Here is a simple parietal arteriovenous malformation in a 26 year old male who presented with a spontaneous intracranial hemorrhage. The location of the malformation is just posterior to the central labial. You can see some of the findings on angiogram. Cerebral arteriogram also demonstrated the typical findings of a cortical arteriovenous malformation in the parietal area primarily fed by the distal MCA branches, and potentially some of the ACA branches. You can see the ACA contribution at the level of the AP view of the Arteriogram. The drainage is via the parasacial veins leading to the superior sagittal sinus. Patient was placed in a supine position. I usually prefer the lateral position for lesions in this area. The supine position can create somewhat of an awkward operative working angle for the surgeon. Nonetheless, here is the sizable skin flap for exposure of this arteriovenous malformation. Obviously this exposure should also identify the superior sagittal sinus. Arteriovenous craniotomy was completed. You can see the location of the superior sagittal sinus. The dura was incised in a curvilinear fashion. And intraoperative ICG angiogram, as well as FLOW 800 analysis was performed to better illustrate the identity of some of the branches. Here you can see some of the normal veins, potentially an arterialized vein here. Also other normal appearing veins bordering the posterior aspect of the malformation. Let's go ahead and look at the color map of the ICG from the FLOW 800 analysis. You can see that all the veins in this area are most likely unaffected and non arterialized. Most likely the veins in this area arterialized and these arteries are the distal MC branches contributing to the malformation. I continued to dissect the arachnoid bands, identify their feeding arteries hidden within the expanded calci. And here is the midline. After some of the the larger feeding vessels are identified, the phase of dissection is continued. The other feeding vessels are controlled more medially. This avion was actually more compact than expected. You can see that I continue to remain around the area of glyotic surfaces around the malformation disconnecting some of the distal MCA branches. Obviously emphasized vessels are carefully protected. Here are some of the distal MC branches leading to the malformation. Here you can see a branch there. Here is an emphasized vessel moving posteriorly. I stay right on the surface of the malformation. It appears that I still remain within a white matter, however, the location of malformation is just a little bit more medial. The dissection of the discloses the arterialized vein as you can see here, joining this superior sagittal sinus. This is an excellent example of a non arterialized vein and an arterialized vein. The color, the caliber, the texture, the thickness of the wall are all quite different. Here you can see it again, arterialized vein and normal vein that is darker. Again, a dark non arterialized vein, a thickened arterialized vein. The entry of the article's vein into this superior sagittal sinus. Portion of AVM here is demonstrated. The architecture is now better understood. After the AVM is disconnected here, I can cut across the draining vein. The medial atmospheric cortical feeding vessels are easily controlled because they own robust walls. The deep white matter feeders always remain problematic and require patience. Here's the portion of the malformation facing the falx. Normal veins are obviously protected. Here's the final distal MC branches remaining that are being coagulated and cut. Now that the AVM is more disconnected, anteriorly and laterally, I continue more inferiorly. You can see the draining vein is now much darker. This vein was arterialized that much brighter before. Here you can see the colors after the AVM is disconnected. Finally, the draining vein is coagulated and cut and the nitus is removed. Final view of the reception cavity. Careful inspection of the cavity demonstrates some bleeding from the white matter feeders. AVM should be suspected. This portion of the resection cavity was heavily coagulated. No obvious nitus was identified. Immaculate hemostasis was secured. Post operative CT, as well as cerebral angiogram sequences, demonstrate complete removal of the malformation without any early arteriovenous shunting. Thank you.
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