11 research outputs found
The policy of conducting patiens with febrile convultions
Π’ΠΎ substantiate the policy of conducting patients with febrile convultions in different phases of rendering aid catamnesis study of one hundred and sixty three children with febrile convulsions in anamnesis were conducted. The duration of catamnesis varied from eight to twelve years. The clinical data as well as the results of additional methods of study (EEG and MRT) of the head brain were analised. Comparison of two groups of children with clinical outcome of febrile convultions into epilepsy (n=24) and benignant outcome (n=139) were conducted. The results of the study testify to the fact that patients with simple febrile convulsions do not need EEG and MRT of the head brain, but children with complex ( atypical) febile convulsions do need conducting these tests. Medical diagnostic and organisation measures in different phases of rendering medical aid to children with febrile convulsions (in the outpatient and hospital setting) recording the phase and stage of the disease have been worked out.ΠΠ»Ρ ΠΎΠ±ΠΎΡΠ½ΠΎΠ²Π°Π½ΠΈΡ ΡΠ°ΡΠΊΠΈ Π²Π΅Π΄Π΅Π½ΠΈΡ Π±ΠΎΠ»ΡΠ½ΡΡ
Ρ ΡΠ΅Π±ΡΠΈΠ»ΡΠ½ΡΠΌΠΈ ΡΡΠ΄ΠΎΡΠΎΠ³Π°ΠΌΠΈ Π½Π° ΡΠ°Π·Π»ΠΈΡΠ½ΡΡ
ΡΡΠ°ΠΏΠ°Ρ
ΠΎΠΊΠ°Π·Π°Π½ΠΈΡ ΠΈΠΌ ΠΌΠ΅Π΄ΠΈΡΠΈΠ½ΡΠΊΠΎΠΉ ΠΏΠΎΠΌΠΎΡΠΈ Π±ΡΠ»ΠΈ ΠΏΡΠΎΠ²Π΅Π΄Π΅Π½Ρ ΠΊΠ°ΡΠ°ΠΌΠ½Π΅ΡΡΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΡ 163 Π΄Π΅ΡΠ΅ΠΉ Ρ ΡΠ΅Π±ΡΠΈΠ»ΡΠ½ΡΠΌΠΈ ΡΡΠ΄ΠΎΡΠΎΠ³Π°ΠΌΠΈ Π² Π°Π½Π°ΠΌΠ½Π΅Π·Π΅. ΠΠ»ΠΈΡΠ΅Π»ΡΠ½ΠΎΡΡΡ ΠΊΠ°ΡΠ°ΠΌΠ½Π΅Π·Π° Π²Π°ΡΡΠΈΡΠΎΠ²Π°Π»Π° ΠΎΡ 8 Π΄ΠΎ 12 Π»Π΅Ρ. ΠΠ½Π°Π»ΠΈΠ·ΠΈΡΠΎΠ²Π°Π»ΠΈΡΡ ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΈΠ΅ Π΄Π°Π½Π½ΡΠ΅, Π° ΡΠ°ΠΊΠΆΠ΅ ΡΠ΅Π·ΡΠ»ΡΡΠ°ΡΡ Π΄ΠΎΠΏΠΎΠ»Π½ΠΈΡΠ΅Π»ΡΠ½ΡΡ
ΠΌΠ΅ΡΠΎΠ΄ΠΎΠ² ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΡ (ΠΠΠ ΠΈ ΠΠ Π’ Π³ΠΎΠ»ΠΎΠ²Π½ΠΎΠ³ΠΎ ΠΌΠΎΠ·Π³Π°). ΠΡΠΎΠ²Π΅Π΄Π΅Π½Ρ ΡΡΠ°Π²Π½Π΅Π½ΠΈΡ Π΄Π²ΡΡ
Π³ΡΡΠΏΠΏ - Π΄Π΅ΡΠ΅ΠΉ Ρ ΠΈΡΡ
ΠΎΠ΄ΠΎΠΌ ΡΠ΅Π±ΡΠΈΠ»ΡΠ½ΡΡ
ΡΡΠ΄ΠΎΡΠΎΠ³ Π² ΡΠΏΠΈΠ»Π΅ΠΏΡΠΈΡ (n=24) ΠΈ Π΄ΠΎΠ±ΡΠΎΠΊΠ°ΡΠ΅ΡΡΠ²Π΅Π½Π½ΡΠΌ ΠΈΡΡ
ΠΎΠ΄ΠΎΠΌ (n=139). ΠΠΎΠ»ΡΡΠ΅Π½Π½ΡΠ΅ ΡΠ΅Π·ΡΠ»ΡΡΠ°ΡΡ ΡΠ²ΠΈΠ΄Π΅ΡΠ΅Π»ΡΡΡΠ²ΡΡΡ ΠΎ ΡΠΎΠΌ, ΡΡΠΎ ΠΏΠ°ΡΠΈΠ΅Π½ΡΡ Ρ ΠΏΡΠΎΡΡΡΠΌΠΈ ΡΠ΅Π±ΡΠΈΠ»ΡΠ½ΡΠΌΠΈ ΡΡΠ΄ΠΎΡΠΎΠ³Π°ΠΌΠΈ Π½Π΅ Π½ΡΠΆΠ΄Π°ΡΡΡΡ Π² ΠΏΡΠΎΠ²Π΅Π΄Π΅Π½ΠΈΠΈ ΠΠΠ ΠΈ ΠΠ Π’ Π³ΠΎΠ»ΠΎΠ²Π½ΠΎΠ³ΠΎ ΠΌΠΎΠ·Π³Π°, Π° Π΄Π΅ΡΡΠΌ ΡΠΎ ΡΠ»ΠΎΠΆΠ½ΡΠΌΠΈ (Π°ΡΠΈΠΏΠΈΡΠ½ΡΠΌΠΈ) ΡΠ΅Π±ΡΠΈΠ»ΡΠ½ΡΠΌΠΈ ΡΡΠ΄ΠΎΡΠΎΠ³Π°ΠΌΠΈ Π½Π΅ΠΎΠ±Ρ
ΠΎΠ΄ΠΈΠΌΠΎ ΠΏΡΠΎΠ²Π΅Π΄Π΅Π½ΠΈΠ΅ ΡΡΠΈΡ
ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΠΉ. Π Π°Π·ΡΠ°Π±ΠΎΡΠ°Π½Ρ Π»Π΅ΡΠ΅Π±Π½ΠΎ-Π΄ΠΈΠ°Π³Π½ΠΎΡΡΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΠΈ ΠΎΡΠ³Π°Π½ΠΈΠ·Π°ΡΠΈΠΎΠ½Π½ΡΠ΅ ΠΌΠ΅ΡΠΎΠΏΡΠΈΡΡΠΈΡ Π½Π° ΡΠ°Π·Π»ΠΈΡΠ½ΡΡ
ΡΡΠ°ΠΏΠ°Ρ
ΠΎΠΊΠ°Π·Π°Π½ΠΈΡ ΠΌΠ΅Π΄ΠΈΡΠΈΠ½ΡΠΊΠΎΠΉ ΠΏΠΎΠΌΠΎΡΠΈ Π΄Π΅ΡΡΠΌ Ρ ΡΠ΅Π±ΡΠΈΠ»ΡΠ½ΡΠΌΠΈ ΡΡΠ΄ΠΎΡΠΎΠ³Π°ΠΌΠΈ (Π°ΠΌΠ±ΡΠ»Π°ΡΠΎΡΠ½ΡΠΉ ΠΈ Π³ΠΎΡΠΏΠΈΡΠ°Π»ΡΠ½ΡΠΉ) Ρ ΡΡΠ΅ΡΠΎΠΌ ΡΠ°Π·Ρ ΠΈ ΡΡΠ°Π΄ΠΈΠΈ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΡ
The prognosis for children's epilepsy with febrile seisures
In search of significant diagnostic criterion to prognosticate epilepsy there has been analysed the role of perinatal pathology, the hereditary load in febrile seisures and epilepsy, the clinical data and results of additional methods of research ( EEG, MRT of the head brain) of children with febrile seisures (FS) in the anamnesis. There has been carried out catamnesis research of 163 children having febrile seisures in their anamnesis. The duration of catamnesis varied from 8 to 12 years old. There has been carried out the comparison of 2 groups - children having febrile seisures with the outcome to epilepsy (n=24) and benign outcome (n=139). In accordance with the research there have been taken the indices in which the groups under tests varied statistically significant- heredity, anamnestic record for epilepsy, focal character of the febrile seisures, abnormalities in neurological status, changes in EEG and MRT of the head brain. They have been used to maintain models for prediction of epilepsy development. The results showed that it is possible to prognose the development of epilepsy on the basis of the results of the EEG and heredity load. The most important diagnostic rate for the development of epilepsy is the epileptiform activity on EEG.ΠΠ»Ρ ΠΏΠΎΠΈΡΠΊΠ° Π΄ΠΎΡΡΠΎΠ²Π΅ΡΠ½ΡΡ
Π΄ΠΈΠ°Π³Π½ΠΎΡΡΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΊΡΠΈΡΠ΅ΡΠΈΠ΅Π² ΠΏΡΠΎΠ³Π½ΠΎΠ·ΠΈΡΠΎΠ²Π°Π½ΠΈΡ ΡΠΏΠΈΠ»Π΅ΠΏΡΠΈΠΈ Π±ΡΠ»Π° ΠΏΡΠΎΠ°Π½Π°Π»ΠΈΠ·ΠΈΡΠΎΠ²Π°Π½Π° ΡΠΎΠ»Ρ ΠΏΠ΅ΡΠΈΠ½Π°ΡΠ°Π»ΡΠ½ΠΎΠΉ ΠΏΠ°ΡΠΎΠ»ΠΎΠ³ΠΈΠΈ, Π½Π°ΡΠ»Π΅Π΄ΡΡΠ²Π΅Π½Π½ΠΎΠΉ ΠΎΡΡΠ³ΠΎΡΠ΅Π½Π½ΠΎΡΡΠΈ ΠΏΠΎ ΡΠ΅Π±ΡΠΈΠ»ΡΠ½ΡΠΌ ΡΡΠ΄ΠΎΡΠΎΠ³Π°ΠΌ ΠΈ ΡΠΏΠΈΠ»Π΅ΠΏΡΠΈΠΈ, ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΈΡ
Π΄Π°Π½Π½ΡΡ
ΠΈ ΡΠ΅Π·ΡΠ»ΡΡΠ°ΡΠΎΠ² Π΄ΠΎΠΏΠΎΠ»Π½ΠΈΡΠ΅Π»ΡΠ½ΡΡ
ΠΌΠ΅ΡΠΎΠ΄ΠΎΠ² ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΡ (ΠΠΠ ΠΈ ΠΠ Π’ Π³ΠΎΠ»ΠΎΠ²Π½ΠΎΠ³ΠΎ ΠΌΠΎΠ·Π³Π°) Ρ Π΄Π΅ΡΠ΅ΠΉ, ΠΈΠΌΠ΅ΡΡΠΈΡ
ΡΠ΅Π±ΡΠΈΠ»ΡΠ½ΡΠ΅ ΡΡΠ΄ΠΎΡΠΎΠ³ΠΈ (Π€Π‘) Π² Π°Π½Π°ΠΌΠ½Π΅Π·Π΅. ΠΡΠΎΠ²Π΅Π΄Π΅Π½Ρ ΠΊΠ°ΡΠ°ΠΌΠ½Π΅ΡΡΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΡ 163 Π΄Π΅ΡΠ΅ΠΉ Ρ ΡΠ΅Π±ΡΠΈΠ»ΡΠ½ΡΠΌΠΈ ΡΡΠ΄ΠΎΡΠΎΠ³Π°ΠΌΠΈ Π² Π°Π½Π°ΠΌΠ½Π΅Π·Π΅. ΠΠ»ΠΈΡΠ΅Π»ΡΠ½ΠΎΡΡΡ ΠΊΠ°ΡΠ°ΠΌΠ½Π΅Π·Π° Π²Π°ΡΡΠΈΡΠΎΠ²Π°Π»Π° ΠΎΡ 8 Π΄ΠΎ 12 Π»Π΅Ρ. ΠΡΠΎΠ²Π΅Π΄Π΅Π½Ρ ΡΡΠ°Π²Π½Π΅Π½ΠΈΡ Π΄Π²ΡΡ
Π³ΡΡΠΏΠΏ - Π΄Π΅ΡΠ΅ΠΉ Ρ ΠΈΡΡ
ΠΎΠ΄ΠΎΠΌ ΡΠ΅Π±ΡΠΈΠ»ΡΠ½ΡΡ
ΡΡΠ΄ΠΎΡΠΎΠ³ Π² ΡΠΏΠΈΠ»Π΅ΠΏΡΠΈΡ (ΠΏ=24) ΠΈ Π΄ΠΎΠ±ΡΠΎΠΊΠ°ΡΠ΅ΡΡΠ²Π΅Π½Π½ΡΠΌ ΠΈΡΡ
ΠΎΠ΄ΠΎΠΌ (ΠΏ=139). ΠΠΎ ΡΠ΅Π·ΡΠ»ΡΡΠ°ΡΠ°ΠΌ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΡ Π±ΡΠ»ΠΈ Π²Π·ΡΡΡ ΠΏΠΎΠΊΠ°Π·Π°ΡΠ΅Π»ΠΈ, ΠΏΠΎ ΠΊΠΎΡΠΎΡΡΠΌ ΠΈΡΡΠ»Π΅Π΄ΡΠ΅ΠΌΡΠ΅ Π³ΡΡΠΏΠΏΡ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² ΡΠ°Π·Π»ΠΈΡΠ°Π»ΠΈΡΡ ΡΡΠ°ΡΠΈΡΡΠΈΡΠ΅ΡΠΊΠΈ Π·Π½Π°ΡΠΈΠΌΠΎ - ΡΡΠΎ Π½Π°ΡΠ»Π΅Π΄ΡΡΠ²Π΅Π½Π½Π°Ρ ΠΎΡΡΠ³ΠΎΡΠ΅Π½Π½ΠΎΡΡΡ ΠΏΠΎ ΡΠΏΠΈΠ»Π΅ΠΏΡΠΈΠΈ, ΡΠΎΠΊΠ°Π»ΡΠ½ΡΠΉ Ρ
Π°ΡΠ°ΠΊΡΠ΅Ρ ΡΠ΅Π±ΡΠΈΠ»ΡΠ½ΠΎΠ³ΠΎ ΠΏΡΠΈΡΡΡΠΏΠ°, Π½Π°ΡΡΡΠ΅Π½ΠΈΡ Π² Π½Π΅Π²ΡΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΎΠΌ ΡΡΠ°ΡΡΡΠ΅, ΠΈΠ·ΠΌΠ΅Π½Π΅Π½ΠΈΡ Π½Π° ΠΠΠ ΠΈ ΠΠ Π’ Π³ΠΎΠ»ΠΎΠ²Π½ΠΎΠ³ΠΎ ΠΌΠΎΠ·Π³Π°. ΠΠ½ΠΈ Π±ΡΠ»ΠΈ ΠΈΡΠΏΠΎΠ»ΡΠ·ΠΎΠ²Π°Π½Ρ Π΄Π»Ρ ΠΏΠΎΡΡΡΠΎΠ΅Π½ΠΈΡ ΠΌΠΎΠ΄Π΅Π»Π΅ΠΉ ΠΏΡΠΎΠ³Π½ΠΎΠ·ΠΈΡΠΎΠ²Π°Π½ΠΈΡ ΡΠ°Π·Π²ΠΈΡΠΈΡ ΡΠΏΠΈΠ»Π΅ΠΏΡΠΈΠΈ. Π Π°ΡΡΠ΅ΡΡ ΠΏΠΎΠΊΠ°Π·Π°Π»ΠΈ, ΡΡΠΎ ΠΏΡΠΎΠ³Π½ΠΎΠ·ΠΈΡΠΎΠ²Π°ΡΡ ΡΠ°Π·Π²ΠΈΡΠΈΠ΅ ΡΠΏΠΈΠ»Π΅ΠΏΡΠΈΠΈ Π²ΠΎΠ·ΠΌΠΎΠΆΠ½ΠΎ Π½Π° ΠΎΡΠ½ΠΎΠ²Π°Π½ΠΈΠΈ Π΄Π°Π½Π½ΡΡ
ΠΎ Π½Π°ΡΠ»Π΅Π΄ΡΡΠ²Π΅Π½Π½ΠΎΠΉ ΠΎΡΡΠ³ΠΎΡΡΠ½Π½ΠΎΡΡΠΈ ΠΏΠΎ ΡΠΏΠΈΠ»Π΅ΠΏΡΠΈΠΈ ΠΈ ΡΠ΅Π·ΡΠ»ΡΡΠ°ΡΠ°Ρ
ΠΠΠ. ΠΠ°ΠΈΠ±ΠΎΠ»Π΅Π΅ Π²Π°ΠΆΠ½ΡΠΌ Π΄ΠΈΠ°Π³Π½ΠΎΡΡΠΈΡΠ΅ΡΠΊΠΈΠΌ ΠΏΠΎΠΊΠ°Π·Π°ΡΠ΅Π»Π΅ΠΌ ΡΠ°Π·Π²ΠΈΡΠΈΡ ΡΠΏΠΈΠ»Π΅ΠΏΡΠΈΠΈ ΡΠ²Π»ΡΠ΅ΡΡΡ ΡΠΏΠΈΠ»Π΅ΠΏΡΠΈΡΠΎΡΠΌΠ½Π°Ρ Π°ΠΊΡΠΈΠ²Π½ΠΎΡΡΡ Π½Π° ΠΠΠ
Febrile children's convulsions and risk of emergence
There has been studies of clinical peculiarities of febrile children's convulsions and the estimation of the additional research data and the factors of the emergence. There has been examined and observed 109 children aged from three months to five having febrile convulsions. Age, sex, genetic predisposition to febrile attacks and epilepsy were analysed along with perinatal anamnesis, the temperature at which the attacks appear, the background diseases, the character of the attacks, the neurological status, the additional methods of research of the head brain (EEG, MRI). The comparison group included the children of the same age suffering epilepsy. Statistically important factor of the risk of the beginning of febrile attacks is the burden of the family anamnesis in febrile convulsions and the marker of the higher probability of the beginning is perinatal pathology (chronic hypoxia of the baby). Additional factors of the risk are frequent acute respiratory diseases.ΠΠ·ΡΡΠ°Π»ΠΈΡΡ ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΠΎΡΠΎΠ±Π΅Π½Π½ΠΎΡΡΠΈ ΡΠ΅Π±ΡΠΈΠ»ΡΠ½ΡΡ
ΠΏΡΠΈΡΡΡΠΏΠΎΠ² Ρ Π΄Π΅ΡΠ΅ΠΉ Ρ ΠΎΡΠ΅Π½ΠΊΠΎΠΉ Π΄Π°Π½Π½ΡΡ
Π΄ΠΎΠΏΠΎΠ»Π½ΠΈΡΠ΅Π»ΡΠ½ΡΡ
ΠΌΠ΅ΡΠΎΠ΄ΠΎΠ² ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΡ, Π° ΡΠ°ΠΊΠΆΠ΅ ΡΠ°ΠΊΡΠΎΡΡ ΠΈΡ
Π²ΠΎΠ·Π½ΠΈΠΊΠ½ΠΎΠ²Π΅Π½ΠΈΡ. ΠΡΠΎΠ²Π΅Π΄Π΅Π½ Π°Π½Π°Π»ΠΈΠ· Π½Π°Π±Π»ΡΠ΄Π΅Π½ΠΈΡ 109 Π΄Π΅ΡΠ΅ΠΉ Ρ ΡΠ΅Π±ΡΠΈΠ»ΡΠ½ΡΠΌΠΈ ΡΡΠ΄ΠΎΡΠΎΠ³Π°ΠΌΠΈ Π² Π²ΠΎΠ·ΡΠ°ΡΡΠ΅ ΠΎΡ 3 ΠΌΠ΅ΡΡΡΠ΅Π² Π΄ΠΎ 5 Π»Π΅Ρ. ΠΠ½Π°Π»ΠΈΠ·ΠΈΡΠΎΠ²Π°Π»ΠΈΡΡ - Π²ΠΎΠ·ΡΠ°ΡΡ, ΠΏΠΎΠ», Π³Π΅Π½Π΅ΡΠΈΡΠ΅ΡΠΊΠ°Ρ ΠΏΡΠ΅Π΄ΡΠ°ΡΠΏΠΎΠ»ΠΎΠΆΠ΅Π½Π½ΠΎΡΡΡ ΠΏΠΎ ΡΠ΅Π±ΡΠΈΠ»ΡΠ½ΡΠΌ ΡΡΠ΄ΠΎΡΠΎΠ³Π°ΠΌ ΠΈ ΡΠΏΠΈΠ»Π΅ΠΏΡΠΈΠΈ, ΠΏΠ΅ΡΠΈΠ½Π°ΡΠ°Π»ΡΠ½ΡΠΉ Π°Π½Π°ΠΌΠ½Π΅Π·, ΡΠ΅ΠΌΠΏΠ΅ΡΠ°ΡΡΡΠ° Π²ΠΎΠ·Π½ΠΈΠΊΠ½ΠΎΠ²Π΅Π½ΠΈΡ ΡΠ΅Π±ΡΠΈΠ»ΡΠ½ΡΡ
ΠΏΡΠΈΡΡΡΠΏΠΎΠ², ΡΠΎΠ½ΠΎΠ²ΡΠ΅ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΡ, Ρ
Π°ΡΠ°ΠΊΡΠ΅Ρ ΠΏΡΠΈΡΡΡΠΏΠΎΠ², Π½Π΅Π²ΡΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΈΠΉ ΡΡΠ°ΡΡΡ, Π΄Π°Π½Π½ΡΠ΅ Π΄ΠΎΠΏΠΎΠ»Π½ΠΈΡΠ΅Π»ΡΠ½ΡΡ
ΠΌΠ΅ΡΠΎΠ΄ΠΎΠ² ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΡ (ΠΠΠ, ΠΠ Π’ Π³ΠΎΠ»ΠΎΠ²Π½ΠΎΠ³ΠΎ ΠΌΠΎΠ·Π³Π°). Π Π³ΡΡΠΏΠΏΡ ΡΡΠ°Π²Π½Π΅Π½ΠΈΡ Π²ΠΎΡΠ»ΠΈ Π΄Π΅ΡΠΈ Ρ ΡΠΏΠΈΠ»Π΅ΠΏΡΠΈΠ΅ΠΉ ΡΠΎΠ³ΠΎ ΠΆΠ΅ Π²ΠΎΠ·ΡΠ°ΡΡΠ°. Π‘ΡΠ°ΡΠΈΡΡΠΈΡΠ΅ΡΠΊΠΈ Π·Π½Π°ΡΠΈΠΌΡΠΌ ΡΠ°ΠΊΡΠΎΡΠΎΠΌ ΡΠΈΡΠΊΠ° Π²ΠΎΠ·Π½ΠΈΠΊΠ½ΠΎΠ²Π΅Π½ΠΈΡ ΡΠ΅Π±ΡΠΈΠ»ΡΠ½ΡΡ
ΡΡΠ΄ΠΎΡΠΎΠ³ Ρ Π΄Π΅ΡΠ΅ΠΉ ΡΠ²Π»ΡΠ΅ΡΡΡ ΠΎΡΡΠ³ΠΎΡΠ΅Π½Π½ΡΠΉ ΡΠ΅ΠΌΠ΅ΠΉΠ½ΡΠΉ Π°Π½Π°ΠΌΠ½Π΅Π· ΠΏΠΎ ΡΠ΅Π±ΡΠΈΠ»ΡΠ½ΡΠΌ ΠΏΡΠΈΡΡΡΠΏΠ°ΠΌ, Π° ΠΌΠ°ΡΠΊΠ΅ΡΠΎΠΌ ΠΏΠΎΠ²ΡΡΠ΅Π½Π½ΠΎΠΉ Π²Π΅ΡΠΎΡΡΠ½ΠΎΡΡΠΈ ΠΈΡ
Π²ΠΎΠ·Π½ΠΈΠΊΠ½ΠΎΠ²Π΅Π½ΠΈΡ - ΠΏΠ΅ΡΠΈΠ½Π°ΡΠ°Π»ΡΠ½Π°Ρ ΠΏΠ°ΡΠΎΠ»ΠΎΠ³ΠΈΡ (Ρ
ΡΠΎΠ½ΠΈΡΠ΅ΡΠΊΠ°Ρ Π³ΠΈΠΏΠΎΠΊΡΠΈΡ ΠΏΠ»ΠΎΠ΄Π°). Π ΠΊΠ°ΡΠ΅ΡΡΠ²Π΅ Π΄ΠΎΠΏΠΎΠ»Π½ΠΈΡΠ΅Π»ΡΠ½ΠΎΠ³ΠΎ ΡΠ°ΠΊΡΠΎΡΠ° ΡΠΈΡΠΊΠ° ΠΌΠΎΠΆΠ½ΠΎ ΡΠ°ΡΡΠΌΠ°ΡΡΠΈΠ²Π°ΡΡ ΡΠ°ΡΡΡΠ΅ ΠΎΡΡΡΡΠ΅ ΡΠ΅ΡΠΏΠΈΡΠ°ΡΠΎΡΠ½ΡΠ΅ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΡ Ρ Π΄Π΅ΡΠ΅ΠΉ
THE RISK FACTORS IN RELAPSE OF FEBRILE CONVULSIONS
The factors of risk in relapse of febrile convulsions have been studied: age, sex, perinatal anamnesis, heredity on febrile attacks, epilepsies, neurological status, the results in analysis (EEG, MRI of the head brain), the temperature, the type of the illness, frequency of the illness, the character of febrile paroxysm. 109 children have been investigated aged from three months to five years suffering from febrile attacks. There has been held the comparison of the groups of children with different quantity of episodes of febrile bouts (with one, two, three and more). The results of the observations testify to high degree of credibility the influence of relapsing course of febrile attacks of the following factors: hereditary burden on febrile attacks, the presence of perinatal pathology, frequent acute respiratory diseases
Risk factors for transition of febrile convulsions to epilepsy
Object: to assess a relationship between febrile convulsions (FC) and epilepsy. Patients and methods. The role of perinatal hereditary diseases, a family history of FC and epilepsy, as well as clinical findings and the results of supplementary studies (electroencephalography and brain magnetic resonance imaging) were analyzed in children with a history of FC. One hundred and sixty-three children with a history of FC were followed up for 8 to 12 years. Two groups of children with transition of febrile convulsions to epilepsy (n=24) and with a good outcome (n=139) were compared. Results and discussion. The findings suggest that factors, such as a family history of epilepsy, the focal pattern of FC, and neurologic changes, highly significantly affect the transformation of FC to epilepsy. Changes in epileptiform EEG activity and abnormal structural neuroimaging are markers for the high probability of transition of febrile convulsions to epilepsy
HEMICONVULSION-HEMIPLEGIA-EPILEPSY SYNDROME (HHE SYNDROME) (A LECTURE)
Hemiconvulsion-hemiplegia-epilepsy syndrome (HHE syndrome) β polyetiologic disease, with onset in childhood, characterized by the triad of symptoms: 1) prolonged convulsive seizures (usually on background of fever), involving one half of the body (hemiconvulsions); 2) acute hemiparesis occurring immediately after seizures (on the side of convulΒsions); 3) symptomatic focal epilepsy, occurring in the sequel. The authors discuss in detail different aspects of the disease, including etiology, pathogenesis, diagnostic approaches, differential diagnosis, and approaches to treatment (including prevention and therapy of the disease) and outcome
CLINICAL AND ELECTROENCEPHALOGRAPHIC SEMIOLOGY OF MYOCLONIC-ATONIC SEIZURES
Abstract: myoclonic-atonic seizures (MAS) β short epileptic generalized seizures in the form of sudden falling spells (or drop attacks). Inour study were vealed MAS in 1.3% of all cases of epilepsy with onset of seizures before 18 years old (n=1261). Predominance of man among the patients was revealed (76.5% men versus 23.5% woman). The most often in the patients with MAS myoclonic-astatic epilepsy (MAE) was diagnosed β 41,2% of cases. Symptomatic and cryptogenic forms of focal epilepsy were diagnosed in 35.2% of the patients. Lennox-Gastaut syndrome was revealed in 23.6% of cases. Onset of epilepsy with MAS varied widely β from 9 month to 6 year soflife; middle age of onset was 3.4 yearsΒ±1.28 years. In all the cases MAS occurred in combination with other types of seizures: there can be any of 9 differenttypes of seizures. The most often myoclonic seizures (70.6% of cases), generalized convulsive seizures (47.1%) and absences (47.1%) were registered. Remission was achieved in 64.7% cases of epilepsy, associated with MAS. Reduction of seizure frequency β₯50% on antiepileptic treatment was achieved in 29.4% of the patients. Only in one patient (5.9%) the therapy was not effective. Our study demonstrated different efficacyof antiepileptic drugs in the treatment of different epileptic syndromes, associated with MAS
ELECTROENCEPHALOGRAPHIC CHANGES WITH DRAVET SYNDROME
Dravet syndrome (DS, severe myoclonic epilepsy of early infancy) is epileptic encephalopathy with onset in the first year of life, manifestedΒ with febrile and afebrile generalized and focal seizures, with the presence of myoclonic paroxysms in typical cases, mental retardation, andΒ resistance to antiepileptic therapy. The disease was for the first time described by Ch. Dravet in 1978 in France, then, in details, by Π‘h. DravetΒ et al. in 1982. In the classification of 1989, DS held a particular place being attributed to the forms of epilepsy that have both generalizedΒ and focal clinical manifestations. According to Proposed diagnostic scheme for people with epileptic seizures and with epilepsy (2001), thisΒ disease is attributed to epileptic encephalopathies of early infancy.Β The main reason of DS development is a mutation in the SCN1A gene revealed with most (but not all) patients. It is assumed that there areΒ certain other mutations that determine DS development, in particular, the GABRG2 mutation.Β Polymorphism of epileptic seizures is typical of the DS: febrile seizures, focal motor (including hemiclonic and secondarily generalized), generalizedΒ tonic and clonic, alternating hemiconvulsions, myoclonic, atypical absences, focal dialeptic seizures, as well as epileptic status.Β The prognosis of the disease is severe. In most cases, seizures continue to occur in adult life but with lower frequency than in childhood.Β The authors review the issues of etiology and pathogenesis in details, as well as clinical manifestations, diagnostics, and treatment of the DS.Β A particular emphasis is given to pathological changes on electroencephalogram (EEG) of patients with DS.Β Distinct slowing of background activity, prevalence of multiregional epileptiform activity, regional slowing, and severe photosensitivity (patternΒ sensitivity) are the most prognostically unfavorable EEG patterns of the DS