenesis, classification, clinical picture, diagnosis, treatment.”

Performed:

Student of group 417

Romanova Ya. Yu.

Teacher:

Zuev A. A.

Saint Petersburg

90% of people have experienced headache at least once

70% go to the doctor.

25-40% suffer from chronic headache.

Hypertension is the leading and sometimes the only complaint in more than 50 diseases. Only 5-14% have serious intracranial pathology.

It is known that sensitivity to pain depends on genetic factors, namely:

Density of nociceptors (pain receptors);

Level of algogenic substances:

Taknevyh (serotonin, histamine, acetylcholine, prostaglandins);

Plasma (bradykinin, kallidin);

Released from nerve endings (glutamate, calcium-tonin-gene-related peptide).

Sensitive to pain:

Skin, subcutaneous fat, mucous membranes,

Muscles, tendons, aponeurosis,

Periosteum, mandibular joint,

Main arteries

Cranial nerves: V, IX, X; roots C2,3; somatic and autonomic ganglia,

Dura mater of the base of the skull and its duplications.

Types of sensitivity.

The epicritic (fast) nociceptive system is responsible for:

Statement of the damaging effects,

Localization and identification of damaging effects,

Implementation of immediate defensive reactions.

Sensitive to temperature and mechanical stimuli.

ENS mediators: glutamate, aspartate, ATP

Average response speed (V)=15m/s.

Having fulfilled the signaling role, epicritic pain is replaced by protopathic pain, which, depending on the degree of damage, occurs in seconds, minutes and even hours.

Protopathic (ancient, slow) nociceptive system:

Constantly reminds you of trouble in the body,

Determines the emotional and autonomic accompaniment of pain,

Meaningful defensive reactions

Sensitive to changes in chemical and physical parameters that occur during inflammation.

This pain is dull, diffuse, and persists until complete recovery.

PrNS mediators: cholecystokinin, somatostatin, substance P.

Average response speed (V)=2m/s.

Antinociceptive system (ANS):

Controls the pain threshold.

Relay systems:

Gate control (islet cells),

Suprasegmental control (central gray matter, raphe nuclei, reticular nucleus of the thalamus)

Somatosensory cortex.

The descending pathways of the ANS through norandenaline, serotonin and, to a lesser extent, dopamine inhibit the flow of pain. GABA and glycine, released from the terminals of inhibitory neurons, block the release of substance P, glutamate and aspartate.

Endogenous opiate system.

The most important part of the ANS. The main role is played by the central gray matter of the brainstem: the brain - b-endorphin and dynorphin, the spinal cord - enkephalins.

Released from the depot, they inhibit the release of substance R.

Blood serotonin stimulates the release of b-endorphins from the anterior pituitary gland.

Cholecystokinin neutralizes the effect of endogenous opiates.

Acute pain (AP) develops when tissue damage and/or smooth muscle function is impaired.

Types of acute pain:

Superficial,

Deep,

Visceral,

Reflected.

The duration of OB is determined by the time of tissue and/or smooth muscle recovery, but no more than 3 months.

After 3 months, the pain transitions from chronic to chronic.

Causes of development of chronic pain (CP):

Chronization of the pathological process,

Dysfunction of the central ANS, metabolism of serotonin, catecholamines, which also determine the psycho-emotional structure of the personality.

The formation of CB depends to a greater extent on psychological factors than on the intensity of exposure. Chronic pain can be purely psychogenic.

Nociceptive pain.

Impact on the receptor apparatus.

Neuropathic pain.

Violation at any level of the somatosensory system (central, peripheral).

Headache (cephalgia).

The main role in the development of cephalgia is played by the trigeminovascular system - a complex of neurons of the trigeminal nerve nucleus and the cerebral vessels innervated by them.

Classification of hypertension (ICD-II, 2004)

14 groups, 86 types.

Primary headache.

1. Tension headache (TTH),

   Tufted headache and trigeminal autonomic cephalgia

   Headaches not associated with structural damage to the nervous system (external influence, cold, orgasmic, cough, physical stress).

Secondary GB.

Vascular pathology,

• Infections, etc.

The most common causes of secondary headache:

Diseases of the cardiovascular system,

Changes in ICP during volumetric processes,

Infections, metabolic disorders,

Neuralgia V, IX, X pairs of the cranial nerve, occipital nerve,

Diseases of the eyes, ears, paranasal sinuses, mandibular joint.

Pathogenetic classification of headache.

Liquorodynamic,

Vascular,

Neuralgic

GB voltage.

Liquorodynamic GB.

Associated with increased or decreased intracranial pressure and dislocation brain. The severity of the pain depends on the rate of change.

Clinic of intracranial hypertension (ICH):

headache, nausea, vomiting “fountain”,

Kocher-Cushing syndrome: Ps, BP,

Mental disorders,

Impaired consciousness

Meningeal symptoms (+/-),

Dizziness (+/-),

Lesion of the VI pair of cranial nerves (+/-),

Congestive optic disc (+/-).

Clinic ICP.

CSF is a “cushion” for the brain.

Anchor formations:

Clinical features:

Strengthens in a vertical position

Shooting when moving,

Accompanied by increased heart rate.

Vascular GB.

Arterial:

Overstretching of the arterial wall at BP>%,

Paretic vasodilation (pressing, bursting, aching pain),

Spastic (local, general). Nausea, lightheadedness, darkening of the eyes.

Tension of the arteries.

Venous:

is caused by excessive blood filling of the veins, associated with a decrease in their tone in the syndrome of autonomic dysfunction, cardiovascular and pulmonary insufficiency, thrombotic veins and sinuses of the brain.

The headache is of a dull, bursting nature, accompanied by a feeling of heaviness in the head, periorbital edema, facial pastiness, and intensifies with venous tests.

Hemorheological:

is caused by increased blood viscosity, which leads to impaired microcirculation, increased blood supply and hypoxia of the brain. The pain can be of varying intensity: dull, diffuse, accompanied by drowsiness, noise and ringing in the ears.

Neuralgic headache.

Damage to the cranial nerve (V, IX), nn. occipitalis.

Paroxysmality,

Trigger zones

Vegetative support (mainly sympathetic),

There are no changes outside the attack!

Tension headache.

Episodic tension headache:

Duration 30 minutes-7 hours, no more than 15 days a month, more often in young people due to anxiety disorders.

Intensity 2-6 points on VAS (visual analogue scale). Paroxysmal autonomic disorders (panic attacks, lipothymia, neurogenic fainting). The most common cause is muscle distress.

Chronic tension headache:

More often in older people with lower educational qualifications due to depression. Intensity 5-6 points or more according to VAS.

Accompanying syndromes: nausea, photo- and phonohypersthesia. Autonomic disorders are permanent (hyperventilation syndrome, diffuse algic syndrome). The most common cause is psychogenia.

EGTH and CGTH may or may not be accompanied by pericranial muscle tension.

Criteria for diagnosing tension-type headache:

Monotonous, compressive, may spread to the collar area,

Diffuse character

The intensity does not increase with normal physical and intellectual stress,

Duration of at least 30 minutes,

Tension and soreness of the pericranial muscles (+/-).

Pathogenesis of tension headaches.

Ivan Drozdov 15.02.2018

A migraine attack is a set of excruciating and painful neurological symptoms that significantly reduce a person’s physical activity and activity. The main cause of development is a pathological narrowing of the blood vessels in the brain, provoked by poor nutrition, stress, overwork, the influence of tobacco and alcohol, as well as a number of neurological diseases. In the first case, it is enough to eliminate the impact of the described factors in order to reduce the number of attacks; in the second, it is necessary to treat diseases and pathologies that provoke the appearance of pain and unpleasant symptoms.

Where do neurological symptoms come from?

In most cases, migraine is accompanied by neurological symptoms, the cause of which is external factors (stress, fatigue, weather dependence) and serious pathological disorders. If focal neurological symptoms appear in aggravated form during migraine attacks, it is necessary to diagnose the causes of their development and begin treatment in a timely manner.

Vertebral artery syndrome and cervical migraine

A pathological disturbance of blood flow directed to the structures of the brain, which is caused by compression of the two main vertebral arteries, is called vertebral artery syndrome (VAS). The cause of these processes may be the presence of osteochondrosis, cartilaginous growths on the bone tissue of the vertebrae, intervertebral hernias, and muscle spasms. The vessels of the brain react with spasm to the decrease in blood flow, as a result of which a person experiences migraine pain.

Facial migraine

The following signs indicate the presence of facial migraine:

• Systematic attacks that occur several times a week lasting from 2-3 minutes to 1-2 hours.
• Aching headache with periodic lumbago radiating to the cervical region, lower or upper jaw, or orbital area.
• Pain in the carotid artery when touched and strong pulsation, swelling of the soft tissues, redness of the skin at its location.
• Psycho-emotional instability during an attack - causeless hysterics, anger, nervous overexcitation, often giving way to apathy, indifference and numbness.

People aged 30-60 years are most susceptible to facial migraine. Common reasons that provoke the development of an attack are stress, prolonged exposure to drafts or cold, injuries and acute dental diseases. Due to the similarity of symptoms, facial migraines are often diagnosed as inflammation of the trigeminal nerve.

Hemiplegic migraine

Diagnosis and treatment of migraine with focal neurological symptoms

In case of obvious neurological focal symptoms, it is necessary to find out the cause of their origin. To do this, the neurologist examines the patient’s complaints and visual manifestations, after which he prescribes a number of the following diagnostic procedures:

• radiography of the cervical and lumbar vertebrae;
• MRI of the neck and brain;
• Doppler ultrasound of the main vessels and arteries of the brain structures;
• Clinical blood test for lipids and cholesterol.

After undergoing diagnosis, the patient is prescribed a comprehensive treatment to reduce the intensity of neurological symptoms, as well as the frequency and duration of migraine attacks. The therapeutic course of treatment may include a number of the following medications and drugs:

• Anti-inflammatory and analgesic tablets (Diclofenac, Imet, Indomethacin, Nurofen).
• A complex of B vitamins that has a positive effect on the central nervous system, metabolic processes, restoration of memory and mental activity.
• Antispasmodics (Spazgan, Spazmalgon), aimed at relieving spasms of cerebral vessels and preventing migraines.
• Tablets that improve blood circulation in the brain vessels (Cinnarizine, Cavinton).
• Neuroprotective drugs (Glycine, Ginkgo Biloba, Thiocetam) have a restorative effect on nerve brain cells, improving their metabolism and protective functions.
• Antidepressants and sedatives (Velafax, Aphazen, Persen) are indicated for prolonged depressive states and stress that provoke migraine attacks.
• Anti-migraine tablets (Sumatriptan, Zomig, Ergotamine) are special medications with an effect aimed at relieving migraine attacks and eliminating additional symptoms.
• Anticonvulsants (Epimil, Valproic acid) are prescribed if migraine attacks are aggravated by epileptic seizures.

Do you have a question? Ask it to us!

Feel free to ask your questions right here on the site.

To prevent attacks with pronounced neurological signs, it is recommended to undergo complex treatment regularly, without waiting for the exacerbation phase. For the effectiveness of drug therapy and as preventive measures, common alternative techniques should be considered - manual procedures. Don’t also forget: proper nutrition and lifestyle are an effective measure to prevent migraine attacks caused by neurological causes.

Migraine is a complex of symptoms and phenomena that cause unpleasant consequences if the lesion is not eliminated in a timely manner. Migraine may have a good combination with focal neurological symptoms. In addition, it is necessary to distinguish between such concepts as migraine with aura, in which neurological disorders are present, and migraine without aura.

Main reasons

Migraine with focal neurological symptoms can be caused by PA-vertebral artery syndrome. They, in turn, are located along the spinal column and pass through the canals, which are formed by the transverse processes of the cervical vertebrae. At the base of the brain stem, the vessel merges into an artery, which branches and at the same time supplies blood to the hemispheres. The cause of the pathology may be nothing more than cervical osteochondrosis. Migraine with focal neurological symptoms can be accompanied by a number of symptoms.

• Paresis of the limbs, which can be partial or complete;
• Nausea;
• Vomiting and dizziness;
• Hearing loss and decreased vision;
• Impaired coordination of movements;
• Amnesia.

A patient suffering from such a disease may experience intense pain that begins in the back of the head and spreads to the parietal region - to the forehead, temples, and neck. During this disease, when turning the head, a crunching or burning sensation may occur.

Headaches that occur in neurology are usually caused by severe compression of the occipital nerves; the pain itself has a shooting character. They can spread along the location of the nerves, and are also distinguished by the fact that they continue for a long time and constantly. If competent treatment is prescribed, it should bring the desired result, but often this does not happen.

Seizures usually limit the patient’s ability to work and take him out of his usual routine of life. There are several main types of migraine with focal neurological symptoms - pharyngeal, facial, hemiplegic. The first is diagnosed less frequently than the others, and the second is represented by pain in the face, which affects overall well-being. The latter type of migraine is quite difficult to detect and diagnose; for this, a specialist must collect all the necessary data and make a diagnosis.

E.G. Filatova, A.M. Wayne

Department of Neurology FPPO MMA named after. THEM. Sechenov

URL

Migraine (M) has been known to mankind for more than 3000 years. In the papyri of the ancient Egyptians, descriptions of migraine attacks were found, as well as prescriptions of medications used to treat this disease. Despite this, much still remains a mystery in the pathogenesis of M. Practitioners and patients suffering from M do not have a clear idea of ​​whether this disease is curable? What modern medications most effectively relieve a painful migraine attack? Do all patients with M need to be treated and how? Does M have any complications? What symptoms should you pay attention to in a patient with M so as not to miss another life-threatening disease (brain tumor, vascular aneurysm, etc.)?

Migraine is a paroxysmal condition manifested by attacks of pulsating headaches in one half of the head, mainly in the orbital-frontotemporal region, or bilateral localization. The attack is accompanied by nausea, vomiting, photo- and phonophobia. Characterized by recurrence and hereditary predisposition.

Epidemiology

Migraine affects 12 - 15% of the population. It is the second most common type of primary headache after tension-type headache (TTH).

Women experience migraine attacks 2 to 3 times more often than men, but in the latter the pain intensity is usually higher.

A characteristic symptom of migraine headache is its occurrence at a young age, up to 20 years. The peak incidence occurs between 25 and 34 years of age. With age, after the onset of menopause, in half the pain goes away, and in the rest, the pain intensity decreases somewhat. In some cases, M transformation occurs with age: the number of attacks increases, the intensity of pain often decreases, and a background interictal headache appears. Such transformed M acquires a chronic daily character. The most common reasons for this transformation include the abuse factor (abuse of analgesics and other anti-migraine drugs), as well as depression. There are known cases of M in 4-8 year old children (0.07% in the population).

There is a hereditary predisposition. If both parents had M attacks, then the disease occurs in 60-90% of cases, only in the mother - in 72%, only in the father - in 20%. Thus, M is more often inherited through the female line and the presence of a family history is an important diagnostic criterion for the disease.

The criteria for diagnosing migraine were defined by the International Headache Society in 1988.

1. Paroxysmal headache lasting from 4 to 72 hours.
2. A headache has at least two of the following characteristics:
   • predominantly unilateral localization, alternating sides, less often bilateral;
   • pulsating character;
   • moderate to severe headache intensity (interferes with daily activities);
   • increased during physical activity.
3. The presence of at least one accompanying symptom:
   • nausea;
   • vomit;
   • phonophobia;
   • photophobia.

To make a diagnosis of M without aura, there must be a history of at least 5 attacks that meet the listed criteria. For M with aura, there must be at least 2 attacks that meet these criteria.

Migraine classification

There are two main forms of migraine: M without aura (simple M) and M with aura (associated M). M without aura is manifested by attacks of pain that meet the listed criteria. This is the most common form, observed in 80% of cases. In M with aura, the pain attack is preceded by a migraine aura. An aura is a complex of focal neurological symptoms that precede an attack of pain or occur at the height of pain. The nature of clinical neurological manifestations depends on the involvement of the carotid or vertebral vascular system in the pathological process.

M with aura is characterized by: 1) complete reversibility of aura symptoms; 2) none of the symptoms should last more than 60 minutes; 3) the duration of the light interval between the aura and headache should be no more than 60 minutes. The greatest difficulties arise in the differential diagnosis of migraine aura with transient ischemic attacks (TIA). The frequency of migraine aura, its temporal characteristics, combination with typical migraine headaches and family history of migraine are of utmost importance.

M with aura is found much less frequently than M without aura (20%). Depending on the nature of the focal neurological symptoms that occur during an aura, several forms are distinguished: ophthalmic (classical), retinal, ophthalmoplegic, hemiparetic, aphasic, cerebellar, vestibular, basilar or syncope. More often than others, the ophthalmic form occurs, which is characterized by flashing bright photopsies in the right or left field of vision, possibly with their subsequent loss. The most severe form of M with aura is basilar or syncopal migraine. This form occurs more often in girls during puberty. Focal neurological symptoms are caused by the involvement of the vertebrobasilar vascular system in the pathological process. There is tinnitus, dizziness, paresthesia in the extremities, there may be photopsia in binasal or bitemporal visual fields, and syncope occurs in 30%, as a result of which this form is called syncope.

A special form of M is vegetative or panic migraine, identified by A.M. Wayne in 1995. In this form, a migraine attack is combined with a panic attack. The disease occurs in patients with affective disorders of an anxiety-depressive nature. The attack begins with a typical migraine attack, it provokes fear (panic), tachycardia, hyperventilation disorders, a possible rise in blood pressure, the appearance of chill-like hyperkinesis, general weakness or lipothymia, polyuria. Panic M is diagnosed when three or more panic-associated symptoms are present in any combination. Panic-associated symptoms are “secondary” in timing to the headache. Headache fully complies with the definition and diagnostic criteria of M. According to our data, the prevalence of “panic” M among other clinical forms of M is about 10%.

There are three phases during a migraine attack. The first phase: prodromal (in 50 - 70%), occurs in all forms of migraine in the form of changes in the emotional state, performance, etc. In M with aura, manifestations depend on the type of aura that is associated with the vascular basin. Second phase: headache with all its features and accompanying symptoms. The third phase is characterized by a decrease in headache, lethargy, fatigue, and drowsiness. Some patients experience emotional activation and euphoria.

"Danger signals" for migraines

They should always be remembered when analyzing a migraine attack and the criteria for its diagnosis. These include:

• No change in the “painful side”, i.e. the presence of hemicrania for several years on one side.
• A patient with M suddenly (in a fairly short time) develops other, unusual in nature, constant headaches.
• Progradiently increasing headache.
• The occurrence of a headache (outside of an attack) after physical exertion, strong stretching, coughing or sexual activity.
• An increase or appearance of accompanying symptoms in the form of nausea, especially vomiting, temperature, stable focal neurological symptoms.
• The appearance of migraine-like attacks for the first time after 50 years.

“Danger symptoms” require a detailed neurological examination with neuroimaging (CT, MRI) to exclude an ongoing organic process.

Factors that provoke a migraine attack

M is a hereditary disease, the course of which (the frequency and intensity of attacks) is influenced by a number of different external and internal factors.

The most important are psychogenic factors: emotional stress, release after positive or negative emotions. It has been noted that people with certain psychological characteristics suffer from M: they are characterized by a high level of aspirations, high social activity, anxiety, and good social adaptation. It is these personal qualities that allow people suffering from M to achieve remarkable success in life. It is known that many outstanding people suffered from M: Carl Linnaeus, Isaac Newton, Karl Marx, Sigmund Freud, A.P. Chekhov, P.I. Tchaikovsky and many others.

Patients with M often note increased meteosensitivity, and changes in weather conditions can provoke a migraine attack in them.

Physical activity, especially extreme physical activity and combined with emotional stress, is also a provocateur of M.

Irregular meals (fasting) or consumption of certain foods can initiate a painful migraine attack in people suffering from M. Approximately 25% of patients associate the occurrence of an attack with eating food rich in tyramine (cocoa, chocolate, nuts, citrus fruits, cheese, smoked meats, etc.). d.). The amino acid tyramine binds to the enzyme monoamine oxidase (MAO) and causes changes in vascular tone (angiospasm). In addition, tyramine competes with the precursor of serotonin, tryptophan, preventing its entry into neurons and thus reducing the synthesis of serotonin in the central nervous system. Alcohol (especially red wine, beer, champagne) and smoking are also provocateurs of a migraine attack.

The influence of female sex hormones on the course of M is well illustrated by the fact that in 60% of women attacks occur on premenstrual days, and in 14% they occur only before or during menstruation - menstrual migraine.

Deviations from the usual sleep formula increase the frequency of M attacks. The trigger can be either lack of sleep or excessive sleep. Patients who manage to fall asleep during an attack relieve headaches in this way. Special studies conducted by our employees have shown that there is a sleep migraine when an attack occurs during night sleep, namely in the most active phase of sleep - REM sleep. During this phase, a person dreams, which is accompanied by activation of vegetative parameters, biochemical and hormonal changes. M of wakefulness occurs in the most active stage of wakefulness - intense wakefulness. More than half of the patients experience M both during sleep and wakefulness.

Complications of migraine

Complications of M include status migraine and migraine stroke.

Status migraine is a series of severe, successive attacks, accompanied by repeated vomiting, with light intervals of no more than 4 hours, or one severe and prolonged attack, lasting more than 72 hours, despite the therapy. Status migraine is a serious condition that usually requires hospital treatment.

The risk of stroke in patients suffering from M without aura is no different from that in the general population. In M with aura, this relationship is different: cerebral stroke occurs 10 times more often than in the population. In migraine stroke, one or more aura symptoms do not completely disappear after 7 days, and neuroimaging studies show a picture of an ischemic stroke. Thus, only with M with aura there is an increased risk of migraine stroke, which is why each attack of M with aura must be promptly and effectively stopped.

Pathogenesis of migraine

The pathogenesis of M is extremely complex, and many of its mechanisms are not fully understood. Modern researchers believe that cerebral mechanisms are leading in the occurrence of a migraine attack. In patients with M, it is assumed that there is a genetically determined limbic-stem dysfunction, leading to a change in the relationship between the anti- and nociceptive systems with a decrease in the influence of the latter. Before an attack, the level of brain activation increases, followed by a decrease during a painful attack. At the same time, the trigeminovascular system is activated on one side or the other, which determines the hemicranial nature of the pain. In the perivascular endings of the trigeminal nerve, when activated, vasoactive substances are released: substance P, calciotonin, causing a sharp dilation of blood vessels, impaired permeability of the vascular wall and initiating the process of neurogenic inflammation (release of nociceptive substances into the perivascular space from the vascular bed: prostaglandins, bradykinins, histamine, serotonin and etc.). The special role of serotonin in M ​​is known. Before an attack, platelet aggregation increases, serotonin is released from them, which leads to a narrowing of large arteries and veins and dilation of capillaries (the most important factor in the development of the 1st phase of an attack). Subsequently, due to the intensive release of serotonin by the kidneys, its content in the blood decreases, which, together with other factors, causes dilatation and atony of blood vessels. Pain in M, therefore, is a consequence of excitation of the afferent fibers of the trigeminal nerve, as a result of the release of a number of biologically active nociceptive substances involved in the formation of neurogenic inflammation. This process is cyclical, in its genesis the leading role belongs to cerebral mechanisms.

Migraine treatment

Significant advances achieved in the study of the pathophysiology of M serve as the basis for modern pharmacotherapy of migraine cephalgia. Treatment of M consists of arresting the attack and preventive treatment in the interictal period. A migraine attack significantly reduces the quality of life of patients and causes significant economic losses. The main requirements for modern means are efficiency, safety, and speed of action.

Stopping an attack

To relieve migraine attacks, 3 groups of drugs are used:

1st group. For mild and moderately intense attacks, paracetamol, acetylsalicylic acid (ASA) and its derivatives, as well as combination drugs: sedalgin, pentalgin, spasmoveralgin, etc. can be effective. The action of this group of drugs is aimed at reducing neurogenic inflammation, suppressing the synthesis of pain modulators (prostaglandins , kinins, etc.), activation of antinociceptive mechanisms of the brain stem. When using them, it is necessary to remember the contraindications to the prescription of ASA: the presence of diseases of the gastrointestinal tract, a tendency to bleeding, increased sensitivity to salicylates, allergies, as well as the possibility of developing abuse headaches with prolonged and uncontrolled use of these drugs.

2nd group. Dihydroergotamine preparations have a powerful vasoconstrictor effect, due to their influence on serotonin receptors localized in the vascular wall, they prevent neurogenic inflammation and thereby stop a migraine attack. Dihydroergotamine is a non-selective serotonin agonist and also has dopaminergic and adrenergic effects. In case of overdose or hypersensitivity to ergotamine drugs, chest pain, pain and paresthesia in the extremities, vomiting, diarrhea (phenomena of ergotism) are possible. Dihydroergotamine nasal spray has the least side effects. The advantage of this drug is its ease of use, speed of action and high efficiency (75% of attacks are stopped within 20 - 45 minutes).

3rd group. Selective serotonin agonists (zolmitriptan, sumatriptan). They have a selective effect on serotonin receptors of cerebral vessels, preventing the release of substance P from the endings of the trigeminal nerve and neurogenic inflammation.

Sumatriptan is used in tablet (100 mg tablets) and injection forms of 6 ml subcutaneously. The effect occurs within 20 - 30 minutes; the most severe attacks are stopped within a maximum of 1 hour.

Zolmitriptan belongs to the second generation of selective serotonin agonists. The drug, in addition to its peripheral effect, which consists in narrowing the vessels dilated during a migraine attack and blocking pain impulses at the level of trigeminal nerve afferents, also has a central effect. The latter is achieved by influencing the interneurons of the brain stem, due to the penetration of the drug through the blood-brain barrier. The advantages of zolmitriptan compared to other triptans are: 1) higher clinical efficacy when taken orally; 2) faster achievement of the therapeutic level of the drug in the blood plasma; 3) less vasoconstrictor effect on the coronary vessels. Zolmitriptan is used in 2.5 mg tablets.

Side effects of serotonin receptor agonists: a feeling of tingling, pressure, heaviness in different parts of the body, facial flushing, fatigue, drowsiness, weakness.

Drugs of groups 2 and 3 are currently the basic drugs used to relieve migraine attacks.

Preventive treatment during the interictal period

Preventive treatment in the interictal period is carried out for patients with a frequency of attacks 2 or more times per month. In this case, a course of treatment lasting 2-3 months is necessary. For patients suffering from infrequent migraine attacks, preventive therapy is not indicated. The main goal of preventive treatment is to reduce the frequency of attacks, reduce their intensity and generally improve the quality of life of patients. The task of curing M is incompetent due to the hereditary nature of the disease.

For preventive therapy, non-drug methods are used, as well as various pharmacological agents. Non-drug methods include a diet limiting foods containing tyramine; gymnastics with an emphasis on the cervical spine; massage of the collar area; water procedures; acupuncture; post-isometric relaxation; biofeedback.

Drug preventive treatment of M includes drugs of various pharmacological groups, which are individually selected for each patient, taking into account provoking factors, concomitant diseases, emotional and personal characteristics, as well as pathogenetic factors of M. The most widely used are b-blockers (propranolol, atenolol, etc.); calcium channel blockers (nimodipine, verapamil); antidepressants (amitriptyline, etc.); serotonin antagonists (methysergide, peritol). It is possible to use small (antiplatelet) doses of ASA (125 - 250 mg daily); in older patients, good results are achieved by prescribing nootropic drugs (pyritinol, etc.); in the presence of allergies, antihistamines are recommended. The presence of muscular-tonic or myofascial syndrome in the pericranial muscles and muscles of the upper shoulder girdle on the favorite side of pain necessitates the administration of muscle relaxants (tizanidine, tolperisone), since activation of the trigger can provoke a typical migraine attack.

The most effective prevention of migraine cephalalgia is a combination of non-drug and medicinal treatment methods. Effective and safe relief of migraine attacks in combination with preventive therapy in patients with frequent attacks can significantly improve the quality of life of patients suffering from this hereditary disease.

1. Vein A.M., Avrutsky M.Ya. Pain and pain relief. M. Medicine. 1997; 277 p.
2. Vein A.M., Kolosova O.A., Yakovlev N.A., Karimov T.K. Headache. M. 1994; 286 pp.
3. Vein A.M., Kolosova O.A., Yakovlev N.A., Slyusar T.A. Migraine. M. 1995; 180 pp.
4. Vein A.M., Voznesenskaya T.G., Danilov Al. B. Effect of aspirin on CNF in healthy subjects. Journal of neuropathology. and a psychiatrist. 1995; 4:45-6.
5. Osipova V.V. Treatment of migraine and cluster headache with sumatriptan. Journal of neuropathology. and a psychiatrist. 1996; 3:100-4.
6. Solovyova A.D., Filatova E.G., Vein A.M. Treatment of acute migraine attacks with digidergot - a nasal aerosol. Journal of Neurology. and a psychiatrist. 1999; 2:21-4.
7. Diener H.C., Ziegler A. Medikamentose Migraineiprophylaxe. Der Schmerz. 1989; 3:227-32.
8. Olesen J. Larsen B. Focal hyperemia followed by spreading oligemia and impaired activation of CBF in classic migraine. Ann. Neurol. 1991; 238:23-7.
9. Olesen J. Clinical and pathophysiological observations in migraine and tension-type headache explained by integration of vascular, supraspinal and myofascial inputs. Pain. 1991; 46:125-32.
10. Ziegler K.D. The Treatment of Migraine./Wolff""s Headache and other Headpain. New York, Oxford. 1987; .87-111.

Medicines Index

Serotonin receptor agonists -
Zolmitriptan: ZOMIG (Zeneca)
Sumatriptan: IMIGRAN (Glaxo Wellcome)

Non-steroidal anti-inflammatory drugs -
Ketoprofen: KETONAL (Lek)

Muscle relaxants -
Tolperisone: MYDOCALM (Gedeon Richter)

Nootropic drugs -
Pyritinol: ENCEPHABOL (Merck)

Combined nootropic drug -
INSTENON (Nycomed)

Most often, middle-aged people, ranging from 30 to 60 years old, suffer from facial migraine. In most cases, pain appears in the lower jaw area, as well as in the neck area, sometimes spreading to the area around the eyes or to the upper jaw. The pain is very deep, unpleasantly aching, throbbing and sometimes unbearable. Against this background, dagger pain appears, attacks of which can be repeated up to several times a week. The duration of an attack of a facial migraine ranges from a couple of minutes to a couple of hours, it all depends on numerous factors.

Phenomena

During a facial migraine, a number of phenomena occur in the body:

• Pain on palpation of the carotid artery;
• Increased pulsation of the artery;
• Swelling of soft tissues;
• The occurrence of throbbing pain in the same part of the head.

Usually the main factor causing the disease is dental trauma. Pain in the carotid artery is noted by patients who suffer from other types of migraine. Their artery is just as painful on the side where the pain appears.

When to see a doctor

Facial migraine is a phenomenon in which you definitely need to see a doctor, but some types of pain do not indicate a migraine, but the presence of more serious ailments, so medical attention is needed in the following cases.

• Headaches occur suddenly and are very painful;
• Pain is associated with stiff neck;
• Unpleasant sensations may be accompanied by fever, convulsions, and confusion;
• Constant pain in people who have not previously complained of such phenomena.

Facial migraine can be accompanied by various pains in different parts of the face - cheeks, jaws, mouth, eyes. Each type of migraine has its own symptoms and is accompanied by its own complications.

Causes

There are several main factors that can trigger migraines:

• Excessive alcohol consumption;
• Changes in weather conditions – temperature, humidity;
• Ingestion of foods high in caffeine;
• Bright light;
• Products with preservatives;
• The presence of hormonal changes;
• Hunger;
• Stress;
• Perfumery;
• Lack of sleep and rest.

In order to eliminate pain, it is necessary to remove all provoking factors, and most likely, the pain will stop. If pain continues, it is recommended to consult a doctor.