蛛网膜下腔出血患者迟发性脑血管痉挛相关因素的临床分析
|
摘要
研究背景:蛛网膜下腔出血(subarachnoid hemorrhage,SAH)是指各种原因引起的脑血管突然破裂,血液流至蛛网膜下腔的统称,占急性脑血管意外的15%左右,具有很高的死亡率和致残率。蛛网膜下腔出血患者转归不良主要有3个重要原因为:1、SAH的直接结果:包括急性缺血性神经功能缺损(acuteischemic neurological deficit,AIND)、血肿和脑水肿;2、再出血:发生率很高,SAH后2周内约为20%;3、迟发性脑血管痉挛(delayed cerebral vasospasm,DCVS):可造成脑缺血或脑损害,蛛网膜下腔出血患者,约70%并发DCVS;36%患者于此基础上继发延迟性缺血性神经功能障碍(delayed ischemicneurological deficit,DIND),是蛛网膜下腔出血后死亡或残疾的最主要原因。在动脉瘤手术或血管内治疗技术和疗效提高的情况下,再出血问题已得到较好解决,对DCVS预防和处理的研究显得越来越重要。因此研究SAH迟发性CVS(DCVS)发生的相关临床因素,对防治DIND并发症的发生,降低SAH患者残疾、死亡率有重要意义。
目的:探讨蛛网膜下腔出血(SAH)患者迟发性脑血管痉挛(DCVS)的临床影响因素,从而为临床上预防蛛网膜下腔出血患者发生迟发性脑血管痉挛提供参考。
材料和方法:回顾性队列分析南方医科大学珠江医院自2005年1月至2008年12月收治的74例动脉瘤性SAH患者的临床资料,判定DCVS,统计患者的年龄、吸烟史、出血次数、Hunt-Hess分级、Fisher分级、白细胞计数峰值等因素的分布,应用SPSS13.0统计软件分析各因素与DCVS的关系,对初步筛选预期变量采用χ~2检验,对可能引起DCVS的预期变量采用非条件多因素Logistic回归分析,以确定影响DCVS的危险因素,以P≤0.05为差异有统计学意义。
结果:本组74例患者中有37例发生DCVS,总发生率50%。其中,≤60岁患者DCVS发生率为56.9%(33/58),出血二次以上患者发生率为81.8%(9/11),吸烟组患者发生率为76.9%(10/13),Hunt-Hess分级Ⅲ级以上患者发生率为68.1%(32/47),Fisher分级Ⅲ以上患者发生率为83.8%(31/37),白细胞计数峰值＞15×10~9/L患者发生率为75.0%(12/16),以上各因素组迟发性脑血管痉挛(DCVS)发生率与相应对照组比较均有统计学差异(P＜0.05)。而高血压、高血糖及性别因素与DCVS的发生无统计学差异(P＞0.05)。根据以上各危险因素分析结果,对有统计意义的6个因素分别赋值进行非条件Logistic回归分析,发现年龄、出血次数、Fisher分级、Hunt-Hess分级均进入最终模型,为DCVS发生的独立危险因素。其中,年龄因素的偏回归系数为—2.702,提示年龄与DCVS的发生呈负相关,年龄越小DCVS发生率越高。整个回归模型对组内病例的判对率为85.1%。
结论:低年龄、出血2次以上及Hunt-Hess分级或Fisher分级Ⅲ级以上患者更易发生迟发性脑血管痉挛,临床上对此类患者应加强监测、及早发现和处理迟发性脑血管痉挛,改善患者预后。
Background:Subarachnoid hemorrhage(SAH)is due to the blood leaking into the subarachnoid space because of the sudden rupture of cerebral vessels,which accouts up to 15%in cerebral vascular diseses,and causes high morbidities and disabilities. poor prognosis mainly result from 3 factors:1.AIND,hemorrhage,brain oedema.2.reoccurence of hemmorrhage.3.DCVS.About 70%patients had the complication of DCVS which eventually results in brain ischemia or brain damage,and 36%of these patients suffered from DIND,which is the main reason of deaths or disabilities of the patients after SAH.With the improvement of aneurysm clipping technique and effect of treatment,the problem of rebleeding has been resolved,but the prevention of DCVS still needs more research,so,it is very important to study the clinical factors causing DCVS and decrease the occurence of DIND so as to decrease the rate of disabilities and death in patients with SAH.
Objective:To explore the risk factors of delayed cerebral vasospasm following aneurysmal subarachnoid hemorrhage.
Methods:The clinical data of 74 patients from Jan 2005 to Dec 2008 with SAH were selected and analysed retrospectively.Six factors including age,history of smoking, number of bleeding,Hunt-Hess grading,Fisher grading and the peak value of white cell count were recorded,The severity of cerebral vasospasm was determined by DSA. The risk factors related to delayed cerebral vasospasm were analysed.All data were dealt with SPSS13.0 software to find the relation between factors and DCVS and select variants using Chi-square.A P value less than 0.05 was considered statistically significant.
Results:37 of 74 patients in this group were diagnosed DCVS,56.9%in patients less than 60 years old,81.8%in patients with history of bleeding more than twice,76.9% in patients with history of somking,68.1%and 83.8%in patients ranked in Hunt-Hess grading or Fisher grading respectively,75%in patients with white cell over 15×10~9/L,So,age,number of bleeding,history of smoking,Hunt-Hess grade, Fisher grade and peak concurrency of white blood cell count are significantly related to the occurrences of delayed cerebral vasospasm.Among above factors,age,number of bleeding,Hunt -Hess grading,Fisher grading are the independent factors of delayed cerebral vasospasm.Hypertensio,sex and hyperglucemia has no significant correlation with DCVS.Age has the negtive correlation with DCVS,the younger the patient is,the higher probability of DCVS occour.The whole model correct judgement is 85.1%.
Conclusions:The patients of lower age,hemorrhage more than twice,Hunt-Hess grading or Fisher grading overⅢare more susceptible to delayed cerebral vasospasm,such patients should be closely monitored and delt with in time in case of delayed cerebral vasospasm.
目的:探讨蛛网膜下腔出血(SAH)患者迟发性脑血管痉挛(DCVS)的临床影响因素,从而为临床上预防蛛网膜下腔出血患者发生迟发性脑血管痉挛提供参考。
材料和方法:回顾性队列分析南方医科大学珠江医院自2005年1月至2008年12月收治的74例动脉瘤性SAH患者的临床资料,判定DCVS,统计患者的年龄、吸烟史、出血次数、Hunt-Hess分级、Fisher分级、白细胞计数峰值等因素的分布,应用SPSS13.0统计软件分析各因素与DCVS的关系,对初步筛选预期变量采用χ~2检验,对可能引起DCVS的预期变量采用非条件多因素Logistic回归分析,以确定影响DCVS的危险因素,以P≤0.05为差异有统计学意义。
结果:本组74例患者中有37例发生DCVS,总发生率50%。其中,≤60岁患者DCVS发生率为56.9%(33/58),出血二次以上患者发生率为81.8%(9/11),吸烟组患者发生率为76.9%(10/13),Hunt-Hess分级Ⅲ级以上患者发生率为68.1%(32/47),Fisher分级Ⅲ以上患者发生率为83.8%(31/37),白细胞计数峰值＞15×10~9/L患者发生率为75.0%(12/16),以上各因素组迟发性脑血管痉挛(DCVS)发生率与相应对照组比较均有统计学差异(P＜0.05)。而高血压、高血糖及性别因素与DCVS的发生无统计学差异(P＞0.05)。根据以上各危险因素分析结果,对有统计意义的6个因素分别赋值进行非条件Logistic回归分析,发现年龄、出血次数、Fisher分级、Hunt-Hess分级均进入最终模型,为DCVS发生的独立危险因素。其中,年龄因素的偏回归系数为—2.702,提示年龄与DCVS的发生呈负相关,年龄越小DCVS发生率越高。整个回归模型对组内病例的判对率为85.1%。
结论:低年龄、出血2次以上及Hunt-Hess分级或Fisher分级Ⅲ级以上患者更易发生迟发性脑血管痉挛,临床上对此类患者应加强监测、及早发现和处理迟发性脑血管痉挛,改善患者预后。
Background:Subarachnoid hemorrhage(SAH)is due to the blood leaking into the subarachnoid space because of the sudden rupture of cerebral vessels,which accouts up to 15%in cerebral vascular diseses,and causes high morbidities and disabilities. poor prognosis mainly result from 3 factors:1.AIND,hemorrhage,brain oedema.2.reoccurence of hemmorrhage.3.DCVS.About 70%patients had the complication of DCVS which eventually results in brain ischemia or brain damage,and 36%of these patients suffered from DIND,which is the main reason of deaths or disabilities of the patients after SAH.With the improvement of aneurysm clipping technique and effect of treatment,the problem of rebleeding has been resolved,but the prevention of DCVS still needs more research,so,it is very important to study the clinical factors causing DCVS and decrease the occurence of DIND so as to decrease the rate of disabilities and death in patients with SAH.
Objective:To explore the risk factors of delayed cerebral vasospasm following aneurysmal subarachnoid hemorrhage.
Methods:The clinical data of 74 patients from Jan 2005 to Dec 2008 with SAH were selected and analysed retrospectively.Six factors including age,history of smoking, number of bleeding,Hunt-Hess grading,Fisher grading and the peak value of white cell count were recorded,The severity of cerebral vasospasm was determined by DSA. The risk factors related to delayed cerebral vasospasm were analysed.All data were dealt with SPSS13.0 software to find the relation between factors and DCVS and select variants using Chi-square.A P value less than 0.05 was considered statistically significant.
Results:37 of 74 patients in this group were diagnosed DCVS,56.9%in patients less than 60 years old,81.8%in patients with history of bleeding more than twice,76.9% in patients with history of somking,68.1%and 83.8%in patients ranked in Hunt-Hess grading or Fisher grading respectively,75%in patients with white cell over 15×10~9/L,So,age,number of bleeding,history of smoking,Hunt-Hess grade, Fisher grade and peak concurrency of white blood cell count are significantly related to the occurrences of delayed cerebral vasospasm.Among above factors,age,number of bleeding,Hunt -Hess grading,Fisher grading are the independent factors of delayed cerebral vasospasm.Hypertensio,sex and hyperglucemia has no significant correlation with DCVS.Age has the negtive correlation with DCVS,the younger the patient is,the higher probability of DCVS occour.The whole model correct judgement is 85.1%.
Conclusions:The patients of lower age,hemorrhage more than twice,Hunt-Hess grading or Fisher grading overⅢare more susceptible to delayed cerebral vasospasm,such patients should be closely monitored and delt with in time in case of delayed cerebral vasospasm.
引文
[1]吴在德主编,外科学,人民卫生出版社,2002年版,315
[2]Mayberg MR.Cerebral vasospasm.Neurosurg Clin N Am,1998,9:615-627.
[3]刘建民,洪波.脑血管痉挛研究进展.《心脑血管病防治》2006年12月第6卷第6期:345-346.
[4]刘承基教授主编。脑血管外科学江苏科技出版社:2000年版,10-21
[5]Echlin FA.Spasm of basilar and vertebral arteries caused by experimental subarachnoid hemorrhage.J Neurosurg.1965 Jul;23(1):1-11.
[6]Arutiunov AI,Baron MA,Majorova NA.The role of mechanical factors in the pathogenesis of short-term and prolonged spasm of the cerebral arteries.J Neurosurg.1974 Apt;40(4):459-72.
[7] Sercombe R,Tran Dinh YR, Gomis P. Cerebrovascular inflammation following subarachnoid hemorrhageJ .Jpn Pharmacol ,2002 ,88 3 :227-249.
[8] Park KW, MetaisC, DaiHB, et al. Microvascular endothelial dysfunction and its mechanism a rat model of subarachnoid hemorrhage. Anesth Aalg, 2001, 92: 990-996.
[9] Onoue H, TsutsuiM, SmithL, etal. Expression and functionof recombinant endothelial nitric oxide synthase gene in canine basilar artery after experimental subarachnoid hemorrhage. Stroke, 1998,29: 1959-1965.
[10]ZimmermannM. Endothelin in cerebral vasospasm. Clinical and experimental results. J Neurosurg, 1997,41: 139-151.
[11]Mascia L, Fedorko L, StewartDJ, et al. Temporal relationship between endothelin-1 concentrations and cerebral vasospasm in patients with aneurysmal subarachnoid hemorrhage. Stroke, 2001,32: 1185-1190.
[12] Wickman G, Lan C, VollrathB. Functional rolesof the rho/rho kinase pathway and protein kinase C in the regulation of cerebrovascular constriction mediated by hemoglobin: relevance to subarachnoid hemorrhage and vasospasm. Circ Res, 2003,92: 809 - 816.
[13]Satoh M, Parent AD, Zhang J H. Inhibitory effect with antisense 驶 mitogen-activated protein kinase oligodeoxynucleotide against cerebral vasospam in rats. Stroke, 2002, 33: 775 - 781.
[14] Sampson LJ, Hinton JM, Garland CJ. Evidence for expression and function of phosphodiesterase type 5(PDE-Ⅴ)in rat resistance arteries. BrJ Pharmacol, 2001,132:13-17.
[15] Gabrielsen TO, Greitz T. Normal size of the internal carotid, middle cerebral and anterior cerebral arteries. Acta Radiol Diagn (Stockh). 1970 Jan;10(1):1-10.
[16] VenkateshB, ShenQ, Lipman J. Continuousmeasurementof cerebral blood flow velocityusing transcranialDoppler reveals significant moment-to-moment variability of data in healthy volunteers and in patientswith subarachnoid hemorrhage. CritCareMed, 2002, 30:563 - 569.
[17]Okada Y, Shima T, Nishida M, et al. Comparison of transcranial Doppler investigation of aneurysmal vasospasm with digital subtraction angiographic and clinical findings. Neurosurgery, 1999, 45:443 - 449.
[18] JabreA, BabikianV, PowsnerRA, et al. Role of single photon emission computed tomography and transcranialDoppler ultrasonography in clinical vasospasm. J ClinNeurosci, 2002, 9: 400 - 403.
[19]Tamatani S, Sasaki O, Takeuchi S, Fujii Y, Koike T, Tanaka R. Detection of delayed cerebral vasospasm, after rupture of intracranial aneurysms, by magnetic resonance angiography. Neurosurgery. 1997 Apr;40(4):748-53; discussion753-4.
[20] Handa Y, Weir BK, Nosko M, Mosewich R, Tsuji T, Grace M. The effect of timing of clot removal on chronic vasospasm in a primate model. J Neurosurg.1987
[21]BiondiA, Ricciardi GK, PuybassetL, et al. Intra-arterial nimodipine for the treatmentof symptomatic cerebral vasospasm after aneurysmal subarachnoid hemorrhage: preliminary results. AJNR Am J Neuroradiol, 2004, 25: 1067-1076.
[22] BadjatiaN, TopcuogluMA, PryorJC, etal. Preliminary experience with intra-arterial nicardipine as a treatment forcerebral vasospasm. AJNR Am J Neuroradiol, 2004, 25: 819 - 826.
[23] TreggiariMM, WalderB, Suter PM, et al. Systematic review of the prevention of delayed ischemic neurological deficitswith hypertension, hypervolemia, and hemodilution therapy following subarachnoid hemorrhage. J Neurosurg, 2003,98: 978 - 984.
[24]Jian-Kang Shen.The PathogenesisofCerebralVasospasm and Its Prevention and Treatment.IntJ CerebrovascDis, July2006, Vol14, No. 7:481-493.
[1] Treggiari MM, Walder B, Suter PM, et al. Systematic review of the prevention of delayed ischemic neurological deficits with hypertension, hypervolemia, and hemodilution therapy following subarachnoid hemorrhage[J]. J Neurosurg, 2003,98(5): 978-984.
[2] Mayberg MR.Cerebral vasospasm. Neurosurg Clin N Am. 1998 Jul;9(3):615-27.
[3] Dietrich HH, Dacey RG Jr. Molecular keys to the problems of cerebral vasospasm[J]. Neurosurgery, 2000,46(3): 517-530.
[4] Friedman J, Goepss SJ, Meyer FB, et al. Volumetric quantification of Fisher Grade 3 aneurysmal subarachnoid hemorrhage: a novel method to predict symptomatic vasospasm on admission computerized topography scans[J]. J Neuresurg, 2002, 97(2): 401-407.
[5] Macdonald RL, Rosengart A, Huo D, et al. Factors associated with the development of vasospasm after planned surgical treatment of aneurismal subarachnoid hemorrhage[J]. J Neurosurg, 2003,99(4): 644-652.
[6] Hirashima Y, Kurimoto M, Hori E, et al. Lower incidence of symptomatic vasospasm after subarachnoid hemorrhage owing to rupture vertebrobas-ilar aneurysms[J]. Neurosurgery, 2005, 57(6): 1110-1116.
[7] Charpentier C, Audibert G, Guillemin F, et al. Multivariate analysis of predictors of cerebral vasospasm occurrence after aneurysmal subarachnoid hemorrhage[J].Stroke. 1999, 30(7): 1402-1408.
[8] Torbey MT, Hauser TK, Bhardwaj A, et al. Effect of age on cerebral blood flow velocity and incidence of vasospasm after aneurismal subarachnoid hemorrhage[J]. Stroke, 2001, 32(9): 2005-2011.
[9] Wilkins RH. Cerebralterial Spasm[M]. Baltimore: Williams &Wilkins, 1980:284-286.
[10] McGirt MJ, Mavropoulos JC, McGirt LY, et al. Leukocytosis as an independent risk factor for cerebral vasospasm following aneurysmal subarachnoid hemorrhage[J]. J Neurosurg, 2003, 98(6): 1222-1226.
[1]Mayberg MR.Cerebral vasospasm.Neurosurg Clin N Am,1998,9:615-627.
[2]刘建民,洪 波.脑血管痉挛研究进展.《心脑血管病防治》2006年12月第6卷第6期:345-346。
[3]Charpentier C,Audibert G,Guillemin F,Civit T,Ducrocq X,Bracard S,Hepner H,Picard L,Laxenaire MC.Multivariate analysis of predictors of cerebral vasospasm occurrence afteraneurysmal subarachnoid hemorrhage.Stroke.1999Jul;30(7):1402-1408.
[4]TorbeyMT,Hauser TK,BhardwajA,et al.Effect of age on cerebral blood flow velocity and incidence of vasospasm after aneurismal subarachnoid hemorrhage.Stroke,2001,32:2005-2011.
[5]陈高,张建民,李珉,蔡菁.动脉瘤性SAH继发重度脑血管痉挛相关因素研究.中华神经外科杂志2005年11月第21卷第11期:665-667.
[6]胡丽葵,任艳.蛛网膜下腔出血后迟发性脑血管痉挛45例分析.中国冶金工业医学杂志2003年第20卷第2期:93.
[7]张忠延,赵凡.蛛网膜下腔出血后迟发性脑血管痉挛42例分析.卒中与神经疾病2001年第8卷第2期:87.
[8]Fisher CM,Kistler JP,Davis JM.Relation of cerebral vasospasm to subarachnoid hemorrhage visualized by computerized tomographic scanning.Neurosurgery.1980 Jan;6(1):1-9.
[9]蔡菁,李吻,陈树大.前交通动脉瘤破裂发生脑血管痉挛的相关因素分析.浙江医学2007年第29卷第6期:579-581.
[10]Friedman J,Goepss SJ,Meyer FB,et al.Volumetric quantification of Fisher Grade 3 aneurysmal subarachnoid hemorrhage:a novel method to predict symptomatic vasospasm on admission computerized topography scans.J Neuresurg,2002,97:401-407.
[11]李丽娟,刘卫彬,张占胜,司建伟.蛛网膜下腔出血后影响脑血管痉挛的因素分析.河南实用神经疾病杂志,2000,(05):20.
[12]张良文,朱树干,见文成,刘玉光,李刚,吴承远.颅内动脉瘤术后脑血管痉挛发生的相关因素分析.临床神经外科杂志2004年第一卷第2期:69-71.
[13]Hirashima Y,Kurimoto M,Hori E,et al.Lower incidence of symptomatic vasospasm after subarachnoid hemorrhage owing to rupture vertebrobasilar aneurysms[J].Neurosurgery,2005,57(6):1110-1116.
[14]罗勇,吴立权,陈谦学,田道锋.动脉瘤性SAH迟发性脑血管痉挛的多元因素分析.中国临床神经外科杂志2007年9月第12卷第9期:525-527.
[15]吴旭,卢刚,王卫余,朱飚,陈书达,胡未伟.高血糖对动脉瘤出血后症状性脑血管痉挛的影响.中华急诊医学杂志2007年3月第16卷第3期:313-315.
[16]Lasner TM,Weil RJ,Riina HA,King JT Jr,Zager EL,Raps EC,Flamm ES.Cigarette smoking-induced increase in the risk of symptomatic vasospasm after aneurysmal subarachnoid hemorrhage.J Neurosurg.1997 Sep;87(3):381-4.
[17]Tsubokawa T,Kuita H,Kaneko N,et al.Clinical significance of natriuretic pep tides in patientswith aneurysmal subarachnoid hemorrhage[J].No To Shinkei,2003,55:953-960.
[18]Sviri GE,Feinsod M,Soustiel JF.Brain natriuretic peptide and cerebral vasospasm in subarachnoid hemorrhage.Clinical and TCD correlations[J].Stroke,2000,31:118-122.
[19]Wijdicks EF,Heublein DM,Bumett JC.Increase and uncoup ling of adrenomedullin from the natriuretic Peptide system in aneurysmal subarachnoid hemorrhage[J].J Neurosurg,2001,94:252-256.
[20]韩陈保,刘洲,王义刚,等.蛛网膜下腔出血后血浆心房钠尿肽与低钠血症及脑血管痉挛的关系[J].中国康复理论与实践,2006,12:329-331.
[21]齐秀珍.蛛网膜下腔出血后低钠血症与脑血管痉挛的关系.中外健康文摘2007年4月第4卷第4期:101.
[22]Dorhout Mees,SvD GW,Algra A,et al.Glucose levels and outcome after subarachnoid hemorrhage[J].Neurology,2003,61(8):1132-1133.
[23]Vora YY,Suarez2Almazor M,Steinke DD,et al.Role of transcranial Doppler monitoring in the diagnosis of cerebral vasospasm after subarachnoid hemorrhage[J].Neurosurgery,1999,44(6):1237-1247.
[24]McCowen KC,Malhotra A,Bistrain BR,et al Stress-induced hyperglycemia[J].Crit Care Clin,2001,17(1):107-124.
[25]刘建民,洪波.脑血管痉挛研究进展.《心脑血管病防治》2006年12月第6卷第6期:345-346.
[26]邵伟,刘卫东.蛛网膜下腔出血脑血管痉挛的研究与治疗进展[J].青岛医药卫生,2004,36(1):41-44.
[27]Milburn JM,Moran C J,Cross DT,et al.Increase in diameters of vasospastic intracranial arteries by intra arterial papaverine administration[J].J Neurosurg,1998,88(1):38-42.
[28]Dumont AS,Dumont RJ,Chow MM,et al.Cerebral vasospasm after subarachnoid hemorrhage:putative role of inflammation.Neuresurgery,2003,53:123-135.
[29]McGirt MJ,Mavropoulos JC,McGirt LY,et al.Leukocytosis as an independent risk factor for cerebral vasospasm following aneurismal subarachnoid hemorrhage.J Neurosurg,2003,98:1222-1226.
[30][李建宏,毛伯镛,杨开勇.脑外伤早期脑血管痉挛的TCD与CT检测的临床意义.华西医科大学学报,1999;30(2):229-230.
[31]Bonilha L,Marques EL,Carelli EF,Fernandes YB,Cardoso AC,Maldaum MV,Borges G.Risk factors and outcome in 100 patients with aneurysmal subarachnoid hemorrhage.Arq Neuropsiquiatr.2001 Sep;59(3-B):676-80.
[2]Mayberg MR.Cerebral vasospasm.Neurosurg Clin N Am,1998,9:615-627.
[3]刘建民,洪波.脑血管痉挛研究进展.《心脑血管病防治》2006年12月第6卷第6期:345-346.
[4]刘承基教授主编。脑血管外科学江苏科技出版社:2000年版,10-21
[5]Echlin FA.Spasm of basilar and vertebral arteries caused by experimental subarachnoid hemorrhage.J Neurosurg.1965 Jul;23(1):1-11.
[6]Arutiunov AI,Baron MA,Majorova NA.The role of mechanical factors in the pathogenesis of short-term and prolonged spasm of the cerebral arteries.J Neurosurg.1974 Apt;40(4):459-72.
[7] Sercombe R,Tran Dinh YR, Gomis P. Cerebrovascular inflammation following subarachnoid hemorrhageJ .Jpn Pharmacol ,2002 ,88 3 :227-249.
[8] Park KW, MetaisC, DaiHB, et al. Microvascular endothelial dysfunction and its mechanism a rat model of subarachnoid hemorrhage. Anesth Aalg, 2001, 92: 990-996.
[9] Onoue H, TsutsuiM, SmithL, etal. Expression and functionof recombinant endothelial nitric oxide synthase gene in canine basilar artery after experimental subarachnoid hemorrhage. Stroke, 1998,29: 1959-1965.
[10]ZimmermannM. Endothelin in cerebral vasospasm. Clinical and experimental results. J Neurosurg, 1997,41: 139-151.
[11]Mascia L, Fedorko L, StewartDJ, et al. Temporal relationship between endothelin-1 concentrations and cerebral vasospasm in patients with aneurysmal subarachnoid hemorrhage. Stroke, 2001,32: 1185-1190.
[12] Wickman G, Lan C, VollrathB. Functional rolesof the rho/rho kinase pathway and protein kinase C in the regulation of cerebrovascular constriction mediated by hemoglobin: relevance to subarachnoid hemorrhage and vasospasm. Circ Res, 2003,92: 809 - 816.
[13]Satoh M, Parent AD, Zhang J H. Inhibitory effect with antisense 驶 mitogen-activated protein kinase oligodeoxynucleotide against cerebral vasospam in rats. Stroke, 2002, 33: 775 - 781.
[14] Sampson LJ, Hinton JM, Garland CJ. Evidence for expression and function of phosphodiesterase type 5(PDE-Ⅴ)in rat resistance arteries. BrJ Pharmacol, 2001,132:13-17.
[15] Gabrielsen TO, Greitz T. Normal size of the internal carotid, middle cerebral and anterior cerebral arteries. Acta Radiol Diagn (Stockh). 1970 Jan;10(1):1-10.
[16] VenkateshB, ShenQ, Lipman J. Continuousmeasurementof cerebral blood flow velocityusing transcranialDoppler reveals significant moment-to-moment variability of data in healthy volunteers and in patientswith subarachnoid hemorrhage. CritCareMed, 2002, 30:563 - 569.
[17]Okada Y, Shima T, Nishida M, et al. Comparison of transcranial Doppler investigation of aneurysmal vasospasm with digital subtraction angiographic and clinical findings. Neurosurgery, 1999, 45:443 - 449.
[18] JabreA, BabikianV, PowsnerRA, et al. Role of single photon emission computed tomography and transcranialDoppler ultrasonography in clinical vasospasm. J ClinNeurosci, 2002, 9: 400 - 403.
[19]Tamatani S, Sasaki O, Takeuchi S, Fujii Y, Koike T, Tanaka R. Detection of delayed cerebral vasospasm, after rupture of intracranial aneurysms, by magnetic resonance angiography. Neurosurgery. 1997 Apr;40(4):748-53; discussion753-4.
[20] Handa Y, Weir BK, Nosko M, Mosewich R, Tsuji T, Grace M. The effect of timing of clot removal on chronic vasospasm in a primate model. J Neurosurg.1987
[21]BiondiA, Ricciardi GK, PuybassetL, et al. Intra-arterial nimodipine for the treatmentof symptomatic cerebral vasospasm after aneurysmal subarachnoid hemorrhage: preliminary results. AJNR Am J Neuroradiol, 2004, 25: 1067-1076.
[22] BadjatiaN, TopcuogluMA, PryorJC, etal. Preliminary experience with intra-arterial nicardipine as a treatment forcerebral vasospasm. AJNR Am J Neuroradiol, 2004, 25: 819 - 826.
[23] TreggiariMM, WalderB, Suter PM, et al. Systematic review of the prevention of delayed ischemic neurological deficitswith hypertension, hypervolemia, and hemodilution therapy following subarachnoid hemorrhage. J Neurosurg, 2003,98: 978 - 984.
[24]Jian-Kang Shen.The PathogenesisofCerebralVasospasm and Its Prevention and Treatment.IntJ CerebrovascDis, July2006, Vol14, No. 7:481-493.
[1] Treggiari MM, Walder B, Suter PM, et al. Systematic review of the prevention of delayed ischemic neurological deficits with hypertension, hypervolemia, and hemodilution therapy following subarachnoid hemorrhage[J]. J Neurosurg, 2003,98(5): 978-984.
[2] Mayberg MR.Cerebral vasospasm. Neurosurg Clin N Am. 1998 Jul;9(3):615-27.
[3] Dietrich HH, Dacey RG Jr. Molecular keys to the problems of cerebral vasospasm[J]. Neurosurgery, 2000,46(3): 517-530.
[4] Friedman J, Goepss SJ, Meyer FB, et al. Volumetric quantification of Fisher Grade 3 aneurysmal subarachnoid hemorrhage: a novel method to predict symptomatic vasospasm on admission computerized topography scans[J]. J Neuresurg, 2002, 97(2): 401-407.
[5] Macdonald RL, Rosengart A, Huo D, et al. Factors associated with the development of vasospasm after planned surgical treatment of aneurismal subarachnoid hemorrhage[J]. J Neurosurg, 2003,99(4): 644-652.
[6] Hirashima Y, Kurimoto M, Hori E, et al. Lower incidence of symptomatic vasospasm after subarachnoid hemorrhage owing to rupture vertebrobas-ilar aneurysms[J]. Neurosurgery, 2005, 57(6): 1110-1116.
[7] Charpentier C, Audibert G, Guillemin F, et al. Multivariate analysis of predictors of cerebral vasospasm occurrence after aneurysmal subarachnoid hemorrhage[J].Stroke. 1999, 30(7): 1402-1408.
[8] Torbey MT, Hauser TK, Bhardwaj A, et al. Effect of age on cerebral blood flow velocity and incidence of vasospasm after aneurismal subarachnoid hemorrhage[J]. Stroke, 2001, 32(9): 2005-2011.
[9] Wilkins RH. Cerebralterial Spasm[M]. Baltimore: Williams &Wilkins, 1980:284-286.
[10] McGirt MJ, Mavropoulos JC, McGirt LY, et al. Leukocytosis as an independent risk factor for cerebral vasospasm following aneurysmal subarachnoid hemorrhage[J]. J Neurosurg, 2003, 98(6): 1222-1226.
[1]Mayberg MR.Cerebral vasospasm.Neurosurg Clin N Am,1998,9:615-627.
[2]刘建民,洪 波.脑血管痉挛研究进展.《心脑血管病防治》2006年12月第6卷第6期:345-346。
[3]Charpentier C,Audibert G,Guillemin F,Civit T,Ducrocq X,Bracard S,Hepner H,Picard L,Laxenaire MC.Multivariate analysis of predictors of cerebral vasospasm occurrence afteraneurysmal subarachnoid hemorrhage.Stroke.1999Jul;30(7):1402-1408.
[4]TorbeyMT,Hauser TK,BhardwajA,et al.Effect of age on cerebral blood flow velocity and incidence of vasospasm after aneurismal subarachnoid hemorrhage.Stroke,2001,32:2005-2011.
[5]陈高,张建民,李珉,蔡菁.动脉瘤性SAH继发重度脑血管痉挛相关因素研究.中华神经外科杂志2005年11月第21卷第11期:665-667.
[6]胡丽葵,任艳.蛛网膜下腔出血后迟发性脑血管痉挛45例分析.中国冶金工业医学杂志2003年第20卷第2期:93.
[7]张忠延,赵凡.蛛网膜下腔出血后迟发性脑血管痉挛42例分析.卒中与神经疾病2001年第8卷第2期:87.
[8]Fisher CM,Kistler JP,Davis JM.Relation of cerebral vasospasm to subarachnoid hemorrhage visualized by computerized tomographic scanning.Neurosurgery.1980 Jan;6(1):1-9.
[9]蔡菁,李吻,陈树大.前交通动脉瘤破裂发生脑血管痉挛的相关因素分析.浙江医学2007年第29卷第6期:579-581.
[10]Friedman J,Goepss SJ,Meyer FB,et al.Volumetric quantification of Fisher Grade 3 aneurysmal subarachnoid hemorrhage:a novel method to predict symptomatic vasospasm on admission computerized topography scans.J Neuresurg,2002,97:401-407.
[11]李丽娟,刘卫彬,张占胜,司建伟.蛛网膜下腔出血后影响脑血管痉挛的因素分析.河南实用神经疾病杂志,2000,(05):20.
[12]张良文,朱树干,见文成,刘玉光,李刚,吴承远.颅内动脉瘤术后脑血管痉挛发生的相关因素分析.临床神经外科杂志2004年第一卷第2期:69-71.
[13]Hirashima Y,Kurimoto M,Hori E,et al.Lower incidence of symptomatic vasospasm after subarachnoid hemorrhage owing to rupture vertebrobasilar aneurysms[J].Neurosurgery,2005,57(6):1110-1116.
[14]罗勇,吴立权,陈谦学,田道锋.动脉瘤性SAH迟发性脑血管痉挛的多元因素分析.中国临床神经外科杂志2007年9月第12卷第9期:525-527.
[15]吴旭,卢刚,王卫余,朱飚,陈书达,胡未伟.高血糖对动脉瘤出血后症状性脑血管痉挛的影响.中华急诊医学杂志2007年3月第16卷第3期:313-315.
[16]Lasner TM,Weil RJ,Riina HA,King JT Jr,Zager EL,Raps EC,Flamm ES.Cigarette smoking-induced increase in the risk of symptomatic vasospasm after aneurysmal subarachnoid hemorrhage.J Neurosurg.1997 Sep;87(3):381-4.
[17]Tsubokawa T,Kuita H,Kaneko N,et al.Clinical significance of natriuretic pep tides in patientswith aneurysmal subarachnoid hemorrhage[J].No To Shinkei,2003,55:953-960.
[18]Sviri GE,Feinsod M,Soustiel JF.Brain natriuretic peptide and cerebral vasospasm in subarachnoid hemorrhage.Clinical and TCD correlations[J].Stroke,2000,31:118-122.
[19]Wijdicks EF,Heublein DM,Bumett JC.Increase and uncoup ling of adrenomedullin from the natriuretic Peptide system in aneurysmal subarachnoid hemorrhage[J].J Neurosurg,2001,94:252-256.
[20]韩陈保,刘洲,王义刚,等.蛛网膜下腔出血后血浆心房钠尿肽与低钠血症及脑血管痉挛的关系[J].中国康复理论与实践,2006,12:329-331.
[21]齐秀珍.蛛网膜下腔出血后低钠血症与脑血管痉挛的关系.中外健康文摘2007年4月第4卷第4期:101.
[22]Dorhout Mees,SvD GW,Algra A,et al.Glucose levels and outcome after subarachnoid hemorrhage[J].Neurology,2003,61(8):1132-1133.
[23]Vora YY,Suarez2Almazor M,Steinke DD,et al.Role of transcranial Doppler monitoring in the diagnosis of cerebral vasospasm after subarachnoid hemorrhage[J].Neurosurgery,1999,44(6):1237-1247.
[24]McCowen KC,Malhotra A,Bistrain BR,et al Stress-induced hyperglycemia[J].Crit Care Clin,2001,17(1):107-124.
[25]刘建民,洪波.脑血管痉挛研究进展.《心脑血管病防治》2006年12月第6卷第6期:345-346.
[26]邵伟,刘卫东.蛛网膜下腔出血脑血管痉挛的研究与治疗进展[J].青岛医药卫生,2004,36(1):41-44.
[27]Milburn JM,Moran C J,Cross DT,et al.Increase in diameters of vasospastic intracranial arteries by intra arterial papaverine administration[J].J Neurosurg,1998,88(1):38-42.
[28]Dumont AS,Dumont RJ,Chow MM,et al.Cerebral vasospasm after subarachnoid hemorrhage:putative role of inflammation.Neuresurgery,2003,53:123-135.
[29]McGirt MJ,Mavropoulos JC,McGirt LY,et al.Leukocytosis as an independent risk factor for cerebral vasospasm following aneurismal subarachnoid hemorrhage.J Neurosurg,2003,98:1222-1226.
[30][李建宏,毛伯镛,杨开勇.脑外伤早期脑血管痉挛的TCD与CT检测的临床意义.华西医科大学学报,1999;30(2):229-230.
[31]Bonilha L,Marques EL,Carelli EF,Fernandes YB,Cardoso AC,Maldaum MV,Borges G.Risk factors and outcome in 100 patients with aneurysmal subarachnoid hemorrhage.Arq Neuropsiquiatr.2001 Sep;59(3-B):676-80.