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Mesial temporal sclerosis. Modern condition of the problem

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

Russian State Medical University, Moscow

Hippocampal sclerosis is the leading cause of the development of temporal epilepsy in people of young age. Villas on the etiopathogenetic bases of the meal temporal sclerosis (MVS) and its neuralization semiology are equally numerous, how much is a synionmatical series of diseases or, more correctly, the pathological state of the basal departments of temporal shares: hippocampal sclerosis, the sclerosis of amygdar, is already connected to the MVS already Hippocampal complex and very exotic incombustal sclerosis. With such a wealth of items, due, obviously, inevitable contradictions in the interpretations between morphologists, neuroradiologists and clinicians, the persistent exploitation of non-specific essentially of the term "sclerosis" is attracted. Indeed, the essence of structural disorders in the temporal fractions with a certain degree of assumption can be described as sclerosis, but the incident shadow of two older brothers - scattered and tuberous - interferes with the cards and makes elements of chaos into a slim system of classification conclusions.

At the same time, symptomatic temporal epilepsy is the most commonly found locally due to the form of epilepsy and, moreover, the most common cause of true resistance to anticonvulsant treatment. Pathological triad - febrile convulsions, hippocampal sclerosis and resistant temporal epilepsy has long been an object of close attention of neurologists, and therefore it seems to us very relevant attempt to the observance of the current state of the problem.

Recently, among the researchers, it applies to the opinion that the neuroradiological diagnosis of the MVS has the right to exist only with histopathological confirmation. This opinion is probably due to the extreme freedom of interpretation of this term and sufficient foundations

for subjective assessment of temporal fractions according to neuralizing data. It is characteristic that exceptionally morphologists are the guides of the mentioned opinion, and neurologists are still inclined to trust the prominent and non-invasive identification of the MVS. We also stand under this banner and in the present work intend to characterize clinical, electroencephalographic and neurovalization aspects of the IMP, and also submit to the algorithm of its comprehensive diagnosis based on the in-project use of EEG data, clinical features and the results of tomographic visualization.

First of all, it should be mentioned that the Patomorphological substrate of the hypochemal sclerosis - glyosis and atrophic reduction of the cortical plate and the subject to the white substance - is found in the material of 50-70% AU-TsSION material obtained after the resistant epileps of partial, subtotal or total amygdal -Hypepocampactomy. And this indicator does not better reflect the situation with the prevalence of hippocampal sclerosis in the population of patients with epilepsy and, in particular, with temporal epilepsy.

In modern pathogenetic schemes of epilepsy, it is an anatomical hippocampal-amigdaryar complex that is considered as the main generator of epileptic activity in patients with temporal epilepsy. The presence of changes in neurovalization and electroencephalography in most cases are combined with typical temporal seven seven semiology.

At the same time, studies conducted by individual authors using functional and histopathological methods make it possible to assert that other areas of the brain can take part in the generation of epileptic activity in patients with neuroradiological signs of mezi-ailic sclerosis. In addition, there is no unambiguous opinion on the nosological independence of the MVS syndrome.

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

On the other hand, the increased sensitivity of hippocampal departments to the effects of nonspecific ex- and endogenous damaging factors has long been known and practically indisputable. These include, before, in total, the hypoxic-ischemic stress factor, by the way, the recognized leader in the initiation of structural potentially epileptogenic cerebral foci is rightfully dividing its leadership with focal cortical dysplasia. This allows us to consider hippocampal sclerosis by the private manifestation of encephalopathy of various etiologies.

And finally, it is impossible to ignore the third, in our opinion, the main structural version of the hippocampal sclerosis, which is a consequence of the coexistence of the prespetively existing paleocortic basal-temporal dysplasia and the secondary gliose-atrophic disorders of the hippocampal structure on it.

Despite the large number of studies of hippocampal sclerosis carried out using the most modern lifetime and Pato morphological methods, there are currently no unambiguous points of view on

causal relationship between exogenous and endogenous factors and atrophic and sclerotic changes in the temporal share.

So, the main theories of the development of hippocam-clutch sclerosis are the following:

Influence of febrile convulsion (or the theory of incombustal post-depths -\u003e Regional disorders of tissue metabolism in the core of the temporal share - the local swelling of the temporal share -\u003e Inci-teuraling -\u003e Regional discirculatory changes -\u003e Neuro-national death - reactive gyosis And atrophy is a decrease in the volume of hippocam-pa, the reactive expansion of the hippocampal groove and the lower horns of the hydraulic-rally side ventricle.

Acute disorders of regional blood circulation in the pool of para-medial and terminal branches of the rear cerebral artery: Spontaneous Embo-lyrics of the artery or resistant angiospaz -\u003e Regional ischemia of basal departments of temporal share - Diapened secondary hemorrhagic "propoteva" -\u003e Local edema - incombustal insertion -\u003e Regional discirculatory changes -\u003e Neuronal death -\u003e reactive glyosis and atrophy - "Reduction of the volume of hippocampus, reactive expansion of the hippocampal groove and the lower horn of a gomolateral side ventricular.

Violations of histogenesis in the paleokortetex of the temporal share (hypochenetic and dysplastic processes): initiating stress factor affecting neurontogenesis in the period from the 17th to the 21st week of gestation -\u003e violation of neural migration, organization and proliferation -\u003e ■ formation of neuronal heterotopions In the white substance of the temporal share and focal or multifocal cortical dysplasia (by the type of "small" forms of FKD, focal pachugiry, focal microhydial 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 the focus of hippocampal sclerosis: initiating a stress factor impassing neurontogenesis in the period from the 17th to the 21st week of gestation - violation of neural migration, organization and proliferation -\u003e Focal or multifocal cortical dysplasia formation -\u003e imperfection of the structure of the bark of basal departments temporal share and vulnerability for secondary discirculatory disorders; The inclination of the damaged temporal share to the rapid local edema -\u003e the local swelling of the temporal share - "■ Incizural insertion -\u003e Regional discirculatory changes - neuronal death -\u003e reactive glyosis and atrophy -\u003e decrease in the volume of hippocampus, reactive expansion of the hippocampal groove and lower horns of the gomolateral side ventricle.

If you trace the pathogenetic stages of the formation of hippocampal sclerosis, some major positions are obvious, which are points of intersection of all four theories. This is, above all, regional ba products and temporal discirculation and swelling of temporal share. The main anatomical condition for the implementation of the pathological mechanisms discussed is the presumptive inferiority of the structure of the temporal share, namely, the cortical dysplasia of the temporal paleocortex.

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

Indeed, the overwhelming majority of researchers indicate the causal nature of the relationship of frequent complicated febrile convulsions and sclerotic disorders of the hypocampal structure. Various authors estimate the frequency of febrile seizures in the population as 2-10%. Most researchers express the view that persistent febrile paroxysms, and in the opinion of some authors, even single febrile seizures,

they lead to irreversible changes in the hippocampus in the form of the selective death of neurons. In favor of this assertion, the fact of the progress of the initiation of atrophic changes in hippocampus may indicate on the background of continuing seizures, which is registered with serial dynamic MR studies.

V.V. William et al. (1997) conducted a study in which the lumetaic indicators of hippocampus patients with epilepsies having peb-rivors in history and patients without anamnestic febrile cramps. In the group of patients with febrile convulsions, the overwhelming majority was discovered a significant bilateral decrease in hippochemical volumes. In the comparison group in patients with epilepsy without febrile seizures in history, such changes were discovered only in 1 of the 19 surveyed. It should be noted that there were no significant differences in epilepsy and demographic indicators between groups. Based on the submitted data, it can be concluded that the volume of hippocampes is reduced due to the influence of febrile paroxysms; And, in turn, it seems obvious that Africral seizures do not affect the morphological state of hippocampal departments.

Other studies illustrate the presence of direct communication between the duration of the epilepsy flow and the degree of hippocampal sclerosis. At the same time, the early debut of epileptic seizures and the presence of febrile convulsions in history corresponds to a more pronounced degree of hippocampal sclerosis.

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

N.F. Moran et al. In its series, they did not find links between the degree of hippocampal atrophy and the number of shared generalized attacks. These data coincide with histological and pathological studies of other authors.

For another version, the presence of damage to the hippocampus due to various exogenous and endogenous factors can contribute to the appearance of febrile seizures. As etiological reasons, genetic, perinatal, hypoxic, infectious, traumatic, and other types of non-specific impacts can be considered. That is, in fact, it is assumed not to initiate the role of febrile convulsions in the initiation of hippocampal sclerosis, but on the contrary, which determines the nature of the damage to the hippocampus in the initiation of febrile seizures. And this is a fundamentally different look at the problem. A glance that has the right to exist, but extremely vulnerable due to the proven fact of the prishability of structural changes in hippocampus, depending on the number and quality of febrile attacks.

Another controversial opinion on the relationship of febrile attacks, hippocampal sclerosis and epilepsy looks view of A. Arzimanoglou and et al. (2002), which, in their observation of patients with febrile seizures, did not reveal the risk of developing subsequent epilepsy when compared with the overall population. An unfavorable prognostic factor in the development of epilepsy was the presence of atypical febrile attacks. According to the authors, long-term convulsions are an indicator of susceptibility to epilepsy, and the intake of anticonvulsant drugs reduces the likelihood of repetition of febrile attacks, but does not reduce the risk of subsequent epilepsy.

Currently, among probable anatomical options for damage to the temporal share with hippocampal sclerosis and epilepsy, increasingly

the role is distinguished by microdiscenesis, that is, by those structural pathological elements, the presence of which is not included in the prerogative of the lifetime visualization, being the subject of studying exclusively histological methods. A large number of publications are devoted to the topic of hippocampal microdisgenesis, among which the study of M. Thom and Co-Auth is particularly presentative. (2001). In their series, the frequency of detection of microdisgenesis, confirmed by a parasorphological study, amounted to 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 substance and the alteration of cortical laminar architecture.

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

The frequency, age priority and specificity of clinical implementation could not not raise the question of the genetic preposition of hippocampal sclerosis. However, established or, at a minimum, no proven opinion, not this account still does not exist. The genetic study of atypical febrile attacks among monosic twins revealed the presence of paroxysis in 15-38% of the examined patients. The detection of similar changes in monosigital twins suggests that the presence of genetic predisposition is one of the leading factors for the formation of hippocampal sclerosis.

According to one of the common histopathological hypotheses, the stimulation of hippocampal pathological neurogenesis occurs under the influence of persistent attacks. NOT. Scharfan et al. It was shown that the formation of granular cells in a toothed overwhelming occurs throughout life. This process is subject to the influence of various incentives, including convulsive status. Strengthening neurogenesis after epileptic status leads to the appearance of ectopic neurons, which, in turn, leads to the reorganization of the S-supplies and the enhancement of epileptogenesis.

In contradiction with the proposed hypothesis there are data on the selective death of neurons in the CA1 fields and the SAZ as a result of the damaging effect of the epileptic status. According to traditional judgments, sclerotic changes are primarily localized in the front of the hippocampus. However, in a number of works, it is expressed that diffuse sclerotic changes in hippocampal sclerosis prevail over a focal lesion. V. Meldrum (1991) in its work results in the ratio of the detected sclerosis of the front departments of hippocampus to diffuse sclerosis as 1: 2.7.

Any neurovalization specialist may indicate the controversial nature of the alilateral character of the hippocampal sclerosis, as in its practice it has repeatedly encountered its bilateral options. In a classic understanding of medobased temporal sclerosis develops only in one temporal share. However, recently, more and more authors report the bilateral lesion of hippocampes. 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 you to conclude that the territorial involvement of various brain zones into the pathological process at the IVS is wider than it seemed earlier.

At the same time, M. Koutrumanidis et al. In a prospective study of patients with hippocampal sclerosis, they did not find a significant effect

the pulp of the epilepsy flow, the frequency and the number of attacks on the degree of arms of the inrophic changes according to MRI.

In addition, the inconsistency of interpretations of detection of hippocampal atrophy is also associated with the fact that similar damage can be detected in patients who do not have an epileptic disease. Thus, the implementation of MRI studies 52 Healthy relatives of patients with verified hippocampal sclerosis revealed the presence of hippocampal atrophy in 18 (34%) of them. In this case, the classic pattern of mesial sclerosis was detected in 14 surveys. This allowed the authors to conclude that the hippocampal sclerosis is not a consequence of repeated cramps. The results of the study show that there is no absolute link between hippocampal sclerosis and epilepsy. The authors suggest that hippocampal atrophy is determined by the presence of genetic predisposition, and the manifestation of epileptic seizures is the resulting exogenous and endogenous factors.

In general, the relationship of hippocampal sclerosis and febrile convulsion can be denoted by the next paradoxical statement: most children with febrile cramps never have epileptic seizures, but many adults with temporal epilepsy and hippocampal sclerosis were a history of febrile seizures.

Another frequently discussed theory is hypoxic damage to the hippocampal structures due to a brain circulation disorder in the perinatal period.

It is proposed to separate three stages of epileptogenesis after the discirculatory lesion of the temporal share: the initial stroke, the latent period of various durability, the stage of epileptic seizures. A large role in epileptogenesis mechanisms belongs to the activation of an exaitotoxic cascade. The activation of calcium channels occurring in the ischemic focus, an increase in the number of exciting amino acids and free radicals leads to electoral cell death in the hippocampus. Electricencephalographic markers chronic stage Epileptogenesis The authors consider an increase in the amplitude of polyspars in the hippocampus.

The effect of hippocampal sclerosis on the development of strokes in old age was noted. In the J. Leverenz and Sovt series. (2002) It is shown that in the group of patients with hippocampal sclerosis, the development of dementia and strokes was more often determined. Comparison of the risk factors of cerebrovascular diseases of the surveyed group with control did not reveal significant differences.

Another etiological factor in damage to the hippocampus is ne-roinfection. Patients undergoing severe meningitis may subsequently have resistant temporal seizures. Patomorphological study after surgical treatment found classic sclerosis of Ammonov Horn.

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

Hippocampal damage is often determined in patients with complex partial attacks.

Other seizures are secondary generalized attacks. Before starting the seizures, the patient may experience a vegetative or limbic aura. The presence of epigastric, flavor and visual aura is much more common in hippocampal sclerosis than when there is a damage to another localization. Extragipocampal arrangement of the epileptic focus is often combined with dizziness. The preservation of the aura in the absence of attacks after surgical treatment is determined in 18.9% of patients. This indicates the spread of the defeat outside the temporal share. For

comparisons, with hippocampal lesion, Aura is stored only in 2.6% operated on.

Concentric loss of vision with hippocampal sclerosis is described. The authors indicate that this phenomenon can also meet with anteri-altanite lesion and damage to the occipient-temporal area.

The frequent manifestation of the attack is the presence of motor automatism and the dystonic installation of the contralateral hand.

Analysis of the lateralization of motor automatism and the dystonic setting of the limbs allows to determine the localization of the epileptic focus.

Half patients with refractory temporal epilepsy detects dystonic settings. With a mesial temporal epilepsy, the focus was located ipsilaterally defeat.

Motor automates were detected in 26 of the 60 patients examined in S. DuPont et al. With mesial epilepsy, the focus was lyocated with ipsilaterally damage, with a neocortical epilepsy only contralaterally.

The combination of ipsilateral motor automatism and the contralateral dystonic installation was found in 14 patients with mesial epilepsy and was not detected during neocortical epilepsy. The authors conclude that the analysis of motor automatism and dystonic plants is a reliable criterion for the differentiation of the mesial and non-Russian localization of the focus.

In addition to the idle manifestations, with hippocampal sclerosis, various intergreacy disorders are determined, indicating the damage to the structures of the temporal share.

In the study mental state Patients with temporal epilepsy as a result of hippocampal sclerosis having complex partial attacks, a significant overall disruption of cognitive functions was found in the form of a decrease in intelligence, visual-spatial functions and speeches. Reducing associative memory and verbal disorders were detected mainly when defeating the left temporal share.

The development of the theory on the role of the mesial temporal sclerosis in epiletto-genes became possible only after the introduction of neurovalization methods into the daily practice of epileptologists. The development of functional methods of neurovalization, 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 share and, specifically, hippocampus.

It should be mentioned that not all methods of neurovalization are equally informative in the diagnosis of structural functional hippocampal lesion.

Computer tomography of the brain does not allow for a diagnosis of mesial sclerosis, but the presence of indirect signs in the form of a decrease in volumetric indicators of the affected temporal share and expansion of the lower horn of the ipsilateral side ventricle to a certain exemplary implies the diagnosis and is a prerequisite for a more in-depth study of the state of the temporal share.

The specificity of MRI in the diagnosis of mesial sclerosis is recognized by the pre-possessing over other visualizing methods and is confirmed by numerous inspections from the standpoint of the "Golden Standard", that is, obtained during the temporal resection regarding the non-developing epilepsy; MRI signs of mesial sclerosis is the detection of the asymmetry of the hippocampal volumes, the focal increase in signal intensity in T2-mode and lowering the intensity in T1 mode.

Currently, the definition of hippocampus volumes is a routine technique in the framework of the pre-crying diagnosis of temporal epilepsy. The relatively new direction in the preoperative preparation of patients with palp patterns-palm sclerosis seems to determine the volume of extremethumporal structures. This direction is relevant, since it has been established that frequent finds during examination of patients with hippocampal sclerosis is a decrease in the volume of not only hippocampes, but also extragipocampal departments, as well as subcortical structures of homo- and contralateral temporal.

According to N.F. Moran et al., The presence of changes in the ratio of white and gray substance in extractable departments is a predictor of adverse outcomes after temporal resection.

Modern research It was shown that morphological and functional changes in hippocampal sclerosis are not limited to the medial temporal departments, but apply to adjacent brain areas.

We have already noted that in patients with drug-refractory epilepsy in hippocampal sclerosis, the conduct of MRI Volumetry detects significant extra-hypocaped atrophic violations. The degree of ext-ragippocampal atrophy correlates with the degree of hippocampal atrophy, but does not have the connection with the course of generalized seizures and the length of the epilepsy flow. The authors suggest that the basis of hippocampal and extragipocampal atrophy are common mechanisms. The presence of an extended atrophic damage zone may explain the lack of effect from temporal lobectomy in a number of patients with hippocampal sclerosis.

Functional MRI with hippocampal sclerosis primarily identifies a significant metabolic asymmetry in temporal fractions.

When using brain mapping methods in the diagnosis of hippocam-forced sclerosis, the informativeness of positron-emission tomography is estimated at 85.7%. The detectable foci of hypoetabolisms corresponded to the areas of anatomical damage in 97% of cases. A feature of metabolic disorders with hippocampal sclerosis is their one-sided localization. Another often detected find was the detection of combined hypoetabolism in the medial and lateral neocortex, which were verified in 19 of 30 patients. Metabolic changes in the lateral neocortex are not accompanied by a structural impairment according to routine MRI.

The use of positron-emission and single-meter-emission tomography in patients with the anatomical signs of hippocampal sclerosis showed that in most cases the functional damage of the brain exceeds the visible anatomical boundaries - and this is the most important fact from the point of view of the prejectional assessment of patients with resistant epilepsy and hippocampal sclerosis. Paesschen et al. Surveyed 24 patients with hippocampal sclerosis and non-develop complex partial seizures. When conducting one-photon-emission tomography, during the seal, changes in the ipsilateral temporal should be detected, at the boundary of the ipsilate-rally medium front and presenter sinking, in both occipital stakes, and small areas of hyperfusion in the contralateral post-central urinet were detected.

The intergreacy single-photon-emission tomography revealed a significant correlation between the detection of hypoperfusion in the ipsilateral temporal and frontal departments, which indicates the functional distribution of the pathological process to the neighboring brain departments.

The use of MP spectroscopy made it possible to detect metabolic dysfunction in the affected area. The inconsistency of the severity of metabolic disorders and the degrees of sclerosis, according to MRI, has suggested that these processes have different pathogenetic bases. The basis of functional disorders in the hippocampal sclerosis is neuronal and global dysfunction, and not the death of hippocampal neurons.

Similar data leads T.R. Henry et al. When examining patients with temporal epilepsy, he found the presence of regional hypoeta-bolosma in the temporal share in 78%, in a mesial-temporal share - in 70%, in the projection of the Talamus (63%), basal ganglia (41%), frontal dollars (30% ), dark (26%) and occipital shares (4%). The authors conclude about the significant role of Talamus in the initiation and distribution of temporal seizures and consider it responsible for the intergreacy cognitive deficit during temporal epilepsy.

In 80-90% of patients with hippocampal atrophy of EEG makes it possible to identify intercreteal activity.

The most frequent finds when conducting a routine scalp EEG are a regional slowdown and regional spike-wave activity. Intergreacy regional slow activity is determined in 57% of patients with temporal epilepsy as a result of hippocampal sclerosis. A characteristic feature is the preferential one-sided localization of slow-wave activity, decreasing when opening the eye.

The maximum amplitude of slow waves is determined in the temporal pieces of the brain, always gomolaterally anatomical damage. The presence of slow-wave activity is associated with hypoetabolism in the lateral temporal non-occort. A strict correlation between the heater of hypoetabolisms, according to the position-throne-emission tomography, and the deceleration zone on the EEG allows the use of neurophysiological research methods to determine the areas and the size of the reduced neuronal oppression. These changes are determined in the intergreacy period and enhanced during the attack.

Regional delta activity, continued and polymorphic or periodic and rhythmic, is often associated with the involvement in the pathological process of white substance and thalamus and reflects the deafferentation located above the brain bark. Intergreacy activity is more often determined in patients with partial attacks, and in this context it is a reliable lateralizing symptom.

The presence of a regional deceleration has no connection with the age of patients and the length of the epilepsy flow, the frequency and the number of attacks.

The authors indicate the presence of combined reduced metabolism in media and lateral temporal fields. The primary neuronal loss in hippocampal formation and amygdale leads to chronic deactivation and metabolic depression in the lateral temporal field.

Another often detected EEG pattern with hippocampal sclerosis is spike-wave activity. When analyzing the characteristics of the spike-wave activity of 61 patients with hippocampal sclerosis with temporal epilepsy and mesial sclerosis, 39 spike-wave complexes were determined to be detected, 22 had bilateral localization. When bilateral localization, the spike-waves of rooting with anatomical damage was not detected.

The presence of one-sided spike-wave activity does not have strict correlations with the localization of hippocampal and amygdalar atrophy.

The scalp EEG data is 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 share.

Long-term post-pruder confusion is always associated with bilateral atrophy and spike activity on EEG.

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

The extensive experience of the surgery of the temporal share showed the high efficiency of the operational treatment of epilepsy associated with palp shlerosis.

In the series O. Nagratptap et al. 50 patients with MWS conducted anterior temporal resection. The effectiveness indicator was 52%, a significant improvement - 88%.

The front temporal lobectomy includes amygdalogipocampal resection and lataolan neocortical resection.

According to classical ideas, the removal of the epileptic focus is the main goal of surgical intervention. However, the temporal resection in half of the operated patients does not have a significant effect on the flow of attacks and this is an indirect evidence of the involvement in epileptogenesis of other, extra-strand or extra-diplochemal cerebral structures.

It should be noted that a thorough pre-commerce examination allows at the initial stage to reduce the likelihood of low outcomes. The identification of b-temporal damage, the presence of ecratagpocampal epileptic foci, according to the results of cortiography, are contraindicated to surgical treatment of epilepsy.

However, even among patients chosen for surgical treatment, the likelihood of low outcome is sufficiently large. Despite the thorough pre-operational training, about 30% of patients with non-develop partial epilepsy due to the hippocampal sclerosis retain the seizures after the corresponding hippocampal resection.

The cause of low outcomes most of the authors consider the presence of hidden extragipocampal structural anomalies that are not detected during the preoperative mapping of the brain. In the katamnestic observation of the operated patients from 27 patients with verified hippocampal sclerosis, 14 subsequently revealed extragipocampal foci. In 10 of them there was a continuation of the seizures. Of 13 patients without extragippoca, a hard injury 11 were free from seizures.

Thus, the hippocampal sclerosis appears before us as a multi-panic and controversial state, which is inherent in certain, characterizing its features: It underlies the resistant temporal epilepsy; is considered as the theoretical address of surgical resection; It is multifact-riala in nature, but a uniform is enough for visualization characteristics; more often he is unilateral, but bilateral representation is possible; In addition to the attacks, he declares itself a slowdown on EEG and probable contralateral dystonic plants. And finally, it is inextricably linked with febrile attacks, as well 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 discussed.

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The hippocampus is located in the medial departments of the temporal share and is as if two nervous tissue attached to each other: a toothed ulusu and the actual hippocampus (Ammonov horn - cornu. Ammonis - CA). The internal structure of the hippocampus is normally shown in Fig. 1. In histological plan, the hippocampar bark refers to the architect, represented by three layers of neurons. The most outer layer of the hippocampus, forming the medial wall of the temporal horns of the side ventricular, is called "Alveus" (tray) and is formed by axons that are coming from the hippocampus. Followed by stratum. oriens. (presented by axons and interneyrone), then layer of pyramidal cells, which are the main cell elements of the hippocampus and, finally, the deepest layer - stratum. lacunosum and moleculare.represented by dendrites, axon and interneyrone (see Fig. 1). It is important for understanding the various types of defeat of Ammonov Horn during its sclerosis is the proposed Lorente de NO separation of the pyramidal layer for 4 sectors (CA1, CA2, CA3 and CA4). The most pronounced layer of pyramidal cells is located in the CA1 sector, which continues into a portion of paragipocampal winding, bearing the name of subcoming (backup). The CA4 segment arrives to the concave part of the toothed overwhelming. The gear shock is a C-shaped structure having three cell layers: an outer molecular, average granular and inner layer of polymorphic cells, which merge with the CA4 sector (see Fig. 1).

Fig. 1. The internal structure of the hippocampus normally (own histological research, Right side). Subiculum is a part of paragapocampal winding, turning into the CA1 sector. The toothed intrigues (highlighted in blue) covers the CA4 sector (highlighted in green). A - Alveus: 1 - Stratum Oriens Hippocampus, 2 - pyramidal layer, 3 - molecular zone of hippocampus, 4 is a molecular layer of gear winding, 5 - granular layer, 6 - polymorphic layer.

Lower drawing demonstrates the same hippocampus. A layer of pyramidal cells S.A. sectors is clearly traced. The toothed convulsion (marked by arrows) covers the SA4 sector, visible layer of granular cells. The triangular arrows indicate a deep part of the hippocampal groove, which shares the SA sectors and toothed ulusu (own histological studies).

Structural changes in the sclerosis of the hippocampus may vary from the minimum, limited by one sector of CA to coarse, spreading beyond the limits of the medial temporal share. The description of the pathological changes in the structure of the brain tissue in the sclerosis of the hippocampus features an exceptional variety of terms and the presence of several classifications with various concepts describing the same histological substrate.

Histological structure of sclerosic hippocampus

Macroscopically sclerosic hippocampus is reduced in volume and has a dense consistency. Among the main microscopic characteristics there is a decrease in the number of pyramidal cells in various layers of Ca and the variable degree of gliosis. In the granular layer of the toothed mulite, the various degree of reducing the density of neurons can be seen, although in general its structure is more stored in comparison with S.A. sectors A distinctive histological feature is that the loss of neurons does not go beyond the SA sectors, which distinguishes the sclerosis of the hippocampus from its atrophy in ischemic damage and neurodegenerative diseases. It is noted that the loss of neurons in the pyramidal layer of hippocampus may occur in several versions, which was the basis for the formation of the classification of this pathology. The classification of the sclerosis of the hippocampus created by the ILAE commission was the greatest distribution. At s.g. 1-th type (pronounced or classic) neuronal loss is observed in all layers of hippocampus (Fig. 2). The second type is characterized by the loss of neurons mainly in the CA1 sector, and at the 3rd type of SG, only the SA4 sector in the transition to the gear winding is amazed (the so-called end. folium. sclerosis). In the literature, along with the term "sclerosis of the hippocampus", a number of definitions are often used, which emphasize that the histological signs of the impaired brain tissue may go beyond the limits of the hippocampus.

Fig. 2. Sclerosic Hippocampus (right side): The absence of a pyramidal layer in all CA segments (sclerosis of the 1st type according to ILAE classification) is determined. The granular layer of the toothed is stored (marked by arrows).

Thus, the term "mesial temporal sclerosis" reflects the fact that, along with the hypocampamp, atrophic and globatic changes are observed in amigdale and hook. When analyzing the histological material obtained during surgery of temporal epilepsy, it became apparent that the sclerosis of the hippocampus is accompanied by pathogistological changes and in the lateral neocortex of the temporal share. M. Thom proposed the term "temporal sclerosis", in which the loss of neurons and glyosis is determined in the 2nd and 3rd layers of the temporal bark. Quite often, heterotoped neurons are detected in the neocortex in the 1st layer of the crust and the white substance, which is indicated by the term "microdiscene". The ILAE Commission in 2011 presented a new classification of focal cortical dysplasia, where the FCD 3A group was isolated when the hippocampum sclerosis can be combined with the dysplasia of the temporal fraction in the form of a violation of its laminar structure, which, in turn, is classified as FCD 1st Type. Microdiscene, the role of which in epileptogenesis is not yet known, are related to the so-called small malformations of the cerebral cortex, and when they are detected with the sclerosis of the hippocampus, the diagnosis is defined as the type 3a. Just like FCD 3A type, the combination of the temporal sclerosis and the sclerosis of the hippocampus is considered. The concept of "double pathology" (Dual Pathology) is often found when the sclerosis of the hippocampus is combined with a potentially epileptogenic lesion of the neocortex, including outside the temporal share, for example, a tumor, vascular malformation, the FCD of the 2nd type, encephalitis of Rasmussen, the glyotic scar . At the same time, the concept of "double pathology" does not include FqD 3A type. Terminology becomes even more comprehensive, since the presence of two epileptogenic brain lesions, but without the sclerosis of the hippocampus denote as a double pathology.

To understand the links between the various departments of the hippocampus and pathogenesis of its sclerosis, it is necessary to have an idea of \u200b\u200bthe structure of a polysinapotic intragippocampal path, which begins on the neurons of the 2nd layer of the entoric cortex (located in the front of the paragipocampal winding and in the hook area). The processes of these neurons form a perforate path, which goes through the sub-paragipocampal coasting of the paragapocampal overhang and in contact with the dendrites of the granular layer cells. The neurons of the granular layer form mossy fibers, innervating pyramidal neurons of CA3 and CA4, which, in turn, through side axons, the so-called collaterals of the shaffer, are in contact with the CA1 sector. Anomalous germination of mossy fibers in a toothed convulsion instead of SA sectors with the formation of exciting synapses is considered one of the pathogenetic links at this year. Of the above segments, the axons are included in Alveus and then in the brain arch through the Fimbria Hippocampus. Considering the anatomical and functional connection between the ammonium horn, a toothed with a sulk, subcuculaum, a number of authors identified them with a term "hippocampal formation" (Fig. 3).

Fig. 3. Internal bonds of hippocampal formation in normal. The pyramidal neurons of the SA sector (marked with a red triangle) with their dendrites are in contact with the dendrites of granular cells of a toothed gingerbread. 1 is a perforant path (marked with a red line) goes through subcuculaum into the molecular layer of a toothed overwhelming, where the granular cells are in contact with dendrites (indicated by a circle); 2 - mossy fibers (marked with purple arrow) go to dendrites of CA3 pyramidal cells and CA4 sectors of hippocampus. 3 - Schaffer collaterals (marked green) innervate apical dendrites of Ca1 pyramidal cells.

Causes of the sclerosis of the hippocampus pathogenesis

The central issue of the etiology of the SG is the clarification of the fact that it appears primary: the structural pathology of the hippocampus, "launching" chronic pharmac-ester epilepsy, or vice versa - long pathological electrical activity with time leads to sclerosis. It is important to note that a substantial part of patients with pharmac-ester epilepsy associated with the SG is transferred in early childhood the status of febrile seizures or another acute pathology of the central nervous system (injury, anoxia, neuroinfection), which received the designation in the literature as the initial precipitating damage. In favor of the acquired nature of the SG, they are also talking to those rare observations when pathology arises only from one of the monosic twins, and, therefore, the genetic factor is not paramount. Nevertheless, the presence of hereditary family forms of temporal epilepsy (for example, a group of epileps associated with the mutations of SCN1A and SCN1B genes encoding sodium channels) indicates that the genetic factor also plays its role, due to the part of such patients with the sclerosis of the hippocampus without febrile attacks . Speaking about the acquired nature of the disease, it should also be borne in mind that not every type of attacks is associated with the development of the SG: these autopsy indicate that a long-term uncontrolled epilepsy with frequent generalized attacks does not lead to neuronal loss in the hippocampus, as well as the Afibrous epileptic status. On the other hand, febrile epileptic status is accompanied by MRI signs of hippocampal edema.

The answer to the question of how often the status of febrile cramps in the child is implemented in the SG and pharmac-escortic epilepsy, it may be possible to promise FEBStat. It has already been established that out of 226 children after the status of febrile convulsions, 22 had MRI signs of hippocampum edema, the most pronounced in the sector of the somer (CA1). Of these 22 patients, repeated MRI were performed at various times in 14, while in 10 cases there were signs of the sclerosis of the hippocampus. Nevertheless, from 226 children, epilepsy was diagnosed only in 16 patients and in most cases was not temporal. Thus, the febrile status does not always lead to epilepsy with the sclerosis of the hippocampus, although the time interval between the precipitating injury of the brain and the appearance of temporal epilepsy can be more than 10 years, and such durability has not yet been studied. Genetic studies also suggest that the ethiology of the SG is heterogeneous. The study of full-hydrogen associations showed that the febrile seizures with the sclerosis of the hippocampus can be genetic syndrome, as they are associated with the presence of a specific allele aloneucleotide sequence located near the gene of the SCN1 sodium channel. Such an association was not detected for cases of epilepsy with SG without febrile attacks. The consensus opinion of epileptologists is the idea that there is a certain initial genetic predisposition, which is implemented in the sclerosis of the hippocampus in the presence of a certain damaging factor (double impact hypothesis).

Hippocampal sclerosis has two fundamental pathological characteristics: the first is a sharp decrease in the number of neurons, the second - hyperoportability of the remaining nervous tissue. One of the key roles in epileptogenesis under the SG plays spruiting of mossy fibers: abnormal axons of granular cells instead of the innervation of sa reinvironment of the molecular neurons of the gear winding through the excitation synapses, thus creating local electrical circuits capable of synchronizing and generating epiprust. An increase in the number of astrocytes, glyosis can also play a role in epileptogenesis, since altered astrocytes cannot sufficiently carry out the reverse seizure of glutamate and potassium. Through the mechanism of increasing glutamate and reduce emissions reverse gripThe inhibitions of gamma-amine oil acid can act and pro-inflammatory cytokines, such as IL-1β, IL-1, TNFα, can act. In this regard, in the pathogenesis of the SG, the role of the Gerpes 6th type virus is discussed, the DNA of which is detected in brain tissue in patients with temporal epilepsy.

Clinic and diagnostics

The history of the disease in epilepsy due to sclerosis of the hippocampus is described mainly on the basis of numerous studies to assess the effectiveness of surgical treatment of temporal epilepsy. It is often a history of an indication of the TSNs transferred in childhood (as a rule, up to 5 years), the status of febrile convulsion, neuroinfection, cranial and brain injury. Stereotypical attacks begin between 6 to 16 years, while the so-called latent period may occur, which falls on the time between the initial precipitating damage and the development of the first epileptic attack. Also, there is also a situation where there is a so-called "silent" period between the first attack and the development of pharmacoresistance. Such a feature of the course of the disease indicates its progressive nature. A characteristic cognitive deficit with SG can be a decrease in memory, especially with uncontrolled attacks.

The diagnosis of epilepsy due to the sclerosis of the hippocampus is based on three basic principles. The first is a detailed analysis of the sequence of symptoms in the epileptic seizure, or semiology, which depends on which epileptic activity of the brain is distributed. The second is the analysis of EEG data and comparing them with the semiology of the attack. And the third is to identify epileptogenic lesions at MRI. Speaking about the semiology of the attack during the temporal epilepsy associated with the SG, it must be remembered that, firstly, each of the symptoms separately is not specific, although there is a typical pattern of attacking. Secondly, the symptoms during the attack appear when the epileptic activity is spreading in the brain departments associated with the hippocampus, which in itself does not give clinical manifestations. The characteristic beginning of the temporal attack is Aura in the form of an ascending sensation in the stomach. Also possible fear or anxiety when engaging at the beginning of the attack Amigdala. At the beginning of the attack, the feeling of "already seen" can be noted (Déjà Vu). In terms of diagnostics, the Aura is in the form of dizziness or noise, which can talk about the extra-hypocaper beginning of the attack. The preserved ability to call the items and speak during the attack is an important lateralizing sign of the defeat of the uncommissioning hemisphere. Change of consciousness is accompanied by stopping actions, while the patient has a frozen eyes with wide eyes (starring). Aura and stopping actions follow Oroalimentary automatons with chewing, Chmokan lips. Also, there is also often a dystonia of the contralateral side of the sclerized hippocampus of the hand (which is associated with the spread of epics in the basal ganglia) and the manual automatons appearing in the form of the items with the fingers of the ipsilateral hand. Among the lateralizing symptoms, the post-sheet paresis is important, which indicates the involvement of the contralateral hemisphere, and percental aphasia during the damage to the dominant hemisphere. These symptoms should be considered in the context of EEG data.

The basis of electroclinic diagnosis in the sclerosis of the hippocampus is video-monitoring, which consists in the simultaneous video recording of the epileptic attack and the electrical activity of the brain.

Video-monitoring solves several tasks:

1. Allows you to eliminate pseudoid acceptances and non-epileptic paroxysms, including when they are combined with really existing epilepsy.

2. It makes it possible to evaluate the semiology of the attack in detail and compare it with the dynamics of its ephatyativity: its lateralization and regional location.

3. Long-term record allows you to find out the lateralization and localization of intergreacy activity. The most successful option in terms of a favorable outcome of epilepsy surgery is the coincidence of lateralizing and localizing symptoms in the attack with the data of the Ictal and Interictal EEG- and MRI picture. The pre-commercial examination is essential is the duration of video -EE-monitoring. It is known that the likelihood of registering paroxysm on a 30-minute EEG at a frequency of attacks 1 time per week is about 1%, and long-term video-monitoring with an average duration of 7 days does not reveal intercreic activity in 19% of patients. The question of the necessary duration of video -EEG monitoring is important from the point of view of the commitment of fixing the Ictal events on EEG in determining the testimony to the operation. A number of epileptologists believe that with characteristic clinical picture and the history of the disease, the painting of the sclerosis of the hippocampus on MRI, the registration of the Icto event is optional with more than 90% of the lateralization of the intercotal epics in the temporal region on the lesion side. In most cases, the resolution of the scalp EEG is sufficient to properly lateralize the zone of the beginning of the attack during temporal epilepsy and, in the context of the consistent semiology of the attack and MRI data, determine the surgical treatment strategy.

The MRI diagnostics of the SG is the following principal phase of pre-governor examination. It must be performed according to the epileptological protocol, among the main characteristics of which you can select a small thickness of the cuts and the high force of the magnetic field. The optimal condition for the implementation of MRI is the interaction between the epileptologist and the x-ray, when research planning is carried out taking into account the alleged localization of the epileptogenic zone. Hippocampal sclerosis on MRI has characteristic features: reduction of the hippocampum volume and disruption of the structure of the Ca layers, a hyperintense signal in T2 and FLAIR mode (Fig. 4). Atrophic changes in the ipsilateral amygdale, a pole of the temporal share, Forks, a Mamillyca body are detected. The tasks of the highly dependent MRI also includes the detection of another epileptogenic pathology of the brain located outside the hippocampus, i.e. double pathology, such as focal cortical dysplasia. Without performing this task, the MRI study will be insufficient to make a decision on the operation, even if it identified signs of sclerosis of the hippocampus.

Fig. 4. MRT-anatomy of normal and sclerized hippocampus. A - T2, coronary cut. Sclerosis of the right hippocampus: the decrease in its volume is determined, the absence of an internal structure compared to the left hypocampum; B - the same slice with explanations. Hippocampuses are circulated with a red line (a decrease in the volume of the right hippocampus), the blue line - to the suburb in the left. The yellow line in the center of the hippocampus was carried out along the deep part of the hippocampal groove (in fig. "A" in the right hippocampus, this furrow is not determined). FG - Fusoform, ITG - Lower temporal convolution; B is a coronary section in Flair mode, a decrease in volume and a hyperintense signal from the right hippocampus are visible.

The fundamental point in the understanding of the electrophysiology of medial temporal epilepsy is the fact that the scalp EEG itself does not reveal epics in the hippocampus, which was demonstrated in numerous studies using intracerebral electrodes. For the appearance of epics in the temporal region on the scalp EEG, it requires its propagation from the hippocampus on the adjacent beater of the temporal share. In this case, the main clinical manifestations The attack with medial temporal epilepsy is associated with the spread of epics in certain brain departments associated with the hippocampus: Déjà Vu is associated with the excitation of the entoring crust, the feeling of fear - with Amgdala, abdominal aura - with an island, oroalimentary automatons - with an island and frontal jaculum, dystonia in contralateral Hand - with the spread of excitement on the ipsilateral basal ganglia. These anatomy-electrophysiological features may determine the presence of seizures in a patient, very similar to temporal paroxysms, but actually having an extra-hypocaped and extra-strand.

As the experience of surgical treatment is accumulated, the peculiar epilepsy has become obvious that the removal of the medial structures of the temporal share allows to get rid of the attacks in a completely 50-90% of patients, but in part of cases the frequency of attacks does not change. These studies of the electrical activity of the brain using intracerebral electrodes and the analysis of unsuccessful outcomes of operations have shown that in some cases the reason for the preservation of the attacks after removal of the SG is the presence of a more extensive epileptogenic zone, which goes beyond the hippocampus. Brain departments, anatomically and functionally related to the hippocampus, such as an island, orbitorrontal cortex, parietal jackets, a dump, temporal and occipital joint, can generate attacks similar by the clinical and EEG picture on temporal paroxysms. The concept of "temporal epilepsy plus" was proposed to describe situations where the sclerosis of the hippocampus exists along with the extra-stranded zone of the initiation of the attack. In this regard, it is important to determine the indications for an invasive EEG study during temporal epilepsy due to this year. Alarming symptoms are the taste of aura, aura in the form of a vertigo, noise. Intericycal epics is often localized bilateral in the temporal areas or in the precentral region. Ictally ephatyativity in the "temporal plus" of the forms is more often noted in the transferful, timing and precent-central regions. Differential diagnosis of temporal epilepsy from "temporal epilepsy plus", conducted by a qualified epileptologist, is key in planning surgical intervention and forecasting treatment.

Treatment of epilepsy associated with sclerosis of hippocampus

Standard provision medical care Patients with pharmac-resistant medial temporal epilepsy is the direction to a specialized center for precomperigial examination and surgical treatment. Among the colossal number of publications confirming the effectiveness of the surgery of temporal epilepsy, it is advisable to note two key studies with the maximum level of evidence. S. Wiebe et al. In 2001, a randomized controlled study was conducted, which showed that the surgery of temporal epilepsy during the sclerosis of the hippocampus makes it possible to get rid of attacks in 58% of cases, and with drug therapy, only 8%. The basis for another study was the fact that the average duration of the disease in patients who received surgical treatment is 22 years, and between the diagnosis of pharmac-resistant epilepsy and surgical treatment takes 10 years and more. J. Engel et al. In a multicenter randomized controlled study, it was shown that the continuation of pharmacotherapy in the inefficiency of two drugs in the medial temporal epilepsy is not accompanied by a remission of seizures, while surgical treatment in such situations can be effective (in 11 of 15 patients are terminated).

Surgery at the temporal epilepsy pursues two obvious objectives: 1) Elemental patient from attacks; 2) Cancellation medicinal therapy or reduced dose of the drug. According to the literature, about 20% of patients after surgery cease to take anticonvulsants, 50% remain on monotherapy and 30% are obtained polyterapia. The third goal, less obvious, but of fundamental importance, is to reduce the risk of sudden inexplicable death in epilepsy (sudep - sudden unexplained death in epilepsy), which is associated with a sharp reflective oppression of cardiorespiratory function in patients with pharmac-escorentent epiprists.

The problem of surgical treatment of temporal epilepsy is included full removal epileptogenic brain cortex with maximum preservation functional plots brain and minimization of neuropsychological deficit. In this regard, there are two surgical approaches: temporal lobectomy and selective amygdalogipocampectomy. Both operations include the removal of the hook, amigdala and hippocampus. Selective access to the medial temple can be performed through several different access. The temporal lobectomy also implies the removal of the lateral neocortion of the temporal share (from 3 to 5 cm, depending on the dominance of the hemisphere). Proponents of the selective approach emanate from the fact that the preservation of the lateral neocortex allows you to minimize the neuropsychological deficit, in particular, a decrease in verbal memory. On the other hand, as already noted, pathological changes may go beyond the limits of the hippocampus in Amigdal, the pole of the temporal share and the lateral neocortex. Invasive EEG studies using deep electrodes showed that under the sclerosis of the hippocampus in 35% of cases, ephatyativity occurs in a pole of the temporal share before in the hippocampus. Also, on the basis of the analysis of these depth electrodes, several types of temporal epileps are allocated: medial, medial-lateral, thermal and mentioned "temporal epilepsy plus" already mentioned. Thus, when choosing a surgical treatment tactics, the likelihood of the presence of a more extensive epileptogenic zone coming beyond the sclerized hippocampus, which can determine the greater efficacy of lobectomy. Nevertheless, today there are no data of the 1st grade of evidence that confirms the advantage of any technique that ensures the control of the attacks, neuropsychological outcome or the need for postoperative intake of anti-epileptic drugs, so the choice of the operation depends on the preferences of the surgeon.

The surgery of temporal epilepsy with sclerosis of the hippocampus with sufficient surgeon experience has the minimum risks of neurological deficit (resistant hemiparesis - less than 1%, complete hemianopsy - 0.4%). An unresolved problem is the risk forecast of memory deterioration after surgery. It is known that after resection of the hippocampus dominant hemispheres, about 35% of patients demonstrate the worst indicators for neuropsychological evaluation of verbal memory. The risk of reducing recloser memory is increased in the case of late beginnings, high preoperative indicators when testing, a Dominant hemisphere CG, minimal changes in hippocampus on MRI - these circumstances indicate that the epileptogenic hippocampus can maintain functional activity. Nevertheless, it is difficult to determine how much the decrease in the verbal memory affects the postoperative quality of life. For greater degree, the quality of the patient's life after the operation depends on the careful control of attacks and eliminate the associated depressive and disturbing disorders. Determining the testimony to operation in high-risk patients should be carried out with special accuracy, since with an unsuccessful epileptological outcome, the patient will also experience a cognitive deficit, sharply reduce the quality of life. In this regard, it should be emphasized that a prerequisite for organizing surgical care patients with epilepsy is the formation of a command approach to each clinical case, close interaction between the epileptologist, surgeon, neurorentgenic and neuropsychologist.

There is no conflict of interest.

Ambulance Ambulance im.N.V. Sklifosovsky participates in the "Complex treatment program of patients suffering from epilepsy" together with the Russian National Research Medical University. N.I. Pirogova, Moscow State Medical and Dental University. A.I. Evdokimova, the Institute of Higher Nervous Activities and Neurophysiology of the Russian Academy of Sciences, a scientific and practical psychoneurological center. Z.P. Solovyov, interwater compartment paroxysmal states №2, urban clinical hospital number12, including a comprehensive examination of patients with epilepsy, selection and correction of conservative therapy, consultation of specialists, observation, surgical treatment of patients suffering from epilepsy.

Epilepsy is one of the most common neurological diseases, its prevalence in the population according to the Russian Federation is 0.34%.

Currently, there are more than 50 million patients with epilepsy. Among the diseases of the nervous system, epilepsy is one of the most frequent causes of disability. Despite the success of pharmacotherapy, the frequency of "uncontrolled" epilepsy in industrialized countries adhering to modern treatment standards is from 30 to 40%. Patients with epilepsy with affordable lesions are the most likely candidates for surgical treatment.

Mortality among patients with constant attacks of 4 - 4.5 times higher than in patients without attacks.

Basic reasons symptomatic epilepsy are:

• brain tumors;
• malformation brain;
• cortical malformations (focal cortical dysplasia, heterotopy, etc.);
• hippocampus sclerosis;
• post-traumatic scar atrophic changes.

Diagnostics.

To solve the issue of the possibility of surgical treatment of epilepsy, it is primarily necessary for a comprehensive "precrurgical" examination, which includes:

1. Clinical study of semiology of attacks;
2. Neuropsychological research;
3. Neuralizing research methods (high-solid magnetic resonance imaging on a capacity of 3.0 Teslas according to a special program "Epilepsy", positron emission tomography).
4. Neurophysiological studies, including both invasive methods (registration of bioelectric activity of the brain with intracranial electrodes), and non-invasive methods (EEG, video EEG monitoring, magnetorencephalography).

Fig. 1. MRI of the brain (coronary sections), arrows indicate the focal cortical dysplasia of the left temporal lobe with the hyperplasia of the left hippocampus.

Fig. 2. Electrodes for the invasive registration of the bioelectric activity of the brain (electrode on the left for installation in the hippocampus, right - cortical subdural electrode).

The main task of treating epilepsy, both drug and surgical, is control over attacks. In patients with constant attacks, resistant to anticonvulsant therapy, the cessation of attacks after surgical treatment significantly improves the quality of life - professional and socially domestic adaptation and leads to a decrease in mortality.

With the continuation of anticonvulsant therapy for control over the attacks, it is possible to achieve no more than 8% of cases. At the same time, in surgical treatment, the control over the attacks is achieved in 58% of patients, and in the group of patients with temporal epilepsy - 67%.

Only after a thorough full survey it is possible to solve the issue of surgical treatment.

The main method of surgical treatment of epilepsy is to remove the epileptogenic zone of the brain under neurophysiological control, using a highly adding microscope, as well as stereotactically navigation methods.

Ambulance Ambulance im.N.V. Sklifosovsky conducts a complete survey, as well as all types of surgical treatment of patients with pharmac-escortient forms of epilepsy.

Examples of surgical treatment

Patient N., 40 years old.

Diagnosis: symptomatic pharmacoresisystem epilepsy. Sclerosis of the right hippocampus. Focal cortical dysplasia of the right-hand front desk. (FKD IIID).

Anamnesis of the disease: For the first time, a convulsive attack was 2 months after the transferred meningoencephalitis. As of 8 years, a generalized epileptic attack with the loss of consciousness was developed for the first time, the frequency of attacks at that time was 1 time per year. Observed at the neurologist, received conservative therapy - without an effect, the number of attacks increased every year. From 17 years of age, the frequency of attacks reached 1 attack a week. At 30 years of age, the number of attacks reached 4-5 per day. 2 years ago, the patient noted the appearance of aura in the form of visual and tactile hallucinations preceded by convulsive supplies. Observed at the neurologist, the dose of anticonvulsant drugs continued to increase, however, despite this, the frequency of attacks increased.

Fig. 3. MRI brain (coronary sections). The arrows indicate the signs of the sclerosis of the right hippocampus in the form of a decrease in the structure of the structure with the expansion of the lower horns of the right side ventricular, the amplification of the signal from the white substance of the brain

The first stage of the patient was operating - the intracranial installation of subdural and intracerebral electrodes with invasive EEG monitoring using the BRAINLAB frameless neuronavigation installation and the Vario Guide system.

Fig. 4 (left). The operation planning step is to install intracranial electrodes using the BrainLab and Varioguide Neuronavigation Installation.

Fig. 5 (right). Step operation - installation of the electrode to the right hippocampia using the BRAINLAB and VARIOGUIDE navigation installation.

With five daily video EEG monitoring in the intergovernmental period, paroxysmal activity was recorded in the patient, the most pronounced on the basal surface of the temporal share on the right. The zone of the attacks of the attacks was localized in the region of the right hippocampus and the basal surface of the right temporal share.

Fig. 6 (left). Holding video EEG monitoring

Fig. 7 (right). Single chamber for video EEG monitoring (an infrared chamber is installed allowing to produce video EEG monitoring around the clock mode).

The patient was performed operation - pedionally-omitous craniotomy, resection of the anterior-medial departments of the right-handed lobe with hippocampectomy. The operation is performed using intraoperative ecog (electrocorticography) - is performed for intraoperative control of the bioelectric activity of the brain, it allows you to confirm the epileptogenic focus, as well as increase the efficiency of surgical treatment.

The patient is discharged for the 12th day in a satisfactory condition, with control EEG data for the presence of paroxysmal activity is not received.

Histological conclusion of ledged departments of the right-handed lobe and right hippocampus): the morphological picture of the FKD (focal cortical dysplasia) type III d (ILAE). Clear picture of the sclerosis of the right hippocampus.

In a patient (katamnez 12 months), after the surgical treatment of epileptic attacks, there was not marked.

Patient N., 25 years old.

Diagnosis: Focal Cortical Dysplasia (FCD IIIA). Sclerosis of the left hippocampus. Symptomatic pharmac-resistant post-traumatic epilepsy. Shkg-15 points.

Complaints: for epileptic attacks with a frequency of 1-2 times a month with loss of consciousness and attacks 1 time per week, without losing consciousness.

Anamnesis of the disease: In 8 months, it suffered a heavy cranmato-brain injury with a long comatose state, subsequently developed weakness in the right limbs. From 6 years, the patient appeared seizures - local cramps of face muscles. From 15 years of age - generalized attacks appeared. Having taken carbamazepine, Topamaks dose rose to the subtoxic, but there was no significant effect.
Currently, the patient has epileptic attacks with a loss of consciousness with a frequency 1-2 times a month duration of up to 1 minute and attacks 1 time per week, without losing consciousness, duration up to 15 seconds.

Fig. 8 (left). MRI brain (coronary cut). The post-traumatic scar-atrophic changes in the left dread lobe of the brain are determined (marked with a red circle).

Fig. 9 (right). MRI brain (axial slice). Arrow 1 marked right hippocampus and arrow 2 left hippocampus. The asymmetric location and decrease in the size of the left hippocampus (arrow 2) attracts attention.

The patient has been fulfilled the daily video EEG monitoring - where paroxysmal activity is revealed, in the left frontal and temporal areas. Irrityactive changes are expressed in the right central region. In a dream, epileptiform activity in the left parallers and the temporal areas is significantly increasing, manifested by continued periods, in most cases is accompanied by twitching the right hand or leg.

The first step in the patient was completed - the intracranial installation of subdural and intracerebral electrodes with invasive EEG monitoring using the BRAINLAB frameless neuronavigation unit and the Vario Guide system.

The patient has been conducted invasive EEG monitoring within 7 days. During the observation, the patient registered three clinical epileptic attacks.

Against the background of the complete well-being and the lack of attacks in the patient, paroxysmal activity in the left hippocampus in the scar zone is constantly registered.

During one of the epileptic attacks, the zone of the beginning of the attack is localized in the region of the post-traumatic scar involving in the subsequent left hippocampus and basal departments of the left temporal share.

During the two other epileptic seizures, the patient registered the zone of the beginning of the attack in the projection of the left hippocampus, followed by the spread to the region of the left temporal share.

Fig. 10 (left). Conducting a round-the-clock invasive video monitoring video (using high-resolution infrared video cameras). The red arrow indicates the zone of registration of paroxysmal activity on the electrode located in the projection of the post-traumatic scar of the left parietal lobe.

Fig. 11 (right). Conducting a round-the-clock invasive video monitoring video (using high-resolution infrared video cameras). The red arrow indicates the zone of registration of paroxysmal activity on the electrode located in the left hippocampus.

Thus, it was revealed that the patient has two zones of the beginning of epileptic attacks - post-traverse scar of the left parietal lobe and the left hippocampus.

Patient holding surgical intervention - bone-plastic trepanation of the skull in the left front-packer - temporal area, selective resection of the left temporal proportion, hippocampectomy on the left, removal of the brainwear of the left parallers and temporal fractions, using intraoperative ecog (electrocorticography).

Fig. 12. Planning operational intervention. Three-dimensional brain model with tractography (built on the brainlab neuronavigation installation using a high-solid MRI 3.0 Tesla with MR-tractography).

Fig. 13. Operational intervention planning, zone operational access Using the brainlab neuronavigation installation.

Fig. 14. Intraoperative corticography after removing the post-traumatic scar. The red arrow marked a subdural electrode. The black arrow is marked with a corticogram from a subdural electrode.

The patient is discharged on the 12th day in a satisfactory condition, with control EEG - single rare paroxysms in the right hemispheres of the brain are recorded, a clear positive trend in the form of a decrease in paroxysmal activity is recorded in the left hemisphere of the brain.

Fig. 15. Holding video-EEG monitoring after surgery. There is a clear positive dynamics of EEG in the form of a decrease in paroxysmal activity in the left hemisphere of the brain, single rare paroxysms are preserved in the right hemispheres of the brain.

Histological conclusion: focal cortical dysplasia (FqD IIIA). Sclerosis of the left hippocampus. Glyomesodermal scar with hemorrhage trails.

In the patient (katamnee 8 months) after the surgical treatment of epileptic attacks was noted.

In this case, it is noted that with the MRI of the brain of clear signs of focal cortical dysplasia of the left temporal share and sclerosis of the hippocampus, it was noted, and only the installation of intracranial electrodes with the subsequent video EEG monitoring allowed the two zones of early epileptic seizures.

This once again confirms the need to carry out a complete comprehensive examination of patients with epilepsy.

& Copy 2009-2020 department of emergency neurosurgery Ambulance to them. N.V. Sklifosovsky

The sclerosis of the hippocampus is a form of epilepsy, which is characterized by severe symptoms. In pathology, there is a loss of neurons and scarring in the deep parts of the temporal share. With sclerosis of the hippocampus, irreversible changes are observed, which is negatively displayed at the patient's living level.

Mesal sclerosis appears in people in various reasons that are subject to the impact of negative environmental factors or diseases in the patient's body. Such a notch is observed at:

• brain tissues. It occurs on the background of respiratory disorders and disorders of metabolism in the body.
• Mechanical injury. Mesial sclerosis is diagnosed in people after fractures of the skull, shocks on the head, collisions that lead to irreversible violations.

• Bad habits. In the risk group there are people who smoke and regularly use alcoholic beverages.
• Poisoning. If during a long period there is no intoxication of the body, then this leads to hippocampal sclerosis.
• Infectious processes. Pathology is diagnosed during the period of meningitis, encephalitis and other inflammation processes in the brain.
• Hereditary predisposition. If a mesial temporal sclerosis occurred in close relatives of the patient, then it is in the risk group.
• Febrile cramps. They lead to disorders in the exchange of substances. Patients diagnose the swelling of the cortex of the temporal share, which leads to the destruction of neurons, tissue atrophing and a decrease in hippocampus in volume.

Circulatory disorders in the brain. If blood circulation is broken in the area of \u200b\u200bthe temporal share, it leads to ischemia and the elimination of neurons. After a certain time, the tissue atrophy and scarring are diagnosed.

Hippocampus sclerosis occurs in patients after a brain stroke. In the risk group there are patients who suffer from hypertension or hypertension. The disease is diagnosed in patients after diabetes. The occurrence of mesial sclerosis is most often observed in elderly patients.

Symptomatics of pathology

In the hippocampal sclerosis in patients, partial epilepsy is diagnosed. This state leads to a variety of features. Native and loved ones notice that human behavior is changing. Mesial temporal sclerosis leads to the emergence of muscle spasms. During the period of leakage of pathology, patients diagnose the occurrence of seizures.

Hippocampus sclerosis is accompanied by memory loss. In case of disease, patients complain about the occurrence of headaches and dizziness. The pathology is evidenced by insomnia. With mesial sclerosis, anxiety increases and the emergence of panic attacks. The patient violates cognitive abilities: memory, thinking, focusing.

When examining the patient, atrophic processes in the front core of the Talamus are observed. The sclerosis of the hippocampus is characterized by atrophy of the waist-sized ispun. In the disease, the ipsilateral brain hypertrophy is diagnosed. In the brain, the white substance decreases in volume.

In the hippocampal sclerosis, controlled cerebeller hemoatrophy appears. Brainmeas are reduced in volume. During the period of the disease, atrophic processes in the neighboring body and the ipsilateral arch appear.

With mesyal sclerosis, patients are diagnosed with seizures, which lead to a violation of the health of the brain. Patients suddenly lose consciousness. They develop vegetative heart dysfunction. In the left-sided sclerosis of the hippocampus, more serious parasympathetic dysfunction is observed.

Hippocampal sclerosis is characterized by pronounced symptoms, when the patient occurs, it is recommended to urgently ask for help to the doctor to ensure full-fledged diagnosis and appointment of effective treatment.

Types and diagnosis of disease

In accordance with the structural changes, the epilepsy of the temporal share may have a surround process or characterized by its absence. In the first case, patients diagnose the development of tumor processes, aneurysms in blood vessels, hemorrhages, congenital pathologies.

All pathological processes are negatively displayed at the work of the limbic system.

To diagnose mesial temporal sclerosis, it is recommended to visit the neurologist. The doctor will inspect the patient and the collection of anamnesis, which will allow him to put a preliminary diagnosis. For its confirmation, the application is recommended:

• Neuroradiological diagnostics;
• Angiography;
• Nuclear magnetorezonance tomography;
• Electroencephalography;
• Computer tomography.

For research, modern equipment is applied, which guarantees the accuracy of the results obtained.

Pathology therapy

Sclerosis is a serious pathological process, which is difficult to amenable to therapy. At the initial stages of hippocampal sclerosis, the use of anti-epileptic drugs is recommended:

• Sodium Valproat

With the use of medication, sodium channel stabilization is carried out. During the use of the medication, a decrease in convulsive activity is ensured. Thanks to the medicine, the mental state and patient mood is ensured. The introduction of the drug is carried out intravenously drip.

Daily dose of medication ranges from 400 to 800 milligrams. It is determined by the doctor in accordance with the severity of the disease. With hypersensitivity to the components of the drug and at child age, its reception is not recommended.

• Phenobarbital.

A medicine from the medial sclerosis in the form of a tablet or solution for injection is made, which allows you to choose the most acceptable option for the patient. Patients are recommended to take 50-100 milligram drugs per day.

If the patient has a liver performance, the amount of medication used is recommended to reduce 2 times.

The drug has a musical, sleeping pills and antiepileptic effect. During the use of the drug, the tone of the smooth muscles of the digestive system is reduced. Improper use of the drug leads to undesirable effects - constipation, inhibition, asthenia, speech lubricant, confusion, arrhythmias, hemorrhages.

• Primidone

It is an antiepileptic medicine that is produced in the form of tablets, which ensures the ease of treatment. After taking the drug, the maximum concentration active substances In the body is observed after 3 hours.

With hypersensitivity to the components of the medication and in old age, its use is not recommended to patients.

Appropriate treatment 2 times a day. The initial dosage of the medication is 125 milligrams. After 3 days, the dosage is raised. The maximum dose of medication is 1500 mg.

• Phenitina

It is a derivative of the hydantoin, which blocks calcium channels. The drug has an appultiarhydric, mioryexizing, anticonvulsant and analgesic effect.

If a person is diagnosed with cachexia, heart failure and porphyria, the use of medicine is not recommended.

In case of violation in the work of the liver and kidneys, the drug is not used for therapy of a mesial temporal sclerosis. With individual intolerance to the medication, its use is not recommended. Patients are recommended to take tablets inside with a calculation of 3-4 mg per kilogram of body weight.

• Sultyama

It is derived sulfonamida. The maximum concentration of the drug is achieved after 2-8 hours after its reception. The drug is highly efficient if the patient flows the temporal type of disease.

With acute liver failure and hypersensitivity, the use of the drug is not recommended.

During pregnancy and breastfeeding Medication is not appointed. Sultyam is a relatively safe drug that is used if the left or right side of the hippocapma is affected.

Selection of medicines and dosage is carried out by a doctor in accordance with the severity of the disease and individual characteristics of the patient. With the inefficiency of drug therapy, it is recommended to use the surgical path of treatment.

Sclerosis in Hippocampus is a serious illness that is difficult to treat, which requires an integrated approach. That is why, if symptoms occur, it is recommended to conduct diagnostics and treatment of pathology.

Mesial temporal sclerosis, sclerosis Hippocampis - The most frequent pathology associated with resistant temporal epilepsy. It is detected in 65% of cases in autopsy, much less often during visualization.

Clinical picture

Most patients suffer from complex partial attacks as a result of temporal epilepsy.

Febrile attacks

Communication (if any) is between mesyal temporal sclerosis and febrile attacks of contradiction: This is due to relative insensitivity during visualization and complexity of establishing the truth of the febrile attack. In a third of patients with an installed temporal epilepsy, a history of fever are present in history. The subsequent observation of children with febrile attacks does not demonstrate a significant increase in the frequency of temporal epilepsy.

Pathology

It is observed uneven damage to the hippocampal formation, with the damage to the toothed is molded, Ca1, Ca4 and to a lesser extent Ca3 of the hippocampal sections. Histologically, the loss of neurons, glyosis and sclerosis occur.

Etiology

There are some contradictions against etiology: whether the mesial temporal sclerosis is caused by epilepsy or the consequence. In children with diagnosed epilepsy, only 1% has radiological signs of mesial temporal sclerosis. Moreover, in adults in 3-10% of cases of MVS, signs of bilateral defeat are observed, despite the unilateral defeat clinic.

Diagnostics

MRI is a selection method to assess the state of hippocampus, however, a certain protocol is needed to achieve good sensitivity. The thin-cut sequences in the coronal plane are required, where the sections will be located at a right angle to the longitudinal axis of hippocampes.

To detect the MVS, the best choice will be the coronal sequences of high resolution T2 / FLAIR.

Among the finds will take place:

• reducing the volume of hippocampus, hippocampal atrophy;
• increased T2-signal;
• anomalous morphology: loss of internal architecture, Stratum RadiaTa is a thin layer of white substance separating toothed cores and ammonium horn.

Since the comparative analysis of the right and left sides is not difficult, it must be remembered that in more than 10% of cases, bilateral defeat, therefore, when evaluating only symmetry, many cases of MVS can be taken for a normal picture.

Also one of the often mentioned, but less specific finds is the expansion of the temporal horns of the side ventricle. In any case, this should not enter the radiologist in confusion, as if the hippocampus is reduced in size.

With a more serious defeat, you can additionally meet:

• atrophy of the ipsilateral arch and the nasty body;
• an increase in signal or atrophy of the front thalala nuclei;
• atrophy of the belt is gyrus;
• an increase in the intensity of the signal from amygdala and / or a decrease in its volume;
• reducing the volume of suburbuum;
• expansion of temporal horns of side ventricles;
• atrophy of collateral BV and the entoring bark;
• atrophy of the Talamus and tailed cores;
• ipsilateral cerebral hypertrophy;
• contractor cerebeller hemiatrophy;
• blur of the border of the compound of gray and white substance in the front template;
• reducing BV in paragipocampal overhang;

Additionally, 3D-volumenical sequences can be performed, although postprocessing may affect sensitivity to subtle changes in hippocampes. Contrast gain is not required.

DWI

As a result of the loss of neurons, extracellular spaces are expanded, and therefore diffusion of water molecules will be larger on the affected side, which will manifest itself a high signal value on ADC.
And on the contrary, as a result of neuronal dysfunction and some edema, diffusion is limited after the attack and, therefore, the signal intensity is reduced.

MP spectroscopy.

MPS changes usually reflect neuron dysfunction.

• reduced NAA and NAA / CR and NAA / CR Relations:
• decrease in mio-inositol in the ipsilateral proportion;
• raising lipids and lactate immediately after the attack;

MP Perfusion

Change on MP perfusion correspond to those in the study of the OTEECT, depending on when scanned.
During the perictal phase, perfusion increases in almost the entire temporal share and even a hemisphere, while the perfusion is reduced into the postal phase.

Peckete and Pat.

• ict of hyperfusion and hypermetabolism;
• interictal period - hypoperphusion and hypoetabolism;

Literature

1. Derek Smith and Frank Gaillard et al. Mesial Temporal Sclerosis. Radiopaedia.org.
2. Shinnar S. Febrile Seizures and Mesial Temporal Sclerosis. Epilepsy Currents. 3 (4): 115-118. DOI: 10.1046 / J.1535-7597.2003.03401.x - PubMed
3. Tarkka R, Pääkkö E, Pyhtinen J, Uhari M, Rantala H. Febrile Seizures and Mesial Temporaal Sclerosis: No Association In A Long-Term Follow-Up Study. Neurology. 60 (2): 215-8. PubMed.
4. Chan s, Erickson JK, Yoon SS. Limbic System Abnormalities Associated with Mesial Temporal Sclerosis: A Model of Chronic Cerebral Changes Due to Seizures. Radiographics: A Review Publication Of The Radiological Society Of North America, Inc. 17 (5): 1095-110.