Article Text

EXCITOXIC BRAIN DAMAGE IN CHILDREN WITH EPILEPSY AND POTENTIAL OF NEUROPROTECTION
  1. O Globa1,
  2. E Sorokina2,
  3. N Semenova3,
  4. L Kuzenkova1,
  5. V Pinelis2
  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 Clinical Diagnostic, Scientific Center of Children’s Health, RAMS, Moscow, Russia

Abstract

Epilepsy is very common in children. Glutamate is the major excitatory neurotransmitter also responsible for triggering excitotoxicity and neurodegeneration through glutamate receptor overactivation in epilepsy, brain ischaemia etc and may leads to autoantibodies (aAB) to glutamate receptors (GluR) synthesis. Determination of GluR–aAB, ionised calcium (Ca2+) in blood, and quantitative measurements of electroencephalogram (EEG) were performed in 101 patients (2 months–16 years) with epilepsy and in 35 children of the control group. GluR–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 the GluR1–aAB serum level was revealed in epilepsy patients versus controls (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 was measured in children with generalised seizures. A significant negative correlation between the GluR1–aAB content and Ca2+ level in blood of children with epilepsy 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 epilepsy patients in addition to anticonvulsant treatment. The GluR1–aAB level in patients treated with glycine was significantly lower than in children with other therapy or without it (p<0.05).

Conclusions In epilepsy glutamate receptors are damaged as a result of excititoxicity, EEG changes reflect this deterioration. Glycine demonstrates the membrane protector quality that may be used as an additional therapy for epilepsy.

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