Table of Content

20 April 2009, Volume 4 Issue 04

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主编手记

The Sight of Back

2009, 4(04):  265-266. 

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热点报道

Highlight Report of International Stroke Conference 2009

2009, 4(04):  267-272. 

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述评

Time Window of Treatment for Acute Ischemic Stroke

2009, 4(04):  273-274. 

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论著

The Features of MRI-PWI Proved Cerebral Blood Flow Uneven Distribution without Corresponding Clinical Signs

2009, 4(04):  275-279. 

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Objective To analyze the characteristics and its possible mechanism on MRI-PWI proved cerebral blood flow uneven distribution without corresponding clinical signs.Methods There were seven cases of one hundred which performed the examination between January 2008 and January 2009 with cerebral blood flow uneven distribution without corresponding clinical signs. All patients underwent lifelong follow-up(varied from 7 days to 14 months). Retrospectively analyzed the clinical manifestation, MRA and PWI features of the 7 cases.Results There were 13 cerebral blood flow uneven distribution regions in 7 cases. One region was consistent with both clinical symptom and MRA features. Two regions were consistent with clinical symptom but weren’t consistent with MRA feature. Four regions were consistent with MRA featurebut weren’t consistent with clinical symptom. Six regions were consistent with neither clinical symptom nor MRA feature. Six regions accorded with PWI grade II, Six regions accorded with PWI grade III, one region accorded with PWI grade IV.Conclusion PWI proved cerebral blood flow uneven distribution not only existed in the ischemic cerebrovascular attack patients. Brain blood flow uneven distribution of this type had no definite correlation with MRA abnormal and clinical symptoms. PWI/DWI mismatch should combine withthe distribution of cerebral blood flow before to assess the patient’s condition.

Role of Chelerythrine Chloride, the Protein Kinase C Inhibitor, on the Cell Damage of SHSY5Y Neuronal Cells from Oxygen-glucose Deprivation

2009, 4(04):  280-283. 

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Objective To investigate the neuroprotective effect of chelerythrine chloride on SHSY5Y neuronal cells against oxygen-glucose deprivation(OGD), and the mechanisms of the neuroprotective effect.Methods SHSY5Y neuroblastoma cells were exposed to OGD, chelerythrine chloride (0.01mol/L) alone or chelerythrine chloride together with diethyldithiocarbamate (100 nmol/L was administrated,cell viability was measured by the MTT assay, intracellular concentration of superoxide anion and calcium were evaluated via the fluorescence intensity of HEt and fluo-3/AM.Results Compared with the sham group, the MTT value decreased significantly in the OGD group (P <0.01), while after OGD, the MTT value was higher significantly in the chelerythrine chloride group than that in the OGD group (P <0.01), the neuroprotective effect of chelerythrine chloride wasblocked by administration of diethyldithiocarbamate; the fluorescence intensity of HEt (P <0.05)and fluo-3/AM (P <0.01) was decreased significantly in the chelerythrine chloride group.Conclusion Chelerythrine chloride protects SHSY5Y neuronal cells against OGD by activating the superoxide dismutase, then reducing the intracellular concentration of superoxide anion and calcium, thereafter inhibiting protein kinase C.

A Study of the Effect of Acute Cerebral Infarction on Left Ventricular Function and the Relationship between Acute Cerebral Infarction and Plasma Brain Natriuretic Peptide

2009, 4(04):  284-288. 

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Objective To observe the changes of left ventricular function in patients with acute cerebral infarction and the relationship between acute cerebral infarction and plasma brain natriuretic peptide(BNP) by using echocardiography and determining plasma BNP concentration. It willpvoide potentile methods for preventing and treating cardiac impairment caused by acute cerebral infarction.Methods Thirty patients within 24 hours after the onset of acute cerebral infarction diagnosed by clinical manifestation and head computed tomography were enrolled. All enrolled patients had no history of heart diseases and no complications such as cardiac insufficiency and arrhythmia. And inthe same period, twenty-one sex and age matched healthy persons were enrolled as control groups.All patients and controls were undergone echocardiographic investigation and plasma determination of BNP concentration.Results (1)The mean of cardiac stroke volume(SV), cardiac output(CO) and cardiac index(CI) in acute cerebral infarction group was much lower than those in control group(38±14 vs 53±12,P <0.01; 3.00±1.39 vs 3.87±1.33, P <0.05; 1.77±0.79 vs 2.37±0.81, P <0.01, respectively). (2)The mean of cardiac left ventricular ejection fraction(LVEF) in acute cerebral infarction group was much lower than those in control group(45±14 vs 68±8, P <0.01). (3)The mean of cardiac peak earlydiastolic velocity E wave/ peak late diastolic velocity A wave (E/A ratio) in acute cerebral infarction group is lower than those in control group(0.97±0.32 vs 1.47±0.23, P <0.01). (4)The plasma BNP concentration in acute cerebral infarction group was higher than that in control group(P <0.01).Conclusion Acute cerebral infarction can induce the decrease of left ventricular systolic and diastolic function. The plasma BNP concentration increases after the onset of acute cerebral infarction, The rise of plasma BNP concentration may be caused mainly by the pathophysiologicmechanism of acute cerebral infarction.

Clinical Analysis of Intravenous Thrombolysis Therapies in Acute Cerebral Infarction with Different Dosage of Reconstructive Tissue Plasminogen Activator(rt-PA)

2009, 4(04):  289-292. 

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Objective FDA recomanded 0.9mg/kg IV rt-PA in thrombolysis treatment for acute ischemic stroke.The trials about IV rt-PA in china have chosen some different dose. To analyze the suitable dosage of rt-PA in Chinese we compared 0.9mg/kg IV rt-PA with 0.6-0.8mg/kg(50mg/person) IV rt-PA.Methods 30 patients were randomly assigned in our study. The NIHSS were from 2 to 26, the stroke onset time is 0.5 to 6 hours, without contraindications to thrombolytic therapy(China cerebrovasculardisease guide contraindication of thrombolysis). The patients were randomly divided into Group A and B, Group A with rt-PA 50mg/person, Group B with rt-PA 0.9mg/kg. To compare between two groups the number of patients with a decrease of 4 or more points on the National Institutes of HealthStroke Scale (NIHSS) at 24 hours and day 14. The intracerebral hemorrhage rate and mortality were also be compared.Results The two groups were well matched on baseline characteristics, including NIHSS (mean of 10.17for both). NIHSS improvement rate of group B at day 14 is signifcient better than group A (86.67% vs 53.3%, P <0.05).The intracerebral hemorrhage rate of two groups were both 6%. Themortality at 14 days in Group A were higher than Group B(26.67% vs 20%, P =0.67).Conclusion This study found significant benefit on 14 days in patients treated by 0.9mg/kg IV rt-PA than (0.6-0.8)mg/kg(50mg/person) IV rt-PA after stroke onset. Risk of intracerebral hemorrhage and mortality was not increased in 0.9mg/kg IV rt-PA. 0.9mg/kg IV rt-PA was suitable for Chinese inthrombolysis treatment for acute ischemic stroke.

Preliminary Investigation on the Role of Hyperglycemia in the Prognosis of Patients with Early Stage Acute Ischemic Stroke

2009, 4(04):  293-297. 

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Objective To investigate the role of hyperglycemia in the prognosis of patients with early stage acute ischemic stroke.Methods 143 consecutive patients with acute ischemic stroke (<72 hours) were involved in this prospective study. All of them had random serum glucose measured at admission, and hyperglycemia was defined as ≥7.2mmol/L.We also evaluated their National Institutes of Health Stroke Scale (NIHSS)when they admitted to hospital. Based on their clinical manifestations and physical examination,ischemic stroke patients were classified according to the TOAST (Trial of Org 10172 in Acute Stroke Treatment) scale.30 days post stroke, by means of Modified Rankin Scales (mRS) scale, we evaluatedthe prognosis of patients with early stage acute ischemic stroke.Results (1) Our data showed that hyperglycemia at admission was present in 85 patients (59.4%).By single variable analysis, age, a prior history of diabetes mellitus, NIHSS were risk factors for acute ischemic stroke patients combined with hyperglycemia (P <0.05). Multivariate stepwiselogistic regression analysis showed that prior history of diabetes mellitus, NIHSS were independent risk factor for acute ischemic stroke patients combined with hyperglycemia (P <0.05).(2) By single variable analysis, the influence of age, infection, hyperglycemia, NIHSS,TOAST on mRS scale werestatistically significant difference (P <0.05). Multivariate stepwise logistic regression analysis showed that hyperglycemia, NIHSS were independent risk factor for poor prognosis (P <0.05).Conclusion Our data indicates the high incidence of hyperglycemia in patients with acute ischemic stroke. Hyperglycemia, which is associated with stroke severity, can be a predictor of more severe stroke at its onset. Hyperglycemia is an independent risk factor for poor prognosis in patients withearly stage acute ischemic stroke.

Secondary Axonal Degeneration Developed in Ipsilateral Thalamus after Rat Cerebral Cortex Infarction

2009, 4(04):  298-304. 

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Objective To approach the course of secondary axonal degeneration in ipsilateral ventroposterior nucleus of the thalamus (VPN) after cerebral cortex infarction in hypertensive rats.Methods Experimental animals were divided into three groups: middle cerebral artery occlusion (MCAO) group, sham-operated group and normal control group. The model of MCAO was duplicated in the stroke-prone renovascular hypertensive rats (RHRSP) with occlusion of right distal middle cerebral artery (MCA). In the sham-operated group, the right MCA of RHRSP only exposed without occlusion. The matched healthy rats served as normal control group. At the end of 1,2 and 4 weeks of MCAO, the animals were killed and the brains were sectioned for Bielschowsky’s silver stainning and immunohistochemistry analysis of the expression of amyloid βA4 precursorprotein (APP), growth associated protein-43 (GAP-43), microtubule associated protein-2 (MAP-2) in the ipsilateral VPN.Results The positive neural fiber of silver stainning were decreased in MCAO group compared with in sham-operated group in ipsilateral VPN at the end of 4 weeks after ischemia (P <0.05). The expression of APP protein was beginning to increase in ipsilateral VPN at the end of 1 week afterischemia, then enhanced to a higher level from 2 through 4 weeks after ischemia (P <0.05). GAP-43,MAP-2 immunoreactivity were beginning to decrease in ipsilateral VPN at the end of 1 or 2 weekafter ischemia (P <0.05), then reduced to a lower level (P <0.05).Conclusion The immuno-detection of protein marker of axons was more sensitive than conventional silver staining which could find the pathological change of axons at the earlier time.Combined with silver staining, it could evaluate in detail the pathological course of axonal anddendritic destroy. This study proved that a long lasting, progressive axonal degeneration developed in ipsilateral VPN after MCAO.

专题论坛

Reaserch on the Strategy of Acute Ischemic Stroke Vascular Recanalization

2009, 4(04):  306-312. 

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The Development of Thrombolytic Therapy for Acute Cerebral Infarction

2009, 4(04):  313-318. 

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病例讨论

Combined therapy of urinary kallikrein and rt-PA on ultra-acute ischemic stroke:appended two cases

2009, 4(04):  319-321. 

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指南与规范

National Clinical Guideline for Diagnosis and Initial Management of Acute Stroke and Transient Ischaemic Attack(TIA)(Part One)

2009, 4(04):  322-341. 

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综述

Research Status in Stem Cell Therapy for cerebral Infarction

2009, 4(04):  342-348. 

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There is no existing effective treatment to repair neurological damage caused by ischemic stroke. Recent studies have highlighted a novel stem cell-based therapeutic approach for the treatment of ischemic stroke. A number of experiments in animal stroke models and a small number of clinical trials have demonstrated that mobilized and recruited endogenous or implanted exogenous stem cells improve neurological outcomes after stroke. Increasing evidence suggests that stem cells implanted locally or intravenously, or mobilized systemically, could migrate and home into ischemic region under the effects of stromal cell-derived factor-1/CXC chemokine receptor-4 (SDF-1/CXCR4)and β2-intergrin. The mechanism that the stem cell therapy might improve neurological deficits after stroke remain uncertain. Transplanted stem cells may provide a microenvironment with rich trophic factors for the ischemic penumbra surrounding the infarcted area, enhance angiogenesis and vasculogenesis, promote survival, migration, and differentiation of the endogenous stem/precursor cells after stroke, and differentiate into neurons to replace lost neurons.