Abstracts

We searched for the immunity changing and autoimmunity correlation in epilepsy patients. Glutamate is a major excitatory neurotransmitter that also triggers a neurodegeneration as a result of excessive stimulation of postsynaptic receptors in epilepsy, brain ischemia and CNStrauma. This process was hypothesized as the major cause for the neuronal loss, chronic inflammatory changes in neurological patients and may leads to the autoantibodies(aAB) to glutamate receptors(GluRs) synthesis. Clinical and experimental data support the role of immune mechanisms during epilepsy pathogenesis., The serum level of lymphocyte subpopulations (obtained by immunocytochemical methods) and the serum level of GluRs-aAB (ELISA, synthetic peptides-analogues of GluR1(AMPA) and NR2A(NMDA) subunits were used as antigens) were estimated in pediatric patients with epilepsy(Epi), mild brain trauma(BT), mitochondrial diseases(MD) and in 20 children of control group(CG)., In Epi(n=60) GluRs-aAB level was significantly higher vs CG(GluR1179[plusmn]15,3c.u.,NR2A161,4[plusmn]14c.u.)(P[lt]0.05). In follow-up studies GluR1aAB level was decreased in E remission, NR2A was still elevated. In acute period of BT(n=20) the GluRs-aAB was high(P[lt]0,05) but the elevation of NR2AaAB was higher than GluR1.In 6-12 mnths follow-up studies GluR1aABlevel was significantly elevated in children with repeated BT and posttraumatic epilepsy. In patients with MD(n=15), even without seizures, the GluRs-aAB was[underline] [/underline]high. Epileptic seizures is the common sign of MD. We have found the significant increase of CD8+lymphocytes, in activation markersCD122+, CD16+56+ and decrease in CD19+ in Epi patients(n=20).We have also found the high level of CD122+, low level of CD19+ in MDpatients(n=5), the decrease in Tlymphocytes subpopulations and the increase of CD122+ in children with BT(n=7). The most immunological deteriorations were related to the temporal lobe focus. We did not find correlation between the immunological changes and the GluRs-aAB levels., Data obtained show that in E, BT and MD glutamate receptors are damaged as a result of excititoxicity. NMDARs dysfunction is observed in all diseases mentioned above. AMPARs damage is more specific for E and the elevation of GluR1aAB level is a risk for E developed in BT and MD. Changes in immological parameters in pediatric patients with epilepsies were not correlated with the glutamate-mediated autoimmunity.,