RU2473333C2 - Method of suppressing epileptiforma activity and relief of epeleptic attacks in case of epileptic syndromes in children with electric epileptic status in phase of slow wave sleep - Google Patents

Abstract

FIELD: medicine.

SUBSTANCE: invention relates to medicine, namely to pediatric neurology, and can be used for suppression of epileptic activity and relief of epileptic attacks in case of epileptic syndromes in children with electric epileptic status in phase of slow wave sleep. For this purpose 0.2-0.3 ml of medication Synacthen-Depot are introduced intramuscularly to patient with confirmed by electroencephalogram electric status in phase of slow wave sleep 2 times per week with gradual 0.2 ml increase of dose until sleep EEG is normalised or dose 2.0 ml is reached, with further gradual medication withdrawal. General duration of treatment course is 3-6 months.

EFFECT: method makes it possible to achieve clinical remission and EEG normalisation without undesirable side effects due to smaller and individually selected doses of medication.

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Description

AREA OF MEDICINE TO WHICH THE INVENTION relates.

The invention relates to medicine, and more specifically to pediatric neurology.

The invention can most effectively be used in pediatric neurology and epileptology for the treatment of epileptic syndromes with electrical status epilepticus in the phase of slow sleep.

BACKGROUND OF THE INVENTION

A known method of treating epileptic syndromes in children with an epileptic status in the phase of slow sleep, selected as an analogue. The essence of the analogue method is as follows. The patient is intramuscularly injected with ACTH at a dose of 80 ME once a day for 3 months. The effectiveness of treatment is evaluated clinically and by recording EEG sleep. A sleep EEG is periodically recorded after the course to detect relapses of electrical status epilepticus during the slow sleep phase (Tassinari CA, Rubboli G, Volpi L, Meletti S, d'Orsi G, Franca M, Sabetta AR, Riguzzi P, Gardella E, Zaniboni A, Michelucci R. Encephalopathy with electrical status epilepticus during slow sleep or ESES syndrome including the acquired aphasia. // Clin Neurophysiol. 2000 Sep; 111 Suppl 2: S94-102).

The disadvantage of this method is the lack of individual selection of the dose of the drug, the high frequency of adverse events and the high cost of treatment.

A known method of treating West syndrome (infantile spasms) in children, selected for the prototype. The essence of the prototype method is as follows. A synthetic analogue of ACTH is administered to the patient intramuscularly - the drug Sinacten-Depot, 1 ml ampoules containing 0.1 mg of active substance (analogue 40 ME ACTH). Injections are carried out 2 times a week, starting with a dose of 0.1-0.2 ml and gradually increasing the dose until the seizure stops or to the maximum tolerated dose, but not more than 1.0 ml. After achieving a clinical effect or after reaching the maximum tolerated dose, the dose of the drug is gradually reduced, until it is completely canceled.

The disadvantage of the prototype method is the lack of experience in children with epileptic syndromes with epileptic status in the phase of slow sleep. These children are older than children with West syndrome and require higher doses of ACTH and longer for treatment.

SUMMARY OF THE INVENTION

The objective of the invention is to develop a new method for the treatment of epileptic syndromes in children with electrical status epilepticus in the phase of slow sleep.

The problem is solved in that a patient with a confirmed electroencephalographically electrical status in the phase of slow sleep is injected intramuscularly 0.2-0.3 ml of the drug Sinacten-Depot. The next injection is carried out every 3-4 days, while the dose is increased by 0.2 ml. After the onset of clinical remission or in the event of adverse events requiring a dose reduction, or when a dose of 2.0 ml is reached, a control study of sleep EEG is performed. Treatment continues with the dose at which clinical remission and normalization of the EEG were achieved, or with the maximum dose achieved. Drug withdrawal is carried out gradually, at least four weeks in advance. A significant difference between the proposed solution and the known one is the use of smaller and individually selected doses of synthetic ACTH - the drug "Sinacten Depot", which significantly reduces the risk of adverse events.

INFORMATION CONFIRMING THE POSSIBILITY OF CARRYING OUT THE INVENTION.

The possibility of carrying out the invention is determined by studies confirming the effectiveness of ACTH in epileptic syndromes in children with electric epileptic status in the slow sleep phase (Inutsuka M, Kobayashi K, Oka M, Hattori J, Ohtsuka Y. Treatment of epilepsy with electrical status epilepticus during slow sleep and its related disorders. // Brain Dev. 2006 Jun; 28 (5): 281-6. Epub 2006 Jan 10).

DETAILED DESCRIPTION OF THE INVENTION

A patient with a confirmed electroencephalographically electrical status is injected intramuscularly with 0.2-0.3 ml of Sinacten-Depot in the phase of slow sleep. The next injection is carried out every 3-4 days, while the dose is increased by 0.2 ml. After the onset of clinical remission or in the event of adverse events requiring a dose reduction, or when a dose of 2.0 ml is reached, a control study of sleep EEG is performed. Treatment continues with the dose at which clinical remission and normalization of the EEG were achieved, or with the maximum dose achieved. Drug withdrawal is carried out gradually, at least four weeks in advance.

EXAMPLES

Example 1. Patient G., 8 years old. Clinical diagnosis: Landau-Kleffner syndrome. Electrical status epilepticus in a phase of slow sleep. It was observed from 12.10.2001 to 05.03.2003.

The hereditary history of epilepsy is not burdened. Early development without features. Speech before the disease developed by age.

She fell ill at the age of 6, when she gradually ceased to understand the addressed speech, and also she stopped speaking. The girl never had epileptic seizures. Examination of the girl on EEG revealed independent foci of epileptiform activity in the back-temporal leads on the right and left, and the girl was sent to hospitalization in the Department of Psychoneurology and Epileptology of the Moscow Research Institute of Pediatrics and Pediatric Surgery.

When examining the somatic and neurological status without features. The girl does not understand the speech addressed, however, the possibility of communicating with gestures remains, the girl understands the meaning of the drawings, there is play activity. Magnetic resonance imaging without features.

On sleep EEG, diffuse epileptiform activity was recorded, occupying more than 85% of the slow sleep phase. Some elements of this activity resembled benign focal epileptiform discharges of childhood.

The child was prescribed valproate (Depakine) and a course of synactene-depot was performed 2 times a week, at a maximum dose of 1.5 mg, lasting 2 months. Epileptiform activity disappeared, speech began to recover. During the year of intensive observation of relapses of electrical status epilepticus in a dream was not observed. The child went to a regular school. Antiepileptic therapy (Depakine) is left until the age of 12 years.

Example 2. Patient Z., 6 years old. Clinical diagnosis: Acquired epileptic opercular syndrome, electrical status epilepticus on the EEG. He was observed in the Department of Psychoneurology and Epileptology from 03.10.02 to 18.14.02 and from 12.03.03 to 15.04.03 Heredity for epilepsy is not burdened. Early development without features. He fell ill at 4 years old (in April 2000). Against the background of complete health, an epileptic seizure developed with loss of consciousness, clonic twitching of the muscles of the face and right limbs, salivation, lasting 3 minutes. After an attack of aphasia, sleep. A month later, atypical absences and orofacial motor seizures from 20 to 50 times a day in the afternoon and single secondary-generalized seizures during sleep joined. Two months later, speech became slurred, behavioral disorders appeared. At the place of residence, he received finlepsin, depakine, sibazon, prednisone, but the attacks did not stop, speech was still illegible.

At admission, dysarthria, salivation, moderate ataxia, and increased irritability attracted attention.

Magnetic resonance imaging of the brain revealed no pathology; focal epileptiform activity in the left parietal, temporal and frontal regions was detected on the waking EEG. According to morphology, the complexes resembled benign focal epileptiform discharges of childhood, however, they were characterized by high amplitude.

During slow sleep, activity became continuous, in the left anterior temporal region, its amplitude reached 600 μV. This activity diffusely spread to all leads and was recorded in both hemispheres, representing a pattern of electrical epileptic status in the phase of slow sleep.

The child was assigned valproate (Depakin chrono) and the Sinacten-Depot course was started according to the scheme we proposed. At a dose of 2 mg 2 times a week, epileptic seizures were stopped and speech began to improve. The child was discharged home to continue the course of hormone therapy at the place of residence.

With repeated hospitalization after 6 months, speech recovered, the child was able to read the poem from memory. The epileptiform activity on the EEG persisted, but the focus shifted to the right anterior temporal region, and Depakin was continued to the patient.

The child was examined in follow-up at 11 years. The boy is studying in a regular school, there are no attacks, there is no epileptiform activity on the EEG.

Claims (1)

A method for the treatment of epileptic syndromes in children with an electric epileptic status in the slow sleep phase, characterized by intramuscular administration of the Sinacten-Depot preparation twice a week, starting from 0.3 ml and gradually increasing the dose until normalization of sleep EEG or until a dose of 2.0 is reached ml with further gradual discontinuation of the drug and the total duration of the course of treatment is 3-6 months.