What do we treat epilepsy. Temporal Epilepsy – Hippocampal Sclerosis Mesial Temporal Sclerosis

The hippocampus is located in the medial parts of the temporal lobe and is like two bent strips of nervous tissue nested into each other: the dentate gyrus and the hippocampus itself (Ammon's horn - cornu Ammonis - CA). The internal structure of the hippocampus is normally shown in Fig. 1. Histologically, the hippocampal cortex belongs to the archicortex, represented by three layers of neurons. The outermost layer of the hippocampus, which forms the medial wall of the temporal horn of the lateral ventricle, is called the alveus (tray) and is formed by axons emerging from the hippocampus. Followed by stratum oriens(represented by axons and interneurons), then a layer of pyramidal cells, which are the basic cellular elements of the hippocampus, and finally the deepest layer - stratum lacunosum and moleculare, represented by dendrites, axons and interneurons (see Fig. 1). Important for understanding the various types of damage to the Ammon's horn in its sclerosis is the division of the pyramidal layer into 4 sectors proposed by Lorente de No (CA1, CA2, CA3 and CA4). The most pronounced layer of pyramidal cells is located in the CA1 sector, which continues into the part of the parahippocampal gyrus, which is called the subiculum (support). The CA4 segment is adjacent to the concave part of the dentate gyrus. The dentate gyrus is a C-shaped structure with three cell layers: an outer molecular layer, a middle granular cell layer, and an inner layer of polymorphic cells that merge with the CA4 sector (see Fig. 1).

Rice. 1. The internal structure of the hippocampus is normal (own histological studies, right side). Subiculum (subiculum) - part of the parahippocampal gyrus, passing into the CA1 sector. The dentate gyrus (highlighted in blue) spans sector CA4 (highlighted in green). a - alveus: 1 - stratum oriens of the hippocampus, 2 - pyramidal layer, 3 - molecular zone of the hippocampus, 4 - molecular layer of the dentate gyrus, 5 - granular layer, 6 - polymorphic layer.

The bottom figure shows the same hippocampus. A layer of pyramidal cells of S.A. sectors is clearly visible. The dentate gyrus (indicated by arrows) covers the CA4 sector, a layer of granular cells is visible. Triangular arrows indicate the deep part of the hippocampal sulcus that separates the SA sectors and the dentate gyrus (own histological studies).

Structural changes in hippocampal sclerosis can vary from minimal, limited to one sector of the SA to gross, extending beyond the medial temporal lobe. The description of pathological changes in the structure of the brain tissue in hippocampal sclerosis is distinguished by an exceptional variety of terms and the presence of several classifications with different concepts describing the same histological substrate.

Histological structure of a sclerosed hippocampus

The macroscopically sclerotic hippocampus is reduced in volume and has a dense texture. Among the main microscopic features are a decrease in the number of pyramidal cells in different layers of the CA and a variable degree of gliosis. In the granular layer of the dentate gyrus, a different degree of decrease in the density of neurons can be noted, although in general its structure is more preserved in comparison with the S.A. sectors. A distinctive histological feature is also that the loss of neurons does not go beyond the SA sectors, which distinguishes hippocampal sclerosis from its atrophy in ischemic injuries and neurodegenerative diseases. It was noted that the loss of neurons in the pyramidal layer of the hippocampus can occur in several ways, which was the basis for the classification of this pathology. The classification of hippocampal sclerosis created by the ILAE commission has received the greatest distribution. Under S.G. Type 1 (pronounced or classic) neuronal loss is observed in all layers of the hippocampus (Fig. 2). The second type is characterized by the loss of neurons mainly in the CA1 sector, and in the 3rd type of SG, only the CA4 sector is affected in the area of ​​transition to the dentate gyrus (the so-called end folium sclerosis). In the literature, along with the term "hippocampal sclerosis", a number of definitions are often used, which emphasize that the histological signs of a disturbed structure of the brain tissue can go beyond the hippocampus.

Thus, the term "mesial temporal sclerosis" reflects the fact that, along with the hippocampus, atrophic and gliotic changes are observed in the amygdala and hook. When analyzing the histological material obtained during surgery for temporal lobe epilepsy, it became obvious that hippocampal sclerosis is accompanied by pathohistological changes in the lateral neocortex of the temporal lobe. M. Thom proposed the term "temporal sclerosis", which defines the loss of neurons and gliosis in the 2nd and 3rd layers of the temporal cortex. Quite often, heterotopic neurons are detected in the neocortex in the 1st layer of the cortex and white matter, which is referred to as "microdysgenesis". In 2011, the ILAE Commission presented a new classification of focal cortical dysplasia, where a group of type 3a FCD was identified, when hippocampal sclerosis can be combined with dysplasia of the temporal lobe cortex in the form of a violation of its laminar structure, which, in turn, is classified as FCD type 1 type. Microdysgenesis, the role of which in epileptogenesis is not yet known, is referred to the so-called small malformations of the cerebral cortex, and if they are detected with hippocampal sclerosis, the diagnosis is defined as FCD type 3a. As well as type 3a FCD, a combination of temporal sclerosis and hippocampal sclerosis is considered. The concept of “dual pathology” is often found in the literature, when hippocampal sclerosis is combined with a potentially epileptogenic lesion of the neocortex, including outside the temporal lobe, for example, a tumor, vascular malformation, FCD type 2, Rasmussen’s encephalitis, gliotic scar . At the same time, the concept of "dual pathology" does not include type 3a FCD. The terminology becomes even more complex, since the presence of two epileptogenic brain lesions, but without hippocampal sclerosis, is referred to as double pathology.

To understand the connections between different parts of the hippocampus and the pathogenesis of its sclerosis, it is necessary to have an idea of ​​the structure of the polysynaptic intrahippocampal pathway, which starts from the neurons of the 2nd layer of the entorhinal cortex (located in the anterior part of the parahippocampal gyrus and in the region of the hook). The processes of these neurons form a perforating pathway that goes through the subiculum of the parahippocampal gyrus to the dentate gyrus and contacts the dendrites of the cells of the granular layer. The neurons of the granular layer form mossy fibers that innervate the pyramidal neurons CA3 and CA4, which, in turn, contact the CA1 sector through lateral axons, the so-called Shaffer collaterals. Abnormal germination of mossy fibers into the dentate gyrus instead of SA sectors with the formation of excitatory synapses is considered one of the pathogenetic links in S.G. From the above segments of the SA, axons enter the alveus and then into the fornix of the brain through the fimbria of the hippocampus. Taking into account the anatomical and functional relationship between the horn of Ammon, the dentate gyrus, and the subiculum, a number of authors have designated them by the term “hippocampal formation” (Fig. 3).

Causes of hippocampal sclerosis, pathogenesis

The central issue of the etiology of SH is to find out what occurs primarily: a structural pathology of the hippocampus, which "triggers" chronic drug-resistant epilepsy, or vice versa - prolonged pathological electrical activity eventually leads to sclerosis. It is important to note that a significant part of patients with pharmacoresistant epilepsy associated with SH suffer in early childhood the status of febrile convulsions or other acute CNS pathology (trauma, anoxia, neuroinfection), which was designated in the literature as initial precipitating damage. The acquired nature of SH is also supported by those rare observations when the pathology occurs only in one of the monozygotic twins, and, therefore, the genetic factor is not paramount. However, the presence of hereditary familial forms of temporal lobe epilepsy (for example, a group of epilepsies associated with mutations in the SCN1a and SCN1b genes encoding sodium channel proteins) indicates that a genetic factor also plays a role, causing hippocampal sclerosis without febrile seizures in some of these patients. . Speaking about the acquired nature of the disease, it should also be taken into account that not every type of seizure is associated with the development of SH: autopsy data indicate that long-term uncontrolled epilepsy with frequent generalized seizures does not lead to neuronal loss in the hippocampus, as well as afebrile status epilepticus. On the other hand, febrile status epilepticus is accompanied by MRI signs of hippocampal edema.

The answer to the question of how often the status of febrile convulsions in a child is realized in FH and drug-resistant epilepsy may be given by the prospective FEBSTAT study. It has already been established that out of 226 children after the status of febrile convulsions, 22 had MRI signs of hippocampal edema, most pronounced in the Sommer sector (CA1). Of these 22 patients, repeated MRI at various times was performed in 14, while in 10 cases signs of hippocampal sclerosis were detected. However, out of 226 children, epilepsy was diagnosed in only 16 patients and in most cases was not temporal. Thus, febrile status does not always lead to epilepsy with hippocampal sclerosis, although the time interval between precipitating brain injury and the onset of temporal lobe epilepsy can be more than 10 years, and a follow-up of such a duration has not yet been studied. Genetic studies also suggest that the etiology of FH is heterogeneous. The study of genome-wide associations showed that febrile seizures with hippocampal sclerosis may be a genetic syndrome, since they are associated with the presence of a specific allele of a single nucleotide sequence located near the SCN1a sodium channel gene. No such association was found for cases of epilepsy with FH without febrile seizures. The consensus opinion of epileptologists is the idea that there is some initial genetic predisposition that is realized in hippocampal sclerosis in the presence of a certain damaging factor (the double whammy hypothesis).

Hippocampal sclerosis has two fundamental pathological characteristics: the first is a sharp decrease in the number of neurons, the second is the 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 SA, 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. Pro-inflammatory cytokines such as IL-1β, IL-1, TNFα can also act through the mechanism of increasing the release of glutamate and reducing reuptake, inhibition of gamma-aminobutyric acid. In this regard, the role of herpesvirus type 6, whose DNA is found in the brain tissue of patients with temporal lobe epilepsy, is discussed in the pathogenesis of FH.

Clinic and diagnostics

The case history of epilepsy due to hippocampal sclerosis is described mainly on the basis of numerous studies evaluating the effectiveness of surgical treatment of temporal lobe epilepsy. Often in the anamnesis there is an indication of an acute pathology of the central nervous system suffered in childhood (usually up to 5 years): 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 a so-called “silent” period to last between the first attack and the development of drug resistance. This feature of the course of the disease indicates its progressive nature. A characteristic cognitive deficit in SH may be memory loss, especially in uncontrolled seizures.

Diagnosis of epilepsy due to hippocampal sclerosis is based on three main principles. The first is a detailed analysis of the sequence of symptoms in an epileptic seizure, or semiology, which depends on which areas of the brain the epileptic activity spreads. The second is the analysis of EEG data and their comparison with the semiology of the attack. And the third is the detection of an epileptogenic lesion on MRI. Speaking about the semiology of an attack in temporal lobe epilepsy associated with SH, it must be remembered that, firstly, each of the symptoms taken separately is not specific, although there is a typical pattern in the course of an attack. Secondly, symptoms during an attack appear when epileptic activity spreads to the parts of the brain associated with the hippocampus, which in itself does not give clinical manifestations. The characteristic beginning of a temporal seizure is an aura in the form of an upward sensation in the abdomen. 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). 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. 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, postictal paresis, which indicates involvement of the contralateral hemisphere, and postictal aphasia, when the dominant hemisphere is affected, are important. These symptoms should be considered in the context of the EEG data.

The basis of electroclinical diagnosis in hippocampal sclerosis is video EEG monitoring, which consists in simultaneous video recording of an epileptic seizure and electrical activity of the brain.

VideoEEG monitoring solves several problems:

1. Allows you to exclude pseudo-attacks and non-epileptic paroxysms, including when they are combined with really existing epilepsy.

2. It makes it possible to assess in detail the semiology of an attack and compare it with the dynamics of its epiactivity: its lateralization and regional localization.

3. Long-term recording allows you to find out the lateralization and localization of interictal activity. The most successful option in terms of a favorable outcome of epilepsy surgery is the coincidence of lateralizing and localizing symptoms in an attack with the data of the ictal and interictal EEG and MRI picture. In pre-surgical examination, the duration of video-EEG monitoring is essential. It is known that the probability of registering paroxysm on a 30-minute EEG with a frequency of attacks once a week is about 1%, and long-term video EEG monitoring with an average duration of 7 days does not reveal interictal activity in 19% of patients. The question of the required duration of videoEEG monitoring is important from the point of view of the mandatory fixation of ictal events on the EEG when determining indications for surgery. A number of epileptologists believe that with a characteristic clinical picture and a history of the disease, a picture of hippocampal sclerosis on MRI, registration of an ictal event is not necessary with more than 90% lateralization of interictal epiactivity in the temporal region on the side of the lesion. In most cases, the resolution of the scalp EEG is sufficient to correctly lateralize the onset of an attack in temporal lobe epilepsy and, in the context of consistent seizure semiology and MRI data, to determine a surgical strategy.

MRI diagnostics of SH is the next fundamental stage of pre-surgical examination. It 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. The optimal condition for performing MRI is the interaction between the epileptologist and the radiologist, when the planning of the study is carried out taking into account the expected localization of the epileptogenic zone. Hippocampal sclerosis on MRI has characteristic features: a decrease in the volume of the hippocampus and a violation of the structure of the layers of the CA, a hyperintense signal in the T2 and FLAIR mode (Fig. 4). Often, atrophic changes are detected in the ipsilateral amygdala, the pole of the temporal lobe, the fornix, and the mamillary body. High-resolution MRI also has the task of detecting another epileptogenic brain pathology located outside the hippocampus, i.e. a dual pathology, such as focal cortical dysplasia. Without this task, an MRI study will not be sufficient to make a decision about the operation, even if it reveals signs of hippocampal sclerosis.

The fundamental point in understanding the electrophysiology of medial temporal lobe epilepsy is the fact that the scalp EEG itself does not detect epiactivity in the hippocampus, which has been demonstrated in numerous studies using intracerebral electrodes. For the appearance of epiactivity in the temporal region on the scalp EEG, it must be spread from the hippocampus to the adjacent cortex of the temporal lobe. At the same time, the main clinical manifestations of an attack in medial temporal epilepsy are associated with the spread of epiactivity to certain parts of the brain associated with the hippocampus: déjà vu is associated with excitation of the entorhinal cortex, a sense of fear - with the amygdala, abdominal aura - with the insula, oroalimentary automatisms - with the insula and frontal operculum, dystonia in the contralateral hand - with the spread of excitation to the ipsilateral basal ganglia. These anatomical and electrophysiological features can cause the patient to have seizures that are very similar to temporal paroxysms, but actually have an extrahippocampal and extratemporal onset.

With the accumulation of experience in the surgical treatment of temporal lobe epilepsy, it became obvious that the removal of the medial structures of the temporal lobe allows you to get rid of seizures completely in 50-90% of patients, however, in some cases, the frequency of seizures does not change at all. Data from studies of the electrical activity of the brain using intracerebral electrodes and an analysis of unsuccessful outcomes of operations have shown that in some cases the reason for the persistence of seizures after removal of the SG is the presence of a larger epileptogenic zone that extends beyond the hippocampus. Parts of the brain that are anatomically and functionally related to the hippocampus, such as the insula, orbitofrontal cortex, parietal operculum, the junction of the parietal, temporal, and occipital lobes, can generate seizures similar in clinical and EEG pattern to temporal paroxysms. The concept of "temporal lobe epilepsy plus" has been proposed to describe situations where hippocampal sclerosis exists along with an extratemporal zone of seizure initiation. In this regard, it is important to determine the indications for invasive EEG examination in temporal lobe epilepsy caused by S.G. Warning symptoms are taste aura, aura in the form of vertigo, noise. Interictal epiactivity is more often localized bilaterally in the temporal regions or in the precentral region. Ictal epiactivity in "temporal plus" forms is more often noted in the anterofrontal, temporoparietal and precentral regions. Differential diagnosis of temporal lobe epilepsy from "temporal lobe epilepsy plus" performed by a qualified epileptologist is key in planning surgical intervention and predicting the outcome of treatment.

Treatment of epilepsy associated with hippocampal sclerosis

The standard of care for patients with drug-resistant medial temporal lobe epilepsy is referral to a specialized center for pre-surgical examination and surgical treatment. Among the huge number of publications confirming the effectiveness of temporal lobe epilepsy surgery, it is worth mentioning two key studies with the highest level of evidence. S. Wiebe et al. in 2001, they conducted a randomized controlled trial, which showed that surgery for temporal lobe epilepsy in hippocampal sclerosis allows you to get rid of seizures in 58% of cases, and with drug therapy - only 8%. The basis for another study was the fact that the average duration of illness in patients who received surgical treatment is 22 years, and 10 years or more elapse between the diagnosis of drug-resistant epilepsy and surgical treatment. J. Engel et al. in a multicenter randomized controlled trial showed that the continuation of pharmacotherapy with the ineffectiveness of two drugs in medial temporal lobe epilepsy is not accompanied by remission of seizures, while surgical treatment in such situations can be effective (in 11 out of 15 patients, seizures stop).

Surgery for temporal lobe epilepsy has two obvious goals: 1) relieving the patient of seizures; 2) canceling drug therapy or reducing the dose of the drug. According to the literature, about 20% of patients stop taking anticonvulsants after surgery, 50% remain on monotherapy, and 30% receive polytherapy. The third goal, less obvious, but of fundamental importance, is to reduce the risk of sudden unexplained death in epilepsy (SUDEP - sudden unexplained death in epilepsy), which is associated with a sharp reflex depression of cardiorespiratory function in patients with drug-resistant epileptic seizures.

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. Both surgeries include removal of the hook, amygdala, and hippocampus. Selective access to the medial temple can be performed through several different approaches. Temporal lobectomy also involves the removal of the lateral neocortex of the temporal lobe (from 3 to 5 cm, depending on the dominance of the hemisphere). Supporters of the selective approach proceed from the fact that the preservation of the lateral neocortex allows minimizing the neuropsychological deficit, in particular, the decrease in verbal memory. On the other hand, as already noted, pathological changes can extend beyond the hippocampus into the amygdala, temporal lobe pole, and lateral neocortex. Invasive EEG studies using deep electrodes have shown that in sclerosis of the hippocampus, in 35% of cases, epiactivity occurs in the pole of the temporal lobe earlier than in the hippocampus. Also, based on the analysis of data from deep electrodes, several types of temporal epilepsy were identified: medial, medial-lateral, temporopolar, and the already mentioned “temporal epilepsy plus”. Thus, when choosing the tactics of surgical treatment, one should take into account the possibility of having a larger epileptogenic zone that extends beyond the sclerosed hippocampus, which may determine the greater effectiveness of lobectomy. However, there is currently no class 1 evidence to support the benefit of any technique in terms of seizure control, neuropsychological outcome, or the need for postoperative antiepileptic medication, so the choice of surgery depends on the preference of the surgeon.

Surgery for temporal lobe epilepsy in hippocampal sclerosis, with sufficient experience of the surgeon, has minimal risks of neurological deficit (persistent hemiparesis - less than 1%, complete hemianopsia - 0.4%). The prognosis of the risk of memory impairment after surgery remains an unresolved problem. It is known that after resection of the hippocampus of the speech-dominant hemisphere, about 35% of patients demonstrate worse performance in the neuropsychological assessment of verbal memory. The risk of decreased verbal memory is increased in the case of late onset of the disease, high preoperative test scores, dominant hemispheric FH, minimal hippocampal changes on MRI - these circumstances indicate that the epileptogenic hippocampus may retain functional activity. However, it is difficult to determine the extent to which a decrease in verbal memory affects postoperative quality of life. To a greater extent, the patient's quality of life after surgery depends on the careful control of seizures and the elimination of concomitant depressive and anxiety disorders. The determination of indications for surgery in high-risk patients should be carried out with particular care, since if the epileptological outcome is unsuccessful, the patient will also experience a cognitive deficit, which drastically reduces the quality of life. In this regard, it should be emphasized that a necessary condition for the organization of surgical care for patients with epilepsy is the formation of a team approach to each clinical case, close interaction between the epileptologist, surgeon, neuroradiologist and neuropsychologist.

There is no conflict of interest.

Of these, 64 had Alzheimer's disease, 44 were diagnosed with mild cognitive impairment, and 34 had no cognitive impairment.

Analysis of the data showed that subjects who did not have dementia at the beginning of the survey, but had a lower volume of the hippocampus and a more significant decrease in volume, were on average three times more likely to develop dementia than the rest. This result allowed scientists to indirectly confirm the assumption that hippocampal atrophy manifests itself already at the stage of moderate cognitive impairment of the hippocampus. In patients with Alzheimer's disease, the loss of nerve cells extends even more widely to other areas of the brain.

Atrophy of the left hippocampus, convulsive syndrome

In July 2007, he bought the American complex of amino acids EXTREME AMINO for pumping up the muscle mass of athletes from ULTIMATE NUTRITION. I took 3 capsules on an empty stomach after training in the gym three times a week. During the intake of amino acids, sleep noticeably worsened, teeth began to grind at night, bad breath and a constant feeling of fatigue appeared. On March 6, 2008, the strongest convulsions of the whole body began at night. He was hospitalized in the medical unit, spent 12 hours in intensive care. Diagnosis - severe poisoning with an unspecified neurotropic substance, convulsive syndrome. On April 29, 2008, after exercising in the gym in the middle of the night, severe vomiting broke out, which turned into convulsions. Since then, I have been taking depakine (6 months at 600 mg, 1.5 months at 1000 mg, last month mg). Seizures occur monthly with a series of seizures. I can’t get out of convulsions without sibazon. I am registered with a neurologist, but I see no way out of my illness. The conclusion of the neurologist: Epilepsy, proceeding in the form of simple partial and nocturnal generalized seizures.

From what you describe, despite taking an antiepileptic drug, you continue to have regular epileptic seizures. This suggests that it is necessary to change the drug. An epileptologist's consultation is needed in order to ask you in more detail, examine you, conduct additional examination methods (electroencephalography and magnetic resonance imaging of the brain), and then, based on the results, decide which drug you need. I will be glad to help you with this. In any case, for now I recommend limiting physical activity: training should be shorter in duration or with longer breaks between sets until normal breathing and heart rate are fully restored!

All rights reserved.

Any use of materials is allowed only with the written consent of the editors.

Causes and types of hippocampal sclerosis

Hippocampal sclerosis is one of the forms of epilepsy, the cause of which is the pathology of the parts of the limbic system of the brain. The main generator of epileptic activity is gliosis in combination with atrophy of the cortical plate of the underlying white matter. To diagnose the disease, neurologists at the Yusupov Hospital use modern methods of instrumental research, perform laboratory tests and minimally invasive diagnostic procedures.

Sclerosis of the hippocampus is accompanied by loss of neurons and scarring of the deepest part of the temporal lobe. Often caused by severe brain injury. It is left handed and right handed. Brain damage due to trauma, neoplasm, infection, lack of oxygen, or uncontrolled spontaneous seizures leads to the formation of scar tissue in the hippocampus. It begins to atrophy, neurons die and form scar tissue.

Based on structural changes, two main types of temporal lobe epilepsy are distinguished:

• with the presence of a volumetric process (tumor, congenital pathology, aneurysm of a blood vessel, hemorrhage) affecting the limbic system;
• without the presence of clearly verified volumetric changes in the area of ​​the medial temporal lobe.

Causes of bilateral sclerosis of the hippocampus

The following causes of hippocampal sclerosis are known:

• hereditary predisposition;
• hypoxia of brain tissue;
• brain injury;
• infections.

Today, the following theories of the development of hippocampal sclerosis are considered the main ones:

• the influence of febrile convulsions leading to regional metabolic disorders and edema of the temporal lobe cortex. Neuronal death occurs, local gliosis and atrophy develop, as a result of which the volume of the hippocampus decreases, reactive expansion of the sulcus and the lower horn of the lateral ventricle.
• acute circulatory disorders in the basin of the terminal and lateral branches of the posterior cerebral artery cause basal ischemia of the temporal lobe, secondary diapedetic sweating, neuronal death, gliosis and atrophy occur.
• violation of the development of the temporal lobe during embryogenesis.

Symptoms of hippocampal sclerosis

Sclerosis of the hippocampus usually leads to focal epilepsy. Epileptic seizures appear in groups or individually. They are complex, starting with strange indescribable sensations, hallucinations or illusions, followed by a numb gaze, food and rotational automatisms. They last about two minutes. With progression, generalized tonic-clonic seizures may occur.

Attacks with sclerosis of the hippocampus may be accompanied by various symptoms:

• behavior change;
• memory loss;
• headaches;
• increased anxiety;
• sleep problems;
• panic attacks.

Patients develop impaired cognitive abilities (memory, thinking, ability to concentrate). Seizures that disrupt brain activity can lead to sudden loss of consciousness, as well as autonomic cardiac dysfunction. Patients with left-sided hippocampal sclerosis have more severe parasympathetic dysfunction compared to patients with right-sided mesial sclerosis.

Epilepsy attacks are accompanied by auditory or vestibular hallucinations, belching or autonomic manifestations, paresthesias, and unilateral facial twitching. Patients note the difficulty of learning, memory impairment. They are conflicted, emotionally labile, have an increased sense of duty.

To diagnose the disease, the doctors of the Yusupov hospital use the following examination methods:

• neuroradiological diagnostics;
• computed tomography;
• nuclear magnetic resonance spectroscopy;
• angiography;
• electroencephalography.

The study is performed on modern equipment from leading world manufacturers.

Treatment of hippocampal sclerosis

To reduce the symptoms of the disease, neurologists at the Yusupov hospital prescribe antiepileptic drugs. The first choice is carbamazepine. Second choice drugs include Valproate, Difenin, and Hexamidin. After treatment, some patients stop having seizures, and a long-term remission occurs.

With resistance to ongoing therapy and progression of hippocampal sclerosis, surgical treatment is performed in partner clinics. It consists in removing the temporal lobe of the brain (lobectomy). After surgery, in 70-95% of cases, the number of seizures decreases. If you are faced with the problem of hippocampal sclerosis and wish to receive qualified specialized medical care, call us. You will be booked in for a consultation with a neurologist at the Yusupov Hospital.

Our specialists

Service prices *

*The information on the site is for informational purposes only. All materials and prices posted on the site are not a public offer, determined by the provisions of Art. 437 of the Civil Code of the Russian Federation. For exact information, please contact the clinic staff or visit our clinic.

Thank you for your feedback!

Our administrators will contact you as soon as possible

LiveInternetLiveInternet

- Tags

-Headings

• 2 Knowledge of the world and yourself (6821)
• Psychology and the Search for the Self (1791)
• Work on yourself (1513)
• Esotericism, philosophy (1336)
• practices, meditations (915)
• Subtle world (696)
• Energy and human structure (583)
• 1 Life without embellishment (5358)
• About men. And women 🙂 (974)
• Unusual. Nature. Secrets. (782)
• Science (472)
• how it was (397)
• World and Ukraine (371)
• World and Earth (353)
• space (345)
• WE and WORLD (309)
• We, World and Ukraine (268)
• World and Earth (162)
• Yellowstone. Petals. Pebbles. (105)
• 3 Wisdom of life (3183)
• practical advice (1917)
• Doctors about medicine (287)
• ONCOLOGY (209)
• Treatments: aroma, color, etc. (182)
• first aid kit: ointments, etc. (150)
• 4 Folk recipes (2253)
• 1 different general tips (371)
• 1 BASKET of useful tips (369)
• joints of the legs, arms, spine (212)
• head, nerves, pressure (159)
• cardiovascular (125)
• kidneys, liver (123)
• gastrointestinal tract (116)
• eyes, vision (115)
• 2 cleaning, cleansing (112)
• 2 general wellness (103)
• ears, throat, nose (93)
• skin problems (92)
• women's and men's problems (78)
• feet, fungus, calluses, bumps (75)
• mouth, teeth and problems with them (62)
• 1 I HEALED MY DISEASE (55)
• cold (51)
• lungs (35)
• 1 From Ancient Knowledge (2092)
• Slavic practices (553)
• amulets (323)
• practices of other nations (302)
• Slavic healing (217)
• plots (201)
• 1 Russia. Slavs. (1891)
• OUR ANCESTORS (567)
• History, legends, fairy tales (376)
• GODS of the Slavs (334)
• Fauna and flora in the Slavs (52)
• SONGS of the bird Gamayun (18)
• HOUSE AND KITCHEN (1483)
• in our kitchen (1247)
• Multicooker and recipes (144)
• Magic (1156)
• practice (579)
• Technologies different (86)
• Elements and Magic (80)
• It's interesting (706)
• Miscellaneous (346)
• Creativity of Alla (59)
• Predictions. Horoscopes. (620)
• Holidays. New Year. (282)
• Svarogy Krug (19)
• Training (611)
• From different books (288)
• space energy (189)
• seminars, lectures (80)
• healing programs (54)
• This video, music (514)
• Day of space stories. (24)
• Movies (18)
• Russian language. (261)
• RUNES (243)
• This is Help for blog and computer (148)
• IT'S PERSONAL (55)

-Music

-Diary search

-Friends

-Regular readers

-Statistics

hippocampus

The hippocampus is an area in the human brain that is primarily responsible for memory, is part of the limbic system, and is also associated with the regulation of emotional responses.

The hippocampus is shaped like a seahorse and is located in the inner part of the temporal region of the brain.

The hippocampus is the main part of the brain for storing long-term information.

The hippocampus is also believed to be responsible for spatial orientation.

At the same time, the main group of neurons shows sparse activity, i.e. in short periods of time, most cells are inactive, while a small part of the neurons show increased activity. In this mode, the active cell has such activity from half a second to several seconds.

Humans have two hippocampi, one on each side of the brain. Both hippocampi are interconnected by commissural nerve fibers. The hippocampus consists of densely packed cells in a ribbon-like structure that runs along the medial wall of the inferior horn of the lateral ventricle in an anteroposterior direction.

The bulk of the nerve cells of the hippocampus are pyramidal neurons and polymorphic cells. In the dentate gyrus, the main cell type is the granular cells. In addition to these types of cells, the hippocampus contains GABAergic interneurons that are not related to any cell layer. These cells contain various neuropeptides, calcium-binding protein and of course the neurotransmitter GABA.

The hippocampus is located under the cerebral cortex and consists of two parts: the dentate gyrus and the horn of Ammon. Anatomically, the hippocampus is a development of the cerebral cortex. The structures lining the border of the cerebral cortex are part of the limbic system. The hippocampus is anatomically linked to the parts of the brain responsible for emotional behavior.

The hippocampus contains four main zones: CA1, CA2, CA3, CA4.

The entorhinal cortex, located in the parahippocampal gyrus, is considered part of the hippocampus due to its anatomical connections.

The entorhinal cortex is carefully interconnected with other parts of the brain. It is also known that the medial septal nucleus, the anterior nuclear complex that combines the nucleus of the thalamus, the supramammary nucleus of the hypothalamus, the raphe nuclei, and the locus coeruleus in the brainstem direct axons to the entorhinal cortex.

The main exit path of axons of the entorhinal cortex comes from the large pyramidal cells of layer II, which perforates the subiculum and protrudes densely into granular cells in the dentate gyrus, the superior dendrites of CA3 receive less dense projections, and the apical dendrites of CA1 receive an even rarer projection. Thus, the pathway uses the entorhinal cortex as the main link between the hippocampus and other parts of the cerebral cortex.

It should be noted that the flow of information in the hippocampus from the entorhinal cortex is significantly unidirectional with signals that propagate through several densely packed cell layers, first to the dentate gyrus, then to the CA3 layer, then to the CA1 layer, then to the subiculum, and then from the hippocampus to the entorhinal cortex, mainly providing a route for CA3 axons. Each of these layers has a complex internal layout and extensive longitudinal connections. A very important large exit tract leads to the lateral septal zone and to the mammillary body of the hypothalamus.

Also in the hippocampus, there are other connections that play a very important role in its functions.

At some distance from the exit to the entorhinal cortex, there are other exits that go to other cortical areas, including the prefrontal cortex. The cortical area adjacent to the hippocampus is called the parahippocampal gyrus or parahippocampus. The parahippocampus includes the entorhinal cortex, the perirhinal cortex, which got its name due to its proximity to the olfactory gyrus. The perirchinal cortex is responsible for visual recognition of complex objects.

There is evidence that the parahippocampus performs a memory function separate from the hippocampus itself, since only damage to both the hippocampus and the parahippocampus leads to complete memory loss.

The very first theories about the role of the hippocampus in human life were that it is responsible for the sense of smell. But anatomical studies have cast doubt on this theory. The fact is that studies have not found a direct connection between the hippocampus and the olfactory bulb. Nevertheless, further studies have shown that the olfactory bulb has some projections to the ventral part of the entorhinal cortex, and the CA1 layer in the ventral part of the hippocampus sends axons to the main olfactory bulb, the anterior olfactory nucleus, and to the primary olfactory cortex of the brain.

As before, a certain role of the hippocampus in olfactory reactions, namely, in remembering odors, is not excluded, but many experts continue to believe that the main role of the hippocampus is the olfactory function.

The next theory, which is currently the main one, says that the main function of the hippocampus is the formation of memory. This theory has been repeatedly proven in the course of various observations of people who were subjected to surgical intervention in the hippocampus, or were victims of accidents or diseases that somehow affected the hippocampus. In all cases, persistent memory loss was observed.

A famous example of this is the patient Henry Molison, who underwent an operation to remove part of the hippocampus in order to get rid of epileptic seizures. After this operation, Henry began to suffer from retrograde amnesia. He simply stopped remembering the events that took place after the operation, but he perfectly remembered his childhood and everything that happened before the operation.

Neuroscientists and psychologists unanimously agree that the hippocampus plays an important role in the formation of new memories (episodic or autobiographical memory). Some researchers regard the hippocampus as part of the temporal lobe memory system responsible for general declarative memory (memories that can be expressed explicitly in words - including, for example, memory for facts in addition to episodic memory).

In each person, the hippocampus has a dual structure - it is located in both hemispheres of the brain. If, for example, the hippocampus is damaged in one hemisphere, the brain can retain almost normal memory function.

It should be noted that damage to the hippocampus does not lead to the loss of opportunities to master certain skills, such as playing a musical instrument. This suggests that such memory depends on other parts of the brain, and not just on the hippocampus.

Not only are age-related pathologies such as Alzheimer's disease (for which the destruction of the hippocampus is one of the early signs of the disease) have a serious impact on many types of perception, but even normal aging is associated with a gradual decline in certain types of memory, including episodic and short-term memory. Since the hippocampus plays an important role in the formation of memory, scientists have associated age-related memory disorders with physical deterioration of the hippocampus.

Initial studies found significant loss of neurons in the hippocampus in older people, but new studies have shown that such loss is minimal. Other studies have shown significant hippocampal shrinkage in older adults, but similar studies have not found this trend in recent studies.

Stress, especially chronic stress, can lead to atrophy of some dendrites in the hippocampus. This is due to the fact that the hippocampus contains a large number of glucocorticoid receptors. Due to constant stress, steroids caused by it affect the hippocampus in several ways: they reduce the excitability of individual hippocampal neurons, inhibit the process of neurogenesis in the dentate gyrus, and cause atrophy of dendrites in the pyramidal cells of the CA3 zone.

Studies have shown that in people who experienced prolonged stress, atrophy of the hippocampus was significantly higher than other areas of the brain. Such negative processes can lead to depression and even schizophrenia. Hippocampal atrophy has been observed in patients with Cushing's syndrome (high levels of cortisol in the blood).

Schizophrenia is seen in people with an abnormally small hippocampus. But to date, the exact relationship of schizophrenia with the hippocampus has not been established. As a result of sudden stagnation of blood in areas of the brain, acute amnesia can occur, caused by ischemia in the structures of the hippocampus.

Liked: 12 users

• 12 Liked the post
• 2 Quoted
• 1 saved
  • 2Add to quote
  • 1Save to links

  That's why I don't go to polyclinics, but the doctor calls me, wants me to go through some kind of medical examination.

  But! As soon as someone finds something, they immediately intervene, and - oops! Man in six months and no!

  Healed to death!

  I'd rather brew volodushki and birch chaga with fireweed. And there - as God wills!

  The most important thing is Faith in the best and not lose heart!

  I went through last year, everything turned out to be more or less normal, only my heart is indulging in something - I drank very light medicines, although it became less likely to hurt.

  But I didn’t get to the oncologist - because of this, they didn’t give me a certificate for the dispensary. Well, okay - I didn’t really want to.

  My husband goes there alone - he likes it: massage, some kind of shower, mountain air and some other nonsense.)))

  human hippocampus

  The hippocampus is an area in the human brain that is primarily responsible for memory, is part of the limbic system, and is also associated with the regulation of emotional responses. The hippocampus is shaped like a seahorse and is located in the inner part of the temporal region of the brain. The hippocampus is the main part of the brain for storing long-term information. The hippocampus is also believed to be responsible for spatial orientation.

  There are two main types of activity in the hippocampus: theta mode and large irregular activity (LNA). Theta modes appear mainly in the state of activity, as well as during REM sleep. In theta modes, the electroencephalogram shows the presence of large waves with a frequency range of 6 to 9 Hertz. At the same time, the main group of neurons shows sparse activity, i.e. in short periods of time, most cells are inactive, while a small part of the neurons show increased activity. In this mode, the active cell has such activity from half a second to several seconds.

  BNA modes take place during the period of long sleep, as well as during the period of calm wakefulness (rest, eating).

  The structure of the hippocampus

  Humans have two hippocampi, one on each side of the brain. Both hippocampi are interconnected by commissural nerve fibers. The hippocampus consists of densely packed cells in a ribbon-like structure that runs along the medial wall of the inferior horn of the lateral ventricle in an anteroposterior direction. The bulk of the nerve cells of the hippocampus are pyramidal neurons and polymorphic cells. In the dentate gyrus, the main cell type is the granular cells. In addition to these types of cells, the hippocampus contains GABAergic interneurons that are not related to any cell layer. These cells contain various neuropeptides, calcium-binding protein and of course the neurotransmitter GABA.

  The hippocampus is located under the cerebral cortex and consists of two parts: the dentate gyrus and the horn of Ammon. Anatomically, the hippocampus is a development of the cerebral cortex. The structures lining the border of the cerebral cortex are part of the limbic system. The hippocampus is anatomically linked to the parts of the brain responsible for emotional behavior. The hippocampus contains four main zones: CA1, CA2, CA3, CA4.

  The entorhinal cortex, located in the parahippocampal gyrus, is considered part of the hippocampus due to its anatomical connections. The entorhinal cortex is carefully interconnected with other parts of the brain. It is also known that the medial septal nucleus, the anterior nuclear complex that combines the nucleus of the thalamus, the supramammary nucleus of the hypothalamus, the raphe nuclei, and the locus coeruleus in the brainstem direct axons to the entorhinal cortex. The main exit path of axons of the entorhinal cortex comes from the large pyramidal cells of layer II, which perforates the subiculum and protrudes densely into granular cells in the dentate gyrus, the superior dendrites of CA3 receive less dense projections, and the apical dendrites of CA1 receive an even rarer projection. Thus, the pathway uses the entorhinal cortex as the main link between the hippocampus and other parts of the cerebral cortex. The axons of the dentate granule cells relay information from the entorhinal cortex on spiny hairs emerging from the proximal apical dendrite of the CA3 pyramidal cells. After that, CA3 axons emerge from the deep part of the cell body and form upward loops to where the apical dendrites are, then all the way back to the deep layers of the entorhinal cortex in the Schaffer collateral, completing the mutual closure. The CA1 area also sends axons back to the entorhinal cortex, but in this case they are rarer than the CA3 outputs.

  It should be noted that the flow of information in the hippocampus from the entorhinal cortex is significantly unidirectional with signals that propagate through several densely packed cell layers, first to the dentate gyrus, then to the CA3 layer, then to the CA1 layer, then to the subiculum, and then from the hippocampus to the entorhinal cortex, mainly providing a route for CA3 axons. Each of these layers has a complex internal layout and extensive longitudinal connections. A very important large exit tract leads to the lateral septal zone and to the mammillary body of the hypothalamus. The hippocampus receives modulating incoming serotonin, dopamine, and norepinephrine pathways, as well as from the thalamic nuclei in the CA1 layer. A very important projection comes from the medial septal zone, sending cholinergic and gabaergic fibers to all parts of the hippocampus. Inputs from the septal zone are essential in controlling the physiological state of the hippocampus. Injuries and disorders in this area can completely stop the theta rhythms of the hippocampus and create serious memory problems.

  Also in the hippocampus, there are other connections that play a very important role in its functions. At some distance from the exit to the entorhinal cortex, there are other exits that go to other cortical areas, including the prefrontal cortex. The cortical area adjacent to the hippocampus is called the parahippocampal gyrus or parahippocampus. The parahippocampus includes the entorhinal cortex, the perirhinal cortex, which got its name due to its proximity to the olfactory gyrus. The perirchinal cortex is responsible for visual recognition of complex objects. There is evidence that the parahippocampus performs a memory function separate from the hippocampus itself, since only damage to both the hippocampus and the parahippocampus leads to complete memory loss.

  Hippocampal Functions

  The very first theories about the role of the hippocampus in human life were that it is responsible for the sense of smell. But anatomical studies have cast doubt on this theory. The fact is that studies have not found a direct connection between the hippocampus and the olfactory bulb. Nevertheless, further studies have shown that the olfactory bulb has some projections to the ventral part of the entorhinal cortex, and the CA1 layer in the ventral part of the hippocampus sends axons to the main olfactory bulb, the anterior olfactory nucleus, and to the primary olfactory cortex of the brain. As before, a certain role of the hippocampus in olfactory reactions, namely, in remembering odors, is not excluded, but many experts continue to believe that the main role of the hippocampus is the olfactory function.

  The next theory, which is currently the main one, says that the main function of the hippocampus is the formation of memory. This theory has been repeatedly proven in the course of various observations of people who were subjected to surgical intervention in the hippocampus, or were victims of accidents or diseases that somehow affected the hippocampus. In all cases, persistent memory loss was observed. A famous example of this is the patient Henry Molison, who underwent an operation to remove part of the hippocampus in order to get rid of epileptic seizures. After this operation, Henry began to suffer from retrograde amnesia. He simply stopped remembering the events that took place after the operation, but he perfectly remembered his childhood and everything that happened before the operation.

  Neuroscientists and psychologists unanimously agree that the hippocampus plays an important role in the formation of new memories (episodic or autobiographical memory). Some researchers regard the hippocampus as part of the temporal lobe memory system responsible for general declarative memory (memories that can be expressed explicitly in words - including, for example, memory for facts in addition to episodic memory). In each person, the hippocampus has a dual structure - it is located in both hemispheres of the brain. If, for example, the hippocampus is damaged in one hemisphere, the brain can retain almost normal memory function. But if both parts of the hippocampus are damaged, there are serious problems with new memories. At the same time, a person perfectly remembers older events, which indicates that over time, part of the memory passes from the hippocampus to other parts of the brain. It should be noted that damage to the hippocampus does not lead to the loss of opportunities to master certain skills, such as playing a musical instrument. This suggests that such memory depends on other parts of the brain, and not just on the hippocampus.

  Long-term studies have also shown that the hippocampus plays an important role in spatial orientation. So it is known that in the hippocampus there are areas of neurons called spatial neurons that are sensitive to certain spatial locations. The hippocampus provides spatial orientation and memorization of certain places in space.

  Hippocampal Pathologies

  Not only are age-related pathologies such as Alzheimer's disease (for which the destruction of the hippocampus is one of the early signs of the disease) have a serious impact on many types of perception, but even normal aging is associated with a gradual decline in certain types of memory, including episodic and short-term memory. Since the hippocampus plays an important role in the formation of memory, scientists have associated age-related memory disorders with physical deterioration of the hippocampus. Initial studies found significant loss of neurons in the hippocampus in older people, but new studies have shown that such loss is minimal. Other studies have shown significant hippocampal shrinkage in older adults, but similar studies have not found this trend in recent studies.

  Stress, especially chronic stress, can lead to atrophy of some dendrites in the hippocampus. This is due to the fact that the hippocampus contains a large number of glucocorticoid receptors. Due to constant stress, steroids caused by it affect the hippocampus in several ways: they reduce the excitability of individual hippocampal neurons, inhibit the process of neurogenesis in the dentate gyrus, and cause atrophy of dendrites in the pyramidal cells of the CA3 zone. Studies have shown that in people who experienced prolonged stress, atrophy of the hippocampus was significantly higher than other areas of the brain. Such negative processes can lead to depression and even schizophrenia. Hippocampal atrophy has been observed in patients with Cushing's syndrome (high levels of cortisol in the blood).

  Epilepsy is often associated with the hippocampus. With epileptic seizures, sclerosis of certain areas of the hippocampus is often observed.

  Schizophrenia is seen in people with an abnormally small hippocampus. But to date, the exact relationship of schizophrenia with the hippocampus has not been established.

  As a result of sudden stagnation of blood in areas of the brain, acute amnesia can occur, caused by ischemia in the structures of the hippocampus.

Mesial and Lateral Temporal Epilepsy - Structural and Genetic Forms of Temporal Epilepsy - Types of Epileptic Seizures - Diagnosis - Treatment - Prognosis - Surgical Treatment

Structural Versus Genetic Forms Temporal Forms of Epilepsy

In structural epilepsy, seizures occur due to physical or metabolic damage to a part of the brain. In the past, this form of epilepsy was also called symptomatic. The most common causes of structural epilepsy are congenital brain anomalies, neuronal migration disorders, arteriovenous malformations, venous angiomas, strokes, tumors, infections, and brain injuries. Temporal lobe epilepsy can begin at almost any age and occurs with equal frequency in both sexes. Genetic and structural forms of epilepsy cause similar types of seizures, however, with a genetic form of temporal lobe epilepsy, MRI should not show significant structural changes in brain tissue. Genetic temporal lobe epilepsy is usually easier to treat with medication than structural temporal lobe epilepsy. On the other hand, neurosurgical treatment is only possible for structural epilepsy. Surgical treatment aims to remove damaged brain tissues that cause the epileptic focus to be maintained. Surgery can significantly reduce the frequency of epileptic seizures and even lead to long-term or final remission in a significant percentage of cases. Some epileptic syndromes tend to progress if left untreated. An example is hippocampal sclerosis. On the other hand, the individual prognosis for epilepsy is unpredictable. The effectiveness of treatment for focal epilepsy depends on the location and cause of the epileptic focus. Prolonged deterioration in the level of consciousness and cognitive abilities after the end of an epileptic seizure, as well as focal status epilepticus, are characteristic of structural temporal lobe epilepsy, especially if left untreated. The nature of epileptic seizures in temporal lobe epilepsy depends on the location of the epileptic focus - mesial or lateral - rather than on the nature of epilepsy - genetic or structural. An exception may be "ascending epigastric discomfort" - the classic aura of mesial temporal lobe epilepsy caused by hippocampal sclerosis.

Mesial Temporal Lobe Epilepsy with Hippocampal Sclerosis

This is one of the most common types of epilepsy, accounting for about 20% of patients with epilepsy and 65% of those suffering from temporal lobe epilepsy. Eighty percent of patients with mesial temporal lobe epilepsy have hippocampal sclerosis. Febrile seizures in childhood are common and occur in 60% of cases of hippocampal sclerosis, of which 35% are complex febrile seizures. Unusually prolonged febrile seizures are characteristic of temporal lobe epilepsy in the future. The development of hippocampal sclerosis may have a genetic component. Hippocampal sclerosis is the most common cause of structural temporal lobe epilepsy. The cause of hippocampal sclerosis remains unknown. There are several hypothesized mechanisms of damage to hippocampal nerve cells: developmental anomalies, an autoimmune mechanism, and damage due to overstimulation resulting from frequent or prolonged epileptic seizures. Studies show that in hippocampal sclerosis, changes in the brain tissue extend beyond the hippocampus.

Symptoms of Structural Mesial Temporal Epilepsy

Ascending Epigastric Discomfort The most typical epileptic phenomenon of the structural form of mesial temporal lobe epilepsy is "ascending epigastric discomfort" in combination with a feeling of fear. Patients describe this sensation as a strange nauseating, emptying, unpleasant sensation that begins in the upper abdomen and gradually moves higher and higher. This specific type of seizure is not typical of the genetic form of mesial temporal lobe epilepsy. automatisms Automatisms are repetitive, stereotypical aimless movements, such as chewing, smacking, fingering, or a movement that mimics picking up small objects with the fingers. Automatisms occur in seventy percent of those suffering from mesial structural epilepsy. Automatisms can be bilateral or limited to one side. Complex Partial Seizures This type of epileptic seizure is a cessation of normal activity. Eyes aimlessly fixed on infinity. At the same time, automatisms are typical. At the time of the seizure, there is no reaction to the environment, as well as there is no awareness of what is happening. Usually, complex partial seizures last from 30 seconds to 2 minutes. They are often confused with absences. Sometimes a seizure can drag on and turn into status epilepticus, i.e. incessant seizure. Other Types of Seizures Phenomena of false perception, such as: deja vu - already seen, jamais vu - never seen, gustatory or olfactory hallucinations, are not typical for mesial temporal lobe epilepsy. Secondary generalized tonic-clonic seizures, usually untreated, and postconvulsive blurred consciousness are typical.

Diagnosis of Mesial Temporal Epilepsy

MRI of the brain demonstrates hippocampal sclerosis. Sometimes, in addition, anomalies in the development of the brain can be detected. Electroencephalography (EEG) shows nothing on the first recording in half of the cases. Only a third of the subjects can detect the classic peak-wave epileptic focus in the temporal lobe. Continuous recording and recording after sleep deprivation increase EEG sensitivity by up to 80%. EEG during a seizure shows rhythmic 4-7 Hz slow wave activity in the temporal lobe.

Prognosis and Treatment of Structural Mesial Temporal Epilepsy

In each case, the forecast is unpredictable. In some patients, the initially good result of treatment with antiepileptic drugs is lost over time, which leads to an increase and aggravation of the severity of epileptic seizures. Severe temporal lobe epilepsy can lead to memory loss, mental decline, and psychological disturbances. However, in most cases, seizures in hippocampal sclerosis can be well controlled for years in most patients. Any of the drugs, or a combination of them, described at the very end of this page can be used in the treatment of structural mesial epilepsy. Carbamazepine, however, is more effective than the others. The choice of drugs is also dictated by age, gender and comorbidities. In the case of uncontrolled structural mesial temporal lobe epilepsy, surgical treatment becomes appropriate. Surgical treatment in 60% of cases leads to complete remission; in 10% - the effect is zero; and in 20% the severity of seizures is reduced to varying degrees. Surgical intervention involves the removal of a significant portion of the temporal lobe. For this reason, surgical complications are not uncommon and account for about 10%. The most frequent are violations of speech, memory and aggravation of the severity of epilepsy.

Structural Lateral Temporal Epilepsy

Lateral localization of structural temporal lobe epilepsy is twice as rare as mesial. The frequency is independent of gender, and the first seizures usually occur in late adolescence.

Symptoms of Structural Lateral Temporal Epilepsy

Hallucinations: various sounds, dizziness, visual hallucinations and illusions, deja vu, jamais vu, etc. Motor convulsions: automatisms in the hand(s), grimacing, twitching in the face, unusual posing in the hand, vocalization, rotation of the body around its axis, speech disturbances. Complex partial seizures or status, as well as generalized seizures, are possible if left untreated. The degree of loss of consciousness is usually less significant than in mesial structural epilepsy.

Diagnosis of Lateral Temporal Epilepsy

Brain MRI shows structural abnormalities in the temporal lobe. EEG between attacks often reveals focal slow wave activity or spikes/sharp waves over the temporal lobe. The EEG at the time of the seizure shows focal 4-7 Hz rhythmic activity or sharp waves over the temporal lobe.

Prognosis and Treatment of Structural Lateral Temporal Epilepsy

The prognosis is largely determined by the cause of the temporal lobe injury and is often unpredictable. Pharmacological treatment is less effective than in the genetic form of temporal lobe epilepsy. Surgery may be a reasonable alternative for severe structural lateral temporal lobe epilepsy.

Inherited Form of Lateral Temporal Epilepsy (Family Autosomal Dominant Lateral Temporal Epilepsy)

Symptoms

Simple auditory hallucinations, such as various noises, ringing, buzzing, clicking, knocking, are the most typical symptom of focal epilepsy that occurs in the lateral part of the temporal lobe. Focal seizures can rarely progress to complex partial seizures or generalized seizures. Seizures that manifest as visual hallucinations, such as various figures or colored spots, speech disturbance, dizziness, smelling, are also possible, although not very typical. The above symptoms indicate an epileptic focus in the lateral part of the temporal lobe. Seizures are often triggered by sleep. The first seizures usually occur between the ages of 10 and 30. The likelihood of the disease does not depend on gender.

Nature of Inheritance

The name of this type of epilepsy speaks for itself - it is inherited in an autosomal dominant manner and occurs in 80% of gene carriers. The cause is a mutation in the LGI1/Epitempin gene on chromosome 10q.

Diagnostics

MRI of the brain and EEG usually do not reveal any abnormalities. Typical symptoms and normal examination findings support the diagnosis of an inherited form of lateral temporal lobe epilepsy.

Prognosis and Treatment

The epileptic seizures described above in the vast majority of cases are short-lived and not very frequent. When treatment is needed, Carbamazepine is very effective. This form of epilepsy does not cause any other neurological or psychiatric symptoms.

Familial Mesial Temporal Lobe Epilepsy

Symptoms

The mesial part of the temporal lobe is responsible for the formation of memory and for retrieving information from the "storehouse" of memory. For this reason, an epileptic focus in this area of ​​the temporal lobe is capable of producing a whole range of sensations: deja vu, jamais vu; feeling as if someone is behind your back; the illusion of "separation" of the soul from the body; feeling of extreme happiness/pleasure, comprehension of some truth or essence. Something like what the Buddhists call "nirvana." The latter is splendidly described by Dostoevsky in The Idiot. On the other side of the spectrum are fear, the feeling of an impending "end of the world", anxiety, and so on. Due to the proximity of the hypothalamus, nausea, vomiting, pallor, and palpitations may occur. Seizures may also manifest as visual and auditory illusions/hallucinations or incomprehensible, indescribable, difficult-to-localize body sensations. Rarely, focal seizures progress to generalized seizures. The first seizures occur between the ages of 10 and 30 (25 years mean age). Hereditary mesial temporal lobe epilepsy is slightly more common in women.

Nature of Inheritance

Autosomal dominant, manifested in 60% of carriers of the gene. Unlike the lateral form of temporal lobe epilepsy, in hereditary mesial temporal lobe epilepsy, there are many different genetic mutations that can cause the genetic form of mesial temporal lobe epilepsy.

Diagnostics

MRI of the brain is usually unremarkable, however, some patients have foci of altered T2 signal in the temporal lobes. FDG-PET can detect a decrease in metabolic rate in the temporal lobes. The main task of the examination is to distinguish the familial form of mesial temporal lobe epilepsy from hippocampal sclerosis, which, in some cases, can also be hereditary. EEG outside seizures is normal in 50%. The rest have either slow wave or peak-slow wave activity over the temporal lobe - usually on one side. At the time of the seizure, typical epileptic activity is observed over the temporal lobes.

Prognosis and Treatment

The prognosis for mesial familial temporal lobe epilepsy is unpredictable. In some cases, the symptoms are so mild that, without a more severe family history, the patient may not even know they have epilepsy. In a small percentage of cases, severe, difficult-to-treat epilepsy is present. In cases of the most typical familial mesial epilepsy, there are obvious focal epileptic seizures described above, which occasionally generalize into complex partial seizures or generalized convulsions. The antiepileptic drugs, carbamazepine and other drugs listed at the bottom of the page, are usually very effective. Long-term remissions lasting for years are not uncommon in familial mesial temporal lobe epilepsy, but sooner or later the seizures recur.

Familial Focal Epilepsy with Variable Epileptic Foci

This is a hereditary epileptic syndrome in which the very fact of focal epilepsy is inherited, but not the localization of the epileptic focus, which is individual for each family member.

Symptoms

Focal epileptic seizures can occur in any part of the cerebral cortex: frontal, temporal, parietal, or occipital. And, although each individual patient has an epileptic focus in a particular place, other family members may have an epileptic focus in a different part of the brain. For this reason, each individual family member suffering from this epileptic syndrome will have their own, individual type of focal epilepsy. The only thing they all have in common is the presence of some variation of focal epilepsy. As with other forms of focal epilepsy, seizures can develop into complex partial or generalized seizures. Most people experience generalized tonic-clonic seizures, at least occasionally. Seizures often occur during sleep. The first seizures may occur between early childhood and 40 years of age. The average age of onset is 10 years. The probability of the disease does not depend on gender.

Nature of Inheritance

Autosomal dominant inheritance pattern with a 60% chance of epileptic seizures in carriers. A variety of genetic abnormalities on chromosomes 2 and 22 are associated with familial focal epilepsy with variable epileptic foci.

Diagnostics

MRI of the brain should be normal. The EEG may be normal outside of seizures, or it may show local epileptic activity corresponding to the location of the epileptic focus, both at rest and at the time of the seizure. The location of the epileptic focus in each individual remains unchanged. EEG abnormalities may be precipitated by sleep deprivation and may be present in family members without any evidence of epilepsy. The severity of EEG abnormalities has no correlation with epilepsy severity or disease prognosis. Prognosis and Treatment The nature, frequency, duration and severity of epileptic seizures varies both between individual families and between members of each individual family. Treatment with anti-epileptic drugs is usually quite effective.

Treatment of Focal Epileptic Syndromes

In most cases, there is a very decent effect of treatment with Carbamazepine. In cases where carbamazepine is not tolerated, is not effective, or is contraindicated, any other drug or combination of drugs designed to control focal epilepsy may be used. Depending on the nature of the side effects, sex, age, other medical problems, or the presence/planning of pregnancy, the following medicines may be used: Oxcarbazepine, Pregabalin, Gabapentin, Lamotrigine, Levetiracetam, Tiagabine, Topiramate, Vimpat, Zonisamide, Valproic acid preparations. Similar drugs are used in the treatment of structural forms of temporal lobe epilepsy, however, as a general rule, structural forms are less amenable to drug treatment.

[email protected]
Content copyright 2018. . All rights reserved.
By Andre Strizhak, M.D. Bayview Neurology P.C., 2626 East 14th Street, Ste 204, Brooklyn, NY 11235, USA

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 with meconium in late 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 surrounding cells, giving an electrical impulse that is unreasonable. 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.

The insular or opercular type is accompanied by twitching of facial muscles, acceleration of the heart rate and an increase in 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 this case, typical signs of inflammation are observed in the general blood test, antibodies to a specific microorganism are determined in the serological examination of plasma, and bacteriological culture provides complete information about the infection and its sensitivity to antibacterial or antiviral agents.

Instrumental modern methods become the most informative. 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, 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 deterioration of 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.

In order to consider this disease in more detail, you need to say a little about the disease provoking it. Temporal lobe epilepsy is a neurological disease that is accompanied by convulsive seizures. Its focus is in the temporal lobe of the brain. Attacks can be both with loss of consciousness, and without.

Mesial sclerosis acts as its complication, and is accompanied by loss of neurons. Due to head injuries, various infections, seizures, tumors, the hippocampal tissue begins to atrophy, which leads to scarring. There is a possibility of aggravating the course of the disease with additional seizures. It can be either right-handed or left-handed.

According to structural changes, hippocampal sclerosis can be divided into two types:

1. Has no volumetric changes in the temporal lobe of the brain.
2. There is a process of increasing the volume (aneurysm, progressive tumor, hemorrhage).

Main reasons

The main reasons include the following:

• genetic factor. If parents or relatives had manifestations of temporal lobe epilepsy or sclerosis, then the likelihood of manifestation in the heirs is extremely high.
• Febrile convulsions. Their influence contributes to various metabolic disorders. The cortex of the temporal lobe swells and the destruction of neurons begins, the tissue atrophies, the hippocampus decreases in volume.
• mechanical injury. Blows to the head, skull fractures, collisions, all this leads to irreversible damage and the development of hippocampal sclerosis.
• Bad habits. Alcoholism and nicotine addiction destroy neural connections and destroy brain cells.
• Childhood trauma. Improper development of the temporal lobe during the prenatal period or various birth injuries.
• Oxygen starvation of brain tissue. Respiratory disorders and metabolic disorders can lead to it.
• Infections. Meningitis, encephalitis and other inflammations in the brain can lead to the activation of mesial sclerosis.
• Poisoning. Intoxication of the body with harmful substances for a long time.
• Circulatory disorders. When blood circulation in the temporal lobe is disturbed, ischemia and death of neurons begin, and then atrophy and scarring.

You will find drugs used for sclerosis, you will find treatment with folk remedies by clicking on the link.

Risk factors

Risk factors include:

1. brain strokes.
2. Hypertension and hypertension.
3. Diabetes.
4. In older people, sclerosis of the hippocampus is recorded more often than in young people.

Sclerosis is a very insidious disease and has various types: disseminated, atherosclerosis.

Symptoms

Reference! Since this disease is provoked by epilepsy, its symptoms can be very similar to its manifestations, or manifestations of Alzheimer's disease.

The signs of hippocampal sclerosis should be considered in more detail, but only a competent specialist can make an accurate diagnosis.

Symptoms include:

During the examination, the following changes can be diagnosed:

• Decreased white matter content in the parahippocampal gyrus.
• Depletion of the tonsils.
• Atrophy of part of the nucleus of the diencephalon.
• Reduction of the singular gyrus.
• Atrophy of the fornix of the brain.

With left-sided mesial sclerosis, the symptoms will be more severe than with right-sided mesial sclerosis, and cause more severe damage to the parasympathetic system. Seizures disrupt the overall activity of all parts of the brain and can even cause disruption of the heart and other organs.

Development

Reference! Approximately 60-70% of patients with temporal lobe epilepsy have some degree of developed sclerosis of the hippocampus.

The clinical signs of the disease are very diverse, but the main ones are febrile convulsions. They can occur even before the onset of epilepsy, due to various neuronal disorders.

With this disease, the hippocampus is destroyed unevenly, the dentate gyrus and several other areas suffer. Histology indicates neuronal death and gliosis. In adults, bilateral degenerative disorders in the brain begin.

Atherosclerosis can develop for various reasons, but the consequences of the disease depend on the pathogenesis, and timely diagnosis and adherence to a certain lifestyle.

Steps to take for treatment

To stop attacks and alleviate the manifestations of temporal sclerosis, special antiepileptic drugs are usually prescribed. Mostly anticonvulsants. The dosage and mode of administration should be selected by a specialist. Can't self-medicate because it is necessary to correlate the manifestation of attacks, their type, the properties of the prescribed medicine and many other things.

If the manifestations of seizures disappear, this indicates that the disease is receding. If seizures do not make themselves felt for two years, then the doctor reduces the dosage of medications. Complete withdrawal of drugs is prescribed only after 5 years of complete absence of symptoms.

Note! The goal of conservative therapy is the complete relief of the manifestations of the disease and, if possible, a complete recovery.

When drug therapy fails, surgery is indicated. There are several types of surgical interventions for this disease, but temporal lobotomy is most often used.