1/11. Stent-assisted angioplasty of intracranial vertebrobasilar atherosclerosis: an initial experience.OBJECT: patients with intracranial vertebrobasilar artery (VBA) atherosclerotic occlusive disease have few therapeutic options. Unfortunately, VBA transient ischemic attacks (TIAs) herald a lethal or devastating event within 5 years in 25 to 30% of patients. The authors report their initial experience with eight patients in whom medically refractory TIAs secondary to intracranial posterior circulation atherosclerotic occlusive lesions were treated with stent-assisted angioplasty. methods: Eight patients (six men), ranging in age from 43 to 77 years, experienced signs and symptoms of VBA insufficiency despite combination therapy with warfarin and antiplatelet agents. Angiographic studies revealed severe distal vertebral (four patients), proximal basilar (one patient), or proximal and midbasilar stenoses (three patients). aspirin and clopidogrel were administered for 3 days before primary angioplasty and stent placement, and this regimen was maintained by the patients on discharge. patients underwent heparinization during the procedure and were given a bolus and 12-hour infusion of abciximab. A neurologist specializing in stroke evaluated all patients before and after the procedure. The VBAs in all patients were successfully revascularized with 7 to 28% residual stenosis. Six patients experienced no neurological complications. One patient died the evening of the procedure due to a massive subarachnoid hemorrhage. Two patients had groin hematomas, one developed congestive heart failure, and one had transient encephalopathy. All surviving patients are asymptomatic up to 8 months postoperatively. CONCLUSIONS: Although primary intracranial VBA angioplasty with stent insertion is technically feasible, complications associated with the procedure can be life threatening. As experience is gained with this procedure, it may be offered routinely as an alternative therapy to patients with medically refractory posterior circulation occlusive disease that may develop into catastrophic VBA insufficiency.- - - - - - - - - - ranking = 1keywords = subarachnoid (Clic here for more details about this article) |
2/11. 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.- - - - - - - - - - ranking = 1keywords = subarachnoid (Clic here for more details about this article) |
3/11. Cerebral aneurysms in the perforating artery manifesting intracerebral and subarachnoid haemorrhage--report of two cases.BACKGROUND: An arteriosclerotic aneurysm in the perforating artery has been focused on as a causative factor for hypertensive intracerebral haemorrhage. However, its pathogenesis remains unknown, and its existence is still a controversy. CASE DESCRIPTION: A 62-year-old female and a 70-year-old male with a history of hypertension suffered from intracerebral haemorrhage accompanied by subarachnoid haemorrhage. Cerebral angiograms demonstrated an aneurysm arising from the perforating artery at the central location of the haematoma in both cases. The aneurysms were confirmed as the cause of bleeding during microsurgery, and were resected. Histological examination of the surgical specimens revealed that the walls of the aneurysms lacked internal elastic lamina and consisted only of the adventitia. CONCLUSION: These findings demonstrate that the aneurysm in the perforating artery can be a causative factor for hypertensive intracerebral haemorrhage, and indicate that the loss of internal elastic lamina induced by hypertension may contribute to the formation of the aneurysm of the perforating artery.- - - - - - - - - - ranking = 28.705448619719keywords = subarachnoid haemorrhage, subarachnoid, haemorrhage (Clic here for more details about this article) |
4/11. Infra-posterior inferior cerebellar artery aneurysm arising after occlusion of the ipsilateral vertebral artery--case report.An 85-year-old woman had subarachnoid hemorrhage due to rupture of a very rare left infra-posterior inferior cerebellar artery (pica) aneurysm, a saccular aneurysm located proximally at the junction of vertebral artery (VA) and pica. Right vertebral angiography demonstrated the aneurysm since the left VA was occluded in the extracranial portion. The aneurysm projected in the opposite direction to common VA-pica aneurysms. The angiographical and intraoperative findings imply this rare aneurysm resulted from the hemodynamic changes caused by the VA occlusion. Detailed exploration of angiography is emphasized to detect such rare aneurysms among the diversity of hemodynamic patterns in elderly patients with subarachnoid hemorrhage.- - - - - - - - - - ranking = 2keywords = subarachnoid (Clic here for more details about this article) |
5/11. Concomitant ectatic posterior communicating artery and tentorial meningioma as a source of oculomotor palsy: case report.OBJECTIVE AND IMPORTANCE: Although non-aneurysmal vascular compression of the oculomotor nerve is rare, it should be considered in the evaluation of unilateral oculomotor palsy. CLINICAL PRESENTATION: A 36-year-old non-diabetic man presented with two months of intermittent retro-orbital headache and third nerve paresis caused by compression of the oculomotor nerve between an ectatic, atherosclerotic posterior communicating artery (PComA) and a small tentorial meningioma. At operation, the subarachnoid portion of the nerve, prevented from migrating posteriorly and laterally by the meningioma, was grooved by the apex of the artery's loop. INTERVENTION: Microvascular decompression (MVD) of the artery loop from the nerve and resection of the meningioma were performed. Postoperatively, the patient's retro-orbital headache and oculomotor paresis, with the exception of mild anisocoria, resolved. Tumor infiltrating the posterior tentorium and lateral cavernous sinus was treated by Cyberknife radiosurgery five months later. One year after surgery, the patient had improvement in his headaches, full extra-ocular movements, and minimal residual anisocoria. CONCLUSION: Only one other report describes MVD of the third nerve from PComA compression. A review is presented of MVD carried out for similar cases of non-aneurysmal vascular compression of the oculomotor nerve. By analogy from cases in which an aneurysm is the compressing vascular structure, prompt surgical treatment is advocated. Complete evaluation of an isolated third nerve palsy should include MRI sequences designed to detect vascular compression of cranial nerves.- - - - - - - - - - ranking = 1keywords = subarachnoid (Clic here for more details about this article) |
6/11. Clinical signs associated with megadolichobasilar artery anomaly.The elongation and ectatic course of the basilar artery (BA), called megadolichobasilar artery anomaly (MDBAA) is a macroscopic description of a neuroradiologic finding. Clinically ischemic brain stem syndromes and peripheral cranial nerve disturbances especially of the trigeminal and facial nerves, cerebellar dysfunction and CSF circulation disturbances are observed. Seldom a subarachnoid hemorrhage is proven. In CT and MRI often a tumorlike mass with a ringlike contrast enhancement combined with a nonhomogeneous lesion due to partial thrombosis, is detected. Angiography in most cases shows fusiform dilatation of the BA, elongation of the top of the basilar trunk, asymmetric tortuosity or dislocation of the irregular shaped wall of the BA. Fifteen patients within the last 12 years are demonstrated. The role of reticular fiber deficiency in the media and defects of the elastic lamina as the basis of these malformations is reported. We discuss coincidental findings of MDBAA with atherosclerosis, congenital factors causing generalized vasculopathy, metabolic disturbances in form of so called inborn errors of metabolism and endocrine deficiencies. In cases with clinical signs the morbidity is remarkably high.- - - - - - - - - - ranking = 1keywords = subarachnoid (Clic here for more details about this article) |
7/11. Morphological changes in human cerebral arteries after percutaneous transluminal angioplasty for vasospasm caused by subarachnoid hemorrhage.light and electron microscopy were used to study morphological changes in cerebral arteries after percutaneous transluminal angioplasty (PTA) for vasospasm in two patients with aneurysmal subarachnoid hemorrhage. One patient died of gastric bleeding 5 days after PTA. Postmortem examination of the inflated middle cerebral arteries revealed heterogeneously extended walls and dilated lumina. Throughout the vessel walls, the extracellular matrix, which was composed of nonmuscle components such as increased collagen, was stretched in conjunction with the medial muscle component. Also, torn and thinned areas of the wall and intramural hemorrhages were caused by overinflation. The second patient died of massive cerebral infarction caused by diffuse vasospasm 5 days after PTA. Prominent stretching of the walls at the atheromatous plaque margin in the dilated vessel was found in addition to the morphological changes observed in the first patient. These observations suggest that characteristic pathological alterations might be present in the vessel wall at the site of angioplasty. The major mechanism of the long-lasting effects of PTA seems to be the stretching and disruption of both the degenerative muscle and the proliferative nonmuscle components, mainly in the media of the vasospastic vessels.- - - - - - - - - - ranking = 5keywords = subarachnoid (Clic here for more details about this article) |
8/11. Sjogren's cerebritis complicated by subarachnoid hemorrhage and bilateral superior cerebellar artery occlusion: case report.We report a case of chronic Sjogren's cerebritis complicated by bilateral superior cerebellar artery occlusion and diffuse subarachnoid hemorrhage. Although primary sjogren's syndrome with chronic leptomeningeal involvement has been well documented and a spectrum of central nervous system disease previously outlined, no case of intracranial subarachnoid hemorrhage with major intracranial vessel occlusion has been reported.- - - - - - - - - - ranking = 6keywords = subarachnoid (Clic here for more details about this article) |
9/11. Unruptured aneurysms associated with ischaemic cerebrovascular diseases. Surgical indication.Out of 3435 patients with ischaemic cerebrovascular disease 2540 cases were investigated using cerebral angiography. In 127 of them (5%) aneurysms were found, but without clinical evidence of subarachnoid haemorrhage (SAH). 45 cases were operated upon and 82 were treated conservatively. Five of these 82 cases (6%) suffered from SAH 3 months to 10 years (mean interval 5.6 years) after the angiographic diagnosis. Four of these 5 patients with SAH died. Among the 45 surgical cases follow-up was uneventful in 29 (64%). The other 16 cases postoperatively showed neurological deterioration (36%), which was transient in 6 but with only minor improvement in 10. Of these 10 cases 2 died from cerebral infarction related to intra-operative temporary vascular occlusion respectively myocardial infarction. Thus surgical mortality was 4% and permanent morbidity 18%. Causes of postoperative neurological deterioration were partly related to general arteriosclerotic changes and special fragility of the ischaemic brain, and partly to operative technique (excessive brain retraction, damage to cortical veins, occlusion of major vessels or damage to perforators, temporary artery occlusion). Apparently in cases with ischaemic cerebrovascular diseases operative procedures, which in other cases as a rule are well tolerated, may produce harmful effects. Therefore, in these cases, the indication for operative treatment of so far silent aneurysms should be restricted to patients who are in good general condition with longer life expectancy as far as the vascular disease is concerned, and without major neurological deficit. Furthermore, the operative technique should be especially gentle and atraumatic.- - - - - - - - - - ranking = 5.6293078366424keywords = subarachnoid haemorrhage, subarachnoid, haemorrhage (Clic here for more details about this article) |
10/11. Intracerebral hemorrhage caused by transmural dissection of the anterior cerebral artery.BACKGROUND AND PURPOSE: Spontaneous dissection of the intracranial carotid artery or its main branches is an unusual condition. CASE DESCRIPTION: A 72-year-old hypertensive woman after an intense nuchal rigidity showed a subarachnoid hemorrhage and an interhemispheric hematoma by computed tomography. The neuropathological study revealed a transmural dissection of the pericallosal artery. CONCLUSIONS: The authors suggest that the dissection origin is an atheromatous plaque that bleeds, producing a dissection plane from the lumen to the adventitial artery.- - - - - - - - - - ranking = 1keywords = subarachnoid (Clic here for more details about this article) |
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