Benign rolandic epilepsy

Generalized convulsive epilepsy (GE) is a group of epilepsies with primary generalized paroxysms: absences, tonic-clonic and myoclonic seizures. Does not include forms with secondary generalized seizures. As a rule, it is idiopathic and less often accompanies other pathologies. Diagnosed based on symptoms and EEG data. Treatment is carried out using anticonvulsants.

To make an appointment with an epileptologist, call tel. 8(969)060-93-93.

Causes

The only etiological factor of the idiopathic variety of the disease is hereditary predisposition. As a rule, the immediate cause is channelopathy, accompanied by instability of nerve cell membranes, which leads to a diffuse spread of epileptiform activity. With primary structural genetic generalized epilepsy in a parent, the risk of having a sick child does not reach 10%.

In 3% of patients, various monogenic variants and polygenic types are detected, resulting from mutations of several genes. Symptomatic HE is provoked by the following circumstances:

• exogenous intoxications: poisoning, some drug addictions;
• neuroinfections: meningitis, encephalitis;
• neoplasms: cerebral lymphomas and gliomas, brain metastases;
• metabolic disorders: hypoxia, lipidosis, hypoglycemia, phenylketonuria.

In childhood, the causes of GE include intrauterine infections, malformations of cerebral structures, fetal hypoxia and birth injuries. Among the generalized forms, idiopathic variants predominate; the symptomatic disorder most often occurs in the form of focal seizures.

Definition

Epilepsy is a chronic brain disease characterized by repeated seizures that arise as a result of excessive neural activity and are accompanied by various clinical and paraclinical manifestations. Among neurological diseases, epilepsy ranks third [5].

The manifestations of epileptic seizures in childhood have significant differences: they often occur atypically, have an abortive course, and changes in the electroencephalogram do not correspond to the clinical picture. For many epileptic syndromes, the genetic nature has been established, new forms of the disease have been described, diagnostic methods have been improved, many antiepileptic drugs have been synthesized and their mechanisms of action have been established, and the effectiveness for individual forms of the disease has been studied. Fortunately, thanks to modern medical advances in the field of epileptology, treatment of most childhood forms has become more effective and allows achieving stable remission in 70-80% of cases. [11,12].

Population-based epidemiological studies suggest that 40–70 people per 100,000 population in developed countries and 100–190 people per 100,000 population in developing countries are diagnosed with epilepsy annually. The Rochester Epidemiology Project, one of the largest and most significant of these databases, found an annual incidence of epilepsy of 52.3 per 100,000 people. In 20-30% of patients, epilepsy is lifelong, despite the fact that the disease is traditionally associated with populations of children and adolescents [1,2,7].

In the pediatric population, epilepsy is more common - 4-5% of the total child population. The highest incidence rates are observed among children of the first year of life [11]. In 70% of patients, epilepsy debuts in childhood and is considered one of the main diseases in pediatric neurology [12]. The frequency of epilepsy in the pediatric population is, according to foreign data, 0.5-0.75% of the child population, and the frequency of febrile seizures (FS) is up to 5%. In Russia, about 800 thousand children and adolescents suffer from active epilepsy, 2/3 of the incidence of epilepsy in our country occurs in childhood

[8,9,13].

Early studies conducted in the United States examining the prevalence of childhood epilepsy in industrial cities found that it varied from 50 to 100 per 100,000 child population. More recent studies have shown a prevalence of 40 per 100,000 population. The highest prevalence of epilepsy is in the first year of life, and is 120 per 100,000 population. Then it decreases and by the age of 10 years it is 40-50 per 100,000 population, and in adolescence - 20 per 100,000 population [20,24,32,34,35,38,43].

Most often, the onset of epilepsy occurs at a young age - up to 16 years with a peak at the age of 9 to 14 years [10]. It is believed that approximately half of all patients become ill before the age of 15. Approximately 75% of patients with epilepsy have seizures in the first 20 years of life. In 29% of cases, epilepsy debuts before the age of 3 years [11,16]. In general, in childhood and adolescence, this disease begins in 70-75% of cases [9,10].

Symptoms

The idiopathic variety first appears in childhood or adolescence. In most patients, the first paroxysm occurs before the age of 21. Cognitive functions are usually preserved. Sometimes there is a transient deterioration, which may have a negative impact on academic performance, but does not entail a significant intellectual decline.

According to the latest data, in children in 3-10% of cases there is a slight deterioration in cognitive functions or mild affective and personality disorders are detected. Focal neurological changes are often absent, and diffuse symptoms are noted.

Secondary GE against the background of anomalies and hereditary pathologies debuts in the first years of life. In other cases, manifestation can occur at any age. The nature and severity of focal and cerebral disorders are determined by the provoking pathology. Adults often show a significant decline in intelligence. Young patients develop oligophrenia.

Symptoms of generalized epilepsy

Based on the previously described types of GE, the following characteristic symptoms can be identified:

• convulsions of varying amplitude and frequency (from simple blinking to spasm of the whole body, followed by twitching of the limbs, with tongue biting and head injuries due to uncontrolled contractions of the neck muscles);
• absence seizures (blackouts);
• disorder of consciousness and memory - with simple seizures, some patients can describe their sensations during an attack, but in other cases they do not remember them. The more often the attacks occur, the faster dementia will occur;
• vegetative manifestations - redness of the face, increased breathing and increased blood pressure;
• the appearance of a migraine-type aura, as described earlier (which is more typical for secondary generalized epileptic seizures).

Tonic-clonic seizures

A tonic spasm is a sharp, prolonged contraction of muscles with the formation of a forced position. Clonic seizures look like short-term, irregular spasms, during which periods of tension and relaxation quickly alternate with each other.

A generalized seizure of epilepsy is accompanied by a fall of the patient followed by the development of a tonic phase lasting from 30 to 40 seconds. After this, a phase of clonic muscle contractions begins, lasting up to 5 minutes. The attack ends with involuntary urination. The whole body relaxes. The patient usually falls asleep.

The first signs of GE

Attacks of generalized epilepsy are completely sudden and impossible to predict. But there are some signs that have manifestations similar to epilepsy, but are not it. They are a consequence of the action of some exogenous factor that adversely affects the functioning of the central nervous system.

• Involuntary muscle twitching, including those that sometimes occur when falling asleep (so-called physiological twitches). Usually at this moment you dream that you stumble or fall from a small height, after which you suddenly wake up, sometimes even screaming.
• Sleep disturbances - nightmares, sleepwalking (sleepwalking) or sleep talking.
• Migraine and accompanying symptoms. It can begin with an aura, during which various perception disturbances occur: visual distortions (atrial fibrillation, flashes, distortion of objects, photopsia, narrowing of visual fields, temporary blindness, etc.), distortion of smell and taste (odors that actually no, a metallic taste appears in the mouth without visible bleeding of the oral mucosa), auditory hallucinations, nausea, numbness/tingling of the extremities.
• Characteristic manifestations of a panic attack are a feeling of fear, a feeling of approaching death, tachycardia, heavy rapid breathing and the feeling that you are watching what is happening as if from the outside.
• Atrioventricular block can be complicated by the occurrence of Morgagni-Adams-Stokes syndrome - fainting caused by a sharp decrease in cardiac output and brain hypoxia, resulting in breathing problems and convulsions.
• The following signs are characteristic of epilepsy - involuntary urination and biting the tongue during sleep. It is possible that the very first attack of generalized epilepsy occurred in a dream.

Diagnostics

Diagnostic measures are carried out by a neurologist or epileptologist. The nature of the disease is established on the basis of anamnesis and electroencephalogram data. In the interictal period with the primary form, the main rhythm is within normal limits, sometimes slightly slowed down. In a secondary disorder, changes are determined by the nature of the causative disease. A distinctive feature of electroencephalograms in both cases is the presence of diffuse peak-wave activity.

To clarify the cause of the disease in symptomatic generalized seizures of epilepsy, additional studies are being conducted. To assess the condition of brain structures, MRI or CT scans are performed. If poisoning is suspected, toxicological tests are performed; in case of dysmetabolic changes, the level of oxygen and sugar in the blood and other parameters are determined. People with a presumably hereditary pathology are referred to a geneticist for consultation and special tests are performed.

GE is differentiated from secondary generalized and focal types of epilepsy, fainting, hypoglycemia, sleepwalking, schizophrenia and hysteria.

The fact of mimicry by focal forms of epilepsy, generalized due to the phenomenon of secondary bilateral synchronization (SBS) and diffuse distribution of epileptic activity with the development of seizures, which can be visually assessed as generalized by kinematics, is widely known. This phenomenon is widespread among symptomatic forms of epilepsy, especially in infancy and early childhood (focal “masks” of Ohtahara, West, Lennox-Gastaut syndromes, etc.), which led to the separation of the group of epileptic encephalopathies from generalized and focal forms in the draft new classification epilepsies and epileptic syndromes and served as the basis for determining the definition of “pseudogeneralized” seizures [3]. At the same time, the opposite phenomenon is also observed - idiopathic generalized epilepsies (IGE) in some cases have focal features in the kinematics of seizures and on the EEG, but their focal nature is excluded with a comprehensive clinical-electro-neuroimaging approach to diagnosis. Most often, such features are observed in patients with juvenile myoclonic epilepsy. In some cases, diagnosing idiopathic generalized epilepsies with focal features is difficult even for an experienced epileptologist. Erroneous prescription of aggravating antiepileptic drugs (carbamazepine) can lead to a significant increase in seizures up to the development of status epilepticus.

The definition of this phenomenon and its definition are proposed for discussion: the phenomenon of secondary focalization

[4] is a clinical-electroencephalographic phenomenon that occurs in idiopathic generalized forms of epilepsy, consisting in the appearance of secondary focal features (clinical and electroencephalographic) in the structure of a generalized epileptic seizure. The criterion for excluding the presence of the phenomenon of secondary focalization is proof of the fact of secondary generalization of the attack with the presence of a regional cortical ictogenic source and establishing a diagnosis of the focal form of epilepsy.

It should be emphasized that the phenomenon of secondary focalization, by definition, is observed exclusively in cases of IGE. This phenomenon contrasts and requires differential diagnosis with the phenomenon of VBS in focal forms of epilepsy, due to which, in particular, “pseudogeneralized” seizures occur - i.e. in fact, it is secondary generalized seizures, but the focal component is often absent due to the rapid generalization of the ictal process. The phenomenon of secondary focalization demonstrates the reverse process - primary generalized activity acquires focal features. With the VBS phenomenon (Tückel-Jasper effect), on the contrary, focal epileptiform activity acquires generalized features due to the involvement of contralateral areas with subsequent diffuse spread [6].

The purpose of the study was to study idiopathic generalized forms of epilepsy with the presence of focal features in the structure of epileptic seizures, identified through the method of video-EEG monitoring.

Material and methods

The study included cases of idiopathic forms of epilepsy in patients undergoing examination and treatment at the clinical sites of the Russian National Research Medical University. N.I. Pirogov over the past 5 years. A total of 180 patients were examined, 100 women and 80 men.

A mandatory criterion for inclusion in the study was the fact of visualization of epileptic seizures during video-EEG monitoring. Patients with IGE in remission or with unrecorded attacks were not included in the study.

Exclusion criteria were idiopathic mixed forms of epilepsy, combining the presence of generalized and focal types of seizures (such as, for example, a combination of childhood absence epilepsy with the rolandic form). Also, in order to avoid double controversial interpretation, cases of double pathology were excluded from the study - a combination of idiopathic and symptomatic components and the genesis of the disease. Exclusion criteria also included persistent regional epileptiform changes in the background recording, identification of the presence of focal epileptic seizures, and establishment of the presence of “pseudogeneralized” seizures. The presence of pronounced cognitive defects, persistent clear focal changes in the neurological status (with the exception of the so-called nonspecific microsymptoms), focal structural defects of the brain during neuroimaging were also exclusion criteria.

Thus, for the “purity” of the study, patients were included in it whose idiopathic nature of epilepsy was not in doubt and was confirmed by a comprehensive clinical and electroneuroimaging diagnostic approach. Strict criteria for selecting patients included in the study minimized the likelihood of mimicry of generalized forms by focal forms of epilepsy (i.e., “pseudogeneralized” masks of IGE were excluded).

Video-EEG monitoring of patients was carried out using a portable video-EEG monitoring system based on the encephalograph-recorder "Encephalan-EEGR-19/26" ABP (Medicom MTD, Taganrog) and in the medical department using video-EEG monitoring systems "Encephalan-121" -03" (Medicom MTD, Taganrog), Grass-Telefactor Aura and Beehive ("Grass-Telefactor", USA).

Results and discussion

The forms of epilepsy identified during the observation of 180 patients with various forms of IGE with recorded epileptic seizures during video-EEG monitoring are presented in Table. 1.

The small number of cases of epilepsy with isolated generalized seizures (GSE) in our study is due to the low probability of recording a generalized clonic-tonic-clonic seizure (GCTS) during video-EEG monitoring (compared to absence and myoclonic seizures in other forms of IGE). All 3 cases of fixation of GCTC were observed exclusively in girls, in 1 of the cases - with a provocation to rhythmic photostimulation (RPS), and in 2 other patients with catamenial course of epilepsy, the fact of fixation of attacks was due to the timing of the study (video-EEG monitoring) being linked to menstrual period phase of the cycle. In the structure of attacks in 2 cases there were no focal features, and a versive component was present in 1 case.

The case of fixation of GCTC in juvenile absence epilepsy (JAE) was a single case and did not have focal features. All patients ( n

=21) typical absence seizures without clinical focal features were observed, although in almost half (
n
=9) of them the initial component of ictal discharges was lateralized in nature with a predominance in the frontal regions.
Moreover, in the group of patients with IGE with phantom absence seizures ( n
= 5), ictal patterns with lateralization phenomena and frontal predominance were noted.

In childhood absence epilepsy (CAE), all 29 patients with this form of the disease had typical absence seizures, mostly complex, while in 5 cases a versive component was observed in the structure of absence seizures, in 1 - rotatory nystagmus, in 6 - pharyngo-oral automatisms, in 2 - gestural automatisms, in 2 cases - stool masturbation and in 2 more cases - urination during attacks.

The high percentage of juvenile myoclonic epilepsy (JME) in this population is due to 2 reasons: firstly, with JME, along with absence forms, there is the highest probability of seizures being recorded by video-EEG monitoring in combination with a high probability of provoking myoclonic seizures in RFS and on background of early awakening. JME is also characterized by frequent “breakdowns” of remission, which sometimes remain unrecognized without the use of video-EEG monitoring (the phenomenon of “pseudo-remission”) [2]. Secondly, in many patients who, before overnight video-EEG monitoring, were diagnosed with JAE and epilepsy with isolated GSP, the presence of myoclonic seizures was proved during the study, and a diagnosis of JME was made.

In all 92 patients with JME, myoclonic seizures were recorded during video-EEG monitoring (in 29 patients there was clear lateralization in the structure of myoclonic seizures, and in 2 cases myoclonic seizures were unilateral in nature). At the same time, in 31 cases the phenomenon of “pseudo-remission” was verified - epileptic seizures were not noticed by patients and their relatives, and a false impression was created about the effectiveness of the antiepileptic drugs (AEDs) taken. In 27 patients, the presence of myoclonic seizures was first established, which ultimately led to a revision of the diagnoses of JAE and epilepsy with isolated GSP in these patients. Fixation of GSP was noted in 8 cases of JME, and these types of seizures should be regarded as myoclonic-tonic-clonic seizures (primary myoclonic phase). In 5 of 8 cases (62.5%) focal features were noted in the structure of attacks in the form of a versive component, while in 1 of these 4 cases, along with the versive component, the phenomena of “staring” (“staring”), automatisms and a dystonic attitude were noted hands, there was also 1 case of lateralization of the clonic component of the attack - a “pseudogemiconvulsive” attack.

The focal features presented in various forms of IGE are summarized in Table. 2

Discussion

Thus, IGE often have focal features in the kinematics of seizures and on the EEG, while their focal nature was excluded with a comprehensive clinical-electro-neuroimaging approach to diagnosis.

As an example of the phenomenon of secondary focalization, we present a clinical observation and a selection of illustrations of the ictal EEG of one of the patients.

Patient C

., 13 years old. Diagnosis: juvenile myoclonic epilepsy.

From the anamnesis: from the 2nd normal pregnancy. The perinatal history is not burdensome. She grew and developed according to her age without any special features. He studies in a regular school, his academic performance is good. At the age of 13 years, a generalized tonic-clonic seizure (GTCS) occurred for the first time while awake (the girl was on the 2nd day of menstruation). The older sister had the onset of GTCS and absence seizures from the age of 13, the presence of myoclonic seizures was not noted, remission for 6 years on Depakine at a dose of 900 mg per day. The presence of other cases of epilepsy in the family is denied.

During video-EEG monitoring 3 weeks after the onset of the first attack, during evening tests, upon presentation of rhythmic photostimulation, provocation of myoclonic attacks was noted, involving the facial, cervical muscles and muscles of the upper shoulder girdle. Against the background of a light stimulus with a frequency of 20 Hz, a provocation of a generalized myoclonic-tonic-clonic attack was noted with the appearance of focal features during the attack. After applying RFS with a frequency of 20 Hz, the appearance of generalized spike-wave and polyspike-wave activity was noted (Fig. 1) with clinical manifestations in the form of myoclonus of the eyelids and upper shoulder girdle.

Figure 1. EEG of patient S., 13 years old. Ictal recording of a generalized myoclonic-tonic-clonic seizure. Myoclonic seizures were the initial (myoclonic) phase in the development of a generalized myoclonic-tonic-clonic seizure, while the initial primary generalized nature of the seizure was beyond doubt. Following the myoclonic phase and before the development of the classical tonic phase, the inclusion of two more phases in the structure of the attack was noted. Following myoclonus, a dialeptic phase began (fixation of posture and gaze), which was accompanied on the EEG by diffuse irregular peak- and polypeak-wave discharges with frontal predominance (Fig. 2).

Figure 2. EEG of patient S., 13 years old. Ictal recording of a seizure (continued). Then the tonic phase of the attack with the presence of a focal right-sided adversive component and “staring” elements. Over a limited period of time, automatisms were noted (fiddle with a handkerchief held in the right hand and a rotational component in the movements of the left hand), which then gave way to dystonic hand settings. On the EEG, against the background of a generalized ictal pattern, the appearance of regionally accentuated alpha-like ictal activity of an arch-like nature was noted with the inclusion of a very fast spike-wave component with “interest” in the left central-parietal-temporal region (contralateral to the versive component of the seizure, which is typical for focal adversive seizures ) - the phenomenon of “secondary focalization” (Fig. 3).

Figure 3. EEG of patient S., 13 years old. Ictal recording of a seizure (continued). There was almost an overlap of the focal ictal pattern in a certain part of the pattern of a generalized myoclonic-tonic-clonic seizure, namely in the initial period of the tonic phase. The subsequent “classical” tonic phase of the attack (Fig. 4) was characterized by the presence on the EEG of generalized polyspike and island wave activity with transformation into fast peak and polyspike wave activity (7-5 ​​Hz).

Figure 4. EEG of patient S., 13 years old. Ictal recording of a seizure (continued). Against the background of the clonic phase of the attack (Fig. 5), the EEG shows a further increase in the amplitude of peak-polypeak-wave complexes with a gradual slowdown of their frequency characteristics (from 5 to 3 Hz).

Figure 5. EEG of patient S., 13 years old. Ictal recording of a seizure (continued). Subsequently, cluster polypeak-wave discharges were observed with a slowdown in frequency characteristics closer to the end of the attack (Fig. 6), which accordingly clinically manifested as cluster clones.

Figure 6. EEG of patient S., 13 years old. Ictal recording of a seizure (end). At the end of the attack, following the last cluster clone, there was a post-attack flattening of the EEG curve leading to diffuse post-attack delta slowing (Fig. 7), against the background of which the patient fell asleep.

Figure 7. EEG of patient S., 13 years old. Post-ictal slowing. An interesting fact is that in the recording of the entire post-attack night sleep, not a single epileptiform discharge was noted, as, indeed, against the background of morning awakening (morning functional tests were not carried out due to the high risk of repetition of the above clinical events). The girl also had preserved background bioelectrical activity with no signs of epileptiform activity in the evening background EEG recording before the start of tests with rhythmic photostimulation.

Thus, the phenomenon of secondary focalization in cases of IGE with the presence of generalized clonic-tonic-clonic and myoclonic-tonic-clonic seizures is clinically expressed in the appearance of focal features (most often in the form of a versive component) in the structure of a primary generalized epileptic seizure. It is as if a focal seizure is superimposed on the kinematic matrix of a generalized clonic (myoclonic)-tonic-clonic seizure. On the EEG, the phenomenon of secondary focalization consists in the appearance in the structure of the pattern of a generalized attack of focal features that correlate with the clinical picture of the attack (namely, the appearance of contralateral focal features).

The clinical phenomenon of secondary focalization in the structure of the GSP can manifest itself in the form of: 1) a versive component (deviation of the eyes, head, arm, body to the side); 2) lateralized tonic-automotor component (up to the identification of dystonic placement of the hands, characteristic of focal attacks of temporal and frontal origin, contralateral to the accentuation of the ictal pattern and ipsilateral automatisms); 3) lateralization of clones in the structure of the clonic phase of a generalized seizure (“pseudo-hemiconvulsive” nature of an epileptic seizure); 4) dialeptic component with the “staring” phenomenon.

Of course, varying degrees of such clinical-electroencephalographic correlation are possible. Dissociation is possible in the form of unilateralization of clinical focal features and regional accentuation in the structure of the generalized ictal pattern, which is actually possible in cases of patterns of focal epileptic seizures.

There may be an isolated clinical phenomenon of secondary focalization without the appearance of a regional accent on the EEG. Or an isolated electrophysiological pattern of secondary focalization in the form of a regional accent of the ictal pattern against the background of a typical symmetrical picture of a generalized seizure.

Simple absence seizures (isolated freezing) cannot clinically demonstrate the phenomenon of secondary focalization by definition. Focal features in the structure of complex absence seizures manifest themselves in the form of a versive component (deviation of the eyes and/or head to the side), lateralization of automatisms during an absence seizure with an automotor component, and the appearance of lateralized myoclonus during myoclonic absence seizures.

With myoclonic seizures (in particular, with JME), a lateral accent or a clear unilateral character of epileptic myoclonus is often noted. Naturally, this fact requires the exclusion of the “symptomatic mask” of JME and the phenomenon of VBS on the EEG. Such patients require high-resolution neuroimaging and correlation of the results obtained with data from continued video-EEG monitoring. During myoclonic seizures and myoclonic absences, cases of unpleasant sensations, current running through the body, visual auras, feelings of fear and epigastric aura were noted (1 patient).

On EEG in cases of absence and myoclonic seizures, the phenomenon of secondary focalization manifests itself in the form of the presence of an unstable initial regional accent in the structure of the ictal pattern, the appearance of a regional accent in the structure of subsequent ictal discharges, post-ictal regional discharges in combination with regional slowing (usually in the frontal regions of the hemispheres). It should be especially emphasized that the presence of a persistent epileptic focus in the background and a regional initial accent of absence and myoclonic seizures indicates the phenomenon of VBS, and the seizures themselves should be regarded as “pseudogeneralized”, according to the definition proposed by K.Yu. Mukhin [3]. The phenomenon of secondary focalization in IGE is a different and essentially opposite process.

The mechanism of the secondary focalization phenomenon is not precisely known and requires continued fundamental research in this area. Probably, the difference in the distribution and persistence of ictal activity in different hemispheres and cortical regions during the course of a generalized attack plays a role in its genesis due to the individual characteristics of neuronal networks, microresidual organic background, the possible presence of microdysgenesis and characteristics of conduction systems, blood supply and biochemical neuronal processes in different hemispheres for each individual patient.

All these facts contribute to the “blurring” of clear taxonomic boundaries of generalized and focal forms of epilepsy and the division of seizures into generalized and focal, and also demonstrate the processes of convergence in epileptology. Currently, the generally accepted classification is being revised in favor of focal and systemic forms of epilepsy. At one time this issue was raised by V.A. Karlov et al. [1], who proved the secondary generalized nature of absence seizures, which were previously considered an absolutely typical example of primary generalized types of seizures. There are works that prove the “interest” and presence of microdysgenesis of the frontal cortex in patients with JME [5].

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Treatment

Idiopathic generalized epilepsy usually responds well to treatment. In 70% of cases, monotherapy with anticonvulsants is sufficient: valproate, levitiracetam, ethosuximide, topiramate. In case of low effectiveness, combination regimens are used, involving the simultaneous use of two drugs. When choosing a drug, take into account that some medications are contraindicated in some forms of HE, but are effective in others.

The type and dose of the antiepileptic drug is determined individually. They begin to reduce the dosage only three years after the complete absence of paroxysms against the background of regular medication use. In secondary forms, the prescription of anticonvulsants is supplemented with the treatment of the underlying pathology.

The outcome is largely determined by the type of GE. In the idiopathic form, the prospects are usually favorable - there is no delay in mental development, patients retain their ability to work. The negative point is the high probability of relapse after reducing the dose or discontinuing medications. The prognosis for the symptomatic variant depends on the course of the causative pathology. A number of patients exhibit high resistance to anticonvulsant therapy.

Prevention of primary HE has not been developed. Measures to reduce the level of injuries, timely diagnosis and treatment of brain diseases that can provoke generalized attacks help reduce the likelihood of a secondary variant.

You can make an appointment with a doctor by phone 8(969)060-93-93.

Prognosis of generalized epilepsy

Epilepsy is still a particularly important pathology that radically changes the life of the person diagnosed with it. At our level of medicine, a cure for this disease has not yet been found; a number of restrictions are imposed on the patient: he cannot drive a vehicle, he should avoid places with unexpected flashes of light. The ability to work of these individuals depends on the frequency and timing of attacks. It is prohibited to work near fire, at heights, in burning workshops, near moving machinery, as well as activities that require quick reaction and attention.

No less important is the problem of stigmatization. Correct therapy with antiepileptic drugs increases the interictal period. The prognosis depends on the form of GE. Idiopathic is the most favorable, since it is not accompanied by mental disorders. Symptomatic completely depends on the disease that caused it. But with the right therapy, it is possible to significantly improve the patient’s quality of life and minimize the number of seizures.

The Yusupov Hospital has many years of experience in treating this disease, which will help choose an individual approach to each patient with epilepsy so that he can lead a normal life even with such an illness. It is necessary to follow all instructions from your doctor and not skip medications to avoid worsening the condition.