丁苯酞联合降纤、抗血小板多靶点治疗进展性脑梗死
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摘要
目的研究进展性脑梗死发病特点,观察丁苯酞联合降纤、抗血小板治疗的临床疗效。
方法选择2009年5月至2009年11月吉林大学中日联谊医院神经内科收治的277例在72小时内发病的急性脑梗死患者,研究梗死分型与进展的关系,并比较进展性脑梗死患者进展时间的特点。记录其中72例进展患者及205例非进展患者的相关临床观测指标,进行危险因素分析。将完成规范治疗的进展患者随机分为A组(丁苯酞联合巴曲酶、奥扎格雷钠组)35例,B组(巴曲酶、奥扎格雷钠组)32例,非进展患者随机分为A组42例,B组45例,对照比较两组患者治疗前后的疗效。
结果完全性前循环、后循环、部分前循环组间及同总体进展率比较均有显著差异(P<0.05),完全性前循环(TACI)进展率最高,后循环(POCI)占所有进展患者的比例最多。颈内动脉系统梗死(ICAS)以24小时内进展多见(P<0.05),椎基底动脉系统梗死(VBAS)在24~72小时及72小时~1周内进展患者比率较前循环有显著差异性(P<0.05)。在进展及非进展患者的单因素分析中,眩晕、颈动脉硬化斑块或狭窄、低密度脂蛋白(LDL)异常、白细胞(WBC)升高在两组间比较有显著差异性(P<0.05),而糖尿病、头痛、发热、甘油三酯(TG)等两组比较无明显差异(P>0.05),并对上述有显著差异的指标进行多因素logistic回归分析显示,颈动脉硬化斑块或狭窄、高血压与进展性脑梗死较其他因素有统计学意义(P<0.05)。进展性脑梗死A、B组在治疗后第3天、第7天NIHSS评分比较无显著差异(P>0.05),在治疗第14天后两组NIHSS评分有显著差异性(P<0.05)。非进展组A、B组在治疗后第3天比较无显著差异(P>0.05),在治疗第7天及14天后两组评分有显著差异(P<0.05)。而Barthel评分和临床疗效评分两组比较均无显著差异(P>0.05)。
结论脑梗死OCSP分型中TACI进展率较高,POCI占所有进展患者的比例较高;按脑血管解剖分型中ICAS梗死以24小时内进展多见,VBAS梗死以发病24小时后至1周内进展多见;高血压病、LDL异常、WBC增高、血管斑块或狭窄、眩晕是PCI的危险因素,其中血管斑块及狭窄、高血压病与PCI关系更为密切;丁苯酞联合降纤、抗血小板多靶点治疗进展与非进展性脑梗死均能有效改善神经功能,联合治疗优于单一降纤、抗血小板治疗。
Progressive cerebral infarction is one of the difficult and hot spots in the field of neurology,due to the pathogenesis of complex,varied clinical manifesta-tions and poor prognosis.More factors of progressive cerebral infarction are mutual interaction and complex,right now the recognized risk factors, including blood pressure, blood glucose,blood lipid abnormalities,obesity,high fibrinogen and other factors,which are closely related to progressive cerebral infarction is still more views in literature.Increase awareness of the status and risk factors for progressive cerebral infarction is important in the level of disease primary prevention and clinical work. Even early risk prediction,early disease assessment and early intervention treatment of progressive cerebral infarction, it is important in reducing the incidence of disease and improving the cure rate of the clinical disease and prognosis.
At present the drug of the treatment for progressive cerebral infarction, ultra-early thrombolytic of the application is more skilled within time window.If the treatment of acute cerebral infarction over time window,in particular treatment to prevent progressive cerebral infarction,including anti-platelet aggregation,defibrase,anticoagulant treatment.But because anti-platelet and fibrinolytic drugs to improve cerebral microcirculation and the promotion of brain cell metabolism are limitedand often only are applicated in acute phase, so improving the PCI neurological improvement is still not satisfactory.Although a significant reduction in the mortality rate and morbidity,but are often limited to the acute phase applications, sub-acute phase of limited application.Therefore, in improve neurological function of patients with progressive cerebral infarction is still not satisfactory.
Butylphthalide is an China's independent property rights of new drugs independent research and development,now has completed phase IV clinical studies.Drugs mechanism include:increasing ischemic district cerebral perfusion, reducing infarct area,improving mitochondrial function,improving cerebral metabolism,especially improving cerebral ischemia District Microcirculation obviously. It has been approved the treatment of cerebral vascular disease applied to 1 line medication. In early large clinical cases observation,the drug's efficacy is recognized.Currently clinical trials of the butylphthalide combined defibrase, antiplatelet drug therapy for progressive cerebral infarction have not been reported at home and abroad.Defibrase,anti-platelet therapy is mainly used to prevent blood clots progress and restore the treatment of ischemic vascular perfusion,if can be used to joint butylphthalide,it can effectively improve ischemic brain microcirculation,may improve the prognosis of patients with effective and guide clinical work.In recent years foreign scholars also have suggest patients to propose the treatment of joint,multi-targeted therapy program,especially those with acute cerebral infarction and a tendency to progress in the early cerebral infarction.
In this paper,we will examine the characteristics of cerebral infarction,and observed the clinical efficacy of Butylphthalide joint defibrase,anti-platelet therapy.277 patients within 72 hours incidence of cerebral infarction,were used to study the relationship between the infarction type and progress, compare the the statistical analysis of time in patients with progressive cerebral infarction.These patients who came form May to November 2009 in Department of Neurology of Jilin University China-Japan Friendship Hospital.Recording 72 progressive patients and 205 cases of clinical non-progress patients,and observing progress indicators, risk factors. Patients of progressive cerebral infarction were randomly divided into A group (butylphthalide combined defibrase ,antiplatelet) 35 cases,B group (defibrase,antiplatelet) 32 cases ,patients of non-progress were divided into A group 42 cases, B group 45 cases, comparisons of the A,B before and after treatment the efficacy of the two groups.
Progress rates of total anterior circulation,posterior circulation,partial anterior circulation group compared with the general progress of the rate was significantly different (P <0.05),complete anterior circulation,has the highest rate of progress , posterior circulation account for the largest proportion of progressiv patients. Patients of carotid infarct within 24 hours to progress were more common (P<0.05), patients of vertebrobasilar infarction in 24 to 72 hours and 72 hours to 1 week compared with the rate of progress of anterior circulation's patients with significant differences (P<0.05).Progress patients and non-progress patients with single-factor analysis,dizziness,arteriosclerosis-prone plaque or stenosis, low-density lipoprotein (LDL) abnormal,white blood cell (WBC) increasing in both groups had significant difference (P<0.05),while diabetes, headache, fever, triglyceride (TG) and other factors showed no significant difference (P>0.05); And multivariate logistic regression analysis of the above significantly different indicators showed that carotid atherosclerosis-prone plaqueor stenosis, hyperten- sion were statistically significant than other factors (P<0.05). NIHSS score of progress infarction A,B group showed no significant difference (P>0.05) on 3 days,7 days after treatment,NIHSS score of 14 days after the two groups was significant difference (P<0.05).Non-progression group A, B group after treatment of 3 days showed no significant difference (P>0.05), in the treatment of 7 days and 14 days after the two rates are significantly different (P<0.05).The Barthel score and clinical score between the two groups had no significant difference (P>0.05).
Based on the characteristics of progressive cerebral infarction,and butylph-thalide combined defibrase,antiplatelet therapy on cerebral infarction progress, reaching the following conclusions:TACI has greater progress rate in infarction OCSP classification,POCI patients accounted for a higher proportion of all;Patients of ICAS infarction within 24 hours were more common by cerebral vascular anatomy typing,VBAS infarction with onset after 24 hours to 1 week was more common progress;Hypertension,LDL abnormal,WBC increasing, vascular plaque or stenosis,dizziness were risk factors for PCI,in which plaques or stenosis,hypertension were more closely with PCI;Butylphthalide combined defibrase,antiplatelet multi-targeted treatment of progressive and non- progressive cerebral infarction can improve neurological function, combination therapy is superior to singled efibrase,anti-platelet therapy.
方法选择2009年5月至2009年11月吉林大学中日联谊医院神经内科收治的277例在72小时内发病的急性脑梗死患者,研究梗死分型与进展的关系,并比较进展性脑梗死患者进展时间的特点。记录其中72例进展患者及205例非进展患者的相关临床观测指标,进行危险因素分析。将完成规范治疗的进展患者随机分为A组(丁苯酞联合巴曲酶、奥扎格雷钠组)35例,B组(巴曲酶、奥扎格雷钠组)32例,非进展患者随机分为A组42例,B组45例,对照比较两组患者治疗前后的疗效。
结果完全性前循环、后循环、部分前循环组间及同总体进展率比较均有显著差异(P<0.05),完全性前循环(TACI)进展率最高,后循环(POCI)占所有进展患者的比例最多。颈内动脉系统梗死(ICAS)以24小时内进展多见(P<0.05),椎基底动脉系统梗死(VBAS)在24~72小时及72小时~1周内进展患者比率较前循环有显著差异性(P<0.05)。在进展及非进展患者的单因素分析中,眩晕、颈动脉硬化斑块或狭窄、低密度脂蛋白(LDL)异常、白细胞(WBC)升高在两组间比较有显著差异性(P<0.05),而糖尿病、头痛、发热、甘油三酯(TG)等两组比较无明显差异(P>0.05),并对上述有显著差异的指标进行多因素logistic回归分析显示,颈动脉硬化斑块或狭窄、高血压与进展性脑梗死较其他因素有统计学意义(P<0.05)。进展性脑梗死A、B组在治疗后第3天、第7天NIHSS评分比较无显著差异(P>0.05),在治疗第14天后两组NIHSS评分有显著差异性(P<0.05)。非进展组A、B组在治疗后第3天比较无显著差异(P>0.05),在治疗第7天及14天后两组评分有显著差异(P<0.05)。而Barthel评分和临床疗效评分两组比较均无显著差异(P>0.05)。
结论脑梗死OCSP分型中TACI进展率较高,POCI占所有进展患者的比例较高;按脑血管解剖分型中ICAS梗死以24小时内进展多见,VBAS梗死以发病24小时后至1周内进展多见;高血压病、LDL异常、WBC增高、血管斑块或狭窄、眩晕是PCI的危险因素,其中血管斑块及狭窄、高血压病与PCI关系更为密切;丁苯酞联合降纤、抗血小板多靶点治疗进展与非进展性脑梗死均能有效改善神经功能,联合治疗优于单一降纤、抗血小板治疗。
Progressive cerebral infarction is one of the difficult and hot spots in the field of neurology,due to the pathogenesis of complex,varied clinical manifesta-tions and poor prognosis.More factors of progressive cerebral infarction are mutual interaction and complex,right now the recognized risk factors, including blood pressure, blood glucose,blood lipid abnormalities,obesity,high fibrinogen and other factors,which are closely related to progressive cerebral infarction is still more views in literature.Increase awareness of the status and risk factors for progressive cerebral infarction is important in the level of disease primary prevention and clinical work. Even early risk prediction,early disease assessment and early intervention treatment of progressive cerebral infarction, it is important in reducing the incidence of disease and improving the cure rate of the clinical disease and prognosis.
At present the drug of the treatment for progressive cerebral infarction, ultra-early thrombolytic of the application is more skilled within time window.If the treatment of acute cerebral infarction over time window,in particular treatment to prevent progressive cerebral infarction,including anti-platelet aggregation,defibrase,anticoagulant treatment.But because anti-platelet and fibrinolytic drugs to improve cerebral microcirculation and the promotion of brain cell metabolism are limitedand often only are applicated in acute phase, so improving the PCI neurological improvement is still not satisfactory.Although a significant reduction in the mortality rate and morbidity,but are often limited to the acute phase applications, sub-acute phase of limited application.Therefore, in improve neurological function of patients with progressive cerebral infarction is still not satisfactory.
Butylphthalide is an China's independent property rights of new drugs independent research and development,now has completed phase IV clinical studies.Drugs mechanism include:increasing ischemic district cerebral perfusion, reducing infarct area,improving mitochondrial function,improving cerebral metabolism,especially improving cerebral ischemia District Microcirculation obviously. It has been approved the treatment of cerebral vascular disease applied to 1 line medication. In early large clinical cases observation,the drug's efficacy is recognized.Currently clinical trials of the butylphthalide combined defibrase, antiplatelet drug therapy for progressive cerebral infarction have not been reported at home and abroad.Defibrase,anti-platelet therapy is mainly used to prevent blood clots progress and restore the treatment of ischemic vascular perfusion,if can be used to joint butylphthalide,it can effectively improve ischemic brain microcirculation,may improve the prognosis of patients with effective and guide clinical work.In recent years foreign scholars also have suggest patients to propose the treatment of joint,multi-targeted therapy program,especially those with acute cerebral infarction and a tendency to progress in the early cerebral infarction.
In this paper,we will examine the characteristics of cerebral infarction,and observed the clinical efficacy of Butylphthalide joint defibrase,anti-platelet therapy.277 patients within 72 hours incidence of cerebral infarction,were used to study the relationship between the infarction type and progress, compare the the statistical analysis of time in patients with progressive cerebral infarction.These patients who came form May to November 2009 in Department of Neurology of Jilin University China-Japan Friendship Hospital.Recording 72 progressive patients and 205 cases of clinical non-progress patients,and observing progress indicators, risk factors. Patients of progressive cerebral infarction were randomly divided into A group (butylphthalide combined defibrase ,antiplatelet) 35 cases,B group (defibrase,antiplatelet) 32 cases ,patients of non-progress were divided into A group 42 cases, B group 45 cases, comparisons of the A,B before and after treatment the efficacy of the two groups.
Progress rates of total anterior circulation,posterior circulation,partial anterior circulation group compared with the general progress of the rate was significantly different (P <0.05),complete anterior circulation,has the highest rate of progress , posterior circulation account for the largest proportion of progressiv patients. Patients of carotid infarct within 24 hours to progress were more common (P<0.05), patients of vertebrobasilar infarction in 24 to 72 hours and 72 hours to 1 week compared with the rate of progress of anterior circulation's patients with significant differences (P<0.05).Progress patients and non-progress patients with single-factor analysis,dizziness,arteriosclerosis-prone plaque or stenosis, low-density lipoprotein (LDL) abnormal,white blood cell (WBC) increasing in both groups had significant difference (P<0.05),while diabetes, headache, fever, triglyceride (TG) and other factors showed no significant difference (P>0.05); And multivariate logistic regression analysis of the above significantly different indicators showed that carotid atherosclerosis-prone plaqueor stenosis, hyperten- sion were statistically significant than other factors (P<0.05). NIHSS score of progress infarction A,B group showed no significant difference (P>0.05) on 3 days,7 days after treatment,NIHSS score of 14 days after the two groups was significant difference (P<0.05).Non-progression group A, B group after treatment of 3 days showed no significant difference (P>0.05), in the treatment of 7 days and 14 days after the two rates are significantly different (P<0.05).The Barthel score and clinical score between the two groups had no significant difference (P>0.05).
Based on the characteristics of progressive cerebral infarction,and butylph-thalide combined defibrase,antiplatelet therapy on cerebral infarction progress, reaching the following conclusions:TACI has greater progress rate in infarction OCSP classification,POCI patients accounted for a higher proportion of all;Patients of ICAS infarction within 24 hours were more common by cerebral vascular anatomy typing,VBAS infarction with onset after 24 hours to 1 week was more common progress;Hypertension,LDL abnormal,WBC increasing, vascular plaque or stenosis,dizziness were risk factors for PCI,in which plaques or stenosis,hypertension were more closely with PCI;Butylphthalide combined defibrase,antiplatelet multi-targeted treatment of progressive and non- progressive cerebral infarction can improve neurological function, combination therapy is superior to singled efibrase,anti-platelet therapy.
引文
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[53]Offner H,Subramanian S,Parker M,et al.Eperimental stroke induces massive,rapid activation of the peripheral immune system[J].J Cereb Blood FlowMetab,2006,26(5):654-665.
[54]Haverkate F.Levels of homeostatic factors, arteriosclaeosis and cardiovascular disease [J]. Vasc Pharmaco,l 2002, 39: 109-112.
[55]Poredos P. Endothelial dysfunction in the pathogensis of atherosclerosis[J]. IntAngio,l 2002, 21: 109-116.
[56]Corrado E,Rizzo M,Tantillo R.Markers of inflammation and infection influence the outcome of patients with baseline asymptomatic carotid lesions[J].Stroke,2006,37(2):482-486.
[57]Blum A,Peleg A,Weinberg M.Anti-cytomegalovirus(CMV) IgG antibody titer in patients with risk factors to atherosclerosis[J].Clin Exp Med,2003,3(3):157-160.
[58]Vroon A, Kavelaars A, LimmrothV, et al. G protein-coupled receptor kinase 2 in multiple sclerosis and experimental autodimmune encephalomyelitis [J]. J Immunol,2005, 174: 4400-4406. [59Hung CH, Chang NC, Cheng BC, et al. Progressive exercise preconditioning protectsagainst circulatory shock during experimental heatstroke [J]. Shock,2005,23: 426-433.
[60]OahL,Misz M,Bereczki D,et al.Low doses of acetylsalicylic acid effectively inhibits thrombocyte aggregation after ischemic stroke[J]. Orv Hetil,1996,137(9):455-459.
[61]Gustafson K,Hagberg H,Bengtsson G,et al.Possible protective role of growth horm- one in hypoxia-ischemia in neonatal rats[J].Pediatr Res,2001,45(3):318-323.
[62]Matsumori A, Takano H, Obata JE. Circulating hepatocyte growth factor as a diagno- sticmarker of thrombud formation in patientswith cerebral infarction [J].Circ J, 2002, 66(2): 216-218.
[63]Haapaniemi E,Soinne L,Syrjala M,et al.Serial changes in fibrinolysis and coagulation activation markers in acute and convalescentphase of ischemic stroke[J].Acta Neurol Scand,2004,110(4):242-247.
[64]Del Sette M,Eliasziw M,Streifler JY,et al.Internal borderzone infarction:a marker for severe stenosis in patients with sympromatic internal carotid artery disease[J]. Stroke,2000,31(3):631-635.
[65]Angeloni U,Bozzao L,Fantozzi L.Internal borderzone infarction following acute middle celebral artery ocdusion[J]. Neurology,1990,40(8):1196-1198.
[66]Momjian M,Baron J.The pathophysiology of watershed infarction in internal carotid artery disease:Review of cerebral perfusion studies[J].Stroke,2005,36(3):567-577.
[67]Chave CJ,Silver B,Schlaug G,et al.Diffusion and perfusion weighted MRI patterns in borderzone infarcts[J].Stroke,2000, 31(5):1090-1096.
[68]Davalos A,Blanco M,Pedraza S,et al.The clinical-DWI mismatch:a new diagnostic approach to the brain tissue at risk of infarction[J] .Neurology,2004,62:2187-2192.
[69]黄如训.良好的脑血循环是脑梗死治疗的根本[J].中国卒中杂志,2008,3(8):547-550.
[70]Krupinskin J,Lssa R,Bujny T,et al.A putative role for platelet derived growth factor in angiogenesis and neuroprotection after ischemic stroke in man[J].Stroke,2004,28:561-657.
[71]Indredqvik B,Bakke F. Treatment in a combined acute and rehabilitation stroke unit: Which aspects are most important[J]. Stroke,2005,30(4):917.
[72]Roquer J,RodriguezCampello A,Gomis M, et al .Acute stroke unit care and early neurological deterioration in ischemic stroke[J]. J Neurol, 2008, 255: 1012-1017.
[73]Rudd AG,Hoffman A,Down C,et al.Access to stroke care in England,Wales and Northern Ireland: the effect of age, gender and weekend admission[J].Age Ageing,2007,36: 247-255.
[74]Terent A,Asplund K,Farahmand B,er al.Stroke unit care revisited-who benefits the most?A cohort study of 105043 patients in Riks-Stroke,the Swedish Stroke Register[J].J NeurolNeurosurg Psychiatry,2009 Mar 29.[Epub ahead of print]
[75]Stroke Unit Trialists’Collaboration.Organised inpatient care for stroke[J].The Coc- hrane Datebase of Systematic Reviwes,2001,issue 3.
[76]Govan L,Weir CJ,Langhorne P,et al.Organized inpatient (stroke unit) care for stroke[J]. Stroke, 2008,39:2402-2408.
[77]Candelise L, Bersano A. Stroke units in Italy[J].Neurol Sci, 2006, 27: 223-224.
[78]Epifanov Y,Dodel R,Haacke C, et al. Costs of acute stroke care on regular neurologicalwards: a comparison with stroke unit setting[J].Health Policy,2007, 81: 339-349.
[1]Christensen H,Boysen G,Johannesen HH.Deteriorating ischemic Stroke cytokines, soluble cytokines receptors,ferritin,systematic blood pressure,body temperature, blood glucose, diabetes,stroke severity and CT infarction volume as predictors of deteriorating ischemic stroke[J]. Neurol Sci,2002,15(1):1-7.
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[53]Offner H,Subramanian S,Parker M,et al.Eperimental stroke induces massive,rapid activation of the peripheral immune system[J].J Cereb Blood FlowMetab,2006,26(5):654-665.
[54]Haverkate F.Levels of homeostatic factors, arteriosclaeosis and cardiovascular disease [J]. Vasc Pharmaco,l 2002, 39: 109-112.
[55]Poredos P. Endothelial dysfunction in the pathogensis of atherosclerosis[J]. IntAngio,l 2002, 21: 109-116.
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[60]OahL,Misz M,Bereczki D,et al.Low doses of acetylsalicylic acid effectively inhibits thrombocyte aggregation after ischemic stroke[J]. Orv Hetil,1996,137(9):455-459.
[61]Gustafson K,Hagberg H,Bengtsson G,et al.Possible protective role of growth horm- one in hypoxia-ischemia in neonatal rats[J].Pediatr Res,2001,45(3):318-323.
[62]Matsumori A, Takano H, Obata JE. Circulating hepatocyte growth factor as a diagno- sticmarker of thrombud formation in patientswith cerebral infarction [J].Circ J, 2002, 66(2): 216-218.
[63]Haapaniemi E,Soinne L,Syrjala M,et al.Serial changes in fibrinolysis and coagulation activation markers in acute and convalescentphase of ischemic stroke[J].Acta Neurol Scand,2004,110(4):242-247.
[64]Del Sette M,Eliasziw M,Streifler JY,et al.Internal borderzone infarction:a marker for severe stenosis in patients with sympromatic internal carotid artery disease[J]. Stroke,2000,31(3):631-635.
[65]Angeloni U,Bozzao L,Fantozzi L.Internal borderzone infarction following acute middle celebral artery ocdusion[J]. Neurology,1990,40(8):1196-1198.
[66]Momjian M,Baron J.The pathophysiology of watershed infarction in internal carotid artery disease:Review of cerebral perfusion studies[J].Stroke,2005,36(3):567-577.
[67]Chave CJ,Silver B,Schlaug G,et al.Diffusion and perfusion weighted MRI patterns in borderzone infarcts[J].Stroke,2000, 31(5):1090-1096.
[68]Davalos A,Blanco M,Pedraza S,et al.The clinical-DWI mismatch:a new diagnostic approach to the brain tissue at risk of infarction[J] .Neurology,2004,62:2187-2192.
[69]黄如训.良好的脑血循环是脑梗死治疗的根本[J].中国卒中杂志,2008,3(8):547-550.
[70]Krupinskin J,Lssa R,Bujny T,et al.A putative role for platelet derived growth factor in angiogenesis and neuroprotection after ischemic stroke in man[J].Stroke,2004,28:561-657.
[71]Indredqvik B,Bakke F. Treatment in a combined acute and rehabilitation stroke unit: Which aspects are most important[J]. Stroke,2005,30(4):917.
[72]Roquer J,RodriguezCampello A,Gomis M, et al .Acute stroke unit care and early neurological deterioration in ischemic stroke[J]. J Neurol, 2008, 255: 1012-1017.
[73]Rudd AG,Hoffman A,Down C,et al.Access to stroke care in England,Wales and Northern Ireland: the effect of age, gender and weekend admission[J].Age Ageing,2007,36: 247-255.
[74]Terent A,Asplund K,Farahmand B,er al.Stroke unit care revisited-who benefits the most?A cohort study of 105043 patients in Riks-Stroke,the Swedish Stroke Register[J].J NeurolNeurosurg Psychiatry,2009 Mar 29.[Epub ahead of print]
[75]Stroke Unit Trialists’Collaboration.Organised inpatient care for stroke[J].The Coc- hrane Datebase of Systematic Reviwes,2001,issue 3.
[76]Govan L,Weir CJ,Langhorne P,et al.Organized inpatient (stroke unit) care for stroke[J]. Stroke, 2008,39:2402-2408.
[77]Candelise L, Bersano A. Stroke units in Italy[J].Neurol Sci, 2006, 27: 223-224.
[78]Epifanov Y,Dodel R,Haacke C, et al. Costs of acute stroke care on regular neurologicalwards: a comparison with stroke unit setting[J].Health Policy,2007, 81: 339-349.
[1]Christensen H,Boysen G,Johannesen HH.Deteriorating ischemic Stroke cytokines, soluble cytokines receptors,ferritin,systematic blood pressure,body temperature, blood glucose, diabetes,stroke severity and CT infarction volume as predictors of deteriorating ischemic stroke[J]. Neurol Sci,2002,15(1):1-7.
[2]Homig CR,Rust DS,Busse O,et al.Space-occupying cerebellar infarction. Clinical course and prognosis[J].Stroke,2004,25(2):372-374.
[3]Shiozaki T,Nakajimay Y,Taneda M,et al.Efficacy of moderate hypotherinia in patients with severe head injury and intracranial hyertension refractory to mild hypothermia[J].J Neurosurg,2003, 99(1):47-51.
[4]Birschel P,Ellul J,Barer D.Progressing stroke:towards an internation ally agreed definition[J].Cerebrovasc Dis,2004,17(2 -3): 242-252.
[5]Hyun-Kil Shin,Kyung-Moo Yoo,HuiMeng Chang,et al.Bilateral intracranial vertebral artery disease in the New England Medical Center posterior circulation registry[J].Arch Neurol,1999,56:1353-1358.
[6]Boyle JJ. Macrophage activation in the roscleros is: Parhogenes is and pharmacology of plaque rupture [J]. Curr Vasc Phamacol 2005, 3: 63-68.
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