$398 Thursday, November 10, 2005 Poster Abstracts

Folic A d d and Vitamin B6 was found in 30.7%, 44%, 5.3% of patients and 43.9%, 34.8%, 4.5% of controls respectively with Hyperhomo- cysteinemia. Conclusion: Hyperhomocysteinemia was seen in more number of patients with haemorrhagic stroke than in the control group. Signi- ficant low levels of Vitamin B12 and Folio Acid were observed in Hyperhomocysteinemia in both patient and control group. The number of persons with low Vitamin B6 were negligible in both patient and control group even in presence of Hyperhomocysteinemia.

I167 Relevance of Coagulopathies in Iscbemie Stroke

Gorthi SP ~, Johri S ~, Kumar V 2, Singh KK, 2 Chopra GS 2, Mukherjee JD 2, Kotwal J~. 1Armed Forces Medical College and Command Hospital (SC) Pune, India; 2Army Hospital Delhi Cantt, New Delhi, India

Background: In approximately 4% of cases cerebral infarcts in the young can be attributed to thrombogenic hematological abnormalities. Recently the association between cerebral infarction and deficiencies of the natural anticoagulant system has been recognized. Methods: One hundred and twenty two subjects (Normal-9, Stroke in young-33, Deep Vein Thrombosis-41, thrombosis in abnormal sites-24, Other disorders- 12 and fanfily members-3) were subjected to screening assays for natural anticoagulants-Protein C-PC, Protein S-PS, Anti thrombin III-AT, Factor V Leiden-FVL and Lupus anticoagnlant-LA. Subsequently another 33 stroke in young patients were systematically studied. Results: Natural anticoagulants were found to be deficient alone or in combination in PC-25, PS-60, Antithrombin-III- 5 Factor V Leiden-17 and Lupus anticoagulant positivity in 13 cases. Results of ANOVA of the parametric data did not show any statistical significance. Post-hoe multiple comparisons with Bonferroni correction showed significant association of antithrombin KI in stroke in young and Protein C in deep vein thrombosis. There was no significance of Factor V Leiden positivity and sex of subjects on contingency table analysis.

After applying strict criteria for diagnosis in 33 cases PC was dia- gnosed in three cases, PS in 6 cases, FVL- land LA in 9 cases and these patients presented with recurrent seizures (112), recurrent hemiparesis (16), ataxic hemiparesis (5). Conclusion: Considering the importance of p rothrombotic state caused by deficiency of PC, PS, AT-KI, FVL and LA in the development of cerebral infarcts, we suggest that it should be looked in every young patient in whom no etiological factor can be determined.

1168 Role o f P2X7 Receptors in Cerebral Iseheinia models - in vitro anti in vivo

Guenther, A l, Franke, H 2, Laemle r , A 1, Wirkner, K 2, Groeger-Arndt, H a, Kruegel, U a, Sperlagh, B 3, Wagner, A a, Illes, pa, Schneider, D ~. 1Department Of Neurology, University Of Leipzig, Germany; 2Rudolf-Boehm-Nstitute for Pharmacology and Toxicology, University Of Leipz&, Germany; 3Institute of E~perimental Medicine, Hungarian Academy of Sciences, Budapest, Hungary

Background: Cerebral ischemia is known to cause a massive release of ATP leading to a stimulation of purinergic receptors. We investigated effects of ischemic stimuli induced modulation of P2X 7 receptor- protein expression and functional characteristics in vitro using rat corticoencephalic cell cultures and in vivo employing a permanent focal cerebral ischenfia model. Methods and Results: Although P2X7 receptor-mRNA and -irnmuno- reactivity (IR) in corticoencephalic cultures were increased by serum- deprivation, only a negligible further enhancement occurred after oxygen-glucose deprivation (OGD). However, OGD markedly increased the ATP- and 2'-3'-O-(4-benzoylbenzoyl)-adenosine 5'-tdphosphate (BzATP)-induced release of [3H]GABA. Brilliant Blue G inhibited the release of [3H] GABA caused by ATP application;

the Brilliant Blue G-sensitive, P2X7 receptor-mediated fraction, was much larger after OGD than after normoxia. Furthermore, BzATP caused a more pronounced increase in the frequency of miniature inhibitory postsynaptic currents (mIPSCs) after OGD than after nor- moxia, assembly by stimulating presynaptic P2X7 receptors situated both at the axon terminals of GABAergic non-pyramidal neurons and at GABA-storing astrocytes. After middle cerebral artery occlyusion (MCAO) spontaneously hypertensive rats showed a time dependent neuronal and glial upregulation of P2Xv immunoreactivity in the periinfarct tissue as shovat by inmmnocytochemistry and laser scanlfing and electron microscopy. Application of P2-antagonJsts (like PPADS; pyridoxal-phosphate-6-azophenyl-2",4"-disulfonic acid) lead to a reduced infarct volume and functional recovery measured by telemetric EEG and behavioural testing (T-labyrinth test and MNSS) compared to untreated controls. Conclusion: Ischemic injury leads to a significant modulation of P2X7 receptors. Thus, neuropharmacological targeting of purinergic recep- tor might be a promising neuroprotective strategy in cerebral ischemia.

1169 Hyperbaric oxygen treatment reduces infarct volume due to differential etteets on Glial Cell activation otter permanent Focal Cerebral Iscbenfia in ~pontaneously Hypertensive rats

Guenther, A l, Kueppers-Tiedt, L a, Rossner, S 2, Schneider, PM a, Kunert, I ~, Wagner, A a, Schneider, D ~. 1Department Of Neurology, University Of Leipzig, Germany; 2Paul-Flechsig-Nstitute for Brain research, Department of Neuroehemistry, University of Leipzig, Germany

Background: Permanent middle cerebral artery occlusion (MCAO) causes neurodegeneration and a robust activation of glial cells pri- marily in sensorimotor brain regions of rats. It has been demonstrated that hyperbaric oxygen (HBO) increases oxygen supply to ischemic areas and reduces neuronal cell loss. The effects of HBO treatment on microgliosis and astrogliosis in permanent cerebral ischemia might be critical for neurodegeneration and neuroprotection, respectively. Methods: We used spontaneously hypertensive rats (SH-rats) with permanent MCAO to investigate the time window to start HBO and to compare the effects of different HBO treatment frequencies on infarct volmne and on differences with regard to microgliosis and astrogliosis. Seven days after MCAO the infarct volume was calculated fl'om Nissl-stained brain sections by image analysis. Microglial cells and astrocytes were detected by cytochemical fluorescent labeling and confocal laser scanning microscopy. Results: HBO significantly decreased the infarct volume when used as early as 15, 90 or 180 rain post MCAO by 24%, 16% and 13%, respectively, in the single-treatment group compared to controls. Repetitive HBO treatment (first HBO session 90 rain after MCAO) was not effective. In the single-treatment group we observed a signi- ficantly higher astrocyte immunoreactivity but decreased microglial density in the periinfarct region. These effects of HBO treatment on glial cells were not present in rats where HBO did not reduce the infarct volmne (360 min after MCAO). Conclusion: HBO-induced suppression of microgliosis and aggravated response of astrocytes might contribute to the reported beneficial effects of early HBO treatment in cerebral ischemia.

1170 A case-control study of tile relationship between ABO blood-group and Stroke

Zhao Han 1, Zhen Wang 1, Liang Feng 1. 2Department of Neurology, First Affiliated Hospital of Wenzhou Medical College Wenzhou, China

Objective: To study the relationship of the four phenotypes of ABO blood-group and stroke. Methods A case-control study was used, 1987 inpatients with stroke (1016 cases with cerebral infarction, 755 cases with cerebral hemorrhage, 216 cases with subarachnoid hemorrhage)