What do we treat epilepsy. Surgical treatment of epilepsy The background of medial temporal sclerosis is observed

MESIAL TEMPORAL SCLEROSIS AND ITS ROLE IN THE DEVELOPMENT OF PALEOCORTAL TEMPORAL EPILEPSY (REVIEW)

MESIAL TEMPORAL SCLEROSIS AND ITS ROLE IN DEVELOPMENT OF PALEOCORTICAL TEMPORAL LOBE EPILEPSY (A REVIEW)

S.H. Gataullina, K.Yu. Mukhin, A.S. Petrukhin

Department of Neurology and Neurosurgery, Faculty of Pediatrics, Russian State Medical University of Roszdrav, Moscow

A review of the literature on the problem of mesial temporal sclerosis is presented. Hippocampal sclerosis was first described by Bouchet and Cazauvieilh in 1825 and is now regarded as a multifactorial, classic epileptogenic brain lesion underlying limbic or mediobasal paleocortical temporal lobe epilepsy, manifested by resistant epileptic seizures. The article highlights the historical aspects of the study of the issue, the anatomy and pathophysiology of hippocampal sclerosis, its role in the development of paleocortical temporal lobe epilepsy.

Key words: epilepsy, mesial temporal sclerosis, etiology, pathogenesis, anatomy, pathophysiology.

The articles gives a review of works on mesial temporal sclerosis. Hippocampal sclerosis was first described by Bouchet and Cazauvieilh in 1825, and is presently classified as a multifactor, classical epileptogenic affection cerebral, underlying limbic or mediobasal paleocortical temporal lobe epilepsy manifested by resistant epileptic seizures. The article highlights historical issues of the subject, anatomy and pathophysiology of hippocampal sclerosis and its role in development of paleocortical temporal lobe epilepsy.

Key words: epilepsy, mesial temporal sclerosis, etiology, pathogenesis, anatomy, pathophysiology.

Definition

Mesial temporal sclerosis (synonyms: hippocampal sclerosis, ammon's horn sclerosis, incisural sclerosis, mesial temporal sclerosis) is a multifactorial, classic epileptogenic brain lesion that underlies limbic or mediobasal paleocortical temporal epilepsy, manifested by resistant epileptic seizures. The term "mesial temporal sclerosis" (MTS) is most often used in the literature, although German authors consider the concept of "Ammon's horn sclerosis" to be more correct. The prevalence and clinical picture of mesial temporal sclerosis in children has not been sufficiently studied to date.

History of study

The Italian anatomist Giulio Cesare Aranzi in 1564 first used the term hippocampus to describe the structure of the brain, clearly similar to a sea horse. Initially, this organ was known only as the center of smell. Later, the neurophysiologist V.M. Bekhterev, based on examinations of patients with severe memory impairment, established the role of the hippocampus in maintaining human memory function. Seizures of a psychomotor nature (complex partial, automotor), which, according to modern concepts, constitute the “core” of the clinical picture of amygdala-hippocampal temporal lobe epilepsy, were described by Hippocrates. There is a legend that the legendary

S.Kh. Gataullina, K.Yu. Mukhin, A.S. Petrukhin

Mesial temporal sclerosis and its role in the development of paleocortical temporal lobe epilepsy (literature review). Rus. zhur. det. Neur.: vol. III, no. 3, 2008.

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Heracles killed his wife and children during a "fit of epileptic madness".

Hippocampal sclerosis was first described by Bouchet and Cazauvieilh in 1825 during an anatomical study of the brain of patients suffering from frequent epileptic seizures. A little later, in 1880, Sommer revealed by microscopy the presence of a characteristic histological pattern in the hippocampus: the death of pyramidal neurons at the base of the temporal horn (Sommer's sector or CAI subfield). Since microscopy created a visual resemblance to the helmet of the Egyptian pharaoh Ammon, which consisted of columns of gold coins, this pathology was called "Ammon's horn sclerosis". But at that time this discovery did not arouse much interest, perhaps because epilepsy was considered a mental (and not morphologically determined) disease. Only at the end of the 19th century, Chaslin (1889) in France and Bratz (1889) in Germany expressed the opinion that the identified changes may play a role in the genesis of epilepsy. A little earlier, in 1880, the great English neurologist John Hughlings Jackson suggested that neurons in damaged areas of the brain have abnormally increased excitability. This further defined the concept of " epileptic focus". Bratz in 1899, studying autopsy materials, found that epileptic seizures at an early age may be one of the causes of hippocampal sclerosis. He also showed that sclerosis of the Sommer sector of the hippocampus can be observed not only in epilepsy, but also in other neurological disorders. According to Bratz, the detected changes in the hippocampus were congenital.

So far, ammon's horn sclerosis and its relationship to epilepsy (cause or effect?) has been a hot topic of discussion. The morphology and topography of changes in hippocampal sclerosis were studied in detail by Spielmayer (1927) and Scholz (1951,1954), who attributed the detected changes to the consequences of frequent convulsive seizures. Gastaut and Roger (1955), as well as Norman (1956, 1957), revealed an increased sensitivity to hypoxia in various parts of the hippocampus and amygdala. According to Gastaut, damage to the mediobasal

parts of the temporal lobe were the result of cerebral edema and subsequent compression of the cerebral vessels. According to Gastaut, Sano and Malamud (1953), febrile status epilepticus played an important role in the development of hippocampal sclerosis. Margerson and Corselli (1966) also hypothesized the significance of epileptic seizures in the genesis of hippocampal sclerosis. In subsequent publications, Falconer (1970) and Oxbury (1987) confirmed the relationship between prolonged febrile convulsions and sclerosis of the ammon's horn by means of clinical and pathological studies.

In 1822, Prichard gave a report of epileptic seizures, bearing the character of ambulatory automatisms. Jackson made a great contribution to the history of temporal lobe epilepsy, who in 1889 first described olfactory hallucinations as an epileptic phenomenon, and proved their appearance when the hook of the hippocampus (uncus) was stimulated. Until now, this type of seizure has retained its historical name "Jackson's uncus attacks".

In 1937 Gibbs F.A. and Gibbs E.L. with Lennox W.G. proposed the term "psychomotor seizures". And 10 years later, Gibbs and Furster (1948) found that when the epileptic focus was localized in the anterior temporal region, seizures with automatisms were predominantly observed. Therefore, to describe this type of seizure, they used the term "automatic", thereby separating them from other "psychomotor" seizures. Gibbs F.A. and Gibbs E.L. in 1938 they presented a description of specific EEG patterns in temporal lobe epilepsy, and later, in 1951, together with Bailey, they came close to solving the issue of surgical treatment of temporal lobe epilepsy. An EEG recording during "psychomotor" seizures showed that rhythmic slow theta activity quickly spreads beyond the temporal region to the entire hemisphere of the same name with a possible capture of the opposite one. This feature prompted Gastaut in 1958 to designate this type of seizure as "partial seizures with diffuse EEG patterns." Other authors, reflecting the localization of the epileptic focus, used the terms "temporo-frontal seizures", "rhinencephalic seizures". Later

studies using video-EEG monitoring and special methods for testing patients have shown that temporal seizures are often accompanied by impaired consciousness. Therefore, the term "complex partial seizures" was introduced, which has been subjected to fierce criticism all the time and was eventually removed from the 2001 Classification Project for Epileptic Seizures.

The term "temporal lobe epilepsy" was proposed in 1941 by the Canadian neurologists Penfíeld and Erickson to describe an epileptic syndrome manifested by seizures with impaired consciousness and automatisms in combination with temporal spikes on the EEG. For the first time, Roger & Roger (1954) became interested in the electroclinical features of temporal lobe epilepsy in children. According to their studies, children had simpler automatisms in the structure of an attack and pronounced autonomic symptoms. However, all the works of that time equated complex partial seizures with temporal seizures, while modern studies have established that some of them are frontal or parietal-occipital, in which the epileptic discharge extends to the mediobasal regions of the temporal lobe.

Despite numerous ongoing studies in the field of temporal lobe epilepsy, there are still no unambiguous answers to the questions: what is the cause of ammon's horn sclerosis? When is it formed? What is the evolution of this pathology?

Anatomical and histological features of the hippocampus

In 1878, Pierce Paul Broca described an area of ​​the central nervous system located in the medial part of both hemispheres of the cerebrum and called it the "limbic lobe" (from Latin "lim-bus" - edge). Later, this structure was named "rhynencephalon", indicating its important role in the sense of smell. In 1937, James Papez proposed another term - "limbic system" - and emphasized the key role of this anatomical substrate in the formation of memory, emotions and behavior (the Peipez circle). The current term "limbic system"

indicates only the anatomical unity of the structures that form it. The central structure of the limbic system is the hippocampus (horn of ammon). Except

Rice. 1. Hippocampus and corpus callosum, top view.

In addition, the limbic system includes the dentate and cingulate gyrus, entorhinal and septal regions, gray shirt (indusium griseum), amygdala (corpus amig-daloideum), thalamus, mastoid bodies (corpus mammillare). In the hippocampus, the head, body, tail, edge, pedicle, and base are distinguished (Fig. 1, 2, 3). Histologically, the following layers are distinguished in the hippocampus (Bogolepova, 1970; Villani et al., 2001):

1. Alveus, contains efferent hippo-campal and subicular axons.

2. Stratum oriens, contains basket cells.

3. Stratum piramidale, contains pyramidal cells, stellate cells and intercalary neurons.

4. Stratum radiatum, consists of apical dendrites of pyramidal cells.

5. Stratum lacunosum, contains perforating fibers.

6. Stratum moleculare, includes a small number of intercalary neurons and a wide branching of the apical dendrites of pyramidal cells.

According to Lorente de No (1934), depending on the location and shape of the pyramidal cells, the hippocampus is divided into 4 subfields (subfíelds): CAI (Sommer's sector) - triangular-shaped neurons, multilayered, of different sizes; CA2 - densely spaced, large pyramidal cells; SAZ - pyramidal cells located

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less tightly packed and mossy fibers (thin, unmyelinated fibers coming from the granular cells of the dentate gyrus); CA4 - large pyramids -

Rice. 2. Hippocampus and corpus callosum, side view.

nye cells, triangular in shape, scattered between mossy fibers (Fig. 4).

In the dentate gyrus (dentate gyrus), 3 layers are distinguished: the molecular layer (long dendrites), the granular layer (granular cells), the polymorphic or subgranular layer, which contains inhibitory neurons of various sizes.

Pathoanatomy and pathophysiology

Rice. 3. Intraventricular part of the hippocampus: 1. body of the hippocampus, 2. head of the hippocampus, 3. tail of the hippocampus, 4. free edge of the hippocampus, 5. peduncle of the hippocampus, 6. base of the hippocampus (subiculum), 7. corpus callosum (splenium), 8. bird spur (calcar avis), 9-collateral triangle, 10. collateral elevation, 11. hook-shaped pocket (recess) of the temporal horn of the lateral ventricle.

According to the description of many authors, selective death of neurons with secondary astroglial proliferation in the CAI zones (Sommer sector), CAZ, CA4, granular cells of the dentate gyrus and the relative preservation of the pyramidal cells of the CA2 zone are pathognomonic for hippocampal sclerosis, according to the description of many authors (Bruton, 1987; Gloor, 1991; Babb, 1997). The anatomical manifestation of cellular damage consists in the death of intercalary neurons in the hilum of the hippocampus and pyramidal cells in the Sommer zone, followed by scarring and atrophy. It is assumed that the death of neurons in the hippocampus leads to the reorganization of synaptic connections between the remaining neurons and, thereby, to dysfunction of the inhibitory and excitatory neurotransmitter systems of the hippocampus. Neuronal death, gliosis, axonal and synaptic reorganization are the main pathological links in the formation of MVS. The sites of gliosis in MVS, like neurons, are able to generate action potentials as a result of the content of pathologically altered astrocytes with a high density of sodium channels. The severity and extent of pyramidal cell death can vary from mild to profound, but the CA2 subfield always remains intact. In many cases, even in the absence of apparent pyramidal cell death in the epileptogenic hippocampus, one can observe selective damage to interneurons containing somatostatin, substance P, and neuropeptide Y.

Often, pathological changes in the hippocampus are bilateral in nature. In some cases, neuronal damage extends to other structures of the limbic system (amygdala, insula, mastoid bodies, thalamus), sometimes involving the lateral cortex and the pole of the temporal lobe.

It is known that the metabolic state of the thalamus is closely dependent on the state of hippocampal neurons in the same hemisphere. Studies by spectroscopic measurement of excitatory amino acids in the hippocampus with frequent recurrent seizures show involvement in the pathological process through neural networks of contralate

Bulb of posterior cornu Calcar avia

Collateral eminence hippocampi

the oral hippocampus and both thalamus. Damage to the functional connections of the hippocampus, as a result of its sclerosis, can affect the maturation processes.

Rice. 4. Fields of the hippocampus.

brain in children.

In the process of studying the hippocampus in children with resistant temporal lobe epilepsy, the following features were identified (Tuxilurn et al., 1997):

1. In the postnatal period, the number of granular cells continues to grow in the hippocampus, the formation of neurons and axons continues.

2. Epileptic seizures that are generated outside the hippocampus (cortical dysplasia, postencephalitic changes, etc.) can contribute to a decrease in the number of granule cells and ammon's horn neurons.

3. Prolonged epileptic seizures in children, unlike adults, do not always lead to severe damage to nerve cells.

It is known that during an epileptic seizure, an excess amount of the excitatory neurotransmitter, glutamate, is released into the synaptic cleft. The hippocampus is the structure most susceptible to glutamate-induced damage, due to the high density of glutamate receptors, especially in the Sommer area. In the hippocampus, in comparison with other parts of the brain, the system of GAM-Kergic recurrent inhibition is relatively poorly developed, but the system of recurrent excitation of pyramidal neurons is maximally represented. During an epileptic seizure, there is a significant influx

calcium ions into the postsynaptic membrane of pyramidal neurons. An increase in the intracellular content of calcium ions triggers a cascade of reactions that cause the activation of proteases, phospholipases and endonucleases, which, in turn, leads to the release of active and potentially toxic metabolites. Deficiency of the main inhibitory neurotransmitter - GABA - is one of the most important factors leading to cytotoxicity.

The limbic system is characterized by the so-called “kindling” process, in which normal brain structures gradually become epileptogenic. In the process of "ignition", mossy fibers (efferent pathways from the granular cells of the dentate gyrus) undergo axonal and synaptic reorganization - sprouting. As a result, return excitatory connections are formed that participate in the progressive development of hypersynchronous discharges. Such synaptic reorganizations are accompanied by the death of pyramidal cells in the hippocampus. Simultaneously with damage to neurons, axons begin to grow to new target cells. Thus, axons of granular cells of the dentate gyrus (mossy fibers) grow in the direction of the inner molecular layer of the dentate gyrus. Because mossy fibers contain glutamate, disruption of synapse formation can lead to a state of hyperexcitability that triggers excessive discharges. Sloviter (1994) found that the most sensitive to excitation are interneurons (mossy fibers), which form synapses with GABA-containing basket cells. As the mossy fibers die, the basket cells become functionally inactive (“dormant”). Deficiency of the functional activity of the inhibitory system contributes to hyperexcitability and the occurrence of epileptic seizures. Normally, mossy fibers (synonyms - intercalary neurons, efferent pathways of granular cells of the dentate gyrus) perform the function of limiting and protecting against excessive activation of their own targets - the pyramidal cells of the SAZ zone of the hippocampus. Abundance return-

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Excitatory synaptic connections in the pyramidal cells of the SAZ zone of the hippocampus and the ability of individual pyramidal cells of the SAZ zone to trigger an active potential in an explosive pattern, explains their role in epileptogenesis. SAS afferents of pyramidal cells - mossy fibers, perform the so-called "gatekeeper" function, limiting excessive activation of SAS of pyramidal cells and preventing the occurrence of seizure activity. Autoradiography has shown that the granule cells of the dentate gyrus actually serve as a barrier protecting the hippocampus from overactivation. Violation barrier function granular cells leads to excessive activation of the SAS of pyramidal cells and hyperexcitability of the hippocampus.

Despite the large number of works devoted to the study and description of pathological changes in hippocampal sclerosis, its etiology is still the subject of debate.

Etiology

Currently, MVS is considered a multifactorial pathology. The main reasons for the development of hippocampal sclerosis according to modern concepts are: atypical febrile convulsions with a high duration of seizures, perinatal ischemia (after the 28th week of gestation), intracranial infections. There is an opinion that genetic predisposition matters in the genesis of hippocampal sclerosis, which is shown in the study of family cases of mesial temporal lobe epilepsy. Of the etiological factors, one can separately note the impact of various metabolic disorders (congenital hyperinsulinism, beta-oxidation anomalies, etc.), which, causing an energy deficit in the brain tissue, can lead to damage to the most sensitive to hypoxia brain structure - the hippocampus.

Bahl (1997) indicates that the epileptic focus is formed when new pathological recurrent, excitatory synapses are formed in the hippocampus.

instead of the dead normal. Although the epileptogenic potential of hippocampal sclerosis is sufficient to form epilepsy, epilepsy and hippocampal sclerosis may be different symptoms the same pathology underlying them, respectively, the development of temporal lobe epilepsy may not depend on cell death and plasticity of the hippocampus.

There are at least 2 types of MVS, which are based on different etiological factors. The first type always includes a unilateral lesion of the hippocampus with a predominant lesion of the CAI zone, the second type is bilateral, with the spread of pathological changes to the SAZ field and other parts of the temporal lobe.

If earlier the relationship of MTS to mesial temporal lobe epilepsy (cause or effect?) caused great controversy, now modern studies prove the post-attack etiology of hippocampal sclerosis. It is believed that prolonged atypical febrile convulsions, status epilepticus, and even a single short generalized tonic-clonic seizure can lead to the formation of MVS. Experimentally provoked prolonged febrile seizures cause axonal reorganization in the immature hippocampus, which leads to its hyperexcitability. Probably, the frequency of seizures does not play a significant role in the formation of hippocampal sclerosis. So, in many patients with a very high frequency of seizures, requiring even surgical functional uncoupling of the hemispheres, hippocampal sclerosis is not detected. On the other hand, prolonged seizures and status epilepticus can contribute to the formation of structural changes ranging from hippocampal sclerosis to hemispheric atrophy. However, only a long duration of seizures is insufficient for the formation of MVS. So, benign occipital epilepsy with an early onset is often accompanied by prolonged seizures (“ictal syncope”, “comatose-like seizures”), but without any structural damage to the brain. Obviously, there are other factors contributing to the formation of structural changes, which are still

not fully identified.

Some authors put forward a hypothesis about the role of angiogenesis in the etiology of hippocampal sclerosis. According to this theory, the process of neovascularization or angiogenesis takes place in the hippocampus, which is accompanied by neuronal-glial reorganization of the epileptogenic focus. It is possible that angiogenesis is stimulated by frequent repeated attacks. Proliferating capillaries in the epileptogenic hippocampus express erythropoietin receptors that are highly immunoreactive. Angiogenesis is maximally expressed in the region of the greatest neuron death and reactive gliosis - in the CAI, CAZ and hilus (chyle) areas of the dentate gyrus. It is possible that erythropoietin enters the brain by receptor-mediated endocytosis. The high content of erythropoietin receptors in the hippocampus in mesial temporal lobe epilepsy suggests a possible role for this cytokine in epileptogenesis.

In mediobasal temporal lobe epilepsy with hippocampal sclerosis, a high incidence of neonatal seizures and a history of perinatal brain lesions was established. It is assumed that, most likely, prolonged febrile convulsions cause damage to the hippocampus in the brain with already existing changes. However, it is possible that febrile seizures are preceded by genetically determined structural disorders in the hippocampus, which facilitate the manifestation of febrile seizures and contribute to the formation of hippocampal sclerosis.

Neuroimaging performed on the first day after febrile seizures reveals hippocampal edema, which decreases after a few days, and in some cases turns into hippocampal atrophy. At the same time, not all children with prolonged atypical febrile seizures subsequently develop temporal lobe epilepsy, which indicates the possibility of joint or isolated influence of genetic, vascular, metabolic and immunological factors.

It has been experimentally shown that in animals it is possible to induce epileptiform activity in the hippocampus

temperature, and also that the febrile seizures themselves can come from the hippocampus or amygdala. Febrile convulsions, mainly with a long duration of seizures, cause hypoxic-ischemic, metabolic changes in the brain and lead to the formation of MVS with the subsequent development of temporal lobe epilepsy. It should be noted that only prolonged atypical febrile convulsions play a role in the genesis of MVS and the subsequent formation of temporal lobe epilepsy. Whereas, epilepsy that develops after typical febrile seizures is more often idiopathic. According to different authors, atypical febrile convulsions in history are observed in 20-38% of patients with temporal lobe epilepsy. A time interval of three years or more (average 8-9 years) is required from the onset of atypical febrile convulsions to the formation of temporal lobe epilepsy. Such a long latent period does not yet find sufficient explanations, but it is most likely that this period of time is necessary for the "maturation" of the hippocampal scar and epileptogenesis.

Previously, some authors proposed a perinatal hypothesis of the occurrence of MVS, which has not yet found any confirmation. According to this theory, mesial temporal sclerosis may be a consequence of pathological childbirth with infringement of the copper-basal parts of the temporal lobe in Bisha's fissure. It was also assumed that hippocampal sclerosis occurs as a result of previous neuroinfections, chronic intoxications, closed craniocerebral injuries, damage to the cervical vertebrae in the neonatal period. The listed pathological conditions in the acute period could cause venous stasis, thrombophlebitis, local diapedetic hemorrhages with subsequent destructive and cicatricial adhesive processes in the brain tissue. Vascular disorders could contribute to chronic cerebral ischemia, causing hypoxia, sclerosis, wrinkling and atrophy of the mediobasal temporal lobes.

It is interesting to note that children with MVS often have a "dual pathology" - a combination of hippocampal sclerosis with another intra- or extra-hippo-

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maple pathology, predominantly cortical dysplasia or less often, neuronal heterotopias, microdysgenesis, gangliogliomas, which suggests a violation of the processes of antenatal brain development in the etiology of MVS. It is possible that the concomitant presence of brain dysgenesis predisposes to more rapid formation of MVS. Clinically, MVS in the structure of "dual pathology" manifests earlier (up to 6 years) than MVS in its "pure form" (the beginning of puberty), and epileptic seizures are more "evil" and resistant to therapy.

It was noted that during the first 5 years of life, the number of granule cells in the dentate gyrus of the hippocampus continues to grow. Emerging granule cells express a particular embryonic form of neuronal adhesion protein, and the number of cells expressing this protein increases during the first 5 years of life. This protein indicates the immaturity of granule cells and their postnatal development, proliferation and migration. Since the process of mitosis and migration continues in the postnatal period in the granular cells of the hippocampus, it is possible that sclerosis of the ammon's horn is the result of impaired neuronal migration. This statement is confirmed by the fact that in the studied groups of patients with neuronal heterotopias of the temporal region and hippocampal sclerosis in isolation, identical patterns of cell death in the hippocampus are found. Animals with experimentally induced neuronal migration disorders were more susceptible to damage to the hippocampus.

AT last years the so-called "devastating epileptic encephalopathy in school-age children" or "pseudoencephalitis" has been described in the literature. This pathology debuts with severe prolonged status epilepticus, fever of unknown etiology and leads to bilateral hippocampal atrophy with the development of severe drug-resistant epilepsy with cognitive impairment. In epileptic syndromes such as severe myoclonic epilepsy of infancy and hemiconvulsive seizures, hemiparesis and epilepsy syndrome (HHE - syndrome), manifested by prolonged febrile seizures and status, Ammon's horn sclerosis is also stated (Nabbout et al., in press).

Interesting observations should be noted, according to which, in the etiology of MVS, persistence may be important herpetic infection(herpes virus type 6) in the mediobasal regions of the temporal lobe. It is noted that the herpetic virus in the brain tissue is detected, even in the absence of inflammatory changes. In some cases, the herpes virus causes encephalitis with a characteristic lesion of the temporal lobe and limbic structures. Herpes simplex virus type 1 predominantly underlies herpes encephalitis in children older than 6 months, while herpes simplex virus type 2 is more often a congenital or perinatal infection. As you know, herpetic encephalitis is often found in children, and it is necessary to remember it as one of the causes of hippocampal sclerosis.

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Bibliography

1. Bogolepova I.N. The structure and development of the hippocampus in prenatal ontogenesis // Zhurn neuropatol and psychiatrist. - 1970. - T. 70, issue 6. - S. 16-25.

2. Minasyan O.Z. Vertebrobasilar circulatory insufficiency in the genesis and treatment of temporal lobe epilepsy: Abstract of the thesis. dis.... doc. honey. Sciences. - 1983.

3. Mukhin K.Yu. Temporal lobe epilepsy // Journal of neurol and psychiatrist. - 2000. - T. 100. - No. 9 - - S. 48-57.

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

5. Arabadzisz D., Fritschy J.M. Reorganization of the GABAergic system during epileptogenesis // Epilepsia - 2004. - Vol. 45, Suppl. 3- - P. 49-51.

6. Arzimanoglou A. Early brain pathology and development of temporal lobe epilepsy // Epilepsia. - 2004. - Vol. 45, Suppl. 3.-P.43-45.

7. Avanzini G. Functional organization of the limbic system. // In: Avanzini G., Beaumanor A., ​​Mira L. Limbic Seizures in Children. - Milan, John Libbey, 2001, - P. 21-29-

8. Babb T.L. Hippocampal sclerosis and dual pathology: experimental and clinical evidence for developmental lesions // In: I. Tuxhorn, H. Holthausen, H. E. Boenigk Paediatric Epilepsy syndromes and their surgical treatment / London, John Libbey, 1997. - P. 227-232.

9. Beaumanoir A., ​​Roger J. Historical notes: from psychomotor to limbic seizures // In: Avanzini G., Beaumanor A., ​​Mira L. Limbic Seizures in Children, Milan, John Libbey, 2001, - P. 1-6 .

10. Bender R.A., Dube C., Gonzalez-Vega R., Mina E.W., Baram T.Z. Mossy fiber plasticity and enhanced hippocampal excitability, without hippocampal cell loss or altered neurogenesis, in an animal model of protracted febrile seizures // Hippocampus. - 2003. - Vol. 13(3). - P. 399-412.

11. Bocti C., Robitaillic Y., Diadori P., Lortie A., Mercier C., Bouthillier A., ​​Carmant L. The pathological basis of TLE in childhood // Neurology. - 2003- - V. 60(2). - P. 162-163-

12. Camfield C., Camfield P. Les crises febriles// In: Roger J., Bureau M., Dravet Ch., Genton P., Tassinari C.A., Wolf P. Les syndromes epileptiques de Tenfant et de G adolescent. - Montrouge, John Libbey, 2005. - P. 159-166.

13. Cendes F., Kanane P., Brodie M., Andermann F. Le syndrome depilepsie mesio-temporale// In: Roger J., Bureau M., Dravet Ch, Genton P., Tassinari C.A., Wolf P. Les syndromes epileptics de Tenfant et de Tadolescent. - Montrouge, John Libbey, 2005. - P. 555-567

14. Chevassus-au-Louis N., Khazipov R. and Ben-Ari Y. Propogation of limbic seizures: experimental studies // In: Avanzini G., Beaumanor A., ​​Mira L. Limbic Seizures in Children. - Milan, John Libbey, 2001. - P. 33-40.

15 D "Incerti L. MRI in limbic structures in the epileptic and non-epileptic child // In: Avanzini G., Beaumanor A., ​​Mira L. Limbic Seizures in Children. - Milan, John Libbey, 2001. - P. 225 -229-

16. Donati D., Akhyani N. et al. Detection of human herpesvirus-6 in mesial TLE surgical brain resections //Neurology. - 2003.-V. 61 (10) - P. 1405-1411.

17. Earle K.M., Baldwin M., Penfield W. Incisural sclerosis and temporal lobe seizures produced by hippocampal herniation // Arch. Neurol. - 1953. - V.63. - P. 27 - 42.

18. Eid T., Brines M.L., Cerami A., Spencer D.D., Kim J.N., Schweitzer J.H. et al. Increased expression of erythropoietin receptor on blood vessels in the human epileptogenic hippocampus with sclerosis // J. Neuropathol. Exp. Neurol. - 2004. - V. 63(1). - P. 73-83-

19- Haas C. Role of migration defects in temporal lobe epilepsy // Epilepsia. - 2004. - Vol. 45, Suppl. 3- - P. 49-51-

20. Hall B.C., Long C.E. et al. Human Herpesvirus-6 Infection in Children. A Prospective Study of Complication and Reactivation // The New England Journal of Medicine. - 1994. - Vol. 331, N. 7. - P. 432-438.

21. Hamelin S., Pallud J., Haussler U., Vercueil L., Depaulis A. Modifications of hippocampal epileptogenesis by progressive hyperthermic seizures in the immature mouse. // Epilepsy. - 2005. - Vol. 46, Suppl. 8. - P. 105-107.

22. Hetherington H., Kenneth P. Vives, Kuzniecky R. I., Spencer D., Pan J.W. Thalamic and hippocampal injury in TLE by NAA spectroscopic imaging // Epilepsia. - 2005. - Vol. 46, Suppl. 8. - P. 107-108.

23. ILAE report. Commission on terminology and classification // Epilepsia. - 2001. - V. 42. - N 6. - P. 796-803.

RUSSIAN JOURNAL OF CHILDREN'S NEUROLOGY

VOLUME III ISSUE 3 2008

24. Kobayashi E. et al. Seizure outcome and hippocampal atrophy in familial mesial temporal lobe epilepsy // Neurology. - 2001. - V. 56. - P. 166-172.

25. Kobayashi E. Magnetic resonance imaging evidence of hippocampal sclerosis in asymptomatic, first-degree relatives of patients with familial TLE, Arch. Neurology. - 2002. - V. 59 (12) - P. 1891 - 1894.

26. Lerner-Nationali M., Rigau V., Crespel A., Coubes P., Rousset M., Baldy-Moulinier M., Bockaert J. Neo-Vascularisation of the Hippocampus in Adult MTLE Patients: Evidens for Angiogenic Processes // epilepsy. - 2005. Vol. 46, Suppl. 6. - P. 276-278.

27. Mathern G.W., Babb T.L., Leite J.P. et al. The pathogenic and progressive features of chronic human hippocampal epilepsy // Epilepsy Res. - 1996. - V. 26(1) - P. 151 - 161.

28. Mikaeloff Y., Jambaqué I., Hertz-Pannier L., Zamfirescu A., Adamsbaum C., Plouin P., Dulac O. and Chiron C. Devastating epileptic encephalopathy in scool-aged children (DESC): a pseudo encephalitis // Epilepsy Res. - 2006. - V. 69(1). - P. 67-79.

29. Muracami N., Ohno S., Oka E., Tanaka A. Mesial temporal lobe epilepsy in childhood // Epilepsia. - 1996. - Vol. 37, Suppl 3. - P. 52-56.

30. Pan J.W., Kuzniecky R.J., Kenneth P. Vives, Hetherington H., Spencer D. Hippocampal glutamate in human MTLE // Epilepsia. - 2005. - Vol. 46, Suppl. 8. - P. 11 - 14.

31. Petroff O.A, Errante L.D., Kim J.H., Spencer D.D. N-Acetil-aspartate, total creatinine, and myo-inosotol in the epileptogenic human hippocampus // Neurology. - 2003. - V. 60 (10). - P. 1645-1651.

32. Scott R.C., King M.D., Gadian D.G., Neville Brain G. R., Connelly A. Hippocampal abnormalities after extensive febrile convulsion: a longitudinal MRI study. // brain. - 2003. - Vol. 126, no. 11, Nov. - P. 2551 - 2555.

33. Scott R.C., Gadian D.G., Cross J.H., Wood S.J., Nevill B.G., Connelly A.: Quantative Magnetic Resonance characterization of Mesial Temporal Sclerosis in Childhood. // Neurology. - 2001. -V.56. - P. 1659-1665.

34. Sloviter R.S. Is Progressive Hippocampal Damage a Cause of Drug Resistant TLE? // Epilepsia. - 2005. - Vol. 46, Suppl. 6.-P.7-9.

35. Sloviter R.S. The functional organization of the hippocampal dentate gyrus and its relevance to the pathogenesis of temporal lobe epilepsy //Ann. Neurol. - 1994. - V. 35 (6) - P. 640-654.

36. Spencer S., Novothy E., de Lanerolle N., Kim J. Mesial temporal sclerosis: electroclinical and pathological correlations and applications to limbic epilepsy in childhood // In: Avanzini G., Beaumanor A., ​​Mira L. Limbic Seizures in Children - Milan, John Libbey, 2001. - P. 41-55.

37. Tuxhorn I., Holthausen H., Boenigk H. Hippocampal pathology in children with severe epilepsy // In: I. Tuxhorn, H. Holthausen, H.E. Boenigk Pediatric Epilepsy syndromes and their surgical treatment. - London, John Libbey, 1997. - P. 234-344.

38. Van Lierde A., Mira L. Aetiological role of febrile convulsive attacks in limbic epilepsy // In: Avanzini G., Beaumanor A., ​​Mira L. Limbic Seizures in Children. - Milan, John Libbey, 2001. - P. 159-163.

39. Villani F., Garbelli R., Cipelletti B., Spreafico R. The lymbic system: anatomical structures and embry-ologic development // In: Avanzini G., Beaumanor A., ​​Mira L. Limbic Seizures in Children. - Milan, John Libbey, 2001. - P. 11-21.

40. Von Campe G., Spencer D.D., de Lanerolle N.C. Morphology of Dentate granule cells in the human epileptogenic hippocampus // Hippocampus. - 1997. - V. 7 (5) - P. 472-488.

41Yu-tze Ng, Amy L. McGregor et al. Childhood Mesial Temporal Sclerosis // Journal of Child Neurology. - 2006. - Vol. 21, Number 6. - P. 512-520.

Hippocampal sclerosis[SG] and mesial temporal sclerosis(MTS) - are the most common histopathological anomalies found in adult patients with drug-resistant form of temporal lobe epilepsy (mesial temporal lobe epilepsy is the most difficult form of epilepsy to treat in adults and in children over 12 years of age).

SG - loss of more than 30% of cells in the CA1 and CA3 regions of the hippocampus with a relative thickening of the CA2 region. The term "MTS" reflects the fact that along with the hippocampus, atrophic and gliotic changes are observed in the amygdala and hook (see figure).

SH has two principal pathological characteristics: [ 1 ] a sharp decrease in the number of neurons, [ 2 ] hyperexcitability of the remaining nervous tissue. Sprouting of mossy fibers plays one of the key roles in epileptogenesis in SH: abnormal axons of granular cells, instead of innervation of the hippocampus (horn of Ammon - cornu Ammonis), reinnervate molecular neurons of the dentate gyrus through excitatory synapses, thus creating local electrical circuits capable of synchronizing and generating an epileptic seizure. An increase in the number of astrocytes, gliosis can also play a role in epileptogenesis, since altered astrocytes cannot sufficiently reuptake glutamate and potassium.

Patients with temporal lobe epilepsy (due to FH/MTS) often have a history of having suffered in childhood (usually before 5 years of age) acute pathology CNS (precipitating damage): the status of febrile seizures, neuroinfection, traumatic brain injury. Stereotypical seizures begin between 6 and 16 years of age, and there may be a so-called latent period, which occurs between the initial precipitating damage and the development of the first epileptic seizure. It is also not uncommon for situations where the so-called "silent" period lasts between the first attack and the development of pharmaco-resistance. This feature of the course of the disease indicates its progressive nature. Also, acute circulatory disorders in the basin of the terminal and lateral branches of the posterior cerebral artery (which cause basal ischemia of the temporal lobe, neuronal death, gliosis and atrophy) and impaired development of the temporal lobe during embryogenesis can also lead to SH. No less relevant is the problem, called dual pathology, which was first described by M.L. Levesque et al. (1991) - a combination of extra-hippocampal lesions (both temporal and extratemporal) with SH. The incidence of this pathology is high: from 8% for tumors to 70% for cortical dysplasia.

SH is often defined in patients with complex partial seizures (secondary generalized seizures are other options). Speaking about the clinical picture of an attack in temporal lobe epilepsy associated with SH, it must be remembered that [ 1 ] each of the symptoms separately is not specific, although there is a typical pattern in the course of an attack; [ 2 ] symptoms during an attack appear when epileptic activity spreads to the brain regions associated with the hippocampus, which in itself does not give clinical manifestations (scalp EEG itself does not detect epiactivity in the hippocampus, which has been demonstrated in numerous studies using intracerebral electrodes; for appearance of epiactivity in the temporal region on the scalp EEG requires its propagation from the hippocampus to the adjacent cortex of the temporal lobe).

Mesial temporal lobe epilepsy has 3 peak age debuts - at 6, 15 and, less often, at 27 years. The characteristic beginning of a temporal seizure is an aura in the form of an upward sensation in the abdomen (associated with the excitation of the islet). There may also be fear or anxiety if the amygdala is involved at the onset of an attack. At the beginning of the attack, there may be a feeling of "already seen" (déjà vu, associated with excitation of the entorhinal cortex). Alarming in terms of diagnosis is the aura in the form of dizziness or noise, which may indicate an extrahippocampal onset of an attack. The preserved ability to name objects and speak during an attack is an important lateralizing sign of damage to the non-dominant hemisphere. The change in consciousness is accompanied by a cessation of actions, while the patient has a frozen look with wide open eyes (starring). The aura and cessation of actions are followed by oroalimentary automatisms with chewing, smacking lips (associated with excitation of the insula and frontal operculum). Also, dystonia of the contralateral side of the sclerotic hippocampus of the hand often occurs (which is associated with the spread of epiactivity to the basal ganglia) and manual automatisms that appear in this case in the form of sorting objects with the fingers of the ipsilateral hand. Among the lateralizing symptoms importance have postictal paresis, which indicates involvement of the contralateral hemisphere, and postictal aphasia, if the dominant hemisphere is affected. These symptoms should be considered in the context of the EEG data. A characteristic cognitive deficit in FH may be memory loss, especially in uncontrolled seizures.

Diagnosis of epilepsy due to FH is based on three main principles:

[1 ] a detailed analysis of the sequence of symptoms in an epileptic seizure, or semiology, which depends on which parts of the brain epileptic activity spreads (see above);

[2 ] analysis of EEG data and their comparison with the semiology of the attack; epileptic activity on the EEG in mesial temporal epilepsy (MTE) may be absent or only indirect conditioned epileptiform elements (rhythmic slow-wave [delta-theta] activity) may be recorded; the study of the bioelectrical activity of the brain during EEG monitoring of sleep significantly increases the likelihood of diagnosing pathological epileptiform activity (regional spike-wave activity); however, for the correct interpretation of sleep EEG in MVE, a highly qualified neurologist-epileptologist is needed, who can assess the complex of clinical and EEG symptoms and establish the correct diagnosis; accurate diagnosis of MVE is possible with the use of intracerebral, subdural and intracisternal (implanted through the foramen ovale) electrodes.

[3 ] detection of an epileptogenic lesion during MRI (should be performed according to an epileptological protocol, among the main characteristics of which one can single out a small thickness of sections and a high strength of the magnetic field): a decrease in the volume of the hippocampus and a violation of the structure of its layers, a hyperintense signal in T2 and FLAIR mode; atrophic changes are often detected in the ipsilateral amygdala, the pole of the temporal lobe, the fornix, and the mamillary body.

Rendering standard medical care patients with drug-resistant MVE is to refer the patient to a specialized center for pre-surgical examination and surgical treatment. Surgery for temporal lobe epilepsy has two obvious goals: [ 1 ] ridding the patient of seizures; [ 2 ] canceling drug therapy or reducing the dose of the drug. The task of surgical treatment of temporal lobe epilepsy includes the complete removal of the epileptogenic cerebral cortex with the maximum preservation of functional areas of the brain and minimization of neuropsychological deficit. There are two surgical approaches in this regard: temporal lobectomy and selective amygdalohippocampectomy. removal of the hook, amygdala and hippocampus. Surgery for temporal lobe epilepsy in SH, with sufficient experience of the surgeon, has minimal risks of neurological deficit (persistent hemiparesis, complete hemianopsia).

Literature:

article "Sclerosis of the hippocampus: pathogenesis, clinic, diagnosis, treatment" D.N. Kopachev, L.V. Shishkina, V.G. Bychenko, A.M. Shkatova, A.L. Golovteev, A.A. Troitsky, O.A. Grinenko; FGAU "Research Institute of Neurosurgery named after N.N. acad. N.N. Burdenko” of the Ministry of Health of Russia, Moscow, Russia; Federal State Budgetary Institution "Scientific Center for Obstetrics, Gynecology and Perinatology named after A.I. acad. IN AND. Kulakov" of the Ministry of Health of Russia, Moscow, Russia (magazine "Issues of neurosurgery" No. 4, 2016) [read];

article “Mesial temporal sclerosis. The current state of the problem” Fedin A.I., Alikhanov A.A., Generalov V.O.; Russian State Medical University, Moscow (magazine "Almanac of Clinical Medicine" No. 13, 2006) [read];

article "Histological classification of mesial temporal sclerosis" Dmitrenko D.V., Stroganova M.A., Schneider N.A., Martynova G.P., Gazenkampf K.A., Dyuzhakova A.V., Panina Yu.S.; SBEE HPE "Krasnoyarsk State Medical University. prof. V.F. Voyno-Yasenetsky" of the Ministry of Health of Russia, Krasnoyarsk (journal "Neurology, neuropsychiatry, psychosomatics" No. 8 (2), 2016) [read];

article "Febrile seizures as a trigger for mesial temporal sclerosis: a clinical case" N.A. Schneider, G.P. Martynova, M.A. Stroganova, A.V. Dyuzhakova, D.V. Dmitrenko, E.A. Shapovalova, Yu.S. Panin; GBOU VPO Krasnoyarsk State Medical University. prof. V.F. Voyno-Yasenetsky Ministry of Health of the Russian Federation, University Clinic (magazine "Problems of Women's Health" No. 1, 2015 [read];

article "Possibilities of magnetic resonance imaging in the assessment of structural changes in the brain in patients with temporal lobe epilepsy" Anna A. Totolyan, T.N. Trofimova; LLC "NMC-Tomography" Russian-Finnish Clinic "Scandinavia", St. Petersburg (magazine "Russian Electronic Journal of Radiation Diagnostics" No. 1, 2011) [read];

article " Surgery symptomatic temporal lobe epilepsy” A.Yu. Stepanenko, Department of Neurology and Neurosurgery of the Russian State Medical University, City Clinical Hospital No. 12 of the Moscow Department of Health (Neurosurgery magazine No. 2, 2012) [read]

© Laesus De Liro

sclerosis called pathological compaction of organs caused by the death of functional elements and their replacement by connective tissue. Sclerosis mainly affects the cardiovascular system.

Multiple or multiple sclerosis called a chronic disease of the nervous system, in which in the head and spinal cord, as well as in the peripheral nerves, multiple lesions develop.

Symptoms: The symptoms of multiple sclerosis depend on which organs and tissues are affected. The onset of the disease is characterized by a decrease in vision (sometimes double vision), weakness and numbness of the limbs, and unsteadiness when walking.

What's happening? The development of sclerosis in most cases is caused inflammatory processes, especially chronic (tuberculosis, syphilis, etc.), and tissue metabolism disorders (with prolonged oxygen starvation due to circulatory disorders or cholesterol metabolism disorders). As a result of the progression of the disease, the normal functions of the affected organs decrease, up to their complete loss.

The reasons

1. Hereditary predisposition.

2. Viral diseases.

The cause of the disease is a virus that is not transmitted from sick to healthy. Typically, multiple sclerosis affects people between the ages of 20 and 40. In the future, all of these disorders increase, then there is a period of improvement, followed by a new outbreak with a progressive deterioration.

Multiple sclerosis is a long-term disease that can last 20 years or more.

Sometimes multiple sclerosis appears suddenly, but more often develops after infectious diseases especially influenza, trauma, pregnancy and childbirth.

It is classified according to the lesion into cerebral, spinal and cerebrospinal.

Signs of the disease

Characterized by weakness of the legs or arms on one side. Changes in gait and coordination of movements. Trembling of the hands, torso or head may be detected.

Muscle tone can be either increased or decreased. Speech becomes slurred and jerky.

With a long course of the disease, personality changes are noted: memory and mental abilities decrease, the patient becomes angry and aggressive, loses criticism of his own condition and behavior.

Diagnosis of the disease

Diagnosis is based on the study of cerebrospinal fluid and computed tomography, which reveals lesions of the spinal cord or brain.

Treatment of the disease

Selected individually. Corticosteroids, immunosuppressors, glucocorticoid hormones are prescribed. Sometimes plasmapheresis is performed and drugs that improve metabolic processes are used. As well as vascular and antihistamines.

Forecast

The prognosis for life is most often favorable.

Eat chokeberry, cottage cheese, vegetables and fruits, horseradish, parsley, apples and wild rose, raspberries and apricots, pomegranate and barberry;

Drink spring water;

Drink a glass of hot water every morning on an empty stomach.

Prevention of sclerosis is the prevention and timely treatment diseases that can potentially lead to sclerotic changes.

Methods traditional medicine it is possible to alleviate the condition of the patient, and under favorable circumstances and a great desire of the sick person, to cure him.

In most cases, the causes of sclerosis are various inflammatory diseases, as well as metabolic disorders due to prolonged oxygen starvation of tissues, disorders of the functions of endocrine organs, etc.

Sclerosis can develop in all human organs and tissues.

• Removes organic salts from the walls of blood vessels and purifies the blood Japanese Sophora: 50 g of flowers or fruits of Sophora insist on 0.5 liters of vodka for a month. Drink 1 teaspoon 3 times a day for 3-4 months. For those who cannot drink alcohol, brew 1 tablespoon of Sophora with 1 cup of boiling water overnight in a thermos. Drink 1-2 tablespoons 3 times a day.
• Removes inorganic salts, soothes, regulates the pressure of mistletoe. Dry the plant, grind into powder. Brew overnight in a thermos 1 teaspoon of the finished powder with 1 cup of boiling water. Drink 2 tablespoons in small sips 15-20 minutes before meals for 3-4 months. The combination of mistletoe and sophora cleanses the vessels well, making them elastic. It is useful to use these plants for those who are over 40 years old.

Decoctions and infusions

Half fill a liter jar with dried pink clover heads, pour 0.5 liters of vodka over them and put them in a dark place for 2 weeks. Drink 1 tablespoon before bed. The course of treatment is 3 months, a break is 2 weeks.

Mix 20 g of yarrow herb, 20 g of mistletoe "white, 50 g of bearded cystoseira. Brew 1 tablespoon of the mixture with a glass of boiling water, insist, wrapped for 2 hours, strain. Drink in sips throughout the day.

Pour 1 teaspoon of Manchurian Aralia 1/2 cup of water or 50 ml of alcohol. Within 1 month, drink 30-40 drops of the obtained tincture of Aralia Manchurian 3 times a day before meals.

Brew 3 tablespoons of crushed dandelion root with 2 cups boiling water, bring to a boil and simmer for 15 minutes over low heat. Drink 1 tablespoon 2 times a day 30 minutes before meals. You need to dig up the roots either in early spring, before flowering, or after the leaves have withered.

Mix 15 g of rue herb, 25 g of hawthorn leaves, 25 g of hawthorn flowers, 10 g of valerian root. Pour 1 glass cold water 1 tablespoon of the mixture, leave for 3 hours, boil for 4 minutes, leave for 20 minutes, strain. Drink sips throughout the day

Mix 30 g of yarrow herb, 15 g of small periwinkle, 15 g of horsetail, 15 g of white mistletoe, 15 g of hawthorn flowers. Pour 1 cup of cold water over 1 cup of the mixture, leave for 1 hour, boil for 5 minutes, strain. Drink sips throughout the day.

Insist 40 g of red clover grass per 0.5 l of 40% alcohol for 10 days. Take before dinner or at bedtime for 20 g.

Mix 10 g of stinging nettle and yarrow herb. Pour 1 tablespoon of the mixture with 0.5 liters of water and boil for 10 minutes. Take 0.5 cup at night. In addition to the main action, the decoction improves metabolism.

Mix 30 g of dandelion root, 30 g of wheatgrass root, 30 g of soapwort root, 30 g of yarrow herb. Infuse 1 tablespoon of the mixture in 1 cup boiling water for 1 hour. Take 1 glass in the morning and evening. The treatment is long.

At multiple sclerosis and atherosclerosis, fresh onion juice mixed with honey is useful (1 glass of juice per glass of honey). For 3 weeks, take 1 tablespoon 3 times a day 1 hour before meals or between meals. If necessary, extend the treatment up to 2 months.

Recipes for the treatment of sclerosis

1. Garlic oil. Peel a medium-sized head of garlic, crush into a pulp. Fold in a glass jar and pour a glass of unrefined sunflower oil. Put in the refrigerator down. The next day, take a lemon, mash, cut off the bump (from the place where it grows), squeeze out a teaspoon lemon juice and pour into a tablespoon. Add a teaspoon of garlic oil there, stir. Take 3 times a day 30 minutes before meals. The course is from 1 to 3 months, then a month break and repeat the course. Relieves spasms of cerebral vessels, cardiac spasms, shortness of breath. An excellent vasodilator.

2. Heather. 1 heaping tablespoon of chopped heather per 0.5 liters of boiling water. Boil for 10 minutes, insist, wrapped, 3 hours, strain. Drink as tea and water at any time of the day, drink with anything. Used for atherosclerosis nervous disorders, insomnia, cardiovascular diseases, circulatory disorders of the brain, liver diseases, stones and sand in the kidneys and bladder. The first week, take 1/2 cup, and then a glass.

3. Garlic. Fill 1/3 bottle with chopped garlic. Pour vodka or 50-60-degree alcohol. Insist 14 days in a dark place, shaking daily. Take 5 drops 3 times a day before meals in a teaspoon of cold water. Cleanses the circulatory system from all kinds of deposits, removes high blood pressure, cleanses the stomach, has a beneficial effect on spasms of cerebral vessels.

4. Honey, onions. Grate onion on a fine grater, squeeze. Mix a glass of onion juice with a glass of honey. Stir well, if the honey is sugared, slightly warm in a water bath. Take a tablespoon 3 times a day one hour before meals or 2-3 hours after meals. It is used for atherosclerosis, especially for cerebral sclerosis.

5. Active lifestyle, weight loss, diet. Restriction in the diet of sugar, sweets, animal fats. Avoid foods rich in cholesterol: brains, egg yolk, caviar, fatty meats and fish, vitamin D, salt and extracts of other substances (meat, broths, fish soup). Recommended: cottage cheese, well-soaked herring, cod, oatmeal, vegetable oils: olive, corn, sunflower, linseed. More vegetables, fruits, rich in vegetable fiber. If you are overweight, fasting days are recommended: apple, kefir, cottage cheese, compote, etc. Walk more in clean air, drink spring, well or tap water passed through filters. A precipitate of chlorine, salts, lime scleroses blood vessels. Cleans well vessels, removes deposits: apples, horseradish, garlic, wild rose, flowers buckwheat, heather, cinquefoil, vitamin P-rutin, sea kale, parsley - greens, roots, red mountain ash. Drink green tea.

6. Red clover (flowering leafy tops collected at the beginning of flowering). 40 g of flowers insist in 500 g of vodka for 2 weeks. Strain, squeeze. Take 20 g before lunch or at bedtime. The course of treatment is 3 months with a break of 10 days. After 6 months, the course can be repeated. It is used for atherosclerosis with normal blood pressure, accompanied by headaches and tinnitus.

7. Hot water. Every morning on an empty stomach drink 200-300 g of hot water, as far as tolerable. This cleanses the blood vessels, cleanses them and removes all kinds of deposits from the body.

8. With sclerosis, accompanied by a noise in the head, a mixture of clover with a stem is taken in equal portions. Brew the mixture like tea and drink throughout the day.

This infusion is also used in the treatment of stomach ulcers, gastritis and colitis.

9. Elecampane. Elecampane tincture on vodka is an ancient remedy for senile sclerosis. 30 g dry root 500 ml of vodka insist 40 days. Accept by 25 drops before meals.

10. Rowan bark. 200 g squiggle 500 ml of boiling water and cook over low heat for 2 hours. Accept by 25 drops before meals.

With senile sclerosis, a thick decoction of mountain ash is taken.

11. Propolis. 20% solution of propolis in 70% ethyl alcohol, 20 drops in warm water 1-2 times a day in the morning and in the afternoon for 20-30 minutes. before meals. The course of treatment is 1-3 months, depending on the individual tolerance of the patient.

Temporal epilepsy is a chronic disease of the central nervous system, namely the brain, one of the types of epilepsy with localization of the pathological focus in the temporal lobe. It is accompanied by convulsive paroxysmal seizures and loss of consciousness. It is the most common form. Pathology is usually associated with a change in the structure of anatomical formations (sclerosis of the hippocampus).

Why temporal lobe epilepsy develops is not precisely established. All the alleged causes of development are divided into two large groups: perinatal, that is, affecting the fetus, and postnatal - factors that disrupt the functioning of the nervous system after the birth of a child.

Perinatal include:

• pathogenic pathogens that have entered the amniotic fluid by transplantation from the mother (rubella, syphilis, and so on);
• hypoxia or asphyxia of the fetus due to entanglement of the umbilical cord or aspiration of the upper respiratory tract meconium on later dates pregnancy;
• spontaneous disturbances in the formation of the nervous tissue of the brain, a violation of the architectonics of the cerebral cortex;
• Prematurity or postmaturity of the fetus.

Postnatal causes include:

• neuroinfections and inflammation of the membranes of the brain;
• skull trauma and concussion
• growth of benign or malignant neoplasms;
• tissue infarction of the temporal lobe due to impaired blood circulation and tissue trophism, stroke;
• sclerosis, replacement of healthy cells with connective tissue under the influence of Mycobacterium tuberculosis;
• intracerebral hematoma;
• toxic effects of certain medicinal substances used in the wrong dosage, various other chemical compounds;
• metabolic disease;
• malnutrition and vitamin deficiency.

Hereditary predisposition to the development of temporal lobe epilepsy has not been proven.

Such structural changes in tissues, such as, for example, sclerosis of the hippocampus (mesial temporal sclerosis), lead to inadequate excitation of the surrounding cells, which give an unreasonable electrical impulse. An epileptic focus is formed, generating a signal and provoking convulsive seizures.

Classification and symptoms

It is classified according to the localization of the focus into 4 types: amygdala, hippocampal, lateral, insular or opercular. In medical practice, the division has been simplified and doctors divide it into lateral and mediobasal epilepsy.

Lethal epilepsy is less common, auditory, visual hallucinations are observed, the patient speaks incoherently and complains of severe dizziness. Spasm of the motor muscles is not typical, consciousness is lost gently, slowly, the person seems to fall into another reality.

The amygdala usually forms in childhood. It is characterized by gastrointestinal disorders, disorders of the autonomic nervous system. Seizures are accompanied by food automatisms, the patient slowly, gradually falls into an unconscious state. In one third of all cases, clonic generalized seizures are observed.

The cause of the hippocampal type is hippocampal sclerosis, which accounts for 80% of cases of all types of temporal lobe epilepsy.

Its feature is hallucinations, illusions, the patient is immersed in a different environment at the level of consciousness. A seizure lasts about two to three minutes on average.

Insular or opercular type is accompanied by twitching of mimic muscles, acceleration of frequency heart rate and increased blood pressure, belching and other digestive disorders. Taste hallucinations are possible.

In temporal lobe epilepsy, symptoms can also recur for all subtypes. So common signs are chills, palpitations (arrhythmia), a feeling of inexplicable fear, memory impairment, a change in the menstrual cycle in girls, and sudden mood swings from aggression to euphoria.

Diagnostics

The diagnosis is quite difficult to make on the basis of the anamnesis of the disease and complaints. Such patients are treated exclusively by epileptologists, psychiatrists and neurologists. It is almost impossible to diagnose such a pathology in the early stages, because the clinical picture is poor and practically does not impair the quality of life.

From a neurological point of view, no abnormalities are observed on general examination. Changes can be only in the case of tumor growth in the temporal lobe and with heavy bleeding. Then pathological reflexes, instability of gait, manifestations of improper functioning of the seventh and twelfth pairs of cranial nerves may appear.

Laboratory diagnostics is important if a neuroinfection is suspected. In that case, in general analysis blood, typical signs of inflammation are observed, with serological study Plasma antibodies to a specific microorganism are determined, and bacteriological culture provides complete information about the infection and its sensitivity to antibacterial or antiviral agents.

The most informative are instrumental modern methods. So the electroencephalogram shows the epileptic activity of the foci in the temporal lobe of the brain. The etiological factor can be determined on computed or magnetic resonance imaging. It can show hippocampal sclerosis, changes in the architectonics of the cerebral cortex, and other pathologies. Positron emission tomography provides complete information about the decrease in metabolism in a particular area and the violation of its functionality.

Treatment and prognosis

Treatment for temporal lobe epilepsy consists in relieving symptoms, that is, reducing the frequency of seizures, as well as eliminating the cause, if it is completely clear to the specialist. Therapy begins with the appointment of one drug, namely karmabzepin, the dose is selected individually and gradually increased. In severe cases, it is rational to use valproates and, in rare cases, difenin.

Polytherapy is rational only in the absence of effects from previous medications. Then two or three antiepileptic drugs are combined with each other. medicines, but in this case, strict control by a neurologist is necessary, since further violations of the structure of the organs of the central nervous system and a deterioration in the patient's well-being are possible.

In most cases, to eliminate the clinical picture, they resort to surgical intervention. So, extensive sclerosis of the hippocampus is removed or destroyed, a growing tumor that compresses neighboring tissues is resected according to indications, the cortex of the epileptogenic zone is aspirated.

Temporal epilepsy gives a disappointing prognosis, especially in childhood. No experienced doctor can give a full guarantee of the elimination of seizures, since with the help of medications the condition improves only in one third of cases, and with the operation performed - in 60%. Complications appear very often in the postoperative period: incoherence of speech, muscle paresis and paralysis, reading disorders, mental disorders.

Prevention is more aimed at eliminating negative effects on the fetus, reducing the incidence of birth injuries and timely treatment of infectious diseases.

3. Bireben A., Doury T., Scarabin Ü.M. // In: Reflex epilepsies: progress in understanding / Ed. P. Wolf, Y. Inoue and B. Ziikin. John Libbey Eurotext; France. -2004. - P. 135-141.

4. Brawn P., Fish D.R., Andermann F. // In: Epilepsy and Movement Disorders / Ed. R. Guerrini et al. - Cambridge University Press, 2002. - P. 141-150.

5. Dubowitz L.M.S., BouzaH., Hird M.F., Jaeken, J.//Lancet. - 1992. - V. 340. - P. 80-81.

6. Fejerman N. // Rev. Neurol. - 1991. - V. 147. - P. 782-97.

7. KokO., Bruyn G.W. // Lancet. - 1962. -V. 1. - P. 1359.

8. Kurczynsky T.W. // Arch. Neurol. - 1983. - V. 40. - P. 246-248.

9. Matsumoto J., Fuhr P., Nigro M., Hallett M., Ann. Neurol. - 1992. - V. 32. - P. 41-50.

10. Manford M.R., Fish D.R., Shorvon S.D. // J. Neurol. neurosurgery. Psychiatry. - 1996. - V. 61. - P. 151-6.

11. Morley D. J., Weaver D. D., Garg B. P., Markand O., Clin. Genet. - 1982. - V. 21. - P. 388-396.

12. Obeso J.A., Artieda J., Luquin M.R. et al. // clinic. Neuropharmacol. - 1986. - V. 9. - P. 58-64.

13. Rees M.I., Andrew W., Jawad S. et al. //Hum. Mil. Genet. - 1994.-V. 3. - P. 2175-2179.

14. Ryan, S. G., Nigro, M. A., Kelts, K. A. et al. // Am. J. Hum. Genet. - 1992. - V. 51 (suppl.). - A200.

15. Stevens H. //Arch. Neurol. - 1965. -V. 12. - P. 311-314.

16. Suhren, O., Bruyn G. W., Tuynman J. A. // J. Neurol. Sei. - 1966. - V. 3. - P. 577-605.

17. Shiang R., Ryan S. G., Zhu Y. Z. et al. // Nature Genet. - 1993. - V. 5. - P. 351-357.

18. Vigevano F., di Capua M., Dalla Bernandina B. // Lancet. - 1989. - V. 1. - P. 216.

MESIAL TEMPORAL SCLEROSIS. CURRENT STATUS OF THE PROBLEM

A. I. Fedin, A. A. Alikhanov, V.O. generals

Russian State Medical University, Moscow

Hippocampal sclerosis is the leading cause of temporal lobe epilepsy in young adults. Views on the etiopathogenetic foundations of mesial temporal sclerosis (MTS) and its neuroimaging semiology are as numerous as the synonematic series of the disease or, more correctly, the pathological state of the basal temporal lobes is diverse: the already mentioned MTS and mediobasal sclerosis are joined by hippocampal sclerosis, sclerosis of the amygdala- hippocampal complex and quite exotic incisural sclerosis. With such a wealth of names, due, obviously, to the inevitable contradictions in the interpretations between morphologists, neuroradiologists and clinicians, the persistent exploitation of the essentially non-specific term "sclerosis" attracts attention. Indeed, the essence of structural disorders in the temporal lobes, with a certain degree of assumption, can be characterized as sclerosis, but the falling shadow of the two older brothers - scattered and tuberous - interferes with the map and introduces elements of chaos into a coherent system of classificatory conclusions.

However, symptomatic temporal lobe epilepsy is the most common form of locally determined epilepsy and, in addition, the most common cause true resistance to anticonvulsant treatment. The pathological triad - febrile convulsions, hippocampal sclerosis and resistant temporal lobe epilepsy has long been the object of close attention of neurologists, and therefore an attempt to review the current state of the problem seems to be very relevant.

Recently, the opinion has been spreading among researchers that the neuroradiological diagnosis of MVS has the right to exist only if it is confirmed histopathologically. This opinion is probably due to the extreme freedom of interpretation of this term and sufficient grounds.

for the subjective assessment of the temporal lobes according to neuroimaging data. It is characteristic that the conductors of the above opinion are exclusively morphologists, specialists in radiation diagnostics and neurologists, as before, tend to trust the intravital and non-invasive identification of MVS. We also stand under this banner and in this paper we intend to characterize the clinical, electroencephalographic and neuroimaging aspects of the MVS, as well as present an algorithm for its complex diagnostics based on the integrative use of EEG data, clinical features and tomographic imaging results.

First of all, it should be mentioned that the pathomorphological substrate of hippocampal sclerosis - gliosis and atrophic reduction of the cortical plate and underlying white matter - is found in the material of 50-70% of autopsy material obtained after partial, subtotal or total amygdalas performed for resistant epilepsy - hippocampusectomy. And this figure perfectly reflects the situation with the prevalence of hippocampal sclerosis in the population of patients with epilepsy and, in particular, with temporal lobe epilepsy.

In modern pathogenetic schemes of epilepsy, it is the anatomical hippocampal-amygdala complex that is considered as the main generator of epileptic activity in patients with temporal lobe epilepsy. The presence of changes in neuroimaging and electroencephalography in most cases is combined with a typical temporal semiology of seizures.

At the same time, studies conducted by individual authors using functional and histopathological methods suggest that other areas of the brain may also be involved in the generation of epileptic activity in patients with neuroradiological signs of mesial sclerosis. In addition, there is no unequivocal opinion about the nosological independence of the MVS syndrome.

From the point of view of some authors, the frequent association of hippocampal sclerosis and microdysgenesis allows us to conclude that hippocampal sclerosis is an independent disease of dysplastic etiology. Thus, a scientific substantiation is provided for the existence of "dysplastic" forms of hippocampal sclerosis, whose neuroradiological and clinical-neurophysiological difference from basal-temporal focal cortical dysplasia is very conditional. And the practical advantages of isolating such a nosologically independent diagnosis from the structure of hippocampal cortical dysplasia are completely non-obvious.

On the other hand, the increased sensitivity of the hippocampal regions to the effects of nonspecific exogenous and endogenous damaging factors has long been known and practically undeniable. These include, first of all, the hypoxic-ischemic stress factor, by the way, the recognized leader in the initiation of structural potentially epileptogenic cerebral foci, rightfully sharing its leadership with focal cortical dysplasia. This allows us to consider hippocampal sclerosis as a particular manifestation of encephalopathy of various etiologies.

And finally, we cannot ignore the third, in our opinion, the main structural variant of hippocampal sclerosis, which is a consequence of the coexistence of the presumptive existing paleocortical basal-temporal dysplasia and the secondary gliosis-atrophic disorders of the hippocampus structure that have “layered” on it.

Despite the large number of studies of hippocampal sclerosis, conducted using the most modern intravital and pathomorphological methods, there are currently no unambiguous points of view on

causal relationships between exogenous and endogenous factors and atrophic and sclerotic changes in the temporal lobe.

So, the main theories of the development of hippocampal sclerosis today are the following:

Influence of febrile convulsions (or the theory of incisural post-edema herniation): febrile convulsions -> regional disorders of tissue metabolism in the temporal cortex - local temporal lobe edema -> incisural herniation -> regional dyscirculatory changes -> neuronal death - reactive gliosis and atrophy - a decrease in the volume of the hippocampus, reactive expansion of the hippocampal groove and the lower horn of the homolateral lateral ventricle.

Acute violations of regional circulation in the pool of para-medial and terminal branches of the posterior cerebral artery: spontaneous embolization of the artery or persistent angiospasm -> regional ischemia of the basal parts of the temporal lobe - diapedetic secondary hemorrhagic "weeping" -> local edema - incisural herniation -> regional discirculatory changes -\u003e neuronal death -\u003e reactive gliosis and atrophy - "decrease in the volume of the hippocampus, reactive expansion of the hippocampal sulcus and lower horn of the homolateral lateral ventricle.

Disorders of histogenesis in the paleocortex of the temporal lobe (hypogenetic and dysplastic processes): an initiating stress factor affecting neurotogenesis in the period from the 17th to the 21st week of gestation -> violation of neuronal migration, organization and proliferation ->■ formation of neuronal heterotopions in the white matter of the temporal lobe and focal or multifocal cortical dysplasias (like "small" forms of FCD, focal pachygyria, focal microgyria or partial temporal hypoplasia), characterized by the presence of a large number of giant primitive neurons and an extremely unstable membrane and prone to stable epileptogenesis.

Superpositional theory of the formation of a focus of hippocampal sclerosis: an initiating stress factor affecting neurotogenesis in the period from the 17th to the 21st week of gestation - a violation of neuronal migration, organization and proliferation -> the formation of focal or multifocal cortical dysplasia -> imperfection of the structure of the cortex of the basal sections temporal lobe and vulnerability to secondary dyscirculatory disorders; the tendency of the damaged temporal lobe to rapid local edema -> local swelling of the temporal lobe -» ■ incisural herniation -> regional dyscirculatory changes - neuronal death -> reactive gliosis and atrophy -> decrease in hippocampal volume, reactive expansion of the hippocampal sulcus and lower horn of the homolateral lateral ventricle.

If we trace the pathogenetic stages of the formation of hippocampal sclerosis, some basic positions become apparent, which are the points of intersection of all four theories. This is, first of all, regional basal-temporal discirculation and temporal lobe edema. The main anatomical condition for the implementation of the discussed pathological mechanisms is the presumptive inferiority of the structure of the temporal lobe, namely, cortical dysplasia of the temporal paleocortex.

The mentioned theories are presented in a certain hierarchical sequence, reflecting the number of their adherents according to the literature data.

Indeed, the vast majority of researchers point to the causal nature of the relationship between frequent complicated febrile seizures and sclerotic disorders of the hippocampus structure. Various authors estimate the frequency of febrile seizures in the population as 2-10%. Most researchers are of the opinion that persistent febrile paroxysms, and according to some authors, even single febrile seizures,

lead to irreversible changes in the hippocampus in the form of selective death of neurons. This statement can be supported by the fact of a progressive increase in atrophic changes in the hippocampus against the background of ongoing seizures, which is recorded during serial dynamic MRI studies.

V.V. William et al (1997) conducted a study comparing hippocampal volumes in patients with epilepsy with a history of febrile seizures and patients without a history of febrile seizures. In the group of patients with febrile seizures the vast majority showed a significant bilateral decrease in hippocampal volumes. In the comparison group, in patients with epilepsy without a history of febrile convulsions, such changes were found only in 1 out of 19 examined. It should be noted that there were no significant differences in the course of epilepsy and demographic parameters between the groups. Based on the presented data, it can be concluded that the volume of the hippocampus decreases due to the influence of febrile paroxysms; and, in turn, it seems obvious that afebrile seizures do not affect the morphological state of the hippocampal regions.

Other studies illustrate the existence of a direct relationship between the duration of the course of epilepsy and the degree of hippocampal sclerosis. At the same time, the early onset of epileptic seizures and the presence of febrile convulsions in history correspond to a more pronounced degree of hippocampal sclerosis.

In hippocampal sclerosis, atrophy is a consequence of neuronal death, which is the result of excitotoxicity and excessive electrical activity in the epileptic focus. Another mechanism for the occurrence of atrophy is metabolic disorders due to persistent seizures.

N.F. Moran et al. in their series, they did not find an association between the degree of hippocampal atrophy and the number of generalized seizures suffered. These data coincide with the histological and pathomorphological studies of other authors.

According to another version, the presence of damage to the hippocampus due to various exogenous and endogenous factors may contribute to the occurrence of febrile seizures. As etiological causes, genetic, perinatal, hypoxic, infectious, traumatic and other types of non-specific effects can be considered. That is, in fact, it is assumed not the initiating role of febrile convulsions in the initiation of hippocampal sclerosis, but, on the contrary, the determining nature of damage to the hippocampus in the initiation of febrile seizures. And this is a fundamentally different view of the problem. A view that has the right to exist, but is extremely vulnerable due to the proven fact of the progression of structural changes in the hippocampus depending on the number and quality of febrile attacks.

Another controversial opinion on the relationship between febrile seizures, hippocampal sclerosis and epilepsy is the point of view of A. Arzimanoglou et al. (2002), who, in their observation of patients with febrile seizures, found no increased risk of subsequent epilepsy when compared with the general population. An unfavorable prognostic factor in terms of the development of epilepsy was the presence of atypical febrile seizures. According to the authors, prolonged convulsions are an indicator of predisposition to epilepsy, and taking anticonvulsants reduces the likelihood of recurrence of febrile seizures, but does not reduce the risk of subsequent epilepsy.

Currently, among the probable anatomical variants of damage to the temporal lobe in hippocampal sclerosis and epilepsy, there is an increasing number of

the role is assigned to microdysgenesis, that is, to those structural pathological elements, the presence of which is not included in the prerogative of intravital imaging, being the subject of study exclusively of histological methods. A large number of publications are devoted to the topic of hippocampal microdysgenesis, among which the study by M. Thom et al. (2001). In their series, the frequency of detection of microdysgenesis confirmed by pathological examination was 67%.

The authors found a set of cytoarchitectonic disorders characteristic of hippocampal sclerosis, which included heterotopic neurons in the molecular layer, an increase in the number of neurons in the white matter, and alteration of the cortical laminar architecture.

An increase in neuronal density occurs due to a decrease in the volume of the hippocampus and depends on the degree of sclerosis. In a number of studies, an increase in the number of neurons in the white matter was a predictor of a poor clinical outcome of epilepsy, in other cases it was combined with a favorable outcome.

The frequency, age priority and specificity of clinical implementation could not but raise the question of the genetic predisposition of hippocampal sclerosis. However, a well-established or, at least, proven opinion on this account still does not exist. A genetic study of atypical febrile seizures among monozygotic twins revealed the presence of paroxysms in 15-38% of the examined patients. The discovery of similar changes in monozygotic twins suggests that the presence of a genetic predisposition is one of the leading factors in the formation of hippocampal sclerosis.

According to one of the widespread histopathological hypotheses, stimulation of hippocampal pathological neurogenesis occurs under the influence of persistent seizures. NOT. Scarfan et al. showed that the formation of granule cells in the dentate gyrus occurs throughout life. This process is influenced by various stimuli, including convulsive status. An increase in neurogenesis after status epilepticus leads to the appearance of ectopic neurons, which, in turn, leads to a reorganization of synaptic connections and an increase in epileptogenesis.

In contradiction with the proposed hypothesis, there are data on the selective death of neurons in the fields CA1 and CAZ as a result of the damaging effect of status epilepticus. According to traditional judgments, sclerotic changes are predominantly localized in the anterior part of the hippocampus. However, a number of works suggest that diffuse sclerotic changes in hippocampal sclerosis prevail over focal lesions. B. Meldrum (1991) in his work gives the ratio of detectable sclerosis of the anterior hippocampus to diffuse sclerosis as 1:2.7.

Any neuroimaging specialist can point out the controversial nature of the statements about the exclusively unilateral nature of hippocampal sclerosis, since in his practice he has repeatedly encountered its bilateral variants. AT classical understanding mediobasal temporal sclerosis develops in only one temporal lobe. Recently, however, more and more authors report bilateral hippocampal lesions. According to various sources, the number of patients with bilateral sclerosis ranges from 8 to 46% of the total number of patients with MVS. This fact allows us to conclude that the territorial involvement of different areas of the brain in the pathological process in MVS is wider than previously thought.

However, M. Koutroumanidis et al. in a prospective study of patients with hippocampal sclerosis, no significant influence length

the severity of the course of epilepsy, the frequency and number of seizures on the degree of atrophic changes according to MRI.

In addition, the inconsistency of interpretations of the detection of hippocampal atrophy is also associated with the fact that similar lesions can be detected in patients who do not have an epileptic disease. Thus, an MRI study of 52 healthy relatives of patients with verified hippocampal sclerosis revealed the presence of hippocampal atrophy in 18 (34%) of them. At the same time, the classic picture of mesial sclerosis was detected in 14 examined patients. This allowed the authors to conclude that hippocampal sclerosis is not a consequence of recurrent seizures. The results of the study show that there is no absolute relationship between hippocampal sclerosis and epilepsy. The authors suggest that hippocampal atrophy is determined by the presence of a genetic predisposition, and the manifestation of epileptic seizures is the resultant of exogenous and endogenous factors.

In general, the relationship of hippocampal sclerosis and febrile seizures can be indicated by the following paradoxical statement: most children with febrile seizures never have epileptic seizures in the future, however, many adults with temporal lobe epilepsy and hippocampal sclerosis had a history of febrile seizures.

Another frequently discussed theory is hypoxic damage to the structures of the hippocampus due to impaired cerebral circulation in the perinatal period.

It is proposed to separate three stages of epileptogenesis after a dyscirculatory lesion of the temporal lobe: an initial stroke, a latent period of various duration, and a stage of epileptic seizures. An important role in the mechanisms of epileptogenesis belongs to the activation of the excitotoxic cascade. The activation of calcium channels occurring in the ischemic focus, an increase in the number of excitatory amino acids and free radicals lead to selective cell death in the hippocampus. Electroencephalographic markers chronic stage epileptogenesis, the authors consider an increase in the amplitude of polyspikes in the hippocampus.

The influence of hippocampal sclerosis on the development of strokes in the elderly was noted. In a series by J. Leverenz et al. (2002) showed that in the group of patients with hippocampal sclerosis, the development of dementia and strokes was more often determined. Comparison of risk factors for cerebrovascular diseases in the examined group with the control did not reveal significant differences.

Another etiological factor in damage to the hippocampus is neuroinfection. Patients who have experienced severe meningitis may subsequently have resistant temporal seizures. Pathological examination after surgical treatment revealed classic sclerosis of the ammon's horn.

Thus, various studies have shown the influence of various exogenous and endogenous, congenital and acquired factors on the development of hippocampal damage.

Hippocampal injury is often seen in patients with complex partial seizures.

Other types of seizures are secondary generalized seizures. Before the onset of seizures, the patient may experience an autonomic or limbic aura. The presence of epigastric, gustatory and visual aura is much more common in hippocampal sclerosis than in damage to other localizations. The extrahippocampal location of the epileptic focus is often associated with dizziness. Preservation of the aura in the absence of seizures after surgical treatment is determined in 18.9% of patients. This indicates the spread of the lesion beyond the temporal lobe. For

In comparison, with hippocampal lesions, the aura persists only in 2.6% of those operated on.

Concentric visual loss in hippocampal sclerosis has been described. The authors point out that this phenomenon can also occur with anteromedial temporal lesions and lesions of the occipitotemporal region.

A frequent manifestation of an attack is the presence of motor automatisms and a dystonic setting of the contralateral hand.

Analysis of the lateralization of motor automatisms and dystonic position of the limbs makes it possible to determine the localization of the epileptic focus.

Half of patients with refractory temporal lobe epilepsy have dystonic attitudes. In mesial temporal lobe epilepsy, the focus was ipsilateral to the lesion.

Motor automatisms were detected in 26 out of 60 examined patients in the study by S. Dupont et al. In mesial epilepsy, the focus was localized ipsilateral to the lesion; in neocortical epilepsy, only contralateral.

The combination of ipsilateral motor automatisms and contralateral dystonic set was found in 14 patients with mesial epilepsy and was not detected in neocortical epilepsy. The authors conclude that the analysis of motor automatisms and dystonic attitudes is a reliable criterion for differentiating the mesial and neocortical localization of the focus.

In addition to ictal manifestations, in hippocampal sclerosis, various interictal disorders are determined, indicating damage to the structures of the temporal lobe.

In the study of the mental state of patients with temporal lobe epilepsy as a result of hippocampal sclerosis, who have complex partial seizures, a significant general impairment of cognitive functions was found in the form of a decrease in intelligence, visual-spatial functions and speech. Decreased associative memory and verbal impairments were found mainly in lesions of the left temporal lobe.

The development of a theory about the role of mesial temporal sclerosis in epileptogenesis became possible only after the introduction of neuroimaging methods in daily practice epileptologists. The development of functional neuroimaging techniques, such as positron emission tomography and functional MRI, has made it possible to obtain dynamic information about the level of metabolism and regional cerebral blood flow in the affected areas of the temporal lobe and, specifically, the hippocampus.

It should be mentioned that not all neuroimaging methods are equally informative in the diagnosis of structural and functional hippocampal lesions.

CT scan of the brain does not allow the diagnosis of mesial sclerosis, but the presence of indirect signs in the form of a decrease in the volumetric parameters of the affected temporal lobe and expansion of the lower horn of the ipsilateral lateral ventricle to a certain extent suggests a diagnosis and is a prerequisite for a more in-depth study of the state of the temporal lobe.

The specificity of MRI in the diagnosis of mesial sclerosis is recognized as prevailing over other imaging methods and confirmed by numerous tests from the standpoint of the "gold standard", that is, obtained during temporal resections for incurable epilepsy; MRI signs of mesial sclerosis are the detection of asymmetry in the volume of the hippocampus, a focal increase in signal intensity in T2 mode and a decrease in intensity in T1 mode.

Currently, the determination of the volume of the hippocampus is a routine technique in the presurgical diagnosis of temporal lobe epilepsy. A relatively new direction in the preoperative preparation of patients with hippocampal sclerosis is the determination of the volume of extratemporal structures. This direction is relevant, since it has been established that frequent findings in the examination of patients with hippocampal sclerosis are a decrease in the volume of not only the hippocampus, but also the extrahippocampal regions, as well as the subcortical structures of the homo- and contralateral temporal lobe.

According to N.F. Moran et al., the presence of changes in the ratio of white and gray matter in the extrahippocampal regions is a predictor of adverse outcomes after temporal resection.

Modern studies have shown that morphological and functional changes in hippocampal sclerosis are not limited to the medial temporal regions, but extend to neighboring areas of the brain.

We have already noted that in patients with drug-refractory epilepsy in hippocampal sclerosis, MRI volumetry reveals significant extrahippocampal atrophic disorders. The degree of extra-hippocampal atrophy correlates with the degree of hippocampal atrophy but has no connection with the course of generalized seizures and the duration of epilepsy. The authors suggest that hippocampal and extrahippocampal atrophy are based on common mechanisms. The presence of an extended zone of atrophic lesions may explain the lack of effect of temporal lobectomy in a number of patients with hippocampal sclerosis.

Functional MRI in hippocampal sclerosis primarily reveals a significant metabolic asymmetry in the temporal lobes.

When using brain mapping methods in the diagnosis of hippocampal sclerosis, the information content of positron emission tomography is estimated at 85.7%. The detected foci of hypometabolism corresponded to the area of ​​anatomical damage in 97% of cases. A feature of metabolic disorders in hippocampal sclerosis is their unilateral localization. Another frequently detected finding was the detection of combined hypometabolism in the medial and lateral neocortex, which were verified in 19 out of 30 patients. Metabolic changes in the lateral neocortex were not accompanied by structural damage according to routine MRI.

The use of positron emission and single photon emission tomography in patients with anatomical signs of hippocampal sclerosis showed that in most cases functional brain damage exceeds visible anatomical boundaries - and this is the most important fact from the point of view of presurgical evaluation of patients with resistant epilepsy and hippocampal sclerosis. Paeschen et al. examined 24 patients with hippocampal sclerosis and untreated complex partial seizures. Single photon emission tomography during a seizure revealed changes in the ipsilateral temporal lobe, at the border of the ipsilateral middle frontal and precentral gyrus, in both occipital lobes, and small areas of hyperperfusion in the contralateral postcentral gyrus.

Interictal single photon emission tomography revealed a significant correlation between the detection of hypoperfusion in the ipsilateral temporal and frontal regions, which indicates the functional spread of the pathological process to the adjacent temporal regions of the brain.

The use of MR spectroscopy made it possible to detect metabolic dysfunction in the affected area. The discrepancy between the severity of metabolic disorders and the degree of sclerosis, according to MRI, suggested that these processes have different pathogenetic bases. The basis of functional disorders in hippocampal sclerosis is neuronal and glial dysfunction, and not the death of hippocampal neurons.

Similar data are provided by T.R. Henry et al. When examining patients with temporal lobe epilepsy, he found the presence of regional hypometabolism in the temporal lobe in 78%, in the mesial-temporal lobe - in 70%, in the projection of the thalamus (63%), basal ganglia (41%), frontal lobe (30% ), parietal (26%) and occipital lobes (4%). The authors conclude that the thalamus plays a significant role in the initiation and spread of temporal seizures and consider it responsible for the interictal cognitive deficit in temporal lobe epilepsy.

In 80-90% of patients with hippocampal atrophy, the EEG reveals interictal activity.

The most common findings during routine scalp EEG are regenar slowing and regional spike-wave activity. Interictal regional slow activity is determined in 57% of patients with temporal lobe epilepsy as a result of hippocampal sclerosis. A characteristic feature is the predominant unilateral localization of slow-wave activity, which decreases when the eyes are opened.

The maximum amplitude of slow waves is determined in the temporal lobes of the brain always homolateral to the anatomical injury. The presence of slow-wave activity is associated with hypometabolism in the lateral temporal neocortex. A strict correlation between the focus of hypometabolism, according to positron emission tomography, and the EEG deceleration zone allows the use of neurophysiological research methods to determine the areas and sizes of reduced neuronal inhibition. These changes are determined in the interictal period and intensify during an attack.

Regional delta activity, continuous and polymorphic or intermittent and rhythmic, is often associated with involvement of the white matter and thalamus and reflects deafferentation of the superior cerebral cortex. Interictal activity is more common in patients with partial seizures, and in this context it is a reliable lateralizing symptom.

The presence of regional slowing has no connection with the age of patients and the duration of the course of epilepsy, the frequency and number of seizures.

The authors point to the presence of a combined reduced metabolism in the medial and lateral temporal fields. Primary neuronal loss in the hippocampal formation and amygdala leads to chronic deactivation and metabolic depression in the lateral temporal field.

Another frequently detected EEG pattern in hippocampal sclerosis is spike wave activity. When analyzing the characteristics of spike-wave activity in 61 patients with hippocampal sclerosis with temporal lobe epilepsy and mesial sclerosis, spike-wave complexes were determined unilaterally in 39 patients, and bilateral localization in 22. With bilateral localization of spike waves, no correlation with anatomical damage was found.

The presence of unilateral spike-wave activity does not have strict correlations with the localization of hippocampal and amygdala atrophy.

The scalp EEG data are confirmed by the results of intraoperative electrocorticography. At the same time, epileptiform activity is determined more often in the medial and lateral regions of the temporal lobe.

Prolonged post-seizure confusion is always associated with bilateral atrophy and EEG spike activity.

Since hippocampal sclerosis is the cause of resistance to drug therapy epileptic seizures, it should be considered through the prism of probable surgical antiepileptic interventions aimed at its total or subtotal excision. The absence of effects from anticonvulsants in the presence of a verified focus of epileptic activity is regarded as an indication for surgical treatment of epilepsy.

The extensive experience of temporal lobe surgery has shown the high efficiency of surgical treatment of epilepsy associated with hippocampal sclerosis.

In a series by O. Hackerman et al. 50 patients with MVS underwent anterior temporal resection. The treatment success rate was 52%, significant improvement - 88%.

Anterior temporal lobectomy includes amygdalohippocampal resection and lateral neocortical resection.

According to classical concepts, the removal of the epileptic focus is the main goal of surgical intervention. However, temporal resection in half of the operated patients does not have a significant effect on the course of seizures, and this is an indirect evidence of the involvement of other, extratemporal or extrahippocampal cerebral structures in epileptogenesis.

It should be noted that a thorough pre-surgical examination allows at the initial stage to reduce the likelihood of low outcomes. Identification of a bitemporal lesion, the presence of extrahippocampal epileptic foci, according to the results of corticography, are a contraindication to the surgical treatment of epilepsy.

However, even among patients selected for surgical treatment, the likelihood of a poor outcome is quite high. Despite careful preoperative preparation, about 30% of patients with untreated partial epilepsy due to hippocampal sclerosis retain seizures after appropriate hippocampal resection.

Most authors believe that the reason for the low outcomes is the presence of hidden extrahippocampal structural anomalies that are not detected during preoperative brain mapping. During the follow-up observation of the operated patients, out of 27 patients with verified hippocampal sclerosis, 14 subsequently revealed extrahippocampal foci. 10 of them had continued seizures. Of 13 patients without extrahippocampal injury, 11 were seizure-free.

Thus, hippocampal sclerosis appears to us as a many-sided and contradictory condition, which has certain features that characterize it: it underlies resistant temporal lobe epilepsy; considered as a theoretical address of surgical resection; it is multifactorial in nature, but fairly uniform in visual characteristics; more often it is unilateral, but bilateral representation is also possible; in addition to seizures, he announces himself by slowing down on the EEG and probable contralateral carpal dystonic settings. And, finally, it is inextricably linked with febrile seizures, just as they are associated with it, and this connection is so strong that it mixes the possible leadership of one of the pathological conditions we are discussing.

LITERATURE

1. Alikhanov A.A. Petrukhin A.S. Neuroimaging in epilepsy. - M., 2001. - 238 p.

2. Arzimanoglou A., Hirsch E., Nehlig A. et al. II epileptic. Discord. - 2002. - V. 3. - P. 173-82.

3. Barr W.B., Ashtari M., Schaul N. // Neurol. neurosurgery. Psychiatry. - 1997. - V. 63. - P. 461-467.

4. Bien C. G, Benninger F. O., Urbach H. et al. // brain. - 2000. V. 123. No. 2. P. 244-253.

5. Burneo J.G., Faught E., Knowlton R. et al. // Associated With Hippocampal Sclerosis. -2003. - V. 6, No. 60. - P. 830-834.

6. Cascino G.D., JackC.R.Jr., Parisi J.E. etal. // Epilepsy Res. - 1992.-V. 11, #1. - P. 51-59.

7. Cendes F, Andermann F, Dubeau F, Gloor P. et al. // Neurology. - V. 43, Issue 6. - P. 1083-1087.

8. Davies K.G., Hermann B.P., Dohan F.C. et al. // Epilepsy Res. - 1996. - V. 24, No. 2. - P. 119-26.

9. Dupont S., Semah F., Boon P., A//Arch. Neurol. - 1999.-V. 8, No. 56. - P. 927-932.

10. Fried I., Spencer D.D., Spencer S.S. // J. Neurosurg. - 1995. - V. 83, No. 1. - P. 60-66.

11. Gambardella A., Gotman J., Cendes F., Andermann F. // Arch. Neurol. - 1995. - V. 52, No. 3.

12. Hardiman O., Burke T., Phillips J. et al. // Neurology. - V. 38, Issue 7. - P. 1041-1047.

13. Henry T.R., Mazziotta J.C., Engel J.//Arch. Neurol. - 1993. - V. 50, No. 6.

14. Hogan R.E., Mark K.E., Wang L. et al. // Radiology. - 2000. - V. 216. - P. 291-297.

16. Kobayashi E., Lopes-Cendes I., Gendes F. // Arch. Neurol. -2002. -V. 59. - P. 1891-1894.

17. Koepp M.J., Labbe C., Richardson M.P., Brooks D.J. et al. // brain. - V 120, Issue 10. -P. 1865-1876.

18. Koutroumanidis M., Binnie C.D., Elwes R. et al. // J. Neurol. neurosurgery. Psychiatry. - 1998.-V. 65.-p. 170-176.

19. Kuzniecky R., Palmer C., Hugg J. et al. // Arch. Neurol. - 2001. - V. 58. - P. 2048-2053.

20. Leverenz J., Agustin C.M., Tsuang D. // Arch. Neurol. - 2002. - V. 59, No. 7. - P. 1099-1106.

21. Martin R.C., Sawin S.M., Knowlton R.C. et al. // Neurology. - 2001. - V. 57. - P. 597-604.

22. McBride M.C., Bronstein K.S., Bennett B. et al. // Arch. Neurol. - 1998.-V. 55, No. 3. - P. 346-348.

23. Meencke H.J. & Janz D. //Epilepsia. - 1984. V. 25, No. 1. - P. 121-133.

24. Meldrum B.// Epilepsy Res. - 1991. - V.10, No. 1. - P. 55-61.

25. Moran N.F., Lemieux L., Kitchen N.D. //Brain. -V. 124, No. 1, - P. 167-175.

26. Nelson K.B., Ellenberg J.H. // J. Med. - 1976. V. 295. - P. 1029-1033.

27. Ounsted C., Glaser G.H., Lindsay J. et al. // Arch. Neurol. - 1985. - V. 42, No. 11.

28. Scharfan H.E., Solan A.E., Goodman J.H. et al. // Neuroscience. - 2003. - V. 121. - P. 1017-1029.

29. Sisodiya S.M., Moran N., Free S.L. etal. //Ann. Neurol. - 1997.-V. 41, no. 4. - P. 490-496.

30. Thorn M., Sisodiya S., Harkness W., Scaravilli F. // Brain. - 2001. - V. 124, No. 11. - P. 2299-2309.

31. William B.B., Manzar A., ​​Neil S. // Neurol. neurosurgery. Psychiatry. - 1997. - V. 63. - P. 461-467.

32. Woermann F.G., Barker G.J., Birnie K.D. // J. Neurol. neurosurgery. Psychiatry. - 1998. - V. 65. - P. 656-664.

33. Wolfa R.L., Alsopa D.C., Levy-Reisa I. et al. // Neurol. neurosurgery. Psychiatry. - 1997. - V. 63. - P. 461-467.