Epilepsy

Epilepsy - a violation of brain function, characterized by repeated spontaneous attacks and accompanied by a variety of clinical and paraclinical symptoms.

Etiology, pathogenesis. In the origin of epilepsy, a combination of predisposition and organic damage to the brain (intrauterine development disorder, birth asphyxia, mechanical damage during labor, infection, craniocerebral trauma, etc.) play a role. In this regard, it is inappropriate to separate epilepsy from the so-called. "Genuine" (hereditarily conditioned) and "symptomatic" (the result of organic brain damage).

An epileptic attack is caused by the spread of excessive neuronal discharges from the focus of epileptic activity to the entire brain (generalized seizure) or part of it (a partial attack). An epileptic focus can occur for a short time in acute brain diseases, for example, in disorders of cerebral circulation, meningitis, which is accompanied by so-called random epileptic attacks. In chronic current brain diseases (tumors, parasitic diseases, etc.), the epileptic focus is more stable, which leads to the occurrence of recurrent seizures (epileptic syndrome). In epilepsy as a disease, repeated seizures are usually the result of the action of a persistent epileptic focus in the form of a sclerotic-atrophic focus. An important link in pathogenesis is the weakening of the functional activity of structures that exert an anti-epileptic influence (the reticular nucleus of the brain bridge, caudate nucleus, cerebellum, etc.), which leads to a periodic "breakthrough" of epileptic excitation, ie, to epileptic seizures. Epileptogenic lesions especially occur in the medial basal parts of the temporal lobe (temporal epilepsy).

Symptoms, course. Generalized seizures are accompanied by loss of consciousness, vegetative symptoms (mydriasis, reddening or pallor of the face, tachycardia, etc.), in some cases - convulsions. The convulsive generalized attack is manifested by common tonic-clonic seizures (large seizure, grand mal), although there can only be clonic or just tonic convulsions. During the attack, patients fall and often get significant damage, often bite the tongue and miss the urine. The seizure usually ends with a so-called epileptic coma, but epileptic stimulation with a twilight confusion of consciousness can also be observed.

The non-convulsive generalized attack (small attack, petit mal, or absence) is characterized by a loss of consciousness and vegetative symptoms (simple absence) or a combination of these symptoms with mild involuntary movements (complex absences). Patients briefly interrupt their actions, and then after the attack continue them, while the memory of the seizure is absent. Less often during an attack there is a loss of a postural tone, and the patient falls (an atonal absence).

In case of partial epileptic seizures, the symptomatology can be elementary, for example, focal clonic seizures-J-xon's attack, turning the head and eyes aside-an adverse attack, etc., or complicated-paroxysmal memory disorders, obsessive-compulsive attacks, psychomotor seizures-automatisms, psychosensory attacks- Complex perception disorders. In the latter cases there are hallucinatory phenomena, the phenomena of depersonalization and derealization of the state of the "seen", "never seen," a sense of alienation of the external world, one's own body,

Any partial attack can go to a generalized (secondarily generalized attack). Secondary generalized seizures also include seizures preceded by an aura (harbinger) - motor, sensory, vegetative or psychic phenomena, from which the attack begins and about which the patient retains the memory.

The course of epilepsy depends largely on its shape. So, in children there are absolutely favorable (Rolandic epilepsy, picnoepilepsy) and unfavorable (children's spasm, Lennox syndrome - Gasto) forms of epilepsy. In adults, the course of epilepsy without treatment in the majority of cases is progredient, which is manifested by the gradual increase in seizures, the appearance of other types of paroxysms (polymorphism), the adherence to daytime bouts of the day, the tendency to develop episodes of seizures or epileptic status, the emergence of characteristic personality changes in the form of stereotypedness and pathological detail Thinking, a combination of affective viscosity with explosivity, importunity, servility, egocentrism, up to the final states defined as epileptic dementia.

Among the additional methods of investigation, the EEG has the greatest value, in which spikes, peaks, and sharp waves are detected, isolated or in combination with a subsequent slow wave (so-called peak-wave complexes). These changes can be caused by special methods of provocation - hyperventilation, rhythmic light stimulation, the introduction of corazole, etc. The most complete provocative effect on the epileptic activity is having a sleep or, conversely, a 24-hour sleep deprivation, which makes it possible to detect epileptic symptoms in 85-100% of cases . EEG studies also contribute to clarifying the localization of the epileptic focus and the nature of epileptic seizures.

Diagnosis of epilepsy is based on the suddenness of seizures, their short duration (seconds, minutes), deep unconsciousness and dilated pupils in generalized attacks, depersonalization and derealization in partial seizures. Typical changes in the EEG confirm the epileptic nature of seizures, although the absence of such does not exclude it. To diagnose epilepsy as a disease, anamnestic data are significant: the disease occurs, usually in childhood, adolescence and adolescence, often there are hereditary complications in the family, a burdened obstetric anamnesis, neuroinfections and cerebral trauma, paroxysmal conditions up to 3 years old.

Treatment is continuous and continuous. Selection of medications and their dosages should be individual, depending on the characteristics of the attacks, their frequency, periodicity, the patient's age, etc. Barbiturates can be prescribed for all kinds of attacks: phenobarbital at the rate of 2-3 mg / kg of body weight of the patient, benzonal for 7- 10 mg / kg. Barbiturates, as well as diphenine in a dose of 5-7 mg / kg, carbamazepine (tegretol, stasepine, finlepsin), 8-20 mg / kg per day, have the greatest impact on convulsive forms of attacks. With absences, ethosuximide (picnoleptsine, suxilep) and valproic acid preparations of carbamazepine are used as the only remedy or in combination with a benzonale. Valproic acid derivatives (depaxin, acetiprol), etc., currently occupy a leading place in the treatment of seizures, since they can act in all kinds of attacks, but the maximum effect is with absences and generalized seizures without a focal start. Doses vary widely - from 15 to 40 mg / kg or more per day.

To avoid toxic effects in polypharmacy, it is necessary to recalculate antiepileptic drugs to the phenobarbital coefficient. It is a conventional unit for phenobarbital, diphenine 0.5, benzonal 0.5, hexamidine 0.35, carbamazepine 0.25, ethosuximide 0.2, trimethine 0.3, valproic acid 0.15.

The total dose in the conventional conversion to phenobarbital should not exceed 0.5-0.6 per day.

Systematic monitoring of the patients' condition is necessary (blood and urine tests at least once a month); When there are signs of intoxication (headache, sleep disturbances, dizziness, changes in blood, etc.), doses of medication are temporarily reduced, additionally prescribed multivitamins and antihistamines (Tavegil, etc.). When complications such as hemorrhalopia (trimethine), hyperplastic gingmvit (diphenin), severe dyspeptic manifestations (ethosuximide), megaloblastic or aplastic anemia, pancytopenia, toxic hepatitis (hexamidine, phenobarbital, diphenine, carbamazepine, ethosuximide), etc., appear Drugs have to be canceled. Any changes in the treatment of antiepileptic drugs should be carried out cautiously and gradually.

Along with drug therapy, depending on the changes identified and underlying the disease, the course is treated by means of resolving, dehydrating, vascular action. The criterion for the abolition of antiepileptic treatment is at least three years of remission with favorable EEG dynamics. Drugs are canceled gradually within 1-2 years (can not be canceled in the puberty period!). The failure of prolonged conservative treatment makes it necessary to decide on the application of a ketogenic diet, vagus stimulation or neurosurgical treatment of epilepsy.

With epilepsy, urgent conditions may arise, requiring immediate action in connection with acute threat to the health and life of the patient or his associates. Such are the status epilepticus (a series of seizures, usually large convulsions, between which consciousness is not completely restored) and acute psychotic conditions. With epileptic status, it is necessary to remove foreign objects from the oral cavity, insert an airway, do an intravenous injection of 10 mg of diazepam in 20 ml of a 40% solution of glucose or in / m 5-10 ml of a 10% solution of sodium thiopental or hexenal. Patients are sent to the resuscitation department of multidisciplinary hospitals, where in case of continuing attacks they are given a long dosed anesthesia. With non-curable status, super-long anesthesia is performed with a nitrous oxide-oxygen mixture on muscle relaxants and controlled respiration, regional craniocerebral hypothermia. Correction of metabolic disorders is mandatory.

In acute psychotic conditions, which occur with or without a disorder of consciousness (dysphoria, twilight states, etc.), one should use neuroleptics - tryptazine IM in 1-2 ml of 0.2% solution, levomepromazine (tizercin) 1-3 ml 2.5% solution in / m with 0.5% solution of novocaine or with 20-40% glucose solution IV, haloperidol 1 ml 0.5% solution IM, etc. In severe depression, antidepressants are administered - Melipramine in 2 ml of a 1.25% solution w / m, amitriptyline in / m or slowly with / in 2-4 ml of 1% solution. Injections of the preparations are repeated if necessary several times a day. All these drugs are used only in combination with antiepileptic drugs.

Prevention includes preventive antiepileptic treatment for children who have undergone perinatal brain damage - if there are EEG changes or characteristic clinical data (nocturnal fears, febrile seizures, etc.), as well as people with a history of traumatic brain injury.