Willis环变异与常见脑血管病的关系：64排CT血管成像研究
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摘要
第一部分颅内交通动脉瘤发生与Willis环变异的关系
目的运用64层螺旋CT血管成像探讨大脑前动脉水平段(A1)发育异常及胚胎型大脑后动脉与颅内交通动脉瘤发生的关系;运用3D-CTA测量大脑前动脉的A1-A2段夹角(外侧夹角),探讨其与前交通动脉瘤形成可能存在的关系。
材料与方法64排螺旋CT脑血管成像诊断为颅内交通动脉瘤患者56例,前交通动脉患者26例、后交通动脉瘤患者30例,选择性别与年龄相匹配的脑血管正常人50例作为对照组;同时运用3维CT血管成像测量25例前交通动脉瘤患者及20例脑血管正常人的大脑前动脉的A1-A2段夹角。
所有数据采用使用SPSS11.0软件包处理,定性资料以频数(率)表示,采用χ2检验;定量资料以均数±标准差表示,采用独立样本t检验。规定p< 0. 05有统计学意义。
结果前交通动脉瘤组一侧大脑前动脉A1段发育异常率达65.4%(17/26),明显高于后交通动脉瘤组16.7%(5/30)及正常对照组16.0%(8/50)(P<0.01),后交通动脉瘤组胚胎型大脑后动脉发生率为31.7%(19/60),明显高于前交通动脉瘤组11.5%(6/52)及正常对照组15.0%(15/100) (P<0.05)。
25例前交通动脉瘤患者(一例无法测量)平均的A1-A2夹角(外侧夹角)为106.27±19.57度(均数±标准差),20例脑血管正常组平均的A1-A2夹角为127.42±15.20度,两组相比有显著差异(P<0.01), 8例双侧A1段基本对称的动脉瘤患者动脉瘤侧平均的A1-A2夹角为95.96±16.38度,无动脉瘤侧平均的A1-A2夹角为133±23.11度,两者相比有显著差异(P<0.01)。
结论一侧大脑前动脉A1段发育异常及胚胎型大脑后动脉与颅内交通动脉瘤发生密切相关;大脑前动脉A1段-A2段夹角大小与前交通动脉瘤的发生关系密切。
第二部分颈内动脉狭窄或闭塞的结局与Willis环变异的关系
目的探讨Willis环变异与颈内动脉狭窄或闭塞的结局之间可能存在的关系。材料与方法64排螺旋CT脑血管成像诊断为重度颈内动脉狭窄或闭塞患者20例,单侧和双侧各10例,根据其临床表现分为大面积脑梗塞组(8例)和非大面积脑梗塞组(12例)。
所有数据采用使用SPSS11.0软件包处理,采用频数(率)的χ2检验,规定P< 0. 05有统计学意义。
结果颈内动脉狭窄或闭塞组发生大面积脑梗塞者前、后循环完整率分别为37.5%(3/8)、12.5%(1/8),明显低于非大面积脑梗塞患者的100%(12/12)、75%(9/12),两组差异有显著性;
结论颈内动脉狭窄或闭塞的结局与Willis环的完整性密切相关。
Part one: The relationship between cerebral aneurysms formation in communicating arteries and anatomic variation of the Willis circle
Objective To study the relation of aneurysm formation on communicating branches with dysplasia of horizontal segment of anterior cerebral artery and fetal type posterior cerebral artery; To study the relation between aneurysm formation in anterior communicating artery and the angel of A1 and A2 segments of anterior cerebral artery Materials and Methods Fifty-six patients harboring communicating aneurysms demonstrated by 64-slice CTA were invovled in this study,among which 26 cases with anterior communicating aneurysms, 30 cases with posterior communicating aneurysms.Fifty healthy matched volunteers were used as controls; A1-A2 angle of anterior cerebral artery were measured by three-dimensional computed tomographic angiography on 25 patients harboring anterior communicating aneurysms and 20 healthy volunteers.
All date were analyzed by SPSS 11.0 statistical software package. Qualitative data express as frequency(rate), Chi-square criterion were performed among groups; Quantitative data express as mean±standard deviation , Independent-Sampler T test were performed among groups. Difference with P<0.05 was considered as significant.
Results. In patients with anterior communicating aneurysms ,65.4%(17/26) had dysplasia (hypoplastic or absent) of the A1 segment, which is higher than those in patients with posterior communicating aneurysms (PCA) and control with great significance. In patients with posterior communicating aneurysms,31.7% (19/60) had fetal type of posterior cerebral artery (FTP ) in PCA, which is higher than those in patients with anterior communicating aneurysms and normal control.
The average A1-A2 angle was determined to be 106.27±19.57 degrees(mean±standard deviation) in 25 patients with anterior communicating aneurysms,which is lower than that(127.42±15.20degrees) in 20 volunteerss without aneurysms (P<0.01). The A1-A2 angle in aneurysm side was 95.96±16.38 degree,which is lower than that (133±23.11 degree)in non-aneurysm side (P<0.01) in 8 patients with aneurysms without morplastic A1 segments.
Conclusions The development of cerebral aneurysms in communicating branches maybe closely related with dysplasia of horizontal segment of anterior cerebral artery and fetal type of posterior cerebral artery;The angle between A1 and A2 segment maybe have important role in the formation of ACoA .
Part two: An investigation on the relationship between end-results of internal carotid artery stenosis or occlusion and anatomic variation of the Willis circle
Objective To study the relationship between end-results of internal carotid artery stenosis or occlusion and anatomic variation of the Willis circle Materials and Methods Twenty patients with internal carotid artery stenosis or occlusion demonstrated by 64-slice CT Angiography (CTA ) were involved in this study. Both unilateral and bilateral lesions are ten cases, They were divided into 2 groups :large area of cerebral infarction group(n=8) and no-cerebral infarction group(n=12) according to the imaging manifestation.
All date were analyzed by SPSS 11.0 statistical software package. Data express as frequency(rate),Chi-square criterion were performed among groups Difference with P<0.05 was considered as significant.
Results. In infarction group,only 37.5%(3/8) demonstrated a complete anterior circulation of the circle and 12.5%(1/8) demonstrated a complete posterior circulation of the circle, which is obvious lower than those in no-infarction group that is 100%(12/12) and 75%(9/12).
Conclusions End-results of internal carotid artery ( ICA) stenosis or occlusion maybe closely related with anatomic variation of the CW.
目的运用64层螺旋CT血管成像探讨大脑前动脉水平段(A1)发育异常及胚胎型大脑后动脉与颅内交通动脉瘤发生的关系;运用3D-CTA测量大脑前动脉的A1-A2段夹角(外侧夹角),探讨其与前交通动脉瘤形成可能存在的关系。
材料与方法64排螺旋CT脑血管成像诊断为颅内交通动脉瘤患者56例,前交通动脉患者26例、后交通动脉瘤患者30例,选择性别与年龄相匹配的脑血管正常人50例作为对照组;同时运用3维CT血管成像测量25例前交通动脉瘤患者及20例脑血管正常人的大脑前动脉的A1-A2段夹角。
所有数据采用使用SPSS11.0软件包处理,定性资料以频数(率)表示,采用χ2检验;定量资料以均数±标准差表示,采用独立样本t检验。规定p< 0. 05有统计学意义。
结果前交通动脉瘤组一侧大脑前动脉A1段发育异常率达65.4%(17/26),明显高于后交通动脉瘤组16.7%(5/30)及正常对照组16.0%(8/50)(P<0.01),后交通动脉瘤组胚胎型大脑后动脉发生率为31.7%(19/60),明显高于前交通动脉瘤组11.5%(6/52)及正常对照组15.0%(15/100) (P<0.05)。
25例前交通动脉瘤患者(一例无法测量)平均的A1-A2夹角(外侧夹角)为106.27±19.57度(均数±标准差),20例脑血管正常组平均的A1-A2夹角为127.42±15.20度,两组相比有显著差异(P<0.01), 8例双侧A1段基本对称的动脉瘤患者动脉瘤侧平均的A1-A2夹角为95.96±16.38度,无动脉瘤侧平均的A1-A2夹角为133±23.11度,两者相比有显著差异(P<0.01)。
结论一侧大脑前动脉A1段发育异常及胚胎型大脑后动脉与颅内交通动脉瘤发生密切相关;大脑前动脉A1段-A2段夹角大小与前交通动脉瘤的发生关系密切。
第二部分颈内动脉狭窄或闭塞的结局与Willis环变异的关系
目的探讨Willis环变异与颈内动脉狭窄或闭塞的结局之间可能存在的关系。材料与方法64排螺旋CT脑血管成像诊断为重度颈内动脉狭窄或闭塞患者20例,单侧和双侧各10例,根据其临床表现分为大面积脑梗塞组(8例)和非大面积脑梗塞组(12例)。
所有数据采用使用SPSS11.0软件包处理,采用频数(率)的χ2检验,规定P< 0. 05有统计学意义。
结果颈内动脉狭窄或闭塞组发生大面积脑梗塞者前、后循环完整率分别为37.5%(3/8)、12.5%(1/8),明显低于非大面积脑梗塞患者的100%(12/12)、75%(9/12),两组差异有显著性;
结论颈内动脉狭窄或闭塞的结局与Willis环的完整性密切相关。
Part one: The relationship between cerebral aneurysms formation in communicating arteries and anatomic variation of the Willis circle
Objective To study the relation of aneurysm formation on communicating branches with dysplasia of horizontal segment of anterior cerebral artery and fetal type posterior cerebral artery; To study the relation between aneurysm formation in anterior communicating artery and the angel of A1 and A2 segments of anterior cerebral artery Materials and Methods Fifty-six patients harboring communicating aneurysms demonstrated by 64-slice CTA were invovled in this study,among which 26 cases with anterior communicating aneurysms, 30 cases with posterior communicating aneurysms.Fifty healthy matched volunteers were used as controls; A1-A2 angle of anterior cerebral artery were measured by three-dimensional computed tomographic angiography on 25 patients harboring anterior communicating aneurysms and 20 healthy volunteers.
All date were analyzed by SPSS 11.0 statistical software package. Qualitative data express as frequency(rate), Chi-square criterion were performed among groups; Quantitative data express as mean±standard deviation , Independent-Sampler T test were performed among groups. Difference with P<0.05 was considered as significant.
Results. In patients with anterior communicating aneurysms ,65.4%(17/26) had dysplasia (hypoplastic or absent) of the A1 segment, which is higher than those in patients with posterior communicating aneurysms (PCA) and control with great significance. In patients with posterior communicating aneurysms,31.7% (19/60) had fetal type of posterior cerebral artery (FTP ) in PCA, which is higher than those in patients with anterior communicating aneurysms and normal control.
The average A1-A2 angle was determined to be 106.27±19.57 degrees(mean±standard deviation) in 25 patients with anterior communicating aneurysms,which is lower than that(127.42±15.20degrees) in 20 volunteerss without aneurysms (P<0.01). The A1-A2 angle in aneurysm side was 95.96±16.38 degree,which is lower than that (133±23.11 degree)in non-aneurysm side (P<0.01) in 8 patients with aneurysms without morplastic A1 segments.
Conclusions The development of cerebral aneurysms in communicating branches maybe closely related with dysplasia of horizontal segment of anterior cerebral artery and fetal type of posterior cerebral artery;The angle between A1 and A2 segment maybe have important role in the formation of ACoA .
Part two: An investigation on the relationship between end-results of internal carotid artery stenosis or occlusion and anatomic variation of the Willis circle
Objective To study the relationship between end-results of internal carotid artery stenosis or occlusion and anatomic variation of the Willis circle Materials and Methods Twenty patients with internal carotid artery stenosis or occlusion demonstrated by 64-slice CT Angiography (CTA ) were involved in this study. Both unilateral and bilateral lesions are ten cases, They were divided into 2 groups :large area of cerebral infarction group(n=8) and no-cerebral infarction group(n=12) according to the imaging manifestation.
All date were analyzed by SPSS 11.0 statistical software package. Data express as frequency(rate),Chi-square criterion were performed among groups Difference with P<0.05 was considered as significant.
Results. In infarction group,only 37.5%(3/8) demonstrated a complete anterior circulation of the circle and 12.5%(1/8) demonstrated a complete posterior circulation of the circle, which is obvious lower than those in no-infarction group that is 100%(12/12) and 75%(9/12).
Conclusions End-results of internal carotid artery ( ICA) stenosis or occlusion maybe closely related with anatomic variation of the CW.
引文
[1]Whyte J, Torres A, Cisneros AI, et al. Structural pecu-liarities of the human cerebral communicating arteries and their repercussion in encephalic vascular pathology[J]. Rev Neurol, 2001, 33: 111-114.
[2]Morimoto M, Miyamoto S, Mizoguchi A, et al. Mouse model of cerebral aneurysm experimental induction by renal hypertension and local hemodynamic changes[J].Stroke, 2002,33:1911一1915.
[3]Fukuda S ,Hashimoto N ,Naritomi H ,et al.P revention of rat cerebral aneurysm formation by inhibition of nitric oxide synthase[J].Circulation,2000,101:2532-2538.
[4]Tateshima S, Murayama Y, Villablanca JP, et al. Intraaneurysmal flow dynamicsstudy featuring an acrylic aneurysm model manufactured using a computerized tomography angiogram as a mold [J] .J Neurosurg,2001,95:1020-1027.
[5]高鹏,陈左权,顾斌贤,等.大脑前动脉A1段优势和前交通动脉瘤相关性研究[J ].同济大学学报,2007,28(4):41-45.
[5]黄永火,李信友,欧阳祖彬,等.前、后交通动脉瘤与Willis环血流变化的分析[J ] .重庆医科大学学报,2004 ,29(3):345-347
[7] Eftekhar B, Dadmehr M, Ansari S, et al. Are the distributions of variations of circle of Willis different in different populations?– Results of an anatomical study and review of literature. BMC Neurology 2006, 6:22
[8]Gonzalez-Llanos F, Pascual JM, Roda JM. Anatomic and hemodynamic study of anterior communicating artery comple?[J].Neurocirugia, 2002, 13(4):285-298.
[9]Kirgis HD,Fisher WL.Aneurysm of anterior communicating artery and gross anatomy of the circle of Willis[J].J Neurosurg,1996,25(1):73.
[10]李建华,贺能树,孙建中,等.颅内交通动脉瘤与Willis环血流动力学变化的关系[J ] .临床放射学杂志,2002 ,21(1):19-22.
[11]胡宁,赵岩,于晓凌,等.Willis环结构与大脑前、后交通动脉瘤形成关系的临床与数字减影分析[J].中国实用内科学杂志,2002,22(10):595-596.
[12]Ingebrigtsen T,Morgan MK,Faulder K,et al.Bifurcation geometry and the presence of cerebral aneurysms[J].J Neurosurgery,2004,101(1):108-113.
[13]Sakamoto S,Ohba S,Shibukawa M, et al. Characteristics of aneurysms of internal carotid artery bifurcation[J].Acta Neurochir,2006,148(2):89-94.
[14]Bor SE,Velthuis BK,Majoie CB, et al.Configuration of intracranial arteries and development of aneurysms[J].Neurology,2008,70:700-705.
[15]Ujiie H,Liepsch DW,Goetz M, et al.Hemodynamic study of the anterior communicating artery [J].Stoke,1996,27(11)2086-2094.
[1]Hoksbergen AW, Fulesdi B, Legemate DA , et al. Collateral configuration of the circle of Willis: transcranial colorcoded duplex ultrasonography and comparison with postmortem anatomy[J]. Stroke , 2000 , 31:1346-1351.
[2]Lippert H,Pabst R. Cerebral arterial circle(circle of Willis). In: Lippert H, Pabst R. Arterial variations in man: classification and frequency[J]. Munich, Germany: Bergmann,1985:92-93.
[3]Bisschops RH, Klijn CJ, Kappelle LJ, et al.Collateral flow and ischemic brain lesions in patients with unilateral carotid artery occlusion Neurology ,2003 ,60 :1435 - 1441.
[4]赵云辉,马著彬,许乙凯.颈内动脉狭窄或闭塞侧支循环途径的DSA和MR血管成像研究[J ] .中华放射学杂志,2004 ,38(10):1056-1061.
[5]赵云辉,马著彬,庄磊,等.单侧和双侧颈内动脉狭窄或闭塞侧支循环途径的研究[J].影像诊断与介入放射学,2006 ,15 :155 -157.
[6] Rodda RA, Path FRC. The arerial pattern sassociated with internal carotid disease and cerebral infarcts[J]. Storke, 1986, 17(1): 69-75.
[7]张艳玲,迟路湘,陈康宁,等.数字减影血管造影下Willis动脉环变异与缺血性脑血管病的关系[J].第三军医大学学报, 2005,27 (5) : 417-421.
[8]黎洪展,刘亚杰,刘振华,等.Willis环变异及其与脑梗死的关系[J].广东医学,2006,27(5):676-678.
[9]李圣贤,朱玉真.基底动脉闭塞致颈内动脉系统短暂性脑缺血发作五例报告[J].中华神经外科杂志, 2003, 19(3): 208.
[10]王拥军.颈内血管狭窄的诊断和治疗[J].中华内科杂志, 2003, 42(8): 531-532.
[1]Whyte J, Torres A, Cisneros AI, et al. Structural peculiarities of the human cerebral communicating arteries and their repercussion in encephalic vascular pathology[J]. Rev Neurol,2001; 33: 111-114.
[2]Morimoto M, Miyamoto S, Mizoguchi A, et al. Mouse model of cerebral aneurysm experimental induction by renal hypertension and local hemodynamic changes[J].Stroke, 2002;33:1911-1915.
[3]Fukuda S ,Hashimoto N ,Naritomi H ,et al.Prevention of rat cerebral aneurysm formation by inhibition of nitric oxide synthase[J].Circulation,2000;101:2532-2538.
[4]Tateshima S, Murayama Y, Villablanca JP, et al. Intraaneurysmal flow dynamics study featuring an acrylic aneurysm model manufactured using a computerized tomography angiogram as a mold. [J]J Neurosurg,2001;95:1020-1027.
[5]黄永火,李信友,欧阳祖彬,等.前、后交通动脉瘤与Willis环血流变化的分析[J ] .重庆医科大学学报,2004 ;29(3):345-347
[6]高鹏,陈左权,顾斌贤,等.大脑前动脉A1段优势和前交通动脉瘤相关性研究[J ].同济大学学报,2007,28(4):41-45.
[7]李建华,贺能树,孙建中,等.颅内交通动脉瘤与Willis环血流动力学变化的关系[J ] .临床放射学杂志,2002 ,21(1):19-22.
[8]Eftekhar B, Dadmehr M, Ansari S, et al. Are the distributions of variations of circle of Willis different in different populations?– Results of an anatomical study and review of literature. BMC Neurology, 2006;6:22
[9]Gonzalez-Llanos F, Pascual JM, Roda JM. Anatomic and hemodynamic study of anterior communicating artery comple[J].Neurocirugia, 2002; 13(4):285-298.
[10]Kirgis HD,Fisher WL.Aneurysm of anterior communicating artery and gross anatomy of the circle of Willis[J].J Neurosurg,1996;25(1):73
[11]胡宁,赵岩,于晓凌,等.Willis环结构与大脑前、后交通动脉瘤形成关系的临床与数字减影分析[J].中国实用内科学杂志,2002,22(10):595-596.
[12]Bisschops RH, Klijn CJ, Kappelle LJ, et al.Collateral flow and ischemic brain lesions in patients with unilateral carotid artery occlusion Neurology ,2003 ,60 :1435 - 1441.
[13]赵云辉,马著彬,许乙凯.颈内动脉狭窄或闭塞侧支循环途径的DSA和MR血管成像研究[J ] .中华放射学杂志,2004 ,38(10):1056-1061.
[14]赵云辉,马著彬,庄磊,等.单侧和双侧颈内动脉狭窄或闭塞侧枝循环途径的研究[J].影像诊断与介入放射学,2006 ,15 :155 -157.
[15] Rodda RA, Path FRC. Thearerial pattern sassociatedwith internal carotid disease and cerebral infarcts[J]. Storke, 1986, 17(1): 69-75.
[16]张艳玲,迟路湘,陈康宁,等.数字减影血管造影下Willis动脉环变异与缺血性脑血管病的关系[J].第三军医大学学报, 2005,27 (5) : 417-421.
[17]黎洪展,刘亚杰,刘振华,等.Willis环变异及其与脑梗死的关系[J].广东医学,2006,27(5):676-678.
[18]李圣贤,朱玉真.基底动脉闭塞致颈内动脉系统短暂性脑缺血发作五例报告[J].中华神经外科杂志, 2003, 19(3): 208.
[2]Morimoto M, Miyamoto S, Mizoguchi A, et al. Mouse model of cerebral aneurysm experimental induction by renal hypertension and local hemodynamic changes[J].Stroke, 2002,33:1911一1915.
[3]Fukuda S ,Hashimoto N ,Naritomi H ,et al.P revention of rat cerebral aneurysm formation by inhibition of nitric oxide synthase[J].Circulation,2000,101:2532-2538.
[4]Tateshima S, Murayama Y, Villablanca JP, et al. Intraaneurysmal flow dynamicsstudy featuring an acrylic aneurysm model manufactured using a computerized tomography angiogram as a mold [J] .J Neurosurg,2001,95:1020-1027.
[5]高鹏,陈左权,顾斌贤,等.大脑前动脉A1段优势和前交通动脉瘤相关性研究[J ].同济大学学报,2007,28(4):41-45.
[5]黄永火,李信友,欧阳祖彬,等.前、后交通动脉瘤与Willis环血流变化的分析[J ] .重庆医科大学学报,2004 ,29(3):345-347
[7] Eftekhar B, Dadmehr M, Ansari S, et al. Are the distributions of variations of circle of Willis different in different populations?– Results of an anatomical study and review of literature. BMC Neurology 2006, 6:22
[8]Gonzalez-Llanos F, Pascual JM, Roda JM. Anatomic and hemodynamic study of anterior communicating artery comple?[J].Neurocirugia, 2002, 13(4):285-298.
[9]Kirgis HD,Fisher WL.Aneurysm of anterior communicating artery and gross anatomy of the circle of Willis[J].J Neurosurg,1996,25(1):73.
[10]李建华,贺能树,孙建中,等.颅内交通动脉瘤与Willis环血流动力学变化的关系[J ] .临床放射学杂志,2002 ,21(1):19-22.
[11]胡宁,赵岩,于晓凌,等.Willis环结构与大脑前、后交通动脉瘤形成关系的临床与数字减影分析[J].中国实用内科学杂志,2002,22(10):595-596.
[12]Ingebrigtsen T,Morgan MK,Faulder K,et al.Bifurcation geometry and the presence of cerebral aneurysms[J].J Neurosurgery,2004,101(1):108-113.
[13]Sakamoto S,Ohba S,Shibukawa M, et al. Characteristics of aneurysms of internal carotid artery bifurcation[J].Acta Neurochir,2006,148(2):89-94.
[14]Bor SE,Velthuis BK,Majoie CB, et al.Configuration of intracranial arteries and development of aneurysms[J].Neurology,2008,70:700-705.
[15]Ujiie H,Liepsch DW,Goetz M, et al.Hemodynamic study of the anterior communicating artery [J].Stoke,1996,27(11)2086-2094.
[1]Hoksbergen AW, Fulesdi B, Legemate DA , et al. Collateral configuration of the circle of Willis: transcranial colorcoded duplex ultrasonography and comparison with postmortem anatomy[J]. Stroke , 2000 , 31:1346-1351.
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