Convulsive readiness. Convulsive readiness symptoms in adults treatment

Atherosclerosis of cerebral vessels is a disease that is characterized by narrowing of the walls of the arteries as a result of the growth of atherosclerotic plaques on them. Most often, the disease appears due to the fact that the human body is disrupted lipid metabolism. In this case, the connective tissue begins to grow, and in the lumen vascular walls Calcium salts are actively deposited.

This leads to the fact that the vessels narrow and sometimes become completely blocked. In the brain, multiple blockages of blood vessels may occur with deposits consisting of cholesterol plaques.

The danger of this disease lies in its extremely slow development. At the initial stages of the disease, a person may not feel any suspicious symptoms at all, but meanwhile a dangerous process continues in the body, in which internal organs are underpaid nutrients and vital oxygen.

Atherosclerotic plaques that fill blood vessels are composed of calcium and fats. The main risk group for this disease is adult men and women aged 50 years and above. Among them, atherosclerosis of cerebral vessels is very common - in every sixth person.

Causes and risk factors

The main cause of atherosclerosis great vessels brain is that normal fat metabolism is disrupted in the body, which leads to the accumulation of cholesterol in the vessels. The age factor of the disease is explained by the fact that in young people excess cholesterol is successfully eliminated from the body. In older people, things are much worse with this - cholesterol accumulates and forms atherosclerotic plaques.

Scientists have not yet come to a consensus on the specific reasons for the development of this pathology. There are only a number of factors that contribute to the occurrence of atherosclerosis:

Forms of the disease

There are two main forms of cerebral atherosclerosis – progressive and cerebral.

Progressive

This type of disease is characterized by:

• memory impairment,
• fatigue,
• poor concentration,
• headaches,
• emotional swings, up to prolonged depressive states,
• sleep disorders,
• fainting,
• dizziness, which can occur when suddenly rising from a sitting or lying position.

If atherosclerosis is progressive, it develops very quickly, and treatment should not be delayed in any case. This form of the disease can affect the mental state of the patient.

Cerebral

This form of the disease affects the central nervous system, disrupting its functionality. The degree of effect on the central nervous system depends on how severely the brain vessels are affected. Blood flow to the brain decreases, oxygen starvation occurs, as a result of which neurons stop functioning normally.

Signs of cerebral atherosclerosis directly depend on which part of the brain is affected. Among them are: memory impairment, tremors in the legs or arms, headaches, depression, insomnia, increased sweating, deterioration of intellectual abilities, hearing and vision impairment, photophobia.

Stages

This vascular disease develops in several stages, each of which is accompanied by its own symptoms:

• First stage. There are no clear signs yet. You can only notice increased fatigue even with light physical exertion, sometimes dizziness and rare pain in the head occur. It becomes difficult for a person to remember some simple things. Symptoms almost always appear in the late afternoon, but disappear completely after sleep.
• Second stage. Symptoms occur much more often, and they are supplemented by such phenomena as: tremors of the limbs, sudden mood swings, depressed emotional state, and speech problems.
• Third stage. At this stage, there are already severe damage to the blood vessels of the brain, which is manifested by frequent cases of memory loss, the inability to perform simple daily actions, hand tremors, and heart rhythm disturbances.

As atherosclerosis progresses, it results in the patient being unable to remember any recent information, but remembering past events quite easily. The person loses control over his actions. There are often cases when he can turn on the water or gas and then go outside.

People with severe stages of atherosclerosis can easily get lost even in familiar areas, because they lose their orientation in space. Patients often cannot remember what day or even year it is. Such patients must be under the supervision of loved ones or in special medical institutions.

What are the dangers and can there be complications?

As a result of the development of atherosclerosis, the lumen of the brain vessels narrows, which leads to insufficient saturation of cells with oxygen. If this condition is chronic, brain tissue begins to partially atrophy, mental and emotional disturbances.

But the greatest danger with atherosclerosis is the possibility of developing a stroke. It occurs when the pressure inside the vessels of the brain reaches a peak value, the walls of the vessel cannot withstand it and burst, which leads to hemorrhage in the brain.

First signs

Any form of atherosclerosis has common clinical manifestations:

• noise in ears;
• headache;
• insomnia;
• anxiety, excitability, nervousness;
• fast fatiguability;
• weakness and drowsiness during the daytime;
• poor concentration;
• memory problems;
• speech impairment, difficulty swallowing food.

Which doctor treats and when to contact him?

At the first signs of atherosclerosis, you should urgently consult a cardiologist. The sooner measures for treatment are taken, the higher the likelihood of a successful outcome.

If a person begins to feel unexplained fatigue even with minimal exertion, noise or tinnitus, frequent attacks of dizziness and headaches that do not go away under the influence of analgesics, you should not delay and consult a doctor.

Diagnostics

Using modern diagnostic methods, it is possible to quickly detect cerebral atherosclerosis in a person. The following examinations are usually prescribed:

• ultrasound scanning of blood vessels;
• blood test for cholesterol levels;
• tomography of cerebral arteries;
• angiography;
• Ultrasound of the heart and internal organs.

For more information about the disease, watch the video:

Treatment methods

Atherosclerosis is a complex disease and its treatment must be comprehensive. In addition to taking medications, a special diet and daily exercise are prescribed to improve blood circulation and strengthen the body.

Medication

Drugs prescribed for atherosclerosis:

• Vasodilators: Cinnarizine, Nimodipine, Corinfar, Cavinton, Eufillin, Papaverine, Isoptin, Vinpocetine, Nicotinic acid, Adalat.
• Drugs that strengthen arterial walls: Selenium, Dihydroquerticin, Potassium.
• Cholesterol-lowering drugs: Simvastatin, Ciprofibrate, Lovastatin, Atorvastatin, Cenofibrate.

In addition to them, tranquilizers and antidepressants may be prescribed. For severe headaches, a course of analgesics is prescribed. Another article talks more about drugs for the treatment of cerebral atherosclerosis.

Diet

The diet during the treatment of this disease must also be adjusted. It is necessary to exclude a number of foods and dishes containing large amounts of cholesterol, namely:

• fatty meats;
• dairy products in which the fat content exceeds 1%;
• sugar, honey, sweet pastries.

Preference should be given to the following products:

• porridge (oatmeal), jelly;
• hawthorn puree;
• low-sweet fruits and vegetables;
• low-fat cottage cheese - you can consume no more than 150 g per day;
• seaweed and seaweed - they are rich in vitamins and microelements that improve blood supply to the blood vessels of the brain.

Find out more about the diet for cerebral atherosclerosis from another material.

Forecasts and preventive measures

Prevention of atherosclerosis of the cerebral arteries is the most important part of treatment, with which you can prevent complications of the disease and improve your well-being. First of all, it is necessary to strictly follow all the doctor’s instructions, give up cigarettes and reduce the consumption of alcoholic beverages to a minimum.

With timely treatment, the prognosis for this disease is very favorable. Adequate therapy, compliance with all medical recommendations and a healthy lifestyle will help to successfully cope with the disease and prevent possible complications.

What is arterial hypertension: causes and treatment of hypertension

Arterial hypertension is a chronic disease that affects a large number of modern people.

The difficulty is that many patients neglect preventive measures and a healthy lifestyle.

Need to know what it is arterial hypertension in order to begin therapeutic procedures in a timely manner, avoiding large-scale complications that can lead to death.

The body's vascular system is like a tree, where the aorta is the trunk, which branches into arteries, which are divided into small branches - arterioles.

Their task is to carry blood to capillaries that supply nutrients and oxygen to every cell of the human body. After oxygen is transferred to the blood, they are again returned to the heart through the venous vessels.

In order for blood to flow through the system of veins and arteries, a certain amount of energy must be expended. The force acting on the walls of blood vessels during blood flow is pressure.

Pressure depends on the functioning of the heart and on the arterioles, which are able to relax if it is necessary to lower blood pressure, or to contract if it is necessary to increase it.

Arterial hypertension is a condition that is defined by a persistent increase in systolic pressure up to 140 mmHg. century or more; and diastolic pressure up to 90 mm Hg. Art. and more.

There are such periods of changes in blood pressure:

1. decreases from 1 to 5 am,
2. rises from 6 to 8 am,
3. decreases from 23 to 00 o'clock at night.

Blood pressure changes with age:

• indicators in children are 70/50 mm Hg. Art.,
• indicators in older people are more than 120/80.

Causes of arterial hypertension

In many cases, it is not possible to understand how arterial hypertension arose. In this case, they talk about primary essential hypertension. Some doctors believe that the stimulating factors of primary hypertension are:

• accumulation of salt in the kidneys,
• the presence of vasoconstrictor substances in the blood,
• hormonal imbalance.

About 10% of people have severe hypertension due to taking certain medications or developing another disease. Such arterial hypertension is called secondary hypertension.

The most common causes of hypertension are:

1. Kidney diseases,
2. Renovascular hypertension,
3. Adrenal tumor
4. Pheochromocytoma,
5. Side effects of drugs
6. Increased blood pressure during pregnancy.

If the kidneys retain a lot of salt, the volume of fluid in the body increases. As a result, blood pressure and volume increase. The kidneys also produce the enzyme renin, which plays a key role in determining blood pressure levels.

Renin also increases the production of aldosterone, a hormone responsible for the reabsorption of water and salt.

Severe renovascular hypertension is quite rare and affects the following groups of people:

• aged people,
• smokers,
• Small children.

Renovascular hypertension is diagnosed by injecting a contrast agent into an artery or vein and then examining the blood flow in the kidneys using X-rays.

The adrenal glands are two glands that secrete many hormones, including aldosterone, located at the top of each kidney. Aldosterone, produced by the adrenal glands, regulates salt and water balance in the body.

In extremely rare cases, a tumor of the adrenal glands provokes an increase in the production of aldosterone, which promotes the retention of water and salt in the body, thereby increasing blood pressure. This type of arterial hypertension most often affects young women. There are additional symptoms:

• strong thirst
• excessive urination.

Another rare type of hypertension is pheochromytoma, which is caused by another type of adrenal tumor. At the same time, the pancreas produces more of the hormone adrenaline.

Adrenaline is a hormone that helps the body respond fully to stressful situations. This hormone has the following properties:

1. accelerates heart rate,
2. increases blood pressure
3. promotes blood transport to muscles lower limbs.

With pheochromocytoma, adrenaline causes:

• rapid heartbeat,
• trembling,
• heat.

Some drugs and substances can increase blood pressure, for example:

1. steroids,
2. antipyretics,
3. glyceric acid.

Symptoms of arterial hypertension

As is known, arterial hypertension has the second name “silent killer”, since its symptoms do not appear for a long time. Chronic hypertension is one of the main causes of strokes and heart attacks.

Arterial hypertension syndrome has the following symptoms:

1. Pressing headache that occurs periodically,
2. Whistling or ringing in the ears
3. Fainting and dizziness,
4. "Floaters" in the eyes,
5. Cardiopalmus,
6. Pressing pain in the region of the heart.

With hypertension, symptoms of the underlying disease may be expressed, especially for kidney diseases. Only a doctor can choose medications for the treatment of hypertension.

Arterial hypertension largely contributes to the hardening of the arteries. Great pressure on the walls of blood vessels leads to their susceptibility to the accumulation of fatty elements. This process is called vascular atherosclerosis.

Over time, the appearance of atherosclerosis provokes a narrowing of the lumen of the arteries and angina pectoris. Narrowing of the arteries of the lower extremities causes the following symptoms:

• pain,
• stiffness while walking.

Also, blood clots occur due to hypertension. So, if a blood clot is in coronary artery, then it leads to a heart attack, and if it is in the carotid artery, to a stroke.

Arterial hypertension, treatment of which long time has not been carried out, often leads to the formation dangerous complication– aneurysms. Thus, the wall of the artery bulges. An aneurysm often ruptures, causing:

1. internal bleeding,
2. brain bleeding,
3. stroke.

A persistent increase in blood pressure is the cause of deformation of the arteries. The muscle layer that makes up the walls of the arteries begins to thicken, compressing the vessel. This prevents blood from circulating inside the vessel. Over time, thickening of the walls of the blood vessels in the eyes leads to partial or complete blindness.

The heart is always affected due to prolonged arterial hypertension. High blood pressure stimulates the heart muscle to work harder to ensure adequate oxygenation to the tissues.

This condition causes an enlargement of the heart. On early stages An enlarged heart has more strength to optimally pump blood into the arteries when pressure is high.

But over time, the enlarged heart muscle can weaken and become rigid, no longer supplying oxygen fully. Circulatory system must ensure a constant supply of nutrients and oxygen to the brain.

If the human body senses a decrease in the amount of blood that enters the brain, then compensatory mechanisms quickly turn on, they increase pressure, and blood from systems and organs is transferred to the brain. The following changes occur:

• the heart starts beating faster,
• blood vessels of the lower extremities and abdominal region contract,
• More blood flows to the brain.

As you know, with hypertension, the arteries that supply the brain with oxygen can narrow due to the accumulation of fat-like substances in them. This increases the risk of strokes.

If the arteries of the brain are blocked for a short time, then there is a break in the blood supply to a separate part of the brain. This phenomenon in medicine is called a microstroke.

Even if the condition lasts only a minute, it requires immediate medical attention. If treatment is not carried out, this is fraught with the development of a full-fledged stroke. Repeated micro-strokes lead to weakening of brain functions. This is how dementia develops in people with arterial hypertension.

Each kidney is made of millions of small filters called nephrons. Every day, over one and a half thousand liters of blood passes through the kidneys, where waste and toxins are filtered and excreted in the urine. Useful material go into the bloodstream.

High blood pressure causes the kidneys to work harder. In addition, damage to small vessels within the nephrons reduces the volume of filtered blood. After some time, this leads to a reduction in the filtering function of the kidneys.

Thus, the protein is excreted in the urine before returning to the bloodstream. Waste that needs to be eliminated can enter the bloodstream. This process leads to uremia, and then to renal failure, which requires constant dialysis and blood purification.

As stated earlier, at the bottom eyeball there are a large number of blood vessels, which are very sensitive to increased blood pressure. After several years of AG, the process of destruction may begin retina. Deformation may be due to:

• accumulation of cholesterol in blood vessels,
• insufficient blood circulation,
• local bleeding.

The diagnosis of arterial hypertension, as a rule, is not made after a single pressure measurement, except when it is above 170-180/105-110 mm Hg. Art.

Measurements are taken over a specified period to confirm the diagnosis. It is necessary to take into account the circumstances during which measurements are taken. The pressure gets higher:

• after smoking or drinking coffee,
• against a background of stress.

If an adult's blood pressure is more than 140/90 mm Hg. Art., then repeated measurements are usually performed after a year. In people whose blood pressure is from 140/90 to 160/100 mm Hg. st, a repeat measurement is carried out after a short time. With high diastolic pressure from 110 to 115 mm Hg. Art. urgent treatment is needed.

In some cases, older people develop rare view arterial hypertension, which is called isolated systolic hypertension. Systolic pressure indicators exceed 140 mmHg. Diastolic pressure remains at 90 mmHg. st or lower. This type The disease is considered dangerous because it provokes strokes and heart failure.

In addition to measuring blood pressure, the doctor should check changes in other organs, especially if pressure readings are constantly at high levels.

The eyes are the only organ of the human body in which blood vessels are clearly visible. Using a bright stream of light, the doctor examines the fundus of the eye with a special device - an ophthalmoscope, which allows you to clearly see the narrowing or dilation of blood vessels.

The doctor can see small cracks and hemorrhages, which are the consequences of high blood pressure.

The inspection also includes:

1. listening to heart rhythm sounds with a stethoscope,
2. measuring heart size by palpation,
3. The use of an electrocardiogram helps to study the electrical activity of the heart and also estimate its size.

In addition to instrumental studies, the doctor prescribes:

• examination of urine to exclude kidney infections,
• blood sugar test,
• blood test for cholesterol.

The fundus, kidneys and blood vessels are the target organs for pathological blood pressure.

Treatment of arterial hypertension

Around the 1950s of the last century, the pharmaceutical industry recorded an increase in the production and synthesis of new groups of antihypertensive drugs.

Previously, treatment for hypertension included:

1. salt-free diet
2. surgical interventions,
3. phenobarbital as a stress reducer.

There is information that at the beginning of the 1940s, every third or fourth bed in the hospital was occupied by a patient with hypertension or its consequences. IN last years A large number of studies have been conducted, which has led to an increase in the effectiveness of therapy for arterial hypertension. Now the number of deaths and serious consequences of the disease has decreased significantly.

The best in Russia and European countries medical workers worked on research and confirmed that only drug treatment of high blood pressure makes it possible to reduce the risk of:

1. cardiovascular diseases,
2. strokes,
3. fatalities.

However, some people are convinced that arterial hypertension cannot be treated with medications, since it reduces the quality of life and leads to the development of various side effects, including depression.

Almost all drugs have side effects, but studies show that when using drugs that lower blood pressure, side effects are reported in only 5-10% of patients.

The existing variety of groups of drugs that lower blood pressure allows the doctor and the patient to choose the most optimal treatment. The doctor is obliged to warn the patient about the possible side effects of the drugs used.

Diuretics or blood pressure diuretics treat blood pressure by increasing the kidneys' excretion of water and salt. This creates relaxation of the blood vessels.

Diuretics are considered the oldest group of antihypertensive drugs. These drugs began to be used in the 50s of the 20th century. They are also now widely used, often in combination with other drugs.

Beta blockers were introduced in the 1960s. The drugs were used to treat angina pectoris. Beta blockers reduce blood pressure by affecting the nervous system. They block the effect of beta nerve receptors on the cardiovascular system.

As a result, the heart rate becomes less active and the volume of blood pumped out by the heart per minute decreases, lowering blood pressure. Beta blockers also reduce the effect of certain hormones, so blood pressure also normalizes.

Because beta blockers can cause peripheral blood vessel narrowing, they are not recommended for people with circulatory problems of the upper or lower extremities.

Calcium channel blockers are part of a group of drugs that block the flow of calcium inside muscle cells. Thus, the frequency of their contractions is reduced. All muscle cells need calcium; if it is absent, the muscles cannot contract normally, the blood vessels relax and blood flow improves, which lowers blood pressure.

Angiotensin II receptor blockers are the most modern group drugs. Angiotensin II is an effective vasoconstrictor; its synthesis is carried out under the influence of renin, a kidney enzyme. Angiotensin II has the main property of stimulating the production of aldosterone, which delays the excretion of water and salt by the kidneys.

Drugs that block angiotensin II receptors. Treatment of hypertension cannot be done without these drugs, because they:

1. prevent further narrowing of blood vessels,
2. facilitate the removal of excess water and salt from the body.

Treatment ACE inhibitors widely used for arterial hypertension. With the help of drugs, the ratio of compounds changes in favor of biologically vasodilating active substances. Medicines in this group are usually prescribed to people with hypertension due to kidney disease or heart failure.

Alpha blockers act on the nervous system, but through different receptors than beta blockers. Alpha receptors promote contraction of arterioles, so they relax and blood pressure decreases. Alpha blockers have a side effect - orthostatic hypotension, that is, a sharp decrease in blood pressure after a person assumes an upright position.

Imidazoline receptor agonists are one of the most promising antihypertensive drugs. Treatment with medications of this group eliminates vascular spasm, as a result of which the pressure begins to decrease.

Imidazoline receptor agonists are used to treat moderate forms of hypertension and are routinely prescribed in combination treatment.

Non-drug treatment

Treatment of arterial hypertension without medications involves, first of all, reducing salt intake. It is also important to reconsider the amount of alcoholic beverages you take. It is known that drinking more than 80 grams of alcohol per day increases the risk of developing cardiovascular diseases and hypertension.

Overweight is considered overweight if it exceeds 20% or more of normal body weight depending on height. Obese people are often susceptible to developing arterial hypertension. Their blood cholesterol levels, as a rule, are increased.

Eliminating excess weight will not only help reduce blood pressure, but also help prevent dangerous diseases:

• atherosclerosis,
• diabetes

It is important to remember that there is no one set diet that will ensure that the lost weight will never come back.

Arterial hypertension can reduce symptoms if you adhere to the following therapy: sports activities,

1. limiting salt intake,
2. dietary diet.

Exercising for half an hour three or four times a week will help you achieve weight loss and normalize blood pressure. The educational video in this article will tell you about the dangers of arterial hypertension.

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How to determine increased intracranial pressure?

If there is a lack of treatment and proper complex, increased ICP (intracranial pressure) can lead to serious complications. There may be a decline in vision up to its loss, disruption of blood circulation in the brain, and problems with the nervous system. With a sharp increase in advanced cases, even death is possible.

For increased intracranial pressure The symptoms are quite characteristic and it is important to pay attention to them promptly. Especially because this pressure acts as an indicator of other ailments with even more serious consequences.

Having discovered the first signs of the disease, you need to visit a doctor as soon as possible to undergo an MRI or other suitable examination methods. This will allow you to make an accurate diagnosis and prescribe a complex of treatment. It is never permissible to ignore signals from the body that indicate that there is some kind of destructive process in the body. Even a headache will not arise out of nowhere.

Definition and causes of the disease

According to the physiological explanation, intracranial pressure occurs due to cerebrospinal fluid (CSF). It accumulates in increased quantities or, conversely, in deficiency in a certain part of the skull. This happens due to problems with its circulation process. The function of the cerebrospinal fluid is to protect the gray matter from overload, as well as mechanical damage.

The substance is under constant pressure, goes through a renewal process and circulates through different areas. It usually takes a week to renew the fluid, but various reasons it can accumulate and for this reason there will be signs of increased intracranial pressure.

Accordingly, ICP is a quantitative characteristic that reflects the degree to which cerebrospinal fluid affects brain tissue. This indicator in normal situation- from 100 to 151 mm. water Art.

Very often the cause of this situation is a head injury, but there can be many other negative factors, including various diseases. The most common conditions when the problem appears:

Symptoms characteristic of most cases

The clinical picture of increased intracranial pressure and symptoms in adults are somewhat different than in children. In most situations, symptoms develop gradually. The main signs of painful processes of this nature:

Headaches usually come to the fore in terms of symptoms, they have a pressing and bursting sensation, and sometimes an unpleasant pulsating feeling appears. The provoking factor due to which pain usually occurs in the morning is a horizontal position of the body, coughing or sneezing, straining, or hyperextension of the head. May be accompanied by nausea, noise in the head, vomiting.

Visual disturbances occur in cases of increased ICP due to swelling in the optic nerve papilla and can lead to blindness. Visual symptoms may include objects appearing in duplicate.

First, peripheral vision deteriorates, and then central vision. In addition, high intracranial pressure can cause symptoms in the form of swelling of the eyelids and face, bruises under the eyes, tinnitus and hearing loss, pain in the upper part of the cervical vertebra, as well as the spinal cord.

In addition to these syndromes may be added autonomic dysfunction accompanied by the following factors:

In severe cases, due to increased ICP, stroke-like conditions occur that seriously threaten the patient's life. Such conditions will occur with impaired consciousness up to falling into a coma, instability when walking and severe dizziness, loss of strength in the limbs, speech disorders, severe incessant vomiting.

Symptoms and causes of high ICP in children

Increased intracranial pressure in a child sometimes manifests symptoms even from the first minutes of birth. In the early period, there is a higher risk of complications, so prompt treatment measures must be taken. For infants, such a diagnosis, unfortunately, is not uncommon. Symptoms indicating higher than normal ICP in children are:

The main factor causing increased intracranial pressure in infants is almost always associated with complications and injuries during childbirth or intrauterine infections, hydrocephalus. A child may be more or less calm all day, and in the evening begin to cry a lot and not calm down, which will cause sleep disturbances.

Repeated regurgitation in a large volume with increased pressure occurs due to irritation of the centers in the medulla oblongata, which is responsible for these symptoms. Enlargement of the head to a size disproportionate to the body, divergence of the sutures in the bones of the skull are caused by stagnation and accumulation of cerebrospinal fluid in those spaces that are responsible for the cerebrospinal fluid ducts.

Increased ICP causes excessive accumulation and stagnation of blood in the venous network of the head and it will be clearly visible under the child’s skin. The manifestation of Graefe's symptom (disturbances in the functioning of the oculomotor nerves, occurring due to birth trauma) in the form of uncontrolled deviations of the eyeballs downward can occur periodically.

Indicators indicating hydrocephalus in a child

Hydrocephalus is excess fluid due to the formation of cerebrospinal fluid and its accumulation. This is also facilitated by the appearance of obstacles in the outflow tract and inflammation in the brain tissue. Increased intracranial pressure in an infant caused by hydrocephalus is accompanied by the following symptoms:

Diagnostic methods

Assess the degree of intracranial pressure for appointment suitable treatment possible using the following studies:

• A catheter with further connection of a pressure gauge is inserted into the area between the spinal canal or the ventricles of the brain - it works according to the scheme of a mercury thermometer;
• Computer and magnetic resonance imaging;
• For children under 1 year of age - neurosonography (ultrasound of the brain);
• Echoencephaloscopy (also used for infants);
• Conducting a fundus examination for blurred contours and papilledema.

Patients who have experienced acute circulatory problems are usually prescribed a tomographic examination or an assessment of the fundus of the eye. For children, it is advisable to use other diagnostic methods - starting with an examination by a neurologist to identify deviations in reflexes, excessive development of the head and checking the fontanelles.

It would also be a good idea to visit an ophthalmologist to determine changes in the bottom of the eye, dilated veins, spasms of the arteries and other negative aspects inherent in this diagnosis. While the fontanelles are still open, an ultrasound of the brain will be the most informative option. In this case, an increase in the size of the ventricles, possible deformations, displacements and other space-occupying formations in the skull will be detected.

According to the requirements of the Ministry of Health, neurosonography must be performed 3 times to check for increased intracranial pressure in children under six months of age and the first time within 30 days from birth. This frequency is required because the situation will constantly change even after the first successful examination.

The procedure and the ultrasound itself are harmless to the baby. When the fontanels are no longer present after a year, it would be advisable to conduct a magnetic resonance or computed tomography scan. One of the biggest misconceptions on this issue is that it goes away on its own with age - this is not true.

Modern methods of treating the disease

When it becomes necessary to decide how to treat increased intracranial pressure in adults, the cause of the disease is first established and it is eliminated. If an increase in ICP is caused by a hematoma or tumor or other problem requiring surgical intervention, then it is performed to remove the space-occupying formation. After this, the second stage begins - drug treatment to correct the degree of pressure. For these purposes, the following types of drugs are used:

1. Osmodiuretics, which reduce fluid volume;
2. Furosemide;
3. Dexamethasone (hormonal drugs);
4. Diacarb;
5. Glycine and others.

The next step will be medicinal manipulations, such as ventricular puncture and other methods of reducing fluid volume. Diet therapy is an obligatory component of complex treatment. The fluid entering the body, as well as salts, should be limited. In order for the cerebrospinal fluid to be eliminated faster and absorbed better, diuretics may be prescribed.

High intraocular pressure - causes, symptomatic manifestations and treatment methods

Increased intraocular pressure is a fairly rare and dangerous disease. The reason for its appearance is associated with the secretion of the natural fluid of the eyeball and pressure on the cornea and sclera. Due to disruptions in the body, secretion increases and this leads to painful sensations. Or the occurrence of the problem may be influenced by the anatomical ocular structure of a person.

It feels like heaviness and bursting pain in the eyes, especially sharp when touching closed eyelids. In advanced cases, without treatment it can lead to deterioration of vision and complete blindness. The situation worsens in the presence of other diseases, such as colds, runny nose, and headaches.

When a doctor has determined increased intraocular pressure, treatment is prescribed depending on the stage at which the disease is located. At the initial stage, regular eye exercises may help, as well as limiting computer work and watching TV.

It will be necessary to eliminate all activities that are too straining on the eyes, such as beadwork and other types of painstaking needlework. With a progressive disease, there may be two solutions: laser excision of the iris or laser stretching of the trabecula. Drug treatment can also be effective in some cases.

From time to time it would not be a bad idea to take a vitamin course. Regular exercise and sufficient exposure to fresh air are essential to maintaining health.

The military registration and enlistment office sent me for all these examinations, after which I was declared unfit for service in the army, category B. Please tell me, I am seriously involved in the sport of boxing. Is it possible to continue this? And what could be the reason for this that I was diagnosed. There are no complaints, like everyone else, sometimes they rarely have a headache, well, in short, everything is like everyone else. and a couple of times when I lost consciousness, once I didn’t eat and fainted from hunger, and the second time I started bleeding on an empty stomach and collapsed. But right now I don’t have any problems, I don’t lose anything, everything is fine. answer. thank you in advance

Ekaterinburg, st. Yasnaya 38

I would like to ask you the following question:

My husband underwent a medical examination in court (they want to deprive him of his rights due to the diagnosis of episyndrome, remission for 5 years), passed tests: no complaints, behavior is adequate to the examination situation, he understands instructions from the first presentation, works at a good pace, denies fatigue, when studying memory using the method memorization of 10 words, memorization curve: 44589 8 words delayed, reveals sufficient abilities for mechanical memorization and retention of information, associative and semantic memory is not impaired, when memorizing 10 pairs of words reproduces 9, 10 words delayed, short story retells after 1 presentation and delayed in full, correctly understands the semantic coloring of the plot, the amount of working memory is within the age norm, repeated 7 characters in direct order, repeated 5 characters in reverse order, the function of active attention is not impaired, the pace of psychomotor reactions is sufficient, uniform , increased fatigue not revealed, the time spent searching for numbers: 40 seconds, 41 seconds, 49 seconds, 45 seconds, 44 seconds; when analyzing the proofreading test, disturbances in the function of attention and increased fatigue are not detected.

personal characteristics: results obtained using the UNP-nE method = +77, pS = -5, l = 3, DISCOVERS A VERY LOW LEVEL of neuroticism and the level of psychopathization - in the zone of an uncertain diagnosis; according to the Leonhard method, a cyclothymic characterological type in combination with anxiety traits was diagnosed .using the ITO method, moderately expressed indicators were obtained on the scales of extraversion, rigidity and emotiveness, which indicates increased sociability, subjectivity, variability of emotional mood, active personal position, thus, during the examination, a decrease in mnestic functions of the organic type was not revealed, increased exhaustion and fatigue does not reveal personal characteristics in the form of expression of characterological traits according to the Cyclothymic type, a very low level of neuroticism, increased sociability, an active personal position,

Based on the above, the expert commission comes to the conclusion that my husband shows signs of an organic personality disorder due to epilepsy, this diagnosis is confirmed by the results of this examination, which revealed his epileptoid character traits (emphasized accuracy, thoroughness, pedantry) he cannot drive vehicles

Do the research results correspond to the expert's conclusions?

On the son’s encephalogram, “against the background of moderate diffuse changes in the biopotentials of the brain, pronounced phenomena of irritation of deep structures in the projection are revealed temporal lobe on the left, the phenomena of irritation of diencephalic structures are expressed (significantly). The threshold of convulsive readiness is reduced. In certain sections of the curve, single complexes of the OMV type are noted (in the frontoparietal lobes). What can you do?

Seizure threshold

Best regards, NDK.

Crap. From what I know in theory, almost in Russian.

There is a concept "convulsive focus" is the area(s) of the cerebral cortex with insufficient blood circulation (ischemia) caused by various possible factors: genetic defects, inheritance, pregnancy complications, birth injuries, TBIs and contusions, a bunch of somatic or infectious diseases, brain tumors, metabolic disorders, strokes, intoxications, and so on, and so on, and so on.

Under certain conditions or provoking factors (there are also a bunch of them - diseases, stress, emotional and mental crises and a lot of other things.) activity convulsive focus the excitation of neurons also increases convulsive focus according to specific neural pathways transmitted to the motor system of the spinal cord, i.e. is being formed convulsive readiness.

Convulsive readiness can be high or low.

High - bad (increased activity in convulsive focus - high probability seizures).

Low - good (reduced activity in convulsive focus- reduced likelihood of seizures).

Reduced convulsive readiness threshold - bad. This means that in order to activate the convulsive focus, and therefore the occurrence of convulsions, it is required not very strong stimulus.

Elevated the threshold of convulsive readiness is not so bad. This means that to activate the convulsive focus, it is required, on the contrary - quite serious stimulus.

The future is vague and depends both on lifestyle and treatment.

“Well, he told me everything he knew” (c) Mikhalych

Clarify the problem, plz.

Apparently, we are talking about either a tendency to epileptic seizures (if we are talking about the conclusion of a neuropathologist) or a tendency to vaginismus (if the conclusion was given by a gynecologist).

Either choose what you like best, or give more specific information.

P.S. I still hope that we are not talking about the second option

So I wanted to go into medical school =)) but it didn’t work out. In the end I went to see a psychologist =)

Gladiator: not about the second one =)) I just want to know what all this threatens and where it came from.

Well, my colleague Butch has already told me what it is.

It’s hard to say what the threat is. Maybe nothing. Well, maybe they won’t take you into aviation. Or maybe a person will go crazy and kill everyone around him with extreme cruelty. Little data. And even if there were enough of them, it would still be difficult to say for sure. You know it yourself - psychiatry is a dark matter.

But where this came from - NO ONE WILL EVER EXPLAIN TO YOU. There are hundreds of reasons, and none of them are 100% reliable.

Sorry for the confusion, but what a question - such an answer!

Where did it come from - you can only theoretically draw a circle possible reasons (I briefly listed above). This is a question for Comrade the Lord God.

Convulsive readiness threatens. convulsive episodes (I can’t say it any other way) of varying degrees of intensity.

What is needed is preventive treatment, prescribed individually by a neurologist with monitoring over time and the establishment of a certain lifestyle - i.e. exclude possible factors provoking convulsive readiness. There are many of them and they are individual.

There are many variations of epileptic seizures, large and small, noticeable to others and not.

For example, a person, in the middle of a conversation, suddenly “withdraws into himself” for a few seconds, and then cannot remember what happened to him.

Or he may start kissing and caressing you, then suddenly hit you with all his might or try to strangle you, then again become affectionate and gentle, and completely forget about his outburst of anger.

Or maybe he’ll live his whole life as a harmless eccentric, and in his old age he’ll pour gasoline on his whole family and set it on fire.

All the options I described happened in practice, and more than once.

However, it is also possible that the epileptic will not show himself in any way until the end of his days. His life is somewhat like Russian roulette.

Modern medicine, with all its grief, can correct the behavior of such people for an indefinite period of time, but no one will give you any guarantees.

By the way, “Reduced seizure threshold” is not a diagnosis. This expert opinion at a certain stage of the examination (EEG?) at the moment and that’s it.

1) Can you say more about cruelty? What did you mean? This interests me. 2) What other data is needed? 3) Regarding the question: I don’t know how it could be asked differently. As soon as the diagnosis was made, that’s what I wrote.

I meant the question was too vague

But seriously, all questions to the moderator of this section

I have to turn to Roman - the most important of the most important - the Admin, in short

Unfortunately, this function is not directly available to the moderator.

I have to turn to [b]Roman - the most important of the most important - the admin, in short

Thanks, it's not worth it

I'm sorry. I myself didn’t know that everything was so complicated (restoring the topic).

Reduced seizure threshold (1)

Convulsive readiness

There is no need to hide the fact that a diagnosis of convulsive readiness will not lead to a degree of extreme disorder for very few parents. Fortunately, in this case, timely detection of the disease, proper treatment and competent specialists will help both desperate parents and the little creature bravely endure all the hardships of the disease. Convulsive readiness is not a fatal diagnosis. You can fight him. The number of people cured of the disease is increasing every day.

Convulsive readiness of the brain

Due to the immaturity of the nervous system, young children may be diagnosed with convulsive readiness of the brain. The seizures with which it is accompanied can occur dozens of times, or they can become an isolated case. Without a full examination, the diagnosis cannot be considered reliable.

Convulsive readiness of the brain is most often diagnosed in children under 5 years of age. Up to 5% of preschool children suffer from it. With proper treatment and medication, and in some cases with the help of alternative medicine, convulsive readiness goes away without a trace. In the first years of life, nerve endings and parts of the brain are in the process of constant formation, as a result the blood-brain barrier is very low, and as a result, excitability occurs faster. The child reacts sharply to irritating factors (external and internal), which leads to convulsive readiness of the brain.

Convulsive readiness: symptoms

The symptoms of the condition are very clear. Often, convulsive readiness symptoms are convulsive. However, they can manifest themselves differently at different stages.

Tonic seizures are characterized by loss of contact with the outside world. The person does not respond or react to any external manifestations. Characteristic muscle contractions can be observed both in one muscle group and throughout the body. The duration of the attack is up to 2 minutes. The head is thrown back, the upper limbs are bent, and the lower limbs are fully straightened.

After the attack of tonic convulsive readiness is over, clonic convulsions occur. The frequency of movements increases greatly. Starting from the face, the spasms spread to the whole body. The speed of inhalation and exhalation increases significantly. The skin becomes very white. Foam often appears from the lips. Based on the duration of a clonic attack, a diagnosis of convulsive readiness is made and the severity of the disease is determined.

Brain seizure threshold

A reduced threshold for convulsive readiness of the brain is typical for children younger age. It is individual for each person and decreases under the influence of a number of factors. The most common ones include:

• severe intoxication;
• heat;
• hereditary predisposition;
• diseases and infections of the brain;
• congenital diseases of the nervous system;
• asphyxia;
• diseases associated with metabolic processes;
• hormonal abnormalities;
• infectious diseases, etc.

Although the brain's seizure threshold is different for each person, an epileptic seizure that persists for more than 30 minutes can lead to serious consequences.

Over time, with proper treatment, the brain's seizure threshold can increase significantly. But, at the same time, it is necessary not to allow the convulsive syndrome to develop into a serious disease and develop into something more than it actually is in the early stages.

Increased convulsive readiness

As noted above, increased convulsive readiness is characteristic primarily of children. Due to the high permeability of brain vessels, the hydrophilicity of tissues and the incomplete process of brain formation, the child reacts much more strongly to many stimuli. It doesn’t take much for his body to go into spasms for a few minutes. A couple of decades ago, the diagnosis of increased convulsive readiness was made late. At the age of 5-8 years. Due to the carelessness of doctors, a person has to take pills all his life and fear a new attack. Now convulsive readiness is just a diagnosis. She is curable. After a well-chosen course of treatment completed for six months, the child may no longer remember his illness.

It is important to remember that a person who has been diagnosed with increased seizure activity should not be disturbed in any way. Even a small pathogen in the focal area can lead to prolonged seizures that worsen the patient's condition.

Reduced seizure activity

In contrast to the previous diagnosis, a decrease in convulsive readiness indicates that the patient may have a seizure at any time. It does not require any irritants. In this case, partial seizures are characteristic. They are shorter lasting and the person remains completely conscious.

The diagnosis of decreased seizure readiness is often made in adulthood. They are surprised to learn about it when undergoing general examinations or doing an MRI. The reasons for the appearance are heredity, previous infectious diseases, and the presence of cancer.

Convulsive readiness in children

It is young creatures who are most susceptible to this disease. As a result birth injuries, insufficient development of nerve endings, brain or heredity, convulsive readiness in children is much more common. As mentioned above, the 5% threshold has not yet been exceeded, but this may soon change, as this diagnosis is being made more and more often.

In order to check the diagnosis or, on the contrary, to drive away all doubts, parents can easily check whether there are preconditions that convulsive readiness is likely in children.

• Take the baby between your elbow and shoulder joints and press a little with your fingers. If the baby's fingers begin to twitch nervously and cramp, then the likelihood of convulsive readiness is high.
• Lightly tap with your finger between the cheekbone and the corner of the mouth. If during or after tapping the baby’s face changes in twitching in the area of ​​the mouth, wing of the nose and eyelid, then this is a reason to contact the pediatrician and tell about your experiences.

It is never possible to draw a clear conclusion that a child has a seizure disorder. And it is not recommended to trust the child’s health to the opinion of only one specialist. Tests are required. Convulsive readiness in children is always accompanied low level serum calcium. Additional MRI and EEG studies are performed as prescribed by a neurologist. With a timely and competent approach, when the child is not yet suffering from prolonged seizures and does not lose consciousness, solving the problem is very simple. In advanced cases, when parents did not pay due attention to obvious symptoms, the children suffer first, and only then their inattentive relatives.

It is not so easy to prepare for seizures. It is more important to deal with them in the early stages. And first of all, parents should monitor the health of their children. Their inattention can result in an unpleasant state when, at first glance, healthy man falls in a fit of convulsions. Convulsive readiness is treatable, but it must be dealt with promptly.

Reducing the seizure threshold

In conclusion, the EEG: Against the background of moderate diffuse changes of a general cerebral nature, irritation of the cortex and signs of dysfunction of the stem-diencephalic parts of the brain are noted, with an emphasis in the right parietal-central-frontal region, which intensify during stress tests. Reducing the threshold of convulsive readiness. To clarify the nature of morpho-functional changes, it is advisable to conduct an MRI of the brain and repeat EEG over time.

I am 34 years old, please answer the following questions:

1.Is it possible to drive a car?

2.What restrictions are there when “lowering the threshold”?

3. Is it possible to somehow “remove” this “lowering the threshold”?

4. And in general, does this mean that at any moment I can have a seizure?

5. Is it necessary to do an MRI?

6.What is cortical irritation and signs of dysfunction of the brainstem-diencephalic sections?

Answered by Ryltsov A. Yu.

Such a conclusion is written according to the norm.

1. Yes, but I don’t give the license, and I don’t decide anything for the bureaucrats from the driver’s commission.
2. None!
3. This is a meaningless set of words - only words can be removed.
4. There is no evidence in the information provided.
5. A meaningless set of words.

Complaints? Reason for EEG?

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Factors that lower the seizure threshold

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

The goal of anticonvulsants is to control seizures (a controversial term, usually understood as reducing the frequency and severity to the extent that the patient can live a normal life without the limitations of epilepsy) with minimal or no toxic effects. ≈ 75.

T.N. Leptomeningeal cysts not associated with post-traumatic leptomeningeal cysts (so-called growing skull fractures) or infection. These are congenital formations that arise during development as a result of splitting of the arachnoid membrane (therefore, in fact, it is an int.

The term "Chiari malformation" is preferred over the traditional "Arnold-Chiari malformation" due to the significantly greater contribution made by Chiari.

Chiari malformation consists of 4 types of hindbrain abnormalities that are probably unrelated. Most cases come.

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Low seizure threshold

A low threshold of convulsive readiness can be detected already in the first days of life due to pathology of intrauterine development, but then we are not talking about an epileptic disease, but about a secondary convulsive syndrome.

Taking into account the differences in pathogenetic mechanisms, all paroxysmal conditions can be divided into three large groups:

Despite the fact that each of these forms has a clear criterion for pathogenetic differentiation, in practice there are significant difficulties when trying to differentiate in each specific case between an epileptic disease and symptomatic epilepsy, between symptomatic epilepsy and epileptiform syndrome.

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Threshold of convulsive readiness of the brain

Epileptic discharge can occur even in a healthy brain; The threshold for convulsive readiness of the brain is individual. For example, a child may develop a seizure against a background of high fever. In this case, no further neurological diseases, including epilepsy, arise in the future. At the same time, febrile seizures develop in only 3-5% of children. This suggests that they have a reduced threshold for convulsive readiness under the influence of endogenous factors. One such factor may be heredity - seizures are more likely to develop in people with a family history of epilepsy. In addition, the threshold for convulsive readiness depends on the degree of maturity of the nervous system.

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lowered seizure threshold

This means that a small irritant is enough to cause convulsions.

On what basis was the diagnosis made?

convulsions can occur due to a SHARP rise in temperature. high temperature is not scary. Reducing any temperature is undesirable for everyone. convulsions are a scary sight, but in themselves they are not dangerous if others act correctly.

The baby was sleeping. Sometimes she jerks her arms and legs too much. Then it goes away. In short, in a nutshell, it was as if she wanted to breathe and could not. There was no temperature, but this condition seemed convulsive to me. Then they turned her over on her tummy and she started drooling. white which were bubbling. And she came to her senses. She was pale. The pediatrician suggested that she burped and choked. They did eeg and echo and said so much. I don't know who to believe now.

I don’t know anything about this, but if the threshold is lowered, then on the contrary the sensitivity should be lowered

I have the same problem(((due to a head injury, an accident. They told me to do a repeat Egg before giving birth in order to make a decision to give birth by soma or CS, has anyone encountered this?? How did they give birth?? What are the consequences??

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Seizure threshold

My 4-month-old son, according to EEG data, was diagnosed with a decrease in the threshold for convulsive readiness of the brain.

The following drugs were prescribed as treatment: Pantogam, glycerol, MgBr.

I strongly doubt the adequacy of the chosen treatment. Please tell me, is it worth giving a baby all these medications? And any medications at all. Why is this diagnosis dangerous?

It is necessary to treat, what to treat, on what basis. unclear.

Comments to the post:

Valery Valerievich Samoilenko

The son was born on October 19. 2007, weight 3200g, height 51 cm. 6/7 apgar. Urgent birth, at 37 weeks, CS due to partial placental abruption. After giving birth, my son had hypoxia, hemorrhagic disease in the form of gastrointestinal bleeding (severe), on vit. B6 anaphylactic shock, etc. a pathological loss of body weight was observed (at discharge, he weighed 2.760 g).

After discharge from the RD, the child is completely breastfed. Weight gain is normal. (now weighs approx. 7200g). Starting from 3 months, there were complaints of restlessness, frequent twitching, a couple of times at night I even called an ambulance, because... the son screamed for several hours, then “rolled over”, convulsions ran through his body.

Traditionally, we were diagnosed with PEP, increased ICP. However, I have read a lot about the overdiagnosis of these “diseases,” which is why I turn to this forum, because I do not want to give my child “extra” medications.

Regarding the surveys carried out. An NSG was performed (increased vascular pulsation was detected, the rest was normal). EEG (lowering the seizure threshold). I don’t have the results of these studies on hand, so I’m writing from memory.

Actually, from the previous answer I understood that we need to look for another doctor, right? How dangerous is the diagnosis we were given based on the EEG?

Let me formulate it even more simply: does my child need to be treated in principle? Or not?

Valery Valerievich Samoilenko

Maybe it makes sense to go for a consultation to the regional hospital.

Regarding the conclusion of the EEG and NSG (which is generally not clear why they did it), what can I, a mere mortal, add to the words of Vasily Yuryevich?

The diagnoses (PEP, ICP) are a myth, so as not to say “nonsense”

The prescribed “treatment” (pantogam, glycerol) is nonsense, to say the least.

The phrase "If" lowering the threshold. “If not treated, there is a risk of developing epilepsy” speaks of the doctor’s wonderful imagination - at best, she was joking.

I don't see any pathology.

Valery Valerievich Samoilenko

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Seizure threshold

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Definition of the concept

An epileptic (convulsive) seizure is a nonspecific reaction of the brain to disturbances of various natures in the form of partial (focal, local) or generalized convulsive seizures.

Status epilepticus is a convulsive seizure lasting more than 30 minutes or repeated seizures without full recovery of consciousness between attacks, life-threatening for the patient (in adults, mortality is 6–18% of cases, in children - 3–6%).

From epilepsy as a disease, one should distinguish epileptic syndromes in current organic diseases of the brain and acute toxic or toxic-infectious processes, as well as epileptic reactions - isolated episodes under the influence of extreme harm for a given subject (infection, intoxication).

Causes

The most common causes of seizures in different age groups are:

Seizures associated with fever (simple or complex)

Congenital metabolic disorders

Phakomatoses (leukoderma and skin hyperpigmentation, angiomas and nervous system defects)

Children's cerebral paralysis(cerebral palsy)

Agenesis of the corpus callosum

Residual epilepsy (brain injury in early childhood)

Brain tumors

25–60 years (late-onset epilepsy)

Residual epilepsy (brain injury in early childhood)

Inflammation (vasculitis, encephalitis)

Brain tumors, brain metastases

A brain tumor

The most common causes of status epilepticus:

• stopping or irregularly taking anticonvulsants;
• alcoholic withdrawal syndrome;
• stroke;
• anoxia or metabolic disorders;
• CNS infections;
• a brain tumor;
• overdose of drugs that stimulate the central nervous system (in particular, cocaine).

Seizures occur paroxysmally, and in the interictal period, in many patients, no disorders are detected for months and even years. Seizures in patients with epilepsy develop under the influence of provoking factors. The same provoking factors can cause a seizure in healthy people. These factors include stress, sleep deprivation, hormonal changes during the menstrual cycle. Some external factors(for example, toxic and medicinal substances) can also trigger seizures. In a cancer patient, epileptic seizures can be caused by tumor damage to brain tissue, metabolic disorders, radiation therapy, cerebral infarction, drug intoxication and central nervous system infections.

Epileptic seizures are the first symptom of brain metastases in 6-29% of patients; in approximately 10% they are observed as a result of the disease. When the frontal lobe is affected, early seizures are more common. In case of defeat cerebral hemispheres the risk of late seizures is higher, and for posterior lesions cranial fossa Seizures are uncommon. Epileptic seizures are often observed with intracranial metastases of melanoma. Occasionally, antineoplastic drugs, in particular etoposide, busulfan and chlorambucil, are the cause of epileptic seizures.

Thus, any epileptic seizure, regardless of etiology, develops as a result of the interaction of endogenous, epileptogenic and provoking factors. Before starting treatment, it is necessary to clearly establish the role of each of these factors in the development of seizures.

Mechanisms of occurrence and development (pathogenesis)

Pathogenesis has not been studied enough. Uncontrolled electrical activity of a group of neurons in the brain (“epileptic focus”) involves significant areas of the brain in the process of pathological excitation. With the rapid spread of pathological hypersynchronous activity over large areas of the brain, consciousness is lost. If pathological activity is limited to a certain area, partial (focal) seizures develop, not accompanied by loss of consciousness. With status epilepticus, continuous generalized epileptic discharges of neurons in the brain occur, leading to depletion of vital resources and irreversible damage to nerve cells, which is immediate cause severe neurological consequences of the status and death.

A seizure is the result of an imbalance between the processes of excitation and inhibition in the central nervous system. Symptoms depend on the function of the area of ​​the brain where the epileptic focus is formed and the path of spread of epileptic excitation.

We still know little about the mechanisms of seizure development, so a generalizing scheme for the pathogenesis of seizures of various etiologies does not exist. However, the following three points help to understand what factors and why can cause a seizure in a given patient:

Epileptic discharge can occur even in a healthy brain; The threshold for convulsive readiness of the brain is individual. For example, a child may develop a seizure against a background of high fever. In this case, no further neurological diseases, including epilepsy, arise in the future. At the same time, febrile seizures develop in only 3-5% of children. This suggests that they have a reduced threshold for convulsive readiness under the influence of endogenous factors. One such factor may be heredity - seizures are more likely to develop in people with a family history of epilepsy.

In addition, the threshold for convulsive readiness depends on the degree of maturity of the nervous system. Some medical conditions significantly increase the likelihood of epileptic seizures. One of these diseases is severe penetrating traumatic brain injury. Epileptic seizures after such injuries develop in 50% of cases. This suggests that trauma leads to changes in interneuronal interactions such that neuronal excitability increases. This process is called epileptogenesis, and factors that reduce the threshold of convulsive readiness are called epileptogenic.

In addition to traumatic brain injury, epileptogenic factors include stroke, infectious diseases of the central nervous system and malformations of the central nervous system. In some epileptic syndromes (for example, benign familial neonatal seizures and juvenile myoclonic epilepsy), genetic disorders have been identified; Apparently, these disorders are realized through the formation of certain epileptogenic factors.

Clinical picture (symptoms and syndromes)

Classification

Forms of seizures

1. Partial (focal, local) - individual muscle groups are involved in convulsions, consciousness, as a rule, is preserved.

2. Generalized - consciousness is impaired, convulsions cover the entire body:

• primary generalized - bilateral involvement of the cerebral cortex;
• secondary generalized - local involvement of the cortex followed by bilateral spread.

• tonic - prolonged muscle contraction;
• clonic - short muscle contractions immediately following each other;
• tonic-clonic.

• Contraction of individual muscle groups, in some cases only on one side.
• Seizure activity may gradually involve new areas of the body (Jacksonian epilepsy).
• Impaired sensitivity of certain areas of the body.
• Automatisms (small movements of the hands, slurping, inarticulate sounds, etc.).
• Consciousness is often preserved (impaired in complex partial seizures).
• The patient loses contact with others for 1–2 minutes (does not understand speech and sometimes actively resists the assistance provided).
• Confusion usually lasts 1–2 minutes after the seizure ends.
• May precede generalized seizures (Kozhevnikov epilepsy).
• If consciousness is impaired, the patient does not remember the seizure.

• Typically occurs in a sitting or lying position.
• Typically occurs in a dream
• May begin with an aura (unpleasant sensations in the epigastric region, involuntary head movements, visual, auditory and olfactory hallucinations, etc.).
• Initial scream.
• Loss of consciousness.
• Falling to the floor. Fall injuries are common.
• As a rule, dilated pupils are not sensitive to light.
• Tonic convulsions for 10–30 seconds, accompanied by cessation of breathing, then clonic convulsions (1–5 minutes) with rhythmic twitching of the arms and legs.
• Focal neurological symptoms are possible (implying focal brain damage).
• Skin color: hyperemia or cyanosis at the beginning of the attack.
• Characterized by biting the tongue on the sides.
• In some cases, involuntary urination.
• In some cases, foam around the mouth.
• After a seizure - confusion, final deep dream, often headache and muscle pain. The patient does not remember the seizure.
• Amnesia for the entire period of the seizure.

• Occurs spontaneously or as a result of rapid withdrawal of anticonvulsants.
• Convulsive seizures follow each other, consciousness is not fully restored.
• In patients in a comatose state, the objective symptoms of a seizure may be erased; attention should be paid to twitching of the limbs, mouth and eyes.
• Often ends fatal, the prognosis worsens with prolongation of the seizure for more than 1 hour and in elderly patients.

Convulsive seizures must be differentiated from:

• It may occur in a sitting or lying position.
• Doesn't occur in a dream.
• Precursors are variable.
• Tonic-clonic movements are asynchronous, movements of the pelvis and head from side to side, eyes tightly closed, opposition to passive movements.
• Facial skin color does not change or facial redness.
• There is no tongue biting or biting in the middle.
• There is no involuntary urination.
• There is no damage from a fall.
• Confusion after an attack is absent or demonstrative in nature.
• Pain in the limbs: various complaints.
• There is no amnesia.

• Occurrence in a sitting or lying position is rare.
• Doesn't occur in a dream.
• Precursors: dizziness, darkening before the eyes, sweating, drooling, tinnitus, yawning are typical.
• There are no focal neurological symptoms.
• Skin color: pale at the beginning or after convulsions.
• Involuntary urination is not typical.
• Fall injuries are not typical.
• Partial amnesia.

Cardiogenic syncope (Morgagni–Adams–Stokes attacks)

• Occurrence in a sitting or lying position is possible.
• Occurrence in a dream is possible.
• Precursors: often absent (with tachyarrhythmias, fainting may be preceded by rapid heartbeat).
• There are no focal neurological symptoms.
• Tonic-clonic movements may occur after 30 seconds of fainting (secondary anoxic seizures).
• Skin color: pale at the beginning, hyperemia after recovery.
• Tongue biting is rare.
• Involuntary urination is possible.
• Damage from falling is possible.
• Confusion after an attack is not typical.
• There is no pain in the limbs.
• Partial amnesia.

A hysterical attack occurs in a certain emotionally stressful situation for the patient in the presence of people. This is a performance that unfolds with the viewer in mind; When patients fall, they never break. Convulsions most often manifest themselves as a hysterical arc; patients take pretentious poses, tear their clothes, and bite. The reaction of the pupils to light and the corneal reflex are preserved.

Transient ischemic attacks (TIAs) and migraine attacks, which cause transient dysfunction of the central nervous system (usually without loss of consciousness), can be mistaken for focal epileptic seizures. Neurological dysfunction due to ischemia (TIA or migraine) often produces negative symptoms, i.e., loss symptoms (eg, sensory loss, numbness, visual field limitation, paralysis), whereas defects associated with focal epileptic activity are usually positive. nature (convulsive twitching, paresthesia, distortion of visual sensations and hallucinations), although such a distinction is not absolute. Brief, stereotypical episodes indicating dysfunction in a specific area of ​​the brain's blood supply in a patient with vascular disease, cardiac pathology, or risk factors for vascular damage (diabetes, hypertension) are more typical of TIA. But, since in older patients a common cause of epileptic seizures is cerebral infarction in the late period of the disease, one should search for a focus of paroxysmal activity on the EEG.

Classic migraine headaches with visual aura, unilateral localization, and gastrointestinal disturbances are usually easy to differentiate from epileptic seizures. However, some migraine sufferers experience only migraine equivalents, such as hemiparesis, numbness, or aphasia, and may not experience headaches afterwards. Such episodes, especially in older patients, are difficult to distinguish from TIAs, but they may also represent seizures of focal epilepsy. Loss of consciousness after some forms of vertebrobasilar migraine and high frequency headaches after epileptic seizures further complicate the differential diagnosis. The slower development of neurological dysfunction in migraine (often over minutes) serves as an effective differential diagnostic criterion. Be that as it may, in some cases, patients who are suspected of having any of the three conditions under consideration need to undergo an examination, including CT, cerebral angiography and specialized EEG, to make a diagnosis. Sometimes, to confirm the diagnosis, trial courses of treatment with antiepileptic drugs should be prescribed (interestingly, in some patients this course of treatment prevents both epileptic and migraine attacks).

Psychomotor variations and hysterical attacks. As noted above, during complex partial seizures, patients often experience behavioral disturbances. This is manifested by sudden changes in the structure of the personality, the appearance of a feeling of impending death or unmotivated fear, pathological sensations of a somatic nature, episodic forgetfulness, short-term stereotypical motor activity such as picking clothes or tapping a foot. Many patients experience personality disorders, and therefore such patients need the help of a psychiatrist. Often, especially if patients do not experience tonic-clonic seizures and loss of consciousness, but have emotional disturbances, episodes of psychomotor seizures are designated as psychopathic fugues (flight reactions) or hysterical attacks. IN similar cases misdiagnosis is often based on a normal interictal EEG and even during one of the episodes. It must be emphasized that seizures can be generated from a focus located deep in the temporal lobe and does not manifest itself in superficial EEG recordings. This has been repeatedly confirmed when recording EEG using deep electrodes. Moreover, deep temporal lobe seizures can manifest themselves only in the form of the above phenomena and are not accompanied by the usual convulsive phenomenon, muscle twitching, and loss of consciousness.

It is extremely rare that patients observed for epileptiform episodes actually have hysterical pseudo-seizures or outright malingering. Often these individuals have actually suffered epileptic seizures in the past or have been in contact with people with epilepsy. Such pseudo-seizures can sometimes be difficult to distinguish from true seizures. Hysterical attacks are characterized by a non-physiological course of events: for example, muscle twitching spreads from one arm to the other without moving to the muscles of the face and legs on the same side, convulsive contractions of the muscles of all extremities are not accompanied by loss of consciousness (or the patient feigns loss of consciousness), the patient tries to avoid injury , for which, at the moment of convulsive contractions, it moves away from the wall or moves away from the edge of the bed. In addition, hysterical attacks, especially in teenage girls, can have an overtly sexual overtones, accompanied by pelvic movements and manipulation of the genitals. If in many forms of seizures in the case of temporal lobe epilepsy the surface EEG is unchanged, then generalized tonic-clonic seizures are always accompanied by disturbances in the EEG both during and after the seizure. Generalized tonic-clonic seizures (usually) and complex partial seizures moderate duration (in many cases) are accompanied by an increase in the level of prolactin in the blood serum (during the first 30 minutes after the attack), whereas this is not noted with hysterical seizures. Although the results of such tests do not have an absolute differential diagnostic value, obtaining positive data can play an important role in characterizing the genesis of attacks.

Diagnostics

Patients with epileptic seizures are admitted to medical institutions both urgently during an attack and routinely several days after the attack.

If there is a history of recent febrile illness accompanied by headaches, mental status changes, and confusion, an acute CNS infection (meningitis or encephalitis) may be suspected; in this case, it is necessary to immediately examine the cerebrospinal fluid. In such a situation, a complex partial seizure may be the first symptom of encephalitis caused by the herpes simplex virus.

A history of headaches and/or mental changes preceding the attack, combined with signs of increased intracranial pressure or focal neurological symptoms, leads to the exclusion of a mass formation (tumor, abscess, arteriovenous malformation) or chronic subdural hematoma. In this case, seizures with a clear focal onset or aura are of particular concern. A CT scan is indicated to clarify the diagnosis.

General examination can provide important etiological information. Gingival hyperplasia is a common consequence long-term treatment phenytoin. Exacerbation of a chronic seizure disorder associated with intercurrent infection, alcohol intake, or discontinuation of treatment is a common reason for patients being admitted to emergency departments.

When examining the skin on the face, capillary hemangioma is sometimes found - a symptom of Sturge-Weber disease (radiography can reveal cerebral calcifications), stigmata of tuberous sclerosis (adenomas sebaceous glands and shagreen patches) and neurofibromatosis ( subcutaneous nodules, café au lait spots). Asymmetry of the trunk or limbs usually indicates hemihypotrophy, a type of somatic developmental delay, contralateral to a congenital or focal brain lesion acquired in early childhood.

Data from anamnesis or general examination can also establish signs of chronic alcoholism. In people suffering from severe alcoholism, seizures are usually caused by withdrawal symptoms (rum seizures), old brain contusions (from falls or fights), chronic subdural hematoma, and metabolic disorders due to malnutrition and liver damage. Epileptic seizures against the background of withdrawal syndrome usually occur 12-36 hours after stopping drinking alcohol and are short-term tonic-clonic, both single and serial in the form of 2-3 seizures. In such cases, after a period of epileptic activity, there is no need to prescribe treatment to the patient, since subsequent seizures usually do not occur. As for patients with alcoholism in whom epileptic seizures develop at a different time (and not after 12-36 hours), they need to be treated, but this group of patients requires Special attention due to their lack of complaints and the presence metabolic disorders that complicate drug therapy.

Standard blood tests can help determine whether seizures are due to hypoglycemia, hypo- or hypernatremia, or hypo- or hypercalcemia. It is necessary to determine the causes of these biochemical disorders and correct them. In addition, other, less common causes of epileptic seizures are established using appropriate tests for thyrotoxicosis, acute intermittent porphyria, lead or arsenic intoxication.

In older patients, epileptic seizures may indicate acute disorder cerebral circulation or be a distant consequence of an old cerebral infarction (even a silent one). The plan for further examination will be determined by the patient's age, the functional state of the cardiovascular system and accompanying symptoms.

Generalized tonic-clonic seizures can develop in individuals without abnormalities in the nervous system after moderate sleep deprivation. Such seizures are sometimes observed in people working double shifts, in university students during exam sessions, and in soldiers returning from short leave. If the results of all tests performed after a single seizure are normal, such patients do not require further treatment.

If a patient who has suffered an epileptic seizure, according to the anamnesis, examination, biochemical tests blood tests fail to detect abnormalities, one gets the impression that the seizure is idiopathic and that there is no underlying serious damage to the central nervous system. Meanwhile, tumors and other space-occupying formations can occur for a long time and manifest themselves asymptomatically in the form of epileptic seizures, and therefore further examination of patients is indicated.

EEG is important for the differential diagnosis of seizures, determining their cause, and correct classification. When the diagnosis of an epileptic seizure is in doubt, for example, in cases of differentiation between epileptic seizures and syncope, the presence of paroxysmal changes in the EEG confirms the diagnosis of epilepsy. For this purpose they use special methods activation (recording during sleep, photostimulation and hyperventilation) and special EEG leads (nasopharyngeal, nasoethmoidal, sphenoidal) for recording from deep brain structures and long-term monitoring even in an outpatient setting. EEG can also detect focal disorders(spikes, sharp waves or focal slow waves), which indicate the likelihood of focal neurological damage, even if the symptomatology of the attack is initially similar to that of generalized seizures. EEG also helps classify seizures. It makes it possible to distinguish focal secondary generalized seizures from primary generalized ones and is especially effective in differential diagnosis short-term lapses of consciousness. Minor seizures are always accompanied by bilateral spike-wave discharges, whereas complex partial seizures may be accompanied by both focal paroxysmal spikes and slow waves or a normal surface EEG pattern. In cases of petit mal seizures, the EEG may demonstrate that the patient is experiencing many more petit mal seizures than are clinically apparent; thus EEG helps in monitoring antiepileptic drug therapy.

Until recently, important additional methods for examining patients with epileptic seizures were lumbar puncture, skull radiography, arteriography and pneumoencephalography.

Lumbar puncture is still performed when acute or chronic CNS infections or subarachnoid hemorrhage are suspected. CT scan and NMR imaging currently provide more definitive information about anatomical disorders than previously used invasive research methods. All adults experiencing a first seizure should have a diagnostic CT scan, either without or with contrast enhancement. If the first examinations give normal results, a repeat examination is carried out after 6-12 months. MRI is particularly useful early in the evaluation of focal epileptic seizures, when it can detect subtle changes better than CT.

Arteriography is performed in case of serious suspicions and for arteriovenous malformation, even if no changes were detected according to CT data, or in order to visualize the vascular pattern in the lesion detected using non-invasive methods.

Treatment

Protect the patient from possible injuries that may occur during a fall and during convulsive twitching of the body, ensure his safety.

Calm those around you. Place something soft (jacket, hat) under the patient's head to avoid head injury during convulsive movements. Unfasten clothing that may impede breathing. You can place a handkerchief twisted into a knot between the teeth of the lower and upper jaw if the attack is just beginning. This is necessary to prevent tongue biting and tooth damage. Turn the patient's head to the side so that saliva can flow freely onto the floor. If the patient stops breathing, begin CPR.

After the seizures have stopped, if the seizure occurred on the street, arrange for the patient to be transported home or to the hospital. Contact the patient's relatives to report the incident. As a rule, relatives know what to do.

If the patient does not report that he suffers from epilepsy, it is better to call " Ambulance", since convulsive syndrome may be a sign significant amount even more serious pathology (cerebral edema, intoxication, etc.). Do not leave the patient unattended.

What not to do during an epileptic seizure

• Leave the patient alone during an attack.
• Try to hold the patient (by the arms, shoulders or head) or transfer him to another, even more convenient place for him, during a convulsive attack.
• Try to unclench the patient’s jaws and insert any objects between them to avoid a fracture of the lower jaw and injury to the teeth.

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 restoring metabolic processes to normal level 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 non-progressive lesions, can cause the development of gliosis and other denervation changes. These changes can lead to the formation of chronic epileptic foci, which cannot be eliminated by removing the primary lesion. In such cases, surgical extirpation of epileptic areas of the brain is sometimes necessary to control the course of epilepsy (see Neurosurgical treatment for epilepsy below).

There is a complex relationship between the limbic system and neuroendocrine function that can have a significant impact on patients with epilepsy. Normal fluctuations in hormonal status affect the frequency of seizures, and epilepsy in turn also causes neuroendocrine disorders. For example, in some women, significant changes in the pattern of epileptic seizures coincide with certain phases of the menstrual cycle (menstrual epilepsy); in others, changes in the frequency of seizures are caused by taking oral contraceptives and pregnancy Yu. In general, estrogens have the property of provoking seizures, while progestins have an inhibitory effect on them. On the other hand, some patients with epilepsy, especially those with complex partial seizures, may show signs of concomitant reproductive problems. endocrine dysfunction. Disorders are common sexual desire, especially hyposexuality. In addition, women often develop polycystic ovary syndrome, and men develop potency disorders. Some patients with these endocrine disorders do not clinically experience epileptic seizures, but have EEG changes (often with temporal discharges). It remains unclear whether epilepsy causes endocrine and/or behavioral disorders or whether these two types of disorders are separate manifestations of the same underlying neuropathological process. However therapeutic effects on endocrine system are in some cases effective in controlling some forms of seizures, and antiepileptic therapy is a good treatment for some forms of endocrine dysfunction.

Pharmacotherapy underlies the treatment of patients with epilepsy. Its goal is to prevent seizures without interfering with normal thinking processes (or the child's normal intellectual development) and without negative systemic side effects. The patient should be prescribed the lowest possible dose of any one anticonvulsant drug as much as possible. If the doctor knows exactly the type of seizures in a patient with epilepsy, the spectrum of action of the anticonvulsants at his disposal and the basic pharmacokinetic principles, he can completely control seizures in 60-75% of patients with epilepsy. However, many patients are resistant to treatment because the drugs chosen are not appropriate for the seizure type(s) or are not prescribed in optimal doses; they develop unwanted side effects. Determining the content of anticonvulsants in blood serum allows the doctor to dose the drug individually to each patient and monitor the administration of the drug. In this case, in a patient who is prescribed drug treatment, after an appropriate period of achieving an equilibrium state (usually taking several weeks, but not less than a period of time of 5 half-life periods), the drug content in the blood serum is determined and compared with standard therapeutic concentrations established for each drug. By adjusting the prescribed dose, bringing it into line with the required therapeutic level of the drug in the blood, the doctor can compensate for the effect of individual fluctuations in the absorption and metabolism of the drug.

Long-term intensive EEG studies and video monitoring, careful determination of the nature of seizures and selection of anticonvulsants can significantly increase the effectiveness of seizure control in many patients previously considered resistant to conventional antiepileptic therapy. Indeed, such patients often have to stop several medications until the most suitable one can be found.

Hospitalizations in neurological department The following categories of patients are subject to:

• With a first-time epileptic seizure.
• With stopped status epilepticus.
• In case of a series of seizures or status epilepticus, it is indicated emergency hospitalization to the neuroreanimation department.
• Patients with TBI are preferably hospitalized in the neurosurgical department.
• Pregnant women with convulsive seizures are subject to immediate hospitalization in an obstetrics and gynecology hospital.
• Patients after a single epileptic attack with an established cause do not require hospitalization.

In case of symptomatic status epilepticus (acute head injury, brain tumor, stroke, brain abscess, severe infections and intoxications), pathogenetic therapy of these conditions is simultaneously carried out with a special emphasis on dehydration therapy - due to the severity of cerebral edema (furosemide, uregitis).

If epileptic seizures are caused by metastases in the brain, phenytoin is prescribed. Prophylactic anticonvulsant therapy is carried out only when the risk of late seizures is high. In this case, the serum concentration of phenytoin is often determined and the dose of the drug is adjusted in a timely manner.

Indications for prescribing specific drugs

Three drugs are most effective for generalized tonic-clonic seizures: phenytoin (or diphenylhydantoin), phenobarbital (and other long-acting barbiturates), and carbamazepine. The condition of most patients can be controlled with adequate doses of any of these drugs, although a certain drug may work better for each patient individually, phenytoin is quite effective in terms of preventing attacks, its sedative effect is very weak, and it does not cause intellectual impairment. However, in some patients, phenytoin causes gingival hyperplasia and mild hirsutism, which is especially unpleasant for young women. With long-term use, coarsening of facial features may occur. Taking phenytoin sometimes leads to the development of lymphadenopathy, and very high doses have a toxic effect on the cerebellum.

Carbamazepine is no less effective and does not cause many of the side effects inherent in phenytoin. Intellectual functions not only do not suffer, but remain preserved to a greater extent than when taking phenytoin. Meanwhile, carbamazepine can provoke gastrointestinal disorders, bone marrow depression with a slight or moderate decrease in the number of leukocytes in the peripheral blood (up to 3.5-4 10 9 / l), which in some cases becomes pronounced, and therefore these changes require careful monitoring . In addition, carbamazepine is hepatotoxic. For these reasons, complete blood counts and liver function tests should be performed before starting carbamazepine therapy and then at 2-week intervals throughout the treatment period.

Phenobarbital is also effective for tonic-clonic seizures and does not have any of the above effects. side effects. However, at the beginning of use, patients experience depression and lethargy, which explains the poor tolerability of the drug. Sedation is dose-related, which may limit the amount of drug prescribed to achieve complete seizure control. In the same case, if the therapeutic effect can be achieved using doses of phenobarbital that do not give a sedative effect, then the mildest regimen of long-term use of the drug is prescribed. Primidone is a barbiturate that is metabolized to phenobarbital and phenylethylmalonamide (PEMA) and may be more effective than phenobarbital alone due to its active metabolite. In children, barbiturates can provoke states of hyperactivity and increased irritability, which reduces the effectiveness of treatment.

In addition to systemic side effects, all three classes of drugs have toxic effects on the nervous system at higher doses. Nystagmus is often observed even at therapeutic concentrations of drugs, while ataxia, dizziness, tremors, inhibition of intellectual processes, memory loss, confusion and even stupor can develop with increasing levels of drugs in the blood. These phenomena are reversible when the concentration of the drug in the blood is reduced to therapeutic levels.

Partial seizures, including complex partial seizures (with temporal lobe epilepsy). Drugs commonly prescribed to patients with tonic-clonic seizures are also effective for partial seizures. It is possible that carbamazepine and phenytoin are somewhat more effective for these seizures than barbiturates, although this has not been definitively established. In general, complex partial seizures are difficult to treat, requiring patients to be prescribed more than one drug (for example, carbamazepine and primidone or phenytoin, or any of the first-line drugs in combination with high doses of methsuximide) and, in some cases, neurosurgical intervention. For these forms of seizures, many epilepsy centers are testing new antiepileptic drugs.

Primary generalized petit mal seizures (absences and atypical). These seizures can be corrected with drugs of various classes, unlike tonic-clonic and focal seizures. For simple absence seizures, ethosuximide is the drug of choice. Side effects include gastrointestinal disorders, behavioral changes, dizziness and drowsiness, but corresponding complaints are quite rare. For more difficult to control atypical petit mal and myoclonic seizures, valproic acid is the drug of choice (it is also effective for primary generalized tonic-clonic seizures). Valproic acid may cause irritation gastrointestinal tract, bone marrow depression (especially thrombocytopenia), hyperammonemia and liver dysfunction (including rare cases of progressive liver failure With fatal, which is more likely a consequence of hypersensitivity to the drug than a dose-dependent effect). General analysis blood count with platelet count and liver function tests should be performed before the start of therapy and during treatment at two-week intervals for a period sufficient to confirm that the drug is well tolerated in a particular patient.

Clonazepam (a benzodiazepine drug) may also be used for atypical petit mal and myoclonic seizures. It sometimes causes dizziness and irritability, but usually does not cause other systemic side effects. One of the first anti-absence drugs was trimethadione, but it is now rarely used due to potential toxicity.

See neurosurgical treatment of epilepsy.

Which doctors should I contact if this occurs?

References

1. Emergency medical care: A guide for doctors. Under the general editorship. prof. V.V. Nikonova Electronic version: Kharkov, 2007. Prepared by the Department of Emergency Medicine, Disaster Medicine and Military Medicine of KhMAPO

“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 his own feelings. In modern medicine, there is even the 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 arises - fear 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; in 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 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. loss of memory, if in the sensorimotor cortex - an attack of twitching of the limbs or unpleasant sensations of “crawling 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”, there are a huge number of manifestations of epilepsy. These may be attacks of unpleasant sensory sensations, disturbances of vision, taste, and 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 outbreak is localized in occipital lobes In the brain, deja vu arises - 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, laureate Nobel Prize in chemistry and the 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 cannot be controlled by conservative methods. The technique, first used in the United States in 1997, becomes a replacement for the previous neurosurgical treatment, the essence of which was the physical removal of the epilepsy focus 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 in this environment an electricity. 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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