同型半胱氨酸与高血压患者轻度认知障碍的相关性

目的 探讨同型半胱氨酸（homocysteine,Hcy）与高血压患者轻度认知障碍的相关性。
方法 回顾性纳入2017年1月-2018年2月邯郸市第一医院神经内科连续收治的原发性高血
压患者,根据其血浆Hcy水平,将患者分为单纯型高血压组（Hcy<15 μm m ol/L）与H型高血压组
（Hcy≥15 μmmol/L）,采用Spearman秩相关分析Hcy与MMSE和MoCA评分的相关性,并采用Logistic回归
分析高血压患者轻度认知功能障碍的影响因素。
结果 共纳入原发性高血压患者113例,其中单纯型高血压组49例,H型高血压组64例。H型高血压
组患者的MMSE和MoCA评分均低于单纯型高血压组（分别为24.94±1.83 vs 27.96±1.54和23.45±2.47
vs 27.24±1.80,均P <0.001）。相关分析显示,Hcy水平与MMSE和MoCA评分存在负相关性（分别为r =-
0.513和r =-0.500,均P＜0.001）。多因素Logistic回归分析显示,高龄（OR 1.236,95%CI 1.124～1.361）、
H型高血压（OR 22.218,95%CI 8.243～59.654）是高血压患者轻度认知功能障碍的独立危险因素。
结论 Hcy水平升高是高血压患者轻度认知功能障碍发生的独立危险因素。     

脑动静脉畸形经立体定向放射治疗后不同时期的组织病理变化

目的研究脑动静脉畸形(AVMs)经立体定向放射治疗后不同时期的组织病理变化。方法对10例脑AVMs立体定向放射治疗后的病理标本进行苏木精-伊红染色,并用平滑肌肌动蛋白(SMA)、血管内皮生长因子(VEGF)及神经胶质酸性蛋白等抗体进行免疫组化研究。结果经立体定向放射治疗后,早期脑AVMs血管病理变化包括内膜层与血管壁分离,细胞外基质增生;中期可见平滑肌细胞增生,血管壁增厚,管腔狭窄至消失,管壁玻璃样变;晚期病理变化包括血管壁进行性增厚,在完全玻璃样变的区域细胞核固缩。早期放射反应的动脉管壁中VEGF呈阳性表达,在中期放射反应的动脉管壁中SMA呈强阳性表达。结论立体定向放射治疗后脑AVMs血管中层的平滑肌细胞增生和变性是血管闭塞的关键因素。     

高压氧治疗未破裂颅内动脉瘤夹闭术后脑梗死疗效及影响因素分析

目的 探讨高压氧治疗未破裂颅内动脉瘤夹闭术后脑梗死疗效及影响因素。
方法 回顾性纳入未破裂颅内动脉瘤夹闭术后脑梗死患者，根据是否进行高压氧治疗（压力
0.2 Mpa，稳压60 min，每日1次）分为高压氧组和对照组。应用NIHSS评分评估患者出院时神经功能缺
损程度，观察高压氧治疗是否有效。将出院NIHSS评分较脑梗死发病24 h内评分下降≥4分作为治疗显
效的标准，应用多因素Logistic回归分析，探讨术后脑梗死疗效的影响因素。
结果 共纳入56例患者，平均年龄53.63±11.02岁，其中男性24例（42.9%）。高压氧组41例，对照
组15例。高压氧组出院NIHSS评分低于对照组[6（4～8）分 vs 12（7～15）分，P =0.001]。纳入患者中治
疗显效22例（39.3%），多因素Logistic回归分析显示，脑梗死发病24 h内NIHSS评分高（OR 1.411，95%CI
1.134～1.756，P =0.002）是未破裂动脉瘤术后脑梗死治疗显效的独立影响因素；与未行高压氧治
疗对比，高压氧治疗1～5次（OR 16.454，95%CI 1.326～204.191，P =0.029），高压氧治疗6～9次（OR
20.966，95%CI 1.996～220.253，P =0.011），高压氧治疗≥10次（OR 47.026，95%CI 3.651～605.774，
P =0.003）与术后脑梗死治疗显效呈独立正相关。
结论 高压氧治疗颅内动脉瘤夹闭术后脑梗死有效，脑梗死发病24 h内NIHSS评分及高压氧治疗是
未破裂颅内动脉瘤术后脑梗死治疗显效独立影响因素。     

以精神行为异常为主要症状的非痴呆型血管性认知障碍临床研究

目的 分析以精神行为异常为主要症状的非痴呆型血管认知障碍（vascular cognitive impairment no
dementia,VCIND）的精神行为特点和认知功能特征。
方法 本研究为横断面研究,收集2011年6月～2013年12月广州市脑科医院以精神行为异常为主要
症状就诊的VCIND18例、伴有精神行为异常的血管性痴呆（vascular dementia,VaD）16例和无认知功能
障碍（no cognitive impairment,NCI）18例作为对照组。采用神经精神科问卷（Neuropsychiatric Inventory,
NPI）和简易精神状态检查量表（Mini-Mental State Examination,MMSE）及蒙特利尔认知评估量表
（Montreal Cognitive Assessment,MoCA）分别评定精神行为和认知状态,并比较各组间精神行为及认
知状态的差异。
结果 VCIND组最多见的精神行为异常表现为易激惹/情绪不稳（66.7%）,睡眠障碍（61.1%）,其
次为激越/攻击行为（55.6%）,幻觉/妄想（44.4%）。VaD组焦虑/抑郁症状与VCIND组相比较多见,差
异具有显著性（75% vs 16.7%;P =0.001）。VCIND组各认知评分介于VaD组和NCI组之间,与NCI组
相比,在视空间/执行能力（2.78±0.73 vs 4.50±0.51）、注意（4.61±0.61 vs 5.33±0.48）、语言
（2.11±0.47 vs 2.67±0.49）、抽象［1（0,1）vs 2（1,2）］、延迟记忆［2（2,3）vs 4（4,4）］方面差异
均具有显著性（P <0.001）。
结论 VCIND可以以精神行为异常为主要表现,尤其是急起的易激惹/情绪不稳、睡眠障碍及激越/
攻击行为。     

小鼠脑出血后不同时间点小胶质细胞极化状态的实验研究

目的 观察小鼠脑出血后不同时间点小胶质细胞M1及M2型的转化，为促炎型M1型小胶质细胞向抗
炎修复型M2型小胶质细胞的转化，减轻脑出血后神经功能损伤提供理论依据。
方法 选取健康雄性ICR小鼠48只，随机分为假手术组、脑出血组，每组按术后时间点不同随机
分为1 d、3 d、7 d三个时间点，每个时间点8只。通过立体定位仪用微量注射器向尾状核注射Ⅳ型胶
原酶0.5 U制备脑出血模型，假手术组注射等量生理盐水。各组于术后对应时间点参照改良Garcia
评分量表进行神经功能缺损评分后灌注取脑，采用蛋白免疫印迹检测M1型小胶质细胞标志物肿瘤
坏死因子α（tumor necrosis factor-α，TNF-α）、白细胞介素6（interleukin-6，IL-6），M2型小胶质细胞
标志物脑源性神经营养因子（brai n-derived neurotrophic factor，BDNF）、胰岛素样生长因子1（insulinlike
growth factor 1，IGF-1）的含量；采用免疫荧光染色标记小胶质细胞M1型（Iba1+CD80）、M2型
（Iba1+CD206），评价出血后血肿周围组织小胶质细胞活化状态。
结果 脑出血组1 d、3 d、7 d各时间点Garci a评分均较假手术组低，TNF-α、IL-6、BDNF及I GF-1的蛋白
表达量均较假手术组增多（均P＜0.01）。脑出血后1 d时M1型高于M2型小胶质细胞数量（38.33±1.53
vs 23.00±3.00，P =0.01）；3 d时M1型同样高于M2型（66.33±3.06 vs 57.33±2.52，P =0.02）；7 d时M1
型低于M2型（33.67±1.15 vs 52.33±0.58，P＜0.01）。
结论 脑出血急性期（1～3 d）以M1型小胶质细胞为主，脑出血亚急性期（7 d）以M2型小胶质细胞
为主。     

特发性高颅压患者脑血流自动调节研究

目的 分析特发性颅内压增高（idiopathic intracranial hypertension，IIH）患者脑血流自动调节机能。
方法 连续入组2018年12月-2019年3月在首都医科大学附属北京天坛医院就诊的IIH患者，并选取年
龄匹配的健康志愿者作为对照组。应用传递函数的算法分析TCD显示的大脑中动脉血流速度及动脉
血压的自然波动以评估脑血流自动调节机能。
结果 入组IIH组10例，对照组13例。所有入组者均完成了双侧大脑半球的脑血流自动调节检测，共
检测了20个高颅压半球及26个正常对照半球。与对照组相比，IIH组大脑中动脉脑血流增益显著降
低[（0.64±0.35）%/% vs（0.37%±0.20）%/%，P =0.004]；相位也显著降低（58.80±20.86°vs
39.16±23.79°，P =0.005），差异有统计学意义。IIH组每秒钟脑血流速度的恢复率较对照更低，但差
异尚未达到统计学意义（[ 26.34±43.29）%/s vs（38.81±20.16）%/s，P=0.240]。
结论 IIH患者脑血流自动调节机能显著受损。     

三维动脉自旋标记评价丁苯酞注射液对急性缺血性卒中患者脑血流的影响

目的 采用MRI 三维动脉自旋标记（3-dimensional arterial spin labeling，3D-ASL）技术观察急性缺血
性卒中患者使用丁苯酞注射液对脑血流灌注的影响。
方法 纳入60例非大动脉狭窄或闭塞性急性缺血性卒中患者，随机分为观察组（30例）和对照组
（30例）。对照组采用常规治疗，观察组在对照组治疗基础上加用丁苯酞注射液，疗程为14 d。治疗前
后均进行头颅3D-ASL检查来测量梗死灶相对脑血流量（relative cerebral blood flow，rCBF）的变化。
结果 观察组和对照组治疗前rCBF差异无统计学意义，治疗后观察组rCBF高于对照组（0.97±0.45
vs 0.35±0.15，P =0.003）。
结论 丁苯酞注射液可以提高急性缺血性卒中患者梗死病灶区域的脑血流灌注水平。     

活性金属基质蛋白酶-9的表达增高可能导致脑动静脉畸形出血风险增加的研究

【摘要】 目的 探讨金属基质蛋白酶-9（matrix metalloproteinase-9,MMP-9）在脑动静脉畸形出血机制中的作用。 方法 收集2010年10月至2011年3月天坛医院住院的脑动静脉畸形（arteriovenous malformation,AVM）患者及颞叶癫痫患者。根据手术切下的动静脉畸形的血管巢及癫痫手术患者术中切除的脑组织,分为脑动静脉畸形出血组（14例）、未出血组（17例）和对照组（25例）。采用Western蛋白印迹检测组织中MMP-9蛋白水平的表达。采用免疫荧光方法检测各组MMP-9的表达,明胶酶谱检测组织中有活性的MMP-2和MMP-9蛋白的表达。 结果 MMP-9蛋白在未出血组中表达高于对照组和出血组（1.21±0.34 vs 0.35±0.06,P =0.0014;1.21±0.34 vs 0.32±0.08,P =0.047）,出血组和对照组之间差异无显著性（0.32±0.08 vs0.35±0.06,P =0.7456）。显示MMP-9蛋白的活性明胶酶谱中,出血组和未出血组及对照组之间的差异有显著性（0.97±0.08 vs 0.40±0.09,P =0.009;0.97±0.08 vs 0.30±0.07,P =0.0034）。在出血组,有活性的MMP-2的表达同样高于未出血组和对照组,差异有显著性（1.36±0.17 vs 0.55±0.12,P =0.019;1.36±0.17 vs 0.36±0.09,P =0.006）。 结论 在脑动静脉畸形组织中活性MMP-9表达增高,在破裂出血的动静脉畸形中MMP-9更多转化为活性的形式出现。     

急进高原的健康人群脑血管反应性研究

【摘要】
目的 探讨健康成年人急进高原低压、低氧环境后脑血管反应性（cerebrovascular reactivity,CVR）的变化及其可能机制。
方法 采用经颅多普勒超声监测仪评估健康成年人从海拔2200 m急进到海拔3800 m前后CVR;用硝酸还原酶法测定该组研究人群血浆一氧化氮（nitric oxide,NO）水平,采用酶联免疫吸附法测定其血浆内皮型一氧化氮合酶（endothelial nitric oxide synthase,eNOs）水平。
结果 研究人群共46例,急进高原后较急进高原前CVR增高,差异有显著性［CVR：2.36±0.74 vs 1.43±0.46,P<0.001;CVR指数（cerebrovascular reserve index,CVRI）：2.56 0.89 vs 1.82 0.71,P<0.001］;血浆NO水平升高,差异有显著性［（44.97± 0.68）μmol/L vs（34.45± 2.86）μmol/L,P<0.001］;血浆eNOS水平升高,差异有显著性［（274.81±13.68）pg/ml vs （209.73±14.34）pg/ml,P<0.001］;急进高原后较急进高原前正常呼吸时双侧大脑中动脉平均脑血流速度明显升高,差异有显著性［（93.78±11.67）cm/s vs （80.85±11.14）cm/s,P<0.001］。
结论 健康成年人急进高原后,CVR、血浆NO及eNOS含量和大脑中动脉平均脑血流速度都明显升高,以适应急进海拔3800 m后的脑缺氧情况。     

多语言任务功能磁共振指导国人语言区动静脉畸形切除手术

目的 观察针对中国人主要汉语语言区的多语言任务功能磁共振（functional MRI,fMRI）指导语言
区动静脉畸形（arteriovenous malformations,AVM）切除手术对术后语言功能的保护作用。
方法 前瞻性纳入首都医科大学附属北京天坛医院神经外科2017年12月-2019年12月收治的语言区
AVM患者31例,术前行多语言任务（包括同义字判断、单字朗读、听力理解）fMRI扫描。使用SPM12软件
明确各个任务的激活区并分析病变与激活区关系（包括二者之间的距离以及是否存在激活区右侧半
球重塑）,借助Brainlab导航系统指导手术,术前、术后一周采用西方失语症语言量表（western aphasia
battery,WAB）评估患者语言功能。
结果 所有患者均得到有效语言区定位。同义字判断任务主要激活左侧半球额中回（24/31,
77.4%）,其中1例（3.2%）患者出现语言区右侧半球优势;单字朗读任务主要激活左侧半球额下回后
部（23/31,74.2%）,7例（22.6%）患者出现语言区右侧半球优势;听力理解任务主要激活左侧半球颞
上回后部（30/31,96.8%）,6例（19.4%）患者出现语言区右侧半球优势。病变距离语言区平均距离为
5.5±3.4 mm。术后WAB量表评分（38.51±2.84分）较术前（39.32±0.64分）无下降（P =0.135）,仅2例
（6.4%）患者术后出现语言功能障碍。
结论 术前采用针对国人主要汉语语言区的多任务fMRI行语言功能定位可有效保护语言功能。     

Relationships between hemorrhage, angioarchitectural factors and collagen of arteriovenous malformations

Objective While associations between the angioarchitecture of arteriovenous malformations (AVMs) in the brain and pathological features have been described, here we investigated the relationship between the angioarchitecture, the pathological features of the vessel wall, and hemorrhagic events. Methods The study was conducted on 43 patients: 16 with ruptured AVM (rAVM), 15 with non-ruptured AVM (nrAVM), 6 with craniocerebral trauma (control) and 6 with epilepsy (control). The diagnosis of AVM was confirmed by preoperative digital subtraction angiography. Tissues were stained with hematoxylin and eosin and Masson’s trichrome (for collagen fibers) to evaluate the vessel wall structure and endothelial integrity. The content and distribution of collagen types I and III in the vessel wall were assessed by immunohistochemical staining. Results In the nrAVM group, the nidus had more draining veins than the rAVM group (P <0.05). Severely damaged endothelial cells, significantly fewer smooth muscle cells in the media, and hyperplasic type-I and -III collagen fibers were found in the rAVM group. The content of collagen types I and III in rAVMs was higher than that in the nrAVM (P <0.05) and control groups (P <0.01). Conclusion There is an association between angioarchitectural features such as the number of draining veins and the pathological structure of the AVM wall. These abnormalities may contribute to AVM rupture.     

Structural fragility and inflammatory response of ruptured cerebral aneurysms. A comparative study between ruptured and unruptured cerebral aneurysms.

BACKGROUND AND PURPOSE: Despite technical advances in endovascular and microsurgical treatment, patients with aneurysmal subarachnoid hemorrhage still have a high mortality and morbidity rate. To improve the treatment results in patients with aneurysms, we must better understand the pathophysiology of cerebral aneurysms and the mechanisms leading to their rupture. Therefore, we studied the pathological differences between unruptured and ruptured aneurysms. METHODS: Ruptured (n=44) and unruptured (n=27) aneurysms were obtained at surgery. The aneurysmal endothelium was scored from 0 (normal) to 5 (complete disruption) by using a scanning electron microscope. The aneurysmal wall was evaluated by immunohistochemical methods. The wall structure was scored from 1 (dense collagen and rich, smooth muscle cells) to 5 (hyaline-like structure). The degree of inflammatory cell invasion into the wall was also scored from 0 (very few cells) to 3 (many cells). RESULTS: Ruptured aneurysms manifested significant endothelial damage (score of 3.7 versus 0.8; Mann-Whitney U test, P<10(-3)), significant structural changes of the wall (3.7 versus 1.7, P<10(-5)), and significant inflammatory cell invasion (2.2 versus 0.8, P<10(-4)) compared with unruptured aneurysms. There was a significant correlation between the score for wall structure and the score for inflammatory cell invasion (Rs=0. 63; Spearman rank correlation test, P<10(-5)). The pathophysiology of several symptomatic unruptured aneurysms was similar to that of ruptured aneurysms. CONCLUSIONS: We conclude that the pathophysiology of unruptured, asymptomatic and ruptured aneurysms is different. The wall of ruptured aneurysms was found to be fragile, possibly because macrophage infiltration into the aneurysmal wall resulted in loss of smooth muscle cells and in degradation of matrix proteins.     

脑动静脉畸形的微观形态学

目的 通过对脑动静脉畸形（cAVM）微观形态学的系统研究，进一步了解cAVM出血发生机制，探讨其相关临床症状发生的结构学基础。方法 应用HE及Masson特殊形态学染色，透射电镜观察及原子力显微镜（AFM）扫描观察15例cAVM的病理组织学及微观形态学改变。结果 HE及Masson染色结果砬示畸形血管管腔大小不一，管壁厚薄不均，畸形血管壁欠完整，管壁各层排列紊乱，胶原纤维断裂，平滑肌纤维不完整。透射电镜扫描显示栓塞的cAVM血管巾，内皮细胞断裂，内膜下层部分缺如；在栓塞与未栓塞的病巢血管壁均显示胶原蛋白束紊乱排列，内皮细胞问紧密连接欠完整，cAVM存在反复出血表现。AFM扫描结果显示畸形血管内皮细胞形态欠完整，内皮细胞之间紧密连接受到一定程度破坏，存在间断的“弹坑样”凹陷和“火山口样”改变。结论 外科切除的cAVM微观组织形态学异常，存在反复出血表现，内皮细胞及细胞间的紧密连接破坏与血管壁各层结构排列紊乱可能是cAVM出血的原因，慢性反复出血后局部脑组织中含铁血黄素的沉积可能是导致癫痫发生的主要原因。     

Treatment of arteriovenous malformations of the brain

The treatment of ruptured and unruptured brain arteriovenous malformations (AVMs) is driven by the need to prevent incident or recurrent intracranial hemorrhages. Improving feasibility of the rapidly developing endovascular, neurosurgical, and radiotherapeutic procedures leads to invasive treatment of an increasing number of neurologically intact patients with accidentally diagnosed AVMs. Recent data confirm that the natural history risk of unruptured AVMs is significantly lower than the risk of those presenting with rupture, and the treatment risk of invasive management of unruptured AVMs seems higher than their natural history risk. The treatment decision algorithm for these patients remains unsettled, as no randomized clinical trial data exist on the benefit of invasive AVM treatment for patients with bled or with unbled AVMs. The recently launched study A Randomized Trial of Unruptured Brain AVMs (ARUBA) will be the first trial randomizing patients with nonhemorrhaged AVMs to invasive versus conservative management.     

不明原因缺血性卒中患者左心房超声检查特点

【摘要】
目的 探讨不明原因缺血性卒中患者左心房超声检查特点。
方法 连续入选我院不明原因缺血性卒中患者36例,选取同期健康志愿者35例作为对照组,两组均行经胸超声心动图检查,比较两组间左心房大小、面积及左心房射血分数、左心房压力等结构及功能指标。
结果 两组左心房内径、左心房面积均无统计学差异。不明原因缺血性卒中组左心房射血分数低于对照组［（61.13±11.42）% vs （65.15±10.12）%,P=0.043］;左心房压高于对照组［（98.76± 21.89）mmHg vs （75.37± 26.98）mmHg,P=0.0414］;左心房中部血流流速低于对照组［（57.50±4.03）cm/s vs （66.56±10.59）cm/s,P=0.035］。
结论 不明原因缺血性卒中患者存在左心房功能异常。     

Is surgical therapy needed for unruptured arteriovenous malformations?

A conservative attitude toward unruptured arteriovenous malformations (AVMs) has been based on the belief that surgical resection is too risky and that their natural history is benign. We have operated on 103 patients with a cerebral AVM. In the 49 patients with unruptured AVMs, there was no mortality, and the morbidity was 14.2%. Similarly, low surgical morbidity has been reported from several centers during the last few years. The chance of hemorrhage for both ruptured and unruptured AVMs is about 3% per year, and the combined morbidity and mortality of each hemorrhage is at least 40%. All patients with an AVM should be individually considered for possible surgical resection, whether or not they have bled.     

Impact of ARUBA trial on trends and outcomes in symptomatic non-ruptured brain AVMs: A national sample analysis

IntroductionThe real-world evolution of management and outcomes of patients with unruptured brain arteriovenous malformations (AVMs) has not been well-delineated following the ARUBA trial findings of no general advantage of initial interventional (surgical/endovascular/radiotherapy) vs. initial conservative medical therapy.MethodsWe analyzed the National Inpatient Sample from 2009-2018, capturing 20% of all admissions in the U.S. Validated ICD-9 and -10 codes defined brain AVMs, comorbidities, and the use of interventional modalities. Analyses were performed by year and for the dichotomized periods of pre-ARUBA (2009-2013) vs. post-ARUBA (2014-2018).ResultsAmong the national projected 88,037 AVM admissions, 72,812 (82.7%) were unruptured AVMs and 15,225 (17.3%) were ruptured AVMs. Among uAVMs, 51.4% admitted pre-ARUBA and 48.6% in post-ARUBA period. The post-ARUBA patients were mildly older (median age 53.3 vs. 51.8 (p = 0.001) and had more comorbidities including hypertension, diabetes, obesity, renal impairment, and smoking. Before the first platform report of ARUBA (2009-2012), rates of use of interventional treatments during uAVM admissions trended up from 31.8% to 35.4%. Thereafter, they declined significantly to 26.4% in 2018 (p = 0.02). The decline was driven by a reduction in the frequency of endovascular treatment from 18.8% to 13.9% and inpatient stereotactic radiosurgery from 0.5% to 0.1%. No change occurred in the frequency of microsurgery or combined endovascular and surgical approaches. Adjusted multivariable model of uAVMs showed increased odds of discharge to a long-term inpatient facility or in-hospital death [OR 1.14 (1.02-1.28), p = 0.020] in post-ARUBA. A significantly increased proportion of ruptured AVMs from 17.0% to 23.3% was observed consistently in post-ARUBA.ConclusionNationwide practice in the management of unruptured AVMs changed substantially with the publication of the ARUBA trial in a durable and increasing manner. Fewer admissions with the interventional treatment of unruptured AVMs occurred, and a corresponding increase in admission for ruptured AVMs transpired, as expected with a strategy of watchful waiting and treatment only after an index bleeding event. Further studies are needed to determine whether these trends can be considered to be ARUBA trial effect or are merely coincidental.     

缺血性卒中患者颈动脉斑块与内皮素-1及丙二醛水平的相关性分析

目的 探讨急性缺血性卒中患者颈动脉粥样硬化斑块与血浆内皮素-1（endothelin-1，ET-1）及丙二醛 （malondialdehyde，MDA）水平的关系。      

破裂与未破裂镜像后交通动脉瘤形态与血流动力学分析

目的探讨破裂与未破裂颅内动脉瘤的血流动力学与形态学差异,分析动脉瘤破裂的危险因素。方法回顾性分析8例镜像后交通动脉瘤病人（均为一侧破裂,一侧未破裂）的临床资料,均行3D—DSA检查,建立数值模型。将16个动脉瘤按是否破裂分组,分析破裂组与未破裂组之间的形态学与血流动力学参数特征。结果破裂组动脉瘤平均擘面切应力（WSS）明显低于未破裂组（P〈0．05）;而低壁面切应力面积（LSA）比率和体颈比值明显高于未破裂组（P〈0．05）。剪切震荡指数（OSI）、动脉瘤直径、大小比率、血管角度和动脉瘤倾角组间差异无统计学意义（P〉0．05）。结论镜像后交通动脉瘤可能是研究动脉瘤破裂风险的理想模型,血流动力学与形态学在判断动脉瘤破裂风险方面同等重要。     

Upregulation of HMGB1 in wall of ruptured and unruptured human cerebral aneurysms: preliminary results

A growing body of evidence suggests that inflammation plays a crucial role in cerebral aneurysm initiation, progression, and rupture. High-mobility group box 1 (HMGB1) is a non-histone nuclear protein that can serve as an alarmin to drive the pathogenesis of inflammatory disease. The purpose of this study was to investigate the expression of HMGB1 in the wall of ruptured and unruptured human cerebral aneurysms. Human cerebral aneurysms (25 ruptured and 16 unruptured) were immunohistochemically stained for HMGB1. As controls, four specimens of the middle cerebral arteries obtained at autopsy were also immunostained. Immunofluorescence double staining was used to determine HMGB1 cellular distribution. HMGB1 was nearly undetectable in the controls. All aneurysm tissues stained positive for HMGB1 monoclonal antibody, and expression of HMGB1 was more abundant in ruptured aneurysm tissue than unruptured aneurysms (p < 0.05). Furthermore, the expression of HMGB1 had no correlation with aneurysm size and time resected after the rupture. HMGB1 nuclear immunoreactivity was co-localized with immunoreactivity of CD3 in T lymphocytes, CD20 in B lymphocytes, CD68 in macrophages, α-SMA in smooth muscle cells, and CD31 in endothelial cells. Cytoplasmic HMGB1 localization was also detected in macrophages and T lymphocytes. Taken together, HMGB1 is expressed in the wall of human cerebral aneurysms and is more abundant in ruptured aneurysms than in unruptured ones. These data indicate a possible role of HMGB1 in the pathophysiology of human cerebral aneurysms.