Objective To investigate the prognosis and its influencing factors of post-encephalitic epilepsy ( PEE) .Methods Fifty viral encephalitis patients with PEE were followed up, which prognosis was observed by whether their no seizures for at least 1 year or not.The clinical data of patients was collected, and the relate risk factors on the poor prognosis of PEE were analyzed.Results The disturbance of consciousness and the seizure presence during acute encephalitis, more than ten seizures in poor prognosis group were much higner than the good one (all P<0.01).The age, sex, seizure type, dysphrenia and neurological defect in acute encephalitis, status epileptisus in acute encephalitis, abnormal EEG and abnormal head CT/MRI had no correlation with poor prognosis ( all P>0.05 ) .Multiple logistic regression analysis demonstrated that disturbance of consciousness during acute encephalitis、seizures presence in acute encephalitis were independent risk factors of poor outcome in PEE ( OR=7.269,95%CI:1.22 -43.35,P=0.029;OR =22.893,95%CI:4.02 -130.43,P=0.000).Conclusion Disturbance of consciousness during acute encephalitis, seizure presence in acute encephalitis both are the single risk factors of poor prognosis in PEE.

Face ; surgery ; Hand Transplantation ; Humans ; Organ Transplantation ; Transplantation, Homologous

Objective To investigate the expression of endothelin converting enzyme (ECE) mRNA in patients with acute cerebral infarction (ACI) and its clinical significance.Methods Blood samples from 40 patients with ACI (patient group) within 72 hours after the onset of ACI and 28 gender and age-matched healthy subjects (control group) were collected on admission. Plasma concentrations of endothelin-1 (ET-1) as well as the serum levels of cholesterol, triglyceride, low density lipoprotein,high density lipoprotein, apoA1, apoB, lipoprotein a and fasting plasma glucose in each sample were measured and analyzed. Additionally, semi-quantitative RT-PCR was performed to check the ECE mRNA level in the blood cells. European stroke scale (ESS) was used to evaluate ACI patients' neurological deficit on admission.Results (1) ECE mRNA could be detected in every blood sample from either patient group or control group. However, the ECE mRNA level increased significantly in the patient group compared with that in the control group (0.31?0.092 versus 0.25?0.10, t=2.46, P=0.016). (2) The plasma ET-1 concentration in patient group was also significantly higher than that of control subjects (183.27?56.63pg/ml versus 156.47?34.24 pg/ml, t=2.23, P=0.029). (3) Plasma ET-1 concentration was negatively correlated with ECE mRNA level in the control group (r=-0.452, P=0.021). However, the result in the patient group was not the same as the control group. (4) The ET-1 concentration and ECE mRNA level in the patients had histories of hypertension, diabetes mellitus and stroke were not significantly different from those in the patients without these histories. (5) No significant correlation existed between plasma ET-1 concentration and ECE mRNA level and age of the patient, ESS score, fasting plasma glucose and serum lipid. Conclusions ECE mRNA level is significantly increased in the early stage of ACI, which may be associated with the acute-phase reaction of cerebral infarction and may have deleterious effects on the development of neuronal injury. Our results suggest the protective reflection in the endothelin system of normal human body may be disturbed by the onset of ACI. The relationship between ECE mRNA level and neurological deficit degree, stroke risk factors is worthy for further study.

Objective To investigate the influence of Levetiracetam(LEV) and Topiramate(TPM) on P-glycoprotein(P-gp) expression at brain in the epileptic rats.Methods The epileptic rat models were made with 1.5 ?g(3 ?l) Kainic acid stereotaxic injected into male SD rats' hippocampi(epilepsy group) and the control group rats were injected with 3 ?l normal saline(NS).The rats in epilepsy group(18 rats) and control group(15 rats) were randomized into TPM,LEV and NS subgroups(6 or 5 rats for each subgroup) to receive once-daily orally feeding of TPM(50 mg/kg),LEV(40 mg/kg) and NS(same amount NS) for 30 d.Immunohistochemistry(EnVision) was used to measure the level of P-gp exprssion in the rats brain.The level of P-gp expression was semi-quantitatively analyzed by mean integrated blue(MIB) value in Leica Qwin imaging analysis & measuring system.Results The expression levels(MIB value) of P-gp in hippocampus and temporal lobe in epilepsy subgroups were significantly higher than those in the corresponding control subgroups(P

Objective To explore the clinical,imaging and pathologic features of hypertrophic cranial pachymeningitis (HCP).Methods The clinical data of one HCP patient who treated in our hospital and other 77 HCP patients from literatures were analyzed retrospectively.Results The clinical manifestation of all the 78 HCP patients had chronic headache,multiple cranial nerves impairment.The secondary was psychiatric disorder(10.3%),ataxia(9.0%) and seizure disorder(6.4%).Hemiplegia,menorrhea and galactosis were found few.Headache was the first onset symptom in the 74 cases (94.9%).HCP was often misdiagnosed subarachnoid hemorrhage,hypotensive cranial pressure headache and cerebral venous sinus thrombosis in early stage.MRI demonstrated local or diffused thickened dura,especially in cerebral falx and/or tentorium of cerebellum,which could be enhanced through reinforced scanning.Pathological evidence indicated an obvious proliferation of dura fiber tissue accompanied with inflammatory cells infiltration.Corticosteroid was effective to all the cases.Conclusions The clinical manifestation of HCP was multiplicity,but it mainly was chronic headache and multiple cranial nerves impairment.MRI demonstrates local or diffused thickened dura especially in cerebral falx and/or tentorium of cerebellum.MRI has an important significance for diagnosis.

Objective To explore the influence and its efficacy of Tong-Xinluo capsule on plasma endothelin levels in the patients with acute cerebral infarction(ACI).Methods 60 patients with ACI enrolled within 72 h of onset were allocated to Tong-Xinluo group(n=30) or control group(n=30) randomly.The control group was treated with Piracetam and aspirin,while Tong-Xinluo was provided 4 tablets tid for 30 d together with Piracetam and aspirin in the other group.Before and at 30th day after treatment,the patients were evaluated by European stroke scale(ESS) and activities of daily living(ADL),and the changes of ESS and ADL were served as the index of efficacy.The plasma level of endothelin-1(ET-1) was tested in the meanwhile.Results 30th day after treatment,there was a significant derease of ET-1 both in Tong-Xinluo group [(40.3?20.5)pg/ml] and control group [(31.5?14.7)pg/ml](P

Objective To observe the roles of nuclear factor-κB (NF-κB) and hypoxia-inducible factor-1 o (HIF-1 α) in hippocampal neurodegeneration of status epilepticus (SE) rats, and explore whether HIF-1α activation is regulated by NF-κB.Methods A total of 110 male Sprague-Dawley rats were randomly divided into seven groups : (1) Control group treated with saline (control, n =15), (2) sham group implanted cannula into lateral ventricle and treated with saline (sham, n =15), (3) SE group treated with pilocarpine (SE, n =20), (4) NF-κB activity inhibitor pyrrolidine dithiocarbamate (PDTC) group treated only with PDTC (PDTC, n =15), (5) SE + PDTC group treated with pilocarpine plus PDTC (SE + PDTC, n =15), (6) SE + HIF-1o siRNA group implanted cannula into lateral ventricle and treated with pilocarpine plus HIF-1 α siRNA (SE + HIF-1α siRNA, n =15), (7) SE + control siRNA group implanted cannula into lateral ventricle and treated pilocarpine plus control siRNA (n =15).SE was induced by injecting lithium chloride and pilocarpine.The seizure of rats was observed.The protein expressions of NF-κB and HIF-1 α in hippocampus of rats were examined by Western blotting.The degenerating neurons in hippocampus were detected by Fluoro-Jade C (FJC) staining.Results Twenty-four hours after termination of SE, the nuclear protein expressions of NF-κB and HIF-1α in hippocampus of rats were increased in SE group (0.57 × 0.06, 0.47 ± 0.07) compared with those in control group (0.23 ± 0.03, 0.20 ± 0.03;P ＜0.05);and compared with SE group PDTC significantly decreased the nuclear protein expressions of NF-κB and HIF-1 α in SE + PDTC group (0.23 ± 0.03, 0.14 ± 0.03;P ＜ 0.05);in SE + PDTC group the numbers of FJC positive cells in CA1 area (28.33 ±5.03) were decreased compared with that in SE group (76.67 ± 13.32);HIF-1 o siRNA injected into lateral ventricle of rats significantly decreased the expression of HIF-1α in hippocampus (0.22 ±0.03) and the number of FJC positive cell in CA1 area (27.34 ±7.02) in SE + HIF-1α siRNA group compared with those in SE group (0.39 ±0.06, 76.67 ± 13.32;P ＜0.05).Conclusions These data suggest that SE can result in activation of NF-κB/HIF-1o pathway in brain.Inhibition of the pathway can attenuate hippocampal neurodegeneration caused by SE, which has the brain protective effect.

[Abstract ] Objective High-mobility group box-1 (HMGB1) is abundantly released in the epileptogenic brain tissue , but few reports are seen about the effect of HMGB 1 on the expression of P-glycoprotein ( P-gp) in the vascular endothelial cells of the epi-leptogenic tissue .This study is to explore whether HMGB 1 can regulate P-gp expression in the brain microvascular endothelial cells of the mouse in vitro . Methods Immortalized brain microvascular endothelial bEnd .3 cells of the mouse were cultured in vitro and al-located to different concentration groups ( treated with culture medium containing 10 , 100 , 500 , and 1000 ng/mL HMGB1 for 8 hours), treatment duration groups (treated with culture medium containing 100 ng/mL HMGB1 for 4, 8, 16, 24, and 32 hours), and a control group ( treated with culture medium without HMGB 1 ) .The mRNA expression of P-gp-encoding gene-multidrug resistance gene 1a (mdr1a) was detected by real-time qPCR, and its protein expression determined by Western blot and immunocytochemistry . Results The results of qPCR manifested that the expressions of mdr 1a mRNA were 1.646 ±0.176, 1.777 ±0.135, 1.617 ±0.043, and 1.398 ±0.182 in the 10, 100, 500, and 1000 ng/mL HMGB1 groups, respectively, significantly higher than 1.030 ±0.284 in the control group (P<0.05), and so were those in the 4, 8, 16, 24 h, and 32 h groups (2.655 ±0.112, 2.168 ±0.212, 1.823 ± 0.232, 1.418 ±0.376, and 1.445 ±0.123) than in the control (1.010 ±0.164) (P <0.05).Western blot showed a significant increase in the P-gp protein expression in all the concentration groups (P<0.05) as well as in the 8 h and 16 h treatment duration groups as compared with the control group (P<0.05).Immunocytochemis-try also revealed a higher P-gp expression in the HMGB1-treated than in the control cells (P<0.01). Conclusion HMGB1 can upregu-late the expressions of mdr1a mRNA and P-gp protein in the brain microvascular endothelial cells of the mouse , which may associated with drug resistance of central nervous system diseases , especially that of epilepsy .

Objective To assess the neuropsychological characteristics in active epileptic patients and investigate itsrisk factors. Methods Ninety adult epileptic patients included 60 active epileptic patients (two or more unprovoked seizures within 12 months) and 30 age-, sex-, education-, course of disease- and seizure type-matched seizure-free subjects (without epileptic seizure for at least 1 year) . The neuropsychological tests including trail making test,digit symbol test, verbal fluency test,digit span test and hamilton depression scale( HAMD) ,were used to detect mental and motor speed, attention, language, working memory and depression symptoms respectively. The neuropsychological tests were compared between active and seizure-free epileptic patients and identified the risk factors of neuropsychological deficits in active epileptic patients. Results Compared to seizure-free subjects, active epileptic patients had significantly worse scores in digit symbol test, verbal fluency test, digit span test ((47.45 ±18. 812) vs(56.40 ±13. 631), (25. 25 ±8. 163) vs(30.40 ±8. 414), (10. 39 ±2. 228) vs( 11. 80 ± 2.074) respectively) ; more time to accomplish the trail making test A and B((64. 35 ±31.710) vs( 45. 47 ± 16. 309) , ( 133. 18 ± 47. 331 ) vs ( 98. 00 ± 35. 003 ) respectively) ; and higher scores in depressive symptoms ((9.12 ±6.219)vs(3.77 ±3.997) ,all P<0.05). Within active epileptic group,significant predictors of neuropsychological deficits were identified in a stepwise linear regression analysis: advancing age was significantly negatively correlated with digit symbol test(β = -0. 468, P = 0. 000) , digit span test (β = -0. 439, P = 0. 000), trail making test A (β =0.365, P = 0.003) and B(β = 0.346, P=0.002) ; higher scores on depressive symptoms was significantly negatively correlated with digit symbol test (β = -0.244, P = 0.015) ; mental work,high-education level and monotherapy were positively correlated with some of the cognitive function subscales. Conclusion This study suggests that active epilepsy can have a direct adverse effect on cognition and depression symptoms. Multi-drug therapy, severity of depression symptoms, advancing age, low-education level and non-mental work are the predictors of neuropsychological impairment in active epilepsy. In addition, good seizure control even after 1 year can have a beneficial impact on cognitive and depression prognosis.

Aim To observe the neuroprotective effect of platelet activating factor receptor antagonist Kadsurenone on rat brain with cerebral ischemia/reperfusion.Methods Animal model was established through middle cerebral artery occlusion(MCAO).we studied the changes of infarct volume,NAA and Lactate in Kadsurenone-treated group with DWI and()~1H-MRS examination after cerebral ischemia 60 min and reperfusion 1,3,6 h.Results Significant reductions in infarct volume were found in the Kadsurenone-treated group as well as in the Ginkgolides-treated group compared with the control group.And Kadsurenone decreased the concentration of lactate and prevented the decline of the concentration of NAA after cerebral ischemia/reperfusion.Conclusion As platelet-activating factor receptor antagonists,both Kadsurenone and Ginkgolides show remarkable neuroprotective effect.And MRI offers exact neuroimaging information for studying the neuroprotective meachnism of Chinese traditional medicine after cerebral ischemia and reperfusion.