Increased convulsive readiness. Symptoms and causes of high ICP in children. The most common causes of status epilepticus

Medicine section:

Neurosurgery and neurology

Factors that lower the seizure threshold

Factors that lower the seizure threshold (i.e., make it easier for a seizure to occur) in patients with or without a history of seizures are quite varied and are listed in the section Etiology of new seizures, as well as:

1. lack of sleep
2. hyperventilation
3. photostimulation (in some cases)

4. infection: systemic (febrile convulsions), central nervous system, etc.
5. metabolic disorders: electrolytes (especially severe hypoglycemia), pH (especially alkalosis), medications, etc.
6. TBI: closed TBI, penetrating TBI
7. cerebral ischemia: NMC

Greenberg. Neurosurgery

Causes

The main reason for the development of VBI is the obstruction of the patency of the main cephalic arteries. First of all, the extracranial sections of the spinal arteries are subject to deviation. Stenosis often affects arterial areas up to the point where the artery enters the bony canal. Sometimes stenosis is localized in the innominate or subclavian arteries. Vessels are mainly affected due to atherosclerotic stenosis. Congenital abnormalities in structure also play an important role. vascular bed. Rarer causes are inflammatory diseases such as arteritis or basilar or vertebral artery dissection.

The risk of developing ischemia in the vertebrobasilar region increases when the possibility of collateral circulation is limited. This is observed with the following deviations:

not the closedness of the Willis circle;
severe hypoplasia of any vertebral artery;
abnormal origin of small branches from the vertebral and basilar arteries.

One cannot help but pay attention to the possibility of compression of the vertebral arteries by the altered vertebrae, which can occur with spondylosis and osteophyte. This situation can be the main reason for the development of VBI. In addition, collateral circulation in the vertebrobasilar region has considerable potential, which is due to the presence of the Zakharchenko ring where the brain stem region is located, the Circle of Willis on the brain base, extra-intracranial connections among the arteries and anastomotic systems on the surface of the brain. Such bypass routes make it possible to completely compensate for pronounced defects in the vascular bed, regardless of their nature, acquired or congenital.

There are several anatomical factors that predispose to severe compression of the vertebral arteries with the risk of developing severe complications, among which there is also cerebral ischemia, which is clearly visible during diagnosis:

exostoses with the formation of a retroarticular canal;
Kimmerle anomaly;
other anomalies in the structure of the cervical vertebral region.

If these factors are present in a person, the role of functional factors increases, which include rotation of the cervical vertebrae with arterial compression and displacement, as well as injuries to the cervical spine.

Intracranial arteries may have a structural variant such as dolichoectasia. Modern non-invasive and invasive methods diagnostics of the cerebral vascular system have made it possible to more often identify such anomalies. Dolichoectasia is a peculiar combination of signs of ischemia of the structures that are supplied with blood from the vertebrobasilar basin and compression of the cranial nerves.

The cause of VBI may lie in damage to small-caliber arteries. This may happen due to diabetes mellitus and arterial hypertension, as well as a combination of these two disorders. Sometimes the reasons lie in cardiogenic emboli, which are usually accompanied by occlusion large vessel and the development of severe neurological deficits. Circulating units may become a prerequisite for the development of VBN blood cells and high ability for aggregation of formed elements.

Vascular disorders of the vertebo-basilar system among adults account for 30% of acute cerebral circulatory disorders and 70% of transient disorders. Approximately 80% of strokes are ischemic, and a quarter of them occur in the vertebrobasilar system (VBS). As noted, VBI also occurs among children. With the help of high-quality diagnostics, this diagnosis is detected in many children from birth, and the cause may be natal damage to the vertebral arteries and spine. Today, the number of such disorders among children and young people is increasing. VBI is chronic.

There are several classifications of this syndrome. One of them was presented in 1989 by Bakulev. He identified three stages in the development of this disorder:

Stage 1 – compensation, when there is an asymptomatic course or there are initial manifestations of the syndrome in the form of focal neurological disorders.
Stage 2 – relative compensation. Here transient ischemic attacks occur, i.e. acute disorder cerebral circulation, combined with rapidly passing cerebral or general symptoms. At the same stage, a small stroke occurs, i.e. completely reversible neurological deficit and discirculatory encephalopathy.
Stage 3 – decompensation. Here a complete ischemic stroke occurs, which has varying degrees of severity, as well as dyscirculatory encephalopathy, but in the third degree, whereas in the previous stage it had the first or second degree.

In accordance with the neurological classification, there are 4 stages:

Angiodystonic stage. In this case, subjective clinical symptoms predominate, rather than symptoms of focal brain damage.
Angiodystonic-ischemic stage.
Ischemic stage, when symptoms of cerebral ischemia in the vertebrobasilar region predominate. Autonomic-irritative symptoms practically disappear.
Stage of residual effects.

Symptoms

Symptoms of VBI can be divided into two groups:

Temporary symptoms usually develop during transient ischemic attacks. Their duration varies from several hours to several days. In this case, the person complains of pain in the back of the head, which has a pressing nature, discomfort in the neck and severe dizziness.
Constant symptoms. They are always present with a person and gradually increase. Exacerbations may occur, during which ischemic attacks occur that can lead to vertebrobasilar strokes. Among permanent signs The syndrome can include frequent headaches in the back of the head, tinnitus, visual and balance disturbances, memory loss, increased fatigue, dizziness, fainting, and a feeling of a lump in the throat.

The most common manifestation of the syndrome is dizziness, which occurs suddenly. Most patients describe the nature of such dizziness as a feeling of straight-line movement or rotation own body or surrounding objects. This may last for several minutes or hours. Dizziness is often combined with hyperhidrosis, nausea, and vomiting.

VBI syndrome can occur even in children aged 3 to 5 years, as well as between 7 and 14 years, although this was previously considered impossible. It has now been clarified that there are no age restrictions. There are specific signs of VBI in children. If they are observed, it is necessary to urgently contact medical institution, get diagnosed and start treatment. Exactly from timely diagnosis and treatment depends on the future of the child. Signs of the development of the syndrome in children include:

poor posture;
frequent tearfulness, increased drowsiness and fatigue;
the child does not tolerate stuffiness, which leads to fainting, nausea and dizziness;
the child sits in an uncomfortable position.

Some diagnoses that are given to children in early age, can provoke the development of the syndrome. These include perinatal encephalopathy and spinal injury during childbirth or during sports.

Diagnostics

Timely diagnosis helps to begin early treatment and avoid serious complications, such as stroke. Diagnostics is of particular importance for children, since timely treatment allows for a favorable prognosis for the development of VBI.

At the very beginning of diagnosis, it is important to determine the damage to the vessels of the vertebrobasilar region based on the clinical picture and the results of functional tests. All patients need to have auscultation of the supraclavicular region. You can confirm the deficiency of blood flow in the pool using several functional tests:

intensive hand work;
de Klein's test;
hautant's test, when the patient sits with a straight back and eyes closed;
vertebral artery test, when the patient lies on his back;
dizziness test, when the patient turns his head to the left and right, turns to the sides only with his shoulders.

Based on the patient's condition during these tests, it is possible to confirm a violation of blood flow in the vertebrobasilar region. Further diagnostics include ultrasound methods, which can be used to determine the location of the lesion and assess the hemodynamic significance of stenosis or pathological tortuosity of the vessels. Such methods help determine functional and structural compensation reserves.

Angiographic diagnostic methods, such as MRI, CT, and radiocontrast angiography, make it possible to most accurately determine the type, extent and localization of a lesion, and to identify multi-level lesions.

After all the necessary studies have been carried out, a diagnosis is made in accordance with ICD-10, then treatment is prescribed and the sooner this is done, the better, as it will avoid complications such as stroke and other consequences and even death.

Treatment

If the syndrome is at the initial stage of development, treatment is carried out on an outpatient basis. If symptoms of acute VBI clearly manifest themselves, the patient is admitted to the hospital for observation and prevention of strokes.

Most often, doctors combine medication with physiotherapy when prescribing treatment. The patient must understand that it is necessary to regularly monitor blood pressure and follow a diet. Given the chronic nature of the disease, it is important to assess the patient’s readiness to systematically use prescribed medications.

Some forms of the disease cannot be treated with medications at all. That is why it is necessary to determine the presence of the disease as early as possible. Individual treatment is selected for each patient. When drug treatment is prescribed, drugs from the following groups are selected:

Vasodilators, i.e. vasodilators to prevent occlusion. Most often, treatment with these drugs begins in the fall or spring. At first, small doses are prescribed, which are gradually increased. If the expected effect is not observed, the drug is sometimes combined with other drugs of similar action.
Antiplatelet agents that reduce blood clotting. It prevents the formation of blood clots. The most popular drug from this group is acetylsalicylic acid. The patient needs to consume 50-100 milligrams per day. However, patients with gastrointestinal diseases need to be careful when taking this drug, because Gastric bleeding may occur, and therefore aspirin should not be taken on an empty stomach.
Nootropic and metabolic drugs that improve brain function.
Antihypertensive drugs that regulate blood pressure.
Painkillers.
Sleeping pills.
Antidepressants.
Antiemetic drugs.
Medicines to reduce dizziness.

The following types of therapies are used:

Massage. It helps improve blood circulation.
Exercise therapy. Regular exercise therapy can help you get rid of spasms, strengthen your spine and improve your posture.
Reflexology. It also helps relieve muscle spasms.
Magnetotherapy.

When complex treatment does not produce results, surgical treatment is prescribed. The operation is performed to improve blood circulation in the vertebral and basilar arteries. In this case, angioplasty is common, in which a special stent is inserted into the vertebral artery. It prevents the arterial lumen from closing and maintains normal blood circulation. For atherosclerosis, endarterectomy is performed, the essence of which is to remove the atherosclerotic plaque. Microdiscectomy helps stabilize the spine.

In children, the syndrome is easily corrected. Drug treatment is practically not used. Rarely, when cases are extremely severe, surgery is performed.

Traditional methods of treatment can also be used, but only as an addition to the main treatment and after consultation with a doctor. A positive effect of vitamin C has been noted. To prevent blood clots, it is recommended to consume viburnum, cranberries, sea buckthorn, currants and other products containing this vitamin.

Forecast

The prognosis of VBI is determined by the nature and severity of the underlying disease and the degree of damage to the vascular bed. If the narrowing of the arteries progresses, persistent arterial hypertension is observed and there is no adequate therapy, the prognosis is poor. Such patients have a high risk of developing stroke. They may also develop dyscirculatory encephalopathy.

A favorable prognosis can be made when the condition of the vascular system of the head is satisfactory, and therapeutic tactics adequate and effective. Much depends on how the patient follows medical recommendations.

Prevention

The following measures will help prevent the onset of the disease or slow down its development:

Diet. It is necessary to give up white bread, sausages, fatty, fried and smoked bread, and canned food. It is worth eating more low-fat cottage cheese, sour berries, garlic, seafood, and tomatoes.
Quit smoking and monitor the amount of alcohol consumed so that it does not exceed the norm, it is natural.
Reduce salt intake.
Exercise in moderation.
Monitor blood pressure.
Don't sit in one position for a long time.
Sleep and sit on a comfortable surface.
Avoid stress.
Walk more in the fresh air, swim more.

VBI is a serious syndrome, but with timely treatment and prevention, its sad consequences can be avoided.

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Bradycardia: symptoms, treatment

Disturbances in the occurrence and conduction of the nerve impulse that ensures the contraction of the heart lead to changes in heart rhythm - arrhythmias. One of the varieties of such pulse deviations is bradycardia - a decrease in the number of heartbeats to less than 55-60 beats per minute in adults and adolescents over 16 years of age, 70-80 in children and 100 in children under one year old. This heart rhythm disturbance is not an independent disease. As a symptom, bradycardia can occur at the most various ailments or appears as a protective physiological reaction in response to external stimuli.

In this article we will introduce you to the physiological and pathological causes, manifestations, methods of diagnosis and treatment of bradycardia. This information will help you make the right decision about the need to see a doctor to identify and treat diseases that provoke this symptom.

Causes

Physiological bradycardia is often found in well-trained individuals

Changes in heart rate can be caused by both natural external factors and diseases of internal organs and systems. Depending on this, bradycardia can be physiological and pathological.

Physiological bradycardia

This slowing of the pulse is a variant of the norm, is not dangerous to human health and can occur after exposure to the following external factors and irritants:

moderate hypothermia or exposure to conditions of high humidity and temperature - the body in such conditions goes into a “saving mode” of energy resources;
age-related changes - after approximately 60-65 years, islands appear in the myocardial tissues connective tissue(age-related cardiosclerosis) and the metabolism as a whole changes, as a result, the body’s tissues need oxygen less, and the heart does not need to pump blood with the same intensity as before;
stimulation of reflex zones - pressure on the eyeballs or pressure on the bifurcation of the carotid arteries when wearing a tie or shirt with a tight-fitting collar affects the vagus nerve and causes an artificial slowdown of the pulse;
good physical training(“training”) – in athletes or during physical labor, the left ventricle increases in volume and is able to provide the body with required quantity blood and with fewer contractions;
night sleep - the body is at rest and does not need frequent heartbeats and large amounts of oxygen;
physical or psycho-emotional fatigue - when tired, the body goes into a “saving mode” of energy resources.

Another type of physiological bradycardia is idiopathic. In such cases, examination of the patient does not reveal any reasons for the slowing of the pulse. The person does not engage in sports or physical labor, does not take medications, does not feel the effects of other contributing factors, and his well-being does not suffer in any way from bradycardia, because it is successfully compensated by the body itself.

Sometimes a decrease in heart rate is considered a physiological norm when taking certain medications that have a similar side effect. But the norm is considered to be a slowing of the pulse only in cases where the patient does not feel worse and the drug is not taken for a long time. In other situations, it is advisable to reduce the dosage, discontinue or replace the medication with another.

In the cases described above, the slowing of the pulse is not dangerous to health and does not cause a decrease in blood supply to the brain and other organs. Treatment to eliminate physiological bradycardia is not required, because it goes away on its own after eliminating the external stimulus. However, with prolonged slowing of the pulse, which occurs in athletes or people over 60-65 years of age, clinical observation by a cardiologist is recommended for the timely detection of possible deviations in health.

Pathological bradycardia

This slowing of the pulse is not normal; it affects a person’s health and can occur due to the following reasons:

heart pathologies - a slow pulse can be provoked by coronary disease, myocardial infarction, focal or diffuse cardiosclerosis, inflammatory diseases (endocarditis, myocarditis), Morgagni-Adams-Stokes syndrome, etc.;
taking medications (especially Quinidine, beta blockers, cardiac glycosides, calcium channel blockers, Morphine, Amisulpride, Digitalis and Adenosine) - usually a slowing of the pulse is caused by improper dosing and administration of such drugs, affects general well-being and can threaten the patient’s life;
poisoning with toxic substances (lead compounds, nicotinic acid and nicotine, narcotic and organophosphorus substances) - under the influence of these compounds the tone of the parasympathetic and sympathetic changes nervous system, various organs and systems are affected (including cells of the cardiac conduction system and myocardial cells);
increased tone of the parasympathetic nervous system - this reaction can be caused by some diseases and pathological conditions(neurosis, depression, peptic ulcer, tumors in the mediastinum, traumatic brain injury, hemorrhagic stroke, increased intracranial pressure, brain tumors, swelling after surgery on the neck, head or mediastinal area);
some infectious diseases - usually infections contribute to the development of tachycardia, but typhoid fever, some viral hepatitis and severe sepsis can cause a slow heart rate, in addition, bradycardia can be observed in severe and protracted infectious diseases that lead to exhaustion of the body;
hypothyroidism - decreased levels of thyroxine and triiodothyronine (hormones thyroid gland) leads to a change in the tone of the nervous system, disruption of the heart and slowing of the pulse; attacks of bradycardia in such conditions occur initially occasionally, and then become constant.

In the cases described above, a slow pulse is dangerous to health and causes a decrease in blood supply to the brain and other organs. Such bradycardia is a symptom of pathology and requires treatment of the underlying disease.

Symptoms

One of the manifestations of bradycardia is dizziness

A slower heart rate affects general well-being only with pathological bradycardia. In addition to signs of the underlying disease, the patient develops symptoms indicating a decrease in heart rate, and their severity will depend on the pulse rate.

Almost all signs of bradycardia occur due to oxygen starvation of the organs and tissues of the body. They usually occur sporadically, but even their periodic occurrence has a significant impact on the quality of life and indicates the presence of a disease that requires treatment.

Dizziness

A significant slowdown in heart rate causes the heart to be unable to maintain blood pressure at the proper level. Due to its decrease, the blood supply to many systems and organs is disrupted. First of all, the brain begins to suffer from ischemia and oxygen starvation, and that is why dizziness becomes one of the first signs of bradycardia. Typically, this symptom appears sporadically and disappears after the number of heartbeats has stabilized.

Fainting

The appearance of such a symptom of bradycardia is caused by the same reason as dizziness. The degree of its severity depends on the level of reduction in blood pressure. With severe hypotension, the brain seems to temporarily switch off, which manifests itself in the form of a presyncope or fainting. Especially often, such symptoms occur against the background of mental or physical fatigue.

Weakness and increased fatigue

These symptoms are caused by a deterioration in the blood supply to skeletal muscles that occurs when the heart rate slows. Due to lack of oxygen, muscle cells are not able to contract with the usual force, and the patient feels weakness or decreased tolerance to physical activity.

Pale skin

When the heart rate slows, blood pressure decreases and insufficient blood flows to the skin. In addition, it is the skin that is a kind of “depot” of blood, and when there is insufficient amount of it, the body mobilizes it from the skin into the bloodstream. Despite this replenishment of blood vessels, the skin, due to hypotension and decreased pulse, continues to suffer from circulatory failure and becomes pale.

Dyspnea

With bradycardia, blood in the body is pumped more slowly and stagnation in the lungs may occur. During physical activity, the patient experiences shortness of breath, because... the vessels of the pulmonary circulation cannot provide complete gas exchange. In some cases, a dry cough may appear in parallel with breathing problems.

Chest pain

Severe bradycardia is always accompanied by disturbances in the functioning of the heart and a deterioration in the blood supply to the myocardium. When the pulse slows significantly, the heart muscle tissues do not receive enough oxygen, and the patient develops angina. Chest pain with bradycardia occurs after physical, psychoemotional stress or a decrease in heart rate to 40 beats per minute or less.

Complications

The prolonged presence of bradycardia and untimely treatment of the underlying disease can cause the following complications:

the formation of blood clots, which increases the risk of myocardial infarction, ischemic stroke and the development of thromboembolism;
heart failure, which increases the likelihood of developing coronary heart disease and myocardial infarction;
chronic attacks of bradycardia, causing weakness, dizziness, deterioration in concentration and thinking.

Diagnostics

The doctor will detect bradycardia by taking the patient's pulse or performing auscultation (listening to the sounds) of the heart

Even the patient himself can find out about the presence of bradycardia. To do this, just feel the pulse in the wrist (radial artery) or in the neck (carotid artery) and count the number of beats per minute. If the number of heartbeats decreases according to age norms, it is necessary to consult a general practitioner for a detailed clarification of the causes of bradycardia and treatment.

To confirm the diagnosis, the doctor will conduct the following examinations:

listening to heart sounds;
phonocardiography.

To identify pathological bradycardia, the doctor performs the following test: the patient is asked exercise stress and the pulse is measured. Its frequency in such cases increases slightly or the patient experiences an attack of arrhythmia.

If pathological bradycardia is confirmed, the following laboratory and instrumental methods diagnostics:

clinical and biochemical blood test;
clinical and biochemical urine analysis;
blood test for hormones;
toxin tests;
bacteriological examinations of blood, urine or feces;
Echo-CG, etc.

The scope of the examination is determined individually for each patient and depends on the associated complaints. After making a preliminary diagnosis, the patient may be recommended to consult a cardiologist, neurologist, gastroenterologist, endocrinologist or other specialized specialists.

Urgent Care

With a sharp slowdown in the pulse and arterial hypotension, the patient may experience a pre-fainting state or faint. In such cases, he needs to provide first aid:

Lay the patient on his back and raise his legs, resting them on a bolster or pillow.
Call an ambulance.
Remove or unfasten clothing that restricts breathing.
Ensure fresh air flow and optimal temperature conditions.
Try to bring the patient to consciousness: sprinkle the face with cool water, rub ears and face soaked in cold water with a towel, lightly pat his cheeks. If the measures provided are not enough, then give the patient to inhale a product with a pungent odor: onion juice, cotton wool soaked in vinegar or ammonia. Remember that sudden inhalation of ammonia vapor may cause bronchospasm or respiratory arrest. To prevent such a complication, cotton wool with ammonia should be applied at a distance from the respiratory tract.
If the patient has regained consciousness, then the pulse should be measured and given to him to drink warm tea or coffee with sugar. Try to find out what medications he takes and, if possible, give them.
After the ambulance team arrives, tell the doctor about all the circumstances of the fainting and the actions performed.

Treatment

Treatment for pathological bradycardia is aimed at treating the underlying disease, leading to a slow heart rate. It can be conservative or surgical. Patients with acute forms of bradycardia require hospitalization.

Conservative therapy

In some cases, to eliminate bradycardia resulting from an overdose or long-term use medications, it may be enough to stop taking the drug or reduce its dosage. For other causes of slow heart rate, a treatment plan is drawn up depending on the severity of the underlying disease.

To eliminate bradycardia, the following medications can be used to increase the number of heart contractions:

ginseng extract - Ginseng tincture, Pharmaton vital, Herbion Ginseng, Gerimax, Doppelgerts Ginseng, Teravit, etc.;
Eleutherococcus extract – Eleutherococcus tincture, Eleutherococcus P (tablets), Eleutherococcus plus (dragees);
preparations based on belladonna extract – thick or dry belladonna extract, belladonna tincture, Corbella, Becarbon, etc.;
Atropine;
Izadrin;
Isoprenyl;
Caffeine;
Eufillin;
Ephedrine;
Ipratropium bromide;
Alupent.

As a rule, taking medications to eliminate bradycardia is recommended when the heart rate drops to 40 beats per minute or less and fainting occurs. The choice of drug, its dosage and duration of administration are determined individually for each patient. Self-medication with such drugs is unacceptable, because their improper use can lead to severe arrhythmias.

In addition to these medications, patients are prescribed drugs to treat the underlying disease: antibiotics for infections, thyroid hormones for hypothyroidism, medications for the treatment of heart disease, peptic ulcers, poisoning, tumors, etc. It is the therapy of the root cause of bradycardia that makes it possible to more effectively eliminate the symptom itself and those unpleasant manifestations which he calls.

In addition to drug treatment, patients with such pulse disturbances should avoid bad habits. This is especially true for smoking, because... It is nicotine that significantly affects heart rate.

With pathological bradycardia, diet is also important. When creating a menu, patients should be guided by the following principles:

limiting products with animal fats;
exclusion of alcoholic beverages;
introduction of vegetable oils and nuts rich in fatty acids into the diet;
the calorie content of food must correspond to energy costs (1500-2000 kcal, depending on the work performed);
reducing the amount of salt and volume of liquid (as recommended by a doctor).

Surgery

Surgical operations to eliminate bradycardia are performed if conservative treatment is ineffective and the underlying disease is accompanied by severe hemodynamic impairment. The technique of such interventions is determined by the clinical case:

for congenital heart defects, corrective cardiac surgery is performed to eliminate the anomaly;
for mediastinal tumors – interventions are performed to eliminate the tumor;
in case of severe bradycardia and ineffectiveness of drug treatment, a pacemaker (a device for normalizing the number of heartbeats) is implanted.

ethnoscience

As an addition to the basic drug therapy plan, your doctor may recommend taking the following folk remedies:

radish with honey;
decoction of rose hips;
yarrow decoction;
garlic with lemon juice;
walnuts with sesame oil;
tincture of pine shoots;
tincture of Chinese lemongrass;
infusion of immortelle flowers;
Tatar decoction, etc.

When choosing a product traditional medicine Possible contraindications and individual intolerance to the components of the recipe must be taken into account.

Bradycardia can be physiological or pathological. This symptom requires treatment only in cases where it is accompanied by a deterioration in health and is caused by various diseases or poisonings. Treatment tactics for pathological bradycardia depend on the clinical case and are determined by the pathology causing the slowing of the pulse. Treatment of such diseases can be medication or surgery.

Union of Pediatricians of Russia, pediatric cardiologist M.A. Babaykina talks about bradycardia in children:

Watch this video on YouTube

Cardiologist D. Losik talks about bradycardia:

Watch this video on YouTube

Intracranial hypertension: symptoms, causes and treatment

Probably every person, at least sometimes, suffered from headache attacks, whether as a result of fatigue and overwork, or as a symptom of a cold. But not everyone knows that the main cause of headaches is intracranial hypertension.

If the pain is episodic and its cause is more or less known, then there is no reason to worry. But if your head hurts more than it doesn’t, then you should consult a doctor to avoid the progression of a much more serious pathology than a common cold.

Mechanism of headache

Our cranium contains, in addition to the brain itself, blood vessels, cerebrospinal fluid, interstitial substance. The cause of intracranial hypertension is the presence of factors that increase the volume of at least one component of the brain system.

A healthy person produces up to 600 ml cerebrospinal fluid(cerebrospinal fluid) per day, which performs protective, nutritional and communication functions between parts of the brain. With edema, enlarged areas of the brain compress the space filled with cerebrospinal fluid and, accordingly, intracranial pressure increases.

If the outflow of cerebrospinal fluid is disrupted or a hematoma forms due to a cerebral hemorrhage, hypertension is also observed. The main reasons include neoplasms or inflammation of the brain tissue, creating abnormal pressure in the skull. And due to the discrepancy between the pressure of different parts of the brain, a dysfunction of the central nervous system occurs.

When hypertension occurs not due to some other disease, but due to the influence of objective factors, for example, obesity, side effects from taking medications, then they talk about benign intracranial hypertension. It is also called a false brain tumor. This condition can also occur in children when taking corticosteroid drugs, drugs of the tetracycline group or those containing an increased dose of vitamin A are stopped.

The normal functioning of the brain is ensured by the following components:

unhindered passage of cerebrospinal fluid between the membranes of the brain and through its ventricles;
good absorption (suction) of cerebrospinal fluid into the venous network of the brain;
complete venous outflow of blood from the brain.

Venous intracranial hypertension occurs due to improper flow of venous blood from the intracranial system due to thrombosis or blockage of the venous ducts, emphysema or mediastinal tumors, causing increased pressure in the chest.

Manifestation of the disease in children and adults

How the syndrome of intracranial hypertension will manifest itself depends entirely on the local location of the causative focus and the speed of development of the disease.

The main signs of intracranial hypertension in adults are headache, most often occurring before lunch, while eating, nausea and vomiting, and possible visual disturbances with pain in the eyeballs up to loss of consciousness. The intensity of the pathology can vary from mild lethargy to falling into a coma.

Symptoms of moderate intracranial hypertension are dulling of consciousness when interest in life is lost, double objects in the eyes, and heart sounds becoming rare as in bradycardia. This state is especially pronounced with a decrease in pressure in the atmosphere. In addition, sleep disturbances possible bleeding from the nose, trembling of the chin, marbling of the skin, as well as changes in behavior indirectly complement the signs of intracranial hypertension in adults.

In women, as a rule, this is associated with the onset of menopause or pregnancy, during which changes occur in the menstrual cycles, as well as with obesity or taking certain medications.

Intracranial hypertension syndrome in children can be caused by the following reasons:

increased size of a child's skull due to excess production of cerebrospinal fluid by the body due to hydrocephalus or hydrocephalus;
consequences of birth trauma;
an infectious disease suffered by the mother during pregnancy.

Intracranial hypertension in infants is diagnosed when there is a developmental delay and the frontal part of the head is too convex. At the same time, the child does not react in any way to bright light and often rolls his eyes. The place of the fontanel on the head is either tense or swollen, the eyeballs are bulging.

In older children, these manifestations include increased drowsiness, constant or frequent headaches, possible strabismus and the inability to catch a visual image that escapes and is not recorded by vision.

Intracranial hypertension in children, which lasts for a long time, can cause pathological changes in brain development. Therefore, when the source of the disease is identified, it is necessary to urgently take all measures for further treatment of the child in order to avoid a worse prognosis.

Treatment methods

Depending on which component common system brain functioning is out of order, the symptoms and treatment of intracranial hypertension in adults and children depend.

So, in order to reduce the amount of cerebrospinal fluid produced, they are prescribed urinary agents, and the corresponding set of exercises, developed by specialists, is designed to reduce intracranial pressure. A special diet and dosage of water consumed per day are prepared for the patient. Engaging a chiropractor and receiving acupuncture sessions help normalize the amount of cerebrospinal fluid.

If the case is severe and the above procedures do not produce the desired effect, they resort to the surgical method. It consists in the fact that by trephination of the skull, a hole is made in it through which a special drainage system is implanted. This system drains excess fluid from the skull.

These methods significantly improve the patient’s health, eliminating the signs of intracranial hypertension syndrome just a few days after the start of treatment. However, the disease can be successfully cured only if the cause that gave rise to hypertension is completely eliminated.

Treatment of intracranial hypertension in children can be carried out using both conservative and radical methods. The choice of treatment method depends entirely on the cause of the disease.

If the pathology is diagnosed in a newborn, then such babies should be observed from birth by a neurologist, who, if necessary, at a certain stage will adjust the treatment to avoid serious complications.

In order to eliminate the consequences of the pathology of pregnancy and the difficult course of labor, it is necessary to breastfeed the baby for as long as possible, punctually observe the daily routine and, especially, sleep, constantly be in contact with the child both emotionally and contactally in order to avoid nervous stress, and regularly take walks outside in any weather.

At the same time, the child must take medications designed to calm the nervous system, improve the circulatory and urinary systems, as well as vitamin preparations to strengthen the immune system.

For older children, the doctor prescribes physiotherapeutic procedures; swimming lessons help in curing the disease.

Any anatomical abnormalities that interfere with the outflow of cerebrospinal fluid from the brain can be resolved surgically.

From traditional methods, as a complementary remedy to the main treatment, you can rub lavender oil into temporal part heads before bed. This remedy not only calms the nervous system, but also promotes strong healthy sleep, which significantly speeds up recovery.

Video about intracranial hypertension:

Existing as a predisposition or acquired as a result of damage, a structural and functional deviation from the norm of brain neurons serves as the basis for a disorder of brain processes that lead to increased excitability, characterized by a preponderance of excitation over inhibition and increasing to convulsive readiness. Against this background, after suppression of inhibitory mechanisms, single, but intense or cumulative irritations cause convulsive phenomena.

Forester sees the essence of convulsive readiness, which fluctuates not only from individual to individual, but also from moment to moment in the same person, in the extremely labile excitability of all motor elements of the nervous system: even weak irritations cause maximum discharges in the pathological focus, and this the reaction lasts longer than the irritation itself, and the excitement, spreading to neighboring areas, can cause generalized convulsions. From the metabolic-physiological point of view, in accordance with the views of Selbach, he characterizes convulsive readiness as an expression of the entire set of metabolic phenomena, which in the period between attacks are determined by the prevalence of assimilatory processes and lead to the need for a central switch in the direction of dissimilation and in the form of a convulsive seizure. Inherited or acquired convulsive readiness weakens in old age, changes depending on the time of day and year and is influenced by the endocrine system.

Factors contributing to a seizure. Factors that increase excitability and its lability can be caused by metabolic or neurophysiological processes, and these processes interact.

Metabolic and physiological processes. In the metabolic-physiological aspect, convulsive readiness is increased by all deviations from the norm, which Selbach reduces to the common denominator of parasympathicotonia with an assimilatory, trophotropic metabolic tendency (increase in body weight, accumulation of fluid in tissues after taking large amounts of table salt, errors in diet, constipation). An increased danger is fraught with the vagototonically directed phase of sleep, and a seizure often occurs on the night following unusual sleep deprivation, when sleep is especially deep. Equally dangerous is the different increased lability a phase of switching from a more awake state during the day to a more restorative state at night and back. Some climatic factors may also have a certain significance, as a result of which vegetative lability may increase.

A decrease in the seizure threshold can also be caused by blood alkalosis as a result of hyperventilation, after which blood pressure decreases, the blood supply to the brain decreases significantly and in many cases disturbances appear on the electroencephalogram. A decrease in carbon dioxide content in the blood at an optimum of 3-5% gradually weakens the activity of reticular neurons, while a limited rise in carbon dioxide enhances it. As for endocrine-metabolic factors, hypoglycemia, hypocalcemia, and in some cases menstruation, pregnancy, and hypothyroidism contribute to seizures.

Nervous processes. Dissimilatory switching becomes necessary as a result of excessive strengthening of the assimilatory metabolic installation. This moment plays a certain role in neurohumoral changes leading, due to increasing excitation, to an epileptic discharge. The inhibitory and activating systems of the brain stem, which, according to Selbach, are the material substrates of tropho- and ergotropic bipolarity, are nevertheless influenced not only by the metabolic system that prevailed at one time or another, but also by nervous processes. Brain damage is also of similar importance: increased intracerebral pressure, mechanical and thermal irritations (heat stroke), encephalitis, meningitis, exogenous and endogenous intoxications, circulatory disorders due to vasospasms, arterial hyper- and hypotension, fluctuations in cerebrospinal fluid pressure, etc. Caused by drugs the increase in cortical seizure excitability is, as Kaspers suggests, (at least in part) a consequence of their direct effect on cellular permeability in the cerebral cortex. Strong sensory stimulation can also contribute to a seizure: photostimulation with intermittent light stimulation and loud sounds.

Psychic influences. They can also increase seizure activity. Strong emotional experiences can take precedence over hormonal, autonomic or vasomotor factors during mental stress, with active concentration, in conditions of responsible work or in a solemn atmosphere, seizures are often suppressed, but then, when mental tension passes, and protective forces weaken and arise with redoubled force. Experts report on children who, by quickly moving their hand and extended fingers between their eyes and a light source, could artificially induce a seizure in themselves, and in one patient, inducing such a seizure was associated with such pleasure that it became a need for her. If, when increasing convulsive readiness with the help of flickering light, we are dealing with a reflex phenomenon, then in this case the psychological factor played a provoking role, as in “musicogenic” epilepsy. This psychological factor can be an experience that is not only emotionally charged, but also associated with a certain meaning. Thus, on the electroencephalogram of one young epileptic patient, convulsive potentials appeared when the name of one of his housemates, with whom he had a strained relationship, was called.

Factors that delay seizures. Factors that delay seizures are, in accordance with their antagonism in relation to factors that lower the convulsive threshold, those whose action is marked by a sympathicotonic, ergotropic and dissimilatory character. True, in conditions of extreme vegetative lability, ergotropic stimulation can also provoke a seizure, without which a seizure does not occur. The convulsive threshold is usually increased by dehydration, acidosis and increased levels of globulins that usually underlie fasting, as well as by drugs that enhance oxidative processes (calcium, ammonium chloride, etc.), and metabolic restructuring due to infectious processes. Sometimes pneumoencephalography leads to this. In one of our patients, seizures stopped during exacerbation of psoriasis. Gottwald reports on one patient with post-traumatic epilepsy, who, after thallium poisoning, developed insomnia and transient parkinsonism, and the seizures stopped. This author refers to the case of Klus, in which a patient, after epidemic encephalitis that affected the vegetative centers of the diencephalon, developed parkinsonism, and the epilepsy disappeared, and explains the cessation of seizures in his patient by the fact that thallium, this “stychnine” sympathetic system", compensated for the vagotropic tendency. Hormonal drugs of the parathyroid and gonads, partly of the pituitary gland and adrenal glands, and of pharmacological drugs - atropine and barbiturates that suppress vagotonia can have a delaying effect on seizures and states of mental stress.
Neurophysiologically normal brain rhythms, which, due to the alternation of excitation and delays, maintain a normal level of readiness, create physiological protection against convulsive discharge. After a seizure, a short-term increase in the seizure threshold is followed by a decrease.

Provoking a seizure. Using a water test with pituitrin (a preparation of the posterior lobe of the pituitary gland), for the effect of which the general vegetative situation is decisive, it is possible to induce adhesions in most patients with epilepsy (but not in healthy people). Diagnostically more reliable and safer than this test are methods aimed at activating convulsive potentials, and above all the already mentioned hyperventilation with its alkalizing and lowering convulsive threshold effect. In case of unclear cerebral focal diseases and in case of activation of traumatic convulsive foci, intravenous use of cardiazol turned out to be advisable. With the help of a slow injection of Cardiazol, in 80% of cases of genuine epilepsy, it is also possible to detect typical phenomena on the electroencephalogram.

In addition to natural sleep, in which many seizure sufferers show seizure potentials on a normal waking electroencephalogram, drug-induced sleep, especially barbiturate sleep, can also serve as a way to provoke a seizure. Since, however, provoking with natural sleep during temporal lobe epilepsy gave better results than pentothal, Mayer preferred largactil (a phenothiazine derivative), which leads to a state very close to physiological sleep, and with its help achieved positive results in 86% of cases.

Using stimulation with flashing light, Schaper caused specific changes in the electroencephalogram in 38% of children suffering from seizures (among adults with an intact brain, only 2%).

The combination of flickering light with cardiazol causes hypersynchronous potentials even at small doses, which, however, according to Hess, are not enough to diagnose epilepsy; Gastout believes that this combination can be used as a test for diencephalic disorders.

Convulsive readiness in childhood. Most authors believe that the reasons for increased convulsive readiness in childhood are the immaturity of the child’s brain, insufficient differentiation of the cerebral cortex and its inhibitory functions, and weak myelination of many pathways. The child's brain, like all rapidly growing tissues in general, should be considered especially vulnerable. Other authors see the reason for this increased convulsive readiness as follows. that the children’s brain is very rich in water, in the increased permeability of the blood-cerebrospinal fluid barrier, in the imbalance of the child’s autonomic system, etc. Forester does not at all consider the fact of increased convulsive readiness in children to be proven, since encephalitis, meningitis and other brain lesions are more often observed at an early age; in addition, infections in a child occur differently than in an adult (smaller lung volume, stronger exhalation of carbon dioxide during hyperthermia, alkalosis).

Based on numerous observations, K. Muller came to the conclusion that the convulsive readiness of children has its own characteristics. In childhood, purulent meningitis is especially common. Among 362 children with meningitis, 173 had convulsions. Of the 21 adults who died, 4 had convulsions during the illness, and of 107 children, 104. Based on the fact that with the same mortality and the same tendency to hyperthermia, children had convulsions more often than in adults, K. Müller concluded that with purulent meningitis, the appearance of convulsive seizures is not due only to the severity of the disease and that convulsive readiness in children has a special character. Forester, like Stertz, believes that irritation leading to convulsions causes a chain of successive reactions, of which each previous one causes the next one, and the final reaction in this chain is a convulsive attack. Since different chains of reactions with their different starting points lead to the same thing convulsive syndrome, we have to assume that at some point their paths converge into one common path. According to Forester, animals with a low seizure threshold for Cardiazol may be resistant to Pyramidone. In patients with numerous clinical seizures, the seizure threshold may be normal, and in rare seizures, it may be low. In twilight states, the seizure threshold is almost always many times higher than normal. The threshold function is probably based on the activity of inhibitory neural systems and synaptic resistance.

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(lat. Epilepsia - seized, caught, caught) is one of the most common chronic neurological diseases of humans, manifested in the body’s predisposition to the sudden occurrence of convulsive attacks. Other common and commonly used names for these sudden attacks- epileptic seizure, falling. Epilepsy affects not only people, but also animals, for example, dogs, cats, mice. Many great ones, namely Julius Caesar, Napoleon Bonaparte, Peter the Great, Fyodor Dostoevsky, Alfred Nobel, Joan of Arc, Ivan IV the Terrible, Vincent Van Gogh, Winston Churchill, Lewis Carroll, Alexander the Great, Alfred Nobel, Dante Alighieri, Fyodor Dostoevsky , Nostradamus and others suffered from epilepsy.

This disease was called “God’s mark,” believing that people with epilepsy were marked from above. The nature of the appearance of this disease has not yet been established; there are several assumptions in medicine, but there is no exact data.

The common belief among people that epilepsy is an incurable disease is wrong. The use of modern antiepileptic drugs can completely relieve seizures in 65% of patients and significantly reduce the number of seizures in another 20%. The basis of treatment is long-term daily drug therapy with regular follow-up studies and medical examinations.

Medicine has established that epilepsy is hereditary disease, it can be transmitted through the mother's line, but more often it is transmitted through the male line, it may not be transmitted at all or may appear after a generation. There is a possibility of epilepsy in children conceived by parents who were drunk or suffering from syphilis. Epilepsy can be an “acquired” disease, as a result of severe fright, head injury, maternal illness during pregnancy, due to the formation of brain tumors, cerebral vascular defects, birth injuries, infections of the nervous system, poisoning, neurosurgery.

An epileptic seizure occurs as a result of simultaneous excitation nerve cells which occurs in a specific area of the cerebral cortex.

Based on their occurrence, epilepsy is classified into the following types:

symptomatic- a structural defect of the brain can be detected, for example, a cyst, tumor, hemorrhage, developmental defects, manifestation of organic damage to brain neurons;
idiopathic- there is a hereditary predisposition, and there are no structural changes in the brain. Idiopathic epilepsy is based on channelopathy (genetically determined diffuse instability of neuronal membranes). Signs organic damage There is no brain in this type of epilepsy, i.e. the patients' intelligence is normal;
cryptogenic- the cause of the disease cannot be identified.

Before each epileptic attack, a person experiences a special state called an aura. The aura manifests itself differently in each person. It all depends on the location of the epileptogenic focus. The aura can be manifested by increased temperature, anxiety, dizziness, the patient feels cold, pain, numbness of some parts of the body, strong heartbeat, a feeling of unpleasant odor, the taste of some food, and sees a bright flickering. It should be remembered that during an epileptic attack, a person not only does not realize anything, but also does not experience any pain. An epileptic attack lasts several minutes.

Under a microscope, during an epileptic seizure, cell swelling and small areas of hemorrhage are visible in this place of the brain. Each seizure makes it easier to carry out the next one, forming permanent seizures. This is why epilepsy must be treated! Treatment is strictly individual!

Predisposing factors:

change in climatic conditions,
lack or excess of sleep,
fatigue,
bright daylight.

Symptoms of epilepsy

Manifestations of epileptic seizures vary from generalized convulsions to changes in the patient’s internal state that are barely noticeable to people around. There are focal seizures associated with the occurrence of an electrical discharge in a certain limited area of the cerebral cortex and generalized seizures, in which both hemispheres of the brain are simultaneously involved in the discharge. During focal attacks, convulsions or peculiar sensations (for example, numbness) in certain parts of the body (face, arms, legs, etc.) may be observed. Focal seizures may also involve short bouts of visual, auditory, olfactory, or taste hallucinations. Consciousness during these attacks can be preserved; in this case, the patient describes his sensations in detail. Partial or focal seizures are the most common manifestation of epilepsy. They occur when nerve cells are damaged in a specific area of one of the brain hemispheres and are divided into:

simple - with such seizures there is no disturbance of consciousness;
complex - attacks with a disturbance or change in consciousness, caused by areas of overexcitation of various localizations and often become generalized;
secondary generalized seizures - typically begin in the form of a convulsive or non-convulsive partial seizure or absence seizure, followed by a bilateral spread of convulsive motor activity to all muscle groups.

The duration of partial attacks is usually no more than 30 seconds.

There are states of the so-called trance - externally ordered actions without conscious control; upon returning consciousness, the patient cannot remember where he was and what happened to him. A type of trance is sleepwalking (sometimes of non-epileptic origin).

Generalized seizures can be convulsive or non-convulsive (absence seizures). For others, the most frightening ones are generalized convulsive seizures. At the beginning of the attack (tonic phase), tension of all muscles occurs, short-term cessation of breathing, a piercing cry is often observed, and tongue biting is possible. After 10-20 seconds. the clonic phase begins when muscle contractions alternate with their relaxation. At the end of the clonic phase, urinary incontinence is often observed. Convulsions usually stop spontaneously after a few minutes (2-5 minutes). Then comes the post-attack period, characterized by drowsiness, confusion, headache and the onset of sleep.

Non-convulsive generalized seizures are called absence seizures. They occur almost exclusively in childhood and early adolescence. The child suddenly freezes and stares intently at one point, his gaze seems absent. Closing of the eyes, trembling of the eyelids, and slight tilting of the head may be observed. The attacks last only a few seconds (5-20 seconds) and often go unnoticed.

The occurrence of an epileptic attack depends on a combination of two factors in the brain itself: the activity of the seizure focus (sometimes also called epileptic) and the general convulsive readiness of the brain. Sometimes an epileptic attack is preceded by an aura (a Greek word meaning “breeze” or “breeze”). The manifestations of the aura are very diverse and depend on the location of the part of the brain whose function is impaired (that is, on the localization of the epileptic focus). Also, certain conditions of the body can be a provoking factor for an epileptic seizure (epileptic seizures associated with the onset of menstruation; epileptic seizures that occur only during sleep). In addition, an epileptic seizure can be provoked by a number of environmental factors (for example, flickering light). There are a number of classifications of characteristic epileptic seizures. From a treatment point of view, the most convenient classification is based on the symptoms of seizures. It also helps to distinguish epilepsy from other paroxysmal conditions.

Types of epileptic seizures

What are the types of seizures?

Epileptic seizures are very diverse in their manifestations - from severe general seizures to imperceptible loss of consciousness. There are also such as: a feeling of a change in the shape of surrounding objects, twitching of the eyelid, tingling in the finger, discomfort in the stomach, short-term inability to speak, leaving the house for many days (trances), rotation around its axis, etc.

More than 30 types of epileptic seizures are known. Currently, to systematize them it is used International classification epilepsy and epileptic syndromes. This classification identifies two main types of seizures - generalized (general) and partial (focal, focal). They, in turn, are divided into subtypes: tonic-clonic seizures, absence seizures, simple and complex partial seizures, as well as other seizures.

What is an aura?

Aura (Greek word meaning “breeze” or “breeze”) is a condition that precedes an epileptic seizure. The manifestations of the aura are very diverse and depend on the location of the part of the brain whose function is impaired. They can be: increased body temperature, feelings of anxiety and restlessness, sound, strange taste, smell, changes in visual perception, unpleasant sensations in the stomach, dizziness, states of “already seen” (deja vu) or “never seen” (jamais vu) , a feeling of inner bliss or melancholy, and other sensations. A person's ability to correctly describe their aura can be of significant help in diagnosing the location of changes in the brain. An aura can also be not only a harbinger, but also an independent manifestation of a partial epileptic seizure.

What are generalized seizures?

Generalized seizures are attacks in which paroxysmal electrical activity covers both hemispheres of the brain. And additional brain studies in such cases do not reveal focal changes. The main generalized seizures include tonic-clonic (generalized convulsive seizures) and absence seizures (short-term blackouts). Generalized seizures occur in about 40% of people with epilepsy.

What are tonic-clonic seizures?

Generalized tonic-clonic seizures (grand mal) are characterized by the following manifestations:

blackout;
tension in the trunk and limbs (tonic convulsions);
twitching of the torso and limbs (clonic convulsions).

During such an attack, breathing may be held for some time, but this never leads to the person’s suffocation. Usually the attack lasts 1-5 minutes. After an attack, sleep may occur, a state of stupor, lethargy, and sometimes a headache.

In the case when an aura or focal attack occurs before an attack, it is regarded as partial with secondary generalization.

What are absence seizures?

Absence seizures (petit mal) are generalized attacks with a sudden and short-term (from 1 to 30 seconds) loss of consciousness, not accompanied by convulsive manifestations. The frequency of absence seizures can be very high, up to several hundred seizures per day. They are often not noticed, believing that the person is lost in thought at that time. During an absence seizure, movements suddenly stop, the gaze stops, and there is no reaction to external stimuli. There is never an aura. Sometimes there may be eye rolling, eyelid twitching, stereotypical movements of the face and hands, and changes in facial skin color. After the attack, the interrupted action is resumed.

Absence seizures are typical for childhood and adolescence. Over time, they can transform into other types of seizures.

What is adolescent myoclonic epilepsy?

Adolescent myoclonic epilepsy begins between the onset of puberty ( puberty) up to 20 years. It manifests itself as lightning-fast twitching (myoclonus), usually of the hands while maintaining consciousness, sometimes accompanied by generalized tonic or tonic-clonic seizures. These attacks mostly occur within 1-2 hours before or after waking up from sleep. The electroencephalogram (EEG) often shows characteristic changes, and there may be increased sensitivity to flickering lights (photosensitivity). This form of epilepsy is highly treatable.

What are partial seizures?

Partial (focal, focal) seizures are seizures caused by paroxysmal electrical activity in limited area brain. This type of seizure occurs in approximately 60% of people with epilepsy. Partial seizures can be simple or complex.

Simple partial seizures are not accompanied by impaired consciousness. They may manifest themselves as twitching or discomfort in the separate parts body, turning the head, discomfort in the stomach and other unusual sensations. Often these attacks are similar to an aura.

Complex partial seizures have more pronounced motor manifestations and are necessarily accompanied by one or another degree of change in consciousness. Previously, these seizures were classified as psychomotor and temporal lobe epilepsy.

In case of partial seizures, a thorough neurological examination is always performed to rule out ongoing brain disease.

What is Rolandic epilepsy?

Its full name is “benign epilepsy of childhood with central temporal (rolandic) peaks.” Already from the name it follows that it responds well to treatment. The attacks appear in early school age and stop in adolescence. Rolandic epilepsy usually manifests as partial seizures (eg, unilateral twitching of the corner of the mouth with drooling, swallowing), which usually occur during sleep.

What is status epilepticus?

Status epilepticus is a condition in which epileptic seizures follow each other without interruption. This condition is dangerous to human life. Even with modern level With the development of medicine, the risk of death of the patient is still very high, so a person with status epilepticus must be immediately taken to the intensive care unit of the nearest hospital. Seizures that are repeated so often that the patient does not regain consciousness between them; distinguish between status epilepticus of focal and generalized seizures; very localized motor seizures are termed “persistent partial epilepsy.”

What are pseudoseizures?

These conditions are intentionally caused by a person and look like seizures. They can be staged in order to attract additional attention or to avoid any activity. It is often difficult to distinguish a true epileptic seizure from a pseudoepileptic one.

Pseudoepileptic seizures are observed:

in childhood;
more often in women than in men;
in families where there are relatives with mental illness;
with hysteria;
if there is a conflict situation in the family;
in the presence of other brain diseases.

Unlike epileptic seizures, pseudo-seizures do not have a characteristic post-seizure phase, a return to normal occurs very quickly, the person smiles often, there is rarely damage to the body, irritability rarely occurs, and more than one attack rarely occurs within a short period of time. Electroencephalography (EEG) can accurately detect pseudoepileptic seizures.

Unfortunately, pseudoepileptic seizures are often mistakenly regarded as epileptic, and patients begin to receive treatment with specific drugs. In such cases, relatives are frightened by the diagnosis, as a result, anxiety is induced in the family and overprotection is formed over the pseudo-sick person.

Convulsive focus

A seizure focus is the result of organic or functional damage to a part of the brain caused by any factor (insufficient blood circulation (ischemia), perinatal complications, head injuries, somatic or infectious diseases, brain tumors and abnormalities, metabolic disorders, stroke, toxic effects various substances). At the site of structural damage, a scar (which sometimes forms a fluid-filled cavity (cyst)). In this place, acute swelling and irritation of the nerve cells of the motor zone may periodically occur, which leads to convulsive contractions of skeletal muscles, which, in the case of generalization of excitation to the entire cerebral cortex, result in loss of consciousness.

Convulsive readiness

Convulsive readiness is the probability of an increase in pathological (epileptiform) excitation in the cerebral cortex above the level (threshold) at which the anticonvulsant system of the brain functions. It can be high or low. With high convulsive readiness, even slight activity in the focus can lead to the appearance of a full-blown seizure. The convulsive readiness of the brain can be so great that it leads to a short-term loss of consciousness even in the absence of a focus of epileptic activity. In this case we are talking about absence seizures. Conversely, convulsive readiness may be absent altogether, and, in this case, even with a very strong focus of epileptic activity, partial seizures occur that are not accompanied by loss of consciousness. The cause of increased convulsive readiness is intrauterine brain hypoxia, hypoxia during childbirth or hereditary predisposition (the risk of epilepsy in the offspring of patients with epilepsy is 3-4%, which is 2-4 times higher than in the general population).

Diagnosis of epilepsy

There are about 40 different forms of epilepsy and different types seizures. Moreover, each form has its own treatment regimen. That is why it is so important for a doctor not only to diagnose epilepsy, but also to determine its form.

How is epilepsy diagnosed?

A complete medical examination includes the collection of information about the patient’s life, the development of the disease and, most importantly, a very detailed description of the attacks, as well as the conditions preceding them, by the patient themselves and eyewitnesses of the attacks. If seizures occur in a child, the doctor will be interested in the course of pregnancy and childbirth in the mother. A general and neurological examination and electroencephalography are required. Special neurological studies include nuclear magnetic resonance imaging and CT scan. The main task of the examination is to identify current diseases of the body or brain that could cause the attacks.

What is electroencephalography (EEG)?

Using this method, the electrical activity of brain cells is recorded. This is the most important test in diagnosing epilepsy. An EEG is performed immediately after the first seizures appear. In epilepsy, specific changes (epileptic activity) appear on the EEG in the form of discharges of sharp waves and peaks of higher amplitude than normal waves. During generalized seizures, the EEG shows groups of generalized peak-wave complexes in all areas of the brain. In focal epilepsy, changes are detected only in certain, limited areas of the brain. Based on EEG data, a specialist can determine what changes have occurred in the brain, clarify the type of seizures, and, based on this, determine which drugs will be preferable for treatment. Also, with the help of EEG, the effectiveness of the treatment is monitored (especially important for absence seizures), and the issue of stopping treatment is decided.

How is an EEG performed?

EEG is a completely harmless and painless study. To carry it out, small electrodes are applied to the head and secured to it using a rubber helmet. The electrodes are connected via wires to an electroencephalograph, which amplifies the electrical signals of brain cells received from them by 100 thousand times, records them on paper or enters the readings into a computer. During the examination, the patient lies or sits in a comfortable diagnostic chair, relaxed, with his eyes closed. Usually, when taking an EEG, so-called functional tests (photostimulation and hyperventilation) are performed, which are provocative loads on the brain through bright flashing light and increased respiratory activity. If an attack begins during an EEG (this happens very rarely), then the quality of the examination increases significantly, since in this case it is possible to more accurately determine the area of impaired electrical activity of the brain.

Are changes in the EEG grounds for identifying or excluding epilepsy?

Many EEG changes are nonspecific and provide only supporting information for the epileptologist. Only on the basis of the identified changes in the electrical activity of brain cells, one cannot speak of epilepsy, and, conversely, this diagnosis cannot be excluded with a normal EEG if epileptic seizures occur. Epileptic activity on the EEG is regularly detected in only 20-30% of people with epilepsy.

Interpreting changes in the bioelectrical activity of the brain is, to some extent, an art. Changes similar to epileptic activity may be caused by eye movement, swallowing, vascular pulsation, respiration, electrode movement, electrostatic discharge, and other causes. In addition, the electroencephalographer must take into account the patient's age, since the EEG of children and adolescents differs significantly from the electroencephalogram of adults.

What is a hyperventilation test?

This is frequent and deep breathing for 1-3 minutes. Hyperventilation causes pronounced metabolic changes in the brain due to intensive removal of carbon dioxide (alkalosis), which, in turn, contribute to the appearance of epileptic activity on the EEG in people with seizures. Hyperventilation during EEG recording makes it possible to identify hidden epileptic changes and clarify the nature of epileptic seizures.

What is EEG with photostimulation?

This test is based on the fact that flashing lights can trigger seizures in some people with epilepsy. During EEG recording, a bright light flashes rhythmically (10-20 times per second) in front of the eyes of the patient being studied. Detection of epileptic activity during photostimulation (photosensitive epileptic activity) allows the doctor to choose the most appropriate treatment tactics.

Why is an EEG with sleep deprivation performed?

Sleep deprivation for 24-48 hours before EEG is carried out to identify hidden epileptic activity in difficult to recognize cases of epilepsy.

Sleep deprivation is a fairly strong trigger for attacks. This test should only be used under the guidance of an experienced physician.

What is EEG during sleep?

As is known, in certain forms of epilepsy, changes in the EEG are more pronounced, and sometimes can only be perceptible during a study during sleep. Recording an EEG during sleep makes it possible to detect epileptic activity in the majority of those patients in whom it was not detected during the daytime, even under the influence of ordinary provocative tests. But, unfortunately, such a study requires special conditions and training of medical personnel, which limits wide application this method. It is especially difficult to carry out in children.

Is it right not to take antiepileptic drugs before an EEG?

This should not be done. Abruptly stopping the medication provokes seizures and can even cause status epilepticus.

When is video EEG used?

This very complex study is carried out in cases where it is difficult to determine the type of epileptic seizure, as well as in the differential diagnosis of pseudo-seizures. Video-EEG is a video recording of an attack, often during sleep, with simultaneous EEG recording. This study is carried out only in specialized medical centers.

Why is brain mapping done?

This type of EEG with computer analysis of the electrical activity of brain cells is usually performed for scientific purposes. Applications this method in epilepsy it is limited to identifying only focal changes.

Is EEG harmful to health?

Electroencephalography is an absolutely harmless and painless study. EEG is not associated with any effect on the brain. This study can be carried out as often as necessary. Carrying out an EEG causes only minor inconvenience associated with putting a helmet on the head and slight dizziness that may occur during hyperventilation.

Do EEG results depend on what device the study is used on?

Equipment for conducting EEG – electroencephalographs, produced by different companies, are not fundamentally different from each other. Their difference lies only in the level of technical service for specialists and in the number of recording channels (electrodes used). EEG results largely depend on the qualifications and experience of the specialist conducting the study and analyzing the data obtained.

How to prepare a child for an EEG?

The child must be explained what awaits him during the examination and convinced that it is painless. The child should not feel hungry before the test. The head should be washed clean. With small children, it is necessary to practice the day before in putting on a helmet and remaining motionless with your eyes closed (you can pretend to play as an astronaut or tank driver), and also teach them to breathe deeply and often under the commands “inhale” and “exhale.”

CT scan

Computed tomography (CT) is a method of studying the brain using radioactive (X-ray) radiation. During the study, a series of images of the brain are taken in different planes, which allows, unlike conventional radiography, to obtain an image of the brain in three dimensions. CT allows you to detect structural changes in the brain (tumors, calcifications, atrophy, hydrocephalus, cysts, etc.).

However, CT data may not have informative value for certain types of attacks, which include, in particular:

any epileptic seizures for a long time, especially in children;

generalized epileptic seizures with the absence of focal changes in the EEG and indications of brain damage during a neurological examination.

Magnetic resonance imaging

Magnetic resonance imaging is one of the most precise methods diagnostics of structural changes in the brain.

Nuclear magnetic resonance (NMR) is a physical phenomenon based on the properties of some atomic nuclei, when placed in a strong magnetic field, to absorb energy in the radio frequency range and emit it after the cessation of exposure to the radio frequency pulse. In its diagnostic capabilities, NMR is superior to computed tomography.

The main disadvantages usually include:

low reliability of calcification detection;
high price;
impossibility of examining patients with claustrophobia (fear of closed spaces), artificial pacemakers (pacemakers), large metal implants made of non-medical metals.

Is a medical examination necessary in cases where there are no more attacks?

If a person with epilepsy has stopped having seizures, but the medications have not yet been stopped, then it is recommended that he undergo a control general and neurological examination at least once every six months. This is especially important for monitoring the side effects of antiepileptic drugs. Usually the condition of the liver, lymph nodes, gums, hair is checked, and lab tests blood and liver tests. In addition, it is sometimes necessary to monitor the amount of anticonvulsants in the blood. Neurological examination this includes a traditional examination by a neurologist and an EEG.

Cause of death in epilepsy

Status epilepticus is especially dangerous due to pronounced muscle activity: tonic-clonic convulsions of the respiratory muscles, inhalation of saliva and blood from the oral cavity, as well as delays and arrhythmias of breathing lead to hypoxia and acidosis. The cardiovascular system experiences extreme stress due to enormous muscular work; hypoxia increases cerebral edema; acidosis increases hemodynamic and microcirculation disorders; secondly, the conditions for brain function are increasingly deteriorating. When status epilepticus is prolonged in the clinic, the depth increases comatose state, convulsions become tonic in nature, muscle hypotonia is replaced by atony, and hyperreflexia is replaced by areflexia. Hemodynamic and respiratory disorders increase. The convulsions may stop completely, and the stage of epileptic prostration begins: the eye slits and mouth are half open, the gaze is indifferent, the pupils are wide. In this condition, death can occur.

Two main mechanisms lead to cytotoxicity and necrosis, in which cellular depolarization is supported by stimulation of NMDA receptors and the key point is the initiation of a cascade of destruction within the cell. In the first case, excessive neuronal excitation results from edema (fluid and cations entering the cell), leading to osmotic damage and cell lysis. In the second case, activation of NMDA receptors activates calcium flux into the neuron with accumulation of intracellular calcium to a level higher than the cytoplasmic calcium binding protein can accommodate. Free intracellular calcium is toxic to the neuron and leads to a series of neurochemical reactions, including mitochondrial dysfunction, activates proteolysis and lipolysis, which destroy the cell. This vicious circle underlies the death of a patient with status epilepticus.

Prognosis for epilepsy

In most cases, after a single attack, the prognosis is favorable. Approximately 70% of patients undergo remission during treatment, that is, they are seizure-free for 5 years. In 20–30 %, seizures continue; in such cases, simultaneous administration of several anticonvulsants is often required.

First aid

Signs or symptoms of an attack are usually: convulsive muscle contractions, respiratory arrest, loss of consciousness. During an attack, those around you need to remain calm - without panic or fuss, provide the correct first aid. Listed symptoms The attack should go away on its own within a few minutes. People around you most often cannot speed up the natural cessation of the symptoms accompanying an attack.

The most important goal of first aid during an attack is to prevent harm to the health of the person experiencing the attack.

The onset of an attack may be accompanied by loss of consciousness and a person falling to the floor. If you fall from the stairs, near objects protruding from the floor level, head bruises and fractures are possible.

Remember: an attack is not a disease transmitted from one person to another; act boldly and correctly when providing first aid.

Entering into an attack

Support the falling person with your hands, lower him to the floor or sit him on a bench. If a person is in a dangerous place, for example, at an intersection or near a cliff, lift his head, take him under the armpits, and move him a little away from the dangerous place.

Beginning of the attack

Sit down next to the person and hold the most important thing - the person’s head; it is most convenient to do this by holding the head of the person lying between your knees and holding it on top with your hands. The limbs need not be fixed, they will not make amplitude movements, and if initially the person lies quite comfortably, then he will not be able to injure himself. No other people are needed nearby, ask them to move away. The main phase of the attack. Holding the head, have a folded handkerchief or part of the person's clothing ready. This may be needed to wipe away saliva, and if the mouth is open, a piece of this material, folded in several layers, can be inserted between the teeth, this will prevent biting the tongue, cheek, or even damaging the teeth against each other during cramps.

If the jaws are closed tightly, there is no need to try to open the mouth by force (this most likely will not work and can injure the oral cavity).

If salivation increases, continue to hold the person's head, but turn it to the side so that saliva can flow onto the floor through the corner of the mouth and does not fall into the mouth. Airways. It's okay if a little saliva gets on your clothes or hands.

Recovery from an attack

Remain completely calm, an attack with respiratory arrest can last several minutes, remember the sequence of symptoms of an attack so that you can later describe them to your doctor.

After the end of the convulsions and relaxation of the body, it is necessary to put the victim in a recovery position - on his side, this is necessary to prevent the root of the tongue from retracting.

The victim may have medications with him, but they can only be used at the direct request of the victim, otherwise criminal liability for causing harm to health may follow. In the vast majority of cases, recovery from an attack should occur naturally, and the right medicine or their mixture and dose will be selected by the person himself after recovering from the attack. Searching a person for instructions and medications is not worth it, as this is not necessary and will only cause an unhealthy reaction from others.

In rare cases, recovery from an attack may be accompanied by involuntary urination, while the person still has convulsions at this time, and consciousness has not fully returned to him. Politely ask other people to move away and disperse, support the person's head and shoulders, and gently discourage them from standing up. Later, the person will be able to cover himself, for example, with an opaque bag.

Sometimes, when recovering from an attack, even with rare convulsions, a person tries to get up and start walking. If you can control the person’s spontaneous impulses from side to side, and the place does not pose any danger, for example, in the form of a road nearby, a cliff, etc., allow the person, without any help from you, to stand up and walk with him, holding him firmly. If the place is dangerous, then do not allow him to get up until the convulsions completely stop or consciousness returns completely.

Usually 10 minutes after the attack, the person completely returns to his normal state and no longer needs first aid. Allow the person to make their own decision about the need to apply for medical care, after recovering from the attack, this is sometimes no longer necessary. There are people who have attacks several times a day, and yet they are completely full-fledged members of society.

Often young people are inconvenienced by the attention of other people to this incident, much more than the attack itself. Cases of an attack under certain irritants and external circumstances can occur in almost half of the patients; modern medicine does not allow pre-insurance against this.

A person whose attack is already ending should not be the focus of general attention, even if, when recovering from the attack, the person emits involuntary convulsive screams. You could, for example, hold the person's head while talking calmly to the person, this helps reduce stress, gives confidence to the person coming out of the attack, and also calms onlookers and encourages them to disperse.

An ambulance must be called in the event of a second attack, the onset of which indicates an exacerbation of the disease and the need for hospitalization, since the second attack in a row may be followed by further ones. When communicating with the operator, it is enough to indicate the gender and approximate age of the victim, in response to the question “What happened?” answer “repeated attack of epilepsy”, give the address and large fixed landmarks, at the request of the operator, provide information about yourself.

In addition, an ambulance should be called if:

attack lasts more than 3 minutes
after an attack, the victim does not regain consciousness for more than 10 minutes
the attack occurred for the first time
the attack occurred in a child or an elderly person
the attack occurred in a pregnant woman
During the attack, the victim was injured.

Treatment of epilepsy

Treatment of a patient with epilepsy is aimed at eliminating the cause of the disease, suppressing the mechanisms of seizure development and correcting the psychosocial consequences that may occur as a result of the neurological dysfunction underlying the disease or in connection with a persistent decrease in working capacity.

If the epileptic syndrome is the result of metabolic disorders, such as hypoglycemia or hypocalcemia, then after the metabolic processes are restored to normal levels, the seizures usually stop. If epileptic seizures are caused by an anatomical lesion of the brain, such as a tumor, arteriovenous malformation or brain cyst, then removal of the pathological focus also leads to the disappearance of seizures. However, long-term lesions, even those that do not progress, can cause the development of various negative changes. These changes can lead to the formation of chronic epileptic foci, which cannot be eliminated by removing the primary lesion. In such cases, control is needed, and sometimes surgical extirpation of epileptic areas of the brain is necessary.

Drug treatment of epilepsy

Anticonvulsants, also known as anticonvulsants, reduce the frequency, duration, and in some cases completely prevent seizures:
Neurotropic drugs - can inhibit or stimulate the transmission of nervous excitation in various parts of the (central) nervous system.
Psychoactive substances and psychotropic drugs affect the functioning of the central nervous system, leading to changes in mental state.
Racetams are a promising subclass of psychoactive nootropic substances.

Antiepileptic drugs are chosen depending on the form of epilepsy and the nature of the attacks. The drug is usually prescribed in a small initial dose with a gradual increase until the optimal clinical effect. If the drug is ineffective, it is gradually discontinued and the next one is prescribed. Remember that under no circumstances should you change the dosage of the medicine or stop treatment on your own. A sudden change in dose can provoke a worsening of the condition and an increase in attacks.

Non-drug treatments

Surgery;
Voight method;
Osteopathic treatment;
Impact Study external stimuli, affecting the frequency of attacks, and weakening their influence. For example, the frequency of attacks may be influenced by the daily routine, or it may be possible to establish an individual connection, for example, when wine is consumed and then washed down with coffee, but this is all individual for each organism of a patient with epilepsy;
Ketogenic diet.

Epilepsy and driving

Each state has its own rules for determining when a person with epilepsy can obtain a driver's license, and several countries have laws requiring physicians to report patients with epilepsy to the registry and inform patients of their responsibility for doing so. In general, patients can drive a car if they have been seizure-free for 6 months to 2 years (with or without drug treatment). In some countries, the exact duration of this period is not defined, but the patient should obtain a doctor's report that the seizures have stopped. The doctor is obliged to warn the patient with epilepsy about the risk he is exposed to when driving with such a disease.

Most people with epilepsy, with adequate seizure control, attend school, enter the workforce, and lead relatively normal lives. Children with epilepsy tend to have more problems at school than their peers, but every effort should be made to enable these children to learn well through additional support in the form of tutoring and counseling.

How is epilepsy related to sex life?

Sexual behavior is an important but very private part of life for most men and women. Studies have shown that approximately a third of people with epilepsy, regardless of gender, have sexual problems. The main causes of sexual dysfunction are psychosocial and physiological factors.

Psychosocial factors:

limited social activity;
lack of self-esteem;
rejection by one of the partners of the fact that the other has epilepsy.

Psychosocial factors invariably cause sexual dysfunction across a variety of chronic diseases, and are also the cause of sexual problems in epilepsy. The presence of attacks often leads to a feeling of vulnerability, helplessness, inferiority and interferes with the establishment of normal relationships with a sexual partner. In addition, many fear that their sexual activity may trigger attacks, especially when attacks are triggered by hyperventilation or physical activity.

There are even known forms of epilepsy when sexual sensations are a component of an epileptic attack and, as a result, form a negative attitude towards any manifestations of sexual desires.

Physiological factors:

dysfunction of brain structures responsible for sexual behavior (deep brain structures, temporal lobe);
change hormonal levels due to seizures;
an increase in the level of inhibitory substances in the brain;
decreased levels of sex hormones due to medications.

Decreased sexual desire occurs in approximately 10% of people receiving antiepileptic drugs, and is more pronounced in those taking barbiturates. A rather rare case of epilepsy is increased sexual activity, which is an equally serious problem.

When assessing sexual dysfunctions, it must be taken into account that they can also be the result of improper upbringing, religious restrictions and negative experience early sexual activity, but the most common reason is a violation of the relationship with a sexual partner.

Epilepsy and pregnancy

Most women with epilepsy are capable of carrying an uncomplicated pregnancy and giving birth healthy children even if they are taking anticonvulsants at the time. However, during pregnancy, the course of metabolic processes in the body changes; special attention should be paid to the levels of antiepileptic drugs in the blood. Sometimes relatively high doses must be prescribed to maintain therapeutic concentrations. Most affected women whose condition was well controlled before pregnancy continue to feel well during pregnancy and childbirth. Women whose seizures are not controlled before pregnancy are at higher risk of developing complications during pregnancy.

One of the most serious complications of pregnancy, toxicosis, often manifests itself as generalized tonic-clonic seizures in the last trimester. Such seizures are a symptom of a severe neurological disorder and are not a manifestation of epilepsy, occurring no more often in women with epilepsy than in others. Toxicosis must be corrected: this will help prevent the occurrence of seizures.

The offspring of women with epilepsy have a 2-3 times increased risk of embryonic malformations; This appears to be due to a combination of the low incidence of drug-induced malformations and genetic predisposition. Among those observed birth defects includes fetal hydantoin syndrome, characterized by cleft lip and palate, heart defects, digital hypoplasia and nail dysplasia.

The ideal for a woman planning a pregnancy would be to stop taking antiepileptic drugs, but it is very likely that in a large number of patients this will lead to a recurrence of seizures, which in the future will be more detrimental to both mother and child. If the patient's condition allows discontinuation of treatment, this can be done at a suitable time before pregnancy. In other cases, it is advisable to carry out maintenance treatment with one drug, prescribing it in the minimum effective dose.

Children chronically exposed to barbiturates in utero often present with transient lethargy, hypotension, restlessness, and often exhibit signs of barbiturate withdrawal. These children should be included in the risk group for the development of various disorders during the neonatal period, slowly removed from the state of barbiturate dependence, and their development should be closely monitored.

There are also seizures that are similar to epileptic, but are not. Increased excitability with rickets, neurosis, hysteria, disturbances of the heart and breathing can cause similar attacks.

Affective - respiratory attacks:

The child begins to cry and at the height of the crying stops breathing, sometimes he even goes limp, falls unconscious, and there may be twitching. Help with affective attacks very simple. You need to take as much air into your lungs as possible and blow on the child’s face with all your might, or wipe his face with cold water. Reflexively, breathing will be restored and the attack will stop. Yactation also occurs, when completely Small child sways from side to side, it seems like he rocks himself to sleep. And those who already know how to sit rock back and forth. Most often, yactation occurs if there is no necessary emotional contact (happens in children in orphanages), rarely - due to mental disorders.

In addition to the listed conditions, there are attacks of loss of consciousness associated with disturbances in the activity of the heart, breathing, etc.

Impact on character

Pathological excitation of the cerebral cortex and seizures do not go away without leaving a trace. As a result, the psyche of a patient with epilepsy changes. Of course, the degree of mental change largely depends on the personality of the patient, the duration and severity of the disease. Basically there is a slowdown mental processes, primarily thinking and affects. As the disease progresses, changes in thinking progress; the patient often cannot separate the important from the unimportant. Thinking becomes unproductive, has a concrete-descriptive, stereotyped character; speech is dominated by standard expressions. Many researchers characterize it as “labyrinthine thinking.”

According to observational data, according to the frequency of occurrence among patients, character changes in epileptics can be arranged in the following order:

slowness,
viscosity of thinking,
heaviness,
hot temper,
selfishness,
rancor,
thoroughness,
hypochondriacity,
quarrelsomeness,
accuracy and pedantry.

The appearance of a patient with epilepsy is characteristic. Slowness, restraint in gestures, taciturnity, sluggish facial expressions, lack of expression on the face are striking; you can often notice a “steel” shine in the eyes (Chizh’s symptom).

Malignant forms of epilepsy ultimately lead to epileptic dementia. In patients with dementia, it manifests itself as lethargy, passivity, indifference, and resignation to the disease. Sticky thinking is unproductive, memory is reduced, vocabulary is poor. The affect of tension is lost, but obsequiousness, flattery, and hypocrisy remain. The result is indifference to everything except own health, petty interests, egocentrism. Therefore, it is important to recognize the disease in time! Public understanding and full support are extremely important!

Is it possible to drink alcohol?

Some people with epilepsy choose not to drink alcohol at all. It is well known that alcohol can provoke seizures, but this is largely due to individual susceptibility, as well as the form of epilepsy. If a person with seizures is fully adapted to full life in society, he will be able to find a reasonable solution to the problem of drinking alcohol. Acceptable doses of alcohol consumption per day are for men - 2 glasses of wine, for women - 1 glass.

Is it possible to smoke?

Smoking is harmful - it is well known. There was no direct connection between smoking and the occurrence of attacks. But there is a fire hazard if an attack occurs while smoking unattended. Women with epilepsy should not smoke during pregnancy, so as not to increase the risk (already high) of malformations in the child.

Important! Treatment is carried out only under the supervision of a doctor. Self-diagnosis and self-medication are unacceptable!

“Then suddenly something seemed to open up before him: an extraordinary inner light illuminated his soul. This moment lasted perhaps half a second; but he, however, clearly and consciously remembered the beginning, the very first sound of his terrible scream, which burst out of his chest of its own accord and which he could not have stopped by any force. Then his consciousness faded away instantly, and complete darkness set in.”

This is a description of the state of Prince Myshkin, the main character of the novel by F.M. Dostoevsky's "Idiot". It is believed that this work is autobiographical, and in the description of Myshkin’s illness, Dostoevsky reflects own feelings. IN modern medicine There is even a term “Dostoyevsky’s epilepsy” - it describes attacks accompanied by pleasant sensations and euphoria. In one of his diaries, the writer says the following: “For several minutes I experienced such happiness that is impossible to feel in ordinary life, such delight that no one else understands. I felt in complete harmony with myself and with the whole world, and this feeling was so strong and sweet that for a couple of seconds of such bliss I would have given ten or more years of my life, and maybe my whole life.”

However, not everyone suffering from epilepsy is as “lucky” as the famous writer. As a rule, the aura, i.e. the sensations that appear a few minutes before the convulsive attack itself are of a different nature. Photo- or phonophobia occurs - fear of bright light and loud sounds, respectively; aversion to surrounding odors. There may also be a distortion of visual perception, a phenomenon called “Alice in Wonderland syndrome”: a person sees objects smaller than they really are (in medicine this is called micropsia). “Floaters” or spots of color appear before the eyes, and sometimes some field of vision “falls out” altogether.

The prevalence of epilepsy is very high. According to the World Health Organization, approximately 50 million people worldwide suffer from epilepsy; V developed countries There are 40 to 70 annual new cases per 100,000 people. This widespread prevalence of the pathology led to the creation of the Global Campaign against Epilepsy: Out of the Shadows by WHO and the International League Against Epilepsy (ILAE).

Ancient disease

One of the first mentions of epilepsy dates back to the times of Ancient Greece and belongs to the pen of Hippocrates. He dedicated an entire treatise “On the Sacred Disease” to this pathology, in which he wrote the following: “The cause of this disease, like other great diseases, is the brain.” And he was right. Modern scientists are closer to understanding the cause of epilepsy, although much remains unclear. For some time it was even believed that this was a disease of people with high intelligence, since, according to historical sources, Julius Caesar, Napoleon Bonaparte, Byron and others suffered from it. However, this assumption about the connection between epilepsy and intelligence is unfounded.

In 1873, John Hughlings Jackson, an English neurologist, proposed that seizures were the result of spontaneous short electrochemical discharges in the brain. He also suggested that the nature of seizures is directly related to the location and function of the source of such activity in the brain. The twentieth century confirmed the scientist’s thoughts. Today it is known that different brain structures have different thresholds of convulsive readiness, i.e. One structure requires less stimulation for a cramp to occur. The hippocampus, a small paired structure responsible for memory and learning, has the lowest threshold for seizure readiness. The most “stable” structures are the cerebellum, striatal complex and sensorimotor cortex. If the focus of epileptic activity is in the hippocampus, then the seizure will be manifested by short-term amnesia, i.e. memory loss, if in the sensorimotor cortex - an attack of twitching of the limbs or unpleasant sensations"Crawling of goosebumps."

What happens at the cellular level?

There are inhibitory and activating systems in the brain. A person suffering from epilepsy has an imbalance between these two systems. If excitatory nerve cells function normally, but inhibitory nerve cells do not function, an attack occurs. If we consider the pathology at the molecular level, it turns out that the work of the inhibitory and activating systems depends on the functioning of potassium channels in the membranes of nerve cells. In 1997, a group of German scientists discovered an exact correspondence in the number of voltage-gated potassium channels in cells of different brain structures. . The largest number of them was found in the hippocampus. Thus, the ideas put forward by Jackson in the 19th century turned out to be correct.

British-born American neurologist and neuropsychologist Oliver Sacks (1933-2015)

In addition to a seizure in its classical sense, i.e. convulsive attack with loss of consciousness, the so-called “grand mal”, exists great amount manifestations of epilepsy. These may be attacks of unpleasant sensory sensations, disturbances of vision, taste, smell. The manifestation depends on in which part of the brain the epileptic focus is located - a group of neurons in which the activity-inhibition balance is disturbed. If it is localized in the temporal lobe, an attack of sudden amnesia may occur. Sometimes, with the same location of the focus, the attack is manifested by a sensation of an unpleasant odor - this can be the smell of burnt hair, rotten fish, etc. When the focus is localized in the occipital lobes of the brain, deja vu occurs - deja vu - or, on the contrary, a feeling of never seen - jamais vu. One of the unusual manifestations may be auditory or visual hallucinations, dreamlike (oneiric) states. This is how they were described by a patient of Oliver Sacks, a famous American neurologist and popularizer of medicine: “I saw India - landscapes, villages, houses, gardens - and instantly recognized the favorite places of my childhood.”

Electroencephalogram of a patient with epilepsy.

There are many causes of epilepsy, and idiopathic epilepsy (that is, without an identified cause) is only one of them. Epileptic seizures can be caused by head trauma, stroke or brain hemorrhage, and even a tumor. Therefore, to diagnose epilepsy, they use the method of magnetic resonance imaging, MRI, which allows, like an X-ray, to look at the state of the brain and exclude the above reasons. Another way to confirm the presence of the disease is to conduct electroencephalography, EEG. This method is absolutely harmless to the body, but allows you to fairly accurately judge the location of the pathological focus, as well as monitor the effectiveness of therapy.

Cure for no reason

Treatment methods for epilepsy can be divided into two classes - conservative and surgical. Today there are a huge number of drugs that suppress pathological activity in the brain and prevent the development of seizures. One of them, barbituric acid, has been used since 1864, when this substance was discovered by Adolf von Bayer, a German chemist, Nobel Prize winner in chemistry and founder of the pharmaceutical company Bayer, now one of the largest companies in the world with a turnover of billions of dollars.

In addition to medications, in some countries patients are put on a special ketogenic diet before radical treatment methods are considered. Its essence lies in the maximum exclusion of proteins and carbohydrates from the diet. At the same time, β-hydroxybutyrate is actively synthesized in the liver, which has an anticonvulsant effect.

DBS technique. The electrode is installed in the area of the brain determined by the neurosurgeon, the wire from the electrode is connected to a generator implanted in the area of the pectoralis major muscle.

However, in about 30% of patients, attacks do not respond to either drug therapy or a ketogenic diet. In March 2010, the journal Epilepsy published the results of a study on stimulation of the anterior thalamic nucleus in epilepsy, which concluded that deep brain stimulation (DBS - deep brain stimulation) is a new treatment option for patients whose seizures not stopped conservative methods. The technique, first used in the USA in 1997, becomes a replacement for the previous neurosurgical treatment, the essence of which was physical removal focus of epilepsy from the brain. Deep stimulation looks like this: an electrode is inserted into a certain area of the brain selected by a neurosurgeon, the wire from which is connected to a matchbox-sized generator placed between the pectoral muscles.The impulses generated by the electrode suppress pathological activity and, as a result, prevent the development of an attack.In addition to epilepsy, DBS is used in the treatment of Parkinson's disease, chronic pain syndrome, dystonia, Tourette's syndrome and many other pathologies.

Transcranial magnetic stimulation technique - TMS.

One of the newest (and still experimental) techniques is transcranial magnetic stimulation of the brain. In 1985, a group of scientists at the University of Sheffield created the first magnetic stimulator capable of stimulating the human motor cortex. The principle of its operation was formulated back in 1831 by Michael Faraday. The TMS machine is a coil. Electric current flowing through the coil produces a magnetic field perpendicular to the direction of the current in the coil. If a conducting medium, such as the brain, enters a magnetic field, then an electric current is induced in this medium. Depolarization of the membrane of nerve cells leads to the appearance of an action potential in them and its further propagation, which leads to the activation or suppression of neurons in various parts of the brain.

Many treatment methods of varying degrees of effectiveness have been invented. However, all of them are symptomatic; they remove only the manifestation of the disease, and not its cause, which still remains unknown even thousands of years after the first description of the disease. The task of the future is to understand what leads to pathology in the brain. Then perhaps we can forget about this disease forever.

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