Takahashi S, Sakuma I, Otani T, Yasuda K, Tomura N, Watarai J, Kinouchi H, Yanagisawa T, Mizoi K
Department of Radiology, Akita University School of Medicine; Japan.
Interv Neuroradiol. 2006 Jan 20;12(Suppl 1):167-73. doi: 10.1177/15910199060120S129. Epub 2006 Jun 15.
Digital subtraction angiography (DSA) and magnetic resonance imaging (MRI) findings in 20 patients with carotid-cavernous fistula (CCF; 3 direct CCFs and 17 indirect CCFs) were retrospectively reviewed to evaluate venous drainage patterns that may cause intracerebral haemorrhage or venous congestion of the brain parenchyma. We evaluated the relationship between cortical venous reflux and abnormal signal intensity of the brain parenchyma on MRI. Cortical venous reflux was identified on DSA in 12 of 20 patients (60.0%) into the superficial middle cerebral vein (SMCV; n=4), the uncal vein (n=2), the petrosal vein (n=2), the lateral mesencephalic vein (LMCV; n=1), the anterior pontomesencephalic vein (APMV; n=1), both the APMV and the petrosal vein (n=1) and both the uncal vein and the SMCV (n=1). Features of venous congestion, such as tortuous and engorged veins, focal staining and delayed appearance of the veins, were demonstrated along the region of cortical venous reflux in the venous phase of internal carotid or vertebral arteriography in six of 20 patients (30.0%). These findings were not observed in the eight CCF patients who did not demonstrate cortical venous reflux. MRI revealed abnormal signal intensity of the brain parenchyma along the region with cortical venous reflux in four of 20 indirect CCF patients (20%). Of these four patients, one presented with putaminal haemorrhage, while the other three presented with hyperintensity of the pons, the middle cerebellar peduncle or both on T2- weighted images, reflecting venous congestion. The venous drainage routes were obliterated except for cortical venous reflux in these four patients and the patients without abnormal signal intensity on MRI had other patent venous outlets in addition to cortical venous reflux. CCF is commonly associated with cortical venous reflux. The obliteration or stenosis of venous drainage routes causes a converging venous outflow that develops into cortical venous reflux and results in venous congestion of the brain parenchyma or intracerebral haemorrhage. Hyperintensity of brain parenchyma along the region of cortical venous reflux on T2-weighted images reflects venous congestion and is the crucial finding that indicates concentration of venous drainage into cortical venous reflux.
回顾性分析20例海绵窦瘘（CCF，3例直接CCF和17例间接CCF）患者的数字减影血管造影（DSA）和磁共振成像（MRI）结果，以评估可能导致脑出血或脑实质静脉充血的静脉引流模式。我们评估了皮质静脉反流与MRI上脑实质异常信号强度之间的关系。20例患者中有12例（60.0%）在DSA上发现皮质静脉反流至大脑中浅静脉（SMCV，4例）、钩静脉（2例）、岩静脉（2例）、中脑外侧静脉（LMCV，1例）、脑桥中脑前静脉（APMV，1例）、APMV和岩静脉（1例）以及钩静脉和SMCV（1例）。20例患者中有6例（30.0%）在内颈动脉或椎动脉造影静脉期的皮质静脉反流区域显示静脉充血特征，如静脉迂曲扩张、局灶性染色和静脉延迟显影。在8例未显示皮质静脉反流的CCF患者中未观察到这些发现。20例间接CCF患者中有4例（20%）MRI显示沿皮质静脉反流区域脑实质信号强度异常。在这4例患者中，1例出现壳核出血，另外3例在T2加权像上脑桥、小脑脚中部或两者均表现为高信号，提示静脉充血。除这4例患者的皮质静脉反流外，静脉引流途径均闭塞，且MRI上无异常信号强度的患者除皮质静脉反流外还有其他通畅的静脉出口。CCF常伴有皮质静脉反流。静脉引流途径的闭塞或狭窄导致静脉流出汇聚，进而发展为皮质静脉反流，导致脑实质静脉充血或脑出血。T2加权像上沿皮质静脉反流区域脑实质高信号反映静脉充血，是提示静脉引流集中至皮质静脉反流的关键表现。
