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1/43. subarachnoid hemorrhage from vertebral artery dissecting aneurysms involving the origin of the posteroinferior cerebellar artery: report of two cases and review of the literature.

    OBJECTIVE AND IMPORTANCE: Few reports have been published on ruptured vertebral artery dissecting aneurysms in which the posteroinferior cerebellar artery (pica) arises from the aneurysm wall, and there is ongoing debate as to the proper management of this type of aneurysm. This article describes two patients. CLINICAL PRESENTATION: Both patients presented with subarachnoid hemorrhage and were admitted to our institution on the day of rupture. Computed tomography revealed that the subarachnoid hemorrhage was located mainly in the posterior fossa. cerebral angiography demonstrated a vertebral dissecting aneurysm involving the origin of the pica. In one patient, the pica was very large. INTERVENTION: One patient was treated by trapping, with the pica involved in the trapped segment. Postoperatively, the patient experienced transient mild hoarseness and dysphasia but recovered completely. The other patient, whose pica was very large, was initially treated by endovascular proximal occlusion. This resulted in marked enlargement of the distal part of the aneurysm, indicating a need for surgical treatment. A clip was applied to the origin of the pica after anastomosis of the occipital artery to the pica. The patient recovered well and was discharged with no neurological deficits. CONCLUSION: The ideal method of treatment for patients with dissecting aneurysms of the vertebral artery involving the pica origin is complete isolation of the aneurysm by trapping, with revascularization of the pica. However, trapping alone is one possible treatment option. If proximal clipping alone is carried out, follow-up angiography is mandatory to observe any changes in the aneurysm.
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ranking = 1
keywords = aneurysm
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2/43. Cerebellar hemorrhage after coil embolization for a ruptured vertebral dissecting aneurysm.

    BACKGROUND: We present a case of ruptured vertebral dissecting aneurysm that exhibited cerebellar hemorrhage after successful embolization of the vertebral artery including the dissected site. CASE PRESENTATION: A 59-year-old man suffered a sudden onset of severe occipital headache when he looked up. Computed tomography demonstrated subarachnoid hemorrhage. Angiography revealed a right vertebral dissecting aneurysm distal to the posterior inferior cerebellar artery. Endovascular embolization of the aneurysm was performed with preservation of the posterior inferior cerebellar artery. The next day, the patient suffered a cerebellar hemorrhage in the vermis. The intracranial pressure was controlled by external ventricular drainage. The patient was discharged with mild cerebellar ataxia and bilateral abducens nerve palsy. CONCLUSION: In a case of vertebral dissecting aneurysm distal to the posterior inferior cerebellar artery, blood circulation in the vertebral arterial system may change after embolization of the aneurysm. In our case, the preserved posterior inferior cerebellar artery might have been hemodynamically stressed postoperatively, resulting in cerebellar hemorrhage. Therefore, strict control of blood pressure is essential in the acute stage after occlusion of the aneurysm.
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ranking = 0.83333333333333
keywords = aneurysm
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3/43. pathology of a dissecting intracranial aneurysm.

    The pathological findings of six autopsy cases of dissecting intracranial aneurysm are studied. Clinically, all cases exhibited systemic hypertension or left ventricular hypertrophy. Macroscopically, all cases exhibited rupture of the vertebral artery and subarachnoid hemorrhage. Two types of lesion were present. First, all cases showed the formation of a dilatated pseudoaneurysm with widespread disruption of the entire arterial wall, which was composed of thin adventitia. Second, a medial disruption of the arterial wall and subadventitial dissecting hemorrhage, which formed a false lumen and stenosis of the 'true' lumen of the artery, was also found. However, these lesions were found to be connected to the site of rupture. The autopsy cases within 1 day of onset of intracranial dissecting aneurysm showed the formation of fibrin thrombus, a marked degree of leukocyte infiltration and necrosis of the arterial wall at the site of the lesion. The cases that survived more than 1 week showed smooth muscle cell proliferation, macrophage accumulation and lymphocytic infiltration. No arteriosclerosis was found in any lesion studied. These data suggest that the disruption of the entire arterial wall might initially occur and cause medial disruption and subadventitial hemorrhage. hypertension and arteriosclerosis might function as causal and protective factors in the pathogenesis of dissecting intracranial aneurysms, respectively.
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ranking = 0.67355326735502
keywords = aneurysm, pseudoaneurysm
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4/43. Remission of hemifacial spasm after proximal occlusion of vertebrobasilar dissecting aneurysm with coils: case report.

    intracranial aneurysm is a rare cause of hemifacial spasm and most of the previously reported cases are treated with surgical microvascular decompression. Authors report a case of hemifacial spasm caused by a dissecting aneurysm located at the vertebrobasilar junction which improved after endovascular obliteration of the affected vertebral artery with coils.The patient was a 69-year-old man with 20 months' history of left hemifacial spasm. A vertebral angiogram showed an irregular dilatation of the right vertebral artery associated with aneurysmal dilatation at the vertebrobasilar junction. Endovascular obliteration of the abnormally dilated right vertebral artery proximal to the vertebrobasilar junction was performed. The hemifacial spasm gradually improved after the embolisation and disappeared 6 months later. Endovascular proximal obliteration of the vertebral artery may have changed the hemodynamic force inside the aneurysm and eliminated the vascular compression at the root exit zone of the facial nerve.
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ranking = 0.66666666666667
keywords = aneurysm
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5/43. 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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ranking = 0.59021993402169
keywords = aneurysm, pseudoaneurysm
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6/43. Pathological mechanism and three-dimensional structure of cerebral dissecting aneurysms.

    OBJECT: The goal of this study was to investigate the pathological mechanism and precise three-dimensional (3D) structure of cerebral dissecting aneurysms in association with their clinical course. methods: Nine aneurysm specimens were excised from eight patients. Of the nine aneurysms, seven arose from the vertebral artery, one from the anterior cerebral artery, and one from the superior cerebellar artery. Eight aneurysms were accompanied with subarachnoid hemorrhage (SAH) and one with infarction. Seven aneurysms were obtained at autopsy and two were obtained during surgery (trapping and bypass). All nine aneurysms were sectioned into serial axial slices measuring 5 to 10 microm in thickness. Taking each slice as an element, we reconstructed the 3D structure of the aneurysm. The true lumen communicated with a pseudolumen through the disrupted portion of the internal elastic lamina (IEL) in all nine aneurysms. The ruptured portion was located just above the disrupted IEL. Two aneurysms had an exit back into the true lumen. but the other seven had no such exit. CONCLUSIONS: The primary mechanism by which a cerebral dissecting aneurysm is created is by the sudden disruption of the IEL. The plane of dissection extends through the media. The majority of aneurysms have one entrance into the pseudolumen (entry-only type). This type is associated with an unstable clinical course. Some cerebral dissecting aneurysms have both an entrance and exit (entry-exit type). This type of aneurysm occasionally contains a constant flow of blood through the pseudolumen and is clinically more stable than entry-only aneurysms.
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ranking = 1.5
keywords = aneurysm
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7/43. A ruptured dissecting aneurysm of the vertebral artery: comparison of angiographic and histological findings.

    We present autopsy findings in a patient with a dissecting aneurysm of the vertebral artery causing subarachnoid haemorrhage. We sectioned the artery longitudinally and compared it with the angiogram, which showed the "pearl-and-string". Histological examination showed a pseudoaneurysm covered by adventitia alone, forming the "pearl". Internal elastic lamina and media were destroyed, and haematoma extended in the subadventitial space of the wall of the pseudoaneurysm. Media thickened by haematoma caused the "string", narrowing the parent artery. alcian blue staining showed that stratified internal elastic lamina in the aneurysm and the parent artery, had undergone marked mucoid degeneration, which may have been responsible for the dissection.
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ranking = 0.68043986804337
keywords = aneurysm, pseudoaneurysm
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8/43. brain stem compression by a giant vertebrobasilar aneurysm mimicking seronegative myasthenia.

    A patient is described with a vertebrobasilar aneurysm who was erroneously thought to have myasthenia gravis on the basis of the clinical presentation and investigations, which were interpreted as supportive of a disorder of the neuromuscular junction. Despite the correct diagnosis being made at a late stage the patient made a full recovery after radiological intervention.
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ranking = 0.41666666666667
keywords = aneurysm
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9/43. Treatment of a ruptured dissecting vertebral artery aneurysm with double stent placement: case report.

    A ruptured dissecting right vertebral artery aneurysm was treated by means of double stent placement with two overlapping stents. Control angiography performed 3 d after stent placement revealed beginning aneurysmal thrombosis. Substantial reduction in aneurysmal size was observed after 4 wk, whereas total occlusion was observed after 3 mo. The reduced stent porosity caused by the overlapping stents, which result in significant hemodynamic changes inside the aneurysmal sac, may accelerate intraaneurysmal thrombosis and may be helpful in achieving a more rapid complete occlusion compared with that achieved by single stent placement.
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ranking = 0.75
keywords = aneurysm
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10/43. Recurrent torticollis caused by dissecting vertebral artery aneurysm in a pediatric patient: results of endovascular treatment by use of coil embolization: case report.

    OBJECTIVE AND IMPORTANCE: torticollis is a symptom that can be related to different pathological mechanisms ranging from simple to life-threatening conditions. We report a child with recurrent torticollis caused by an intracranial dissecting vertebral artery aneurysm. This is a very rare condition in childhood, and it was resolved successfully with endovascular treatment. CLINICAL PRESENTATION: The patient was a 10-year-old boy with a 4-year history of left recurrent torticollis, followed by hemiparesis, dysarthria, dysmetria, and tremor. Brain magnetic resonance imaging and digital angiography detected a dissecting aneurysm involving the fourth segment of the left vertebral artery. INTERVENTION: The patient underwent endovascular treatment. Coil embolization, followed by histoacryl injection into the lesion, provided complete obliteration of the aneurysmal sac. CONCLUSION: The patient's postoperative course was characterized by a dramatic disappearance of symptoms and signs within a few hours of the intervention. No relapses of symptoms occurred during a follow-up period of 18 months. This is the first report of a child in whom recurrent torticollis was related to a dissecting vertebral artery aneurysm. Although long-term results of vertebral artery coil embolization remain to be elucidated, the method seems reliable and effective in treatment of these vascular lesions in pediatric patients.
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ranking = 0.66666666666667
keywords = aneurysm
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