Cases reported "Intracranial Aneurysm"

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1/39. Giant fusiform aneurysm of the basilar artery: consideration of its pathogenesis.

    BACKGROUND: We tried to determine the pathogenesis of a fusiform aneurysm of the basilar artery based on the findings of two patients who had pontine infarctions due to thrombosis within the aneurysm. CASE REPORT: The patients were female, aged 75 and 62 years. At autopsy of the first case, the dilated basilar artery was filled with fresh and old thrombus. The wall was extremely thin on the left side, where a fresh red thrombus was evident, and thick on the right side, where an old white thrombus appeared. The thick wall had a thickened and hyalinized intima, and a deposition of atheromatous plaque disrupted both the internal elastic lamina and muscle layer. The left vertebral artery was atherosclerotic and its lumen was severely compromised, but the right vertebral artery was hypoplastic. On angiogram of the second case, the dilated basilar artery presumably was filled with thrombus on the left side, contralateral to the dilated and tortuous vertebral artery. The left vertebral artery was hypoplastic. CONCLUSION: atherosclerosis may be the essential factor in the pathogenesis of a fusiform aneurysm of the basilar artery in elderly patients. The disrupted internal elastic lamina and muscle layer may be susceptible to mechanical injury by hemodynamic strain, causing progressive attenuation of the arterial wall. Stenosis of the vertebral artery on the dominant side probably produces a jet stream within the basilar artery on the stenotic side and a stagnant zone on the opposite side, promoting the initial thrombus formation.
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2/39. basilar artery occlusion due to spontaneous basilar artery dissection in a child.

    basilar artery occlusion (BAO) causing brainstem infarction occurred in a 7-year-old boy without any basic disorders. A diagnosis of BAO due to basilar artery dissection (BAD) was suspected at angiography, and this was confirmed by gadolinium-enhanced magnetic resonance imaging (MRI). These investigations clearly showed all the typical diagnostic signs such as a pseudolumen, double lumen and intimal flap, and a pseudolumen in resolution. The spontaneous healing of the dissection was clearly demonstrated during 10 months of follow-up. We stress that BAD can occur in young children and that combined diagnosis with gadolinium-enhanced MRI and angiography is conclusive for diagnosis of dissecting aneurysms. Wider use of these combined diagnostic methods will allow the detection of less severe basilar artery dissection, thus extending the spectrum of presentation and prognosis.
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3/39. Late hemorrhage from persistent pseudoaneurysm in vertebral artery dissection presenting with ischemia: case report.

    BACKGROUND: vertebral artery dissection lesions tend to resolve spontaneously, but abnormal findings such as aneurysmal-dilatation occasionally persist. However, the clinical features and pathological findings in such cases have never been verified. CASE DESCRIPTION: A 62-year-old man presented with left cerebellar infarction. Angiography showed the "pearl and string sign" in the left vertebral artery, and he was diagnosed as having left vertebral artery dissection. Repeated angiography showed persistent aneurysmal dilatation with irregular stenosis. Eleven years after the cerebellar infarction, the patient presented with a subarachnoid hemorrhage from an aneurysm of the left vertebral artery, and the lesion was explored via the left suboccipital approach. The vertebral artery was firm, making the placement of a clip impossible, so the lesion was treated by coating of the bleeding point. The patient died of pneumonia and hyperglycemia on postoperative day 15. Postmortem examination revealed an organized intramural hematoma, thickening of the intima, and fibrous degeneration of the media of the vertebral artery, a fusiform, distended thin arterial wall with intimal disruption at the aneurysmal dilatation, and arteriosclerosis of all cerebral arteries. CONCLUSION: This case indicates that persistent aneurysmal dilatation of a dissection is a pseudoaneurysm prone to rupture, and that healing of the affected vessels might be severely compromised in the presence of pathological conditions such as arteriosclerosis and disturbed intraluminal blood flow in the dissected lesions.
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4/39. De novo formation of an aneurysm in a case of unusual intracranial fibromuscular dysplasia.

    Intracranial fibromuscular dysplasia (FMD) is a vascular disease of unknown origin occurring predominantly in young women. The internal carotid artery is most often involved, but other cerebral arteries may also be affected. We report the case of a young woman presenting with an unusual angiographic appearance of intracranial FMD of the internal carotid artery (ICA) that could not be categorized into any type of the Osborn-Anderson classification. During follow up the patient presented with an intracerebral and subarachnoid hemorrhage. Repeated angiography revealed multiple aneurysms in the pathologic segment of the vessel. The patient underwent surgical treatment with clipping of the aneurysms, wrapping of the pathologic segment of the ICA and biopsy of the superficial temporal artery. Histopathological sections revealed FMD of the intimal type. alpha(1)-antitrypsin blood levels were normal. Cases of intracranial FMD previously reported in the literature are reviewed and various aspects of this rare disease are discussed.
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5/39. Different roles of arteriosclerosis in the rupture of intracranial dissecting aneurysms.

    AIMS: Although intracranial dissecting aneurysm (IDA) is a newly described variant of the brain aneurysms that affects mainly the vertebrobasilar arterial system, its pathogenesis remains obscure. We aimed to clarify the role of arteriosclerosis in the pathogenesis of IDA based on histopathological findings in seven autopsy cases of IDA. methods AND RESULTS: All cases exhibited systemic hypertension or left ventricular hypertrophy. Macroscopically, all cases exhibited subarachnoid haemorrhage. Two types of dissection were recognized in the vertebral artery. Six of seven IDA cases showed a widespread disruption of the entire thickness of the arterial wall with the formation of a dilated pseudoaneurysm, which consisted of thin adventitia (arterial wall disruption type). Medial disruption of the arterial wall and subadventitial dissecting haemorrhage were also found, resulting in the formation of a false lumen and stenosis of the 'true' lumen of the artery. However, these lesions were connected to the site of rupture of the entire arterial wall. Within 1 day after onset of IDA, the autopsy cases showed formation of fibrin thrombus, marked leucocyte infiltration and necrosis of the arterial wall at the site of the lesion. Cases that survived more than 1 week showed smooth muscle cell proliferation, macrophage accumulation and lymphocytic infiltration in the lesions. These cases showed no atherosclerotic plaque, but non-atherosclerotic fibrocellular intima. The thickness of intima and media was significantly less in the vertebral artery of IDA patients than that of non-IDA patients with systemic hypertension. On the other hand, the remaining case showed severe atherosclerosis with haemorrhage into the lipid core without connection to the arterial lumen (intra-atheromatous plaque haemorrhage type). However, unusual arterioles and neovascularization of the intra-and peri-arterial walls were observed. CONCLUSIONS: Our results suggest that disruption of the entire arterial wall may be a critical event in the development of IDA and result in the medial disruption and subadventitial haemorrhage. Non-atheromatous intima might function as a protective factor in arterial wall disruption. On the other hand, atherosclerosis may predispose to intra-atheromatous plaque haemorrhage type of IDA through intramural haemorrhage originating from the newly formed vessels.
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6/39. Dissecting aneurysms of the middle cerebral artery: neuroradiological and clinical features.

    There are few reported cases of nontraumatic dissecting aneurysms of the middle cerebral artery (MCA), and their neuroradiological and clinical features have not been analysed. We looked at these aspects in a collaborative study. We reviewed 13 patients diagnosed as having a dissecting aneurysm of the MCA based on clinical signs and neuroradiological findings in 46 stroke centres between 1995 and 1999. There were four patients who presented with cerebral ischaemia, and nine who presented with bleeding. Of the former group, three were aged less than 15 years. cerebral angiography showed extensive stenosis and a double lumen of the M1 portion in all four patients. High signal on T1-weighted images around the arterial flow void, due to intramural haematoma, was often seen in the second week. MR angiography showed findings corresponding those of intra-arterial angiography in all four cases. We saw an infarct on CT or MRI in territory of the perforating branches of the M1 segment in all four patients. In the patients presenting with bleeding, pure subarachnoid haemorrhage or a sylvian fissure haematoma was seen on initial CT, and the predominant angiographic finding was dilatation with stenosis, but the site of the lesions was not uniform. A double lumen or intimal flap was seen in about half the cases. Rebleeding occurred within 14 days of the onset in five of the nine patients, with a poor prognosis.
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7/39. Giant fusiform aneurysms in the middle cerebral artery presenting with hemorrhages of different origins. Report of three cases and review of the literature.

    Three cases of giant fusiform aneurysms in the middle cerebral artery (MCA) presenting with hemorrhages of different origins are reported, and appropriate literature is reviewed to investigate the characteristics of these lesions. Two patients had suffered a subarachnoid hemorrhage and the other had an intramural hemorrhage (dissection). Pathologically, these aneurysms presented with hemorrhages of different origins; classic rupture type (Case 1), dissection type (Case 2), and atherosclerosis-related thrombosis type (Case 3). Based on surgical and pathological investigations in these three cases and a review of the reported literature, the authors propose that giant fusiform aneurysms in the MCA are characterized by weaknesses in the internal elastic lamina with intimal thickening. Therefore, these lesions have the potential to present with hemorrhage in each of the three types. This finding indicates that there is a strong relationship between the pathological features of giant fusiform aneurysms and their clinical course, and that it is necessary to determine appropriate therapy for giant fusiform aneurysms in the MCA by evaluating cerebral blood flow, even if the lesions are found incidentally.
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8/39. Rapid development of giant aneurysm at the base of the brain in an 8-year-old boy with perinatal hiv infection.

    An 8-year-old boy with perinatal hiv infection developed a large fusiform aneurysm in the circle of willis two years prior to death which was confirmed by radiological studies. The postmortem examinations revealed a predominantly intimal, proliferative lesion, and partial destruction of the internal elastic lamina in the involved arteries. Within the intima hyperplasia of fibroblasts and smooth muscle cells was observed. No inflammatory alterations, no granulomas and no multinucleated giant cells could be noted in the vascular walls and in the cerebral parenchyma. A small ischemic infarct was present in the left thalamus. cerebellum, brainstem and medulla showed multiple areas of progressive multifocal leukoencephalopathy (PML). immunohistochemistry with anti-gp41, a monoclonal antibody against hiv envelope did not exhibit any positive results. These findings implicate that the vascular lesion might be attributed to primary infection of the brain by hiv which led to a defect of elastic lamina and consecutive intimal hyperplasia. A second hypothesis could be based on the effect of extremely high dose AZT therapy avoiding inflammatory reaction after hiv infection.
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9/39. "Dolichoectatic" intracranial vertebrobasilar dissecting aneurysm.

    We report five patients with intracranial vertebrobasilar dissecting aneurysms, all of whom had ischemic symptoms. Angiographically, four of the five cases revealed distention and elongation of the vertebrobasilar artery like dolichoectasia and one irregular stenosis, the so-called "string sign". Magnetic resonance imaging disclosed all dolichoectatic dissecting lesions by demonstrating intimal flaps, double lumen, or subacute clot in the false lumen. We also present a successful demonstration of slow flow in the false lumen by gradient refocused magnetic resonance imaging scan with partial flip angle by the cardiac gating method. It is suggested that many of the classical "dolichoectasia" may include dissecting lesions.
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10/39. Dissecting aneurysm of the posterior communicating artery.

    A 36-year-old male presented with an extremely rare dissecting aneurysm of the posterior communicating artery manifesting as severe occipital headache. Magnetic resonance (MR) imaging revealed a partially thrombosed aneurysm of the right posterior communicating artery and angiography showed the pearl and string sign. Three months later, repeat angiography showed that the aneurysm was completely thrombosed and the posterior communicating artery was occluded. Magnetic resonance (MR) imaging showed an intimal flap. These neuroradiological findings demonstrated that the aneurysm was a dissecting aneurysm of the right posterior communicating artery. He was discharged with no neurological deficit.
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