Transcript

- Colleagues and friends, thank you for joining us for another session of the Virtual OR. Our guests today is Dr. Robert Spetzler from Barrow Neurological Institute. Again, he requires no introduction. He truly has been a role model for so many of us. Today, he will be talking about updated management strategies for arteriovenous malformations, especially after introduction of the ARUBA study. Dr. Spetzler, thank you again, and looking forward to learning from you.

- Thank you, Aaron. This is clearly one of my favorite topics and we have learned so much from encountering these impressive lesions. I think from a surgical perspective, a surgeon really requires a position that he or she is comfortable in in order to really provide the best surgical techniques for their patients. I personally like to be seated with arm rests because they gave me the greatest ability for fine hand movements. I couldn't operate without the mouthpiece, once you're used to it, it's very hard to give up. And then very good use of the foot pedals, and obviously all the extra Slidell that come along to enhance our visualization and monitoring. So this is an actual picture, mouthpiece. When we look at AVMs, we need to be reminded that they really are incredible dynamic lesions. And, I wanna just point out that this particular patient had a small trauma for which she received an MRI scan, may be a little bit of a change right here, but not much else. And then 44 months later, he developed a seizure disorder. And you can see that now there is a significant change in the MRI scan with the development of an obvious arteriovenous malformation. And if you look back at the previous MRI scans, really, even in retrospect, there's not the slightest abnormality in that region. And when an angiogram is performed, one can see the deep arteriovenous malformation, and this was treated with embolization and gamma knife. And it nicely resolved. This again is where the lesion was. The reverse also happens. This is a patient that had this arteriovenous malformation, and this arteriovenous malformation, which is readily visible on angiography and CT scan. And then an update almost 20 years later reveals that the AVM which used to be right side here is completely gone. Although on the MRI scan, you do see a involuted abnormality. Most dramatic is this case. I think when we see this MRI scan and we look at the edematous region around this lesion, and we see this classic large vein, we would certainly diagnose a cavernous malformation. This was treated, in my mind most inappropriately with radiation, gamma knife radiation. And here you are looking at this scan and this lesion has turned into what is an obvious arteriovenous malformation. And this is what it looks like. A lesion that considering the fact that he'd already been radiated in this region is in my mind an inoperable arteriovenous malformation, how this evolved remains unclear. When we talk about AVMs, we need to look at the natural history because obviously any treatment we do has to compare favorable to the natural history. And these numbers are well-recognized. Some of these have been higher. Some of these have been lower, varying degree. There is no doubt that once you have ruptured, your risk of rupture over the next year is at least double of what it was beforehand. And that with each subsequent hemorrhage, you have a greater chance of a mortality. Presentation, increasingly incidental now with the introduction and the wide use of the MRI and CT scans, but still the most common is hemorrhage or seizure. Less common naturally neurologic deficit. When we look at treatment options, observation is a treatment option that's appropriate for quite a few patients, microsurgery, the gold standard for getting rid for the appropriately selected AVM, embolization, radiosurgery, and sometimes only symptom control like seizures or treating hydrocephalus. This grading system which we published in 86 has been widely utilized in comparing various series of AVMs. And whenever I talked about AVMs, I always grouped one and two together and grade four and five together. And so we modified the grading system in 2010 and made an A, B, C, where we basically had grade one or two in A, Grade three in B, and grade four and five in C. The advantage of that naturally is that they had similar treatment strategies and similar surgical outcomes. And so it becomes easier. An easier classification is one that really is much more easy to use and it predicts accuracy of the outcome because the outcomes were very similar between the two groups. And now you have much larger numbers in each group and therefore statistical power becomes enhanced. So we have grade A, four variations. We have grade B, four variations, and grade C, all depending on size, eloquence and venous drainage. When we talk about arteriovenous malformation, obviously radiation is an important adjunct for the appropriately selected arteriovenous malformation. It is also important than radiation, the recognition that radiation is not benign needs to be emphasized because when the patient leaves the radiation suite on the same day of surgery or the same day of radiation, it seems like such a benign treatment. Here's a patient that was treated elsewhere, has this small meningioma. The neurosurgeon decided that this was an inoperable lesion and went ahead and used stereotactic radiosurgery for this meningioma. This is two years. Severe compromise of the visual pathway with the patient going completely blind by two years. This is a patient of mine, left side, family refused surgery. So we offered radiosurgery, which was performed. Year three, patient returned with a hemorrhage. At this point, she was unable to speak. Her husband said, please take it out. And we did, fortunately she recovered some of her neurologic function, but remained permanently aphasic. Here's a patient that I recommended radiosurgery for, with the gamma knife. And then this is what evolved, radiation necrosis. Some of it naturally disappears very readily with steroids, but here's a bad case with significant shift. We'd had to do a decompressive craniotomy. She has survived, but is greatly incapacitated. So what do we really call success? Well, AVMs are a problem that really lasts your entire life. So the risk of an annual problem persists. Our treatments have to be compared long-term, not just the next year or even two years to three years. So here's an example of 44 year old male, received gamma knife in 97, had an MRI scan that was considered negative and published in a series for AVMs. And five years later develop new refractory seizures. And in 2011, 15 years delay, he presented with a bleed, cysts and a negative arteriogram. And I will show you what that looked like. So this is it. You can see the edematous region around the abnormality with enhancement in the middle of this cavity. And these have been well described. Angiogram was negative. This is the surgery. And as you open into that cavity, you can see the AVM sitting right in the middle. You see the hemosiderin blood, which was the cause of the most recent surgery. Very easy to resect. In fact, is surgery for AVMs after they've been radiated, I find significantly easier than without radiation because obviously we have thickened the wall. So what have we learned? ARUBA was really the first randomized trial of a unruptured arteriovenous malformation. And their main finding is that the natural history is not benign. If you look at a follow-up of two and almost close to three years, the primary end point was reached in 10% of patients, secondary end point in 15% of patient. And that was neurologic deficit or death, and any sort of a problem from the AVM. I'm not gonna go into detailed analysis because we've published this and it has been pointed out over and over again. But what have we learned? In that study, there was an incredible lack of uniform treatment. This was at a time when embolization was running rampant and 30% had embolization alone. And I'll address that in a minute. Radiotherapy has a delayed effect, and yet the followup was only 33 months. And so that included as a treatment, an effective treatment. And then my biggest concern is that they offered gamma knife to grade one and two or arteriovenous malformation. When the morbidity and mortality of microsurgery their treatment is significantly lower. In our series, and also in Morgan's series, prospective study, the surgical risk was just less than 1% for grade one and two arteriovenous malformations. And 33 months followup for a disease that continues all the time is naturally way too short. So it was a good try, but it was a bad study Onyx, which was the main embolize aid that was utilized in the ARUBA trial is I think an excellent addition to our armamentarium. It can be cut. You can reset ultra, use an ultrasonic aspirator for resection. But when you look at LINNC, a very aggressive review of utilizing embolization in a conference that is sponsored by Moray, in 2007, embolization alone, they had greater than 8% severe complication with only a 60%. And that is a questionable cure in my mind. And I'll get back to that a little bit later. In 2008, morbidity in embolization had gone up as they became more aggressive at the benefit of a higher cure rate. Again, questionable. But they did a lot of grade two AVMs. Look at this. And 57% of that group alone had a drop of one on the ranking scale. Now, when we had a first international AVM meeting in England Shock Moray, who organized the LINNC conferences had a fellow review, his unruptured AVMs, and found that the morbidity and mortality of treating these unruptured AVMs was 17%. And he got up on the stage and said he no longer embolizes unruptured AVMs. Remember that 30% of the patients in ARUBA had this treatment. So if we look at long-term, embolization 99, radiosurgery, 2000, 2010, an angiogram interpreted as AVM obliterated, in 2012, the patient presents with a repeat hemorrhage when we saw them. And when you look at this hemorrhage, it's a big intraventricular hemorrhage, so the patient looks terrible, but always has the ability to recover. I've always made a teaching point is when you have blood in the fourth ventricle, a patient can look like they are brain dead, and yet have the complete ability for recovery just as if it was drug induced or hypothermic. So actually when you did the angiogram, there is a little bit of AVM sitting right here. We took it out, not very difficult. And then we had the post-op angiogram and this patient actually over time made a very good recovery. When we look at more of the surgical adjuncts, we have ICG developed by Andreas Robbie for neurosurgery, who spent a lot of time with us when we introduced it to the neurosurgical community, has the advantage of being quick, safe, inexpensive, high resolution. However, the disadvantage for AVMs is you only see the surface view. You will miss deep residual. So it's important to remember what it's good for, but also what it lacks. So if you look at this here, you see the surface of an AVM. Here's the ICG, here's the delayed flow, this beautiful laminar flow pattern that we see. And if you look, it really is a very nice to check your anatomy against your angiogram and against other studies. So it is clearly helpful, of benefit, and we use it continuously. And here it is, post-op after resection, there are special circumstances. I'm not gonna show you a large series of AVMs, except those that really have a profound teaching point. This is an 18 week old with a Bruit, a little Israeli girl. She has this, what we can see on MRI scan. We perform no angiography. We perform no CT scan in order to avoid radiation to this developing brain. And this is what we saw at surgery. We see a large aneurysm and with an AVM underneath. So we are going around, cutting the arachnoid, separating it from the brain. ICG demonstrates the flow into the lesion. And then we see the nidus of the AVM down just below. So when we did, as we put clips on the feeding vessels, and then, we sort of compressed the AVM as much as, the aneurysm as much as possible. Now you see the ICG no longer any flow so that we didn't lose a lot of blood and then took out the rest of the AVM. And if you look at the post-op, the AVM is gone. So the AVM selected for treatment depend on obviously presentation, hemorrhage, age, accessibility. It all has to do with selection, selection, selection. So here is a very young infant, small girl who presents now with heart failure. And the residents reminded me very much that the total volume was only 950 CCs. And when you did the angiogram, you see that there's absolutely no filling of the normal brain. Everything is shunted through this high flow arteriovenous malformation explaining the onset of cardiac failure, high output failure. My colleague embolized as much as was possible. And now you're beginning to see some normal vessels appearing. And we did this in steps so that we wouldn't suddenly change the intolerable change in blood flow. And then we operated on this little girl. You can see from the ICG, the portion of the AVM that have already been obliterated. The problem with infants and AVMs or babies and infants and young children is that the vessels are incredibly fragile, much more fragile than an adult. And so here, we're going between the AVMs trying to get the appropriate feeders. And one of the lessons I teach is many of you have bleeding, don't cover it up. Don't Tamponade it so you can't see it, work on it until you have it resolved. Most of the time when we have bleeding, it's because we are getting into the AVM rather than being on the edge. With each drop of blood I lose, I'm thinking back again at the small blood volume in this little infant, and now I'm sort of terrified that I'm gonna lose her on the table. Finally, I get control over this, and then continue the resection. And just keep going to the vessels. ICG helps me identify where I'm still getting feeders from, and now you really don't have any flow anymore. It's all dead. It's just coming back and forth. And then getting the last bit of the arteriovenous malformation, cutting across it to make sure we have it completely occluded. And now with the fine line CG, again, we only see this pulsating and no flow or shunting through the AVM. We did interoperative angiography, and you can see how helpful that is. Dr. Albuquerque was my endovascular surgeon and the interoperative angiographer. And then finally, fortunately, she had a normal exam. You see those big vessels that we had beforehand, all shrunk. There's a little bit of a large vessel yet that hasn't shrunk all the way, but she had a normal lab exam. What did we do when we have deep AVMs that are associated to the midline? This is a professor's daughter, an A student. And she had selective arteriography with embolization. There wasn't much to embolize because these feeding vessels were so small. But the problem is here, how do you get to the most distal or lateral portion of the AVM that is on the left side? If you come in ipsilateral, you're going to do great harm to get to this point. So we came in contralateral, image guidance helping us when we look at the falx to stay away from the actual AVM. So this is what we did. Obviously we went across the midline as I like to do, and just pull the sagittal sinus over a little bit. Patient's head is horizontal, and now we open the falx at the edge of the falx. And you can see the vascularity of the falx itself. Once we have this, then the direction of our approach is to go to the most lateral portion after reef removed all the feeders from the anterior cerebral artery. And this is just a continuation of this dissection, and we just keep going lateral. You don't see a retractor, no reason for a retractor except to hold off the brain on the contralateral side as we slide down along the length of the arteriovenous malformation, and then once we're at the most distal portion, then it becomes relatively easy to bring it around. Notice we've kept intact the large draining vein so that the AVM would not get larger with interference of the drainage. See, the use of the tractor only to hold over the contralateral portion. Post op, lesion has gone, and she returned to being an A student. I wanted to show one more. Again, one midline. You can see the drainage, pre embolization, post embolization. So here we are, again, horizontal. Now I'm going down the ipsilateral side because this was so attached to the falx. And so I'm separating it ipsilaterally, putting gel foam in between the AVM and the brain, and then going to the contralateral side. So I have that better angle like we had before, and then opening the falx and just resecting the falx to the point so that I've got complete control. Now I have this very, very fortuitous angle that comes in by going contralateral. The most difficult portion is most lateral portion of this AVM. And so I wanna have good visualization. I'm using our sucker with the light on it, by Kojin so that we can see the most distal portion of the AVM, and cutting it, and cutting it. You can always test whether you've gotten it all by temporarily occluding the venous drainage. And if it doesn't get larger, you know you've got all the vessels, no retractor at any time for this lesion. And there it comes up. And the post-op angiogram. This patient, which is really, I believe the last case I'm gonna show was a big lesson for me. In 2007, this young lad presented with a severe hemorrhage. You can see origin of the hemorrhage right here. And obviously from this relatively small and diffuse arteriovenous malformation And had another hemorrhage. And this is what happened. This AVM turned into this massive arteriovenous malformation, and he was now four years later, He was embolized, we considered surgery at this point, but Dr. McDougall embolized him. We thought we had obliterated the intranidal aneurysm, which we thought was the culprit for the repeat hemorrhage. And so we canceled surgery, unfortunately. This is the comparison, 2007, 2012. This AVM has resulted in this, demonstrating the dynamic nature of this. So we cancel surgery, but he re-bled a few weeks later. And so we scheduled him for surgery. And both patient and mother were fully aware that the patient would be hemiplegic after surgery. So we did the operation. It was a relatively easy. The patient had received previous radiation had these multiple hemorrhages, which created space where the hematomas were located. The AVM was really ripped into two portions. So we just worked in the space that the hematomas created here, Some residual of the hematoma from the last hemorrhage. And we just resected it like any other AVM. But remember this was in the thalamus. Patient that presented with a hemiplegia from which he recovered. It wasn't normal, but it was very, very functional. And we take out the arteriovenous malformation. And with image guidance, we knew we were at the end, sort of a nice way. And this was the other portion which was looked at, but we took that out as well, to be sure that he was free of this arteriovenous malformation. So what did this tell us? It also emphasizes that with children, a diffuse arteriovenous malformation can grow dramatically. And here we're going into the cistern which was normal. And that for children, you need to be very, very observant as to recurrence, especially when they're diffuse and restudy them every year with MRA to see if there's any suspicion before we go on to angiography. What was unique about him? He started off antigravity three to five on the left and postoperatively, despite my telling the mother and him that he would be hemiplegic, his exam was unchanged, reminding me that an AVM location varies a great deal when you have associated hematomas and radiation, which obviously affect, I mean, here should be the internal capsule, affect the function and the rerouting of the function. And so that was a big lesson learned for me so that my prediction fortunately, did not come true. We did a prospective study after we published our radiation, our grading system. And Dr. Hamilton, who was a fellow at the time, we did 120 patients with complete AVM removal, and they were followed up six weeks, six months, and one year with a mean followup of one year. And this is, these are the results. Just, if you look again, emphasizing that for grade one and two, we have excellent results. For grade three, we have 2.8% permanent deficit. And four grade four and five, with four actually being a little bit higher, we had just below a 20% permanent deficit. A significant portion of our deficits came from embolic treatment. And that is when you report AVM results. It's gotta be management results, not surgery, not embolization, but the combination of whatever treatment we use. So this is the way it looks, obviously the early results, when you look at the light blue bars are always worse. And with time AVM deficits really resolved very nicely in a significant portion of patients. While when we published our series, we had an editorial letter that came from the Henry Ford, the Ausman Group. And basically they said inherent bias in their patients selection for surgery. The morbidity and mortality they reported is really very low for this sort of surgery is special for removal of grade five lesions. And remember, I mentioned that we had basically just under 20% To me, that's a horrible complication rate, but those patients were selected and I'm gonna address this. So the similar results between when we published our classification system, which was a retrograde study, and then our prospective study, clearly depends on selection of patients. It is not that we selected every patient that was sent to us with grade four or five for surgery that we operated on. So we initiated a study that I'm very pleased about. It's not a question of can you, but should you? And that can't be overemphasized. So we initiated this study, Dr. Han was a chief resident when this was published, did the grunt work on this. And so we prospectively looked at every patient that was sent to us of grade four and five for surgery and see what we actually decided to do. We recommended no treatment in 80% of our grade four and five AVMs that were sent to us for surgery. 15% partial treatment. So those, for example, that came with fluctuating symptoms where we thought flow was a problem, embolization was used. Or if they had an associated aneurysm that looked worrisome, it was just cleaved. Only 5% of the patients that were sent to us had complete obliteration. And that's what we recommended for them. Naturally, these were highly selected patients. And so when you think of a great five AVM, and you say, well, maybe a 20% risk is not high, that totally misses the point that the selection of those patients is very, very specific and either their symptoms or their number of hemorrhages are so significant and the risk is so high to accept a complication rate of 20%. But the reason we only had a 20% complication rate because of this incredible selective process. So what do we recommend? Well, for grade A, I think surgical resection with rare preoperative embolization is the appropriate treatment. For grade B, you gotta use everything, surgery, embolization, radiosurgery, or nothing, and for great C, multimodality treatment only if repetitive or significant hemorrhage or progressive neurologic deficit, very important not to be aggressive because you have to beat the natural history of this disease. So I appreciate your attendance. And I'm open to a question from Aaron.

- Pleasure to watch. Obviously, beautiful lecture. So illuminating. I wanna talk to you about a couple of things. If you have AVMs that are very close in the vicinity, or partially within the Wernicke's and Broca's area versus sensory motor cortex, just talking about function right now. It's been my practice that if you really stay close to the nidus, very tight. The Broca's and Wernicke's area, you'll be very well to recover full function after episode of temporary deficit without necessarily awake craniotomy or anything else because Broca's and Wernicke's are very diffuse functions later in evolution. So because usually the bold MRI sequence is affected by the hemo AVM in the close vicinity, I don't even do a functional MRI. I just removed the AVM, make sure they know that they're gonna have a short deficit that will recover as long as I'm really only removing the AVM. Do you agree with that strategy or do you have a different perspective?

- No, absolutely. First of all, I don't like operating on an awake patient. Second of all, I think functional MRI scan is terrific, but for AVMs, there is no functioning brain within the nidus of the AVM. So your philosophy is exactly shared by myself. You stay at the edge of the AVM. And yes, you can create a temporary deficit, but you can be very, very confident in the vast majority of cases that recovers. I didn't talk specifically about AVMs, for example, in the brainstem or deep in the brain because of the length of time. But the secret for an AVM is to get there. And if you can get there without causing harm, then you can take it out. And then patience, patience, patience. Again, the emphasis on the point of we follow our patients for their entire life. Once they get in their adulthood, we get a scan first three years after they have a negative scan, and then every five years for the rest of their lives. And try to use non x-ray monitoring. So that with MRA and MRI, as good as they are today, I think you can decide whether you have a MRI scan that is suspicious enough to warrant further studies.

- Well said. I also, I kinda agree with you. And I know a number of surgeons have advocated awake craniotomy for AVMs. AVMs are there such vascular lesions, obviously. There are so well innervated. I just can't imagine how uncomfortable that would be for a patient to undergo surgery for an awake craniotomy, where there's no function in the AVM. It's all about technical skills disconnecting the feeding vessels very early on, so the bulk of the AVM becomes less turgor, and you really retract only on the AVM because it's not decompressed and leave all the functional banks very much intact, even from any retraction, and patients do very well. Let me ask you a question about an AVM that encroaches or partially engulfs, which are very rare, the motor cortex or sensory cortex. What I have done is that one of the strategies has been downgrading it via partial radiation. In other words, if they're unruptured, which are otherwise, they would have some deficits you're gonna operate anyways. So why not downgrade that just piece into the motor cortex with radiation and come back and remove the surgery after a couple of years or so? What are your thoughts there?

- Yes, I've utilized that technique, especially with the AVMs that truncate down toward the ventricle. And we target only the bottom of the AVM, where you have the fragile vessels that drain under the deep venous system, and then come back a couple of years later and remove them. Yeah, I like that technique. You just have to recognize that you're still having risk for a couple of years while you're waiting for that deep portion that disappear. And you have to not use it without considering the extra risk that you're taking. But I like that technique. In fact, this I've published our own thoughts on that, and I agree completely. I mean, radiotherapy is very effective as long as we have small AVMs. And so you're taking a larger AVM and you're targeting only a small portion of the AVM where it's most effective and where it affects the risk of surgery very significantly.

- I got you. Let me ask you another one that's very controversial. Something I feel strongly about, but you may not, but we'll see what your opinion is. If the patient presents with a hemorrhage and as ruptured autonomous malformation, if the neurological status is relatively okay. In other words, there could be hemiplegic, but there's not significant brain edema or really the brain does not look hostile environment to operate at, which is very rare. In other words, most of the time I operated on hemorrhagic AVMs within 24 hours. I do that for two reasons. Number one, with removing the clot, I have seen so many patients improve dramatically after surgery from zero to five to three to five. I mean, immediate, it's magical. Number two is I remove the AVM and the clot at the same time and believe it or not, as I'm sure you have done, I've done it a number of times without an angiogram, because these AVMs, you read the books. If you do enough of them with time, you'll have a pretty good understanding where their vasculature comes from. So acute hemorrhage, I operate 24 hours, remove the clot, remove the AVM. What is most important to me is that the patient recovers from the hemorrhage and the AVM surgery at the same time, rather than you remove the hemorrhage and the patient comes back for another surgery for the AVM, or you let them recover from the hemorrhage and then come back, get hurt again from the AVM surgery. What are your thoughts there?

- Well, I've operated on many AVMs with an acute hemorrhage. And clearly the benefit that you're accepting is when you remove the source of the neurologic deficit, which happens to be the clot, you're much more of a hero than if you have waited and then hurt the patient afterwards, they have a deficit that otherwise would have been masked by the acute hemorrhage. It varies. So there are, I think with the larger clots, even without angiography, and you're going, you will often find an AVM that's torn apart so that you have part of it on one side of the wall of the hematoma and the other side on the other side, clearly those require surgery. And when you find them, you found the source of the hemorrhage. So in atypical patients, young people, without hypertension, et cetera, that is certainly the way to go. There are patients that have a deep hematoma in which the patient benefits by allowing the hematoma to liquefy because the liquid hematomas obviously easy to remove. In general, I was always in a position where, when I got the patient in was either acute and local, in which case we operated right away, or if it was somebody that was sent to me, then by that time, the hematoma had already liquefied and resolved. I think I wouldn't be completely one sided on this, but really utilize the benefit of a liquification depending on the specific patient and the complexity of their AVM.

- Okay, fair enough. I think those are really the main points that I wanted to run by you and get your opinion. Do you have any other closing thoughts about future AVM surgery, specifically, we're getting these amazing presentations from our European colleagues of a transvenous embolization of the malformation. I'm sure people present cases that have looked good. It's just a tendency for all of us. Do you really? What is the role of transvenous, which obviously is trans-arterial to do the full job? In other words, curing with embolization alone, what do you expect is the future?

- Yeah. Venous embolization is not new. Although now it's in heyday. I think the advantage of Venous embolization is that it usually is much easier to define than arterial input. And if you can get rid of an AVM by embolizing the venous outflow in a safe fashion, I find that attractive. The question is the risk. I've seen a number of venous complications with the, I mean, you're changing flow very quickly and very suddenly. So now you're going from a low pressure, but high flow system to normal blood pressure system. And some of those fragile vessels are not gonna be able to tolerate that. So I think we have to wait and see, I know that in the older days where alcohol was used in attempt for this, it has been stopped, and the complications have been significant. I think we have to wait and see. Finally, I think what we, what ARUBA has taught us is that the natural history is not benign. However, neither is the treatment. And if treatment is used indiscriminately, whether it's radiation, embolization or surgery without achieving complete obliteration of the AVM, we have added risk without the benefit of getting rid of the AVM. So I think if we're gonna treat AVMs with a rare exception of the giant ones with flow related neurologic deficit, our goal has to be complete obliteration. Anything less than that has not changed the natural history of the disease, but added on the treatment morbidity and mortality.

- Well, with that very elegant statement, which really summarizes the role of the neurosurgeon in AVM surgery so beautifully. I wanna thank you, thank you, and thank you so much for great supporter of the Virtual OR series being such a huge mentor for so many years, for so many of us, including myself. I look forward to having you with us next time.

- Thank you, Aaron. And I appreciate what you really do for neurosurgical education. Great job.

- Thank you, sir. Have a great evening.

- Thank you.

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