Development of 'De novo' Aneurysm after Therapeutic Carotid Occlusion

Carotid occlusion is an inevitable therapeutic modality for the treatment of complex aneurysms such as giant, traumatic, and intracavernous aneurysms. Late complications of carotid occlusion include ''de novo'' aneurysm formation at a distant site because of hemodynamic changes in the circle of Willis. We report a case of de novo aneurysm in a vessel that appeared to be normal on initial angiography. The patient developed an anterior communicating artery aneurysm and marked growth of a basilar bifurcation aneurysm 9 years after trapping of the left internal carotid artery for the treatment of a ruptured large saccular aneurysm involving ophthalmic and cavernous segments. We propose that patients who undergo therapeutic carotid occlusion should be periodically followed by magnetic resonance angiography or computed tomographic angiography to evaluate the possibility of de novo aneurysm formation; this advice is in line with previous reports.     

The anatomy of aneurysm-bearing circles of Willis

The circle of Willis is known to exhibit considerable anatomical variability. The incidence of variations of the circle is said to be greater when an aneurysm is present, particularly one of the anterior communicating artery. In this study 40 circles of Willis bearing 51 saccular aneurysms were dissected and examined macroscopically. Forty circles from patients with other neurological diseases served as controls. Ninety-seven per cent of circles bearing aneurysms showed variations from a hypothetical "normal" structure, as did 85% of controls. The aneurysm group as a whole, and circles bearing anterior communicating aneurysms, showed a higher incidence of anterior cerebral artery asymmetry than controls (p less than 0.001), as did the latter when compared with circles bearing aneurysms at other sites (p less than 0.01), but there were no other significant differences.     

Cerebral aneurysms and variations in the circle of Willis

In order to obtain information about the relationship between variations in the circle of Willis and aneurysms, 44 complete circles of Willis with aneurysm were studied macroscopically. The incidence of variations was significantly higher in the aneurysm series than in the control circles without aneurysm. There was a definite correlation between asymmetric proximal segments of the anterior cerebral artery and aneurysms of the anterior communicating artery, and a tendency to correlation was found in the case of asymmetric posterior communicating arteries and aneurysms on the internal carotid artery-posterior communicating artery junction. In the light of these findings it seems likely that through hemodynamic changes variation in the circle of Willis plays some role in the development of cerebral aneurysms.     

Moyamoya病患者颅内出血原因探讨——75例Moyamoya病分析

目的 探讨Moyamoya病(MMD)发生颅内出血的原因.方法 收集作者近期收治的21例有颅内出血的MMD患者的临床资料,并结合文献中报道的54例MMD患者进行回顾性分析.结果 75例患者中,CT显示MMD患者脑内出血位于脑实质内47例,脑室内出血22例,蛛网膜下腔出血6例,表现为蛛网膜下腔出血的MMD患者均经DSA证实为伴发颅内动脉瘤.结论 MMD出血主要位于脑实质内或脑室内,有蛛网膜下腔出血时,应考虑并存颅内Willis环附近主要动脉动脉瘤可能.     

烟雾病颅内血流相关性动脉瘤的血管内治疗

目的探讨烟雾病患者颅内血流相关性动脉瘤的临床特点及血管内治疗方法。方法回顾性分析11例经全脑血管造影证实的烟雾病合并颅内血流相关性动脉瘤患者的临床表现和血管内栓塞治疗方法。结果 11例中7例表现为颅内出血,4例表现为缺血症状;9个动脉瘤位于Willis环周围,1个位于大脑后动脉顶枕支,1个位于脉络膜后内侧动脉;11个动脉瘤除1例外周型动脉瘤因超选困难外其余10例均成功行血管内栓塞治疗,随访均获良好疗效。结论烟雾病患者颅内血流相关性动脉瘤可有出血或非动脉瘤性临床表现,此类动脉瘤可分为累及Willis环的主要动脉型动脉瘤和累及侧支为主的外周动脉型动脉瘤;血管内栓塞治疗烟雾病患者的颅内动脉瘤是安全有效的,对外周动脉型动脉瘤可予对症保守治疗。     

烟雾病伴发颅内动脉瘤的诊断和治疗

目的 探讨烟雾病伴发颅内动脉瘤的诊断和治疗.方法 回顾性分析78例烟雾病患者的临床表现、影像学特点及治疗方法 .结果 78例烟雾病中,8例合并动脉瘤(10.3%),其中6例表现为颅内出血,2例表现为缺血症状;其中2例位于Willis环远端血管,6例位于Willis环.3例行显微外科手术夹闭,3例行血管内栓塞治疗,2例保守治疗.平均随访26个月(8-40个月),1例在右侧后交通动脉动脉瘤栓塞治疗12个月后,再次出现左侧外囊出血死亡,7例无再次颅内出血.结论 烟雾病患者应行全脑血管造影检查,部分烟雾病可伴发动脉瘤.位于Willis环的动脉瘤可行显微外科手术治疗或血管内栓塞治疗,位于Willis环远端血管的动脉瘤治疗,有待进一步探讨.     

Configuration of the circle of Willis,direction of flow,and shape of the aneurysm as risk factors for rupture of intracranial aneurysms

Background   Improved knowledge on risk factors for rupture of intracranial aneurysms may lead to more tailored aneurysm management. We studied whether configuration of the circle of Willis, direction of flow towards the aneurysm, and shape of the aneurysm are risk factors for rupture. Methods   We reviewed CT angiograms of 126 patients with 75 ruptured and 75 unruptured aneurysms, matched for site of the aneurysm, gender and age of the patient, and year of CT angiogram. For the characteristics studied, we calculated odd ratios (ORs) with corresponding 95 % confidence intervals (CIs) for risk of rupture. Configuration of the circle of Willis (incompleteness, asymmetry or dominance) was analyzed on a per site basis. Non-spherical shape was subdivided into elliptical (oval and oblong) and multilobed. In additional analyses, we adjusted for size by means of multivariable logistic regression. Results   Flow straight into the aneurysm (OR 2.0; 95 % CI 1.0–4.1) and non-spherical shape (OR 2.8; 95 % CI 1.5–5.5) were associated with rupture. Both elliptical shape, with increasing ORs for oval (OR 1.8; 95 % CI 0.8–4.0) to oblong shape (OR 6.2; 95 % CI 1.9–21), and multilobed shape (OR 4.1; 95 % CI 1.2–14) were associated with rupture. These ORs decreased after adjustment for size. Configuration of the circle of Willis was not associated with a strong risk of rupture; moderate risk could not be excluded. Conclusion   Direction of flow into the aneurysm and nonspherical (both elliptical and multilobed) shape may contribute to the risk of rupture, but are related to aneurysm size and may warrant more frequent follow-up.     

Analysis of phospholipase C gene in patients with subarachnoid hemorrhage due to ruptured intracranial saccular aneurysm

Abstract

This study is designed to determine whether patients with aneurysmal subarachnoid hemorrhage have mutations in the phospholipase C-dl (PLC-51) gene, which was identified as a gene responsible for hypertension in spontaneously hypertensive rats. Seventy-two cases (31 male and 4 1 female) with intracranial saccular aneurysms were analyzed. The mean age was 60.1 ± 11.5 years (mean± SD) (range 24-85 years). There were 35 patients (48.6%) with hypertension, 5 (6.9%) with diabetes mellitus, 72 (16.7%) with hyperlipidemia, 8 (11.1%) with ischemic heart disease, and 25 (34.7%) who were active smokers. The location of aneurysm was distributed as follows: 33 (33%) were at anterior cerebral artery, 23 (23%) were at middle cerebral artery, 28 (28%) were at internal carotid artery, and 16 (16%) were at vertebro-basilar artery. Six patients (8.3%) had a family history of intracranial aneurysms. There were 20 patients (27.8%) with multiple aneurysms, and 8 patients (11.1 %) with a large or giant aneurysm. The four regions of PLC-51 gene (bases 1099-1271, 1254-1401, 1343-1481, and 1882-2023) where genetic mutations were found in spontaneously hypertensive rats, were screened by PCR-SSCP analysis and their nucleotide sequences of all patients were determined. However, no mutations were detected in all patients. These results suggest that mutations ofPLC-d 1 gene previously implicated in hypertensive factor in rats may not be the case with human patients and therefore may be poorly related with aneurysmal subarachnoid hemorrhage. [Neurol Res 1999; 21: 368-372]     

Saccular Aneurysm of the Azygos Anterior Cerebral Artery: Three Case Reports

The azygos anterior cerebral artery, a rare anomaly in the circle of Willis in which only a single vessel supplies the medial aspects of both anterior cerebral hemispheres, is closely associated with saccular aneurysms. We present three cases of azygos anterior cerebral artery aneurysms among the 781 cerebral aneurysms surgically treated at our institution in an 11-year period. These three cases all involved elderly women who presented with subarachnoid hemorrhage. Conventional cerebral angiography and CT angiography revealed small saccular aneurysms at the distal ends of the azygos anterior cerebral arteries. These aneurysms were clipped successfully using a bifrontal interhemispheric approach. Hence, the pathogenesis of these particular aneurysms relating to hemodynamic change, associated anomalies, and surgical pitfalls is discussed with review of literature.     

Pipeline血流导向装置治疗颅内动脉瘤的安全性及疗效分析

目的探讨Pipeline血流导向装置(PED)治疗颅内动脉瘤的安全性和疗效。方法回顾性分析2015年2月至2020年2月郑州大学第一附属医院神经介入科收治的采用PED治疗的颅内动脉瘤患者103例(108个动脉瘤)。其中颈内动脉颅内段小型动脉瘤65例,Willis环远端动脉瘤23例,椎-基底动脉动脉瘤15例;囊状动脉瘤83例,夹层和梭形动脉瘤20例;破裂动脉瘤9例,未破裂动脉瘤94例。术后采用O′Kelly Marotta(OKM)分级标准判断动脉瘤的闭塞程度,采用改良Rankin量表评分(mRS)评估临床预后。结果103例患者(108个动脉瘤)共置入109枚支架,支架置入成功率为100%。术后即刻动脉瘤闭塞OKM分级A级45例(43.7%)、B级42例(40.8%)、C级6例(5.8%)、D级10例(9.7%)。103例患者中,围手术期9例(8.7%)发生并发症,其中出血性事件1例(1.0%),缺血性事件8例(7.8%),死亡1例(1.0%)。术后12个月,102例患者中,mRS评分≤2分者99例(97.1%),3~5分3例(2.9%);79例行数字减影血管造影检查,其中OKM分级B级和C级各7例(各占8.9%),D级65例(82.2%),无一例患者的动脉瘤复发。结论采用PED治疗颈内动脉颅内段小型动脉瘤、椎-基底动脉动脉瘤及Willis环远端动脉瘤,围手术期并发症少,手术效果好。     

脑动脉瘤模型制作及高血压对其影响的实验研究

目的 建立脑动脉瘤动物模型并初步探讨高血压对脑动脉瘤的影响.方法 45只雄性SD大鼠按随机数字表法分为高血压组、正常血压组和正常对照组.高血压组行脑动脉瘤模型制作+双侧肾动脉狭窄术:正常血压组只建立脑动脉瘤模型:正常对照组不予任何处理.各组在术前,术后6周、12周三个时间点分别测量各组大鼠动脉收缩压.术后12周测量脑动脉瘤大小,并灌注固定,取脑动脉瘤部位血管组织,应用HE染色、Van Geson染色和Verhoeff染色进行病理检查.结果 高血压组在处死前血压明显升高[(197.48±15.44)mm Hg],与手术前的血压[(104.40±14.70)mm Hg]相比差异有统计学意义(P<0.05);处死前脑动脉瘤的长度[(2.38±0.31)mm]和宽度[(1.89±0.35)mm]与脑动脉瘤制作完成时的长度[(1.62±0.18)mm]和宽度[(1.36±0.09)mm]相比差异有统计学意义(P<0.05);正常血压组和正常对照组无明显变化.病理检查显示高血压组血管内膜消失,弹力层完全断裂;正常血压组尚存部分弹性纤维;正常对照组血管组织无改变.结论本实验采用的脑动脉瘤模型稳定性好,制作方便,具有与人类脑动脉瘤相似的形态和病理结构.高血压对脑动脉瘤的弹力蛋白和胶原蛋白有明显影响,是影响脑动脉瘤增大的重要因素之一.     

儿童颅内动脉瘤的诊断和治疗

目的探讨儿童颅内动脉瘤的临床特点和治疗策略。方法回顾性分析了7例儿童颅内动脉瘤的临床资料。7例儿童动脉瘤中,4例位于后循环,3例位于前循环;1例伴有AVM。仅1例是女童。开颅手术治疗1例,血管内治疗4例,2例未治。结果治疗的5例中,3例经血管内栓塞治愈。1例经开颅手术治愈,1例基底动脉主干梭形动脉瘤经血管内栓塞部分瘤体,症状好转。无死亡。结论儿童颅内动脉瘤罕见,其临床状态常较好,经过积极治疗后大多数可以获得良好的预后。     

Expressions of PDGF-B and collagen type III in the remodeling of experimental saccular aneurysm in rats

The essential etiologic factors of intracranial berry aneurysm may be the hemodynamic stress on the arterial wall. Vascular remodeling triggered by abnormal hemodynamic stress on the blood vessels may play an important role in the formation, development and rupture of intracranial aneurysms. However, the specific causative mechanisms associated with this remain elusive. In this study, we look for the possible mechanism of platelet-derived growth factor B (PDGF-B) on the pathogenesis of saccular aneurysms in rats. Direct microsurgical destruction of the arterial intima and internal elastic lamina at the bifurcation of the carotid artery was performed in 30 rats to induce saccular aneurysms and the contralateral carotid arteries were ligated in half of them. After 4-5 months, the size of the aneurysms was determined. The expressions of PDGF-B and collagen type III on the walls of the normal carotid arteries and the saccular aneurysms were determined by in situ hybridization and immunohistochemistry. Saccular aneurysms could be induced immediately by destroying the intima and internal elastic lamina at the bifurcation of the carotid artery in rats. Saccular aneurysms grew significantly due to the hemodynamic stress in 4-5 months, and much bigger after the ligation of the contralateral carotid artery which enhanced the hemodynamic stress. There was no PDGF-B expression on the walls of the normal carotid arteries in rats, but it was expressed on the aneurysmal walls and more distinctly with the growth of the saccular aneurysms. However, there was collagen type III expression on the media of the normal carotid artery, but its expression decreased on the aneurysmal walls and further reduced with the growth of the saccular aneurysms. So, PDGF-B may induce the expression of MMP for the degradation of collagen type III on the wall of the saccular aneurysms. This may be one of the important mechanisms on the pathogenesis of the saccular aneurysm.     

Cerebral artery aneurysms in infancy, childhood and adolescence.

From this series of 16 cerebral artery aneurysms in the paediatric age group the following points can be made: (a) aneurysms in the paediatric age group may be found in unusual locations, more peripherally than usually seen in the adult population, (b) in seven patients, the aneurysm was of giant size; two of these produced symptoms by mass effect, (c) in two patients with subacute bacterial endocarditis the aneurysm was mycotic; the inflammatory fusiform dilatation of the entire circle of Willis in one case was associated with generalized candidiasis, (d) an antecedent head injury in a child may so prejudice the initial clinical assessment that the possibility of haemorrhage from aneurysm is overlooked, and (e) gradual vertebral artery ligation, to reduce the pressure-head in fusiform aneurysms, is well tolerated by the young patient, even when done bilaterally.     

A nonlinear biomathematical model for the study of intracranial aneurysms

The formation and rupture of aneurysms is a significant medical problem, but is not clearly understood. Most intracranial aneurysm are located in the circle of Willis. We consider a nonlinear mathematical model that simulates the blood flow inside the aneurysm, one of the relevant factors in the evolution of an aneurysm. Different techniques from nonlinear analysis are used in order to obtain, from the model, several consequences that would help to understand some medical aspects of aneurysms of the circle of Willis.     

Nontraumatic arterial dissection of the anterior cerebral artery: six cases report]

Nontraumatic arterial dissection of the anterior cerebral artery (NAD-ACA) is a relatively rare disease entity, although case reports have recently been increased. We treated 6 patients suffering from NAD-ACA from January 1996 to December 2003, and the neuroradiological findings together with the clinical courses were reviewed. There were 3 males and 3 females with a mean age of 57.7-year-old, ranging from 41 to 65. Five patients had a past history of hypertension and one diabetes mellitus. At the onset, all patients presented with clinical manifestations of cerebral ischemia. Among them, all exhibited contralateral hemiparesis with greater weakness of the lower extremity, and two patients exhibited headache. Initial angiography revealed the pearl and string sign in four patients and string sign, tapered occlusion in each one. Follow-up angiographies revealed sequential changes in all patients; four improved and two progressed. Main anatomic site of the lesion was as follows; five in the A2 and one in the A1 portion, in addition, one patient was complicated by saccular aneurysm, one by PCA dissection, and two had with saccular aneurysm contralateral ACA & MCA and VA dissection each other. Four patients were treated conservatively by intravenous administration of argatroban, one by intravenous administration of Dextrane and one by anti-platelet agent in the acute stage. All patients were treated by anti-platelet agents in the chronic stage. Good recovery was achieved in five patients, but one who suffered from severe subarachnoid hemorrhage in the chronic stage died. Our experience suggests that hypertension and/or the succeeding abnormal structural changes in the arterial wall may contribute to the occurrence of this disease. NAD-ACA showing clinical manifestations of cerebral ischemia could result in a relatively good prognosis; however, attention should be paid to patients treated conservatively with a very closed follow-up angiography to prevent a possibility of severe hemorrhage.     

Pathological changes in experimental saccular aneurysms in the carotid artery of the rat

Abstract

Although the reason for development of saccular aneurysms in humans has still not been elucidated\ the process might be observed and explained using a reproducible aneurysm model in vivo. In this paper, a sequential pathological study of the experimental saccular aneurysms was made. No additional influential factors were applied. At all stages of the development between the induction and 6 months, the histology of the aneurysm wall was similar to that of human aneurysms. The imbalance of the degeneration and regeneration processes during the development of these experimental aneurysms is discussed according to the pathological findings in different periods. Haemodynamic stress and different regenerative speeds in different arterial tissues must be responsible for the saccular aneurysm formation and growth.     

Clinicopathological features of non‐atherosclerotic cerebral arterial trunk aneurysms

Internal elastic lamina (IEL) is the most vital structure of the cerebral arterial wall. Longstanding weakness of the IEL due to hemodynamic stress is compensated by adaptive intimal thickening. Formation of cerebral arterial trunk aneurysm is assumed to be the result of a break in the equilibrium between hemodynamic stress and the condition of the IEL and intima. Cerebral arterial trunk aneurysms unrelated to the branching zones have several lesional patterns of IEL and the state of intima. There is a strong relationship between the pathological features of aneur‐ ysms and their clinical courses. We attempt to delineate the concept of cerebral arterial trunk aneurysms including ‘dissecting aneurysms’ and ‘fusiform aneurysms’.     

A method for temporary and repeated increase of blood pressure in the rat, using intraperitoneal adrenaline injections.

In experimental studies, permanent hypertension has been considered to be an important factor in aneurysm formation and growth. However, in clinical studies it has been found that saccular aneurysms often develop and rupture in some patients without persistent hypertension. Environmental events that temporarily and repeatedly increase blood pressure do not take an equivalent length of time in vivo but have been noted as factors in the growth or rupture of saccular aneurysms. In order to test the effect of intermittent blood pressure elevations on saccular aneurysm formation and growth, a reliable method for temporarily and repeatedly increasing blood pressure should be developed first and in this paper, such a model is described. It is based on the intraperitoneal injections of adrenaline in rats, a route which does not seem to have been used so far.     

The relationship of blunt head trauma, subarachnoid hemorrhage, and rupture of pre-existing intracranial saccular aneurysms

Patients with a history of closed head trauma and subarachnoid hemorrhage are uncommonly diagnosed with an intracranial saccular aneurysm. This study presents a group of patients in whom a pre-existing aneurysm was discovered during work-up for traumatic subarachnoid hemorrhage. Without an accurate pre-trauma clinical history, it is difficult to define the relationship between trauma and the rupture of a pre-existing intracranial saccular aneurysm. We retrospectively reviewed 130 patients who presented to Detroit Receiving Hospital between 1993 and 1997 with a diagnosis of subarachnoid hemorrhage (SAH). Of these 130 patients, 70 were spontaneous, and 60 had a history of trauma. Mechanisms of trauma include motor vehicle accident, assault, or fall from a height. Of the 60 patients with subarachnoid hemorrhage and a history of trauma, 51 (86%) did not undergo conventional four-vessel angiography, and had no further neurological sequelae. Nine patients (14%) had a suspicious quantity of blood within the basal cisterns or Sylvian fissure and had a four-vessel angiogram. Five patients (8%) were diagnosed with a saccular intracranial aneurysm, and all underwent surgical clipping of the aneurysm. We conclude that the majority of patients (92%), with post-traumatic SAH do not harbor intracranial aneurysms. However, during initial evaluation, a high level of suspicion must be entertained when post-traumatic subarachnoid hemorrhage is encountered in the basal cisterns or Sylvian fissure, as 8% of our population were diagnosed with aneurysms.