Myoclonic spasms are characterized by short-term muscle contractions of the body. This syndrome is accompanied by sudden shudders, convulsions, hiccups, etc. Convulsive spasms can occur both during sleep and during active physical activity of a person. Provocateurs of a sudden attack can be sharp sounds, bright light and even a sudden touch. In children, a similar reaction most often occurs when they are very frightened.

Reasons for the development of the disease

Currently, there are quite a lot of diseases that are accompanied by short-term seizures. If such symptoms occur, the reasons for its development should be found out.

The most common factors that contribute to the occurrence of myoclonic seizures are:

• increased physical activity;
• stress and emotional distress;
• insufficient intake of vitamins and minerals into the body;
• long-term use of caffeine-containing drugs;
• nicotine addiction;
• negative reaction to certain medications (estrogen, corticosteroids).

Quite often, cramps that are provoked by such reasons affect the fingers, eyelids and calves of the legs. As a rule, such a cramp is short-lived and stops on its own, without requiring serious treatment.

In addition, there are more serious factors that provoke myoclonus. These include:

• dystrophic changes in muscle tissue;
• the development of amyotrophic sclerosis, which is accompanied by the death of nerve cells;
• spinal muscular atrophy;
• muscle nerve injuries;
• autoimmune diseases (Isaac syndrome), etc.

Despite the fact that myoclonic seizures, in most cases, do not pose a danger, any manifestations of this nature require consultation with a doctor and a thorough examination of the patient to exclude more serious symptoms.

Symptoms of an attack

A feature of myoclonic spasms is the absence of pain. Spasms can affect one or a group of muscles.

Visually, slight twitching of the face, hands, eyelids, etc. is observed. Their duration does not exceed 1 minute and most often such manifestations appear in a dream.

The following symptoms are observed with myoclonic spasms:

• numbness and muscle tension in the head and neck area;
• upper eyelid tic;
• involuntary muscle contractions;
• slight tremor of the limbs;
• symptom of “restless legs” (swelling, cramps, etc.).

A myoclonic cramp in the calf area resembles a regular one, but there is a significant difference between them: with myoclonus there is no loss of consciousness, unlike a convulsive syndrome.

Course of an attack in childhood

In children, myoclonic spasms can be much more severe than in adult patients. Often myoclonus is accompanied by a generalized seizure, reminiscent of minor epilepsy with short-term loss of consciousness and convulsions.

Myoclonic epilepsy, in addition to seizures, can occur with absence seizures (symptoms of a type of short-term epilepsy), which are most often observed at the age of 4 years, but disappear as they grow older. These attacks are characterized by a short-term stupor of the patient, with his eyes open, but the person loses consciousness. Often, absence seizures in children can be a harbinger of juvenile myoclonic epilepsy.

In childhood, myoclonus is accompanied by tearfulness, emotional instability, and heightened impressionability, but with timely treatment this condition quickly stabilizes and the prognosis for recovery is favorable.

Classification of convulsive syndrome

Currently, there is the following classification of myoclonus:

• Physiological. This type of myoclonic spasm is caused by physical fatigue, emotional and sensory outbursts. As a rule, physiological myoclonus is manifested by an attack of hiccups, night shudders and calf cramps.
• Epileptic. The main factors in the development of epileptic myoclonus are diseases that can be accompanied by seizures. The symptoms of the disease manifest themselves quite clearly and gradually progress.
• Essential. In this case, the cause of the myoclonic attack is a hereditary factor. The first symptoms of the disease appear at an early age, and their peak occurs during puberty.
• Symptomatic. In this form, the main symptom of myoclonus is persistent ataxia of the soft palate. Based on localization, cortical, subcortical, peripheral and segmental foci are distinguished. The distribution of muscles is produced by segmental, focal and multifocal myoclonus with rhythmic and arrhythmic contractions.

Diagnostic methods

In order to prescribe adequate treatment, it is necessary to carry out diagnostic measures that will help exclude serious diseases, since in some cases myoclonus can be disguised as other, more severe manifestations. This condition especially affects children, as their symptoms are much more severe.

At the first visit to the doctor, a visual examination of the patient is performed and a detailed medical history is obtained, determining the possibility of genetic transmission, duration and frequency of myoclonic attacks, which makes it possible to differentiate seizures and their causes.

For a more accurate diagnosis, the following examination methods may be prescribed:

• blood sampling for biochemical analysis;
• X-ray examination of the head area;
• electroencephalography.

Based on the data obtained and external examination, the neurologist makes a final diagnosis and prescribes all necessary therapeutic measures.

Treatment strategy

If myoclonic seizures are benign, if the attack occurs in response to natural stimuli (overexertion, fear, etc.), serious treatment is not required. For episodic manifestations, it is recommended to take sedative medications that normalize the nervous system. Sometimes taking tincture of valerian, motherwort or valocordin is quite enough.

For negative symptoms, which are aggravated by serious problems in the functioning of the brain and central nervous system, complex therapy with anticonvulsants is prescribed:

• in order to block the transmission of nerve impulses, nootropics are prescribed (Piracetam, Cinnarizine, Phenotropil, Nootropil, etc.);
• muscle relaxation and reduction of central nervous system activity can be achieved with the help of muscle relaxants and sedatives (Andaxin, Seduxen, etc.);
• for severe and frequent seizures, as well as to prevent new seizures, injections of Oxybutyrate, Haloperidol and Droperidol are prescribed;
• in severe cases, corticosteroids are prescribed, but only for a short course and under the supervision of the attending physician.

It must be remembered that preventing the development of convulsive syndrome, as well as eliminating the causes that provoke this condition, is of great importance. For example, if children experience frequent nighttime shudders, it is recommended to watch only calm TV shows before bed, as well as avoid active games that increase nervous excitability.

Correctly administered therapy and constant monitoring of the patient can reduce the frequency of myoclonic attacks several times. At the same time, a person leads a full life, without feeling discomfort when communicating with loved ones. In this case, the prognosis for recovery is favorable.

ormyoclonic seizures — These are sharp, momentary, sudden, involuntary, repeated flexion contractions (or twitches) of muscle groups, like a wince, that involve the whole body or part of it, most often the arms or upper torso.

Myoclonic seizure is a generalized .

Myoclonic seizures cause a person to suddenly fall, the so-called attacks of falls " The falling attack lasts 1-2 seconds, starts and stops abruptly. During a fall attack, there is a high risk of getting a traumatic brain injury or fractures or bruises.

For myoclonic spasms in the arms a person suddenly drops objects, for example, spills sugar, throws away a spoon. Sometimes only slight contractions occur in the hands, felt only by the sufferer himself. Characteristically, myoclonus intensifies in the morning (1-1.5 hours after waking up), especially with lack of sleep. People around associate such twitching with neurotic disorders. More often they consult a doctor only after the onset of generalized tonic-clonic seizures with a fall and loss of consciousness. Already at a neurologist's appointment, when questioning patients, it is possible to identify previous myoclonic attacks. Next, myoclonus should be recorded and noted daily.

Such myoclonic spasms characteristic of myoclonic epilepsy .

On myoclonic seizures in myoclonic epilepsy we see discharge polypik - wave . On video-EEG monitoring, the polypik-wave discharge synchronously coincides with a myoclonic attack.

The video from YouTube demonstrates an example of myoclonic seizures.

Benign myoclonus

The presence of myoclonus does not always mean that the patient has epilepsy.

Non-epileptic myoclonus or benign myoclonus can be detected in some neurological pathological conditions and in healthy people.

Causes of benign myoclonus may be: severe progressive degenerative diseases of the brain, damage to the brain stem and spinal cord, as well as acute ischemic-hypoxic damage to the brain.

Most often, almost every person observes myoclonus in himself or in others when falling asleep ( hypnagogic myoclonus or night shudders ). They are considered an absolutely normal physiological symptom. Some people are like this shuddering when falling asleep significantly expressed. In such cases, it comes to the need for video - EEG - monitoring to exclude the epileptic genesis of myoclonus. Myoclonus of sleep onset does not require any medications.

Myoclonus cause

What diseases can be manifested by myoclonic seizures?

- In patients with diffuse damage to the gray matter of the brain: storage diseases, infectious diseases (for example, Creutzfeldt-Jakob disease, subacute sclerosing panencephalitis).
- Against the background of metabolic disorders (uremia, hypoxia, hyperosmolar conditions, paraneoplastic syndromes).
— Against the background of progressive neurological diseases: progressive myoclonic epilepsy with or without Lafora bodies.
Manifestation of primary generalized epilepsy: juvenile myoclonic epilepsy, or absence seizures with a myoclonic component.
In newborns, they are associated with neurodegenerative conditions (for example, gangliosidoses: Tay-Sachs disease, Alpers disease).

What conditions should myoclonic seizures be distinguished from?

Differential diagnosis myoclonus is carried out between symptoms:

myokymia,

focal motor seizures in epilepsy,

tic hyperkinesis,

benign myoclonus when falling asleep,

hyperreaction (hyperexflexion) when frightened.

Tremor(lat. tremor- trembling) - fast, rhythmic, short movements of the limbs or torso caused by muscle contractions. May be normal with fatigue, strong emotions; as well as in pathologies, for example, in Parkinson's disease.

Tiki- These are fast, stereotyped and short-term movements. Tics are conditionally voluntarily controlled, violent: a person is not able to overcome or stop them. For a few minutes, patients can stop the tic, making efforts to overcome significant internal tension.

T iki look as normal, but involuntary or obsessive movements: blinking, sniffing, coughing, scratching, facial movements (wrinkling the forehead, twisting the mouth), adjusting clothes or hairstyles, shrugging, vocalisms in the form of involuntary sounds, shouting. These are very common symptoms, so almost anyone can be diagnosed with Tiki. Tiki increase with excitement, decrease with distraction, physical work, concentration on something else, disappear in sleep.

Hyperexlexia - a pathologically enhanced reaction that occurs to an unexpected stimulus (shuddering from fear).

Every person shudders periodically. But with hyperexlexia, people almost jump from a slight rustle. This is an innate feature of the nervous system.

Myokymia(twitching) eyelids are repeated contractions of the orbicularis oculi muscle, located in the thickness of the eyelids. Blinking is often called a tic in everyday life, but it is not so. Tics can be demonstrated (in response to a request to show what kind of tics the patient has, he easily depicts them). Myokymia cannot be shown arbitrarily. The small muscles of the eye contract involuntarily. Patients say: “My eye twitches.”

Tetany(ancient Greek τέτανος - cramp, tension) - convulsive attacks caused by a violation of calcium metabolism in the body, associated with a deficiency of the function of the parathyroid glands (usually when they are damaged during surgery) or due to dehydration due to repeated vomiting or diarrhea.

Tetany is a common complaint in children, adolescents and adults - “cramping the calf muscles” during the day and more often during sleep. Painful cramps in the legs, stop on their own or after rubbing or shaking the limb. They are observed in almost all people at different periods of life. They often go away after using calcium supplements.

Focal seizures - the most common manifestation of epilepsy. Partial seizures occur when neurons in a specific area of ​​the brain hemisphere are damaged. Focal seizures are simple partial, complex partial and secondary generalized:

• simple focal seizures - with simple partial seizures there is no impairment of consciousness
• complex focal seizures - attacks with loss or change of consciousness are caused by certain areas of overexcitation and can become generalized.
• secondary generalized seizures - characteristically begins in the form of a simple partial seizure, followed by the spread of epileptic activity to the entire brain and manifested by muscle spasms of the whole body with loss of consciousness.

If epiactivity comes from the motor cortex, then seizures manifest themselves as clones in individual muscle groups. These clonic simple partial seizures in focal epilepsies are clinically similar to myoclonic seizures in myoclonic epilepsies.

Benign myoclonus on sleep – physiological shudders of the whole body or parts of it at falling asleep(hypnic twitching). Typical for most people.

In young children, startling during sleep interferes with restful sleep. Children wake up abruptly and cry. Simple actions help improve sleep: swaddling babies tightly, covering them with a heavier blanket, and you can also tuck the edges of the blanket under the mattress.

In the video taken from YouTube you can see an example of normal physiological sleep accompanied by benign sleep myoclonus.

So, we found out what it is myoclonic spasms, causes of myoclonic seizures; what types of non-epileptics are there? benign myoclonus. Revealed differences between myoclonus for various pathological conditions: tremor, myokymia, focal motor seizures in epilepsy, tic hyperkinesis, tetany, benign sleep myoclonus, hyperreaction (hyperexlexia) in fear.

Looked at video myoclonic spasms in juvenile myoclonic epilepsy and video Physiological startles during sleep in a healthy child . And all these different conditions are similar to simple twitches; an epilepsy specialist can figure out the diagnosis. If myoclonus occurs, consult a neurologist.

Catad_tema Epilepsy - articles

Levetiracetam in the treatment of juvenile myoclonic epilepsy (preliminary results)

K.Yu. Mukhin, M.D. Tysyachina, A.S. Petrukhin
Department of Neurology and Neurosurgery, State Educational Institution of Higher Professional Education, Russian State Medical University of Roszdrav; Center for Pediatric Neurology and Epilepsy, Moscow

Levetiracetam In Treatment Of Juvenile Myoclonic Epilepsy (Preliminary Results)

K.Yu. Mukhin, M.D. Tysyachina, A.S. Petrukhin

The aim of this study was to investigate the efficacy and tolerability of levetiracetam (Keppra, UCB) in patients with juvenile myoclonic epilepsy (JME). We examined 12 patients with an established diagnosis of JME aged 14–22 years, 4 men and 8 women. Keppra was prescribed in combination with other AEDs (valproate, suxilep) in 3 cases and in monotherapy in 9 cases (of which in 3 - in initial monotherapy). Follow-up period was from 7 months. up to 3 years. Persistent relief of epileptic seizures was found in 100% of cases, complete blocking or a pronounced decrease in the index of interictal epileptiform discharges on the EEG - in 75%. In 5 out of 6 patients, Keppra significantly reduced the manifestations of photosensitivity, both according to the clinical picture and according to EEG results. The effect of Keppra on epileptiform activity was less pronounced in the group of patients receiving polytherapy (combination with valproate or suxilep) and in the presence of absence seizures (2 patients). Side effects of Keppra therapy were noted in only one patient (8%) in the form of the Landolt phenomenon of forced normalization.

Keywords: epilepsy, juvenile myoclonic epilepsy, treatment, levetiracetam.

The aim of the study was to investigate the efficacy and tolerance of levetiracetam (keppra, UCB) in patients with juvenile myoclonic epilepsy (JME). Twelve patients diagnosed with JME, aged 14 to 22, were examined, including 4 males and 8 females. Keppra was combined with other anti-epileptic drugs (valproates, suxilep) in 3 cases, while in 9 cases it was administered as monotherapy (including initial monotherapy in 3 cases). The follow-up period varied from 7 months to 3 years. A stable relief of epileptic seizures was acknowledged in 100% cases; a complete blocking or an expressed reduction of the interictal epileptiform discharge index in EEG was achieved in 75% of patients. Keppra definitely reduced manifestations of photosensitivity in 5 out of 6 patients, which was proven both by the clinical presentation and EEG data. The impact of keppra on epileptiform activity was less expressed in the group of patients receiving polytherapy (combined with valproates or suxilep) and in cases with absences (2 patients). Side effects of keppra therapy were observed only in 1 female patient (8%), in the form of the Landolt’s forced normalization phenomenon.

Key words: epilepsy, juvenile myoclonic epilepsy, treatment, levetiracetam.

Juvenile myoclonic epilepsy (JME) or Janz syndrome is a form of idiopathic generalized epilepsy characterized by its onset in adolescence with the onset of massive myoclonic seizures, occurring mainly after the patient awakens. In modern literature, the disease was first described by D. Janz and W. Christian in 1957 under the name “impulsive petit mal.” Since then, a large number of publications on this syndrome have been published in our country and abroad, however, establishing an accurate diagnosis is still very difficult. The main mistake of doctors is a superficially collected anamnesis, focusing attention in the medical history on generalized convulsive seizures (GSE) and losing sight of myoclonic seizures (MS). Panayiotopoulos S.P. et al. (1991) in London conducted a special statistical study of errors in the diagnosis of JME. The authors noted that out of 70 patients they examined, the correct diagnosis was not established in 66 (91.4%!). Moreover, 1/3 of these patients were repeatedly examined and treated in leading neurological clinics in the UK. According to the authors' observations, JME was correctly diagnosed only after an average of 8.3 years from the onset of the disease and 17.7 months later. from the moment of visiting a specialized neurological clinic. However, JME is a very common form of epilepsy and probably one of the most common within generalized epilepsies. Its frequency among all forms of epilepsy is 5–12%, and among idiopathic generalized forms - up to 23%.

The onset of JME varies from 7 to 21 years with a maximum in the age range of 11–15 years. MP is an obligate type of seizures in this disease. Myoclonic paroxysms are characterized by lightning-fast twitching of various muscle groups; they are often bilateral, symmetrical, single or multiple, varying in amplitude; often occurring in a series of salvos. Myoclonus is localized mainly in the shoulder girdle and arms, mainly in the extensor muscle groups. In 30% of patients, myoclonic attacks involve the muscles of the legs, while the patient feels a sudden blow to the knees and slightly squats or falls (myoclonic-astatic attacks). Consciousness was preserved during myoclonic attacks. Myoclonic seizures occur or become more frequent in the first minutes and hours after patients awaken. Decreased level of wakefulness, drowsiness, yawning, closing the eyes - these factors often increase the likelihood of attacks occurring in the morning. In 90% of cases, myoclonic seizures are combined with hypersensitivity awakening. A generalized seizure may be preceded by a series of myoclonic paroxysms. This type of seizure is called clonic-tonic-clonic. In 40% of patients, short absence seizures of the juvenile (non-picnoleptic) type occur. The most important factors provoking attacks in JME are sleep deprivation and sudden violent awakening. In some patients, myoclonic seizures occur solely due to lack of sleep. Approximately 1/3 of JME patients (most often female) have photosensitivity. There may be an increase in the frequency of GSP and myoclonic seizures in the perimenstrual period. During a neurological examination of patients, there are no pathological changes, and cognitive impairment is not typical. Some patients have a high level of anxiety and neuroticism, and a tendency to depressive reactions. A characteristic EEG pattern in patients with JME is short discharges of generalized fast peak/polypeak-wave activity, sometimes with some advance in the frontal leads (Fig. 1). It is provoked by rhythmic photostimulation and closing the eyes. Epileptiform activity on EEG is detected in 80–95% of patients in the interictal period. The main background recording activity is always preserved. There are no changes on neuroimaging.

Rice. 1. Patient G.A., 17 years old. Diagnosis: Juvenile myoclonic epilepsy.

JME has a favorable prognosis: patients have no cognitive impairment, and attacks in the vast majority of cases are controlled by treatment with antiepileptic drugs (AEDs). At the same time, patients are forced to take AEDs for many years, since discontinuation of therapy, even with many years of remission, in the highest percentage of cases leads to relapse of attacks. The frequency of relapses after discontinuation of treatment in patients with JME is, according to various authors, from 50% to 100%.

Traditionally, the treatment of JME in the twentieth century was carried out with valproic acid drugs. However, in recent years, new highly effective broad-spectrum AEDs (lamotrigine, topiramate, levetiracetam) have been synthesized, and their effectiveness in JME has been shown in individual publications. In addition, a large amount of data has accumulated indicating the lack of effectiveness of valproates and their high toxicity, especially in women. All this predetermined the search for optimal AEDs in the treatment of JME.

The aim of this study was to investigate the effectiveness and tolerability of levetiracetam (Keppra, UCB) in patients with juvenile myoclonic epilepsy.

We examined 12 patients with an established diagnosis of JME aged 14–22 years, 4 men and 8 women. Keppra was prescribed in combination with other AEDs (valproate, suxilep) in 3 cases and in monotherapy in 9 cases (of which 3 in initial monotherapy). In 6 out of 9 cases, monotherapy with Keppra was prescribed instead of valproic acid (Depakine). The effect of Keppra on the frequency and nature of various types of attacks, EEG data, as well as drug tolerability were analyzed. All patients underwent video-EEG monitoring (VEM) before the examination and over time. Follow-up period was from 7 months. up to 3 years.

results

The age of onset of attacks in the examined patients ranged from 7 to 16 years (average - 11.7 years). All 12 patients had an obligate type of seizures in JME - myoclonic paroxysms. Generalized tonic-clonic and clonic-tonic-clonic seizures were observed in 9 cases, and typical absence seizures - in 2 cases. Also, 3 patients had a special type of seizure - epileptic myoclonus of the eyelids.

Thus, exclusively myoclonic seizures were diagnosed in only two patients, and a combination of MP, DBS and absence seizures was diagnosed in one case. In the majority of cases (8 patients), the typical phenotype of JME was a combination of MP and GSP. Photosensitivity, both clinical and according to EEG data, was observed in 50% of patients (6 cases). In all cases, the attacks were provoked by sleep deprivation.

In all patients, neurological examination and indicative neuropsychological testing did not reveal any abnormalities. 3 female patients were diagnosed with a high level of neuroticism and a tendency to depressive reactions.

In all cases, at least once, a routine EEG study revealed generalized (diffuse) epileptiform activity. This activity was manifested mainly by short discharges of generalized peak- or polypeak-wave complexes in the background, during rhythmic photostimulation and/or within 3 seconds after closing the eyes. In 2 patients with absence seizures, the EEG showed generalized highly synchronized regular peak-wave activity with a frequency of 3–4 Hz with a discharge duration of up to a maximum of 4 seconds. In 6 patients, epileptiform activity was exclusively or predominantly detected during rhythmic photostimulation at frequencies of 15–20 Hz and/or when closing the eyes. It is important to note that it was in this group of patients that 3 out of 6 patients had epileptic myoclonus of the eyelids (Fig. 2).

Rice. 2. Patient G.A., 17 years old. Diagnosis: Juvenile myoclonic epilepsy. When conducting video-EEG monitoring during sleep, epileptiform activity was recorded in the form of short (up to 1 sec) discharges of generalized peak/polypeak-wave activity, with amplitude predominance in the frontal regions.

The therapeutic history of the patients was as follows. In 3 cases, Keppra was prescribed as initial monotherapy for newly diagnosed JME. In 6 cases, Keppra was also used in monotherapy when replacing valproic acid drugs (Depakine): in 3 cases due to lack of effectiveness (2 - ongoing seizures and 1 - high index of epileptiform activity in the form of interictal discharges on the EEG) and in 3 due to severe side effects at the request of patients. In the remaining 3 cases, Keppra was added to other AEDs (2 - Depakine and 1 - Suxilep) due to the insufficient effectiveness of previous therapy. Doses of Keppra in patients with JME ranged from 1500 to 4500 mg/day in 2 divided doses. In all cases, a gradual dose titration was carried out, taking from 3 to 8 weeks.

When examining patients at follow-up, the effect of Keppra on the course of epilepsy and EEG data were analyzed; as well as drug tolerability. In all 3 cases of initial monotherapy, a positive effect reaching 100% was obtained: complete relief of all types of attacks and gradual normalization of the bioelectrical activity of the brain according to VEM data. In all 6 patients switched from monotherapy with Depakine to Keppra, no epileptic seizures were observed. In 5 cases, complete blocking of epileptiform activity was observed according to VEM data, and in 1 case there was no effect on epileptiform discharges. In 3 patients, Keppra was added to suxilep (1 case) and Depakine (2 cases). Epileptic seizures were completely stopped, including epileptic myoclonus of the eyelids, which was resistant to many other AEDs. However, a significant improvement in VEM results in reducing interictal epileptiform activity was achieved only in 1 out of 3 cases. Thus, in the general group of patients, persistent relief of epileptic seizures was observed in 100% of cases, and complete blocking or a significant decrease in the index of interictal epileptiform discharges on the EEG was observed in 75%. In 5 out of 6 cases, Keppra significantly reduced the manifestations of photosensitivity, both according to clinical manifestations and according to EEG data.

Side effects (AE) of Keppra therapy were noted in only 1 patient (8%). Patient G.A., 17 years old, with the onset of attacks at 9 years old, MP + GSP phenotype, had previously taken phenobarbital, clonazepam, suxilep, Depakine, Topamax in various combinations. Epileptic seizures were stopped with a combination of Depakine 1750 mg/day and Topamax 150 mg/day. However, epileptiform activity on the EEG in the form of frequent generalized interictal discharges of polypeak-wave complexes in the background was constantly observed, with a high index. In addition, various PE therapies were registered in the patient: a sharp decrease in appetite and body weight, amenorrhea, hypochromic anemia, neutropenia. Due to the catastrophic loss of body weight, the presence of other AEs, as well as the unsatisfactory result of the effect on epileptiform activity, it was decided (together with the patient’s family) to change the treatment. Topamax was discontinued, the dose of Depakine was reduced to 1000 mg/day, and Keppra was simultaneously introduced at a final dose of 3500 mg/day (dose titration was carried out over 3 weeks). No epileptic seizures occurred, and a positive effect was noted in the form of a sharp decrease in the index of interictal epileptiform activity on the EEG. However, after 1 week. After taking the full dose of Keppra, the patient developed Landolt's forced normalization syndrome. This manifested itself as severe irritability, anger, insomnia, aggression (verbal and non-verbal) towards parents; a pronounced decrease in background mood. The Keppra dose was reduced to 2000 mg/day. Currently, the patient is receiving Depakine Chrono 1000 mg/day and Keppra 2000 mg/day. There are no attacks, side effects are completely stopped: weight and menstrual cycle are restored, blood counts are normalized. She is emotionally labile, but tries to avoid conflicts and is critical. However, the EEG continues to record pronounced epileptiform activity in the form of diffuse polypik-wave discharges in the interictal background.

The duration of follow-up observation for patients taking Keppra ranged from 7 months. up to 3 years (in 92% of cases - more than 1 year). Treatment retention is currently 100%. None of the patients discontinued Keppra due to ineffectiveness, poor tolerability, or any other reasons. Relapse of HSP was observed once only in 1 patient when taking medications (Suxilep + Keppra) was missed and after severe sleep deprivation. A persistent, prolonged effect of Keppra in blocking interictal epileptiform activity on the EEG was also noted.

Discussion

The modern history of treatment for JME goes back 50 years. D. Janz and W. Christian, who described this disease in 1957, were the first to use barbituric acid derivatives in therapy: phenobarbital and primidone (hexamidine). Paradoxically, complete remission of attacks was achieved by the authors in 86% of cases! They also used phenytoin and found that this drug is not very effective in patients with JME and causes aggravation of attacks in 33% of cases.

Thus, already half a century ago it was shown that epileptic seizures in JME are relatively easily controlled by antiepileptic drugs, in particular barbiturates. The problem was the high incidence of barbiturate AEs, primarily affecting cognitive function and the neuroendocrine system, especially in men.

Since the 80s last century, valproic acid preparations (Konvulex, Depakine) became firmly established in clinical practice. Valproates (VPA) have been shown to be highly effective in relieving all types of seizures in patients with JME (myoclonus, HSP, absence seizures), and they have firmly established themselves as the first choice drugs in the treatment of this form of epilepsy. Complete drug remission when prescribing valproates is achieved in 80–87% patients, and in the vast majority of cases - on monotherapy. Given the insufficient effectiveness of valproates, they have always remained the basic drugs in combination therapy: VPA + suxilep (for resistant absence seizures); VPA + phenobarbital (for resistant GSP); VPA + clonazepam (for severe myoclonus and photosensitivity).

However, with the accumulation of extensive clinical experience with valproic acid derivatives over the past 20 years, serious problems have become apparent. Firstly, valproates, which are highly effective for myoclonus and absence seizures, are significantly less effective for GSP and epileptic myoclonus of the eyelids. Second, valproate is not effective enough to block interictal epileptiform activity on the EEG. It is with JME that it is important to achieve complete blocking of epileptiform discharges on the EEG, since their preservation is one of the most important factors in the recurrence of attacks when the AED dose is reduced and therapy is discontinued. And finally, thirdly (and most importantly!), evidence has accumulated indicating a high incidence of serious side effects of valproate during long-term therapy.

In our first publication devoted to the side effects of AEDs in the treatment of idiopathic generalized epilepsy, in 154 patients taking valproic acid drugs, various AEs were found in 49% of cases. In our 2008 publication, in 100 patients with epilepsy receiving valproate monotherapy, side effects were observed in 62% of cases! This concerns, first of all, the effect of valproates on the neuroendocrine system, liver function, and cosmetic side effects. Many authors consider it extremely undesirable to prescribe valproate to girls and women of childbearing age. These drugs can lead to obesity, carbohydrate metabolism disorders (hyperglycemia), menstrual cycle disorders, and polycystic ovary syndrome. In addition, valproate has been shown to have a more pronounced teratogenic effect compared to other AEDs.

All of the above predetermined the search in the 21st century for new drugs in the treatment of JME - effective and relatively safe. Some publications discuss the possibility of using lamotrigine and topiramate in JME. Lamotrigine, although well tolerated, is not effective enough in monotherapy for JME; in addition, in some cases it can lead to aggravation of attacks, in particular myoclonus. Topamax is highly effective for generalized seizures, however, it is less effective for absence seizures and myoclonus. In general, the drug shows fairly high effectiveness in the treatment of patients with JME and, of course, is promising.

Since the beginning of the century, a broad-spectrum drug, levetiracetam (Keppra), began to be used in clinical practice. Currently, Keppra has been proven to be highly effective in treating most epileptic seizures in children and adults, as well as the drug is well tolerated. By 2008, evidence had accumulated indicating the selective effectiveness of levetiracetam in idiopathic generalized epilepsy, in particular in JME. Sharpe et al. (2008) conducted a study of levetiracetam in the treatment of juvenile myoclonic epilepsy in 30 patients. The drug was prescribed in monotherapy (in 12 patients - initial therapy) at a dose of 500–3000 mg/day (10–59 mg/kg/day). The average duration of treatment was 27 months. As a result of monotherapy with levetiracetam, 24 of 30 patients (80%) achieved stable drug remission, and another 2 had a significant reduction in the frequency of attacks. The authors note that among the 20% of patients in whom remission was not achieved, patients with an atypical course of the disease predominated. In addition, the therapeutic effect was worse in a small group of patients with absence seizures. As a result of the study, the authors obtained another important conclusion: the effectiveness of levetiracetam does not depend on the effect of previous therapy. Most patients received valproate before being prescribed levetiracetam. PE was observed only in 1 case out of 30 - “behavioral disorder”.

In a study by N. Specchio et al. (2008) studied the effect of levetiracetam on interictal epileptiform activity and photoparoxysmal response to EEG in patients with JME. 48 patients were examined, 10 of them with a newly diagnosed JME. The mean dose of levetiracetam was 2200 mg/day, and the mean follow-up period was 19.3 months. Before treatment, interictal epileptiform activity on the EEG was detected in 91% of patients, and a photoparoxysmal response in 35%. During levetiracetam therapy, complete normalization of the EEG was observed in 56% of cases, and blocking or marked reduction of the photoparoxysmal reaction was observed in 76%. As a result of the study, the authors concluded that levetiracetam is highly effective in blocking interictal epileptiform discharges and photoparoxysmal response to EEG. Previously Kasteleijn-Nolst Trenite D.G. et al. (1996) showed the effectiveness of levetiracetam in blocking photosensitivity in patients with epilepsy.

Our study includes only preliminary results based on the use of levetiracetam (Keppra) in the treatment of 12 patients with JME. In the general group, stable relief of epileptic seizures was found in 100% of cases, and complete blocking or a pronounced decrease in the index of interictal epileptiform discharges on the EEG in 75%. In 5 out of 6 patients, Keppra significantly reduced the manifestations of photosensitivity, both according to clinical manifestations and according to EEG data. The effect of Keppra on epileptiform activity was less pronounced in the group of patients receiving polytherapy (combination with valproate or suxilep) and in the presence of absence seizures (2 patients). This is consistent with the results of the study by D.V. Sharpe et al. (2008), who showed the insufficient effect of levetiracetam in the atypical course of JME and the presence of absence seizures in patients.

We have shown the high effectiveness of Keppra in a special type of seizure within JME - epileptic myoclonus of the eyelids. This type of attack often occurs in patients with photosensitivity and is triggered by closing the eyes; auto-induction of seizures often occurs. Myoclonus of the eyelids can be combined with other types of seizures, in particular absence seizures and DBS; its resistance to most AEDs was noted. In the publication of P. Striano et al. (2008) noted the high effectiveness of levetiracetam in mono- and polytherapy in the treatment of patients with Jeavons syndrome - epileptic myoclonus of the eyelids with or without absence seizures. The positive effect of levetiracetam was observed in 80% of 35 patients with Jeavons syndrome. Blocking of diffuse epileptiform activity on the EEG that occurs when the eyes are closed was observed in 57% of cases.

All publications show good tolerability of levetiracetam, including high doses of the drug. In the 12 JME patients we examined who took Keppra, only in 1 case was PE observed in the form of the phenomenon of forced Landolt normalization. In a study by Sharpe D.V. et al. (2008) PE was also observed in 1 out of 30 patients and manifested itself, as described by the authors, as a “behavioral disorder.” Thus, adverse effects of levetiracetam are reported very rarely. However, we should not forget about the possibility of the phenomenon of forced normalization in adult patients taking levetiracetam, especially in cases of high clinical effectiveness of the drug and with complete blocking of interictal epileptiform discharges on the EEG.

In conclusion, I would like to emphasize that most patients diagnosed with JME must take AEDs for a very long time. The problem is the high rate of seizure recurrence after AED discontinuation. Canceling drugs even after 4–5 years of complete electroclinical remission causes relapse of attacks in at least 75% of patients. In this case, it is important to completely block interictal epileptiform activity according to VEM data, including recording during sleep. For this reason, long-term treatment should be carried out with a highly effective and well-tolerated AED, preferably in monotherapy.

This preliminary study and literature data strongly suggest that levetiracetam (Keppra) may be the drug of choice in the treatment of juvenile myoclonic epilepsy. It has been shown that Keppra is not inferior in effectiveness to valproate and has significant advantages over them in terms of safety. Keppra is also highly effective in blocking interictal epileptiform activity on the EEG and the phenomenon of photosensitivity. The best effect of the drug is achieved with monotherapy, especially with initial therapy. Currently, the prescription of valproates as a basic drug for many forms of epilepsy is caused not so much by their greater effectiveness, but by their better knowledge. Further research is needed on the effectiveness of levetiracetam in idiopathic generalized epilepsy and, in particular, in JME.

Bibliography
1. Voronkova K.V., Petrukhin A.S., Pylaeva O.A., Kholin A.A. Rational antiepileptic pharmacotherapy // Moscow, Binom, 2008. - 192 p.
2. Mironov M.B., Mukhin K.Yu., Petrukhin A.S., Kholin A.A. Monitoring the effectiveness of treatment of patients with juvenile forms of idiopathic generalized epilepsy and the state of “pseudo-remission”. - Journal of neurol and psychiat. - 2005. - T. 105. - No. 8. - pp. 24–28.
3. Mukhin K.Yu., Nikanorova M.Yu., Levin P.G. Juvenile myoclonic epilepsy // Journal of neurol and psychiat. - 1995. - T.95. - N.3. - pp. 17–21.
4. Mukhin K.Yu., Petrukhin A.S., Rykova E.A. Side effects of anticonvulsants in the treatment of idiopathic generalized epilepsy // Journal of neurol and psychiat. - 1997. - T. 97. - N.7. - P. 26–30.
5. Mukhin K.Yu., Petrukhin A.S. Idiopathic forms of epilepsy: taxonomy, diagnosis, therapy. - M., 2000. - 319 S.
6. Mukhin K.Yu., Glukhova L.Yu., Petrukhin A.S., Mironov M.B., Sobornova A.M. Topamax in monotherapy of epilepsy // Journal of neurol and psychiat. - 2004. - T. 104. - N. 8. - P. 35–40.
7. Mukhin K.Yu., Pilia S.V., Chadayev V.A., Mironov M.B., Petrukhin A.S. Keppra in the treatment of epilepsy: effectiveness and tolerability // Journal of neurol and psychiat. - 2005. - T.105. - N. 1. - P. 49–51.
8. Mukhin K.Yu., Tysyachina M.D., Mironov M.B., Pilia S.V., Petrukhin A.S. Keppra in monotherapy for epilepsy: electro-clinical efficacy and tolerability // Russian Journal of Child Neurology. - 2007. - T. 2. - No. 3. - P. 14–23.
9. Mukhin K.Yu., Petrukhin A.S., Mironov M.B., Dolinina A.F. Sodium valproate (Depakine) in achieving remission in patients with idiopathic generalized 10. Mukhin K.Yu., Tysyachina M.D., Mukhina L.N., Petrukhin A.S. Comparative effectiveness and tolerability of topiramate, valproate and carbamazepine in monotherapy for epilepsy in children and young adults // Rus. zhur. det. neur. - 2008. - T. 3. - No. 2. - P. 3–48.
11. Petrukhin A.S., Mukhin K.Yu., Medvedev M.I. Basic principles of treatment of epilepsy in children // Neurological Bulletin - 1997. - T. 29. - N 1–2. - pp. 95 - 97.
12. Petrukhin A.S., Demikova N.S., Mukhin K.Yu. Teratogenicity of antiepileptic drugs // Current problems of modern clinical genetics / ed. G.R. Mutovin, L.F. Marchenko. - Moscow, 2001. - P. 205–213.
13. Petrukhin A.S., Mukhin K.Yu., Kalinina L.V., Pylaeva O.A. Lamictal: poly- and monotherapy for epilepsy / Psychiat and psychopharmacoter. - 2004 / appendix 1. - pp. 20–26.
14. Gallagher M.J., Eisenman L.N., Brown K.M., Erbayat-Altay E., Hecimovic H., Fessler A.J., Attarian H.P., Gilliam F.G. Levetiracetam reduces spike-wave density and duration during continuous EEG monitoring in patients with idiopathic generalized epilepsy. // Epilepsy. - 2004. - V. 45. - P. 90–91.
15. Genton P., Gelisse P., Thomas P. Juvenile myoclonic epilepsy today: current definitions and limits // In: Eds. B. Schmitz, T. Sander / Juvenile myoclonic epilepsy: the Janz syndrome. - 2000. - Petersfield, WBP. - P. 11–32.
16. Janz D., Christian W. Impulsive petit mal // Dtsch. Z. Nervenheilk. - 1957. - V. 176. - P. 346–386.
17. Kasteleijn-Nolst Trenité D.G., Marescaux C., Stodieck S., Edelbroek P.M., Oosting J. Photosensitive epilepsy: a model to study the effects of antiepileptic drugs. Evaluation of the piracetam analogue, levetiracetam. //Epilepsy Res. - 1996. - V. 25. - P. 225–30.
18. Kellett M.W., Smith D.F., Stockton P.A., Chadwick D.W. Topiramate in clinical practice: first year’s post-licensing experience in a specialist epilepsy clinic // J. Neurol. Neurosurg. Psychiatry. - 1999. - V. 66. - P. 759–763.
19. Meador K.J., Baker G.A., Finnell R.H. et al. In utero antiepileptic drug exposure. Fetal death and malformations // Neurology. - 2006. - V. 67. - P. 407–412.
20. Panayiotopoulos C.P. The epilepsies: Seizures, Syndromes and Management // Bladon Medical Publishing, 2005. - 540 P.
21. Panayiotopoulos C.P., Obeid T., Tahan R. Juvenile myoclonic epilepsy: a 5-year prospective study // Epilepsia. - 1994. - V. 35. - P. 285–296.
22. Panayiotopoulos C.P., Tahan R., Obeid T. Juvenile myoclonic epilepsy: factors of errors involved in the diagnosis and treatment // Epilepsia. - 1991. - V. 32 - P. 672–676.
23. Prasad A., Kuzniecky R.I., Knowlton R.C., Welty T.E., Martin R.C., Mendez M., Faught R.E. Evolving antiepileptic drug treatment in juvenile myoclonic epilepsy. // Arch Neurol. - 2003. - V. 60. - P. 1100–1105.
24. Sharpe D.V., Patel A.D., Abou-Khalil B., Fenichel G.M. Levetiracetam monotherapy in juvenile myoclonic epilepsy. //Seizure. - 2008. - V. 17. - P. 64–68.
25. Specchio N., Boero G., Michelucci R., Gambardella A., Giallonardo A.T., Fattouch J., Di Bonaventura C., de Palo A., Ladogana M., Lamberti P., Vigevano F., La Neve A. ., Specchio L.M. Effects of levetiracetam on EEG abnormalities in juvenile myoclonic epilepsy. // Epilepsy. - 2008. - V. 49. - P. 663–9.
26. Striano P., Sofia V., Capovilla G., Rubboli G., Di Bonaventura C., Coppola A., Vitale G., Fontanillas L., Giallonardo A.T., Biondi R., Romeo A., Viri M., Zara F., Striano S. A pilot trial of levetiracetam in eyelid myoclonia with absences (Jeavons syndrome). // Epilepsy. - 2008. - V. 49. - P. 425–30.
27. Sundqvist A., Nilsson B.Y., Tomson T. Valproate monotherapy in juvenile myoclonic epilepsy: dose-related effects on electroencephalographic and other neurophysiological tests // Ther. Drug Monit. - 1999. - V. 21. - P. 91–96.
28. Thomas P., Genton P., Gelisse P., Wolf P. Juvenile myoclonic epilepsy // In: Epileptic syndromes in infancy, childhood and adolescence. 3rd edition/Eds. J. Roger, M. Bureau, Ch. Dravet, P. Genton, C.A. Tassinari, P. Wolf - London: John Libbey, 2005. - P. 367–388.
29. Wallace S. Myoclonus and epilepsy in childhood: a review of treatment with valproate, ethosuximide, lamotrigine and zonisamide // Epilepsy Res. - 1998. - V. 29. - P. 147–154.

The disease is a syndrome, the clinical picture of which is expressed by a complex of myoclonic and epileptic seizures. This type of epilepsy is hereditary or acquired and can be caused by many factors.

Myoclonic epilepsy is most often diagnosed in children and adolescents. Boys are more susceptible to the disease.

Juvenile myoclonic epilepsy, abbreviated as JME, is also called Janz syndrome. It refers to a form of benign idiopathic epilepsy. This disease is age-related and is associated with the pubertal development of a teenager.

• All information on the site is for informational purposes only and is NOT a guide to action!
• Can give you an ACCURATE DIAGNOSIS only DOCTOR!
• We kindly ask you NOT to self-medicate, but make an appointment with a specialist!
• Health to you and your loved ones!

This type of epilepsy is characterized by seizures with massive bilateral manifestations. Thus, the disease affects paired organs: eyes, limbs.

Disease history

For the first time, a disease such as childhood myoclonic epilepsy was described in 1981. Dravet and Bior conducted a study on seven-year-old children.

The syndrome of benign myoclonic epilepsy in children acted as a phenomenon of myoclonic seizures. At the same time, no other types of seizures were observed.

Such manifestations were treatable in the first three years of life, but at older ages they appeared extremely rarely or did not appear at all. Psychomotor development in these children was stated to correspond to age standards. There were no psychological deviations noted.

In 1989, Benign Myoclonic Epilepsy Syndrome in Children was included in the international classification along with generalized idiopathic epilepsy.

To date, 98 cases of the disease have been described in the medical literature.

Causes

A sudden and violent awakening can trigger an attack.

A number of scientists have also identified some anthropometric features of patients with myoclonic epilepsy.

These include:

• high growth;
• absence of dysplastic features in physical development;
• high level of emotional mobility;
• presence of neurotic traits.

Types of myoclonic epilepsy

Epilepsy of the myoclonic type is a brain pathology accompanied by seizures.

The disease can manifest itself in three types of attacks:

Myoclonic	Associated with twitching of the limbs and upper body. Occurs in the morning immediately after waking up. If severe fatigue occurs, they may appear in the evening.
Tonic-clonic	More than 70% of patients with myoclonic epilepsy experience such attacks. Their occurrence in most cases is provoked by non-compliance with the “sleep-wake” regime.
Absence seizures	With this type of attack, the patient loses consciousness. This period lasts a few seconds, while convulsions are completely absent. Absence seizures occur in one third of those suffering from myoclonic epilepsy and can occur at any time of the day.

Determining the type of seizure is possible only in a hospital setting. The photostimulation method is most effective in making a diagnosis.

Differential diagnosis

Myoclonic seizures in myoclonic epilepsy are massive and bilaterally synchronous. They are characterized by sporadic manifestations, multiple disorders of fat metabolism and postanoxic myoclonus.

In juvenile myoclonic epilepsy, consciousness functions without impairment.

To make an accurate diagnosis, it is necessary to collect a detailed history and examine typical clinical features with appropriate indicators.

Symptoms

The main symptom of juvenile myoclonic epilepsy is a seizure.

It has the following properties:

• muscles in the arms and upper body twitch uncontrollably;
• the patient is conscious;
• a seizure most often occurs in the morning upon awakening;
• The time periods between seizures can be long and sometimes amount to months and years.

The intensity of a myoclonic seizure can be more or less intense. In some cases, the attack consists only of twitching of the eyelid, in others it is severe convulsions of the upper body.

A mild form of a seizure may not attract attention, but in severe forms it is possible to develop absence seizures associated with a loss of attention.

The patient's neurological status remains within normal limits. No cognitive impairment was observed.

Most often, juvenile myoclonic epilepsy manifests itself at the age of 12-14 years. But the age range can be wider and cover children from 8 years old. Cases of the disease have also been recorded in newborns.

Diagnostics

Symptoms of myoclonic epilepsy are often interpreted as some kind of nervousness. For this reason, we talk about epilepsy as such when generalized seizures appear.

EEG abnormalities may be noted with the use of photostimulation methods and sleep deprivation. Measuring the EEG at the moment of awakening can be informative.

Subtle, mild disorders can be determined using EEG video. The method is effective when reading aloud and during a conversation.

First aid for a seizure

Relatives should understand that a patient can have an attack at any time. For this reason, it is important to know what actions to take.

During an exacerbation, seizures can be quite frequent and occur at any time of the day.

The attack poses the greatest danger to the patient himself due to the fact that any injuries can be caused.

It is impossible to completely eliminate or speed up the end of an attack.

But knowing some rules of first aid for epilepsy will help you avoid concomitant harm to health:

In any case, seeking medical help would be advisable.

Forecast

Sudden remission of juvenile myoclonic epilepsy is extremely rare. Resumption of seizures occurs in every 9 out of 10 cases after stopping antiepileptic drugs.

Currently, medicine has data on the need for lifelong treatment and regular monitoring of the patient’s condition.

Seizures can also occur during treatment (about 50% of cases). But timely and competent treatment gives a fairly favorable prognosis for recovery and leading a normal lifestyle.

Treatment

Treatment of juvenile myoclonic epilepsy comes down to two postulates:

• taking medications;
• adjusting the patient's lifestyle.

Valaproate has proven effectiveness. Monotherapy with their help helps control attacks.

Drug therapy produces significant results. Medicines help reduce the intensity and frequency of seizures. In some cases, complete recovery is possible.

The treatment program is prescribed by the doctor. This takes into account the individual characteristics of the patient, the etiology and clinical picture of the disease. Drug withdrawal is also carried out under the supervision of a specialist.

A sustainable therapeutic effect is achieved by following all the doctor’s instructions. As a rule, long-term and continuous treatment is required.

During the treatment process, periodic monitoring is carried out in order to adjust the course and identify improvements.

The treatment prognosis is based on the following points:

This treatment forecast was created by French experts on juvenile myoclonic epilepsy in 2011.

The patient’s life requires proper rest, adherence to the regime, the elimination of stressful conditions and sleep problems.

Juvenile myoclonic epilepsy is one of the forms. This type of pathology is characterized by its onset in adolescence, associated with massive bilateral myoclonic seizures, localized mainly in the upper extremities.

Juvenile epilepsy is one of the first forms of epilepsy with a known genetic defect.

The disease has a favorable prognosis if detected early and promptly seek medical help.

Insufficient maturity of the brain and the entire nervous system are the conditions against which convulsions can occur in children under one year of age. At the same time, seizures can be detected in 3% of children born on time and in 20% of premature babies. Therefore, parents of babies born prematurely should be especially attentive to their health. Myoclonic spasms are sharp, sudden involuntary contractions that involve a group of muscles or the entire body (most often the upper part and arms). Most often, such cramps occur during the period of falling asleep or sleeping and are sometimes called nocturnal shudders. In some children, such twitching is quite intense. It is necessary to find out the cause of this condition. In some people, this condition continues into adulthood and is not a symptom of any disease. In this case, no special treatment is required. Myoclonic spasms when falling asleep may have a genetic cause. If the nighttime shudders are quite strong, they can wake up and frighten the baby. For children up to 5–6 months old, swaddling may be an alternative, at least for the period of falling asleep.

However, there are other causes of myoclonic seizures in children. In order to find out this, you need to seek qualified medical help and undergo a thorough examination using modern research methods, such as electroencephalography and magnetic resonance imaging. Let's consider the possible causes of seizures in newborns.

1. Various metabolic disorders.

For example, hypoglycemia. Hypoclecemia is a condition in which the blood glucose level is below 2.7 mmol/l. Its main cause is hyperinsulinism. Hyperinsulinism is a pathology caused by excess insulin, causing a significant decrease in blood sugar. A lack of glucose can provoke oxygen starvation of the brain, which leads to disruption of its activity and can provoke seizures.

Hyponatremia and hypocalcemia can cause seizures. Hyponatremia is a low serum sodium level, less than 135 mEq/L. Hypocalcemia is a low level of calcium in the blood. Treatment of these pathologies requires qualified medical care. Usually the prognosis of treatment is favorable, no consequences are observed.

2. Encephalopathy – non-inflammatory brain damage. In newborns it can be congenital or acquired during labor. Medications may be prescribed to treat encephalopathy. To relieve symptoms - physiotherapy and massage.

3. Meningitis and encephalitis. Meningitis is an inflammation of the lining of the brain or spinal cord. The disease is infectious - it is infection of the body by a certain bacterium that leads to the formation of purulent cavities in the brain. It is important to start treatment on time and follow all recommendations of your doctor. Encephalitis is a group of brain diseases caused by the penetration of an infectious pathogen into the body. For treatment, antiviral and anti-inflammatory drugs, bed rest and plenty of fluids are prescribed. Urgent hospitalization of the child is necessary. The main thing in the diagnosis of meningitis and encephalitis is a lumbar puncture, with the help of which cerebrospinal fluid is taken for analysis.