Subcortical ischemic vascular dementia is a subtype of vascular cognitive impairment. Its major pathological features are lacunar infarcts and deep white matter changes, and its major clinical manifestation is executive function impairment. Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) provides an opportunity for the study of pure subcorticai ischemic vascular dementia in the absence of Alzheimer's disease. There is currently lack of the gold standard for diagnosing subcortical ischemic vascular dementia. Imaging examination plays an important role in its diagnosis, while the treatment must first consider the control of vascular risk factors, especially hypertension.

The main cause of subcortical ischemic vascular dementia is small vessel disease, including lacunar state, strategic infarct dementia, and Binswanger' s syndrome. The clinical manifestations are subcortical syndrome and cognitive impairment. The positive diagnosis and treatment of subcortical ischemic vascular dementia may help to reduce the risk of cognitive impairment in the elderly.

Objective To investigate the effect and safety of Batroxobin (DF-521) combined with Aspirin (ASA) in the treatment of acute cerebral infarction. Methods 102 patients with acute cerebral infarction were enrolled in the study and all the patients were divided into three groups: ASA group (n=23), Batroxobin group (n=35) and ASA combined with Batroxobin group (n=44). Platelet count, blood viscosity, platelet aggregation test (PAgT), fibrinogen, coagulation studies (PT, APTT, INR), TXB2, imaging, National Institutes of Health Stroke Scale (NIHSS) and Modified Barthel Index (MBI) were measured or assessed before and after treatment, respectively. Hemorrhage rate (including brain and other organs) as one of complication was also investigated.Results After treatments, ASA combined with Batroxobin group showed the strongest inhibition of platelet aggregation among the three groups (all P0.05). A follow up of 3 months showed that the scores of NIHSS and MBI in ASA combined with Batroxobin group were better than those in the other two groups (all P

Objective To explore the correlation between the glucose variability and the death of critically ill patients in neurology department.Methods Clinical characteristics of 231 patients admitted to neurointensive care unit (N-ICU) were analyzed retrospectively.The patients were divided into two groups:survival group(n =190)and death group (n =41).The baseline data,such as gender,age,mechanical ventilation,acute physiology and chronic health evaluation Ⅱ (APACHE Ⅱ) score were recorded.All data of blood glucose measured during hospitalization in N-ICU were collected.Standard deviation (SD),coefficient of variability (CV),maximum successive change and mean amplitude of glycemic excursions (MAGE) were used as glucose variability index.Logistic regression analysis was used to study the association between the glucose variability and the death.Receiver operating characteristic (ROC) curve was adopted to evaluate the application value of each glucose variability index on predicting mortality.Results Glucose variability,APACHE Ⅱ score (deleting the age component) and mechanical ventilation were significantly correlated with death (OR =4.959,1.444,5.472 ; 95％ CI 2.015 ～ 12.202,1.240 ～ 1.681,1.455 ～20.574;P =0.000,0.000,0.012).The predictive value was high and same when using SD and APACHE Ⅱ score (deleting the age component) as predictor (area under the ROC curve =0.910,0.957 ;Z =1.396,P =0.163).The application value of CV,maximum successive change and MAGE was moderate (area under the curve =0.847,0.856,0.872).Conclusion There is significant association between the glucose variability and the death of critically ill patients in neurology department.

Objective To study the effects of the monomers of ginsenoside Rb1 (GSRb1) on the concentrations of intracellular calcium in ischemic neurons of rats.Methods Hippocampus neurons from embryo of rats were cultured in vitro, then placed into normal extracellular fluid (normal control group), simulated ischemic extracellular fluid (ischemia group), simulated ischemic extracellular fluid without calcium (ischemia without calcium group) and simulated ischemic extracellular fluid with different concentration of GSRb1. The fluorescence intensity of intracellular calcium in each group was measured by laser scanning confocal microscope technique, and the corresponding percentage was calculated by comparison with normal control.Results Compared with normal control group, fluorescence intensity of intracellular calcium increased by ( 73.5?10.31)% in ischemia group, ( 4.5?2.58)% in ischemia without calcium group,( 20.2?3.41)%, ( 13.6?2.98)%,( 10.5?3.62)% and ( 12.7?4.51)%, respectively, in simulated ischemic extracellular fluid with different concentration of GSRb1 groups (20, 40, 60 and 80 ?mol/L). The decreases of fluorescence intensity of intracellular calcium in simulated ischemic extracellular fluid with different concentration of GSRb1 groups were significantly different compared with ischemia group (all P