How epilepsy develops from hippocampal sclerosis. Hippocampal sclerosis: causes, symptoms, diagnosis, choice of treatment method, recovery period and medical advice. Structural versus Genetic Forms of Temporal Temporal Epilepsy

A) Terminology:
1. Abbreviations:
Mesial temporal sclerosis (MTS)
2. Synonyms:
Ammon's horn sclerosis, hippocampal sclerosis (HS)
3. Definition:
Seizure syndrome-associated loss of neurons in the hippocampus and adjacent structures in combination with their gliosis

b) Visualization:

1. :
Best diagnostic criterion:
o Main features: abnormal increase in signal intensity on T2-WI from the hippocampus, decrease in its volume/its atrophy, unclearness of its internal architectonics of structure o Secondary features: atrophy of the ipsilateral fornix and ipsilateral mammillary body, widening of the ipsilateral temporal horn of the lateral ventricle and choroidal fissure
o Additional signs: loss of fingers of the head (peduncle) of the ipsilateral hippocampus, atrophy of the white matter of the parahippocampal gyrus, signal intensity from the white matter of the anterior temporal lobe on T2-weighted images
Localization:
o Mesial parts of the temporal lobe(s), in 10-20% of cases there is bilateral damage
o Hippocampus > amygdala > fornix > mammillary bodies
Dimensions:
o ↓ mild to severe hippocampal volume
Morphology:
o Abnormal shape, size of the affected hippocampus

2. CT signs of mesial temporal sclerosis:
Non-contrast CT
o Usually normal picture; CT is an insensitive method for diagnosing MVS

3. MRI signs of mesial temporal sclerosis:
T1-VI:
o ↓ size of hippocampus
o Lack of normal differentiation between gray and white matter in the hippocampus
o ± atrophy of the homolateral parts of the fornix, ipsilateral mastoid body
o Hippocampal volumetry: sensitivity to detect SWS (especially bilateral SWS)
T2-VI:
o Hippocampal atrophy
o Unclearness of the internal architectonics of the hippocampus structure
about signal intensity from the hippocampus
o ± atrophy of the ipsilateral parts of the fornix, ipsilateral mastoid body, expansion of the temporal horn of the ipsilateral lateral ventricle
o ± abnormal increase in signal intensity, decrease in volume in the anterior part of the ipsilateral temporal lobe
FLAIR:
o Increased signal intensity from the altered hippocampus
DVI:
about signal intensity on DWI ("T2-transillumination" effect)
about the diffusion coefficient on the ICD map
Post-contrast T1-weighted images
o No contrast enhancement
MR spectroscopy:
o ↓ NAA peak in the hippocampus, temporal lobe
o For ↓ NAA/Cho and ↓ NAA/Cho+Cr assume MBC
o ± peak lactate/lipids 24 hours after prolonged seizure

4. Angiography of mesial temporal sclerosis:
Preoperative Wada test: neuropsychological testing after intracarotid injection of amobarbital (Amytal):
o Determination of lateralization of memory function and language/speech functions
o Allows you to predict postoperative memory loss and the feasibility of the operation itself
o May be useful in determining seizure lateralization at seizure onset
fMRI mapping replaces the Wada test

5. Radionuclide diagnostics:
FDG PET: hypometabolism in altered mesial parts of the temporal lobe
SPECT: hypoperfusion (in the interictal period) or hyperperfusion (during an attack) in the epileptogenic zone:
o Sensitivity: during an attack > in the interictal period

6. Imaging Guidelines:
Best visualization tool:
o High resolution MRI
o MR spectroscopy, volumetry can be useful in determining the lateralization of the MVS in difficult cases
Study Protocol Advice:
o Thin-slice coronal T2WI and FLAIR images (3 mm) perpendicular to the long axis of the hippocampus
o Thin-slice coronal 3D SPGR images (1-2 mm) perpendicular to the long axis of the hippocampus

V) Differential diagnosis mesial temporal sclerosis:

1. Status epilepticus:
Clinical history of multiple seizures or status epilepticus
Temporary increase in signal intensity on T2-WI ± gyral contrast pattern in the affected areas of the cortex, hippocampus

2. Low grade astrocytoma:
Hyperintense mass in the white matter of the temporal lobe (usually non-contrast enhancing)
± typical convulsive syndrome, young adult age

3. Choroidal fissure cyst:
Asymptomatic choroidal fissure cyst with CSF signal intensity and causing change normal architectonics of the hippocampus structure:
o Round shape on axial, coronal sections
o Oval shape, parallel to the long axis of the temporal lobe on sagittal sections
Absence of abnormal increase in signal intensity from the mesial parts of the temporal lobe on T2-weighted images

4. Remnant of the hippocampal sulcus:
Disruption of normal involution of the hippocampal sulcus →
asymptomatic cyst between the dentate gyrus and ammon's cornu
A common (10-15% of cases) variant of the norm

5. Cavernous malformation:
Heterogeneous, hyperintense lesion with a “popcorn” pattern surrounded by a dark, closed ring of hemosiderin deposition
± convulsive syndrome

6. Dysembryoplastic neuroepithelial tumors (DNETs):
Volumetric formation of a “foamy” structure with a variable pattern of contrast accumulation, located in the cortex ± regional cortical dysplasia
Complex partial seizures

7. Cortical dysplasia:
The most common comorbidity associated with MWS
Increased signal intensity on T2-weighted images from the white matter of the anterior temporal lobes

G) Pathology of mesial temporal sclerosis:

1. General characteristics mesial temporal sclerosis:
Etiology:
o Conflicting evidence about whether this condition is acquired or develops:
- Acquired genesis: occurs after complex febrile seizures, status epilepticus, encephalitis
- Formation during development: in 15% of cases, a concomitant developmental disorder is detected
- “Double hit” hypothesis: the first is the initially provoking injury (such as a complex seizure), the second is increased susceptibility (such as genetic predisposition, developmental anomalies)
- In most cases, MBC is the outcome of both acquired and developmental processes
o Febrile seizures (FS) are most often observed among children (2-5%):
- Long-term PS can lead to acute damage to the hippocampus → followed by its atrophy
Genetics:
o There are reports of familial cases of mesial temporal lobe epilepsy (TLE), FS
o Recent studies suggest that the relationship between PS and late-onset epilepsy may be genetically determined
o Association with syndrome-specific FS genes (channelopathies) is observed in a small number of FS cases
Associated anomalies:
o Concomitant developmental disorder (15%)

2. Macroscopic and surgical features:
The hippocampus is normally anatomically divided into a head (pedicle), body and tail:
o Divided into ammon's cornu, dentate gyrus, hippocampal sulcus, fimbria, tray, base, parahippocampal gyrus, collateral sulcus
Atrophy of the mesial part of the temporal lobe: body (88%), tail (61%), head (51%) of the hippocampus, amygdala (12%)
No hemorrhage or necrosis

3. Microscopy:
Chronic astrogliosis with a dense fibrillar network of astrocyte nuclei and a reduced number of intact neurons
Ammon's horn, cornu ammonis (CA) contains four zones of granular cells: CA1, CA2, CAZ, CA4:
o Layers of pyramidal cells in areas CA1, CA4 are most susceptible to ischemia
o Variable neuronal loss may be observed in all areas of the hippocampus

d) Clinical picture:

1. Manifestations of mesial temporal sclerosis:
Most common signs/symptoms:
o Complex partial convulsive seizures, automatisms:
- Simple at a younger age with increasing complexity and discreteness of attacks with age
Other signs/symptoms:
o Possible progression to generalized tonic-clonic seizures
Clinical profile:
o There is often a history of febrile or drug-resistant seizures in childhood
- If you have a history of complex or prolonged febrile seizures, there is a risk of developing damage to the hippocampus, MWS
o Surface electro- (EEG) or magnetoencephalography (MEG) is useful for localizing the epileptogenic focus (60-90%)
o Intracranial EEG (subdural or deep electrode) may be indicated in cases of conflicting results from non-invasive studies

2. Demography:
Age:
o Disease in older children, young adults
Floor:
o No gender bias
Epidemiology:
o MWS is observed in the majority of patients who have undergone temporal lobectomy for epilepsy

3. Course and prognosis:
Anterior temporal lobectomy is effective in 70-95% of cases if the submitted MRI shows signs of MWS
Anterior temporal lobectomy is effective in 40-55% of cases if the submitted MRI shows a normal picture
↓ efficiency surgical treatment when involved in pathological process tonsils

4. Treatment of mesial temporal sclerosis:
Clinical tactics for patient management are based on the phenotypic characteristics of the initial manifestations of febrile and subsequent convulsive attacks
Initially - drug treatment
Temporal lobectomy is used to correct seizures that are resistant to drug therapy, as well as in cases of intolerance to the side effects of drugs:
o The resection area includes the anterior temporal lobe, most of the hippocampus, and variable portions of the amygdala

e) Diagnostic checklist:

1. note:
The most common cause of complex partial epilepsy in adults
Bilateral damage is observed in 10-20% of cases; difficult to detect without volumetry, except in severe cases

2. Tips for interpreting images:
Coronal T2-VI, high-resolution FLAIR images are most sensitive for diagnosing MWS
Double combined pathology in 1 5%
In children, low-grade neoplasms and cortical dysplasia are the most common cause of complex partial epilepsy (compared to MWS)

and) Bibliography:
1. Azab M et al: Mesial Temporal Sclerosis: Accuracy of NeuroQuant versus Neuroradiologist. AJNR Am J Neuroradiol. ePub, 2015
2. HamelinSetal: Revisiting hippocampal sclerosis in mesial temporal lobe epilepsy according to the "two-hit" hypothesis. Rev Neurol (Paris). 171 (3):227-3 5, 2015
3. French JA et al: Can febrile status cause hippocampal sclerosis? Ann Neurol. 75(2): 173-4, 2014
4. Thom M: Review: Hippocampal sclerosis in epilepsy: a neuropathology review. Neuropathol Appl Neurobiol. 40(5):520-43, 2014
5. Blumcke I et al: Defining clinico-neuropathological subtypes of mesial temporal lobe epilepsy with hippocampal sclerosis. Brain Pathol. 22(3):402-1 1, 2012
6. Malmgren K et al: Hippocampal sclerosis-origins and imaging. Epilepsy. 53 Suppl 4:19-33, 2012

Epilepsy is a disease that occurs as a result of excessive abnormal electrical activity of certain parts of the brain, which leads to periodic seizures. Seizures can be different. Some people simply freeze in place for a few seconds, while others experience full-blown convulsions.

An epileptic seizure is a condition that is associated with excessive hypersynchronous electrical discharges of brain neurons.

Approximately 2 out of 100 people in Ukraine experience unprovoked seizures at least once in their life. However, single seizures do not mean that a person has epilepsy. To make a diagnosis of epilepsy, it is usually necessary to have at least two unprovoked seizures.

Even minor seizures require treatment, as they can be dangerous while driving and other Vehicle, swimming, work at height, underwater, electrical work, etc.

Treatment usually includes drug therapy. However, if it is ineffective, surgical treatment is used. Surgical treatment of epilepsy is one of the latest achievements of modern medical science.

Symptoms

Since epilepsy is caused by abnormal electrical activity of brain cells, a seizure can involve any process brain controlled. For example:

• Speech and pronunciation disorders
• Temporary inhibition
• Spasms of facial muscles
• Uncontrollable twitching of arms and legs
• Loss of consciousness or impairment

Symptoms vary depending on the type of seizure. In most cases, the seizures are almost identical to each other.

The two anamnestic features most specific to epileptic seizures are the aura associated with the focal onset of the seizure and postictal confusion or sleep that develops after a generalized tonic-clonic seizure.

Aura is the initial part of a seizure, preceding loss of consciousness, of which the patient retains some memories. An aura is sometimes the only manifestation of an epileptic seizure.

It is customary to classify seizures into focal And generalized, depending on how the seizure begins.

Focal (partial) seizures

These are seizures that result from abnormal activity in one specific part of the brain. These seizures are divided into two subcategories:

Simple partial seizures.

These seizures do not result in loss of consciousness. They can change emotions or change the way we see things, smell, feel, hear. They may also lead to involuntary twitching of body parts or spontaneous sensory symptoms such as tingling or dizziness.

Simple partial seizures are stereotypical (identical) and are caused by one focal focus of pathological activity.

Jacksonian motor seizures arise as a result of irritation of the precentral gyrus of the cortex and are manifested by clonic twitching of the muscles of the face, arms or legs with possible spread to other areas (march).

When adverse seizures (irritation of the frontal adversus field) the head and eyes turn in the direction opposite to the hearth.

Phonatory seizures occur when the lesion is localized in Broca's area (speech center). The patient cannot speak or shouts out individual distorted words.

Sensory seizures arise in the form of auditory, visual, olfactory hallucinations.

Somatosensory seizures occur during discharges in the postcentral gyrus and are manifested by local sensitivity disorders (paresthesia).

Vegetative-visceral seizures arise from discharges in the temporal lobe and limbic system. This results in attacks of abdominal pain, respiratory disorders (shortness of breath, difficulty breathing), palpitations and pharyngo-oral attacks with drooling, involuntary chewing, smacking, licking, etc.

Known attacks of mental dysfunction and thinking.

Complex partial seizures.

They begin as simple ones, followed by a disturbance of consciousness and an inadequate perception of the world. Their main difference is the memorization of the seizure in a distorted form as a consequence of the absence of a complete blackout of consciousness.

These seizures can affect consciousness, causing confusion for a period of time. Complex partial seizures often result in non-purposeful movements such as rubbing hands, chewing, swallowing, or walking in circles.

The occurrence of complex partial seizures is associated with the formation of secondary and even tertiary foci of epileptic activity, which are cloned outside the primary focus. At first, secondary lesions are functionally dependent on the primary lesion, and over time they can function independently. The spread of epileptic foci is the reason for the progression of the disease and changes in its manifestations.

Generalized seizures

Generalized seizures are characterized by loss of consciousness and occur when the entire brain is involved in the pathological process. Seizures can be primarily generalized, when excitation occurs simultaneously in both hemispheres of the brain, or secondarily generalized, as a consequence of partial seizures. In this case, the aura of such a seizure is a partial seizure.

There are six main types of generalized seizures:

• Absence seizures (minor epileptic seizures).
• Tonic convulsions.
• Clonic seizures.
• Myoclonic spasms.
• Atonic seizures.
• Tonic-clonic seizures(so called the great epileptics seizures).

When to see a doctor immediately

You should seek immediate medical attention if a seizure occurs in conjunction with any of the following:

• The seizure lasts more than five minutes.
• Normal breathing and consciousness do not return after the seizure ends.
• After one seizure ends, the next one begins immediately.
• The seizure is accompanied by a high fever.
• You have experienced heatstroke.
• You are pregnant.
• You have diabetes.
• You were injured during an attack.

Causes

In half of the cases, it is not possible to establish the causes of epilepsy. In the other half of cases, epilepsy can be caused by various factors, for example:

Risk factors

Certain factors can increase the risk of epilepsy.

• Age. The most common time of onset of epilepsy is early childhood and age after 65 years.
• Floor. Men have a little more risk development of epilepsy than in women.
• Family history of epilepsy.
• Head injuries.
• Stroke and other vascular diseases.
• Infections nervous system . Infections such as meningitis, which causes inflammation of the brain or spinal cord, may increase the risk of developing epilepsy.
• Frequent seizures in childhood. Heat in childhood it can sometimes cause seizures, which can subsequently lead to the development of epilepsy at a later age, especially if there is a family predisposition to epilepsy.

Complications

Sometimes a seizure can lead to circumstances that pose a danger to the patient or others.

• A fall. If you fall during a seizure, you may injure your head or break something.
• Drowning. People with epilepsy are 13 times more likely to drown while bathing or swimming than the rest of the population due to the risk of having a seizure in water.
• Car crashes. Having a seizure while driving a car can lead to an accident.
• Complications during pregnancy. Convulsions during pregnancy pose a danger to mother and baby. Taking some antiepileptic drugs increases the risk congenital anomalies in children. If you have epilepsy and are planning a pregnancy, talk to your doctor. Most women with epilepsy can become pregnant and have healthy child. But it is very important to consult a doctor when planning a pregnancy.
• Emotional health problems. People with epilepsy are more likely to have psychological problems, in particular depression.

Other life-threatening complications of epilepsy are less common:

• Status epilepticus. During status epilepticus, the patient is in a state of constant convulsive activity lasting more than five minutes, or he has frequent epileptic seizures that repeat one after another, between which he does not regain full consciousness. People with status epilepticus have an increased risk of permanent brain damage and death.
• Sudden unexplained death in epilepsy. People with poorly controlled epilepsy also have a small risk of sudden unexplained death. Overall, fewer than 1 in 1000 people with epilepsy (especially those with generalized tonic-clonic seizures) will die suddenly.

Examination methods and diagnostics

Your doctor may use a range of tests to diagnose epilepsy, from neurological tests to sophisticated imaging tests such as MRI.

Neurological and behavioral methods examinations. The doctor tests the patient's motor abilities, behavior, and intellectual potential to find out how the seizures affect him.

Blood tests. A blood sample is tested for signs of infection, electrolyte imbalance, anemia, or diabetes, which may be associated with seizures.

Conservative treatment

Treatment of epilepsy begins with medications. If they are ineffective, surgery or another type of treatment is offered.

Most people with epilepsy live seizure-free while using one of the antiepileptic drugs. Other drugs may reduce the frequency and intensity of epileptic seizures. More than half of children with drug-controlled epilepsy can eventually stop taking their medications and live seizure-free. Many adults can also stop treatment after two or more years without attacks. Finding the right medication and dosage can be challenging. Initially, one drug is prescribed in relatively low doses, increasing the dose gradually as needed to control attacks.

All antiepileptic drugs have side effects . Milder side effects include fatigue, dizziness, weight gain, loss of density bone tissue, skin rashes, loss of coordination, speech problems.

More severe but rare side effects include depression, suicidal thoughts and behavior, disorders of the kidneys, pancreas or liver, impaired blood formation.

To achieve better control of epileptic seizures with medication, you must:

• take medications strictly as prescribed;
• Always tell your doctor if you are switching to generic medications or taking other prescription drugs, brand-name drugs, or herbal remedies;
• never stop taking medications without consulting your doctor;
• Tell your doctor if you experience new or worsening feelings of depression, suicidal thoughts, or unusual changes in mood or behavior.

At least half of people newly diagnosed with epilepsy live seizure-free while taking the first antiepileptic drug they are prescribed. With ineffective drug treatment The patient is offered surgery or other types of therapy.

Ketogenic diet. Some children with epilepsy are able to reduce seizures by maintaining a strict high-fat, low-carbohydrate diet. This diet is called a ketogenic diet, forcing the body to break down fats instead of carbohydrates for energy. Some children can stop this diet after a few years without having seizures.

Consult your doctor if you or your child decide to follow the ketogenic diet. It is important to ensure that the child does not become malnourished while using the diet. Side effects of a fat-rich diet may include dehydration, constipation, slow growth due to deficiency nutrients and a buildup of uric acid in the blood, which can cause kidney stones. These side effects are rare if the diet is used properly and under medical supervision.

Surgical treatment of epilepsy

Epilepsy surgery is indicated when studies show that seizures occur in small, well-defined areas of the brain that do not interfere with vital functions. important functions, such as speech, language or hearing. These surgeries remove areas of the brain that cause seizures. 20% of patients with epilepsy undergo surgical treatment.

The goal of surgical treatment is to significantly reduce the frequency of attacks and improve the quality of life of such patients.

Indications for surgery:

• Mesial temporal sclerosis;
• Partial seizures with aura (at the beginning of the attack, consciousness is preserved);
• Partial seizures with secondary generalization and loss of consciousness;
• Drop attacks (atonic attacks) (sudden falls of patients without convulsions).

Primary generalized seizures with primary loss of consciousness are not subject to surgical treatment .

Half of all surgical cases involve the removal of brain tumors. The second part of surgical epilepsy is most often associated with sclerosis of the hippocampus of the temporal lobe (mesial sclerosis). Temporal lobectomy is the treatment of choice for such patients. Operations for localizing epilepsy foci outside the temporal lobe (extratemporal operations) require long-term pre- and postoperative EEG monitoring using electrodes installed directly on the cerebral cortex. Removal of pathologically functioning areas of the cerebral cortex - the main task such operations.

If seizures occur in areas of the brain that cannot be removed, your doctor may recommend various types of surgery in which surgeons make a series of incisions in the brain to prevent seizures from spreading to other parts of the brain (commissurotomy of the corpus callosum, functional hemispherectomy).

In many patients, epilepsy disappears forever after surgery. However, even after successful surgery, some patients still need medication to prevent rare attacks, although the doses may be much lower. In a small number of cases surgical intervention in case of epilepsy, it can cause complications associated with the removal of functioning areas of the cerebral cortex.

Lifestyle

Take your medications correctly. Do not adjust the dosage of medications yourself. Instead, talk to your doctor if you feel something needs to be changed.

Proper sleep. Sleep deprivation is a powerful trigger for seizures. Get adequate rest every night.

Wear a medical bracelet. This will help you with medical care.

Uncontrolled seizures and their impact on life can lead to depression at times. It is important not to let epilepsy isolate you from society. You can lead an active social life.

A person with epilepsy, his friends and family members should know about epilepsy and understand the patient's condition. Study epilepsy, use scientific, not fantastic ideas about this disease.

Try to eliminate negative emotions and maintain a sense of humor.

Live independently as much as possible, continuing to work if possible. If you are unable to travel due to your seizures, use the public transportation options available to you.

Find a good doctor who will help you and with whom you feel comfortable.

Try not to think about seizures.

If the attacks are so severe that you cannot work outside the home, you may have other options, such as working from home through the use of special computer programs. Find a hobby and connect online with other people who are interested in the same thing. Be active in finding friends and contacts with other people.

First aid for an epileptic seizure

• Gently turn the patient onto his side.
• Place something soft under it and under your head.
• Loosen tight fitting parts of the tie.
• Don't try to open your mouth with your fingers. No one has ever “swallowed” their tongue during an attack - this is physically impossible.
• Do not try to lift the patient, shout or shake him.
• If you observe seizures, remove dangerous objects that could injure him.
• Stay with the patient until medical personnel arrive.
• Observe the patient so that you can provide detailed information about what happened.
• Determine the onset time and duration of the seizure.
• Remain calm and reassure others nearby.

To take a closer look at this disease, we need to say a little about the disease that provokes it. Temporal lobe epilepsy is neurological disease which is accompanied by convulsive attacks. Its focus is in the temporal lobe of the brain. Seizures can occur with or without loss of consciousness.

Mesial sclerosis acts as a complication and is accompanied by loss of neurons. Due to head injuries, various infections, seizures, tumors, the tissue of the hippocampus begins to atrophy, which leads to the formation of scars. There is a possibility that the course of the disease will be aggravated by additional seizures. It can be either right- or left-handed.

Based on structural changes, the hippocampus can be divided into two types:

1. There are no volumetric changes in the temporal lobe of the brain.
2. There is a process of increasing 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 seizures. Their influence contributes various violations metabolism. The cortex of the temporal lobe swells and the destruction of neurons begins, the tissue atrophies, the hippocampus decreases in volume.
• Mechanical injuries. 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. Incorrect development of the temporal lobe during the prenatal period or various birth injuries.
• Oxygen starvation of brain tissue. It can be caused by respiratory and metabolic disorders.
• Infections. Meningitis, encephalitis and other inflammations in the brain can lead to activation of mesial sclerosis.
• Poisoning. Intoxication of the body with harmful substances over a long period of time.
• Circulatory disorders. When blood circulation in the temporal lobe is impaired, ischemia and neuronal death begin, followed by atrophy and scarring.

You will find medications used for sclerosis, treatment folk remedies you will find by going to .

Risk factors

Risk factors include:

1. Brain strokes.
2. Hypertension and hypertension.
3. Diabetes.
4. In older people, hippocampal sclerosis is recorded more often than in young people.

Symptoms

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

The signs of hippocampal sclerosis should be examined in more detail, but only a competent person 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 amygdala.
• Atrophy of part of the diencephalon nucleus.
• Reduction of the singular gyrus.
• Atrophy of the cerebral vault.

In the presence of left-sided mesial sclerosis, symptoms will be more severe than with right-sided mesial sclerosis and cause more serious damage to the parasympathetic system. Seizures are disrupting general activities all parts of the brain and can even cause problems with 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, and this is associated with various neural disorders.

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

Atherosclerosis can develop in different ways, but the disease depends on timely and specific compliance.

Measures to be taken for treatment

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

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

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

When drug therapy does not bring results, surgical intervention is prescribed. There are several types of surgical interventions for this disease, but the most commonly used is temporal lobotomy.

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 examination, but had lower hippocampal volume and more significant dynamics of volume reduction, were on average three times more likely to develop dementia compared to others. 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 spreads even more widely to other areas of the brain.

Atrophy of the left hippocampus, seizure syndrome

In July 2007, I bought the American complex of amino acids EXTREME AMINO for pumping muscle mass athletes from ULTIMATE NUTRITION. I took 3 capsules on an empty stomach after training in the gym three times a week. While taking amino acids, my sleep noticeably worsened, my teeth began to clench at night, I had bad breath and a constant feeling of fatigue. On March 6, 2008, at night, severe convulsions of the whole body began. He was hospitalized in the medical unit and spent 12 hours in intensive care. Diagnosis: severe poisoning with an unspecified neurotropic substance, convulsive syndrome. On April 29, 2008, after working out at the gym in the middle of the night, severe vomiting began, 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). The seizures occur monthly in a series of attacks. I can’t get out of cramps without Sibazon. I am registered with a neurologist, but I don’t see a way out of my illness. Neurologist's conclusion: Epilepsy occurs in the form of simple partial and nocturnal generalized seizures.

Judging by what you describe, despite taking an antiepileptic drug, you continue to have regular epileptic seizures. This indicates that it is necessary to change the drug. You need a consultation with an epileptologist in order to question you in more detail, examine you, and conduct additional methods examinations (electroencephalography and magnetic resonance imaging of the brain), and then, based on the results obtained, decide which drug you need. I will be glad to help you with this. In any case, for now I recommend limiting physical exercise: workouts should be shorter in duration or with longer breaks between approaches until normal breathing and heart rate are completely restored!

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Causes and types of hippocampal sclerosis

Hippocampal sclerosis is a form of epilepsy caused by pathology of the limbic system of the brain. The main generator of epileptic activity is considered to be gliosis in combination with atrophy cortical plate underlying white matter. Neurologists at the Yusupov Hospital use modern methods to diagnose the disease. instrumental research, perform lab tests and minimally invasive diagnostic procedures.

Hippocampal sclerosis is accompanied by loss of neurons and scarring of the deepest part of the temporal lobe. Often caused by serious brain injuries. It can be left-handed or right-handed. Brain damage due to injury, neoplasm, infection, lack of oxygen, or uncontrolled spontaneous seizures results in the formation of scar tissue in the hippocampus. It begins to atrophy, neurons die and form scar tissue.

Based structural changes There are two main types of temporal lobe epilepsy:

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

Causes of bilateral hippocampal sclerosis

Known following reasons hippocampal sclerosis:

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

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

• the influence of febrile seizures, leading to regional metabolic disorders and swelling of the temporal lobe cortex. Neuronal death occurs, local gliosis and atrophy develop, resulting in a decrease in the volume of the hippocampus and a reactive expansion of the sulcus and the inferior 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.
• disruption of the development of the temporal lobe during embryogenesis.

Symptoms of hippocampal sclerosis

Hippocampal sclerosis usually leads to focal epilepsy. Epileptic seizures appear in groups or individually. They can be complex, starting with strange indescribable sensations, hallucinations or illusions, followed by numbness of vision, eating and rotatory automatisms. Lasts about two minutes. As it progresses, generalized tonic-clonic seizures may occur.

Attacks with hippocampal sclerosis can be accompanied by various symptoms:

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

Patients develop impairment of 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, paresthesia and unilateral facial twitching. Patients note learning difficulties and memory impairment. They are conflict-ridden, emotionally labile, and have a heightened sense of duty.

To diagnose the disease, doctors at the Yusupov Hospital use the following examination methods:

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

The study is carried out using modern equipment from leading global manufacturers.

Treatment of hippocampal sclerosis

To reduce the symptoms of the disease, neurologists at the Yusupov Hospital prescribe antiepileptic drugs. The drug of first choice is Carbamazepine. Second-choice drugs include Valproate, Diphenin and Hexamidine. After treatment, some patients stop having attacks and go into long-term remission.

In cases of resistance to therapy and progression of hippocampal sclerosis, surgical treatment is performed in partner clinics. It involves removing the temporal lobe of the brain (lobectomy). After surgery, the number of attacks decreases in 70-95% of cases. If you are faced with the problem of hippocampal sclerosis and want to get a qualified specialized medical care, call by phone. You will be scheduled for a consultation with a neurologist at the Yusupov Hospital.

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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.

In this case, the main group of neurons shows sparse activity, i.e. During short periods of time, most cells are inactive, while a small proportion of neurons exhibit 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 connected by commissural nerve fibers. The hippocampus consists of densely packed cells in a ribbon structure that extends along the medial wall of the inferior horn of the lateral ventricle of the brain 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 granule cells. In addition to the cells of these types, the hippocampus contains GABAergic interneurons, which 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. From an anatomical point of view, 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 connected to the parts of the brain responsible for emotional behavior.

The hippocampus contains four main areas: 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, the integrating nucleus of the thalamus, the supramammillary nucleus of the hypothalamus, the raphe nuclei, and the locus coeruleus in the brainstem send axons to the entorhinal cortex.

The main outgoing tract of axons in the entorhinal cortex comes from the large pyramidal cells of layer II, which perforate the subiculum and project densely into the granule cells in the dentate gyrus; the superior dendrites of CA3 receive less dense projections, and the apical dendrites of CA1 receive an even sparse 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 propagating through a somewhat dense layer of cells, first to the dentate gyrus, then to layer CA3, then to layer CA1, then to the subiculum and then from the hippocampus to the entorhinal cortex. cortex, mainly providing routes for CA3 axons. Each of these layers has a complex internal circuit and extensive longitudinal connections. A very important large exit pathway goes to the lateral septal zone and to the mammillary body of the hypothalamus.

There are also other connections in the hippocampus that play a very important role in its functions.

At some distance from the exit to the entorhinal cortex, there are other exits going 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 received its name due to its close location with the olfactory gyrus. The perirhinal cortex is responsible for visual recognition of complex objects.

There is evidence that the parahippocampus has a separate memory function from the hippocampus itself, since only damage to both the hippocampus and the parahippocampus results in 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. However, further research has shown that the olfactory bulb has some projections to the ventral entorhinal cortex, and layer CA1 in the ventral hippocampus sends axons to the main olfactory bulb, the anterior olfactory nucleus and the primary olfactory cortex.

A certain role of the hippocampus in olfactory reactions, namely in the memorization of odors, is still 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 memory formation. This theory has been proven many times in various observations of people who have undergone surgery on the hippocampus, or have been 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 Molaison, who underwent surgery 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 happened 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 explicitly expressed in words - including, for example, memory for facts in addition to episodic memory).

In every 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 the ability to master certain skills, for example, playing a musical instrument. This suggests that such memory depends on other parts of the brain, not just the hippocampus.

Not only age-related pathologies such as Alzheimer's disease (for which destruction of the hippocampus is one of early signs diseases) have profound effects on many types of perception, but even normal aging is associated with gradual decline in some types of memory, including episodic and short-term memory. Because the hippocampus plays an important role in memory formation, scientists have linked age-related memory impairment to physical deterioration of the hippocampus.

Initial studies found significant neuronal loss in the hippocampus in older adults, but new research suggests that such loss is minimal. Other studies have shown that the hippocampus shrinks significantly in older adults, but similar studies again found no such trend.

Stress, especially chronic stress, can cause 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 associated with 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 dendritic atrophy in the pyramidal cells of the CA3 area.

Studies have shown that in people who experienced long-term stress, hippocampal atrophy 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 level cortisol in the blood).

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

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  That’s why I don’t go to clinics, but the doctor calls me and wants me to undergo some kind of medical examination.

  But! As soon as they find something on someone, they immediately intervene, and - OP! Six months later the person is gone!

  Healed to death!

  I’d rather brew volodushki and chaga birch with fireweed. And then - as God willing!

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

  I went through it last year, everything turned out to be more or less normal, only my heart was playing around with something - I took very light medications, although I started getting sick less often.

  But I didn’t get to the oncologist - so 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 (GIA). Theta modes appear mainly in a state of activity, as well as during REM sleep. In theta modes, the electroencephalogram shows the presence of large waves with a frequency range from 6 to 9 Hertz. In this case, the main group of neurons shows sparse activity, i.e. during short periods of time, most cells are inactive, while a small proportion of neurons exhibit increased activity. In this mode, the active cell has such activity from half a second to several seconds.

  BNA-regimes take place during the period long sleep, as well as during periods of quiet wakefulness (rest, eating).

  The structure of the hippocampus

  Humans have two hippocampi, one on each side of the brain. Both hippocampi are connected by commissural nerve fibers. The hippocampus consists of densely packed cells in a ribbon structure that extends along the medial wall of the inferior horn of the lateral ventricle of the brain 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 granule cells. In addition to the cells of these types, the hippocampus contains GABAergic interneurons, which 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. From an anatomical point of view, 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 connected to the parts of the brain responsible for emotional behavior. The hippocampus contains four main areas: 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, the integrating nucleus of the thalamus, the supramammillary nucleus of the hypothalamus, the raphe nuclei, and the locus coeruleus in the brainstem send axons to the entorhinal cortex. The main outgoing tract of axons in the entorhinal cortex comes from the large pyramidal cells of layer II, which perforate the subiculum and project densely into the granule cells in the dentate gyrus; the superior dendrites of CA3 receive less dense projections, and the apical dendrites of CA1 receive an even sparse projection. Thus, the pathway uses the entorhinal cortex as the main link between the hippocampus and other parts of the cerebral cortex. Dentate granule cell axons convey information from the entorhinal cortex to spiny hairs emerging from the proximal apical dendrite of CA3 pyramidal cells. CA3 axons then emerge from the deep part of the cell body and loop upward to where the apical dendrites are located, then extend all the way back into the deep layers of the entorhinal cortex in the Schaffer collaterals, completing the mutual closure. Area CA1 also sends axons back to the entorhinal cortex, but in this case they are sparser than the outputs of CA3.

  It should be noted that the flow of information in the hippocampus from the entorhinal cortex is significantly unidirectional with signals propagating through a somewhat dense layer of cells, first to the dentate gyrus, then to layer CA3, then to layer CA1, then to the subiculum and then from the hippocampus to the entorhinal cortex. cortex, mainly providing routes for CA3 axons. Each of these layers has a complex internal layout and extensive longitudinal connections. A very important large exit pathway goes to the lateral septal zone and to the mammillary body of the hypothalamus. The hippocampus receives modulatory inputs from serotonin, dopamine and norepinephrine pathways, as well as from the thalamic nuclei in layer CA1. 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 critical to control physiological state hippocampus Injuries and disturbances in this area can completely shut down the theta rhythms of the hippocampus and create serious memory problems.

  There are also other connections in the hippocampus that play a very important role in its functions. At some distance from the exit to the entorhinal cortex, there are other exits going 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 received its name due to its close location with the olfactory gyrus. The perirhinal cortex is responsible for visual recognition of complex objects. There is evidence that the parahippocampus has a separate memory function from the hippocampus itself, since only damage to both the hippocampus and the parahippocampus results in complete memory loss.

  Functions of the hippocampus

  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. However, further research has shown that the olfactory bulb has some projections to the ventral entorhinal cortex, and layer CA1 in the ventral hippocampus sends axons to the main olfactory bulb, the anterior olfactory nucleus and the primary olfactory cortex. A certain role of the hippocampus in olfactory reactions, namely in the memorization of odors, is still 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 memory formation. This theory has been proven many times in various observations of people who have undergone surgery on the hippocampus, or have been 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 Molaison, who underwent surgery 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 happened 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 explicitly expressed in words - including, for example, memory for facts in addition to episodic memory). In every 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 when both parts of the hippocampus are damaged, serious problems arise with new memories. At the same time, a person remembers older events perfectly, which suggests that over time, part of the memory moves 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 the ability to master certain skills, for example, playing a musical instrument. This suggests that such memory depends on other parts of the brain, not just the hippocampus.

  Long-term studies have also shown that the hippocampus plays an important role in spatial orientation. So we know 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 memory of specific places in space.

  Hippocampal pathologies

  Not only do age-related pathologies such as Alzheimer's disease (for which hippocampal destruction is one of the early signs of the disease) have profound effects on many types of perception, but even normal aging is associated with a gradual decline in some types of memory, including episodic and short-term memory. Because the hippocampus plays an important role in memory formation, scientists have linked age-related memory impairment to physical deterioration of the hippocampus. Initial studies found significant neuronal loss in the hippocampus in older adults, but new research suggests that such loss is minimal. Other studies have shown that the hippocampus shrinks significantly in older adults, but similar studies again found no such trend.

  Stress, especially chronic stress, can cause 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 associated with 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 dendritic atrophy in the pyramidal cells of the CA3 area. Studies have shown that in people who experienced long-term stress, hippocampal atrophy 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. During epileptic seizures, sclerosis of certain areas of the hippocampus is often observed.

  Schizophrenia occurs in people with an abnormally small hippocampus. But to date, the exact connection between schizophrenia and the hippocampus has not been established.

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

Research Institute of Emergency Medicine named after N.V. Sklifosovsky participates in the “Program complex treatment patients suffering from epilepsy" together with the Russian National Research medical university them. N.I. Pirogov, Moscow State Medical and Dental University named after. A.I. Evdokimov, Institute of Higher Nervous Activity and Neurophysiology of the Russian Academy of Sciences, Scientific and Practical Psychoneurological Center named after. Z.P. Solovyova, Interdistrict Department of Paroxysmal Conditions No. 2, City clinical hospital No. 12, which includes a comprehensive examination of patients with epilepsy, selection and correction of conservative therapy, consultations with specialists, observation, and surgical treatment of patients suffering from epilepsy.

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

Currently, there are more than 50 million people with epilepsy in the world. Among diseases of the nervous system, epilepsy is one of the most common reasons disability. Despite the successes of pharmacotherapy, the incidence of “uncontrolled” epilepsy in industrialized countries that adhere to modern standards of treatment ranges from 30 to 40%. Patients with epilepsy with lesions that can be removed are the most likely candidates for surgical treatment.

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

The main causes of symptomatic epilepsy are:

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

Diagnostics.

To resolve the issue of the possibility of surgical treatment of epilepsy, first of all, a comprehensive “presurgical” examination is necessary, which includes:

1. Clinical study of seizure semiology;
2. Neuropsychological research;
3. Neuroimaging research methods (high-resolution magnetic resonance imaging on a 3.0 Tesla device using a special “epilepsy” program, positron emission tomography).
4. Neurophysiological studies, including both invasive methods (registration of bioelectrical activity of the brain using intracranial electrodes) and non-invasive methods (EEG, video-EEG monitoring, magnetoencephalography).

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

Rice. 2. Electrodes for invasive recording of bioelectrical activity of the brain (electrode on the left for installation in the hippocampus, on the right - the cortical subdural electrode).

The main goal of epilepsy treatment, both medical and surgical, is seizure control. In patients with persistent seizures resistant to anticonvulsant therapy, cessation of seizures after surgical treatment significantly improves the quality of life - professional and social adaptation and leads to a decrease in mortality.

With continued anticonvulsant therapy, seizure control can be achieved in no more than 8% of cases. At the same time, with surgical treatment, seizure control is achieved in 58% of patients, and in the group of patients with temporal lobe epilepsy - in 67%.

Only after a thorough, complete examination is it possible to decide on surgical treatment.

The main method of surgical treatment of epilepsy is removal of the epileptogenic zone of the brain under neurophysiological control, using a high-resolution microscope, as well as stereotactic navigation methods.

At the Research Institute of Emergency Medicine named after N.V. Sklifosovsky is held full examination, as well as all types of surgical treatment of patients with drug-resistant forms of epilepsy.

Examples of surgical treatment

Patient N., 40 years old.

History of the disease: The first convulsive attack occurred at 2 months after meningoencephalitis. At the age of 8 years, a generalized epileptic attack with loss of consciousness developed for the first time; the frequency of attacks at that time was 1 time per year. She was observed by a neurologist, received conservative therapy - without effect, the number of attacks increased every year. From the age of 17, the frequency of attacks reached 1 attack per week. At the age of 30, the number of attacks reached 4-5 per day. 2 years ago, the patient noted the appearance of an aura in the form of visual and tactile hallucinations preceding convulsive seizures. She was observed by a neurologist, the doses of anticonvulsants continued to increase, however, despite this, the frequency of attacks increased.

Rice. 3. MRI of the brain (coronal sections). Arrows indicate signs of sclerosis of the right hippocampus in the form of a decrease in the size of the structure with expansion of the lower horn of the right lateral ventricle, increased signal from the white matter of the brain

Rice. 4 (left). The planning stage of the operation is the installation of intracranial electrodes using the neuronavigation unit BrainLab and VarioGuide.

Rice. 5 (right). The stage of the operation is the installation of an electrode in the right hippocampus using the BrainLab and VarioGuide navigation system.

Rice. 6 (left). Conducting video-EEG monitoring

Rice. 7 (right). Single room for video-EEG monitoring (an infrared camera is installed that allows video-EEG monitoring to be carried out around the clock).

The patient was discharged on the 12th day in satisfactory condition; the control EEG showed no evidence of paroxysmal activity.

Histological conclusion of the resected sections of the right temporal lobe and the right hippocampus): morphological picture of FCD (focal cortical dysplasia) type III d (ILAE). A clear picture of sclerosis of the right hippocampus.

The patient (follow-up 12 months) did not experience any epileptic seizures after surgical treatment.

Patient N., 25 years old.

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

History of the disease: at 8 months he suffered a severe traumatic brain injury with a prolonged coma, and subsequently developed weakness in the right limbs. At the age of 6, the patient began to experience seizures—local convulsions of the facial muscles. From the age of 15, generalized seizures appeared. He took carbamazepine, Topamax doses were increased to subtoxic, but no significant effect was achieved.
Currently, the patient has epileptic seizures with loss of consciousness with a frequency of 1-2 times a month lasting up to 1 minute and attacks once a week, without loss of consciousness, lasting up to 15 seconds.

Rice. 8 (left). MRI of the brain (coronal section). Post-traumatic scar-atrophic changes in the left parietal lobe of the brain are determined (marked with a red circle).

Rice. 9 (right). MRI of the brain (axial section). Arrow 1 marks the right hippocampus and arrow 2 the left hippocampus. Noteworthy is the asymmetric location and decrease in size of the left hippocampus (arrow 2).

The first stage of the operation was 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 underwent invasive EEG monitoring for 7 days. During observation, the patient had three clinical epileptic seizures.

Against the background of complete well-being and the absence of attacks, the patient constantly recorded paroxysmal activity in the left hippocampus and in the scar area.

During one of the epileptic seizures, the seizure onset zone is localized in the area of ​​the post-traumatic scar, subsequently involving the left hippocampus and the basal parts of the left temporal lobe.

During two other epileptic seizures, the patient had a seizure onset zone in the projection of the left hippocampus with subsequent spread to the area of ​​the left temporal lobe.

Rice. 10 (left). Conducting round-the-clock invasive video-EEG monitoring (using a high-resolution infrared video camera). The red arrow indicates the zone where paroxysmal activity began to be recorded on the electrode located in the projection of the post-traumatic scar of the left parietal lobe.

Rice. 11 (right). Conducting round-the-clock invasive video-EEG monitoring (using a high-resolution infrared video camera). The red arrow indicates the zone where paroxysmal activity began to be recorded on an electrode located in the left hippocampus.

The patient underwent surgical intervention - osteoplastic craniotomy in the left fronto-parietal-temporal region, selective resection of the left temporal lobe, hippocampectomy on the left, removal of the brain scar of the left parietal and temporal lobes, using intraoperative ECoG (electrocorticography).

Rice. 12. Planning of surgical intervention. Three-dimensional model of the brain with tractography (built on the BrainLab neuronavigation unit using high-resolution 3.0 Tesla MRI with MR tractography).

Rice. 13. Planning of surgical intervention, surgical access zones using the BrainLab neuronavigation unit.

Rice. 14. Intraoperative corticography after removal of a post-traumatic scar. The red arrow marks the subdural electrode. The black arrow marks the corticogram from the subdural electrode.

Rice. 15. Conducting video-EEG monitoring after surgery. There is a clear positive EEG dynamics in the form of a decrease in paroxysmal activity in the left hemisphere of the brain; isolated rare paroxysms in the right hemisphere of the brain persist.

The patient (follow-up 8 months) did not experience any epileptic seizures after surgical treatment.

In this case, it is noteworthy that during MRI of the brain, no clear signs of focal cortical dysplasia of the left temporal lobe and hippocampal sclerosis were noted, and only the installation of intracranial electrodes with subsequent video-EEG monitoring made it possible to identify two zones of the onset of epileptic seizures.

This once again confirms the need for a complete comprehensive survey patients with epilepsy.

© 2009-2020 emergency neurosurgery department Research Institute of Emergency Medicine named after. N.V. Sklifosovsky