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Objective At present, the risk factors for cognitive impairment in epilepsy patients are not quite clear.This study was to explore the impacts of the clinical features, emotional health and quality of life (QOL) on the cognitive function of the adult patients with mild cognitive impairment (MCI).Methods Using the Montreal Cognitive Assessment (MoCA) and Mini Mental State Examination (MMSE) scales, we evaluated the cognitive functions of the 109 adult epileptics of the outpatient clinic of neurology in Jinling Hospital.We assessed their emotional health with Hamilton Depression Scale-24 (HAMD-24), estimated their QOL with Quality Of Life in Epilepsy-31 (QOLIE-31), and collected their baseline clinical data by questionnaire survey.Results There were 67 cases of MCI (61.5%) among the 109 patients.The residential area was the strongest predictor of MCI in the adult epileptics (OR=0.226, 95% CI: 0.082-0.627).Among other risk factors of post-epileptic MCI were the total scores of HAMD-24 (OR=0.770, 95% CI: 0.644-0.921) and QOLIE-31 (OR=0.712, 95% CI: 0.575-0.880), QOL (OR=1.070, 95% CI: 1.015-1.128), cognitive function (OR=1.120, 95% CI: 1.043-1.203), and social function (OR=1.103, 95% CI: 1.035-1.175).Conclusion The incidence of MCI is high in adult patients with epilepsy.The development and progression of post-epileptic MCI can be delayed by more emphasis on the evaluation of cognitive function, emotional health, and quality of life.
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Objective Ischemic stroke with elevated serum immunoglobulin E ( IgE) in some young patients is regarded as cerebral vasculitis clinically though without sufficient pathological evidence .This study was to investigate the characteristics of vascular lesions in these patients by temporal artery biopsy . Methods We performed histopathologic examinations on the temporal arteries of 32 young ischemic stroke patients with unknown etiology , 16 with normal and the other 16 with elevated serum IgE .We observed inflammatory cells infiltration and mast cells by HE staining and toluidine blue stai-ning respectively and determined the expressions of matrix metalloproteinase -9 (MMP-9), monocyte chemotaxis protein -1 (MCP-1) and serum IgE by immunohistochemistry . Results Compared with the patients with normal IgE , those of the elevated IgE group showed a significantly higher rate of inflammatory cells infiltration (12.5%vs 62.5%, P0.05).Nor was any signifi-cant difference observed in the number of the mast cells between the normal and elevated IgE groups (2.8 ±1.5 vs 3.6 ±2.3, P>0.05). Conclusion The infiltration and necrosis of inflammatory cells and fibrin exudation in the temporal artery of the young pa-tient with elevated serum IgE are likely to be the manifestations of vasculitis , and MCP-1 may play a role in the pathogenesis of the disease.
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Objective Inflammation response is involved in the whole pathological process of acute cerebral infarction ( ACI) , but few reports are seen on its clinical implication in ACI patients .The purpose of this study was to investigate the predictive value of the differential count of leukocytes for stroke severity and early clinical outcomes in the acute phase of cerebral infarction . Methods We collected the clinical and laboratory data of 635 patients diagnosed with ACI within 72 hours of symptom onset and eval-uated the association between the differential count of peripheral blood leukocytes and stroke severity at admission and within 3 days af-ter admission as well as the clinical outcomes at discharge .The neural function impairment scores of the patients were obtained with The NIH Stroke Score ( NIHSS) at admission and on the third day after admission , and the therapeutic results evaluated with the modi-fied Rankin Scale ( mRS) , mRS >2 as poor prognosis .Analyses were performed on the correlation of the differential count of leuko-cytes with NIHSS and mRS scores and its influence on the ACI patients . Results At discharge , the mRS related influencing factors included the total count of leukocytes (OR=1.147, 95% CI:1.038-1.268), count of neutrophil cells (OR=1.227, 95% CI:1.00-1.369 ), count of lymphocytes ( OR =0.508, 95% CI:0.342-0.753), and neutrophil to lymphocyte ratio (NLR) (OR=1.150, 95%CI:1.008-1.314).the NIHSSs were correlated with the counts of leucocytes (r=0.078, P=0.024), neutrophil cells (r=0.083, P=0.019), and lymphocytes (r=0.010, P=0.004) at admission, and with the counts of leucocytes ( r =0.238, P <0.001), neutrophil cells (r=0.335, P<0.001), lymphocytes (r=-0.269, P<0.001), and NLR (r=0.423, P<0.001) on the third day after admission. Conclusion In the acute phase of cer-ebral infarction , the differential count of leukocytes and NLR are valuable for predicting the severity of neurologic impairment and early poor functional outcome .
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Objective It remains to be confirmed whether tissue kallikrein has neuroprotective effect in diabetes-induced stroke.This study was to investigate the neuroprotection of tissue kallikrein against cerebral ischemia-reperfusion injury in diabetic rats. Methods Healthy male SD rats were randomly divided into a sham operation, a saline control, and a tissue kallikrein group.Diabetes mellitus was induced in the animals by intraperitoneal injection of streptozotocin and the model of focal cerebral ischemia-reperfusion was made with an intraluminal vascular occlusion method. At 24 hours after modeling, we obtained the neurological deficit score, in-farct size, and brain water content, counted Iba1-and MPO-positive cells by immunohistochemistry, and determined the expressions of ICAM-1 and VCAM-1 by real-time PCR. Results In comparison with the saline controls, the rats treated with tissue kallirein showed significant decreases in the neurological deficit score (P<0.01), the infarct size ([23.57 ±5.79] vs [47.97 ±1.19]%, P<0.01), brain edema ([81.73 ±2.10] vs [84.94 ±2.34]%, P<0.05), the counts of Iba1-and MPO-positive cells (12.33 ±4.46 vs 31.83 ±8.13 and 13.83 ±4.49 vs 37.50 ±7.64, both P<0.01), and the expressions of ICAM-1 and VCAM-1 (both P<0.05). Conclusion Tissue kallikrein has a neuroprotective effect against cerebral ischemia-reperfusion injury in diabetic rats, which may be associated with its anti-inflammation property.
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Objective There is little research focusing on the expression and function of bradykinin 1 receptor ( B1R ) and bradykinin 2 receptor ( B2R) after cerebral ischemia/reperfusion on the basis of diabetes .The aim of this study was to compare the ex-pression difference and function change of B 1R and B2R in non-dia-betic and diabetic rats . Methods The cerebral ischemia/reperfu-sion model was established on 41 non-diabetic and type 2 diabetic rats, the weight and the biochemical index were measured on these two types of rats .8 non-diabetic rats and 8 diabetic rats were respec- tively assigned to two groups according to random number tables:control group and I/R 24 h group, 4 in each group.Real-time PCR was performed to observe the expressions of two receptors at 24 h after reperfusion .Then, 33 non-diabetic rats and 33 diabetic rats were randomly divided into 4 groups respectively, including sham group (n=6), saline group (n=9), B1R antagonist group (n=9) and B2R antagonist group (n=9).At 24 hours after cerebral I/R, neurological deficiency was evaluated by neurological severity scores ( NSS);infarct volume was observed by TTC staining;cell apoptosis was determined by TUNEL staining;neuron degeneration was de-tected by Fluoro-Jade C staining. Results Glucoses of diabetics at 3, 7, 14 d after model establishment [(23.45 ±5.01), (23.71 ±4.87), (22.72 ±4.11) mmol/L] were obviously elevated compared with non-diabetics [(5.77 ±0.75), (6.05 ±0.69), (7.15 ±1.09) mmol/L];blood cholesterin [(4.59 ±3.43) mmol/L] and insulin [(67.26 ±12.02) pmol/L] at 14 d after model establishment were evidently incresaed in comparison to those in non-diabetics [(1.58 ±0.37) mmol/L, (25.34 ±4.88) pmol/L] (P0.05).Compared with non-diabetics, diabetics suffered from more apparent up-regulation of B1R mRNA (P<0.01) but relatively less B2R mRNA (P<0.05) at 24 h after I/R.NSS score, infarction volume, damaged and apoptotic cells in B2R antagonis-treated non-diabetic rats at 24 h after I/R conspicuously decreased compared with saline-treated non-daibetic rats.Those indicators in B1R antagonis-treated diabeics were strikingly lessened compared with saline-treated daibetics . Conclusion I/R induced distinct up-regulation of B2R mRNA in non-diabetics and inhibiton of B 2R effectively ameliorated the infarct volume and cell injury after I/R in non-diabetics; I/R induced more notable up-regulation of B1R mRNA in diabetics and B1R antagonist exerted neuroprotective effects instead of B 2R antagonist af-ter I/R in diabetics.
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Kallikrein-kinin system consists of kininogen , kallikrein, bradykinin and kinin .Kinins, derived from kininogen by tissue kallikrein , play their biological effects via bradykinin 1/2 receptors or protease activated receptors .Existing researches suggest that kinins exert various effects through different intracellular and mitochondrial signal pathways such as MAPK , PI3K/Akt/GSK3 be-ta, NO, JAKs/STATs.This review aims to elucidate the roles and the intracellular signal pathways of KKS in different diseases .
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Objective To investigate the enlarged perivascular space (EPVS) and its clinical significance in patients with cerebral small vessel disease (CSVD).Methods One hundred seventy-four patients with CSVD and 86 patients without CSVD admitted to Jinling Hospital,Clinical School of Nanjing University School of Medicine from October 2011 to February 2012 were recruited.All patients underwent cranial MRI examination (including diffusion-weighted imaging and fluid attenuated inversion recovery sequences).The numbers of EPVS and anatomic distribution in all the subjects of both groups were analyzed.The receiver operator characteristic (ROC) curve was used to investigate its diagnostic critical value of anatomic distribution.Results Multivariate logistic regression analysis showed that EPVS in basal ganglia region (odds ratio [OR] 1.491,95％ confidence interval [CI] 1.165-1.909; P =0.002) and EPVS in centrum semiovale (OR 1.279,95％ CI 1.022-1.601;P=0.032) were independently associated with CSVD.EPVS in the basal ganglia region and the centrum semiovale in patients with CSVD was significantly more than that in patients with non-CSVD (all P ＜0.001).Its corresponding diagnosis cut-off points of CSVD were 4 and 6 respectively.The area under the ROC curve and the diagnostic sensitivity and specificity were 0.859,72.4％,93.0％ and 0.808,65.5％,95.3％,respectively.Conclusions EPVS contributes to the diagnosis of CSVD.When using EPVS to diagnose CSVD,the anatomical sites need to be distinguished and establish appropriate diagnostic critical value.
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Transcranial Doppler (TCD) is a non-invasive,convenient and inexpensive method for cerebral hemodynamic assessment widely used in clinical practice.Monitoring of cerebrovascular reserve capacity with TCD can provide relevant information for clinical decision making in the treatment of carotid stenosis.During carotid angioplasty and stenting,TCD can be used to evaluate effect of stenting on hemodynamics,and predict major complications,particularly postoperative hyperperfusion.
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Vascular smooth muscle cell (VSMC) proliferation and migation play important roles in the occurrence and development of atherosclerosis and restenosis after intravascular stenting.The studies in recent years have shown that kallikrein-kinin system (KKS) is closely correlated with VSMC proliferation and migration in cytokines and transduction pathways.Therefore,investigating the roles of KKS in the VSMC proliferation and migation process has great significance in clinical prevention and treatment of atherosclerosis and restenosis after intravascular stenting.
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Objective To compare the clinical efficacy and angiographic outcomes of balloon dilation angioplasty,balloon-expandable stent implantation and self-expanding stent implantation in the treatment of intracranial arterial stenosis.Methods The patients with intracranial arterial stenosis who met the indications of surgical intervention treated with balloon dilatation angioplasty and stent placement were selected from Nanjing Stroke Registry Program.According to the different interventional procedures,the patients were divided into the balloon expandable stenting goup,the self-expanding stents group and the balloon dilatation angioplasty group.The success rate of surgery,the perioperative complication rate and the significant residual stenosis rate were compared among the three groups.The clinical and angiographic assessments were performed through 1-,3-,6-,12- and 24-month regular outpatient or inpatient follow-up after procedure.The incidences of ischemic stroke and/or death and restenosis within 2 years were compared.Multivariate Cox proportional hazards analysis was used to analyze the risk factors for recurrent ischemic stroke and/or death and restenosis.Results A total of 183 patients with 192 stenoses performed balloon dilatation angioplasty or stenting,in which 92 were in the balloon expandable stenting goup,42 were in the self-expanding stents goup and 49 in the balloon dilatation angioplasty group.Their preoperative stenosis rates were 80.2 ±12.8％ 、76.3 ± 11.9％ and 89.7 ± 10.2％,respectively (F =15.863,P =0.000).There were no significant differences in other baseline data.The success rates of surgery in the balloon expandable stenting group,self-expanding stents group and balloon dilatation angioplasty group were 96.7％,95.2％ and 91.8％,respectively (x2 =1.646,P =0.439).The perioperative complication rates were 6.5％,14.3％ and 10.2％,respectively (Fisher exact test,P=0.334).The imaging follow-up showed that the restenosis rate in the balloon dilatation angioplasty group was 48.5％.Although it was high than 27.7％ in the balloon expandable stenting group and 34.8％ in the self-expanding stents group,there were no significant differences (x2 =4.176,P =0.124).Multivariate Cox proportional hazards analysis showed that balloon dilatation angioplasty was an independent risk factor for restenosis after procedure (hazard ratio 2.490,95％ confidence interval 1.247- 4.969,P=0.010).Conclusions Compared to the balloon expandable stenting,the balloon dilatation angioplasty is more likely to have restenosis,but it is not associated with the risks of postoperative recurrent ischemic stroke and/or death.
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Objective To investigate the relationship between isehemic lesion patterns and Suzuki's vessel grades in adult moyamoya disease(MMD).Methods Forty-four consecutive MMD patients,12 with transient ischemic attack(TIA),30 with cerebral infarct(CI)and 2 with combined TIA and CI,who were diagnosed in Jinling hospital between January of 2004 and July of 2009,were retrieved from Nanjing Stroke Registry Program.Ischemic lesions patterns of CI type of MMD were further divided into two paired subgroups including subcortical subgroup versus cortical subgroup, and subgroup of anterior cerebral circulation versus subgroup of posterior cerebral circulation.In addition,the ipsilateral vessel grades of all symptomatic hemispheres were evaluated by Suzuki's 6-grade system according to the results of cerebral angiography of internal carotid arteries.The percentage of number of hemispheres with ischemic events among the paired groups,including TIA group versus CI group,subcortical subgroup versus cortical subgroup,and subgroup of anterior cerebral circulation versus subgroup of posterior cerebral circulation,were analyzed respectively with changes of the Suzuki's grading.Results For above-mentioned each paired groups.the percentage of number of hemispheres with ischemic events was gradually decreased in the former (namely,11/26,2/13,1/8,0 and 0;15/15,9/11,1/7,0 and 0;15/15,10/11,4/7,0 and 0)and increased in the latter(namely,15/26,11/13,7/8,2/2 and 1/1;0,2/11,6/7,2/2 and 1/1;0,1/11,3/7,2/2 and 1/1 ) from grade 2 to grade 6, and the differences were statistically significant (Z = -2. 33 and P =0. 019,Z = - 4.49 and 0. 00, Z = - 3.66 and 0. 01, respectively ). Moreover, the mean value of Suzuki' s grade was lower in the former than the latter for above-mentioned three groups (2. 29 vs 2. 97, 2. 44 vs 4. 18 and 2. 62 vs 4. 13, respectively). Conclusion The ischemic lesion patterns of adult MMD is changing with the change of Suzuki' s vessel grading. The higher the Suzuki' s grade, the greater the likelihood of ischemic lesions involving the cortical areas of posterior cerebral circulation.
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Objective To investigate the relationship between the "prominent laterality of the posterior cerebral artery (PLPCA)" found on magnetic resonance angiography (MCA) and the size and distribution of cerebral infarction and the National Institutes of Health Stroke Scale (NIHSS)scores in patients with occlusion of the M1 segment of the middle cerebral artery (MCA).Methods Fifty patients with acute cerebral infarction caused by the occlusion of the M1 segment of MCA were divided into PLPCA positive group (n =24) and PLPCA negative group (n =26) according to MRA manifestation.the NIHSS scores,size of cerebral infarction scores,and constituent ratios of distribution in all the feeding subregions of MCA in both groups were compared.Results The proportions of the patients with ≥3 risk factors (9/24 vs.18/26,P =0.046),NIHSS scores (5.4 4.4 vs.10.4 ±4.9,t = -3.690,P =0.001),and the size of cerebral infarction scores (1.92 ± 1.10vs.2.88 ± 1.37,t = -3.690,P =0.001) in the PLPCA positive group were significantly lower than those in the PLPCA negative group.The proportions of the patients with cerebral infarction involying the middle branch of the MCA territory (6/24 vs.19/26,P =0.002) and the posterior branch of the MCA territory (2/24 vs.5/26,P ＜0.001) in the PLPCA positive group were significantly lower than those in the PLPCA negative group.The proportions of the patients whose infarction involving the area of the posterior watershed zone were significantly higher than those in the PLPCA negative group (6/24 vs.1/26,P =0.045),and the proportions of complete infarction were significantly lower than those in the PLPCA negative group (0/24 vs.6/26,P =0.023).Conclusions When MCA M1segment was occluded,if PLPCA were observed on MRA,it indicated that the infarct size was smaller and the NIHSS score was lower.The infarction was less involved in the middle and post branches of MCA,and it is prone to have posterior watershed infarction.
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Objective:To analyze the independent and comprehensive effects of the sites and mechanisms of middle cerebral artery(MCA)occlusion on cerebral infarction patterns and the National Institutes of Health Stroke Scale (NIHSS)scores andto investigate the possible related mechanisms and their potential values to the selection of patieras for thrombolysis.Methods:Sixty-six patients with new cerebral infarction caused by MCA occlusion were enrolled.The sites of MCA occlusion were classified into the origin of the MCA(type Ⅰ),the MCA trunk distal to the lenticulostriate arteries(type Ⅱ)and the branches of the MCA(type Ⅲ):the mechanisms of cerebral infection were categorized as thrombotic and embolic.Cerebral infarction lesion patterns were determined according to diffusion-weighted image(DWI).NIHSS scores were evaluated within 24 hours after stroke onset.The independent and comprehensive effects of the sites and mechanisms of MCA occlusion on cerebral infarction lesion patterns and the NIHSS were analyzed.Results:Cerebral infarction involved a larger range and NIHSS scores were higher in patients with occlusion at the origin of MCA and embolic occlusion of the MCA trunk distal to the lenticulostriate arteries.The analysis of the combination of the sites and mechanisms of occlusion could conduct further stratification for patients with cerebral infarction caused by MCA occlusion compared with univariate analysis.Conclusion:The analysis of the combination of the sites and mechanisms of occlusion better stratifies patients with cerebral infarction caused by MCA occlusion.It may be help to select patients for thrombolytic therapy.
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In recent years, multicenter studies have confirmed that intra-arterial thrombolysis is an effective approach in the treatment of acute cerebral infarction. This article reviews the study status quo of the time window, pretreatment assessment, and selection of patients and drugs for intra-arterial thrombolysis.
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Objective:To investigate neuroprotection of calcitriol in LPS-induced rat systemic inflammation and underlying mechanism. Methods:Adult male Sprague-Dawley rats were randomized into three groups: blank group(6 rats),calcitriol group [23 rats,4?g/(kg?d)?14d] and control group [23 rats,fat milk,4ml/(kg?d)?14d].46 rats were induced systemic inflammation by intraperitoneal injection of LPS(10mg/kg) on day 14th,1 hour after the administration.On post-injection 3,6,9 hour,36 rats were anesthetized to death and obtained rat brain tissue to detect activity of NF-?B by EMSA and to assess TNF-?,IL-10 concentration by ELISA.HE staining was used to determine brain injury. Results:LPS effectively activated NF-?B,enhanced TNF-? expression,induced sporadic neurons damage in brain in the control group and in time-dependent,compared with blank group rats.Calcitriol significantly down-regulated NF-?B activity,TNF-? expression but enhanced IL-10 expression at all time point evaluated,compared with the control group rats. Conclusion:Intraperitoneal injection of LPS can induce brain damage,Calcitriol modulate the inflammatory-antiinflammatory cytokine balance by downregulating activation of NF-?B,reducing over express of TNF-? and elevating IL-10 concentration.
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Objective:Atherosclerotic reanal artery stenosis(RAS) exists as one manifestation of more generalized atherosclerosis.It is important to find RAS in the population of carotid artery stenosis.The aim of the present study was to evaluate the prevalence of RAS in patients with carotid artery stenosis and to identify the risk factors for RAS.Methods:A total of 126 patients were carried out renal artery angiography after cerebral angiography.A univariate and multivariate Logistic regression analysis was performed to investigate the association of the clinical variables with RAS.Results: Renal artery stenosis was identified in 23(21.4%) patients.Multivariate predictors included coronary artery disease(OR=6.34,95%CI: 2.20-18.26) and peripheral vascular disease(OR=3.67,95%CI: 1.29-10.46). Conclusion: Coronary artery disease and peripheral vascular disease may be clinical predictors for RAS.