RU2767271C1 - Method for diagnosing neuroimmune disorders in young children with epilepsy - Google Patents

Abstract

FIELD: medicine.

SUBSTANCE: invention relates to medicine, namely to neurology, and can be used to diagnose neuroimmune disorders in young children with epilepsy. The child's blood serum is examined. In full-term newborns and children at the 1st year of life in the first month, at 3 and 6 months, the level of antibodies to myelin basic protein (AB to MBP) and antibodies to myelin-associated glycoprotein (AB to MAG) are determined in the blood serum. When the concentration of antibodies to myelin basic protein is 1.5 conventional optical density units (o.d.c.u.) and higher, and antibodies to myelin-associated glycoprotein are 172.4 pg/ml and higher, the development of neuroimmune disorders is diagnosed.

EFFECT: method provides the possibility of accurate specific diagnosis of neuroimmune disorders in children with epilepsy in the 1st year of life, which makes it possible to choose an adequate therapeutic and diagnostic tactics and improve the prognosis of the course of the disease, due to the early detection of brain-specific antibodies to MBP and MAG, which can serve as one of the prognostically significant tools for the occurrence of neuroimmune disorders in epilepsy in children.

1 cl, 1 tbl, 3 ex

Description

The invention relates to medicine, namely to pediatric neurology, and can be used to diagnose neuroimmune disorders in children of the 1st year of life with epilepsy.

It is known that the neuroendocrine and immune systems in the human body are a single integrative functional basis with their various multiple connections.

Their interdependence and interdependence is based on the mediator and antigenic community, the ability to form memory, network relationships, self-regulation and the leading role in the processes of maintaining functional dynamic homeostasis and adaptation, providing a certain reliability of intersystem relations. At the same time, the functioning of a complex neuro-endocrine-immune organization is fraught with the possibility of developing dysregulatory disorders in case of disruption of compensatory mechanisms and pathology of its constituent links.

Neuroimmunopathology is characteristic of almost any nosological form of brain disease, while neuroimmunological disorders are not only an important link in pathogenesis, but can also be a risk factor for the development of a chronic process, its atypical course with the formation of resistance to pharmacotherapy. The pathology of the nervous regulation of the immune system can manifest itself in two main types of functional disorders: immunological deficiency, up to a severe immunodeficiency state, or excessive activation of immune responses, including autoimmune processes.

In domestic and foreign literature of recent years, there are indications of destabilization of not only cerebral cell membranes with posthypoxic changes in metabolism in the brain, but also damage to the membrane structures of cells that form the blood-brain barrier (BBB) as a result of ischemia and subsequent hypoxia, manifested by expansion of tight endothelial junctions. , edema and swelling of the processes of astrocytes, with a violation of the constancy of the internal environment and diffusion processes (Bradbury M., 1983, Gusev E.I., 2011). At the same time, it is believed that violations of the integrity of the BBB occur instantly, within a few minutes after cerebral hypoxia-ischemia or a more delayed phenomenon of barrier destruction.

Damage to the BBB causes a whole cascade of immune-dependent reactions leading to both the induction of the epileptic syndrome and its progression. Over the past decades, numerous experimental and clinical data have been obtained that have made it legitimate to consider the inflammatory theory of epileptogenesis. It is believed that the activation of microglia and astrogliosis, accompanied by damage to neurons, contributes to the chronicity of the inflammatory process in epilepsy (Vezzani A. et al., 2002). The main conclusion of this kind of work is the position that inflammation in the central nervous system (CNS) is based on damage to the BBB.

Under these conditions, the method of routine EEG and EEG video monitoring, being a non-invasive, "gold standard", method of in vivo diagnostics with visualization of the lesion in the brain, becomes a valuable source of information about the functional state of the brain and the neuroimmune system controlled by it. The possibility of obtaining a timely qualitative assessment of these changes is valuable in terms of determining the clinical situation as a whole. Quantitative changes in a number of EEG parameters can detect a tendency to move towards critical values and, therefore, have a prognostic value, which serves as a guideline for the doctor for appropriate preventive therapy. There is experimental confirmation of the dependence of the nature of the electrical activity of brain structures on the level of immunodeficiency (Kryzhanovsky G.N., et al., 1987). However, in the vast majority of cases, it only allows diagnosing and fixing the current epileptiform pathological process, without affecting the deeper pathophysiological essence of this phenomenon.

The main advantage of these methods is their high accuracy, however, the disadvantages of their wide use are the technical difficulties of implementation, taking into account the contingent of patients examined, including the use of medical techniques that require the child to be motionless (lack of voluntary movements) throughout the entire procedure of the study.

There is a known method for predicting the risk of developing symptomatic epilepsy in neuroinfections in children (RF patent No. 2652967 dated 03.05.2018), including the identification of the causative agent of the disease and the determination of epileptiform activity on the EEG, characterized in that in the acute period of the disease after verification of the etiology of the disease, the content of alpha-1 is determined -antitrypsin in the cerebrospinal fluid and a 2-hour EEG monitoring is carried out and when establishing the etiology of the disease caused by herpes simplex viruses types 1 and 2 or the human herpes virus type 6, the level of alpha-1-antitrypsin in the cerebrospinal fluid is above 0.045 g/l and registration on the EEG focal epileptiform activity predict the development of symptomatic epilepsy.

The disadvantages of the method are:

1. The use of an invasive technique (lumbar puncture) for the collection of biological material in order to determine the declared parameters.

2. Technical difficulties of implementation using labor-intensive diagnostic procedures and specially trained medical personnel, taking into account the contingent of the examined children.

3. The indicators used for prognosis are not always precisely defined and unambiguously interpreted in young children with various forms of symptomatic epilepsy.

4. Examination is carried out in already ill children with neuroinfections with a different nature of convulsive seizures.

The diagnosis of clinical and neuroimmunological disorders in patients with epilepsy with the syndrome of encephalopathy is known (Diagnosis of clinical and neuroimmunological disorders in patients with epilepsy with the syndrome of encephalopathy, their immunocorrection and treatment: Methodological recommendations of the NIPNI named after V.M. Bekhterev, S.A. Gromov, L.V. Lipatova.-SPb., 2010-27 p.). The authors developed clinical and laboratory immunopathological syndromes with an assessment of the neuroantigenic landscape and immune status, the type of immune response in conditions of autosensitization to neurospecific antigens. The use of the proposed methodology makes it possible to draw up individual immunocorrection programs taking into account the identified immunopathological syndromes in order to optimize antiepileptic therapy and overcome drug resistance in patients.

The disadvantages of this method are:

1. A method that is cumbersome in its form, content and interpretation of the obtained results is used, requiring labor-intensive specialized approaches, including questionnaires, to objectify clinical symptoms in patients with epilepsy, which is not applicable in young children.

2. As additional instrumental tests, labor-intensive diagnostic neuroimaging techniques (CT, MRI of the brain) are used, which require special preparation of the patient (long-term sedation) and medical personnel.

3. A multi-stage, time-consuming, expensive laboratory method for determining the immunological parameters of blood is used.

4. The studied laboratory blood parameters are not precisely determined and unambiguously interpreted for the diagnosis of neuroimmune disorders in patients with epilepsy complicated by encephalopathy.

Known assessment of the neuroimmune status in children with perinatal pathology (Morozov S.G., Kozhevnikova E.N., Petkevich N.P., Inshakova V.M., Klyushnik T.P., Sidyakin A.A. / Issues of gynecology, obstetrics and perinatology, 2014, vol. 13, no. 5, pp. 33-39). Assessment of neuroimmunological features in children with the consequences of perinatal CNS lesions is carried out on the basis of a number of indicators of congenital (activity of leukocyte elastase (LE), its inhibitor of α-1 proteinase (α1-PI) and acquired (level of autoantibodies (aAT1) and anti-idiotypic antibodies (aAT2) to 4 nervous tissue proteins: S-100 protein, myelin basic protein (MBP), specific astrocyte protein (GFAP), nerve growth factor (NGF).It has been shown that a persistent increase in the concentration of aAT and aAT2 of this specificity is above certain values starting from 1 -th month of life and then for several subsequent months and even years, it accompanies or precedes the development of clinically pronounced disorders of the nervous system from psychomotor developmental delays to epilepsy and autism.

The disadvantages of this method are:

1. Labor intensity and low accuracy of determining several (6) immunological parameters at the same time, requiring the collection of a sufficient volume of peripheral venous blood.

2. The need for repeated dynamic control of these parameters in the dynamics of clinical observation not only in the 1st year of life, but also in subsequent age periods of postnatal ontogenesis.

3. This method allows only to fix the development of the pathological process at its various stages, not allowing to predict the further clinical situation.

4. The inability to use these diagnostic markers only in epilepsy.

It is known to assess the features of immune status disorders in newborns with perinatal hypoxia (Safarova A.F., Kuliev N.D. Features of the defeat of the immune status of newborns with perinatal hypoxia. Medical news - 2010 - No. 2 - p. 23-25). The authors state an undoubted and stable pathogenetic relationship between the development of ischemic brain damage and an autoimmune process with the activation of the release of pro-inflammatory cytokines, which have an additional damaging effect on various brain structures.

The disadvantages of the immunological markers used in clinical practice include:

1. The nonspecificity of these parameters for the diagnosis of neonatal seizures and/or epilepsy as one of the severe, in some cases, prognostically unfavorable clinical manifestations of perinatal hypoxia in the neonatal period.

2. Lack of clear laboratory criteria for diagnosing ischemic brain damage in the indicated group of children.

3. Restriction on the age period. The authors do not discuss a possible further clinical and laboratory scenario in the detection of immune status disorders in newborns in the later periods of postnatal ontogenesis.

Based on the foregoing, we can conclude that, despite the wide range of methods for diagnosing neuroimmune disorders in various pathological conditions in young children, they only allow us to state the fact of their presence, without making it possible to predict the nature of the course of the main pathological process in the nervous tissue.

Closest to the claimed invention is a method for diagnosing neuroimmune disorders in patients with epilepsy (RF patent No. 2329762 dated July 27, 2008), including electroencephalographic (EEG) monitoring, characterized in that the EEG is recorded from the surface of the head and when slow waves are detected at rest, the amplitude which exceeds background values by 1.5-2.0 times and a decrease in the index of alpha activity in the posterior leads, as well as a decrease in the alpha index after functional tests in all leads of the left hemisphere and an increase in the anterior areas of the brain, diagnose neuroimmune disorders in patients with epilepsy.

The disadvantages of this method include:

1. The inability to directly diagnose neuroimmune disorders, since the registration of these EEG parameters determined by the standard method (from the cerebral cortex) does not allow one to unambiguously judge the state of its deep structures (hypothalamus, pituitary gland, limbic system), which are directly involved in the regulation of immune responses in the body as a whole.

2. The need to use a labor-intensive technique and specially trained personnel in the absence of voluntary movements and / or medical sedation of the child during the study.

3. The need for functional tests with hyperventilation, which is technically difficult to implement in young children.

These disadvantages are eliminated in the present invention.

The objective of the claimed invention is to develop a simpler method for diagnosing neuroimmune disorders in young children with epilepsy in the 1st year of life while maintaining high accuracy.

The problem is solved by the fact that the method for diagnosing neuroimmune disorders in infants with epilepsy consists in the fact that in newborns and children in the first year of life in the first month, and at the age of 3 and 6 months, the factors of neuroimmune disorders are examined in the blood serum by determining the concentration of antibodies to myelin basic protein (AT to MBP) and the concentration of antibodies to myelin-associated glycoprotein (AT to MAG) and at the concentration of antibodies to myelin basic protein equal to 1.5 arbitrary units of optical density (c.u.o.p.) and higher , and the concentration of antibodies to myelin-associated glycoprotein 172.4 pg/ml and above, diagnose the development of neuroimmune disorders.

The technical result of the proposed method consists in the possibility of choosing an adequate treatment and diagnostic tactics and improving the prognosis of the course of the disease, by providing accurate, specific diagnosis of neuroimmune disorders in children with epilepsy in the 1st year of life.

The pathogenesis of neurodysregulatory pathology is associated with the formation of pathological integrations in the damaged nervous system (Abramov V.V., 1991) due to impaired inhibitory control. The initial link in this process is the formation of an aggregate of hyperreactive neurons, which produces an increased uncontrolled stream of impulses, that is, a generator of pathologically enhanced excitation. In turn, the latter hyperactivates the CNS structure in which it originated or with which it is functionally connected, as a result of which it significantly changes the functional state of other CNS structures and together with them forms a complex pathological integration system (IPS). The pathological chain of formation of IPS after CNS damage represents the following stage mechanisms: the formation of a generator - the occurrence of pathological determinants - the formation of a pathological system. If the IPS has access to the periphery, its effector link is the altered somatic structures, which are the final link of the IPS.

It is known that paroxysmal EEG changes are associated with high sensitization to neurospecific antigens (NAG). A relationship has been established between the concentration of neurospecific proteins and the severity of the clinical picture in patients with CNS diseases. The standard response of a neuron to NAH is a significant depolarization of the cell membrane, a decrease in the threshold of action potentials, and an increase in the amplitude of the depolarization spike that occurs in hippocampal neurons in response to electrical stimulation of Stefer's collaterals. Thus, the immunological induction of a pathologically enhanced excitation generator is associated with a typical mechanism of neuronal hyperactivation - membrane depolarization, the basis of which is the activation of sodium and especially calcium channels.

The occurrence of paroxysmal depolarization shifts is a characteristic sign of epileptization of neurons, which ultimately leads to the formation of a generator of pathologically enhanced excitation from these neurons. Neuroantibodies AT (HAT) can induce the generator or maintain and increase its power. Thus, antibodies to synaptic vesicles of the brain cause an increase in the frequency of discharges of pacemaker neurons and initiate the activity of previously silent neurons. When analyzing the HAT effect, it is emphasized that their main electrographic variant is epileptiform activity and it is believed that their main target is the synaptic structures and functions of the neuron (Shtark M.V., 1985).

Thus, early detection of brain-specific antibodies can serve as one of the prognostic tools for the occurrence of neuroimmune disorders in epilepsy in children.

It is known that myelin proteins perform structural, stabilizing and transport functions, showing pronounced immunogenic properties. About 30 proteins of this group have been isolated, 80% of them are myelin basic protein (MBP), proteolipid complex and myelin-associated glycoprotein (MAG). MBP and MAG are the main protein components of myelin contained in the membrane of oligodendrogliocytes - the main structural elements of the BBB, participating in the organization, assembly and maintenance of the integrity of the myelin of nerve fibers, stimulate the growth of astroglia, inactivating a number of inhibitors of serine proteinases (for example, a 1-antitrypsin), having pronounced immunogenic and encephalitogenic properties of degenerative demyelination and intercellular immunopathological inflammation.

The formation of an epileptic system is impossible without the participation of pathways in it, that is, white matter, since the main cause of brain epileptization is the development of stable pathological interneuronal connections. The phenomenon of demyelination of the pathways in the projection of epileptic foci is manifested by defibration, homogenization and complete disintegration of myelin with exposure of axons. In areas of demyelination, pronounced changes in lipids (cerebrosides, sphingomyelin and phospholipids) that make up myelin are found, as well as the phenomenon of gliosis, which is regarded as a compensatory-adaptive reaction, possibly aimed at restoring impaired (due to demyelination) insulation of nerve conductors. Based on these morphological findings, it was suggested that the altered white matter is the epileptogenic focus, and the modules of the cortex and hippocampus in the form of an epileptic focus can be included in the "functional" epileptic system. Thus, the results obtained made it possible to develop the concept that in the pathogenesis of an epileptic seizure, an important role is played not only by damage to the neurons of the cortex, but also by damage to the myelin sheaths of the pathways, the so-called "epileptic leukoencephalopathy", which can lead to the development of various types of disorders in the conduction of nerve impulses, creating zones of increased irritation.

In turn, the violation of BBB resistance causes the release of neurospecific proteins with high antigenicity into the blood. In response, the immune system reacts with the production of antibodies, leading to the emergence and maintenance of neuroimmune disorders, disruption of the normal metabolism of target cells, myelin formation and destruction of neurons. Organ-specific antibodies are capable of causing neuronal activation and death of CNS neurons due to disruption of their trophic supply, which may play a leading role in the occurrence of epileptic seizures.

The existence of a certain amount of autoantibodies to various neuroantigens has been proven, the penetration of which into the brain, by binding to the corresponding targets, can disrupt the functioning of neural networks and / or synaptic transmission, which at the clinical level is reflected in the violation of behavioral functions and cognitive reactions (Klyushnik T.P. , Morozov S.G., 2010, Morozov S.G. et al., 2014).

In our studies, it was found that in young children with epilepsy, an increase in AT to MBP up to 1.5 c.u.o.p. and higher and AT to MAG up to 172.4 pg/ml and higher, involved in the occurrence and course of neuroimmune disorders, is associated with an aggravation of the course of the disease. In this regard, early diagnosis of the processes of neuroimmune disorders in the first 1-3-6 months of a child's life can help optimize further treatment and diagnostic tactics and improve the prognosis of the course of the disease.

Detailed description of the method and examples of its clinical implementation.

In full-term newborns and children with epilepsy in the first month, and at the age of 3 and 6 months of life, the level of antibodies to myelin basic protein (MBP) and antibodies to myelin-associated glycoprotein (MAG) is determined in 2 ml of blood serum by enzyme immunoassay using test systems from the company " Navin (Moscow) and Buhlmann (Germany), respectively. The reaction was recorded on a multifunctional programmable counter for immunological studies with a computer and software 1420 Multilabel Counter Victor (Finland).

If the concentration of antibodies to MBP is 1.5 c.u.o.p. and above, and antibodies to MAG is 172.4 pg/ml and above diagnose the development of neuroimmune disorders in epilepsy in children of the 1st year of life. The efficiency of this method is confirmed by the following clinical examples:

Example 1

The D-s child was born from the 3rd pregnancy (1st pregnancy - medical abortion, 2nd pregnancy - non-developing), which proceeded with the threat of termination in the first half, low placentation, signs of premature maturation of the placenta in the second half. Childbirth in the period of 38-39 weeks by caesarean section, due to complete placenta previa, weighing 4100, length 52 cm in a state of asphyxia with an Apgar score of 4-6 points. At the age of 4 days, convulsions were first noted in the form of rhythmic clonic twitching of the muscles of the upper and lower extremities on the right, accompanied by a violation of the rhythm and frequency of breathing, a “marble” skin pattern, perioral and acrocyanosis, which were stopped by intravenous administration of sibazon at an age dosage. The neurosonogram (NSG) revealed a significant depletion of the pattern of sulci and convolutions against the background of increased echogenicity of the brain perenchyma with moderate expansion and asymmetry of the lateral ventricles. On the 7th day of life, the child was transferred to the Department of Neonatal Pathology (ARN) to clarify the diagnosis and therapy. On the 15th day of life, a repeated attack of convulsions of a similar nature was recorded within 15-20 seconds. An examination was carried out in the department: EEG signs of regional epileptiform activity were detected in the fronto-central leads against the background of a slowdown in the main activity of the background recording. MRI of the brain revealed signs of focal cerebral cortical dysgenesis: polymicrogyria, schizencephaly with signs of heterotopia. Based on the results of a comprehensive clinical and instrumental examination, a consultation with a neurologist, the diagnosis was made: Congenital malformation of the brain: focal cerebral cortical dysgenesis: polymicrogyria, schizencephaly with signs of heterotopia. Structural epilepsy with motor onset, bilateral tonic-clonic seizures with focal onset.

At the age of 17 days, peripheral venous blood was taken. The concentration of AT to MBP was 1.5 c.u.p., and AT to MAG was 172.4 pg/ml, which, according to the claimed method, indicates the possible development of neuroimmune disorders. The child was discharged from the department with recommendations for observation and therapy at the place of residence. At 3 months of age, peripheral blood sampling was performed. The concentration of AT and MBP was 1.7 c.u.o.p. and AT to MAG 182.7 pg/ml. At 5.5 months of life, an attack of tonic-clonic convulsions was noted in the right upper limb, accompanied by hypersalivation for 2 minutes, which stopped on its own. At the age of 6 months, repeated peripheral blood sampling was performed. The concentration of AT and MBP was 1.9 c.u.o.p. and AT to MAG 199.1 pg/ml, which, according to the claimed method, testified to the progressive course of neuroimmune disorders and the need to make adjustments to the diagnostic and treatment process.

Example 2

Child K-th was born from 1 pregnancy that proceeded with mild anemia of the I and II half, uterine fibroids, 1 urgent birth through the natural birth canal with discoordination of labor, the imposition of exit obstetric forceps weighing 3750, 51 cm long with 2-fold entanglement umbilical cord around the neck, with an Apgar score of 7-7 points. By the end of the 3rd day of life, attacks of clonic twitching of the muscles of the trunk and extremities were noted twice during the day, accompanied by adversion of the eyes to the left, cyanosis of the face, oramandibular hyperkinesis, which stopped on their own. During the NSG at the stage of the maternity hospital, signs of hypoxic-hemorrhagic brain damage were revealed. On the 4th day of life, blood was taken to determine AT to MBP and AT to MAG, which revealed their values of 1.4 c.e.p. and 169.2 pg/ml, respectively, which, according to the claimed method, indicated the absence neuroimmune disorders. In order to optimize further tactics of observation and therapy, on the 7th day of life, the child was transferred to the neonatal pathology department with a diagnosis of cerebral hypoxic-hemorrhagic lesion of the central nervous system. Symptomatic post-hemorrhagic epilepsy. During the stay in the department of repeated convulsive seizures were not recorded. Based on the results of the examination, EEG signs of mild cerebral changes with irritation of the cerebral cortex, dysfunction of the median structures, and a decrease in the seizure threshold were revealed. MRI of the brain revealed signs of focal glial lesions of the subcortical structures of the brain in combination with asymmetry of the lateral ventricles. The child was discharged from the department with a diagnosis of cerebral hypoxic-hemorrhagic lesion of the central nervous system, structural epilepsy with focal seizures with a motor onset. At the age of 3 and 6 months, peripheral blood sampling was performed again, where the concentration of AT to MBP was 1.2 and 1.3 c.u.p. respectively, a AT to MAG 154.8 and 157.6 pg/ml, respectively, which, according to the claimed method, indicated the absence of neuroimmune disorders in a child with epilepsy.

Example 3

G-ko's child was born from 2 pregnancies (1st pregnancy - a child of 4 years old - healthy), which proceeded physiologically, 2 urgent births through the natural birth canal weighing 3400, 50 cm long, with an Apgar score of 8-8 points. The early neonatal period proceeded smoothly and on the 5th day the child was discharged from the maternity ward. On the 20th day of life, convulsions were first noted in the form of a series of flexor-extensor infantile spasms. The child was hospitalized to the hospital, where, according to the results of the examination (EEG-diffuse typical hypsarrhythmia with no regional changes, generalized epilepsy, brain MRI-moderately pronounced asymmetry of the lateral ventricles), the diagnosis was made: West's syndrome. Produced by the sampling of peripheral blood with the determination of the level of AT to MBP, amounting to 1.6 c.u.p. and AT to MAG, amounting to 185.1 pg/ml, which, according to the claimed method, indicates possible neuroimmune disorders. At the age of 3 months, there was a resumption of seizures with the addition of a myoclonic component. Taken peripheral blood for research: the level of AT to MBP was 1.7 c.u.p., the level of AT to MAG 202.8 pg/ml, which, according to the claimed method, indicates the preservation of neuroimmune disorders. An EEG study (video EEG monitoring) showed an increase in the index of specific paroxysmal activity, which required correction of the anticonvulsant therapy regimen, against which convulsive seizures became less frequent and shorter. The level of AT to MBP at 6 months of life was 1.9 c.u.p., and the level of AT to MAG was 225.6 mg/ml, which, according to the claimed method, indicated the preservation and increase of neuroimmune disorders requiring correction of treatment diagnostic tactics of patient management.

In this way, 150 children were examined. The data obtained are shown in the table.

Statistical processing of research results

Thus, the claimed method for diagnosing neuroimmune disorders in infants with epilepsy in the 1st year of life is quite simple, accessible and has high accuracy, reliability and objectivity, which allows them to carry out not only timely dynamic prospective clinical and laboratory monitoring with advanced immunological examination , but also taking into account its results, include immunotropic drugs in the treatment regimen that contribute to more effective treatment of the underlying disease.

The advantages of this method:

1. The possibility of diagnosing neuroimmune disorders in young children with epilepsy will make it possible to take into account the parameters of the immune status along with clinical and instrumental, including video-EEG monitoring, which will contribute to both adequate treatment tactics and control over the course of epilepsy.

2. Does not require special training of the child.

3. Use minimally invasive diagnostic methods available in clinical practice.

4. High accuracy - 81.2%. Sensitivity - 84.6%. Specificity - 89.1%.

The inventive method for diagnosing neuroimmune disorders in young children with epilepsy has been tested in a hospital and can be recommended for clinical practice.

Claims (1)

A method for diagnosing neuroimmune disorders in young children with epilepsy, including a study of the child's blood serum, characterized in that in full-term newborns and children at the 1st year of life in the first month, at 3 and 6 months, the level of antibodies to the main protein is determined in the blood serum myelin (AT to MBP) and antibodies to myelin-associated glycoprotein (AT to MAG) and at a concentration of antibodies to myelin basic protein of 1.5 conventional optical density units (c.e.o.p.) and higher, and antibodies to myelin-associated glycoprotein 172 .4 pg / ml and above diagnose the development of neuroimmune disorders.