Deep Basal Frontal AVM

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Let's discuss resection of high-risk arteriovenous malformations, and in this case, a basal frontal arteriovenous malformation. This is a 16 year-old female who presented with intractable epilepsy. MRI evaluation demonstrated a large AVM encompassing the posterior basal frontal lobe infiltrating the septal region. There is a draining vein leading more posteriorly, which is deep seated. Here's another view of the deep draining vein. Most of the perforating vessels are expected to originate from A1, M1, as well as ICA bifurcation. Next, the angiogram confirmed our suspicion regarding the origin of the feeding vessels. Early arterial phase, AP angiogram demonstrates very small arterial feeders from proximal A1, proximal M1 in the ICA bifurcation. There is a large draining vein leading more posteriorly and another more superficial one, joining the anterior superior sagittal sinus. These small feeding vessels are amenable to coil embolization for sure underwent a right frontotemporal craniotomy, sylvian fissure, basal frontal lobe, temporal lobe. First, the sylvian fissure was widely dissected. The operative strategy involves early exposure of the A1, M1 and ICA bifurcation and disconnection of the feeding vessels from these larger arteries. Here's the opening of the sylvian fissure. Dissection is continued more medially along the sphenoid wing until the ICA bifurcation is identified. Here is one of the large arterialized veins over the malformation within the fissure that is carefully protected. Here's the malformation that is being mobilized. Sylvian fissure dissection is continued more medially. Gentle elevation of the frontal lobe should expose the ICA bifurcation. Here's the ICA and its bifurcation. The optic nerve should be carefully protected. The arachnoid bands are widely split. I continue more dissection medially until the A1 branch is exposed. The AVM is gently elevated by the retractor blade and pulmona of the CSF is drained via the basal cisterns. Here's the optic nerve. Here's the arachnoid band over the ICA. Dissection is continued along the anterior wall of the internal carotid artery. Here's the A1 and the feeding vessels toward the malformation. The contralateral optic nerve. The chiasm, lamina terminalis. Here are some of the feeding vessels from A1. Now that most of the feeding vessels are exposed, I start with a circumferential disconnection on the malformation. You can see the feeding vessels from the ICA bifurcation, locate at the tip of the arrow. Bipolar coagulation disconnects the cortical feeding vessels along the basal frontal lobe. I use intraoperative CTA navigation to disconnect the perimeter of the malformation from the basal frontal lobe. An orbitozygomatic craniotomy is most likely unnecessary. The edge of the craniotomy is quite flat with the roof of the orbit. Here's the section of the MCA feeders toward the posterior border of the malformation. I continue to also disconnect the malformation entirely. Here's again, the A1 feeding vessels to the malformation from the A1, en passage vessels are carefully protected. The artery of Heubner is also identified and protected. Now white matter dissection continues at relatively equal depths around the perimeter of the malformation. Gliotic borders are also removed. White matter feeders can be quite problematic, especially in this area near the periventricular region. These white matter feeders have to be pursued slightly away from the nidus where the walls are more robust so that they can be controlled via bi-polar electro coagulation. In this case, small pieces of absorbent cotton was used to achieve hemostasis in the face of relatively minimal bleeding. Temporal node of aggressive arterial bleeders should be avoided to minimize the risk of remote intercranial hemorrhage. I continue to disconnect the malformation more posterosuperiorly. One has to remain outside the nidus. Here's one of the draining veins moving posteriorly. I continue to control the arterial feeders around the vein. There's often two or three very robust arterial feeders around the draining veins. Next, I continue with circumferential isolation and disconnection of the arteriovenous malformation from the white matter feeders around the frontal horn of the lateral ventricle. Again, some bleeding was encountered along the posterior border of the malformation. The draining vein moving posteriorly was again protected. One has to remain patient, avoid over aggressive indiscriminate coagulation, in this case, temporal occlusion of the vein did not reveal any swelling of the nidus. I felt it would be safe to sacrifice this draining vein so that the malformation can be more easily mobilized as circumferentially disconnected. Again, continuing more medially, the MCA feeding vessels are disconnected. The M1 should be protected. Those perforating vessels that are traveling more superiorly should be also preserved. Most of the AVM appears isolated. Here again is continuation of our disconnection, in this uphill fashion toward the ICA bifurcation. The gliotic borders are apparent. The medial arachnoid membranes are now violated to protect the en passage A1 branches. Here's the M1. Some of the feeding vessels are also carefully protected in this area and their identity is first confirmed before they are coagulated and cut. Now moving toward A1. The nidus appears free and is extracted. Thrombin solution is used to achieve hemostasis along the inflamed brain. Patience is required to achieve the necessary hemostasis. Aggressive coagulation can lead to additional bleeding from the peri AVM inflamed brain. Intraoperative angiogram demonstrated complete exclusion of the malformation without any residual AV shunting. Post operative CT angiogram similarly confirmed these findings. Three months MRI evaluation revealed gross total removal of the malformation without any untoward side effects, and this patient has remained seizure-free since her surgery, thank you.

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