Yuh W T, Simonson T M, Wang A M, Koci T M, Tali E T, Fisher D J, Simon J H, Jinkins J R, Tsai F
Department of Radiology, University of Iowa College of Medicine, Iowa City.
AJNR Am J Neuroradiol. 1994 Feb;15(2):309-16.
To study MR patterns of venous sinus occlusive disease and to relate them to the underlying pathophysiology by comparing the appearance and pathophysiologic features of venous sinus occlusive disease with those of arterial ischemic disease.
The clinical data and MR examinations of 26 patients with venous sinus occlusive disease were retrospectively reviewed with special attention to mass effect, hemorrhage, and T2-weighted image abnormalities as well as to abnormal parenchymal, venous, or arterial enhancement after intravenous gadopentetate dimeglumine administration. Follow-up studies when available were evaluated for atrophy, infarction, chronic mass effect, and hemorrhage.
Mass effect was present in 25 of 26 patients. Eleven of the 26 had mass effect without abnormal signal on T2-weighted images. Fifteen patients had abnormal signal on T2-weighted images, but this was much less extensive than the degree of brain swelling in all cases. No patient showed abnormal parenchymal or arterial enhancement. Abnormal venous enhancement was seen in 10 of 13 patients who had contrast-enhanced studies. Intraparenchymal hemorrhage was seen in nine patients with high signal on T2-weighted images predominantly peripheral to the hematoma in eight. Three overall MR patterns were observed in acute sinus thrombosis: 1) mass effect without associated abnormal signal on T2-weighted images, 2) mass effect with associated abnormal signal on T2-weighted images and/or ventricular dilatation that may be reversible, and 3) intraparenchymal hematoma with surrounding edema.
MR findings of venous sinus occlusive disease are different from those of arterial ischemia and may reflect different underlying pathophysiology. In venous sinus occlusive disease, the breakdown of the blood-brain barrier (vasogenic edema and abnormal parenchymal enhancement) does not always occur, and brain swelling can persist up to 2 years with or without abnormal signal on T2-weighted images. Abnormal signal on T2-weighted images may be reversible and does not always indicate infarction.
通过比较静脉窦闭塞性疾病与动脉缺血性疾病的表现及病理生理特征,研究静脉窦闭塞性疾病的磁共振成像(MR)模式,并将其与潜在的病理生理学联系起来。
回顾性分析26例静脉窦闭塞性疾病患者的临床资料和MR检查结果,特别关注占位效应、出血、T2加权像异常以及静脉注射钆喷酸葡胺后实质、静脉或动脉增强异常。如有随访研究,评估萎缩、梗死、慢性占位效应和出血情况。
26例患者中有25例存在占位效应。26例中有11例占位效应但T2加权像信号正常。15例患者T2加权像信号异常,但在所有病例中其范围远小于脑肿胀程度。无患者实质或动脉增强异常。13例进行对比增强检查的患者中有10例静脉增强异常。9例T2加权像高信号的患者出现脑实质内出血,其中8例血肿主要位于周边。急性窦血栓形成观察到三种总体MR模式:1)占位效应且T2加权像无相关异常信号;2)占位效应伴T2加权像相关异常信号和/或脑室扩张,可能可逆;3)脑实质内血肿伴周围水肿。
静脉窦闭塞性疾病的MR表现与动脉缺血性疾病不同,可能反映不同的潜在病理生理学。在静脉窦闭塞性疾病中,血脑屏障的破坏(血管源性水肿和实质增强异常)并不总是发生,脑肿胀可在有或无T2加权像异常信号的情况下持续长达2年。T2加权像异常信号可能可逆,并不总是提示梗死。