Role of estrogen deficiency in the formation and progression of cerebral aneurysms. Part II: experimental study of the effects of hormone replacement therapy in rats

OBJECT: The increased incidence of cerebral aneurysms in postmenopausal women appears to be related to low levels of circulating estrogen. Using a rat model of aneurysm induction, the authors found that oophorectomy increased the incidence of experimental cerebral aneurysms (Part I in this issue). In the current study they examined the effects of hormone replacement therapy (HRT) on the formation of cerebral aneurysms in rats. METHODS: Forty-five female Sprague-Dawley rats were divided into three equal groups. The animals in Groups A and B were subjected to a cerebral aneurysm induction procedure (renal hypertension and right common carotid artery ligation) followed 1 month later by bilateral oophorectomy. After an additional week the rats in Group A received 17beta estradiol continuous-release pellets. The rats in Group C served as controls. Three months after the aneurysm induction procedure, all the rats were killed and vascular corrosion casts of their cerebral arteries were prepared and checked for aneurysmal changes. Using a scanning electron microscope, the authors recorded aneurysmal changes as endothelial changes alone (Stage I), endothelial changes with intimal pad elevation (Stage II), and saccular aneurysm formation (Stage III). Aneurysmal changes (Stages I, II, and III) occurred in one third of rats that had undergone oophorectomy and were receiving HRT (Group A), compared with 87% of the rats that had undergone oophorectomy but did not receive HRT (Group B). Although most of the aneurysmal changes identified in Group A rats were limited to Stage I or II, most changes in Group B animals were identified as saccular dilation (Stage III). CONCLUSIONS: The findings demonstrated the significant protective role of estrogen against the formation and progression of cerebral aneurysms. It appears to be related to the beneficial effects of estrogen on the function and growth of endothelial cells, which play a major role in preserving the integrity of the vascular wall.     

Vascular corrosion casts mirroring early morphological changes that lead to the formation of saccular cerebral aneurysm: an experimental study in rats

OBJECT: The formation of cerebral aneurysms involves complex processes and little is known about the mechanisms by which they originate, grow, and rupture. The purpose of this study was to identify early ultrastructural morphological changes that lead to the formation of experimental cerebral aneurysms. METHODS: Twenty male Sprague-Dawley rats were subjected to cerebral aneurysm induction (renal hypertension and right common carotid artery ligation); 10 intact rats served as the control group. The animals were killed after 2 months, and a vascular corrosion cast of their cerebral arteries was prepared and screened for aneurysm development by using a scanning electron microscope. Sequential morphological changes observed at the cerebral artery bifurcation in response to hemodynamic shear stress included endothelial changes, intimal pad elevation, and saccular dilation. Endothelial cell changes were the first observed morphological changes; they were followed by various degrees of artery wall dilation. No aneurysmal changes developed in any of the control rats. Of the 20 surgically treated rats, 11 displayed aneurysmal changes. In five of these animals only changes in the endothelial cell imprints could be identified. In the other six rats morphological changes in endothelial cells were associated with different stages of aneurysmal dilation. CONCLUSIONS: This is the first study to demonstrate in vivo early morphological changes that lead to the formation of cerebral aneurysms. The morphological findings indicate the principal role of endothelial cells in the pathogenesis of cerebral aneurysms and suggest that hemodynamic shear stress and blood flow patterns may precipitate these early changes.     

血管内皮细胞间连接蛋白VE-cadherin和β-连环蛋白在颅内动脉瘤中的表达

目的 观察血管内皮钙黏蛋白(VE-cadherin)和β-连环蛋白(β-catenin)在SD大鼠和人颅内动脉瘤壁中的表达,探讨血管内皮细胞连接受损与颅内动脉瘤形成的关系.方法 建立肾性高血压诱导的SD大鼠颅内动脉瘤模型,获取8个SD大鼠颅内动脉瘤.另取15例颅内动脉瘤组织标本,应用免疫组织化学方法检测VE-cadherin在大鼠脑动脉瘤壁中的表达,以及VE-cadherin和β-catenin在人脑动脉瘤壁的表达.按照Martina的方法对血管内皮层免疫反应强度进行评分.结果 正常SD大鼠和人的脑动脉血管壁上内皮层完整,VE-cadherin呈棕褐色线样均匀表达.SD大鼠颅内动脉瘤壁上VE-cadherin表达减少,呈间断性非均匀分布.正常SD大鼠脑动脉血管壁和颅内动脉瘤壁免疫反应强度评分分别为2.40 ±0.55和1.38±0.51,两组间差异有统计学意义(t=3.41,P＜0.01).人颅内动脉瘤壁内皮排列紊乱,VE-cadherin和β-catenin表达也明显减少,分布不均匀或表达缺失.正常脑动脉与颅内动脉瘤VE-cadherin和β-catenin免疫反应强度评分分别为2.60±0.54/1.33±0.49和2.80±0.45/1.33±0.49,VE-cadherin和β-catenin在两者间差异均有统计学意义(t分别为4.88和5.91;P＜0.01).结论 颅内动脉瘤的形成过程中存在内皮细胞连接受损.

Abstract：

Objective To verify whether vascular endothelial intercellular gap injury takes part in the formation of intracranial aneurysms by assaying the expression of vascular endothelial intercellular gap proteins VE-cadherin and β-catenin in the rat experimental intracranial aneurysms and human intracranial aneurysms. Methods Twenty Sprague-Dawley rats were used for establishing a model of hypertension-induced experimental intracranial aneurysm. Eight aneurysmal changes were found in the junction of the anterior cerebralartery (ACA) and the olfactort artery (OA) of rats, and immunohistochemistry was performed to detect the expression level of VE-cadherin. The expression of VE-cadherin and β-catenin was also assayed by using immunohistochemistry in fifteen human intracranial aneurysms. Results The VE-cadherin expression was reduced obviously in the intracranial aneurysms of rats as compared with the nomal cerebral artery ( 1.38 ±0. 51 vs 2.40 ±0. 55 ,P ＜0. 01 ). In human intracranial aneurysms, the expression of VE-cadherin was lower than that in the human superficial temporal artery ( 1.33 ± 0. 49 vs 2. 60 ± 0. 54, P ＜0. 01 ). And the expression of β-catenin was also reduced obviously as compared with the controls ( 1.33 ±0. 49 vs 2. 80 ± 0. 45 ,P ＜0. 01 ). Conclusion Vascular endothelial intercellular gap injury may involve in the formation of intracranial aneurysms.     

An autopsy case of persistent primitive hypoglossal artery with multiple cerebral aneurysms

An autopsy case of persistent primitive hypoglossal artery (PPHA) with multiple cerebral aneurysms is reported. A 54-year-old man with subarachnoid hemorrhage was admitted to Kuwana Hospital three days after the onset. The patient was stuporous and had stiffness of the neck. A computed tomogram showed hematoma in the interhemispheric fissure, subarachnoid hemorrhage in the basal cisterns and bilateral Sylvian fissures, and maxked dilatation of ventricles. Cerebral angiogram revealed the left PPHA and multiple aneurysms at the right anterior cerebral artery (A 2) (ruptured), anterior communicating artery, left anterior cerebral artery (A 1), left internal carotid-anterior choroidal artery junction, right internal carotid artery (C 1), and right middle cerebral artery. Neck clipping of the ruptured aneurysm and ventricular drainage were performed on the day of admission. Eight days after admission he died of rupture of the residual aneurysm. In pathological study, the PPHA was originated from the extracranial portion of the left internal carotid artery, 2 cm distal from the cervical carotid bifurcation, entered the intracranial space through the hypoglossal foramen, and turned into the basilar artery. There were six aneurysms which were shown on cerebral angiogram and another aneurysm on the left anterior inferior cerebellar artery. Microscopic examination revealed atherosclerotic change of the PPHA, true aneurysmal changes of the seven aneurysms and defect of tunica media (Forbus' medial gap) at all of the arterial bifurcations without early aneurysmal changes.     

Role of estrogen deficiency in the formation and progression of cerebral aneurysms. Part I: experimental study of the effect of oophorectomy in rats

OBJECT: Estrogen has been shown to play a central role in vascular biology. Although it may exert beneficial vascular effects, its role in the pathogenesis of cerebral aneurysms remains to be determined. To elucidate the role of hormones further, the authors examined the effects of bilateral oophorectomy on the formation and progression of cerebral aneurysms in rats. METHODS: Forty-five female, 7-week-old Sprague-Dawley rats were divided into three equal groups. Group I consisted of intact rats (controls). To induce cerebral aneurysms, the animals in Groups II and III were subjected to ligation of the right common carotid and bilateral posterior renal arteries. One month later, the rats in Group II underwent bilateral oophorectomy. Three months after the experiment began all animals were killed and cerebral vascular corrosion casts were prepared and screened for cerebral aneurysms by using a scanning electron microscope. Plasma was used to determine the level of estradiol and the gelatinase activity. Hypertension developed in all rats except those in the control group. The estradiol level was significantly lower in Group II than in the other groups (p < 0.01). The incidence of cerebral aneurysm formation in Group II (60%) was three times higher than that in Group III (20%), and the mean size of aneurysms in Group II (76 +/- 27 microm, mean +/-standard deviation) was larger than that in Group III (28 +/- 4.6 microm) (p < 0.05). No aneurysm developed in control animals (Group I), and there was no significant difference in plasma gelatinase activity among the three groups. CONCLUSIONS: The cerebral aneurysm model was highly reproducible in rats. Bilateral oophorectomy increased the susceptibility of rats to aneurysm formation, indicating that hormones play a role in the pathogenesis of cerebral aneurysms.     

Digital subtraction angiography and dynamic computed tomography for evaluating the hemodynamics in cases of giant intracranial aneurysm

Dynamic computed tomography (CT) and digital subtraction angiography were used for postoperative evaluation of the hemodynamic changes in five patients with giant or large intracranial aneurysms. The lesions in four of these cases were giant or large aneurysms of the internal carotid artery, and were treated by occlusion of the cervical internal carotid artery and superficial temporal-middle cerebral artery anastomosis. The lesion in the fifth case was a giant aneurysm of the right vertebral artery, which was treated by proximal clipping of the vertebral artery. Preoperative digital subtraction angiography revealed aneurysmal staining, and dynamic CT scanning indicated the rapid transit of contrast medium in the dome of the aneurysm. Dynamic CT scanning immediately after operation indicated a low flow state in all of the aneurysms, suggesting that they were thrombosed. Although within a few months the peripheral edges of the aneurysms became enhanced, dynamic CT scanning revealed a slower transit of contrast medium through the centers of the aneurysms than in the basilar artery, and digital subtraction angiography failed to demonstrate aneurysmal staining, suggesting that the aneurysms remained thrombosed. The present data indicate that dynamic CT scanning and digital subtraction angiography may be useful for relatively noninvasive evaluation of the hemodynamic changes in patients with giant intracranial aneurysms.     

Aneurysm growth and enlargement of pre-aneurysmal lesions

Three patients with cerebral aneurysms newly growing and enlarging for 2 to 10 years are reported. Case 1, a 54-year-old woman, had subarachnoid hemorrhage due to rupture of an intracranial aneurysm, growing from a small residual aneurysmal neck on the left internal carotid artery 10 years after the repair of the aneurysm. Case 2, a 63-year-old man, had a junctional dilatation on the left internal carotid-posterior communicating artery, developing into ruptured aneurysm about 10 years after the first hemorrhage. Case 3, a 52-year-old man, had multiple aneurysms on the bilateral bifurcations of middle cerebral arteries and left anterior cerebral artery-frontopolar artery junction. Angiography 2 years after the repair of the aneurysms revealed the new growth of a small aneurysm on the anterior cerebral artery at the junction of the fronto-orbital artery, developing from a localized vascular dilatation which had been recognized by the preoperative angiography. The existence of pre-aneurysmal lesions in arterial wall and the addition of hemodynamic impingement were thought to be one of the precipitating factors of aneurysmal formation. The pre-aneurysmal lesions in our study are as follows; a small part of thin wall of residual aneurysmal neck, a junctional dilatation, and a small evagination of arterial wall. It is necessary to discriminate a junctional dilatation and a small evagination of arterial wall from a small aneurysm with observation from multiple directions by the preoperative angiographic study. Our observations suggest that preaneurysmal lesions of the cerebral artery may develop into aneurysm and rupture, and hence the follow-up angiography is recommended for the cases with a preaneurysmal lesion or a small aneurysm for many years.     

Factors associated with aneurysm size in patients with subarachnoid hemorrhage: effect of smoking and aneurysm location

OBJECTIVE: Intracranial aneurysm size is an important determinant of risk of rupture and outcome after rupture. Risk factors influencing aneurysm formation and growth are not well defined. In this study, we examined the association between known risk factors for cerebrovascular disease and size of intracranial aneurysms in patients with aneurysmal subarachnoid hemorrhage. METHODS: We analyzed prospectively collected data from the placebo-treated group in a multicenter clinical trial conducted at 54 neurosurgical centers in North America. The presence, location, and size of intracranial aneurysms were determined by review of the admission angiograms. Pertinent information regarding the presence of various cerebrovascular risk factors was collected for each patient. Using logistic regression analysis, we identified independent determinants of aneurysm size from demographic, clinical, and angiographic characteristics of the participants. The impact of aneurysm size on 3-month mortality was analyzed after adjusting for potential confounding factors. RESULTS: For 298 patients admitted with subarachnoid hemorrhage, the ruptured aneurysms were graded as small (<13 mm) in 235 patients (79%) and large (> or =13 mm) in 63 patients (21%). In the logistic regression model, both smoking at any time (odds ratio, 2.2; 95% confidence interval, 1.1-4.5) and middle cerebral artery origin (odds ratio, 2.5; 95% confidence interval, 1.3-4.9) were independently associated with large aneurysms. Neither hypertension, diabetes mellitus, nor alcohol and illicit drug use were associated with large-sized aneurysms. After adjusting for initial Glasgow Coma Scale score and age in the logistic regression model, the presence of large-sized aneurysms was independently associated with 3-month mortality (odds ratio, 2.3; 95% confidence interval, 1.1-4.8). CONCLUSION: Cigarette smoking and middle cerebral artery origin seem to increase the risk for developing large aneurysms in patients predisposed to intracranial aneurysm formation. Further studies are required to investigate the mechanism underlying the association between cigarette smoking and intracranial aneurysm formation.     

Two cases of persistent primitive artery associated with anterior communicating aneurysm

Two aneurysm patients who have persistent primitive artery are reported. Both patients were admitted to our hospital under the diagnosis of subarachnoid hemorrhage. Carotid angiograms revealed saccular aneurysms in the anterior communicating artery. One case had the right persistent trigeminal and the other had the right persistent hypoglossal artery. Both patients were treated by aneurysmal neck clipping successfully. The incidence of association of persistent primitive trigeminal artery with intracranial vascular disease is 25%, in which 14% of cases have the intracranial aneurysms. Other congenital anomalies of the intracranial artery co-existent with intracranial aneurysm have been considerably reported so far. Our cases might suggest that congenital factors have taken part in the formation of the intracranial aneurysm.     

Spontaneous saccular cerebral aneurysm in a rat

Summary A saccular cerebral aneurysm was incidentally found at the bifurcation of a fenestrated anterior cerebral artery of 35-week-old Sprague-Dawley rat. The animal had been fed a normal laboratory diet. The internal lamina extended for a short distance into the neck of the aneurysm and then suddenly disappeared. The medial layer ended abruptly at the neck of the aneurysm. The aneurysmal wall consisted mainly of connective tissue, and of some poorly stained fragments of elastic lamina. No evidence of polyarteritis nodosa or any other inflammatory reaction was obtained. These findings were the same as those observed in man. Therefore, this aneurysm proved to be of truly spontaneous origin.In contrast to experimental aneurysms in rats and in monkeys, in which aneurysms are observed very often, degenerative changes of the elastic lamina in spontaneous aneurysm in the rat were confined to the neck of the aneurysm. This fact may explain partly the difference in frequency between spontaneous and experimental aneurysms in animals. The present study indicates that degenerative changes of the elastic lamina play a very important role in the development of saccular cerebral aneurysms.     

Clinicopathological study of bacterial intracranial aneurysms.

The authors report the clinicopathological findings in six cases of bacterial intracranial aneurysms. All patients received appropriate high-dose antibiotics, and four were treated surgically. One patient with multiple aneurysms of the main trunks died of disseminated intravascular coagulation. Autopsy disclosed no apparent aneurysm or inflammatory cell infiltration, but a partially interrupted internal elastic lamina and thickened intima were disclosed at the angiographical aneurysm sites. These findings suggest that 1) appropriate high-dose antibiotics are effective against inoperable bacterial aneurysms in the main trunks, 2) new aneurysms may be formed in patients with cyanotic congenital heart disease, because bacterial emboli can directly reach the cerebral circulation and reimplant on the fragile arterial walls after vasculitis. Histological examination of aneurysmal walls revealed inflammatory cell infiltration after resolution of clinical endocarditis. This suggests that both appropriate high-dose antibiotic therapy and surgery should be considered in patients with distal bacterial aneurysms.     

Pathology of laser-induced experimental aneurysms

Aneurysms were produced in the common carotid artery of 35 rats by milliwatt CO2 laser welding of an adventitia patch over a hole. The aneurysmal sac was formed by collagen; the lumen was covered by an endothelial-like lining and partially thrombosed. The pathology of these aneurysms is similar to spontaneously occurring intracranial human aneurysms. This aneurysm model has properties (reliability, spontaneous bleeding tendency, minimal vessel manipulation, and pathological features) that make it theoretically advantageous for the induction of experimental intracranial aneurysms in larger animals.     

Delayed post-traumatic pseudoaneurysmal formation of the intracranial ophthalmic artery after closed head injury. Case report

A 42-year-old male presented with a rare case of delayed aneurysmal formation of the intracranial ophthalmic artery after closed head injury manifesting as subarachnoid hemorrhage. Initial magnetic resonance angiography revealed no aneurysmal formation, but angiography 7 days after the injury demonstrated an intracranial ophthalmic artery aneurysm. Follow-up computed tomography angiography demonstrated enlargement of the aneurysm. The aneurysm was successfully treated by surgical resection. Histological examination revealed that the aneurysm was a pseudoaneurysm. Traumatic intracranial aneurysm (TICA) is rare and usually occurs in the peripheral arteries of the cerebral circulation or the basal portion of the internal carotid artery. The present case shows that failure to demonstrate an aneurysm on the initial angiography in the acute stage does not exclude the presence of traumatic aneurysm. This case clearly shows the time course of development of a TICA of the ophthalmic artery after closed head injury.     

Subarachnoid hemorrhage from a ruptured anterior cerebral artery aneurysm caused by polyarteritis nodosa. Case report.

Polyarteritis nodosa (PAN) is a rare systemic necrotizing arteritis that involves small- and medium-sized arteries in various organs. Although aneurysm formation in visceral arteries is a typical finding in PAN, intracranial aneurysms are much less common, and only a few cases of aneurysm rupture associated with this disease have been documented. In this paper, the authors report on a ruptured PAN aneurysm of the anterior cerebral artery; the lesion was trapped and resected. On histological examination, extensive fibrinoid necrosis and an inflammatory infiltration of leukocytes were seen in the aneurysm wall. To the authors' knowledge this is the first report of subarachnoid hemorrhage from a histologically confirmed PAN aneurysm.     

Dissecting aneurysm of the intracranial vertebral artery associated with proximal focal degeneration of the elastica: a comparative pathological study of the vertebral artery in patients with and without aneurysms

BACKGROUND: The pathogenesis underlying intracranial dissecting aneurysms remains unclear. We performed a detailed study using vertebral artery specimens obtained at autopsy from patients with and without aneurysms to identify the primary abnormality resulting in weakness of the elastica. We compared our observations with those made in specimens manifesting the normal atherosclerotic process. METHODS: Using histologic methods, we examined intracranial vertebral artery specimens from two autopsied aneurysm patients and 13 autopsied control cases to compare the state of atherosclerosis and the weakness of the elastica at this aneurysm predilection site. RESULTS: Case 1: A 54-year-old woman with 2 dissecting aneurysms of the bilateral vertebral arteries (VA) who died from recurrent subarachnoid hemorrhage (SAH). Case 2: A 53-year-old woman who died from SAH. Microscopically, all 3 vertebral aneurysms were typical transmural dissecting aneurysms. They manifested areas of focal, severe degeneration of the elastic lamina and calcification at VA sites proximal to the aneurysms. These lesions could be differentiated from secondary changes attributable to the aneurysms because of their separate location only proximal to the site of aneurysmal rupture. Atherosclerotic changes were minimal in both cases. In the controls, the degenerative state of the elastic lamina of the VA reflected an atherosclerotic process. CONCLUSIONS: We postulate that focal degeneration of elastic tissue not involved in the atherosclerotic process was the vasculopathy resulting in aneurysm formation in our SAH cases.     

Epidemiological features and diagnostic evaluation of intracranial aneurysms

Female gender and cigarette smoking appear to be risk factors for the development of multiple intracranial aneurysms. An acquired nature is likely in this form. The mechanism of aneurysm formation in patients with sickle cell anemia is apparently different. These patients also present multiple aneurysms that show propensity for vertebrobasilar territory and appear at a younger age. Familial cerebral aneurysms are diagnosed once heritable connective tissue disorders have been excluded. The age of patients tends to be lower and the size of aneurysm to be smaller at the time of rupture in the familial form. These aneurysms are less frequently found in the anterior communicating artery than the sporadic aneurysms. A high incidence of asymptomatic familial aneurysms was detected in people with family histories of intracranial aneurysms studied by means of magnetic resonance angiography. Furthermore, familial aneurysms are more likely to rupture in families having members with aneurysmal subarachnoid hemorrhage (SAH) than in those without. The results of an interesting study using color "power" transcranial Doppler ultrasound in patients with aneurysmal SAH suggest that as the intracranial pressure diminished, the size of the aneurysm increased, and there was relatively little change between maximum and minimum dimensions during the cardiac cycle, i.e., the pulsatility is reduced. The use of postoperative angiography after clipping is a matter of debate. The indication more widely accepted is in large aneurysms with a wide neck, in which incomplete clipping can be suspected. Taking into account the current low risk of angiography in centers of excellence, its routine use may be recommended. Aneurysm remnants, vessel occlusion, vasospasm, and newly identified aneurysms are the main findings that were reported.     

A ruptured distal aneurysm, thought to be a mycotic aneurysm, associated with acute subdural hematoma: case report and review of the literature

A case is described of a ruptured intracranial mycotic aneurysm in the distal middle cerebral artery associated with an acute subdural hematoma. A 55-year-old woman, with a history of tuberculous meningitis at the age of 7, presented left hemiparesis. She was in a state of semi-coma. Computed tomography scan showed a right acute subdural hematoma. Magnetic resonance angiography revealed no cerebral aneurysm. Emergency external decompression was performed and a distal central artery aneurysm was found and was resected during the operation. Numerous areas of hemosiderin pigmentation were recognized around the aneurysm and in the subarachnoid space. Microscopic examination of the aneurysmal sections showed neither elastic lamina nor membranous structures and no infiltration of any inflammatory cells. We think this aneurysm is a pseudoaneurysm. The incidence of ruptured mycotic aneurysms presenting with acute subdural hematoma is extremely low. There have been only four previously reported cases as far as I can ascertain. This case and a review of the literature are discussed.     

Antegrade recanalization of a completely embolized vertebral artery after endovascular treatment of a ruptured intracranial dissecting aneurysm. Report of two cases

Occlusion of the parent artery is a traditional method of treatment of unclippable cerebral aneurysms. Surgical or endovascular occlusion of the parent artery proximal to the aneurysm has been recommended for the treatment of dissecting aneurysms located in the vertebrobasilar circulation. Nevertheless, occlusion of the parent artery may not result in permanent exclusion of the aneurysm from the systemic circulation because, occasionally, postoperative rebleeding occurs after proximal occlusion. Alternatively, endovascular occlusion of the affected site, including the aneurysmal dilation, and parent artery, is a safe and reliable treatment for dissecting aneurysms. The authors present two rare cases of ruptured vertebral artery (VA) dissecting aneurysms that were treated by endovascular occlusion of the affected site including the aneurysm and parent artery by using Guglielmi detachable coils. In both cases the VA recanalized in an antegrade fashion during the follow-up period. Based on these unique cases, the authors suggest that a careful angiographic follow up of dissecting aneurysms is required, even in patients successfully treated with endovascular occlusion of the affected artery and aneurysm.     

Traumatic aneurysm occurring after surgical procedure of large cerebral aneurysm

A case of intracranial traumatic aneurysms occurring after surgical treatment of a large cerebral aneurysm is reported. A 56-year-old man was admitted to our department with complaints of headache, nuchal pain and nausea. Left carotid angiography (Lt-CAG) revealed a large aneurysm, measuring 20 mm in maximum diameter, of the azygos anterior cerebral artery. Successful clipping operation was performed on day 17 of subarachnoid hemorrhage. Unfortunately, small cortical branches were pulled out during the procedure from the right pericallosal artery. The postoperative Lt-CAG showed formation of two other aneurysms. Second operation was done on day 28 after the first operation. These aneurysms were located at the previously injured sites on the right pericallosal artery. From the history sited above, we diagnosed them as traumatic aneurysms. The second operation resulted in successful obliteration of these two traumatic aneurysms. Literature review yielded 25 similar cases, and the authors discuss the etiologic factors of the traumatic aneurysm due to surgical procedure.