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Teaching NeuroImages: reversible pontomesencephalic edema caused by traumatic carotid cavernous fistula.教学神经影像学:创伤性颈动脉海绵窦瘘引起的可复性桥脑正中脑脚水肿。
Neurology. 2014 Jul 8;83(2):e18. doi: 10.1212/WNL.0000000000000562.
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本文引用的文献

1
Basal cerebral venous drainage from cavernous sinus dural arteriovenous fistulas.海绵窦硬脑膜动静脉瘘的大脑基底静脉引流
Neuroradiology. 2009 Mar;51(3):175-81. doi: 10.1007/s00234-008-0486-3. Epub 2008 Dec 23.
2
The anterior medullary-anterior pontomesencephalic venous system and its bridging veins communicating to the dural sinuses: normal anatomy and drainage routes from dural arteriovenous fistulas.延髓前部-脑桥中脑前部静脉系统及其与硬脑膜窦相通的桥静脉:正常解剖结构及硬脑膜动静脉瘘的引流途径
Neuroradiology. 2008 Dec;50(12):1013-23. doi: 10.1007/s00234-008-0433-3. Epub 2008 Jul 18.

教学神经影像学:创伤性颈动脉海绵窦瘘引起的可复性桥脑正中脑脚水肿。

Teaching NeuroImages: reversible pontomesencephalic edema caused by traumatic carotid cavernous fistula.

机构信息

From the Department of Neurology, Miller School of Medicine, University of Miami, FL.

出版信息

Neurology. 2014 Jul 8;83(2):e18. doi: 10.1212/WNL.0000000000000562.

DOI:10.1212/WNL.0000000000000562
PMID:25002572
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4117172/
Abstract

A 45-year-old man presented with a painful bulging right eye and blindness 6 weeks after a motorcycle accident and traumatic brain injury. He had a complete right oculomotor nerve palsy and only perception of light. MRI revealed ipsilateral pontomesencephalic edema (figure, A and B). Catheter angiography showed a direct right carotid-cavernous fistula (figure, C). Two months after coil embolization, the ptosis, proptosis and ophthalmoplegia resolved. MRI revealed resolution of pontomesencephalic edema (figure, D). The presumed mechanism was transmission of arterialized pressures of the cavernous sinus via a bridging vein to the anterior pontomesencephalic vein, generating venous hypertension and vasogenic edema.

摘要

一位 45 岁男性,在摩托车事故和外伤性脑损伤后 6 周出现右眼疼痛性突出和失明。他出现完全性右侧动眼神经麻痹,仅能感知光。MRI 显示同侧桥脑被盖水肿(图 A 和 B)。导管血管造影显示右侧颈动脉-海绵窦直接瘘(图 C)。线圈栓塞治疗 2 个月后,上睑下垂、眼球突出和眼肌麻痹均得到缓解。MRI 显示桥脑被盖水肿消退(图 D)。推测的发病机制是通过桥前吻合静脉将海绵窦动脉化压力传递到前桥脑正中静脉,导致静脉高压和血管源性水肿。