Childhood absence epilepsy, causes of absence seizures, forms of childhood epilepsy

Authors: Mukhin K.Yu., Petrukhin A.S.

Part 1:

• Introduction
• Definition, classification of epilepsy
• Idiopathic generalized epilepsy
• Pediatric absence epilepsy.
• Juvenile absence epilepsy.
• Epilepsy with isolated generalized seizures.
• Juvenile myoclonic epilepsy
• Idiopathic partial epilepsy
• Rolandic
• Idiopathic partial epilepsy with occipital paroxysms.

Part 2:

• Cryptogenic generalized epilepsy
• Lennox-Gastaut syndrome.
• Epilepsy with myoclonic-astatic seizures.
• Epilepsy with myoclonic absence seizures
• Symptomatic partial epilepsy
• Symptomatic temporal lobe epilepsy
• Symptomatic frontal lobe epilepsy
• General principles of treatment of epilepsy

Introduction

The rapid development of neuropharmacology in recent decades, the synthesis of new highly effective antiepileptic drugs (AEDs), a radical revision of many principles of treatment of epilepsy, has now made it possible to classify epilepsy as a curable disease. According to generalized data from the leading antiepileptic centers in the world, a pronounced therapeutic effect is achieved in 75-85% of patients suffering from epilepsy. Epilepsy is one of the most pressing problems in pediatric neurology. According to foreign data, the frequency of epilepsy in the pediatric population is 0.5-0.75% of the child population, and febrile seizures up to 5%. There are no exact statistics on this disease in Russia. Firstly, not all doctors are widely familiar with the modern International Classification of Epilepsy. In this regard, the statistics of epilepsy did not include such diagnoses as “epileptiform syndrome”, “convulsive syndrome”, which are not used in any country in the world and, in fact, are the same disease - epilepsy. Secondly, in our country, epileptic people are observed by both neurologists and psychiatrists, which significantly distorts the statistics. In all countries of the world, epilepsy is a neurological disease.

Over the past decade, there has been a very rapid accumulation of new knowledge on the problem of epilepsy. Both experimental and clinical studies have contributed to a better understanding of the underlying pathophysiological mechanisms of the disease. New research methods have significantly changed our ability to diagnose epilepsy and identify etiological factors of the disease. In addition, great advances have been made in the development of medical and surgical treatment approaches.

Definition, classification of epilepsy

Definition. Epilepsy is a chronic disease of the brain characterized by repeated unprovoked attacks of disturbances in motor, sensory, autonomic, mental or mental functions resulting from excessive neural discharges. The presented definition contains two important provisions. Firstly, epilepsy does not include single seizures, regardless of their clinical manifestations. Only repeated seizures are the basis for a diagnosis of epilepsy. Secondly, epilepsy includes spontaneous, unprovoked seizures (with the exception of reflex forms). By definition, febrile seizures, as well as seizures that occur in acute diseases of the brain (for example, encephalitis, subdural hematoma, acute cerebrovascular accident, etc.) are not epilepsy. Classification. The manifestations of epilepsy are extremely diverse, which from the very beginning of studying the disease made it difficult to create a unified classification. The modern classification of epileptic seizures was adopted by the International League Against Epilepsy in 1981 in Kyoto (Japan). Unlike previous classifications, it takes into account both clinical and neurophysiological (EEG) criteria for most types of epileptic seizures (Table 1). The classification divides all types of epileptic seizures into partial (focal, focal, local, localization-related), generalized and unclassified. Partial seizures are diagnosed when, at the onset of paroxysm, there are clear clinical and electrophysiological criteria for the involvement of certain brain structures. For example, clonic convulsions of one half of the face and arm (faciobrachial seizures) usually indicate the presence of an epileptic focus in the middle-lower parts of the anterior central gyrus; olfactory hallucinations – in the area of ​​the hook; photopsia – in the occipital lobe cortex, etc. If the attack begins as a partial attack, and then involves the entire musculature of the trunk and limbs and signs of involvement of both hemispheres on the EEG, then it should be classified as focal with secondary generalization. The classification clarifies the concept of simple and complex partial seizures. Previously, complex partial seizures were defined as paroxysms with a change in consciousness, and simple ones - without change. According to the Kyoto classification, complex partial seizures should be understood as paroxysms not with a change, but with a complete shutdown of consciousness. Consequently, according to the modern classification, all attacks that occur with phenomena of depersonalization, dream states, cognitive disorders, etc., are not classified as complex, but as simple partial, since the patient’s consciousness during these paroxysms is changed, but not turned off, and the memory of the attacks is preserved . Also, the 1981 classification stipulates that one patient may have several different types of seizures. For example, an attack, starting as a simple partial, can transform into a complex partial, and then into a secondary generalized one. The term “polymorphic seizures” has been removed from the classification, which does not carry any information and is not recommended for use. Thus, the Kyoto classification is at this stage the most complete systematization of epileptic seizures. With the accumulation of clinical experience, the introduction of video-EEG monitoring into practice, the development of neuro-radiological diagnostic methods (CT, MRI, PET), molecular genetics and other sciences, it became obvious that there are a number of special forms of epilepsy, which are characterized by their own clinic (typical types of attacks), course and prognosis. Some of these forms have been known for a long time, such as West syndrome, Lennox-Gastaut syndrome, and Rolandic epilepsy. Others - benign familial neonatal seizures, severe myoclonic (in infancy), juvenile absence epilepsy - have been identified only in recent years. These forms of epilepsy, or according to the International Classification, epileptic syndromes, as a rule, are manifested not by any one type of seizure, but by a combination of them. Epileptic syndromes are defined as separate, independent forms of epilepsy, characterized by a limited age of onset of seizures, the presence of a special type of seizures, specific changes in the EEG (characteristic of a given syndrome), patterns of course and prognosis. For example, one type of seizures - absence seizures - can be part of a number of epileptic syndromes: childhood and adolescent absence epilepsy, juvenile myoclonic epilepsy, with myoclonic absence seizures and others, and the course and prognosis for all of these syndromes are different. A fundamentally new step in the development of epileptology was the creation of a modern classification of “epilepsies, epileptic syndromes and diseases associated with seizures.” This classification was adopted by the International League Against Epilepsy in October 1989 in New Delhi and is currently generally accepted by epileptologists around the world (Table 2). The classification of epileptic syndromes is based on the following principles: 1. Localization principle:

• localization-related (focal, local, partial) forms of epilepsy;
• generalized forms;
• forms that have features of both partial and generalized.

2. Principle of etiology:

• symptomatic,
• cryptogenic,
• idiopathic.

3. Age of onset of attacks:

• newborn shapes,
• infant,
• children's,
• youthful,
• adults.

4. The main type of attacks that determines the clinical picture of the syndrome:

• absence seizures,
• myoclonic absence seizures,
• infantile spasms, etc.

5. Features of the course and forecast:

• benign,
• severe (malignant).

The principles of localization and etiology in classification require clarification. The classification is based on classical ideas about focal and generalized forms of epilepsy. Localization-related forms are determined if the nature of the paroxysms, EEG data and neuroradiological examination confirm the local origin of the attacks. This applies not only to forms with a clearly identified structural defect of the brain (temporal lobe epilepsy), but also to syndromes in which the nature of the seizures and EEG indicate a local onset, but changes on CT are usually absent (rolandic epilepsy, benign occipital epilepsy). It is also possible that there are multifocal forms of epilepsy, in which seizures originate from several foci within one or both hemispheres. In generalized forms of epilepsy, seizures must be generalized from the very beginning, which is confirmed by EEG data (bilateral synchronous spread to both hemispheres). The pathogenesis of generalized forms of epilepsy is still not clear enough. A corticothalamic hypothesis for the occurrence of primary generalization is proposed. In cases where the nature of the attacks and examination data do not allow us to confidently state the local or primary generalized onset of paroxysms, these epileptic syndromes are defined as not amenable to clear classification, that is, having signs of both locality and generalization. The classification divides all epileptic syndromes into symptomatic, idiopathic and cryptogenic. Symptomatic forms mean epileptic syndromes with a known etiology and verified morphological disorders (tumors, scars, gliosis, cysts, dysgenesis, etc.). In idiopathic forms, there are no diseases that could be the cause of epilepsy, and epilepsy is, as it were, an independent disease. Currently, the genetic determination of idiopathic forms of epilepsy has been established. The term “cryptogenic” (hidden) refers to those syndromes whose cause remains hidden and unclear. These syndromes do not meet the criteria for idiopathic forms, but there is no evidence of their symptomatic nature. For example, in the case of a combination of epilepsy with hemiparesis or oligophrenia, the symptomatic nature of the disease is assumed, but CT and MRI studies do not visualize changes in the brain. This case is classified as cryptogenic. It is obvious that with the improvement of the technical capabilities of neuroimaging (for example, PET), most cryptogenic forms will be transferred to the category of symptomatic. Symptoms. The semiology and clinic of various epileptic seizures are described in detail in many manuals on epilepsy. At the same time, the diagnosis of certain forms of epilepsy (epileptic syndromes) has received insufficient attention in the literature. Let us dwell on the diagnostic criteria and principles of treatment of the main epileptic syndromes of childhood and adolescence.

Diagnostic methods

Absence attacks can be identified at home, but for a detailed diagnosis, it is important to consult a doctor. The Clinical Brain Institute offers comprehensive screening programs for patients suspected of having any type of epilepsy. Methods are selected individually, taking into account the patient’s age, clinical manifestations of the disease and concomitant pathologies.

1. Electroencephalography is the main method for diagnosing various types of epilepsy, including absence seizure. During the examination, the patient is asked to look at a bright light to provoke an attack. The results will show changes in brain activity under normal conditions and during an attack.
2. Doppler ultrasound is a specific technique for examining blood vessels located in the neck and brain. Their narrowing, damage, as well as impaired ability to contract and relax leads to a deterioration in blood supply to the brain. This factor is often included in the list of causes of epilepsy.
3. Computed tomography and magnetic resonance imaging are informative ways to examine all parts of the brain if epilepsy is suspected. Special equipment allows you to visualize any organic changes and obtain a full three-dimensional image. Such images will help identify tumors, circulatory disorders and other diseases. In addition, it is possible to conduct an examination with a contrast agent to diagnose cerebral vessels.

Doctors at the Clinical Institute of the Brain emphasize that one examination is not enough. During the treatment period, it is necessary to update the data, on the basis of which you can adjust the dosage of drugs, cancel them or replace them with other drugs.

Idiopathic generalized epilepsy

All forms of idiopathic epilepsy are characterized by:

• Genetic predisposition (often a family history of epilepsy).
• Limited age of disease onset.
• No changes in neurological status.
• Normal intelligence of patients.
• Preservation of the basic rhythm on the EEG.
• Absence of structural changes in the brain during neuroimaging.
• The drugs of choice for treatment are valproic acid derivatives.
• Relatively favorable prognosis with therapeutic remission achieved in the vast majority of cases.

Main symptoms of seizures (psychogenic non-epileptic)

Pseudo-seizures, as a rule, completely imitate an epileptic attack - they can be accompanied by various characteristic physical and somatic symptoms:

• dilated pupils;
• involuntary urination;
• defecation;
• tongue bite;
• angina attack;
• asthma attack and much more.

And most importantly, they are also felt by patients as a true seizure.

You can understand whether this is an attack or not only by recording this event during video EEG monitoring.

Symptoms of psychogenic non-epileptic seizures are most often a reflection of a psychological personality conflict or mental disorder.

Most patients with pseudoseizures have psychiatric comorbidities

• anxiety-depressive disorder,
• somatoform disorder,
• conversion disorder,
• panic attacks,
• chronic pain and others.

Pediatric absence epilepsy.

Absence seizures are a type of generalized nonconvulsive seizures, characterized by a high frequency and short duration of paroxysms with loss of consciousness and the presence of a specific pattern on the EEG - generalized peak-wave activity with a frequency of 3 Hz. Absence seizures are one of the most common types of epileptic seizures in children and adolescents. The onset of absence seizures in childhood absence epilepsy (CAE) is observed in the age range from 2 to 9 years, averaging 5.3 ± 0.3 years. The peak age of manifestation is 4-6 years, with a predominance of girls by gender. Clinically, absence seizures are characterized by a sudden short cessation (or significant decrease in the level) of consciousness with absence or minimal motor phenomena. An aura, as well as post-ictal confusion, are not typical. The duration of absence seizures ranges from 2-3 to 30 seconds, averaging 5-15 seconds. A characteristic feature of absence seizures is their high frequency, reaching tens and hundreds of attacks per day. It is important to divide absence seizures into simple and complex ones. Simple absence seizures are characterized by the cessation of all activity, “freezing”, “freezing” of patients, a fixed “absent” gaze, and a confused, hypomimic facial expression. Simple absence seizures account for only 20% of the clinical picture of DAE. DAE is more characterized by complex absence seizures that occur with a minimal motor component. The following types of complex absences are distinguished: with myoclonic, tonic, atonic, vegetative components, as well as with automatisms and focal phenomena. The most common absence seizures are those with myoclonic and tonic components. Absence seizures with a myoclonic component are observed in 40% of patients with DAE. Manifested by: myoclonus of the eyelids; perioral myoclonus (rhythmic stretching of the lips, like a “goldfish”); perinasal myoclonus (rhythmic twitching of the wings of the nose). During an attack, a number of patients experience a single shudder or several short weak twitches of the muscles of the shoulder girdle and/or arms. Absence seizures with a tonic component are most typical for DAE, observed in 50% of patients. They are manifested by deviation of the head, and sometimes the body, backwards (retropulsive absence seizures), tonic abduction of the eyeballs upward or to the side. Sometimes during an attack there is a slight tonic tension (usually asymmetrical) in the muscles of the upper extremities. Absence seizures with an atonic component are not typical for DAE and are observed only in isolated cases, mainly in atypical forms. They manifest themselves as a sudden loss of muscle tone in the muscles of the arms (loss of objects), neck (passive nod), and legs (atonic-astatic attacks). Atonic absence seizures are more often referred to as atypical absence seizures (peak-wave complex frequency less than 2.5 Hz) within Lennox-Gastaut syndrome. Absence seizures with a vegetative component are observed, on average, in 5% of patients with DAE. They manifest themselves as urinary incontinence during an attack, mydriasis, discoloration of the skin of the face and neck with the appearance of an urticarial rash on the skin of these areas. Absences with a focal component are found in 15% of patients and significantly predominate in patients with tonic absences. During an attack, mild unilateral tension in the muscles of the arm or face appears, sometimes with isolated myoclonic twitches; turning your head and eyes to the side. It should be remembered that the appearance of pronounced focal phenomena during attacks is alarming regarding the presence of partial paroxysms in patients. Automatisms in the structure of absence seizures are observed in 35% of patients suffering from DAE. The most common automatisms that occur are gestures, pharyngo-oral and speech. The status of absence seizures in DAE is noted with a frequency of about 10%. This condition is manifested by a sharp increase in absence seizures, following one after another directly or with a very short interval. Amymia, drooling, and motor retardation (stupor) are observed. The duration of the status ranges from several hours to several days. Generalized convulsive seizures (GSE) are found in 1/3 of patients with DAE. Several months or years pass from the debut of absence seizures to the joining of SHGs. In most cases, SHGs join 1-3 years after the onset of the disease (65% in the group of patients with SHGs), less often - in the range of 4-13 years (35%). Rare generalized tonic-clonic convulsive paroxysms predominate. Factors that provoke an increase in absence seizures include the following: hyperventilation; sleep deprivation; photostimulation; menstruation; intense mental activity or, conversely, a relaxed, passive state. Hyperventilation is the main trigger for absence seizures. Carrying out 3-minute hyperventilation in untreated patients with DAE causes absence seizures in almost 100% of cases; and in patients receiving AEDs, it serves as one of the criteria for the effectiveness of drug therapy. The frequency of detection of epileptic activity in the interictal period with DAE is high and amounts to 75-85%. The main background recording activity is preserved. The most typical EEG pattern is bursts of generalized spike-wave activity. The frequency of peak-wave complexes varies from 2.5 to 4-5 per second. (usually 3 Hz – typical absence seizures). Treatment. Complete therapeutic remission in DAE is achieved in 70-80% of cases and a significant reduction in attacks in the remaining patients. Treatment should always begin with valproic acid preparations (Depakine, Convulex, Apilepsin). Average dosages are 30-50 mg/kg/day Depakine Enterik in 3-4 doses or chrono in 2 doses. Suxilep has also been shown to be highly effective in relieving absence seizures. The average dosage of the drug is 15 mg/kg/day in 2-3 doses. A significant negative aspect of suxilep therapy is the complete lack of effect of the drug on GSP. If absence seizures are resistant to monotherapy with valproate and succinimides, a combination of valproate and suxilep, or valproate and lamotrigine (Lamictal) is prescribed. The average daily dose of Lamictal when combined with valproate is 0.2-5.0 mg/kg/day in 2 divided doses. The use of carbamazepine (finlepsin, tegretol, timonil) is strictly contraindicated in all forms of absence epilepsy due to the high likelihood of increased frequency of attacks.

It is well known that absence is a sudden and short-term loss of consciousness. Atypical absence seizures (AA) are epileptic absence seizures associated on the EEG with patterns of irregular slow peak-wave activity with a frequency of less than 2.5 Hz or paroxysmal fast activity when the main activity of the background recording is slowed down [15].

In 1939, F. Gibbs et al. [12] were the first to describe slow diffuse discharges of acute-slow wave complexes with a frequency of less than 2.5 Hz on the EEG, which they called “petit mal variant”. In 1950, W. Lennox and D. Davis [13] showed significant differences in the clinical picture of seizures, development and prognosis of epilepsy between patients with absence seizures caused by generalized peak-wave discharges with a frequency of 3 Hz and diffuse discharges slower than 2.5 Hz (“ petit mal variant").

In this work, the term “atypical absence seizures” was first proposed - seizures accompanied on the EEG by slow discharges of acute-slow wave complexes. H. Gastaut et al. [11] described in detail the clinical features of the course of epilepsy with a severe prognosis in patients with AA, accompanied by slow acute-slow wave complexes with a frequency of less than 2.5 Hz on the EEG, in combination with tonic seizures and low-amplitude fast-wave activity. This form of epilepsy later became known as Lennox-Gastaut syndrome.

The term “atypical absence seizures” was formed as an antipode to typical absence seizures. At the same time, absence seizures began to characterize not only the electroclinical characteristics of generalized seizures, but also forms of generalized epilepsy with a diametrically different prognosis. The main criterion at that time, which made it possible to distinguish between the two types of seizures, was the particular characteristics of ictal discharges: 3 Hz or more - typical absences; diffuse discharges of peak-wave complexes with a frequency of less than 2.5 Hz characterize AA. Later, other epileptic syndromes were described (myoclonic-astatic epilepsy, epilepsy with myoclonic absence seizures, etc.), the structure of which also included AA, which further complicated their taxonomic position.

At the same time, in the 50s, the concept of secondary bilateral synchronization (BSS) was formulated: “We call the bilateral synchronous discharge emanating from a unilateral cortical focus the phenomenon of secondary bilateral synchronization.” This classic definition was presented by K. Tukel and H. Jasper in a 1952 publication [17]. This article presented a medical history of a patient with seizures that had the clinical and electroencephalographic characteristics of typical absence seizures - freezing with the appearance of generalized discharges with a frequency of 3 Hz on the EEG, in which, during the examination, a space-occupying formation was revealed in the parasagittal frontal regions. Thus, another semantic meaning of AA was formulated - seizures that have the kinematic characteristics of generalized, diffuse ictal EEG patterns, but are focal in terms of the mechanism of occurrence. Further work confirmed the existence of AA associated with structural local disorders of the cerebral cortex in symptomatic focal epilepsy [1, 4, 10]. The development of medical technologies in recent decades has made it possible to show that AA in Lennox-Gastaut syndrome in most cases are pseudogeneralized (within the framework of VBS), and the syndrome itself is often a phenocopy, a “mask” of symptomatic focal/multifocal epilepsies associated with organic brain damage or with hereditary genetic diseases [4].

AA are often detected in patients with a special group of epileptic encephalopathies associated with the so-called benign epileptiform patterns of childhood and electrical status of slow-wave sleep. These include Landau-Kleffner syndrome (LKS), pseudo-Lennox syndrome (PLS), and epilepsy with electrical status epilepticus of slow-wave sleep (ESES syndrome). In this group of diseases, AA are considered pseudogeneralized attacks.

Recently, publications have appeared showing the possibility of the occurrence of AA in idiopathic focal forms of epilepsy within the framework of the phenomenon of VBS on the EEG, in particular within the framework of the syndrome “idiopathic focal epilepsy with pseudogeneralized seizures”.

The purpose of the study was to study the anamnestic, clinical, electroencephalographic and neuroimaging characteristics of patients with AA.

Material and methods

The study included 1261 patients with various forms of epilepsy, whose disease debuted at different ages - from the first day of life to 18 years. Patients were observed from 1999 to 2010.

The study was conducted at the clinical sites of the Department of Neurology and Epileptology, Faculty of Advanced Training for Physicians, Russian Medical University. N.I. Pirogov and at the clinical base of the Institute of Child Neurology and Epilepsy named after. Saint Luke.

Diagnosis of epileptic syndromes was based on the criteria of the International Classification of Epilepsies, Epileptic Syndromes and Similar Diseases (1989), and was also based on the report of the ILAE Commission on Classification and Terminology (2001).

All patients were examined clinically by a neurologist; A routine EEG study was performed; also in all cases, continued video-EEG monitoring was carried out 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 (Sigma Infinity GE magnetic resonance system with a magnetic field voltage of 1.5 Tesla).

results

Absence seizures were detected in 231 (18.3%) patients. Of these, AA during the course of the disease was recorded in 129 (10.2%) patients from all patients with epilepsy or 55.8% of cases among patients with absence seizures.

Among the examined patients with AA, there was a predominance of male patients - 55% of cases versus 45% in female patients.

It is of interest to analyze the structure of forms of epilepsy associated with AA (Table 1).

The study showed that AA occurs in 13 types of epileptic syndromes. Cryptogenic and symptomatic focal forms of epilepsy were most often detected, in 20.8 and 18.6% of cases, respectively. Idiopathic focal epilepsy with pseudogeneralized seizures (IFE-PGS) was observed in 13.8% of patients. With equal frequency, in 7.0% of cases, syndromes such as Lennox-Gastaut syndrome, focal epilepsy of childhood with structural changes in the brain and benign epileptiform patterns of childhood (FEDSIM-DEPD), epilepsy with electrical status epilepticus of slow-wave sleep (ESES-) were observed. syndrome). SLS and epilepsy with myoclonic absence seizures (EMA) were detected in 6.2% of cases. 4.7% of patients had SPL, 3.9% had myoclonic-astatic epilepsy (MAE). In rare cases (1.6% of patients), AA was recorded in progressive myoclonus epilepsy, severe myoclonic epilepsy of infancy (Dravet syndrome), epilepsy with epileptic myoclonus of the eyelids with absence seizures.

The onset of epilepsy in patients with AA varied over a wide age range from 1 month of life to 12 years. The average age of onset was 3.4±2.92 years. It is important to note that if epilepsy occurred over the age of 12 years, then AA was not observed.

AA at the onset of epilepsy was noted in 32.6% of cases among patients in this group. Moreover, the average age of onset of AA was 4.33±2.45 years. It should be noted that the age of onset varied significantly among different epileptic syndromes (see Table 1).

Other types of seizures at the onset of the disease in patients with AA were noted with different frequencies: febrile seizures - in 13.2% of cases, secondary generalized convulsive seizures (SGSP) - in 12.4%, hemiclonic - in 9.3%, epileptic spasms - in 7.6%, focal motor - in 4.6%, tonic - in 3.1%, myoclonic - in 3.1%, generalized convulsive seizures (GSP) - in 3.1%, occipital - in 2, 3%, negative myoclonus - in 2.3%, focal atonic (temporal syncope) - in 2.3%, generalized atonic - in 1.6%, epileptic myoclonus of the eyelids - in 1.6%, focal automotor seizures - in 0 .8% of cases.

AA as the only type of attacks in the clinical picture was observed in 20.9% of cases and most often with IFE-PGP (40.8%). In other cases, AA was combined with other types of attacks. Two or more types of seizures in the structure of epilepsy were observed in 79.1% of cases; three types or more - in 60.5%; four or more - in 24.0%.

When analyzing anamnestic data and the results of video-EEG monitoring, it was revealed that in epilepsy associated with AA, numerous types of seizures can be observed. A total of 16 types of attacks were identified, taking into account semiological features (Table 2).

The most common types of seizures recorded in patients with AA were SHSP (33.3% of cases), tonic seizures (21.7%), hemiclonic (18.6%), myoclonic (17.1%) and negative myoclonus (15.5%). It is of interest that among all types of seizures in the studied group, focal seizures significantly predominated.

In all patients, AA was verified during video-EEG monitoring. It is important to note that parents and others did not always notice AA, and in 36.4% of cases this type of attack was first identified during video-EEG monitoring.

AA was manifested by a decrease in the level of consciousness, suspension of the patients’ motor activity, and general “lethargy.” The consciousness of patients during an attack often fluctuates; Drooling may occur during attacks. Most often, AA was accompanied by an atonic component, which manifests itself in the form of nodding, lowering of the shoulders, bending of the body, and cascading falls. Less frequently, the myoclonic component (twitching of the limbs and facial muscles, nodding) and automatisms were detected.

AA were accompanied by diffuse continuous discharges of acute-slow wave complexes of varying degrees of bilateral synchronization. There was significant variation in the frequency characteristics of ictal discharges from 1.5 to 4 Hz (mean 2.5 Hz). It was noted that the frequency of diffuse discharges depends not only on the syndromic identity, but also on the age of onset of epilepsy. Thus, at the onset at the age of 4 years and older, there is an increase in the frequency of acute-slow wave complexes. Slow acute-slow wave complexes were most often detected in groups of patients with cryptogenic/symptomatic focal epilepsy, Lennox-Gastaut, Dravet, FEDSIM-DEPD syndromes.

In all cases, in patients with AA, during video-EEG monitoring, diffuse epileptiform activity was detected, which was represented by diffuse discharges of acute-slow wave complexes, diffuse discharges of peak-wave complexes, diffuse discharges of polypeak-wave complexes, diffuse discharges of slow acute-slow complexes wave (see picture).

Figure 1. Diffuse bilateral-asynchronous discharges of slow sharp-slow wave complexes with regional onset in the left temporoparietal region. In 21.7% of cases, the EEG recorded a pattern of “diffuse low-amplitude fast-wave activity” (LAFA), which clearly correlated with the presence of tonic seizures or epileptic spasms in the patients’ clinical picture. It should be noted that in the vast majority of cases there was an increase in the index of diffuse discharges during sleep compared to wakefulness. Continued diffuse epileptiform activity during the slow-wave sleep phase was observed in 26.4% of cases.

In most cases, diffuse epileptiform activity occurred as part of the VBS phenomenon.

During the interictal period, regional/multiregional epileptiform activity was detected in 98.4% of cases. It is important to note the high percentage of benign epileptiform patterns of childhood (BEPD), recorded in 38.8% of cases among all patients with AA. DEPD in 100% of cases were detected in the following syndromes: FEDSIM-DEPD, IFE-PGP, SLK, SPL, ESES syndrome.

Neuroimaging revealed changes in the brain in 66 patients—in 51.2% of cases. Among them, local disorders that arose in the perinatal period prevailed - 47 (71.2%) cases. The most common findings were local atrophic changes - in 37.9% of cases, focal glial changes - in 27.2% of patients, arachnoid/porencephalic cysts - in 16.7% of cases. In 8 (12.1%) cases, various types of neuronal migration disorders were identified, of which focal cortical dysplasia was detected in 4 (6.1%) cases. Asymmetric ventriculomegaly of varying severity was noted in 4 (6.1%) cases. Diffuse atrophic/subatrophic changes were recorded in 28.8% of cases.

Despite the high percentage of neurological and intellectual impairments in patients with AA, in 48.8% of cases there were no abnormalities in the brain according to neuroimaging data. This dissociation allows us to conclude that the attacks themselves and continued epileptiform activity play an important role in the pathogenesis of cognitive impairment associated with AA.

When antiepileptic therapy was prescribed with either one or several drugs in various combinations, complete remission was achieved only in 53.5% of cases of epilepsy associated with AA. A decrease in the frequency of attacks with antiepileptic drugs (AEDs) was observed in 38.0% of patients. No effect was noted in 8.5% of cases. Relief of attacks with monotherapy was achieved in 16.3% of patients. In these cases, remission was observed in 85.7% of patients while taking valproic acid derivatives and in 14.3% when taking succinimides. The study showed varying effectiveness of AEDs in the treatment of individual epileptic syndromes associated with AA (see Table 1). A high percentage of remission was observed in the following forms of epilepsy: MAE, EEMV (in 100% of cases), IFE-PGP, SPL (83.3% of patients), FEDSIM-DEPD (77.8%). In the largest groups of patients in our study - with cryptogenic and symptomatic focal forms of epilepsy - remission was achieved only in 40.7 and 41.7% of patients. In severe myoclonic epilepsy of infancy and progressive myoclonus epilepsy, remission was not achieved in any case.

In 3 cases of resistant symptomatic focal epilepsy (FCD, pachygyria, porencephalic cyst) with the phenomenon of VBS, surgical treatment was performed after a complex of presurgical diagnostics.

In all these cases, long-term follow-up after surgery showed complete remission of attacks.

Discussion

The study identified various forms of epilepsy and epileptic syndromes associated with AA, but cryptogenic/symptomatic forms of epilepsy with the phenomenon of VBS on the EEG predominated.

The results of the study confirm the work of various authors who noted that AA can occur in symptomatic focal forms of epilepsy as part of pseudogeneralized seizures with the phenomenon of VBS on the EEG. These cases are most typical for frontal lobe epilepsy, especially originating from the supplementary motor area [7-9]. In this case, AA are combined with focal motor, versive seizures and VGSP. Classic studies by W. Blume and N. Pillay [10] showed that the phenomenon of VBS on the EEG most often arises from a focus in the frontal cortex (51%), while in temporal lobe epilepsy it forms in only 28% of cases. Most authors emphasize the predominant occurrence of pseudogeneralized seizures (including AA) and VBS on the EEG in cryptogenic frontal lobe epilepsy, i.e. in the absence of a verified structural defect in the brain according to neuroimaging data [4, 9, 14].

It is of interest that the third most common form of epilepsy in patients with AA is idiopathic focal epilepsy with pseudogeneralized seizures, a new form of epilepsy described in 2009 by Prof. K.Yu. Mukhin [5]. IFE-PHP debuts in childhood; characterized by a combination of focal motor seizures that occur upon awakening and falling asleep (as in rolandic epilepsy) and pseudogeneralized seizures: AA, atonic and myoclonic (including epileptic myoclonus of the eyelids) [5]. A combination of regional epileptiform activity of the DEPD with diffuse peak-wave discharges is characteristic. It is important to note the absence of an increase in epileptiform activity during sleep. The disease has a favorable prognosis with remission occurring at the onset of puberty. Our study is consistent with publications showing the possibility of AA occurrence in idiopathic focal forms of epilepsy.

The study revealed a high frequency of benign epileptiform childhood EEG patterns in patients with AA, which can be observed in SLS, ESES syndrome, IFE-PHP, FEDSIM-DEPD syndrome, SPL, which is consistent with the data of other authors [5, 6, 16].

The results obtained during the study showed that AA can be combined with 16 different types of epileptic seizures in different forms of epilepsy. At the same time, the correct interpretation of the semiology of all types of attacks in the clinical picture allows us to significantly narrow the diagnostic search even at the early stages of diagnosis (see Table 2). In this regard, in our opinion, it is unacceptable to use the term “epilepsy with polymorphic seizures”, which does not allow us to clarify the diagnosis and, therefore, to adequately prescribe AEDs.

The study showed the great importance of video-EEG monitoring in the diagnosis of epilepsy with AA. This can be explained by several reasons. In 36.4% of cases, this type of seizure was first identified during video-EEG monitoring and had not previously been noticed by others. This leads to an incorrect interpretation of the condition of a patient with epilepsy (the phenomenon of “pseudo-remission” - a state of imaginary well-being) and, accordingly, incorrect treatment [2]. The large nosological spectrum of epileptic syndromes with different courses and prognosis, the variety of other types of seizures associated with AA, show that correct diagnosis based only on anamnestic and clinical data is impossible, which dictates the need for additional detailed study of electroencephalographic features, both ictal and and interictal.

If AA is suspected, in our opinion, a special scenario for conducting video-EEG monitoring should be followed. It is extremely important to test the patient during the period of diffuse discharges. The difficulty of recording AA should be taken into account, since children with this type of seizure may have reduced intelligence. In the absence of contact with the patient, it becomes necessary to create situations in which the fact of a decrease in the level of consciousness will be established. In our laboratory, we achieve this by playing the patient with parents or medical staff. During the game, the cessation of the started activity, freezing, hypomimia, and fixed gaze, which appear against the background of a diffuse peak-wave discharge on the EEG, will indicate in favor of AA. In order to identify the atonic component in the structure of AA, patients should be tested in the Bare test. In children, this test can be created in the form of a game with the transfer of toys into the hands of the patient. Also important is a test with a long-term orthostatic position of the patient and a change in position from vertical to horizontal. This makes it possible to identify a hidden atonic component, not noticeable in a supine position, and also to differentiate negative myoclonus from the myoclonic component. A prerequisite for video-EEG monitoring of patients with AA is sleep recording. This is due to several reasons. First, other types of seizures can be detected during sleep, for example, tonic or myoclonic in Lennox-Gastaut syndrome, as well as AA during sleep [3]. Secondly, AA are often observed in epileptic encephalopathies associated with continued epileptiform activity during the slow-wave sleep phase.

When antiepileptic therapy was prescribed both in monotherapy and polytherapy in various combinations, complete remission was achieved only in 53.5% of cases of epilepsy with AA.

The study showed an extremely wide range of effectiveness of AEDs in the treatment of selected epileptic syndromes associated with AA. A high percentage of remission was observed in the following forms of epilepsy: MAE, EEMV (in 100% of cases), IFE-PGP, SPL (83.3% of patients), FEDSIM-DEPD (77.8%). In the largest groups of patients in our study - with cryptogenic and symptomatic focal forms of epilepsy - remission was achieved only in 40.7 and 41.7% of patients. In severe myoclonic epilepsy of infancy and progressive myoclonus epilepsy, remission was not achieved in any case.

Significant differences in the prognosis of individual epileptic syndromes associated with AA dictate the need to use the entire range of diagnostic measures, which should include a thorough history taking, clinical examination, video-EEG monitoring with sleep inclusion, MRI of the brain, and genetic consultation.

Juvenile absence epilepsy.

Juvenile absence epilepsy (JAE) is a type of idiopathic generalized epilepsy, which is characterized by the main type of seizures - absence seizures, debuting in the pubertal period with a high probability of the addition of DBS and characteristic EEG changes in the form of generalized peak-wave activity with a frequency of 3 Hz or more. The onset of absence seizures in JAE varies from 9 to 21 years, with an average of 12.5 years. In the vast majority of patients (75%), absence seizures begin in a relatively short time period - 9-13 years. An important feature of JAE is the frequent onset of the disease with GSP - 40% of cases. Absence seizures in patients suffering from JAE are manifested by a short loss of consciousness with freezing and hypomimia. Characterized by a significant predominance of simple absences, that is, attacks without any motor component. The duration of attacks ranges from 2 to 30 seconds, on average 5-7 seconds. At the same time, half of the patients experience very short absence seizures, not exceeding 3 seconds. A characteristic feature of JAE is the relatively low frequency of attacks compared to DAE. In most patients, single absence seizures predominate during the day or 1 attack every 2-3 days. Generalized convulsive seizures are observed in the majority of patients – 75%. In the group of patients with GSP, the disease most often debuts not with absence seizures, but with tonic-clonic convulsive paroxysms. GSPs are characterized by short, infrequent tonic-clonic seizures, usually occurring upon awakening or falling asleep. Unlike DAE, hyperventilation provokes absence seizures in no more than 10% of patients with JAE. HSP in 20% of patients is provoked by sleep deprivation. During an EEG study in the interictal period, results close to normal are found in 25% of patients. The main EEG pattern is generalized peak-wave activity with a frequency of 3 Hz or more (4-5 per second), which is predominantly symmetrical and bilaterally synchronous. Treatment. The effectiveness of treatment for JAE is significantly lower than for DAE. Therapeutic remission is achieved, on average, in 60% of patients, a significant reduction in attacks - 35%, no effect - 5%. Treatment begins with monotherapy with valproic acid. The average dosage is 30-50 mg/kg/day. Due to the extremely high probability of the addition of GSP in JAE, starting treatment with succinimides, as well as using them as monotherapy, is strictly contraindicated. If there is no significant effect from monotherapy with valproate in sufficiently high doses, a combination of valproate with succinimides or lamictal is used. Average doses of suxilep are 20 mg/kg/day; Lamictal – 1-5 mg/kg/day.

Classification of the disease

Types of absence seizures are distinguished based on the clinical picture (the presence or absence of muscle and movement disorders in the patient). The type of pathology can be diagnosed after visual observation of the seizure. Complex absence seizure is accompanied by a change in a person’s muscle tone for 10–20 seconds. Muscle-motor episodes form several subtypes of pathology: atonic, myoclonic, tonic and automatic.

A simple absence seizure develops as a one-time blackout of the consciousness of a person suffering from pathology for 25-30 seconds. There are no other symptoms or signs of the disease. A flash of light or a loud sound helps to bring the patient out of the absensive state. Mild forms of the disease allow a person to continue dialogues or actions interrupted by an attack.

Epilepsy with isolated generalized seizures.

Epilepsy with isolated GSP is defined as a syndrome of idiopathic generalized epilepsy, manifested by a single type of seizure - primary generalized tonic-clonic convulsive paroxysms in the absence of an aura and a clear focus on the EEG. The onset of the disease is observed in a very wide age range: from 1 to 30 years with a maximum in the puberty period (average - 13.5 years). Clinically, GSP is manifested by a sudden (without aura) loss of consciousness with the patient falling, convulsions, eyeballs turning, and pupils dilating. First, there is a short tonic phase, which turns into a longer clonic phase, followed by post-ictal stunning. The duration of the GPS ranges from 30 seconds to 10 minutes (average 3 minutes). The frequency of attacks is low - from single per year to 1 time per month, without a tendency to a serial and status course. It is extremely characteristic that most attacks coincide with the period of awakening and, less often, falling asleep. The most significant provoking factor is sleep deprivation and sudden violent awakening. There may be an increase in attacks during the perimenstrual period. An EEG study in the interictal period may be within normal limits in half of the patients. Characterized by generalized peak-wave activity with a frequency of 3 Hz and higher, often with amplitude asymmetry or bifrontal predominance. Different regional patterns may emerge. Treatment. Remission is achieved in 75-80% of patients. Basic drugs are carbamazepine and valproate. In the absence of generalized peak-wave activity on the EEG, treatment begins with carbamazepine, which is more effective than valproate. When generalized convulsive attacks are accompanied by absences or myoclonic paroxysms, or when generalized peak-wave activity appears on the EEG, the basic drug is only valproate. The average dosage of carbamazepine is 15-25 mg/kg/day in 3 divided doses; valproate 20-50 mg/kg/day in 3 divided doses. Reserve drugs include barbiturates (phenobarbital 1.5-3.0 mg/kg/day in 1-2 doses; hexamidine, benzonal), hydantoins (difenin 4-8 mg/kg/day in 2 doses). In rare resistant cases, combinations are possible: carbamazepine + valproate; carbamazepine + barbiturates; valproate + barbiturates; barbiturates + hydantoins. With inadequate treatment, it is possible that absence seizures or myoclonic seizures may be added to GSP with transformation into juvenile myoclonic epilepsy.

Causes and risk factors

Absence is a disease typical of children. The attacks often recur from the ages of 4 to 11 years, after which they stop. According to statistics, girls get sick more often than boys. However, the disease may first develop in young people between 15 and 30 years of age. The main cause of absence seizure is an imbalance in the processes of excitation and inhibition in the cerebral cortex, resulting in incorrect repetitive signals. Due to their occurrence, it is customary to distinguish two main types of absence seizure:

• secondary - associated with infectious diseases, injuries, inflammatory changes in the cerebral cortex, cerebral palsy and other pathologies that affect the bioelectrical activity of the nervous system;
• primary - the cause of the attacks cannot be determined; there are no organic pathologies or brain damage.

Predisposing factors to the manifestation of another attack are considered to be physical or mental fatigue, lack of rest, as well as deep breathing and hyperventilation. The role of genetic factors in the formation of non-convulsive epileptic seizures, along with various gene failures, has been traced. In addition, the disease can occur in a previously healthy person due to infectious diseases or traumatic brain injuries.

Juvenile myoclonic epilepsy.

Juvenile myoclonic epilepsy (JME) is one of the forms of idiopathic generalized epilepsy, characterized by onset in adolescence with the occurrence of massive bilateral myoclonic seizures, mainly in the arms, during the period after patients awaken. JME is one of the first forms of epilepsy with a known genetic defect. A two-locus model of inheritance (dominant-recessive) is assumed, with the dominant gene localized on the short arm of chromosome 6. The onset of JME varies from 7 to 21 years with a maximum in the age range of 11-15 years. The disease can begin at an earlier age with absence seizures or DBS, followed by the addition of myoclonic seizures during puberty. Myoclonic seizures are characterized by lightning-fast twitching of various muscle groups; they are often bilateral, symmetrical, single or multiple, varying in amplitude. They are localized mainly in the shoulder girdle and arms, mainly in the extensor muscle groups. During attacks, patients drop objects from their hands or throw them far to the side. In 40% of patients, myoclonic attacks also involve the leg muscles, while the patient feels a sudden blow to the knees and slightly squats or falls (myoclonic-astatic attacks); then immediately gets up. Consciousness is usually preserved during attacks. Myoclonic seizures occur or become more frequent in the morning, after the patient awakens. In 90% of cases they are combined with GSP awakenings and in 40% with absence seizures. The main triggers for attacks are sleep deprivation and sudden violent awakening. Approximately 1/3 of JME patients (usually females) exhibit photosensitivity. Epileptic activity on EEG is detected in 85% of patients in the interictal period. The most typical is generalized fast (from 4 Hz and above) polypeak-wave activity in the form of short bursts. Peak-wave activity of 3 Hz may also occur. Treatment. Along with drug therapy, it is necessary to strictly adhere to sleep and wakefulness; Avoid lack of sleep and photostimulation factors in everyday life. Basic drugs are exclusively derivatives of valproic acid. The average daily dosage is 40-60 mg/kg. If the effectiveness is insufficient, polytherapy is prescribed: depakine + suxilep (for resistant absence seizures); depakine + phenobarbital or hexamidine (for resistant GSP); depakine + lamictal or clonazepam (for resistant myoclonic attacks and severe photosensitivity). Complete drug remission is achieved in 75% of patients, in most cases with valproate monotherapy. However, subsequently, when AEDs are discontinued, relapses are observed in half of the patients. For this form of epilepsy, it is recommended to discontinue AEDs after at least 4 years from the onset of remission.

Treatment for absence seizures

Absence seizure therapy requires careful selection and includes several areas. It is necessary to eliminate all provoking and irritating factors. For example, it is necessary to give up night work, ensure sufficient night sleep, and protect yourself from emotional stress. Anticonvulsant therapy and anticonvulsants are used as treatment. Absence seizures are treated like other forms and types of epilepsy. At the same time, experts emphasize that absence is often explained by lack of sleep, and therefore special attention should be paid to this factor.

Currently, there are no methods that provide effective prevention of absence seizures, since the causes that cause them are mostly unpredictable. However, therefore, the opinion of scientists is ambiguous. There is an opinion that in isolated cases of absence seizure, the progression of the disease can be prevented if you do not drink alcohol and avoid rhythmic photostimulation. It is also necessary to avoid hyperventilation and head injuries. As with any disease, therapy will be more successful if you do not delay your visit to the doctor and start treatment in a timely manner.

Rolandic

Benign childhood partial epilepsy with central temporal peaks (rolandic epilepsy).

Rolandic epilepsy (RE) is an idiopathic partial epilepsy of childhood, characterized by predominantly short hemifacial motor nocturnal seizures, often preceded by somatosensory aura and typical EEG changes. The onset of RE varies in the age range from 2 to 14 years. In 85% of cases, attacks begin between the ages of 4 and 10 years, with a maximum at 9 years. Simple partial (motor, sensory, autonomic), complex partial (motor) and secondary generalized seizures are observed. The most typical are simple partial motor and/or sensory paroxysms. The attack begins with a somatosensory aura: a tingling sensation, numbness on one side in the pharynx, tongue, and gums. Then motor phenomena appear: unilateral tonic, clonic or tonic-clonic convulsions of the muscles of the face, lips, tongue, pharynx, larynx; pharyngo-oral attacks, often combined with anarthria and hypersalivation. At the same time, in their sleep, patients make peculiar throat sounds such as “gurgling”, “grunting”, “gargling”. In 20% of patients, seizures may spread from the facial muscles to the homolateral arm (brachiofacial seizures) and involve the leg in approximately 8% of cases. As the disease progresses, attacks may change direction. Secondary generalized seizures are observed in 20-25% of patients with EC. The duration of attacks with RE is short: from a few seconds to 2-3 minutes. The frequency is usually low - on average 2-4 times a year. In the first months after the onset of the disease, attacks may be more frequent, but over time they occur less and less often, even without treatment. RE paroxysms are “rigidly” connected to the sleep-wake rhythm. The most typical attacks are at night, occurring mainly when falling asleep and waking up. Only 15-20% of patients experience attacks both during sleep and while awake. On the EEG in the interictal period, characteristic “Rolandic” peak-wave complexes are detected with high frequency while the basic activity is necessarily preserved. These complexes are slow, diphasic, high-amplitude peaks or sharp waves (150-300 μV), often followed by slow waves, with a total duration of about 30 ms. These complexes resemble the QRS waves of an ECG. Rolandic complexes are usually localized in the central and temporal region; can be observed both unilaterally (usually contralateral to hemifacial seizures) and bilaterally independently. Typical is the instability of EEG patterns, their variability from one recording to another. Treatment. The basic drug is valproate. The average dosage is 20-40 mg/kg/day in 3 divided doses. If ineffective, switch to carbamazepine - 10-20 mg/kg/day in 2-3 doses. Polytherapy is unacceptable! Complete therapeutic remission is achieved in almost 100% of cases. After 14 years of age, attacks disappear (with treatment or spontaneously) in 93% of patients, and after 16 years - in 98%. Given the absolutely favorable prognosis, some authors suggest not prescribing treatment if a diagnosis of EC is established. This point of view is debatable. We recommend the use of AEDs for patients suffering from endometrial cancer. If the doctor has chosen observation tactics without prescribing AEDs, then all the following conditions must be met:

• absolute confidence of the doctor (better than 2 expert epileptologists) in the diagnosis of EC,
• clinical and EEG manifestations of RE are typical,
• both parents are aware of the diagnosis and agree not to give the child AEDs,
• the patient himself agrees not to undergo treatment, knowing that he may experience epileptic seizures for several years.

Idiopathic partial epilepsy with occipital paroxysms.

Idiopathic partial epilepsy with occipital paroxysms - benign occipital epilepsy (BOE) - is a form of idiopathic localization-related epilepsy of childhood, characterized by simple partial seizures with visual disturbances and the presence of specific peak-wave activity in the occipital leads on the EEG. The disease begins at the age of 2-12 years with two peaks of onset - around 3 and 9 years. Simple partial sensory paroxysms with visual disturbances are typical. Characteristic are simple visual hallucinations, photopsia, visual illusions (macro-, micropsia). Transient amaurosis and homonymous quadrant hemianopsia may occur. During an attack, a versive component with forced turning of the eyes and head is often observed. A focus in the occipital lobe often radiates excitation anteriorly (to the temporal and frontal lobe) with the appearance of complex structural hallucinations; switching off consciousness and the occurrence of secondary generalized convulsive attacks. Typically, attacks occur during sleep, especially when patients awaken. Attacks are often accompanied by migraine symptoms: headache and vomiting. The first attacks in young children are the most severe and lasting (up to several hours or even days). The EEG determines the appearance of high-amplitude peak-wave activity in one of the occipital leads or bioccipital leads independently. The morphology of the patterns resembles that of rolandic epilepsy. Characteristic is the disappearance of epiactivity when recording EEG with eyes open. Differential diagnosis. It should be differentiated, first of all, from symptomatic occipital epilepsy, which occurs with structural damage to the occipital lobes. With symptomatic occipital epilepsy, the age of onset of seizures is not limited; complex partial and secondary generalized seizures are more often observed. The morphology of peak-wave complexes on the EEG is different than in idiopathic occipital epilepsy, and it does not change with eye opening. Neuroradiological examination reveals morphological changes in the occipital lobes of the brain. The prognosis is less favorable. Treatment. The drugs of choice are carbamazepine derivatives. The average daily dose is about 20 mg/kg. If ineffective, valproate is used - 30-50 mg/kg/day. Reserve drug phenytoin – 3-7 mg/kg/day. Treatment is carried out only with monotherapy. Resistant cases must be differentiated from symptomatic occipital epilepsy. Complete therapeutic remission is observed in 95% of cases. At the same time, attacks are more difficult to stop and the doses of AEDs are higher than for rolandic epilepsy.

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Treatment

Therapy for the combination of absence seizures with attacks of other diseases involves prescribing anticonvulsants to the patient. These drugs effectively prevent the development of paroxysms. Treatment of ordinary absence seizures is carried out with the use of ethosuximide, a low-toxic drug of the antiepileptic spectrum. The daily dose is determined based on the patient’s age, weight and clinical picture of the pathology.

Side effects from taking antiepileptic drugs include gastrointestinal disorders, headaches, dizziness, and skin lesions with dermatitis. For this reason, medications are prescribed only after a full cycle of diagnostic studies. Self-administration of pharmacological drugs by a patient can provoke depression of the functions of the central nervous system and respiratory organs.

Treatment of concomitant injuries that occur when the patient falls during attacks is carried out by a therapist, traumatologist or surgeon. Painkillers are prescribed taking into account the pharmacotherapy of the underlying disease to exclude incompatibility of the active substances.