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Vascular dementia is the primary cause of senile dementia in our country,which is the only preventable type of dementia now.qqais article reviews the advances in research on pathophysiology and imaging of vascular dementia.
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Objective To study the relationship between generalized tonic clonic epilepsy of different frequence seizure and erythrocyte ATPase activity.Methods We measured Na +/K + ATPase,Mg 2+ ATPase,Ca 2+ ATPase activity of 68 patients with generalized tonic clonic seizure who were divided into 3 groups by different frequence:Status epilepsy group (SE) for 26 cases,Frequency epilepsy (FE) group for 22 cases,epilepsy (EP) group for 20 cases and the normal controls for 35 cases.Results Erythrocyte Na +/K + ATPase in SE, FE group decreased,as compared with EP group,the normal control group, there was remar kable difference( P
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Objective To investigate the clinical characteristics of Landau-Kleffner syndrome.Methods The clinical data of 3 patients with Landau-Kleffner syndrome was analyzed retrospectively.Results The clinical features of 3 cases presented acquired aphasia,epileptic attack and psychical behaviour abnormality.The EEG showed foci spike wave discharge,while the CT and MRI examination were normal.The epileptic attacks were controlled after treatment,but the recovery of aphasia and psychical behaviour abnormality was poor.Conclusions Acquired aphasia and epileptic attack are the clinical characteristics of Landau-Kleffner syndrome.The EEG shows spike wave dischargeis.Partial recovery can be obtained post-treatment.
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Objective To explore the expression and significance of adhesion molecules ?2 integrin CD11c, CD18 in the polymorphonuclear neutrophils (PMN) and mononuclear leukocytes (MNL) of peripheral blood in patients with acute ischemic stroke (AIS).Methods Using indirect immunofluorescence and adopting a flow cytometry, the expressions of CD11c, CD18 in PMN and MNL in peripheral blood were measured within 72 h and 7 d after onset in 28 patients and 28 healthy controls.Results In AIS group, the expressions of CD11c, CD18 in PMN and MNL within 72 h ( 20.82?5.88, 218.25?89.00, 34.78?14.56 and 286.75?95.50, respectively) and at 7 d ( 18.60?5.52, 185.52?68.44, 31.97?14.47and 247.00?88.06, respectively) were significantly higher than those of normal control group ( 15.63?3.01, 150.76?41.20, 20.20?8.50 and 186.38?52.97, respectively)(all P
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Objective To investigate the role of apoptosis and apoptotic proteins p53,p21 and Bax in mechanisms of brain ischemic tolerance in rats.Methods In our study the models of focal-focal type brain ischemic preconditioning were maded by occlusion middle cerebral artery using an intraluminal filament method. Infarct sizes were measured by image analysis system.Neuronal apoptosis was identified by TUNEL staining and expressions of p53, p21 and Bax were analyzed by immunohistochemistry.Results Compared with the lethal ischemic group, the volume of infarct was greatly reduced when MCAO 20 minutes was performed as ischemic preconditioning( P
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Objective To detect the levels of MBP and IL 16 in cerebrospinal fluid(CSF) and serum, investigate the correlation between them and the role in multiple sclerosis attacking process.Methods The levels of MBP and IL 16 of cerebral fluid and serum of 31 patients with MS were detected by ELISA and compared with those of 24 cases of inflammatory demyelinating polyneuropathy or 22 cases of healthy persons.Results CSF and serum levels of MBP were found increaed significantly in MS patients compared with those in IDP and in healthy controls(HC)(all P 0.05).The concentrations of MBP in CSF of MS significantly correlated with that of IL 16 in CSF( r =0.468, P 0.05).The concentration of MBP in CSF of MS significantly correlated with CSF that in serum( r =0.505, P 0.05).Conclusion MBP is one of the autoantigens that induce MS,IL 16 may be mainly produced in CNS due to MBP stimulation; IL 16 may act within CNS.
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Objective To investigate the effects of Topiramate(TPM) on activity of SOD and concentration of MDA in blood serum and the changes of the nerve function scores after cerebral ischemia/perfusion in rats. Methods Male Sprague-Dawley rats were randomly divided into ischemia/perfusion group, TPM group and sham-operation group. Rat models of transient focal cerebral ischemia were made by 2 h occlusion of right middle cerebral artery occlusion and reperfusion for 24 h.Rats in TPM group were injected TPM(8 mg/ml,80 mg/kg)in the beginning of the artery occlusion and the reperfusion. The rats were sacrificed after they were evaluated by the nerve function deficiency scores. The activity of SOD and concentration of MDA in blood serum were measured.Results The activity of SOD and concentration of MDA in blood serum in ischemia/perfusion group were (157.72?19.04)U/ml and (7.45?0.84 )nmol/ml, those in TPM group were ( 171.25?15.72)U/ml and (( 6.10?0.98) nmol/ml,those in sham-operation group were (179.74?7.95)U/ml and (5.90?0.72 )nmol/ml. Compaired with sham-operation and TPM groups, the activity of SOD in ischemia/perfusion group was significantly lower, the concentration of MDA was obviously higher (all P
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Objective To investigate the neuroprotective effects of Topiramate (TPM) on rat brain with ischemia-reperfusion damage and its mechanisms.Methods The 30 male SD rats were randomly assigned to sham operated group, ischemia-reperfusion group and TPM treated group.The cerebral ischamia and reperfusion model was made by suture occlusion of right middle cerebral artery(MCAO).Rats in TPM treated group were intraperitoneally injected TPM (80 mg/kg) twice. At 24 h following onset of MCAO,the nerve function score was evaluated with Neurological Grading Scale. The infarction volume was measured with TTC staining. The contents of glutamate (Glu) and gamma-aminobutyric acid (GABA) of cerebral cortex were tested by the high performance liquid chromatography with fluorescent detection. GABAA receptors were observed by immunohistochemistry.Results (1) Compared with the ischemia-reperfusion group, the Neurological Grading Scale of TPM treated group was significantly higher(P
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Objective To observe the expressions of apoptosis-related proteins Bcl-2 and Bax in cerebral ischemic preconditioning-perfusion models of rats. Methods Ischemic preconditioning was induced by 20 minutes of monolateral middle cerebral artery occlusion using an intraluminal filament method in rats. The animals were perfused 6 h, 12 h, 1d, 3 d, 5 d and 7 d respectively before they were sacrificed. The expressions of Bcl-2 and Bax were analyzed by immunohistochemistry staining. Results Bcl-2 positive cells increased significantly at 1 d after perfusion, reached their peak at 3 d, and maintained high level until 7 d. They were all higher than that of control group (all P 0.05). Conclusion Upregulation of Bcl-2 but not Bax may play a role in ischemic preconditioning protection .
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Objective Study the expressions of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) in rat models of cerebral ischemia reperfusion and the protective effect of ?-Sodium Aescinate.Methods Rat models of cerebral ischemia-reperfusion were made using an intraluminal monofilament method and ?-Sodium Aescinate was given peritoneally to observe its protective effect. The histochemical change and the expression of ICAM-1, VCAM-1 were detected by HE staining and immunohistochemistry ways.Results (1) ?-Sodium Aescinate could obviously reduce the brain damage after ischemia reperfusion. (2) The expressions of ICAM-1, VCAM-1 in endothelial cells in ischemic territory increased after cerebral ischemia reperfusion. ICAM-1 immunoreactivity peaked at 24 h after reperfusion and VCAM-1 immunoreactivity peaked at 24～48 h after reperfusion. Both of them decreased gradually, but remained a higher level than normal 72 h after reperfusion. (3) ?-Sodium Aescinate could decrease the expressions of ICAM-1, VCAM-1 remarkably 24 h and 48 h after reperfusion.Conclusions High expressions of ICAM-1, VCAM-1 may be involved in the mechanism of cerebral ischemia reperfusion injury. ?-Sodium Aescinate may play its protective role by reducing the expressions of ICAM-1 and VCAM-1.