Interv Neuroradiol
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Valavanis A, Pangalu A, Tanaka M. Endovascular treatment of cerebral arteriovenous malformations with emphasis on the curative role of embolisation. Schweiz Arch Neurol Psychiatr 2004;155:341-7. ⋯ Precise angiographic analysis of the vascular composition and intrinsic angioarchitecture of the nidus of the arteriovenous malformation by super-selective microcatheterisation is required to identify the types of feeding arteries and patterns of their supply, the number and vascular connections of nidal compartments, the types of arteriovenous shunts, the morphology of the vascular spaces composing the nidus and the number and exit patterns of draining veins. Complete angiographic investigation for recognition of secondarily induced phenomena of the cerebral vasculature, such as arterial and venous high-flow angiopathy and so-called perinidal angiogenesis is essential for a comprehensive evaluation and assessment of the associated haemorrhagic risk. Based on a precise topographic classification, detailed angioarchitectural analysis, application of superselective multimicrocatheterisation techniques along with a controlled intranidal injection of non-absorbable liquid embolic materials, nearly 40% of cerebral arteriovenous malformations can be completely and stably obliterated and therefore curatively treated by single session or multistaged embolisation with a morbidity of 1.3% and a mortality of 13%. which arc lower than the known natural history of this disease.
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In this case presentation we describe a patient with an anomalous origin of the right vertebral artery arising from the right common carotid artery in combination with an aberrant right subclavian artery and a left vertebral artery originating from the arch between the left common carotid artery and left subclavian artery. Hence there were five vessels originating from the aortic arch. The possible embryological mechanism as well as a postulation on the importance of the level of entrance of the vertebral artery in the cervical transverse foramen is discussed.
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This study evaluated: 1) the effect of recanalization on changing clinical outcome, 2) the relationship between dose of Urokinase (UK) and incidence of recanalization and intracranial haemorrhage, and 3) the efficacy and feasibility of balloon disruption (BD) in the treatment of acute cerebral embolism. Sixty-one patients with acute embolism of the major cerebral arteries treated by endovascular approaches over the past nine years were retrospectively evaluated. Among them, 30 cases were treated by BD alone or in conjunction with intra- arterial fibrinolysis in the last five years. ⋯ Concerning morbidity and mortality of BD, there was one death caused by dissection of the M2 portion of the middle cerebral artery (MCA) that happened during BD on a distally migrated embolus. Although no conclusions can be drawn from our study, a favorable outcome for acute embolism of the major cerebral arteries is expected by attaining good recanalization. In addition, BD is an effective technique that can achieve high-grade recanalization alone, or reducing the dose of fibrinolytic agent.
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Hyperdynamic therapy, consisting of hypervolemia, haemodilution, and hypertension, is an established treatment for cerebral vasospasm following subarachnoid haemorrhage. Angioplasty has emerged as an additional, effective treatment for symptomatic vasospasm. Loss of autoregulation, however, can occur despite effective angioplasty, underscoring the need for treatment with hyperdynamic therapy in combination with angioplasty. ⋯ Autoregulation is disturbed during vasospasm. Although angioplasty can improve large artery blood flow during vasospasm, hyperdynamic therapy is also needed to maintain cerebral perfusion, particularly in the face of impaired autoregulation. Quantitative CBF measurement permits the maintenance of optimal CBF and monitoring of response to therapy.
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Anticoagulant therapy is usually used after endovascular operations like coil embolization of aneurysms, or for thromboembolic diseases such as myocardial infarction. Few data exist regarding hemorrhage from benign brain tumors during systemic heparinization with the exception of pituitary adenomas (1,2). We experienced two cases of hemorrhage from benign brain tumors during systemic heparinization. ⋯ The second patient had a suprasellar tumor and was heparinized prophylactically for myocardial infarction. He had an intratumoral hemorrhage on the fifth day after the start of the heparinization. This small series suggests that systemic heparinization with brain tumors, even when they are benign, is very dangerous, and further studies with a larger patient base are warranted.