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Role of vascular endothelial growth factor in the pathophysiology of intracranial arteriovenous malformations

机译:血管内皮生长因子在颅内动静脉畸形的病理生理中的作用

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I have read, with great interest, a recently published article in the British Journal of Neurosurgery by Kashiwazaki et al. titled "Increasing expression of vascular endothelial growth factor (VGEF) and its receptor (VEGFR) in enlarging brain arteriovenous malformations - a case report".1 The authors describe a unique case of an intracranial arteriovenous malformation (AVM) located in the motor cortex of a 26-year-old patient which grew markedly in size. The patient initially presented with a seizure which led to the diagnosis of a Spetzler-Martin grade III AVM which was fed by the middle meningeal artery as well as by distal branches of the anterior cerebral and middle cerebral (MCA) arteries. After failing medical therapy with anticonvulsants and experiencing functional decline, follow-up angiography at 5 years showed significant AVM growth to a classification of Spetzler-Martin grade IV. Two years later, the AVM ruptured and was treated with hematoma evacuation and subtotal excision of the nidus. Postoperative angiography 18 months after resection demonstrated a residual nidus which had recruited deep arterial feeders from the lenticu-lostriate branches of the proximal MCA. At this time, the remainder of the nidus was surgically extirpated. The AVM endothelial cells (EC) and adjacent dura were subjected to immunohistochemical analysis and stained positively for VEGF and VEGFR.
机译:我非常有兴趣地阅读了柏崎等人在《英国神经外科杂志》上最近发表的一篇文章。标题为“在扩大脑动静脉畸形中增加血管内皮生长因子(VGEF)及其受体(VEGFR)的表达-病例报告”。1作者描述了颅内动静脉畸形(AVM)位于运动皮层的一例一名26岁的患者,其大小明显增长。患者最初表现为癫痫发作,导致诊断为Spetzler-Martin III级AVM,该病由脑膜中动脉以及大脑前和大脑中动脉(MCA)的远端分支供血。抗惊厥药物治疗失败并出现功能下降后,随访5年的血管造影显示AVM显着增长,达到Spetzler-Martin等级IV级。两年后,AVM破裂并接受血肿疏散和病灶次全切除术治疗。切除后18个月的术后血管造影显示残留的病灶,已从近端MCA的扁los-小枝分支募集了深层动脉供血器。这时,其余病灶已通过外科手术切除。对AVM内皮细胞(EC)和邻近硬脑膜进行免疫组织化学分析,并对VEGF和VEGFR染色呈阳性。

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