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NEUROCHEMICAL INVESTIGATION IN CHILDREN WITH EPILEPSY
  1. O Globa1,
  2. E Sorokina2,
  3. N Semenova3,
  4. O Maslova1,
  5. L Kuzenkova1,
  6. V Pinelis1
  1. 1Department of Neurology, Scientific Center of Children’s Health, RAMS, Moscow, Russia
  2. 2Laboratory of Membranology and Genetic Group, Scientific Center of Children’s Health, RAMS, Moscow, Russia
  3. 3Division of Neurophysiology, Scientific Center of Children’s Health, RAMS, Moscow, Russia

Abstract

Objective Epilepsy (E) is very common in children. Glutamate (Glu) is the major excitatory neurotransmitter also responsible for triggering excitotoxicity and neurodegeneration through glutamate receptor overactivation in E, brain ischemia etc. and may lead to the autoantibodies (aAB) to glutamate receptor (GluRs) synthesis.

Method Determination of GluRs-aAB, ionized calcium (Ca2+) in blood, and quantitative measurements of electroencephalogram (EEG) were performed in 101 patients (2 months–16 years) with E and in 35 children of control group (CG). GluRs-aAB were estimated by ELISA, synthetic peptide-analogues of GluR1 subunit were used as antigens.

Results A significant increase of more than 1.5–2 times of GluR1-aAB serum level was revealed in E patients vs CG (p<0.05) and was observed in 92% of cases. The serum level of GluR1 was directly correlated with frequency of seizures and epileptiform activity on the EEG. The highest levels of spectral power and aAB were measured in children with generalized S. A significant negative correlation between the GluR1-aAB content and Ca2+ level in blood of children with E was also revealed. These results led us to consider a new therapeutic strategy to reduce neurotransmitter imbalance for activation of an inhibitory system by using sublingual glycine in 45 E patients in addition to the anticonvulsant treatment. The GluR1-aAB level in patients treated with glycine was significantly lower than in children without it (p<0.05).

Conclusion In E glutamate receptors are damaged as a result of excititoxicity; EEG changes reflects this deterioration. Gly demonstrates the membrane protector quality which may be used as an additional therapy for epilepsy.

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