Great to be here, good to see everyone. I'm going to talk about ABM, as Errol mentioned. And it's a disease that I really encourage treating, because it really pushes you to think very creatively about all the tools that we have, just like you saw in Lewis Kim's talk, and Errol and Adam's, and so on. Some disclosures. So, cartoons are nice to look at, they're simplified, but they do tell you a little bit about ABMs, but not everything. This is a good cartoon as a checklist of what you need to think about when you look at an AVM. You need to consider associated aneurysms, you need to understand the nidus. But don't forget the draining veins. I think the real secret sauce in understanding AVMs is actually on the venous side. Venous stenoses, I think, affect natural history of AVMs. They can also affect treatment planning, and so on. So, pay special attention to the venous side, don't forget that. But remember that AVMs are actually three-dimensional animals, they're not two-dimensional cartoons. And this is a rather simple AVM, so as they get more complicated, and as you go beyond the angiogram, you need to be thinking about the white matter tracks around an AVM, you need to be thinking about perforators, you need to be thinking about the cortical representation around them. And beyond that, you need to think on the molecular level and physiological level, what is the AVM doing to the surrounding brain tissue on many levels. So, I'm going to talk about a couple myths out there. One myth is that AVMs, when they bleed, they don't really cause much harm. That's espoused by some of our colleagues in neurology, that the hemorrhages are rather benign, and most people do okay. Well, that hasn't been my experience. I've seen many people maimed, disabled, and killed by AVMs. And when you look at series, keep in mind that you're looking at a certain bias. People who can't make it to the hospital don't get counted in that history, so people who die at home don't make it to the natural history study. But people, we think that this is probably a very conservative estimate. 10-20% are moderately disabled, 3% of patients are severely disabled, and 30-50% have a neurological deficit after bleeding. 10% mortality after hemorrhage, I think that's an underestimate, based on who makes it to the hospital, So this is Adam Arthur, back from college. But myth number one is that all AVMs are embryological. There's a certain mythology, actually I believed when I was a resident, an AVM, you're born with it, it's a static lesion, and you die with it. And it's not true. AVMs evolve, they change over time. This is actually a little older, but there are about a dozen reported cases of de novo AVM formation. And if you watch AVMs carefully over time, they do change. This is Howard Rina, back in college. But all AVMs are static, and actually they're not static. It's a bias from the old angio era, where people at most had one angiogram, and what you saw is what you had. But when you're born, you typically don't have a venous stenosis, yet Howard and I see patients in their 50s, so something happened there along the way. So here's a young kid, a 12-year-old, with this AVM, presented with a seizure. You can almost miss it, right up here in the premotor area. And he was advised to have gamma knife. I had not seen him at that point, and he was lost to follow-up. He did not undergo treatment, lost to follow-up, had another seizure at age 18. I'll show you here. And now this AVM looks quite a bit different. This is six years later. This is not a rare phenomenon, actually. It's not well-documented literature, but if you follow people long enough, it's a much more, an easier AVM not to miss, so to speak. And so now, we'll come back to that later. So, as with all these diseases, where you need to start, and where things start in the clinic, is in natural history. It doesn't make sense to talk about pipeline or bypass if you don't really understand the natural history of what you're treating. And so that's very important to start with that. And I'm not going to go into, natural history could be its own separate talk, where it's two to four percent, but in reality, the natural history is probably a much wider range. Remember that when you look at numbers in literature, you're looking at averages. But when you're seeing somebody in the clinic, you're seeing a patient, not an average person. So, when you actually start looking deeper at the question of natural history, this is a nice table from the New York data. If you look at no prior hemorrhage versus prior hemorrhage, and you start to dial in deep venous drainage versus not, you start to see a wide variation. So, when you look at an AVM, don't just look at them and say, oh, that's an AVM, and walk in and say, you've got a four percent annual risk of hemorrhage. What if they have an associated aneurysm? What if that aneurysm is ugly and big? What if it's multilobular? What if they have deep venous drainage? What if it's in the posterior fossa, where we think that the risk of hemorrhage is higher? I think that deep venous drainage may actually be a surrogate marker for outflow obstruction, quote unquote, relative to your arterial input. That's why, as I said earlier, look at the veins because they may give you some clues as to the natural history. Posterior fossa AVMs, I think, likely carry worse natural history. We don't know a lot about them because the numbers are small, but I think they behave more aggressively than anterior circulation, or supratentorial AVMs, I should say. What about grading scales? As you move from natural history, your next step as you're sitting in a clinic looking at an AVM is to understand the grading scales. Some insight, grading scales were the first attempt at precision medicine, which has become a popular term. Obviously, Spitzer-Martin being the first grading scale that looks at size, location, quote unquote, eloquence, although the brain is not technically eloquent, but you know what I mean. The frontal lobe is probably the most eloquent piece of tissue in the universe, yet we insult the frontal lobe by calling it a quiet zone. I've seen many patients with severe depression with frontal lobe with cavernomas or AVMs. Is there a relationship, perhaps? We've seen some of those patients get better after treatment, interestingly. Lawton has since gone on to refine the grading scale by dialing in two important issues that I like about the scales. One, the deep perforating arteries. I think that's an important determinant. Perforator involvement is an important determinant of risk of treatment. Remember, these scales relate to surgical treatment, by the way. Age is another one. We know age. An 80-year-old versus an 80-year-old has a big impact on outcome. This is another attempt to look at that issue. Spetzler went in the opposite direction and simplified the grading scale. Again, the grading scale war will go on. The bottom line is, study these grading scales because they give you great insight into how you should be thinking about an AVM. It's not where you should end your thinking, but it's where you should start. The AVM folks have also come up with a grading scale that looks at risk of treatment vis-a-vis volume of the AVM. Don't think of AVMs in terms of diameter anymore because when you're talking about radiosurgery, and even surgery, think about it volumetrically. Remember, think 3D, not 2D. Thinking in diameter is an oversimplification of what you're looking at because risk probably goes up exponentially, not linearly, with volume increase. Remember, we treat patients, not scale. Scales are helpful. They're a good framework for you to start thinking, but they're not the end game. What about to treat or not to treat? The big elephant in the room is the ARUBA trial. I love talking about ARUBA. I have a lot to say about it, but I'll try to keep it to just two or three slides. With ARUBA, it was basically a study looking at quote-unquote medical management, whatever that means, versus interventional treatment, whatever that means. In this study, it meant anything you wanted. That's kind of an odd thing for a randomized trial to have that. For unruptured AVM, remember it's asymptomatic, unruptured AVMs. Which AVMs are we talking about in this trial? We know from Spetzer's grading scale and others that grade 1 and 2 AVMs do spectacularly well with surgery. Most of them do. There are some nuances to patient selection, but most of them do really, really well with surgical treatment. 76% were grade 1 and 2, 20% were grade 3, and 8% were grade 4 and 5. Grade 4 and 5 AVMs, we should not have been included in ARUBA. These are not AVMs that have low risk of treatment with any modality. In fact, you could argue an asymptomatic grade 5 AVM is something you should observe. Right there, you've got an 8-10% bias. Grade 3 is actually a diverse subset that also you can select off patients who will do well and those who may not do as well. Keep in mind, a large proportion were grade 1 and 2. These patients are great in Lewis's hands and Adam's hands and Errol Howard's to resect surgically. They do very well. What were the treatments? Only 5 patients received microsurgery alone. Kind of odd when you look at 80% were microsurgery. Embolization in 30, radiosurgery in 31, microsurgery plus embolization in 12, embolization plus radiosurgery in 15. All 3 in 1. I want to emphasize, if you look at embolization, you've got 5, almost about half the cohort. Remember that this study mostly shifted to Europe where the philosophy in Europe has been in most centers, particularly in France, to embolize until you get to a cure. In fact, they're moving away from that. Interestingly, their reaction to Aruba in France, some of my friends out there, is we shouldn't be treating AVMs based on Aruba. Because they were looking at it from the prism of you embolize until you either cure it in one session or eventually cure it. Now what they're thinking actually, because they again emphasize embolization and isolation in most cases, that if you can cure it in one session, that's a good AVM to do. If you cannot, then that's a patient you don't treat. I think that's a limited way. When you only have one tool, there's a danger of looking at the world from that prism. Towards precision medicine, there's a call now for precision medicine. It's not a new concept. It's become a sexy term. It's not completely new. If you look at the progression of healthcare from Hippocrates to the sterile era, population science, we look at averages. But in the clinic we have patients. What we really need to move towards, and what you're seeing today actually, if you listen to Louis' talk carefully, about precision medicine, which treatment is going to fit with which patient to give the best outcome. We need to innovate. We need to go beyond the grading scales. I'll talk a little bit about that. We use functional imaging. You can walk in a clinic and say, yeah, this is an AVM, 2% risk of hemorrhages in motor cortex, next patient. Or you can say, well, let's look a little bit deeper. I love the detective work that we do in clinic. What about the functional imaging? Where is the motor cortex? It can often be displaced in patients with AVMs, but functional imaging is only the start of the story. You really want to get interesting in your detective work, you need to be looking at the white matter tracks. When you talk to epilepsy surgeons and people who do a lot of mapping, the cortex doesn't bother them as much. People can resect the actual superficial cortical layer of the motor cortex and get away with it. It's the deeper layer. If you injure the white matter track, that's where you don't get away with it and you get into a lot of trouble. I don't only care about where the motor cortex is, but I want to see the cortical spinal tract. I'm not very good at looking in two-dimensional images and seeing that. I need the help of a guy named Tom Gallagher at Northwestern who does a really nice job with this. I can sit down with him in 3D glasses. We can look at the tracks and look at where the cortical spinal tract is relative to a certain lesion. Now we can get more precise. We can take Spetzer's work and incorporate what is eloquent. Here's where we can make it a little bit more precise. It's nice to do this before the OR, to sit down in three dimensions and incorporate this into your image guidance system as to where those tracks are because that's what I'm really worried about. I'm worried about the cortex, don't get me wrong, but the white matter tracks make me even more nervous. The perforators also make me a little nervous. It's good to be very educated about that before you go to the surgery or if you're planning embolization or radiosurgery. Beyond that, there's the fourth dimension. The fourth dimension is hemodynamics. We can now, with 4D MRI, look at the flow in every single AVM feeder, in every outflow vein. If you're embolizing an AVM, we always talk about hemodynamic reduction of the volume of an AVM. Why not quantify it? Ali can embolize an AVM. He'll tell you that it's 20-30%. He's fudging a little bit because it's an estimate based on a 2D image. Why not quantify it so you can get to a certain metric? Maybe we'll define one day that taking out 80% of an AVM is where you need to get to hemodynamically to protect the surrounding brain for surgery. Here, you can get a nice map and every color represents a certain flow parameter. This is still in the research realm, but it's, again, trying to make sense of this 3D tangle makes us maybe a little bit smarter about how to treat an AVM. Now with time resolve, this is not an angiogram, this is time resolve, 12 frames per second, faster than Howard can do on his angio machine, where you can actually get this. It's getting close to what an angiogram can do. Maybe this is a nice way to follow an AVM. Maybe Howard sees them in 2010 without a venous stenosis. Maybe in 2015 they have a venous stenosis. Maybe now there's a biomarker for selecting a patient for treatment. This is actually maybe 10 years from now with molecular imaging. This is from a mouse brain with antibodies tagged with MRI. Maybe we need to start studying AVMs molecularly to see maybe when certain MMPs get upregulated, maybe that's the time to treat an AVM. Again, that's getting a little bit futuristic. Let's shift gears and talk a little bit about treatment, embolization, radiosurgery, and microsurgery are the tools. My key, if you only take one message from this talk, is don't make up a plan as you go along. It always makes me nervous when people say, well, we'll start embolizing and see what happens. You have to have a plan. You need to be a little flexible to change, but it's good to have a battle plan that you can modify. Think wisely about all the tools, but it doesn't mean you need to use all of them for every case. You need to be wise and not overuse the tools. Let's talk a little bit about endovascular treatment. My main message from this part of the talk is don't think of embolization as one thing. It always irritates me when a junior resident or somebody says, well, patient embolized, what does that mean? What does embolization mean? In 2014, it's art and science. This is just a short list of what embolization could mean. You may be embolizing an AVM to reduce its volume for surgery. You may be targeting a rupture site, and I'll show you that. You may be securing proximal aneurysm. You may be embolizing for cure in select cases. You may be embolizing pre- and post-radio surgery. You may be embolizing for paleation. An 80-year-old with severe meningeal headaches may benefit from a meningeal artery embolization. Venous stenting, and I'll show you a case of that. You need to be precise. I don't like the term, the patient got a craniotomy. What does that mean? What exactly was done? These are some of the tools we use. Embolizing for cure. What is the data? you can actually predict somebody's outcome in a series based on which AVMs they select. So this is a series where they selected all sorts of AVMs. Their cure rate was quite low, and their morbidity was quite high because they were not good at patient selection. And this is in the MBCA era, and this is our literature review. And the cure rate is quite low. This group, wow, they have an 84 percent cure rate. Why? Because are they, were they technical geniuses? No. They were just a lot shrewder about picking cases. All their AVMs were tiny. They were very careful about which AVMs they picked. So which AVMs you pick, like a thermostat, I can dial in your complication rate and your cure rate. So you've got to be wise. That's precision medicine. And let's move on to Onyx era. The occlusion rates are a bit better, but not, still not great. You're still only getting up to 30, 40, 50 percent occlusion rates, depending on how selective you are. This group favored lower-grade AVMs. They got a bit better occlusion rate. Again, you can titrate this based on your selection. We don't, long-term recanalization, we don't know. What about embolization after gamma knife? My bias is to embolize an AVM after radiosurgery, if that's what you're going to do with a very specific goal in mind. I don't like to embolize AVMs before gamma knife, but that is a controversial topic that we can debate. One thing I would caution against that, I'll skip over that, is there was a, and this was actually popular in Europe, to embolize higher-grade AVMs, come back once a year, get it embolized, and see what happens over time. The hemorrhage rate may be, this is not known for sure, but may be higher if you partially treat an AVM than if you just leave it alone. So be cautious about partial treatment of the AVM, unless you have a very specific goal in mind, like you're knocking out an aneurysm, or, you know, so you're doing something like that. I'll skip over this just to show that. Now let's just show a preoperative embolization. This is a 51-year-old gentleman with a cerebellar AVM, he came in with ataxia. This is a challenging AVM, you're working in the small confines of the posterior fossa, it's a large AVM, not a simple one to treat, but it does have a compactinitis. So you can have a blood bath and try to treat this with a lot of reperfusion issues if you do this without embolization, or you can take your time over several sessions, start to get access via microcatheters, and start to knock this down to something more manageable. And you're going to see over time we're injecting Onyx, and over time we're creating a cast of this AVM, and eventually it becomes more like a vascular tumor than a blood bath, and I think it becomes more manageable. Here it's actually pleasurable to resect something like this, it's been kind of defanged, the dragon has been slayed to a large degree. Still bloody, but not to the degree it would have been had you not embolized this. What about securing a deep feeder? This is an 18-year-old young kid who had been galvanized three times in Europe, I have a lot of European friends but I like to beat up on them a little bit, three times in Europe for a quote-unquote cavernoma, he came to us with another hemorrhage, has this hemorrhage, and deep to here there's some funny-looking vessels, turns out he has an AVM, not a cavernoma, and normally we don't like to operate in such deep AVMs, but he now has a highway down to the, there's a cavity that takes you right down to the AVM, but there's this one bothersome deep feeder, if that snaps during surgery, you know, you could lose track of it and you may be chasing it, that may not be a good thing, so I catheterized this, injected it with NBCA, and now it becomes a much simpler problem, this was just basically a tuft of little vessels in the depth of that cavity, it was a very simple operation, and taking out that feeder really helped, so you can do that to help yourself. What about securing a proximal aneurysm? Here's a 52-year-old lady with this occipital AVM, not a very difficult one, but has this, a floated basilar aneurysm, this was from a number of years back before pipeline, and so we basically partially coiled this, resected the AVM and brought her back for a stent coil, and I've seen her now at her eight-year follow-up, she's doing terrific, again, you wouldn't want to treat that AVM before securing that aneurysm because you could decrease outflow and cause it to rupture. Here's a 71-year-old gentleman who comes in with new frontal headaches, and in a small AVM, on the GRE there was a little bit of blood around it, this is an ideal case morphologic, now this would be very simple to treat surgically, but he's a 71-year-old with multiple comorbidities, this is ideal morphologically for, quote-unquote, curing with glue, you basically get a nice cast with Onyx and he goes home the next day. Targeting a rupture site, this is a case where you need to bring in all your knowledge, critical care knowledge as well, 32-year-old female with a grade 4-5 AVM that was managed conservatively, appropriately, but she kept hemorrhaging and kept having progressive hemiparesis, from this AVM, the hemorrhages have done part of the work for us here, you can see there's an enlarged CSF spaces around the AVM, still not an easy AVM, you wouldn't want to resect this without embolization, this is also, pay attention to these deep feeders, that could be problematic surgically, and so what we did is we embarked on staged embolization for this with a plan to eventually remove it surgically, first embolization went great, second embolization, she emerges to the ICU in a bit of this kind of posture, she's extensor posturing and with this, and for those of you, most of you here have suffered with these kinds of patients, these patients don't do well, when you have casted ventricles, you play with the EVD all night, you're just kidding yourself, this has a 90% mortality, TPA has been found to be very effective for these, it's not in phase 3 data yet, but we have phase 2 data, but with a recent rupture, you can't just infuse TPA, so we brought the patient back to the, we put an EVD in, brought the patient back to the angio suite, on the CTA, we identified this as the rupture site, we correlated it with the angio, we catheterized that vessel, embolized that, and then started TPA, and we see here that this is day 3, day 4, day 5, day 6, blood cleared, she went back to neurological baseline, we took out the AVM and she did great, I think she would have died had we not been able to infuse TPA into that ventricle, but we had to seal the rupture site first, so here you had to use all your knowledge to help this patient. What about venous stenting, that's an odd thing for an AVM, this is a lady that I learned a lot about from, actually this case got me interested in the venous side, 19 year old female, with progressive headaches over 2 years, not relieved by narcotics, we weren't smart enough to realize that her headaches were from something I'm about to show you, and she has this AVM, and that's not an easy AVM, I'm not showing you actually enough, I'm sorry I didn't bring all the angiograms, but it's a big occipital lobe AVM, and we also embarked on staged embolization with a plan to eventually remove it because it was becoming progressively symptomatic, and after her second or third embolization I came up to the ICU and she was slipping into a coma, she was becoming unresponsive, there was no hemorrhage on the CAT scan, scratching my head, I looked at the MRI and she had a Chiari, and I looked back at the angiogram, this was something that wasn't picked up, she had an occluded IJ on one side and a highly stenotic IJ on the other, so we could, at that point we said well she's basically going down the tubes from high ICP, we basically took her down the angiosuite and stented her, and I don't have, oh here's the AVM, we stented her sigmoid sinus, sorry, and this is the Chiari at the time, I'm sorry I don't have the right images in order here, but she basically developed this downward herniation, this is pre-stenting, we stented her IJ, and I couldn't find the venous angiogram for this to show you, but this is post-stenting, she immediately woke up after the angiogram, we had restored her venous outflow, this was a venous outflow problem that we had fixed, it wasn't the arterial side that was her problem, this patient had progressive headaches and lethargy and eventually near a coma from venous hypertension and high ICP. What about radiosurgery, just briefly, radiosurgery is not a magical tool, it is a nice tool to have, but it's not magic, it takes time to occlude an AVM, it's great for surgically inaccessible lesions, staged radiosurgery I have a question mark about, we've used it successfully in a number of patients, but the complication rate is not benign and it doesn't always work. The concept of downgrading an AVM is fascinating, where if you could take an AVM and knock out the dangerous part of it and then bring the patient back a couple years later, it's still a research kind of approach, but it's an interesting concept. I won't belabor the data on this, but make sure you know the data, if you look at Greenberg it says a three centimeter AVM is okay at a gamma knife, well it turns out that when you look at the Pittsburgh data, the 3, 4, 5, and 10 year occlusion rates with SRS are 58, 87, 90, 93%, but that's for AVMs that have a volume, a median volume of 1.9 centimeters, these are relatively small AVMs, so when you look in Greenberg it says 3 centimeters, that's the upper limit of what you have, that doesn't mean for a 3 centimeter AVM you're going to get this kind of result, just keep that in mind. It's not a bad treatment, I use it routinely for AVMs that aren't inaccessible surgically, but I don't think it's a good replacement for a 2 to 3 centimeter AVM that's easily treatable surgically. And remember that there are some long-term complications that you need to keep in mind that I won't belabor. This is just to show you a case where you really need to think carefully before treating an AVM. There's a 20 year old beautiful, intelligent young lady who has progressive headaches and probably migraines and or seizures with intermittent facial weakness from a significant AVM here that you see. And this is an AVM that is very tempting, you say, wow, this is an AVM that's on the surface, I'd love to resect this. What bothered me about this AVM is this. These deep feeders that cross the white matter tracks, you have a high chance of leaving this patient hemiplegic if you're going to operate on this, in my opinion. And so we, she had also an ACOM that I clipped, she has these deep feeders, this is problematic, this is crossing the deep white matter. And so we treated this with staged radiosurgery. She's now at her 5 year follow-up, her AVM is gone and she's intact. Another way to approach this perhaps is to treat the deep component with radiosurgery and bring her back and then resect it a number of years later. But we, at the time we did staged radiosurgery, two session radiosurgery, and she did well from that. Just to skip over this. So let's talk in the last remaining time about microsurgery. The beautiful thing about microsurgery is it gives you an immediate cure. It's a great treatment for select patients. There's minimal chance of recurrence if you get a clean postoperative angioma, with the exception of children. You have to monitor children more carefully because they do have a higher rate of recurrence. The technique for surgical resection, I mean study your angiogram very carefully, understand the feeding arteries, draining veins. Yesterday I talked about the spiral technique. Don't dig a hole when you're resecting an AVM. You need to progressively detach the AVM in a spiral circumferential fashion, keeping the vein alive until the end. And just to show you, this is a posterior fossa AVM, a 51 year old gentleman who comes in with this hemorrhage. I love these cases. This patient came to the ER. We see this about a couple times a year. They come in dead. 51 year old male in the ER, posturing, blown pupils. Do not call hospice. Do not give up on this patient. This is a Lazarus procedure. You can save these people. This patient needs ideally a quick CTA to know exactly what you're dealing with on the way to the OR. In the OR you put a ventriculostomy in and don't open it until you have the dura exposed or the dura open. And this turned out to be, this is an angiogram that was done after surgery. What we did at that time is we did a craniectomy, partial hematoma evacuation, duroplasty, kept the EVD and took the patient down to the angio suite. And here's your rupture site. It's this aneurysm. Very easy to catheterize in this case. We catheterized it, coiled it. Now you've taken away the acute re-hemorrhage risk. You're an ICP doctor. You've taken care of the ICP issue. And then you can bring the patient back a couple months later and manage the AVM surgically or with radiosurgery or EMBLs, whatever your technique is. But remember in the acute period, there's nobody better positioned to take care of these patients than you as a neurosurgeon because you have all the tools at your disposal. Don't let anybody convince you to be passive about this kind of patient. I have a whole series of these patients in my practice that I've saved and I love seeing them back because they were dead on arrival. Make the craniectomy wide. Here's another case, a slightly different type of case, where you need to, this is a large frontal lobe AVM, sorry, this is a 21-year-old female with a premotor AVM, nursing student, who was very concerned about her, she had a seizure. So hopefully this video will run. I want to show you just something here. This is, I'm sorry it skipped over the angiogram, but this is a premotor AVM. Here you see a grid mapping the motor and sensory cortex with phase reversal. All you see on the surface is draining veins. The AVM is deep to you. The key, the trick here is this may look daunting if you haven't done one of these before. Where is the AVM? The key is to carefully skeletonize these draining veins and you can get into these corridors to start devascularizing the AVM deep to the veins and keep the veins alive until the end. Hopefully this will play. I'm sorry, I can show it to you on my laptop later. I'm sorry this case is not playing well. This is a large AVM. This looks also daunting, but with staged embolization you can make this manageable. The key here is you need a big craniotomy. Don't think about minimally invasive craniotomies when you're thinking about AVMs. This is an intraoperative ICG angiogram. This is a patient who presented with severe depression and interestingly her depression resolved after, it's not clear whether it was related to this AVM, but I think there is something about frontal lobe and psychiatric diseases in AVMs that we don't really fully understand yet. But with sequential devascularization you can very nicely treat this AVM and a patient can have a great outcome even though it's a very large AVM. I'm just going to show two more cases. This is back to that growing 18-year-old with this premotor AVM. Here's the preop angiogram. We did one stage embolization prior to, two stage embolization to dry it up only because it was close to motor cortex. And here it is at surgery. When you look at this, the first thing you need to do is open up the subarachnoid space, thickened arachnoid. Just take your time. Open up every arachnoid space you can find around the AVM. You can use image guide. There's your draining vein and you open up those channels and all of a sudden now you've got working ports to get into the AVM. You can start to work around the AVM and sequentially and carefully devascularizing it. We have a grid on the motor cortex. We're monitoring motor and sensory evoked potentials from the cortical surface. You see it's under the dura, actually, now. And we're just sequentially. And usually you can get into a sulcus, but sometimes the AVM can cross a sulcus. In this case, it jumped over a sulcus so we got into this gyrus. I try to work in the subarachnoid space whenever possible, but sometimes you do have to go transcortical. And here we're just sequentially and carefully devascularizing the AVM, keeping the vein alive. And you see the vein progressively turn darker, clearing some of the white matter. And then eventually you get to the point where you feel the dragon has been slayed and you can bring the whole AVM out just on its venous pedicle. And there it is. The AVM is just lying on the brain, but the vein is still alive, and then you can divide the vein. I'm just going to show this one, can I show one last case? So this is, this is just something we did last week. We've done now two awake AVM cases. It's an interesting concept. I don't think it's for every AVM, but I think it has some advantages. There's a 36 year old female presented with a new onset seizures. They were refractory to medical management with a lot of gradient echo around this small AVM. It's superficial and small, which is why we consider it awake, but a lot of gradient echo around it in a relatively eloquent area. So it's not a very big AVM, but it's in somewhat of an eloquent area with severe seizures despite medical management. And you look here on the T2, and what you'll see here is a lot of GRE signal around the AVM. So if we're going to resect this, it's not just about the AVM, it's also about this GRE iron laden tissue around the AVM. So we thought we'd do this awake. And here is we're mapping the cortical surface, a bigger craniotomy than we need here, only because we wanted to map the language all around the AVM. And the patient is awake now. iPhone camera, not Hollywood here, but. Using an ozumen to map the cortical surface around the AVM and talking to the patient throughout the case, putting letters on where they belong, just skip through this. And here we're using iPad just to keep testing her language function. And here we've mapped the, every letter here represents a different function. Here we have it mapped out around the AVM. The AVM is actually down there. So actually the area around the AVM was quite quiet, which was nice to know. So I could be a little bit more aggressive in that iron-laden tissue around the AVM. And here it, yeah, we did, we did. And it looked like broke, Wernicke was just in front of the AVM, and the arcuate fasciculus was just deep and in front. So this was a nice additional confirmatory modality. And again, I wouldn't consider this for a big AVM, but this was a relatively superficial AVM. And here we're just devascularizing it. And we kept a grid on the brain during the procedure, and we kept talking to her. We sedate, we have a great anesthesiologist who does a great cranial block. They feel nothing. He does a beautiful cranial block for us. And I'll show you here just the two seconds of, this is ICG during the case. And there was a normal labay right in front of the AVM that we had to keep track of. And there's an unpassage vessel that I'm gonna show you here. So this artery's coming in, but it continues on as a normal artery. So it gives off branches to the AVM. So we carefully skeletonize that. And actually I, I didn't notice that until during the surgery. I should have studied the pre-op angiogram a little bit more carefully. So you see here this, see how that transitioned from a large artery to a smaller artery? At this point, it's no longer related to the AVM. It just gives off branches up to this point. So you can use your ICG to study that. And here it is, we're in the final phases of devascularizing the AVM. There was some hemo-siderin-laden brain just deep to the AVM that we cleaned up a little bit. And here we're carefully working circumferentially to devascularize it. It's not a very big AVM. But I just wanna show you here one thing, and then we'll move on. So here we're just completely devascularizing the AVM. Just devascularizing the nidus. The vein was very tortuous, but I completely skeletonized the vein. We, we're gonna pull it out in, in, in one piece. So here you see the AVM now has been elongated. Because we've, it was in a circle before. And now we're looking at the vein completely, all the way back until it connects back with the labate transverse, transverse sinus junction. We're seeing the entire length of the vein. We're inspecting it circumferentially, then dividing it. And here's an ICD showing reversal flow in the draining vein, confirming that there's no more arterialization. And the nice thing is that she went home the next day because without that anesthetic effect, she was just, you know, feeling great. You know, it was, you know, she could have gone on the floor post-op. A lot of what we attribute to our surgery sometimes is the anesthesia. Post-op angiogram. I just wanna show you this really cool post-op angiogram, lateral, where, this is something I should have noticed pre-op. But notice how, there's the on-passage vessel that we preserved. Now, could, could we have gotten away with taking that artery? Sure, but it's good practice to try to preserve arteries that you don't need to take. See how that artery's large, and then it transitions right at that point you saw in surgery. This is the on-passage vessel we're continuing on as a normal vessel. Up to that point, it's enlarged because it was in the habit of supplying the AVM. But from this point on, it's a normal vessel. Again, would it have been the end of the world to take that artery? No, but sometimes, you know, getting in the habit of paying attention to that could save somebody a stroke. Thank you.

arteriovenous malformations

venous side

natural history

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precision medicine

embolization

microsurgery