Detectability of brain metastases with Ms-EPI-FLAIR (+) is almost similar to that with SE-T1WI (+). Ms-EPI-FLAIR (+) could be an alternative to SE-T1WI (+) in the depiction of brain metastases.

The termination of the superficial middle cerebral vein (SMCV) has been described as entering or being partially equivalent to the venous sinus coursing under the lesser sphenoid wing, which has classically been called the sphenoparietal sinus. However, the recent literature reports that the SMCV is not connected to the sphenoparietal sinus. In this study, the venous anatomy was evaluated to clarify the anatomy of the sphenoparietal sinus and the termination of the SMCV. Magnetic resonance imaging (MRI) was performed on 1.5-T superconductive units using a three-dimensional fast spoiled gradient-recalled acquisition in the steady state (3-D fast SPGR) sequence with fat suppression in a total of 48 sides of 24 patients. Coronal source images and reconstructed axial images were displayed on the Advantage Window Console, and connections to the cavernous sinus were then evaluated for the venous sinus coursing under the lesser sphenoid wing (hereafter called the sinus of the lesser sphenoid wing), the middle meningeal vein, and the SMCV. The following findings were observed bilaterally in all patients. The sinus of the lesser sphenoid wing was connected medially with the cavernous sinus and laterally with the anterior branch of the middle meningeal vein near the pterion. The anterior branch of the middle meningeal vein entered the bony canal laterally above the junction with the sinus of the lesser sphenoid wing and coursed along the inner table of the skull or emerged into the diploic vein, indicating its parietal portion. Although the termination of the SMCV had several patterns, the SMCV was not connected with the sinus of the lesser sphenoid wing in any of the patients. The sphenoparietal sinus is considered to consist of the sinus of the lesser sphenoid wing and the parietal portion of the anterior branch of the middle meningeal vein; these were identified as venous structures distinct to the SMCV.

The aim of this study was to establish the role played by jejunal veins in hepatopetal flow after biliary-enteric anastomosis and to evaluate the helical CT features of hepatopetal flow through the anastomosis. We retrospectively analyzed helical CT images of the liver in 31 patients with biliary-enteric anastomosis who underwent hepatic angiography with (n=13) or without (n=18) CT arterial portography within 2 weeks of the CT examination during the last 4 years. Arterial portography showed hepatopetal flow through small vessels located (communicating veins) between the elevated jejunal veins and the intrahepatic portal branches in two (9%) of 22 patients with a normal portal system. Helical CT showed focal parenchymal enhancement around the anastomosis in these two patients. All nine patients with extrahepatic portal vein occlusion (100%) had hepatopetal flow through the anastomosis, and four of the nine had decreased portal flow. CT revealed small communicating veins in two of these four patients. In five patients with normal portal perfusion despite extrahepatic portal vein occlusion, CT detected dilated communicating veins and elevated jejunal veins. The presence of communicating veins and/or focal parenchymal enhancement around the anastomosis indicates hepatopetal flow through the elevated jejunal veins.

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.

No abstract

No abstract

No abstract

167nous 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 T2weighted 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.