颅内囊性动脉瘤瘤壁的组织结构变化及其临床意义

目的观察颅内囊性动脉瘤瘤壁超微病理性结构,预测颅内囊性动脉瘤进展。方法在光学显微镜及电子显微镜下观察12例颅内多发动脉瘤（19个标本）、15例单发动脉瘤及9例重型颅脑损伤患者（对照组）脑血管标本的血管壁组织结构。同时采用免疫组化方法检测各组血管壁标本中的Ⅳ型胶原表达情况。结果在动脉瘤标本中可见动脉瘤壁的内皮细胞损伤、弹力板不完整或缺失及平滑肌细胞坏死,与正常大脑中动脉动脉壁有明显的差异;动脉瘤壁Ⅳ型胶原表达较对照组显著减低（P〈0.05）。结论颅内囊性动脉瘤壁中各层结构的形态及分布特点与正常大脑中动脉动脉壁存在较大差异,这可能是颅内囊性动脉瘤容易破裂的原因。     

Ⅲ型胶原蛋白在大鼠实验性囊性动脉瘤中的表达

目的　探讨Ⅲ型胶原蛋白在大鼠实验性囊性动脉瘤生长塑形过程中的作用。方法　通过显微手术方法破坏大鼠颈动脉分叉部位的内膜和内弹力层诱导囊性动脉瘤 ,在结扎及未结扎对侧颈动脉的情况下 ,观察 4～ 5个月 ,在长、宽、高三个径线上测量动脉瘤的大小。通过免疫组化方法 ,研究Ⅲ型胶原蛋白在正常动脉及动脉瘤壁上的表达。结果　破坏大鼠颈动脉分叉部位的内膜和内弹力层可诱导出囊性动脉瘤 ,在长期血流应力作用下 ,动脉瘤逐渐增大生长塑形 ,并且结扎对侧颈总动脉增加同侧血流冲击 ,可使动脉瘤生长更加明显。在正常动脉壁中膜平滑肌细胞周围有Ⅲ型胶原蛋白的明显表达 ,而在动脉瘤壁上其表达减少 ,并且随着动脉瘤生长塑形其表达进一步减少。结论　囊性动脉瘤在长期血流应力作用下 ,有Ⅲ型胶原蛋白的降解 ,使动脉壁力学性能下降 ,无法抗衡血流应力作用而逐渐生长塑形。     

颅内破裂动脉瘤的血流动力学特征:基于流固耦合技术的计算流体力学模拟分析

目的 探讨颅内破裂动脉瘤破裂点和瘤囊处血流动力学特征。方法 选择2018年1月至2019年6月收治的颅内破裂动脉瘤21例，根据术前CTA、DSA数据三维重建动脉瘤模型，采用ANSYS软件计算动脉瘤破裂点和瘤囊处血流动力相关参数[壁剪切应力（WSS）、切应力震荡指数（OSI）]。结果 动脉瘤破裂点WSS[（0.215±0.047）Pa]明显低于瘤囊WSS[（0.464±0.148）Pa；P<0.001]。动脉瘤破裂点OSI[（0.035±0.024）]与瘤囊OSI[（0.030±0.016）]无统计学差异（P>0.05）。在一个心动周期中，随着血流动力学的变化，动脉瘤形态出现规律的变化，载瘤动脉及动脉瘤的形态变化存在明显差异，即动脉瘤两侧壁的形态变化相对较小，动脉瘤破裂点处形态变化明显。结论 颅内动脉瘤破裂点较动脉瘤囊WSS更低而形态变化更大，颅内动脉瘤破裂与WSS呈负相关，而与形态变化呈正相关。     

囊性动脉瘤动物模型的建立及应用

颅内囊性动脉瘤是自发性蛛网膜下腔出血最常见的原因之一,其病死率、致残率极高.尸检证明人群中至少5%的人患有该病.临床观察发现：动脉瘤多有内皮细胞损伤和内弹力膜、中膜、平滑肌层缺失,仅由纤维性增厚的内膜和结缔组织外膜构成.本文回顾了囊性动脉瘤动物模型建立的各种技术及其应用,并将国内外研究现状和进展综述如下.     

脑动脉瘤的病理发生

脑动脉瘤的病理发生机制尚有争议。现有先天性或中膜缺损以及退行性变和内弹力膜缺损病因学理论。动脉瘤的家族性和Willis环解剖变异与动脉瘤发生的关系还有待进一步研究。近年来的研究表明血流动力学压力所引起的血管壁损伤和退行性改变可导致动脉瘤的发生;动脉瘤进一步生长和破裂的机制可能与动脉瘤壁的慢性炎性增生性反应和动脉壁对损伤的修复过程,以及蛋白水解酶调节的分解和合成代谢失衡有密切关系。     

基于64排CTA技术的颅内单发囊性动脉瘤破裂风险研究

目的探讨颅内单发囊性动脉瘤破裂的形态学风险因素。方法收集我院2012-01—2016-01诊断为颅内单发囊性动脉瘤的53例患者的影像学资料,根据动脉瘤是否破裂分为破裂组和未破裂组。比较2组CTA检查所示动脉瘤分布部位、瘤体高度、瘤体宽度、瘤颈宽度、瘤高与瘤颈比值(AR)、载瘤动脉直径、瘤高与载瘤动脉直径比值(SR)、瘤颈与载瘤动脉直径比值(NPR)、入射夹角等参数。结果破裂组动脉瘤主要分布于后交通动脉及前交通动脉,未破裂组动脉瘤多位于大脑中动脉及后交通动脉,2组分布部位差异无统计学意义(P0.05);未破裂组瘤颈宽、AR及入射夹角均小于破裂组,差异均有统计学意义(P0.05)。结论颈宽、AR及入射夹角为颅内单发囊性动脉瘤破裂的形态学风险因素。     

颅内动脉瘤易感或可能相关致病基因的研究进展

颅内动脉瘤系颅内动脉壁的囊性膨出，多发生于颅内动脉分又处，在破裂之前大多无临床症状，破裂后可以导致蛛网膜下隙出血，具有较高的发病率和病死率，颅内动脉瘤的发病原因至今尚不十分清楚，其形成、发展和破裂是多种环境因素和多个基因共同作用的结果，其中颅内动脉瘤的易感基因在发病机制中起着重要作用。本文对近年来发现的可能与颅内动脉瘤发病密切相关的易感基因作综述。     

PDGF-B在大鼠实验性囊性动脉瘤塑形机制中作用的初步探讨

动脉瘤的形成、生长与破裂就是血管塑形的过程.Skirgaudas首先研究发现在颅内动脉瘤瘤壁上有正常动脉壁上并不存在的血管内皮细胞生长因子与碱性成纤维细胞生长因子的表达,提出了血管因子在动脉瘤发病过程中可能起到一定作用.因此,本实验在建立大鼠实验性囊性动脉瘤生长塑形模型的基础上,研究了在其塑形过程中,局部生成的血小板衍化生长因子-B（platelet-derived growth factor B PDGF-B）及Ⅲ型胶原蛋白在动脉瘤中的表达,探讨其在囊性动脉瘤发病机制中的可能作用.     

60例大脑中动脉瘤破裂临床分析

<正>颅内动脉瘤是指颅内动脉壁的囊性膨出,是造成蛛网膜下腔出血的最常见的原因,在脑血管疾病中仅次于脑血栓和高血压脑出血。颅内动脉瘤好发于中老年人,青少年较少见[1],大脑中动脉瘤约占颅内动脉瘤的20%,约50%的大脑中动脉瘤破裂后引起颅内血肿,75%左右的大脑中动脉动脉瘤一旦破裂都会对周围的神经造成不同程度的损害,所以,一旦颅内动脉瘤破裂应立即行手术治疗。     

颅内囊性动脉瘤破裂形态学的危险因素分析

目的研究颅内囊性动脉瘤破裂的形态学危险因素。方法回顾性分析551例（共611个）颅内囊性动脉瘤的病例资料,以动脉瘤破裂作为最后评定指标,分为破裂组（341个动脉瘤）和未破裂组（270个动脉瘤）,使用SPSS17.0统计软件包分析数据。结果两组之间动脉瘤长、瘤颈宽、载瘤动脉平均直径、载瘤动脉近端与动脉瘤长轴夹角（IA）、瘤体长与瘤颈宽之比（AR）、瘤体最大径与载瘤动脉平均直径之比（SR）、动脉瘤面积与瘤颈处动脉面积之比（S1/S2）、存在子瘤有显著差异（P〈0.05）。多因素Logistic回归分析显示：瘤颈宽〈1.7 mm（OR=2.318,95%CI=1.381-3.893,P=0.001）、存在子瘤（OR=12.512,95%CI=7.827-20.002,P〈0.001）、S1/S2〉2.1（OR=2.460,95%CI=1.408-4.300,P=0.002）为颅内囊性动脉瘤破裂的独立危险因素。结论动脉瘤长、瘤颈宽、载瘤动脉平均直径、IA、AR、SR、S1/S2、存在子瘤是动脉瘤破裂的形态学危险因素。     

The incidence of berry aneurysm in the Iranian population: an autopsy study

Intracranial berry aneurysms are the most common kind of aneurysms in the brain, and are caused by head trauma in 1% of cases. They may remain asymptomatic for a long time or may rupture and cause intracranial hemorrhage. These aneurysms are associated with a high mortality rate. A definitive diagnosis can be made by angiography or autopsy. We studied the cadavers of 425 people who passed away accidentally. The number and location of berry aneurysms were recorded. Twelve cases (2.82%) were found to have a single berry aneurysm and two (0.47%) had multiple aneurysms. The aneurysms had a tendency to occur in the frontal half of the Circle of Willis and in approximation of the bifurcation of arteries. The main characteristics of cases of berry aneurysm in the Iranian population were in agreement with that reported in previous Western studies.     

Extracranial vertebral and carotid dissection occurring in the course of subarachnoid hemorrhage

The pathogenesis of both intracranial aneurysms and spontaneous cervical artery dissection may be related to an underlying vasculopathy. Seven cases of spontaneous cervical artery dissection in the course of ruptured berry aneurysms are reported here.     

Aneurysm of the distal portion of the posterior and inferior cerebellar artery in a child]

The case of a 7-year-old boy presenting with recurrent episodes of subarachnoid hemorrhage due to a distal posterior inferior cerebellar artery aneurysm (PICA), successfully operated, is reported. The low incidence of intracranial aneurysms in the first decade of life and the rare occurrence of distal PICA aneurysms are unusual features of this case. The theories regarding the origin of intracranial berry aneurysms are discussed.     

Diagnosis of cerebral arterial aneurysms in acute and subacute subarachnoid hemorrhage

The paper pools experience in using computed tomographic and magnetic resonance angiographies in patients with intracranial berry aneurysms in different periods following subarachnoid hemorrhage. The new low-invasive techniques for visualization of arterial vessels have been found to detect the aneurysm and to define its topographic and anatomic location in most cases (as high as 90%) by being on a par with direct cerebral angiography and to compare favourably with the latter. Based on the analysis of complex studies (angiography, CT- and MR-angiographies), the authors have developed algorithms for diagnosing intracranial aneurysms by the stage of subarachnoid hemorrhage.     

Traumatic production of an intracranial berry-like aneurysm in a monkey

A berry-like dissecting intracranial aneurysm resulted from inadvertent puncture of the internal carotid artery during trans-palatal section of a monkey's optic nerve. The light and ultrastructural features are rather similar to those of human berry aneurysms supporting the notion that the latter are degenerative rather than congenital in origin.     

Direct evidence of hypertension and the possible role of post-menopause oestrogen deficiency in the pathogenesis of berry aneurysms

Summary To determine the significance of hypertension in the pathogenesis of berry aneurysms, 113 patients with subarachnoid haemorrhage (SAH) and verified aneurysm and 63 patients with SAH without aneurysm were compared. Of those patients with angiographically verified aneurysms, 61.9% were found to have elevated blood pressure (>160/95 mmHg) and 19.5% showed electrocardiographic signs of left ventricular hypertrophy (SV1+RV5 (6) >3.5 mV). The percentages for patients without aneurysm were 36.5% and 6.4% respectively. A significant correlation was found between anterior aneurysms and left ventricular hypertrophy (P<0.01). The mean Sokolow index values were also significantly elevated in cases of aneurysm (P<0.01). There was a complementary relationship between the extent of left ventricular hypertrophy and the percentage of females with regard to localization of an aneurysm and age group. The predominance of females in the total aneurysm population, in the 50- to 59-year-old age group, and among patients with internal carotid aneurysms indicates that a sex-specific hormonal factor may also play a role in the pathogenesis of aneurysms in addition to hypertension. The collagen wasting commonly observed in bone and skin in the post-menopausal period due to decreased oestrogen levels could possibly be responsible for the formation of aneurysms in the proximal segments of the cerebral arteries, as occurs in various connective tissue diseases.     

Effects of antihypertensive drugs on blood velocity: implications for prevention of cerebral vascular disease.

The treatment of high blood pressure prevents death from congestive heart failure, hypertensive nephropathy, and encephalopathy, and strokes from cerebral arteriolar disease (lacunes, hemorrhage from microaneurysms). However, atherosclerosis, manifested as coronary artery disease is just as frequent a cause of death in well-controlled hypertensives as in poorly-controlled patients. Increasing evidence suggests that increased blood velocity, by causing turbulence and high shear rates at the endothelial surface of arteries, may be important in the pathogenesis of atherosclerosis. Turbulence has been observed in cerebral berry aneurysms. In order to measure the effects of antihypertensive agents on blood velocity, a new method of analysing Doppler ultrasound velocity recordings has been developed. Studies in Rhesus monkeys show the following: In doses which reduce diastolic pressure by 13-28%, propranolol decreased mean blood velocity (MV) by 17%, clonidine decreased MV by 14%, while methyldopa increased MV 12%, and hydralazine increased MV by 52%. (p less than .00001). It is hypothesized that enlargement of berry aneurysms, the progression of cerebral atherosclerosis, and embolism from carotid lesions might all be decreased by the selection of antihypertensive agents which decrease blood velocity.     

Pattern of reticular fibres of the major cerebral arteries in cases of unexplained subarachnoid haemorrhage

Summary The pattern of reticular fibres was studied in the intracranial arteries of six patients who did of subarachnoid haemorrhage without demonstrable cause. In each patient, the media of all of the major intracranial arteries contained much fewer reticular fibres than those of individuals without vascular disease. These fibres were mainly sparser in the outer part of the media, resembling the pattern seen in patients with ruptured berry aneurysms. It is concluded that the deficiency in reticular fibres may predispose to rupture even at the early stage of aneurysm formation.     

Age changes at cerebral artery bifurcations and the pathogenesis of berry aneurysms

Cerebral artery bifurcations with and without aneurysms were studied in postmortem brains by histology (1-μm resin sections) and by scanning electron microscopy. Specimens were taken from 20 patients without aneurysms with an age range of 1 month-80 years. Gaps in the tunica media at the carina and the lateral wall of the bifurcations were observed in 60% of specimens from arteries at all ages, but they were larger in older patients. A more striking change with age was the development of inelastic pads of intimal thickening in relation to bifurcations. Intimal pads were observed at and distal to the carina of bifurcations, but scanning electron microscopy also revealed intimal pads proximal to bifurcations in 60% of patients over the age of 30 years and in 2 out of 9 (22%) patients under 10 years. Similar pads covered a much wider area of vessel wall proximal to the necks of berry aneurysms in the 15 patients studied. Contralateral bifurcations in these patients showed no difference from non-aneurysm patients. It is suggested that the inelastic intimal pads form as a result of haemodynamic stress and that the presence of such pads may alter the stresses and strains at vessel bifurcations. Together with the presence of a gap in the tunica media, the pattern of inelastic intimal pad formation may be a major predisposing factor in the formation of cerebral artery aneurysms.     

PROGNOSTIC FACTORS IN RUPTURED ANEURYSMS OF THE CIRCLE OF WILLIS: THE SIGNIFICANCE OF SYSTEMIC HYPERTENSION

The incidence of essential hypertension has been retrospectively studied in a group of sixty-four fatal cases of ruptured berry aneurysm, and compared with a non-fatal group. Hypertension is more frequent in the fatal group, and is associated with a higher incidence of multiple aneurysms, a smaller size of aneurysm at rupture and a poorer survival after two haemorrhages when comparison is made with normotensive patients. The possible role of hypertension in the development and rupture of aneurysms is discussed, and it is concluded that it may contribute to both. Following rupture it carries a poor prognosis with a resulting over emphasis of its significance in autopsy series. Possible mechanisms for this effect include diffuse vascular disease, and an increased liability to oedema or spasm following rupture of an aneurysm.