Can taurine help with symptoms of derealization

Epilepsy foci in the brain what is it? Epileptic foci in the brain What are epileptiform foci?

Epileptic focus

A group of neurons that are involved in the onset of a partial seizure. For widespread or generalized seizures, O.E. The neurons from which discharge began are counted. The presence of O.E. is detected in the EEG and outside of the seizure by the presence of local epileptic activity with the corresponding leads.


. V. M. Bleikher, I. V. Kruk. 1995.

See what "Epileptic Focus" is in other dictionaries:

    Epileptic focus - - a nerve structure (group of neurons), the excitation of which leads to a focal or generalized attack of epilepsy. The activity and theme of such a focus can often be found in the clinical structure of epileptic seizures and in the EEG in ... ...

    Epileptical attack - Epilepsy ICD 10 G40. G41. ICD 9 345 DiseasesDB ... Wikipedia

    A seizure in epilepsy that occurs due to excessive excitation and discharge in the neurons of the brain, including in the area of ​​the epileptic focus. SPORTS. The abdomen is characterized by discomfort or pain in the umbilical cord and ... ... Explanatory dictionary of psychiatric terms

    epilepsy - I Epilepsy (epilepsy; Greek epilepsy fit, epileptic fit) is a chronic polyetiological disease that manifests itself through seizures and other seizures, mental disorders and characteristic personality changes. E. One of ... ... Medical Encyclopedia

    epilepsy - ICD 10 G40.40. G41.41. ICD 9 345 ... Wikipedia

    EPILEPSY - EPILEPSY. Contents: History ......................... 531 Etiology .................... .... 532 Distribution .................... 536 Pathological Anatomy ............... 5 37 Experimental Pathology .. ........... 539 Pathogenesis ... Great Medical Encyclopedia

    Focal or partial seizure - - are manifested in paroxysms of an isolated violation of a function. The consciousness in this case may be deaf ("complex partial seizure"), but often or even most of the time it remains more or less clear. Some partial seizures ... Encyclopedic Dictionary of Psychology and Education

    EPILEPSY - - a chronic disease caused by damage to the central nervous system; manifests itself in convulsive seizures and specific personality changes. Seizures are divided into large and small. A major (generalized) seizure that occurs acutely ... ... Encyclopedic Dictionary of Psychology and Education

    - (Greek epilepsy - seizure, epileptic fit). Chronic endogenous organic disease that occurs with repeated paroxysmal disorders (convulsive and non-convulsive) and the formation of dementia with characteristic ... .... Explanatory Dictionary of Psychiatric Terms

    Seizure - - sudden and strong manifestation of what l. Feelings (anger, hysteria). Marry impulse, seizure. * * * - a short-term and mostly recurring painful condition with a sudden loss of consciousness, often with convulsions, other ... ... Encyclopedic Dictionary of Psychology and Education

LECTURE 15

According to the definition by WHO experts, epilepsy is a chronic brain disease with various causes, characterized by repeated epileptic seizures as a result of excessive neuronal discharges and accompanied by a variety of clinical and paraclinical symptoms.

It is necessary to make a strict distinction between an epileptic seizure and epilepsy as a disease. Individual epileptic seizures or epileptic reactions according to the terminology of local researchers that occur in a certain situation, or accidental according to the terminological dictionary of epilepsy, will not be repeated in the future. An example are some cases of febrile convulsions in children. Epilepsy should not include recurrent seizures in acute cerebral disorders, such as: B. in cerebrovascular accidents, meningitis, encephalitis. At the suggestion of SN Davidenkov, in such cases it is advisable to use the term “epileptic syndrome”.

Etiology. The development of epilepsy requires a sustained focus of epileptic activity caused by organic brain damage. At the same time, the epileptization of neurons, that is, a special state of neurons that determines the "convulsive readiness" of the brain in the foci of its organic lesion and the degree of epileptic influence of this foci on the structures of the brain depends on the premorbid properties of the organism, and in particular epileptic predisposition to genetics or an acquired character that determines the greater likelihood of an epileptic seizure in the patient with brain damage.

The importance of the genetic factor can be seen most clearly in typical absences (short-term loss of consciousness, followed by amnesia), which are inherited in an autosomal dominant manner with incomplete gene penetrance, in primary generalized epilepsy that begins in childhood. The role of the genetic factor in partial seizures is less pronounced. As mentioned earlier, in this case, seizures are more common in close relatives of patients than in the general population.

Exogenous factors influencing the development of the disease include perinatal and postnatal neuroinfections, neurotoxicosis, and traumatic brain injury, which are of paramount importance. This does not exclude the role of other factors - intrauterine, vascular, toxic. In perinatal pathology (from the 27th week of the fetus to the 7th day of life of a newborn), the main factors here are traumatic (discrepancy between the sizes of the head and pelvis of the fetus, use of obstetric benefits, etc.) and anoxic (suffocation of the Fetus) in prolonged labor, the umbilical cord that wraps around the fetal neck, etc.).


Pathogenesis. In the pathogenesis of epilepsy, both changes in the functional state of part of neurons in the area of ​​epileptogenic lesions (epileptogenic focus), the entirety of which represents an epileptic focus, and features of the interaction of the population of epileptic neurons are important. The electrical activity of epileptic neurons is characterized by the appearance of a paroxysmal depolarization shift (PDS) of the membrane potential, followed by a phase of hyperpolarization. At the same time, the neurons surrounding the epileptic focus are in a state of constant hyperpolarization, which prevents the epileptic activity from spreading out of the focus.

The main pathophysiological mechanism of epilepsy is the hypersynchronization of neural activity, i. H. The simultaneous coverage of a large number of epileptic and neighboring neurons with excitation. The hypersynchronization, which not only determines the formation of an epileptic focus, but also its effect on the brain, can be based on various mechanisms - an increase in synaptic conduction, an epileptic (extra-synaptic) effect of the electrical field of an epileptic neuron on neighboring cells , in-phase discharges, etc.

There are three concepts to explain the epileptization of neurons: 1) violation of the neuron membrane or its metabolism; 2) a change in the environment of the neuron; 3) pathological changes in the population of neurons associated with a lack of inhibitory processes. All disorders are detected at both the metabolic and neurotransmitter levels as well as the structural level.

In the epileptic focus, the loss of dendritic spines by the neurons, the reduction of dendritic ends, their varicose veins, glial proliferation and the selective loss of GABAergic terminals are determined. These changes are seen as morphological manifestations of partial nerves; Afferentiation, which may explain the increase in spontaneous neural activity and hypersensitivity of postsynaptic receptors.

The variability of the membrane potential of epileptic neurons and their rhythmic fluctuations can be caused by a violation of the maintenance of an appropriate concentration gradient of K, Na, Ca and Mg ions on both sides of the nerve cell membrane, as well as a change in the distribution of ions within the cell (especially by the Accumulation of K ions in mitochondria). Disorders of the energy mechanisms were also noted: a decrease in the activity of cytochrome oxidase, which leads to a decrease in the formation of ATP, a violation of the function of the Krebs cycle.

The role of biogenic amines in the occurrence of epilepsy has now been established. A decrease in the levels of DOPA, dopamine and norepinephrine in epileptogenic herds, as well as a weakening of the reactivity of the DOPA-dopamine-norepinephrine system, which can affect the epileptic activity of the brain and cause failure of the anti-epileptic defense system, has been noted. A disruption of the serotonin metabolism, in particular a decrease in the content of 5-hydroxyindole acetic acid, can have a certain influence on epileptogenesis. In addition, a decrease in the content of amino acids involved in the Krebs cycle, glutam and gamma-aminobutyric acid (GABA), was found in the focus of epileptic activity. The latter is known to have a pronounced antispasmodic effect. Apparently, as part of hypovitaminosis B6 (pyridoxine), seizures are precisely linked to a deficiency in GABA, since it is formed from glutamic acid with the participation of decarboxylase with the participation of pyridoxine phosphate. Pyridoxine deficiency epilepsy is an example of biochemical disorders that can be caused by genetic factors or exogenous lesions that increase the brain's epileptic readiness. There is also evidence of a possible role for the excitatory neurotransmitter glutamate in triggering epileptic seizures. The inhibiting mediators taurine and glycine, the content of which is reduced in the epileptic focus, can also have a certain effect.

Extrafocal factors can also spread the influence of epileptic focus on the brain. In epilepsy, they form a special functional state of the brain called increased epileptic readiness, “convulsive reactivity” of the brain, and so on. It is the brain's increased epileptic readiness that helps create an epileptic focus and spread its influence to other parts of the brain.

According to P. M. Sarajishvili, an epileptic focus cannot cause an epileptic seizure without encompassing the functional system in which apparently specific and unspecific nuclei of the optical hill are invariably involved. For the mechanism of generalization of paroxysmal activity from the primary cortical epileptic focus, “generalizing formations of the subcortex”, which include the structures of the limbic brain, medial thalamus, subthalamus, and reticular formation of the midbrain, are of primary importance.

The structures and mechanisms that ensure the spread of the epileptic discharge from the place of origin make up the epileptic system.

At the same time, the brain has structures that inhibit epileptogenesis and counteract the spread of the influence of the epileptic focus on the brain. Such formations include the caudate nucleus, the caudal nucleus of the pons, the lateral nucleus of the hypothalamus, the orbitofrontal cortex, the cerebellum, and the region of the single bundle. Their influence takes place both in the form of a direct inhibitory effect and in the form of a return inhibition that develops under the influence of an epileptic focus. This system is also described as a negative feedback system that works through a population of intercalar neurons. An interneuron triggered by impulses from the epileptic focus can interrupt the flow of these impulses by hyperpolarizing the epileptic neuron.

The recurrent inhibition of neurons along the periphery of the epileptic focus is also of some importance in blocking the epileptic focus. Structures and mechanisms that prevent epileptogenesis are called the anti-epileptic system.

The facts disclosed in recent years confirm the assumption that the desynchronization devices of the brain have an anti-epileptic effect and the synchronization devices can contribute to the activation of epileptic foci. At least electropolygraphic studies of nocturnal sleep in humans have shown that the activation of the epileptic focus takes place in the second stage of slow sleep, that is, in the stage of the carotid spindles, in which the recruitment of the thalamocortex is facilitated and, accordingly, the spread of epileptic activity is facilitated .. Conversely, REM sleep suppresses the generalization of epileptic activity that largely applies to delta sleep.

Schematically, the sequence of "events" in the development of a generalized tonic-clonic seizure can be represented as follows. Under certain conditions, the amplitude and frequency of epileptic neuron discharges begin to increase. After the intensity of the charges exceeds a certain threshold, the epileptic activity overcomes the inhibitory effects of the surrounding neurons and spreads to the nearby areas of the cortex and subcortical structures (basal ganglia, thalamic nucleus, nucleus of reticular stem formation). The activity of the latter spreads both in the rostral direction, which additionally stimulates neurons in the epileptic focus and other areas of the cortex as well as in the caudal (along the corticospinal and reticulospinal tract) to the spinal neurons. The spread of excitation to the subcortical, thalamic and stem nuclei corresponds to the tonic phase of the attack, accompanied by unconsciousness, pronounced vegetative manifestations (hypersalivation, mydriasis, tachycardia, arterial hypertension, sometimes short-term respiratory failure), characteristic discharges (peaks) with high amplitude over the EEG over the surface of the entire cortex. The subsequent activation of the diencephalic-cortical inhibition system, however, periodically interrupts the spread of the epileptic discharge, which corresponds to the transition from the tonic phase to the clonic; In the EEG, rhythmic discharges are converted into “peak wave” complexes. Clonic twitching and causing their discharges become less and less pronounced and infrequent, eventually disappearing, reflecting the "exhaustion" of the neurons of the epileptic focus, also manifested in some cases by the paralysis after Todd's attack. At the same time, diffuse slow waves are recorded in the EEG.

When the epileptic focus cannot be stably blocked, which is usually manifested in the manifestation of epileptic seizures, a number of new pathophysiological mechanisms for the formation and development of epilepsy as a disease arise. The most important of them is the appearance of secondary epileptic foci. In their emergence, the mechanism of secondary recurring generalization is of great importance, that is, the excitation of the generalization apparatus of the subcortex under the influence of the cortical epileptic focus, followed by a secondary “reflection” of the excitation into the cortex. This "reflection" occurs most often at the symmetrical point of the cortex of the "healthy" hemisphere. Transcallosal effects also play a role. The secondary epileptic focus goes through the stage of dependent focus during its formation and later becomes independent of the influence of the primary focus and plays the role of an independent epileptogenic factor.

Another important mechanism of "epileptization" of the brain is a violation of the information function of neurons, which undergo considerable restructuring. As a result, they recode afferent stimuli in specific epileptic ways.

The mechanism of occurrence of primary generalized epilepsy is not clear enough, in which it is not possible to establish an epileptogenic lesion, seizures do not have a focal onset, and epileptic activity is characterized by generalized synchronous and symmetrical discharges. The importance for the development of this form of epilepsy can be seen in the inadequacy of the activating influences of the brain stem, an increase in the excitability of the cortex and an increase in the tendency to produce sustained vibrations. The question of the pacemaker of epileptic activity and the role of organic brain damage in primary generalized epilepsy remains open.The presence of dysontogenesis in this form of epilepsy (impaired development of the body in the prenatal period or in early childhood) in the form of ectopy of nerve cells has been demonstrated; This suggests that structural changes in the brain underlie primary generalized epilepsy and that its mechanism is apparently reduced to a denervation hypersensitivity of ectopic neurons, which acquires epileptic properties.

Clinic.The main clinical symptom of the disease is epileptic seizures. The International Classification of Epilepsy distinguishes between generalized and partial (focal) epileptic seizures. Generalized seizures are accompanied by loss of consciousness and vegetative manifestations, the severity of which depends on whether or not they are accompanied by convulsions. Differentiate between convulsive and non-convulsive forms. Generalized epileptic seizures in the EEG are characterized by bilateral symmetrical and synchronous epileptic discharges.

The convulsive forms of generalized epileptic seizures include major epileptic seizure and its variants. A major epileptic seizure ("major illness", grand mal) is characterized not only by unconsciousness and autonomic disorders (mydriasis, hyperhidrosis, tachycardia, etc.), but also by convulsions in which both sides of the body are involved at the same time. Tonic seizures occur first, and then clonic seizures. In rarer cases, seizures may only be tonic or only clonic (called non-triggered seizures). As a rule, due to the involvement of the respiratory muscles in the process, apnea occurs, patients bite their tongue, involuntary urination is observed (if there was urine in the bladder at the time of the attack), and when falling, patients often suffer traumatic injuries. The seizure ends in an epileptic coma that turns into sleep, after which amnesia is diagnosed. Patients experience a feeling of weakness, muscle pain, and weakness. In other cases, psychomotor agitation, a twilight state of consciousness, and other mental disorders may develop after a seizure.

A major epileptic seizure in the EEG is characterized by the appearance of rhythmic discharges with a frequency of 8 to 14 per second of low amplitude, followed by an increase in the latter (recruitment) to 100 to 200 μV (tonic seizure phase) and a transition to peak waves and Polypeak wave discharges (clonic phase)).

The second type of generalized epileptic seizure is absenteeism. It is characterized by turning off consciousness without convulsions and without falling of the patient and vegetative manifestations (pallor or redness of the face, mydriasis, salivation, etc.). The EEG shows discharge paroxysms with the structure of peak wave complexes with a discharge frequency of 3 per second. The type of seizure described is called "simple absence", its electroencephalographic picture is called "typical absence". This type of epileptic seizure is more common in people with a pronounced hereditary load, can easily be caused by light flickering and hyperventilation, and has a relatively good prognosis. In so-called complex absences, the disconnection of consciousness and autonomic disorders are associated with various motor phenomena, e.g. B. myoclonic twitching (myoclonic absence), involuntary contractions of the facial muscles, rolling of the eyeballs, turning off the posture tone causing the patient to fall (atonic absence). A complicated absence in the EEG manifests itself in rhythmic peak wave complexes with a frequency of 3 discharges per second (usually this is a myoclonic absence), but more often these discharges have a frequency of 1.5-2.5 per second (the so-called atypical absence). This form of absence is usually observed in children aged 2 to 8 years with pronounced organic symptoms and delayed mental and physical development and has a poor prognosis (Lennox-Gastaut syndrome).

Absences are often referred to as minor seizures ("minor illness", petit mal). However, these terms are not the same, as small seizures sometimes also refer to some forms of partial epileptic seizures that occur when the patient is unconscious without convulsions and falling, such as pseudo-temporal falls.

It is believed that the epileptic focus of generalized seizures is in the oral parts of the brain stem. However, such seizures can be caused by pathological foci in the mediobasal parts of the cerebral hemispheres with immediate generalization.

ANTI-EPILEPTIC LEAGUE CLASSIFICATION OF EPILEPTIC SEASTS (1981)

I. Partial (focal) seizures.

Partly easy

1. Drive by March (Jacksonian); without march - controversial, attitude, language (vocalization or language stasis).

2. Sensory (somatosensory, visual, auditory, olfactory, taste, epileptic vertigo).

3. Vegetative.

4. With psychopathological manifestations (dysphasic, dysmnestic, cognitive, affective, illusions and hallucinations).

Partial complex

1. Start as simply as possible with a subsequent disturbance of consciousness (with and without automatism).

2. Starting with a violation of consciousness (with and without automatism).

Partial seizures with secondary generalization

P. Generalized seizures

1. Easy

2. Complex (clonic, tonic, atonic, with vegetative manifestations, with automatisms)

Seizures

Tonic-clonic

tonic

Clonic

Myoclonic (localized myoclonus)

Atonic (akinetic).

Unclassified seizures.

The second group of epileptic seizures is partial (focal). With partial seizures, the epileptic focus is always in the cerebral cortex, only part of the brain is involved in the process, while, as noted, the involvement of subcortical structures is mandatory, partial seizures into simple (without disturbances of consciousness) and complex (with disturbances of consciousness) are divided. In addition, a distinction is made between partial seizures with secondary generalization. Among the sometimes simple seizures, a distinction is made between motor, sensitive, autonomous, psychopathological manifestations.

Most ostentatious of the partial motor seizures is Jackson's or somatomotor seizure, which occurs when the epileptic focus is in the projection motor cortex. It is characterized by clonic seizures that involve the muscles of the face, hand, foot, etc. Spasms can be localized or widespread depending on the features of the cortical somatotopic localization of motor functions (Jackson's March). Consciousness remains. In some cases, convulsions spread to the entire half of the body, and sometimes they are generalized, which is accompanied by loss of consciousness.

An oculomotor epileptic seizure is manifested by a tonic abduction of the eyeballs, an adverse - by turning the eyes and head in the opposite direction, and a fit of epileptic rotation - by turning the trunk to the side. These seizures are caused by epileptic foci in the premotor cortex.

A special type of partial motor seizure is observed in Kozhevnikov's epilepsy - constant myoclonus in a limited group of muscles, which periodically turns into generalized seizures.

Partial sensory seizures are primarily Jackson sensory or somatosensory seizures. These are attacks of paresthesia with limited localization, a Jackson march is possible, consciousness is preserved. They occur when foci appear in the sensory projection cortex. A somatosensory seizure often turns into a somatomotor seizure (called a sensorimotor seizure). Sensory seizures also include visual, auditory, olfactory and taste attacks, which manifest themselves in the form of stimulus phenomena of the corresponding projection cortex (photopsia, wrong taste, smell, etc.).

In epileptic seizures, psychopathological manifestations are seldom without impairment of consciousness and are therefore more often observed in the context of partially complex seizures. A change in consciousness during partially complex seizures manifests itself in a lack of reaction to external stimuli or a violation of the awareness of what is happening.

In the case of perceptual disorders caused by foci in the projection-associative cortex, illusory or hallucinatory experiences arise - lively visual scenes, complex melodies. These seizures are psychosensory. The latter also include seizures with cognitive and dysmnestic manifestations accompanied by impaired sensory synthesis such as derealization or depersonalization, which usually occurs with impaired consciousness. These are the syndromes deja vu - "already seen", deja entendu - "already heard", deja vecu - "already experienced", jamais vu - "never seen", jamais entendu - "never heard", jamais vecu - "never" the past ". In all of these cases, what the patient can see, hear, and experience appears to be visible, audible, and experienced beforehand. Or on the contrary, situations and phenomena that the patient repeatedly encounters and which he has experienced appear completely new to him, never seen before, not experienced. With these paroxysms there is one degree or another of impaired consciousness. In severe cases, in Jackson's terminology, there are "dream states" which the patient experiences as if in a dream. Such paroxysms can include pharyngo-oral symptoms (swallowing, sucking, smacking, etc.) combined with olfactory and gustatory hallucinations, violent memories.

Less common seizures, defined as bouts of memory impairment and ideational seizures, usually manifest themselves in the form of thought interruptions, often compulsive memory of something, etc., and are caused by epileptic discharges in the temporal or frontal lobes of the brain.

Partial seizures include vegetative-visceral paroxysms. They are diverse and are caused by epileptic discharges in the orbital-insulotemporal area and possibly in the rostral part of the trunk. Tachycardia, increased blood pressure, shortness of breath, mydriasis, sweating are observed clinically. The most studied are epileptic digestive seizures caused by discharges in the pararinal area - pharyngo-oral, epigastric, abdominal. Pharyngo-oral epileptic seizures are manifested in hypersalivation, often in combination with the movement of the lips, tongue, licking, swallowing, chewing, etc. An epileptic seizure in the abdomen is characterized by various sensations in the epigastric area (epigastric seizure), often rumbling in the Abdominal cavity, vomiting, etc., is often accompanied by a change in consciousness.

Vegetative-visceral seizures are characterized by the same signs as other epileptic seizures: short duration, stereotypical manifestations in the same patient, they are often accompanied by changes in consciousness.

The literature describes the so-called diencephalic or hypothalamic epilepsy, which is characterized by vegetative crises or vegetative-visceral paroxysms that last from tens of minutes to hours or longer. In this case, the short duration of loss of consciousness and seizures, which develop only at the height of the seizure, is characterized. Seizures are clinically different from epileptic seizures. Electrographically, it is not possible for them to register the phenomena characteristic of an epileptic seizure. Hypothalamic paroxysms do not respond to anti-epileptic drugs. Therefore, in the Terminological Dictionary of Epilepsy and in the work of a number of local researchers, the validity of the isolation of diencephalic epilepsy is questioned.

In epilepsy, psychomotor seizures occur no less often than psychosensory paroxysms or, according to the terminological dictionary, epileptic seizures of automatism, which are characterized by paroxysmal disorders of consciousness and motor activities in the form of automatisms and therefore also refer to complex partial seizures. The behavior of patients is characterized by externally ordered actions, which, however, are not appropriate to the given situation. During psychomotor seizures, there is a clouding of consciousness, followed by amnesia.

All types of psychomotor seizures are most commonly caused by epileptic discharges in the anterior temporal lobe. The International Classification provides for the allocation of affective seizures - various paroxysmal mood disorders, usually an unmotivated feeling of fear, more rarely - fits of laughter (helolepsy), states of happiness, etc. Normally, such paroxysms are accompanied by a change in consciousness. They are caused by discharges in the anteromedial temporal lobe.

Partial (focal) seizures with simple and complex symptoms can lead to generalized seizures. In these cases they speak of secondary generalized seizures. Secondary generalized seizures should also include generalized seizures preceded by an aura (“symptom signal”). Aura (Latin aura - "breath") is a term that denotes pathological sensations of a different kind that occur in patients at the beginning of a seizure (in addition to secondary generalized seizures, it can also be observed with partially complex seizures).

Usually the same patient has a stereotypical aura when a severe seizure recurs. Its nature is determined by the location of the epileptic focus. During the aura, for example, the patient can feel every smell (olfactory aura), every taste (taste aura), see different images or whole images (visual aura), etc.

There are the following types of aura: sensory, sensitive, motor, speech, autonomous and mental. Visual and auditory auras are examples of sensory auras. The sensitive aura manifests itself in the form of various senestopathies (dry mouth, numbness, distorted perception of one's own body, etc.). The motor aura is a stereotypical movement performed by the patient before a seizure occurs. The language aura manifests itself in the interruption of language (inability to speak) or, conversely, in the violent involuntary pronunciation of certain words. In addition to the motor language aura, there may also be a sensory language aura - patients either do not understand the language addressed to them or hear words that no one really speaks. The vegetative aura is perhaps the most diverse. These and various unpleasant sensations in the area of ​​the heart (heart aura), abdominal organs (abdominal aura), sensations of respiratory arrest or lack of air, feeling of hunger, etc.

Particularly peculiar is the psychic aura, in which the patient experiences an unusual emotional state, sometimes an incredible bliss. An example of such an aura can be found in the excellent description of F. M. Dostoevsky has a fit in Prince Myshkin. The writer himself suffered from epilepsy and apparently experienced similar sensations.

The aura lasts for a moment and is the only, often very vivid, memory that the patient subsequently retains about the attack. Very often the aura can be the only clinical manifestation of an epileptic seizure. Usually, however, after the aura, there is a loss of consciousness and seizures occur. The aura always indicates the focal onset of the seizure.

As mentioned earlier, epilepsy is characterized by paroxysmal manifestations and non-paroxysmal chronic changes in the patient's personality. Epilepsy is characterized by slowness and rigidity of mental processes, as well as pathological thoroughness of thinking. Patients in a conversation are detailed, but they cannot highlight the main thing, express the main idea, give a brief answer, get stuck on secondary details.

Excessive punctuality, pedantry, insignificant sensitivity, impatience, nonsense, importance and at the same time fear, submissiveness, flattery, shyness, sweetness, exaggerated respect, gentleness in dealing, the desire to please the interlocutor (so-called defense). The circle of interest gradually narrows, memory deteriorates, egocentrism grows, features of epileptic dementia are revealed.

These changes are due to many factors: organic brain damage, impairment of normal functional activity of the brain under the influence of epileptic discharges, chronic stress due to recurrent seizures and family and social difficulties caused by the disease, hereditary predisposition and the adverse effects of long-term antiepileptic Therapy.

In addition to chronic changes in the personality and mental manifestation of the patient during an attack (mnestic, ideal, affective symptoms), epilepsy often causes periodic mental disorders in the form of dysphoria or psychoses of varying duration.

In addition to the international classification of epileptic seizures, there is an international classification of epilepsy, according to which forms of epilepsy are differentiated according to two main criteria: etiology and type of seizure. With an established etiological factor and the localization of an epileptogenic lesion, epilepsy is classified as symptomatic. When the etiology cannot be established and organic damage to the brain is evident, epilepsy is called cryptogenic. In the absence of data on organic brain damage and unknown etiology, epilepsy is classified as idiopathic. The type of seizure distinguishes between focal and generalized epilepsy. The forms of focal epilepsy are: benign Rolandic and occipital epilepsy, reading epilepsy (idiopathic forms); Kozhevnikovskaya epilepsy and epilepsy with specific forms of provocation (symptomatic forms). Generalized forms include: benign neonatal seizures, benign childhood myoclonus epilepsy, pycnolepsy, juvenile myoclonus epilepsy, epilepsy with generalized tonic-clonic seizures of awakening; West and Lennox-Gastaut syndrome, epilepsy with myoclonic-astatic seizures, epilepsy with myoclonic seizures (cryptogenic and symptomatic forms); early myoclonic encephalopathy and other symptomatic forms.

In addition, a distinction is made between undifferentiated epilepsy with generalized and partial seizures (newborns, myoclonus epilepsy in infancy, acquired epilepsy aphasia, etc.) and special forms, in particular situational seizures (feverish, dysmetabolic).

Diagnosis.Anamnesis must be obtained from both the patient's words and his / her immediate family. Evidence of perinatal pathology and early cerebral processes raise the suspicion of residual brain damage that can lead to epilepsy. There is often evidence of epileptic seizures in relatives in the medical history.

Particular attention should be paid to paroxysmal episodes in childhood - seizures during the neonatal period, the so-called spasmophilia, in which epileptic seizures are often confused, convulsions during febrile states (febrile convulsions). This also includes the so-called stomach crises. - Paroxysms of short-term abdominal pain that occur regardless of food intake and are accompanied by autonomic disorders (pallor, nausea, change in pulse, etc.)

Less studied is the role of some paroxysmal conditions that occur during sleep - night terrors, myoclonus, tonic convulsions, etc., which are often seen in children.

Epilepsy is characterized by the stereotype and regularity of seizures, relative independence from the latter from external influences, which are often limited to a certain time of the day (nocturnal seizures - "sleep epilepsy"; morning seizures - "awakening epilepsy", daytime - "wakefulness epilepsy", etc.) .) the presence of the corresponding changes in character and intelligence in patients.

When formulating a diagnosis, the form of epilepsy, the type of seizures, their frequency, peculiarities of their distribution in the "wakefulness - sleep" cycle, the presence or absence of mental changes, e.g. B. Epilepsy with frequent polymorphic seizures (complex psychosensory, secondary generalized) states of sleep and wakefulness, dysphoric states, and pronounced personality changes.

Early manifestations of epilepsy have certain features: incomplete, rudimentary, abortive, partial forms of paroxysms, a high frequency of sleepwalking and sleeping, muscle tremors. At this point, seizures can still be episodic in nature and caused by various external influences, e.g. B. Anxiety, which is observed especially often in children, overwork, etc. However, the type and rhythm of the seizures, which are characteristic of each patient, are gradually formed. As the disease worsens, new symptoms gradually appear: increased frequency of seizures, often a tendency to serial manifestation or development of status epilepticus. At this point, mental changes can increase. Therefore, epilepsy shows certain progressive patterns, the investigation and analysis of which are important for the diagnosis and prognosis of the disease.

Epilepsy is characterized by certain changes in the EEG. Similar changes can be found in epileptic syndromes, but in these cases they are combined with EEG changes caused by the main process.

Most typical of epilepsy are the so-called epileptic signs - peaks, sharp waves, and peak-wave complexes. With epilepsy, paroxysmal rhythms are also recorded in the EEG - rhythmic discharges of increased voltage with a frequency of 8-12. 14-16, 20-30 per second. Electrographic epileptic signs are, however, by far not always recognized under normal recording conditions - in about 1/3 of the cases. Therefore, various methods of provocation are used: rhythmic light stimulation (flashes of light with a rhythm of 4 to 50 per second), hyperventilation (3 minutes of deep breathing), in some cases - the introduction of pharmacological agents with a convulsive effect (Corazol, Bemegrid, etc.). At the same time, the percentage of epileptic phenomena found in the EEG increases. The most powerful activator of epileptic activity is sleep, namely the carotid spindle stage, which is associated with the recruitment mechanism of the thalamic cortex. However, electrographic recording during natural or pharmacological sleep can only be used in specialized institutions. A widely used and highly effective method of inducing epileptic activity is 24-hour sleep deprivation followed by conventional EEG recording. Repeated EEG registration at short intervals also increases the likelihood of detecting pathological changes in epilepsy. The type of electrographic phenomena detected in epilepsy largely depends on the form of epilepsy, the type of seizure and the location of the epileptic focus. The most characteristic changes occur in generalized forms of epilepsy, mainly in generalized seizures.

Partial seizures, usually of cortical origin, are characterized by the appearance of multiple peaks and sharp waves in the EEG. However, other partial seizures - olfactory, auditory, visual, dizzying, psychomotor, and psychosensory seizures - may have other electrographic characteristics that are not clearly defined.

This is how bilateral, often asymmetrical, more or less pronounced sharp and slow waves are described. Very often, paroxysmal rhythms are observed with a discharge frequency of 4 to 7 per second or at some other frequency recorded or generalized in the temporal or frontal leads.

In secondary generalized seizures, the EEG changes described usually become an electrographic image of a major seizure. In addition to these changes characteristic of epilepsy, other EEG changes are usually found that are focal, unilateral or generalized in nature (hypersynchronous α rhythm, deformation of normal rhythms, appearance of slow oscillations - δ and ε waves), etc.

When epilepsy is unfavorably current, so-called hypsarrhythmia (from the Greek hypsos - "high") is often observed, the presence of slow waves and rhythmic discharges in the l and e wavelength range of increased amplitude in combination with epileptic phenomena without normal rhythms. Hypsarrhythmia is characteristic of childhood cramp.

Research methods such as CT and MRI are of great importance for the diagnosis of epilepsy.

In recent years, video and teleelectroencephalographic monitoring of patients have been used, which greatly improves the accuracy of diagnosis.

The changes that occur in the body during ontogenesis shape not only the features of its function in different periods of age, but also the clinical manifestations of various pathological conditions.

The paroxysmal readiness of the child's brain is much higher than that of the adult. The reasons for this are varied: high hydrophilicity of the brain tissue, other cortical-subcortical relationships, immaturity of the inhibition systems, lability of homeostasis, etc.

Late epilepsy (late-onset epilepsy) is characterized by the prevalence of major seizures and psychomotor paroxysms. Seizures usually occur with pronounced vegetative manifestations (fluctuations in blood pressure, breathing disorders). The coma after the attack is longer. The aura is more often linguistic, affective, migraine-like. Seizures are usually monomorphic, and there is a tendency towards a serial course. Epileptic activity in the EEG is detected less often and is more local. The course of the disease (with idiopathic epilepsy) is usually benign; epileptic dementia is rare. However, it should be emphasized that idiopathic epilepsy rarely manifests itself in adulthood and in old age. Therefore, a particularly thorough examination of such patients is necessary in order to exclude focal pathology (mainly a brain tumor or other volumetric process).

Differential diagnosis of epilepsy. If the patient has epileptic seizures, the first thing to do is to exclude the current cerebral process. In this case, in addition to the symptoms characteristic of certain diseases of the brain (tumors, encephalitis, etc.), it is worth taking into account the peculiarities of the manifestation and course of the epileptic seizures themselves.

Jackson's seizures are therefore rare in epilepsy and, conversely, often the first manifestation of tumors in the Roland region of the hemispheres of the brain. The dynamics of seizures in tumors is characterized by a number of features. More often, the first seizures are generalized and the subsequent ones are partial, often starting with a series of seizures. It is characteristic that the seizures become rarer and more limited, and then completely disappear when the hypertensive syndrome appears and increases.

Epileptic seizures in acute disorders of the cerebral circulation, as a rule, are convulsive in nature, the features of their manifestations correspond to the zone of cerebral circulatory disorders. Generalized seizures are observed in the circulation in the vertebrobasilar pelvis, and Jacksonian and secondary generalized seizures are observed in the carotid pelvis. Subsequently, seizures recur due to repeated acute disorders of the brain circulation as well as a decompensation of the blood circulation in the area of ​​old herds.

In some patients, seizures can occur under the influence of certain external stimuli (so-called reflex epilepsy): mostly visual (flashes of light, some images, various color sensations, especially red), less often acoustically (unexpected noise or certain noises, voices, music) somatosensory (unexpected touch or sustained stimulation of a specific part of the body); Also, they sometimes appear while reading and eating. Seizures can be partial (in the area of ​​the brain stimulated by the stimulus), but are more often primarily generalized. They usually start in childhood and adolescence and become less pronounced as you get older. Seizures are more common when watching TV, in a disco with flickering lights, and also when moving on an escalator. Covering one eye can sometimes help prevent a light stimulation-induced seizure. It is necessary to use anticonvulsants only when it is impossible to avoid the action of provoking factors, but these funds are often ineffective. In rare cases, focal brain damage is found in reflex epilepsy. In most patients, however, the reasons for such a selective increase in convulsiveness are unknown.

Sometimes women have more seizures just before and during menstruation (called menstrual epilepsy), which may be associated with water retention in the body and / or with cyclical changes in hormone levels. Treatment in this case is carried out only the evening before and during the "dangerous" period and includes the use of diacarb, oral contraceptives (consultation of a gynecologist required), as well as anticonvulsants (it is obviously preferable to use benzodiazepines - clonazepam or nitrazepam, but other drugs can also be used used). ...

Seizures are common in people with alcoholism who suddenly stop drinking. 90% of these seizures occur in the first 7-48 hours after withdrawal. More commonly, a series of 2-6 seizures occurs (over 4-12 hours), after which the seizures usually stop. As a rule, generalized tonic-clonic seizures are observed.

Focal seizures are more likely to indicate simultaneous damage to the focal brain (e.g. head injury). Alcohol can also trigger seizures if you already have epilepsy.

Seizures can occur with sudden withdrawal from phenobarbital, as well as a range of hypnotics, usually against a background of other manifestations of withdrawal symptoms.

It should be noted that seizures that occur in the first year of life are more often caused by congenital malformations, birth trauma, infections, anoxia, metabolic disorders (hypocalcemia, hypoglycemia, vitamin B6 deficiency, phenylketonuria) or childhood convulsions. Childhood seizures are usually caused by perinatal anoxia or birth trauma, infection, thrombosis of the cerebral arteries and veins, or are manifestations of idiopathic epilepsy. Seizures that begin in adolescence are usually associated with idiopathic epilepsy (especially genetic epilepsy) or trauma. From a young age (18-25 years), they can also be caused by idiopathic epilepsy, trauma, tumors, and alcohol withdrawal syndrome. Middle-aged (35-60 years old) seizures are more commonly caused by trauma, tumors, vascular disease, and chronic alcoholism. In old age, vascular diseases and tumors are the most common causes of seizures, less often degenerative diseases and injuries.

Treatment.During a generalized tonic-clonic seizure, support is reduced in order to protect the patient as much as possible from possible harm (trauma). It is placed on a bed or on the floor, sideways if possible, all surrounding objects that can cause damage are removed. One should not try to prevent a tongue bite by placing an object between the patient's jaws, as broken teeth are undoubtedly a more uncomfortable consequence of an attack than a bitten tongue.

In symptomatic epilepsy, the underlying disease must be treated first. However, sometimes even after successful treatment (e.g. removal of a tumor or abscess) the need for antispasmodic therapy remains.

The organization of a rational work and rest regime, as well as psychotherapy, is of great importance. The patient should lead an active lifestyle whenever possible. Moderate exercise is helpful. Activity is a seizure antagonist. At the same time, excessive emotional and physical stress, prolonged exposure to the sun and alcohol consumption should be avoided. However, experience shows that in patients with a favorable course of the disease, episodic consumption of small doses of alcohol, as a rule, does not lead to the occurrence of seizures. It is necessary to establish good sleep on a regular basis. It is necessary to overcome the feeling of inferiority that often occurs in patients, which is often associated with overprotection in the family, especially in children. On the other hand, it should be taken into account that patients often suffer from social isolation. Since the majority of patients with epilepsy are either mentally safe or have only minor distinctive features, children can and should go to school, adults - continue their professional activities, if not with driving a car, working with mechanisms of movement, at height, with fire etc. related. It is necessary to identify provoking factors in each patient in order to rule out their effect if possible (some patients are unusually sensitive to stress, hyperventilation, sleep disorders, alcohol or drugs).

The mainstay of treatment is the use of anticonvulsants. The right choice of drug and the choice of its dose, the continuity and duration of treatment, as well as good contact between patient and doctor all contribute to a successful therapy.

The choice of drug depends on the type of seizure.For generalized and simple partial seizures, 4 main drugs are used: phenobarbital, diphenine, carbamazepine, sodium valproate (Table 7), their effectiveness in theory being approximately the same, and the selection of a specific drug is made (by trial and error) taking into account the individual sensitivity of the patient , Side effects, as well as the availability of the drug.

In practice, phenobarbital is more commonly used in adults at a dose of 2 to 4 mg / (kg * day) and in children at 3 to 8 mg / (kg * day). In sleep epilepsy, however, it is advisable to avoid this, as it suppresses the phase of depressive effect on epileptic activity, shortens in patients with sleep epilepsy. In children, the drug can cause paradoxical hyperactivity and irritability and disrupt the learning process. Drowsiness (the main side effect of the drug) usually decreases a few days or weeks after you start taking the drug. If it doesn't, it sometimes needs to be canceled. However, phenobarbital is generally well tolerated and can be effective for all types of epilepsy.

With prolonged use, diphenin can cause hypertrichosis, coarsening of facial features, gingival hyperplasia and impaired concentration. These side effects limit its use in children and young women. Chronic diphenine poisoning is sometimes associated with neuropathy and cerebellar degeneration. The drug has an adverse effect on the metabolism of folic acid and vitamin K.

When using carbamazepine (finlepsin), emotional lability, drowsiness and difficulty falling asleep, concentration disorders, loss of appetite, vomiting, headache, allergic reactions, leukopenia and thrombocytopenia can occur. However, as the effect of the auto induction increases, these phenomena usually disappear. The most beneficial side effects of the drug are associated with bone marrow suppression and liver damage. Therefore, patients need to have a clinical blood test and liver function tests regularly (at the beginning of treatment - once a month). If there are signs of bone marrow suppression or liver dysfunction, the drug should be discontinued. In most cases these phenomena are reversible, although fatal irreversible aplastic anemia can occasionally occur. However, it should be emphasized that these complications are rare. Due to the fact that carbamacepia inhibits cognitive function to a lesser extent than other anticonvulsants, some epileptologists consider it the drug of choice for generalized seizures (especially sleep epilepsy). If its effectiveness is insufficient, then phenobarbital or hexamidine should be prescribed at the same time.

For the treatment of partial attacks of movement, in addition to the drugs listed above, benzonal (benzobarbital) can be prescribed at a dose of 5-10 mg / kg. For the treatment of partial complex seizures, the following drugs are used in order of importance: carbamazepine at 15 to 20 mg / (kg * day), diphenine at 5 to 10 mg / (kg * day). Hexamidine at 10-15 mg / (kg * day). It should be noted that anticonvulsants are less effective for this type of seizure than for generalized tonic-clonic seizures.

To treat absences, ethosuximide is mainly used at a dose of 10-25 mg / (kg day). The drug can provoke the occurrence of large seizures that require the use of phenobarbital. If it is ineffective, sodium valproate and diacarb are used. In atypical absences, sodium valproate is the drug of choice. If no effect is achieved, sodium valproate should be used with ethosuximide or lamictal.

To treat myoclonic seizures, sodium valproate is used in an amount of 10 to 50 mg / (kg day), benzodiazepine derivatives - clonazepam in an amount of 0.05 to 0.1 mg / (kg day) and sibazone (2 to 4 mg / day used in children). 5-10 mg / day in adults, followed by a slow increase in dose). If they are ineffective, diphenine and phenobarbital can be prescribed. The use of valproic acid supplements, which increase GABA levels in the brain, as well as Lamictal, significantly improved the outlook for the treatment of a number of severe forms of epilepsy, including childhood convulsions. To treat the latter, GABA preparations are used, for example, synacts, administered intramuscularly at a dose of 1 mg per year of life (usually 12-15 injections per course); If the disease relapses, a second treatment is carried out. Use corticosteroids, Lamictal, Nitrazepam (2-3 mg 1-3 times a day), a ketogenic diet, or Diacarb (Fonurit).

It should be noted that long-term use of clonazepam in patients at different times of treatment will develop a tolerance to the drug that requires a "medical leave".

Diacarb (Fonurit), a carbonic anhydrase inhibitor, is prescribed to improve anticonvulsant therapy even in epileptic seizures against the background of hydrocephalus with menstrual epilepsy and seizures caused by hyperventilation. It has potassium-removing properties that require appropriate correction; Paresthesia, anorexia, drowsiness and, rarely, agranulocytosis may occur with use. Dosages of the drug - from 250 mg 2 times a day to 0.5 g 3 times a day. Since tolerance to Diacarb develops quickly, intermittent treatment is optimal.

Treatment should always begin with medication, gradually increasing the dose from initial to medium and then, if the seizures persist and no toxic effects occur, then maximally. If the frequency of seizures has not changed, the drug should be canceled while another drug is prescribed. In cases where only a partial therapeutic effect has been achieved, especially when the seizures are of a mixed nature and when none of the anticonvulsants had the correct effect separately, the second drug is added to the first drug or a combination of drugs is prescribed. It should be noted that the combination of drugs increases the likelihood of side effects due to their interaction. However, a combination of drugs sometimes makes it possible, by reducing the dose of one of them, to reduce the phenomenon of intoxication while maintaining the therapeutic effect.

Treatment for epilepsy should be continuous and long-term. The question of the abolition of antiepileptic drugs can be raised in patients who have been in remission of the drug for at least 3 years. The refusal of drugs occurs gradually over 1-2 years by reducing the doses under careful clinical and electroencephalographic control. Treatment should not be discontinued during puberty. Since anti-epileptic treatment is carried out over a long period of time, special attention should be paid to the possible side effects of drugs. Signs of their intolerance manifest themselves in the form of drowsiness, weakness, nausea, ataxia, changes in the blood count and other symptoms. Therefore, it is first necessary to have the blood checked regularly. In addition, you should consider the characteristics of the side effects of individual drugs.

A low effectiveness of anticonvulsant therapy is to be expected with pronounced psychological changes in adult patients and in children - with intellectual disabilities, the presence of malformations, pronounced focal neurological symptoms, prolonged seizures, the presence of partial seizures (especially complex partial seizures) and significant changes in the EEG ... At the same time, factors such as the number of seizures before treatment and the family history have no influence on the success of the treatment.

It should be remembered that in some cases, psychological changes in patients (including overt dementia) may be associated with inadequate treatment: chronic drug intoxication (including folic acid deficiency, which often occurs with prolonged use) with inadequate control of seizures (especially) partially complex seizures ); A combination of both reasons is often observed. Correction of therapy in these cases can lead to a significant improvement in the patient's condition.

In the absence of improvement from conservative treatment, the question of surgical treatment should be raised in a timely manner, that is, before the onset of severe mental changes and secondary epileptic foci. At present, many methods of surgical treatment of epilepsy are successfully used to remove epileptic foci (hypocampectomy, anterior temporal lobectomy, etc.), disrupt the pathways of epileptic discharge (fornicotomy, commissurotomy, etc.) and activate inhibitory structures (stimulation of the tooth nucleus of the cerebellum) etc.). Methods for the bioelectrical treatment of epileptic seizures are being developed.

Epilepsy is a chronic brain disease characterized by recurrent unprovoked seizures with various clinical manifestations. During an epileptic seizure, various disorders of motor, sensory, mental, mental and autonomic functions can be detected. These disorders are caused by excessive neuronal discharges in the gray matter of the cerebral cortex.

Traditionally, all forms of epilepsy can be divided into two broad groups: hereditary epilepsy and acquired epilepsy. Developing a single seizure is not indicative of epilepsy. There are statistics that suggest that around 10% of the population has had a seizure at least once in their life. Two points are critical to the diagnosis of epilepsy: the development of repeated seizures and the development of spontaneous, unprovoked seizures. The exception is epileptic reflex attacks. Classic examples of reflex seizures are characteristic of photosensitive epilepsy, when a light stimulus can cause an epileptic seizure.

Epilepsy and epileptic syndrome

It is necessary to distinguish between epilepsy as a disease and as a syndrome. Epilepsy is an independent chronic neurological disorder. Epileptic syndrome is a manifestation of various diseases, accompanied by convulsive tonic-clonic seizures, loss of consciousness and other symptoms that can be triggered by external factors such as high fever.

Epilepsy usually begins in childhood. One of the main reasons for the development of the disease is a violation of the activity of genes responsible for the work of the sodium, potassium, hydrogen and chloride channels in the nerve cell. As a result of these deviations, the polarization of the nerve cell membrane is disturbed and the activity of the neuroglial cells changes. As a result, neuronal cells greatly increase their activity. For example, epilepsy is caused by genetic changes that lead to an increase in the activity of the nerve cell and the cells around it - neuroglia cells. However, there are other types of epilepsy associated with specific genes that are monogenic in inheritance. A specific gene and a specific problem associated with disrupting the activity of that gene lead to the disease. However, in most cases, epilepsy is polygenic, that is, a combination of changes in gene activity is required for its development, which leads to the phenomenon of hyperexcitability of the cerebral cortex and the development of epileptic seizures.

Disease development

In 60–70% of cases, epilepsy develops in childhood. The disease is divided into several groups according to age categories: Epilepsy in infancy occurs in the first year of life; Childhood epilepsy develops up to 6 years old; Adolescent epilepsy occurs between the ages of 12-14 years. The disease begins to develop depending on when the activity of a group of certain genes changes. In Russia, 0.5–1% of the total child population suffer from epilepsy. Different forms of epilepsy work differently. Some forms of children proceed with a gross violation of the child's development. The earlier epilepsy develops and the later it is diagnosed, the worse the prognosis for the child's development.

Each epileptic syndrome is unique but has its own distinctive clinical features. One of the classifications of epilepsy was made on the basis of the clinical manifestations of seizures. Epilepsy is linked to the "paroxysmal brain" problem. The brain in epilepsy works differently: it can periodically produce discharges with the strongest activity without provocateurs, which manifest as seizures. A person can be born with a predisposition, that is, a predisposition to this disease. In the future, the influence of various factors can realize this predisposition. One of the examples when a predisposition to epilepsy is revealed is febrile seizures, that is, seizures in children that occur when the temperature is high. The presence of such seizures does not mean that the child necessarily has epilepsy. However, it has been found that some children with febrile seizures have altered activity in the hippocampus, a part of the brain that may play a significant role in the development of paroxysmal impulse activity. And in this group of children, the risk of developing epileptic syndrome is higher than in children who have never had a high temperature seizure.

Adolescent forms of epilepsy are also "benign". Such forms cannot affect development and can be effectively controlled by anti-epileptic drugs. In general, modern therapy methods can effectively help patients 60–70% of the time. The claim that epilepsy is incurable is a myth. The combination of drug treatment with surgical methods and neuromodulation can in most cases be helpful even in difficult situations.

Epileptic seizures

Epileptic seizures can vary widely - from convulsive tonic-clonic seizures to seizures with altered consciousness and visual hallucinations. When the excitation of brain activity is triggered in the occipital cortex, which is responsible for vision, seizures with impaired vision and headaches can manifest. In a generalized seizure, patients lose consciousness. There are rare forms of seizure, when the patient changes consciousness, but he can perform various actions: walking, talking, making some stereotypical movements.

Another common manifestation of epilepsy is tonic-clonic seizures (“tonic” is tension, “clonic” is twitching). Tonic-clonic seizures are generalized when all muscles are tense and partial when in certain parts of the body, e.g. B. in the right arm or in the left leg, tension or twitching occur. Also, convulsions can only be clonic when there is no tension, or tonic when there is no twitching.

Epilepsy is rarely fatal. However, there is a concept of status epilepticus - a condition in which epileptic seizures are repeated one after the other. Serious complications can occur at the time of status epilepticus.

Improper patient care during an attack can also lead to a poor outcome. The seizure occurs suddenly, and the patient's fall can lead to retraction of the tongue and suffocation - respiratory failure. There is a myth that if you have severe seizures you have to stick something in a person's mouth, but doing so can injure the teeth and tongue, and add an additional cause of suffocation. To help a person during an attack, all you need to do is turn them on their side and remove the surrounding objects that can cause the injury.

Treatment of the disease

There are several approaches to treating epilepsy: medical and surgical methods, and the use of neuromodulation. These methods are often combined with one another. A special ketogenic diet is used in some forms of epilepsy. The mechanism of this diet is not fully understood, but it is believed that ketone bodies can trigger a variety of biochemical processes, thereby suppressing epileptic discharges. The ketogenic diet drastically reduces the amount of carbohydrates while increasing the fat content.

In drug therapy, a group of anti-epileptic drugs is used - anticonvulsants. Neurosurgery is used in forms resistant to drug therapy to create a stable focus of epileptic activity in the brain.

Recently, neurostimulation has been actively developing. Methods such as vagus nerve stimulation, transcranial magnetic stimulation are used.

Epilepsy research

Epilepsy was first described before our time.Many famous historical figures suffered from this disease, for example, Alexander the Great, Julius Caesar. However, research into epilepsy as a disease began on a larger scale in the 19th century. In 1888, John Jackson gave one of the earliest definitions of epilepsy. Russian doctors Aleksey Kozhevnikov and Vladimir Bekhterev made a significant contribution to the development of an understanding of the causes and clinical manifestations of epilepsy. They described the clinical manifestations of seizures and identified epilepsy as a disease in its own right. A major breakthrough in epilepsy research came in the 20th century when electroencephalography, a method of studying the bioelectrical activity of the brain, appeared. Electroencephalography shows all of the electrical activity of the brain, the work of the cortex, and the deep structures of the brain. Using this method, scientists recorded epileptic electrical discharges that coincided with epileptic seizures. Then the rapid development of epileptology began as an independent direction in neurology. With the method of electroencephalography different types of epileptic seizures could be distinguished. In recent years a major breakthrough in the study of this disease has been associated with the development of functional imaging and genetics techniques.

The content of the article

epilepsy - a chronic brain disease characterized by repeated epileptic seizures due to excessive neuronal discharges and accompanied by a variety of clinical and paraclinical symptoms.

Etiology of Epilepsy

According to modern concepts, the development of epilepsy apparently requires the presence of a sustained focus of epileptic activity associated with damage to the organic brain. At the same time, the epileptization of neurons in herds of organic brain damage and the degree of the epileptic influence of this herd on the brain structures depend on the premorbid properties of the organism and in particular on the epileptic predisposition. The latter is defined as a constitutional or acquired condition that predisposes a person to various forms of epileptic seizures with brain damage.
Among the exogenous pathogenic factors of disease origin, perinatal as well as neuroinfections and traumatic brain injuries are of the greatest importance. This does not exclude the role of other points: intrauterine, vascular, toxic. In perinatal pathology, traumatic factors (inconsistency in the size of the head and pelvis, use of obstetric benefits, etc.) and anoxic-fetal asphyxia (prolonged labor, entanglement with the umbilical cord, etc.) play the greatest role.
Epilepsy can occur as a result of traumatic brain injury or neuroinfection.

Pathological anatomy of epilepsy

Pathological studies show that epileptogenic lesions usually have an atrophic-sclerotic character. The zone of occurrence of epileptic discharges (epileptic focus) is usually located on the periphery of traumatic scars, cysts, areas of dysontogenesis (hamartomas, etc.) and other lesions.
Changes in the concave surface of the ammonium horn (summer sector) are particularly common, in connection with which the concept of the particular vulnerability of this part of the brain during childbirth was presented. Obviously, each epileptic seizure is accompanied by the development of significant changes in brain tissue (dystonic changes in blood vessels, stasis, perivascular edema, micro-bleeding, acute changes in neurons, etc.). The status epilepticus is particularly severe.
Repeated acute disorders associated with repeated seizures lead to the gradual formation of vascular-hypoxic encephalopathy: exhaustion of gray matter cells, progressive changes in neuroglia. At the same time, in addition to the ammonia horn, the cerebral cortex (especially the frontal cortex), the Purkinje cells of the cerebellum, the unspecific nuclei of the optical mound, etc. are affected.
As the morphological substrate of an epileptic discharge, a special state of synapses in an epileptic focus is described - activation, accumulation of synaptic vesicles, expansion of synaptic clefts, etc. [Chubinidze A. P., 1973, etc.], detected by electron microscopic examination.

Epilepsy pathogenesis

In the pathogenesis of epilepsy, changes in the functional state of neurons in the area of ​​epileptogenic lesions (epileptogenic focus) are of great importance.
The discharges of such new cells (the so-called epileptic neurons) are characterized by a very high frequency and a relatively low amplitude, which is a consequence of the tendency of these neurons to a prolonged and pronounced depolarization, the so-called paroxysmal depolarization shifts of the membrane potential [Okudzhava VM, 1975 ]. The collection of epileptic neurons forms an epileptic focus. In this case, a number of new pathophysiological features are important that show up in the epileptic focus as a result of the interaction of populations of epileptic neurons. The most important one should be recognized as hypersynchronization of neural activity i.e. H. The simultaneous involvement of a large number of epileptic and neighboring neurons in the excitation. Apparently not all mechanisms of hypersynchronization are established, but many of them are known, namely: increased synaptic conduction [Jasper, 1954]; epileptic excitation, that is, the direct (extra-synaptic) effect of the electric field of an epileptic neuron on neighboring cells, in-phase discharges, an increase in the number of actively functioning neurons, etc. Hypersynchronization of neuronal activity is the main pathophysiological mechanism of epilepsy, since it is not only the basis for the formation of epilepsy is focus, but also the effects of the latter on the brain.
The spread of the influence of the epileptic (epileptogenic) focus on the brain can be facilitated by this particular functional state of the brain called increased epileptic readiness, "convulsive reactivity" of the brain, and so on. It is the increased epileptic readiness of the brain that contributes to the formation of an epileptic focus and the spread of its influence to other parts of the brain.
According to P. M. Saradzhishvili (1971), the epileptic focus cannot cause an epileptic seizure without including the functional system in which the specific and unspecific nuclei of the visual mound seem to be invariably involved. For the mechanism of generalizing epileptic activity from the primary cortical epileptic focus, “generalizing formations of the subcortex”, which include the structures of the limbic brain, medial thalamus, subthalamus, and reticular formation of the midbrain, are of primary importance. At the same time, the brain has structures that inhibit epileptogenesis and counteract the spread of the influence of the epileptic focus on the brain. Such formations include the caudate nucleus, the caudal nucleus of the pons, the lateral nucleus of the hypothalamus and some others, especially the cerebellum, the region of the single bundle. The influence of these structures takes place both in the form of a direct inhibitory effect and in the form of a return inhibition, which develops under the influence of an epileptic focus. This system is also described as a negative feedback system that works through a population of intercalar neurons. Intercalary neurons excited by impulses from the epileptic focus can interrupt the flow of these impulses by hyperpolarizing epileptic neurons [Okudzhava VM, 1969 etc.]. The recurrent inhibition of neurons along the periphery of the epileptic focus is also of some importance in blocking the epileptic focus.
It can be assumed that the desynchronization devices of the brain have an anti-epileptic effect, while the synchronization devices can promote the activation of epileptic foci. At least polygraphic studies on night sleep in humans have shown that the activation of the epileptic focus takes place in certain stages of slow sleep, while the REM sleep, in which EEG desynchronization takes place, suppresses epileptic activity [Sarajishvili P. M., 1972; Wayne AM, 1974, etc.].
It should be noted that the extrafocal brain apparatus itself is under the influence of certain extracerebral factors - humoral, reflexive, etc. For example, it has long been known that acalosis promotes and acidosis, on the contrary, prevents the development of a seizure.
When the epileptic focus cannot be stably blocked, which is usually manifested in the manifestation of epileptic seizures, a number of new pathophysiological mechanisms for the formation and development of epilepsy as a disease arise. The most important of these is the emergence of secondary epileptic foci. In their emergence, the mechanism of secondary recurrent generalization is of great importance, that is, excitation under the influence of the cortical epileptic focus of the generalization apparatus of the subcortex, followed by a secondary "reflection" of excitation into the cortex. Such a "reflection" occurs most often in the symmetrical point of the cortex of the "healthy" hemisphere. Transcallosal effects also play a role. With the formation of a secondary epileptic focus, it goes through the stage of a dependent focus and later becomes independent of the influence of the primary focus and plays the role of an independent epileptogenic factor.
The question naturally arises as to whether the study of metabolism in epilepsy can shed light on some aspects of its pathogenesis. A large number of studies that have been carried out over a period of a hundred years and dealt with various aspects of metabolism (water-salt, nitrogen-protein, carbohydrates, acid-base balance, etc.) have proven to be ineffective, to refute the position expressed by Fischer. In epilepsy, there are no regular changes in metabolism, only excessive fluctuations in the various indicators in one direction or another. These fluctuations in biochemical parameters depend to a certain extent on the phases of the epilepsy cycle (pre-epileptic, post-epileptic, interepileptic). In recent years, it has been shown that they relate not only to biochemical constants such as the acid-base balance of blood, the content of nitrogenous compounds, sodium, potassium, and others, but also cover almost all aspects of metabolism. The instability of the membrane potential and its rhythmic fluctuations were also noted, which is associated with a violation of the maintenance of an adequate gradient in the ion concentration of electrolytes on both sides of the nerve cell membrane in the form of excessive intracellular accumulation of sodium ions. Disturbed ion distribution and within the cell where an unusually large amount of potassium ions accumulate in the mitochondria. These disorders underlie the paroxysmal shift in depolarization of the membrane potential of the epileptic neuron.
In the focus of epileptic activity, a decrease in the content of amino acid glutamus and gamma-aminobutyric acid (GABA), which are metabolically related and directly related to the Krebs cycle, was found. The latter is known to have a pronounced antispasmodic effect. Apparently, a seizure as a component of hypovitaminosis B6 (pyridoxine) is associated with a deficiency of GABA, since the latter is formed from glutamic acid with the participation of paridoxine phosphate under the action of decarboxylase.
Pyridoxine deficiency epilepsy is an example of biochemical disorders that arise under the influence of genetic factors or exogenous lesions and that can increase the brain's epileptic readiness. Recently, attention has been drawn to the possible role of disturbances in the functioning of brain systems such as noradrenergic and serotonergic systems which exert an inhibitory function [Bekhtereva NP et al., 1979 and others]. Attempts are made to treat epilepsy by correcting these disorders. The well-known role of the violation of acetylcholine (ACh) metabolism can also be considered proven. ACh has a pronounced convulsive effect. The ability to retain ACh in an unbound active form in an epileptic neuron has been found to be reduced.
An excess of free ACh in the postsynaptic membrane immediately leads to depolarization. It is possible that this phenomenon is mainly due to a lack of glutamic acid, which is necessary for the binding of ACh, and an excess of sodium ions, which is necessary for the release of active ACh.

Epilepsy Clinic

As can be seen from the definition of epilepsy, epileptic seizures are the main clinical symptom of the disease. In the international static classification of epilepsy, all epileptic seizures are divided into generalized, partial (focal) and unilateral seizures. Generalized seizures are clinically manifested as loss of consciousness, massive vegetative manifestations and, depending on whether they are accompanied by convulsions or not, are divided into convulsive and non-convulsive forms. In the EEG, generalized epileptic seizures are characterized by bilateral symmetrical and synchronous epileptic discharges.
The convulsive forms of generalized epileptic seizures include major epileptic seizure and its variants. A major epileptic seizure (severe illness, grand mal), as well as unconsciousness and autonomic disorders (mydriasis, hyperhidrosis, tachycardia, etc.) are characterized by seizures in which both sides of the body are involved at the same time. Tonic convulsions follow first, and then clonic convulsions. In rarer cases, seizures may only be tonic or clonic in nature (the so-called non-triggered seizure). As a rule, apnea occurs due to the involvement of the respiratory muscles; Patients bite their tongues and urine passes involuntarily; Patients often suffer traumatic injuries when they fall. The seizure ends in an epileptic coma that turns into sleep. After that, amnesia, a feeling of weakness, muscle pain, and weakness are noted. In other cases, psychomotor agitation, a twilight state of consciousness, and other mental disorders may develop after a seizure.
A major epileptic seizure is electroencephalographically characterized by the occurrence of rhythmic discharges of 8 to 14 per second and low amplitude, followed by an increase in the latter (recruitment) to 100 to 200 μV (tonic seizure stage) and a transition to peak wave and polypeak wave discharges (clonic Stage). ... The second type of generalized epileptic seizure is absence. Clinically, it is characterized by a shutdown of consciousness without convulsions and a fall of the patient (absence - absence) and vegetative manifestations (pallor or reddening of the face, mydriasis, salivation, etc.), electroencephalographic - by paroxysms of discharges with a structure of peak wave complexes with a frequency of 3 per second. The type of seizure described is called simple absence, the EEG image is called typical absence. This type of epileptic seizure is more common in people with a pronounced hereditary load, can easily be caused by flashes of light and hyperventilation, and has a relatively good prognosis.
In so-called complex absences, the disconnection of consciousness and autonomic disorders are associated with various motor phenomena, e.g. B. myoclonic twitching (myoclonic absence), involuntary contractions of the facial muscles, rolling of the eyeballs or turning off the posture tone causing the patient to fall (atonic absence). Complex absence in the EEG is manifested in rhythmic complexes of the peak wave 3 per second (usually with myoclonic absence), but more often these discharges have frequencies from 2 to 2.5 per second (the so-called atypical absence). This form of absence is characterized by resistance to flashes of light and hyperventilation, which are usually observed in children aged 2 to 8 years with pronounced organic symptoms and delayed mental and physical development. Has a poor prognosis (Lennox-Gastaut syndrome).
Often absences are referred to as minor seizures (minor illness, petit mal), but these two terms are not the same, as minor seizures also refer to some forms of partial epileptic seizures that occur with loss of consciousness without seizures, such as pseudo temporal falls. It is believed that in generalized seizures, the epileptic focus is on the oral parts of the brain stem (called centracephalic epilepsy). Recently, however, evidence has been obtained that such seizures can be caused by foci in the medial-basal parts of the cerebral hemispheres [Karlov VA, 1974; Saradzhishvili P. M., Geladze T.Sh., 1976; Banco et al., 1976 and others].
The second group of epileptic seizures is partial. In partial seizures, the epileptic focus is always in the cerebral cortex, only part of the brain is involved in a seizure, while, as has since been established, the involvement of subcortical structures and especially the optic mound is mandatory. There are partial seizures with motor, sensory, vegetative-visceral symptoms, seizures with impaired perception, epileptic automatisms and a few others.
The most ostentatious manifestation of partial motor seizures is a Jacksonian or somatomotor seizure, which occurs when there is an epileptic focus in the projection motor cortex. It is characterized by clonic seizures that begin on the face, hand, foot, etc. Spasms can remain localized or spread with a pattern determined by the peculiarity of the cortical somatotopic localization of motor functions ("Jackson's March"). Consciousness remains. In some cases, convulsions spread to the entire half of the body, and sometimes they are generalized, which is accompanied by loss of consciousness.
An oculomotor epileptic seizure manifests itself as a tonic abduction of the eyeballs, an adverse seizure of the eyes and head in the opposite direction, and a seizure of epileptic rotation in the trunk as well. These seizures are caused by epileptic foci in the premotor cortex.
Kozhevnikov's epilepsy is a special type of partial motor seizure: persistent myoclonus in a limited muscle group that periodically turns into generalized seizures. Partial sensory seizures primarily include Jackson's sensory or somatosensory seizures. These are attacks of paresthesia with limited localization, but the "Jackson march" is also possible while maintaining consciousness. They are located in focal points in the sensory projection cortex. A somatosensory seizure often turns into a somatomotor seizure (called a sensorimotor seizure).
Sensory seizures also include visual, auditory, olfactory and taste attacks, which manifest themselves in the form of stimulus phenomena of the corresponding projection cortex (photopsia, wrong taste, smell, etc.). These seizures are also known as sensory seizures with simple symptoms. In addition, a distinction is made between sensory seizures with complex symptoms - epileptic perception disorders or psychosensory seizures, which are usually caused by foci in the projection-associative cortex. They appear in the form of corresponding illusory or hallucinatory experiences - vivid visual scenes, complex melodies, etc.
Illusory and hallucinatory (psychosensory) epileptic seizures also include seizures of impaired sensory synthesis due to the type of derealization or depresonalization that usually occurs in disorders of consciousness. These are the syndromes deja vu - "already seen", deja entendu - "already heard", deja vecu - "already experienced", jamais vu - "never seen", jamais entendu - "never heard", jamais vecu - "never" Experienced. "In all of these cases, the patient's visible, audible, and experienced experience appears to be already visible, audible, experienced. Or, on the contrary, situations and phenomena that the patient has repeatedly encountered and experienced appear completely new to him, never seen before , not experienced.
Apparently there are some degrees of impaired consciousness in these paroxysms. In severe cases there are "dream states" in Jackson's terminology, in which the above-mentioned states are experienced by patients as in a dream. Such paroxysms can include operative symptoms (swallowing, sucking, smacking, etc.) combined with olfactory and taste hallucinations, violent memories.
No less and perhaps more often than psychosensory paroxysms occur in epilepsy psychomotor seizures or epileptic seizures of automatism, which are characterized by paroxysmal disturbances of consciousness and motor activities in the form of automatisms. The behavior of the patient is expressed in terms of externally ordered actions, which, however, are not appropriate to the given situation. Confusion develops during psychomotor seizures, followed by amnesia. All types of psychomotor seizures are most commonly caused by epileptic discharges in the anterior temporal lobe.
The International Statistical Classification of Diseases, Injuries and Causes of Death of the 9th revision (1975) also provides for the allocation of affective attacks - various paroxysmal mood disorders, mostly unmotivated feelings of fear, less often fits of laughter (helolepsy), states of happiness, etc. Usually such paroxysms are accompanied by a change in consciousness . They are caused by discharges in the anteromedial temporal lobe.
It should be borne in mind that all types of partial (focal) seizures, both simple and complex symptoms, can lead to generalized seizures and in these cases are referred to as secondary generalized seizures. Secondary generalized seizures should also include generalized convulsive seizures with a preceding aura. Usually the same patient has a stereotypical aura when a severe seizure recurs. Its nature is determined by the location of the epileptic focus. During the aura, the patient experiences certain sensations, e.g. B. Smell (olfactory aura), taste (taste aura), visual sensations, images or whole images (visual aura), auditory (auditory aura), abdominal pain (abdominal aura), etc. According to SN Davidenkov, the following types of auras are distinguished: sensory, sensitive, motor, linguistic, vegetative and mental.
The visual and auditory auras mentioned above are examples of sensory auras. The sensitive aura manifests itself in the form of various senestopathies (dry mouth, numbness, distorted perception of one's own body, etc.). The motor aura is a stereotypical movement performed by the patient before a seizure occurs. The vegetative aura is perhaps the most diverse. These are various unpleasant sensations in the area of ​​the heart (aura cordialis), gastrointestinal tract (aura abdominalis), sensations of respiratory arrest or lack of air, feeling of hunger, etc.
Particularly peculiar is the psychic aura, in which the patient experiences an extraordinary emotional state, often an incredible bliss. An example of such an aura can be found in Dostoyevsky's excellent description of an attack in Prince Myshkia. The writer himself suffered from epilepsy and apparently experienced similar sensations.
The aura lasts for a moment and is the only, often very vivid, memory that the patient subsequently retains about the attack. Very often, the aura in general can be the only clinical manifestation of an epileptic seizure. Usually, however, after the aura, there is a loss of consciousness and seizures occur. The aura always indicates the focal onset of the seizure. Finally, the classification provides for a third type of seizure - one-sided seizures. These seizures mainly occur in children. The most frequently studied hemiconvulsive seizures with tonic-clonic seizures that directly affect the patient are associated with unconsciousness and post-seizure disorders (coma, stupor, etc.). However, unlike a major seizure, seizures are one-sided.