Vascular closure staple clips made of titanium were originally developed for microvascular anastomosis. Clinical applications for these clips include arteriotomy closure for carotid endarterectomy, extracranial-intracranial bypass, and dural closure. This is the first report in which vascular closure staple clips have been used successfully for direct repair of a tear on the internal carotid artery (ICA). This report involves a 65-year-old man who presented with sudden onset of headache. Admission computerized tomography scans demonstrated a diffuse and thick subarachnoid hemorrhage in the basal cisterns. Cerebral angiograms demonstrated a broad-based, small bulge on the superomedial wall of the left ICA. Intraoperatively, an extremely thin-walled aneurysm was seen on the segment of the ICA at the C-2 vertebral level. The aneurysm ruptured abruptly, although no surgical manipulation was being performed on the aneurysm itself. After temporary clips were applied on the vessel, a large tear of the ICA was repaired with vascular closure staple clips. Reconstruction with the vascular closure staple clips required only a short period of temporary occlusion of the ICA. Postoperative angiograms revealed reduction of the aneurysm bulge and good patency of the ICA. The postoperative course was uneventful, and the patient has been free of symptoms. The vascular closure staple clipping procedure is useful for urgent repair of an aneurysm tear. This method is a new treatment option for these fragile aneurysms in cases in which other options, such as encircling clips or bypass procedures, may have drawbacks or be impossible.
Simultaneous monitoring with the microscope and endoscope is extremely useful in applying clips to ICA aneurysms. This combined method allows for direct dissection of the aneurysm, perforating vessels, and the main trunk in an area not visible through the microscope's eyepiece and promises better surgical results.
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.
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.
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