Paroxysmal activity of brainstem structures during hyperventilation. Epilepsies associated with benign epileptiform discharges in children. EEG patterns in clinical epileptology

08.04.2004

Rodriguez V.L.

The modern classification of epilepsies and epileptic syndromes also includes EEG criteria, which already implies the need for close interaction between the clinician and the functional diagnostician.

We collected 150 cases of epilepsy and 150 cases of non-epileptic paroxysmal and non-paroxysmal conditions in which the diagnosis by the clinician after the conclusion of the functional diagnostician was incorrectly made, and in almost all of these cases anticonvulsants were prescribed. How we collected such an array is very simple - we checked the archives.

Our general conclusion about the cause is poor interaction between the clinician and the functional diagnostician. How this was reflected in more detail:

1. In overdiagnosis of epilepsy , (more often this was associated with the conclusion of a functional diagnostician about the presence of “epileptiform activity”, or the presence of “paroxysmal activity”, although it was not there.) Neurologists in such cases only read the conclusion, but did not look at the curve, often because they were unfamiliar with EEG. Recordings on ink devices were not looked at, because it is inconvenient and time-consuming, printouts of digital EEG curves - because what is printed by a computer is already perceived as dogma - you never know what a living, sinful neurophysiologist said - that’s what the computer said! Moreover, he showed me some beautiful hearth, and in color!

Overdiagnosis was significantly higher in cases of using machines with automatic conclusions.

Most often, bursts of slow waves during hyperventilation (uneven, the quality of which is not controlled in shielded chambers) were mistaken for epileptiform activity.

Somewhat less often, although quite often - normal phenomena of children's EEG (polyphasic potentials - sailing waves)

Somewhat less frequently, bursts of local slow waves or short-lived local decelerations were called epileptiform activity.

Somewhat less often – physiological artifacts (the so-called “blinkers” or artifacts from short sudden movements, which also cannot be controlled in a screened chamber)

Even less frequently, EEG sleep phenomena (vertex potentials, K-complexes, acute transient vertex potential) were mistaken for epileptiform phenomena.

In last place, the reason for the overdiagnosis of epilepsy was the registration of real epileptiform activity in the EEG, which was honestly noted by the functional diagnostician as epileptiform or paroxysmal, but without further clarification. And although there were no clinical epileptic manifestations (for example, there were only headaches, hyperactivity, enuresis, tics), a neurologist or psychiatrist was subordinate to a functional diagnostician.

2. Underdiagnosis of epilepsy was associated with the problems of neurologists who followed the lead of functionalists in cases where epileptiform activity was not recorded. But it was also associated with ineffectiveness associated with poor quality of functional diagnostics: improper preparation of the patient, ignoring or incorrectly conducting functional tests, the inability to assess the typical morphology of this activity due to the “cutting” of high-amplitude activity recorded on ink-writing devices.

Lack of typing of epileptiform activity was more common when recording EEG on old ink-writing devices.

If we were faced with a seemingly ideal case - the coincidence of a neurologist’s conclusion about the presence of epilepsy and the presence of epileptiform activity on the EEG, there was still room for a therapeutic marriage (for example, the frequent absence of truly significant, pathognomonic epileptiform activity in Janz syndrome, but the frequent presence of random focal paroxysmal phenomena). As a result, the prescription of carbamazepine, which is contraindicated for this syndrome.

We defined this phenomenon as a lack of typification of epileptiform activity.

In the course of the work, the existence of some “myths” that were characteristic of different EEG rooms or that were characteristic of clinicians also unexpectedly emerged.

Functionalist myths:

normal low-amplitude EEGs in adults were interpreted as pathological background activity and could be interpreted as “whole-brain changes”, more often defined as “diffuse” or, in conclusion, interpreted as manifestations of encephalopathy;

The % increase in the level of slow-wave activity during hyperventilation was for some reason considered as a criterion for the success or failure of treatment. This was based on the idea of ​​“convulsive readiness,” which is supposedly higher if there is more slow-wave activity during hyperventilation;

unusual conclusions that, in addition to stating the presence or absence of epileptiform activity and correct or incorrect assessment of the background, contain conclusions about the presence of intracranial hypertension and, for example, “severe vasospasm in the middle cerebral artery system of the left hemisphere”;

Some functionalists have avoided problems altogether, because they are allowed to do so by the lack of awareness of clinicians and their own, perhaps, laziness. We are talking about automatic conclusion, which the EEG system should do itself (!?). One such system was rejected by the Crimean republican functional diagnostician - the electroencephalograph "Neuron-Spectrum" manufactured in Ivanovo, the other works well and finds epileptic activity in healthy people in 80% of cases - "Encephalan", Taganrog).

Myths of clinicians

if an epileptic does not have epileptiform activity, it means that the device is bad or the diagnostician is a bad functional person, or we are talking about simulation or, at worst, aggravation of the disease (the latter is more typical for medical experts);

if there is epileptiform activity, then there must be epilepsy;

computer visualization of the epileptic focus can indicate the extent of neurosurgical intervention.

The result was 300 incorrect diagnoses.

This depressing picture forced us to create instructions for functional diagnosticians and instructions for neurologists, which are almost, but not quite, identical. For functional diagnosticians, it is simply presented with a framework of terminology, age norms and illustrations, and for clinicians it is supplemented with a brief description of epileptic syndromes, recommendations on the specifics of preparing and conducting EEG in patients with various epileptic syndromes, reporting data on the epidemiology of various epileptiform phenomena, their evolution (under the influence of drugs , or natural).

Where the clinician and the functional diagnostician began to speak the same language, good results were not long in coming - they were noted within about a month.

Here is an approximate generalized version of the instructions for both:

The use of EEG in epileptology has various purposes:

identification of epileptic activity - in order to confirm the epileptic nature of seizure disorders;

identification of features of detected epileptic activity - such as locality, morphological features, temporal connection with external events, evolution over time, both spontaneous and under the influence of treatment;

determination of the characteristics of the electrical activity background against which epileptic activity was recorded;

monitoring the effectiveness of treatment.

The main task of EEG in clinical epileptology– detection of epileptic activity and description of its features – morphology, topography, dynamics of development, connection with any events. There is no doubt that the most reliable and informative EEG is during the attack itself.

Epileptic activity– the term is used when the patient’s condition and the EEG picture do not raise doubts about the presence of epilepsy (for example, recorded during the attack itself or status epilepticus).

Epileptic seizure pattern- a phenomenon consisting of repeating discharges that begin and end relatively suddenly, have a characteristic dynamics of development, lasting at least several seconds.

This is the activity that usually coincides with an epileptic seizure. If the patterns of an epileptic seizure at the time of their recording are not accompanied by clinical symptoms of epilepsy, they are called subclinical.

However, it is clear that such a rare and, most importantly, short event as an attack almost excludes the possibility of its registration. In addition, interference-free EEG recording during seizures is almost impossible.

Therefore, in practice, EEG recording of only the interictal period is almost always used, and hence the logically correct, although somewhat “diplomatic” term:

Epileptiform activity - certain types of oscillations in the EEG, characteristic of those suffering from epilepsy and observed in the interictal period.

In the interictal period in the waking EEG it is detected in 35-50% of patients with known epilepsy. The name “epileptiform” is also determined by the fact that such activity can occur not only in patients with epilepsy, but in approximately 3% of healthy adults and 10% of children. In neurological patients and patients with obviously non-epileptic seizures, it is recorded in 20-40% of cases.

It follows that the EEG recorded during an attack has a high diagnostic value, and the EEG of the interictal period, unfortunately, is quite low.

Electroencephalography in the field of clinical epileptology operates with a simple and rather limited set of terms that neurophysiologists must adhere to and are useful for clinicians to know. Terminology (and this is the common language of communication between a clinician and a neurophysiologist) must comply with the standards of the glossary International Federation of Electroencephalography Societies (since 1983).

According to the standards of the glossary of the International Federation of Societies of Electroencephalography, the most common EEG term in our conclusions is “ convulsive readiness » no since 1983

A very long time ago, a certain ethics developed in functional diagnostics: the result should be given not only in the form of a description and conclusion, but also with factual material, and everything that is referenced in the conclusion should be illustrated.

So, epileptiform activity includes:

Spike

Polyspike (multiple spike)

sharp wave

Peak-Slow Wave Complex

Complex “Acute wave-Slow wave”

Complex "Polyspike-Slow Wave"

And it's all!

Discharge called an outbreak of epileptiform activity.

Flash- a group of waves with sudden appearance and disappearance, clearly distinguished from background activity frequency, shape and/or amplitude. It is not a sign of pathology, and is not synonymous with the term " paroxysm"(flare of Alpha waves, flash of slow waves, etc.).

Paroxysmal activity– thus a broader, and therefore less precise, term than “epileptic” or “epileptiform.” Includes EEG phenomena with completely different specificity in relation to epilepsy - both a recording of the seizure itself (epileptic activity), epileptiform activity of the interictal period, and a number of phenomena not related to epilepsy, such as, for example, a “flare”

Paroxysmal is an EEG phenomenon that occurs suddenly, quickly reaches a maximum and ends suddenly, clearly different from background activity.

The term " Epileptic activity " is used in 2 cases:

1. When it is registered during the attack itself.

This activity may or may not contain epileptiform phenomena - Epileptic seizure patterns:

ongoing polyspike, rice. 1;

psychomotor seizure pattern, Fig.2;

Paradox – no epileptiform activity.

Fig.1. Recording during a partial seizure. Child 8 years old, hemophilia, partial seizures. Pattern of a focal epileptic seizure: a continuing polyspike of increasing amplitude.

2. When the schedule of paroxysmal activity is beyond doubt, even if it is recorded outside the attack.

The only example is EEG graphics typical absence seizure , Fig.3

When describing epileptiform activity we took as a basis Hereditary EEG patterns associated with epilepsy.

Rice. 2. Psychomotor seizure pattern

Fig.3. A typical absence seizure pattern.

Certain specific combinations of genetic EEG signs can mark the manifestation of various epileptic syndromes. Of the 5 such most significant patterns (according to H. Doose), the most studied and least disputed are 3:

Generalized spike-wave complexes at rest and during hyperventilation (FSV)

Photoparoxysmal reaction– FPR (GSV caused by rhythmic photostimulation). The peak prevalence of FPR is between 5 and 15 years of age.

Focal benign sharp waves- FOV. Most common in children aged 4 to 10 years.

These EEG patterns do not indicate a mandatory clinical manifestation of epilepsy, but only indicate the presence of a genetic predisposition. Each of them occurs with a certain frequency in phenotypically healthy individuals in the general population.

1. GSW - generalized spike waves.

The hereditary nature of FGP was proven by W. Lennox in twin studies in 1951. Later, the independent nature of inheritance of spontaneous FGP and FGP during photostimulation was proven. The mode of inheritance is polygenic, with age-dependent expressivity.

The incidence of FGPs has 2 age peaks: the first - from 3 to 6 years, the second - from 13 to 15 years. In a population of healthy children from 1 to 16 years of age, the phenomenon occurs most often (2.9%) at the age of 7-8 years.

FGPs are usually associated with primary generalized idiopathic epilepsies that begin in the first decade or early second decade of life.

Typical examples: Calp's pycnolepsy, Herpin-Jantz syndrome, "Grand mal awakening" (Gowers-Hopkins) syndrome.

Fig.4. FGP. Herpin-Jantz syndrome: against a generally normal background of electrical activity - spontaneous bilaterally synchronously primary generalized discharges of polyspike waves without the correct repetition period.

2. PPR - photoparoxysmal reaction. Covers a wide range of manifestations: from acute waves to generalized regular or irregular Spike-Wave complexes. Actually, FPR is defined as the occurrence of irregular Spike-Wave complexes in response to rhythmic photostimulation (Fig. 5).

Fig.5. GSV during photostimulation - FPR in response to rhythmic photostimulation with a frequency of 16 Hz. The only Grandmal at the disco with a working strobe light

Representation in the population of healthy children from 1 to 16 years old is 7.6%. Expressiveness peaks between 5 and 15 years of age.

Clinical manifestations in individuals with FPR are very diverse. More often, FPR is detected in photogenic epilepsy that occurs in adolescence, in children with idiopathic generalized seizures without photogenic provocation, with symptomatic and idiopathic partial epilepsies, with febrile seizures. In general, epilepsy occurs rarely in individuals with FPR - in approximately 3% of cases. In addition to epilepsy, FPR is associated with other paroxysmal conditions: syncope, nightmares, anorexia nervosa, migraine. Increased paroxysmal readiness after alcohol intake manifests itself in the form of significantly increased photosensitivity to flashes and a photomyoclonic response to rhythmic photostimulation. This correlates with hypomagnesemia, arterial pH shifts to alkaline side, varying from 7.45 to 7.55. Photosensitivity does not persist for a long period. EEG recorded in the 6 - 30 hour period after last appointment alcohol, demonstrates a massive photomyoclonic response, the escalation of which can lead to the development of a typical grand mal, which can continue even several minutes after the cessation of photostimulation (Fig. 6).

Fig.6. Manifestation of the “photomyoclonic response.”
EEG 12 hours after the last alcohol consumption.

3. FOV - focal benign sharp waves.

Characteristic of idiopathic benign partial epilepsy (“ Rolandic» - Neurac-Bissart-Gastaut syndrome).

Central temporal commissures may be found in 5% of people in the general population healthy population, most common between the ages of 4 and 10 years. In the presence of this pattern, epilepsy develops in only 8% of children, however, the spectrum of clinical manifestations in FOV carriers can vary from severe mental retardation to mild functional disorders, from febrile seizures and rolandic epilepsy to atypical benign partial epilepsy ( pseudo-Lennox syndrome ), epilepsy with continuous peak waves during slow-wave sleep ( ESES syndrome), Patry's syndrome, Landau-Kleffner syndrome(Fig. 7).

There are also a few rather specific, consistently occurring and important phenomena in various epileptic syndromes:

Hypsarrhythmia pattern – Fig.8 ;

Flash-Suppression pattern – Fig.9 .

The difficulties of using EEG in epileptology are objectively related to:

with the extreme rarity of the possibility of recording the seizure itself;

with artifacts from movements during a seizure;

with a rather low percentage of detection of epileptiform activity in epilepsy;

with a fairly frequent occurrence of the same activity in non-epileptic conditions and even in healthy people.

Fig.7. FOV (focal benign sharp waves). Morphologically – “rolandic” epileptiform activity localized in the occipital leads. Idiopathic benign childhood epilepsy, Gastaut syndrome (early version - Panayotopoulos)

Fig.8. Pattern "Hypsarrhythmia"

Fig.9. Flash-Suppression Pattern

What can improve detection rates for epilepsy?

1.Repeated EEG recordings.

Statistics say that the 2nd and 3rd repeated EEGs can increase the percentage of detection of epileptiform activity from 30-50% to 60-80%, and subsequent registrations no longer improve this indicator. The need for re-registration is also determined by the following specific tasks:

• ascertaining the stability of the focus of epileptic activity (in the first and only registration, focality may be “random”);
• when selecting an effective dose of ACTH for hypsarrhythmia (2 weeks);
• assessing the effectiveness of vitamin B-6 therapy (3-5 days);
• reactions of “rolandic” epi-activity to Ospolot (Sultiam) – 2-3 days;
• to assess dose sufficiency of older (“baseline”) AEDs (after 3–4 months) or risk of treatment-related side effects
• sufficiency of the dose of valproate (or suxilep) for typical absence seizures;
• overdose of barbiturates - Fig. 10;
• aggravation of epileptiform activity, and then seizures during treatment with carbamazepine (myoclonic forms of epilepsy).

2.Duration of EEG recording

Firstly, lengthening the time seems to replace repeated recordings; on the other hand, repeated registrations are carried out under different conditions (time of day, season, patient’s condition - whether he had enough sleep or not, on an empty stomach, etc.). According to German standards, a regular EEG must be recorded for at least 30 minutes; in our practice, we record 5 trials of 1 minute each: background with eyes closed, background with eyes open, 3 minutes of hyperventilation, rhythmic photostimulation of 2 Hz and 10 Hz).

Fig. 10. Barbiturate overdose: slowing of background activity, disorganization of the Alpha rhythm, high-frequency activity of 15-25 Hz in the anterior leads

3.Proper Use and Interpretation the most complete, varied, and even better, targeted set of functional tests used:

opening and closing eyes not only depression of the Alpha rhythm must be taken into account, but also photosensitivity, reaction of polyphase potentials;

photostimulation, (photosensitivity, and not just a reaction of rhythm assimilation);

Matsuoka sample– proposed in 1994;

presenting the patient with an attack;

organization of a specific provocation for reflex epilepsies or non-epileptic paroxysmal conditions. For example, ocular-heart reflex during pale attacks of holding one's breath, causing Chvostek's sign or touching the bridge of the nose when hyperexlexia);

reading epilepsy: Not worth talking about due to the rarity of the syndrome.

4. Sleep deprivation.

To use it, you need to take into account the distribution of seizures by time of day (only during sleep, upon awakening, provoked by sleep deficiency - suspicion of temporal forms, Rolandic, Landau-Kleffner syndrome, Janz syndrome, Grand mal awakening syndrome).

It is possible to take into account not only the daily distribution of seizures, but also their dependence on the phase of the moon or the menstrual cycle. The anticonvulsant effect of progestins and androgens, as well as the convulsogenic effect of estrogens, are well known. The maximum frequency of attacks is observed in the perimenstrual period, when there is a drop in progesterone and an increase in estradiol.

5.EEG recording in a state of natural sleep - for epilepsy only during sleep, ESES syndrome, Landau-Kleffner and in special cases differential diagnosis – Ohtahara syndromes, hypsarrhythmias and so on.

6. Fasting EEG.

Thank you

The site provides background information for informational purposes only. Diagnosis and treatment of diseases must be carried out under the supervision of a specialist. All drugs have contraindications. Consultation with a specialist is required!

The activity of the brain, the state of its anatomical structures, the presence of pathologies are studied and recorded using various methods - electroencephalography, rheoencephalography, computed tomography, etc. A huge role in identifying various abnormalities in the functioning of brain structures belongs to methods of studying its electrical activity, in particular electroencephalography.

Electroencephalogram of the brain - definition and essence of the method

Electroencephalogram (EEG) is a recording of the electrical activity of neurons in various brain structures, which is made on special paper using electrodes. Electrodes are placed on different parts of the head and record the activity of a particular part of the brain. We can say that an electroencephalogram is a recording of the functional activity of the brain of a person of any age.

The functional activity of the human brain depends on the activity of the median structures - reticular formation And forebrain, which determine the rhythm, general structure and the dynamics of the electroencephalogram. A large number of connections of the reticular formation and forebrain with other structures and the cortex determine the symmetry of the EEG, and its relative “sameness” for the entire brain.

An EEG is taken to determine the activity of the brain in case of various lesions of the central nervous system, for example, with neuroinfections (poliomyelitis, etc.), meningitis, encephalitis, etc. Based on the EEG results, it is possible to assess the degree of brain damage due to various causes, and clarify specific location that has been damaged.

The EEG is taken according to a standard protocol, which takes into account recordings in a state of wakefulness or sleep (infants), with special tests. Routine tests for EEG are:
1. Photostimulation (exposure to flashes of bright light on closed eyes).
2. Opening and closing eyes.
3. Hyperventilation (rare and deep breathing for 3 to 5 minutes).

These tests are performed on all adults and children when taking an EEG, regardless of age and pathology. In addition, additional tests may be used when taking an EEG, for example:

• clenching your fingers into a fist;
• sleep deprivation test;
• stay in the dark for 40 minutes;
• monitoring the entire period of night sleep;
• taking medications;
• performing psychological tests.

Additional tests for EEG are determined by a neurologist who wants to evaluate certain functions of a person's brain.

What does an electroencephalogram show?

An electroencephalogram reflects the functional state of brain structures in various human states, for example, sleep, wakefulness, active mental or physical work, etc. The electroencephalogram is absolutely safe method, simple, painless and not requiring serious intervention.

Today, the electroencephalogram is widely used in the practice of neurologists, since this method makes it possible to diagnose epilepsy, vascular, inflammatory and degenerative lesions of the brain. In addition, EEG helps to determine the specific location of tumors, cysts and traumatic damage to brain structures.

An electroencephalogram with irritation of the patient by light or sound makes it possible to distinguish true visual and hearing impairments from hysterical ones, or their simulation. EEG is used in intensive care units for dynamic monitoring of the condition of patients in a coma. The disappearance of signs of electrical activity of the brain on the EEG is a sign of human death.

Where and how to do it?

An electroencephalogram for an adult can be taken in neurological clinics, in departments of city and regional hospitals, or at a psychiatric clinic. As a rule, electroencephalograms are not taken in clinics, but there are exceptions to the rule. It is better to go to a psychiatric hospital or neurology department, where specialists with the necessary qualifications work.

Electroencephalograms for children under 14 years of age are taken only in specialized children's hospitals where pediatricians work. That is, you need to go to the children's hospital, find the neurology department and ask when the EEG is taken. Psychiatric clinics, as a rule, do not take EEGs for young children.

In addition, private medical centers specializing in diagnostics and treatment of neurological pathology, also provide EEG services for both children and adults. You can contact a multidisciplinary private clinic, where there are neurologists who will take an EEG and decipher the recording.

An electroencephalogram should be taken only after a full night's rest, in the absence of stressful situations and psychomotor agitation. Two days before the EEG is taken, it is necessary to exclude alcoholic drinks, sleeping pills, sedatives and anticonvulsants, tranquilizers and caffeine.

Electroencephalogram for children: how the procedure is performed

Taking an electroencephalogram in children often raises questions from parents who want to know what awaits the baby and how the procedure goes. The child is left in a dark, sound- and light-proof room, where he is placed on a couch. Children under 1 year of age are kept in their mother's arms during EEG recording. The whole procedure takes about 20 minutes.

To record an EEG, a cap is placed on the baby's head, under which the doctor places electrodes. The skin under the electrodes is wetted with water or gel. Two inactive electrodes are placed on the ears. Then, using alligator clips, the electrodes are connected to the wires connected to the device - the encephalograph. Since electrical currents are very small, an amplifier is always needed, otherwise brain activity will simply not be recorded. It is the small current strength that is the key to the absolute safety and harmlessness of EEG, even for infants.

To begin the examination, the child's head should be placed flat. Anterior tilt should not be allowed as this may cause artifacts that will be misinterpreted. EEGs are taken for infants during sleep, which occurs after feeding. Wash your child's hair before taking the EEG. Do not feed the baby before leaving the house; this is done immediately before the test so that the baby eats and falls asleep - after all, it is at this time that the EEG is taken. To do this, prepare formula or express breast milk into a bottle that you use in the hospital. Up to 3 years of age, EEG is taken only in a state of sleep. Children over 3 years old can stay awake, but to keep your baby calm, take a toy, book, or anything else that will distract the child. The child should be calm during the EEG.

Typically, the EEG is recorded as a background curve, and tests with opening and closing the eyes, hyperventilation (slow and deep breathing), and photostimulation are also performed. These tests are part of the EEG protocol, and are performed on absolutely everyone - both adults and children. Sometimes they ask you to clench your fingers into a fist, listen to various sounds, etc. Opening the eyes allows us to assess the activity of inhibition processes, and closing them allows us to assess the activity of excitation. Hyperventilation can be carried out in children after 3 years of age in the form of a game - for example, asking the child to inflate a balloon. Such rare and deep inhalations and exhalations last for 2–3 minutes. This test allows you to diagnose latent epilepsy, inflammation of the structures and membranes of the brain, tumors, dysfunction, fatigue and stress. Photostimulation is carried out with the eyes closed and the light blinking. The test allows you to assess the degree of mental, physical, speech and mental development child, as well as the presence of foci of epileptic activity.

Electroencephalogram rhythms

The electroencephalogram must show a regular rhythm of a certain type. The regularity of rhythms is ensured by the work of the part of the brain - the thalamus, which generates them and ensures the synchronization of the activity and functional activity of all structures of the central nervous system.

The human EEG contains alpha, beta, delta and theta rhythms, which have different characteristics and reflect certain types of brain activity.

Alpha rhythm has a frequency of 8 – 14 Hz, reflects a state of rest and is recorded in a person who is awake, but with his eyes closed. This rhythm is normally regular, the maximum intensity is recorded in the region of the back of the head and the crown. The alpha rhythm ceases to be detected when any motor stimuli appear.

Beta rhythm has a frequency of 13 – 30 Hz, but reflects the state of anxiety, restlessness, depression and the use of sedative medications. The beta rhythm is recorded with maximum intensity over the frontal lobes of the brain.

Theta rhythm has a frequency of 4–7 Hz and an amplitude of 25–35 μV, reflecting the state of natural sleep. This rhythm is a normal component of the adult EEG. And in children this type of rhythm on the EEG predominates.

Delta rhythm has a frequency of 0.5 - 3 Hz, it reflects the state of natural sleep. It can also be recorded in a limited amount during wakefulness, a maximum of 15% of all EEG rhythms. The amplitude of the delta rhythm is normally low - up to 40 μV. If there is an excess of amplitude above 40 μV, and this rhythm is recorded for more than 15% of the time, then it is classified as pathological. Such a pathological delta rhythm indicates a dysfunction of the brain, and it appears precisely over the area where pathological changes develop. The appearance of a delta rhythm in all parts of the brain indicates the development of damage to the structures of the central nervous system, which is caused by liver dysfunction, and is proportional to the severity of the disturbance of consciousness.

Electroencephalogram results

The result of the electroencephalogram is a recording on paper or in computer memory. The curves are recorded on paper and analyzed by the doctor. The rhythm of EEG waves, frequency and amplitude are assessed, characteristic elements are identified, and their distribution in space and time is recorded. Then all data is summarized and reflected in the conclusion and description of the EEG, which is pasted into medical card. The EEG conclusion is based on the type of curves, taking into account the clinical symptoms present in a person.

Such a conclusion must reflect the main characteristics of the EEG, and includes three mandatory parts:
1. Description of the activity and typical affiliation of EEG waves (for example: “The alpha rhythm is recorded over both hemispheres. The average amplitude is 57 μV on the left and 59 μV on the right. The dominant frequency is 8.7 Hz. The alpha rhythm dominates in the occipital leads.”).
2. Conclusion according to the description of the EEG and its interpretation (for example: “Signs of irritation of the cortex and midline structures of the brain. Asymmetry between the hemispheres of the brain and paroxysmal activity were not detected”).
3. Determination of Compliance clinical symptoms with EEG results (for example: “Objective changes in the functional activity of the brain were recorded, corresponding to manifestations of epilepsy”).

Decoding the electroencephalogram

Decoding an electroencephalogram is the process of interpreting it taking into account the clinical symptoms present in the patient. In the process of decoding, it is necessary to take into account the basal rhythm, the level of symmetry in the electrical activity of brain neurons of the left and right hemispheres, the activity of the commissure, EEG changes against the background of functional tests (opening - closing the eyes, hyperventilation, photostimulation). The final diagnosis is made only taking into account the presence of certain clinical signs that concern the patient.

Decoding the electroencephalogram involves interpreting the conclusion. Let's consider the basic concepts that the doctor reflects in the conclusion and their clinical significance (that is, what these or those parameters can indicate).

Alpha - rhythm

Normally, its frequency is 8–13 Hz, the amplitude ranges up to 100 μV. It is this rhythm that should prevail over both hemispheres in healthy adults. Alpha rhythm pathologies are the following:

• constant registration of the alpha rhythm in the frontal parts of the brain;
• interhemispheric asymmetry above 30%;
• violation of sinusoidal waves;
• paroxysmal or arc-shaped rhythm;
• unstable frequency;
• amplitude less than 20 μV or more than 90 μV;
• rhythm index less than 50%.

What do common alpha rhythm disturbances indicate?
Severe interhemispheric asymmetry may indicate the presence of a brain tumor, cyst, stroke, heart attack or scar at the site of an old hemorrhage.

High frequency and instability of the alpha rhythm indicate traumatic brain damage, for example, after a concussion or traumatic brain injury.

Disorganization of the alpha rhythm or its complete absence speaks of acquired dementia.

About delayed psycho-motor development in children they say:

• alpha rhythm disorganization;
• increased synchrony and amplitude;
• moving the focus of activity from the back of the head and crown;
• weak short activation reaction;
• excessive response to hyperventilation.

A decrease in the amplitude of the alpha rhythm, a shift in the focus of activity from the back of the head and crown, and a weak activation reaction indicate the presence of psychopathology.

Excitable psychopathy is manifested by a slowdown in the frequency of the alpha rhythm against the background of normal synchrony.

Inhibitory psychopathy is manifested by EEG desynchronization, low frequency and alpha rhythm index.

Increased synchronization of the alpha rhythm in all parts of the brain, a short activation reaction - the first type of neuroses.

Weak expression of the alpha rhythm, weak activation reactions, paroxysmal activity - the third type of neuroses.

Beta rhythm

Normally, it is most pronounced in the frontal lobes of the brain and has a symmetrical amplitude (3–5 μV) in both hemispheres. Pathology of the beta rhythm is the following signs:

• paroxysmal discharges;
• low frequency, distributed over the convexital surface of the brain;
• asymmetry between hemispheres in amplitude (above 50%);
• sinusoidal type of beta rhythm;
• amplitude more than 7 μV.

What do beta rhythm disturbances on the EEG indicate?
The presence of diffuse beta waves with an amplitude no higher than 50-60 μV indicates a concussion.

Short spindles in the beta rhythm indicate encephalitis. The more severe the inflammation of the brain, the greater the frequency, duration and amplitude of such spindles. Observed in a third of patients with herpes encephalitis.

Beta waves with a frequency of 16 - 18 Hz and high amplitude (30 - 40 μV) in the anterior and central departments brain - signs of delayed psychomotor development of a child.

EEG desynchronization, in which the beta rhythm predominates in all parts of the brain, is the second type of neurosis.

Theta rhythm and delta rhythm

Normally, these slow waves can only be recorded on the electroencephalogram of a sleeping person. In a state of wakefulness, such slow waves appear on the EEG only in the presence of degenerative processes in the tissues of the brain, which are combined with compression, high blood pressure and lethargy. Paroxysmal theta and delta waves in a person in a state of wakefulness are detected when the deep parts of the brain are damaged.

In children and young people under 21 years of age, the electroencephalogram may reveal diffuse theta and delta rhythms, paroxysmal discharges and epileptoid activity, which are normal variants and do not indicate pathological changes in brain structures.

What do disturbances of theta and delta rhythms on the EEG indicate?
Delta waves with high amplitude indicate the presence of a tumor.

Synchronous theta rhythm, delta waves in all parts of the brain, bursts of bilateral synchronous theta waves with high amplitude, paroxysms in the central parts of the brain - indicate acquired dementia.

The predominance of theta and delta waves on the EEG with maximum activity in the occipital region, flashes of bilateral synchronous waves, the number of which increases with hyperventilation, indicates a delay in the psychomotor development of the child.

A high index of theta activity in the central parts of the brain, bilateral synchronous theta activity with a frequency of 5 to 7 Hz, localized in the frontal or temporal regions of the brain indicate psychopathy.

Theta rhythms in the anterior parts of the brain as the main ones are an excitable type of psychopathy.

Paroxysms of theta and delta waves are the third type of neuroses.

The appearance of high-frequency rhythms (for example, beta-1, beta-2 and gamma) indicates irritation (irritation) of brain structures. This may be due to various cerebrovascular accidents, intracranial pressure, migraines, etc.

Bioelectric activity of the brain (BEA)

This parameter in the EEG conclusion is a complex descriptive characteristic regarding brain rhythms. Normally, the bioelectric activity of the brain should be rhythmic, synchronous, without foci of paroxysms, etc. At the conclusion of the EEG, the doctor usually writes what specific disturbances in the bioelectrical activity of the brain were identified (for example, desynchronized, etc.).

What do various disturbances in the bioelectrical activity of the brain indicate?
Relatively rhythmic bioelectrical activity with foci of paroxysmal activity in any area of ​​the brain indicates the presence of some area in its tissue where excitation processes exceed inhibition. This type An EEG may indicate the presence of migraines and headaches.

Diffuse changes in the bioelectrical activity of the brain may be normal if no other abnormalities are detected. Thus, if in the conclusion it is written only about diffuse or moderate changes in the bioelectrical activity of the brain, without paroxysms, foci of pathological activity, or without a decrease in the threshold of convulsive activity, then this is a variant of the norm. In this case, the neurologist will prescribe symptomatic treatment and put the patient under observation. However, in combination with paroxysms or foci of pathological activity, they speak of the presence of epilepsy or a tendency to seizures. Reduced bioelectrical activity of the brain can be detected in depression.

Other indicators

Dysfunction of midbrain structures – this is a mildly expressed disturbance in the activity of brain neurons, which is often found in healthy people, and indicates functional changes after stress, etc. This condition requires only a symptomatic course of therapy.

Interhemispheric asymmetry May be functional impairment, that is, not evidence of pathology. In this case, it is necessary to undergo examination by a neurologist and a course of symptomatic therapy.

Diffuse disorganization of the alpha rhythm, activation of diencephalic-stem structures of the brain against the background of tests (hyperventilation, closing-opening of eyes, photostimulation) is the norm, if the patient has no complaints.

Center of pathological activity indicates increased excitability of this area, which indicates a tendency to seizures or the presence of epilepsy.

Irritation of various brain structures (cortex, middle sections, etc.) is most often associated with impaired cerebral circulation due to various reasons (for example, atherosclerosis, trauma, increased intracranial pressure, etc.).

Paroxysms They talk about increased excitation and decreased inhibition, which is often accompanied by migraines and simple headaches. In addition, there may be a tendency to develop epilepsy or the presence of this pathology if a person has had seizures in the past.

Reducing the threshold for seizure activity indicates a predisposition to seizures.

The following signs indicate the presence of increased excitability and a tendency to convulsions:

• changes in electrical potentials of the brain according to the residual-irritative type;
• enhanced synchronization;
• pathological activity of the midline structures of the brain;
• paroxysmal activity.

In general, residual changes in brain structures are the consequences of damage of various types, for example, after injury, hypoxia, viral or bacterial infection. Residual changes are present in all brain tissues and are therefore diffuse. Such changes disrupt the normal passage of nerve impulses.

Irritation of the cerebral cortex along the convexial surface of the brain, increased activity of the median structures at rest and during tests can be observed after traumatic brain injuries, with a predominance of excitation over inhibition, as well as with organic pathology of brain tissue (for example, tumors, cysts, scars, etc.).

Epileptiform activity indicates the development of epilepsy and an increased tendency to seizures.

Increased tone of synchronizing structures and moderate dysrhythmia are not pronounced disorders or pathologies of the brain. In this case, resort to symptomatic treatment.

Signs of neurophysiological immaturity may indicate a delay in the child’s psychomotor development.

Pronounced changes in residual organic type with increasing disorganization during tests, paroxysms in all parts of the brain - these signs usually accompany severe headaches, increased intracranial pressure, attention deficit hyperactivity disorder in children.

Disturbance of brain wave activity (appearance of beta activity in all parts of the brain, dysfunction of midline structures, theta waves) occurs after traumatic injuries, and can manifest itself as dizziness, loss of consciousness, etc.

Organic changes in brain structures in children are a consequence of infectious diseases such as cytomegalovirus or toxoplasmosis, or hypoxic disorders that occur during childbirth. A comprehensive examination and treatment is necessary.

Regulatory cerebral changes are registered in hypertension.

The presence of active discharges in any part of the brain , which intensify with exercise, means that in response to physical stress a reaction may develop in the form of loss of consciousness, visual impairment, hearing loss, etc. The specific reaction to physical activity depends on the location of the source of active discharges. In this case, physical activity should be limited to reasonable limits.

In case of brain tumors, the following are detected:

• the appearance of slow waves (theta and delta);
• bilateral synchronous disorders;
• epileptoid activity.

Changes progress as the volume of education increases.

Desynchronization of rhythms, flattening of the EEG curve develops in cerebrovascular pathologies. A stroke is accompanied by the development of theta and delta rhythms. The degree of electroencephalogram abnormalities correlates with the severity of the pathology and the stage of its development.

Theta and delta waves in all parts of the brain; in some areas, beta rhythms are formed during injury (for example, with a concussion, loss of consciousness, bruise, hematoma). The appearance of epileptoid activity against the background of brain injury can lead to the development of epilepsy in the future.

Significant slowing of alpha rhythm may accompany parkinsonism. Fixation of theta and delta waves in the frontal and anterior temporal parts of the brain, which have different rhythms, low frequencies and high amplitudes, is possible in Alzheimer's disease

EEG patterns in clinical epileptology

The most studied patterns:

• focal benign sharp waves (FOW);
• photoparoxysmal reaction (PPR);
• generalized spike waves (during hyperventilation and at rest).

FOV is more often registered in childhood, between 4 and 10 years, and FPR in children under 15-16 years of age.

With FOV, the following negative deviations are observed:

• mental retardation;
• febrile seizures;
• development of Rolandic epilepsy;
• mental disorders;
• various functional disorders.

Develops in approximately 9%.

In the presence of FPR, the following are revealed:

• photogenic epilepsy;
• symptomatic partial epilepsy;
• idiopathic partial epilepsy;
• febrile seizures.

In the absence of attacks, even against the background of pathological waves on the EEG, treatment should not be prescribed, since pathological changes can be recorded without symptoms of diseases of the nervous system (observed in approximately 1% of healthy people).

In the presence of Landau-Kleffner syndrome, ESES, and various non-convulsive epileptic encephalopathies, antiepileptic drugs are prescribed, since these diseases cause memory and speech impairment, mental disorders, and, in children, growth retardation and learning difficulties.

The article presents a group of patients with focal epilepsy associated with DEPD in children with perinatal organic brain damage, which, according to its clinical, electro-neuroimaging characteristics, occupies a special “intermediate” position between idiopathic and symptomatic epilepsy. We observed 35 patients aged from 2 to 20 years. Based on the results obtained, diagnostic criteria for the syndrome are proposed. The disease is characterized by: a predominance of male patients; debut epileptic seizures under the age of 11 years with a maximum in the first 6 years (82.9%) with two peaks: in the first 2 years of life and at the age of 4 to 6 years; often debuts with infantile spasms; predominance of focal hemiclonic seizures, focal occipital seizures and SHSP. A combination of focal and pseudogeneralized seizures is possible (epileptic spasms, negative myoclonus, atypical absence seizures). Characterized by a relatively low frequency of focal and secondary generalized attacks confined to sleep (occurring upon awakening and falling asleep). Neurological deficits are present in most patients, including motor and cognitive impairment; Cerebral palsy is common. It is typical to detect a DEPD pattern on the EEG. In all cases, signs of perinatal brain damage, predominantly of hypoxic-ischemic origin, are stated. Remission of attacks is achieved in all cases; later epileptiform activity on the EEG is blocked. Neurological (motor and cognitive) impairments generally remain unchanged.

According to modern concepts, focal epileptic seizures arise as a result of local discharges in neuronal networks limited to one hemisphere, with greater or lesser spread (Engel J. Jr., 2001, 2006). Focal (localization-related) epilepsies are traditionally divided into symptomatic, cryptogenic (synonym - probably symptomatic) and idiopathic forms. By symptomatic we mean forms of epilepsy with a known etiological factor and verified structural changes in the brain that are the cause of epilepsy. As the name implies, symptomatic epilepsy is a manifestation of another disease of the nervous system: tumors, brain dysgenesis, metabolic encephalopathy, a consequence of hypoxic-ischemic, hemorrhagic brain damage, etc. These forms of epilepsy are characterized by neurological disorders, decreased intelligence, and resistance to antiepileptic therapy (AED). Probably symptomatic (synonym cryptogenic, from Greek criptos - hidden) forms of epilepsy are called syndromes with unspecified, unclear etiology. It is understood that cryptogenic forms are symptomatic, however, at the present stage, when using neuroimaging methods, it is not possible to identify structural disorders in the brain [ 26]. In idiopathic focal forms, there are no diseases that can cause epilepsy. Idiopathic epilepsies are based on a hereditary predisposition to disorders of brain maturation or genetically determined membrane and channelopathies. In idiopathic focal forms of epilepsy (IFE), neurological deficits and intellectual impairment are not detected in patients, and neuroimaging shows no signs of structural brain damage. Perhaps the most important feature of IFE- absolutely favorable prognosis of the disease with spontaneous cessation of attacks when patients reach puberty. Idiopathic focal epilepsies are classified as “benign epilepsies.” Many authors do not accept the term “benign” to characterize a disease such as epilepsy. However, it is generally accepted that benign epilepsy includes forms that satisfy two main criteria: mandatory relief of seizures (medical or spontaneous) and the absence of intellectual and mnestic disorders in patients, even with a long course of the disease.

For idiopathic focal forms of epilepsy, a characteristic feature is the appearance on the EEG of “ benign epileptiform patterns of childhood» - DEPD, specific graph elements consisting of a five-point electric dipole.

The characteristic features of DEPD on EEG are (Mukhin K.Yu., 2007):

• The presence of a five-point electric dipole consisting of an acute and a slow wave.
• The maximum “positivity” of the dipole is in the frontal leads, and the maximum “negativity” is in the central temporal leads, which is most typical for Rolandic epilepsy.
• The morphology of the complexes resembles QRS waves on an ECG.
• Regional, multiregional, lateralized or diffuse nature of activity.
• Instability of epileptiform activity with possible movement (shift) during subsequent EEG recordings.
• Activation during I - II stages of slow-wave sleep.
• Lack of clear correlation with the presence of epilepsy and the clinical picture of epilepsy.

DEPDs are easily recognizable on EEG due to their unique morphological characteristic: a high-amplitude five-point electric dipole. At the same time, we emphasize the importance of the morphological characteristics of this EEG pattern, and not the localization. Previously, we presented the classification of “DEPD-associated conditions”. It has been shown that DEPD are nonspecific epileptiform disorders that occur in childhood, which can be observed in epilepsy, diseases not associated with epilepsy, and in neurologically healthy children.

In recent years in clinical practice We observed a special group of pediatric patients with focal epilepsy, which, according to its clinical and electroneuroimaging characteristics, occupies a special “intermediate” position between idiopathic and symptomatic. We are talking about focal epilepsy associated with DEPD in children with perinatal organic brain damage. This group of patients has clearly defined clinical, electroencephalographic and neuroimaging criteria, response to AED therapy and prognosis.

The purpose of this study: to study the clinical, electroencephalographic, neuroimaging characteristics, features of the course and prognosis of focal epilepsy associated with DEPD in children with perinatal brain damage; establishing diagnostic criteria for the disease and determining optimal methods of therapeutic correction.

PATIENTS AND METHODS

We observed 35 patients, of which 23 were male and 12 were female. The age of the patients at the time of publication ranged from 2 to 20 years (mean, 10.7 years). The vast majority of patients ( 94.3% of cases ) was a child's age: from 2 to 18 years. The observation period ranged from 1 year to 8 months. up to 14 years 3 months (on average, 7 years 1 month).

Criteria for inclusion in the group:

— presence of focal epilepsy in patients;

— anamnestic, clinical and neuroimaging signs of brain damage of perinatal origin;

— registration of regional/multiregional epileptiform activity, morphologically corresponding to “benign epileptiform patterns of childhood” on the EEG.

Criteria for exclusion from the group:

— progression of neurological symptoms;

— verified hereditary diseases;

— structural disorders in neuroimaging acquired in the postnatal period (consequences of traumatic brain injuries, neuroinfections, etc.).

All patients were examined clinically by a neurologist, neuropsychologist; A routine EEG study was carried out, as well as continued video-EEG monitoring with the inclusion of sleep (electroencephalograph-analyzer device EEGA-21/26 “ENCEPHALAN-131-03”, modification 11, Medicom MTD; video-EEG monitoring “Neuroscope 6.1.508”, Biola). All patients underwent an MRI examination (magnetic resonance system Sigma Infinity GE with a magnetic field voltage of 1.5 Tesla). To monitor antiepileptic therapy over time, the content of AEDs in the blood was studied using gas-liquid chromatography; General and biochemical blood tests were performed (Invitro laboratory).

RESULTS

Among the patients we examined there was a significant predominance in the group of male patients (65.7% of cases); the male to female ratio was 1.92:1.

Onset of seizures . The onset of seizures in our group was observed over a wide age range. The earliest occurrence of seizures was observed in the patient on the 3rd day of life, the latest age of onset of epilepsy - 11 years. After 11 years, the attacks did not debut.

Most often, epileptic seizures occurred in patients in the first year of life - in 28.6% of cases. At older ages, the onset of epileptic seizures was noted: at the 2nd and 4th years of life - 11.4% of cases, at the 1st and 5th years - 8.6% of cases, at the ages of 6, 7, At 8 and 9 years old, respectively, the probability of seizures was 5.7%. The onset of attacks was observed least often at the ages of 3, 10 and 11 years - 2.9% each, respectively (1 patient each) (Fig. 1).

Analyzing the age intervals of onset in our group of patients, we can note a significant predominance of the frequency of attacks during the first 6 years of life - 82.9% of cases with two peaks. Most often, attacks began during the first two years of life. In this interval, debut was noted in 37.1% of cases. The second peak is observed in the range from 4 to 6 years - in 20%.

As patients grow older, there is a gradual decrease in the likelihood of a first attack from 48.6% in the first 3 years of life to 11.4% in the age range from 9 to 11 years.

Seizures at the onset of epilepsy . At the onset of epilepsy in our group of patients, focal seizures predominated - 71.4%. Focal motor seizures were noted in 51.4% of cases, secondary generalized convulsive seizures - 14.3%. Other types of focal seizures were observed much less frequently: focal hypomotor in 1 case and negative myoclonus - also in 1 case.

Epileptic spasms at the onset of epilepsy were observed in 17.1% of patients; Serial tonic asymmetrical seizures predominated, often in combination with short focal versive seizures. In 1 case, myoclonic spasms were detected. In all cases, the onset of epileptic spasms was observed in children in the first year of life.

In 14.3% of cases, epilepsy debuted with the appearance of febrile seizures: in 3 cases - typical, and in 2 - atypical. Generalized convulsive seizures were observed in only 8.6% of patients at the onset of the disease; myoclonic - in 1 case.

Epileptic seizures in the advanced stage of the disease. Analyzing the occurrence of epileptic seizures in our group, we can note a significant predominance of focal and secondary generalized seizures in the clinical picture. Among the focal seizures, the most frequently recorded focal clonic seizures, characteristic in kinematics for Rolandic epilepsy: hemifacial, faciobrachial, hemiclonic - 34.3% of cases. In 28.6% of cases, focal seizures were identified, which, based on clinical features and electroencephalographic characteristics, can be classified as focal occipital. In this group, attacks of simple visual hallucinations predominated, with vegetative phenomena (headache, nausea, vomiting), versive and paroxysms of limpness, often followed by a transition to a secondary generalized convulsive attack. Focal versive tonic seizures were observed in 11.4% of patients. Secondary generalized seizures occurred in 40% of cases, including focal onset in most cases. Pseudogeneralized seizures were observed in 31.4% of patients, of which epileptic spasms were more common - 20.0%; in isolated cases, atypical absences and atonic seizures occurred. Focal automotor seizures were detected only in 2 cases.

In 45.7% of cases, only one type of seizure was detected in patients, and also in 45.7% - a combination of two types. In patients who experienced type 1 seizures throughout the entire period of the disease, focal motor seizures predominated (in 17.1% of cases), secondary generalized seizures (14.3% of cases) and focal paroxysms emanating from the motor cortex (8.6% of cases). %). In the group of patients with two types of seizures, attention was drawn to the frequent association of focal motor (25.7% of cases), secondary generalized (20% of patients) and focal seizures emanating from the occipital regions (17.1% of patients) with other types of seizures . A combination of 3 and 4 types of attacks was observed in isolated cases (in 1 and 2 cases, respectively). The most common combination of focal motor seizures and epileptic spasms was detected - in 11.4% of cases, focal motor and secondary generalized seizures - 8.6%, secondary generalized and focal, emanating from the occipital cortex - in 8.6%.

Based on the frequency of occurrence, we divided epileptic seizures into single ones (1 -3 for the entire period of the disease), rare (1-3 times a year), frequent (several attacks per week) and daily. In 57.6% of cases, attacks were rare (27.3%) or single (30.3%). Attacks occurring several times a month were observed in 15.2% of patients. Daily seizures were detected in 27.3% of patients and were represented mainly by pseudogeneralized paroxysms: epileptic spasms, atypical absence seizures, negative myoclonus.

The duration of epileptic seizures varied among patients. In 56.6% of cases, the attacks ended spontaneously within 1 -3 minutes, while short attacks (up to 1 minute) were observed in 33.3% of cases (mostly pseudogeneralized). The high percentage of prolonged attacks is noteworthy. So attacks lasting 5-9 minutes, noted in 13.3% of patients. In 36.7% of cases, the duration of the attacks exceeded 10 minutes, and in some patients the paroxysms were of the nature of status epilepticus.

The study showed a high chronological dependence of epileptic seizures on the sleep rhythm —wakefulness,” which was observed in 88.6% of patients in our group. Most often, attacks were observed during the period of awakening or falling asleep - in 42.9%. Seizures occurred during sleep in 25.7% of cases; in wakefulness and sleep - 17.1%. In only 11.4% of patients, epileptic seizures did not have a clear connection with sleep.

Neurological status. In 100% of cases, focal neurological symptoms were detected. Pyramidal disorders were observed in 82.9% of cases, of which 40% of patients had paresis or paralysis. From others neurological symptoms ataxia was the most common - in 20% of cases, muscular dystonia - 11.4%, tremors in the limbs - 8.6%. A decrease in intelligence of varying degrees of severity was detected in 57.1% of cases. Cerebral palsy syndrome was found in 40% of patients. Of these: the hemiparetic form was observed in 57.2% of cases of all forms of cerebral palsy, spastic diplegia - in 21.4% of cases, double hemiplegia - in 21.4% of cases.

EEG study results. The main activity was close to or corresponded to the age norm in 57.2% of cases. However, in most cases, even against the background of a preserved alpha rhythm, a diffuse or biocipital theta slowdown of the background rhythm was determined. Delta deceleration with an emphasis in the posterior regions was detected in 14.3% of cases, mainly in children with epileptic spasms and the onset of seizures in the first year of life. In this case, delta waves were combined with multiregional epileptiform activity in the occipital regions. In more than 50% of cases, the EEG during wakefulness and sleep showed an increased index of exalted beta activity (excessive fast). In general, for patients in our group, the characteristic EEG pattern in the waking state was theta slowdown of the main activity in combination with an acceleration of cortical rhythms.

A mandatory criterion for inclusion in the group was the identification of benign epileptiform patterns of childhood (BECP) on EEG. DEPD were presented in the form of regional/multiregional epileptiform activity in 100% of cases, as well as in the form of lateralized, and much less often, bilateral and diffuse discharges.

In 75% of cases, regional epileptiform activity was noted in the central-temporo-frontal regions (p is. 2), in 30% of cases, DEPD were recorded in the occipital leads (Fig. 3). It should be noted that in our group a focus was often detected in the vertex areas. In 57.1% of cases, regional/multiregional epileptiform activity was limited to one hemisphere; in 42.9%, independent foci of epileptiform activity were noted in two hemispheres (Fig. 4). In 57.1% of patients, a bilateral distribution of epileptiform activity was noted, which included: cases of continued discharges in symmetrical areas in the two hemispheres with the formation of a picture of bilateral asynchronous complexes ( rice. 3), bilateral spread of discharges from one focus to homologous parts of the contralateral hemisphere, bilateral acute-slow wave complexes, diffuse discharges of acute-slow wave complexes.

The study showed a high chronological association of DEPD with sleep. In 100% of cases, DEPD was recorded during sleep, in 77.1%, epileptiform activity was detected both during sleep and wakefulness. It is important to note that in no case was the appearance of epileptiform activity of the DEPD isolated in a state of wakefulness noted.

Analysis of the results of video-EEG monitoring made it possible to identify the characteristic features of epileptiform activity in the examined group. Benign epileptiform patterns of childhood were characterized by a tendency to form groups in the form of doublets, triplets and longer groups (pseudo-rhythmic discharges). The DEPD index increased in the state of passive wakefulness and was maximum during the transition to the state of drowsiness and in sleep. In a state of active wakefulness, the DEPD index was significantly blocked. In sleep, the representation of DEPD is maximum in the stages of slow-wave sleep, during In REM sleep, a significant reduction in this EEG pattern was observed. It was in our patients’ sleep that we recorded continuous peak-wave epileptiform activity in slow-wave sleep (PEMS) and electrical status epilepticus in slow-wave sleep - PEMS with an index of more than 85% of the sleep recording.

The study showed that there was no significant relationship between the DEPD index and the frequency of focal motor seizures. DEPD were not an EEG pattern of focal seizures. However, in the case of lateralized or diffuse discharges, the likelihood of epileptic negative myoclonus or atypical absence seizures was high.

The dynamics of epileptiform activity in patients during treatment is of interest. Having appeared on the sleep EEG once, DEPD continued to be recorded continuously in all subsequent EEG recordings for many months or years. In all cases, relief of epileptic seizures was first noted, and only then — disappearance of DEPD. During AED therapy, a decrease in the index and amplitude of epileptiform complexes was gradually observed over time. In cases of PEMS, epileptiform activity and especially the electrical status gradually “faded” and “released” more and more epochs of EEG recording for a normal rhythm. PEMS became less regular and rhythmic, and increasingly large gaps appeared, free from epileptiform activity. At the same time, regional patterns somewhat intensified, both in sleep and wakefulness, replacing diffuse activity. At first, epileptiform activity completely disappeared when recording while awake, and then during sleep. By the onset of puberty, epileptiform activity was not recorded in any of the cases.

Neuroimaging data When conducting neuroimaging, various structural disorders in the brain were identified in 100% of cases. The most frequently detected signs of hypoxic-ischemic perinatal encephalopathy (62.8% of cases): diffuse atrophic/subatrophic changes of varying severity - 31.4%, periventricular leukomalacia - 31.4% (Fig. 5). Arachnoid cysts (Fig. 6) were detected in 13 (37.1%) patients, of which cysts were found in 7 cases temporal lobe(53.9% among patients with cysts), in 4 patients - the parietal lobe (30.8%), in 2 patients - the frontal lobe (15.4%), in 2 - the occipital region (15.4%). Changes in the cerebellum (hypoplasia of the cerebellar vermis, cerebellar atrophy) were detected in 11.4% of cases. Cortical tubers were observed in 1 patient; in 2 cases signs of polymicrogyria were detected.

Clinical-electro-neuroimaging correlations. Separately, we analyzed the correlations of clinical, electroencephalographic and neuroimaging data in the examined patients. The degree of correlation was based on a comparison of survey data indicating a common focus. The relationship between 4 main parameters was assessed: neurological status (side of the lesion), seizure semiology (localization of the lesion), EEG data and neuroimaging results:

• 1st degree of correlation: coincidence of all clinical, electroencephalographic and neuroimaging parameters (4 parameters indicated above).
• 2nd degree of correlation: coincidence of three out of four parameters.
• 3rd degree of correlation: coincidence of 2 out of 4 parameters.
• Lack of clear correlation.

The frequency of occurrence of diffuse symptoms in the structure of the above parameters was separately assessed. We included the following: bilateral neurological symptoms, pseudogeneralized seizures, diffuse discharges on the EEG and diffuse changes in the brain during an MRI study.

A clear correlation (coincidence of all 4 parameters) was observed only in 14.3% of patients; 2nd degree of correlation — 25.7% of cases; 3rd degree - 22.9%. A significant lack of correlation was found in 37.1% of patients. Various diffuse symptoms were noted in 94.3% of cases. However, there was not a single patient who experienced exclusively diffuse symptoms.

Therapy and prognosis The study showed a good prognosis for the control of epileptic seizures and high effectiveness of antiepileptic therapy. During treatment, seizure relief was achieved in all but one patient - 97.1%! In 28.6%, complete electro-clinical remission was achieved, which is 32.3% of all patients with clinical remission for more than a year. In 1 case, a patient with hemiclonic and secondary generalized seizures and signs of hypoxic-ischemic perinatal encephalopathy on MRI achieved seizure remission that lasted for 3 years. Further, a recurrence of attacks was noted. Currently, after correction of AEDs, the attacks have been stopped, but at the time of publication, the duration of remission was 1 month. Remission for more than 1 year was observed in 31 patients, which was 88.6% of cases. It should be noted that, despite such a high percentage of remissions, in most cases, at the initial stages of therapy, the disease was resistant to seizures and epileptiform activity on the EEG. Only in 8 cases (22.9%) attacks were stopped with monotherapy. In other cases, remission was achieved with duo- and polytherapy, including the use of corticosteroids. The most effective drugs in the treatment of patients in the examined group were: valproate (Convulex) and topiramate (Topamax), both in monotherapy and in combination. When using carbamazepine in monotherapy, high efficiency was noted in a number of cases, but aggravation phenomena were often observed in the form of an increase in focal seizures and the appearance of pseudogeneralized paroxysms, as well as in the form of an increase in the index of diffuse epileptiform activity on the EEG. When focal attacks were resistant, a good response was obtained when prescribing combinations: Convulex + Topamax, Convulex + Tegretol or Trileptal. Succinimides (suxilep, petnidan, zarantin), which were used only in combination, mainly with valproate, were highly effective. Succinimides were effective against both pseudogeneralized seizures and epileptiform activity on the EEG. Sulthiam (oppolot) has also been used successfully in combination with valproate. In resistant cases, mainly in patients with infantile spasms, as well as in the presence of “electrical status epilepticus of slow-wave sleep” on the EEG, we prescribed corticosteroid hormones (synacthen depot, hydrocortisone, dexamethasone) with the highest effect: stopping attacks, blocking or significantly reducing the index epileptiform activity in all cases. The use of hormones was limited by the high frequency of side effects of therapy.

Analysis of the results showed that at the initial stages of treatment, in most cases it is not possible to block or even reduce the DEPD index on the EEG. Cases of diffuse spread of DEPD with the formation of a picture of continued epileptiform activity during the slow-wave sleep phase were particularly resistant. In these cases, the addition of succinimides or oppolot to the basic AEDs showed the greatest effectiveness. The administration of these drugs significantly blocked regional and diffuse epileptiform activity on the EEG. The use of corticosteroids has also shown high effectiveness against DEPD.

It should be noted the positive effect of AEDs observed in the examined patients in relation to cognitive functions and motor development. This effect, first of all, can be associated with the “freeing” of the brain from seizures and epileptiform activity, as well as with more intensive rehabilitation assistance, which became possible after seizure control was established. However, complete or significant restoration of motor and cognitive functions was not observed in any case, even after complete relief of seizures and blocking of epileptiform activity.

DISCUSSION

The study of the described group of patients was carried out at the Center for Pediatric Neurology and Epilepsy (K.Yu. Mukhin, M.B. Mironov, K.S. Borovikov), together with German colleagues (H. Holthausen et al.) from 2002 to 2009 . Currently, there are more than 130 patients under our supervision who meet the criteria described in the article. In our opinion, this group represents a completely special epileptic syndrome with a favorable course of epilepsy, but with severe neurological disorders. We called it " focal epilepsy of childhood with structural changes in the brain and benign epileptiform patterns on the EEG", abbreviated — FEDSIM-DEPD. A not entirely successful synonym used earlier is “double pathology”; by this term, different authors mean various pathological conditions, in particular, a combination of mesial temporal sclerosis with dysplastic changes in the hippocampus.

I would like to draw your attention to the fact that we did not find such studies in the domestic and foreign literature available to us. Some publications describe only isolated observations of patients with focal motor seizures reminiscent of those in IFE, a favorable prognosis for the course of epilepsy, and the presence of structural changes in the brain. The authors call these cases “idiopathic copies of symptomatic focal epilepsies.” In fact, these isolated cases are identical to the group of patients with FEDSIM-DEPD that we described. However, the fundamental difference is in the name, which radically changes the idea of ​​this syndrome.

FEDSIM-DEPD is not, in the strict sense, symptomatic epilepsy. Firstly, in many cases, the ictogenic zone does not coincide with the localization of structural changes in the brain, not only within the brain lobe, but even within the hemisphere. In 28.6% of the patients we examined, diffuse cortical atrophy was observed, and there were no local structural changes in the brain. Secondly, epileptiform activity in patients of this group is represented mainly by multiregional and diffuse DEPD, and not by clearly regional EEG patterns, as in symptomatic focal epilepsies. Moreover, if the phenomenon of secondary bilateral synchronization occurs, then the zone of discharge generation does not always coincide with the zone of the pathological substrate. Thirdly (this - the main thing!), in the overwhelming majority of cases, epileptic seizures disappear during puberty, despite the persistence of the morphological substrate in the brain.

The lack of a clear correlation of the ictogenic zone and the localization of epileptiform activity with the localization of structural changes in the brain, the eventual disappearance of epileptic seizures in almost all patients, casts doubt on the symptomatic nature of epilepsy, that is, its development directly as a result of exposure to the morphological substrate. On the other hand, there is a high incidence of epilepsy in families of probands; onset of epilepsy exclusively in childhood; attacks identical in nature to IFE with their timing at the time of awakening and falling asleep; presence of DEPD on EEG; relief of seizures in puberty (under the influence of therapy or spontaneously) - clearly indicate the idiopathic nature of epilepsy. However, in idiopathic focal epilepsy there are no structural changes in the brain, no focal neurological symptoms and intellectual deficits, no slowing of the underlying background EEG activity and no continued regional slowing. Also, IFE is not characterized by prolonged attacks, often with a status course and the formation of Todd's palsy. In our opinion, these symptoms are not caused by epilepsy, but are the result of perinatal pathology. Thus, we are talking about a unique syndrome in which epilepsy is inherently idiopathic, and associated symptoms(neurological and intellectual deficits) are caused by structural damage to the brain. It follows from this that FEDSIM-DEPD is not an “idiopathic copy of symptomatic epilepsy,” but, most likely, idiopathic focal epilepsy, developing in patients with morphological changes in the brain of perinatal origin. This form is idiopathic, but by no means benign. The concept of “benign epilepsy” includes not only the possibility of stopping (or self-limiting) seizures, but also the absence of neurological and cognitive impairment in patients, which does not happen with FEDSIM-DEPD, by definition. FEDSIM-DEPD is idiopathic (by the nature of the attacks and the characteristics of the course) epilepsy in children with local or diffuse changes in the brain of perinatal origin. This a group of patients, taking into account clinical, electro-neuroimaging features, in our opinion, is a separate, clearly defined epileptic syndrome in children, which occupies a special intermediate place in a number of focal forms of epilepsy of various etiologies.

The pathogenesis of the development of such a unique epileptic syndrome will likely be the subject of further study. We would like to discuss some possible mechanisms for the occurrence of FEDSIM-DEPD. From our point of view, the development of FEDSIM-DEPD is based on two mechanisms: congenital disorder brain maturation and pathology of the perinatal period, mainly hypoxic-ischemic damage to the central nervous system. The term “ hereditary impairment of brain maturation” - a congenital disorder of brain maturation - was first used by the famous German pediatric neurologist and epileptologist Hermann Doose. The Doose hypothesis, which we wholeheartedly support, lies in the existence in a number of patients of a genetically determined disorder of brain maturation in the prenatal period. In our opinion, there are 3 main diagnostic criteria for the condition designated as “congenital disorder of brain maturation.”

1. The presence of “pathology of neuropsychic development” in patients: global impairment of cognitive functions, mental retardation, dysphasia, dyslexia, dyscalculia, attention deficit hyperactivity disorder, autistic-like behavior, etc.

2. The combination of these disorders with interictal epileptiform activity, corresponding in morphology to benign epileptiform patterns of childhood.

3. Improvement in the course of the disease and complete disappearance of epileptiform activity when patients reach puberty.

A variety of endogenous and exogenous factors acting in the prenatal period can cause congenital disorders of brain maturation processes. In this case, it is possible that “genetic predisposition” plays a leading role. H. Doose (1989), H. Doose et al. (2000) showed that benign epileptiform patterns of childhood on the EEG (isolated, in combination with epilepsy or other “developmental pathology”) are genetically determined, inherited in an autosomal dominant manner with low penetrance and variable expressivity. Each gene locus or allelic genes influences the synthesis of a specific polypeptide or enzyme. The developmental pathology is based on a violation of the prenatal differentiation of neurons, the formation of the dendritic tree and the reorganization of synaptic contacts, due to which neurons must be connected into “cellular ensembles” or neuronal networks. Under the influence of various damaging factors, erroneous neuronal connections may occur. - aberrant synaptic reorganization. According to some researchers, impaired plasticity (aberrant sprutting) is most characteristic of childhood and may be one of the causes of epilepsy, as well as the development of cognitive disorders. Impaired neuronal plasticity during brain development leads to the formation of “broken,” “perverted” cellular ensembles of cortical neurons, which is clinically expressed as persistent congenital impairments of cognitive functions. Phylogenetically, the youngest parts of the brain - the frontal lobes - are especially vulnerable to disorders of neuronal organization.

A congenital disorder of brain maturation, manifested by various “developmental pathologies” ( table 1). These pathological conditions arise mainly from birth. However, the appearance of epileptiform activity, and in some cases seizures, occurs, as a rule, during a certain “critical” period of child development - most often between the ages of 3 and 6 years. It is important to note that as the child grows and the brain matures, there is a gradual improvement in mental development, relief of attacks and complete blocking of DEPD with the onset of puberty. Sex hormones play a critical role in brain development. A.S. Petrukhin (2000) believes that disturbances in exposure to hormones in the prenatal period can induce mechanisms leading to perverted differentiation of the brain. On the other hand, the onset of the functioning of sex hormones during puberty leads to a “smoothing out” of the symptoms of cognitive epileptiform disintegration and, in many cases, to complete normalization of the electroencephalogram. We believe that the mechanism of congenital disorders of brain maturation processes is the main one in the development of the symptom complex “idiopathic focal epilepsy”. At the same time, it is more correct to consider benign epileptiform patterns of childhood not as markers of epilepsy, but as a sign of brain immaturity.

The second mechanism for the development of FEDSIM-DEPD is the presence of morphological changes in the brain caused by the pathology of the prenatal period. H. Holthausen (2004, personal communication) proposed the term “ dual pathology" We are talking about patients with two pathological conditions: morphological changes in the brain and the presence of DEPD on the EEG and/or epileptic seizures. Structural changes, according to MRI, are always congenital in nature, caused by pathology of the prenatal period. On the other hand, epileptic seizures in patients with “double pathology” and epileptiform activity of the DEPD type do not have a clear localization relationship with morphological substrates in the brain. Among the patients we examined, grade 1 correlation (coincidence of the localization of the lesion according to the neurological examination, the nature of the attacks, EEG and MRI results) was observed only in 14.3% of cases. And a complete lack of correlation was found in 34.3% of patients, that is, in more than 1/3 of patients!

Epilepsy that occurs in these patients has all the features of idiopathic focal (more often - rolandic, less often - occipital), and DEPD activity is usually observed multiregionally. The most typical occurrence is pharyngo-oral, hemifacial, facio-brachial, versive and secondary generalized seizures. Attacks occur almost exclusively upon awakening and falling asleep, their frequency is low, and they necessarily (!) disappear by puberty - as a result of therapy or spontaneously. During the treatment of our patients, seizure relief was achieved in all, with the exception of one patient - 97.1%!

Thus, despite the presence of morphological changes in the brain, both local and diffuse, the clinical picture (the nature of the attacks, EEG data) and the course of epilepsy are identical to those in idiopathic focal epilepsy. However, the problem is that, despite the absolutely favorable course of epilepsy (meaning obligate relief of seizures), the prognosis for motor and cognitive functions in this category of patients can be very difficult. In this regard, FEDSIM-DEPD cannot in any way be called a “benign” form of epilepsy. While maintaining the first criterion of benign epilepsy (obligate relief of seizures), the second criterion (normal motor and mental development of children) - usually absent. This is the fundamental difference between FEDSIM-DEPD and IFE.

The most common congenital morphological substrates in patients with FEDSIM-DEPD are: arachnoid cysts, periventricular leukomalacia, diffuse cortical atrophy of hypoxic-ischemic origin, polymicrogyria, congenital occlusive shunted hydrocephalus. When visualizing on MRI periventricular leukomalacia (premature children with hypoxic-ischemic perinatal encephalopathy) and shunted occlusive hydrocephalus, the development of cerebral palsy (atonic-astatic form or double diplegia) with epilepsy and/or multiregional DEPD on the EEG is typical. In the presence of polymicrogyria, a clinical picture of a hemiparetic form of cerebral palsy with epilepsy and/or DEPD is formed. In patients with arachnoid and porencephalic cysts, it is possible to detect congenital hemiparesis, speech, behavioral (including autism) and intellectual-mnestic disorders in combination with DEPD on the EEG. Once again, it should be noted that the course of epilepsy in patients in this group is always favorable. At the same time, movement disorders and intellectual-mnestic disorders can be very serious, leading to severe disability.

Some publications indicate the role of early organic damage to the thalamus as a result of hypoxic-ischemic disorders in the perinatal period. Structural abnormalities in the thalamus can lead to hypersynchronization of neurons, their “firing,” helping to maintain “increased convulsive readiness” until the onset of puberty. Guzzetta et al. (2005) presented a description of 32 patients with thalamic lesions in the perinatal period; Moreover, 29 of them showed electro-clinical signs of epilepsy with electrical status epilepticus in the slow-wave sleep phase. It has been suggested that the ventrolateral and reticular nuclei of the thalamus, as well as an imbalance of the GABA-transmitter systems, are responsible for the development of constant ongoing epileptiform activity (by morphology - DEPD) in the slow-wave sleep phase. According to H. Holthausen ( Holthausen, 2004, personal communication), DEPD are an electroencephalographic reflection of perinatal leukopathy. It is damage to the white matter (conducting pathways) of the brain that leads to the development of “idiopathic” focal epilepsy, combined with DEPD. Therefore, FEDSIM-DEPD often occurs in premature infants with cerebral palsy and periventricular leukomalacia on MRI. However, this does not explain the appearance of DEPD in neurologically healthy children and in IFE, in cases where there are no motor disorders, that is, there is no damage to the white matter.

Cognitive impairment in FEDSIM-DEPD is due to three main reasons. Firstly, morphological changes in the brain that occur in the prenatal period. These changes are irreversible, we cannot influence them with medication, however, they do not progress. Secondly, frequent epileptic seizures and, especially, constant continued epileptiform activity can lead to severe disturbances in praxis, gnosis, speech, and behavior. Forming in the developing brain of a child, epileptiform activity leads to constant electrical “bombardment” of the cortical centers of praxis, gnosis, speech and movements; leads to their “overexcitation”, and then functional “blocking” of these centers. A functional rupture of neuronal connections occurs due to long-term epileptiform activity. At the same time, what is important for us is the index of epileptiform activity, its prevalence (the diffuse nature and bifrontal distribution are the most unfavorable), as well as the age at which this activity manifests itself.

There is a third mechanism for the formation of cognitive impairment in patients with FEDSIM-DEPD. From our point of view, an important factor in the development of cognitive deficit in this category of patients is “ congenital disorder of brain maturation processes" The etiology of this process is unknown. Apparently, it is determined by a combination of two reasons: genetic predisposition and the presence of various stress factors affecting the intrauterine development of the child. Specific marker of brain immaturity - appearance on the EEG of “benign epileptiform patterns of childhood” - DEPD. In this regard, the use of steroid hormones, promoting “brain maturation”, and not AEDs, have the most effective effect in improving cognitive functions in patients with FEDSIM-DEPD. Doose H., Baier W.K. (1989) suggested that the EEG pattern of DEPD is controlled by an autosomal dominant gene with age-dependent penetrance and variable expressivity. Unfortunately, antiepileptic therapy, while affecting epileptiform activity, does not always have a clear positive effect on reducing neuropsychological disorders. As they grow and mature (primarily - puberty) there is a gradual improvement in cognitive functions, learning abilities and socialization of patients. However, impairment of cognitive functions, of varying severity, can persist throughout life, despite the relief of seizures and blocking of epileptiform activity.

Based on the results obtained and literature data, we developed diagnostic criteria for FEDSIM-DEPD syndrome.

1. Predominance of male patients by gender.

2. Onset of epileptic seizures before the age of 11 years with a maximum in the first 6 years (82.9%) with two peaks: in the first 2 years of life and at the age of 4 to 6 years. Often debuts with infantile spasms.

3. The predominance of focal motor seizures (hemifacial, brachiofacial, hemiclonic), focal seizures originating from the occipital cortex (visual hallucinations, versive seizures, limp seizures) and secondary generalized convulsive seizures.

4. A combination of focal and pseudogeneralized seizures is possible (epileptic spasms, negative myoclonus, atypical absence seizures).

5. Relatively low frequency of focal and secondary generalized attacks.

6. Chronological association of focal attacks with sleep (occurrence upon awakening and falling asleep).

7. Neurological deficits in most patients, including motor and cognitive impairment; often the presence of cerebral palsy.

8. Background EEG activity: characterized by theta slowdown of the main activity against the background of an increased index of diffuse beta activity.

9. The presence on the EEG, mainly in the central temporal and/or occipital leads, of a specific EEG pattern - benign epileptiform patterns of childhood, which more often arise multiregionally and diffusely with an increase in the slow-wave sleep phase.

10. Neuroimaging in all cases reveals signs of perinatal brain damage, predominantly of hypoxic-ischemic origin. These morphological changes can be both local and diffuse, with predominant defeat white matter (leukopathy).

11. Remission of epileptic seizures is achieved in all cases; later epileptiform activity on the EEG is blocked. Neurological (motor and cognitive) impairments generally remain unchanged.

Thus, 5 main criteria remain in all cases of FEDSIM-DEPD syndrome: onset of epileptic seizures in childhood; the presence of focal seizures (variants of hemiclonic or focal, emanating from the occipital cortex) and/or secondary generalized seizures confined to sleep; the presence of benign epileptiform patterns of childhood (BEPD) on the EEG; the presence of structural changes in the brain of perinatal origin during neuroimaging; complete relief of epileptic seizures before patients reach adulthood.

Rice. 1. Frequency of onset of attacks in each annual interval (%).

Rice. 2. Patient Z.R.

Video-EEG monitoring: During sleep, multiregional epileptiform activity is recorded: in the right central-temporal region spreading to the right parietal-occipital region, in the frontal-central-parietal vertex regions, in the left frontal region in the form of single low-amplitude spikes. Epileptiform changes have the morphology of benign epileptiform patterns of childhood (BECP).

Rice. 3. Patient M.A., 8 years. Diagnosis: FEDSIM-DEPD. Delayed psycho-speech development.

Video-EEG monitoring: Epileptiform activity is recorded, presented in the form of bilateral DEPD discharges with an amplitude of up to 200-300 μV of varying degrees of synchronization in the occipito-posterior temporal regions with a pronounced spread to the vertex regions with an alternative onset both in the right posterior regions (more often) and in the left departments

Fig.4. Patient A.N., 10 years. Diagnosis: FEDSIM-DEPD. Right-sided hemiconvulsive seizures.

Video-EEG monitoring : Regional epileptiform activity (READ) is recorded, presented independently in the left temporo-central-frontal region with periodic spread to the left posterior regions and in the right central-frontal region with a tendency to spread to all electrodes of the right hemisphere.

Rice. 5. Patient Z.R., 2 years. Diagnosis: FEDSIM-DEPD. Left-sided hemiclonic seizures with Todd's palsy.

MRI of the brain: Phenomena of residual post-hypoxic leukopathy of the periventricular white matter of both parietal lobes: clearly limited areas of increased T2 signal, hyperintense in FLAIR, localized in the white matter of the fronto-parietal and parieto-occipital lobes. Secondary ventriculomegaly of the lateral ventricles.

5. Zenkov L.R. Non-paroxysmal epileptic disorders. - M.: MEDpress-inform., 2007. - 278 p.

6. Karlov V.A. Epilepsy. - M., 1990. - 336 p.

7. Karlov V.A. Epileptic encephalopathy // Journal of neurol and psychiat. - 2006. - T. 106(2). - P. 4-12.

8. Kryzhanovsky G.N. Plasticity in the pathology of the nervous system // Journal of neurol and psychiat. - 2001. - T. 101(2). — P. 4-7.

9. Mukhin K.Yu. Benign epileptiform disorders of childhood and their specificity // K.Yu. Mukhin, A.S. Petrukhin, L.Yu. Glukhova / Epilepsy: atlas of electrical clinical diagnostics. - 2004, M.: Alvarez Publishing. - pp. 277-288.

10. Mukhin K.Yu. Idiopathic focal epilepsy with pseudogeneralized seizures is a special form of epilepsy in childhood // Rus. zhur. det. neur. - 2009. - T. 4(2). - P. 3-19.

11. Mukhin K.Yu. The concept of idiopathic epilepsy: diagnostic criteria, pathophysiological aspects // In the book: K.Yu. Mukhin, A.S. Petrukhin / Idiopathic forms of epilepsy: taxonomy, diagnosis, therapy. - M.: Art-Business Center, 2000. - P. 16-26.

12. Mukhin K.Yu., Petrukhin A.S., Mironov M.B. Epileptic syndromes. Diagnostics and therapy. A reference guide for doctors. System solutions. - M., 2008. - 224 p.

13. Mukhin K.Yu., Petrukhin A.S., Mironov M.B., Kholin A.A., Glukhova L.Yu., Pilia S.V., Volkova E.Yu., Golovteev A.L., Pylaeva O.A. Epilepsy with electrical status epilepticus of slow-wave sleep: diagnostic criteria, differential diagnosis and treatment approaches. - M., 2005. - 32 p.

14. Mukhin K.Yu., Petrukhin A.S. Idiopathic forms of epilepsy: taxonomy, diagnosis, therapy. - M: Art-Business Center, 2000. - P. 176-192.

15. Nogovitsyn V.Yu., Nesterovsky Yu.E., Osipova G.N., Sandukovskaya S.I., Kalinina L.V., Mukhin K.Yu. Polymorphism of the electroencephalographic pattern of benign epileptiform disorders in childhood // Journal of neurol psychiat. - 2004. - T. 104(10). - pp. 48-56.

16. Petrukhin A.S., Mukhin K.Yu., Blagosklonova N.K., Alikhanov A.A. Epileptology of childhood. - M.: Medicine, 2000. - 623 p.

17. Ambrosetto G. Unilateral opercular macrogyria and benign childhood epilepsy with centrotemporal (rolandic) spikes: report of a case // Epilepsia. - 1992. - V. 33(3). - P. 499-503.

18. Beaumanoir A., ​​Bureau M., Deonna T., Mira L., Tassinari C.A. Continuous spikes and waves during slow sleep. Electrical status epilepticus during slow sleep. Acquired epileptic aphasia and related conditions. - London: John Libbey, 1995. - 261 p.

19. Ben-Zeev B., Kivity S., Pshitizki Y., Watemberg N., Brand N., Kramer U. Congenital hydrocephalus and continuous spike wave in slow sleep - a common association? // J. Child Neurol. - 2004. - V. 19 (2). - P. 129-134.

20. Caraballo R.H., Cersosimo R., Fejerman N. Symptomatic focal epilepsies imitating atipical evolutions of idiopathic focal epilepsies in childhood // In: Eds. N. Fejerman, R.H. Caraballo / Benign focal epilepsies in infancy, childhood and adolescence. - J.L., UK., 2007. - P. 221-242.

21. De Negri M. Hyperkinetic behavior, attention deficit disorder, conduct disorder and instabilite psychomotrice: identity, analogies, and misunderstandings // Brain Dev. - 1995. - V. 17(2). - P. 146-7; discussion 148.

22. Doose H. EEG in childhood epilepsy. - Hamburg, John Libbey, 2003. - P. 191-243.

23. Doose H. Symptomatology in children with focal sharp waves of genetic origin // Eur. J. Pediatr. - 1989. - V. 149. - P. 210-215.

26. Dreifuss F. Classification and recognition of seizures // Clin. Ther. - 1985. - V. 7. - N. 2. - P. 240-245.

27. Engel J. Jr. A proposed diagnostic scheme for people with epileptic seizures and with epilepsy: Report of the ILAE Task Force on Classification and Terminology // Epilepsia. - 2001. - V. 42(6). — P. 796—803.

28. Engel J. Jr. Report of the ILAE Classification Core Group // Epilepsia. —2006. - V. 47(9). — P. 1558—1568.

29. Fejerman N., Caraballo R.H. Definition of syndromes, seizure types and nosologic spectrum // In: Eds. N. Fejerman, R.H. Caraballo / Benign focal epilepsies in infancy, childhood and adolescence. - J.L., UK., 2007. - P. 3-13.

30. Guerrini R., Genton P., Bureau M. et al. Multilobar polymicrogiria, intractable drop attack seizures, and sleep-related electrical status epilepticus // Neurology. - 1998. - V. 51. - P. 504-512.

31. Guzzetta F., Battaglia D., Veredice Ch., Donvito V., Pane M., Lettori D., Chiricozzi F., Chieffo D., Tartaglione T., Dravet Ch. Early thalamic associated injury with epilepsy and continuous spike-wave during slow sleep // Epilepsia. - 2005. - V. 46/6. — P. 889—900.

32. Holthausen H., Teixeira V.A., Tuxhorn I. et al. Epilepsy surgery in children and adolescents with focal cortical dysplasia // In: I. Tuxhorn, H. Holthausen, H-E Boenigk / Pediatric epilepsy syndromes and their surgical treatment. - London, JL., 1997. - P. 199-215.

33. Kim H.L., Donnelly J.H., Tournay A.E. et al. Absence of seizures despite the high prevalence of epileptiform EEG abnormalities in children with autism monitored in a tertiary care center // Epilepsia. - 2006. - V. 47(2). - P. 394-398.

34. Luders H.-O., Noachtar S. Epileptic seizures. Pathophysiology and clinical semiology. - Churchill Livingstone, N.Y., 2000. - 796 p.

35. Sutula T.P. Mechanisms of epilepsy progression: current theories and perspectives from neuroplasticity in adulthood and development // Epilepsy Res. - 2004. - V. 60(2-3). - P. 161-171.

Electroencephalography helps to clarify the localization of the pathological focus in organic brain lesions, the severity of general changes in its functional state, as well as the dynamics of local and general changes in electrical activity. The most informative are EEG data for various forms of epilepsy, tumors, vascular disorders of the brain (especially acute cerebrovascular accidents), and traumatic brain injury.

Electroencephalography as a method of clinical diagnosis has its own specific sign language, which establishes a correspondence between changes in electrical potentials recorded on the EEG and the terms that are used to designate them.

The main characteristics of the EEG are frequency, amplitude and phase.

Frequency is determined by the number of oscillations in 1 s.

Amplitude is the range of electrical potential fluctuations on the EEG; it is measured from the peak of the previous wave in the opposite phase.

The phase defines the current state of the process and indicates the direction of its changes. Monophasic is an oscillation in one direction from the isoelectric line with a return to the initial level; biphasic is an oscillation when, after completing one phase, the curve passes the initial level, turns in the opposite direction and returns to the isoelectric line.

In clinical neurology, visual analysis of the EEG is most often used, which makes it possible to identify the main frequency bands present in the EEG. The term “rhythm” in EEG refers to a type of electrical activity that corresponds to a certain state of the brain and is associated with corresponding cerebral mechanisms.

The main EEG rhythms of an adult who is not in a state of sleep are as follows:

1. Alpha (α) rhythm. Its frequency is 8-13 oscillations per 1 s, amplitude up to 100 μV. Registered in% of healthy adults. It is best expressed in the occipital leads; towards the frontal lobe of the hemispheres, its amplitude gradually decreases. The largest amplitude of the α rhythm is in a person who is in a calm, relaxed state.

EEG of an adult in a state of wakefulness: a regular α-rhythm, modulated in the spindles, is best expressed in the occipital region; activation reaction to a flash of light (irritation indicator on the lower channel).

2. Beta (β) rhythm. Oscillation frequency is 1 s, amplitude is up to 15 µV. This rhythm is best recorded in the area of ​​the anterior central gyri.

1 - the most common type; 2 - low amplitude; 3 - flat

Rhythms and phenomena that are pathological for an adult include the following:

1. Theta (θ) rhythm. The frequency of oscillations is 1 s, the amplitude of the pathological θ-rhythm is most often higher than the amplitude of normal electrical activity and exceeds 40 μV. In some pathological conditions it reaches 300 μV or more.

2. Delta (Δ) rhythm. The frequency of oscillations is 1 s, its amplitude is the same as the θ rhythm; Δ- and Θ-oscillations can be observed in small quantities on the EEG of an adult who is awake, with an amplitude not exceeding the a-rhythm, which indicates a slight shift in the level of functional activity of the brain. EEGs containing Δ- and Θ-oscillations, which exceed 40 μV in amplitude and cover no more than 15% of the total recording time, are considered pathological.

Epileptic (epilentiform, convulsive, convulsive) activity. In epilepsy, the brain is characterized by certain functional changes at the macro- and microstructural levels. One of the main features of the brain in this pathology is the property of neurons to give more active excitation reactions and enter into synchronized activity. The process of activation of neurons causes an increase in the amplitude of waves on the EEG due to the summation over time of the amplitudes of in-phase oscillations. If the discharges of individual neurons are very densely grouped in time, in addition to an increase in amplitude, a decrease in the duration of the total potential may be observed due to a shortening of time dispersion, which leads to the formation of a high-amplitude but short phenomenon - a peak.

A peak or spike (from the English spike) is a peak-shaped potential. Its duration is 5-50 ms, the amplitude exceeds the amplitude of background activity and can reach hundreds and even thousands of microvolts.

A phenomenon of similar origin, characteristic of epileptic syndrome, is an acute wave. Outwardly, it resembles a peak and differs from it only in its extension in time. The duration of the acute wave is more than 50 ms. Its amplitude can reach the same values ​​as the amplitude of the peaks.

Sharp waves and peaks are most often combined with slow waves, forming a stereotypical complex.

A peak wave is a large amplitude complex resulting from the combination of a peak and a slow wave.

Main types of epileptic activity:

1 - peaks; 2 - sharp waves; 3 - sharp waves in the β rhythm; 4 - peak wave; 5 - multiple peak-wave complexes; 6 - sharp wave - slow wave.

A sharp wave - a slow wave is a complex that is similar in shape to a peak-wave complex, but has a longer duration. Features of the EEG associated with the passage of time, when analyzed, are defined by the terms “periods”, “flashes”, “discharges”, “paroxysms”, “complexes”.

A period is a more or less long period during which relatively uniform activity is recorded on the EEG. Thus, periods of desynchronization and periods of temporary α-rhythm against the background of desynchronized EEG are distinguished.

Discharges are compact groups of electrical phenomena that last a relatively short time, arise suddenly and significantly exceed the amplitude of the general background activity. The term “discharges” is used mainly in relation to pathological manifestations on the EEG. There are discharges of high-amplitude waves of the α- or β-rhythm type, discharges of high-amplitude polyphasic oscillations, discharges of Δ- and Θ-waves, peak-wave complexes, etc.

1 - high amplitude α-waves; 2 - high amplitude β-waves; 3 - sharp waves; 4 - polyphase oscillations; 5 - Δ-waves, 6 - Θ-waves; 7 - peak-wave complexes.

Complexes are short discharges of the type described above, which last more than 2 s and usually have a stereotypical morphology.

Topographical features of the EEG are described in spatial terms. One of the main such terms in EEG analysis is symmetry.

EEG symmetry is understood as a significant coincidence of frequencies, amplitudes and phases of the EEG of homotopic sections of both hemispheres of the brain. Differences in amplitude between the EEG of homotopic sections of both hemispheres, amounting to 50%, are considered diagnostically significant.

A normal EEG of an adult who is awake. In the majority (85-90%) of healthy people, a dominant α rhythm is recorded on the EEG during eye closure at rest. Its maximum amplitude is observed in the occipital regions. Towards the frontal lobe, the α rhythm decreases in amplitude and combines with the β rhythm. In 1% of healthy subjects, the regular α-rhythm on the EEG does not exceed 10 μV, and high-frequency low-amplitude oscillations are recorded throughout the brain. This type of EEG is called flat, and EEG with an oscillation amplitude that does not exceed 20 μV is called low-amplitude. Flat low-amplitude EEGs, according to modern data, indicate the predominance of desynchronized nonspecific systems in the brain. Such EEGs are a variant of the norm.

Clinical interpretation of EEG in neurological pathology. It can now be considered generally accepted that the detection of obvious pathological changes on the EEG is a manifestation of abnormal functioning of brain tissue and, consequently, cerebral pathology. Even with complete external clinical health of the subject, the presence of pathological changes on the EEG should be considered as a sign of latent pathology, residual or not yet manifested lesion.

There are three EEG groups: normal; borderline between normal and pathological; pathological.

Normal EEGs are those containing α- or β-rhythms, which in amplitude do not exceed 100 and 15 μV, respectively, in the zones of their physiological maximum severity. On a normal EEG of an adult awake person, Δ- and Θ-waves can be observed, the amplitude not exceeding the main rhythm, not having the character of bilaterally synchronous organized discharges or clear locality, and covering no more than 15% of the total recording time.

EEGs that go beyond the specified limits, but do not have the nature of obvious pathological activity, are called borderline. EEGs in which the following phenomena are observed can be classified as borderline:

• α-rhythm with an amplitude above 100 μV, but below 150 μV, having a normal distribution that gives normal fusiform modulations over time;
• β-rhythm with an amplitude above 15 μV, but below 40 μV, recorded within the lead;
• Δ- and Θ-waves, not exceeding the amplitude of the dominant α-rhythm and 50 μV, in an amount of more than 15%, but less than 25% of the total recording time, not having the nature of bilateral synchronous bursts or regular local changes;
• clearly defined bursts of α-waves with an amplitude greater than 50 μV or β-waves with an amplitude within the μV range against a background of flat or low-amplitude activity;
• a-waves of a pointed shape as part of the normal α-rhythm;
• bilaterally synchronous generalized Δ- and Θ-waves with an amplitude of up to 120 μV during hyperventilation.

EEGs that go beyond the above boundaries are called pathological.

EEG changes in major diseases of the central nervous system. In epilepsy, a number of electrographic signs have been established that make it possible to clarify the diagnosis of this disease, and in some cases, determine the type of attack. A large attack causes an acceleration of EEG rhythms, a psychomotor attack causes a slowdown in electrical activity, and a small attack causes alternating periods of fast and slow oscillations. One of the main signs of epilepsy recorded on the EEG is the presence of convulsive activity, the main types of which are described above: acute high-amplitude waves, peaks, peak-wave complexes, acute wave, slow wave.

EEG of a patient with generalized generalized convulsive seizures and absences: generalized bilateral synchronous peak-wave complexes are observed in response to intermittent

In the period between attacks, the EEG of patients with epilepsy, regardless of the type of attack, usually records paroxysmal activity - high-voltage pointed electrical potentials in the Δ- and Θ- and α-range, and sometimes fast paroxysmal rhythms of 1 s. These bilaterally synchronous oscillations occur simultaneously in all areas of the brain.

The paroxysmal type of activity on the EEG of patients with epilepsy is associated with the occurrence of a synchronous discharge extremely large quantity groups of neurons. A normal EEG in epilepsy during the period between attacks can be observed in 5-20% of patients. These include mainly patients with infrequent seizures or with a deeply located epileptic focus (in the hypocapal area, etc.). Therefore, a normal EEG is not a categorical denial of clinically manifested epilepsy.

When recording the electrical activity of the brain under resting conditions, the so-called epileptic activity may not be detected. In these cases, functional electroencephalography recording is used during the application of various functional loads. Important and to some extent specific tests for patients with epilepsy are hyperventilation and photostimulation. The most common photostimulation, which is carried out using a special device. A pulsed gas-discharge lamp is installed at a distance of cm from the eyes along the midline, and it operates at a given rhythm from 1 to 35 Hz; The duration of the procedure is up to 10 s. In a similar study on the EEG, a reaction of assimilation of the flickering rhythm is observed mainly in the occipital regions of the brain. At the beginning of stimulation, depression of the α-rhythm is observed, then the amplitude of the reproduced rhythm gradually increases, especially in the range of 8-13 oscillations per 1 s.

The hyperventilation test consists of recording an EEG during deep and regular breathing (20 breaths per 1 minute for 2 minutes) followed by breath holding. During tests in patients with epilepsy, pathological waves may become more frequent, a-rhythm synchronization may increase, paroxysmal activity may appear or intensify under the influence of a progressive decrease in the level of CO 2 in the blood and the resulting increase in the tone of nonspecific brain systems.

With brain tumors, in 50% of patients, the EEG shows a pronounced interhemispheric asymmetry with the presence of a focus of pathological activity in the form of polymorphic D-waves corresponding to the affected area. In the unaffected hemisphere of the brain, changes in the EEG are either absent or insignificantly expressed.

EEG of a patient with convexital astrocytoma of the right frontal lobe growing into the cerebral cortex: a clearly limited focus of Δ-waves in the right frontal lobe.

Subcortical tumors, especially those involving the hypothalamus, are almost always accompanied by the presence (sometimes dominance) of slow waves of the Δ- and Θ type, paroxysmal activity of the a-, Θ- and, less commonly, Δ-range. Bilateral symmetrical discharges of high-amplitude Δ-waves are most often recorded when the pathological process spreads to the hypothalamus. Often, in the presence of a tumor of this location, slow waves predominate in the frontal lobes.

Tumors in the posterior cranial fossa in most cases are not accompanied by any changes in brain potentials. EEG changes are mainly expressed in sharpening and hypersynchronization of the main electroencephalographic a-rhythm, sometimes in combination with slow Δ- and Θ-waves. In% of cases of a tumor of this localization, paroxysmal discharges of a hypersynchronous Θ-rhythm with a predominance in the occipital or frontal regions are recorded on the EEG.

In acute stroke, the pattern of bioelectrical activity of the brain is determined mainly by the localization and extent of the pathological focus and, to a lesser extent, by the nature of the cerebrovascular accident (hemorrhage, infarction).

When the lesion is localized in the cerebral hemispheres, in most cases (80%), the EEG shows pronounced interhemispheric asymmetry due to the predominance of pathological forms of activity in the affected hemisphere; At the same time, focal changes in the bioelectrical activity of the brain in the corresponding area of ​​the lesion can be recorded. In 20% of cases, in the presence of foci in the hemispheres, the EEG reveals only diffuse changes of varying degrees of manifestation.

With brainstem localization of the lesion, changes in the EEG are not as significant as due to damage to the cerebral hemispheres. The structure of the EEG is changed more clearly in case of damage upper sections brain stem either by the type of increased rhythm desynchronization reaction, or with the presence of bilateral synchronous a-, Θ-activity. As a result of damage to the lower parts of the brain stem, EEG changes are insignificant.

With traumatic brain injury, changes in the EEG depend on its severity. If the injury is mild, there may be no changes or only minor disturbances in brain potentials are recorded in the form of increased frequent oscillations and uneven a-rhythm. In this case, there may be interhemispheric asymmetry, as well as electrographic signs of damage to the brain stem. In severe traumatic brain injury (with profound loss of consciousness), the EEG is characterized by dominance in all areas of high-amplitude Θ-waves, against the background of which discharges of rough Δ-activity are determined (1.5-2 oscillations per 1 s), indicating significant changes in the functional states of the brain and, first of all, its medial structures. In some cases, against the background of significant diffuse changes in the bioelectrical activity of the brain, interhemispheric asymmetry and focal disorders in a specific area of ​​impact of injury.

What is the focus of pathological activity?

Many changes in the EEG are not specific, but still some of them are quite definitely associated with specific diseases, such as epilepsy, herpetic encephalitis and metabolic encephalopathies. In general, neuronal damage or dysfunction can be judged by the presence of slow waves (theta or delta rhythm) recorded diffusely or over a specific brain region, while diffuse or focal sharp waves or spikes (epileptiform activity) indicate a tendency to development of convulsive seizures.

Focal slowing is highly sensitive and of great value in diagnosing focal neuronal dysfunction or focal brain damage, but the disadvantage is that it is nonspecific because the type of lesion cannot be determined. Thus, cerebral infarction, tumor, abscess, or trauma on the EEG can cause the same focal changes. Diffuse slowing is more likely to indicate an organic rather than a functional nature of the lesion, but is also not a specific sign, since it can be observed without any significant toxic, metabolic, degenerative or even multifocal pathology. EEG is a valuable diagnostic tool in patients with impaired consciousness and in some circumstances can provide prognostic information. In conclusion, it should be noted that EEG recording is important for establishing brain death.

1. Some types of interictal EEG patterns are designated by the term “epileptiform” because they have a distinct morphology and are observed on the EEG in most patients with seizures, but are rarely recorded in patients without clinical symptoms typical of epilepsy. These patterns include sporadic spikes, sharp waves, and spike-slow wave complexes. Not all spike patterns are indicative of epilepsy: 14 Hz and 6 Hz positive spikes; sporadic spikes recorded during sleep (gate spikes), 6 Hz spike-wave complexes; psychomotor pattern - these are all spike patterns, the clinical significance of which is not fully understood. Interictal data should be interpreted with caution. Although some pathological patterns may support a diagnosis of epilepsy, even epileptiform changes, with some exceptions, weakly correlate with the frequency and likelihood of recurrence of epileptic seizures. You should always treat the patient, not the EEG.

2. The majority of patients with undiagnosed epilepsy have a normal EEG. However, epileptiform activity is highly correlated with clinical manifestations of epilepsy. Epileptiform EEG is recorded in only 2% of patients without epilepsy, while this EEG pattern is recorded in 50-90% of patients with epilepsy, depending on the circumstances of the recording and the number of studies performed. The most convincing evidence in favor of a diagnosis of epilepsy in patients with episodic clinical manifestations can be obtained by recording an EEG during a typical episode.

3. EEG helps determine whether seizure activity during a seizure is widespread throughout the brain (generalized seizures) or limited to a specific area (focal or partial seizures) (Fig. 33.2). This distinction is important because the causes of different types of seizures may be different with the same clinical manifestations.

4. In general, detection of epileptiform EEG activity can help in classifying the type of seizures a patient is experiencing.

Generalized seizures of nonfocal origin are usually associated with bilateral synchronous bursts of spikes and spike-wave complexes.

Persistent focal epileptiform activity correlates with partial, or focal, epilepsy.

Anterior temporal commissures correlate with complex partial epileptic seizures.

Rolandic spikes correlate with simple motor or sensory epileptic seizures.

Occipital spikes correlate with primitive visual hallucinations or decreased vision during seizures.

5. EEG analysis allows further differentiation of several relatively specific electroclinical syndromes.

Hypsarrhythmia is characterized by a high voltage, arrhythmic EEG pattern with a chaotic alternation of long duration, multifocal spike waves and sharp waves, as well as numerous high voltage arrhythmic slow waves. This infantile EEG pattern is usually recorded in pathology characterized by infantile spasms, myoclonic jerks and mental retardation (West syndrome) and usually indicates severe diffuse brain dysfunction. Infantile spasms are tonic flexion and extension of the neck, trunk and limbs with abduction of the arms to the sides, usually lasting 3-10 seconds. EEG and clinical examination data do not correlate with any specific disease, but indicate the presence of severe brain damage before the age of 1 year.

The presence of 3 Hz spike-wave complexes on the EEG is associated with typical absence seizures (petit mal epilepsy). This pattern is most often seen in children between three and fifteen years of age and is exacerbated by hyperventilation and hypoglycemia. Such EEG changes are usually accompanied by certain clinical symptoms, such as the appearance of a fixed gaze straight ahead, short clonic movements, lack of response to stimuli and lack of motor activity.

Generalized multiple spikes and waves (polyspike-wave pattern) are usually associated with myoclonus epilepsy or other generalized epileptic syndromes.

Generalized slow spike-wave patterns with a frequency of 1-2.5 Hz are observed in children aged 1 to 6 years with diffuse brain dysfunction. Most of these children have mental retardation and seizures are not treatable with medication. A triad of clinical signs consisting of mental retardation, severe epileptic seizures, and a slow spike-wave EEG pattern is called Lennox-Gastaut syndrome.

Central-midtemporal spikes observed in childhood are associated with benign rolandic epilepsy. These epileptic seizures often occur at night and are characterized by focal clonic movements of the face and hands, twitching of the corner of the mouth, tongue, cheeks, stoppage of speech and increased salivation. The occurrence of attacks can be easily prevented by taking anticonvulsants, and the manifestations of the disease disappear by age. ? Periodic lateralized epileptiform discharges are high-voltage spiky complexes recorded over one of the cerebral hemispheres; The frequency of appearance of complexes is 1-4 seconds. These complexes are not always epileptiform and are associated with the occurrence of acute destructive brain damage, including infarction, rapidly growing tumors and encephalitis caused by the herpes simplex virus.

6. Focal slowing (delta activity) in the interictal period usually indicates the presence of structural brain damage as the cause of epileptic seizures. However, such focal slowing may be a transient consequence of a partial seizure and does not indicate significant structural damage. This slowing may clinically correlate with transient postictal neurological deficits (Todd's phenomenon) and resolve within three days after the attack.

7. The diagnosis of a patient can be based on EEG data when recording a prolonged epileptiform EEG pattern, only briefly replaced by a normal EEG rhythm, which is a sign of non-convulsive status epilepticus.

8. Outpatient EEG monitoring is an EEG recording in conditions of free movement of the patient outside the EEG laboratory, as with Holter monitoring when recording an ECG. The main indication for use of this method is to document the occurrence of a seizure or other phenomenon, especially in patients whose seizures occur spontaneously or in connection with specific events or activities. The result of ambulatory EEG monitoring depends on the patient's behavior, but the absence of epileptiform activity on the EEG during an attack does not completely exclude the diagnosis of epilepsy, since recording through surface electrodes may not reflect epileptic paroxysms arising in the midtemporal, basal frontal or deep midsagittal structures brain

9. The lack of effect from the treatment of focal epileptic seizures is sometimes an indication for surgery to remove the pathological focus. Accurate determination of the localization of the epileptogenic region of the brain requires specialized stationary equipment that allows simultaneous video recording and EEG recording. The technique using the same equipment is often used to determine whether the seizures observed in a patient are epileptic or whether they are functional (psychogenic) in nature.

We welcome your questions and feedback:

Please send materials for posting and wishes to:

By sending material for posting you agree that all rights to it belong to you

When quoting any information, a backlink to MedUniver.com is required

All information provided is subject to mandatory consultation with your attending physician.

The administration reserves the right to delete any information provided by the user

Pathological electroencephalogram

I - diffuse changes in deep brain tumor (spongioblastoma);

II - focus of pathological (slow) activity in the fronto-central lead on the right in a patient with ischemic softening in the anterior cerebral artery basin;

III - focus of pathological (epileptiform) activity in the parieto-occipital lead on the left in a patient with consequences of a brain contusion, d - lead of the right hemisphere; s - lead of the left hemisphere; F - C - fronto-central leads; R - O - parieto-occipital leads.

An EEG that has deviations from the age norm is called pathological. These deviations (changes) can be diffuse, homolateral (widespread in only one hemisphere) or focal.

In case of a brain tumor, the EEG is characterized by slow activity, which in the leads closest to the tumor has the longest period of fluctuation. Sometimes, at some distance from the tumor, pointed oscillations with a relatively high amplitude for them can be recorded. A high prevalence of synchronous slow activity indicates a deep location of the tumor. The addition of generalized paroxysmal activity to focal changes indicates involvement in pathological process median structures.

Spondylogram of the lumbar spine (a, b): Spondylography is used to diagnose diseases of the spine (deforming osteochondrosis and spondylosis, syringomyelia, tuberculous spondylitis, hemangioma, sarcoma, cancer metastases, etc.) and spinal cord (extramedullary and intermedullary tumors), as well as anomalies development. Angiography is a special method for studying cerebral vessels by introducing into them contrast agents(cardiotrast, torotrast, diodon, hypaque, verografin, conrey...

Angiographic diagnosis is based on taking into account the following data: changes in the normal topography of cerebral vessels, the appearance of newly formed vessels, changes in the shape and width of their lumen, etc. With a saccular aneurysm, an additional shadow (aneurysmal protrusion) appears along the course of the arterial vessel. Menovascular tumors are characterized by the appearance of an additional network of newly formed vessels, and intracerebral tumors are characterized by displacement of vascular trunks. The nature…

Contraindications to angiography: severe atherosclerosis, severe forms of hypertension, diabetes mellitus, kidney and liver diseases, as well as cardiopulmonary failure and advanced age of patients. Pneumoencephalography (PEG) is the introduction of air or oxygen into the cerebrospinal fluid spaces of the brain through lumbar or suboccipital punctures followed by craniography. Pneumoencephalography allows you to simultaneously identify the state of the ventricular system and the subarachnoid space of the brain...

Ventriculography - the introduction of contrast agents (oxygen, air, mayodil, etc.) directly into the ventricles of the brain by ventricular puncture to identify the level of occlusion in tumors of the posterior cranial fossa, III ventricle and cerebral aqueduct, occurring with severe symptoms of hydrocephalus. It is prescribed before the operation itself, as the last way to clarify the process and its localization. The method is not safe, especially when...

Due to the increasing use of active treatment methods (anticoagulants, fibrinolytics, enzymes, hormones) and surgical operations on the brain and spinal cord, the requirements for completeness and reliability of diagnosis in neurology are continuously increasing. This leads to the widespread introduction of various additional methods studies - electrophysiological (EEG, thermography, EMG, REG, EchoEG, ultrasound) and non-contrast and contrast...

The information on the site is for informational purposes only and is not a guide for self-medication.

EEG (Electroencephalogram) - interpretation

Electroencephalogram of the brain - definition and essence of the method

1. Photostimulation (exposure to flashes of bright light on closed eyes).

2. Opening and closing the eyes.

3. Hyperventilation (rare and deep breathing for 3 – 5 minutes).

• clenching your fingers into a fist;
• sleep deprivation test;
• stay in the dark for 40 minutes;
• monitoring the entire period of night sleep;
• taking medications;
• performing psychological tests.

Additional EEG tests are determined by a neurologist who wants to evaluate certain functions of a person's brain.

What does an electroencephalogram show?

Where and how to do it?

Electroencephalogram for children: how the procedure is performed

Electroencephalogram rhythms

Electroencephalogram results

1. Description of the activity and typical affiliation of EEG waves (for example: “The alpha rhythm is recorded over both hemispheres. The average amplitude is 57 µV on the left and 59 µV on the right. The dominant frequency is 8.7 Hz. The alpha rhythm dominates in the occipital leads”).

2. Conclusion according to the description of the EEG and its interpretation (for example: “Signs of irritation of the cortex and midline structures of the brain. Asymmetry between the hemispheres of the brain and paroxysmal activity were not detected”).

3. Determining the correspondence of clinical symptoms with EEG results (for example: “Objective changes in the functional activity of the brain were recorded, corresponding to manifestations of epilepsy”).

Decoding the electroencephalogram

Alpha - rhythm

• constant registration of the alpha rhythm in the frontal parts of the brain;
• interhemispheric asymmetry above 30%;
• violation of sinusoidal waves;
• paroxysmal or arc-shaped rhythm;
• unstable frequency;
• amplitude less than 20 μV or more than 90 μV;
• rhythm index less than 50%.

What do common alpha rhythm disturbances indicate?

Severe interhemispheric asymmetry may indicate the presence of a brain tumor, cyst, stroke, heart attack or scar at the site of an old hemorrhage.

• alpha rhythm disorganization;
• increased synchrony and amplitude;
• moving the focus of activity from the back of the head and crown;
• weak short activation reaction;
• excessive response to hyperventilation.

A decrease in the amplitude of the alpha rhythm, a shift in the focus of activity from the back of the head and crown, and a weak activation reaction indicate the presence of psychopathology.

Beta rhythm

• paroxysmal discharges;
• low frequency, distributed over the convexital surface of the brain;
• asymmetry between hemispheres in amplitude (above 50%);
• sinusoidal type of beta rhythm;
• amplitude more than 7 μV.

What do beta rhythm disturbances on the EEG indicate?

The presence of diffuse beta waves with an amplitude not higher than V indicates a concussion.

Theta rhythm and delta rhythm

Delta waves with high amplitude indicate the presence of a tumor.

Bioelectric activity of the brain (BEA)

Relatively rhythmic bioelectrical activity with foci of paroxysmal activity in any area of ​​the brain indicates the presence of some area in its tissue where excitation processes exceed inhibition. This type of EEG may indicate the presence of migraines and headaches.

Other indicators

• changes in electrical potentials of the brain according to the residual-irritative type;
• enhanced synchronization;
• pathological activity of the midline structures of the brain;
• paroxysmal activity.

In general, residual changes in brain structures are the consequences of damage of various types, for example, after injury, hypoxia, or a viral or bacterial infection. Residual changes are present in all brain tissues and are therefore diffuse. Such changes disrupt the normal passage of nerve impulses.

• the appearance of slow waves (theta and delta);
• bilateral synchronous disorders;
• epileptoid activity.

Changes progress as the volume of education increases.

Electroencephalogram: cost of the procedure

Read more:

Reviews

1) On a flattened background EEG, general cerebral BEA disturbances of moderate severity with cortical dysrhythmia, mild irritation, reduction of the d-rhythm and fragmentation of brain stem structures, which intensify during loading tests

2) noting an increase in B-activity in all parts of the cerebral cortex.

What does this mean?

Male, 24 years old.

Beta rhythm of low index, low frequency, diffusely distributed, more pronounced in the fronto-central regions.

When opening the eyes, there is a slight depression of the alpha rhythm

Upon photostimulation, absorption of rhythms in the alpha frequency range is observed.

In response to hyperventilation, a slight increase in the severity of the alpha rhythm is observed in the form of periods of synchronization of alpha activity at a frequency of 10 Hz.

Mild cerebral changes in the bioelectrical activity of the brain of a regulatory nature.

signs of dysfunction of nonspecific mid-stem structures.

No local or paroxysmal activity was recorded.

Rhythmic photostimulation in the frequency range 1-25 Hz: increase in the index and amplitude of a-activity, sharp waves in the a-groups in the parietal-central, occipital and posterior temporal regions, emphasis in amplitude on the right.

Hyperventilation: rhythmic disorganization, sharp waves and reduced EMV complexes in the right temporal region.

EEG during sleep: no physiological sleep patterns were recorded.

Beta activity in the form of groups of waves of high index (up to 75%), high amplitude (up to 34 μV), low frequency, most pronounced in the right occipital-parietal region (O2 P4). A myogram may be present.

slow activity in the form of a rhythm, high amplitude (up to 89 μV).

In OH there is a clear depression of the alpha rhythm.

ZG alpha rhythm has recovered completely.

EEG changes during provoking AF: FT-3 delta activity: increased power; rhythm amplitude increased

FT-5 Alpha activity: rhythm amplitude decreased

FT-10 delta activity: rhythm amplitude increased

FT-15 Alpha activity: rhythm amplitude decreased

PP Alpha activity: increased power, rhythm amplitude increased.

no significant interhemispheric asymmetry was recorded at the time of the study. Thanks a lot

The main rhythm corresponds to age according to the index, but at a reduced frequency, signs of a moderate slowdown in the rate of formation of the cortical rhythm, moderate regulatory changes with slight disorganization of the cortical rhythm. No local pathological activity was detected.

There are no dynamics of maturation of cortical activity; the frequency and index of cortical rhythmics have not increased in comparison with the results of 2 years and 6 months.

Thank you in advance! I hope for your possible help!

Moderate diffuse changes in the bioelectrical activity of the brain. In a state of wakefulness, during a hyperventilation test, generalized discharges of theta waves lasting 2 seconds were recorded. In the structure of theta waves, sharp-slow wave complexes were periodically recorded in the frontal sections of both hemispheres.

The superficial stages of slow-wave sleep have been reached. The physiological phenomena of slow-wave sleep have been formed. No pathological epileptiform activity was recorded during sleep.

Thanks in advance for your answer

Leave feedback

You can add your comments and feedback to this article, subject to the Discussion Rules.